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171 TABLE 8. 2 Estimated Number and Percentage of Diagnosed and Undiagnosed Diabetes Among Adults Aged 18 Years and Older, United States, 2015 Characteristic Diagnosed Diabetes No. in Millions (95% CI)a Undiagnosed Diabetes No. in Millions (95% CI)a Total Diabetes No. in Millions (95% CI)a Total 23. 0 (21. 1-25. 1) 7. 2 (6. 0-8. 6) 30. 2 (27. 9-32. 7) Age in years 18-44 3. 0 (2. 6-3. 6) 1. 6 (1. 1-2. 3) 4. 6 (3. 8-5. 5) 45-64 10. 7 (9. 3-12. 2) 3. 6 (2. 8-4. 6) 14. 3 (12. 7-16. 1) =65 9. 9 (9. 0-11. 0) 2. 1 (1. 4-3. 0) 12. 0 (10. 7-13. 4) Sex Women 11. 7 (10. 5-13. 1) 3. 1 (2. 4-4. 1) 14. 9 (13. 5-16. 4) Men 11. 3 (10. 2-12. 4) 4. 0 (3. 0-5. 5) 15. 3 (13. 8-17. 0) Percentage (95% CI)b Percentage (95% CI)b Percentage (95% CI)b Total 9. 3 (8. 5-10. 1) 2. 9 (2. 4-3. 5) 12. 2 (11. 3-13. 2) Age in years 18-44 2. 6 (2. 2-3. 1) 1. 3 (0. 9-2. 0) 4. 0 (3. 3-4. 8) 45-64 12. 7 (11. 1-14. 5) 4. 3 (3. 3-5. 5) 17. 0 (15. 1-19. 1) =65 20. 8 (18. 8-23. 0) 4. 4 (3. 1-6. 3) 25. 2 (22. 5-28. 1) Sex Women 9. 2 (8. 2-10. 3) 2. 5 (1. 9-3. 2) 11. 7 (10. 6-12. 9) Men 9. 4 (8. 5-10. 3) 3. 4 (2. 5-4. 6) 12. 7 (11. 5-14. 1) Note:a Numbers for subgroups may not add up to the total because of rounding. b Data are crude, not age adjusted. CI, confidence interval. Data source: 2011-2014 National Health and Nutrition Examination Survey and 2015 U. S. Census Bureau data. Source: National Center for Chronic Disease Prevention and Health Promotion. (2017). National diabetes statistics report, 2017: Estimates of diabetes and its burden in the United States. Retrieved from https://www. cdc. gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report. pdf TABLE 8. 3 Prevalence of Diagnosed and Undiagnosed Diabetes Among Adults Aged 18 Years and Older, United States, 2011-2014 Characteristic Diagnosed Diabetes Percentage (95% CI)Undiagnosed Diabetes Percentage (95% CI)Total Percentage (95% CI) Total 8. 7 (8. 1-9. 4) 2. 7 (2. 3-3. 3) 11. 5 (10. 7-12. 4) Race/Ethnicity Asian, non-Hispanic 10. 3 (8. 6-12. 4) 5. 7 (4. 0-8. 2) 16. 0 (13. 6-18. 9) Black, non-Hispanic 13. 4 (12. 2-14. 6) 4. 4 (3. 0-6. 2) 17. 7 (15. 8-19. 9) Hispanic 11. 9 (10. 3-13. 7) 4. 5 (3. 2-6. 2) 16. 4 (14. 1-18. 9) White, non-Hispanic 7. 3 (6. 6-8. 1) 2. 0 (1. 5-2. 6) 9. 3 (8. 4-10. 2) Note: CI, confidence interval. Data source: 2011-2014 National Health and Nutrition Examination Survey. Source: National Center for Chronic Disease Prevention and Health Promotion. (2017). National diabetes statistics report, 2017: Estimates of diabetes and its burden in the United States. Retrieved from https://www. cdc. gov/diabetes/pdfs/data/statistics/national-diabetes-statistics-report. pdf 5. Frequent urinary tract infections (UTIs) or vaginal candidiasis. 6. Poor wound healing. B. Common/typical scenario. 1. Patients frequently complain of fatigue and weakness. They may have muscle cramps, blurred vision, and signif-icant polyuria, polydipsia, and polyphagia. 2. Weight loss occurs over time despite normal or increased appetite. C. Family and social history. 1. Ask about family history since there is a strong link to family history. 2. Ask about type of occupation, if the person is a shift worker, use of alcohol, smoking, or recreational drug use. 3. Review how much exercise the person gets. D. Review of symptoms. 1. HEENT. a. Dental issues. Periodontal disease is associated with diabetes. Diabetes Mellitus—Type 2
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172 2. Psychologic. a. Depression. b. Anxiety. c. Disordered eating. d. Psychosocial barriers/support. e. Barriers to self-management. 3. Microvascular complications. a. Neuropathy. b. Nephropathy. c. Retinopathy. 4. Macrovascular complications. a. Coronary artery disease. b. Cerebrovascular disease. c. Peripheral arterial disease. Physical Examination A. Height, weight, BMI, waist circumference. B. Vital signs. C. Funduscopic examination. D. Thyroid palpation. E. Skin examination. 1. Acanthosis nigricans (see Figure 8. 1). 2. Lipohypertrophy. 3. Diabetic dermopathy. 4. Skin tags. F. Foot examination. 1. Inspection, noting mycotic changes to nail or skin. 2. Vascular examination. a. Hair patterns or lack of hair growth. b. Pulses (dorsalis pedis and posterior tibial). c. Temperature/color. 3. Reflexes. a. Patellar. b. Achilles. 4. Proprioception, vibration, and monofilament sensa-tion. Diagnostic Tests A. Hemoglobin A1C (Hgb A1C), fasting glucose, random glucose, or 2-hour glucose tolerance test to diagnose. 1. Hgb A1C greater than 6. 5%. 2. Fasting glucose greater than 126 mg/d L. 3. Random glucose greater than 200 mg/d L with classic symptoms of hyperglycemia. 4. 2-hour glucose tolerance test greater than 200 mg/d L. B. Hgb A1C on admission to hospital if no result available for past 3 months. C. Yearly lab work for patients with diabetes. 1. Fasting lipid panel. 2. Liver function tests. 3. Urine albumin-to-creatinine ratio. 4. Serum creatinine and glomerular filtration rate ( GFR). Differential Diagnosis A. Prediabetes. B. Metabolic syndrome. C. Stress hyperglycemia. D. Medication-induced hyperglycemia. E. Posttransplant diabetes. F. MODY type diabetes. G. Latent autoimmune diabetes. H. Type 1 diabetes. I. Ketosis-prone diabetes. J. Pancreatitis. K. Pancreatic insufficiency. Evaluation and Management Plan A. General plan. The recommended outpatient compre-hensive treatment plan most helpful in treating type 2 diabetes according to the American Association of Dia-betes Educators consists of the following seven self-care behaviors. 1. Healthy eating: The patient should see a registered dietician for medical nutrition therapy counseling. 2. Being active: At least 150 minutes of moderate to vig-orous intensity physical activity spread out over a week. This can include resistance exercises and flexibility exer-cises. 3. Glucose monitoring. a. Oral agents recommended one to two times a day before meals; can vary which meals. b. Insulin recommended before meals and bedtime. 4. Medications: Oral agents, insulin, non-insulin (injectable). a. Delivery method options: Pens, vial and syringe, pump. b. Proper storage. c. Preparation, administration, and site rotation. d. Disposal of sharps. e. Hypoglycemia symptoms. 5. Problem solving. 6. Healthy coping. 7. Reducing risks. B. Patient/family teaching points. 1. Inpatient education focuses on survival skills only. a. Checking glucose. b. Taking medications. c. Diet. d. Hypoglycemia treatment. 2. Outpatient education is more comprehensive and uses guidelines by the American Association of Diabetes Edu-cators to direct the education. The patient should be referred to outpatient diabetes education at the time of diagnosis, yearly thereafter, and as needed or if therapy changes. C. Pharmacotherapy. 1. Oral agents (see Table 8. 4). a. Metformin: First-line agent. b. Sulfonylureas such as glimepiride. c. Meglitinides such as repaglinide. d. Thiazolidinediones such as pioglitazone. e. Alpha glucosidase inhibitors such as acarbose. f. Dipeptidyl peptidase-4 (DPP-4) inhibitors such as sitagliptin. g. Sodium glucose cotransporter-2 (SGLT2) inhibitors such as canagliflozin. h. Glucagon-like peptide-1 (GLP-1) receptor ago-nists such as exenatide. 2. Insulin. a. Mainstay of therapy in hospital. b. Initiate therapy using one of three different calcu-lations. i. For renal patients or those new to insulin: Start with 0. 3 units/kg/day total daily dose. ii. For most patients: Start with 0. 5 units/kg/day total daily dose. iii. For obese patients, insulin resistant patients, or those on steroids: Start with 0. 7 units/kg/day total daily dose. c. 50/50 rule. i. Give one-half of the total daily dose as basal insulin (glargine, detemir, degludec). 8. Endocrine Guidelines
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173 TABLE 8. 4 Oral Agents Used to Treat Diabetes Oral Agent Side Effects Benefits and Considerations Metformin (first-line agent)GI side effects; start low and go slow in titrating up dose Extended-release form used to prevent GI side effects Benefits ºInexpensive ºDoes not lead to hypoglycemia Considerations ºRenally cleared ºGenerally stop when hospitalized ºPossible vitamin B 12deficiency when used long term ºLactic acidosis risk (rare: 1/30,000 patients) ºContraindications: Estimated GFR <30 m L/min/1. 73 m2, use with caution if estimated GFR <30 m L/min/1. 73 m2, acidosis, hypoxemia, and alcohol abuse Sulfonylureas such as glimepiride Can cause hypoglycemia Can cause weight gain Benefits ºInexpensive Considerations ºHepatically metabolized ºRenally cleared ºCaution required in renal and cardiac patients; have active metabolites ºGenerally stopped while in hospital Meglitinides such as repaglinide Short action reduction in postprandial glucose May cause hypoglycemia Benefits ºModerate cost ºCan use in hospital ºEffective treatment for steroid-induced hyperglycemia such as once a day prednisone Considerations ºHepatically metabolized ºRenally cleared ºFrequent dosing Thiazolidinediones such as pioglitazone Edema/weight gain/CHF exacerbation ºContraindicated in New York Heart Association classes III and IV heart failure ºIncreased risk of MI in rosiglitazone; risk has not been shown in pioglitazone Benefits ºDoes not cause hypoglycemia ºInexpensive Considerations ºNot used in hospital ºDelayed onset: Can take up to 12 weeks to achieve peak effect Alpha glucosidase inhibitors such as acarbose GI side effects: Gradual dose titration helps prevent Benefits ºMinimal systemic absorption ºMarked reduction in MI rates ºModerate cost Considerations ºNot used in hospital ºFrequent dosing DPP-4 inhibitors such as sitagliptin Minimal side effects Rarely causes hypoglycemia Benefits ºGood oral agent for hospital use Considerations ºRenal dose adjustment (except for linagliptin) ºContraindicated in patients with history of pancreatitis ºHigh cost (continued ) Diabetes Mellitus—Type 2
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174 (continued ) TABLE 8. 4 Oral Agents Used to Treat Diabetes Oral Agent Side Effects Benefits and Considerations SGLT2 inhibitors such as canagliflozin Causes glucosuria Increased risk of genitourinary infections Polyuria, especially when also on diuretics Can cause volume depletion, dehydration, dizziness, and hypotension Cases of DKABenefits ºShown to improve cardiovascular disease outcomes ºEmpagliflozin (Jardiance) considered best at reducing cardiovascular events Considerations ºNot for use in hospital ºHigh cost GLP-1 receptor agonists such as exenatide Once-a-week preparations. Prolonged decreased appetite may occur in patients taking these preparations who are admitted to the hospital because medication is likely still having an effect Benefits ºCan aid in weight loss ºCan improve cardiovascular risk factors ºVictoza (liraglutide) considered best at reducing cardiovascular events Considerations ºShould not be used in patients with history of medullary thyroid cancer or history of pancreatitis ºUse in the hospital is being studied, but not currently recommended ºUse with narcotic pain medications: Ileus has occurred with GLP-1 receptor agonist use postoperatively in conjunction with narcotic pain medications. Patients should wait until off narcotic pain medications and having no issues with constipation CHF, congestive heart failure; DKA, diabetic ketoacidosis; DPP-4, dipeptidyl peptidase-4; GFR, glomerular filtration rate; GI, gastrointestinal; GLP-1, glucagon-like peptide-1; MI, myocardial infarction; SGLT2, sodium glucose co-transporter-2. ii. Give one-half of the total daily dose as prandial insulin divided evenly between three meals (lispro, aspart, glulisine). iii. Add a correction scale using the same rapid-acting insulin used previously. D. Discharge instructions. 1. Verify the patient understands how to take the medi-cation as prescribed. a. Dose. b. Route. c. Frequency. d. Relationship to meals. e. Proper disposal of sharps (for injectables). f. Rotation of sites for subcutaneous injections. g. Storage. 2. Make sure the patient is familiar with dietary restric-tions. a. The patient should aim for consistent amounts of carbohydrates per meal at first. Then the goal will be to learn to dose insulin to the amount of carbohydrates using carbohydrate counting. 3. Verify the patient is familiar with how to monitor glu-cose on an ongoing basis. a. For oral agents that do not typically cause hypo-glycemia. i. One to two times a day before meals; can vary which meal. ii. Also acceptable: Have Hgb A1C checked every 3 to 6 months with provider as an alternative to checking daily. b. For oral agents that can cause hypoglycemia. i. Consider initially checking glucose before each meal. ii. After a period of time, the patient may go to one to two times a day. c. For non-insulin injectable agents such as exe-natide, one to two times a day (hypoglycemia is rare). d. For insulin. i. Before meals and bedtime. ii. Before and after exercise. iii. Before driving. iv. More often as needed. Follow-Up A. Recommend annual eye examination and podiatry exam-ination. B. Recommend outpatient education if appropriate. C. Follow-up with endocrinologist or primary care provider. Specify how soon patient should be seen. Specify when to call provider. D. Outline hypoglycemia treatment. 1. Rule of 15: 15 grams of carbohydrates every 15 min-utes until glucose above 70 mg/d L (e. g., 1/2 cup pop, 1/2 cup juice, glucose gel, glucose tablets). 2. Carry glucose tablets or gel at all times. 3. Instruct the patient (if on insulin) to carry a glucagon kit that can be administered by a friend or family member if the patient is unresponsive. 8. Endocrine Guidelines
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175 Consultation/Referral A. Refer the patient to endocrinology for new diagnosis, uncontrolled Hgb A1C, multiple complications of diabetes, and comorbid conditions affecting diabetes control. B. Refer the patient to nephrology for nephropathy. C. Refer the patient to ophthalmology every 2 years if nega-tive examinations. D. Refer the patient to podiatry for issues and/or yearly examination. E. Refer the patient to a dentist for evaluation of gums and oral health problems associated with diabetes such as xeros-tomia, gingivitis, or signs of infection. F. Refer the patient to psychology for coping with chronic disease. Special/Geriatric Considerations A. More than 25% of U. S. population older than 65 years has diabetes. B. Diabetes in older adults is associated with higher mortal-ity and reduced functional status. C. Older adults with diabetes have a higher risk of microvas-cular and cardiovascular complications of the disease. Bibliography Cefalu, W. T. (2017). Standards of medical care in diabetes-2017. Diabetes Care, 40 (Suppl. 1), s1-s135. doi:10. 2337/dc17-S003 Garber, A. J., Abrahamson, M. J., Barzilay, J. I., Blonde, L., Bloomgarden, Z. T., Bush, M. A.,... Umpierrez, G. E. (2017). Consensus statement by the American Association of Clinical Endocrinologists and Amer-ican College of Endocrinology on the comprehensive type 2 diabetes management algorithm—2017 executive summary. Endocrine Practice, 23(2), 207-238. doi:10. 4158/EP161682. CS Menke, A., Orchard, T., Imperatore, G., Bullard, K., Mayer-Davis, E., & Cowie, C. (2013). The prevalence of type 1 diabetes in the United States. Epidemiology, 24, 773-774. doi:10. 1097/EDE. 0b013e31829ef01a Mensing, C. (2011). The art and science of diabetes self-management education desk reference (2nd ed. ). Chicago, IL: Publisher American Association of Diabetes Educators. National Center for Chronic Disease Prevention and Health Promotion. (2017). National diabetes statistics report, 2017: Estimates of diabetes and its burden in the United States. Retrieved from https://www. cdc. gov/ diabetes/pdfs/data/statistics/national-diabetes-statistics-report. pdf Statistics About Diabetes. (n. d. ). Retrieved from http://www. diabetes. org/ diabetes-basics/statistics/ Diabetic Ketoacidosis Julie Stone Definition A. Life-threatening emergency. B. Absolute insulin deficiency. C. Severe hyperglycemia. D. Ketone body production. E. Systemic acidosis. F. Develops over 1 to 2 days. Incidence A. 18% of cases of diabetic ketoacidosis (DKA) in hospitals are children with type 1 diabetes. B. 48% of cases of DKA in hospitals are adults with type 1 diabetes. C. 34% of cases of DKA in hospitals are adults with type 2 diabetes. D. Higher rate of DKA for persons age less than 45. E. One to five episodes per 100 people per year. F. Average mortality 5% to 10%. Pathogenesis A. Unchecked gluconeogenesis leads to hyperglycemia. 1. Increased glucose production. 2. Decreased glucose uptake. B. Osmotic diuresis leads to dehydration. C. Unchecked ketogenesis leads to ketosis. D. Dissociation of ketone bodies into hydrogen ions and anions leads to anion gap metabolic acidosis; electrolyte abnormalities. Predisposing Factors A. Illness/Infection. B. Myocardial infarction (MI)/cerebrovascular accident (CVA). C. Omission of insulin. D. Minority populations. E. Newly diagnosed with type 1 diabetes. F. Poor social support. G. Mental illness. Subjective Data A. Common complaints/symptoms. 1. Thirst. 2. Polyuria. 3. Abdominal pain. 4. Nausea and vomiting. 5. Profound weakness. 6. Fatigue. 7. Dyspnea. B. Common/typical scenario. Patients with any form of dia-betes who present with certain symptoms should be evalu-ated for DKA. These symptoms are abdominal pain, nausea, fatigue, and/or dyspnea. Physical Examination A. Fruity breath. B. Vital sign assessment. 1. Kussmaul respirations. 2. Supine or orthostatic hypotension. 3. Diminished peripheral pulses. 4. Tachycardia. 5. Hypothermia. C. Skin examination. 1. Dry mucous membranes. 2. Poor skin turgor. Diagnostic Tests A. Glucose usually greater than 250 mg/d L. B. Positive blood and urine ketones. C. Elevated beta hydroxybutyrate. D. High anion gap ( >12 m Eq/L). E. Low arterial p H ( <7. 3). F. Low bicarbonate ( <15 m Eq/L). G. Serum hyperosmolality greater than 280 m Osm/L. Differential Diagnosis A. Lactic acidosis. B. Other metabolic acidosis. C. Starvation ketosis, ketogenic diet. D. Euglycemic acidosis. 1. Normal glucose. 2. Clinical presentation of DKA. 3. Seen with sodium-glucose cotransporter 2 (SGLT2) inhibitors. Diabetic Ketoacidosis
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176 E. Hyperglycemia without ketosis. F. Hyperosmolar hyperglycemic syndrome. Evaluation and Management Plan A. Fluid replacement. 1. Normal saline (NS) 1 to 2 L over 1 to 2 hours. 2. Calculation of corrected serum sodium. a. High or normal serum sodium: 1/2 NS at 250 to 500 m L/hr. b. Low serum sodium: NS at 250 to 500 m L/hr. 3. When glucose less than 250 mg/d L: D5%NS or 1/2 NS. 4. Suggested rate for fluid replacement. a. First hour: 1 to 2 L. b. Second hour: 1 L. c. Third to fifth hours: 500 to 1,000 m L/hr. d. Sixth to 12th hours: 250 to 500 m L/hr. B. Correction of hyperglycemia/metabolic acidosis. 1. Intravenous regular insulin infusion. a. Bolus: 0. 1 to 0. 15 units/kg. b. Drip rate: 0. 1 units/kg/hr. c. Check glucose every hour. i. If glucose does not decrease by 10% in the first hour, a second loading dose is indicted. ii. When glucose less than 250 mg/d L, slow rate to 0. 05 to 1 units/kg/hr until resolution of ketoaci-dosis. d. Continue insulin infusion until anion gap closes (<14 m Eq/L). e. Initiate subcutaneous basal insulin 2 hours prior to stopping drip. f. Refer to hospital DKA protocol. 2. Acceptable to use subcutaneous insulin to treat DKA as well. a. Use insulin analogs: Lispro, aspart, or glulisine. b. Check glucose every 2 hours and give bolus of ana-log. i. Initial dose 0. 2 to 0. 3 units/kg. ii. Then 0. 1 to 0. 2 units/kg every 2 hours until glucose less than 250 mg/d L. iii. When glucose less than 250 mg/d L add dex-trose to intravenous fluids as earlier. iv. Continue to give 0. 05 to 0. 1 unit/kg every 2 hours until anion gap closes. C. Replacement of electrolyte losses. 1. Watch for life-threatening hypokalemia, which can occur as insulin is infused. 2. Monitor potassium closely and treat potassium losses aggressively. Anticipatory potassium replacement during treatment of DKA is usually required. a. If potassium is greater than 5. 5 m Eq/L, then no supplementation is immediately required. Reassess within 2 to 4 hours. b. If potassium is 4 to 5. 4 m Eq/L, give 20 m Eq of replacement potassium. c. If potassium is 3. 3 to 4 m Eq/L, give 40 m Eq of replacement potassium. d. If potassium is less than 3. 3 m Eq/L, hold start-ing insulin until potassium is replaced. Give potas-sium 20 to 30 m Eq/hr until potassium is greater than 3. 3 m Eq/L. 3. A sharp drop in serum phosphorus can also occur with insulin infusion. T reatment is usually not required. 4. Bicarbonate is not usually given unless p H less than 7. 0 mol/L. D. Identification and treatment of precipitating causes. 1. Nonadherence to insulin regimen or psychiatric issues. 2. Insulin administration error or insulin pump mal-function. 3. Poor sick day management. a. Patients often omit insulin when not eating or hav-ing nausea or vomiting. b. Patients often forget to check their glucose levels when feeling ill. 4. Infections. a. Intra-abdominal. b. Pyelonephritis. c. Urinary tract infections (UTIs). d. Pneumonia. e. Influenza. 5. MI. 6. Pancreatitis. 7. Steroid therapy prescribed with no instructions about adjusting insulin. 8. CVA. E. Conversion to a maintenance diabetes regimen; transi-tion to subcutaneous insulin when glucose is less than 200 mg/d L and the anion gap is less than 14 m Eq/L. F. Patient/family teaching points. 1. Sick day management. 2. Survival skills. 3. Glucose monitoring. 4. Insulin administration. 5. Use of ketone strips. 6. Medical alert bracelet. 7. Preventing DKA. a. Recognizing signs and symptoms. b. Frequency of glucose testing. c. Urine ketone testing. d. When to call for help. G. Discharge instructions. 1. Ensure the patient has prescriptions for insulin pen, insulin vial, and needles or syringes. 2. Ensure the patient has prescriptions for glucometer, test strips, and lancets. 3. Ensure the patient has ketone strips. 4. Confirm that a follow-up appointment has been made. 5. Give the patient physician contact phone numbers. Follow-Up A. Follow-up should occur with the endocrinologist for a management plan to regulate diabetes. B. Patients may need to follow-up with social services for assistance with medications. Consultation/Referral A. Refer the patient to psychology/social work for assistance with purchasing medications and equipment and for emo-tional support. B. Refer the patient to endocrinology for optimized man-agement of diabetes. Special/Geriatric Considerations A. End-stage renal disease patients on dialysis. 1. Absence of osmotic diuresis. 2. Less volume depleted. 8. Endocrine Guidelines
Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
177 3. High serum potassium. 4. Insulin infusion: Only treatment required in a major-ity of patients. 5. Emergency hemodialysis: Possible treatment in cases where there is pulmonary edema, profound metabolic acidosis, or severe hyperkalemia with ECG changes. B. DKA in pregnancy. 1. DKA can occur rapidly and at a much lower glucose level in pregnant women with diabetes compared to non-pregnant women with diabetes. 2. The effects of DKA on the fetus are not known. Ketoacids and glucose cross the placenta. 3. There is a direct relationship between plasma ketone levels in pregnant diabetic women and lower IQ levels in the child. 4. Presenting symptoms and treatment are the same as in women who are not pregnant. 5. Certain metabolic changes predispose to ketosis. a. Increased insulin resistance. b. Insulin requirements that rise during pregnancy. c. More cases of DKA in second and third trimesters. 6. Accelerated starvation. a. Use of large amounts of glucose for energy by fetus/placenta. b. Lower maternal glucose, leading to relative insulin deficiency. c. Increase in free fatty acids, which undergo con-version to ketones in liver. 7. Emesis. 8. Stress and fasting state: Can increase insulin antago-nistic hormones, which along with dehydration can pro-mote development of ketosis. 9. Lowered buffering capacity. 10. Increased minute alveolar ventilation in pregnancy leading to respiratory alkalosis, which is compensated by increased renal excretion of bicarbonate. Bibliography Cefalu, W. T. (2017). Standards of medical care in diabetes-2017. Diabetes Care, 40 (Suppl. 1), s1-s135. doi:10. 2337/dc17-S003 Menke, A., Orchard, T., Imperatore, G., Bullard, K., Mayer-Davis, E., & Cowie, C. (2013). The prevalence of type 1 diabetes in the United States. Epidemiology, 24, 773-774. doi:10. 1097/EDE. 0b013e31829ef01a Mensing, C. (2011). The art and science of diabetes self-management education desk reference (2nd ed. ). Chicago, IL: Publisher American Association of Diabetes Educators. Statistics About Diabetes. (n. d. ). Retrieved from http://www. diabetes. org/ diabetes-basics/statistics/ Hyperglycemic Hyperosmolar State Julie Stone Definition A. Severe relative insulin deficiency, resulting in profound hyperglycemia and hyperosmolality. B. Absence of acidosis. C. Develops over days to weeks. D. Typically presents in type 2 diabetes or in patients with no prior diagnosis of diabetes. Incidence A. Hyperglycemic hyperosmolar state (HHS) represents less than 1% of hospital admissions of patient with diabetes. B. Mortality is between 10% and 20%, which is 10 times higher than mortality for diabetic ketoacidosis (DKA). C. Condition has been reported in children and young adults. Pathogenesis A. Extreme elevations in glucose. B. Insulin deficiency. C. Increased levels of counterregulatory hormones. 1. Glucagon. 2. Catecholamines. 3. Cortisol. 4. Growth hormone. D. Increased gluconeogenesis. E. Decreased use of glucose by peripheral tissues. F. Higher hepatic and circulating insulin concentrations as well as lower glucagon in HHS compared to DKA. G. Prevention of ketogenesis. H. Severe hyperglycemia associated with a severe inflamma-tory state. Predisposing Factors A. Elderly patients with type 2 diabetes. B. Patients with more comorbidities. C. Infection. 1. Pneumonia. 2. Urinary tract infection (UTI). D. No prior diagnosis of diabetes. E. Stroke. F. Myocardial infarction (MI). G. T rauma. H. Medications. 1. Glucocorticoids. 2. Thiazide diuretics. 3. Phenytoin (inhibits endogenous insulin secretion). 4. Beta-blockers. 5. Atypical antipsychotics. Subjective Data A. Common complaints/symptoms. 1. Dehydration presenting as a shock-like state. 2. Mental confusion. 3. Thirst. 4. Polyuria. 5. Nausea and vomiting. 6. Weakness and fatigue. Physical Examination A. Ill appearing, likely with decreased level of consciousness. B. Vital sign assessment. 1. Tachycardia. 2. Hypotension. 3. Tachypnea. 4. Decreased core temperature. C. Neurologic findings. When HHS causes neurologic dys-function, treatment of the HHS results in resolution of neu-rologic findings. When neurologic events cause HHS the neurologic findings remain after the resolution of the HHS. 1. Seizures. 2. Drowsiness and lethargy. 3. Delirium to coma. 4. Hemianopsia. 5. Aphasia. 6. Paresis. 7. Positive Babinski sign. 8. Myoclonic jerks. 9. Nystagmus. Hyperglycemic Hyperosmolar State
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178 D. Dermatological findings. 1. Acanthosis nigricans (see Figure 8. 1). 2. Diabetic dermopathy. 3. Dry mucous membranes. 4. Decreased skin turgor. 5. Necrobiosis on pretibial surfaces. E. Funduscopic examination: Retinopathy, premature cataracts, xanthelasma. F. Decreased urine output. Diagnostic Tests A. Plasma glucose: Greater than 600 mg/d L. B. Arterial p H: Greater than 7. 30 mol/L. C. Serum bicarbonate greater than 18 m Eq/L. D. Urine or serum ketones: Absent or small. E. Serum beta hydroxybutyrate less than 3 mmol/L. F. Effective serum osmolality greater than 320 m Osm/L. G. Anion gap variable. H. Hemoglobin and hematocrit elevated due to volume con-traction. I. Leukocytosis usually present. J. Hemoglobin A1C (Hgb A1C). K. Look for underlying cause using the following. 1. Chest x-ray. 2. Urine analysis. 3. Blood and urine cultures. 4. ECG. Differential Diagnosis A. DKA. B. Hyperglycemia without DKA or HHS. C. Dehydration. D. Mental status changes or even coma. E. Intoxication. F. Sepsis. G. Postictal state. H. Diabetes insipidus. Evaluation and Management Plan A. Replacement of fluids. 1. T reatment of HHS requires more free water and greater volume replacement than in DKA: Can be as much as 10 L fluid deficit. 2. Rapid and aggressive intravascular volume replace-ment is necessary. a. Use isotonic sodium chloride initially. b. Replace one-half of volume in first 12 hours and then remainder over next 12-hour period. c. When glucose reaches 250 to 300 mg/d L, switch to D5%NS or 1/2NS. 3. Use caution in patients with heart failure and kidney disease as well as in those who are elderly. B. Correction of hyperglycemia. 1. Use intravenous insulin or subcutaneous insulin in doses similar to DKA. 2. Understand that the use of insulin without concomi-tant vigorous fluid replacement increases the risk of shock. 3. Recheck glucose every 1 to 2 hours. C. Replacement of electrolytes. 1. Potassium is not usually significantly elevated on admission. 2. Replacement of potassium is required as insulin drops are used. Add potassium to intravenous fluids starting at 5 m Eq/L or less. 3. Recheck electrolytes every 2 to 4 hours as clinically indicated. 4. Phosphate, magnesium, and calcium are not routinely replaced. D. Hospitalization. 1. All patients diagnosed with HHS require hospitaliza-tion and virtually all require ICU admission. 2. Neurological monitoring, with “neuro” checks every 2 hours, is important. E. Detection and treatment of underlying pathology. 1. Some sources advocate prophylactic heparin treat-ment and broad-spectrum antibiotics until the underly-ing cause can be established. F. Conversion to maintenance diabetes regimen prior to discharge. 1. The patient's extreme hyperglycemia usually indicates extensive beta cell dysfunction. 2. Initially patients require discharge on full insulin therapy. 3. Use Hgb A1C to help determine glucose control prior to admission. 4. Make transition to subcutaneous insulin when glu-cose less than 200 mg/d L and the anion gap is less than 14 m Eq/L. G. Patient/family teaching points. 1. Sick day management. 2. Survival skills. 3. Glucose monitoring. 4. Insulin administration. 5. Medical alert bracelet. H. Discharge instructions. 1. Ensure that the patient has prescriptions for insulin pen, insulin vial, and needles or syringes. 2. Ensure that the patient has prescriptions for glucome-ter, test strips, and lancets. 3. Confirm that a follow-up appointment has been made. 4. Give the patient physician contact phone numbers. Follow-Up A. Follow-up should occur with the endocrinologist for a management plan to regulate diabetes. B. Patients may need to follow-up with social services for assistance with medications. Consultation/Referral A. Refer the patient to psychology for improving adherence to the diabetes regimen. B. Refer the patient to social work and case management to assist with obtaining medications and resources as needed. Special/Geriatric Considerations A. Diabetes in older adults is associated with higher mortal-ity and reduced functional status. B. Older adults with diabetes have a higher risk of microvas-cular and cardiovascular complications of the disease. Bibliography Azoulay, E., Chevret, S., Didier, J., Neuville, S., Barboteu, M., Bornstain, C.,... Schlemmer, B. (2001). Infection as a trigger of diabetic ketoacido-sis in intensive care unit patients. Clinical Infectious Disease, 32, 30-35. doi:10. 1086/317554 Joint British Diabetes Societies Inpatient Care Group. (2010, March). The management of diabetic ketoacidosis in adults. Retrieved from http://www. diabetes. nhs. uk/document. php?o =13368. Endocrine Guidelines
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179 Kamalakannan, D., Baskar, V., & Barton, D. M. (2003). Diabetic ketoacidosis in pregnancy. Postgraduate Medical Journal, 79, 454-457. doi:10. 1136/pmj. 79. 934. 454 Kitabchi, A. E., Umpierrez, G. E., Murphy, M. B., Barrett, E. J., Kreisberg, R. A., Malone, J. I., & Wall, B. M. (2004, January). Hyperglycemic crises in diabetes. Diabetes Care, 27 (Suppl. 1), S94-S102. doi:10. 2337/ diacare. 27. 2007. S94 Pasuel, F. J., & Umpierrez, G. E. (2014). Hyperosmolar hyperglycemic state: A historic review of the clinical presentation, diagnosis, and treatment. Diabetes Care, 37, 3124-3131. doi:10. 2337/dc14-0984 Wordsworth, G., Robinson, A., Ward, A., & Atkin, M. (2014). HHS—Full or prophylactic anticoagulation? British Journal of Diabetes and Vascular Disease, 14, 64-66. doi:10. 15277/bjdvd. 2014. 011 Metabolic Syndrome Julie Stone Definition A. Also called insulin resistance syndrome. B. A group of traits linked to obesity that puts people at risk for both cardiovascular disease (CVD) and type 2 diabetes. C. Must have three of the following. 1. Waist circumference greater than 40 inches in men; greater than 35 inches in women (varies somewhat by eth-nicity depending on which guidelines are used). 2. T riglyceride level of 150 mg/d L or higher or taking medication for elevated triglyceride levels. 3. High-density lipoprotein (HDL) below 40 mg/d L for men and below 50 mg/d L for women or taking medica-tion for low HDL. 4. Blood pressure above 130/85 mm Hg or taking antihy-pertensives. 5. Fasting glucose greater than 100 mg/d L or taking med-ication for elevated blood glucose. D. Linked to type 2 diabetes, obesity, CVD, polycystic ovar-ian syndrome, nonalcoholic fatty liver disease, and chronic kidney disease. E. Patients with metabolic syndrome are at twice the risk of developing CVD over the next 5 to 10 years as individuals without the syndrome. The risk of developing diabetes is five times higher for individuals with metabolic syndrome. Incidence A. About 34% of American adults are thought to have metabolic syndrome. B. Risk increases as people age. C. Prevalence is higher in non-Hispanic white men than Mexican American and non-Hispanic black men. D. The condition is more common in Mexican American women than non-Hispanic black or non-Hispanic white women. E. Prevalence is increasing globally due to increased obesity and sedentary lifestyles. Pathogenesis A. Contributing factors include increased free fatty acid lev-els, inflammatory cytokines from fat, and oxidative factors. B. Patients with the characteristics of metabolic syndrome demonstrate a prothrombotic state and a proinflammatory state. C. Elevated triglycerides and low HDL cholesterol is an atherogenic dyslipidemia condition. D. The mechanism of how this constellation of risk factors contributes to development of type 2 diabetes and CVD is not completely understood. Predisposing Factors A. Sedentary lifestyle. B. Western diet high in carbohydrates and fats, including saturated fats. C. Obesity. D. Family history of diabetes, heart disease, and hyperlipi-demia. Subjective Data A. Typically, asymptomatic. B. Patient presentation for a routine physical or a preopera-tive examination. Physical Examination A. Look for abdominal obesity: Record height, weight, body mass index (BMI), waist circumference, and waist to hip ratio. B. Perform thorough cardiovascular examination. C. Note skin findings consistent with obesity and insulin resistance. 1. Skin tags. 2. Acanthosis nigricans (see Figure 8. 1). D. Note presence of xanthelasma on medial aspect of eyelids, which is suggestive of hyperlipidemia. Diagnostic Tests A. Fasting lipid panel. B. Fasting glucose. Differential Diagnosis A. Type 2 diabetes. B. Prediabetes. C. Hyperlipidemia. D. Hypertension. E. Obesity. Evaluation and Management Plan A. General plan. T reatment centers on two principles. 1. Identify individuals with metabolic syndrome. 2. Use risk factor modification to prevent CVD and type 2 diabetes. B. Weight loss. 1. Routinely measure weight and anthropometric mea-surements. C. Healthy diet. 1. Recommend saturated fat less than 7% of total calo-ries. 2. Reduce trans fats. 3. Limit dietary cholesterol to less than 2,000 mg/d. 4. Restrict total fat to 25% to 35% of total calories. 5. Choose unsaturated fats. 6. Limit simple sugars. D. Increased physical activity. 1. Encourage 30 to 60 minutes of moderate inten-sity aerobic activity, preferably daily, supplemented by increase in daily lifestyle activities. E. Monitoring of blood glucose, lipoproteins, and blood pressure. F. T reatment of individual risk factors following guidelines for hypertension, hyperlipidemia, and hyperglycemia. G. Smoking cessation. Follow-Up A. Follow-up with primary care providers to monitor under-lying problems and to treat cardiovascular risk factors. Metabolic Syndrome
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180 Consultation/Referral A. Endocrinology to manage any underlying problems with diabetes. B. Cardiology to manage cardiovascular risk factors. Special/Geriatric Considerations A. The risk of metabolic syndrome increases with age. B. People with metabolic syndrome are at increased risk of CVDs. Bibliography Aguilar, M., Bhuket, T., & Torres, S. (2015). Prevalence of the metabolic syndrome in the United States, 2003-2012. Journal of the American Medical Association, 313, 1973-1974. doi:10. 1001/jama. 2015. 4260 Alberti, K. G., Eckel, R. H., Grundy, S. M., Zimmet, P. Z., Cleeman, J. I., Donato, K. A.,... Smith, S. C., Jr. (2009). Harmonizing the metabolic syndrome: A joint interim statement of the International Dia-betes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and Interna-tional Association for the Study of Obesity. Circulation, 120, 1640-1645. doi:10. 1161/CIRCULATIONAHA. 109. 192644 American Association of Diabetes Educators. (2008). AADE7 self-care behaviors. Diabetes Educator, 24, 445-449. American Diabetes Association. (2010, January). Diagnosis and classifica-tion of diabetes mellitus. Diabetes Care, 33 (Suppl. 1), S62-S69. doi:10. 2337/dc10-S062 American Diabetes Association. (2012, January). Standards of medical care in diabetes—2012. Diabetes Care, 35 (Suppl. 1), S11-S63. doi:10. 2337/ dc12-s011 American Diabetes Association Professional Practice Committee. (2013, January). American Diabetes Association clinical practice recommenda-tions: 2013. Diabetes Care, 36 (Suppl. 1), S1-S110. Pheochromocytoma Kathryn Evans Definition A. A catecholamine-secreting tumor that typically produces one or more of the following hormones: Epinephrine, nore-pinephrine, or dopamine. B. Cardiovascular morbidity and mortality may be high for undiagnosed pheochromocytomas (PCCs) due to cate-cholamine secretion. C. PCCs enlarge over time and may cause mass effect if undi-agnosed. Incidence A. 0. 2% to 0. 6% of patients in an outpatient setting with hypertension have a PCC. B. Autopsy studies suggest that 0. 05% to 1% of patients have undiagnosed PCCs. C. Peak incidence is between the fourth and fifth decades of life. D. Approximately 5% of adrenal incidentalomas are PCCs and 10% to 17% of PCCs may be malignant. E. PCC should be considered in the workup for malig-nant hypertension, particularly when the patient reports paroxysmal symptoms, has an adrenal incidentaloma, or has a hereditary predisposition to PCC. Pathogenesis A. Catecholamine-producing neuroendocrine tumors aris-ing from the adrenomedullary chromaffin cells. B. Germline mutations: Present in at least one-third of patients presenting with PCC. C. PCCs may be related to a hereditary condition. Predisposing Factors A. 30% of patients have a PCC as part of a genetic disorder. B. Several genetic conditions predispose patients to PCC, including: 1. Multiple endocrine neoplasia (MEN) type 2A. 2. MEN type 2B. 3. Von Hippel-Lindau syndrome. 4. Neurofibromatosis type 1. Subjective Data A. Common complaints/symptoms. 1. Signs and symptoms are present in about 50% of patients. 2. Symptoms are typically paroxysmal. 3. Classic triad of symptoms includes: a. Headache. b. Sweating. c. Tachycardia. B. Other signs and symptoms. 1. Cardiovascular (palpitations). 2. Anxiety/panic attacks. 3. Nausea. 4. Abdominal/chest pain. 5. Flushing. 6. Weight loss. 7. Weakness. 8. T remor. 9. Pallor. 10. Shortness of breath. Physical Examination A. Vital signs. 1. Tachycardia. 2. Hypertension. 3. Weight loss. B. Complete cardiovascular examination. C. Skin examination. 1. Pallor. 2. Flushing. Diagnostic Tests A. Testing for PCC is necessary if there is: 1. Previous history of PCC. 2. Symptoms of PCC, especially if they occur in a parox-ysmal manner. 3. Adrenal incidentaloma. 4. Hereditary predisposition to PCC. B. Initial testing involves two types of metanephrine tests. 1. Urinary fractionated metanephrines should be a 24-hour urine collection and include a creatinine level. 2. Plasma-free metanephrines should be drawn with the patient in the supine position. a. Sympathetic activation occurs in the upright posi-tion and can falsely elevate catecholamine levels. b. Ideally, patients should be in the supine position for 30 minutes prior to blood draw. C. False positive results are common. 1. Physiologic stress such as hospitalization may elevate hormones and should be considered contributing factors to elevations. 2. Multiple drugs can cause false positive results, includ-ing: a. Acetaminophen. b. Beta-blockers: Labetalol, sotalol. 8. Endocrine Guidelines
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181 c. T ricyclic antidepressants. d. Sympathomimetics. e. Buspirone. f. Monoamine oxidase (MAO) inhibitors. g. Cocaine. 3. Confirmatory testing is needed if positive results are believed to be influenced by any of these factors. D. When biochemical results suggest a PCC, imaging is nec-essary. A CT scan should be ordered to locate the mass (CT preferred over MRI). E. An MRI should be used in patients when a CT scan cannot be performed (e. g., allergy to CT contrast, or when attempting to limit radiation, such as in pregnant women). F. All patients with PCCs should consider genetic testing to assess for other related conditions such as the MEN syn-dromes. Differential Diagnosis A. Labile essential hypertension. B. Malignant hypertension. C. Illegal drug use such as phencyclidine or cocaine. D. Combining multiple pharmacologic agents such as MAO inhibitors, decongestants, or sympathomimetics. E. Stroke. F. Myocardial infarction. G. Anxiety disorder. H. Hyperthyroidism. I. Hypoglycemia (including insulinoma). J. Alcohol withdrawal. Evaluation and Management Plan A. General plan. T reatment involves surgery. 1. Preoperative management. a. Preoperative medical treatment should occur for 7 to 14 days if possible to stabilize blood pressure (BP) and heart rate. b. Patients with hormonally active PCCs should undergo preoperative blockage with an a-adrenergic receptor blocker such as phenoxybenzamine or doxazosin. Calcium channel blockers can be used as secondary agents for further BP control. c. Beta-blockers can be added after initiation of an a-adrenergic receptor blocker to control heart rate. They should not be added before a-adrenergic recep-tor blockers due to the potential for hypertensive crisis if the a-adrenergic receptors are unopposed. d. a-Methyl-paratyrosine (metyrosine) can be used for a short time preoperatively in combination with ana-adrenergic receptor blocker to further stabilize BP and reduce blood loss and volume depletion dur-ing surgery. e. Initiating a continuous saline infusion the evening before surgery is another helpful approach to mini-mize volume depletion. f. Preoperative diet should include high sodium and high fluid intake to prevent hypotension after the tumor removal. g. Monitor heart rate, BP, and blood glucose in the pre-and postoperative periods. 2. Operative procedure. a. Most PCCs can be removed via minimally invasive adrenalectomy. b. Open resection is recommended for large tumors greater than 6 cm or for invasive tumors. 3. Postoperative management. a. The most common postoperative complications include hypertension, hypotension, and rebound hypoglycemia. b. Heart rate, BP, and glucose should be monitored for 24 to 48 hours. c. For patients who are at risk for adrenal insuffi-ciency (AI) after surgery, particular attention should be paid to signs and symptoms of AI. B. Patient/family teaching points. 1. Consider genetic testing, if not already completed, for other potential family members at risk. C. Discharge instructions (if standard accepted guidelines exist please use discharge template). 1. Monitor BP at home, counseling particularly on the potential for low or labile BP. 2. Monitor postoperative incision for any signs of infec-tion. 3. Discuss the symptoms of PCC and the recommenda-tion for annual biochemical monitoring to ensure long-term disease remission. Follow-Up A. Biochemical testing should be repeated 2 to 4 weeks after surgery to ensure complete tumor resection. B. Annual biochemical monitoring is recommended to assess for recurrent disease. Consultation/Referral A. Consultation with an endocrinologist and an endocrine surgeon is preferred for optimal patient outcomes. B. It is recommended that patients with PCCs be treated by multidisciplinary teams at centers with expertise in this con-dition. Some studies suggest that there is lower postoperative mortality and shorter hospital stays in high-volume centers, but these data are not conclusive. Special/Geriatric Considerations A. Patients with metastatic disease or general complexity should always be referred to high-volume centers with exper-tise in the management of PCCs. Bibliography Lenders, J. W., Duh, Q.-Y., Eisenhofer, G., Gimenez-Roqueplo, A.-P., Grebe, S. K., Murad, M. H.,... Young, W. F., Jr. (2014). Pheochromo-cytoma and paraganglioma: An endocrine society clinical practice guide-line. Journal of Clinical Endocrinology & Metabolism, 99 (6), 1915-1942. doi:10. 1210/jc. 2014-1498 Young, W. F., Jr. (2018, December 11). Clinical presentation and diagnosis of pheochromocytoma. In K. A. Martin (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/clinical-presentation-and-diagnosis-of-pheochromocytoma Prediabetes Julie Stone Definition A. Failing pancreatic islet beta cells. B. State of insulin resistance. C. Caused by excess body weight, usually abdominal/visceral obesity. D. Dyslipidemia. E. Elevated triglycerides. F. Low high-density lipoprotein (HDL) cholesterol. G. Hypertension. Prediabetes
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182 Incidence A. In 2012, 86 million Americans age 20 and older had pre-diabetes; this is up from 79 million in 2010. Pathogenesis A. Insulin resistance. There is a marked decrease in insulin sensitivity 5 years prior to diagnosis of type 2 diabetes. B. Relative insulin deficiency; beta cell dysfunction. Beta cell function is increased 3 to 4 years prior to the diagnosis of diabetes and then decreased immediately prior to the diabetes diagnosis. Predisposing Factors A. Obesity. 1. Body mass index (BMI) greater than 25 in all but Asians. 2. BMI greater than 23 in Asian Americans. B. First-degree relative with diabetes. C. Higher risk in certain ethnic populations. 1. African Americans. 2. Latino. 3. Native Americans. 4. Asian Americans. 5. Pacific Islanders. D. Women with history of gestational diabetes. E. History of cardiovascular disease. F. Hypertension greater than 140/90 mm Hg. G. HDL less than 35 mg/d L. H. T riglycerides greater than 250 mg/d L. I. Women with history of polycystic ovary syndrome. J. Women who have given birth to a baby weighing over 9 lbs. K. Physically inactive. L. Physical findings of insulin resistance. 1. Skin tags. 2. Acanthosis nigricans (see Figure 8. 1). M. Obstructive sleep apnea. N. Can have patient take American Diabetes Association risk test at www. diabetes. org. Subjective Data A. Common complaints/symptoms. B. Usually asymptomatic. C. Patient may present for routine physical or preoperative assessment. Physical Examination A. Record height, weight, BMI, waist circumference, waist to hip ratio. B. Monitor for abdominal obesity. C. Assess for signs of cardiovascular disease and peripheral vascular disease. D. Check for the following signs/symptoms. 1. Premature arcus cornealis. 2. Xanthelasma. 3. Polycystic ovarian syndrome symptoms. a. Acne. b. Hair loss. c. Hirsutism. 4. Acanthosis nigricans (see Figure 8. 1). 5. Presence of skin tags. Diagnostic Tests A. Hemoglobin A1C (Hgb A1C): 5. 7% to 6. 4%. B. Fasting glucose: 100 to 125 mg/d L. C. Random glucose: 140 to 199 mg/d L. Differential Diagnosis A. Metabolic syndrome. B. Type 2 diabetes. C. Obesity. D. Hypertension. E. Hyperlipidemia. Evaluation and Management Plan A. General plan: Lifestyle therapy. 1. T reat cardiovascular risk factors. a. Dyslipidemia. b. Hypertension. 2. Weight loss/management. a. This can be achieved through lifestyle, pharma-cotherapy, surgery, or a combination of treatments. b. Bariatric surgery can be very effective in preventing progression of prediabetes to type 2 diabetes. 3. Nutrition therapy. 4. Physical activity. 5. Sleep. 6. Community engagement. 7. Alcohol moderation. 8. Smoking cessation. B. Pharmacotherapy. 1. No medications are approved by the Food and Drug Administration solely for the management of prediabetes and the prevention of type 2 diabetes. 2. Medications should not be considered the only ther-apy. All medications should be combined with lifestyle modifications. 3. Metformin reduces risk of type 2 diabetes mellitus (T2DM) in prediabetes patients by 25% to 30%. 4. Acarbose reduces risk of T2DM in prediabetes patients by 25% to 30%. 5. Consider with caution use of thiazolidinediones (pre-vent development of type 2 diabetes by 60%-75%) or glucagon-like peptide-1 (GLP-1) receptor agonists. Follow-Up A. Follow-up with primary provider as needed to manage risk factors. Consultation/Referral A. Refer the patient to a registered dietician for diet educa-tion/counseling. B. Refer the patient to a psychologist/counselor for stress reduction and life coaching. C. An exercise physiologist may help with planning a realis-tic exercise program. D. Refer the patient to a lipid clinic for management of hyperlipidemia. Special/Geriatric Considerations A. The risk of diabetes increases with age. B. Microvascular and cardiovascular complications are more common in the elderly and should be monitored closely. Bibliography Bock, G., Dalla Man, C., Campioni, M., Chittilapilly, E., Basu, R., Toffolo, G.,... Rizza, R. (2006). Pathogenesis of pre-diabetes: Mechanisms of fasting and postprandial hyperglycemia in people with impaired fasting glucose and/or impaired glucose tolerance. Diabetes, 55, 3536-3549. doi:10. 2337/db06-0319 Grundy, S. M. (2012). Pre-diabetes, metabolic syndrome, and cardiovascu-lar risk. Journal of the American College of Cardiology, 59 (7), 635-643. doi:10. 1016/j. jacc. 2011. 08. 0808. Endocrine Guidelines
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183Thyroid Disorder—Euthyroid Sick Syndrome Lisa Coco Definition A. Term designated for those patients with nonthyroid ill-nesses who have abnormal thyroid tests and can be classified into the following categories. 1. Low T3 syndrome (most common). 2. Low T3 and low T4 syndrome. 3. High T4 syndrome. 4. Mixed form in which a combination of abnormalities may be found. Incidence A. Euthyroid sick syndrome can affect people of all races. B. It affects both sexes equally. C. It occurs in people of any age. Pathogenesis A. Almost 90% of the hormones secreted by the thyroid gland are T4 and approximately 10% are T3. Most of T4 is converted into T3 in the peripheral tissues, accounting for 90% of the production of T3. The more physiologically active hormone is T3, which is four times more potent than T4. B. The most common factor in these conditions is reduced extrathyroidal conversion of T4 to T3. C. With low T3 syndrome, the FT3 is low and the FT4 is normal. D. The patient is clinically euthyroid and the leading cause in many circumstances is from systemic illness. E. The low T3 resolves when the underlying illness clears. F. The low T3 and low T4 syndrome is usually identified in severely ill patients. G. The TSH early in the illness may be low or normal. 1. As the illness progresses and recovery ensues, the thyroid-stimulating hormone ( TSH) is often above normal. 2. Patients who have severely low T3 and T4 levels gen-erally do not do well; mortality approaches 84%. 3. High T4 syndrome is caused by increased concen-trations of thyroid-binding globulin produced in certain liver diseases causing high T4 levels. T4 usually returns to normal within 6 to 8 weeks as the disease stabilizes. Predisposing Factors A. Acute or chronic illness. B. Medications. C. Other endocrine disorders. D. Burns. E. Extreme heat or cold. F. Starvation. Subjective Data A. Common complaints/symptoms. 1. Most often, there are no associated symptoms. Care-ful history and physical examination will not reveal the typical features of hypothyroidism. Lab values will be abnormal. 2. If there are symptoms, they are specific to each case. B. Common/typical scenario. 1. Patients are usually symptomatic. The condition is found typically during routine screening for thyroid disease. C. Family and social history. 1. No relevant family or social history. D. Review of systems. 1. Negative review of systems. Physical Examination A. There are no particular findings for patients with nonthy-roidal illness. B. The examination findings in each patient reflect the char-acteristics of the nonthyroidal disease. Diagnostic Tests A. Total T4. B. Total T3. C. TSH. D. Free T4. E. Reverse T3. F. Free T3. Differential Diagnosis A. Hashimoto's thyroiditis. B. Hyperthyroidism. C. Hypopituitarism. D. Hypothyroidism. E. Thyroid dysfunction induced by amiodarone. Evaluation and Management Plan A. General plan. 1. Monitor thyroid levels as needed if patient becomes symptomatic. Refer to healthcare provider. B. Patient and family teaching. 1. If symptoms of hypothyroidism or hyperthyroidism occur, call your healthcare provider. C. Pharmacology. 1. There is no evidence to date demonstrating the benefit of thyroid replacement in nonthyroidal illness. D. Discharge instructions. 1. No clear agreement on treatment exists. Hormone replacement with levothyroxine may not help these patients. Allowing for recovery time of the illness and checking thyroid function weeks after the illness resolves are the best treatment for euthyroid sick patients. Follow-Up A. Follow-up with primary care provider after release from the hospital. B. Refer to endocrinology. Consultation/Referral A. Referral to an endocrinologist is recommended for moni-toring of thyroid function tests both during and after recovery from nonthyroidal illness. Bibliography American Association of Clinical Endocrinologists. (2016). Hyperthyroidism: Information for patients. Retrieved from http://thyroidawareness. com/ sites/all/files/hyperthyroidism. pdf Brenner, Z., & Porsche, R. (2006). Amiodarone-induced thyroid dysfunc-tion. Critical Care Nurse, 26 (3), 34-41. Burch, W. (1994). Endocrinology (3rd ed. ). Baltimore, MD: Williams & Wilkins. Burman, K., Ellahham, S., Fadel, B., Lindsay, J., Ringel, M., & Wartofsky, L. (2000). Hyperthyroid heart disease. Clinical Cardiology, 23 (26), 402-408. doi:10. 1002/clc. 4960230605 Carroll, R., & Matfin, G. (2010). Endocrine and metabolic emergencies: Thyroid storm. Therapeutic Advances in Endocrinology and Metabolism, 1(3), 139-145. doi:10. 1177/2042018810382481 Thyroid Disorder—Euthyroid Sick Syndrome
Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
184 Chowdhury, S., Ghosh, S., Mathew, V., Misgar, R., Mukhopadhyay, P., Mukhopadhyay, S.,... Roychowdhury, P. (2011). Myxedema coma: A new look into an old crisis. Journal of Thyroid Research, 2011, 1-7. doi:10. 4061/2011/493462 Dahlen, R., & Kumrow, D. (2002). Thyroidectomy: Understanding the potential for complications. MEDSURG Nursing, 11 (5), 228-235. Francis, J., & Jayaprasad, N. (2005). Atrial fibrillation and hyperthyroidism. Indian Pacing and Electrophysiology Journal, 5 (4), 305-311. Holcomb, S. (2002). Thyroid diseases: A primer for the critical care nurse. Dimensions of Critical Care Nursing, 21 (4), 127-133. doi:10. 1097/ 00003465-200207000-00003 Lee, S. (2018, March 15). Hyperthyroidism and thyrotoxicosis. In R. Khardori (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/121865-overview Manzullo, E. F., & Ross, D. S. (2019, February 26). Nonthyroid surgery in the patient with thyroid disease. In J. E. Mulder (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/nonthyroid-surgery-in-the-patient-with-thyroid-disease Merrill, E. (2013). A devastating storm. The Medicine Forum, 14 (12), 24-25. doi:10. 29046/TMF. 014. 1. 012 The Nurse Practitioner: The American Journal of Primary Healthcare. (2005). Thyroid Disorders, 30 (6), 51-52. Roman, S. (2017). Current best practices in the management of thy-roid nodules and cancer. (Power Point slides). Retrieved from https://reachmd. com/programs/cme/current-best-practices-in-the-management-of-thyroid-nodules-and-cancer/8470/transcript/16717/ Ross, D. (2018, September 27). Thyroid function in nonthyroidal illness. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/thyroid-function-in-nonthyroidal-illness Ross, D., & Sugg, S. (2018, September 25). Surgical management of hyperthyroidism. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/surgical-management-of-hyperthyroidism T uttle, R. (2018, January 17). Differentiated thyroid cancer: Clinico-pathologic staging. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/differentiated-thyroid-cancer-clinicopathologic-staging/print Umpierrez, G. (2002). Euthyroid sick syndrome. Southern Medical Journal, 95(5), 506-513. doi:10. 1097/00007611-200295050-00007 Thyroid Disorder—Hyperthyroidism Lisa Coco Definition A. If the thyroid-stimulating hormone (TSH) level is too low, the thyroid is producing too much hormone, specifically T3 and possibly T4. This is called hyperthyroidism. B. Set of disorders that involve excess synthesis and secretion of thyroid hormones by the thyroid gland, which leads to the hypermetabolic state of thyrotoxicosis. C. The main autoimmune cause of hyperthyroidism is Graves' disease. D. Three main causes. 1. Diffuse toxic goiter (Graves' disease). 2. Toxic multinodular goiter. 3. Toxic adenoma. Incidence A. Hyperthyroidism affects approximately 3 million people. B. Graves' disease. 1. This is the most common form of hyperthyroidism in the United States, causing approximately 60% to 80% of cases of thyrotoxicosis. 2. Its peak occurrence is at age 20 to 40 years. C. Toxic multinodular goiter causes approximately 15% to 20% of thyrotoxicosis, occurring more frequently in regions of iodine deficiency. Toxic adenoma is the cause of approxi-mately 3% to 5% of cases {9}. Pathogenesis A. Hyperthyroidism results from excess production of thy-roid hormone from the thyroid gland. B. Untreated toxicosis can increase the incidence of cardio-vascular and pulmonary complications, skin and bone con-ditions, and eye disease. Predisposing Factors A. Genetic factors: Graves' disease often occurs in multiple members of a family. B. Autoimmune thyroid disorders. C. Hashimoto's disease. Subjective Data A. Common complaints/symptoms. 1. Palpitations, sweating, extreme fatigue, may have presence of goiter, and weight loss. B. Common/typical scenario. 1. Patient presents with extreme fatigue or anxiety and/or significant weight loss over a short period of time and often complains of palpitations. C. Family and social history. 1. May have a genetic or familial history. D. Review of systems. 1. Cardiovascular: Ask about palpitations or recent increases in blood pressure medications. 2. Head, eyes, ears, nose, and throat (HEENT: Hair loss. 3. Psych: Insomnia, anxiety, irritability, nervousness, increased perspiration. 4. Endocrine: Menstrual irregularities, weight loss, heat intolerance, thinning skin. 5. Musculoskeletal—muscle weakness, myalgias, arthralgias. Physical Examination A. Constitutional—appears toxic. B. Cardiovascular—systolic hypertension with a wide pulse pressure, tachycardia, atrial fibrillation. C. HEENT: Palpable diffuse goiter, thyroid bruit, exoph-thalmos, periorbital edema, proptosis, lid lag. D. Neurological/musculoskeletal—tremors, hyperreflexia. E. Dermatological—warm moist skin, pretibial myxedema. F. Psychological—anorexia, difficulty focusing. Diagnostic Tests A. TSH level: Most reliable screening measure. It is usually suppressed to an immeasurable level ( <0. 05 m IU/L) in thy-rotoxicosis. B. Free T4—may or may not be elevated. C. Free T3—will be elevated. D. Thyroid-stimulating immunoglobulin (TSI) or thy-rotropin receptor antibodies (G1) to establish Graves' disease. Thyroid peroxidase (TPO) level or antimicrosomal antibod-ies are usually elevated with Graves' disease but are usually low or absent in toxic multinodular goiter and toxic ade-noma. E. Thyroid uptake scan to determine the pattern of uptake, which varies with the underlying disorder. Normal radioac-tive iodine uptake after 6 hours is 2% to 16%; after 24 hours, it is about 8% to 25%. In hyperthyroidism there will be markedly increased uptake. Differential Diagnosis A. Euthyroid sick syndrome. B. Thyroiditis. C. Goiter. D. Struma ovarii. E. Graves' disease. 8. Endocrine Guidelines
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185 Evaluation and Management Plan A. General plan. 1. Symptom management—help the patient to establish symptom control with medications. 2. Further laboratory studies. a. Repeat TSH every 6 weeks or as needed until symptoms controlled. b. Check TSI and TPO to rule out Graves' disease or Hashimoto's thyroiditis, respectively. 3. Nuclear thyroid scanning to differentiate hyperthy-roidism from thyroiditis. B. Patient and family teaching. 1. Definitive treatment plan must be established and coordinated with endocrinology. 2. Reinforce need to see endocrinology on a regular basis. 3. If you develop flu-like symptoms while on antithyroid medications, call your provider immediately and stop your medications completely. C. Pharmacotherapy. 1. T reatment consists of symptom relief with the follow-ing drugs. a. Beta-blockers—titrate to heart rate less than 90 beats per minute and to reduce the sympathetic response associated with peripheral conversion of T4 to T3. Effects of beta-blockers are dramatic and rapid (within 10 minutes). i. Propranolol best studied in this class of medi-cations. ii. Other beta-blockers have similar effects and can be used. b. Antithyroid medications—prevents thyroid hor-mone synthesis. i. Methimazole (Tapazole) is considered the first-line drug therapy. ii. Propylthiouracil (PTU) is preferred in thyroid storm and first trimester of pregnancy. c. Corticosteroids. i. Dexamethasone contributes to blocking T4 to T3 conversion, which will control symptoms. Use-ful in emergencies, but has long-term complica-tions to consider. 2. Radioactive iodine-131 therapy ablates thyroid tissue. a. Thyroid cancer. b. Hyperthyroidism not controlled with medical therapy. 3. Thyroidectomy: May be preferable to radioactive iodine-131 therapy. a. May be required for large goiters causing airway constriction and severe dysphagia. b. Thyroid cancers not responsive to radioactive iodine 131 therapy. D. Imaging studies: Ultrasound, CT scan, and chest x-ray are routine. Fine needle aspiration for biopsy, vocal cord evalua-tion, or esophageal evaluation may be needed depending on the patient's presentation. 1. Monitor for thyroid storm, particularly in the first 18 hours postsurgery. a. T reat with antithyroid medications until euthy-roid. b. Beta-blockers: Atenolol should be taken 1 hour before surgery to maintain blockade. E. Discharge instructions. 1. Before discharge, refer the patient to outpatient endocrinology and to ophthalmology, if needed, for eye disease. Follow-Up A. Continue to monitor symptoms and thyroid levels. B. Check TSH 6 weeks after discharge. Consultation/Referral A. Refer to endocrinology to manage symptoms and disease progression. Special/Geriatric Considerations A. In the acute care setting, the focus should be on the adverse effects of antithyroid medications. 1. Rash. 2. Urticaria. 3. Arthralgia. B. Monitoring of results of lab studies is also important. 1. Complete blood count (CBC) for agranulocytosis if patient develops a fever or sore throat. Routine monitor-ing not recommended. 2. Hepatic profile for hepatitis. C. In addition, monitor the development of fever (>100. 5∘F) or a sore throat; the medication will need to be stopped. Bibliography American Association of Clinical Endocrinologists. (2016). Hyperthyroidism: Information for patients. Retrieved from http://thyroidawareness. com/ sites/all/files/hyperthyroidism. pdf Brenner, Z., & Porsche, R. (2006). Amiodarone-induced thyroid dysfunc-tion. Critical Care Nurse, 26 (3), 34-41. Burch, W. (1994). Endocrinology (3rd ed. ). Baltimore, MD: Williams & Wilkins. Burman, K., Ellahham, S., Fadel, B., Lindsay, J., Ringel, M., & Wartofsky, L. (2000). Hyperthyroid heart disease. Clinical Cardiology, 23 (26), 402-408. doi:10. 1002/clc. 4960230605 Carroll, R., & Matfin, G. (2010). Endocrine and metabolic emergencies: Thyroid storm. Therapeutic Advances in Endocrinology and Metabolism, 1(3), 139-145. doi:10. 1177/2042018810382481 Dahlen, R., & Kumrow, D. (2002). Thyroidectomy: Understanding the potential for complications. MEDSURG Nursing, 11 (5), 228-235. Francis, J., & Jayaprasad, N. (2005). Atrial fibrillation and hyperthyroidism. Indian Pacing and Electrophysiology Journal, 5 (4), 305-311. Holcomb, S. (2002). Thyroid diseases: A primer for the critical care nurse. Dimensions of Critical Care Nursing, 21 (4), 127-133. doi:10. 1097/ 00003465-200207000-00003 Lee, S. (2018, March 15). Hyperthyroidism and thyrotoxicosis. In R. Khardori (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/121865-overview Manzullo, E. F., & Ross, D. S. (2019, February 26). Nonthyroid surgery in the patient with thyroid disease. In J. E. Mulder (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/nonthyroid-surgery-in-the-patient-with-thyroid-disease Mathew, V., Misgar, R. A., Ghosh, S., Mukhopadhyay, P., Roychowdhury, P., Pandit, K.,... Chowdhury, S. (2011). Myxedema coma: A new look into an old crisis. Journal of Thyroid Research, 1-7. doi: 10. 4061/2011/ 493462 Merrill, E. (2013). A devastating storm. The Medicine Forum, 14 (12), 24-25. doi:10. 29046/TMF. 014. 1. 012 The Nurse Practitioner: The American Journal of Primary Healthcare. (2005). Thyroid Disorders, 30 (6), 51-52. Roman, S. (2017). Current best practices in the management of thy-roid nodules and cancer. (Power Point slides). Retrieved from https://reachmd. com/programs/cme/current-best-practices-in-the-management-of-thyroid-nodules-and-cancer/8470/transcript/16717/ Ross, D. (2018, September 27). Thyroid function in nonthyroidal ill-ness. In J. E. Mulder (Ed. ), Up To Date. Retrieved from Retrieved from https://www. uptodate. com/contents/thyroid-function-in-nonthyroidal-illness Ross, D., & Sugg, S. (2018, September 25). Surgical management of hyperthyroidism. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/surgical-management-of-hyperthyroidism T uttle, R. (2018, January 17). Differentiated thyroid cancer: Clinico-pathologic staging. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/differentiated-thyroid-cancer-clinicopathologic-staging/print Thyroid Disorder—Hyperthyroidism
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186 8. Endocrine Guidelines Umpierrez, G. (2002). Euthyroid sick syndrome. Southern Medical Journal, 95(5), 506-513. doi:10. 1097/00007611-200295050-00007 Thyroid Disorder—Hypothyroidism Lisa Coco Definition A. If the thyroid-stimulating hormone ( TSH) level is too high, the thyroid gland is not producing enough thyroid hor-mone, specifically T4 and possibly T3. This is called hypothy-roidism. B. Develops when the thyroid gland produces less than the normal amount of thyroid hormones. This leads to low serum levels of T4. C. Results in the slowing of several bodily functions. D. The main autoimmune cause of hypothyroidism is Hashimoto's disease. Incidence A. Hypothyroidism affects approximately 10 million people. B. It affects approximately 10% of women and 3% of men in the outpatient setting. C. Inhibits natural mechanism of metabolism in the body affecting many organ systems. Also associated with increased serum cholesterol levels, which may increase the risk for atherosclerosis and heart disease. Pathogenesis A. Insufficient production of thyroid hormone from thyroid gland. B. Three causes. 1. Primary: Occurs at the thyroid. 2. Secondary: Results from problems with the pituitary. 3. Tertiary: Results from problems at the level of the hypothalamus. Predisposing Factors A. Age and sex. B. Family history. C. Any autoimmune disorder: Autoimmune thyroiditis. D. Subacute thyroiditis. E. Radioactive iodine treatment. F. Spontaneous onset. G. Thyroid surgery or medications. H. Postpartum thyroiditis. I. Congenital condition. Subjective Data A. Common complaints/symptoms. 1. Weight gain, fatigue, forgetfulness, dry hair/nail changes, cold intolerance, menstrual irregularities. B. Common/typical scenario. 1. Patient presents with persistent fatigue and inability to lose weight. The patient will complain that he or she just does not feel right. C. Family and social history. 1. May have a familial link. D. Review of systems. 1. Constitution—ask about recent viral infections, per-vasive fatigue, drowsiness, forgetfulness, learning difficul-ties. 2. Dermatological—dry brittle hair and nails, itchy skin. 3. Psychological—recent depression, feeling sadness, decreased libido, irritability. 4. Endocrine—cold intolerance, menstrual irregulari-ties, miscarriages. 5. Musculoskeletal—muscle cramps, soreness. Physical Examination A. Cardiovascular—low blood pressure, bradycardia, fluid retention. B. HEENT—periorbital edema, assess for presence of goi-ter, dysphagia, eyebrow hair loss, possible scalp hair loss. C. Neuro/musculoskeletal—lower extremity fluid retention, myalgia, arthralgia, hyporeflexia. D. Dermatological—dry skin, coarse. Diagnostic Tests A. TSH (0. 4-5 u IU/m L). B. Free T4 (0. 8-1. 8 ug/d L). C. Thyroid antibodies. 1. Thyroid peroxidase (TPO) level ( <35 IU/m L). Differential Diagnosis A. Anemia. B. Addison's disease. C. Anovulation. D. Dysmenorrhea. E. Cardiac tamponade. F. Pericardial effusion. G. Chronic fatigue syndrome. H. Depression. I. Thyroiditis. J. Euthyroid sick syndrome. K. Goiter. L. Hypothermia. M. Constipation. N. Infertility. O. Iodine deficiency. P. Menopause. Q. Hyperlipidemia. R. Pituitary disorders. Evaluation and Management Plan A. General plan. 1. Normalize thyroid levels by starting thyroid hormone replacement therapy. 2. Routine laboratory testing every 6 weeks to adjust dose accordingly until stabilized. B. Patient and family teaching. 1. Teach patient signs and symptoms of hypothyroidism and when to call provider, including increase in fatigue, unexplained weight gain and fluid retention, increase in hair loss, arthralgias, and myalgias. 2. Labs must be checked every 6 weeks for a period of time until the medications can be normalized to patient tolerance and TSH goal is reached. C. Pharmacology. 1. T reatment consists of administering the synthetic thy-roid hormone levothyroxine. a. Dose is based on weight in kilograms multiplied by 1. 6 and can be administered orally or intravenously in the hospital setting at 50% to 80% of the PO dose. It should be taken on an empty stomach with no food, no other medications or caffeine for 1 hour, and no supplements for 4 hours. Follow-Up A. Ensure patient adherence to treatment regimen. B. Stress the importance of taking medication daily at approximately the same time.
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187 C. Stress the importance of laboratory checks of TSH level every 6 to 8 weeks. Consultation/Referral A. Once discharged, referral to an outpatient endocrinolo-gist is recommended. Special/Geriatric Considerations A. Keep TSH levels for geriatric patients in the midrange to avoid the incidence of cardiac side effects such as atrial fibrillation or tachycardia. Bibliography American Association of Clinical Endocrinologists. (2016). Hyperthyroidism: Information for patients. Retrieved from http://thyroidawareness. com/ sites/all/files/hyperthyroidism. pdf Brenner, Z., & Porsche, R. (2006). Amiodarone-induced thyroid dysfunc-tion. Critical Care Nurse, 26 (3), 34-41. Burch, W. (1994). Endocrinology (3rd ed. ). Baltimore, MD: Williams & Wilkins. Burman, K., Ellahham, S., Fadel, B., Lindsay, J., Ringel, M., & Wartofsky, L. (2000). Hyperthyroid heart disease. Clinical Cardiology, 23 (26), 402-408. Carroll, R., & Matfin, G. (2010). Endocrine and metabolic emergencies: Thyroid storm. Therapeutic Advances in Endocrinology and Metabolism, 1(3), 139-145. doi:10. 1177/2042018810382481 Chowdhury, S., Ghosh, S., Mathew, V., Misgar, R., Mukhopadhyay, P., Mukhopadhyay, S.,... Roychowdhury, P. (2011). Myxedema coma: A new look into an old crisis. Journal of Thyroid Research, 2011, 1-7. doi:10. 4061/2011/493462 Dahlen, R., & Kumrow, D. (2002). Thyroidectomy: Understanding the potential for complications. MEDSURG Nursing, 11 (5), 228-235. Francis, J., & Jayaprasad, N. (2005). Atrial fibrillation and hyperthyroidism. Indian Pacing and Electrophysiology Journal, 5 (4), 305-311. Holcomb, S. (2002). Thyroid diseases: A primer for the critical care nurse. Dimensions of Critical Care Nursing, 21 (4), 127-133. doi:10. 1097/ 00003465-200207000-00003 Lee, S. (2018, March 15). Hyperthyroidism and thyrotoxicosis. In R. Khardori (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/121865-overview Manzullo, E. F., & Ross, D. S. (2019, February 26). Nonthyroid surgery in the patient with thyroid disease. In J. E. Mulder (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/nonthyroid-surgery-in-the-patient-with-thyroid-disease Merrill, E. (2013). A devastating storm. The Medicine Forum, 14 (12), 24-25. doi:10. 29046/TMF. 014. 1. 012 The Nurse Practitioner: The American Journal of Primary Healthcare. (2005). Thyroid Disorders, 30 (6), 51-52. Roman, S. (2017). Current best practices in the management of thyroid nod-ules and cancer. (Power Point slides). Retrieved from https://reachmd. com/programs/cme/current-best-practices-in-the-management-of-thyroid-nodules-and-cancer/8470/transcript/16717/ Ross, D. (2018, September 27). Thyroid function in nonthyroidal ill-ness. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https:// www. uptodate. com/contents/thyroid-function-in-nonthyroidal-illness Ross, D., & Sugg, S. (2018, September 25). Surgical management of hyperthyroidism. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/surgical-management-of-hyperthyroidism T uttle, R. (2016). Differentiated thyroid cancer: Clinicopatho-logic staging. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/differentiated-thyroid-cancer-clinicopathologic-staging/print Umpierrez, G. (2002). Euthyroid sick syndrome. Southern Medical Journal, 95(5), 506-513. doi:10. 1097/00007611-200295050-00007 Thyroid Disorder—Myxedema Coma Lisa Coco Definition A. A rare (0. 22/one million annually) but severe life-threatening form of decompensated hypothyroidism associ-ated with a high mortality rate. B. Major precipitating factors: Infection and discontinua-tion of thyroid supplements. Incidence A. At present, there are over 300 cases reported in the lit-erature. Myxedema coma is rare and generally unrecognized, with 80% of patients older than 60 years of age. B. Myxedema coma can occur in younger women with 36 known cases occurring with pregnant females. C. A commonly ignored background factor in myxedema coma/crisis is the discontinuation of thyroid supplements in critically ill patients. Pathogenesis A. Low intracellular T3 secondary to hypothyroidism is the basic underlying pathology. Predisposing Factors A. Certain medications. B. Infection and septicemia. C. T rauma. D. Withdrawal of thyroid supplements. E. Underlying cardiovascular disease. Subjective Data A. Complaints/symptoms. 1. Decreased mentation and extreme lethargy. B. Common/typical scenario. 1. Very few cases have occurred in the United States, but usually related to having underlying hypothyroidism. Most likely to be seen in the ICU after hypothyroid medi-cation is discontinued for an extended period of time and a precipitating event occurs, such as sepsis. C. Family and social history. 1. Ask about discontinuation of thyroid medications. D. Review of systems. 1. Unable to assess due to mental status. Physical Examination A. Cardiovascular—hypotension, bradycardia, ECG changes. B. Respiratory—decreased breath sounds, respiratory depression. C. Neurological—poor cognitive function, generalized weakness. Diagnostic Tests A. Thyroid-stimulating hormone (TSH). B. Free T4. C. Nonspecific labs to rule out other disorders including complete blood count, urinalysis, blood and urine culture, and serum electrolytes. Differential Diagnosis A. Cerebrovascular accident. B. Acute psychosis. C. Hypoglycemia. D. Hypoxia. E. Sepsis. F. Hypothermia. G. Acute myocardial infarction (MI). H. Intracranial hemorrhage. I. Panhypopituitarism. J. Adrenal insufficiency. Thyroid Disorder—Myxedema Coma
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188 K. Hyponatremia. L. Gastrointestinal (GI) bleeding. M. Conversion disorder. Evaluation and Management Plan A. General plan. 1. Consult with endocrinologist. This is a medical emer-gency with a high (25% to 60%) risk of mortality. If an endocrinologist is not available, confer with a critical care specialist. The advanced practice provider (APP) should not manage this type of patient alone. 2. Be aware that cardiovascular morbidity occurs, including cardiogenic shock, respiratory depression, hypothermia, and coma. 3. Achieve normothermia. Warming occurs with admin-istration of thyroid hormone, in most cases both T3 and T4, with gradual slow rewarming via a warming blanket. 4. Focus on stabilization of cardiac status. Cardiac support is given through the administration of thyroid hormone and intravenous fluids with the stabilization of electrolytes and blood glucose. 5. Achieve optimum ventilation. Ventilation is given through administration of oxygen and, if needed, central or bilevel positive airway pressure or mechanical ventila-tion. B. Patient and family teaching. 1. Explain to the patient and family the severity of myxedema crisis and the course of treatment in the inten-sive care setting. C. Pharmacology. 1. Give intravenous triiodothyronine and thyroxine replacement with gradual slow rewarming. 2. Resuscitation and ICU management should be a mul-tidisciplinary team approach. D. Discharge instructions. 1. Poor outcomes are associated with myxedema coma; may need nursing home placement, long-term acute care hospital, or even palliative care/hospice if clinical course is complicated. Follow-Up A. Follow-up is dependent on individual outcome. Consultation/Referral A. Consultation with an endocrinologist. B. May need to consider a palliative care consult due to high mortality rate. C. Social work consult for placement or family support may be needed. Special/Geriatric Considerations A. Poor outcomes are associated with myxedema coma in all age groups. B. Myxedema coma is rare, with fewer than 40 cases reported and presentation of advanced hypothyroidism in pregnancy is very unusual. Bibliography American Association of Clinical Endocrinologists. (2016). Hyperthyroidism: Information for patients. Retrieved from http://thyroidawareness. com/ sites/all/files/hyperthyroidism. pdf Brenner, Z., & Porsche, R. (2006). Amiodarone-induced thyroid dysfunc-tion. Critical Care Nurse, 26 (3), 34-41. Burch, W. (1994). Endocrinology (3rd ed. ). Baltimore, MD: Williams & Wilkins. Burman, K., Ellahham, S., Fadel, B., Lindsay, J., Ringel, M., & Wartofsky, L. (2000). Hyperthyroid heart disease. Clinical Cardiology, 23 (26), 402-408. Carroll, R., & Matfin, G. (2010). Endocrine and metabolic emergencies: Thyroid storm. Therapeutic Advances in Endocrinology and Metabolism, 1(3), 139-145. Chowdhury, S., Ghosh, S., Mathew, V., Misgar, R., Mukhopadhyay, P., Mukhopadhyay, S.,... Roychowdhury, P. (2011). Myxedema coma: A new look into an old crisis. Journal of Thyroid Research, 2011, 1-7. doi:10. 4061/2011/493462 Dahlen, R., & Kumrow, D. (2002). Thyroidectomy: Understanding the potential for complications. MEDSURG Nursing, 11 (5), 228-235. Francis, J., & Jayaprasad, N. (2005). Atrial fibrillation and hyperthyroidism. Indian Pacing and Electrophysiology Journal, 5 (4), 305-311. Holcomb, S. (2002). Thyroid diseases: A primer for the critical care nurse. Dimensions of Critical Care Nursing, 21 (4), 127-133. doi:10. 1097/ 00003465-200207000-00003 Lee, S. (2018, March 15). Hyperthyroidism and thyrotoxicosis. In R. Khardori (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/121865-overview Manzullo, E. F., & Ross, D. S. (2019, February 26). Nonthyroid surgery in the patient with thyroid disease. In J. E. Mulder (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/nonthyroid-surgery-in-the-patient-with-thyroid-disease The Nurse Practitioner: The American Journal of Primary Healthcare. (2005). Thyroid Disorders, 30 (6), 51-52. Roman, S. (2017). Current best practices in the management of thyroid nod-ules and cancer. (Power Point slides). Retrieved from https://reachmd. com/programs/cme/current-best-practices-in-the-management-of-thyroid-nodules-and-cancer/8470/transcript/16717/ Ross, D. (2018, September 27). Thyroid function in nonthyroidal illness. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/thyroid-function-in-nonthyroidal-illness Ross, D., & Sugg, S. (2018, September 25). Surgical management of hyperthyroidism. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/surgical-management-of-hyperthyroidism T uttle, R. (2018, January 17). Differentiated thyroid cancer: Clinico-pathologic staging. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/differentiated-thyroid-cancer-clinicopathologic-staging/print Umpierrez, G. (2002). Euthyroid sick syndrome. Southern Medical Journal, 95(5), 506-513. doi:10. 1097/00007611-200295050-00007 Thyroid Disorder—Thyroid Storm Lisa Coco Definition A. State of severe hyperthyroid crisis that causes organ dys-function. B. An acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones. C. The severe end of the spectrum of thyrotoxicosis. Incidence A. Thyroid storm is most often seen in the context of under-lying Graves' hyperthyroidism. B. Although quite rare, it can complicate thyrotoxicosis of any etiology and has a high mortality rate that may approach 10% to 20%. C. Thyroid marker levels do not adequately address the dif-ferences between thyroid storm and hyperthyroidism. To dif-ferentiate the severity and potential morbidity of the disease, the Burch-Wartofsky Point Scale (BWPS) can predict the risk of thyroid storms independently from thyroid levels. D. Thyrotoxicosis is three to five times more common in females, predisposing them to this condition. Pathogenesis A. Patients with thyroid storm have relatively higher levels of free thyroid hormones. 8. Endocrine Guidelines
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189 Predisposing Factors A. Regardless of the underlying etiology, the transition to a state of thyroid storm usually requires a second superimposed insult. Most often, this is infection. B. Other associated causes are: 1. T rauma. 2. Surgery. 3. Thyroid surgery. 4. Myocardial infarction (MI). 5. Diabetic ketoacidosis (DKA). 6. Pregnancy. 7. Parturition. 8. Abrupt cessation of antithyroid medications. 9. Excessive ingestion of thyroid hormone. Subjective Data A. Common complaints/symptoms. 1. Irritability, emotional lability, and anxiety. 2. Increased appetite with poor weight gain. 3. Heat intolerance and excessive sweating. 4. Fatigue. 5. Respiratory distress. 6. Nausea and vomiting, diarrhea, and abdominal pain. B. Common scenario. 1. Severe florid hyperthyroidism evidenced by extreme irritability, high heart rate, cardiac arrhythmia, nausea, and/or vomiting; in addition, the patient may present with a possible psychosis. C. Family and social history. 1. None. D. Review of systems. 1. May be difficult to speak to during the acute phase. 2. Ask about extreme irritability, fatigue, anxiety. 3. Ask about palpitations. Physical Examination A. General: Appears toxic. B. Cardiovascular—hypertension with pulse pressure, car-diac arrhythmias, fever. C. HEENT—goiter, exophthalmos. D. Neurological—tremors, seizure activity, hyperflexia. Diagnostic Tests A. Thyroid-stimulating hormone (TSH). B. Free T4. C. Free T3. D. Liver function tests. E. Complete blood count (CBC). F. Comprehensive metabolic panel. G. Imaging studies, which may include: 1. Chest x-ray (CHF). 2. Head CT (exclude other neurological conditions). 3. ECG (cardiac arrhythmias). Differential Diagnosis A. Anticholinergic or adrenergic drug intoxication. B. Anxiety disorders. C. Central nervous system infections. D. Heart failure. E. Hypertension. F. Hypertensive encephalopathy. G. Hyperthyroidism. H. Malignant hyperthermia. I. Panic disorder. J. Pheochromocytoma. K. Septic shock. Evaluation and Management Plan A. General plan. 1. Medical treatment of thyroid storm aims to stop thy-roid hormone production within the gland, inhibit the release of thyroid hormone, and inhibit conversion of T4 to T3. 2. An acute care or ICU is most appropriate for manage-ment. 3. Antithyroid treatment should be continued until euthyroidism is achieved, at which point a final decision regarding oral medications, surgery, or radioactive iodine therapy can be made. a. Occasionally, patients may be severely agitated, limiting further intervention. b. Sedatives such as haloperidol or benzodiazepine can be given. 4. Management of airway, breathing, circulation, dis-ability, and examination (ABCDE) is crucial. 5. With high fever, acetaminophen is preferable to aspirin, which can increase serum T4 and T3 concentra-tions by interfering with protein binding. 6. Cooling blankets can also be used with close attention to slow cooling to decrease metabolic demand. 7. Other elements of supportive care: Intravenous fluids, electrolyte replacement, and nutritional support. 8. Intubation or noninvasive positive pressure ventila-tion may also be needed with arterial blood gas (ABG) analysis. B. Patient and family teaching. 1. Explanation of what thyroid storm is and the impor-tance of management should be discussed with the patient and family. The need for the ICU is the most appropriate for management to provide careful moni-toring. C. Pharmacotherapy. 1. Beta-blockers. Propranolol is the first-line choice for beta-blockers providing antiadrenergic effects and inhibits peripheral conversion of T4 to T3. 2. Propylthiouracil (PTU) is the thionamide of choice in severe, life-threatening thyroid storm because it blocks conversion of T4 to T3. a. PTU should be administered orally or via nasogas-tric tube in the awake or unresponsive patient with a loading dose of 600 mg followed by a dose of 200 to 250 mg every 4 to 6 hours. b. PTU is preferred in the first trimester because it causes less severe birth defects. 3. Methimazole. a. Methimazole is recommended for severe non-threatening thyroid storm because it has a longer half-life than PTU, normalizes T3 more rapidly, and has less hepatotoxicity. b. Methimazole is administered in a loading dose of 40 mg po with a dose of 20 to 30 mg every 4 to 6 hours (max 120 mg/d). 4. Potassium iodine (SSKI): 5 ggts po q6h. 5. Steroids: 100 mg hydrocortisone IV; then 100 mg q8h. D. Definitive therapy: Thyroidectomy. Consultation/Referral A. Endocrinology should be consulted on all cases. Follow-Up A. Follow-up care with an endocrinologist posthospitaliza-tion is recommended. Thyroid Disorder—Thyroid Storm
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190 Special/Geriatric Considerations A. With pregnancy, lithium carbonate at a dose of 300 mg every 8 hours can be used when there is a contraindication to thionamide therapy. Lithium inhibits thyroid hormone release from the thyroid gland. Bibliography American Association of Clinical Endocrinologists. (2016). Hyperthyroidism: Information for patients. Retrieved from http://thyroidawareness. com/ sites/all/files/hyperthyroidism. pdf Brenner, Z., & Porsche, R. (2006). Amiodarone-induced thyroid dysfunc-tion. Critical Care Nurse, 26 (3), 34-41. Burch, W. (1994). Endocrinology (3rd ed. ). Baltimore, MD: Williams & Wilkins. Burman, K., Ellahham, S., Fadel, B., Lindsay, J., Ringel, M., & Wartofsky, L. (2000). Hyperthyroid heart disease. Clinical Cardiology, 23 (26), 402-408. Carroll, R., & Matfin, G. (2010). Endocrine and metabolic emergencies: Thyroid storm. Therapeutic Advances in Endocrinology and Metabolism, 1(3), 139-145. doi:10. 1177/2042018810382481 Chowdhury, S., Ghosh, S., Mathew, V., Misgar, R., Mukhopadhyay, P., Mukhopadhyay, S.,... Roychowdhury, P. (2011). Myxedema coma: A new look into an old crisis. Journal of Thyroid Research, 2011, 1-7. doi:10. 4061/2011/493462 Dahlen, R., & Kumrow, D. (2002). Thyroidectomy: Understanding the potential for complications. MEDSURG Nursing, 11 (5), 228-235. Francis, J., & Jayaprasad, N. (2005). Atrial fibrillation and hyperthyroidism. Indian Pacing and Electrophysiology Journal, 5 (4), 305-311. Holcomb, S. (2002). Thyroid diseases: A primer for the critical care nurse. Dimensions of Critical Care Nursing, 21 (4), 127-133. doi:10. 1097/ 00003465-200207000-00003Idrose, A. M. (2015). Acute and emergency care for thyrotoxicosis and thy-roid storm. Acute Medicine and Surgery, 2 (3), 147-157. Published online 2015 May 12. doi:10. 1002/ams2. 104 Lee, S. (2018, March 15). Hyperthyroidism and thyrotoxicosis. In R. Khardori (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/121865-overview Manzullo, E. F., & Ross, D. S. (2019, February 26). Nonthyroid surgery in the patient with thyroid disease. In J. E. Mulder (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/nonthyroid-surgery-in-the-patient-with-thyroid-disease Merrill, E. (2013). A devastating storm. The Medicine Forum, 14 (12), 24-25. doi:10. 29046/TMF. 014. 1. 012 The Nurse Practitioner: The American Journal of Primary Healthcare. (2005). Thyroid Disorders, 30 (6), 51-52. Roman, S. (2017). Current best practices in the management of thy-roid nodules and cancer. (Power Point slides). Retrieved from https://reachmd. com/programs/cme/current-best-practices-in-the-management-of-thyroid-nodules-and-cancer/8470/transcript/16717/ Ross, D. (2018, September 27). Thyroid function in nonthyroidal illness. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/thyroid-function-in-nonthyroidal-illness Ross, D., & Sugg, S. (2018, September 25). Surgical management of hyperthyroidism. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/surgical-management-of-hyperthyroidism T uttle, R. (2018, January 17). Differentiated thyroid cancer: Clinico-pathologic staging. In J. E. Mulder (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/differentiated-thyroid-cancer-clinicopathologic-staging/print Umpierrez, G. (2002). Euthyroid sick syndrome. Southern Medical Journal, 95(5), 506-513. doi:10. 1097/00007611-200295050-000078. Endocrine Guidelines
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191 9 Psychiatric Guidelines Dawn Vanderhoef Bipolar Disorder Dawn Vanderhoef Definition A. Manic episode (see Table 9. 1). 1. Distinct period of abnormal and persistent elevated, expansive, or irritable mood and abnormally and persis-tent increase in goal-directed activity or energy, lasting at least a week and nearly all day. 2. During the period of mood disturbance and increased energy or activity, three of the following symptoms (four if mood is irritable) are present to a significant degree and represent a noticeable change from usual behavior. a. Inflated self-esteem or grandiosity. b. Decreased need for sleep. c. More talkative. d. Flight of ideas. e. Distractibility. f. Increase in goal-directed activities. g. Excessive involvement in activities that have a high risk for painful consequences. 3. The mood disturbance is sufficiently severe to cause marked impairment in social, occupational functioning, or to necessitate hospitalization to prevent harm to self or others. 4. The episode is not attributable to the physiological effects of a substance or to another medical condition. 5. NOTE: A full manic episode that emerges during antidepressant treatment but persists at a fully syndromal level beyond the physiological effect of treatment is suffi-cient evidence for a manic episode. B. Hypomanic episode (see Table 9. 1). 1. Distinct period of elevated expansive or irritable mood, lasting at least 4 days, that is clearly different from non-depressed mood. 2. Three or more (four if mood is irritable): Grandiosity, decreased sleep, pressured speech, racing thoughts, hyper-verbal, distractible, increase in goal-directed activity, and excessive involvement in pleasurable activities that may have negative consequences. 3. Change in behavior is uncharacteristic for the person. 4. Other people notice the change in mood and func-tioning. 5. Episode does not cause marked impairment in social or occupational functioning, it does not require hospital-ization, and there is no psychosis. 6. Symptoms are not due to substance use or a general medical condition. C. Bipolar depression. 1. Prolonged sadness. 2. Pessimism. 3. Changes in appetite. 4. Indifference. 5. Loss of energy. 6. Persistent lethargy. 7. Inability to concentrate. 8. Recurring thoughts of death or suicide. D. Bipolar I or bipolar II disorder. 1. Bipolar I: Has one or more manic episodes or mixed episodes: A distinct period of abnormally and persistently increased goal-directed activity or energy lasting at least 1 week and present nearly every day, for most of the day, with three or more of the following: Grandiosity/inflated self-esteem, decreased need for sleep, more talkative/ pressured speech, flight of ideas/racing thoughts, distractibility, increase in goal-directed behavior, or exces-sive engagement in high-risk activities. The Diagnostic and Statistical Manual of Mental Disorders (5th ed. ; DSM-5 ) has six separate criteria sets. a. bipolar disease (BPD) I single manic episode. b. Most recent episode hypomanic. c. Most recent episode manic. d. Most recent episode mixed. e. Most recent episode depressed. f. Most recent episode unspecified. 2. Bipolar II: Has one or more major depressive episodes and at least one hypomanic episode. a. Specifiers are used to indicate the nature of the current episode: hypomanic or depressed. b. If depressed, specifiers are mild, moderate, severe without psychotic features or severe with psychotic features, chronic, with catatonic features, with melancholic features, with atypical features, or with postpartum onset. Incidence A. 12-month prevalence for bipolar I disorder is 0. 6% with lifetime male-to-female ratio of 1:1. Age of onset is about 18 years of age, earlier than in major depressive disorder. B. 90% of individuals with a single manic episode have a recurrent mood episode. C. 60% of manic episodes occur immediately before a major depressive episode. D. 12-month prevalence for bipolar II disorder is 0. 3%. Bipolar Disorder
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192 Pathogenesis A. Up to 70% to 80% heritability. B. Brain changes. 1. Decreased size and activity in the prefrontal cortex with limbic hyperactivity and decreased hippocampal volume. 2. The amygdala is larger and more active in bipolar dis-order. 3. Disrupted glutamate and gamma-aminobutyric acid (GABA) regulation with greater norepinephrine and dopamine activity in mania. Predisposing Factors A. Environmental: Separated, widowed individuals have higher rates. B. Genetics: Family history is one of the strongest and most consistent predictors for bipolar disorder. Individuals with psychiatric features likely have subsequent episodes with psy-chotic features. C. Gender: Females are more likely to have rapid cycling and mixed states and are more likely to have depressive episodes along with a greater likelihood of alcohol use disorders. D. Suicide: Lifetime risk is 15 times greater than that in the general population. Subjective Data A. Common complaints/symptoms. 1. Mania. a. Racing thoughts. b. Flight of ideas. c. Increased focused activity. d. Thoughts of grandiosity. e. Excessive talking or pressured speech. 2. Depressive episodes. a. Depressed mood. b. Loss of energy or fatigue. c. Diminished interest in anything. d. Weight loss. e. Feelings of worthlessness. B. Common/typical scenario. 1. A typical scenario starts with an unusual shift in mood and energy. The person may have excessively elevated mood for about a week and then become depressed. C. Family and social history. 1. Inquire about family history of mental illness. 2. Inquire about periods of depression or manic episodes. 3. Inquire about patterns of prolonged sleep alternating with excessively elevated mood. 4. Inquire about lifestyle and stressful life events. D. Review of systems. 1. Noncontributory. Mental State Examination A. Conduct a Mental State Examination. B. General description: Manic patients are excited, talkative, and sometimes amusing. Hyperactivity is common and at times is psychotic and disorganized. C. Mood and affect: Mood is euphoric but also can be irrita-ble. A low frustration tolerance is common as is labile mood with shifts from laughing to crying to irritability. D. Perceptual disturbances. 1. Delusions are common in manic patients. 2. Mood-congruent manic delusions have themes of wealth, extraordinary abilities, or power. 3. Hallucinations may also be present. E. Thought: Distractibility and flight of ideas are common. F. Impulse control: 75% of manic patients are assaultive and threating. G. Judgment and insight: Impairment is a hallmark. H. Reliability: Commonly unreliable historians. Diagnostic Tests A. Used to rule out a medical cause of the psychiatric symptoms. B. Endocrine disorders. 1. Hyperthyroid. 2. Diabetes. 3. Cushing's syndrome. 4. Addison disease. C. Neurological disorders. 1. Epilepsy. 2. Cerebrovascular disease. 3. T umors. 4. Head trauma. 5. Lupus. 6. Multiple sclerosis. D. Infectious disease. 1. HIV/AIDS. 2. Lyme disease. 3. Syphilis. E. Medications/substances associated with mania. 1. Amphetamines. 2. Cocaine. 9. Psychiatric Guidelines TABLE 9. 1 Mania and Hypomania Comparisons Manic Episode Hypomanic Episode Duration 1week or more 4days or more Mood Abnormally and persistently high, irritable, or expansive Activity/energy Persistentlyincreased Symptomsthat arechanges from usualbehavior Three or more of grandiosity, ↓need for sleep, ↑talkativeness, flight of ideas or racing thoughts, distractibility (self-report or that of others), agitation, ↑goal-directed activity, poorjudgment Severity Resultsin psychotic features, hospitalization, or impairment at work, social, and personal levels Clearchange fromusual functioning and others notice this change and NO psychosis, hospitalizations, or impairment Other Ruleout substance/medication-induced symptoms with mixed features,if appropriate Source:Adapted with permission from Morrison, J. (2014). DSM-5 made easy: The clinician's guide to diagnosis. New York,NY:Guilford Press.
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193 3. Corticosteroids. 4. Hallucinogens. 5. Levodopa. 6. Opiates. 7. Phencyclidine (PCP). F. Screening instruments: Positive screen DOES NOT indi-cate a disorder; REQUIRES validation with comprehensive interview/assessment. 1. Mood Disorder Questionnaire (MDQ). 2. Young Mania Rating Scale. 3. Bipolar Depression Rating Scale (BDRS). 4. Hypomania Checklist (HCL-32): Self-report. Differential Diagnosis A. Major depressive disorder. B. Schizophrenia. C. Generalized anxiety disorder. D. Posttraumatic stress disorder. E. Substance-induced mood disorder. F. Attention deficit hyperactivity disorder. G. Personality disorders. Evaluation and Management Plan A. General plan. 1. T reatment of bipolar disorders is complex— antidepressants should be avoided unless an individual has refractory depression unresponsive to an atypical antipsychotic (AA) and mood stabilizer. Antidepressant treatment can make an individual cycle or become refrac-tory to treatment. 2. If an antidepressant is used to treat the depressive episode it should be discontinued after 6 to 9 months of sustained remission of the episode. 3. Refer to AAs in the Posttraumatic Stress Disorder section. B. Patient/family teaching points. 1. Compliance with treatment plan can be challenging. 2. Teach patient and family warning signs and symptoms. 3. Teach patient coping skills to deal with life stressors. 4. Encourage patient to learn more about biology behind the disease to increase compliance. 5. Provide information on local support groups and other national resources. C. Pharmacotherapy. 1. Gold standard is Lithium, which has an indication for acute mania, prophylaxis of depression and suicide, and is adjunct to antidepressant treatment in unipolar depres-sion. a. Elimination is almost entirely by the kidneys; there-fore, once a day dosing is recommended. Lithium 300 mg =0. 3 m Eq/L plasma concentration. b. Therapeutic range 0. 5 to 1. 0 m Eq/L. c. Drug-drug interactions: Diuretics, angiotensin-converting enzyme (ACE) inhibitors, digoxin, nonsteroidal anti-inflammatory drugs (NSAIDs), Flagyl. d. Pregnancy: Avoid use due to risk of Ebstein's anomaly. e. Laboratory tests: Prior to treatment, check preg-nancy test in females, creatinine, thyroid profile, and complete blood count (CBC; can cause leukocytosis) and repeat every 6 months. Patients over 40 years of age should have an EKG. f. Side effects of lithium at different levels can be seen in Table 9. 2. TABLE 9. 2 Lithium Toxicity and Side Effects Lithium Level (m Eq/L) Side Effects 1. 0-1. 5 Tremor 1. 5-2. 0 Cog-wheeling, tremor,nausea, drowsiness 2. 0-3. 0 Ataxia, confusion >3. 0 Delirium, coma, seizures,death 2. Valproate (Depakote) is indicated for acute mania and rapid cycling. Also used in prophylaxis. It is highly pro-tein bound and metabolized by the liver. Extended release has about 8% to 20% lower bioavailability than interven-tion radiology (IR). a. Drug-drug interactions: ASA, CYP2D6 and 3A4, avoid with heavy alcohol consumption. b. Box warning: Pancreatitis. c. Laboratory tests: Liver function tests, CBC, and pregnancy test in females. Recheck liver function tests, CBC, and valproic acid (VPA) level every 6 months. Response is based on evaluation of patient; laboratory ranges were developed in persons with seizure disorders. 3. Carbamazepine (Tegretol) is indicated for acute mania and prophylaxis. a. Highly protein bound, interaction with CYP3A4, and is a strong autoinducer. b. Lowers the effectiveness of oral birth control pills. c. Laboratory tests: Liver function tests, CBC, preg-nancy test in females, and follow-up testing every 6 months with carbamazepine level. 2007 Food and Drug Administration (FDA) Alert: Genetic testing required in persons with human leukocyte antigen (HLA) allele, which occurs in individuals from Asia, including South Asian Indians. 4. Lamotrigine (Lamictal) is indicated for bipolar main-tenance; it has been found effective in bipolar II disorder as well. a. Follow recommended dosing and guidelines if a patient is on valproate. b. Risk of Stevens-Johnson syndrome if a patient missed more than 5 days; need to be retitrated. c. Oral contraceptives lower lamotrigine levels. Follow-Up Patients with bipolar disorder should be followed by a psychiatric specialist. Consultation/Referral A. Consultation and referral to a primary care provider is warranted if there are comorbid physical health conditions. Special/Geriatric Considerations A. Support group. 1. Depression and Bipolar Support Alliance. 2. National Alliance on Mental Illness (NAMI). Bibliography American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed). Arlington, VA: American Psychiatric Pub-lishing. Morrison, J. (2014). DSM-5 made easy: The clinician's guide to diagnosis. New York, NY: Guilford Press. Bipolar Disorder
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194 Pliszka, S. R. (2016). Neuroscience for the mental health clinician (2nd ed. ). New York, NY: Guilford Press. Sadock, B. J., Sadock, V. A., & Ruiz, P. (2015). Kaplan & Sadock's synopsis of psychiatry: Behavioral sciences/clinical psychiatry (11th ed. ). Philadelphia, PA: Wolters Kluwer. Stahl, S. M. (2013). Stahl's essential psychopharmacology: Neuroscientific basis and practical applications ( 4th ed. ). New York, NY: Cambridge Univer-sity Press. Stahl, S. M. (2014). Stahl's essential psychopharmacology: Prescriber's guide (5th ed. ). New York, NY: Cambridge University Press. Major Depressive Disorder Dawn Vanderhoef Definition A. Five (or more) of the following symptoms present during the same 2-week period and represent a change from previ-ous functioning. At least one of the symptoms must be either (a) depressed mood or (b) loss of interest or pleasure. 1. Depressed mood most of the day, nearly every day, by subjective report (sad, empty, hopeless) or observed by others (appears tearful). 2. Markedly diminished pleasure in all or most activities. 3. Significant weight loss (more than 5% in a month) or decrease or increase in appetite nearly every day. 4. Insomnia or hypersomnia nearly every day. 5. Psychomotor agitation or retardation nearly every day (observable by others, not merely subjective feelings of restlessness or being slowed down). 6. Fatigue or loss of energy nearly every day. 7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day. 8. Diminished ability to think or concentrate, indeci-siveness, nearly every day (subjective or observed). 9. Recurrent thoughts of death (not just dying), recur-rent suicidal ideation without a specific plan, or a suicide attempt or a specific plan. B. Symptoms cause clinically significant distress or impair-ment in social, occupational, or other areas of functioning. C. The episode is not attributable to the physiological effects of a substance or to another medical condition. D. With postpartum onset: If symptoms are within 4 weeks postpartum. Commonly includes psychosis. E. Mnemonic: SIGE CAPS. 1. Sleep disturbance. 2. Interest and pleasure decrease. 3. Guilt. 4. Energy lower. 5. Concentration decrease. 6. Appetite increase or decrease. 7. Psychomotor agitation or retardation. 8. Suicidal/hopeless. Incidence A. 12-month prevalence is approximately 7% with increase in 18-to 29-year-olds. B. Females have 1. 5-to 3-fold higher rates than males begin-ning in early adolescence. C. Mean age of onset is 40 years of age with 50% of persons having an onset between the ages of 20 and 50 years. Pathogenesis A. Heritability: 50%. B. 8% to 17% risk if first degree relative has diagnosis. 1. Neurochemical imbalance: Most basic level is the monoamine hypothesis, an imbalance in the following neurotransmitters. a. Norepinephrine. b. Dopamine. c. Serotonin. Predisposing Factors A. No close interpersonal relationships. B. Divorced or separated. C. More common in rural than urban areas. D. Stressful life events precede first episode. E. Depression in older persons is common. Individuals with the following are at higher risk of developing depression: Lower socioeconomic status, loss of spouse, current physical illness, and social isolation. Subjective Data A. Common complaints/symptoms. 1. Agitation or restlessness. 2. Psychomotor retardation. 3. Flat affect. 4. Loss of energy. 5. Feeling of worthlessness. 6. Diminished ability to concentrate. 7. Loss of pleasure in activities. 8. Recurrent thoughts of death. B. Common/typical scenario. 1. Patients may not seek attention for depression but typically complain of other symptoms, such as insom-nia, headaches, abdominal upset, and difficulty concen-trating. C. Family and social history. 1. Depression can be familial. 2. Social history is noncontributory. D. Review of systems. 1. Noncontributory. Mental State Examination A. General description: Psychomotor retardation, hand wringing, stooped posture, downcast gaze. B. Mood and affect: 50% persons deny depressed feelings/ constricted affect. C. Speech: Decreased rate and volume with limited response to questions. D. Perceptual disturbances: Assess for hallucinations (audi-tory are most common), delusions, paranoia. E. Thought content: Negative worldviews, rumination, and guilt. Assess for suicidal (10%-15% commit suicide) and homicidal ideation. F. Cognition: Cognitive impairment seen in 50% to 70% of depressed patients. G. Impulse control: If the patient has psychotic symptoms, may consider harming others. HIGH RISK for self-harm exists when energy is improving; the individual can carry out the plan. H. Suicide assessment. 1. Ask about ideation: Onset, duration, frequency, active thoughts, lethality, stressors, use of substances. 2. Ask about plan: Wish to die, means, and understands consequences. 3. Ask about means: Access to carry out plan, taken steps to prepare to end life, lethality. 4. Ask about intent: Protective or risk factors. 5. Screening instrument: Columbia Suicide Severity Rating Scale. I. High risk populations for suicide. 1. Older single white males. 2. Divorced/widowed. 9. Psychiatric Guidelines
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195 3. Unemployed. 4. Psychosis. 5. Homeless. 6. LGBT. 7. Veterans. 8. Comorbid physical and/or substance use disorder. 9. Previous attempt and/or family history. 10. Access to lethal means. J. Homicidal assessment. 1. Ideation, means, plan, and intent. 2. Assess for anger, rage, and interpersonal conflict. 3. If actively homicidal: Inpatient psychiatric hospital-ization, notify law enforcement and Duty to Warn: Tarasoff v. Regents of the University of California (1976)—must notify victim. Diagnostic Tests A. Thyroid profile. B. Complete blood count. C. Comprehensive metabolic panel. D. And based on history: Vitamin D level, folate level, B12, or thiamine level. E. Medical rule outs. 1. Endocrine disorders: Hypothyroidism, diabetes, adrenal dysfunction. 2. Neurological disorders: Dementia, seizures, tumors, Parkinson's disease, sleep apnea, cerebrovascular accident (CVA), neoplasms. 3. Cardiac disease: Congestive heart failure, hyperten-sion. 4. Infection: Mononucleosis, HIV/AIDS, pneumonia, TD. 5. Nutrition deficits: Anemia, low vitamin D/folate/ B12/thiamine. 6. Other: Side effects of medications such as cardiac medications, hypnotics, antibacterial medica-tions, antineoplastic medications, analgesics, antiepilep-tics, or antiparkinsonian drugs. F. Screening instruments (in public domain): Positive screen DOES NOT indicate a disorder; REQUIRES validation with comprehensive interview/assessment. 1. Patient Health Questionnaire (PHQ)—2. 2. Patient Health Questionnaire (PHQ)—9. 3. Mood Disorders Questionnaire (MDQ). 4. Edinburgh Postnatal Depression Scale (EPSD). 5. Geriatric Depression Scale. Differential Diagnosis A. Bipolar disorder, depressed phase. B. Mood disorder due to general medical condition. C. Eating disorder. D. Substance-induced mood disorder. E. Adjustment disorder. Evaluation and Management Plan A. General plan. 1. Meets criteria for major depressive disorder, single episode or recurrent, and, if postpartum onset, psychosis or suicide/homicidal ideation. 2. If patient is not actively suicidal, homicidal, or psychotic, discuss treatment options. 3. Psychotherapy for mild symptoms or if patient refuses medication. 4. Prior to starting antidepressant treatment, bipolar disorder has been ruled out. B. Patient/family teaching points. 1. Teach patients about early signs of relapse and ratio-nale of treatment choices made. 2. Family members need to be taught about depression and how to be supportive. 3. Encourage patient to learn more about biology behind the disease to increase compliance. 4. Provide information on local support groups and other national resources. C. Pharmacotherapy. 1. Medication treatment options. a. Selective serotonin reuptake inhibitors. i. Boxed warning for increase in suicidal think-ing up to age 24 (for all antidepressants in all classes). ii. Risk of serotonin syndrome. iii. Discontinuation syndrome—abrupt discon-tinuation of medication that is more common in medications with short half-lives. 1)Mnemonic FINISH. a)Flu-like symptoms. b)Insomnia. c)Nausea. d)Imbalance. e)Sensory disturbance. f)Hyperarousal. 2)T reatment: Place back on medication. iv. Serotonin syndrome (risk with any medication that increases serotonin levels). 1)Mnemonic HARMED (medical emer-gency). a)Hyperthermia. b)Autonomic instability. c)Rigidity. d)Myoclonus. e)Encephalopathy. f)Diaphoresis. 2)T reatment. a)Stop medication. b)Supportive measures and cyprohepta-dine (Periactin) can be helpful. b. Serotonin norepinephrine reuptake inhibitors (SNRIs). c. Other antidepressants. i. Noradrenergic and specific serotonergic antidepressant (Na SSA) more sedating at lower doses; increased appetite; can lower white blood cell (WBC); Sol Tab. ii. Norepinephrine dopamine reuptake inhibitor (NDRI). 1)Avoid with history of seizure disorder or eating disorder; weight neutral and little to no sexual dysfunction. 2)Attention deficit/hyperactivity disorder (ADHD) off label; less likely to switch into mania/DOSE BASED ON FORMULA-TION. 3)Zyban—smoking cessation. 4)Serotonin antagonist reuptake inhibitor (SARI): Sleep agent; risk of priapism; orthostasis; QTc prolongation. 5)Multimodal antidepressant. a)SSRI—5HT1a agonist (low sexual dysfunction). b)5HT1a partial agonist. c)5HTc, 1D (improved cognition). Major Depressive Disorder
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196 d)7 antagonist—vortioxetine (T rin-tellix): Little/no sexual dysfunction, improved cognition, gastrointestinal (GI) upset, hyponatremia, bleeding. 6)Serotonin partial agonist reuptake inhibitor (SPARI). d. Tricyclic Antidepressants (TCAs). i. Side effects: Sedation, weight gain, hypoten-sion, anticholinergic toxicity (treatment with physostigmin), and QTc prolongation (EKG over 40 or with history of cardiovascular disease). ii. Lethal in overdose. iii. Use caution when given with anticoagulants, which increases risk for bleeding. iv. Need to check blood levels (therapeutic ranges). e. Monoamine oxidase inhibitors (MAOIs). i. Not used as first-or second-line treatment due to need for dietary changes and drug-drug inter-actions. ii. Risk for hypertensive crisis with tyramine (treatment with phentolamine). iii. Need education on tyramine free diet, such as to avoid dairy, fish, and processed meats. iv. Many drug-drug interactions: Demerol, OTC flu/cold medications, lithium, serotonergic agents, stimulants. v. Even with MAOI patches, dietary changes should be made. Follow-Up A. Weekly follow-up for the first month. B. High risk of suicide as energy improves and mood stays low. Consultation/Referral A. Consultation with or referral to a psychiatric specialist if patient fails two full (adequate trial both time and dose) antidepressant trials. B. Referral for psychotherapy as appropriate. Special/Geriatric Considerations A. Women of childbearing age: Assess Food and Drug Administration (FDA) pregnancy risk (with all psychotropic medications). B. Postpartum depression: Important to assess for postpar-tum depression (PPD) with psychosis. C. Older adults: Assessment of depression in older adults with cognitive problems, as pseudodementia may be present. White, widower, older males are at high risk of suicide. Con-siderations related to aging and drug-drug interactions. Bibliography American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Arlington, VA: American Psychiatric Pub-lishing. Caplan, J. P., & Stern, T. A. (2008). Mnemonics in a nutshell: 32 aids to psychiatric diagnosis. Current Psychiatry, 7 (10), 27-33. Pliszka, S. R. (2016). Neuroscience for the mental health clinician (2nd ed. ). New York, NY: Guilford Press. Sadock, B. J., Sadock, V. A., & Ruiz, P. (2015). Kaplan & Sadock's synopsis of psychiatry: Behavioral sciences/clinical psychiatry (11th ed. ). Philadelphia, PA: Wolters Kluwer. Stahl, S. M. (2013). Stahl's essential psychopharmacology: Neuroscientific basis and practical applications ( 4th ed. ). New York, NY: Cambridge Univer-sity Press. Stahl, S. M. (2014). Stahl's essential psychopharmacology: Prescriber's guide (5th ed. ). New York, NY: Cambridge University Press. Posttraumatic Stress Disorder Dawn Vanderhoef Definition A. Exposure to actual or threatened death, serious injury, or sexual violation in one (or more) of the following ways. 1. Directly experiencing the traumatic event(s). 2. Witnessing, in person, the event(s) that occurred to a close family member or close friend, resulting in actual or threatened death. 3. Learning that the traumatic event(s) occurred to a close family member or close friend. In cases of actual or threatened death of a family member or friend, the event(s) must have been violent or accidental. 4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (e. g., first responders col-lecting human remains; police officers repeatedly exposed to details of child abuse). B. Presence of one (or more) of the following intrusive symp-toms associated with the traumatic event(s), beginning after the traumatic event(s) occurred. 1. Recurrent, involuntary, and intrusive distressing sto-ries or memories of the traumatic event(s). 2. Recurrent distressing dreams in which the content and/or affect of the dream related to the traumatic event(s) are expressed. 3. Dissociative reactions (flashbacks) in which the individual feels or acts as if the traumatic event(s) were recurring. 4. Intense or prolonged psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event(s). 5. Marked physiological reactions to internal or external cues that symbolize or resemble an aspect of the traumatic event(s). C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the traumatic event(s) occurred, as evidenced by one or both of the following. 1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s). 2. Avoidance of or efforts to avoid external reminders (people, places, conversations, activities, objects, situ-ations) that trigger distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s). D. Negative alterations in cognition and mood associated with the traumatic event(s) beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following. 1. Inability to remember an important aspect of the trau-matic event(s) (typically due to dissociative amnesia and not the other factors such as head injury, alcohol, or drugs). 2. Persistent and exaggerated negative beliefs or expecta-tions about oneself, others, or the world. 3. Persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the individual to blame himself/herself or others. 4. Persistent negative emotional state (horror, fear, anger, guilt, shame). 5. Markedly diminished interest or participation in significant activities. 6. Feelings of detachment or estrangement from others. 7. Persistent inability to experience positive emotions. 9. Psychiatric Guidelines
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197 E. Marked alterations in arousal and reactivity associated with the traumatic event(s) beginning or worsening after the traumatic event(s) occurred, as evidenced by two (or more) of the following. 1. Irritable behavior and angry outbursts typically expressed as verbal or physical aggression toward others/ objects. 2. Reckless or self-destructive behavior. 3. Hypervigilance. 4. Exaggerated startle response. 5. Problems with concentration. 6. Sleep disturbances (falling/staying asleep or restless sleep). F. Duration of the disturbance is more than 1 month. G. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. H. The disturbance is not attributed to the physiological effects of a substance or another medical condition. Incidence A. 9% to 15% lifetime incidence, and lifetime prevalence is about 8% of the general population. B. Lifetime prevalence is 10% in women and 4% in men and is more common in young adults. C. More common in single, divorced, widowed, and socially withdrawn individuals. D. Risk factor is severity, duration, and proximity of the person's exposure to the trauma. E. Symptoms usually develop within the first 3 months of the trauma, but a delay can exist. Pathogenesis A. Activation of the amygdala, increase in epinephrine and norepinephrine, and changes in cortisol production. B. Activation of the hypothalamus-pituitary-adrenal axis (HPA) and reduction of the hippocampus/frontal cortex. Predisposing Factors A. Childhood trauma. B. Intimate partner violence. C. Personality disorder. D. Female. E. Genetic vulnerability. F. Recent life change. G. Perception of external locus of control. H. Alcohol and substance use. I. Rape, military combat, and ethnically motivated genocide. J. Medical rule out: Posttraumatic stress disorder (PTSD) commonly exists with chronic pain syndromes and irritable bowel syndrome. K. Other psychiatric disorders commonly coexist with PTSD and all other disorders. Subjective Data A. Common symptoms. 1. Patients who have PTSD have considerable stress that interferes with their ability to interact in society. B. Common or typical scenario. 1. May involve the patient withdrawing from society, job loss, divorce, or even substance abuse. C. Family/social history. 1. Ask about family situation, support system, or use of any drugs or alcohol. D. Review of systems. 1. Psychiatric: Ask about depression, anxiety, constant fear, suicidal thoughts, or complaints of chronic pain. Mental State Examination A. General. 1. Agitated. 2. Anxious. 3. Irritable. B. Attitude. 1. Describe if patient is friendly, cooperative, hostile, or defensive. C. Mood. 1. General mood of patient. D. Affect. 1. Can be described as expansive, euthymic, constricted, or blunted. E. Speech. 1. Quantity, rate, and volume. F. Thought process and content. 1. How is the patient thinking? Diagnostic Tests A. Screening instruments. 1. Posttraumatic Stress Disorder Checklist for Diagnos-tic and Statistical Manual of Mental Disorders (5th ed. ; DSM-5 ) (PCL-S). 2. Clinician-Administered PTSD Scale for PTSD (CAPS-5). 3. T rauma Screening Questionnaire (TSQ). 4. Short Screening Scale for PTSD. 5. Short Form of the PTSD Checklist. Differential Diagnosis A. Adjustment disorder. B. Acute stress disorder—Distinguished from PTSD based on time frame: Duration is restricted to 3 days to 1 month. C. Anxiety/obsessive-compulsive disorder. D. Major depression. E. Personality disorders. F. Conversion disorder. G. Psychotic disorders. H. T raumatic brain injury. Evaluation and Management Plan A. General plan. 1. Psychotherapy. a. T rauma-focused therapy. b. Cognitive behavioral therapy (CBT). c. Exposure therapy. d. Eye movement desensitization and reprocessing (EMDR). B. Pharmacotherapy. 1. Selective serotonin reuptake inhibitors (SSRIs) are the only Food and Drug Administration (FDA) approved treatment for PTSD and have the strongest evidence: Paroxetine (Paxil) and sertraline (Zoloft) are the only medications with FDA approval. 2. Benzodiazepines are not indicated in the treatment of PTSD. 3. Serotonin norepinephrine reuptake inhibitors (SNRIs) like venlafaxine XR (Effexor SR) and mirtazap-ine (Remeron) have been shown to be helpful. 4. Prazosin has been studied to treat nightmares: Starting dose 1 mg with range up to 40 mg. Posttraumatic Stress Disorder
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198 Follow-Up A. Coordination with a psychiatric specialist for ongoing treatment and follow-up. B. T rauma-informed care and interventions have the best outcomes. Consultation/Referral A. Consider referral for integrative treatments (Confusion Assessment Method [ CAM]): Mindfulness, yoga, acupunc-ture, and massage. Special/Geriatric Considerations A. Adaptive coping in elderly patients may be impaired and lead them to engage in substance abuse to manage PTSD symptoms. B. Older adults may not identify symptoms in the context of a psychological framework, making them less likely to seek treatment. C. There may be a stigma in older adults about seeking psychological assistance. Bibliography American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Arlington, VA: American Psychiatric Pub-lishing. Pliszka, S. R. (2016). Neuroscience for the mental health clinician (5th ed. ). New York, NY: Guilford Press. Sadock, B. J., Sadock, V. A., & Ruiz, P. (2015). Kaplan & Sadock's synopsis of psychiatry: Behavioral sciences/clinical psychiatry (11th ed. ). Philadelphia, PA: Wolters Kluwer. Stahl, S. M. (2013). Stahl's essential psychopharmacology: Neuroscientific basis and practical applications (4th ed. ). New York, NY: Cambridge Univer-sity Press. Stahl, S. M. (2014). Stahl's essential psychopharmacology: Prescriber's guide (5th ed. ). New York, NY: Cambridge University Press. Schizophrenia Dawn Vanderhoef Definition A. Psychiatric disorder that affects behavior. B. People with varying degrees of schizophrenia can have chronic and severe alterations in the way they think, feel, and behave. Incidence A. 1% with a lifetime prevalence of 0. 6% to 1. 9%. B. Equally prevalent in men and women, but onset differs with more men having onset before age 25 with a peak age of 10 to 25 years of age and a peak in females age 25 to 35 with up to 10% of women having onset after age 40. Pathogenesis A. The pathogenesis of schizophrenia is unknown. B. It is a uniquely human condition that appears to be caused by a complex interaction of genes and environment. C. Genetic studies have shown a strong hereditary associ-ation, but the understanding of why or how schizophrenia occurs is unknown. Predisposing Factors A. Decreased cortical volume in temporal cortex and increased ventral size with decrease in gamma-aminobutyric acid (GABA) interneurons. Genetic estimates of up to 46% in monozygotic twins. B. Born in winter or spring. C. Raised in urban areas. D. Early or prenatal infections. E. Birth complications. F. Substance use disorders. Subjective Data A. Common complaints/symptoms. 1. One of the top three +one for 1 month. a. Delusions. b. Hallucinations (auditory and visual are most common; gustatory, olfactory, and tactile are more common due to an organic etiology). c. Disorganized speech. d. Grossly disorganized or catatonic behavior. e. Negative symptoms (restricted affect, poverty of speech, decreased interests, decrease dsense of pur-pose, decreased social drive). 2. Impairment in function such as work, interpersonal relations, self-care, academic, or occupational issues. 3. Continuous symptoms that last for 6 months or longer. B. Common/typical scenario. 1. Patients commonly present with hallucinations or dis-organized speech. 2. Symptoms may be vague in the beginning stages. 3. The first psychotic episode may start in the teen years up to the mid-30s. C. Family and social history. 1. Family and close friends may describe a noticeable change in personality. 2. Family history of schizophrenia may be pertinent, but the link is not very strong. D. Review of systems. 1. Rule out schizoaffective disorder, major depressive disorder, and bipolar disorder. 2. Rule out due to substance use or general medical condition. 3. Positive and negative symptoms. a. Positive symptoms: Hallucinations, delusions, dis-organized behavior, paranoia. b. Negative symptoms: Affect flattening, alogia, avo-lition, apathy, anhedonia, abstract thinking loss. Mental State Examination A. General description: Disheveled, agitated, obsessively groomed, silent, or immobile. B. Mood and affect: Reduced emotional responsiveness and/or overly active and inappropriate emotions (extremes of rage, happiness, and anxiety). C. Perceptual disturbances. 1. Auditory hallucinations are most common (voices threating, accusatory, or insulting). 2. Command hallucinations put the patient and others at risk of harm. 3. Visual hallucinations are also common. 4. Tactile, olfactory, and gustatory disturbances are unusual and often associated with an underlying medi-cal/neurological cause. D. Thought. 1. Content: Delusions (persecutory, grandiose, religious, somatic). 2. Belief that outside sources control thoughts or behavior. 3. Process: Way ideas form, including flight of ideas, thought blocking, impaired attention, poverty of thought, poor abstraction, clang associations, thought9. Psychiatric Guidelines
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199 broadcasting (others can hear their thoughts), or thought insertion (people place thoughts into their minds). E. Violence. 1. Delusions may lead to violent behavior. 2. In an acute setting, intramuscular medication may be needed (benzodiazepine such as lorazepam or antipsy-chotic medication). 3. Suicide is common; 20% to 50% of persons with schizophrenia attempt suicide. 4. Homicide is no more likely than in the general popu-lation: Associated with bizarre hallucinations or delusions with predictors of previous violence, dangerous behavior, or hallucinations/delusions with violent content. F. Orientation/memory/cognitive impairment: Usually ori-ented to person, place, and time. Memory and cognition are likely to be impaired. G. Judgment and insight: Poor insight may lead to poor adherence along with poor judgment in the acute phase of illness. H. Reliability: Dependent on the phase of illness. I. Medication protective in suicidal ideation clozapine (Clozaril). Diagnostic Tests A. Broad screening: Complete blood count (CBC), blood glucose, comprehensive metabolic panel, urine drug screen, liver function tests. B. Exclude specific disorders: Thyroid panel, vitamin B12, folate, HIV, RPR (with prevalence of syphilis, this should be part of screening). C. Other tests: EEG, chest x-ray, CT scan/MRI (first episode scan is part of the work up). D. Screening instruments. 1. Brief Psychiatric Rating Scale (BPRS). 2. Scale for Assessment of Negative/Positive Symptoms (SANS / SAPS). 3. Positive and Negative Symptoms Syndrome Scale (PANSS). Differential Diagnosis A. Schizophreniform (less than 6 months of symptoms). B. Schizoaffective disorder. C. Brief psychotic disorder. D. Delusional disorder. E. Bipolar disorder. F. Major depressive disorder. G. Substance-induced disorder. H. Psychotic disorder due to general medical condition (as with all psychiatric disorders, onset of symptoms is more commonly insidious: An abrupt change in mental status is likely related to an organic cause). I. Medical rule outs. 1. Epilepsy. 2. Neoplasm. 3. AIDS. 4. Vitamin B 12deficiency. 5. Heavy metal poisoning. 6. Diabetes mellitus. 7. Cardiovascular disease. 8. Lung disease and cancer (due to high rates of nicotine use in up to 90% of patients—due in part to impairment of nicotine receptors in the brain). Evaluation and Management Plan A. General plan. 1. Risk of neuroleptic malignant syndrome (NMS) on antipsychotic medication. 2. Mnemonic FEVER. a. Fever. b. Encephalopathy. c. Vital sign instability. d. Enzyme elevation and creatinine phosphokinase (CPK). e. Rigidity. 3. Cardinal signs/symptoms of NMS: Acute mental sta-tus changes with fluctuating consciousness, lead pipe rigidity, autonomic instability. 4. Labs: Leukocytosis and increased CPK, aspartate aminotransferase (AST), alanine aminotransferase ( ALT), and myoglobinuria. 5. T reatment: Stop offending agent. Supportive care often in ICU setting. B. Pharmacotherapy treatment of NMS. 1. Bromocriptine: Dopamine agonist used to restore lost dopaminergic tone. 2. Dantrolene: Direct acting skeletal muscle relaxant. 3. Antipsychotic medications. a. Medication class box warning : Increase mortality in elderly patients with dementia-related psychosis. Warning for increased risk of hyperglycemia and dia-betes mellitus. b. Expert guidelines on screening for all persons treated on AA medications: At baseline, assess family and per-sonal history of cardiovascular disease, weight (body mass index [ BMI]), blood pressure, waist circumfer-ence, and fasting lipid/glucose; weight is done every 4 weeks; and blood pressure and fasting labs are com-pleted again in 12 weeks. Glucose and lipid changes can occur in the absence of weight gain. c. Risk of tardive dyskinesia on both atypical and typ-ical antipsychotics exists and assessment of abnor-mal movements using the Abnormal Involuntary Movement Scale (AIMS) is recommended every 6 months. d. Risk of dystonic reactions: Cervical, torticollis, ocu-logyric crisis, blepharospasms, larynogospasm. Acute treatment: Intermuscular benzotropine (Cogentin), diphenhydramine (Benadryl), or IV benzodiazepine. Follow-Up A. Follow-up with a psychiatric specialist: Should not be treated in primary care setting. B. Smoking cessation programs. Consultation/Referral A. Consultation with primary care providers and referral for ongoing medical follow-up given the high prevalence of medical comorbidities. B. Referral to psychosocial intervention/training programs and National Alliance on Mental Illness (NAMI). C. Referral for cooccuring disorders treatment may be neces-sary given the high rates of comorbid substance use disorders. Special/Geriatric Considerations A. More than two-fifths of older adults with schizophrenia show clinical signs of depression and rates of suicide may be higher. Bibliography American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Arlington, VA: American Psychiatric Pub-lishing. Pliszka, S. R. (2016). Neuroscience for the mental health clinician (2nd ed. ). New York, NY: Guilford Press. Schizophrenia
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200 Sadock, B. J., Sadock, V. A., & Ruiz, P. (2015). Kaplan & Sadock's synopsis of psychiatry: Behavioral sciences/clinical psychiatry (11th ed. ). Philadelphia, PA: Wolters Kluwer. Stahl, S. M. (2013). Stahl's essential psychopharmacology: Neuroscientific basis and practical applications (4th ed. ). New York, NY: Cambridge Univer-sity Press. Stahl, S. M. (2014). Stahl's essential psychopharmacology: Prescriber's guide (5th ed. ). New York, NY: Cambridge University Press. Tasman, A., & Mohr, W. (2011). Fundamentals of psychiatry. Hoboken, NJ: Wiley-Blackwell. Substance Use Disorders Dawn Vanderhoef Definition A. Abuse: Maladaptive pattern of use as evidenced by one or more of the following occurring within a 12-month period. 1. Recurrent substance use with failure to fulfill major role obligations. 2. Recurrent use in physically hazardous situations. 3. Recurrent substance-related legal problems. 4. Continued use despite persistent or recurrent social or interpersonal problems. B. Dependence: Maladaptive pattern of use as evidenced by three or more of the following occurring at any time within the same 12-month period. 1. Tolerance. 2. Withdrawal. 3. Substance taken in larger amounts over a longer period of time. 4. Persistent desire/effort to cut down or control use. 5. Increasing time spent obtaining, using, and recovering from use. 6. Important social, occupational, or recreational activi-ties given up. 7. Continued use despite knowledge of adverse effects. 8. With physiological dependence: Evidence of tolerance or withdrawal. 9. Without physiological dependence: No evidence of tolerance or withdrawal. C. Substances of addiction: Alcohol; caffeine; cannabis; hallucinogens; inhalants: opioids; sedatives/hypnotics/anxi-olytics; stimulants; tobacco; other/unknown substances. Incidence A. Alcohol abuse 9. 4% versus dependence 14%. B. Cannabis 8. 5%. C. Opioids 1. 4%. D. Sedatives 1%. E. Amphetamines 2%. F. Cocaine 2. 8%. G. Hallucinogens 1. 7%. Pathogenesis A. Has both a genetic and environmental risk with complex neurobiology. Predisposing Factors A. Age of first use matters: Odds of alcoholism as an adult go down by 14% for each year a youth does not drink after age 14. B. Access. C. Peer groups. Subjective Data A. Common complaints/symptoms. 1. Craving, irrepressible urge to seek and consume drug substance. B. Common/typical scenario. 1. Patients commonly present for either another medical condition or a complication associated with use of the substance. C. Family and social history. 1. Behaviors may be learned or there may be a genetic predisposition to addictive substances. D. Review of systems. 1. Psychological—irritable, anxious, restless. 2. Cardiac—racing heart rate, feeling of palpitations. Mental State Examination A. General. 1. Agitated. 2. Anxious. 3. Irritable. B. Attitude. 1. Describe if patient is friendly, cooperative, hostile, or defensive. C. Mood. 1. General mood of patient. D. Affect. 1. Can be described as expansive, euthymic, constricted, or blunted. E. Speech. 1. Quantity. 2. Rate. 3. Volume. F. Thought process and content. 1. How is the patient thinking? Diagnostic Tests A. Comprehensive metabolic panel (CMP). B. Liver function tests. C. Blood alcohol level. D. Serum drug screen. E. Pregnancy test. F. HIV. G. EKG. H. Screening. 1. Screening, brief intervention, and referral to treat-ment (SBIRT). a. Screening: A healthcare professional assesses for risky substance use behaviors using standardized screening tools such as CAGE. b. Brief intervention: A healthcare professional engages a patient showing risky substance use behav-iors in a short conversation. 2. A standard drink. a. 2 oz of beer/ale/malt liquor. b. 1. 5 oz of spirits such as vodka, tequila, gin, whiskey, or rum. c. 5 oz of wine. 3. Positive screen for at-risk drinking. a. Men: Greater than 14 drinks a week or greater than 4 on occasion. b. Women: Greater than 7 drinks a week or greater than 3 drinks on occasion. c. Elders: Greater than 7 drinks a week or greater than 1 drink on occasion. 9. Psychiatric Guidelines
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201 4. CAGE assessment: One yes is a positive screen and needs further assessment. a. Have you ever felt the need to CUT down on your substance use? b. Have people ANNOYED you by criticizing your substance use? c. Have you ever felt GUILTY about your substance use? d. Have you ever felt the need to drink/use first thing in the morning as an EYE opener? Differential Diagnosis A. Attention deficit hyperactivity disorder (ADHD). B. Bipolar disorder. C. T rauma-related disorders. D. Major depression. E. Anxiety disorders. F. Other substance use disorders. Evaluation and Management Plan A. Motivational interviewing to assess readiness and increase ambivalence. B. T reatment is based on severity, individual motivation taking into account abstinence, or harm reduction. C. Withdrawal. D. Hierarchy of detoxification: Sedative/hypnotics, alcohol, then opioids. E. Assessment of alcohol withdrawal and providing inter-vention: Risk of seizures after 48 hours of last drink and risk of DTs after 72 hours of last drink. F. Alcohol withdrawal assessment: Clinical Institute for Withdrawal Assessment for Alcohol (CIWA-AR) and detox is most commonly attempted with a benzodiazepine. G. Opioid withdrawal assessment: Clinical Opiate With-drawal Scale (COWS) and detox commonly with opiates such as buprenorphine or phenobarbital. H. Alcohol cravings: Naltrexone/Vivitrol, acamprosate, ondansetron, or disulfiram (Antabuse)—need to provide education about products to avoid adverse reactions. I. Opioid replacement: Methadone, buprenorphine (can be prescribed by nurse practitioners [NPs] with additional training), Suboxone. J. Nicotine replacement: NRT options (patch, gum, inhaler), bupropion (Zyban) same as Wellbutrin, varenicline (Chantix) Follow-Up A. Follow-up with a substance use disorder specialist for medications and therapy. Consultation/Referral A. Consultation for medical comorbidities. B. Referral to outpatient support groups such as Alcoholics Anonymous (AA), Narcotics Anonymous (NA), Cocaine Anonymous (CA), Opioids Anonymous (OA). C. Referral to treatment: A healthcare professional provides a referral to brief therapy or for additional services. Special/Geriatric Considerations A. Substance abuse in the elderly is a rapidly growing problem and may be triggered by retirement; death of a close family member, friend, or even pet; financial strains; or men-tal or physical decline. B. Elderly patients may have a decreased ability to metabo-lize drugs or alcohol. Bibliography American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Arlington, VA: American Psychiatric Pub-lishing. Morrison, J. (2014). DSM-5 made easy: The clinician's guide to diagnosis. New York, NY: Guilford Press. Sadock, B. J., Sadock, V. A., & Ruiz, P. (2015). Kaplan & Sadock's synopsis of psychiatry: Behavioral sciences/clinical psychiatry (11th ed. ). Philadelphia, PA: Wolters Kluwer. Substance Abuse and Mental Health Services Administration. (2019). Recovery and recovery support. Retrieved from https://www. samhsa. gov/find-help/recovery Psychiatric Patient Medical Clearance Dawn Vanderhoef Definition A. Guidelines exist, but no clear definition of what “medical clearance” should include. B. Review local institutional guidelines. 1. Purpose: Clearance of a psychiatric patient to transfer to a setting with fewer medical resources. 2. Guideline: Within reasonable medical certainty, there is no contributing medical condition causing the psychi-atric complaints. C. Assessment for risk of violence STAMP—Staring and eye contact, Tone and volume of voice, Anxiety, Mumbling, and Pacing. D. T raining in nonviolent crisis intervention and de-escalation. Subjective Data A. Common complaints/symptoms. 1. Delirium. 2. Confusion. 3. Agitated behavior. B. Common/typical scenario. 1. Patients come to the ED or are brought by family or medical services because of an alteration in disposition. C. Family and social history. 1. Inquire about drug use, or any medications. 2. Inquire about falls. 3. Inquire about family history of mental illness. 4. Biopsychosocial history. a. What led to ED presentation? b. Risk to self/others or inability to care for self due to mental status changes. c. Rule out organic or substance-induced causes. d. Identify needed medical treatments. 5. History. a. History taking will provide guidance as to what medical testing should occur. Collateral data from a family member, caseworker, group home staff, or someone who knows the patient is critical. b. Is this an existing or new psychiatric illness? c. Assessment of mental status for acute (more commonly organic in nature) or insidious (more commonly psychiatric in nature) onset, drug inter-action, or toxicity (new medication/medication change/overtaking medication). d. Relapse of a psychiatric disorder due to nonadher-ence. D. Review of systems. 1. Dermatologic—ask about bruising or breaks in skin. 2. Neurological—ask about dizziness, confusion, or weakness. Psychiatric Patient Medical Clearance
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202 Mental State Examination A. Mental State Examination: Assessment of risk to self, risk to others, or risk of violence (see suicide/homicide risk assess-ment noted previously). B. Quick confusion scale. 1. Five items: What year is it? What month is it? About what time is it? Count backward from 20 to 1. Repeat a phrase. 2. Correlation with Mental State Examination. Diagnostic Tests A. No high yield laboratory tests. B. Consider. 1. Drug screen and blood ethanol level. 2. Anything triggered by return of spontaneous circula-tion (ROSC) to include American Society of Anesthesi-ologists (ASA) or acetaminophen level. 3. Human chorionic gonadotropin (HCG). 4. Basic metabolic panel (BMP). 5. Complete blood count (CBC). 6. Liver function test (LFT). 7. HIV. 8. Rapid plasma reagin (RPR). 9. Unstable angina (UA). Differential Diagnosis A. Fasting glucose/metabolic disorders. B. Meningitis (drop coin to see if patient can look down). C. Substance use (look up nose for substance use). D. Seizure—postictal (assess tongue for lacerations) E. T raumatic brain injury. F. Delirium. G. Drug overdose. H. Syphilis. Evaluation and Management Plan A. Assess capacity: Consent to treatment and competency: Does this patient have a legal guardian (incompetence can only be determined by the court)? B. Involuntary commitment: Know your state laws about the process AND transportation. C. Duty to protect (see earlier) and duty to report (children, older adults, and those without capacity). D. Inpatient/outpatient or referral to community resource. Consultation/Referral A. Psychiatry if available in the hospital or one can use telemedicine. ED protocols for evaluation of psychiatric cases have been developed by the American College of Emergency Physicians. B. Consult case management to help the patient find needed resources for outpatient management. C. Consult social work if drugs are involved or the patient is homeless. Special/Geriatric Considerations A. Geriatric patients are more likely to present with delirium to the ED related to medical conditions. B. Elderly patients with psychiatric disorders are more likely to have multiple psychotic disorders, mood disorders, and dementia and less likely to have schizophrenia or substance disorders. Bibliography American College of Emergency Physicians. (2009). Massachusetts med-ical clearance guidelines. Retrieved from https://www. acep. org/global assets/uploads/uploaded-files/acep/advocacy/state-issues/psychiatric-hold-issues/ma-medical-clearance-guidelines-toxic-screen-ma. pdf American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Arlington, VA: American Psychiatric Pub-lishing. Boudreaux, E. D., Niro, K., Sullivan, A., Rosenbaum, C. D., Allen, M., & Camargo, C. A. (2011). Current practices for mental health follow-up after psychiatric emergency department/psychiatric emergency service visits: A national survey of academic emer-gency departments. General Hospital Psychiatry, 33 (6), 631-633. doi:10. 1016/j. genhosppsych. 2011. 05. 020 New Jersey Hospital Association. (2011). Consensus statement: Medi-cal clearance protocols for acute psychiatric patients referred for inpa-tient admission. Retrieved from http://www. njha. com/media/33107/ Clearance Protocolsfor Acute Psy Patients. pdf Nordstrom, K., Zun, L. S., Wilson, M. P., Stiebel, V., Ng, A. T., Bregman, B.,... Nouri, T. (2012). Medical evaluation and triage of the agitated patient: Consensus statement of the American Asso-ciation for Emergency P sychiatry project BETA medical evaluation workgroup. Western Journal of Emergency Medicine, 13 (1), 3-10. doi:10. 5811/westjem. 2011. 9. 6863 Tang, S., Patel, P., Khubchandani, J., & Grossberg, G. (2014). The psy-chogeriatric patient in the emergency room: Focus on management and disposition. ISRN Psychiatry, 2014, 5. doi:10. 1155/2014/4135729. Psychiatric Guidelines
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203 10 Infection Guidelines Rose Milano Colitis: Infective Jennifer W. Parker Definition A. Inflammation of the colon caused by an infectious agent (i. e., bacteria, virus, or parasites). Colitis is diagnosed when the patient has diarrhea (passage of three or more unformed stools per day and has evidence of inflammation in the colon based on at least one of the following. 1. Positive fecal markers: Elevated leukocytes, positive lactoferrin, or positive calprotectin. 2. Dysentery: Many small volume stools containing obvious blood or mucus (often associated with fever and abdominal pain). 3. Mucosal inflammation as identified by colonoscopy or sigmoidoscopy. B. Duration of symptoms. 1. Acute: 14 days or fewer (most are infectious and self-limiting). 2. Persistent: 14 to 30 days. 3. Chronic: 30 or more days (most are noninfectious). C. Pseudomembranous colitis caused by the bacteria Clostridioides difficile in the acute care setting: Of special concern; to be highlighted in this chapter. Incidence A. The vast majority of colitis is viral; only 1. 5% to 5. 6% of stool cultures produce positive results. B. Severe diarrhea (four or more liquid stools/day for more than 3 days) is generally bacterial. C. In the past 10 years, C. difficile infection (CDI) has been increasing in the United States—not only in the healthcare setting but also in community. Here are the 2011 estimated incidence rates in the United States for CDI, which can no longer be considered just a healthcare-acquired disease. 1. Community-acquired CDI: 51. 9 cases per 100,000. The rate of first recurrence was 13. 5%, and the death rate within 30 days was 1. 3%. 2. Healthcare-acquired CDI: 95. 3 cases per 100,000. The rate of first recurrence was 20. 9%, and a death rate within 30 days was 9. 3%. Pathogenesis A. Diarrhea represents altered changes in the flow of water and electrolytes within an osmotic gradient. Normally the gastrointestinal (GI) tract absorbs about 8 to 9 L of fluid a day, excreting about 200 m L of water in stool. B. Enteric pathogens, acting primarily on transporter cells or the lateral spaces between cells (which are regulated bytight junctions), alter the balance toward significantly greater excretion and less absorption. C. Pathogens can alter absorption by either direct or indirect modulation. 1. Direct modulation involving. a. Epithelial ion transport processes. i. Evidence from the literature proposes that the rapid onset of diarrhea induced via enteropathogenic Escherichia coli (EPEC) may result from direct effects on intestinal epithelial ion transport processes. b. Barrier function. 2. Indirect modulation involving. a. Inflammation. i. Shigella and Salmonella species cause an inflammatory diarrhea characterized by fever and polymorphonucleocytes (PMNs) in the stool. ii. PMNs regulate absorption through cytokine secretion but also have a more direct role through the secretion of a precursor to adenosine, activat-ing certain transmembrane conductance regula-tors. b. Neuropeptides. i. C. difficile and rotavirus infection also work indirectly through modulation of ion transport subsequent to cytokine secretion and activation of enteric nerves via neuropeptides. c. Loss of absorptive surface. i. Giardia lead to the loss of brush border absorptive surface and diffuse shortening of villi. ii. Similarly, EPEC cause effacement of microvilli, which decreases the surface area for nutrient absorption and causes increased osmolar-ity of the intestinal contents and malabsorption. iii. Major causes in the United States. 1)Viruses: Norovirus, rotavirus, aden-oviruses, and astrovirus. 2)Bacteria: Salmonella, Campylobacter, Shigella, enterotoxigenic E. coli, and C. diffi-cile. 3)Protozoa: Cryptosporidium, Giardia, Cyclospora, and Entamoeba. D. CDI (nosocomial and community acquired) account for almost all cases of pseudomembranous colitis (acute colitis characterized by the formation of an adherent inflammatory membrane that overlays injury site). 1. There is multifactorial activation with enterotoxin A and cytotoxin B. In addition, there is a new strain with increased productions of enterotoxin A and cyto-toxin B, as well as binary toxin, with fluoroquinolone resistance. Colitis: Infective
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204 2. Besides the direct effect of the toxins on tight junc-tions, and in contrast to other pathogens, C. difficile leads to activation of neuropeptides, resulting in inflammation via a necroinflammatory reaction, which activates mast cells, nerves, vascular endothelium, and immune cells. Predisposing Factors A. Hospitalization, previous CDI, greater than 65 years of age, recent abdominal surgery, use of proton pump inhibitors (PPI), and living conditions (long-term care facilities). B. International travel: Shigella, Campylobacter, Salmonella, enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), and others. C. Foodborne: Staphylococcus aureus, Bacillus cereus, Clostrid-ioides perfringens, or E. coli. D. Other risk factors. 1. Antibiotic exposure, healthcare exposure. 2. Exposure to C. difficile. 3. HIV or other immune deficiency. 4. Chemotherapy. 5. Enteric tube feeding or other GI tract manipulation. 6. I nflammatory bowel disease (IBD) or other chronic GI disease. Subjective Data A. Common complaints/symptoms. 1. Mild: Watery diarrhea three or more times a day, abdominal cramping. 2. Severe: Watery diarrhea 10 or more times a day with abdominal cramping and pain. May also be associated with fever, dehydration, and rapid heart rate. B. Common/typical scenario. 1. Careful, detailed history of present illness: Important because it can suggest likely cause of the diarrhea. a. Duration—acute, persistent, chronic, or change in periodicity. b. Frequency and characteristics of stool. i. Small bowel origin—watery, large volume, abdominal cramping, bloating, or gas. ii. Large bowel origin—frequent, regular small volume stools, often tenesmus with bowel move-ments, and inflammatory signs (i. e., fever and bloody or mucoid stools) are common. iii. Inflammatory signs suggest enteric viruses (e. g., cytomegalovirus [CMV], adenovirus), invasive bacteria (e. g., Salmonella, Shigella, Campylobacter ), or cytotoxic pathogen such as C. difficile. C. Family and social history. 1. Food exposure—raw or undercooked meat, seafood, unpasteurized dairy products. Timing is important. a. Less than 6 hours with nausea and vomiting, likely S. aureus or B. cereus. b. 8-16 hours—likely C. perfringens. c. Greater than 16 hours—viral or possibly E. coli enterotoxigenic pathogen. 2. Other exposures. a. Animals (e. g., poultry, petting zoos): Salmonella. b. T ravel to resource limited areas (increased risk of pathogens and certain bacteria). c. Occupation—Day-care centers likely for Giardia, Shigella, or Cryptosporidium. d. Recent hospitalizations—increased likelihood of CDI. e. Antibiotic use—increased likelihood of CDI. f. Use of PPI—can increase risk of infectious diar-rhea. D. Review of systems. 1. Neurologic—lightheadedness, dizziness. 2. Dermatologic—dry skin. 3. Genitourinary—frequency of urination and color. 4. Abdominal—diarrhea, nausea, pain anywhere in the abdomen, bloody stools, loss of appetite, bloating, or dis-tension. Physical Examination A. Volume status: Hypovolemia. 1. Dry mucous membranes. 2. Tenting of skin or diminished skin turgor. 3. Change in mental status. 4. Dizziness, lightheadedness, and orthostatic blood pressure. 5. Hypotension. B. Complications: Ileus or peritonitis. 1. Abdominal distention. 2. Abdominal tenderness with percussion or gentle pal-pitation. 3. Rebound tenderness. 4. Abdominal rigidity. Diagnostic Tests A. Blood studies: Often not needed for patients with infec-tious diarrhea but helps determine status of the acutely ill patient. 1. Serum electrolytes if volume depletion is a con-cern: Screening for hypokalemia and acute kidney injury (AKI). 2. Complete blood count (CBC)—may be of limited help. a. Platelet count—concern for hemolytic uremic syndrome. b. Leukocytosis—consistent with CDI. 3. Blood cultures—if high fever is present, or sepsis is a concern. 4. Lactate, CPR, procalcitonin (PCT) level if patient has signs and symptoms of sepsis. B. Stool studies: Often unnecessary if patients have no comorbidities: Infectious colitis generally resolves on its own. However, these tests should be completed for those with severe illness, high-risk comorbidities, or suggestive history. 1. Fecal leukocytes—findings of white blood cell (WBC) count on a test result does notdifferentiate between IBD and infectious colitis. 2. Acute bloody diarrhea: Bacterial colitis. a. and Entamoeba. b. Shiga toxin direct testing: For many strains of Shiga toxin-producing E. coli (STEC). 3. Stool culture. a. Shigella, Salmonella, and Campylobacter are rou-tinely sought. b. If STEC, noncholera Vibrio, or Yersinia is sus-pected, alert the lab to look for these, because spe-cialized techniques are required. 4. Ova and parasites (O&P): For patients with persis-tent diarrhea or who are immunocompromised. Unlike bacterial pathogens, which are shed continuously, O&P are shed intermittently. 5. C. difficile toxin: For patients who currently take or have recently taken antibiotics orhave been hospitalized or recently been in a healthcare facility. 10. Infection Guidelines Cultures for enterohemorrhagic E. coli (EHEC)
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205 C. Imaging (CT): Not usually warranted unless patient is presenting with acute abdomen. D. CDI. 1. Leukocytosis: Can be marked in severe disease (>15,000 cells/ 𝜇L). 2. Volume depletion—elevated creatinine (Cr), blood urea nitrogen (BUN), reduced estimated glomerular fil-tration rate (GFR). 3. Elevated lactate. 4. Predictors of mortality. a. WBC greater than 35,000 cells/ 𝜇L or less than 4,000 cells/ 𝜇L. b. Significant banding ( >10%). c. Immunosuppression. d. Cardiorespiratory failure. 5. Need to differentiate C. difficile colonization from infection. a. Only perform CDI testing on loose stools (unless concern for ileus) when there is a reasonable likeli-hood of CDI. b. Stool studies. i. Culture: Gold standard for identification of C. difficile. 1)Sow times; requires follow-up with toxi-genic testing, because not all strains produce toxins. 2)Usually reserved for epidemiologic stud-ies. ii. Enzyme immunoassay—rapid. 1)Sensitivity of 75% to 94% and specificity of 83% to 98% for identification of toxins A and B. 2)Low sensitivity may require further diag-nostic testing in face of high clinical suspicion and negative test results. iii. Polymerase chain reaction—superior to enzyme immunoassay. 1)Used by most U. S. hospitals. 2)High sensitivity and specificity—single sample is sufficient. 3)Generally 24 to 48 hours turnaround. 4)Does not differentiate colonization from infection. Differential Diagnosis A. IBD (i. e., ulcerative colitis, Crohn's disease). B. Ischemic colitis—vasculitis common in Henoch-Schönlein purpura. C. Immunodeficiency syndromes (e. g., common vari-able immunodeficiency, chronic granulomatous disease, Wiskott-Aldrich syndrome, and immunodysregulation polyendocrinopathy enteropathy X-linked [IPEX] syn-drome). D. Irritable bowel syndrome. E. Celiac disease. Evaluation and Management Plan A. General plan. 1. Supportive care. a. Fluid and electrolyte administration to keep up with losses. i. Oral is preferred hydration. Severe disease may require oral rehydration solution. ii. Monitor electrolytes and repletion as neces-sary. 2. Low fat, low dairy (except yogurt or other fermented dairy items) diets: Preferred; banana, rice, applesauce, and toast (BRAT) diet. 3. Holding of anti-motility therapy (e. g., loperamide, bismuth subsalicylate): Can be harmful with some pathogens; generally all right with inflammatory diarrhea. B. Pharmacotherapy. 1. Antibiotics. 2. Empiric therapy. a. Not widely recommended (despite reducing length of illness) because of promotion of antibiotic resistance, likely changes in gut flora, and increased risk of CDI. b. However, recommended for certain conditions: i. Severe disease: Greater than six stools per day, fever, hypovolemia requiring hospitalization. ii. Bloody or mucoid stools (likely invasive bac-terial infection) unless fever is low or absent. iii. Comorbidities (especially immunocompro-mising and cardiac diseases), including age greater than 70. c. Oral fluoroquinolones for 3 to 5 days: Preferred treatment for empiric therapy for acute diarrhea of unknown source. i. Ciprofloxacin: 500 mg BID. ii. Levofloxacin: 500 mg daily. iii. Fluoroquinolone intolerant patients: Oral azithromycin 500 mg PO daily for 3 days or ery-thromycin 500 mg PO BID for 5 days. 3. History of antibiotic therapy or recent hospitaliza-tions: T reatment for CDI. a. Discontinuation of offending antibiotic (if possi-ble). b. Avoidance of anti-motility medications. c. Enhanced contact precautions: Handwashing before and after patient contact. d. Antibiotic therapy: Best to wait for diagnostic con-firmation if possible; no treatment if positive toxin assay but asymptomatic. i. Mild-moderate. 1)Vancomycin 125 mg PO QID ×10 to 14 days. 2)Fidaxomicin 200 mg BID ×10 days. 3)Metronidazole 500 mg PO TID ×10 to 14 days (not first-line treatment; use only if other options not available. ) Not for use in recurrent CDI infections. ii. Severe (WBC >15,000 cells/ 𝜇L×serum albumin <3 g/d L, and /or Cr ≥1. 5 baseline). 1)Vancomycin 125 mg PO QID ×10 to 14 days. iii. Fulminant or complicated. 1)Vancomycin 125 mg PO QID ×10 to 14 days, plus. 2)Metronidazole 500 mg IV q 6 to 8 hours, plus. 3)Vancomycin via nasogastric tube or rec-tally. iv. Recurrent, antibiotic resistant (but recur-rent is not equivalent to resistant); after initial treatment, recurrence in 15% to 20% of cases generally 5 to 8 days after treatment. It is impor-tant to distinguish a spontaneous recurrence ver-sus antibiotic triggered resistance. 1)Repeat same or alternate antibiotic. Recurrences beyond the second infection Colitis: Infective
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206 should not be treated with metronidazole due to possible neurotoxic effects with prolonged use and decreased effectiveness. 2)Vancomycin pulses and/or tapers for extended duration. 3)Vancomycin for 2 weeks, then rifaximin for 2 weeks (generally not used now that fecal microbiota treatment is available). 4)High dose vancomycin in combination with Saccharomyces boulardii (notin immuno-suppressed patients). 5)Fecal microbiota treatment: Used in cases of multiple recurrent CDI, moderate CDI with no response to standard antibiotic ther-apy for 1 week, or severe or fulminate CDI with no response to treatment in 48 hours; relatively high success rate (nearly 90% for recurrent CDI). It involves fecal enemas, colonoscopy with delivery of fecal material, and nasogastric tube delivery of fecal material. 6)Colectomy. v. Probiotics: Generally, not appropriate for patients being treated for CDI. 4. Probiotics: Should be started within 48 hours of ini-tiation of antibiotic treatment on any patient receiving antibiotics other than for CDI to lower risk of C. diffi-cile. C. Patient/family teaching points. 1. Prevent the spread of C. difficile with aggressive hand-washing. Do not rely on hand sanitizers because they are ineffective in destroying C. difficile spores. 2. Patients need to have a private room. 3. All staff and visitors must wear isolation gowns and gloves while in the room. D. Discharge. 1. Avoid unnecessary antibiotics. 2. Report new or worsening symptoms. 3. Clean surfaces at home with chlorine-based disinfec-tants. 4. Drink fluids to prevent dehydration. Follow-Up A. There is generally no role for repeat laboratory test-ing/testing for a cure with C. difficile. B. Assays may remain positive during recovery. Consultation/Referral A. In severe, unresponsive cases, gastroenterology and/or surgery may need to be consulted. Special/Geriatric Considerations A. Elderly patients are generally characterized as having decreased immune function. B. Short-and long-term hospitalizations have become a crit-ical risk factor in the development of colitis in this popula-tion. C. Mortality rates are also significantly higher in elderly patients. Bibliography Barkley, T. W., Jr., Myers, C. M. (2014). Practice considerations for adult-gerontology acute care nurse practitioners. West Hollywood, CA: Barkley and Associates. Du Pont, H. L. (2012). Approach to the patient with infectious colitis. Current Opinion in Gastroenterology, 28, 39-46. doi:10. 1097/MOG. 0b013e32834d3208Encephalitis Dominick Osipowicz Definition A. Inflammation of the brain parenchyma. B. Viral encephalitis: An acute viral infection of the brain parenchyma, characterized by a moderate elevation of white blood cells in the cerebrospinal fluid (CSF) and focal neuro-logical deficits. These include but are not limited to altered mental status, cognitive impairments, aphasia, hemiparesis, paresthesias, and behavioral changes. C. Bacterial or fungal encephalitis: Rare. D. Paraneoplastic and autoimmune encephalitis: Beyond the scope of this text but should be considered in the setting of known history of or concern for cancer and a sterile CSF analysis. Etiology of disease is related to an inflammation of the brain parenchyma secondary to an antibody attack of the neuronal surface cells and/or synaptic proteins. Incidence A. Despite its rarity in contrast to bacterial meningitis, encephalitis remains a significant health concern associated with a high rate of morbidity and mortality. B. Incidence is related to global distribution patterns of viral infections with the herpes virus and arthropod-borne viruses. Pathogenesis A. Encephalitis is characterized as an inflammation of the brain parenchyma due to infectious, postinfectious, or non-infectious etiology with symptoms of altered mental status, focal neurological deficits, and seizures. B. Viral infection is the most common cause of encephalitis in adults. Herpes simplex virus (HSV) is the leading cause of encephalitis worldwide. C. In addition to HSV, common causes of infectious encephalitis are varicella herpes zoster virus (VZV), cytomegalovirus (CMV), West Nile Virus, influenza, HIV,10. Infection Guidelines Hodges, K., & Ravinder, G. (2010). Infectious diarrhea: Cellular and molecular mechanisms. Gut Microbes, 1 (1), 4-21. doi:10. 4161/gmic. 1. 1. 11036 Kelly, C. P. Lamont, J. T., & Bakken, J. S. (2019, March 1). Clostrid-ioides (formerly clostridium) difficile infection in adults: T reat-ment and prevention. In E. L. Baron (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/clostridioides-formerly-clostridium-difficile-infection-in-adults-treatment-and-prevention Lamont, J. T. (2018, October 25). Clostridioides (formerly clostridium) difificile infection in adults: Clinical manifestations and diagnosis. In E. L. Baron (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/clostridioides-formerly-clostridium-difficile-infection-in-adults-clinical-manifestations-and-diagnosis Liubakka, A., & Vaughn, B. P. (2016). Clostridioides difficile infection and fecal microbiota transplant. Advanced Critical Care, 27 (3), 324-337. doi:10. 4037/aacnacc2016703 Mc Donald, L. C., Gerding, D. N., Johnson, S., Bakken, J. S., Carroll, K. C., Coffin, S. E.,... Wilcox, M. H. (2018). Clinical practice guidelines for Clostridioides difficile in adults and children: 2017 update by the Infec-tious Disease Society for Healthcare Epidemiology of America (SHEA). Clinical Infectious Disease, 66, 987. doi:10. 1093/cid/ciy149 Piccoli, D. A. (2019, January 4). Colitis. In C. Cuffari (Ed. ), Med-scape. Retrieved from http://emedicine. medscape. com/article/927845-overview Shen, N. T. (2017). Timely use of probiotics in hospitalized adults prevents Clostridioides difficile infection: A systematic review with meta-regression analysis. Gastroenterology, 152, 1889-1900. doi: 10. 1053/j. gastro. 2017. 02. 003 Wedro, B. (2016, June 20). Colitis. Retrieved from http://www emedicinehealth. com/colitis/article_em. htm.
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207 mumps, rabies, and measles. Also, more than a dozen species of arthropod-borne viruses are known to cause encephalitis. Predisposing Factors A. Recent viral illness. B. Mosquito bites. C. Tick bites. D. Exposure to pig, bat, duck, and rodent feces. E. Rabid animal bites. F. T ravel to areas with known infective vectors. G. Immunocompromised state. H. Immunosuppressive therapy. I. Organ transplantation. Subjective Data A. Common complaints/symptoms. 1. Presentation varies from mild confusion and inappro-priate behavior to comatose state. 2. Affected patients present with cortical findings as viruses gravitate toward the brain parenchyma. 3. Cortical symptoms include but are not limited to altered mental status, cognitive impairment, aphasias, hemiparesis, paresthesias, and behavioral changes. 4. Meningeal irritation should not be a symptom. How-ever, it may be seen in patients with meningoencephalitis. B. Family and social history. 1. Familial history is often noncontributory. 2. Social history may reveal recent viral illness and travel abroad, particularly to sub-Saharan Africa and exposure to rodents, ticks, and mosquitoes. 3. History of cancer or concern for cancer diagnosis may be a factor. C. Review of systems. 1. General: Fatigue, weakness, fever, or chills. 2. Head, ear, eyes, nose, and throat (HEENT): Headaches. 3. Neurological: Lethargy, syncope, seizures, muscle weakness, altered sensation, altered speech, or disorien-tation. Physical Examination A. Altered mental status: Presence or absence of normal brain function. This is the important distinguishing feature between encephalopathy and meningitis. B. Focal neurological deficits: Including, but not limited to, cognitive impairments, aphasia, hemiparesis, paresthesias, and behavioral changes. C. Seizure activity. D. Nuchal rigidity (unlikely): Including tenderness to palpa-tion and pain with flexion and extension. Diagnostic Tests A. A noncontrast CT of the head: Required. 1. Patients will likely have altered mental status, focal neurological deficits, and new onset seizures, which raise concern for elevated intracranial pressure; this allows for ruling out a space occupying lesion. 2. CT scan of the head with temporal lobe edema that does not follow a vascular pattern is the classic presenta-tion of HSV encephalitis. B. MRI: Shows demyelination, which may be present in other clinical states with similar presentation. C. Lumbar puncture: Gold standard for a diagnosis of viral encephalitis. 1. CSF analysis. a. Cell count/differential, glucose, protein and gram stain, and bacterial culture. b. Abnormal CSF suggestive of viral encephalitis. i. Elevated opening pressure. ii. CSF white blood cell (WBC) count elevated but l ess than 250/ 𝜇L and lymphocyte dominant. iii. present in HSV encephalitis. iv. CSF glucose greater than 60 mg/d L and CSF/serum ratio of greater than 0. 6. v. CSF protein elevated but l ess than 150mg/d L. vi. Culture and polymerase chain reaction (PCR) test for virus. 1)If culture is negative but strong clini-cal and radiological suspicion for HSV/VZV encephalitis remains, repeat lumbar puncture in 3 to 5 days and continue treatment. 2. Contraindications to lumbar puncture. a. Systemic anticoagulation. b. Thrombocytopenia. c. Coagulopathy. d. Open sacral wound at level L3 to L5. e. CT head with evidence of increased intracranial pressure and/or mass lesion. D. EEG: Often abnormal in acute encephalitis. E. Relevant blood work: CBC, basal metabolic profile (BMP), partial thromboplastin time (PTT)/prothrombin time (PT)/international normalized ratio (INR), lactate, and arterial blood gas. F. Blood cultures. Differential Diagnosis A. Viral encephalitis. B. Bacterial meningitis. C. Epidural abscess. D. Nonconvulsive status epilepticus. E. Subarachnoid hemorrhage. Evaluation and Management Plan A. General plan: Viral encephalitis. 1. Rule out bacterial meningitis due to high risk of mor-bidity and mortality. 2. Patient presentation suggestive of c entral nervous system (CNS) infection. 3. Follow SEPSIS 3. 0 guidelines for fluid resuscitation management of septic shock. 4. Begin broad-spectrum antibiotics as well as antiviral therapy and glucocorticoids if appropriate. 5. Obtain a “Stat” CT head without contrast to rule out alternative diagnoses. 6. Use lumbar puncture with CSF analysis for definitive treatment, and if available meningitis/encephalitis PCR for rapid identification of causative pathogen. 7. Arrange for hemodynamic management and sup-portive care. 8. Admit to ICU for appropriate level of care. 9. Consider MRI of the brain in patients who fail to improve despite treatment to evaluate alternative diag-noses. 10. Consider EEG brain for patients with fluctuating neurological examination or a suppressed level of con-sciousness. B. Patient/family teaching points. 1. Worsening neurological examination may lead to acute respiratory failure requiring intubation and mechanical ventilation. Encephalitis CSF red blood cells (RBC) count may be
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208 2. Seizures may require treatment with anti-epileptics and in severe cases intubation and mechanical ventilation for treatment with potent sedatives. 3. Evidence of cerebral edema on head CT may prompt aggressive medical management with mannitol and hypertonic saline, including surgical decompression. 4. Evidence of hydrocephalus on head CT may prompt neurosurgical evaluation and intervention. 5. Long-term neurological sequelae are likely with encephalitis. C. Pharmacotherapy. 1. Definitive diagnosis of encephalitis: Based on CSF analysis and culture data. 2. HSV/VZV encephalitis: Acyclovir 10 mg/kg IV q8 hours for a duration of 21 days. a. Kidney function should be assessed because acy-clovir is nephrotoxic. 3. CMV encephalitis: Ganciclovir 5 mg/kg IV q12 hours +Foscarnet 60 mg/kg q8 hours until symptoms improve. 4. HIV encephalitis. a. Highly Active Antiretroviral Therapy (HAART): Resume or initiate. b. Patient-specific treatment plan: Refer to infectious disease guidelines for treatment of HIV/AIDS. 5. De-escalation of antimicrobial therapy based on negative cultures or preferably definitive meningitis/ encephalitis PCR test. 6. Patients presenting with seizure activity: Prompt initiation of antiepileptics and discontinuation of med-ications known to reduce seizure potential. D. Discharge instructions. 1. Patients should be instructed to seek emergency care if they experience signs and symptoms of fever, headache, neck pain, confusion, and muscle weakness. Follow-Up A. Patients with neurological sequelae on discharge are to obtain follow-up with a neurologist. Consultation/Referral A. Consider infectious disease consult for atypical pathogens or patients who do not respond to traditional therapy. B. Consult neurology for patients with neurological sequelae. Special/Geriatric Considerations A. Viral encephalitis in elderly patients may often present with mild confusion, lethargy, and nonspecific neurological findings. The provider must be vigilant to recognize patients at high risk for CNS infection and promptly initiate treat-ment. Bibliography Dalmau, J., & Rosenfeld, M. R. (2018, December 10). Paraneoplastic and autoimmune encephalitis. In A. F. Eichler (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/paraneoplastic-and-autoimmune-encephalitis Gaieski, D. F., Nathan, B. R., & O'Brien, N. F. (2015). Emergency neuro-logical life support: Meningitis and encephalitis. New York, NY: Springer Science +Business Media. Gluckman, S. J. (2017, October 15). Viral encephalitis in adults. In J. Mitty (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/ contents/viral-encephalitis-in-adults Wijdicks, E. F. M., & Rabinstein, A. A. (2012). Neurocritical care. (pp. 27-43). New York, NY: Oxford University Press. Endocarditis: Infective Robin Miller Definition A. An infection involving the cardiac valves (native or pros-thetic), mural endocardium, or intracardiac devices. B. Termed a vegetation. C. Acute endocarditis. 1. Rapid damage to cardiac structures with extracardiac seeding; fulminant illness can develop in days to 2 weeks. 2. If untreated, can lead to death within weeks. D. Subacute endocarditis. 1. Indolent course. 2. Slow and progressive damage to cardiac structures. 3. Gradually progressive unless associated with embolic event or ruptured mycotic aneurysm. E. Short incubation period ( <6 weeks) and long incubation period ( >6 weeks) are preferred classifications. F. Heart side used for classification. 1. Right sided—generally from intravenous (IV) drug use. 2. Left sided—more common in IV drug use and non-drug users. Incidence A. Uncommon; 3 to 7 per 100,000 person-years. B. Life-threatening infection; third to fourth most common after fatal infective (IE) process after sepsis, pneumonia, and intra-abdominal abscess. C. 5% to 15% of affected patients have negative blood cul-tures. Pathogenesis A. Endothelial injury allows either direct infection or the development of a platelet and fibrin thrombus that serves as a site of bacterial attachment. B. Primary portals of entry include: 1. Oral cavity. 2. Skin. 3. Upper respiratory tract. 4. Sites of focal infection. C. Microorganisms adhere to endothelium, which is often abnormal or damaged. Platelets aggregate at the site. D. If the organism is resistant to normal bactericidal activity of serum and microbicidal peptides released by platelets, pro-liferation will occur with formation of microcolonies. Platelet deposition is induced. E. Tissue factor is elicited from the endothelium and causes a localized procoagulant state. F. Fibrin deposition occurs. This together with platelet aggregation and microorganism proliferation all generate a vegetation. 1. Organisms deep within vegetation are metabolically inactive and resistant to antimicrobials. 2. Surface microorganisms are shed into the bloodstream continuously. G. Clinical manifestations of IE are a result of cytokine release. H. Microorganisms associated with IE are dependent on classification (see Table 10. 1). Predisposing Factors A. IV drug use predominantly. B. Advanced age. 10. Infection Guidelines
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209 TABLE 10. 1 Classification of Microorganisms Associated With Infective Endocarditis Native Valve Endocarditis Prosthetic Valve Endocarditis. Time of Onset Related to Salve surgery in Months Implantable Cardiac Device Intravenous Drug Use Hospital-acquired Community-acquired<2 2-12 >12 Organism Staphylococcus aureus. Enterococci. Streptococci Streptococci. S. aureus. Entero-cocci Coagulase-negative Staphylo-cocci. Staphylo-coccus aureus. Coagulase-negative Staphylo-cocci. Staphylo-coccus aureus. Enterococci Streptococci. Staphylo-coccus aureus. Enterococci. Coagulase-negative Staphylococci Staphylococcus aureus. Coagulase-negative staphylo-cocci Staphylococcus aureus. Strepto-cocci. Source:Brusch,J. L. (2007). Infectiveendocarditisanditsmimicsinthecriticalcareunit. In B. A. Cunha(Ed. ), Infectious diseases in critical care (2nded., pp. 261-262). New York,NY:Informa Healthcare;Thuny,F.,Grisoli, D., Collart, F.,Habib, G., & Raoult, D. (2012). Management of infective endocarditis: Challenges and perspectives. Lancet, 379 (9819), 965-975 doi:10. 1016/S0140-6736(11)60755-1 C. Degenerative valve disease. D. Prosthetic valves or other cardiac devices. E. Chronic rheumatic heart disease (especially in developing countries). F. Impaired immune system. G. Hemodialysis. H. Unrepaired cyanotic congenital heart defect. Subjective Data A. Common complaints/symptoms. 1. Flu-like symptoms, including fever and chills. 2. Night sweats. 3. Anorexia and weight loss. 4. Chest pain with breathing. 5. Shortness of breath. B. Common/typical scenario. 1. Depends on the type of IE, location, and patient risk factors. 2. Fever: Common in most types of IE. 3. Physical examination findings: Can vary based on location of lesion. 4. Need to identify if there has been a recent surgery or illness. C. Family and social history. 1. IV drug use. D. Review of systems. 1. General: Malaise, chills, or sweats. 2. Cardiovascular: Recent surgery, dyspnea, or chest pain or pressure. 3. Respiratory: Dyspnea or cough. 4. Skin: Discoloration of fingers and toes, pain in fingers and toes, or cutaneous lesions. 5. Musculoskeletal: Generalized musculoskeletal pain. 6. Neurological: Vision changes or headache. 7. With arterial emboli, review of systems (ROS) can include: a. Flank pain. b. Hematuria. c. Abdominal pain. Physical Examination A. Cardiac manifestations. 1. New regurgitant cardiac murmurs (85% of cases): Indicates valve involvement. 2. S3 heart sound (with heart failure). B. Noncardiac manifestations. 1. Janeway lesions: Red spots on palms of hands or soles of feet. 2. Osler's nodes: Red tender spots under the skin of fin-gers or toes. 3. Subungual hemorrhage. 4. Discoloration of skin, distal phalanges, or extremities (especially with arterial occlusion from emboli). 5. Conjunctival hemorrhage. 6. Petechiae. Diagnostic Tests A. Blood cultures. 1. Three sets of blood cultures. 2. Peripheral venipuncture, different sites. 3. First and third sets drawn at least 1 hour apart. B. Other cultures. 1. Serologic testing for organisms difficult to identify by blood culture alone (i. e., Bartonella, Legionella ). 2. At time of surgery, detection of pathogens from valve tissue by polymerase chain reaction (PCR) is validated. C. Other tests. 1. Complete blood count (CBC) with differential. 2. Complete metabolic panel. 3. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), procalcitonin (PCT). 4. Chest radiograph. 5. EKG. a. With abscess formation, progressive heart block can occur. D. Echocardiogram. 1. T ransthoracic echocardiogram (TTE) in all suspected cases l ess than 12 hours after initial evaluation. 2. T ransesophageal echocardiogram (TEE) in the follow-ing circumstances. a. Inability to assess valve adequately in TTE. b. Suspected IE but negative TTE. c. High likelihood for IE: TEE first. d. For recurrent IE. e. If vegetation is noted. f. Clinical suspicion for 3 to 5 days after initial TEE. E. Other imaging modalities. 1. Coronary CT angiography (chest CT angiography [CTA] coronary). a. In those undergoing surgery for IE. b. Preoperative screening: Evaluation for central ner-vous system (CNS) and intra-abdominal lesions. Endocarditis: Infective
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210 c. Limitations. i. Radiation exposure. ii. Nephrotoxicity associated with contrast dye. iii. Lack of sensitivity to evaluate valve lesions. 2. MRI. a. Tool to detect cerebral embolic events (typically silent) and evaluate for mycotic aneurysms. b. Not routinely used. F. Modified Duke criteria for diagnosis. 1. Based on clinical, laboratory, and echocardiographic findings. a. Definite IE. i. T wo major criteria or ii. One major criterion and three minor criteria or iii. Five minor criteria. b. Possible IE. i. One major criterion and one minor criterion or. ii. Three minor criteria. c. Rejected. i. Firm alterative diagnosis. ii. Resolution of IE syndrome with antibiotic therapy l ess than 4 days. iii. No pathological evidence of IE at surgery/ autopsy with antibiotics l ess than 4 days. iv. Does not meet the previous criteria. 2. Major criteria. a. Positive blood culture. i. Typical microorganisms identified on two sep-arate blood cultures. 1)Viridans streptococci, Streptococcus bovis, HACEK group (fastidious gram-negative coccobacillary organisms. HACEK stands for Haemophilus species, Aggregatibac-terspecies, Cardiobacterium hominis, Eikenella corrodens, and Kingella species), Staphylococcus aureus. 2)Community-acquired enterococci in the absence of a primary focus. ii. Persistently positive blood culture, consistent with IE. 1)At least two positive cultures of blood samples drawn greater than 12 hours apart or all of three cultures or, 2)A majority of four or more separate cul-tures of blood (with first and last sample drawn at least 1 hour apart). iii. Single positive blood culture for Coxiella bur-netii or anti-phase 1 Ig G antibody titer of 1:800 or more. iv. Evidence of endocardial involvement: Echocardiogram positive for IE. 1)Oscillating intracardiac mass on valve or supporting structures, in the path of regur-gitant jets, or on implanted material in the absence of an alternative anatomic explana-tion. 2)Abscess. 3)New partial dehiscence of prosthetic valve or new valvular regurgitation (worsening or changing or preexisting murmur not suffi-cient). 3. Minor criteria. a. Predisposing factors, or IV drug use. b. Fever: Temperature greater than 38∘C. c. Vascular phenomena: Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranialhemorrhage, conjunctival hemorrhages, and Janeway lesions. d. Immunological phenomena: Glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor. e. Microbiological evidence: Positive blood culture but does not meet a major criterion as previously noted or serological evidence of active infection with organism consistent with IE. Differential Diagnosis A. Bacteremia from other focal infection. B. Heart failure. C. Valve dysfunction not associated with IE (e. g., cord rup-ture). D. Peripheral arterial disease. E. Pulmonary embolism. F. Heart block related to conduction disease. G. Mesenteric ischemia. H. Chronic obstructive pulmonary disease (COPD). I. Leukemia. Evaluation and Management Plan A. General plan. 1. Empiric antimicrobial coverage (see Pharmacother-apy) is warranted if acute IE is suspected. 2. Blood cultures need to be repeated every 24 to 48 hours until negative. 3. Surgical intervention needs to be considered, espe-cially in the patients indicated here. Definitive treatment may not be possible without valve replacement and/or removal of implantable cardiac devices. a. Indications for surgical intervention. i. Moderate to severe refractory heart failure due to valve regurgitation. ii. Partially dehisced and unstable prosthetic valve. iii. Persistent bacteremia despite optimal antimi-crobial therapy. iv. S. aureus prosthetic valve IE with intracardiac complications. v. Prosthetic valve endocarditis relapse despite optimal antimicrobial therapy. vi. Ruptured abscess. vii. Valve obstruction by vegetation. b. Considerations for surgical intervention. i. Perivalvular abscess with or without progres-sive conduction delays. ii. Large ( >10 mm) hypermobile vegetation noted on TTE (known increased risk of embolic events); recommendation increases strength with associated prior embolic events or valvular regur-gitation. iii. Persistent unexplained fever ( >10 days) in culture-negative valve endocarditis. iv. Poorly responsive or relapsed endocarditis associated with highly resistant microorganisms, such as enterococci or S. aureus. B. Patient/family teaching points. 1. Discussion about potential complications and pro-gression of disease. 2. Early therapy warranted; will need adherence to antimicrobial therapy to prevent resistant organisms. 3. Surgical options need to be discussed, especially as they relate to possible removal of implantable cardiac devices. 4. Education regarding need for central line and long-term IV antibiotics, likely at home; or skilled nursing facility (SNF) if IV drug use is a concern. 10. Infection Guidelines
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211 5. Education around abstinence from IV drugs, if indicated. C. Pharmacotherapy. 1. Primary goal: To eradicate infection by sterilizing veg-etations. 2. Prolonged IV antimicrobial therapy: Required. 3. Empiric antimicrobial therapy: To be initiated when IE is suspected, after initial blood cultures have been drawn. 4. Typical length of parenteral therapy: 4 to 6 weeks. 5. For patients who undergo surgery, intraoperative tis-sue cultures should be obtained, with antimicrobial cov-erage narrowed to identified organisms. 6. For IE associated with implantable cardiac device, antimicrobial therapy is instituted but considered adjunct to device removal (if possible). 7. For common antimicrobial coverage based on the identified microorganism (see Table 10. 2). D. Discharge instructions. 1. Instructions about IV antibiotics and central line care, if indicated, should be provided. Follow-Up A. Follow-up depends on what therapy is initiated and needed interventions. 1. A visit with the patient's primary care physician should occur within 3 weeks of discharge. 2. If surgical intervention was required, a visit with the surgical team should occur within 1 to 2 weeks of dis-charge. 3. Depending on the length of antimicrobial therapy and patient factors, a visit with an infectious disease provider should occur within 1 week of planned antimicrobial dis-continuation. Consultation/Referral A. An infectious disease consult should be obtained to deter-mine appropriate antimicrobial therapy as well as needed duration and follow-up. B. A cardiac surgery consult may be warranted when surgical indications are present. C. If indicated, a substance abuse/addiction team consult may be needed. TABLE 10. 2 Antimicrobial Coverage in Infectious Endocarditis Based on Causal Microorganism Organism Antibiotic Duration Notes Streptococcus Penicillin G 12-24 million U/24 hr (continuouslyorin4-6divideddoses)IV orceftriaxone 2 g/24 hr IV or vancomycin 30 mg/kg per 24 hr IV in 2 divided doses plusgentamicin 3 mg/kg per 24 hr IV (if prostheticvalve) for first 2 weeks4-6weeks Forrelativepenicillin resistance,use higherdose of penicillin G. Vancomycinshould be used in patientswho cannot tolerate penicillin. If microorganismis susceptibleto ceftriaxone, use as first-lineagent. Staphylococcus (mostcommon is Staphylococcus aureus ) Methicillin-susceptible S. aureus (MSSA) of native valve (no foreign devices)Nafcillin,oxacillin 12 g/24 hr IV in 4-6 equally divided doses ORcefazolin 6 g/24 hr IV in 3 divided doses OR vancomycin 30 mg/kg per 24 hr IV in 2 divided doses ORdaptomycin >8 mg/kg/dose IV6weeks Usepenicilliniforganismissensitive; dosingbased on sensitivity and renalfunction; check creatinine kinase Methicillin-resistant S. aureus(MRSA)of native valve (no foreign devices)Vancomycin30 mg/kg per 24 hr IV in 2 divided doses6weeks MSSAof prosthetic valve Nafcillin,oxacillin 12 g/24 hr IV in 6 equally divided doses PLUSgentamicin 3 mg/kg per 24/h IV in 2-3 divided doses (2 weeks) PLUSrifampin 900 mg/24hr PO in 3 divided doses6-8weeks Usegentamicin for 2-week period to determinesusceptibility prior to addingrifampin MRSAof prosthetic valve Vancomycin30 mg/kg per 24 hr IV in 2 divided doses PLUSgentamicin 3 mg/kg per 24/hr IV in 2-3 divided doses (2 weeks) PLUSrifampin 900 mg/24 hr PO in 3 divided doses6-8weeks Usegentamicin for 2-week period to determinesusceptibility prior to addingrifampin Enterococcus Penicillin G 18-30 million U/24 hr IV continuously or in 6 divided doses PLUSgentamicin 3 mg/kg (ideal body weight) per 24/hr IV in 2-3 divided doses4-6weeks Ampicillin2 g IV every 4 hr PLUS gentamicin 3 mg/kg (IBW) per 24/hr IV in 2-3 divided doses4-6weeks (continued ) Endocarditis: Infective
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212 (continued ) TABLE 10. 2 Antimicrobial Coverage in Infectious Endocarditis Based on Causal Microorganism Organism Antibiotic Duration Notes Vancomycin30 mg/kg per 24 hr IV in 2 divided doses. PLUSgentamicin 3 mg/kg (IBW) per 24/hr IV in 2-3 divided doses4-6weeks Forpenicillin allergicpatients Ampicillin2 g IV every 4 hr PLUS ceftriaxone 2 g IV every 12 h6weeks For Enterococcus faecalis strains withhigh level of resistance (ampicillin +gentamicinpreferable) IV,intravenous; MRSA, Methicillin-resistant S. aureus ;MSSA, Methicillin-susceptible S. aureus. D. For those with persistent bacteremia without surgical options, it is appropriate to consider a palliative care consul-tation. Special/Geriatric Considerations A. Prophylaxis should be targeted at the viridans group of streptococci. B. Antibiotic prophylaxis should be considered for patients with the following conditions. 1. Prosthetic cardiac valve or prosthetic material used for cardiac valve repair. 2. Previous IE. 3. Congenital heart disease (CHD). 4. Unrepaired cyanotic CHD including palliative shunts and conduits. 5. Repaired congenital heart defect with prosthetic mate-rial or device within past 6 months. 6. Repaired CHD with residual defects at site or adjacent to site of a prosthetic patch or device. 7. Cardiac transplantation recipients with cardiac valvu-lopathy. C. Prophylactic antimicrobials should be considered when patients with the conditions listed in B undergo the following procedures. 1. Dental procedures that involve manipulation of gin-gival tissue or the periapical region of the teeth or perfo-ration of the oral mucosa. 2. Invasive procedures of the respiratory tract that involve incision or biopsy of the respiratory mucosa, such as tonsillectomy and adenoidectomy. 3. Elective cystoscopy or other urinary tract manipula-tion in those with an enterococcal urinary tract infection or colonization. D. General treatment principle: Single dose administered prior to procedure (if not administered before, must be given within 2 hours of procedure). E. Pharmacotherapy. 1. Standard oral regimen: Amoxicillin 2 g PO, 30 to 60 minutes prior to procedure. 2. If unable to take oral therapy: Ampicillin 2 g IV, 30 to 60 minutes prior to procedure. 3. Penicillin allergy: Cephalexin 2 g PO OR clin-damycin 600 mg PO OR azithromycin 500 mg PO, 30-60 minutes prior to procedure. Bibliography Brusch, J. L. (2007). Infective endocarditis and its mimics in the critical care unit. In B. A. Cunha (Ed. ), Infectious diseases in critical care (2nd ed., pp. 261-262). New York, NY: Informa Healthcare. Cahill, T. J., Baddour, L. M., Habib, G., Hoen, B., Salaun, E., Pettersson, G. B.,... Prendergast, B. D. (2017, January). Challenges in infectiveendocarditis. Journal of the American College Cardiology, 69 (3), 325-344. doi:10. 1016/j. jacc. 2016. 10. 066 Karchmer, A. W. (2005). Infective endocarditis. In R. O. Bonow, D. L. Mann, D. P. Zipes, & P. Libby (Eds. ), Braunwald's heart disease: A text-book of cardiovascular medicine (7th ed., pp. 1633-1658). Philadelphia, PA: WB Saunders. Slipczuk, L., Codolosa, J. N., Davila, C. D., Romero-Corral, A., Yun, J., Pressman, G. S., & Figueredo, V. M. (2013). Infective endocarditis epidemiology over five decades: A systematic review. PLOS ONE, 8 (12), e82665. doi:10. 1371/journal. pone. 0082665 Thuny, F., Grisoli, D., Collart, F., Habib, G., & Raoult, D. (2012, March 10). Management of infective endocarditis: Challenges and perspectives. Lancet, 379 (9819), 965-975. doi:10. 1016/S0140-6736(11)60755-1 Influenza David Bergamo Definition A. An acute respiratory illness caused by the influenza virus, an orthomyxovirus. Incidence A. 3 to 5 million severe cases and 250,000 to 500,000 deaths annually worldwide. B. Annually, since 2010, in the United States. 1. Between 9. 2 and 35. 6 million related illnesses. 2. Hospitalization rate between 140,000 and 710,000. 3. Death rates range between 12,000 and 56,000. Pathogenesis A. A single-stranded RNA virus attaches to the epithelial cells in the respiratory tract and replicates inside of them. Ongoing destruction and eradications of these cells occurs. B. Infectious particles are released through “budding,” caus-ing rapid invasion of neighboring cells and a cyclical process. Predisposing Factors A. All individuals are at risk. Influenza vaccination can decrease risk. However, this decrease changes annually, pend-ing vaccination efficacy. B. Those at higher risk for complications include children younger than 5 years of age, adults older than 65 years old, pregnant women, long-term care facility residents, Alaskan Natives, and American Indians. C. Other high risk groups include patients with underlying neurological, cardiac, or pulmonary conditions; immunosup-pressed individuals (with conditions such as hypogamma-globulinemia, HIV, or cancer); obese patients; and those with other significant comorbid conditions. 10. Infection Guidelines
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213 Subjective Data A. Common complaints/symptoms. 1. Fever. 2. Diffuse myalgias. 3. Fatigue. 4. Cough and respiratory symptoms, including rhinor-rhea and sore throat. 5. Headache. B. Common/typical scenario. 1. Symptoms: Abrupt in onset; some patients may remember exact time. 2. Abrupt onset of fever with myalgia and respiratory symptoms during influenza season (late fall to early spring): High likelihood for influenza. C. Family and social history. 1. Positive comorbid conditions or hereditary immun-odeficiencies. 2. Recent exposure to individuals with symptoms of influenza: Symptoms generally appear 2 days after expo-sure (airborne, touching contaminated surfaces). 3. Crowded environments. D. Review of systems. 1. Neuro: Anorexia, dizziness, or weakness. 2. Gastrointestinal (GI) symptoms: Uncommon in adults. 3. Respiratory: Nonproductive cough (productive cough is more common in pneumonia). 4. HEENT: Runny nose, sore throat. Physical Examination A. Relatively benign, with nonspecific findings. B. Constitutional: Ill appearing, fatigued appearing. C. Fever: Usually 100∘F-104∘F; rarely much higher other than in complicated cases. D. Possible hyperemia or cervical lymphadenopathy (more common in younger patients). E. Mild tachycardia from hypoxia, dehydration, and fever. F. Pharyngitis. G. Conjunctivitis. H. Pulmonary findings: Possibly dry cough, focal wheezing, or rhonchi. I. Skin: May appear flushed, warm to hot, with diaphoresis depending on the core body temperature. Diagnostic Tests A. Clinical diagnosis in patients with influenza symptoms during influenza season or during outbreaks. The combi-nation of fever with cough, sore throat, and myalgia can improve diagnostic accuracy. In periods of outbreak, patients with combinations of any of these symptoms may be reason-ably treated with neuraminidase inhibitors without testing. B. Rapid influenza tests. 1. P olymerase chain reaction (PCR): Most sensitive and specific and can differentiate subtypes. 2. Rapid antigen tests: Result obtained in 15 minutes; less sensitive. 3. Gold standard: Viral culture; may take 72 hours to obtain results. Differential Diagnosis A. HIV. B. Pneumonia. C. Cytomegalovirus (CMV). D. Legionnaires' disease. E. Hantavirus pulmonary disease. F. Acute respiratory distress syndrome (ARDS). G. Other viral upper respiratory infections (URIs). H. Tick-and mosquito-borne illnesses. 1. However, these tend to present in different seasons or patients have exposure history or travel history. Evaluation and Management Plan A. General plan. 1. Usually self-limited; duration can be shortened with the use of neuraminidase inhibitors. 2. Airborne isolation. 3. Supportive care. B. Patient/family teaching points. 1. Handwashing is key to help prevent spread. 2. Annual influenza vaccines for all those who can receive them (most individuals). C. Pharmacotherapy. 1. Neuraminidase inhibitors. a. Oseltamivir (Tamiflu). i. Most commonly used agent; can cause nausea and vomiting. ii. T reatment: 75 mg BID for 5 days, starting within 48 hours of symptom onset. iii. Prophylaxis: 75 mg daily for 10 days within 48 hours of contact with infected person. b. Zanamivir (Relenza). i. Inhaled agent that should not be used in patients with pulmonary disease. ii. Should be avoided in lactose intolerant patients (powder mixture contains lactose/milk proteins). c. Peramivir (Rapivab). i. Intravenous formulation for those who cannot use oral route. ii. T reatment: 600 mg IV 1 dose. d. Laninamivir. i. Still under development: Nasal spray. e. All neuraminidase inhibitors: Can cause neu-ropsychiatric effects based on their mechanism of action. Less commonly, they may cause skin reactions, including erythema multiforme or Stevens-Johnson syndrome. f. Adamantane antivirals (amantadine and rimanta-dine). i. Target M2 protein of influenza A and there-fore not active against influenza B; little to no activity against current influenza A strains. ii. Amantadine and rimantadine not currently recommended for treatment of influenza A, due to high levels of resistance among many circulat-ing strains of influenza. iii. Amantadine and rimantadine are safe in chil-dren older than 1 year of age. g. Ribavirin. i. Nucleoside analog active against influenza A and B. ii. Not Food and Drug Administration (FDA) approved; rarely used except with consulta-tion of infectious disease specialists via inhaled route. h. Baloxavir marboxil. i. FDA approved. ii. Influenza treatment 40 to less than 80 kg: 40 mg as a single dose within 48 hours of onset of influenza symptoms. iii. 80 kg: 80 mg as a single dose within 48 hours of onset of influenza. Influenza
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214 Follow-Up A. Follow-up other than regular visits with primary care physician is usually not required. Consultation/Referral A. If hospitalized, consider consultation with infectious dis-ease and pulmonary specialists. B. If illness is significant, a critical care specialist may be required. C. In general, influenza tends to be an outpatient illness cared for by primary care and urgent care providers. Special/Geriatric Considerations A. Annual influenza vaccination is indicated in all patients who are at least 6 months of age except : 1. Patients who have had a severe allergic reaction to prior influenza vaccine (this does not include minor flu-like symptoms). 2. Those with a severe allergic reaction to egg proteins if receiving the live attenuated vaccine (nasal). B. Immunocompromised patients, pregnant women, and patients 50 years of age or older should notreceive live atten-uated vaccine. C. Adults under the age of 65 with no significant comorbidi-ties generally have self-limiting disease. D. Children younger than 5 years of age, but especially under 2 years, are at higher risk of influenza complications. E. Patients older than 65 years have an increased risk of developing complications. Bibliography Centers for Disease Control and Prevention. (2016). National and state healthcare associated infections progress report. Retrieved from http://www. cdc. gov/HAI/pdfs/progress-report/hai-progress-report. pdf Centers for Disease Contro and Prevention. (2019, February 19). Disease burden of influenza. Retrieved from https://www. cdc. gov/flu/about/ disease/burden. htm Longo, D., Fauci, A., Kasper, D., Hauser, S., Jameson, J., & Loscalzo, J. (Eds. ). (2015). Harrison's principles of internal medicine (19th ed. ). New York, NY: Mc Graw Hill. Meningitis Dominick Osipowicz Definition A. Inflammation of the meninges, the three membranes sur-rounding the brain and spinal cord. B. Types of meningitis. 1. Bacterial meningitis: Acute infection of the meninges and cerebrospinal fluid (CSF), characterized by an ele-vated number of white blood cells and positive bacte-rial cultures in the CSF. This type of meningitis has the highest rate of morbidity and mortality of all forms of disease. 2. Viral meningitis: Acute viral infection of the meninges and CSF, characterized by a moderate elevation of white blood cells in the CSF with negative bacterial cultures. Often referred to as aseptic meningitis due to lack of growth in CSF cultures, it is often self-limiting without treatment. 3. Fungal meningitis: Acute fungal infection of the meninges and CSF, characterized by a moderate elevation of white blood cells in the CSF, generally with negative bacterial cultures but positive for antibodies offungal organisms. Like bacterial meningitis, it is associ-ated with significant morbidity and mortality. 4. Drug-induced meningitis (rare): Acute inflammation of the meninges, characterized by a moderate eleva-tion of white blood cells in the CSF with negative blood cultures and history of using nonsteroidal anti-inflammatory drugs (NSAIDs), certain antibiotics, intra-venous immune globulin, and antiepileptic drugs. Incidence A. In 2015, there were 8. 7 million cases of meningitis world-wide. B. More than one million cases of bacterial meningitis occur every year, worldwide. C. Meningitis is one of the top 10 causes of death from infec-tion. Fatalities from meningitis are in excess of 100,000 every year. D. Like bacterial meningitis, fungal meningitis is associated with a significant morbidity and mortality. Pathogenesis A. Many pathogens responsible for meningitis, including bacteria, possess surface components that enhance mucosal colonization. 1. After bacterial colonization, invasion across the epithelium occurs by intra-or inter-cellular pathways, often mediated by specific adhesions of the bacterial sur-face. 2. Following invasion, bacteria survive normal immuno-logical forces via evasion of the complement system, often due to polysaccharide capsules, and then cross the blood-brain barrier. Complement activation may occur in the CSF, often causing meningeal tissue damage. In the CSF, bacteria can multiply to high concentrations due to the low humoral immunity activity in CSF. The clinical disease process is due to the interaction of the host inflam-matory response and bacterial components once the bac-teria enter the CSF. 3. Once inflammation is present, a series of injuries to the blood-brain barrier epithelium lead to vasogenic brain edema, loss of cerebrovascular regulation, and increased intracranial pressure (ICP), ultimately leading to motor, sensory, or cognitive deficits. B. Bacterial meningitis: Characterized as a rapidly progress-ing systemic bacterial illness presenting with fever, headache, and neck stiffness. C. Cortical brain function: Generally remains intact as brain parenchyma is spared. D. Types of meningitis and associated causal pathogens. 1. Bacterial meningitis. a. Misdiagnosed, undiagnosed, or untreated bacte-rial meningitis: Associated with a high rate of mor-bidity and nearly 100% mortality. b. Most common bacterial pathogens: Streptococcus pneumoniae, Listeria monocytogenes, Neisseria meningi-tis, Haemophilus influenzae, and Staphylococcus aureus. i. Adults: Most common pathogen is S. pneumo-niae. ii. Elderly (age >60): Highly susceptible to L. monocytogenes. 2. Viral meningitis. a. Diagnosis of exclusion given the limited diagnostic tools for isolating individual pathogens. b. Most common viral pathogens: Human simplex virus (HSV), varicella-zoster virus (VZV), HIV, West Nile Virus (WNV), and enteroviruses. 10. Infection Guidelines
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215 3. Fungal meningitis. a. Most common fungal pathogens: Cryptococcus neo-formans and Coccidioides immitis. 4. Drug-induced meningitis. a. Proposed mechanism of action: Combination of delayed hypersensitivity reaction and direct meningeal irritation. b. Common causative agents: NSAIDs, certain antibiotics, intravenous immune globulin, and antiepileptic drugs. Predisposing Factors A. Immunocompromised state. B. Use of immunosuppressive therapy. C. Organ transplantation. D. Environmental exposure. E. Use of intravenous drugs. F. Lack of immunizations for meningococcus ( Neisse-ria meningitides ), pneumococcus ( S. pneumoniae ), and H. influenzae. G. Recent brain surgery or trauma (concern for S. aureus ). H. Bacterial meningitis is more likely to affect the elderly and individuals who are immunocompromised. Subjective Data A. Common complaints/symptoms. 1. Severe headache. 2. Nuchal rigidity: Inability to flex neck forward pas-sively due to increased muscle tone and stiffness; present in 70% of cases of bacterial meningitis. 3. Hyperthermia/hypothermia. 4. Altered mental status. B. Common/typical scenario. 1. Classic triad of meningitis: Fever, neck stiffness, and headaches. a. Found in less than 50% of patients. b. However, two out of three symptoms should raise suspicion for meningitis. 2. Nonspecific symptoms: Altered mental status, lethargy, malaise, nausea, vomiting, diarrhea, photo-phobia, muscle aches, cough, and sore throat. C. Family and social history. 1. Family history: Generally noncontributory. 2. Social history: Recent illness; travel abroad, partic-ularly sub-Saharan Africa; exposure to rodents, ticks, mosquitos; or individuals residing in close quarters (e. g., students in dormitory housing). 3. Medication history positive for NSAIDs, certain antibiotics, intravenous immune globulin, or antiepilep-tic drugs. D. Review of systems. 1. General: Fatigue, weakness, fever, or chills. 2. Head, ear, eyes, nose, and throat (HEENT): Head-aches, neck pain, or neck stiffness. 3. Neurological: Lethargy. 4. Skin: Rash. Physical Examination A. Nuchal rigidity, including tenderness to palpation and pain with flexion or extension. B. Kernig test: Pain induced by attempting full extension of the knee while the hip is flexed at 90∘. Specificity is high, but sensitivity is limited. C. Brudzinski test: Passive flexion of the neck induces flexion of the hips. Specificity is high, but sensitivity is limited. D. Lethargy and suppressed level of consciousness. E. Focal neurological deficits, including cranial nerve palsies. F. Papilledema. G. Petechial or ecchymotic rash. Petechial rash is relatively specific for meningococcal meningitis, which is caused by N. meningitides. Diagnostic Tests A. Lumbar puncture: Gold standard for diagnosis of bacte-rial meningitis (ideally performed prior to or simultaneously with antibiotic administration) with CSF analysis. 1. CSF analysis. a. Assessment of cell count/differential, glucose, pro-tein gram stain, and bacterial culture. b. Normal CSF. i. Normal opening pressure l ess than 20 mm Hg. ii. CSF WBC l ess than 5/ 𝜇L. iii. CSF RBC (absent). 1)CSF Glucose greater than 60 mg/d L and CSF/serum ratio of greater than 0. 6. iv. CSF Protein l ess than 50 mg/d L. v. Sterile culture. c. Abnormal CSF suggestive of bacterial meningitis. i. Elevated opening pressure. ii. CSF WBC greater than 1,000/ 𝜇L and neu-trophil dominant. iii. CSF RBC (absent). iv. CSF Glucose l ess than 40 mg/d L and CSF/serum ratio of l ess than 0. 4. v. CSF Protein greater than 200 mg/d L. vi. Culture results in a positive growth for bacte-rial organism. d. Abnormal CSF suggestive of viral/aseptic meningi-tis. i. Elevated opening pressure. ii. CSF WBC l ess than 250/ 𝜇L and lymphocyte dominant. iii. CSF RBC (absent). iv. CSF Glucose greater than 60 mg/d L. v. CSF Protein l ess than 150 mg/d L. vi. Sterile culture. e. Abnormal CSF suggestive of fungal meningitis (results may be nonspecific). i. Elevated opening pressure. ii. CSF WBC l ess than 500/ 𝜇L and lymphocyte dominant. iii. CSF RBC (absent). iv. CSF Glucose l ess than 40 mg/d L and CSF/serum ratio of l ess than 0. 4. 1)Bacteria ingest glucose, causing a decreased level associated with bacterial meningitis. v. CSF Protein greater than 250 mg/d L. vi. Sterile culture. 1)Proceed with fungal cultures and fungal antibody testing. f. WBC/RBC adjustment. i. A false positive WBC elevation: Often noted in a traumatic lumbar puncture or a patient with subarachnoid bleed. ii. Acceptable ratio of WBC/RBC should be approximately 1:700. 2. Relative contraindications to lumbar puncture. a. Systemic anticoagulation. b. Thrombocytopenia. c. Coagulopathy. d. Open sacral wound at level L3 to L5. Meningitis
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216 e. CT of the head with evidence of increased ICP and/or mass lesion. B. Laboratory tests. 1. Relevant blood work including complete blood count (CBC), basal metabolic profile (BMP), partial thrombo-plastin time (PTT)/prothrombin time (PT)/international normalized ratio (INR), lactate, and arterial blood gas. 2. Blood cultures. C. A noncontrast CT of the head: Required for certain patients. 1. Those who present with signs and symptoms concern-ing for elevated ICP, altered level of consciousness, new-onset seizures, or focal neurological deficits. 2. Those with immunocompromised status. 3. Those with a history of prior c entral nervous sys-tem (CNS) infection, trauma, stroke, cancer, and surgery. Differential Diagnosis A. Viral encephalitis. B. Epidural abscess. C. Nonconvulsive status epilepticus. D. Subarachnoid hemorrhage. E. Meningeal tear or CSF leak. Evaluation and Management Plan A. General plan. 1. Bacterial meningitis. a. Blood cultures. b. Broad spectrum antibiotic therapy and glucocorti-coids if appropriate. c. Administration of antivirals if there is concern for encephalitis. d. Obtain “Stat” CT of the head if altered mental sta-tus, focal neurological deficit, immunocompromised status, or new onset seizures. e. Lumbar puncture (ideally performed prior to or simultaneously with antibiotic administration) with CSF fluid analysis for definitive treatment, includ-ing meningitis/encephalitis polymerase chain reaction (PCR) for rapid identification of causative pathogen if available. f. Continued hemodynamic management and sup-portive care. g. MRI of the brain should be considered if the patient fails to improve despite appropriate therapy. 2. Viral meningitis. a. Spinal fluid suggestive of viral meningitis. b. De-escalation of antibiotic therapy. c. Supportive treatment, including but not limited to: i. Rest. ii. Fluid resuscitation. iii. Antipyretics and analgesics as needed. 3. Fungal meningitis. a. Spinal fluid analysis is likely to be abnormal but may be nonspecific, sending CSF for fungal cultures and fungal antibody testing. b. Addition of antifungal medication to antibiotic therapy for bacterial meningitis. c. Supportive treatment as previously noted. 4. Drug-induced meningitis. a. T reatment as previously noted pending results of lumbar puncture. b. De-escalation of antibiotic and antiviral therapy. c. Immediate cessation of causative agent. d. Supportive treatment. B. Patient/family teaching points. 1. Worsening neurological examination may lead to acute respiratory failure requiring intubation and mechanical ventilation. 2. Seizures may require treatment with antiepileptics and, in severe cases, intubation and mechanical ventila-tion for treatment with potent sedatives. 3. Evidence of cerebral edema on head CT may prompt aggressive medical management with mannitol and hypertonic saline, as well as surgical decompression. 4. Evidence of hydrocephalus on head CT may prompt neurosurgical evaluation and intervention. 5. Neurological sequelae including hearing loss and visual symptoms are very likely post recovery in bacterial meningitis. C. Pharmacotherapy. 1. Dexamethasone 10 mg IV q6 hours (prior to initia-tion of antibiotics if able). a. Evidence is inconclusive, but certain studies sug-gest that dexamethasone correlates with a decrease in mortality and mitigates incidence of hearing loss in patients with S. pneumoniae meningitis. 2. Ceftriaxone 2 g IV q12 hours ( N. meningitidis, H. influenzae ). a. Lactam allergy: Substitute with chloramphenicol 50 to 100 mg/kg/day IV divided q6 hours. b. Has good meningeal coverage. 3. Vancomycin 20 mg/kg IV q12 hours ( S. pneumoniae ). 4. Ampicillin 2 g IV q6 hours (if suspicious for Listeria monocytogenes). a. B-lactam allergy: Substitute with trimethoprim-sulfamethoxazole 5 mg/kg IV q6 hours. 5. Acyclovir 10 mg/kg IV q8 hours (if suspicious for HSV encephalitis). 6. Imipenem 1 gram IV q6 hours (if trauma or neuro-surgical manipulation). 7. Fluconazole 400 mg IV daily (if suspicious for C. neo-formans and C. immitis ). Dosing can be increased to 800 to 1,200 mg daily for critically ill patients. D. Discharge instructions. E. Instruct patient to seek emergency care if presenting with fever, headache, and stiff neck because this may indicate a worsening infection. Follow-Up A. Patients with neurological sequelae on discharge are encouraged to follow-up with a neurologist. Consultation/Referral A. Consider an infectious disease consult for patients with atypical pathogens or patients who do not respond to tradi-tional therapy. Special/Geriatric Considerations A. Gerontology patients with a fulminant bacterial meningi-tis may present with atypical symptoms and deny neck pain or headache. Confusion and lethargy may be the only pre-senting symptoms. B. Provider must be vigilant to recognize high-risk patient for CNS infection so that treatment is not delayed. 10. Infection Guidelines
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217 Bibliography Gaieski, D. F., Nathan, B. R., & O'Brien, N. F. (2015). Emergency neuro-logical life support: Meningitis and encephalitis. New York, NY: Springer Science +Business Media. T unkle, A. R. (2018, August 30). Clinical features and diagnosis of acute bacterial meningitis in adults. In J. Mitty (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/clinical-features-and-diagnosis-of-acute-bacterial-meningitis-in-adults Wijdicks, E. F. M., & Rabinstein, A. A. (2012). Neurocritical care. New York, NY: Oxford University Press. Necrotizing Fasciitis Dana A. Albinson Definition A. Severe bacterial infection of the fascia (connective tis-sue that covers and separates the muscles and other internal organs) and overlying subcutaneous fat that causes extensive tissue death. Incidence A. Necrotizing fasciitis can occur at any age; however, the mean age is around 50 years. B. Hospitalizations due to necrotizing fasciitis are gender neutral. C. Necrotizing fasciitis occurs randomly and is not linked to similar infections in others. Pathogenesis A. The most common way of getting necrotizing fasciitis is when the bacteria enter the body through a break in the skin, such as a cut, scrape, burn, insect bite, or puncture wound. B. The infection spreads along the muscle fascia as a result of its relatively poor blood supply, and muscle tissue may be spared. In addition, overlying tissue can appear unaffected. C. Necrotizing fasciitis is typically classified based on the microbial source of infection. 1. Type I—polymicrobial with aerobic and anaerobic bacteria, such as Clostridioides, Peptostreptococcus, and Bacteroides species. 2. Type II—monomicrobial and generally caused by group A streptococcus (GAS; also known as hemolytic streptococcal gangrene). Predisposing Factors A. Type I: Certain comorbid conditions. 1. Diabetes. 2. Obesity. 3. Cardiovascular disease. 4. Peripheral vascular disease. 5. Liver disease. 6. Kidney disease. 7. Cancer. 8. Other chronic health conditions that weaken the body's immune system. B. Type II: Risk factors in healthy individuals (no past med-ical history). 1. Skin injury—laceration or burn. 2. Blunt trauma. 3. Surgery. 4. Childbirth. 5. Varicella. 6. Intravenous drug use. Subjective Data A. Common complaints/symptoms. 1. Pain—usually out of proportion to how the area looks; followed by anesthesia (due to thrombosis of small vessels). 2. Swelling. 3. Redness. 4. Fever. 5. Chills. 6. Fatigue. B. Family and social history. 1. A detailed history is important, as it can suggest the likely cause of the infection. 2. A careful history, including several factors, should be taken. a. Indicate if any trauma occurred at the site. b. Onset and duration of symptoms. c. Speed at which erythema is spreading. d. Existence of any comorbid conditions (past medi-cal history). e. Any recent swimming in lakes, ponds, or areas of concern. Physical Examination A. Early on, healthy appearance, but possible rapid progres-sion to ill/septic appearance. B. Acute tenderness at site of infection. C. Skin with area of rapidly increasing erythema, bullae, skin necrosis, and/or crepitus; sometimes with dusky or purplish discoloration. 1. Skin color can change in a few days from red/purple to patchy blue/gray, followed in 3 to 5 days with skin breakdown with bullae with thick pink/purple fluid and frank cutaneous gangrene. D. Increased warmth and induration at site. E. Possible crepitus at site. F. Difficult to palpate muscle groups due to induration, with edema of subcutaneous tissue. G. If the skin is open, gloved fingers can pass easily between the two layers and may reveal yellowish-green necrotic fascia. H. If the skin is not open, a scalpel may be needed to open the site. Diagnostic Tests A. Lab work. 1. Complete blood count (CBC), basal metabolic profile (BMP), and blood and tissue cultures are necessary. 2. Lab findings are often nonspecific but may include leukocytosis with a marked left shift; coagulopathy; and elevated creatine kinase (CK), lactate, and creatinine. B. Imaging: Noncontrast CT and MRI scans (especially in abdominal wall infections). 1. These can be helpful if gas is identified in the soft tissue and/or fascial planes. 2. MRI can be overly sensitive. C. Surgical exploration. 1. Donotdelay surgical exploration for results from blood, skin, or wound cultures. 2. Surgical exploration is the only way to confirm diag-nosis. Histopathology of tissue will show extensive tissue damage, including: a. Thrombosis of blood vessels. b. Abundant bacteria along fascial planes. c. Infiltration of acute inflammatory cells. Necrotizing Fasciitis
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218 Differential Diagnosis A. Acute epididymitis. B. Cellulitis. C. Orchitis. D. Toxic shock syndrome. E. Deep vein thrombosis (DVT). F. Brown recluse spider bite. Evaluation and Management Plan A. Surgical emergency. Debridement needs to be done early to minimize tissue loss and possible amputation, and debride-ment will require review in the operating room every 24 hours. B. Empiric antibiotics. These should be started immediately. Agents should be broad based to cover gram-negative and gram-positive organisms and anaerobes. More target-specific antibiotics may be started once tissue cultures and sensitivi-ties are available. 1. Clindamycin is the antibiotic of choice to cover necro-tizing fasciitis for its antitoxin effects. 2. In addition, the patient requires carbapenems (e. g., imipenem, meropenem, or ertapenem—please note that ertapenem does not cover pseudomonas) or beta lac-tamase inhibitor (e. g., piperacillin/tazobactam, ampi-cillin sodium/sulbactam sodium, or Ticarcillin/clavulanic acid), as well as an agent active against methicillin-resistant Staphylococcus aureus (MRSA; e. g., vancomycin, daptomycin, or linezolid). C. Intravenous fluids. Massive fluids may be necessary due to diffuse capillary leak and hypotension. Also, nutritional support needs to be implemented to help support wound healing. Follow-Up A. Repeat imaging of area to make sure there is no lingering infection. B. Follow-up with infectious disease after completion of antibiotics. C. Follow-up with surgery as needed. Consultation/Referral A. Consult surgery emergently for surgical intervention. B. Infectious disease for antibiotic duration. C. Depending on extent of injury, may need plastics consult for flap. D. Wound care. Special/Geriatric Considerations A. Necrotizing fasciitis is the most frequently overlooked infectious process of the skin in the elderly. B. Skin and soft tissue represent a common site of infection, and it is a recognized focus of sepsis in the elderly. Bibliography Centers for Disease Control and Prevention. (n. d. ). Necrotizing fasciitis: A rare disease, especially for the healthy. Retrieved from https://www. cdc. gov/features/necrotizingfasciitis Edlich, R. (2018, October 17). Necrotizing fasciitis workup. In M. S. Bronze (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/2051157-workup Ghosh, A., & Johnstone, J. (2013). Necrotizing fasciitis in an immuno-compromised elderly woman. Canadian Journal of Infectious Diseases and Medical Microbiology, 24 (1), 38-39. doi:10. 1155/2013/489587 Goh, T., Goh, L. G., Ang, C. H., & Wong, C. H. (2013). Early diagno-sis of necrotizing fasciitis. British Journal of Surgery, 101 (1), e119-e125. doi:10. 1002/bjs. 9371Misiakos, E. P., Bagias, G., Patapis, P., Sotiropoulos, D., Kanavidis, P., & Machairas, A. (2014). Current concepts in the management of necrotiz-ing fasciitis. Frontiers in Surgery, 1, 36. doi:10. 3389/fsurg. 2014. 00036 Oud, L., & Watkins, P. (2015). Contemporary trends of the epidemiology, clinical characteristics, and resource utilization of necrotizing fasciitis in Texas: A population-based cohort study. Critical Care Research and Prac-tice, 2015, 1-9. doi:10. 1155/2015/618067 Southwick, F. S. (2008). Infectious diseases: A clinical short course (2nd ed, pp. 268-271). New York, NY: Mc Graw-Hill Professional Publishing. Osteomyelitis Rose Milano Definition A. Represents a wide spectrum of inflammatory bone disor-ders due to bacteria, mycobacteria, or fungi. B. Multifaceted presentations of bone infection; no univer-sally accepted system of classification. C. Classification is most commonly based on the pathogen-esis, chronicity, or location. D. Known as a disease of the very young and the very old. Incidence A. The incidence of osteomyelitis in the United States is largely unknown. It may be as high as 16% after foot punc-ture (30%-40% in patients with diabetes). The rate of occur-rence of vertebral osteomyelitis is estimated at 2. 4 cases per 100,000. The prevalence of osteomyelitis is estimated as 1 case per 5,000 in children. B. The prevalence of bone and joint infections in adults is increasing because of (1) longer life expectancy, (2) increasing use of bone fixation and prosthetic implants, and (3) higher rate of diabetes. Pathogenesis A. Hematogenous source: Spread by seeding from bacteria in blood. 1. Primary sources of initial infection: Urinary tract, skin and soft tissue, and intravascular catheters, as well as endocarditis. 2. Usually monomicrobial. 3. Most common in children due to seeding in the meta-physis of long bones, particularly the femur and tibia. Such osteomyelitis is rare in adults, but when it does occur it is most frequent in the vertebrae of the spine. B. Contiguous source: Spread from adjacent soft tissues and joints. 1. Exogenous: Often spread following surgery or trauma with direct inoculation. 2. Generally polymicrobial, but can be monomicrobial. 3. Accounts for 80% of chronic osteomyelitis infection. 4. Bimodal age distribution with differing sources. a. Older individuals: Decubitus ulcers, chronic soft tissue injuries, dental infections, and joint arthroplas-ties. b. Younger individuals: Open fracture or bone surgery. C. Secondary disease: From vascular insufficiency or periph-eral neuropathy. 1. Most often related to diabetes. 2. Results from chronic, progressive deep skin/soft tissue infection, generally in the foot from diabetic foot syn-drome. D. Infectious causes: Multifactorial mechanisms in hosts at high risk. 1. Most commonly due to hematogenous seeding. 10. Infection Guidelines
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219 2. Intravenous drug abuse. 3. HIV infection. 4. Sickle cell disease: Accounts for about one third of cases. E. Histological changes. 1. Infection: Results in bone edema and vascular conges-tion, leading to small vessel thrombosis. 2. Medullary and periosteal blood supplies: Compro-mised; bone becomes necrotic. 3. Sequestra: Fragments of dead bone that detach from living bone. 4. Dead bone: Becomes colonized by a biofilm of bac-teria that is often resistant to antibiotics, so debridement in addition to antibiotics is necessary for chronic, well-established osteomyelitis. F. Microorganisms: Often a function of the location of the osteomyelitis infection. 1. Staphylococcus aureus: Most frequent cause of all types of osteomyelitis. 2. Coagulase-negative staphylococci: Most common cause of prosthetic-associated infection. 3. Streptococci and other anaerobic bacteria: Associated with diabetic foot lesions and decubitus ulcers. 4. Aspergillus spp., Candida albicans, and Mycobacteria spp. most common in immunocompromised hosts. 2. Symptoms develop over days to weeks. C. Family and social history. 1. Past medical history: Comorbidities leading to increased risk. 2. Recent surgeries, implants, and so on. 3. History of diabetes with ulcers. 4. Decubitus ulcers. 5. Peripheral vascular disease. 6. I ntravenous (IV) drug abuse. 7. Sickle cell disease. 8. Recent trauma. 9. Urinary tract infection (UTI) or pyelonephritis. D. Review of systems. 1. Constitutional: Possible night sweats, fatigue, malaise, or lethargy. 2. Genitourinary: Signs and symptoms of UTI; loss of bowel or bladder control. 3. Musculoskeletal: Pain, swelling, or redness at site. 4. Skin: Purulent drainage from open wound. 5. Musculoskeletal: Weakness in lower extremities. Physical Examination A. Location of any skin lesions (in case of diabetic foot ulcers [ >2×2 cm] or exposed bone, osteomyelitis is likely). B. Positive neurological examination with areas of weakness or sensory loss (particularly in suspected spinal osteomyeli-tis). C. Presence of vascular and arterial insufficiency. D. Probe to the bone in pedal ulcers using sterile, blunt metal tool. 1. Positive result: Hard, gritty surface of bone. Diagnostic Tests A. Laboratory studies: Generally nonspecific initially. 1. CBC. a. Leukocytosis: Common in acute osteomyelitis but less common in chronic cases. 2. ESR greater than 70 mm/h: Indicative of osteomyeli-tis. 3. CRP elevated. 4. Blood cultures: Most useful when patient is febrile. B. Imaging studies. 1. Accuracy dependent on intensity of the inflammation, chronicity of the infection, site, vascularity, and associated pathology. 2. Simply support or refute clinical suspicion. 3. Plain films generally used for the initial study. a. Most sensitive but least specific of all the diagnostic modalities. b. Cortical abnormality with periosteal new bone for-mation: Suggestive of osteomyelitis. c. Most useful when symptoms have persisted for more than 2 weeks. 4. MRI: High negative predictive value and highly sen-sitive. a. First choice for suspected spinal osteomyelitis. 5. Radionuclide bone skeletal scintigraphy (i. e., three-phase bone scan) combined with CT: May be used if MRI is not possible due to indwelling hardware. C. Bone biopsy: Combined with histologic findings of inflammation and bone necrosis. 1. May be done using open or percutaneous approach, with open being preferable because the sensitivity of per-cutaneous biopsy is poor. Osteomyelitis Predisposing Factors A. Compromised host. B. Immunocompromise (HIV: High correlation secondary to unsterilized needles. The very young experience mostly in the long bones while the very old have more occurrences in the vertebrae). C. Intravenous drug abuse or alcohol abuse. D. Diabetes. E. Malignancies. F. Impaired circulation. G. Liver cirrhosis. H. Sickle cell disease. I. Chronic steroid use. J. Bone or joint surgery. K. T raumatic injury involving the bone. Subjective Data A. Common complaints/symptoms. 1. Gradual onset of symptoms over several days. 2. Spinal osteomyelitis. a. Pain: Determined by the location of the infection in the spine; generally dull pain with and without movement. b. Fever (only in 64% of cases, due to degree of immunocompromise and age). c. Local tenderness, warmth, erythema, and swelling. d. Motor weakness or radicular pain. e. Spinal deformity in patients with prolonged course of treatment. 3. Long bone and pelvis. a. Acute osteomyelitis: Can present as septic arthritis because it affects the metaphysis to the joint. b. Tenderness, warmth, erythema, and swelling. 4. Chronic osteomyelitis. a. Pain, erythema, and swelling. b. Occasional draining sinus tract. c. More likely with presence of prosthetic material, extensive tissue ulceration, or vascular insufficiency. B. Common/typical scenario. 1. Complaints of pain, swelling, and possibly low-grade fever.
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220 Differential Diagnosis A. Spinal osteomyelitis with symptoms of backache. 1. Influenza, or virus with flu-like symptoms. 2. Pyelonephritis. 3. Pancreatitis. 4. Osteoporotic fracture. 5. Disc herniation. B. Long bone osteomyelitis. 1. Septic arthritis. 2. Bone tumor. 3. Occult or pathological fracture. 4. Soft tissue infection. 5. Charcot arthropathy. 6. Bursitis. 7. SAPHO syndrome (synovitis, acne, pustulosis, hyper-ostosis, and osteitis). 8. Gout. C. Infectious disease consult to determine type and duration of antibiotics. Special/Geriatric Considerations A. Incidence peaks in geriatric patients because of prosthetic implants and chronic health diseases such as peripheral vas-cular disease and diabetes. B. The most common sites of infection in the elderly are in joint replacements and the spine. Bibliography Calhoun, J. H., & Manring, M. M. (2005, December). Adult osteomyeli-tis. Infectious Disease Clinics of North America, 19 (4), 765-786. doi:10. 1016/j. idc. 2005. 07. 009 Paluska, S. A. (2004). Osteomyelitis. Clinics in Family Practice, 6, 127-156. doi:10. 1016/S1522-5720(03)00130-210. Infection Guidelines Evaluation and Management Plan A. General plan. 1. Bone probing for foot ulcerations suspected of being osteomyelitis. 2. Prolonged duration of antibiotic treatment is necessary. 3. Bone biopsy: Open approach preferable to needle biopsy. a. Identification of causative organism with gram stain and culture, including aerobic, mycobacterial, and fungal culture. 4. Surgical debridement: May be required for chronic osteomyelitis. 5. Removal of hardware: May be required. 6. Adjunctive therapies: Hyperbaric oxygen therapy. B. Patient/family teaching points. 1. Prolonged duration of antibiotic treatment is neces-sary. 2. Recurrence is common. C. Pharmacotherapy. 1. Antibiotic selection based on cultures identi-fying causative agent and susceptibilities. Empiric treatment against methicillin-resistant Staphylococcus aureus (MRSA) should be completed when culture data are available (piperacillin-tazobactam, ampicillin-sulbactam, ticarcillin-clavulanate; penicillin allergic: clin-damycin, metronidazole, ciprofloxacin, levofloxacin; if MRSA is suspected, vancomycin). 2. Prolonged duration of treatment; generally outpatient parenteral antibiotic therapy. a. Measurement of C-reactive protein (CRP) weekly: To determine serial trends. D. Discharge instructions. 1. Complete the course of antibiotics as prescribed. 2. Follow wound care instructions as prescribed. 3. Avoid injury to the area where the infection is located. 4. Report new or worsening symptoms, especially pain, redness, swelling, or drainage in the affected area. Follow-Up A. Based on the location of disease and duration of treat-ment. 1. Long-term oral antibiotic therapy (3-6 months) may be required if orthopedic hardware must remain in place. Consultation/Referral A. Orthopedic consult. B. Radiology consult to assist with determining the best mode of diagnostics. Peritonitis Jennifer W. Parker Definition A. Inflammation of the peritoneum: The thin layers (visceral and parietal) of tissue that line the inner wall of the abdomen, covering most of the organs. B. Considered an acute abdomen. C. Types. 1. Primary peritonitis: Most often seen as spontaneous bacterial peritonitis (SBP). a. Considered to be infection of peritoneum/ascitic fluid without a surgically treatable source. 2. Secondary peritonitis: Most common form. a. Considered to be inflammation of the peritoneum secondary to a surgically treatable source. 3. Tertiary peritonitis: Recurring or chronic peritonitis after adequate treatment of the original disease. Incidence A. May be difficult to establish and varies with disease pro-cess and type of peritonitis. 1. Patients with an all cause diagnosis of cirrhosis were reported. 2. Patients with ascites have an incidence rate as high as 18%. 3. Patients with peritoneal dialysis may have rates as high as 12%. Pathogenesis A. Peritonitis may be generalized or localized (i. e., abscesses, the leading cause of persistent infection/tertiary peritonitis), and infectious or sterile (i. e., chemical or mechanical). B. Primary peritonitis (generally SBP) is an acute infec-tion of ascitic fluid, resulting from translocation of bacte-ria across the gut wall and/or mesenteric lymphatics or, less frequently, due to hematogenous seeding in the presence of bacteremia. 1. SBP is a complication of any disease that causes ascites, including cirrhosis, heart failure, and Budd-Chiari syndrome. From 10% to 30% of patients with liver cirrhosis develop SBP. 2. Majority ( >90%) of SBP is monomicrobial, with most commonly gram-negative organisms including Escherichia coli (40%) and Klebsiella pneumoniae (7%); or gram-positive organisms such as Streptococcus pneumoniae
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221 (15%), other Streptococcus strains (15%), and Staphylococ-cusspecies (3%). C. Secondary peritonitis is intra-abdominal sepsis generally from a perforated viscus resulting from direct spillage of the luminal organ into the peritoneum. 1. Causes include perforated peptic ulcer, diverticulitis, appendicitis, necrotizing pancreatitis, or iatrogenic perfo-ration. 2. Pathogens differ from the proximal to distal end of the gastrointestinal (GI) tract (gram-positive is predom-inant in the upper GI tract, unless the patient is on long-term proton pump inhibitor (PPI) treatment, when gram-negative may become more populous). Contamina-tion from distal small bowel or colon is generally polymi-crobial and may include fungi. 3. Women can experience localized peritonitis from an infected fallopian tube or a ruptured ovarian cyst, as well as pelvic inflammatory disease. D. Peritoneal-dialysis-associated peritonitis. 1. Causes include and are almost always due to catheter-related infection and are related to touch contamination with pathogenic skin bacteria. 2. Abdominal pain, cloudy peritoneal effluent due to white cell counts greater than 100 cells/mm3, purulent drainage at catheter site, or a swollen, tender tunnel site may appear. E. Secondary peritonitis: Acute or chronic. 1. Onset can be sudden as when secondary to appendici-tis or cholecystitis, or it can be associated with chronic diseases (especially GI) such as Crohn's disease or peptic ulcer disease (PUD); trauma; or recent surgery. a. Primary peritonitis (SBP): Cirrhosis of the liver; hepatitis C, now with ascites. C. Social history. 1. Alcohol dependency. 2. I ntravenous (IV) drug use. 3. Blood transfusion. D. Review of systems. 1. Primary peritonitis (SBP). a. Constitutional: Feeling poorly, fever, loss of appetite, or generalized weakness. b. Neurological: Change in mental status or dizzi-ness/lightheadedness (secondary to hypotension). c. Respiratory shortness of breath, dyspnea on exer-tion, and inability to take a deep breath. d. GI: Diffuse abdominal pain, abdominal tender-ness, fever, and often ascites. 2. Secondary peritonitis. a. Constitutional: Fever, chills, diaphoresis, or loss of appetite. b. Neurological: Lightheadedness/dizziness (sec-ondary to hypotension). c. Cardiac: Tachycardia secondary to pain. d. Respiratory: Shortness of breath, dyspnea (secondary to pain). e. GI: Acute abdominal pain (worse with move-ment), nausea and vomiting, and constipation or diarrhea. Peritonitis Predisposing Factors A. Primary peritonitis (SBP): Cirrhosis of the liver with ascites. 1. Any diagnosis of cirrhosis. 2. Contaminated dialysate. B. Secondary peritonitis: Peritonitis with surgically treatable source. 1. Perforation of intestinal tract, abdominal organs. 2. T rauma. 3. Peritoneal dialysis. 4. Previous history of peritonitis. Subjective Data A. Common complaints/symptoms. 1. Primary peritonitis (SBP): Fever and abdominal pain, often accompanied by change in mental status from hep-atic encephalopathy and/or sepsis. 2. Secondary peritonitis: Acute abdominal pain, worse with movement, variable location of pain, high fever, and nausea and vomiting. a. Pain can be generalized and dull initially (visceral peritoneum involvement) and then become more localized and severe (parietal layer involvement). B. Common/typical scenario. 1. Diagnosis of peritonitis is primarily clinical; thus, his-tory is important. 2. Specific historical factors include knowledge of previous peritonitis, causes of immunosuppression including the use of immunosuppressive agents, recent abdominal surgery or trauma, presence of diseases (e. g., inflammatory bowel disease, diverticulitis, PUD) that may predispose to intra-abdominal perforations/infec-tions, and travel history. Physical Examination A. General appearance: Ill and in severe discomfort. 1. Peritonitis can often proceed quickly to septic shock and multiple organ dysfunction syndrome (MODS). B. Vital signs. 1. Temperature: Often greater than 38∘C, but if patient is in shock, may become hypothermic. 2. Tachycardia from presence of inflammatory media-tors; fever and hypovolemia from vomiting/shock/third spacing. 3. Hypotension: Primarily as patients progress with dehydration and shock. C. Abdominal (patient should be supine, with a pillow underneath knees; this may allow for improved relaxation of abdominal wall). 1. Tenderness to palpitation. a. The region of greatest tenderness overlies the site of maximal irritation/pathologic process, even with gen-eralized pain. 2. Rigidity: Voluntary in anticipation to or response to palpitation or involuntary from peritoneal irritation. a. Involuntary rigidity makes peritonitis highly likely. 3. Increased pain with movement: Possible severe pain caused by coughing or flexing of the hips. 4. Rebound tenderness (i. e., positive Bloomberg sign): As peritoneum snaps back into place with sudden removal of pressure. 5. Distension. 6. Hypoactive to absent bowel sounds: Reflecting gener-alized ileus (less likely with highly localized infection). 7. Masses or hernias (occasionally). 8. Ascites: Especially in SBP. D. Genitourinary: Oliguria or anuria as patient becomes hypotensive. E. Integumentary: Presence of signs of liver failure such as jaundice or angiomata if SBP results from cirrhosis.
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222 Diagnostic Tests A. For all patients. 1. Paracentesis: For all patients with new ascites and/or hospitalization of cirrhotic patients prior to receiving antibiotics. a. A cell count of 250 or more polymorphonuclear leukocytes (PMN) suggests infection. Patients should be started on broad-spectrum antibiotics immedi-ately, with narrowing of antibiotic treatment follow-ing results of culture of ascitic fluid. b. Analysis of ascitic fluid should also include Gram's stain; fluid chemistries; serum-ascites albumin gra-dient; ascitic fluid total protein concentration; and ascitic fluid glucose, lactate dehydrogenase, amylase, and bilirubin concentrations. All of these can help the diagnosis of SBP and/or differentiate SBP from sec-ondary peritonitis. 2. Plain and upright abdominal films: Evaluation for free air or dilation of large or small bowel. a. Free air is present in most cases of anterior gas-tric and duodenal perforation, less frequent with small bowel and colonic perforations, and rarely present with perforations of the appendix. b. Upright films are useful for identifying free air under the diaphragm (usually on the right), which is indicative of viscus perforation. 3. Chest x-ray: Elevated diaphragm. 4. CT of abdomen with enteral and IV contrast: Evi-dence of surgically treatable source, ascites, or mass. CT is the optimal diagnostic study for peritoneal abscess and related visceral pathology. 5. Blood cultures: Often positive. B. For patients on peritoneal dialysis. 1. Peritoneal fluid analysis: With WBC greater than 100 cells/mm3; more than 50% of those are polymorphonu-clear leukocytes. a. Low WBC is found even in cases of peritonitis, usually due to the short length of dialysate dwell time, or a poor host immune response. b. Gram's stain of fluid should be completed. 2. Peritoneal fluid culture: Most commonly gram-positive organisms, such as coagulase-negative Staphylo-coccus. 3. Peripheral WBC and blood cultures. 4. Culture of purulent drainage from exit site. Differential Diagnosis A. Primary peritonitis (SBP). 1. Important to differentiate from secondary peritoni-tis because of high mortality associated with unnecessary versus postponed surgery. 2. Other conditions to be considered with ascitic patients: Peritoneal carcinomatosis, tuberculous peritoni-tis, and alcoholic hepatitis. B. Secondary peritonitis: Associated with many thoracic and abdominal conditions. 1. Thoracic conditions leading to diaphragmatic irrita-tion (e. g., empyema). 2. Retroperitoneal processes: Renal abscess, pyelonephri-tis, cystitis, and urinary retention. 3. External hernia with intestinal incarceration. 4. Familial Mediterranean fever. 5. Gynecological disorders: Salpingitis, endometriosis, teratoma, and dermoid cysts. 6. Neoplasms. 7. Vascular conditions: Mesenteric embolus or nonoc-clusive ischemia, ischemic colitis, and portal or mesen-teric vein thrombosis. 8. Splenosis. 9. Vasculitis: Systemic lupus erythematosus and allergic vasculitis. Evaluation and Management Plan A. All types of peritonitis: Essential to provide aggressive fluid management to maintain hemodynamic stability. 1. If at all possible: Avoid vasopressors. B. Primary peritonitis (SBP). 1. Empiric antibiotic therapy should be given as soon as possible (but preferably after paracentesis for culture). a. Cefotaxime 2 g every 8 hours is recognized to pro-duce good results in ascitic fluid. b. Other third generation cephalosporins and fluo-roquinolones may also be appropriate, although resis-tance to fluoroquinolones is an increasing concern. 2. Any nonselective beta blocker should be discontin-ued. 3. IV albumin (1. 5 g/kg body weight within 6 hours of diagnosis and 1. 0 g/kg on day 3) is beneficial with renal dysfunction (Cr >1. 0 mg/d L, BUN >30 mg/d L or total bilirubin is >4 mg/d L). 4. Diuretic therapy concentrates ascitic fluid, thereby raising opsonic activity, which limits recurrence of SBP. 5. Use of PPIs, which are associated with increased risk of SBP, should be limited. C. Secondary peritonitis. 1. Prompt initiation of empiric antibiotic treatment after all cultures have been drawn is necessary to cover gram-negative aerobes, enteric streptococci, and anaer-obes (e. g., Cefotaxime 2 g IV every 8 hours with metron-idazole 500 mg IV every 8 hours). 2. Emergent operative management to eliminate the contamination source is important. 3. Frequently, patients must be nil per os (NPO) with possible nasogastric tube placement—depending on the source of infection. 4. Nutritional demands need to be met; many patients develop an ileus after surgery. Consideration of enteral versus parenteral feeding should take place early in the course of treatment. Sepsis will increase nutritional demands. Follow-Up A. Primary peritonitis (SBP). 1. Repeat paracentesis is generally not necessary if patient has cirrhosis and monomicrobial infection. a. With an atypical course of SBP, repeat paracentesis in 48 hours. 2. Prophylaxis is recommended for the many ascitic patients to prevent repeat SBP, including: a. Patients with ascites with GI bleed. b. Patients with low protein levels in ascitic fluid (<1 g/d L). c. Patients with history of SBP. 3. Prophylactic regimens include: a. Ciprofloxacin—750 mg weekly. b. T rimethoprim-sulfamethoxazole five doses (Mon-day to Friday) of double strength tablets weekly. c. Norfloxacin—400 mg daily (Note: Long-term prophylaxis with fluoroquinolones is recognized to lead to high level fluoroquinolone resistance). 10. Infection Guidelines
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223 Consultation/Referral A. Peritonitis, with the associated high mortality rates, often requires multiple consults, including: 1. Surgery (secondary peritonitis). 2. Infectious disease. 3. GI. 4. Nutrition. 5. Critical care. 6. Renal (for peritoneal-dialysis-associated peritonitis). Special/Geriatric Considerations A. Elderly patients may not present with profound guard-ing and/or abdominal rigidity, which are classic findings of peritonitis. B. Fever and tachycardia are more common, although these signs are much less specific to peritonitis. C. Careful history should be taken, and peritonitis cannot be ruled out with just a physical examination in elderly patients. Bibliography Barkley, T. W., Jr., & Myers, C. M. (2014). Practice considerations for adult-gerontology acute care nurse practitioners. West Hollywood, CA: Barkley and Associates. Burkart, J. M. (2018, June 1). Clinical manifestations and diagnosis of peritonitis in peritoneal dialysis. In S. Motwani (Ed. ), Up To Date. Retrieved from www. uptodate. com/contents/clinical-manifestatiosn-and-diagnsosis-of-peritonitis-in-peritoneal-dialysis Daley, B. J. (2017, January 11). Peritonitis and abdominal sepsis. In P. K. Roy (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/ article/180234-overview Runyon, B. A. (2018, April 11). Spontaneous bacterial peritoni-tis in adults: Diagnosis. In K. M. Robson (Ed. ), Up To Date. Retrieved from www. uptodate. com/contents/spontaneous-bacterial-peritontis-in-adults-diagnosis Runyon, B. A. (2018, September 21). Spontaneous bacterial peritoni-tis in adults: T reatment and prophylaxis. In K. M. Robson (Ed. ), Up To Date. Retrieved from www. uptodate. com/contents/spontaneous-bacterial-peritontis-in-adults-treatments-and-prophylaxis Sabatine, M. S. (Ed. ). (2017). Pocket medicine: The Massachusetts Gen-eral Hospital handbook of internal medicine (6th ed. ). Philadelphia, PA: Wolters Kluwer. Systemic Inflammatory Response Syndrome (SIRS)/Bacteremia/Sepsis Rose Milano Definition A. Systemic Inflammatory Response Syndrome (SIRS): Clinical syndrome that is a form of dysregulated inflamma-tion; can be present with or without infection; considered the clinical expression of host response to inflammation resulting from nonspecific insult. 1. SIRS is considered to be present when two or more of the following signs are present: a. Temperature greater than 38∘C (100. 4∘F) or less than 36∘C (96. 8∘F). b. Heart rate more than 90 beats per minute. c. Respiratory rate greater than 20 breaths per minute or arterial carbon dioxide (Pa CO2) of less than 32 mm Hg. d. Abnormal white blood cell count ( >12,000/ 𝜇L or <4,000/ 𝜇L or>10% immature forms; i. e., bands). B. Bacteremia: T raditionally, essentially synonymous with septicemia; today, defined as the presence of viable bacteria in the blood. 1. Signs and symptoms range from asymptomatic, non-infectious to full blown sepsis. C. Sepsis (general): A continuum of severity ranging from infection and/or SIRS, to sepsis, severe sepsis, and septic shock. D. Sepsis: T raditionally, clinical syndrome with a collection of signs (objective) and symptoms (subjective); patient meets SIRS criteria and has a source of infection (this definition has been changed). Severe sepsis: Usually defined as sepsis with persistently low blood pressure, despite fluid resuscitation. 1. According to the Surviving Sepsis 2016 Campaign, sepsis is a life-threatening dysfunction caused by a dysreg-ulated host response to infection (and category of severe sepsis has been removed). 2. Organ dysfunction is defined by an increase over base-line in the sequential organ failure assessment (SOFA) score (see Table 10. 3). In critically ill patients, SOFA has a higher predictive value of in-hospital mortality than the SIRS criteria. Patients who meet SOFA criteria have greater than 10% predicted mortality. a. SOFA score. i. Mortality prediction score based on evalua-tion of organ dysfunction. ii. Based on six different criteria: Respiratory, cardiovascular, hepatic, coagulation, renal, and neurological. iii. Calculated on day of admission to the ICU and daily thereafter, until discharged from the ICU. iv. Recommended that one uses the worst value to calculate the patient's daily score. b. Quick SOFA score (q SOFA). i. System used as a prompt to recognize patients with infections who are likely to be septic, yet not in the ICU. ii. Developed with the intention to be used in the prehospital, ED, non-ICU floors in a hospital. iii. Bedside scoring system that assesses three components. 1)1 point: Systolic blood pressure less than or equal to 100 mm Hg, 2)1 point: Respiratory rate greater than or equal to 22 breaths per minute. 3)Altered mental status: Glasgow Coma Score of less than 15. iv. Per the Surviving Sepsis Guidelines: A patient with an infection and a q SOFA score of 2 or more has a higher risk of death or prolonged ICU stay. E. Septic shock: Sepsis, a vasodilatory or distributive shock, defined by the 2016 Surviving Sepsis Campaign as including the criteria for sepsis, and even with adequate fluid resuscita-tion meets the following conditions: 1. Unresponsive to fluid resuscitation. 2. Serum lactate levels more than 2 mmol/L. 3. Need for vasopressors to maintain mean arterial pres-sure (MAP) of 65 mm Hg or more. Incidence A. SIRS. 1. The incidence of SIRS increases as the level of care unit acuity increases. 2. Progression of SIRS was noted to be: 26% developed sepsis, 18% developed severe sepsis, and 4% developed septic shock within 28 days of admission. Systemic Inflammatory Response Syndrome/Bacteremia/Sepsis
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224 TABLE 10. 3 Sequential Organ Failure Assessment SOFA Score 0 1 2 3 4 Respiratory Pa02/Fi02 ≥400 <400 <300 <200 (+) respiratory support<100 (+) respiratory support Coagulation ≥150,000 Platelets ×103/mm3<150,000 <100,000 <50,000 <20,000 Hepatic Bilirubinmm/d L <1. 2 1. 2-1. 9 2. 0-5. 9 6. 0-11. 9 >12 Cardiovascular Catecholamine doses ug/kg/min for at least 1 hour. MAP ≥70mm Hg MAP <70 mm Hg Dopamine <5 OR dobutamine (anydose)Dopamine 5. 1-15 ORepinephrine OR norepinephrine. Dopamine >15OR. epinephrine OR norepinephrine >0. 1 Neurological Glasgow Coma Score 15 13-14 10-12 6-9 <6 Renal Creatininemg/d L OR Urine Output m L/day<1. 2 1. 2-1. 9 2. 0-3. 4 3. 5-4. 9 <500 m L/day>5. 0<200 m L/day B. Bacteremia. 1. Often asymptomatic, transient, and without conse-quences. 2. 25% to 45% with significant bacterial counts develop sepsis. C. Sepsis. 1. One of the leading causes of death in the United States; between 230,000 and 370,000 people die of sepsis annually in the United States. 2. Sepsis is diagnosed in more than 25% of all hos-pitalized patients. The incidence of sepsis diagnosis has increased over the past 10 years. 3. Septic shock is associated with higher mortality than sepsis alone (40% vs. 10%). 4. Sepsis develops in 80% of patients prior to being admitted to a hospital. 5. 7 out of 10 patients diagnosed with sepsis had recently seen a healthcare worker or had a chronic disease requir-ing frequent medical care. Pathogenesis A. SIRS. 1. An insult/injury occurs, followed by local cytokine production, a local inflammatory response. a. Inflammatory cascade is an important piece of pathophysiology. b. Local cytokines are released to the systemic circu-lation, further provoking local response. 2. This leads to growth factor stimulation, with the recruitment of platelets and macrophages. 3. The acute phase of the response is controlled by a decrease in proinflammatory mediators and release of endogenous antagonists. If homeostasis is not restored with cytokine release into the systemic circulation, sig-nificant reaction occurs. 4. Continued exposure to injury/illness results in contin-uation of this inflammatory cascade, leading to progres-sive illness. B. Bacteremia. 1. Sources of gram-negative bacteremia: Gastrointesti-nal (GI) tract, genitourinary tract, or from the skin on patients with decubitus ulcers. 2. Staphylococcal bacteremia: Common in patients with intravenous (IV) catheters and IV drug abusers. 3. Infection above the diaphragm causing bacteremia: Most likely gram-positive organism. 4. Infection below the diaphragm causing bacteremia: Most likely gram-negative bacillus. C. Sepsis. 1. Sources of infections most likely associated with sep-sis: Infections of the respiratory tract, gastrointestinal tract, genitourinary tract, and the skin. If the nervous sys-tem becomes involved, the mortality is greatest. 2. Bacterial infections: Most common cause of sepsis. a. Common causal bacteria: Staphylococcus aureus, group A Streptococcus, Escherichia coli, Klebsiella species, Enterobacter species, and Pseudomonas aerug-inosa. b. Fungal and viral sources: Also possible causes. 3. Immunocompromised patients: Susceptible to fungal bloodstream infections from Candida species. 4. Culture Negative Severe Sepsis (CNSS). a. Sepsis without a documented microbiological source. b. Affects 28% to 49% of hospitalized patients with sepsis. 5. Sepsis: A complex interaction between a host's response to an invading pathogen and the pathogen itself. a. Most of the time, the response to an invading pathogen is a normal reaction in order to maintain overall integrity of the host. The normal host response may include fever and leukocytosis. b. Any pathogen that violates at the tissue level is potentially able to evade the host's humeral and cel-lular immune system leading to widespread, systemic infection. c. Although the early phases of sepsis are pro-inflammatory in nature, if not controlled, these may progress to a significant immunosuppressed phase where the host is at an increased risk for secondary infections, along with reactivation of latent viruses. i. Initially, pro-inflammatory molecules enter the bloodstream in an effort to ward off the pathogen. 10. Infection Guidelines
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225 ii. With sepsis, an overactive immune response to an infection causes the natural checks and bal-ances to fail. Rather than dissipating, the activated inflammatory forces spread beyond the infected area. iii. As these pro-inflammatory molecules travel they cause dilation and endothelial damage, lead-ing to leakage of fluid out of the intravascular sys-tem and interstitial edema accumulation. iv. This vascular leakage causes disruption of oxy-gen, nutrients, waste products, and fluids through the capillary walls. v. If left unchecked, eventually organs become hypoxic and begin to fail. d. A patient's response to sepsis is highly dependent on a variety of both host variables (i. e., age, comor-bidities, genetics) and pathogen factors (i. e., viru-lence, susceptibility to treatment). Predisposing Factors A. SIRS. 1. Infection. 2. Autoimmune disorders. 3. Pancreatitis. 4. Vasculitis. 5. Thromboembolism. 6. Burns. 7. Surgery. B. Bacteremia. 1. IV drug user. 2. Presence of indwelling catheter (i. e., urinary catheter, IV catheter). 3. Presence of multiple abscesses. 4. History of structural heart disease and/or prosthetic heart valve. 5. History of recent dental procedure. 6. History of recent surgical treatment of an abscess or infected wound. C. Sepsis. 1. Younger than 1 year or over 65 years of age. 2. Weakened immune system. 3. Comorbid diseases. 4. Unrecognized, untreated, or undertreated infection. 5. Any condition listed under bacteremia. Subjective Data A. Common complaints/symptoms. 1. Condition specific. a. SIRS. i. Temperature greater than 100. 4∘F. ii. Heart rate greater than 90. iii. Respiratory rate greater than 20. iv. Abnormal WBC count ( >12,000 or <400,000). b. Bacteremia. i. Possibly asymptomatic or only a mild fever. ii. Other symptoms: Tachypnea, shivering, chills, persistent fever, altered sensorium, hypotension, and GI symptoms. This suggests development of sepsis and should be treated as such. iii. Thus, the remainder of this section will be directed toward sepsis specifically. c. Sepsis. i. Acute fever with or without chills. ii. Altered mental status (related to fever or hypoxia). iii. Hypotension. iv. Tachycardia (unless on beta-blockers, cal-cium channel blockers, or if presenting late with systemic organ failure). v. Tachypnea with hypoxia. vi. Cool, clammy skin (depending on status of end organ perfusion). vii. Abdominal pain if intra-abdominal source of infection. B. Common/typical scenario. 1. Possibly asymptomatic. 2. q SOFA score: 2 or more. 3. Nonspecific symptoms such as weakness, fatigue, malaise. C. Family and social history. 1. Use of IV drugs. 2. Family history of diabetes, hepatic disease, cardiovas-cular disease, or immunosuppression. 3. Medical history: Important because it can suggest a likely source of the infection as the cause of the inflam-matory response. It helps to identify the following: a. Comorbidities. b. Recent infections. c. Recent procedures/medical treatments. d. Implanted devices. D. Review of systems: Highly variable depending on source of infection. 1. Constitutional—fever, chills, malaise, or fatigue. 2. Respiratory—dyspnea, cough, or increased oxygen needs. 3. Cardiovascular—chest pain or palpitations. 4. Gastrointestinal—ocalized or diffuse abdominal pain. 5. Genitourinary—dysuria or decreased urine output. 6. Neurological—altered mental status. 7. Integumentary—cool/cold clammy skin, rash at IV sites, purulent wound, erythema, or warmth. Physical Examination A. General: Asymptomatic or generally ill appearing, com-plaining of fever, chills, or shivering. B. Neurological: Altered mental status from baseline, rang-ing from confusion, malaise, and fatigue to lethargic to obtunded to comatose. C. Respiratory: Tachypnea, dyspnea, cough, respiratory dis-tress, or sputum production. D. Cardiovascular: Tachycardia with or without murmur; jugular vein distention. E. Gastrointestinal: Diffuse severe abdominal pain with peritonitis; pain localized depending on source of infection. 1. Right upper quadrant with gallbladder source. 2. Right lower quadrant with appendix source. 3. Left lower quadrant with diverticulitis. F. Genitourinary: Costovertebral angle tenderness with acute pyelonephritis or tender prostate on examination, with possible prostatitis. G. Musculoskeletal: Swelling, joint tenderness, or warmth from septic arthritis. H. Dermatological. 1. Cool, clammy, and diaphoretic—septic shock. 2. Rash, erythema, and induration—cellulitis. Diagnostic Tests A. Laboratory. 1. Complete blood count (CBC) to check for leukocy-tosis with left shift, anemia, and thrombocytopenia. Systemic Inflammatory Response Syndrome/Bacteremia/Sepsis
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226 2. Blood cultures, at least two sets aerobic and anaerobic prior to antibiotic administration. 3. Urinalysis with culture if indicated. 4. Chemistry panel to check renal and hepatic function. 5. Cardiac enzymes to rule out cardiac cause. 6. Lactate level (marker of tissue perfusion). 7. Procalcitonin level to guide length of antimicrobial therapy. a. Low levels may indicate reduction of the likelihood of bacterial infection. B. Imaging. 1. Chest x-ray. 2. Abdominal ultrasound if suspect biliary tract obstruc-tion. 3. Possible CT scan or MRI: Superior to ultrasound when looking for any potential sources of infection, except those related to the biliary tree. a. Consider specific CTs if suspect concomitant trau-matic injury; useful in base workup on mechanism of injury. C. Miscellaneous. 1. EKG if suspect cardiac cause. 2. Possible lumbar puncture if suspect infection of the neurological system. Differential Diagnosis A. Pulmonary embolism. B. Acute myocardial infarction. C. Acute pancreatitis. D. Diabetic ketoacidosis. E. Massive aspiration. F. Upper or lower GI hemorrhage. G. Diuretic-induced hypovolemia. H. Systemic vasculitis. I. Cholecystitis. J. Renal calculi. Evaluation and Management Plan A. General plan. 1. Based on recommendations from the 2016 Surviving Sepsis Campaign: International Guidelines for Manage-ment of Sepsis and Septic Shock. 2. Sepsis and septic shock are medical emergencies, and it is recommended that treatment and resuscitation begin immediately. 3. The source of insult should be identified to prevent progressive dysfunction (SIRS). Recommend source con-trol for infection should occur as soon as medically and logistically possible. 4. Surviving sepsis interventions, or “Bundles. ” “Time of presentation” is defined as the time of triage in the ED or, if presenting from another care venue, from the earli-est chart annotation consistent with all elements of severe sepsis or septic shock ascertained through chart review. a. Tasks to be accomplished within 3 hours of pre-sentation. i. Measure lactate level. ii. Obtain blood cultures prior to administering antimicrobials. iii. Administer broad spectrum antimicrobials. iv. Administer 30 m L/kg crystalloids for hypotension or lactate 4 mmol/L or more. b. Tasks to be accomplished within 6 hours of pre-sentation. i. In the event of persistent hypotension after initial fluid administration (MAP <65 mm Hg) orif initial lactate was 4 mmol/L or more, reassess volume status and tissue perfusion and document findings. ii. Give vasopressors (for hypotension that does not respond to initial fluid resuscitation) to main-tain a MAP of 65 mm Hg or more. iii. Remeasure lactate if initial lactate elevated. c. Assessment of volume status and tissue perfusion indicators. i. Perform a focused examination including vital signs, cardiopulmonary status, capillary refill, pulse, and skin findings ORtwoofthefollowing. ii. Measure central venous pressure (CVP). iii. Measure central venous oxygen saturation (Scv O2). iv. Obtain a bedside cardiovascular ultrasound. v. Perform dynamic assessment of fluid respon-siveness with passive leg raise or fluid challenge. d. Fluid therapy. i. Resuscitate patients with sepsis-induced hypotension using at least 30 m L/kg of IV crys-talloid solution over 3 hours. ii. If additional fluids are required after initial resuscitation, base IV crystalloid infusion rates on frequent assessment of hemodynamic status. e. Antimicrobial therapy. i. Start administration of IV antimicrobials as soon as possible, within 1 hour, after diagnosis. ii. Administer empiric combination antimicro-bial therapy using drugs from at least two differ-ent antimicrobial classes to target the most likely pathogens for initial management, pending cul-ture results. 1)Do not use combination therapy for rou-tine treatment of neutropenic sepsis. iii. Narrow empiric antimicrobials as soon as pathogens have been identified by culture/sen-sitivity results and/or adequate clinical improve-ments are noted. iv. 7 to 10 days of antimicrobial therapy is ade-quate for most serious infections associated with sepsis. v. Perform daily assessment for de-escalation of antimicrobial therapy. vi. Understand that procalcitonin levels can be used to support shortening the duration of antimicrobial therapy. f. Vasoactive agent therapy (recommended). i. Aim for an initial target MAP of 65 mm Hg. ii. Select norepinephrine as a first choice of vaso-pressor. g. Corticosteroids. i. Understand that these agents are not recom-men ded if adequate fluid resuscitation and vaso-pressor therapy are able to restore hemodynamic stability. ii. Recognize that if fluids and vasopressors are not successful, then a daily dose of hydrocortisone 200 mg can be attempted. h. Mechanical ventilation. i. Strongly recommend prone over supine posi-tioning of adult patients with sepsis-induced adult respiratory distress syndrome (ARDS). ii. Strongly recommend a Pa O 2/FIO 2ratio of less than 150. iii. Do not use high frequency oscillatory ventila-tion (HFOV) in adult sepsis-induced ARDS. 10. Infection Guidelines
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227 iv. Do not use beta-2 agonists to treat adult sepsis-induced ARDS without bronchospasms. v. Suggest using lower over higher tidal volumes in adult sepsis-induced respiratory failure without ARDS. i. Glucose control. i. Initiate an insulin infusion once blood glucose levels are more than 180 mg/d L for two consecu-tive readings. ii. Aim for an upper glucose limit that targets less than or equal to 180 mg/d L. iii. Monitor blood glucose levels every 1 to 2 hours until stable, then every 4 hours, while on insulin infusion in the ICU. j. Nutrition. i. Start early enteral feeding as soon as patient can tolerate. ii. Use enteral feeding as opposed to parenteral feeding. iii. Within the first 7 days of caring for a criti-cally ill adult septic patient, start IV glucose and advance enteral feedings as tolerated over admin-istering parenteral feedings. iv. Give trophic/hypocaloric enteral feedings according to patient tolerance. v. Do not routinely monitor gastric residual vol-umes in adult septic patients, unless they are at a high risk for aspiration. vi. Suggest use of prokinetics for adult septic patients with feeding intolerance. k. Renal replacement therapy. i. Do not recommend for adult sepsis with acute kidney injury, unless there are other definitive indications for dialysis. B. Patient/family teaching points. 1. To be completed within 72 hours of ICU admission. 2. Goals of care. 3. Prognosis. 4. End-of-life care planning. Follow-Up A. Follow-up with the discharging provider and infectious disease provider. Consultation/Referral A. Consult critical care team to manage patients with sepsis. B. Consult infectious disease provider to assist in managing antibiotic selection. C. Consult appropriate surgical service for source control if sepsis is related to a structure in the body. Special/Geriatric Considerations A. Pregnancy. 1. Most common cause of sepsis in pregnant patients is obstruction of the urinary tract. a. This may be caused by either hormonal effects of the pregnancy (hydroureters) or the mechanical obstruction of the uterus impinging on the ureters. B. Geriatrics. 1. Blunted responses: May have insult without meeting criteria. 2. Medication effects: Blunt heart rate, respiratory rate, and temperature. 3. Possible peritonitis without rebound tenderness. Septic Arthritis Rose Milano Definition A. Infection of a joint, generally caused by bacteria, but can be caused by fungi or mycobacteria. B. Devastating form of acute-onset arthritis; considered an orthopedic emergency. C. Although all types of septic arthritis are infectious, not all types of infectious arthritis are classified as septic. Systemic diseases that can trigger an inflammatory response in joints include: 1. Lyme disease. 2. Chikungunya: Mosquito-borne illness (in the family of alphaviruses). 3. Rubella. 4. Parvovirus. 5. Hepatitis B and C. Incidence A. Incidence is 2 to 10 per 100,000 in general population. B. The incidence is increased in patients with rheumatoid arthritis or joint prostheses, 30 to 70 per 100,000. C. The prevalence has been estimated to range from 8% to 27% in adults presenting with one or more acutely painful joints. Septic Arthritis Bibliography Abraham, E. (2016). New definitions for sepsis and septic shock: Continuing evolution but with much still to be done. Journal of American Medical Association, 315 (8), 757-758. doi:10. 1001/jama. 2016. 0290 Centers for Disease Control and Prevention. (2016). National and state healthcare associated infections progress report. Retrieved from http://www Delinger, R. P., Schorr, C. A., & Levy, M. M. (2017). A user's guide to the 2016 Surviving Sepsis Campaign. Intensive Care Medicine, 43 (3), 299-303. doi:10. 1007/s00134-017-4681-8 Gaieski, D. F., Edwards, J. M., Kallen, M. J., & Carr, B. G. (2013). Bench-marking the incidence and mortality of severe sepsis in the United States. Critical Care Medicine, 41 (5), 1167-1174. doi:10. 1097/CCM. 0b013e31827c09f8 Gupta, S., Sakjuja, A., Kumar, G., Mc Grath, E., Nanchal, R. S., & Kashani, K. B. (2016). Culture negative severe sepsis: Nationwide trends and out-comes. Chest, 150 (6), 1251-1259. doi:10. 1016/j. chest. 2016. 08. 1460 Head, L. W., & Coopersmith, C. M. (2016). Evolution of sepsis manage-ment: From early goal directed therapy to personalized care. Advances in Surgery, 50 (1), 221-234. doi:10. 1016/j. yasu. 2016. 04. 002 Longo, D., Fauci, A., Kasper, D., Hauser, S., Jameson, J., & Loscalzo, J. (Eds. ). (2015). Harrison's principles of internal medicine (19th ed. ) New York, NY: Mc Graw Hill. Mac Claren, A., & Spelman, G. (2018, July 6). Fever in the intensive care unit. In G. Finlay (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/fever-in-the-intensive-care-unit Marino, P. M. (2014). The ICU book (4th ed). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins. O'Grady, N. M., Barie, P. S., Bartlett, J. G., Bleck, T., Carroll, K., Kalil, A. C.,... Masur, H. (2008). Guidelines for evaluation of new fever in critically ill adult patients: 2008 update from the American Asso-ciation of Critical Care Medicine and the Infectious Diseases Society of America. Critical Care Medicine, 36 (4), 1330-1349. doi:10. 1097/ CCM. 0b013e318169eda9 Rhodes, A., Evans, L. E., Alhazzani, L. E., Levy, M. M., Antoneilli, M., Ferrer, R., & Dellinger, P. (2017). Surviving sepsis campaign: Interna-tional guidelines for management of sepsis and shock: 2016. Intensive Care Medicine, 43 (3), 304-377. doi:10. 1007/s00134-017-4683-6 Singer, M., Deutschman, C. S., Seymour, C. W., Shankar-Hari, M., Annane, D., Bauer, M., & Angus, D. A. (2016). The third international consensus definitions for sepsis and septic shock (Sepsis-3). Journal of the American Medical Association, 315 (8), 801-810. doi:10. 1001/jama. 2016. 0287. cdc. gov/HAI/pdfs/progress-report/hai-progress-report. pdf
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228 D. Mortality has been at the persistent rate of 5% to 15% over the past 25 years. Pathogenesis A. Hematogenous seeding from bacteremia. Bacteria cause acute synovitis after entering the closed joint space within hours. The synovium is very vascular with no membrane bar-riers, making it susceptible to seeding by bacteria. 1. Synovial reaction: Results in swift entry of acute and chronic inflammatory cells. 2. Release of cytokines and proteases, which causes car-tilage degradation. 3. Bone loss: Evident within a few days. 4. Generally monomicrobial. 5. Most cases (75%): Involvement of only one joint (monoarticular). a. Polyarticular infection is commonly seen in rheumatoid arthritis. B. Joint surgery, joint aspiration, or local steroid injections: Often polymicrobial infections. C. Puncture wounds or bites: Also possibly inoculant into the joint. D. Bacteria most often involved. 1. Staphylococcus aureus: Primary cause. 2. Beta hemolytic streptococci: Next most common. 3. Neisseria gonorrhoeae: Most common pathogen among younger, sexually active adults, causing more than 75% of septic arthritis cases. E. In intravenous (IV) drug users, gram-negative bacilli implicated most often. 1. Klebsiella pneumoniae. 2. Escherichia coli. 3. Pseudomonas aeruginosa. Predisposing Factors A. Age greater than 80 years. B. Immunocompromised status. C. Preexisting joint disease (gout, systemic connective tissue disorders). D. Diabetes mellitus. E. Rheumatoid arthritis. F. Disseminated gonococcal infections in young healthy adults. Develops in 1% to 3% of untreated cases of gonor-rhea. G. All substance abuse, particularly IV drug use. H. Skin infections; cutaneous ulcers. I. Previous intra-articular corticosteroid injections. Subjective Data A. Common complaints/symptoms. 1. Native joints: Acute joint pain, swelling, warmth, ery-thema, decreased range of motion, fever, or malaise. 2. Prosthetic joints: Possibly minimal symptoms. B. Common/typical scenario. 1. History of joint swelling, pain, fever, general malaise, or chills of acute onset. 2. Other recent infection (e. g., u rinary tract infection [ UTI], cellulitis; cutaneous infections from IV drug use; sexually transmitted diseases, particularly gonorrhea; endocarditis). 3. Recent orthopedic surgery or joint replacement: Can be early onset, delayed onset (3-24 months), or late onset (24 months after surgery). 4. History of rheumatoid arthritis; receiving anti-tumor necrosis factor (TNF). a. Anti-TNF therapy associated with doubling of risk of septic arthritis. b. Can result in higher mortality because septic arthritis can be mistaken for an acute rheumatoid arthritis flare up and lead to delay in treatment. 5. History of immunosuppressive diseases, including: a. Liver disease. b. Diabetes. c. Solid tumors. d. Lymphomas. e. HIV. C. Family and social history. 1. History of IV drug use. 2. Smoking history. 3. Sexually active with multiple partners (gonococcal bacterial arthritis). D. Review of systems. 1. Constitutional: Fatigue, malaise, lethargy, decreased appetite, or recent trauma. 2. Gastrointestinal: Unintentional weight loss, or diar-rhea. 3. G enitourinary (GU): Frequent infections. 4. Musculoskeletal: Pain in joint(s), joint swelling, decreased range of motion, or arthritis. 5. Skin: Lesions, erythema, cutaneous wounds, needle marks, or bites. 6. Hematologic/lymphatic: Swollen lymph nodes or exposure to Lyme disease. Physical Examination A. Low grade fever. 1. Chills and spiking fever atypical. 2. Fever less likely in older adults. B. Possible joint swelling, warmth, erythema, and limited range of motion. C. Generally monoarticular. Polyarticular disease is present in about 20% of cases, generally in patients with rheumatoid arthritis or other systemic connective tissue disease. 1. Knee most common (50%). 2. Hip (20%). 3. Ankle (7%). 4. Wrists (7%). 5. Sacroiliac joints (1%-4%). 6. Axial joint septic arthritis (sternoclavicular, ster-nomanubrial joints): Most common in IV drug abuse. D. Joint effusion. E. Limited active and passive range of motion. F. Prosthetic joint infections: Later physical findings often minimal. 1. Slight to no swelling. 2. May have draining sinus. Diagnostic Tests A. Synovial fluid aspiration. 1. Synovial fluid leukocyte count and neutrophil per-centage: Reliable measure before cultures available. Syn-ovial fluid leukocyte count greater than 50,000/mm3 with polymorphonuclear leukocyte predominance is usu-ally indicative of septic arthritis but can also be seen in gout. 2. Cytology: Used to exclude gout or other crystal arthri-tis types. Mycobacteria and fungi may also be identified by cytology. 3. Cultures. a. Complete blood count. 10. Infection Guidelines
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229 i. Leukocytosis present in most cases but has low sensitivity and specificity. b. Inflammatory markers. i. E rythrocyte sedimentation rate (ESR): Useful only in patients with native joint infections with-out underlying hematological or rheumatological conditions. ii. C-reactive protein (CRP): Typically elevated, but also lacks specificity. c. Radiologic studies. i. Plain films not usually helpful except to rule out an injury that might produce similar symp-toms. ii. CT better than plain films in identifying joint effusion, soft tissue swelling, and abscesses. iii. MRI sometimes useful in native joint infec-tions. Newer machines may allow for assessment of prosthetics. 4. Bone scintigraphy: Sensitive in identifying joint infec-tions but is not specific enough to distinguish infection from other pathologies. B. Other diagnostics. 1. CT or ultrasound guided biopsy: Used in axial skeletal joints and sternoclavicular joints. 2. Open biopsy: Highest sensitivity and specificity but is rarely done. 3. Arthroscopy: Useful to evaluate for septic arthritis of the knee. Differential Diagnosis A. T raumatic effusion. B. Hemarthrosis. C. Bursitis. D. Cellulitis. E. Acute synovitis (inflammation of synovial membrane). F. Gout or pseudo gout. G. Viral arthritis (rubella, hepatitis B and C, HIV). H. Lyme disease. I. Reactive arthritis—seronegative spondyloarthropathies such as Reiter's syndrome, psoriatic arthritis, ankylosing spondylitis, inflammatory bowel disease-related arthritis. J. Endocarditis—can present with sterile synovitis or joint pain similar to septic arthritis. Fifteen percent of patients with infective endocarditis have concomitant septic arthritis or osteomyelitis. Evaluation and Management Plan A. General plan. 1. Considered a medical emergency. 2. Early treatment ( <7 days from onset): Improved out-come. 3. Antibiotics: First-line treatment. a. Empiric treatment aimed at most common bacte-ria of staphylococci and streptococci. b. Concomitant infections such as UTIs: Possible use of antibiotics for gram-negative bacteria. c. Prosthetic joint infections: Vancomycin if methicillin-resistant coagulase-negative staphylo-cocci. 4. Drainage. a. Hip, shoulder, and sacroiliac joints: Not easily drained with needle aspiration; may require open arthrotomy. b. Sternomanubrial and sternoclavicular joints: Gen-erally managed with open irrigation and debridement. 5. Splinting. a. Knees splinted in extension. b. Elbows splinted at 90∘. c. Hips in balanced suspension with no rotation. d. Joint range of motion to begin when infection improved. 6. Removal of prosthetic joint often necessary. 7. Dental prophylaxis: Should be considered in patients who have prosthetic joints and immunosuppression, dia-betes, or rheumatoid arthritis. B. Pharmacotherapy. 1. Antibiotic therapy: Initiated empirically, then tailored based on gram stain/cultures after joint aspiration. a. Most common pathogens: S. aureus, Staphylococ-cus epidermidis, and methicillin-resistant Staphylo-coccus aureus (MRSA), so empiric coverage can be initiated for gram-positive organisms (vancomycin). b. Ceftriaxone: Empiric coverage for gonococcal infection. 2. Symptom management with acetaminophen and ibuprofen if no contraindications. C. Patient/family teaching. 1. Antibiotics are used to treat the infection in septic arthritis. 2. If source control is not achievable with antibiotics alone, the fluid in the joint may be drained. 3. If there is extensive fluid, reaccumulation of fluid, or treatment is ineffective, surgery may be an option. D. Discharge. 1. Rest painful joints as needed. 2. Elevate joints to reduce swelling and pain. 3. Exercise may help keep joints flexible and reduce pain, but once joints become painful remember to rest them. 4. N onsteroidal anti-inflammatory drugs (NSAIDs) help reduce swelling, pain, and fever. Follow-Up A. Follow-up with the orthopedics team. B. Infectious disease. C. Physical therapy may be helpful. Consultation/Referral A. Consult rheumatology for assistance with diagnosis. B. Consult orthopedics for anticipated surgical intervention. C. Infectious disease consult for duration, route, and type of antibiotics. Special/Geriatric Considerations A. Immunocompromised patients. 1. Fungal septic arthritis: More common with Can-dida species, Aspergillus, Histoplasma, Cryptococcus, and Sporothrix. 2. Fungal infections: Challenging to diagnose and treat. B. Geriatric patients. 1. Inflammatory response: Possibly blunted due to age. Patients may not have overt symptoms such as fever and significant joint swelling, which could delay diagnosis. 2. Advanced age: Significant risk factor for poor out-come. 3. Female predominance after age 80. 4. Removal of prosthetics in patients with advanced age: May not be possible. 5. High index of suspicion: Warranted in geriatric patients in any recently symptomatic joint or worsening of preexisting joint disease. Septic Arthritis
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230 Bibliography Del Pozo, J. L., & Patel, R. (2009, August 20). Clinical practice. Infec-tion associated with prosthetic joints. New England Journal of Medicine, 361(8), 787-794. doi:10. 1056/NEJMcp0905029 Garcia-De La Torre, I. (2003, February). Advances in the management of septic arthritis. Rheumatic Disease Clinics of North America, 29 (1), 61-75. doi:10. 1016/S0889-857X(02)00080-7. Retrieved from https: //www. sciencedirect. com/science/article/pii/S0889857X02000807 Osmon, D. R., Berbari, E. F., Berendt, A. R., Lew, D., Zimmerli, W., Steck-elberg, J. M.,... Wilson, W. R. (2013, January). Executive summary: Diagnosis and management of prosthetic joint infection: Clinical prac-tice guidelines by the Infectious Diseases Society of America. Clinical Infectious Diseases, 56 (1), 1-10. doi:10. 1093/cid/cis966 Zimmerli, W., T rampuz, A., & Ochsner, P. E. (2004, October 14). Prosthetic-joint infections. The New England Journal of Medicine, 351(16), 1645-1654. doi:10. 1056/NEJMra040181 Tuberculosis Rose Milano Definition A. An infectious disease characterized by the growth of tubercles (nodules). B. One of the oldest diseases known to affect humans, most frequently affecting the lungs, although up to 1one third of cases occur outside of the pulmonary system. Incidence A. One of the top 10 leading causes of death worldwide, tuberculosis ( TB) ranks higher than malaria and HIV. TB is a leading killer of HIV-positive individuals; in 2015, 35% of deaths in those with HIV were due to TB. Pathogenesis A. General information. 1. Cause: Bacterium Mycobacterium tuberculosis. 2. Dispersion: Spread by M. tuberculosis bacilli-infected airborne droplets, through coughing, sneezing, speaking, and singing. B. Primary tuberculosis. 1. Active disease that develops in previously unexposed patients. 2. Almost always starts in the alveoli of the lungs. C. Latent tuberculosis infection (LTBI). 1. Exposure to M. tuberculosis without development of active disease. M. tuberculosis can stay dormant in the exposed host for decades. 2. Noncontagious: Can turn into active TB disease if left untreated. About 5% to 10% of persons who do not receive treatment for LTBI infection develop active TB disease at some time in their lives. D. Extra-pulmonary TB: Can affect any organ/system in the body. It may occur in 10% to 40% of infected individuals; the most common sites are: 1. Lymph nodes (tuberculous lymphadenitis). 2. Pleura. 3. Upper airways. 4. Genitourinary tract. 5. Skeletal. 6. Central nervous system (CNS/meninges). 7. Gastrointestinal (GI). 8. Pericardium (tuberculous pericarditis). 9. Miliary/disseminated TB. E. Drug-resistant TB. 1. Certain strains of M. tuberculosis bacillus are resistant to the drugs normally used to treat the disease. F. Previous exposure. 1. Individuals with positive tuberculosis skin test (TST) are less susceptible to a new M. tuberculosis infection than individuals with a negative TST. 2. Previous latent or active TB infections may not confer protective immunity. Predisposing Factors A. Decreased immune status of the host. 1. HIV. 2. Posttransplant patient on immunosuppressive ther-apy. 3. Cancer patient on chemotherapy. 4. Intravenous (IV) drug abuse history. B. Malnutrition. C. History of smoking tobacco/alcohol abuse/intravenous drug use. D. Chronic renal failure/hemodialysis. E. Recent infection with pulmonary fibrotic changes. F. Post jejunoileal bypass/gastrectomy. G. Elderly individuals with comorbidities and inconsistent immune response. H. Crowded living conditions. I. Healthcare workers. J. Migration from/travel to a country with a high volume of TB cases. K. Extremes in age: Very young and very old. Subjective Data A. Common complaints/symptoms. 1. Early active TB disease: May be asymptomatic. 2. Fever. 3. Unexplained productive cough for more than 2 weeks (cough is seldom a presenting symptom in HIV patients). 4. Hemoptysis: Sign of advanced infection. 5. Loss of appetite/weight loss. 6. Malaise/fatigue. 7. Night sweats. B. Common/typical scenario. 1. Generally, exposure from infected droplets by cough-ing, sneezing, speaking, or singing. 2. Slow symptom progression (over months). a. Worsening productive cough. b. Low grade fever. c. Night sweats. d. Fatigue. e. Weight loss. 3. Hemoptysis and/or pleuritic pain, which indicates severe disease. 4. Detailed medical history: TB. a. Presence of TB symptoms: If so, for how long?. b. Known exposure to individuals with infectious TB disease: When? c. Residence in high-risk congregate settings, such as prisons, long-term care facilities, and homeless shel-ters. d. Past medical diagnosis of latent TB or previous known TB disease and previous treatment. e. Comorbid diseases, which may increase risk of TB progression, including: i. HIV. ii. Diabetes mellitus. C. Family and social history. 1. TB: An infectious disease with no known genetic pre-disposition. 2. Social stigma/poor knowledge about TB: Possibly dif-ficult to obtain accurate history. 10. Infection Guidelines
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231 3. Recent travel to areas of known high prevalence of TB, such as Central/South America, Russia, Africa, Eastern Europe, and Asia. D. Review of systems. 1. General: Fever, night sweats, weight loss, and fatigue. 2. Vision: Icteric sclera. 3. Head/neck: Headache, neck pain, swelling/soreness of lump in throat, and hoarseness. 4. Respiratory: Shortness of breath, cough, coughing up blood, and pleuritic chest pain. 5. Neurological: Change in level of consciousness/ mental status, generalized weakness. 6. Endocrine: Fatigue, polyuria, polydipsia, polyphagia, and weight loss. 7. Musculoskeletal: Bone/joint pain. E. Mental health: Alcohol/drug abuse. F. Skin/hair: Presence/change in lesions/lumps. Physical Examination A. General. 1. Many individuals with primary TB are asymptomatic (about 90% early onset). 2. Once symptoms present, constitutional symptoms include weakness, fatigue, fever, chills, night sweats, loss of appetite, and jaundice. B. Head, ear, eyes, nose, throat (HEENT; TB of eyes, mouth, nose). 1. Headache (meningeal TB). 2. Nonhealing oral ulcers/dysphagia (GI tract TB). 3. Icteric sclera. 4. Bleeding gums. 5. Epistaxis. 6. Hoarseness. C. Neck (lymphatic TB/pericardial TB). 1. Lymphadenitis. 2. Jugular venous distention (late sign of pericardial tam-ponade). D. Neurological (meningeal TB). 1. Altered mental status, confusion. 2. Coma. E. Respiratory (pulmonary TB). 1. Decreased, absent, coarse breath sounds. 2. Dyspnea, tachypnea, sputum production, cough, and hemoptysis (pulmonary TB). F. Skin. 1. Jaundice. 2. Pruritic rash, which may lead to ulcers and abscesses. 3. Various stages of bruising. Diagnostic Tests A. Mantoux TST. 1. Small “wheel” of tuberculin fluid is injected under the skin. 2. Positive skin test means the individual has been infected with the TB bacteria. a. Greater than 5 mm induration is positive for: i. HIV. ii. Recent exposure. iii. Fibrotic changes on chest x-ray. iv. Organ transplant. v. Patients on immunosuppression medications. b. Greater than 10 mm induration is positive for: i. IV drug users. ii. Recent immigrants from high-risk areas. iii. Residents/employees of high-risk congregate settings. iv. Microbial lab personnel. c. Greater than 15 mm or more induration is positive for: i. Any individual, even with no risk factors. 3. A negative skin test does not exclude a diagnosis of latent TB or active TB disease. 4. Targeted TST programs are recommended for use only in high-risk groups. B. Approved TB blood tests in the United States: Interferon gamma release assays (IGRAs). 1. Quanti FERON-TB test. 2. T-SPOT TB test. C. Acid-fast bacilli (AFB) testing: Smear and culture. 1. Culture remains the gold standard for diagnosis and identifying drug susceptibility and genotyping. 2. Sputum specimens should be obtained from all individuals suspected of having active TB disease, both pulmonary and extra-pulmonary, with or without respi-ratory symptoms. a. At least three sputum specimens should be col-lected at consecutive intervals, 8 to 12 hours apart. b. At least one of the specimens should be an early morning specimen. D. Imaging: Cannot be used alone to distinguish active TB from latent TB. 1. Chest x-ray with a posterior-anterior view is the stan-dard approach. a. Although abnormalities may be seen anywhere on a chest x-ray, TB lesions are most often noted in the apical and posterior sections of the upper lobes or superior sections of the lower lobes. b. Chest x-rays can be used to rule out active pul-monary TB in an asymptomatic, immunocompetent individual with a positive TST or IGRA. 2. Chest CT is recommended if any suspicions for TB are noted after chest x-ray. Differential Diagnosis A. Pulmonary TB. 1. Nontuberculous mycobacterial (NTM) infection. 2. Fungal infections. 3. Sarcoidosis. 4. Lung abscess. 5. Septic emboli. 6. Lung cancer. 7. Lymphoma. 8. Actinomycosis. B. Extra-pulmonary TB. 1. Fungal infections. 2. Non-TB bacterial infections. 3. Syphilis. 4. Nodular vasculitis. 5. Leprosy. 6. Cat-scratch disease. 7. Rheumatoid arthritis. 8. Lupus vulgaris. 9. Pott disease. 10. Histoplasmosis. 11. Constrictive pericarditis. 12. Bronchiectasis. Evaluation and Management Plan A. General plan: If properly treated, TB caused by drug-susceptible strains is curable in the vast majority of cases. If untreated, the disease may be fatal within 5 years in 50% to 65% of cases. Tuberculosis
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232 1. Medical evaluation for TB disease. a. Medical history. b. Physical examination. c. Test for M. tuberculosis infection (IGRA or TST). d. Chest x-ray. e. Bacteriologic examination of clinical specimens. 2. Goals of treatment if active TB disease has been diag-nosed. a. Curing the individual. b. Preventing morbidity and mortality. c. Preventing emergence of multidrug resistant (MDR)-TB. d. Interrupting transmission of disease by making patients with active TB disease become patients with latent noninfectious TB. 3. LTBI: Who should receive treatment? a. Individuals with positive IGRA or TST and greater than 5 mm induration. i. Those with HIV. ii. Those who have had recent contact with per-son who has active TB disease. iii. Those with fibrotic chest x-ray findings and history of prior TB disease. iv. Those with organ transplants or other known immunosuppressive conditions, including those who have been receiving the equivalent of 15 mg of prednisone daily for longer than 1 month. b. Individuals with positive IGRA or TST and greater than 10 mm induration. i. Those who have recently (less than 5 years) arrived in the United States from areas where prevalence of TB is high (Asia, Africa, Eastern Europe, Russia, and Latin America). ii. Those who are known IV drug users. iii. Those who are residents/employees of high-risk cluster/congregate settings (prisons, nursing homes, homeless shelters, hospitals). iv. Those who work in a mycobacteriology lab set-ting. v. Those individuals with comorbidities known to increase the risk of infection to active disease (leukemia, diabetes, cancer, renal failure, gastrec-tomy). vi. Those with an un-accounted weight loss of 10%. c. Direct observation therapy (DOT): For individu-als who have active TB disease or are at high risk for TB disease ifthey are suspected to be noncompliant with prescribed medications. B. Patient/family teaching points. 1. Provide information about the disease process. 2. Explain the prescribed medication regimen and the importance of completing the entire treatment, even if the patients are asymptomatic. 3. Give information about possible side effects of the LTBI medications prescribed and when to call the medi-cal provider. Possible side effects include: a. Fever. b. Unexplained anorexia. c. Coffee or cola-colored urine. d. Icterus. e. Skin rash. f. Paresthesias of upper/lower extremities. g. Fatigue/weakness. h. Abdominal tenderness, especially right upper quadrant. i. Easily bruisable. j. Joint pain. k. Nausea/vomiting. C. Pharmacotherapy. 1. Latent TB. a. It is imperative to rule out active TB disease prior to initiating LTBI therapies. If mono-therapy with Isoniazid is prescribed for active TB disease, drug resistance may develop. b. Mono-therapy with Isoniazid (INH): 6-month dosing regimen. c. Mono-therapy with INH: 9-month dosing regi-men. d. INH and rifapentine (RPT) regimen: 12 doses. e. Rifampin (RIF) mono-therapy: 4 month regimen. i. Active TB disease. ii. T reatment must be for at least 6 months. iii. Most, but not all, of the M. tuberculosis bacilli are killed within the first 8 weeks of treatment. iv. Undertreatment of the bacilli surviving the initial 8 weeks of treatment can cause the individ-ual to become ill again, potentially with MDR-TB. v. Although the Food and Drug Administration has approved 10 medications to treat active TB disease, four core medications are used as first-line drugs. 1)INH. 2)RIF. 3)Ethambutol (EMB). 4)Pyrazinamide (PZA). vi. Dosing regimens: Available at the Centers for Disease Control and Prevention website: www. cdc. gov/tb/topic/treatment/tbdisease. htm. D. Discharge instructions. 1. Provide documentation of the following. a. TST or IGRA results. b. Medications to be taken (dose and timing). c. Possible side effects of medications to watch for. d. Duration of drug treatment, with date of last dose. 2. Give details of when individual is required to be tested for TB. 3. Name signs and symptoms of active TB disease and stress the importance of seeking medical care if symptoms should arise. 4. Give information about the consequences of noncom-pliance with the prescribed medication regimen. 5. Describe TB infection control measures and the potential need for isolation. Follow-Up A. Assess the state of infection and the infection's response to therapy. 1. Negative culture results are the most important objec-tive measure of response to treatments. 2. Individuals with previously reported positive culture are considered positive until two consecutive negative monthly specimens can be obtained. B. Check individuals monthly during treatment. 1. Monitor compliance with prescribed medication reg-imen. 2. Monitor for signs and symptoms of active TB disease. 3. Monitor for signs and symptoms of side effects of medications, especially hepatitis. a. Jaundice. b. Loss of appetite. c. Fatigue. d. Muscle and/or joint aches. 10. Infection Guidelines
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233 C. Recognize that active hepatitis and/or end-stage liver disease is a relative contraindication for use of INH or RIF. 1. Individuals with baseline abnormal liver function tests (LFTs) need regular monitoring with physical examina-tion and laboratory evaluation of LFTs. D. Understand that follow-up recommendations after treat-ment for active TB disease has been completed include the following: 1. Individuals with a positive response to a 6-to 9-month treatment regimen with both INH and RIF do not require routine follow-up but they should be educated to promptly report a prolonged cough, fever, or weight loss to their medical provider. 2. Individuals with TB bacilli who were resistant to INH and RIF should be monitored for 2 years after completing the alternative treatment option. Consultation/Referral A. TB disease treatment regimens for specific situations require special management and should be administered in consultation with a TB expert. B. Certain individuals with known or suspected TB should be evaluated by a TB specialist. 1. Pregnant women. 2. Breastfeeding women. 3. Infants and children. 4. HIV-infected individuals. 5. Individuals with known hepatic disease. 6. Individuals with extra-pulmonary TB disease. 7. Individuals with drug-resistant TB disease. 8. Individuals with culture-negative TB disease. 9. Individuals with renal insufficiency or end-stage renal disease. Special/Geriatric Considerations A. Individuals are no longer considered contagious when they meet all three of the following criteria. 1. Three consecutive negative AFB sputum smears col-lected at 8-to 24-hour intervals with at least one being an early morning specimen. 2. Symptoms have improved clinically. 3. Compliance with prescribed treatment regimen for at least 2 weeks or longer. B. Special consideration for treatment interruption during initial phase. 1. Interruption is equal to or greater than 14 days; restarting the treatment from the beginning is recom-mended. 2. Interruption is less than 14 days; continuing treat-ment to complete the total number of doses as originally planned, as long as they are completed within 3 months, is recommended. C. Special consideration for treatment interruption during the continuation phase. 1. If greater than or equal to 80% of the doses have been given andsputum AFB is negative on initial testing, then further dosing may not be needed. 2. If greater than or equal to 80% of the doses have been given andsputum AFB is positive on initial testing, then continue and complete therapy as initially prescribed. 3. If less than 80% of the doses have been given andthe interruption is less than 3 months duration, then con-tinue and complete therapy as initially prescribed. 4. If less than 80% of the doses have been given and the interruption is more than 3 months in duration, then restart therapy from the beginning of the initial phase. D. The rate of TB increases in elderly individuals who live at home. E. There is a two-to three-fold additional increased inci-dence rate of active TB among nursing home residents. F. Atypical presentation is not uncommon in older individ-uals. 1. Approximately 75% present with lung involvement. 2. Miliary TB, meningitis TB, skeletal TB, and geni-tourinary TB increase with advanced age. 3. Many do not present with cough, hemoptysis, fever, night sweats, or weight loss. 4. Many present with a change in functional capacity, chronic fatigue, cognitive impairment, anorexia, or unex-plained low grade fever. 5. Nonspecific, unexplainable symptoms that persist for weeks to months should alert medical providers to con-sider the possibility of unrecognized TB. Bibliography Centers for Disease Control and Prevention. (2013). Core curriculum on tuberculosis: What the clinician should know (6th ed. ). Atlanta, GA: Author. Retrieved from https://www. cdc. gov/tb/education/corecurr/ pdf/corecurr_all. pdf Centers for Disease Control and Prevention. (n. d. ). T uberculosis. Retrieved from https://www. cdc. gov/tb/default. htm Ehlers, S., & Schaible, U. E. (2013). The granuloma in tuberculosis: Dynam-ics of a host-pathogen collusion. Frontiers in Immunology, 3 (411), 1-9. doi:10. 3389/fimmu. 2012. 00411 Ellner, H. J. (2016). T uberculosis. In L. Goldman & A. L. Schafer (Eds. ), Goldman-Cecil medicine (25th ed. ). 2030-2039. Philadelphia, PA: Else-vier Saunders. Lewinsohn, D. M., Leonard, M. K., Lo Bue, P. A., Cohn, D. L., Daley, C. L., Desmond, E.,... Woods, G. L. (2016). Official American Thoracic Society/Infectious Diseases of America/Centers for Disease Control and Prevention clinical practice guidelines: Diagnosis of tuber-culosis in adults and children. Clinical Infectious Diseases, 64 (2), e1-e33. doi:10. 1093/cid/ciw694 Marino, P. M. (2014). The ICU book (4th ed. ). Philadelphia, PA: Wolters Kluwer/Lippincott, Williams & Wilkins. Mason, P. H., Roy, A., Spillane, J., & Singh, P. (2016). Social, historical and cultural dimensions of tuberculosis. Journal of Biosocial Science, 48 (2), 206-232. doi:10. 1017/S0021932015000115 Mathew, A. S., & Takalkar, A. M. (2007). Living with tuberculosis: The myths and the stigma from the Indian perspective. Clinical Infectious Diseases, 45 (9), 1247. doi:10. 1086/522312 Mattu, A., Grossman, S. A., & Rosen, P. L., (Eds. ). (2016). Geriatric emer-gencies: A discussion-based approach. Hoboken, NJ: John Wiley & Sons. Rajagopalan, S. (2001). T uberculosis and aging: A global health problem. Clinical Infectious Disease, 33, 1034-1039. doi:10. 1086/322671 Raviglione, M. C. (2015). Mycobacterial diseases: T uberculosis. In D. L. Kasper, S. L. Hauser, L. J. Jameson, A. S. Fauci, D. L. Longo, & J. Loscalzo (Eds. ), Harrison's principles of internal medicine. (pp. 1102-1122). San Francisco, CA: Mc Graw-Hill. Weber, C. G. (2014, July 11). Clinical infectious disease-2017 (The clinical medicine series) [Kindle] Pacific Primary Care Software PC. World Health Organization. (2018). Tuberculosis fact sheet. Retrieved from http://www. who. int/mediacentre/factsheets/fs104/en Tuberculosis
Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
235 11 Peripheral Vascular Guidelines Fiona Unac Acute Limb Ischemia Fiona Unac Definition A. Acute limb ischemia (ALI) is a sudden decrease in limb perfusion that causes a potential threat to limb viability. Incidence A. The incidence of ALI is approximately 1. 5 cases per 10,000 persons per year. Pathogenesis A. Arterial emboli that travel to the extremities predomi-nantly originate from the heart. B. Paradoxical emboli occur when venous thrombus traverse a cardiac defect and lodge in the arterial circulation. C. Arterial thrombosis can occur where there is an atherosclerotic plaque or arterial aneurysm at sites of prior revascularization or in patients with thrombophilic condi-tions. D. Arterial trauma can occur with interventional catheteri-zation procedures, as well as blunt or penetrating injuries. Predisposing Factors A. Atrial fibrillation. B. Recent myocardial infarction. C. Aortic atherosclerosis. D. Large vessel aneurysmal disease (e. g., aortic aneurysm, popliteal aneurysm). E. Prior lower extremity revascularization (angioplasty/ stent, bypass graft). F. Risk factors for aortic dissection. G. Arterial trauma. H. Deep vein thrombosis (paradoxical embolism). Subjective Data A. Common complaints/symptoms. 1. The “Six P's” is the classic presentation of ALI in patients without underlying occlusive vascular disease. a. Paresthesia. b. Pain. c. Pallor. d. Pulselessness. e. Poikilothermia (cold). f. Paralysis. 2. The sudden and dramatic development of ischemic symptoms in a previously asymptomatic patient is most consistent with an embolus. B. Common/typical scenario. 1. Other signs and symptoms. a. Patients with known peripheral artery disease or those who have undergone prior revasculariza-tion may develop symptoms slower (hours to days), depending if collateral channels provide flow around the occlusion. b. Upper limb ischemia is seldom limb threatening. Patients often present with a cold feeling and numb-ness, rather than pain in the arm. Duplex ultrasonog-raphy can confirm diagnosis. The arm often improves with anticoagulation. There should be a low thresh-old to undertake embolectomy if there is doubt about limb viability. c. Blue toe syndrome is typically due to embolic occlusion of digital arteries with atherothrombotic material from proximal arterial sources. There is often a strong pedal pulse and a warm foot. Identifica-tion and eradication of the embolic source should be undertaken. C. Family and social history. 1. Elicit onset, duration, and intensity of the “Six P's” of ALI (paresthesia, pain, pallor, pulselessness, poikilother-mia, and paralysis). 2. Question the patient about previous peripheral artery disease, prior lower extremity revascularization, and aor-tic or popliteal aneurysm. 3. Question the patient about atrial fibrillation, coronary artery disease, recent myocardial infarction, valve disease, and deep vein thrombosis. 4. Inquire into the patient's history of limb trauma. 5. Ask the patient about any condition that is a con-traindication for administering pharmacological throm-bolytic agents. D. Review of systems. 1. Musculoskeletal: Ask about the following. a. Temperature and pain of extremity. b. Any numbness, tingling, or weakness. Physical Examination A. Check temperature, pulse, respirations, and oxygen satu-ration. B. Take blood pressure on both arms. C. Inspect: Observe affected limb and compare with con-tralateral limb for mottling, pale, rubra, or necrosis. D. Auscultate. 1. Heart and lungs. 2. Carotid, abdominal aorta pulses. 3. Pulse of affected limb with the contralateral limb. a. Arm: Brachial. b. Leg: Femoral, popliteal. Acute Limb Ischemia
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236 E. Palpate. 1. Palpate and compare the pulses of the affected limb with the contralateral limb. a. Arm: Brachial, radial, ulnar pulses. b. Leg: Femoral, popliteal, dorsalis pedis, post tibial pulses. 2. Check capillary refill of affected limb and compare with contralateral limb. 3. Check limb strength and movement of affected limb and compare with contralateral limb. 4. Check limb sensation of affected limb and compare with contralateral limb. F. Handheld Doppler. 1. Assess pulses of affected limb with the contralateral limb and note if the pulse is monophasic, biphasic, or triphasic. a. Arm: Brachial, radial, ulnar pulses. Diagnostic Tests A. 12-Lead ECG to assess for underlying atrial fibrillation or myocardial infarction. B. If distal leg pulses detected on handheld Doppler, obtain an ankle-brachial index (ABI). An ABI of about 0. 3 is diag-nostic of subcritical acute ischemia (refer to lower extremity peripheral artery disease for measuring ABI). C. Full serum chemistry panel, including urea, creatinine, complete blood count, and baseline coagulation studies. D. Vascular imaging. 1. The availability of specific imaging modality and the time required to perform and interpret the study should be weighed against the urgency for revascularization. 2. Patients should be anticoagulated prior to and during imaging. 3. CT is the investigation of choice. 4. Percutaneous angiography is the best choice when an endovascular solution to the arterial occlusion is likely. Differential Diagnosis A. Chronic critical limb ischemia. B. Acute extremity compartment syndrome. C. Extensive deep vein thrombosis. D. Raynaud phenomenon. E. Nonischemic limb pain from acute gout, neuropathy, spontaneous hemorrhage, or traumatic soft tissue injury. Evaluation and Management Plan A. General plan. 1. Systemic anticoagulation with unfractionated hep-arin. a. Anticoagulation minimizes the risk of further clot propagation and prevents microvascular thrombosis of underperfused distal vessels. 2. Supportive measures. a. Keep NPO by mouth until a definitive treatment plan has been determined. b. Intravenous hydration, supplemental oxygen, and analgesia. c. Results of vital signs, EKG, and serum panel will guide further therapy. 3. T reatment selection. a. ALI treatment depends on the extent of limb ischemia (refer to Table 11. 1). b. Class I: ALI may require medical therapy only. Revascularization if contemplated can be performed electively. c. Class II: ALI may require revascularization to pre-serve the affected extremity. i. Class IIa: Percutaneous endovascular options are more effective in patients with ischemia of less than 2 weeks duration. Surgical revascularization is more effective in patients with ischemia of more than 2 weeks. ii. Class IIb: Requires emergency revasculariza-tion. T reatment options will depend on timeli-ness, personnel, and resource availability. d. Class III ALI. Revascularization is usually futile, and primary amputation should be considered. 4. Endovascular treatment options. a. Catheter-directed thrombolysis. b. Pharmacomechanical thrombectomy. c. Catheter-directed thrombus aspiration. d. Percutaneous mechanical thrombectomy. 5. Surgical revascularization options. a. Balloon catheter thrombectomy or embolectomy. b. Bypass procedures. c. Endarterectomy. d. Hybrid procedures combining open and endovas-cular techniques. B. Pharmacological. 1. There are no pharmacological treatment options for ALI. 2. This is a surgical emergency. 3. Systemic anticoagulation with a heparin drip may be started to minimize further clot propagation and to pre-vent microvascular thrombosis. 4. Administer an initial bolus of 100 mg/kg followed by an intravenous infusion of 1,000 U/hr. 5. If an urgent operation is not undertaken, the heparin should be titrated to maintain an activated partial throm-boplastin (a PTT) between 60 and 100 seconds. 6. Postoperatively, patients will need to be started on long-term oral anticoagulation. C. Discharge. 1. Patients will need to be maintained on anticoagula-tion after surgery and will need to follow-up with vas-cular surgery for the surgical wound. Patients need to be taught about side effects of anticoagulation therapy and signs and symptoms of effective wound healing. Follow-Up A. Outpatient vascular specialty after 4 to 6 weeks. B. Outpatient cardiology (if emboli likely to have originated from the heart) after 4 to 6 weeks. Consultation/Referral A. ALI is an emergency. B. Immediate transfer to hospital for urgent vascular con-sult. Special/Geriatric Considerations A. Patients with ALI are usually elderly. Bibliography Cronenwett, J. L., & Johnston, K. W. (2014). Rutherford's vascular surgery (8th ed). Philadelphia, PA: Elsevier Saunders. Gerhard-Herman, M. D., Gornick, H. L., Barrett, C., Barshes, N. R., Corriere, M. A., Drachman, D. E.,... Walsh, M. E. (2016). 2016 AHA/ACC guideline on the management of patients with lower extrem-ity peripheral artery disease: A report of the American College of Car-diology/American Heart Association Task Force on Clinical Practice Guidelines. Journal of the American College of Cardiology, 69, 1465-1508. doi:10. 1016/j. jacc. 2016. 11. 00811. Peripheral Vascular Guidelines
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237 TABLE 11. 1 Factors Affecting Risk of AAA Rupture Low Risk Average Risk High Risk Diameter <5cm 5-6cm >6 cm Expansion <0. 3cm/y 0. 3-0. 6 cm/y >0. 6 cm/y Smoking/COPD None,mild Moderate Severe/steroids Familyhistory Norelatives Onerelative Numerousrelatives Hypertension Normalblood pressure Controlled Poorly controlled Shape Fusiform Saccular Veryeccentric Wallstress Low(35 N/cm2/Medium (40 N/cm2/High (45 N/cm2) Sex... Male Female AAA, abdominal aortic aneurysm; COPD, chronicobstructive pulmonary disease. Source:Rahimi, S. A. (2019, January 8). Abdominal aortic aneurysm. In V. L. Rowe (Ed. ), Medscape. Retrieved from https://emedicine. medscape. com/article/1979501-overview Mitchell, M. E., & Carpenter, J. P. (2018, March 15 ). Clinical features and diagnosis of acute lower extremity ischemia. In K. A. Collins (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/ clinical-features-and-diagnosis-of-acute-lower-extremity-ischemia Rasmussen, T. E., Clouse, W. D., & Tonnessen, B. H. (2011). Handbook of patient care in vascular diseases (5th ed. ). Philadelphia, PA: Wolters Kluwer Health. Aortic Vessel Diseases: Aneurysms of the Aorta Ponrathi Athilingam Definition A. An aortic aneurysm is an abnormal enlargement or bulging of the wall of the aorta. B. An aneurysm can occur anywhere in the vascular tree. C. The bulge or ballooning may be defined as a: 1. Fusiform: Uniform in shape, appearing equally along an extended section and edges of the aorta. 2. Saccular aneurysm: Small, lopsided blister on one side of the aorta that forms in a weakened area of the aorta wall. D. An aneurysm can develop anywhere along the aorta. 1. Abdominal aortic aneurysms (AAAs): Occur in the section of the aorta that runs through the abdomen (abdominal aorta). 2. Thoracic aortic aneurysms: Occur in the chest area and can involve the aortic root, ascending aorta, aortic arch, or descending aorta. 3. Thoracoabdominal aortic aneurysms: Involve the aorta as it flows through both the abdomen and chest. Incidence A. Approximately three to four per 100,000 per year. 1. Intraperitoneal rupture (20%). 2. Retroperitoneal rupture (80%). 3. Aortocaval fistula (3%-4%). 4. Primary aortoduodenal fistula (less than 1%). Pathogenesis A. Once the aorta reaches a critical diameter (about 6 cm in the ascending aorta and 7 cm in the descending aorta), it loses all distensibility, so that a rise in blood pressure to around 200 mm Hg (as can occur physiologically during stress orexertion) can exceed the arterial wall strength and may trig-ger dissection or rupture. This is an emergency that warrants immediate intervention; often surgical. B. Often occurs as: 1. Retroperitoneal leak or rupture: If blood leaks into the space around the aorta behind the gut cavity then the leak is “contained” by the tissues and the patient is more likely to survive long enough to get to the hospital. 2. Free intraperitoneal rupture: If the rupture is into the gut cavity (the peritoneal cavity) then there are no tissues to “contain” the escape of blood from the aorta, and it is much less likely that the patient will survive long enough to be taken to the hospital. Virtually all the blood in the circulation can escape into the peritoneal cavity. Predisposing Factors A. Genetic: Familial thoracic aortic aneurysm and dissection (TAAD). B. Connective tissue disorders (Marfan's syndrome, Ehlers-Danlos syndrome type IV, and Loeys-Dietz syndrome, which partly resembles Marfan's syndrome). C. Aortitis from giant cell arteritis. D. Rheumatoid arthritis. E. Behçet's disease. F. Takayasu's arteritis or retroperitoneal fibrosis. G. Infection, such as syphilis and HIV. H. T rauma. I. Weightlifting. J. Cocaine and amphetamine use. Subjective Data A. Common complaints/symptoms. 1. Most people are unaware that they have an aneurysm because, in most cases, there are no symptoms. However, as aneurysms grow, symptoms may include: a. Pulsating enlargement or tender mass felt by a physician when performing a physical examination. b. Pain in the back, abdomen, or groin that may be prolonged and not relieved with position change or pain medication. 2. A ruptured aneurysm usually produces sudden, severe pain and other symptoms, such as loss of consciousness or shock, depending on the location of the aneurysm and the amount of bleeding. Aortic Vessel Diseases: Aneurysms of the Aorta
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238 B. Common/typical scenario. 1. Thoracic aneurysm dissection rupture. a. TAAs are easily missed or misdiagnosed for cardiac ischemia. b. Patients complain of sudden intense and persistent chest or back pain, pain that radiates to the back, trou-ble breathing, low blood pressure causing feelings of fainting, loss of consciousness, and trouble swallow-ing. 2. Abdominal aneurysm dissection or rupture. a. With AAA rupture patients complain of a sudden onset of severe lower back pain that may radiate to the groin, hypotension, or transient lower limb paralysis. b. Classic triad of symptoms: Pain, hypotension, and a pulsatile mass. c. Most abdominal aneurysms rupture into the retroperitoneal cavity. d. Rarely, AAA may rupture into the abdominal veins or the bowel. This may or may not be associated with retroperitoneal rupture. e. Emergent surgery is warranted once diagnosis is confirmed with echocardiogram, CT scan, or MRI. f. Rupture of an aneurysm is one of the most fatal surgical emergencies, with an overall mortality rate of 90%. C. Family/social history. 1. Family history is an independent risk factor for more rapid growth of aortic aneurysms and should be assessed. 2. First-degree family history of aortic aneurysm or bicuspid aortic valve also elevates risk. 3. Ask about smoking, which also increases risk of aortic aneurysm. D. Review of systems. 1. HEENT: Ask about any hoarseness or difficulty swal-lowing. 2. Respiratory: Ask if the patient is having any shortness of breath, coughing, difficulty breathing, or chest pain. 3. Musculoskeletal: Ask about back pain. Physical Examination A. T ransient lower limb paralysis. B. Right hypochondrial pain. C. Nephroureterolithiasis. D. Groin pain. E. Testicular pain. F. Testicular ecchymosis (blue scrotum sign of Bryant). G. Iliofemoral venous thrombosis. H. Inguinoscrotal mass mimicking a hernia. I. Patient may show decreased red blood cell (RBC) or hemoglobin due to internal blood loss and increased white blood cell (WBC). Diagnostic Tests A. An echocardiogram, MRI, or CT scan may help to dif-ferentiate the diagnosis. 1. Echocardiogram. 2. CT and MRI only if the aorta is calcified. B. Aortic angiogram or arteriogram: An arteriogram or angiogram accurately and directly depicts the vasculature; therefore, it clearly delineates the vessels and any abnormali-ties. 1. An abdominal aneurysm would only be visible on an x-ray if it were calcified. 2. CT scan and ultrasound don't give a direct view of the vessels and don't yield as accurate a diagnosis as the arteriogram. Differential Diagnosis A. Acute gastritis. B. Appendicitis. C. Urinary tract infection (UTI). D. Diverticulitis. E. Pancreatitis. F. Cholelithiasis. G. Small bowel obstruction. H. Myocardial infarction. Evaluation and Management Plan A. General plan. 1. Uncomplicated aneurysm. a. The goals of treatment include: i. Preventing the aneurysm from growing. ii. Preventing or reversing damage to other body structures. iii. Preventing or treating a rupture or dissection. iv. Allowing the patient to continue doing nor-mal daily activities. v. Follow-up and screening for risk to prevent occurrence, which is key. vi. Evaluation of risk factors. b. Primary management is rigorous blood pressure control. c. Smoking cessation. d. Antiplatelet therapy where appropriate. B. Dissecting or ruptured aneurysm. 1. Rupture of aneurysm is an emergency: Patient is often in shock and needs immediate intervention. a. Open repair when a rupture occurs as an emer-gency surgery. b. Emergency endovascular repair for ruptured AAA, thanks to new technology, is now feasible? c. Operative risk is based on patients' comorbidities and hospital factors (Table 11. 1). 2. Type of repair. a. Open repair of an AAA involves an incision of the abdomen to directly visualize the aortic aneurysm. b. Endovascular aneurysm repair (EVAR). C. Patient/family teaching points. 1. Patients should seek attention if they feel chest pain or they just suddenly “don't feel right. ” 2. A strong pulse sensation near the navel or bulge from the abdomen is also a reason to contact a provider right away. Deep constant or severe back or flank pain may be the only symptom a patient has of an expanding aneurysm. D. Pharmacotherapy. 1. Uncomplicated aneurysm. a. Statins: The role of statin therapy in AAA is unproven, but statins are advised because AAA patients have increased cardiovascular disease (CVD) risk. b. Other medical treatment: There is some evidence that the following may reduce the rate of expan-sion of small aneurysms, but their role is not yet clear. i. Doxycycline or roxithromycin. ii. Angiotensin-converting enzyme (ACE) inhi-bitors or losartan. iii. Statins. iv. Low-dose aspirin. v. Evaluate annually for risk of rupture, and follow-up. 11. Peripheral Vascular Guidelines
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239 E. Discharge instructions. 1. Patients with incidentally discovered AAA should be taught to recognize signs and symptoms of an emergency and be given instructions on what to do next. 2. Patients who undergo surgery should be taught effec-tive wound care and to assess for signs and symptoms of healing. Follow-Up A. Surgical intervention for aneurysm (abdominal or tho-racic). 1. Patients with an incidentally discovered AAA that is less than 3 cm in diameter require no further follow-up. 2. With AAAs 4 to 5 cm in diameter, elective repair may be of benefit for patients who are young, have a low oper-ative risk, and have a good life expectancy. 3. If the AAA is 3 to 4 cm in diameter, annual ultrasound imaging should be used to monitor for further dilatation. AAAs 4 to 4. 5 cm in diameter should be evaluated with ultrasonography every 6 months, and patients with AAAs greater than 4. 5 cm in diameter should be referred to a vascular surgeon. 4. The decision to treat an unruptured AAA is based on: a. Operative risk. b. Risk of rupture. c. Patient's estimated life expectancy. Consultation/Referral A. Consultation should be made immediately to vascular surgery or cardiothoracic surgery for evaluation and general management of patients. Special/Geriatric Considerations A. Age is an important predictor of mortality in patients with aortic dissection with or without surgical intervention. B. T reatment with endovascular aortic aneurysm repair should be strongly considered, particularly in octogenarians. Bibliography Bown, M. J., Fishwick, G., Sayers, R. D., & Bell, P. R. (2007). Repair of rup-tured abdominal aortic aneurysm by endovascular technique. Advances in Surgery, 41, 63-80. doi:10. 1016/j. yasu. 2007. 05. 005 Hiratzka, L. F., Bakris, G. L., Beckman, J. A., Bersin, R. M., Carr, V. F., Casey, D. E., Jr.,... Williams, D. M. (2010). 2010 ACCF/AHA/AAT-S/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. Circulation, 121(13), e266-e369. doi:10. 1161/CIR. 0b013e3181d4739e Le Fevre, M. L. (2014, August 19). Screening for abdominal aortic aneurysm: U. S. Preventive Services Task Force recommendation statement. Annals of Internal Medicine, 161 (4), 281-290. doi:10. 7326/M14-1204 Moulakakis, K. G., Mylonas, S. N., Dalainas, I., Kakisis, J., Kotsis, T., & Liapis, C. D. (2014, May). Management of complicated and uncompli-cated acute type B dissection: A systematic review and meta-analysis. Annals of Cardiothoracic Surgery, 3 (3), 234-246. doi:10. 3978/j. issn. 2225-319X. 2014. 05. 08 Mussa, F. F., Horton, J. D., Moridzadeh, R., Nicholson, J., T rimarchi, S., & Eagle, K. A. (2016). Acute aortic dissection and intramural hematoma: A systematic review. Journal of the American Medical Association, 316, 754-763. doi:10. 1001/jama. 2016. 10026 Rahimi, S. A. (2019, January 8). Abdominal aortic aneurysm. In V. L. Rowe (Ed. ), Medscape. Retrieved from https://emedicine. medscape. com/article/1979501-overview Svensson, L. G., Kouchoukos, N. T., Miller, D. C., Bavaria, J. E., Coselli, J. S., Curi, M. A., & Sundt, T. M., 3rd. (2008). Expert consensus document on the treatment of descending thoracic aortic disease using endovascular stent-grafts. The Annals of Thoracic Surgery, 85 (1), S1-S41. doi:10. 1016/j. athoracsur. 2007. 10. 099 Westaby, S., & Bertoni, G. B. (2007, February). Fifty years of thoracic aortic surgery: Lessons learned and future directions. The Annals of Thoracic Surgery, 83 (2), S832-S834. doi:10. 1016/j. athoracsur. 2006. 10. 098Carotid Artery Disease Ponrathi Athilingam Definition A. Atherosclerosis (waxy substance) plaque builds up inside the carotid arteries and causes carotid artery disease. B. There are two common carotid arteries, one on each side of the neck. They each divide into internal and external carotid arteries. 1. The internal carotid arteries supply oxygen-rich blood to brain. 2. The external carotid arteries supply oxygen-rich blood to face, scalp, and neck. Incidence A. Carotid artery stenosis is one of the risk factors for stroke. The overall prevalence of asymptomatic carotid artery steno-sis≥50% in the general population is estimated. B. The prevalence is higher in patients who harbor additional atherosclerotic lesions such as coronary artery disease. C. Patients with severe asymptomatic carotid stenosis have an annual risk of 2% to 5% for stroke. D. Among those 70 years and older, prevalence is increased to 12. 5%. Pathogenesis A. Atherosclerosis of the carotid arteries is a diffuse, degen-erative disease of the arteries resulting in plaques that consist of necrotic cells, lipids, and cholesterol crystals in the intima of carotid arteries. B. Arterial narrowing leads to locally increased velocities. A hemodynamic effect is reached when pressure and flow vol-ume are diminished in the poststenotic segment. C. These plaques can cause stenosis, can crack, or cause injury, allowing platelets to stick to the site to form thrombi and/or rupture, causing embolization, which can cause stroke. Predisposing Factors A. Smoking. B. High cholesterol levels in the blood. C. High blood pressure. D. Family history of atherosclerosis. E. Sedentary lifestyle. F. Diabetes or metabolic syndrome. Subjective Data A. Common complaints and symptoms. 1. Amaurosis fugax (fleeting or transient ipsilateral visual loss). 2. T ransient ischemic attacks (TIAs). 3. Crescendo TIAs. 4. Stroke-in-evolution. 5. Cerebral infarction. B. Common/typical scenario. 1. Patients may be asymptomatic with carotid artery dis-ease. 2. Sometimes it is found on routine surveillance. 3. Patients oftentimes present with stroke symptoms which depend on the location of the brain. Carotid Artery Disease
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240 4. Typically the patient with a stroke from carotid artery disease presents with weakness of extremities and speech difficulties. C. Family and social history (pertinent findings—positive/ negative). 1. Ask about family history, which has a strong associa-tion. 2. Ask about smoking, dietary habits, and physical activity. D. Review of systems (pertinent findings—positive/ negative). 1. Neurology—ask about the following: a. Numbness. b. Tingling or weakness. c. Speech difficulties. d. Confusion. e. T rouble swallowing. f. Visual disturbances. Physical Examination A. Thorough history. B. Carotid bruit heard on auscultation. C. Fundoscopic examination, if patient presents with amau-rosis fugax, hypertensive, or history of TIAs. D. Cardiac auscultation for murmur. Diagnostic Tests A. Imaging of the carotid artery is recommended in all patients with symptoms of carotid territory ischemia. This recommendation is based on the significant incidence of clin-ically relevant carotid stenosis in this patient group and the efficacy of carotid endarterectomy (CEA) for clinically sig-nificant lesions in reducing overall stroke (Grade 1, level of evidence A). B. Imaging should be strongly considered for patients who present with amaurosis fugax, evidence of retinal artery embolization on fundoscopic examination, or asymptomatic cerebral infarction and are candidates for CEA. This recom-mendation is based on the intermediate stroke risk in this group of patients and the efficacy of CEA in reducing the risk of subsequent stroke (Grade 1, level of evidence A). C. Routine screening is notrecommended to detect clinically asymptomatic carotid stenosis in the general population. D. Diagnosis. 1. Carotid duplex ultrasonography, with or without color: Screening test of choice to evaluate for carotid stenosis. 2. Computed tomographic angiography (CTA) is prefer-able to MRI/magnetic resonance angiography (MRA) for delineating calcium. 3. Carotid angiography. 4. Carotid MRA: May be useful in collaborating the finding of an occluded carotid with duplex sonography; however, this modality tends to overstate the significance of the stenosis. 5. Aortic arch and carotid arteriography: To evaluate the percentage of stenosis. Differential Diagnosis A. Stroke. B. Intracerebral hemorrhage. C. Neck trauma. D. Headache. E. Vertebral dissection. F. Vertigo. Evaluation and Management Plan A. General plan. 1. For neurologically symptomatic patients with 50% stenosis or asymptomatic patients with 60% stenosis diameter reduction, optimal medical therapy is indicated (Grade 1, level of evidence B). a. Grading carotid artery stenosis by ultrasound. i. Low degree stenosis 0% to 40%. ii. Moderate stenosis 50% to 60%. iii. Hemodynamically relevant stenosis greater than 70%. iv. Other simplistic grade is mild stenosis (less than 50%), moderate stenosis (50%-70%), and severe stenosis (70% or greater). 2. Antiplatelet therapy in asymptomatic patients with carotid atherosclerosis is recommended to reduce overall cardiovascular morbidity although it has not been shown to be effective in the primary prevention of stroke. 3. Surgical management. a. Carotid artery angioplasty and stenting. i. Indication for carotid angioplasty and stenting (CAS). 1)Symptomatic patients with a high-grade stenosis ( >70%) who are at high risk for CEA. 2)Patients who are at high risk for CEA and have asymptomatic carotid stenosis greater than 80%. 3)CAS is preferred over CEA in symptomatic patients with 50% stenosis and prior ipsi-lateral operation, tracheal stoma, or external beam irradiation resulting in fibrosis of the tis-sues of the ipsilateral neck. b. CEA. i. Indications for CEA. 1)Symptomatic patients with greater than 70% stenosis—clear benefit was found in the North American Symptomatic Carotid Endarterectomy T rial (NASCET). 2)Symptomatic patients with greater than 50% to 69% stenosis—benefit is marginal; appears to be greater for male patients. 3)Asymptomatic patients with greater than 60% stenosis—benefit is significantly less than for symptomatic patients with greater than 70% stenosis. 4)Generally, symptomatic patients with greater than 50% stenosis and healthy, asymptomatic patients with greater than 60% stenosis warrant consideration for CEA. 5)Patients who present with repetitive (crescendo) episodes of transient cerebral ischemia unresponsive to antiplatelet therapy should be considered for urgent CEA. 6)CEA is preferred over CAS in patients 70 years of age, with long ( >15 mm) lesions, pre-occlusive stenosis, or lipid-rich plaques that can be completely removed safely by a cervical incision in patients who have a virgin, nonra-diated neck. 7)Patients with symptomatic carotid steno-sis will benefit from CEA prior to or con-comitant with coronary artery bypass graft. The timing of the intervention depends on clinical presentation and institutional experience. 11. Peripheral Vascular Guidelines
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241 8)Patients with severe bilateral asymp-tomatic carotid stenosis (including stenosis and contralateral occlusion) should be consid-ered for CEA prior to or concomitant with coronary artery bypass graft. ii. Contraindications for CEA. 1)Patients with a severe neurological deficit following a cerebral infarction. 2)Patients with an occluded carotid artery. 3)Concurrent medical illness that would significantly limit the patient's life expectancy. 4)Anatomic issues that would be unfavor-able for CEA include the following: a)Lesions that extend above C2. b)Prior irradiation of the neck. c)Prior neck operation. B. Patient/family teaching points. 1. Review lifestyle changes. a. Smoking cessation. b. Weight loss. c. Increasing physical activity. d. Consuming a healthy diet low in fat and choles-terol. 2. Remind patients to take medication daily. 3. Blood pressure management. 4. Optimum blood sugar control in diabetes. 5. Manage comorbid conditions. 6. Educate patient on warning for stroke and regular follow-up. 7. Patients should be instructed to seek help immediately if they have any worsening symptoms or signs and symp-toms of a stroke. C. Pharmacotherapy. 1. Perioperative medical management of patients under-going carotid revascularization should include blood pressure control ( <140/80) or beta-blockade (HR 60-80). 2. Management of cholesterol with statin therapy (low-density lipoprotein [ LDL] 100 mg/d L). 3. Perioperative antithrombotic therapy for CEA should include aspirin (81-325 mg). a. Antiplatelet agents (e. g., aspirin, ticlopidine, clopidogrel). b. Anticoagulants (e. g., warfarin)—Note that use of warfarin in patients with noncardiac emboli is contro-versial. Anticoagulation is not recommended for the treatment of TIA or acute stroke unless there is evi-dence of a cardioembolic source. D. Discharge instructions. 1. Eat a healthy diet. 2. Limit salt. 3. Maintain a healthy weight. 4. Exercise as directed. 5. Limit alcohol. 6. Smoking cessation. Follow-Up A. Medical therapy recommendation by guideline after intervention. 1. Aspirin (30-325 mg/d) irreversibly acetylates the cyclooxygenase of platelets, thus inhibiting platelet syn-thesis of thromboxane. 2. Ticlopidine (250 mg q12h) is a thienopyridine that irreversibly alters the platelet membrane and inhibits platelet aggregation. It is approximately 10% more effec-tive than aspirin. Toxicity includes neutropenia and diar-rhea. 3. Clopidogrel (75 mg/d) is used if the risk of neutrope-nia is low. 4. Warfarin (titrated international normalized ratio [INR] 2-3) use in patients with noncardiac emboli is con-troversial. 5. Antiplatelet therapy with cilostazol may reduce the progression of carotid artery stenosis after stent implan-tation. B. Other recommendations for follow-up. 1. A postoperative duplex ultrasound, within 30 days, is recommended to assess the status of the endarterec-tomized vessel. 2. Imaging after CAS or CEA is indicated to follow con-tralateral disease progression in patients with contralateral stenosis 50%. 3. In patients with multiple risk factors for vascular disease, follow-up duplex may be indicated with lesser degrees of stenosis. The likelihood of disease progression is related to the initial severity of stenosis (Grade 2, level of evidence C). 4. Risk factor modification: Lifestyle or medical inter-ventions are implemented in order to address the follow-ing risk factors: Hypertension, hypercholesterolemia, and smoking. Consultation/Referral A. Referral to a cardiologist. B. Vascular surgeon is recommended. C. Intervention cardiologist. Special/Geriatric Considerations A. Benefits of CAS versus CEA should be strongly consid-ered in the elderly. B. While elderly patients who had CEA had fewer incidents of stroke than those who had CAS, mortality, they had an increased risk of mortality and an increased rate of AMI. Bibliography Brown, K., Itum, D. S., Preiss, J., Duwayri, Y., Veeraswamy, R. K., Salam, A., & Brewster, L. P. (2015). Carotid artery stenting has increased risk of external carotid artery occlusion compared with carotid endarterectomy. Journal of Vascular Surgery, 61 (1), 119-124. doi:10. 1016/j. jvs. 2014. 06. 008 Mas, J. L., T rinquart, L., Leys, D., Albucher, J. F., Rousseau, H., Viguier, A., & Chatellier, G. (2008, October). Endarterectomy Versus Angio-plasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial: Results up to 4 years from a randomised, multicentre trial. Lancet Neurology, 7 (10), 885-892. doi:10. 1016/S1474-4422(08)70195-9 Moore, W. S., Popma, J. J., Roubin, G. S., Voeks, J. H., Cutlip, D. E., Jones, M., & Brott, T. G. (2016, April). Carotid angiographic char-acteristics in the CREST trial were major contributors to periproce-dural stroke and death differences between carotid artery stenting and carotid endarterectomy. Journal of Vascular Surgery, 63 (4), 851-858. e1. doi:10. 1016/j. jvs. 2015. 08. 119 Ricotta, J. J., Aburahma, A., Ascher, E., Eskandari, M., Faries, P., Lal, B. K., & Moore, W. S. (2011, September). Updated Society for Vascular Surgery guidelines for management of extracranial carotid disease. Jour-nal of Vascular Surgery, 54 (3), e1-e31. doi:10. 1016/j. jvs. 2011. 07. 031 von Reutern, G. M., Goertler, M. W., Bornstein, N. M., Del Sette, M., Evans, D. H., Hetzel, A.,,... Yasaka, M. (2012). Grading carotid stenosis using ultrasonic methods. Stroke, 43, 916-921. doi:10. 1161/ STROKEAHA. 111. 636084 Carotid Artery Disease
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242Peripheral Artery Disease: Lower Extremity Fiona Unac Definition A. Lower extremity peripheral artery disease (PAD) is the obstruction of blood flow in the lower extremity arteries. Incidence A. The incidence of lower extremity PAD increases with age. 1. 5% of adults over 50 years of age. 2. 14. 5% of adults over 70 years of age. Pathogenesis A. Lower extremity PAD is frequently caused by atheroma in the walls of the arteries. B. PAD, coronary artery disease, and cerebral artery disease are all manifestations of atherosclerosis and commonly occur together. Predisposing Factors A. Age 70 years and older. B. Age 50 to 69 years with a history of smoking or diabetes. C. Age 40 to 49 with diabetes and at least one other risk factor for atherosclerosis. D. Known atherosclerosis at other sites (e. g., coronary, carotid, renal artery disease). E. Hypertension. F. Smoking. G. Hyperlipidemia. H. Homocysteinemia. I. Diabetes. Subjective Data A. Common complaints/symptoms. 1. The PAD Fontaine Classification score lists the com-mon symptoms in accordance with disease progression. B. Common/typical scenario. 1. Patient will report painful cramping during walking or exercise. 2. Elicit onset, duration, location, and intensity of pain. (Intermittent claudication pain is typically a muscle tight-ness in the buttock, thigh, or calf that comes on with exer-cise and is relieved at rest. ) 3. Inquire what aggravates and relieves the pain. a. Is the leg pain worse when legs are elevated or down? b. Is there resting pain or nocturnal cramping? (With critical limb ischemia, resting leg pain is aggravated when the legs are elevated. ) 4. Question the patient about cardiovascular-related conditions: Coronary artery disease, myocardial infarc-tion, carotid artery disease, trans-ischemic attack, or strokes. 5. Question the patient about other medical conditions such as diabetes, chronic kidney disease, heart failure, chronic obstructive pulmonary disease, and hematology conditions. 6. Inquire about musculoskeletal conditions such as osteoarthritis and spinal degeneration. C. Review of systems. 1. Musculoskeletal. a. Inquire about aching, tightness, or squeezing pain in the calf, thigh, or buttocks. b. Ask about pain before walking versus pain that starts during walking. Physical Examination A. Atherosclerotic disease is a diffuse process. Therefore, the examination, regardless of the complaint (intermittent clau-dication, angina, transient ischemic attack), should include the entire arterial system. 1. Check blood pressure in both arms, heart rate, and rhythm. 2. Inspect full length of upper and lower extremities: Dry, shiny hairless skin, muscle atrophy, color, necrotic and/or gangrenous ulcers, or evidence of distal emboliza-tion in the fingers and/or toes (blue toe syndrome). 3. Auscultate. a. Heart to listen for arrhythmias, gallops, and mur-murs. b. Carotid, brachial, abdominal aorta, femoral, and popliteal pulses to listen for bruits. c. Lung fields. 4. Palpate. a. Abdomen to assess for a pulsatile mass (aortic aneurysm). b. Leg: Femoral, popliteal, dorsalis pedis, and post tibial pulses. c. Arm: Brachial, radial, ulnar pulses. d. Check capillary refill, strength, and sensation of upper and lower extremities. 5. Beurger test to assess for positional rubra (with signif-icant PAD, foot is paler with elevation and then rubrous or cyanotic in the dependent position). 6. 10 g monofilament foot test to assess for peripheral neuropathy. Diagnostic Tests A. Ankle-brachial index has a high sensitivity and specificity for the identification of PAD. Inclusion of the toe-brachial index or continuous wave Doppler (if tissue is intact) assess-ment increases detection of serious PAD. B. Radiological imaging of arterial leg circulation such as ultrasound, CT, or MRI is best reserved for vascular services as part of the treatment decision and workup. C. Abdominal aorta screening is recommended due to the correlation between PAD and abdominal aortic aneurysm. Ultrasound is the modality of choice. D. Hematologic evaluation: Complete blood count, fasting blood glucose, fasting lipids, serum creatinine, urinalysis. Differential Diagnosis A. Arterial aneurysm. B. Arterial dissection. C. Embolism. D. Popliteal entrapment syndrome. E. Adventitial cystic disease. F. Thromboangitis obliterans (Buerger's disease). G. Limb trauma. H. Nonarterial etiologies for limb pain: Neurogenic, muscu-loskeletal causes, pathologic. Evaluation and Management Plan A. General plan. 1. Peripheral arterial disease management is dependent on symptom severity, comordid condition, and whether or not a patient will experience a meaningful benefit from a technically successful procedure. 11. Peripheral Vascular Guidelines
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243 2. Patients with PAD should have a cardiovascular risk reduction plan. a. Smoking cessation is critical. b. T reatment of diabetes if applicable to achieve an Hb A1c less than 5. 5 mmol/L. c. Healthy diet and exercise. d. Hematologic evaluation (see section “Diagnostics Tests”). Results will guide further therapy. e. Additional management plan for patients with intermittent claudication (Fontaine IIa and IIb) includes: i. Structured exercise program. ii. Referral to vascular service if intermittent clau-dication is lifestyle limiting and patient may ben-efit from revascularization treatment. 3. Critical limb ischemia (Fontaine III) and necrosis and gangrene (Fontaine IV) management plan will depend on progression of limb symptoms, comorbid conditions, and conduit availability. a. Supportive measures may include: i. Wound management. ii. Antibiotic therapy if underlying cellulitis or wound infection (consider Flucloxacillin). iii. Pain management. b. Vascular treatment may include: i. Endovascular revascularization. ii. Bypass surgery. iii. Digit or limb amputation. B. Patient/family teaching points. 1. Patients should seek out a provider if they experience pain, numbness, tingling, weakness, or significant tem-perature change in their extremities. 2. Patients should also report open sores that do not heal. C. Pharmacotherapy. 1. Antiplatelet therapy with long-term low-dose aspirin. 2. T reatment of hyperlipidemia with a statin to achieve a low-density lipoprotein level less than 100 mg/d L ( <70 mg/d L if PAD and a history of coronary or cerebral artery disease). 3. T reatment of hypertension to achieve a blood pressure less than 140/90 mm Hg ( <130/80 mm Hg for patients with diabetes or renal failure). 4. Consider pharmacology therapy. In the United States only pentoxifylline and cilostazol have achieved Food and Drug Administration (FDA) approval for the treatment of intermittent claudication. D. Discharge. 1. Patients need to be taught to make healthy dietary changes, keep cholesterol levels down, maintain a healthy weight, and stop smoking. Follow-Up A. Three-month primary care review of cardiovascular risk management. B. If treated percutaneously or surgically, outpatient vascular review after 4 to 6 weeks. Consultation/Referral A. Consultation and referral are dependent on symptom sta-tus. Patients with lower extremity PAD have a wide spectrum of symptoms. 1. Fontaine Classification I: Asymptomatic. Conserva-tive management. 2. Fontaine Classification IIa: Intermittent claudication greater than 200 m (and nonlifestyle limiting). Conser-vative management. 3. Fontaine Classification IIb: Intermittent claudication less than 200 m (or lifestyle limiting). Refer to vascular service. 4. Fontaine Classification III: Nocturnal or resting pain. Referral to vascular service. 5. Fontaine Classification IV: Necrosis and gangrene. For hospital admission, vascular consult. Special/Geriatric Considerations A. Patients with PAD are usually elderly. B. Younger patients are usually diabetic. Bibliography Cronenwett, J. L., & Johnston, K. W. (2014). Rutherford's vascular surgery (8th ed. ). Philadelphia, PA: Elsevier Saunders. Mitchell, M. E., & Carpenter, J. P. (2017). Overview of acute arterial occlusion of the extremities (acute limb ischaemia). Retrieved from www. uptodate. com Neschis, D. G., & Golden, M. A. (2018, June 11). Clinical features and diagnosis of lower extremity peripheral artery disease. In K. A. Collins (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/clinical-features-and-diagnosis-of-lower-extremity-peripheral-artery-disease Rasmussen, T. E., Clouse, W. D., & Tonnessen, B. H. (2011). Handbook of patient care in vascular diseases (5th ed. ). Philadelphia, PA: Wolters Kluwer Health. Tehan, P. E., Bray, A., & Chuter, V. H. (2016). Non-invasive vascular assessment in the foot with diabetes: Sensitivity and specificity of the ankle brachial index, toe brachial index and continuous wave Doppler for detecting peripheral arterial disease. Journal of Diabetes and Its Com-plications, 30 (1), 155-160. doi:10. 1016/j. jdiacomp. 2015. 07. 019 Peripheral Artery Disease: Upper Extremity Fiona Unac Definition A. Upper extremity arterial disease is the obstruction of blood flow in the large and/or small arterial vessels of the upper extremity arteries. Incidence A. Upper extremity arterial disease is relatively rare. It accounts for less than 5% of patients presenting with limb ischemia. Pathogenesis A. Arterial vasospasm: Raynaud's phenomenon, ergotism, vinyl chloride exposure. B. Arterial obstruction. 1. Atherosclerosis (main cause of upper extremity arte-rial disease). 2. Thoracic outlet compression. 3. Embolic (e. g., cardiac or thoracic outlet in origin), aneurysms. 4. Arteritis (e. g., Takayasu arteritis or giant cell arteri-tis). 5. Fibromuscular disease. 6. Hypersensitivity angiitis. 7. Iatrogenic, cold, or vibration injury. 8. Dialysis steal syndrome. 9. Connective tissue disease (e. g., scleroderma, rheumatoid arthritis, systemic lupus). 10. Myeloproliferative disorders and hypercoagulable states. 11. Infection from injection of drugs and arterial procedures. Peripheral Artery Disease: Upper Extremity
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244 C. Bilateral symptoms may be from a systemic cause such as a connective tissue disorder. D. Unilateral symptoms may be from a discrete occlusive lesion. Predisposing Factors A. Dependent on pathogenesis. B. Patients who present with upper extremity ischemia range from young adults with nonatherosclerotic causes to elderly patients with atherosclerosis. C. Risk factors include smoking, hypercholesterolemia, hypertension, diabetes, and age. Subjective Data A. Common complaints/symptoms. 1. Most patients with upper extremity arterial disease are asymptomatic; the condition is only detected by finding asymmetric arm blood pressures. B. Common/typical scenario. 1. Raynaud's phenomenon: Predictable sequence of color changes in finger and/or hand. a. Pallor (white), followed by cyanosis (blue) and then rubor (red). b. Often associated with finger numbness. c. Pain is generally not severe, unless ulceration is present. d. Symptoms are activated by exposure to cold and emotional stimuli. 2. Arm intermittent claudication is an unusual presenta-tion of arm ischemia due to excellent collateral blood flow around the shoulder. However, active adults, particularly manual laborers, may experience arm claudication from subclavian or brachial artery stenosis. 3. Dizziness, or even syncope, during arm exertion may be from subclavian steal syndrome. 4. Patients with chronic upper extremity ischemia may complain of change in sensation, hand temperature, and muscle pain with use. 5. Tissue necrosis includes gangrene and poorly heal-ing ulcerations of the fingers. (Patients may dismiss small ulcers caused by microemboli as inconsequential bruises or sores. ) 6. Acute limb ischemia is covered previously. C. Family and social history. 1. Elicit onset, duration, location,and intensity; aggra-vates and relieves pain. 2. Inquire about signs and symptoms of connective tis-sue disease such as dry eyes, difficulty swallowing, dry mouth, and arthritis. 3. Question the patient about any history of trauma, including upper extremity access for peripheral or coro-nary catheterization. 4. Inquire about occupational and recreational history regarding exposure to vibrating tools or toxins, as well as repetitive trauma. 5. Question the patient about cardiovascular-related conditions: Coronary artery disease, myocardial infarc-tion, carotid artery disease, transient ischemic attack, or strokes. 6. Question the patient about other medical conditions such as diabetes, chronic kidney disease, heart failure, chronic obstructive pulmonary disease, or hematology conditions. 7. Inquire about musculoskeletal conditions such as osteoarthritis or rotator cuff injury. D. Review of systems. 1. Musculoskeletal: Ask about arm pain with movement and at rest; ask about any swelling. 2. Dermatology: Ask about ulceration of fingers or dis-coloration. Physical Examination A. Take blood pressure in both arms. 1. 10 mm Hg or more difference suggests a hemody-namically significant innominate, subclavian, or axillary artery stenosis. 2. In cases of suspected claudication, arm blood pressure, should be measured at rest and after 2 to 5 minutes of exercise. B. Inspect. 1. Hands and fingers and note temperature, color, cap-illary refill, ulcers, and any other lesions. 2. Fingers for clubbing, which is associated with chronic pulmonary disease. (Patients with clubbing and cold fin-gers may have low arterial oxygen levels as the basis for their complaint). 3. Fingers for telangiectasia and sclerodactyly, which is commonly seen with advanced scleroderma as well as other connective tissue diseases. 4. Check for splinter hemorrhages in the nail beds, which is seen with emboli. C. Auscultate. 1. Heart to listen for arrhythmias, gallops, and murmurs. 2. Supraclavicular and infraclavicular fossa to listen for bruits which may indicate a possible subclavian artery stenosis. A supraclavicular pulsatile mass is associated with a subclavian aneurysm or cervical rib. D. Palpate. 1. Upper extremity pulses. a. Axillary and proximal brachial artery: The upper medial arm in the groove between the biceps and tri-ceps muscles. b. Brachial artery: The antecubital fossa just medial to the biceps tendon. c. Radial artery: The wrist over the distal radius. d. Ulnar artery: The wrist over the distal ulna. 2. Carotid, abdominal aorta, femoral, popliteal, dorsalis pedis, post tibial pulses. E. Handheld Doppler. 1. Assess upper extremity pulses including digital pulses and note if the pulse is monophasic, biphasic, or triphasic. F. Neurological examination, including muscle mass, mus-cle strength, and sensation to assess for compression of the neurovascular bundle (see section “Thoracic Outlet Syn-drome”). G. Additional bedside examination. 1. Allen's test is recommended if there is a difference in arm blood pressure or if there is a reduced radial or ulnar pulse. a. Allen's test should be conducted on both arms. b. A positive Allen's test suggests that there is ade-quate dual blood supply to the hand. i. Elevate the hand and ask the patient to clench his or her fist for 30 seconds. ii. Pressure is applied over the ulnar and radial arteries to occlude both of them. iii. The hand is then opened. It should appear blanched. iv. One artery is tested by releasing the pressure over that artery to see if the hand flushes (color should return within 5-15 seconds). 11. Peripheral Vascular Guidelines
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245 v. The other artery is then tested in a similar fashion. 2. Adson's test and Roos test can assist in assessing for thoracic outlet syndrome (see section “Thoracic Outlet Syndrome”). Diagnostic Tests A. Vascular laboratory: Segmental pressure measurements of the upper extremity and finger pressure measurements and waveforms. B. Radiological imaging of arterial arm circulation such as duplex ultrasound, CT, and MRI is best reserved for vascular services as part of the treatment decision and workup. C. Hematologic evaluation. 1. Erythrocyte sedimentation rate, C-reactive protein, antiphospholipid antibodies, antinuclear antibody titer, and rheumatoid factor to screen for underlying autoim-mune disease. 2. Platelet count, since thrombocytosis can mimic Ray-naud's phenomenon. 3. Serum protein electrophoresis since serum protein abnormalities may be associated with vasospasms. 4. For patients at risk of or with suspected atheroscle-rotic disease, fasting lipids, fasting glucose, or serum creatinine. Differential Diagnosis A. Multiple etiologies; see “Pathogenesis” section. B. Differential diagnosis includes neurogenic, musculoskele-tal, and pathological causes. Evaluation and Management Plan A. General plan. 1. All patients with upper extremity arterial disease should have a cardiovascular risk reduction plan based on their 5-year cardiovascular risk assessment. 2. T reat underlying cause. a. Primary Raynaud's phenomenon. i. Conservative management; patients advised to minimize cold exposure and stress. b. Emboli: Manage arrhythmia and anticoagulate. c. Connective tissue diseases: Management of disease process. d. Occupational and recreational factors: Advise patients to minimize exposure. 3. Supportive measures. a. Wound management. b. Antibiotic if underlying cellulitis or wound infec-tion (consider Flucloxacillin). c. Pain management. 4. Vascular treatment may include: a. Endovascular revascularization. b. Bypass surgery. c. Digit or limb amputation. B. Patient/family teaching points. 1. Patients should seek out a provider if they experience any pain, numbness, tingling, weakness, or significant temperature change in their extremities. 2. Patients should also report open sores that do not heal. C. Pharmacotherapy. 1. Frequent or severe symptoms. a. Nifidipine 30 to 180 mg/d or amiodipine 5 to 20 mg/d. 2. Start with lowest dose and gradually increase, if needed, depending upon the response. D. Discharge instructions (if standard accepted guidelines exist, please use discharge template). 1. Make healthy dietary changes. 2. Keep cholesterol levels down. 3. Maintain a healthy weight. 4. Smoking cessation. Follow-Up A. Depend on pathogenesis: Outpatient follow-up with vas-cular, cardiology, or rheumatology service. B. Three-month primary care review of cardiovascular risk management. Consultation/Referral A. Consultation and referral is dependent on pathogenesis and severity of symptoms. 1. If clinical presentation is suggestive of large vessel dis-ease, refer to vascular service. 2. If hematological screening is positive for autoimmune disease, refer to rheumatology service. 3. Acute limb ischemia for urgent hospital admission (see “Acute Limb Ischemia” section). 4. Necrosis and gangrene. For hospital admission, seek a vascular consult. Special/Geriatric Considerations A. Elderly patients may not report or experience intermit-tent claudication. B. Elderly patients may have decreased blood flow and other circulatory problems that put them at special risk of being unaware of any issues or problems. Bibliography Barshes, N. R. (2017, November 22). Overview of upper extremity periph-eral artery disease. In K. A. Collins (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-upper-extremity-peripheral-artery-disease Cronenwett, J. L., & Johnston, K. W. (2014). Rutherford's vascular surgery (8th ed. ). Philadelphia, PA: Elsevier Saunders. Mitchell, M. E., & Carpenter, J. P. (2017). Overview of acute arterial occlusion of the extremities (acute limb ischaemia). Retrieved from www. uptodate. com Rasmussen, T. E., Clouse, W. D., & Tonnessen, B. H. (2011). Handbook of patient care in vascular diseases (5th ed. ). Philadelphia, PA: Wolters Kluwer Health. Peripheral Vascular Disease Ponrathi Athilingam Definition A. Peripheral vascular disease (PVD) refers to diseases of the blood vessels located outside the heart and brain. B. Peripheral arterial disease (PAD) develops only in the arteries. PAD is the most common form of PVD. Incidence A. The Centers for Disease Control and Prevention (CDC) reports approximately 12% to 20% of people over age 60 develop PAD; it affects 15% to 20% of persons older than 70 years of age. B. PAD affects about 8. 5 million Americans. C. The prevalence of PAD, both symptomatic and asymp-tomatic, is greater in men than in women, especially in young persons. At very advanced ages almost no differences exist Peripheral Vascular Disease
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246 between the sexes. However, age remains the main marker of PAD risk. D. The estimated prevalence of intermittent claudication in persons aged 60 to 65 years is 35%. However, the prevalence in persons 10 years older (70-75 years) rises to 70%. Pathogenesis A. PVD is a slow and progressive circulation disorder caused by narrowing, blockage, or spasms in a blood vessel. PAD is considered a set of chronic or acute syndromes, gen-erally derived from the presence of occlusive arterial disease, which causes inadequate blood flow to the limbs. B. On most occasions, the underlying disease process is arte-riosclerotic disease, mainly affecting the vascularization to the lower limbs. C. From the pathophysiologic point of view, ischemia of the lower limbs can be classified as functional or critical due to an imbalance between the needs of the peripheral tissues and the blood supply. D. Functional ischemia occurs when the blood flow is nor-mal at rest but insufficient during exercise, presenting clini-cally as intermittent claudication. E. Critical ischemia is produced when the reduction in blood flow results in a perfusion deficit at rest and is defined by the presence of pain at rest or trophic lesions in the legs. Predisposing Factors A. Age over 50. B. Postmenopausal women have a higher risk. C. Overweight and obesity. D. Dyslipidemia. E. Hyperhomocysteinemia. F. History of cerebrovascular disease or stroke. G. History of heart disease. H. History of diabetes. I. High blood pressure. J. Family history of high cholesterol, high blood pressure, or PVD. K. Kidney disease on hemodialysis. L. Lifestyle choices that can increase risk of developing PVD include: 1. Sedentary lifestyle or not engaging in physical exer-cise. 2. Unhealthy dietary habits. 3. Smoking increases risk by seven times. 4. Drug use. 5. Excessive alcohol. Subjective Data A. Common complaints/symptoms. 1. The first signs of PVD begin slowly and irregularly. 2. Fatigue or cramping in legs and feet that gets worse with physical activity due to the lack of blood flow are the earliest signs the patients often report. 3. Leg cramps when lying in bed may occur. 4. Poor hair growth often below knees. 5. Legs and arms may turn reddish blue or pale. 6. Skin in the extremities may appear pale and thin. 7. Pulses in the extremities may be weak. 8. Ulcers and wounds in legs and toes that will not heal. 9. Toes may appear blue in color and the toenails become thick and opaque. 10. Patient often experiences severe burning in toes. 11. In severe cases, pain may occur even at rest, particu-larly at night when the legs are raised in bed. 12. In a small number of cases (often untreated), tissue death (gangrene) of a foot may result. 13. If an artery higher upstream is narrowed, such as the iliac artery, pain may be experienced in the thighs or but-tocks while walking. B. Common/typical scenario. 1. Patients will typically present with intermittent clau-dication, which is cramping with exercise that resolves with rest. 2. If the patient has severe disease progression, he or she may present with pain in the legs that occurs at rest. C. Family and social history. 1. Ask about family history of any vascular disease or dia-betes. 2. Ask about smoking, if the patient has a sedentary lifestyle or poor eating habits. D. Review of systems. 1. Musculoskeletal: Ask about leg cramps, pain at rest, or if patients raise their legs at night. 2. Neurology: Ask about numbness or severe burning in toes. 3. Dermatology: Ask about discoloration of extremities, ulcers, or wounds that don't heal, and/or nails that have become thick and opaque. Physical Examination A. Basic examination of PVD includes assessment for the presence of pulses in the lower limbs including the femoral, popliteal, pedal, and posterior tibial arteries. B. Auscultation of the abdomen will enable identification of the presence of murmurs, which are indicative of disease in the aorta or the iliac arteries. Auscultation of the inguinal region may reveal the presence of lesions in the external iliac or femoral bifurcation vessels. C. Check the temperature, color, and capillary refill of the foot. Patients with claudication do not usually show a reduc-tion in temperature or capillary filling. D. Leg dangling test: A reduction in temperature and pale-ness, with or without cyanosis or dangling erythrosis, are common in patients with critical ischemia. E. Patients with PAD have a higher risk for developing crit-ical limb ischemia (CLI). 1. The patients with CLI should undergo expedited eval-uation and treatment of factors that are known to increase the risk of amputation. 2. Patients with CLI in whom open surgical repair is anticipated should undergo assessment of cardiovascular risk. 3. Patients with CLI and skin breakdown should be referred to healthcare providers with specialized expertise in wound care. 4. Patients at risk for CLI (those with diabetes, neuropa-thy, chronic renal failure, or infection) who develop acute limb symptoms represent potential vascular emergencies and should be assessed immediately and treated by a spe-cialist competent in treating vascular disease. F. Chronic foot and leg ulcers (see Table 11. 2). G. Stages of PVD. 1. Stage I is characterized by the absence of symptoms. It includes patients who have an extensive occlusive arte-rial lesion in the legs, or have high risk but present no symptoms of arterial failure. In these situations, the patients may present with critical ischemia straight from an asymptomatic stage. 2. Stage II is characterized by the presence of intermit-tent claudication. The intermittent claudication that is11. Peripheral Vascular Guidelines
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247 TABLE 11. 2 How to Differentiate Foot Ulcer and Pain Neuropathic Ulcer Ischemic Ulcer Oftenpainless Extremelypainful Normalpulses Absentpulses Typicallypunched-out appearance Irregularmargins Oftenlocated on sole or edge offoot or metatarsal head Commonlylocated or startson toes Presenceof calluses Callusesabsent or infrequent Lossof sensation, reflexes, andvibration sense Variablesensory findings present Increasein blood flow (arteriovenous shunting)Decreasein blood flow Dilatedveins Collapsedveins Dry,warm foot Coldfoot Bonedeformities Nobony deformities Redappearance Pale,cyanotic Sources: Armstrong,D. G., & Lavery,L. A. (1998, March15). Diabetic foot ulcers: Prevention,diagnosis and classification. American Family Physician, 57 (6):1325-1332. Retrieved fromhttps://www. aafp. org/afp/ 1998/0315/p1325. html; Cleveland Clinic. (n. d. ). Leg and foot ulcers. Retrieved fromhttp://my. clevelandclinic. org/heart/disorders/vascular/ legfootulcer. aspx;Frykberg,R. G. (2002, November 1). Diabetic foot ulcers: Pathogenesis and management. American Family Physician, 66(9), 1655-1663. Retrieved fromhttp://www. aafp. org/afp/2002/1101/ p1655. html;Jeffcoate,W. J.,&Harding,K. G. (2003). Diabeticfootulcers. The Lancet, 361(9368), 1545-1551. doi:10. 1016/S0140-6736(03)13169-8 typical in patients with PAD is defined as the appearance of pain in muscle masses caused by walking and which ceases immediately after stopping exercise. Of note: A great number of patients report pain in the legs associ-ated with walking, but not with the presence of arterial disease. The stage II is itself divided into groups. a. Stage IIa includes patients with non-invalidating claudication that impedes walking long distances. b. Stage IIb refers to patients with short claudica-tion or claudication that impedes activities of daily living. 3. Stage III constitutes a more advanced phase of ischemia and is characterized by the presence of symp-toms at rest. The predominant symptom is usually pain, although the patient often reports paresthesia and hypoesthesia. 4. Stage IV is characterized by the presence of tropical lesions. It is due to the critical reduction of distal per-fusion pressure, which is insufficient to maintain tissue tropism. These lesions are situated in the more distal areas of the limb, usually the toes, although on occasions they may present in the malleolus or the heel. Diagnostic Tests A. The diagnosis is usually made by the typical symptoms, history, and physical examination. B. Homocysteine level to rule out hyperhomocysteinemia. C. An ankle-brachial index (ABIs), toe-brachial index (TBI), and/or exercise ABI must be ordered. D. Pulse volume recording or plethysmography: Recording the pulse wave volumes along the limb byplethysmography is particularly useful in patients in whom arterial calcification prevents a reliable recording of sys-tolic pressures. T ransmetatarsal or digital recording provides important information about the state of the vascularization in this zone. E. Segmental pressure examination or Doppler recording of velocimetric wave can also provide very useful information by means of evaluating the changes in the different components of the arterial velocimetric wave. F. Duplex ultrasound of the extremities is useful to diag-nose anatomic location and degree of stenosis of PAD. May be used in select candidates for endovascular intervention, surgical bypass, and to select the sites of surgical anastomo-sis. This may also be used for surveillance following femoral-popliteal bypass using venous conduit (but not prosthetic grafts). G. Imaging techniques are indicated if surgical or endovascu-lar repair is contemplated after identification of a susceptible lesion. 1. Computed tomography angiography (CTA) produces an excellent arterial picture; however, it requires iodinated contrast. CTA may be considered to diagnose anatomic location and presence of significant stenosis in patients with lower extremity PAD and as a substitute for mag-netic resonance angiography (MRA) for those patients with contraindications to MRA. 2. MRA has virtually replaced contrast arteriography for PAD diagnosis. The advantages of MRA include: a. Excellent arterial picture and no ionizing radia-tion; noniodine-based intravenous contrast medium rarely causes renal insufficiency or allergic reac-tion. However, about 10% of patients cannot utilize MRA because of claustrophobia, having a pacemak-er/implantable cardioverter-defibrillator, or because they are obese. b. The major challenge with MRA is: Gadolin-ium use in individuals with an estimated glomeru-lar filtration rate ( e GFR) less than 60 m L/min has been associated with nephrogenic systemic fibrosis (NSF)/nephrogenic fibrosing dermopathy. c. The MRA is useful to diagnose anatomic location and degree of stenosis of PAD as well as in selecting patients with lower extremity PAD as candidates for endovascular intervention. Differential Diagnosis A. For leg pain or claudication with normal physiological testing, a provider needs to consider (not PAD related). 1. Symptomatic Baker's cyst. 2. Chronic compartment syndrome. 3. Spinal stenosis. 4. Nerve root compression: Arthritis—hip, ankle, or foot. Evaluation and Management Plan A. General plan. 1. The two main goals of PVD treatment are to stop the disease from progressing and manage pain and symptoms so patients can remain active. The treatments are aimed to lower risk for serious complications. 2. Antiplatelet therapy. 3. Smoking cessation, as well as avoiding environmental smoking and secondhand smoking. 4. Good glycemic control. 5. Surgical management. a. Endovascular revascularization. Peripheral Vascular Disease
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248 i. Endovascular procedures are effective as a revascularization option for patients with lifestyle-limiting claudication. ii. Endovascular procedures are recommended to establish in-line blood flow to the foot in patients with nonhealing wounds or gangrene. A staged approach may be done in patients with ischemic rest pain. b. Surgical revascularization: Bypass or graft to restore blood flow. Surgical revascularization is performed; bypass to the popliteal artery with autogenous vein is recommended in preference to prosthetic graft material. c. Angioplasty of the blocked peripheral artery is a procedure to open narrowed or blocked blood ves-sels that supply blood to your legs. Fatty deposits can build up inside the arteries and block blood flow. B. Patient/family teaching points. 1. Pain management to enhance activity. 2. Exercise and physical activity. Structured exercise pro-gram and home-based exercise program. a. Any exertional limitation of the lower extrem-ity muscles or any history of walking impairment, described as fatigue, aching, numbness, or pain. b. The primary site(s) of discomfort in the buttock, thigh, calf, or foot, and relation of such discomfort to rest or exertion. 3. Look for any poorly healing or nonhealing wounds of the legs or feet. 4. Note any pain at rest localized to the lower leg or foot and its association with the upright or recumbent posi-tions. 5. Watch for postprandial abdominal pain that repro-ducibly is provoked by eating and is associated with weight loss. 6. Family history of a first-degree relative with an abdominal aortic aneurysm. 7. Pulse intensity should be assessed and should be recorded numerically from 0 to 3 (0 =absent, 1 =dimin-ished, 2 =normal, and 3 =bounding). C. Pharmacotherapy. 1. Statin therapy. 2. Antihypertensive therapy: Angiotensin-converting enzyme (ACE) inhibitors. 3. Oral anticoagulation (warfarin) in improving lower extremity bypass patency demonstrated improved patency among the subgroup of patients with autoge-nous vein bypass grafts. 4. Cilostazol increases blood flow and relieves symptoms of claudication. D. Discharge instructions. 1. Patients should be encouraged to maintain a healthy diet, stop smoking, control diabetes, and begin an exercise program. Follow-Up A. PVD is a lifelong chronic medical condition. Ongoing care focuses on cardiovascular risk reduction with medical therapy, optimizing functional status with structured exercise and, when indicated, revascularization. B. Patients with PVD who have undergone lower extrem-ity revascularization (surgical and/or endovascular) should be followed up with periodic clinical evaluation and ABI mea-surement. C. Duplex ultrasound is recommended for routine surveil-lance after femoral-popliteal or femoral-tibial-pedal bypass with a venous conduit. Minimum surveillance intervals are approximately 3, 6, and 12 months, and then yearly after graft placement. Consultation/Referral A. Interdisciplinary care team members must be included. B. Care team members may include: 1. Vascular medical and surgical specialists (i. e., vascu-lar medicine, vascular surgery, interventional radiology, interventional cardiology). 2. Orthopedic surgeons and podiatrists. 3. Endocrinologists. 4. Infectious disease specialists. 5. Radiology and vascular imaging specialists. 6. Physical medicine and rehabilitation clinicians. 7. Orthotics and prosthetics specialists. 8. Social workers. 9. Exercise physiologists. 10. Physical and occupational therapists. 11. Nutritionists/dieticians. Special/Geriatric Considerations A. Elderly may not experience intermittent claudication because of comorbidities that limit walking such as arthritis, spinal stenosis, heart failure, and pulmonary disease. Hence, management of comorbidities is vital in management of PAD. B. Elderly also need a more sensitive diagnostic test for PAD for the identification of patients with asymptomatic PVD. C. They may also benefit from early diagnosis by screening for asymptomatic PAD. D. It would be beneficial for the elderly to have an estab-lished structured or supervised exercise program rather than an unsupervised exercise program. E. Cilostazol increases maximal walking distance, pain free walking distance, and quality of life for the elderly popula-tion. Bibliography Alonso-Coello, P., Bellmunt, S., Mc Gorrian, C., Anand, S. S., Guzman, R., Criqui, M. H.,,... Spencer, F. A. (2012, February ). Antithrom-botic therapy in peripheral artery disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed. : American College of Chest Physi-cians Evidence-Based Clinical Practice Guidelines. Chest, 141 (2 Suppl. ), e669S-e690S. doi:10. 1378/chest. 11-2307 Armstrong, D. G., & Lavery, L. A. (1998, March 15). Diabetic foot ulcers: Prevention, diagnosis and classification. Amer-ican Family Physician, 57 (6), 1325-1332. Retrieved from https://www. aafp. org/afp/1998/0315/p1325. html Cleveland Clinic. (n. d. ). Leg and foot ulcers. Retrieved from http://my. clevelandclinic. org/heart/disorders/vascular/legfootulcer. aspx Frykberg, R. G. (2002, November 1). Diabetic foot ulcers: Pathogenesis and management. American Family Physician, 66 (9), 1655-1663. Retrieved from http://www. aafp. org/afp/2002/1101/p1655. html Gerhard-Herman, M. D., Gornick, H. L., Barrett, C., Barshes, N. R., Corriere, M. A., Drachman, D. E.,... Walsh, M. E. (2016). 2016 AHA/ACC Guideline on the management of patients with lower extremity peripheral artery disease: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Prac-tice Guidelines. Journal of the American College of Cardiology, 69, 1465-1508. doi:10. 1016/j. jacc. 2016. 11. 008 Jackson, E. A., Munir, K., Schreiber, T., Rubin, J. R., Cuff, R., Gallagher, K. A.,... Grossman, P. M. (2014, June 17). Impact of sex on morbid-ity and mortality rates after lower extremity interventions for peripheral arterial disease: Observations from the Blue Cross Blue Shield of Michi-gan Cardiovascular Consortium. Journal of American College of Cardiol-ogy, 63 (23), 2525-2530. doi:10. 1016/j. jacc. 2014. 03. 036. 11. Peripheral Vascular Guidelines
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249 Jeffcoate, W. J., & Harding, K. G. (2003). Diabetic foot ulcers. The Lancet, 361, 1545-1551. doi:10. 1016/S0140-6736(03)13169-8 Suzuki, J., Shimamura, M., Suda, H., Wakayama, K., Kumagai, H., Ikeda, Y.,... Morishita, R. (2016, April). Current therapies and investigational drugs for peripheral arterial disease. Hypertension Research, 39 (4), 183-191. doi:10. 1038/hr. 2015. 134 Thoracic Outlet Syndrome Cara M. Staley Definition A. Thoracic outlet syndrome (TOS) is a constellation of signs and symptoms that arise from compression of the neu-rovascular bundle just above the first rib and behind the clav-icle, within the confined space of the thoracic outlet. Incidence A. TOS is uncommon and its true incidence is unknown. B. Most patients are 20 to 50 years old, less than 5% are teenagers, and 10% are older than 50. C. 70% are female. Pathogenesis A. Neurogenic (n TOS) arises from brachial plexus compres-sion. 1. It accounts for more than 95% of TOS cases. 2. Associated with developmental anomalies of the tho-racic outlet and fibrosis of the scalene muscle. 3. Most common causes are hyperextension neck trauma (motor vehicle accident whiplash) and repetitive stress injuries. B. Venous (v TOS) arises from subclavian vein compression. 1. It accounts for 3% of TOS cases. 2. Often a result of developmental anomalies of the cos-toclavicular space and repetitive arm activities. 3. In v TOS a focal area of scarred subclavian intima nar-rows the lumen. Thrombus is the final event that occludes the vein. 4. Typically asymptomatic until a venous thrombolytic event occurs. C. Arterial (a TOS) arises from subclavian artery compres-sion. 1. It accounts for 1% of TOS cases. 2. Almost always associated with a cervical rib or anoma-lous rib. 3. a TOS subclavian artery stenosis is accompanied by poststenotic dilatation that gives the appearance of an aneurysm. Thrombus forms in the dilatation. 4. Usually asymptomatic until the arterial emboli dis-lodges. Predisposing Factors A. Cervical rib or anomalous rib. B. Congenital cervical fibrocartilaginous band associated with an incomplete cervical rib. C. Muscular anomalies. D. Chronic inflammatory change due to trauma. E. Fractured first rib or clavicle. F. Neck mass, for example, goiter, apical lung cancers, thy-roid cancers, lymphoma. G. Repetitive occupational overhead arm movements (e. g., box stacking), or sporting movements (e. g., pitching, swim-ming). Subjective Data A. Common complaints/symptoms. 1. Neurogenic TOS: Pain, dysesthesia, numbness, and weakness, which may not be localized in specific nerve distribution. Symptoms are reproducibly aggravated by elevation or sustained use of the arms or hands. 2. Venous TOS: Pain, cyanosis, edema. Paresthesia in the fingers is typically from swelling in the hand rather than nerve compression. Collateral venous patterning over the ipsilateral shoulder, neck, and chest wall indicates com-pensatory superficial venous flow from subclavian vein stenosis or occlusion. 3. Arterial TOS: Pain, pallor, paresthesia, coldness to hand. Symptoms develop spontaneously unrelated to work or trauma. B. Common/typical. 1. Common causes of TOS include physical trauma from car accidents, sports, or repetitive injuries. 2. Sometimes having an anatomical defect such as an extra rib can cause this. 3. Patients may complain of numbness or tingling in their arm or fingers and have a weak grip. C. Family and social history. 1. Elicit onset, duration, location, intensity, aggravators, and relievers of symptoms. 2. Ask about occipital headaches and pain over the trapezius, neck, chest, and shoulder. (Patients with symp-toms confined to the forearm and hand are more likely to have carpal or cubital tunnel syndrome, not n TOS). 3. Enquire about any history of neck trauma (e. g., whiplash, clavicle fracture, fall on slippery surface, or trip-ping down stairs). 4. Enquire about occupational and recreational history of repetitive stress injury (e. g., hours on keyboards, assem-bly lines). 5. Rule out any secondary causes of upper extremity deep vein thrombosis or arterial thrombosis such as cen-tral venous catheters, pacemakers, or peripheral or coro-nary catheterization. D. Review of systems. 1. Musculoskeletal: Ask about arm pain or swelling. 2. Cardiovascular: Ask about cold fingers. 3. Dermatology: Ask about any changes in skin color such as lack of color or bluish discoloration. 4. Neurology: Ask about numbness, tingling, or weak-ness of extremity. Physical Examination A. Perform a standard neurological test. B. Take blood pressure in both arms. Lower systolic pressure in the affected arm may suggest a TOS. C. Inspect. 1. Neck and supraclavicular area for pulsatile and non-pulsatile mass. 2. Hands and fingers: Swelling and cyanosis (v TOS), pale, cold, ischaemic changes (a TOS). 3. Skin overlying the ipsilateral shoulder, neck and chest wall for collateral venous patterning (v TOS). D. Auscultate. 1. Heart to listen for arrhythmias, gallops, and murmurs. 2. Supraclavicular and infraclavicular fossa to listen for bruits or a thrill (a TOS). Thoracic Outlet Syndrome
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250 E. Palpate. 1. Carotid and upper extremity pulses. Reduced or absent (a TOS). 2. Palpate scalene muscle to assess for tenderness (n TOS). F. Perform provocative maneuvers. 1. Adson test. a. Palpate the radial pulse and then move the patient's upper extremity into an extended, abducted, and externally rotated position. b. Patient then rotates and laterally flexes the neck to the ipislateral side while inhaling deeply. c. A positive test results in reduction or obliteration of the radial pulse. 2. Elevated arm stress test (EAST) or Roos test. a. Patient seated with arms abducted at 90∘in exter-nal rotation, elbows flexed to 90∘, head in neutral position. b. Patient opens and closes hands. c. The test has a high negative predictive value for n TOS if the patient performs the maneuver for 3 min-utes. Diagnostic Tests A. The predominant clinical signs and symptoms direct the nature of further evaluation depending on the type of TOS. 1. Cervical spine x-ray: Identify bony abnormalities such as cervical ribs, anomalous ribs, or rib/clavicular fracture calluses. 2. Ultrasound: The initial imaging test to evaluate a TOS or v TOS. Provocative shoulder/arm maneuvers are per-formed under ultrasound. 3. Cross sectional imaging (CT or MR) and/or elec-tromyography is best reserved for TOS specialists. 4. Hematologic evaluation: There are no specific blood tests for TOS. However, hematologic tests are helpful in ruling out other causes. See the “Diagnostic Test” section “Upper Extremity Arterial Disease. ” Differential Diagnosis A. Neurogenic TOS. 1. Carpal tunnel syndrome. 2. Ulnar nerve compression. 3. Rotator cuff tendinitis. 4. Neck strain/sprain. 5. Fibromyositis. 6. Cervical disc disease. 7. Cervical arthritis. 8. Brachial plexus injury. B. Arterial TOS. 1. Embolization from other sources. 2. Vasculitis. 3. Radiation arteritis. 4. Connective tissue disorders. 5. Arterial dissection. 6. Atherosclerotic upper extremity disease. 7. Thromboangiitis obliterans. 8. T raumatic. C. Venous TOS. 1. Acute thrombosis. 2. Lymphedema. 3. Rheumatologic disorders. 4. Cellulitis and allergic reactions. 5. Metabolic or global causes of limb swelling such as heart failure or myxedema. Evaluation and Management Plan A. General plan. 1. T reatment is indicated only for symptomatic patients. Having a cervical rib or other rib anomaly does not indi-cate a need to intervene. 2. Prevention and rehabilitation: Minimizing work-related overuse syndromes. Input from physical thera-pists. 3. Thrombolysis. 4. Severe arterial ischemia usually requires surgical embolectomy (with or without intraoperative thrombol-ysis). 5. Thoracic outlet decompression. B. Patient/family teaching points. 1. Patients need to avoid repetitive movements and heavy lifting. 2. Diet and exercise can improve symptoms as well. 3. Stretching daily can keep muscles strong and prevent increased pressure on the thoracic outlet. C. Pharmacotherapy. 1. Medical therapy: Interscalene injection of anesthetic agents, steroids, or botulinum toxin type A. 2. Anticoagulation. D. Discharge instructions. 1. Patients should follow-up with their primary care provider. 2. Surgery may be indicated if medical treatment and physical therapy are not effective. 3. Untreated symptoms can lead to permanent nerve damage, so patients should report any worsening symp-toms. Follow-Up A. As guided by appropriate specialist services (neurology, vascular, or general surgery). Consultation/Referral A. Acute ischemia: For hospital admission, seek vascular consult. B. Non-acute, progressive symptoms referral to TOS specialist. 1. Such as complaints of shoulder, neck, head, chest, and arm problems with activity, elevation, or dangling; with supraclavicular or intraclavicular tenderness, and the absence of obvious cervical disc, rotator cuff, or carpal tunnel pathology. Special/Geriatric Considerations A. TOS is a complex disease in terms of its etiologies, patho-physiology, diagnosis, and management. B. TOS is associated with a high incidence of insurance claims and worker compensation issues. C. Early identification that TOS potentially exists and refer-ral to specialist services is important. Bibliography Goshima, K. G. (2019, January 31). Overview of thoracic outlet syn-dromes. In K. A. Collins (Ed. ), Up To Date.. Retrieved from https://www. uptodate. com/contents/overview-of-thoracic-outlet-syndromes Illig, K. A., Thompson, R. W., Freischlag, J. A., Donahue, D. M., Jordon, S. E., & Edgelow, P. I. (Eds. ). (2013). Thoracic outlet syndrome. Philadel-phia, PA: Springer Publishing Company. 11. Peripheral Vascular Guidelines
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251 12 Hematology Guidelines Mary L. Wilby Anemia Mary L. Wilby Definition A. Anemia is characterized by a lower than normal number of red blood cells (RBCs) and/or level of hemoglobin causing decreased oxygen-carrying capacity. Incidence A. Iron deficiency is the most common cause of anemia worldwide with women and children most often affected. B. Other causes of anemia vary based on age, gen-der, and geographical region. Anemias in high income North American countries, including the United States, are most frequently the result of gastrointestinal hemorrhage, hemoglobinopathy, and chronic kidney disease. C. Approximately 240,000 ED visits in the United States result in anemia as the primary hospital discharge diagnosis. Pathogenesis A. Anemia can be a consequence of bleeding, hemolysis, or inadequate bone marrow function, or nutritional deficiency. B. Blood loss anemia results in a loss of iron containing RBCs. Hemolysis results in destruction of RBCs but iron is retained in the body. C. Microcytic anemia is characterized by RBCs of reduced size. While most commonly associated with iron deficiency, microcytic anemia can be associated with anemia of chronic disease (ACD), thalassemia, and sideroblastic anemia. D. Macrocytic anemias are characterized by greater than nor-mal mean corpuscular volume. Causes are most often associ-ated with vitamin B12and folate deficiency; antimetabolite drugs, including methotrexate; and other causes that inter-fere with cell metabolism. E. Pernicious anemia is associated with vitamin B12defi-ciency caused by the absence of intrinsic factor, a glyco-protein secreted by parietal cells needed for absorption of vitamin B12. Absence of intrinsic factor may be congeni-tal, but is most often caused by an autoimmune-mediated atrophic gastritis. F. Normocytic anemia, characterized by normal size RBCs, may be associated with ACD, hemolysis, acute blood loss, and volume overload. In the acute care setting, hemolysis may be associated with hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), or heart valve abnormali-ties. Predisposing Factors A. Use of nonsteroidal anti-inflammatory drugs (NSAIDs). B. Peptic ulcer disease. C. Chronic kidney disease. D. Uterine fibroids/menorrhagia. E. Family history of thalassemia, sickle cell disease, or hered-itary spherocytosis. F. Recent blood transfusion. G. Nutritional deficiency. H. Alcohol abuse. I. Cancer. J. Connective tissue diseases. K. Chronic infection such as HIV or tuberculosis (TB). L. Pregnancy. M. Intestinal disorders including diverticulosis, inflamma-tory bowel disease, or celiac disease. Subjective Data A. Common complaints/symptoms. 1. Signs and symptoms of anemia may vary depending on the severity, speed of development, age, and comor-bidities of the individual. Tissue hypoxia and the patho-logic process contribute to complaints. 2. Fatigue, weakness, headache, shortness of breath, pal-pitations, and angina may occur. 3. Decreased oxygen to the brain often results in confu-sion, visual changes, and fainting. 4. Chronic blood loss may not cause symptoms until hemoglobin drops below 8 g/d L. B. Common/typical scenario. 1. Other signs and symptoms. a. Pale skin, nail beds, conjunctiva, and mucous membranes result from shifting of blood away from cutaneous tissues. b. Flow-type systolic murmurs may be associated with altered blood viscosity. High output heart failure and ventricular hypertrophy may occur with severe anemia, especially individuals with established heart disease. c. Hemolytic anemia may be associated with increased bilirubin causing jaundice, splenomegaly, and dark-colored urine. C. Family and social history. 1. Onset and duration of symptoms. 2. Family history of blood disorder. 3. Associated abdominal pain. 4. Changes in diet, bowel habits. 5. Menstrual history including timing and amount of bleeding. 6. Medication history. Anemia
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252 D. Review of systems. 1. Head, ear, eyes, nose, and throat (HEENT): Ask about premature graying of hair or burning sensation of tongue. 2. Neurology: Ask about numbness or tingling sensa-tions. 3. Genitourinary: Ask about urine color. 4. Gastrointestinal: Ask about stool color, any blood in stool, abdominal pain, or cramping. 5. Ask about dietary habits or unusual habits such as pagophagia. 6. Dermatology: Ask about any rashes or redness of skin. 7. Psychiatric: Ask about fatigue. Physical Examination A. Check vital signs including pulse, respirations, and blood pressure. B. Oral mucosa may be cracked or dry; tongue may be thick-ened and smooth with vitamin deficiency. C. Cardiac examination, noting rate, rhythm, and presence of murmurs. D. Lung examination, noting rate and adventitious sounds. E. Abdominal examination, noting evidence of bleeding, distension, peristalsis, abnormal bowel sounds, tenderness, and masses. F. Rectal examination, noting presence of blood in stool. G. Skin and mucous membrane examination, noting petechiae, bruising, or pallor of skin, nail beds, and mucous membranes including conjunctiva. H. Neurological disturbances may be associated with long-standing vitamin B12deficiency; peripheral neuropathy, alterations in deep tendon reflexes, impaired vibratory sensa-tion, alterations in balance, and impaired mental status may be present. Diagnostic Tests A. Complete blood count (CBC) including RBC indices. B. Reticulocyte count. C. Hemoglobin electrophoresis. D. Coombs test (antiglobulin test). E. Serum ferritin. F. Serum iron. G. Vitamin B12level. H. Folate level. I. Haptoglobin. Differential Diagnosis A. Acute blood loss. B. Chronic blood loss. C. Hemolysis. D. Aplastic anemia. E. Leukemia. Evaluation and Management Plan A. General plan. 1. See Figure 12. 1 for overview of anemia evaluation. 2. T reatment of anemia is based on identifying and elim-inating or ameliorating the cause. 3. The severity of the anemia and its accompanying symptoms determine treatment. 4. T ransfusion is often indicated if/when hematocrit drops to 27% or less. 5. Risks associated with transfusion include fluid over-load, transfusion reaction, and iron overload, which must be taken into consideration. 6. Iron deficiency may be treated with increased intake of dietary iron and supplemental iron. Dietary sources are frequently insufficient and oral and/or intravenous sup-plementation are often required. 7. ACD may require treatment when patients become symptomatic with use of medication to stimulate ery-thropoiesis such as erythropoietin alpha and darbepoietin alfa. B. Patient/family teaching points. 1. Nutritional deficiencies of iron, vitamin B12, and folic acid should be corrected with changes to diet. 2. If taking ferrous sulfate, patients should avoid tea and coffee, which can affect absorption of the drug. C. Pharmacotherapy. 1. T reatment of anemia is to correct the underlying con-dition and supplement with ferrous sulfate until anemia is corrected and for several months after it is corrected. 2. Ferrous sulfate 325 mg three times a day is the stan-dard pharmacological treatment. 3. Vitamin C 500 units per day can promote absorption of ferrous sulfate. 4. Patients with severe anemia from chronic kidney fail-ure, chemotherapy, or HIV can benefit from epoetin injections. a. Dose of epoetin will depend on the severity of anemia, but typically starts at 50 to 100 units per kilogram administered subcutaneously three times per week. Patient will require adequate iron stores prior to starting epoetin injections. D. Discharge instructions (If standard accepted guidelines exist please use discharge template). 1. Patients are not routinely admitted for anemia unless they are hemodynamically unstable. 2. Discharge planning for a patient who is found to be anemic in the hospital would be to follow-up with the primary care provider for a further evaluation and workup of anemia in nonacute setting. Follow-Up A. Once iron stores have been replenished, there is no need to retest iron studies unless there is evidence of a change in the patient's symptoms or physical examination. B. Follow-up to identify the cause of the anemia is discussed in the following. C. Conditions that are unresolved warrant follow-up. D. ACD often requires ongoing treatment and follow-up under specialist care depending on the cause of the under-lying disease. E. Patients with aggressive forms of thalassemia should be under care of a hematologist. F. Patients with vitamin B12deficiency require ongoing care for monitoring B12levels and monitoring of liver function if taking parenteral therapy. G. Follow-up for patients with folic acid deficiency should consist of periodic monitoring of CBC and serum folate levels. Consultation/Referral A. Iron deficiency associated with occult blood loss often requires referral to a gastroenterologist for upper endoscopy and/or colonoscopy as well as additional testing to identify the source of bleeding. B. In the case of menorrhagia, referral for follow-up gyneco-logic care may be needed. Follow-up care of individuals with ACD is dependent on the underlying cause. 12. Hematology Guidelines
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253FIGURE 12. 1 Overview of anemia evaluation. LDH, lactate dehydrogenase. Anemia Vitamin B12 and folate levels Normal One or both abnormal Smear shows reticulocytes, spherocytes, target cells Smear shows anisocytosis, oval macrocytes, nuclear abnormalities Consider hemolysis, liver disease, or heavy alcohol use Consider bone marrow disease Nutritional de/f_iciency Macrocytic Offending medications?Anemia Normocytic Microcytic Evaluate possible causes Bleeding Check fecal occult blood Nutritional Check ferritin, B12, folate Hemolysis Check haptoglobin, LDH, bilirubin, reticulocytes Renal disease Check serum creatinine Yes-consider anemia of chronic disease Is microcytosis new?Check serum ferritin No-likely thalassemia Hemoglobin electrophoresis Low-iron de/f_iciency Normal or elevated
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254 C. Referral for care by nephrology, rheumatology, hematol-ogy, oncology, gastroenterology, or other specialists may be required. D. Use of erythrocyte stimulating factors should be directed by a hematologist or other qualified specialist. E. Thalassemia may require consultation with hematology for ongoing monitoring. F. Evidence of sideroblastic anemia should prompt consul-tation with hematology. Special/Geriatric Considerations A. Adults over 50 with occult blood in the stool or iron defi-ciency anemia should be referred for colonoscopy given the increased risk for gastrointestinal malignancy associated with aging. B. In some cases the risk associated with the procedure, including perforation, may outweigh the benefits. Bibliography Centers for Disease Control and Prevention National Center for Disease Statistics. (2017). Anemia or iron deficiency. Retrieved from https: //www. cdc. gov/nchs/fastats/anemia. htm Grossman, S. (2014). Disorders of hemostasis. In S. C. Grossman & C. M. Porth (Eds. ), Porth's pathophysiology: Concepts of altered health states (9th ed., pp. 648-664). Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins. Kassebaum, N., Jasrasaria, R., Naghavi, M., Wulf, S., Johns, N., Lozano, R.,... Murray, C. (2014). A systematic analysis of global anemia burden from 1990 to 2010. Blood, 123, 615-624. doi:10. 1182/blood-2013-06-508325 Porter, B. O., & Winland-Brown, J. E. (2015). Hematological and immune problems. In L. M. Dunphy, J. E. Winland-Brown, B. O. Porter, & D. J. Thomas (Eds. ), Primary care the art and science of advanced practice nursing (4th ed., pp. 920-1025). Philadelphia, PA: F. A. Davis. Rote, N., & Mc Cance, K. (2014). Structure and function of the hematolog-ical systems. In K. Mc Cance & S. Huether (Eds. ), Pathophysiology: The biologic basis for disease in adults and children (7th ed., pp. 945-981). St. Louis, MO: Elsevier. Bleeding Diatheses Mary L. Wilby Definition A. Bleeding disorders may occur as a result of abnormalities in platelet number or function, coagulation factors, fibrinol-ysis, and blood vessel integrity. B. Deficiencies or inhibitors of clotting factors, whether acquired or inherited, can result in bleeding disorders. Incidence A. Bleeding disorders occur frequently in seriously ill patients, and causes may vary from prolonged global clot-ting tests or isolated thrombocytopenia to composite defects, such as consumption coagulopathies. B. A prolongation of global clotting times, such as the pro-thrombin time (PT) or the activated partial thromboplastin time (a PTT), may be apparent in 14% to 28% of critically ill patients. C. The incidence of a low platelet count (platelet count <150,000 per microliter) in an intensive care population is 35% to 44%. Platelet counts of less than 100,000 per micro-liter may be seen in another 30% to 50% of patients. Pathogenesis A. Hemostasis is the process of clot formation at the site of blood vessel injury. Abnormal bleeding is often a result of theabsence or dysfunction of one or more of the elements needed in clot formation. B. Most clotting factors are synthesized by the liver. A final step dependent on vitamin K is required for Factors II, VII, IX, and X, and procoagulant proteins C and S. Factor VIII, von Willebrand factor (v WF), and tissue plasminogen acti-vator are produced in the endothelium, including that of the liver. The liver reticuloendothelial system is responsible for metabolizing most clotting factors and fibrin degradation products (FDPs ). C. Coagulation factor inhibitors are antibodies that neutral-ize a specific clotting factor's function. Alloantibodies occur in patients with inherited factor deficiency. Autoantibodies arise in patients without an inherited factor deficiency. The most commonly inhibited factor is Factor VIII. D. Low platelet counts in critically ill individuals are fre-quently the result of increased platelet turnover due to thrombin generation, platelet activation, and enhanced platelet-vessel wall interaction. Sepsis is a frequent cause for thrombocytopenia in seriously ill patients. The severity of sepsis may be correlated with the reduction in the platelet count. E. Drug-induced thrombocytopenia has been associated with a variety of prescription and over-the-counter (OTC) medications including quinine and some sulfa-containing antibiotics. Antigen-antibody responses lead to the destruc-tion of platelets. F. Immune thrombocytopenic purpura (ITP) occurs as a result of antibody-induced destruction of platelets. Primary ITP can occur without any known risk factors while sec-ondary ITP is a result of an acute or chronic underlying disor-der, such as AIDS, systemic lupus erythematosus, lymphoma, or hepatitis C. G. Thrombotic thrombocytopenic purpura (TTP) is a rare condition that manifests with a combination of low platelet count, hemolytic anemia, renal failure, neurological abnor-malities, and fever. This rare disorder stems from introducing certain platelet aggregating substances into the circulation. In many cases this is triggered by a lack of an enzyme that breaks down v WF, causing platelet aggregation and adherence to vascular endothelium. While this condition may occur in otherwise healthy people, it is also found in individuals with autoimmune disorders, HIV infection, and pregnancy. H. Disseminated intravascular coagulation (DIC) is a systemic process that can cause both thrombosis and hemorrhage. The processes associated with coagulation and fibrinolysis become abnormally activated within the vessels and promote ongoing coagulation and fibrinolysis. Con-sumption of platelets is associated with constant generation of thrombin. Microvascular thrombi, along with inflamma-tion, may cause injury to the microvasculature, resulting in organ dysfunction. Consumption of platelets and low levels of other factors increase the risk for hemorrhagic complica-tions, especially in perioperative patients or those undergoing other invasive procedures. Thrombin generation is triggered and promoted by a lack of thrombin-generating inhibitory mechanisms. Impaired fibrin degradation, due to elevated circulating levels of plasminogen activator inhibitor-type 1 (PAI-1), further promotes intravascular fibrin deposition. Patients with DIC have a low or decreasing platelet count, prolongation of coagulation tests, low plasma levels of coag-ulation factors and inhibitors, and increased markers of fibrin formation or degradation, including D-dimer or FDPs. No single diagnostic test is used to confirm DIC. The presence of a condition associated with DIC and a combination of labo-ratory tests are necessary to confirm the diagnosis. 12. Hematology Guidelines
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255 I. Von Willebrand disease (VWD) is the most com-mon form of inherited bleeding disorder, resulting from a deficiency or defect of v WF. Individuals with VWD have defects in both platelet function and the coagulation path-way. J. Hemophilia A is the most common form of hemophilia, accounting for approximately 85% of hemophilia cases. Caused by an x-linked recessive gene, it affects males most often. Although it is a genetic disorder, a number of cases occur without a family history of bleeding. Deficiency or defects of Factor VIII are associated with excessive bleeding, most often occurring in soft tissue, joints, and the gastroin-testinal (GI) tract. Bleeding may be spontaneous or associated with trauma. Predisposing Factors A. TTP. B. Hemolytic-uremic syndrome. C. Chemotherapy-induced microangiopathic. D. Hemolytic anemia. E. Severe malignant hypertension. F. Hemolysis, elevated liver enzymes, low platelet count (HELLP) syndrome of pregnancy. G. Preeclampsia. H. Retained products of conception. I. Malignancy, especially leukemia. J. Blood transfusion reaction. K. Systemic infection. L. Connective tissue disease. M. Pancreatitis. N. Liver disease. O. Surgery or trauma. P. Burns. Q. Snake venom. Subjective Data A. Common complaints/symptoms. 1. Bruising. 2. Nose bleeds. 3. Bleeding gums. 4. Menorrhagia. 5. Weakness. 6. Fatigue. 7. Abdominal discomfort. B. Common/typical scenario. 1. Other signs and symptoms. a. Immediate bleeding after vessel injury is frequently associated with platelet disorders. b. Large ecchymoses and large, diffusely spreading deep tissue hematomas are common with coagulation disorders. c. Bleeding into synovial joints is characteristic of inherited coagulation disorders such as hemophilia. d. Petechiae. e. Oozing from venipuncture sites. f. Uncontrolled postpartum bleeding. C. Family and social history. 1. History of HIV infection and malignancy. 2. History of liver or kidney disease, or malabsorption that is often associated with bleeding. 3. Medication history including anticoagulants, non-steroidal anti-inflammatory drugs (NSAIDs), oral con-traceptives, antibiotics, alcohol, and dietary vitamins K and C. 4. Response to previous hemostatic challenges, including trauma, tooth extraction, pregnancy, surgery, sports, and menstruation. 5. Family history of bleeding disorders. D. Review of systems. 1. Hematological: Ask about past bleeding problems, any history of anemia, bleeding after any type of surgi-cal procedure or dental procedure, or any transfusions. 2. GI: Ask about dietary habits or antibiotic use which might contribute to vitamin K deficiency; ask about liver disease or black tarry stools. 3. Genitourinary: Ask about any kidney diseases or hematuria. 4. Endocrine. a. Ask women about menses. b. Ask about medications the patient is taking for other conditions. 5. Dermatological: Ask about bruising or ecchymosis. Physical Examination A. Signs of bleeding (e. g., petechiae, mucosal bleeding, soft tissue bleeding, ecchymoses). In hospitalized patients, bleed-ing from multiple sites can indicate DIC or TTP. Acute extensive mucocutaneous bleeding in a patient previously without symptoms should suggest ITP. B. Organ enlargement. C. Joint abnormalities. D. Signs of systemic disease including fever and lympha-denopathy. Diagnostic Tests A. Complete blood count (CBC). B. Bleeding time. C. PT. D. a PTT. E. Platelet function analysis. F. Examination of a peripheral blood smear. The following may be required in the presence of abnormalities in screening tests described earlier. G. Factor deficiencies and inhibitors. H. Fibrinogen. I. Fibrin and FDPs. Differential Diagnosis A. Anticoagulant overdose. B. Acquired Factor VIII inhibitors. C. Local surgical complications. D. Physical abuse. Evaluation and Management Plan A. General plan. 1. Bleeding associated with deficiency of vitamin K can be treated with parenteral vitamin K. Normalization of clotting studies usually follows within several hours. Fresh frozen plasma may be needed in the event of hemorrhage or if emergency surgery is necessary. 2. Individuals with acute or chronic liver disease may require treatment of alterations in clotting functions, fibrinolytic systems, or platelet function. When multi-ple coagulation factors are involved, infusion of fresh frozen plasma is a preferred treatment. Additional treat-ments may include exchange transfusion and platelet infusion. Bleeding Diatheses
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256 3. DIC treatment should be directed at reducing the bur-den of the underlying disease, controlling thrombosis, and preserving organ function. Controlling the under-lying condition is necessary to reduce the stimulus for abnormal clotting and restoring a normal balance of clot-ting factors. The role of heparin is limited but has been effective when DIC is associated with retained products of conception and when acute promyelocytic leukemia is present. It is contraindicated when there is evidence of central nervous system (CNS), GI, or postoperative bleeding. Interventions for restoring the balance of coag-ulation factors and platelets include infusion of fresh frozen plasma, cryoprecipitate, and platelets. 4. Individuals with hemophilia should avoid trauma whenever possible. Medications that interfere with platelet function, including NSAIDs, should be avoided. 5. VWD type 1 and some forms of type 2 can be treated with desmopressin to promote hemostasis, treat mucocutaneous bleeding, and prevent bleeding associated with minor procedures. Therapy with antifib-rinolytic agents such as tranexamic acid is also benefi-cial in VWD. T reatment with oral contraceptives or a levonorgestrel-releasing intrauterine device can be very beneficial for women with VWD experiencing menor-rhagia. Infusion of von Willebrand concentrate is also an option when desmopressin is not effective. B. Patient/family teaching points. 1. Patients should contact their primary care provider prior to any dental procedures or surgical interventions. 2. Bruising may be spontaneous or recurrent and patients may experience prolonged bleeding after minor cuts or abrasions. 3. Women of childbearing age will need high risk obstet-rics and should carefully plan pregnancies. C. Pharmacotherapy. 1. Pharmacological treatment will be based on the underlying cause of bleeding diathesis and is fairly lim-ited. 2. In the acute setting, blood products can be used to control bleeding disorders. 3. Avoidance of medications that interfere with platelet function should be evaluated. 4. Hypoprothrombinemia can be treated acutely with parenteral vitamin K. 5. Minor bleeding or elevated international normalized ratio (INR)—2. 5 to 5 mg oral vitamin K one time may be sufficient, or can be repeated in 24 hours if needed. 6. Patients who have internal bleeding or who are at high risk for bleeding can be given intravenous vitamin K 5 to 10 mg diluted in IVF and infused over 20 minutes. These patients should also receive prothrombin complex concentrate (PCC). D. Discharge instructions (If standard accepted guidelines exist please use discharge template). 1. Patient should be instructed on how to recognize signs and symptoms that warrant immediate attention. 2. Patients should also be given instructions on how to control a bleeding source. Follow-Up A. In general, medications such as aspirin and NSAIDs should be avoided in patients with abnormal bleeding. B. Conditions that may pose special risks for individuals with bleeding disorders, including hypertension that may lead to intracranial bleeding, need close monitoring and treat-ment. C. Procedures necessary for preventive care and screening should be planned in cooperation with the patient's hema-tologist. D. Dental care and screening colonoscopy can usually be performed with decreased risk for bleeding when supervised carefully and given appropriate hemostatic coverage. Consultation/Referral A. T reatment of underlying conditions is important in con-trolling bleeding in individuals with bleeding diatheses. B. Consultation with a gastroenterologist/hepatologist is important in management of advanced liver disease. C. When thrombocytopenia is present, consultation with a hematologist is warranted. D. If DIC or thrombocytopenia is associated with sepsis, consultation with an infectious disease specialist is indicated. E. Bleeding associated with malignancy requires referral to hematology oncology. F. Bleeding in the setting of pregnancy-related complica-tions requires immediate referral to OB/GYN. Special/Geriatric Considerations A. Bleeding disorders in the elderly pose special challenges. B. A number of acquired disorders can present in older adults as a result of alterations in coagulation factors, medi-cations, and comorbid conditions more common with aging. C. Older adults are more likely to be receiving medications to treat thrombotic disorders and evidence of bleeding may be dismissed as a side effect of anticoagulants and antiplatelet drugs. D. Increased risk for bleeding associated with anticoagulants as well as NSAIDs accompanies many physiological changes of aging. E. Thrombocytopenia in the elderly may be associated with ITP, leukemia, or DIC associated with malignancy or sepsis. F. Though rare, there is risk for acquired hemophilia and acquired von Willebrand syndrome in older adults. Bibliography Baz, R., & Mekhail, T. (2013). Bleeding disorders. Cleveland Clinic Center for Continuing Education, Disease Management. Retrieved from http://www. clevelandclinicmeded. com/medicalpubs/ diseasemanagement/hematology-oncology/bleeding-disorders/ Capriotti, T., & Frizzell, J. P. (2016). Pathophysiology: Introductory concepts and clinical perspectives (pp. 285-304). Philadelphia, PA: F. A. Davis. Drews, R. E. (2017). Approach to the adult patient with bleeding diathesis. In L. Leung (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/approach-to-the-adult-with-a-suspected-bleeding-disorder Grossman, S. (2014). Disorders of hemostasis. In S. C. Grossman & C. M. Porth (Eds. ), Porth's pathophysiology: Concepts of altered health states (9th ed., pp. 648-664). Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins. Kruse-Jarres, R. (2015). Acquired bleeding disorders in the elderly. ASH Education Book, 2015 (1), 231-236. Kruse-Jarres, R., Singleton, T. C., & Leissinger, C. A. (2014). Iden-tification and basic management of bleeding disorders in adults. Journal of the American Board of Family Medicine, 27 (4), 549-564. doi:10. 3122/jabfm. 2014. 04. 130227 Leung, L. (2018, November 12). Overview of hemostasis. In P. Mannucci (Ed. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-hemostasis Levi, M., & Sivapalaratnam, S. (2015). Hemostatic abnormalities in criti-cally ill patients. Internal and Emergency Medicine, 10, 287-296. doi:10. 1007/s11739-014-1176-2 Lillicrap, D. (2013). Von Willebrand disease: Advances in pathogenetic understanding, diagnosis, and therapy. Blood, 122 (23), 3735-3740. doi:10. 1182/blood-2013-06-498303 Schwartz, A., & Rote, N. S. (2014). Alterations in leukocyte, lymphoid, and hemostatic function. In K. L. Mc Cance, S. E. Huether, V. L. Brashers, & N. S. Rote (Eds. ), Pathophysiology: The biologic basis for disease in adults and children (pp. 1008-1054). St. Louis, MO: Elsevier/Mosby. 12. Hematology Guidelines
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257Coagulopathies Mary L. Wilby Definition A. Strictly speaking, coagulopathy describes a condition that disturbs the blood's ability to clot. For purposes of this text, coagulopathy will refer to hypercoagulability. Bleeding dis-orders are described elsewhere in this chapter. B. Hypercoagulability, sometimes referred to as throm-bophilia, is an enhanced state of hemostasis that increases the risk for thrombosis and blood vessel occlusion. C. These conditions are typically created in the presence of increased platelet function or increased activity of the coagu-lation system. Arterial thrombi are most often associated with turbulent blood flow and are composed of platelets. D. Hypercoagulability disorders have been characterized as primary (hereditary) or secondary (acquired). Incidence A. Approximately 30% of those who present with deep vein thrombosis or pulmonary emboli are found to have Factor V Leiden. Factor V Leiden is seen primarily in individuals of European descent and in approximately 5% of whites in the United States. B. Antiphospholipid antibodies are present in 3% to 5% of the general population and are more prevalent in individuals with systemic lupus erythematosus. C. Venous thromboembolism (VTE) is not uncommon in the presence of malignancy. T umor type and stage, location of the tumor, treatment, and comorbid conditions influence risk. It is estimated that as many as 10% of cancer patients develop VTE. Pathogenesis A. Most hereditary thrombophilic disorders are associated with mutations in coagulation proteins, fibrinolytic proteins, platelet receptors, and various other factors. Factor V Leiden, a condition in which a Factor V mutation interacts with pro-tein C, leading to increased clot formation, is the most com-mon hereditary condition. B. Other inherited hypercoagulable states are rarer and include prothrombin gene mutation, hyperhomocysteine-mia, antithrombin deficiency, and protein C and protein S deficiency. C. Antiphospholipid syndrome is the most com-mon acquired hypercoagulable condition. When present, antiphospholipid antibodies are directed against phospholipid-protein complexes causing risk for both arte-rial and venous thrombus formation. D. Protein C and protein S deficiency may also become acquired in some disease states. E. Increased platelet function may manifest as enhanced platelet adhesion, with clot formation and decreased blood flow. Disturbances in blood flow, as with a therosclerotic plaques, cause endothelial tissue damage. Increased sensitiv-ity of platelets to substances that influence platelet aggrega-tion may increase platelet activity. F. Elevation in platelet counts above 1,000,000/ μL, referred to as thrombocytosis, is associated with both thrombosis and bleeding. Primary thrombocytosis is a myeloprolifer-ative disorder associated with a disorder of hematopoietic cells in the bone marrow. Secondary thrombocytosis is often associated with disease states that trigger thrombopoietin production, increasing platelet production. These conditions include surgery, cancer, and chronic inflammatory disorders. Predisposing Factors A. Surgery. B. Cancer. C. Chronic inflammatory disorders. D. Atherosclerosis. E. Diabetes mellitus. F. Smoking. G. Pregnancy. H. Oral contraceptive use. I. Estrogen replacement therapy. J. Obesity. K. Heart failure. L. Nephrotic syndrome. M. Polycythemia. N. Sickle cell disease. Subjective Data A. Common complaints/symptoms. 1. Patients with thrombocytosis may experience painful burning and throbbing in digits associated with arteriole occlusion. 2. Painful, swollen extremity (usually unilateral). B. Common/typical scenario. 1. Other signs and symptoms. a. Neurological impairment consistent with tran-sient ischemic attack or stroke. b. Chest pain associated with cardiac ischemia. c. Dyspnea associated with pulmonary emboli. d. Visual disturbance with retinal ischemia. C. Family and social history. 1. History of fetal loss in women with antiphospholipid syndrome. 2. History of unprovoked thrombosis in adults under 45 years of age. 3. Family history of multiple individuals with VTE. D. Review of systems. 1. Hematologic: Ask about bruising or previous clotting episodes of the arterial or venous system, such as stroke, myocardial infarction, or small vessel thrombosis. 2. Rheumatology: Ask about autoimmune disorders. 3. Obstetrics: Ask about spontaneous abortions. 4. Dermatology: Ask about skin discoloration. Physical Examination A. Physical examination may yield nonspecific findings. B. Evidence of arterial thrombosis may manifest in signs of stroke, myocardial infarction, DVT, PE, or digital ischemia. C. Skin necrosis is associated with warfarin therapy. Diagnostic Tests A. Complete blood count (CBC). B. Prothrombin time. C. Activated partial thromboplastin time. D. Antiphospholipid antibodies. E. Protein C—may be low in acute thrombosis. F. Protein S—may be low in acute thrombosis. G. Antithrombin III—may be low in acute thrombosis. Differential Diagnosis A. Paroxysmal nocturnal hematuria. B. Homocysteinemia. C. Heparin-induced thrombocytopenia. D. Atherosclerosis. E. Sickle cell disease. F. Myeloproliferative diseases. Coagulopathies
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258 Evaluation and Management Plan A. General plan. 1. Not all thrombotic episodes are associated with hyper-coagulable risk factors and not all individuals with risk factors develop thrombosis. 2. Workup for coagulopathy is indicated with the pres-ence of idiopathic or recurrent VTE, VTE before the age of 40, VTE with strong family history, VTE in an atypi-cal site, or warfarin-induced skin necrosis. 3. T reatment involves reducing or eliminating factors that lead to thrombosis. B. Patient/family teaching points. 1. Women need to avoid oral contraceptives or hormone replacement therapy. 2. Patients may need to be treated with lifelong antico-agulation to prevent further clotting. 3. Patients must be instructed on how to manage bleed-ing diathesis if on anticoagulation agents. C. Pharmacotherapy. 1. Acute events require treatment with anticoagulants including heparin, warfarin, and other agents. 2. Immune suppression may be needed in some cases when the condition is refractory to anticoagulants. D. Discharge instruction. 1. Patients will need to follow-up with hematology. 2. Any dental procedures or surgical interventions must be done in conjunction with the patient's primary care provider. Follow-Up A. Monitoring of anticoagulation therapy posthospitaliza-tion is critical to preventing recurrence. B. Patients should be cautioned to avoid trauma while receiving anticoagulant therapy. C. Patients with modifiable risk factors including tobacco use or use of estrogen-containing oral contraceptives should be counseled about their use. Consultation/Referral A. Consultation with a hematologist is critical in the diag-nosis and management of patients with hypercoagulable dis-orders. B. It is also important that laboratory testing is completed at a facility with experience in utilizing specialized tests. Special/Geriatric Considerations A. Aging is accompanied by increased risk of both arterial and venous thrombosis. B. While mechanisms are not entirely clear, a number of coagulation factors, including Factors V, VII, VIII, IX, and von Willebrand factor (v WF), increase with aging. This cou-pled with other comorbid conditions such as malignancy and structural changes in vascular endothelium contribute to an increased risk for thrombosis in older adults. C. Special consideration is given for the use of anticoagula-tion in older adults to minimize the risk for bleeding. Careful monitoring of vitamin K antagonists is necessary. D. Use of direct oral anticoagulants (DOAs) may be an alter-native in some cases. E. Education and monitoring to decrease risk for falls and other forms of trauma are essential for older adults receiving anticoagulation therapy. Bibliography Bauer, K. A. (2019, February 27). Risk and prevention of venous thromboembolism in adults with cancer. In L. Leung (Ed. ), Up To-Date. Retrieved from https://www. uptodate. com/contents/risk-and-prevention-of-venous-thromboembolism-in-adults-with-cancer Grossman, S. (2014). Disorders of hemostasis. In S. C. Grossman & C. M. Porth (Eds. ), Porth's pathophysiology: Concepts of altered health states (9th ed., pp. 648-664). Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins. Hogan, C. (2015). Thrombophilia and hypercoagulable states. In F. J. Domino, R. A. Baldor, J. Golding, & M. B. Stephens (Eds. ), The 5 minute clinical consult premium, 2016 (24th ed., pp. 1092-1093). Philadelphia, PA: Wolters Kluwer Health. Nakashima, M. O., & Rogers, H. J. (2014). Hypercoagulable states: An algorithmic approach to laboratory testing and update on monitoring of direct oral anticoagulants. Blood Research, 49 (2), 85-94. doi:10. 5045/ br. 2014. 49. 2. 85 Previtali, E., Bucciarelli, S., Passamonti, S. M., & Martinelli, I. (2011). Risk factors for venous and arterial thrombosis. Blood Transfusion, 9, 120-138. doi:10. 2450/2010. 0066-10 Robert-Ebadi, H., & Righini, M. (2010). Anticoagulation in the elderly. Pharmaceuticals, 3 (12), 3543-3569. doi:10. 3390/ph3123543 Schick, P. (2018, January 5). Hereditary and acquired hyper-coagulability. In S. Nagalla (Ed. ), Medscape. Retrieved from https://emedicine. medscape. com/article/211039-overview Schwartz, A., & Rote, N. S. (2014). Alterations in leukocyte, lymphoid, and hemostatic function. In K. L. Mc Cance, S. E. Huether, V. L. Brashers, & N. S. Rote (Eds. ), Pathophysiology the biologic basis for disease in adults and children (pp. 1008-1054). St. Louis, MO: Elsevier Mosby. Deep Vein Thrombosis Mary L. Wilby Definition A. Deep vein thrombosis (DVT) describes clot formation in the deep veins, most often in the lower extremities. B. DVT increases the risk for venous thromboembolism (VTE) to the pulmonary circulation. C. See Figure 12. 2. Incidence A. More than 900,000 VTE events occur each year in the United States. Nearly one-third of these result in death. B. Up to 50% of cases are believed to be idiopathic, with an additional 15% to 25% associated with cancer, and 20% associated with surgery. C. Pulmonary embolism (PE) can occur in up to 50% of patients with untreated DVT. D. The mortality rate associated with PE is 25% to 30%. Pathogenesis A. Three factors often referred to as Virchow's triad promote venous thrombosis. These three factors are (a) venous stasis, (b) damage to venous endothelium, and (c) hypercoagula-ble states. Buildup of clotting factors and platelets promotes thrombus formation in the vessel, often adjacent to a valve. Inflammation associated with the clot promotes additional platelet aggregation, causing the clot to grow proximally. B. Bed rest and/or immobility are factors often associated with venous stasis. C. Hypercoagulability may be associated with increased activity of clotting factors or inherited or acquired conditions in which factors that would normally inhibit clotting are defi-cient. D. Venous injury can result from surgery, trauma, and venous catheters. 12. Hematology Guidelines
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259 FIGURE 12. 2 Diagnosis of DVT. DVT, deep vein thrombosis; PE, pulmonary embolism. E. Localized symptoms are the result of inflammation and venous obstruction, but symptoms may not be apparent if the vein is deep within the leg because of incomplete occlusion and collateral circulation. Predisposing Factors A. Immobility. B. Obesity. C. Prolonged dependency (including air travel). D. Age. E. Heart failure. F. T rauma. G. Medications. H. Malignancy. I. Central venous catheters. J. Pregnancy. K. Oral contraceptives. L. Hormone replacement. M. Nephrotic syndrome. N. Antiphospholipid antibody syndrome. O. Hospitalization (especially orthopedic surgery, trauma, spinal cord injury, gynecologic disorders). P. Inherited clotting disorders including Factor V Leiden mutation, prothrombin mutations, antithrombin deficiency,hyperhomocysteinemia, elevated Factor VIII activity, protein C deficiency, and protein S deficiency. Subjective Data A. Common complaints/symptoms. 1. Pain. 2. Swollen extremity. 3. Muscle tenderness. B. Common/typical scenario. 1. Other signs and symptoms. a. Fever. b. Increased erythrocyte sedimentation rate. c. Increased white blood cell count. C. Family and social history. 1. History of recent surgery or trauma. 2. History of cancer, liver disease, autoimmune disorder, or cardiovascular disease. 3. Previous history of blood clotting or bleeding prob-lems. 4. Family history of stroke or other thrombosis. 5. Immobility. 6. Recent prolonged travel. D. Review of systems. 1. Musculoskeletal: Ask about extremity pain with or without movement, edema, and redness. Deep Vein Thrombosis Diagnosis of DVT Algorithm Suspicion of DVT Risk factors that increase risk-+ clinical signs of DVT, recent surgery or immobility, malignancy, previous history DVT, symptoms that might indicate PE 1 or less risk factors (low risk) D-dimer Negative DVT excluded Positive or unable to test Compression ultrasonography Negative DVT excluded Positive DVT con/f_irmed Negative Positive Compression ultrasonography2 or more risk factors (moderate to high risk)
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260 Physical Examination A. Physical examination alone is less reliable than when cou-pled with thorough history. B. Unexplained extremity swelling, pain, warmth, or ery-thema may be noted. Pain is frequently described as a cramp or ache in the calf or thigh. C. The location of the thrombus may influence physical findings. Swelling in the foot and ankle and calf pain are associated with thrombi in the venous sinuses in the soleus muscle and posterior tibial and peroneal veins. Thrombi in the femoral vein are associated with pain in the popliteal area and distal thigh while those in the ileofemoral veins are man-ifested by pain and swelling involving the whole leg. D. Upper extremity swelling along with pain and venous dis-tention may indicate upper extremity DVT. Diagnostic Tests A. Serum D-dimer concentration. B. Lower extremity ultrasonography. C. CT. D. MRI. E. Venogram. Differential Diagnosis A. T rauma. B. Infection. C. Peripheral artery disease. D. Chronic venous insufficiency. E. Postthrombotic syndrome. F. Lymphedema. G. Erythema nodosum. H. Insect bites. I. Muscle strain. Evaluation and Management Plan A. General plan. 1. Prompt diagnosis of DVT is facilitated by combin-ing medical history and physical examination, D-dimer testing, and appropriate use of imaging studies. 2. Hospitalized patients are typically treated with intra-venous heparin and monitored for signs of bleeding. 3. Thrombolytic therapy should be reserved for massive PE or extensive DVT. 4. Contraindications to outpatient management of DVT include surgery within 7 days, cardiopulmonary instability, and severe symptomatic venous obstruction. 5. Additional contraindications for outpatient treat-ment include platelet count less than 50,000/l L, other medical or surgical conditions requiring inpa-tient management, medical nonadherence, geographical or telephone inaccessibility, impaired hepatic function, impaired renal function (e. g., rising serum creatinine), and inadequate home healthcare support. 6. The optimal duration of therapy is dictated by the presence of modifiable risk factors for thrombosis. 7. Long-term anticoagulation is an important consider-ation for individuals with unprovoked VTE or ongoing prothrombotic risk factors such as cancer and antiphos-pholipid antibody syndrome. 8. Short-term therapy is sufficient for most patients with VTE associated with transient triggers such as major surgery. 9. Inferior vena cava (IVC) filters should be consid-ered for patients with acute VTE and contraindications to anticoagulation. Retrievable filters are preferable. 10. Warfarin is contraindicated in pregnancy while low molecular weight heparin (LMWH), dalteparin, and fon-daparinux are pregnancy Category B. B. Patient/family teaching points. 1. Patients must be taught to recognize concerning signs for bleeding diathesis while on anticoagulation. 2. Depending on the medication ordered, patients may need to have routine blood work completed. 3. Patients need to set reminders to take the medications the same time each day to optimize efficacy of the medi-cation. C. Pharmacotherapy. 1. Low dose fractionated or nonfractionated heparin given subcutaneously is the mainstay of treatment. 2. The availability of LMWH, fondaparinux, and direct oral anticoagulants (DOACs) has increased the options for acute outpatient treatment of DVT and PE. a. DOACs can be as effective as LMWH and vitamin K antagonists such as warfarin. D. Discharge instructions (If standard accepted guidelines exist please use discharge template). 1. Patients will need to follow-up with hematology as an outpatient. Follow-Up A. Patients with DVT should gradually resume activity and avoid immobility. B. Monitoring of anticoagulation and bleeding risk can be done as an outpatient. C. Individuals receiving warfarin need regular monitoring of prothrombin time and international normalized ratio (INR). D. Platelets should be monitored in patients receiving LMWH and fondaparinux. Consultation/Referral A. Consultation with interventional radiology is neces-sary when considering use of thrombolytics, thrombectomy, stents, or placement of IVC filter. B. Ongoing follow-up should be provided for patients requiring IVC filter to reduce risks for filter thrombosis. Special/Geriatric Considerations A. Increasing age and renal impairment increase risk for VTE in older adults while at the same time increasing risk for bleeding associated with anticoagulant therapy. B. DOAs may offer an acceptable alternative to warfarin as monitoring is simpler. C. Alteration in renal function may necessitate dose adjust-ments or serve as a contraindication for their use. Bibliography Behravesh, S., Hoang, P., Nanda, A., Wallace, A., Sheth, R. A., Deipolyi, A. R., & Oklu, R. (2017). Pathogenesis of thromboembolism and endovascular management. Thrombosis, 2017, 1-14. doi:10. 1155/2017/ 3039713 Brashers, V. L. (2014). Alterations in cardiovascular functioning. In K. L. Mc Cance, S. E. Huether, V. L. Brashers, & N. S. Rote (Eds. ), Pathophys-iology the biologic basis for disease in adults and children (pp. 1129-1193). St. Louis, MO: Elsevier Mosby. Conelius, J. (2014). Disorders of blood flow in the systemic circulation. In S. C. Grossman & C. M. Porth (Eds. ), Porth's pathophysiology: Concepts of altered health states (pp. 739-765). Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins. Geldhof, V., Vandenbrielem, C., Verhamme, P., & Vanassche, T. (2014). Venous thromboembolism in the elderly: Efficacy and safety of non-VKA oral anticoagulants. Thrombosis Journal, 12, 21. doi:10. 1186/ 1477-9560-12-2112. Hematology Guidelines
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261 Keller, K., Prochaska, J. H., Coldewey, M., Gobel, S., Ullmann, A., Jünger, C.,... Wild, P. S. (2015). History of deep vein thrombosis is a discrimi-nator for concomitant atrial fibrillation in pulmonary embolism. Throm-bosis Research, 136 (5), 899-906. doi:10. 1016/j. thromres. 2015. 08. 024 Streiff, M. B., Agnelli, G., Connors, J. M., Crowther, M., Eichinger, S., Lopes, R.,... Ansell, J. (2016). Guidance for the treatment of deep vein thrombosis and pulmonary embolism. Journal of Thrombosis and Thrombolysis, 41, 32-67. doi:10. 1007/s11239-015-1317-0 Talfur, D. V., & Talfur, A. (2015). Deep vein thrombosis. In F. J. Domino, R. A. Baldor, J. Golding, & M. B. Stephens (Eds. ), The 5 minute clinical consult premium, 2016 (24th ed., pp. 1092-1093). Philadelphia, PA: Wolters Kluwer Health. Weber, J. (2014). Venous thromboembolic disease. Journal of the American Osteopathic College of Radiology, 3 (3), 2-7. Wilbur, J., & Shian, B. (2012). Diagnosis of deep vein thrombosis and pulmonary embolism. American Family Physician, 86 (10), 913-919. Retrieved from https://www. aafp. org/afp/2012/1115/p913. html Sickle Cell Crisis Mary L. Wilby Definition A. Vaso-occlusive crisis (VOC) involving the bones is the most consistent and characteristic feature of sickle cell dis-ease (SCD). B. VOCs and their accompanying pain present most fre-quently in the extremities, chest, and back, although multiple sites may be involved. Incidence A. Approximately 5% of the world's population carries an abnormal hemoglobin gene, with SCD being the most pre-dominant form. B. The greatest burden of the disease lies in sub-Saharan Africa. SCD affects nearly 100,000 individuals in the United States, the majority of whom are African American. Pathogenesis A. SCD occurs as a result of change in the amino acids of the beta globin chain of the hemoglobin molecule. Under circumstances where deoxygenation occurs, causing a reac-tion leading to “sickling” of the red blood cell, reoxygena-tion allows the cell to return to its normal shape; however, repeated sickling damages the cells, leaving them perma-nently sickled. B. Chronic hemolysis and high viscosity and vascular occlu-sion are the two main pathologic processes leading to the symptom most often associated with SCD. Infarction occurs as a result of stasis of the rigid sickle cells in the vascular beds of organs as a result of decreased blood flow. Sickled cells lose their flexibility and are unable to pass through the capillaries. Additionally, sickle cells tend to exhibit more adhesiveness to vascular endothelium and other blood cells, contributing to the obstruction of blood flow. C. Bone pain crisis is one of the most common manifesta-tions of SCD. Pain occurs as a result of activating afferent nerves in bones experiencing ischemia. Long bones includ-ing the femur and humerus, as well as ribs, vertebrae, pelvis, and sternum, are common sites of pain, often with multiple sites affected at once. Painful crises may vary in intensity. D. When arising in other sites, pain can be confused with, or can be an early indication of, another acute complication such as stroke, liver or splenic sequestration, or constipation associated with opioid use. The etiology of the pain must be identified in order to rule out potential causes of pain other than an uncomplicated VOC, such as cardiac ischemia, pneu-monia, or other abdominal complications. VOC can occur inthe presence of other complications, making diagnosis more challenging. No diagnostic test is able to rule in or to rule out a VOC. Diagnostic tests are most useful in ruling out other causes of pain. E. Acute abdominal pain may result from vaso-occlusion of mesenteric vasculature, sequestration of blood in the spleen, biliary tract disease, or non-SCD related conditions. Sequestration most often occurs in the spleen, but the liver and lymph nodes may also be sites of sequestration. If not recognized and treated rapidly, acute sequestration may result in shock and death. Mesenteric syndrome is a rare complication. The patient may present with gen-eralized abdominal pain, localized or rebound ten-derness, and rigidity. Paralytic ileus with vomiting, distention, and absence of bowel sounds along with dilated bowel loops, and air-fluid levels on abdominal x-ray are hallmarks. Predisposing Factors A. Exposure to cold. B. Dehydration. C. Infection. D. Physical exertion. E. Tobacco smoke. F. Alcohol use. G. Drug abuse. H. High altitude. I. Hypoxic conditions. J. Physical pain. K. Pregnancy. L. Hot weather. M. Emotional stress. N. Onset of menses. Subjective Data A. Common complaints/symptoms. 1. Extremity pain. 2. Chest pain. 3. Back pain. B. Common/typical scenario. 1. Other signs and symptoms. a. Abdominal pain. b. Tachycardia. c. Tachypnea. d. Fever. e. Pallor. f. Jaundice. C. Family and social history. 1. Recent history of precipitating factors. 2. Previous VOC. 3. Comorbid conditions. 4. Current treatment regimen, including analgesics and other medications, as well as transfusions. D. Review of systems. 1. Ask about pain and where it is located. a. Pain can affect any part of the body. 2. Ask about any infections, cough, or fever. 3. Cardiac. a. Chest pain. b. Palpitations. 4. Neurology. a. Any weakness or shaking. Physical Examination A. Vital signs. B. Oxygen saturation. Sickle Cell Crisis
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262 C. Skin and mucous membranes, noting pallor or jaundice. D. Hydration status. E. Cardiac examination. F. Lung examination. G. Abdominal examination. H. Neurological examination. Diagnostic Tests A. Complete blood count (CBC). B. Blood and urine cultures if febrile. C. Chest x-ray if pulmonary symptoms. D. EKG to rule out ischemia. E. Chemistry panel. F. Liver function testing. G. Urinalysis. Differential Diagnosis A. Avascular necrosis. B. Acute chest syndrome. C. Gout. D. Bone infarction. E. Osteomyelitis. F. Joint infection. G. Cerebrovascular accident. H. Pneumonia. I. Asthma. Evaluation and Management Plan A. General plan. 1. T reatment of bone pain crisis includes providing ade-quate analgesia, hydration, prophylactic or therapeutic antibiotics after collection of appropriate cultures, and oxygenation when hypoxia is evident. 2. Oral hydration may be inadequate, making intra-venous hydration necessary. 3. Pain management is best directed by the patient's report of pain. a. Analgesia should be offered within 30 minutes of presentation with an acute painful event. b. Before prescribing analgesics for an acute painful sickle cell episode, the provider should inquire about and consider any analgesia taken by the patient for this painful episode prior to his or her arrival at the hospital. i. The effectiveness of pain relief should be assessed frequently. If the patient with severe pain has not had relief, a second dose of strong opi-oid should be offered. Patient-controlled analgesia should be considered if repeated boluses of strong opioid medications are needed within a 2-hour period. ii. Frequent monitoring for adverse events asso-ciated with strong opioids, including respiratory depression and excessive sedation, is advised. iii. An alternative diagnosis should be considered if the patient does not respond to standard treat-ment for an acute crisis. iv. Consideration of exchange blood transfusion should be given in situations where pain is unre-lieved with conventional measures. v. Nonpharmacologic measures include: 1)Physical therapy. 2)Relaxation. 3)Distraction techniques. 4)Music therapy. 5)Meditation, which may be beneficial. 6)Prophylactic incentive spirometry, which is recommended to reduce the risk for acute chest syndrome. B. Patient/family teaching points. 1. Preventing sickle cell crises is the keystone manage-ment approach. 2. Patients need to be taught how to recognize their own triggers and to have a self-assessment and treatment plan at home. 3. Prevention of infection is also important. a. Reinforcing proper hygiene is key. b. Reinforcing universal precautions is essential. 4. Remind patients that the use of live vaccines is con-traindicated in sickle cell due to the immunosuppressive therapy they receive. C. Pharmacotherapy. 1. A dose of a strong opioid should be offered to all patients with severe pain (7 or greater on a 0-10 scale) and those with moderate pain (4-7 on a 0-10 scale) who have already received some analgesia before their arrival at the hospital. 2. Severe VOC requires parenteral opioid analgesia and hydration in a hospital setting. 3. The dose of the analgesia should be titrated with the severity of the pain until adequate control is achieved with a scheduled dose regimen, with short-acting agents for breakthrough pain. 4. Meperidine should be avoided because of neurotoxic-ity associated with high doses. 5. A weak opioid may be considered for those with mod-erate pain who have not yet received some form of anal-gesic. Except when contraindicated, acetaminophen, or nonsteroidal anti-inflammatory drugs (NSAIDs), should be offered to all patients via a suitable route in addition to opioids. 6. All patients receiving opioids should receive laxatives on a regular basis as well as antiemetics and antipyretics as needed. D. Discharge instructions (If standard accepted guidelines exist please use discharge template). 1. Long-term follow-up is essential. 2. Teach patients to recognize signs of infection and what to do when the signs manifest. Follow-Up A. Patients with SCD should have regular follow-up with their hematologist. B. Those with frequent readmissions for painful crises should be considered for treatment, with hydroxyurea used to increase fetal hemoglobin. C. Routine laboratory evaluation should include CBC, elec-trolytes, renal, and liver function tests. D. Adults should receive all age-appropriate immunizations including pneumococcal vaccines, influenza, and meningo-coccal vaccines. Consultation/Referral A. Referral for pain management services may be warranted for individuals with chronic pain and when there is concern for opioid abuse. B. Referral to ophthalmology for annual retinal examination should be considered for all patients. Special/Geriatric Considerations A. Improved treatment of patients with SCD has progres-sively increased their survival over the past 30 years. 12. Hematology Guidelines
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263 B. While the average life expectancy of patients with SCD in the 1970s was less than 20 years, mean life expectancy in the 1990s among those with the most severe form of the disease increased to 42 years for men and 48 years for women. C. Cases of individuals living into their 50s and 60s have been well documented, with additional recent cases indicat-ing some individuals lived into their 80s. D. Those who survive into later life are more likely to have long-term disease complications including renal insuffi-ciency. Bibliography Adewoyin, A. S. (2015). Management of sickle cell disease: A review for physician education in Nigeria (sub-Saharan Africa). Anemia, 2015, 791498. doi:10. 1155/2015/791498Ballas, S. K., Pullte, D. E., Lobo, C., & Riddick-Burden, G. (2016). Case series of octogenarians with sickle cell disease. Blood, 128, 2367-2369. doi:10. 1182/blood-2016-05-715946 Field, J. J., Vichinsky, E. P., & De Braun, M. R. (2018, September 7). Overview of the management and prognosis of sickle cell dis-ease. In S. L. Schrier & D. H. Mahoney, Jr. (Eds. ), Up To Date. Retrieved from https://www. uptodate. com/contents/overview-of-the-management-and-prognosis-of-sickle-cell-disease Lanzkron, S., Carroll, C. P., & Haywood, C., Jr. (2013). Mortality rates and age at death from sickle cell disease: U. S., 1979-2005. Public Health Reports, 128, 110-128. doi:10. 1177/003335491312800206 National Heart, Lung, and Blood Institute. (2014). Evidence-based manage-ment of sickle cell disease: Expert panel report, 2014. Washington, DC: U. S. Department of Health and Human Services. Porter, B. O., & Winland-Brown, J. E. (2015). Hematological and immune problems. In L. M. Dunphy, J. E. Winland-Brown, B. O. Porter, & D. J. Thomas (Eds. ), Primary care the art and science of advanced practice nursing (4th ed., pp. 920-1025). Philadelphia, PA: F. A. Davis. Sickle Cell Crisis
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Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf
13 Oncology Guidelines Jerrad M. Stoddard Brain/Central Nervous System Malignancies Jerrad M. Stoddard Definition A. Brain tumors most commonly arise from distant metas-tasis of other primary malignancies. B. Subtypes and classification: Primary brain tumors are classified according to the histologic pattern of cell differen-tiation. 1. Gliomas. a. Most commonly occurring primary brain tumors. b. Several types, including: i. Glioblastomas (most common). ii. Astrocytomas. iii. Oligodendrogliomas. iv. Ependymomas. 2. Meningiomas. 3. Nerve sheath tumors. 4. Pituitary tumors. 5. Primary central nervous system (CNS) lymphoma (associated with HIV/AIDS and immunosuppression). Incidence A. The U. S. incidence rate of primary brain and CNS tumors in patients 20 years of age and older is 28. 6 per 100,000 persons. B. The incidence rate for children (ages 0-19) is much lower, 5. 6 per 100,000 persons. C. The 5-year overall survival rate for all malignant brain tumors is ∼34%. D. Survival rates depend on histologic subtype. For exam-ple, the 5-year overall survival rates for anaplastic astrocytoma and glioblastoma are 28% and 5%, respectively. Pathogenesis A. Primary brain tumors proliferate from brain tissue most commonly from glial tissue. 1. T umors that arise from glial tissue include astrocy-tomas, oligodendrogliomas, and ependymomas. 2. Nonglial primary type brain tumors are meningiomas, schwannomas, craniopharyngiomas, germ cell tumors, and pineal region tumors. B. Typically primary brain tumors do not metastasize, although they can. C. Secondary or metastatic brain tumors originate from another part of the body and spread to the brain. 1. Several types of secondary brain tumors spread quickly to the brain, including lung, breast, melanoma, colon, and kidney cancer. Predisposing Factors A. Ionizing radiation. B. Exposure to cured foods. C. HIV/AIDS. D. Immunosuppression. E. Cytomegalovirus (CMV) infection. F. Familial predisposition. 1. Neurofibromatosis type 1 (NF1) and type 2 (NF2). 2. Li-Fraumeni syndrome. 3. T urcot syndrome. Subjective Data A. Common complaints/symptoms. 1. Patients with low-grade tumors may initially be asymptomatic. 2. Symptoms are related to compression of intracranial structures and/or increased intracranial pressure (ICP). 3. Nausea and/or vomiting may occur due to increased ICP. 4. Neurological symptoms. a. Seizures. b. Headaches. c. Focal neurological deficits. d. Syncope. e. Visual changes. f. Gait instability. 5. Symptoms/signs associated with pituitary tumors (e. g., prolactinomas). a. Bitemporal hemianopsia due to compression of the optic chiasm. b. Spontaneous bilateral nipple discharge. c. Hypogonadism. Physical Examination A. Assess for evidence of primary tumors (most commonly lung followed by melanoma, renal cell, breast, and colorec-tal). B. A full neurological exam must be performed in all patients with suspected brain tumors. 1. Mini-Mental State Exam. 2. Motor strength in all extremities. 3. Sensory testing. 4. Visual field testing. 5. Reflexes. 6. Cranial nerve testing. 7. Gait and cerebellar assessment. 8. Rectal tone. Diagnostic Tests A. Contrast enhanced MRI (diagnostic standard). Brain/Central Nervous System Malignancies265
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B. Single photon emission CT (SPECT) imaging may be used to detect defects in the blood-brain barrier and may be considered to distinguish benign from malignant brain lesions. C. Consider lumbar puncture (contraindicated if evidence of elevated intracranial pressure). D. Hormone evaluation for pituitary tumors. E. Consider metastatic disease. 1. If metastatic disease is suspected, search for primary tumor (most commonly lung primary). 2. Biopsy of brain lesion is not necessary if metastatic disease is confirmed. Differential Diagnosis A. Gliomas. B. Meningiomas. C. Nerve sheath tumors. D. Pituitary tumors. E. Primary CNS lymphomas. Evaluation and Management Plan A. General plan. 1. Management of brain tumors is dependent on defini-tive pathology for diagnosis. 2. Biopsy or total resection (if possible) is recommended for all suspected brain malignancy. 3. The blood-brain barrier limits CNS penetration of many chemotherapies. 4. T reatment approach varies depending on grade. a. Low-grade glioma (grade I or II). i. Maximal safe resection is recommended for all patients. ii. Low-risk patients. 1)Observation postoperatively is reasonable due to slow growth. 2)MRI should be obtained every 3 to 6 months for the first 5 years, then annually. iii. High-risk patients. 1)Age greater than 40, subtotal resection, or unfavorable molecular features. 2)Consider radiation and adjuvant chemo-therapy. b. High-grade glioma (grade III or IV). i. Maximal safe resection. ii. Combination therapy with adjuvant radiation therapy and chemotherapy following resection. iii. Chemotherapy. iv. Targeted therapy. 5. Seizure prophylaxis. a. Patients with no prior history of seizures generally do not require prophylactic anticonvulsants. b. Patients undergoing surgical resection of supraten-torial tumors should be placed on prophylactic anti-convulsants. B. Acute care issues in brain/CNS cancers. 1. Seizures. 2. Cerebral edema. Follow-Up A. Follow-up with the team on a regular basis is impor-tant, including medical oncology, radiation oncology, and the neurosurgeon. Consultation/Referral A. Referral to a neurosurgeon for biopsy/resection. 1. Histologic review of the biopsy is the most crucial component of diagnosing brain tumors. 2. Histologic classification dictates therapeutic approach. 3. Pathologic review. Special/Geriatric Considerations A. Prognosis of the patient is highly dependent on tumor location, the ability to resect it, tumor type, and age of patient. B. Patients may develop seizures related to the location or aggressiveness of the tumor. Bibliography Ostrom, Q. T., Gittleman, H., Fulop, J., Liu, M., Blanda, R., Kromer, C.,... Barnholtz-Sloan, J. S. (2015). CBTRUS Statistical Report: Primary brain and central nervous system tumors diagnosed in the United States in 2008-2012. Neuro Oncology, 17 (Suppl. 4), iv1-iv62. Breast Cancer Alicia John Definition A. Uncontrolled growth of breast cells, usually forming a tumor that can be felt as a lump or seen on a x-ray. B. Malignant tumors invade the surrounding tissues or metastasize to distant body areas. C. Breast cancer can be curable, and early detection yields a favorable prognosis. Incidence A. Breast cancer is the most commonly diagnosed cancer in American women, and approximately 12. 4% of women in the United States will develop invasive breast cancer during their lifetime. B. After increasing for more than 20 years, breast cancer inci-dence rates in women have stabilized since 2000, possibly related to fewer women using hormone replacement therapy after menopause. C. Breast cancer is the second leading cause of cancer deaths in women, second only to lung cancer. D. The chance that a woman will die from breast cancer is about 1 in 36 ( ∼3%). E. The median age of diagnosis of breast cancer for women in the United States is 68. F. Fewer than 5% of women diagnosed with breast cancer in the United States are younger than 40. G. Risk of breast cancer increases with age, and is highest for women over the age of 70. H. Breast cancer is much less common in men than in women, with men in the United States experiencing a 1 in 1,000 lifetime risk of developing breast cancer. Pathogenesis A. Ductal carcinoma in situ (DCIS). 1. DCIS is considered noninvasive or preinvasive breast cancer. 2. The cells that line the ducts of the breast have become dysplastic but remain contained within the walls of the ducts and have not spread into the surrounding breast tissue. 3. DCIS accounts for approximately 20% of new diag-noses of breast cancer. 13. Oncology Guidelines266
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B. Lobular carcinoma in situ (LCIS). 1. LCIS is a collection of abnormal cellular growth inside one or more of the milk-producing glands in the breast (called lobules). 2. As the abnormal cells have not grown outside of the lobules, it is considered “in situ. ” 3. Although it is not considered cancer, it is associated with a higher risk of developing invasive cancer in the future. 4. LCIS is not very common and usually occurs in pre-menopausal women. 5. LCIS is considered higher risk as it typically does not cause symptoms and can be difficult to see on imaging, making it difficult to detect. 6. It is usually found incidentally when the breast is biop-sied for some other reason. C. Invasive ductal carcinoma (IDC). 1. This is the most common type of breast cancer and accounts for approximately 80% to 85% of all new breast cancer diagnoses. 2. IDC (or infiltrating) starts within the duct and grows into the adipose tissue of the breast. 3. Breaking beyond the ductal wall means it now has the capability to spread to other areas of the body through lymphatic spread. D. Invasive lobular carcinoma (ILC). 1. ILC starts in the milk-producing glands (lobules) and has invaded into the adipose tissue of the breast and there-fore can metastasize to other parts of the body. 2. Accounts for about 10% of breast cancers. 3. It is considered higher risk as it can be difficult to see on imaging, making detection and monitoring for recur-rence difficult. E. Inflammatory breast cancer (IBC). 1. IBC is a rare but aggressive form of invasive breast cancer, and accounts for about 1% to 3% of all breast cancers. 2. There may not be a palpable mass or tumor, so it may not be seen on imaging. Sometimes skin thickening can be seen on mammogram. 3. Often mistaken as cellulitis of the breast, as it presents with redness, warmth, and edema to the skin of the breast, often causing an orange peel appearance. a. This is caused not by infection but by cancer cells blocking lymph vessels in the skin, causing congestion. b. If cellulitis is suspected and the patient fails to respond after a course of antibiotics, timely or prompt mammogram and biopsy should be considered. 4. Time is of the essence with IBC given the strong potential for rapid progression. 5. IBC is considered a more aggressive breast cancer and is associated with poorer prognosis when compared to IDC. F. Other less common breast cancers and tumors: Angiosar-coma, medullary, mucinous, Paget's disease, papillary, phyl-lodes, tubular. Predisposing Factors A. Nonmodifiable. 1. Family history. 2. Genetic mutation or diagnosis (including BRCA1/2 gene mutations, Cowden syndrome, and Li-Fraumeni syndrome). 3. Race (white women are more likely to develop breast cancer than other ethnicities). 4. Gender (women >men). 5. Personal history of breast cancer. 6. Breast cellular changes (such as hyperplasia). B. Modifiable. 1. Smoking. 2. Obesity (fat cells produce estrogen). 3. Increased alcohol consumption (alcohol can limit your liver's ability to control blood levels of the hormone estrogen). 4. Sedentary lifestyle. 5. Exposure to estrogen (nulliparity, early onset of men-orrhea, delayed onset of menopause, hormone replace-ment therapy, never breastfeeding). 6. Use of oral contraceptives (there is an immediate increased risk, but that risk resolves over time after dis-continuation). 7. Prior radiation to the breast or chest wall. Subjective Data A. Common complaints/symptoms. 1. Localized disease. a. Pain, swelling, or redness in the breast. b. Nipple changes, inversion, or discharge. c. Skin changes, thickening, dimpling, or scaling in the breast or nipple. d. With lymphatic spread, patients may experience painful or enlarged lymph nodes in the axilla, chest, or neck. 2. Metastatic disease. a. Weight loss and/or change in appetite. b. Persistent, nagging, or worsening pain (visceral or bone/joint). c. Shortness of breath or cough. d. Headache. e. Fatigue. B. Common/typical scenario. 1. Due to increased awareness and screening, breast can-cer can frequently be found on screening mammograms, by self-breast examination, or by providers performing breast surveillance examinations. 2. When patients present with symptoms outside of the breast, they likely have already developed metastatic dis-ease. Physical Examination A. In addition to evaluating for disease in the primary site (breast), evaluate for possible metastatic disease. B. The most common sites of breast cancer metastases are brain, bone, liver, and lung. C. Check vital signs including pulse oximetry. D. A thorough baseline cardiac examination is important, as some chemotherapies used to treat breast cancer are associ-ated with risk for cardiotoxicity. Many chemotherapies used to treat breast cancer can cause neuropathies, so it is impor-tant to assess for any preexisting neuropathies at baseline that may not be related to cancer (such as diabetic neuropathy or prior nerve damage due to injury). E. Breast examination. 1. Should be performed in the sitting position with arms at side and raised above head, and again while lying supine with the same arm positions. If a patient has a self-palpated mass, ask the patient in which position he or she was best able to feel the mass. Do not forget to also exam-ine the nipple-areolar complex. 2. Once the mass is located, measure with a disposable measuring tape by isolating the mass between the thumb Breast Cancer267
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and forefinger and noting the distance between your dig-its. Note which quadrant of the breast the mass is in. 3. Assess the skin of the breast, including skin overlying the mass and the nipple for changes such as redness, peau d'orange appearance, edema, scaliness, or even an open lesion. 4. If the patient notes nipple discharge, the breast can be gently pressed to try and elicit the discharge so the out-put can be evaluated. If unable to easily express discharge, do not utilize increasing pressure. Sometimes the patient will have discharge that has collected in a bandage or her bra that can be evaluated. Note the color, amount, and consistency. 5. Lymph nodes should also be evaluated in the sit-ting and supine positions. Include bilateral evaluation of axilla, supraclavicular, infraclavicular, cervical, and mandibular regions. If lymph nodes are palpated, note size, consistency, if fixed or mobile, and if patient reports tenderness with palpation. F. Evaluate for metastatic disease. 1. Pulmonary: Observe for signs of dyspnea, increased work of breathing, or retractions; evaluate for pleural effu-sions (auscultation, percussion, and cacophony). 2. Musculoskeletal: Bone tenderness, impaired range of motion. 3. Abdomen: Assess for hepatomegaly, ascites, mass, or tenderness. 4. Neurological: Incoordination, focal deficits, visual changes, hearing changes, decreased strength. Diagnostic Tests A. History and physical examination. B. Diagnostic bilateral mammogram with tomosynthesis, which provides higher resolution when evaluating someone who has a known mass or breast abnormality; ultrasound of the breast as necessary (or as recommended by the radiolo-gist). C. Breast biopsy and clip placement. Ultrasound of nodal basin on the ipsilateral side. D. Pathology review; determination of hormone receptor status (estrogen/progesterone receptor and human epidermal growth factor receptor 2 [HER2]). E. Breast MRI when indicated. This is usually recommended by the radiologist if dense breast tissue obscures the mass, there is a question of the size of the mass, or concern is observed for involvement of the chest wall. F. Breast cancer is predictable. It starts in the breast, moves to the regional lymph nodes, and then metastasizes to dis-tant sites in the body. If nodal ultrasound is negative and there are no findings on physical examination to suggest metastasis, systemic staging is not indicated (per National Comprehensive Cancer Network [NCCN] guidelines). If a suspicious node is noted on imaging or examination, pro-ceed with biopsy of lymph node. If positive, proceed with metastatic workup. 1. Complete blood count (CBC), comprehensive metabolic panel (CMP). 2. CT chest, abdomen, pelvis with contrast. 3. Bone scan. 4. PET scan, if indicated. G. Diagnosis. 1. Tissue sample or biopsy is required for diagnosis. Pathology results will help guide the next step of workup, referral/provider evaluation, and recommended interven-tions. 2. It is imperative to send biopsy sample(s) for estrogen/ progesterone (ER/PR) and HER-2/neu testing, as theseresults are required for prognostication and therapy rec-ommendations. H. Staging: Breast cancer is staged utilizing the American Joint Committee on Cancer (AJCC) tumor, node, metastasis (TNM) system. Differential Diagnosis A. DCIS. B. LCIS. C. IDC. D. ILC. E. IBC. F. Paget's disease. G. Abscess. H. Fibroadenoma. Evaluation and Management Plan A. General plan. 1. Unless there is metastatic disease at the time of presen-tation, all patients that can tolerate surgery will be offered surgical intervention. 2. Depending on stage, some patients will also be offered chemo and/or radiation. 3. If the cancer is estrogen or progesterone positive, they may also be offered adjuvant hormone therapy. 4. Surgery. 5. Radiation therapy. 6. Chemotherapy. 7. Hormone therapy. a. About two out of three breast cancers are hormone receptor-positive. b. These cells have estrogen (ER-positive) and/or pro-gesterone (PR-positive) receptors on the cell surface that stimulate cell proliferation in the presence of estrogen or progesterone, respectively. B. Acute care issues in breast cancer. 1. Breast cancer patients are typically only admitted for surgical resection. a. Some procedures, such as segmental mastectomy, are outpatient procedures. b. More involved procedures, such as total mastec-tomy or those receiving immediate breast reconstruc-tion, may require postoperative admission. 2. Neutropenic fever (also see sections on Leukemias). a. Neutropenia may occur as a chemotherapy side effect, and neutropenic patients are highly susceptible to infection. b. Neutropenic fever can be life-threatening and can rapidly lead to sepsis. c. Diagnostics include CBC with differential, blood cultures, urinalysis with culture, chest x-ray, sputum culture (if appropriate), intravenous (IV) fluid sup-port (if appropriate), antipyretics, and empiric broad-spectrum antibiotics. d. Use of granulocyte stimulating colony factor (G-CSF) may be considered for neutropenia. 3. Metastatic symptoms. a. The most common sites of metastatic spread from breast cancer are bone, brain, liver, and lung. b. Patients with metastatic disease may be admitted for pain management or symptoms resulting from an organ system being affected by disease such as: i. Fluid retention or transaminitis from hepatic metastasis. ii. Confusion related to brain metastasis. iii. Pain and/or fracture from metastasis to the bone. 13. Oncology Guidelines268
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TABLE 13. 1 Breast Cancer Follow-Up NCCN ACS/ASCO History physical examination Year 1, every 3-4 mo Year 2, every 4 mo Year 3-5, every 6 mo Year 6 +, annually Year 1-3, every 3-6 mo Year 4-5, every 6-12 mo Year 6 +, annually Signs of recurrence No recommendation Educated and counseled about signs and symptoms Mammography 6 mo after post-BCS radiation therapy Annually thereafter Annually MRI No recommendation Not recommended for routine screening unless patient meets high-risk criteria for increased surveillance Pelvic examination Annually, for woman on tamoxifen Annual exam if uterus present No recommendation Routine blood tests No recommendation No recommendation Imaging studies No recommendation No recommendation Tumor marker testing No recommendation No recommendation ACS, American Cancer Society; ASCO, American Society of Clinical Oncology; BCS, Breast Cancer Society; NCCN, National Comprehensive Cancer Network. Follow-Up A. See Table 13. 1. Consultation/Referral A. Medical oncology. B. Breast surgical oncology. C. Radiation oncology (can be done prior to or after surgery and/or chemotherapy; or for palliation if metastatic). D. Fertility specialist, if appropriate. E. Cardiology referral may be indicated prior to chemother-apy or surgery as chemotherapeutic regimens (i. e., anthracy-clines) can cause cardiotoxicity or lead to evaluate for anes-thesia clearance. F. Genetic counseling: If indicated according to NCCN guidelines. G. Any patient with suspected breast cancer needs to be seen urgently by a specialist or breast clinic. H. Consider referrals to support groups and psychiatry for assistance in coping. Special/Geriatric Considerations A. T reatment guidelines for elderly patients with breast can-cer are limited. B. T reatment recommendations should be decided in con-junction with the patient and based on life expectancy as well as the patient's functional status, comorbidities, and social support. Bibliography National Cancer Institute. (n. d. ). Fast stats. Retrieved from https://seer. cancer. gov/faststats/selections. php?series=cancer NCCN. (2017, November 10). Clinical practice guidelines in oncology. Breast cancer (Version 3. 3017). Fort Washington, PA: National Com-prehensive Cancer Network. Runowicz, C. D., Leach, C. R., Henry, N. L., Henry, K. S., Mackey, H. T., Cowens-Alvarado, R. L., & Ganz, P. A. (2016). American Can-cer Society/American Society of Clinical Oncology breast cancer sur-vivorship care guideline. CA: A Cancer Journal for Clinicians, 66, 43-73. doi:10. 3322/caac. 21319Gastrointestinal Cancers: Colorectal Cancer Definition A. Cancer that forms in the tissues of the colon. B. Most colon cancers are adenocarcinomas and develop from polyps. Incidence A. Colorectal cancer is the third most common cancer in both men and women, and is also the third leading cause of cancer deaths. B. In 2016, there were an estimated 134,490 cases diagnosed in the United States: 39,220 cases of rectal cancer and 95,270 cases of colon cancer. C. The incidence of colon cancer has continued to decline over the past three decades, likely associated with improved screening and treatment of colorectal polyps. Despite this decline, there were still an estimated 49,140 deaths from colon and rectal cancer in 2016. D. Greater than 90% of new cases of colorectal cancer occur in patients over the age of 50, with the median onset age at 73. E. While the risk of colorectal cancer increases with age, in recent years there has been a significant increase in the inci-dence of colorectal cancer in younger patients. Pathogenesis A. Colorectal cancer is a complex process that derives from the epithelial cells lining the colon. B. Genetic mutations, either inherited or acquired, are thought to occur that irritate the lining, causing inflamma-tion and necrosis of the colon. C. Over time, lesions can develop which can disrupt cellular DNA and cause dysplasia, which can lead to the development of cancer. Gastrointestinal Cancers: Colorectal Cancer269 Cheryl Pfennig, Karen A. Beaty, Erin Michelle Dean, Rae Brana Reynolds, and Leigh A. Samp
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Predisposing Factors A. Approximately 2% to 5% of colorectal cancers are hered-itary, while the majority of cases are sporadic. B. Risk factors associated with the development of colorectal cancer include: 1. Dietary factors including the consumption of red meat, processed meat, and animal fat. 2. Cigarette smoking. 3. Inflammatory bowel disease (e. g., ulcerative colitis). 4. History of a prior colorectal cancer or adenomatous polyps. 5. Obesity. 6. Familial syndromes: Familial adenomatous polypo-sis (FAP) or hereditary nonpolyposis colorectal cancer (HNPCC). Subjective Data A. Common complaints/symptoms. 1. Colorectal cancer is often asymptomatic, with symp-toms appearing once the disease has become more advanced. Screening colonoscopies often detect early, asymptomatic colorectal cancers. 2. The most common presenting signs and symptoms include: a. Abdominal pain. b. Anorectal pain. c. Iron deficiency anemia. d. Weight loss. e. Fatigue. f. Hematochezia. g. Melena. h. Bowel changes. i. Constipation. ii. Diarrhea. iii. Urgency. iv. Frequency. v. Tenesmus. vi. Mucous discharge. i. Nausea/vomiting. j. Urinary dysfunction. k. Erectile dysfunction. Physical Examination A. Gastrointestinal. 1. Percussion. a. Dull areas may be present over the tumor site. b. A protuberant, tympanic abdomen may be indica-tive of an obstruction. 2. Auscultate for bowel sounds in all four quadrants. a. Absent or decreased bowel sounds are often indica-tive of obstruction. 3. Palpate for tenderness and/or masses in all four quad-rants. a. Larger tumors of the colon are often palpable on physical examination in nonobese patients. b. Liver is one of the two most common sites for col-orectal metastasis, and patients with advanced liver metastasis may have tender hepatomegaly. 4. Digital rectal examination to assess for tumor loca-tion, circumferential nature, and sphincter tone. B. Gynecologic examination in females with rectal cancer is important secondary to the proximity of the rectum to the vagina. Vaginal examination should be performed to evaluate for posterior vaginal wall involvement and to rule out recto-vaginal fistula. C. Evaluate for metastatic disease: Primarily liver, lung, and/or lymph nodes. Diagnostic Tests A. The workup for colorectal cancers includes diagnostic studies to help determine the extent of disease, as well as the presence of metastatic disease. B. Colon cancer workup. 1. Colonoscopy, complete to the cecum with adequately prepped colon. 2. Pathology review of biopsies. 3. Laboratory studies: Complete blood count (CBC), comprehensive metabolic panel (CMP), carcinoembry-onic antigen (CEA) level. 4. CT scan of the chest, abdomen, and pelvis with intra-venous (IV) and oral contrast. C. Rectal cancer workup. 1. Colonoscopy, complete to the cecum with adequately prepped colon. 2. Pathology review of biopsies. 3. Laboratory studies: CBC, CMP, CEA. 4. CT scan of the chest, abdomen, and pelvis with IV and oral contrast. 5. Pelvic MRI is the preferred staging study; however, if not available, perform endorectal ultrasound. 6. Flexible sigmoidoscopy or rigid proctoscopy is often performed by a surgeon to verify the tumor location for radiation treatment planning and surgery planning. 7. Enterostomal therapist referral is made for patient education and ostomy site marking. D. Diagnosis and staging. 1. Colorectal cancer diagnosis is established via tis-sue biopsy. Colonoscopy is the most common mode to obtain a tissue diagnosis, although an image-guided biopsy of a tumor may confirm the diagnosis. 2. Adenocarcinomas are the most common histologic subtype, accounting for greater than 90% of all cases. Less common histologic subtypes include: Mucinous car-cinoma, signet-ring cell carcinoma, squamous cell carci-noma, and undifferentiated carcinoma. 3. Confirmed tissue diagnosis and a complete workup provide the necessary data to clinically stage colorectal cancer. Proper clinical staging is important, as it influ-ences treatment planning and serves as an indicator for prognosis. 4. Staging for colorectal cancer is similar to the staging of many cancers, and utilizes the tumor, node, metastasis (TNM) system. Differential Diagnosis A. Inflammatory bowel disease. B. Ileus. C. Ischemic bowel. D. Diverticulosis. Evaluation and Management Plan A. General plan. 1. The primary treatment for colorectal cancer is surgery; however, disease stage and presence of metastatic disease can alter the treatment modalities offered as well as their sequencing. 2. Chemotherapy agents are commonly administered in the adjuvant setting; however, they may be adminis-tered in patients with locally advanced disease or with metastatic disease at presentation. 3. Radiation therapy. 4. Surgical management for colorectal cancers. a. Should include resection of the primary tumor, as well as the lymphatic, venous, and arterial supply. 13. Oncology Guidelines270
Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf