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PMC4217353_01 | Male | 66 | A 66-year-old male presented to his primary care physician with the right upper chest pain, progressive malaise, generalized weakness, loss of appetite, and a 10 lb weigh loss for 2 months. Past medical history was significant for rheumatoid arthritis, chronic pulmonary obstructive disease, and 60-pack-year of cigarette smoking. He had been treated for rheumatoid arthritis with weekly subcutaneous injection of etanercept for 10 months, and symptoms of rheumatoid arthritis were well-controlled. He denied cough, dyspnea, fever, chills, night sweat, or known tuberculosis exposure. Physical examination was unremarkable, and routine laboratory tests did not reveal significant abnormalities. A chest radiograph showed a right upper lobe density. Etanercept therapy was subsequently discontinued because of the concern of opportunistic infections secondary to etanercept. The tuberculin skin test (TST) was noted 2 mm prior to initiation of etanercept treatment. The patient underwent chest computed tomography (CT) which was reported a pleura-based consolidated mass (1.5 x 2 x 1 cm) on the lateral aspect of the right upper lobe and a thick-walled cavitary lesion (2.5 x 3 x 3.5 cm) on the superomedial side of the right lung apex, highly suggestive of a Pancoast tumor (Figures 1 and 2). There were background emphysematous pulmonary changes, without bronchiectasis, mediastinal, or hilar lymphadenopathy. It was followed by the 18F-FDG PET study, which demonstrated hypermetabolic uptake foci in these areas located within the right upper lobe (Figures 3 and 4). The standardized uptake values (SUVs) of the lesions were ranging from 7.4 to 12.8, consistent with pulmonary malignancy.
The bronchoscopy with bronchoalveolar lavage (BAL) was performed to establish the diagnosis of lung cancer. The bronchoscopy did not reveal endobronchial tumors. BAL cytology examination failed to demonstrate malignant cells. BAL Gomori methenamine-silver (GMS) stain and fungal culture was negative. The Ziehl-Neelsen acid-fast bacilli (AFB) smears of several BAL samples were positive. BAL Mycobacterium tuberculosis complex DNA probe and Mycobacterium avium intracellulare DNA probe were performed, and they were negative. Mycobacterium kansasii DNA probes on multiple BAL specimens reported positive, and a clinical diagnosis of pulmonary M. kansasii infection was then entertained. His HIV serology was negative. A triple drug regimen:isoniazid 300 mg/day, rifampin 600 mg/day, and ethambutol 1200 mg/day:was initiated while awaiting the final culture result. Chest pain and malaise were resolved in a week, and appetite returned in two weeks from the initiation of antimicrobial therapy. M. kansasii was eventually isolated from the culture after 6 weeks. The isolate was susceptible to rifampin, ethambutol, clarithromycin, rifabutin, ciprofloxacin, moxifloxacin, and amikacin. Serial CT chest imaging studies at the 6-week and the 6-month of antimycobacterial therapy revealed significant radiological improvement of pulmonary lesions (Figures 5 and 6). The patient continued to improve clinically, and a total resolution of pulmonary lesions was achieved (Figure 7) on completion of a 12-month course of triple drug therapy. | null | Not supported with pagination yet | null |
PMC9858565_01 | Female | 8 | An 8-year-old girl presented to a hospital pediatric emergency department with a 1-week history of cough, fever for 4 days, and dyspnea for 5 h, without any response to oral cephalosporins. When she was admitted to the hospital, she had shortness of breath, 50 beats per minute, fever, 38.3 C, tachycardia, 154 beats per minute, and hypoxemia, 72% in ambient air. Physical examination revealed moist rales in the left lung and diminished breath sounds over the right lung. Leukocyte count was 19 x 109/L, indicating leukocytosis of mainly neutrophils, and C-reactive protein level was 0.2 mg/dl. Blood biochemical analysis showed that the level of alanine aminotransferase was 516 U/L, lactate dehydrogenase was 2113 U/L, and sodium ions was 122 mmol/L. Chest x-ray photograph showed diffuse opacification on the left lung, Atelectasis was observed in the right lung with a large effusion in the right pleural cavity (Figure 1). She received a combination of antibiotics (azithromycin and ceftriaxone) to treat severe pneumonia and was transferred to the pediatric intensive care unit (PICU) for further treatment. There, she was given high-flow warm humidified oxygen through the nose. A computed tomography (CT) scan of the chest showed bilateral lung infection and right lung consolidation density; Multiplelymph nodes in the mediastinum show that the area is slightly larger; Bilateral pleural effusion (Figure 2A). Ultrasonic examination also showed a large amount of pleural effusion in the right lung. Lower chest puncture drainage was performed under ultrasound guidance, and antibiotic therapy was escalated to cefoperazone sodium, sulbactam sodium, and azithromycin. Analysis of pleural effusion showed that a protein level of 38.2 g/L, glucose of 6.57 mmol/L, lactate dehydrogenase of 3082 U/L, and mononuclear phagocyte predominance was observed. Negative bacterial culture results for blood, endotracheal aspirate and pleural effusion. Antigen testing for respiratory pathogens (including adenovirus, respiratory syncytial virus, influenza virus and EB virus) is suggestive of negative results. Polymerase chain reaction (PCR) showed that MP was positive in endotracheal aspirate and pleural effusion. MP-specific IgM and IgG antibodies from blood showed negative results. Acquired mutations on the ribosomal macrolide target were negative, suggesting that it was not a macrolide-resistant strain. Further medical history obtained from family members did not indicate any risk factors for tuberculosis; however, a gamma release assay was also sent for analysis. On the first day of admission, patient was found to have abnormal coagulation function, and bleeding spots appear on the skin the next day. In the coagulation profile, the international normalized ratio was 1.67, with a partial thromboplastin time of 31.5 s and a prothrombin time of 17.5 s. Thrombin time was 60.0 s. The fibrinogen function K value was 18.1 min, the fibrinogen and platelet function (angle) were 27.9, the platelet function was 21.2 mm, and the comprehensive index of coagulation function was -14.5. In order to exclude hematologic diseases, coagulation factors and plasma correction tests were added, and fresh frozen plasma and fibrinogen infusions were given, and the coagulation function was slightly improved. After 48 h, she remained febrile with worsening tachypnea and hypoxic respiratory failure, hemoptysis, and required intubation and ventilation. Blood was visible in the airway, and bronchoscopy and bronchoalveolar lavage revealed DAH. Therefore, a diagnosis of severe MP in conjunction with DAH, severe pediatric acute respiratory distress syndrome (ARDS), and acute hypoxic respiratory failure was established. Human blood immunoglobulin, epinephrine endotracheal instillation, and intravenous application of glucocorticoids were administered.
Because of ongoing hypoxia, she was cannulated onto veno-venous extracorporeal membrane oxygenation (VV-ECMO) on hospitalization day 3. The results of pleural fluid and blood tests for metagenomic next-generation sequencing (mNGS) suggested MP infection, with no other viral or bacterial infections. She was screened for rheumatological conditions, tuberculosis, autoimmune diseases, and tumour. Results did not suggest these situations.The patient stayed on ECMO for 5 d; Due to the significant prolongation of PT and APTT, anticoagulation was given without heparin or low-dose heparin regimen, and the anticoagulation target was gradually adjusted on the basis of fresh frozen plasma supplementation to prevent thrombosis in the extracorporeal membrane lung and pipeline. Laying in the prone position for for 10 h + per day during this period improved oxygenation. Ultrasound was used to assess lung exudation. The patient was ventilated for ten days. During this period, she received methylprednisolone 1-2 mg/kg/d and a 14-day tapering regimen for acute respiratory distress syndrome and azithromycin was given intravenously, for inflammation, three times a week. Simultaneously, further testing revealed that the patient's humoral and cellular immune function was disorder, the TBNK lymphocyte subsets were suggested that CD3 799 x 106/L(normal 960-3640), CD4 344 x 106/L(normal 550-2190), CD8 440 x 106/L(normal 260-1380), CD4/CD8 0.78(normal 0.72-2.88),natural killer cell 60 x 106/L(normal 80-680); Cytokine detection suggested that IL-6 1.33 pg/ml(normal 0-20), IL-10 27.56 pg/ml(normal 0-5.9); Immunoglobulins and complements were shown that IgA0.37 g/L(normal 0.52-2.16), IgM0.46 g/L(normal 6.09-12.85), C3 0.25 g/L(normal 0.79-1.52), C4 0.09 g/L(normal 0.12-0.36). Hemophagocytic lymphohistiocytosis was negative. Mycoplasma DNA continued to test positive on repeat workups.
On the 9th day, the patient had low-grade fever; sputum culture, blood mNGS testing, and G test suggested Candida albicans infection, and fluconazole antifungal therapy was administered for 10 d. Other infectious organism was not found in repeated respiratory tract, blood cultures andpleural cultures. After 8 d of therapy, CT of the chest revealed exudative changes in both lungs, partial consolidation in the right lung, similar to the range of lesions as before, interstitial changes in the right lower lung with multiple bronchial cystic changes, and reactive lymphadenopathy (Figure 2B). After 12 d of therapy, the patient clinically improved and became afebrile. Ventilator use was discontinued, and she was discharged from the hospital 15 d after extubation without supplemental oxygen. Pulmonary CT review 45 days after discharge indicated that the lesion was significantly absorbed compared to the lesion in the previous CT scan (Figure 2C).
Written informed consent to participate in this study was provided by the participant's legal guardian/next of kin. We obtained informed written consent from the patient's parent authorizing the publication of this clinical case and images. | acute respiratory distress syndrome, diffuse alveolar hemorrhage, mngs, mycoplasma pneumoniae, pediatric, veno-venous extracorporeal membrane oxygenation | Not supported with pagination yet | null |
PMC3959514_01 | Male | 47 | A 47-year-old Indian male, presented with high-grade fever and left-sided pleuritic chest pain of 3-week duration. He complained of anorexia and significant weight loss of 6 kg in the last 1 month. There were no other respiratory symptoms, jaundice or bowel symptoms. The patient was diagnosed with diabetes and was on insulin therapy for the past 5 years. Two years ago, the patient was evaluated for hemoptysis, diagnosed as sputum-negative pulmonary TB on the basis of X-ray finding suggestive of right upper lobe fibrosis. He was treated with Isoniazid (H), Rifampicin (R), and Pyrazinamide (Z) for 2 months and with H, R and Z for 4 months. He was treated for small joint arthritis for 3 months prior to presentation. There was no history of recent exposure to pulmonary TB. There was no history of malignancies in the family. He is a reformed smoker and a chronic alcoholic. No history of recent travel to North Australia or Southeast Asia. There is no history of exposure to soil. There was no history of sexual promiscuity.
On examination his vitals were stable and he had a body mass index of 17.8 kg/m2. Abdominal examination revealed tenderness in the left hypochondrium and moderate hepatosplenomegaly. Per rectal examination did not reveal bleeding or deposits. On chest examination, there were fine crepitations and diminished air entry in the right upper chest. Examination of other systems was within normal limits.
His hemogram showed polymorphonuclear leukocytosis and an erythrocyte sedimentation rate of 70 mm/h. He had a fasting blood sugar value of 236 mg/dL and a postprandial value of 300 mg/dL with a urine sugar of 2%. His renal function and electrolytes were normal. His liver function tests and prothrombin time were within normal limits (WNL). His amylase and lipase levels were WNL. His chest X-ray showed right upper zone fibrosis. His upper and lower gastrointestinal endoscopies were normal. Ultrasonography of the abdomen showed a collection of heterogeneous echogenicity near the inferior pole of spleen suggestive of a perisplenic abscess. Contrast-enhanced CT scan of the abdomen revealed a splenic abscess with a breech in the capsule and extension of abscess into the perisplenic area (Fig. 1). His viral serology was negative for hepatitis B, C and human immunodeficiency virus.
The possibilities considered in this middle-aged gentleman presenting with fever, weight loss and arthritis with evidence of right upper lobe fibrosis, hepatosplenomegaly and perisplenic abscess were TB, brucellosis, melioidosis, lymphoma, salmonellosis and connective tissue disorders. His sputum was negative for acid-fast bacillus. Infectious screen was negative for enteric fever, malaria and brucella serology. He had positive rheumatoid factor and anti-cyclic citrullinated protein was negative. Anti-nuclear antibodies were absent and tumor markers were WNL. Trephine biopsy of the bone marrow was normal. The aspirate from the abscess revealed catalase- and oxidase-positive, gram-negative bacillus with bipolar staining and violet colonies with central umbonation in Ashdown's selective agar (Fig. 2), diagnostic of Burkholderia pseudomallei. Polymerase chain reaction for TB was negative in the aspirate. Blood, sputum and urine cultures were sterile.
The patient was diagnosed as melioidosis and treated with 2 weeks of parenteral ceftazidime (2 g t.i.d.) followed by oral co-trimoxazole (160/800 mg t.i.d.) for 12 weeks upon which he became symptom-free. His fever and arthritis subsided and follow-up ultrasound showed resolution of abscess. Chest X-ray showed improvement in the right upper lobe lesion. The response to the therapy confirmed our diagnosis of melioidosis. | burkholderia pseudomallei, splenic abscess, melioidosis | Not supported with pagination yet | null |
PMC3785362_01 | Female | 35 | The patient was a 35 year old woman with an extensive past medical history including pemphigus vulgaris. She had a previous diagnosis of Castleman disease confirmed by pathology following excision approximately 10 years earlier. She subsequently developed bronchiolitis obliterans and underwent bilateral lung transplantation. Subsequent CT follow up demonstrated a soft tissue mass in the mediastinum that remained stable for a number of years. Unfortunately in the decade after her lung transplant she again developed a clinical picture of bronchiolitis obliterans, this time attributed to chronic allograft rejection. Repeat double lung transplant was contemplated and she underwent coronary angiography as part of the pre-surgical work up. At catheterization a vascular mediastinal mass was discovered and MRI examination of the thorax was requested.
Pre-contrast imaging demonstrated a 5 x 3.8 x 5.2 cm solid mass in the middle mediastinum. This appeared homogenous and of slightly higher signal than skeletal muscle on T1 weighted images, with moderate signal intensity on fat-suppressed T2 weighted images (Figs. 1a/b). Subtle serpiginous areas of signal void were identified within the mass.
A dynamic multi-slice first pass perfusion sequence was performed in the coronal plane (for imaging parameters see Table 1). Image acquisition was commenced immediately before an injection of 10 ml of gadolinium-DTPA and continued for approximately 80 heart beats. During this acquisition dramatic enhancement of the mass was seen to occur, with peak signal intensities only slightly less than those of the surrounding vascular structures and peak enhancement occurring 1-2 heartbeats after contrast appeared in the thoracic aorta (Figs. 2a-e images/movie).
Post-contrast T1 weighted imaging confirmed a persistent increase in signal intensity within the mass (Fig. 3). Phase velocity mapping also appeared to demonstrate flow within the areas of tubular signal void described (not shown). | castleman disease, first pass perfusion, gadolinium | Not supported with pagination yet | null |
PMC3569976_01 | Male | 75 | We report a 75-year-old male with a 10-year history of progressive OT and unsuccessful medical treatment. He used a portable stool or cane when he had to stand in place. Upon standing, he would have the immediate onset of fine tremors in both legs. He could only stand in place for 20 seconds at most before needing to sit, lean, or hold on to something. The patient had been initially trialed on acetazolamide and primidone over the course of 5 years prior to his referral to our institution. He tolerated the medications, but they were discontinued because of ineffectiveness. He was then started on topiramate, up to 50 mg twice per day, but discontinued because of side effects of anorexia and significant weight loss. He was subsequently begun on clonazepam, up to 0.5 mg twice per day, but was discontinued because of sedation. Gabapentin and then valproic acid were trialed without any improvement in his symptoms. The severity of the side effects of the clonazepam and topiramate and the ineffectiveness of the other medications resulted in referral for consideration of DBS surgery.
Pre-operative surface EMG showed 13 Hz tremors of the lower extremities upon standing, which spread upwards to his paraspinal, truncal, and upper limb muscles. The patient underwent bilateral thalamic DBS. The target coordinates were based upon the midcomissural point and 11.5 mm lateral to the wall of the ipsilateral third ventricle. Intraoperative electrophysiology was performed to locate and confirm the leg portion of the Vim nucleus. Microelectrode recordings were followed by microstimulation looking for sensory side effects in the contralateral leg. In the right brain, leg side effects were noted at 13 mm lateral to the ipsilateral wall of the third ventricle, whereas in the left brain, final laterality was 11.5 mm. Macrostimulation was carried out to further refine final electrode placement based upon intraoperative improvement of contralateral leg tremor. This was assisted by surface EMG recordings of the legs, asking the patient to push down on each leg against resistance or on a footboard (Figure 1). Final electrode placement per side was determined based on stimulation side effects (sensory symptoms in the contralateral leg) and improvement of the contralateral leg tremor on surface EMG with macrostimulation (Figure 2).
One month following surgery, initial programming was done. The left Implantable Programmable Generator (IPG) settings were: contacts 0 and 1(-); contact 2(+); amplitude 4 volts; pulse width 60 milliseconds; and frequency 185 Hz. The right IPG settings were: contact 4(-); contact 5(+); amplitude 2.5 volts; pulse width 90 milliseconds; and frequency 185 Hz.
He reported an 80% subjective improvement of his OT in the left leg and 50% improvement in the right leg. He was able to stand in place for 7 minutes before needing to sit. He no longer required his portable stool/cane. A repeat surface EMG study was performed 3 months post-DBS. On standing from a seated position, there was immediate onset of tremor in the lower extremities on surface EMG, although the tremor bursts were less continuous, less rhythmic, and often showing bursts of slower frequency than the previous 13 Hz tremor seen pre-operatively (Figures 3-4). At 11 months post-DBS, the patient developed an infection and skin erosion around the IPG, which required removal of the pulse generator. Interestingly, it took 1 month before he returned to baseline severity of his OT. A new pulse generator was placed 2 months later, resulting in prompt improvement of his OT. The patient has been followed at our institution by the treating movement disorders neurologist and implanting neurosurgeon. Since surgery, the patient has had 19 visits to the DBS clinic demonstrating continued improvement. At last follow-up 30 months following DBS, he continued to experience a good response to stimulation alone (with no anti-tremor medications). He was able to stand in place at least 7 minutes or more before needing to sit or lean on something. The left IPG settings on last follow-up were: contacts 4 and 5(-); contact 6(+); amplitude 2.2 volts; pulse width 90 milliseconds; and frequency 185 Hz. The right IPG settings were: contact 0(-); contact 1(+); amplitude 2.7 volts; pulse width 90 milliseconds; and frequency 185 Hz. | orthostatic tremor, deep brain stimulation, thalamus | Not supported with pagination yet | null |
PMC7171607_04 | Female | 62 | A 62-year-old female patient presented to the emergency department with chief complaints of breathlessness for 10 years, cough with expectoration, and lower limb swelling since last 4 days. The breathlessness was associated with history of orthopnea, paroxysmal nocturnal dyspnoea (PND), and palpitations. There was a gradual increase in difficulty in breathing over the past 4 days with progression from grade 2 to grade 3. The cough was gradual in onset and was associated with yellowish expectoration and no haemoptysis. The pain in the lower limbs was seen along with abdominal swelling and facial puffiness. The patient was a known case of type 2 DM but was on irregular mediation. There was no history of HTN, PTB, or any other comorbidities. On examination, she was febrile; heart rate was 116 beats/min; respiratory rate was 27 breaths/min; blood pressure was 130/90 mm Hg; and oxygen saturation was 915 while breathing room air. The patient had pallor and bilateral pedal oedema. Systemic examination including respiratory system did not reveal any significant findings. The total leukocyte count was 8520/mm3 with 90% neutrophils and 3% lymphocytes. The haemoglobin was 9.6 g/dl, and the erythrocyte sedimentation rate was 102/hr. Serum urea was 75 mg, and creatinine was 2.5 mg/dl. An empirical antibiotic, modified dose of piperacillin and tazobactam was started along with other supportive treatment.
Sputum sample was sent to microbiology laboratory for KOH examination which incidentally revealed weak, acid-fast, and filamentous bacilli resembling Nocardia spp. She was immediately initiated on modified dose of trimethoprim/sulfomethaxozole and linezolid. As the patient showed gradual improvement in his condition, he was discharged on the same drugs. He successfully completed 3 months of antibiotics with satisfactory clinico-radiological improvement. | null | Not supported with pagination yet | null |
PMC7171607_05 | Male | 73 | A 73-year-old male patient presented to the Pulmonary Medicine OPD with chief complaints of fever, difficulty in breathing, palpitations, and increased frequency of urination since the last 5 days. The fever was low grade in nature and was associated with evening rise of temperature. He also complained of passing blood in urine along with dribbling of the same. He was a known case of type 2 diabetes mellitus and pulmonary tuberculosis since last 10 years and 2 years, respectively. Detailed history revealed that he had taken antitubercular drugs for 6 months and left by himself months back. There was no history of HTN or any other comorbidities. On examination, he was febrile; heart rate was 86 beats/min; respiratory rate was 27 breaths/min; blood pressure was 100/60 mm Hg; and oxygen saturation was 91% while breathing room air. The patient had pallor and bilateral pedal oedema. Respiratory system examination revealed crepitations on the right side of the chest. Other systemic examinations did not reveal any significant findings. The total leukocyte count was 8795/mm3 with 70% neutrophils and 18% lymphocytes. His fasting and postprandial blood sugar levels were 185 mg/dl and 439 mg/dl, respectively, whereas HbA1c was recorded as 8.5%. Sputum samples were sent for Gram stain, acid-fast bacilli stain, culture, and KOH mount. AFB stain and GeneXpert was done, both of which came negative. KOH mount revealed branching filament-like structures, which were confirmed by modified acid-fast staining as Nocardia spp. The sputum sample was also cultured on blood agar and it revealed white, dry colonies with rough surface after 48 hours of incubation. These colonies were identified by MALDI-TOF as Nocardia araoensis with a confidence interval of 1.50. He was started on Tab Trimethoprim-Sulphamethoxazole for a period of 15 days. On follow-up after a period of 15 days, the patient had improved symptomatically. | null | Not supported with pagination yet | null |
PMC6745118_01 | Male | 5 | A forty-five-year-old male resident of Saile Sikhar Municipality, Ward no. 5, Darchula District, was admitted to Sukraraj Tropical and Infectious Disease Hospital on 24 January 2019. Prior to visitation to our center, the patient had already been treated with LAMB (5 mg/kg daily for 3 days) against the first episode while LAMB 5 mg/kg stat and paromomycin 15 mg/kg IM for 10 days against the second episode. Finally, the patient was treated with miltefosine (50 mg) twice daily directly observed treatment for 28 days (Figure 1).
The patient presented to a local hospital in Nepalgunj on 25 January 2018 with a history of abdominal pain, anorexia, and fever with chills and sweating for 3 months. Clinically, the patient showed pallor with hepatosplenomegaly. The following information was available in his case file: his rK39 test was positive; glucose level 109.8; urea 17.64; creatinine 0.75; total bilirubin 62; direct B 0.28 mg%; alanine aminotransferase 20.3 U/L; aspartate aminotransferase 21.5 U/L; and alkaline phosphatase 118.6 U/L. He was admitted and treated with three doses of LAMB, 5 mg/kg daily for 3 days in the hospital.
The patient went to the Zonal Hospital of Western Development Region on 20 August 2018. Bone marrow aspiration cytology was performed showing cellularity which was normal for age; myeloid : erythroid ratio was 1 : 2. There was normal maturation and morphology of normoblasts. Myeloblasts were not identified in the smears studied. The megakaryocyte was normal in morphology and distribution. There was an increase in plasma cells and macrophages. Rare histiocytes showed intracellular amastigotes (LD bodies). Sparse clusters and singly dispersed extracellular amastigotes (LD bodies) were also identified. His total blood count was 1630; neutrophils 11.1%; lymphocytes 68.4%; monocytes 8.9%; eosinophils 0.9%; basophils 10.7%; hemoglobin level 6.8 g/dl; platelet count 104,000; creatinine 0.8 mg/dl; glucose 108.4 mg/dl; alanine aminotransferase 13.8 U/L; urea 30.4.
At the time of admission, the patient had had a history of fever and loss of appetite for 4 weeks, vomiting for 2 weeks, constipation for 4 days, productive cough for 4 days, and bilateral pitting pedal and chest pain for 4 days. Laboratory parameters revealed a hemoglobin level of 5.4 g/dl; total count 800; platelet count 54,000; prothrombin time 10 sec with international normalized ratio 0.91; rK39-positive; malaria- and leptospira-negative; urea and creatinine 20/0.4 mg/dl; total bilirubin 0.7 mg/dl; direct bilirubin 0.02 mg/dl; HIV serology negative; acid-fast bacilli-negative sputum; serum albumin 1.1 mg/dl; and total protein 6.9 mg/dl; urine routine microscopy showed 18-20 pus cells and 8-10 red blood cells. The patient was treated with ceftriaxone, blood transfusion (2 pints), and LAMB 5 mg/kg single dose in day one followed by paromomycin 15 mg/kg IM for 10 days. On the basis of X-ray findings, antitubercular treatment category 1 was also started. Hospital stay was uneventful with no fever, and vitals were stable.
After a week of treatment, his laboratory parameters improved with hemoglobin 8.4 g/dl; total count 2000; platelet count 131,000; and creatinine 0.2 mg/dl. The liver function test showed alanine aminotransferase 24 U/L; aspartate aminotransferase 21 Units/L; total bilirubin 0.6 mg/dl; and direct bilirubin 0.1 mg/dl. Blood transfusion was performed on August 28 and 29. He received 3 units of blood in the hospital and was referred to our center.
Upon arrival, the patient complained about an intermittent fever and vague abdominal pain for the past one week. He also had epistaxis for 4 days. Clinically, he looked emaciated, pale, lean, and thin. There was massive splenomegaly crossing the midline extending below the umbilicus up to the right iliac fossa. Vitals were within normal limits (blood pressure 90/60 mm of Hg, temperature 96.2 F, and pulse 84/min). Laboratory parameters revealed a hemoglobin level of 5.8 g/dl; total count 400 cells/cumm; neutrophils 69%; lymphocytes 27%; monocytes 4%; and platelet count 29,000 cells/cumm. Peripheral blood smear showed anisopoikilocytosis; hypochromic red blood cells; very low white blood cell count with normal morphology; no abnormal cells; and very low platelet count with normal morphology. rK39 was positive. Sputum for acid-fast bacilli was negative. Lipid profile showed a cholesterol level of 67 mg/dl; triglyceride 136 mg/dl; high-density lipoprotein 20 mg/dl; and low-density lipoprotein 20 mg/dl. Serum albumin was 1.0 mg/dl; total protein 7.9; prothrombin time 15 sec; and international normalized ratio 1.3. Sputum for GeneXpert MTB/RIF was negative. Ferritin level was increased to 766 ng/ml. Bone marrow cytology was performed which showed parasitic Leishman-Donovan (LD) bodies. Chest X-ray was normal. Ultrasonography revealed massive splenomegaly measuring 26 cm. There was hepatomegaly with coarse echotexture. Portal vein caliber distended with mild portal hypertension. There was no lymphadenopathy with minimal ascites. Malarial parasite and HIV serology were negative.
The patient was treated with miltefosine 50 mg twice daily directly observed treatment for 28 days in hospital. The patient's general condition improved with 3 kg weight gain within a month. The spleen regressed and could be felt left to the midline six fingers below the costal margin. His total count improved and increased up to 2000 cells/cumm while the platelet count increased to 190000 cells/cumm. Liver function tests and renal function tests were normal, and bone marrow reports showed markedly hypercellular marrow showing adequate iron stores and no abnormal cells. The LD bodies were not visible in the bone marrow 30 days after treatment with miltefosine.
First follow-up after miltefosine treatment was done six weeks after discharge. The patient had 7 kg weight gain. His blood parameters showed a hemoglobin count of 9.6 gm/dl, total count 3200 cells/cumm, platelet count 189,000 cells/cumm, creatinine level 0.9 mg/dL, alanine aminotransferase 70 U/L, aspartate aminotransferase 30 U/L, serum albumin 3.2 mg/dl, and total protein 11.4 mg/dl. Abdominal ultrasound showed minimal hepatomegaly with coarse echotexture and moderate splenomegaly measuring 17 cm in size. Six-month follow-up of the patient showed the patient was healthy and free of VL. | null | Not supported with pagination yet | null |
PMC9087846_03 | Female | 5 | A 5-year-old female spayed, 18 kg German Shepherd-cross dog developed acute behavior changes, panting, and ataxia. CBC, serum biochemistry panel, urinalysis, thoracic, and abdominal radiographs were unremarkable. Toxin exposure was considered possible. Activated charcoal with sorbitol (43 mL), IV lipid emulsion therapy (288 mL total), and 24 h of IV fluids were administered, transient improvement was seen, and the dog was discharged. Upon subsequent worsening of clinical signs, the dog was re-presented 4 days after the initial onset of clinical signs. The dog was obtunded with intermittent dysphoria, moderate generalized ataxia, circling to the left, and low head carriage. Other than an inconsistent menace response of the right eye (oculus dextrus: OD) and postural reaction deficits in all limbs, the neurological examination was normal. Due to concern for diffuse, potentially left-sided thalamocortical disease, MRI of the brain was performed (Figure 3) and revealed diffuse, bilaterally symmetrical T2W, T2W-FLAIR hyperintensity of the cerebral white matter tracts with no contrast enhancement. The white matter appeared hyperintense on DWI and hypointense on ADC maps (Figure 3). Abnormalities were most prominent in the CST, corona radiata, internal capsule, and corpus callosum. These findings suggested diffuse leukoencephalopathy, such as bromethalin toxicosis. Slight flattening of the caudal cerebellum was noted, with no signs of herniation. CBC, PT, and PTT were normal. Cisternal CSF analysis showed 4 nucleated cells/uL and total protein content of 30.4 mg/dL. Polymerase chain reaction (PCR) testing (Neurologic REALPCR PANEL, IDEXX, Westbrook, ME) of CSF for rickettsial, viral, fungal, and protozoal pathogens was negative. A serum sample was submitted to CAHFS for desmethylbromethalin testing.
The dog was treated with dexamethasone sodium phosphate (0.1 mg/kg IV), maropitant (1 mg/kg IV), and hospitalized overnight on IV fluid therapy. Mentation was improved but an inconsistent menace response OD, postural reaction deficits in all limbs, and intermittent circling to the left persisted. Desmethylbromethalin testing was positive with a semi-quantitative estimated concentration between 25 and 100 ng/g based on comparison with a standard curve. Following discharge on prednisone (0.5 mg/kg PO daily) for cerebral inflammation, maropitant (2 mg/kg PO daily) as an antiemetic and omeprazole (20 mg total PO q12 h) to reduce the risk of gastrointestinal ulceration, the dog returned to normal within 18 days of the initial onset of signs. Prednisone dose was tapered over 2 weeks, and the dog was neurologically normal with normal MRI 6 months later (Figure 3). | biopsy, bromethalin, canine, corticospinal tract, desmethylbromethalin, leukoencephalopathy, restricted diffusion | Not supported with pagination yet | null |
PMC9360766_01 | Male | 31 | For this observational study we had the participation of a 31-year-old client diagnosed with borderline personality disorder (BPD) for the last 8 years; and a 35-year-old clinical psychologist (a master's degree in General Health Psychology and a master's degree in Behavior Therapy). Both participants came from a public-funded Vocational Rehabilitation and Employment center (VR&E) in the Community of Madrid. The client has been referred to this center due to mood problems (i.e., emotional lability) and substance use problems that directly interfere with the client's chances of accessing employment/training opportunities; and once obtained, problems in keeping his job or completing the required training. Also, this study involved the participation of two trained observers. Both observers are predoctoral students that have been trained in the same research group (i.e., the ACOVEO research group). Observer 1 and Observer 2 have, respectively, 4 and 2 years of experience working with the observational coding system used in this research and they helped in the development of it. Before recording the clinical session, the client and clinician have been informed about the use of the data and the purpose of the research. All participants have signed the study informed consent.
We used the Functional Coding System for Verbal Interaction in Clinical Contexts to code the verbal interaction between the client and the psychologists. This coding system, which focuses on the putative functions of the verbal behavior, has five coding categories for the clinician verbalizations: Clinical Discriminative Stimulus (CD) and Instructional Discriminative Stimulus (ID), Conditioned Motivating Operation (CMO), and Positive Reinforcer (R+) and Aversive Stimulus (AS). The observational system assumes that the verbal behavior of the client has a response function it is not established any specific categories in the observational system. To code the client's verbal behavior in this case we used eight categories based on the response topography Giving Information (GI), Asking for Information (AI), Following Instructions (FI), Not Following Instructions (NFI), Well-Being (WB), Discomfort (D), Target Behavior (TB) and Problem Behavior (PB). See Table 1 for a brief description of the coding categories, also more details of the coding system are available in the additional materials.
Recordings of 16 clinical sessions were obtained through the camera installed on the VR&E psychologist's computer. The recordings were sent to the ACOVEO research group and were treated following the protocol used in the research group in which the recordings are anonymized following the ethical and legal guidelines of the Organic Law 3/2018 on Personal Data Protection and guarantee of digital rights. These recordings were stored on external hard drives kept under lock and key in the group's laboratory at the Autonomous University of Madrid.
The recording of the clinical sessions, the observation project, and the analysis of inter-observer reliability were carried out with The Observer XT 12 observation software. The data analysis was done in R (RStudio Team, 2020) and Microsoft Excel. GSEQ was the software used to conduct the sequential analysis of the data. We selected this software because it is generally employed in observational research (e.g.,); it was specifically used in previous research in the study of verbal interaction in clinical cases; and it was specially developed to calculate sequential patterns in observational data. Finally, we used ThemeEdu software for automatic pattern detection. ThemeEdu was selected because it has been successfully applied in different research areas (i.e., neuronal interactions, behavioral interactions, etc.), but it was not employed in the study of verbal interactions in clinical settings. Both programs allowed us to conduct the data analysis described in the section below (see "Data Analysis").
In this observational study, we used an intra-subject design with three different phases: Evaluation (EVA.), Treatment Phase 1 (T1), and Treatment Phase 2 (T2). These phases were not experimentally manipulated and have been divided considering the protocols and procedures of the VR&E center (i.e., EVA, first three sessions; TP1, 4-9 sessions; and TP2, 10-16 sessions). The division between the two treatment phases is arbitrary and responds to a need to divide the treatment into, at least, two phases to evaluate differences between various time points.
After the study, both observers received specific training in the observational instrument. The training process was completed when a stable reliability index (k > 0.70) was achieved while coding similar clinical sessions. These sessions were from the research team's clinical sessions archive.
After training was completed, observer 1 individually recorded all treatment sessions. Observer 2, also individually, recorded 4 random sessions out of the 16 treatment sessions, representing 25% of the sample, which is above the usual 10% for studies of this type. The inter-observer reliability calculation was carried out after the end of the recording of both observers. One month after the end of the recording phase, observer 1 recorded again two randomly selected treatment sessions to allow the calculation of intra-observer reliability.
The kappa coefficient (k) was used to calculate the inter-observer and intra-observer reliability of the records. Once the records were obtained, the rate per minute of each variable recorded in each session was calculated. Descriptive data (e.g., count, rate per minute, etc.) were obtained to allow a visual inspection of the variables and the patterns through time. To analyze the interaction between variables, we used two types of statistical analysis, which are part of the family of statistical tools for the sequential analysis of temporally distributed data. First, we calculated the Yule's Q, a contingency index of 2x2 tables, using the GSEQ software. This index allows us to calculate the Lag +1 correlation between a given behavior and the one that follows it. The Lag-1 correlation tells us which behavior precedes the behavior we are analyzing. This index allows descriptive and analytical analysis of the association and its scores can also be interpreted in the same way as Cohen's r. To study the association between specific pairs of behaviors we calculated the adjusted residuals (z), which are a normalized index of the extent to which the values of the frequencies observed in each cell of the matrix deviate from their expected values: a value greater than 1.96 indicates that this behavior occurs significantly more than expected and, conversely, a value less than -1.96 implies that it occurs significantly less than expected by chance (p < 0.05; see for an advance mathematical description).
Moreover, we used a pattern recognition model T-Pattern Model, using ThemeEdu software. This model allows us to recognize patterns (T-Patterns) from observational data (T-Data) using the T-Pattern detection algorithm. Pattern detection works in a bottom-up fashion, from the data to the pattern detection. The T-Pattern is a hierarchical, multi-ordinal, and self-similar pattern type that comprises m ordered components (i.e., behavioral events), X1.m, recurring in a single discrete dimension, where each component is a T-data category (or pattern primitive, called event-type) or a T-pattern.
In this case, patterns of interaction between client and therapist have been detected in all three phases of observation. We used the pattern recognition default settings with some specifications. We have required that the patterns must be repeated at least three times in each session and all sessions of each phase, with this we want to make sure that the pattern is a characteristic of this phase not a characteristic of one of the sessions. Also, we have excluded the patterns made by the repetition of the same variable and the patterns made by an interaction of variables of the same subject, because we want to study the interaction between variables. Finally, we have required a maximum of 4 levels for the analysis of the interaction, because more than four levels could be interpreted as chains made of contingencies of two or three members.
To assess the effect of the treatment on the client's behaviors we calculated the effect size, in this study we used the Non-overlap of All Pairs (NAP) which is an index focused on identifying the differences between two phases of a design (A and B). | clinical psychology, pattern analysis, principle-based therapy, process-based therapy, sequential analysis, verbal interaction | Not supported with pagination yet | null |
PMC5851328_01 | Male | 91 | A 91-year-old man presented with abdominal pain and was followed up to 2 days. On physical examination, periumbilical tenderness was found, but there were no peritoneal irritation signs or other obvious abnormal findings of the ears, nose, or skin. The blood test results showed a high inflammatory reaction (white blood cell (WBC) count 13,800/microL; C-reactive protein (CRP) level 33.5 mg/L) and acute kidney injury (creatinine (Cre) 1.11 mg/dL). Urinalysis was normal. The chest radiography demonstrated no remarkable change. The computed tomography (CT) scan was negative for any infectious focus or other abnormal findings, such as cavitating nodules in the lungs or other site neoplasms. Antibiotics (tazobactam/piperacillin 13.5 g/day) were administered as empiric therapy.
After hospitalisation, the patient developed fever over 39 C. Results of the blood cultures and other cultivation tests were all negative, including the tuberculosis test. Additional analyses demonstrated a negative ANCA titer, proteinase 3- (PR3-) ANCA, and myeloperoxidase- (MPO-) ANCA. Two days later, the patient showed a new peritoneal irritation sign at the periumbilical and right lower abdomen. The CT scan showed an increased CT value of the greater omentum and ileocolic mesentery, and ascites (Figure 1). Blood test results showed that the inflammatory reaction was still high (WBC count 20,700/microL; CRP level 29.3 mg/L), although renal function returned to normal (Cre level 0.93 mg/dL). The antibiotics were changed (meropenem 3 g/day), but the fever and abdominal pain did not disappear, and inflammatory reaction remained at a high level.
Because there was no sign of infectious focus for fever and abdominal pain, except for an increased CT value of the omentum and ascites, examination laparotomy was planned. Laparotomy revealed diffuse redness and swelling of the greater omentum and pale haemorrhagic ascites (Figure 2). Histological examination of the resected omentum demonstrated both arteritis and more severe venulitis, focal necrotizing vasculitis of the venules, and palisading granuloma (Figures 3(a) and 3(c)).
The patient was diagnosed as having GPA based on the Chapel Hill Consensus Conference 2012 definitions and treated with intravenous methylprednisolone pulse therapy (1000 mg/day for 3 days). Subsequently, daily prednisolone was administered, and the dose was gradually tapered to 15 mg over 1 month. The patient was discharged without relapse.
One year later, the patient did not show any symptoms, and the follow-up CT scan showed no sign of vascular inflammation. | null | Not supported with pagination yet | null |
PMC9036100_01 | Female | 28 | Case: The 28-year-old client, Julia, comes to therapy with depressive symptoms that she has experienced since her teenage years. Julia has been dating Ben for 2 years, and they plan to move in together. Julia works as a dental assistant in a large practice. She is the oldest of four sisters and was used to helping her parents, who are self-employed with a bakery and take care of her younger sisters. She also helps every Saturday with the bookkeeping and orders for the bakery. The parents' marriage was and still is characterized by quarrels, which scared Julia a lot as a child. Father and mother had little time for the children and demanded, as they did of themselves, daily smooth functioning and a willingness to work hard. "That's the only way to make it in life," Julia's father always said. Julia therefore received a lot of appreciation when she decided a few years ago to study part time beside her job. Since then, she spends every free minute studying. Her relationship with Ben, who prefers to enjoy his hobbies and meet friends in his free time, has deteriorated significantly. He has given up asking her to come along. Julia often feels misunderstood by Ben and withdraws from him more and more.
The Trigger for Her Current Crisis: Two months ago, Julia's mother suffered a severe slipped disk and since then can no longer stand behind the counter as much. Julia now works not only on Saturdays in the office but also early in the morning for 3 h at the counter of the bakery before she goes to her own work. She sleeps very little and therefore can hardly concentrate on studying in the evenings. She fluffed two exams and failed. Since then, Julia has had the feeling of losing the ground under her feet. She feels more and more overwhelmed. Physically, she now suffers from severe back pain every day. In the evening, she lies awake ruminating for a long-time despite of being very tired.
Exploration means choosing an option which has less information, and outcome is associated with a certain risk. Exploitation means staying with an option that one knows well and is believed to produce expected results. Ultimately, it is learning history that determines what choices are made in these situations. At the beginning of therapy, the client relies on what she knows. Following the internal model, we term it as a survival strategy, refers to the old priors and the attempt to fit incoming data. Her self-regulation is controlled by a survival strategy which, for the purpose of satisfying needs, prescribes relatively narrow behavioral paths by means of its commands and prohibitions. The more stressful the personal developmental conditions were experienced, the smaller the behavioral repertoire. Accordingly, behavioral tendencies used for psycho-emotional "survival" are rigidly maintained to prevent occurrence of the feared. At best, more effort is invested to fulfill specifications of the survival strategy even more precisely. It is like squeezing a lemon that contains no more juice: Quite a bit of effort still yields a few drops. Indeed, it is now well established that both acute and chronic stress leads to the over-selection of exploitative strategies, even though little is accomplished. Under the influence of this kind of stress experience, situation at hand is more likely to be appraised as threatening, which furthermore makes selection of exploratory strategies unlikely. The maladaptive impact of stress is now what makes stress response no longer context specific.
Case (Continuation): In our case Julia behaves the way she learned it in the strict environment of her childhood. She works harder and does no questioning. Thus, even in current situations, their specificity and differences are not sufficiently addressed. Instead of situation-specific, schematic action is taken. Julia reacts as she has learned in her family. She tries in vain to satisfy her need for appreciation with the same attempts at low-maintenance and performance-oriented behavior. Without need fulfillment, there is a sharp drop in security. The exploration of alternative possibilities of the real adult world is thus omitted, instead the contact to the body is lost more and more: She feels her exhaustion only when she gets a lot of pain.
This "clinging" to the previous schema is considered by in the context of a predictive processing mechanism. The authors develop a perspective according to which many affective and cognitive features (e.g., worry, rumination, impaired anxiety learning, reduced specificity of autobiographical memory, somatic symptoms) of a wide variety of diagnoses can be traced back to a common underlying processing strategy. This they refer to as the "better-safe-than-sorry strategy." The associated style of information processing is essentially top-down oriented with a tendency toward low sensory-perceptual detail. Here rumination can be seen as a process of maintaining the old dysfunctional priors and policies. Clients also no longer rely on their body signals, for example. As a result, bodily signals are suppressed and cannot update the priors by "active inference." This happens in favor of rapid categorization of threat-related stimuli, but at expense of an update of threat-related priors. These priors are held with high precision and as such represent learned critical safety-related aspects. In our specific case, they are all those features that are addressed in the four lines of the survival strategy.
Case (Continuation): The survival strategy is elaborated on the basis of a concrete problem situation, so that it is not only cognitively understandable but also emotionally tangible for the client.
Julia's Survival Strategy:
-Only if I always perform, function smoothly, and act dutifully
-and if I never enter into conflicts and separate myself from others
-then I maintain security through appreciation and affiliation,
-and prevent losing control and failing.
Since these precise threat-related expectations dominate processing, noticeable deviations are very often ignored in the current situation. This mode of operation is thus not very context-specific, so that effective error minimization and thus a clear update of priors is omitted. At the same time, active inference generates perceptions and actions that are consistent with prior expectations but do not necessarily match the current situation. Here, this update does not easily succeed, the PEs remain and free energy remains permanently increased. In the longer term, this gradually leads to more and more free energy, i.e., PEs, and ultimately to chronic uncertainty or chronic stress (Figure 1, left). In this respect, a more adaptive internal model can hardly be developed.
However, if there are changes in the environment, i.e., if a new context arises, the previously very successful strategies may fail.
Case (Continuation): The context changed dramatically for Julia, when her mother falls ill and she starts working significantly more than usual in the bakery. Due to this overload, Julia experiences a failure of previously successful strategies. This produces massive stress and thus leads to an increase in "free energy": selected actions no longer produce rewarding energy boost by satisfying the client's central needs. On the contrary, all threads slip away from her and she is confronted with loss of control and failure:her central fear from line 4.
This context leads to stronger prioritization of safety, so that a higher-level control is controlled by this prior. It is now provided with stronger precision.
How should client Julia deal with this situation?
The client's internal model is summarized in her survival strategy. It is worked out right at the beginning of therapy and provides a precise "blueprint" for an initial shaping of affective alliance. This is intended to replenish safety reservoir, since the "better-safe-than-sorry strategy" generates stress and thus increasing insecurity and hopelessness due to stagnating error reduction process. To understand these relationships more precisely, let us take a closer look at safety regulation. In respect, it will become clear how satisfaction of various needs is related to the extent of perceived safety. The dynamics of safety regulation are explored in more detail in the Zurich Model of Social Motivation. In Figure 2, the safety reservoir is ideally always well-filled. Its target level is subjective and varies according to personality. If the level is far below the target value, then the person feels too little security and experiences anxiety. Conversely, too much security leads to boredom.
A favorable safety level can be established by means of various sources:
From the Outside
Protection and security by close, familiar people, such as partners, dear relatives, friends, appreciative colleagues, etc.
From the Inside
By internalized good experiences of attachment. Because of positive early childhood experiences, "basic trust" is formed. This corresponds to an internal working model of secure attachment.
Security based on self-confidence, which in turn is associated with high autonomy needs.
We are dealing here with two major sets of needs:
Needs related to attachment and social relationships, e.g., security, belonging, caring, harmony, feeling valued and welcome, etc., as well as
Needs related to the self, e.g., self-worth, self-actualization, expansion of the self through the exercise of power, through new experiences, knowledge, achievement.
Looking at the client's survival strategy, we can see in the third line, strong attachment-related needs. Her willingness to perform should make her attractive as an attachment partner, i.e., she fills her security reservoir primarily by satisfying needs that can be thematically assigned to the attachment motivation.
Based on our client's needs profile and Figure 2, it is clear that an increase in the level of felt safety is achieved by the therapist satisfying the specific attachment-oriented needs for being seen and belonging in the therapeutic relationship.
Case (Continuation): Julia's therapist gives her a warm welcome from the beginning and asks her what she needs to feel comfortable in therapy. She expresses appreciation for her willingness to take on responsibility, shows empathy for her exhaustion and tireless dedication to the family business. In addition, the therapist acknowledges Julia's commitment to therapy. For here, Julia's dutiful nature is also very helpful, as she also practices therapy-promoting behavior regularly and therefore achieves success quickly, e.g., improvement of her sleep quality.
This puts the client in a realm of experience:a kind of ecological niche:in which her internal model receives sensory input that it in turn predicts as probable. This leads to a lowering of uncertainty or free energy.
The successful shaping of affective alliance depends both on accuracy with which the therapist grasps her client's need structure and, on her caution, and flexibility in acting on it in a need-satisfying way with her behavior. Here, the application of relationship rules is particularly important (Table 1). By designing the relationship complementary to her needs, the therapist provides experience that correspond to the expectation or priors of the client. In this respect, the therapist tries to actively establish and reinforce goals and experiences that are outlined in the survival strategy. Conditions and experiences that the client perceives as bad or avoids are not activated for the moment, if possible.
Case (Continuation): In the first phase of therapy, Julia's therapist therefore avoids questioning her client or criticizing her approach. This was a fear that Julia had also expressed at the very beginning of therapy. She said at the time, "I'm afraid that you (the therapist) will just say that I shouldn't help my parents anymore and finish my studies. But it's not all that simple for me." Julia experienced it as very beneficial to be understood and seen with her needs in this way. This allows her to open up more and express the full extent of her stresses.
In principle, complementary relationship design shows empirically high effectiveness in terms of therapy outcome. With this form of relationship design, the therapist creates space for processes of active inference according to client's previous familiar pattern. This enables him or her to adopt a PE-minimizing and thus self-informing policy. In other words, this strategy for minimizing free energy looks like this: The therapist engages with the client in a dance in which the client leads and the therapist responds in ways that the client expects.
The goal-achievement alliance serves to reduce the problem behavior itself by means of effective methods as well as to promote goal behavior. In our chosen perspective, this means establishing and supporting directed exploration. The goal achievement alliance can be labeled in therapy as a kind of expedition, in the course of which difficult situations have to be mastered but also important discoveries can be made. This requires a shared map, good preparation, and a coordinated approach.
Typically, people use a mix of undirected and goal-directed exploration. Goal-directed, information-seeking exploration is guided and motivated by uncertainty in the agent's world model. This means that agents typically selectively choose options that are informative, i.e., those associated with greatest uncertainty. Undirected exploration is defined as a deviation from current most valuable strategy by unplanned selecting a different option. What does this mean for therapy? Clients are unlikely to spontaneously choose the option associated with most uncertainty. Nevertheless, targeted experiences must be provided to selectively help erase uncertainty in this respect. To address client's fear/uncertainty, experiments are constructed along a difficulty hierarchy. The client is encouraged to "question reality" and is supported in trusting his or her own experience. Undirected exploration:understood as a client's unplanned and impulsive actions:should be limited at the outset so that what has been achieved is not risked carelessly. Once a certain level of safety has been reached, then undirected exploration can later lead to a pleasurable journey of discovery.
The previous outline of directed exploration will now be made more concrete. Directed exploration means searching for and reflecting on specific information. This information concerns both client's view of himself and his view of the world: Who am I and how do I react in a certain situation, what are my emotions and impulses for action? On the other hand, clients need information about the efficacy of their actions, possible reactions of their environment, and an assessment of how they are likely to cope with consequences of their actions. Typically, the internal model includes beliefs about future states and policies, with the most likely policies leading to preferred outcomes. In this sense, behavior is also understood here as fulfillment of optimistic predictions. Clients who are asked to test new situations do not necessarily share this optimism, as they lack adaptive priors about future states, effective policies, and clarity about preferred outcomes. Here, importance of therapeutic interaction in establishing optimism and hope becomes clear. The updating process should be handled in a manner which is free of judgment and within the context of a benevolent error culture that promotes learning. In the service of an acceptable level of certainty and controllability, the goal-achievement alliance provides the following methodological rules: (1) selection of an appropriate small-step approach, (2) joint determination of the level of stress to be tolerated, and (3) development of plans and strategies to prepare for emerging uncertainties. The precise content of these aspects is again guided by the model of safety regulation specific to the client (Figure 2).
In order to keep the free energy during exploration reasonably limited from the very start, goal-achievement alliance additionally provides for a limited selection of future-related priors. These are obtained based on a variety of tasks, joint observations, and hypotheses. To this end, we thematize two foci of work for the goal attainment alliance: (1) emotional work and (2) behavioral experiments.
Emotional experience can be understood as a somatic change that occurs in response to stimuli that affect our physical or mental well-being. More current theories of emotion focus primarily on the perception and recognition of various bodily changes, although traditional basic assumptions such as "appraisal" may also be included as important components of emotion. Within their integrative model, describe three processes:
Current situations, thoughts, and memories elicit changes in the brain and body (e.g., changes in attention, changes in heart rate, etc.).
Physical changes are registered and classified in terms of causation (e.g., I feel shaky because I drank too much coffee or because I am scared).
Finally, it is decided to what extent attention is paid to such feelings.
Appropriate evaluations are based on learning experiences. Even if bodily feelings are present, they may remain implicit because, for example, it was "forbidden" in the learning history to feel and express feelings of being overwhelmed. The model highlights the importance of interoceptive processes for emotional experience. Namely, interoception describes the perception and representation of internal body signals (e.g., heartbeat, breathing activity, feelings of satiety). It contributes to body awareness, defined as attentional focus on and awareness of internal body sensations, and is critically involved in the regulation of emotions.
How is this conceptualized within the framework of FEP?
In order to represent emotional events, the internal model includes interoceptive priors in addition to exteroceptive priors. They result from previous experiences of similar situations. They form the basis not only of predictions about upcoming interoceptive and exteroceptive signals but also about the most appropriate action to deal with the upcoming sensory flow. All of this is processed in a single inference process. In this respect, these predictions are compared with sensory input from body and context. Minimizing the prediction errors results in the perception of body sensations and action impulses. The meaning emerges by mapping the response patterns to learned emotion concepts ("this feels like anger"). However, minimizing PEs or free energy in this respect may encounter problems:
Emotion concepts are too diffuse and provide inaccurate predictions regarding body feelings, context, and action,
There are hyper-precise priors that dominate interoceptive and/or exteroceptive perception,
Learning history has caused selective attentional biases that now ignore bodily or contextual cues.
All these questions are addressed by our work in the so-called "Emotional Field". In this respect, two important methodological rules of the goal achievement alliance are applied. They refer to the practice of focusing attention on the body and maintaining an agreed-upon level of negative affect. We repeatedly encounter clients who have difficulty naming emotional categories. This is facilitated if attention is first selectively drawn to body signals when an emotional episode occurs. Subsequently, this can be reflected upon and usually emotion concepts can be named and reflected upon (see). Our working format is essentially bottom-up and provides for a clear separation between experiencing specific bodily sensations and talking about them. arguably refer to the same thing when they speak methodologically of "decoupling."
Case (Continuation): In the Emotional Field Julia works with her therapist on a problematic situation with her father. The argument arose when Julia wanted to explain to him that she cannot help out in the bakery on Saturdays as well because she needs time to study. The father, however, had shown no understanding at all and insisted that he needed her for bookkeeping on Saturdays as well. In order to ensure an intensive emotional activation of Julia, she is first asked to portray her father as vividly as possible. For this, Julia, guided by her therapist, chooses a typical body posture, a frequently heard phrase and the corresponding facial expressions. So, Julia's father becomes tangible as the central reference person in the room. Julia then positions herself in front of the wall that shows her "visualized" father. Julia chooses a middle distance and a smaller position, because she has always felt inferior to her dominant father, although he is physically much smaller than she is. Supported by the therapist, Julia now begins to describe how she feels in her body. Julia reports a heaviness in her chest that makes her breathing shallow. In addition, she feels an impulse to make herself even smaller. Julia should now give in to this impulse. She crouches down very tightly and can hardly breathe. Julia should now wait for the next body impulse and give in to it. After a short time, she reports a heat rising in her head and a tension in her arms. Julia feels the urgent desire to get up. When Julia stands in front of her father again, however, heat and tension immediately disappear. Julia wants to make herself small again. At this point, the therapist asks Julia to move to the so-called expert position, a reflection point in the room located away from the experience space in front of the wall. Here Julia and her therapist try to give a name to the different emotional states just experienced. The first emotion that emerges is very familiar to Julia. It is fear, which takes away her breath and helps her to hide. Julia is familiar with this strange heat, but she cannot think of a more concrete name for it. The therapist writes down the two terms fear and heat on one note each. Julia places both pieces of paper accordingly in front of her visualized father. After this short conversation, the therapist asks Julia if she feels ready to go into the experience again and find out more about this heat. Julia agrees. Both start again with the confrontation of Julia in front of the wall with her father. As in the first run, Julia's fear shows up first, which:if intensified:again creates erection impulse, heat in the head and tension in the arms. The therapist asks Julia to reinforce these body signals as well. Julia now also feels a strong desire to move closer to her father and reports an impulse to yell at him. She yells, "You bully make us all sick!" Now Julia feels significantly taller. To reinforce this feeling, her therapist gives her a wooden stool to stand on. From here she can now look down on her father, but at that moment all courage leaves Julia and she immediately wants to make herself small again and back away. The therapist lets Julia follow her body impulses and then discusses this with her again on the expert position. In this way, Julia experiences her survival strategy first hand. The body impulses take up a lot of space and make it easier for Julia to understand what happens to her in conflicts. The so-called reaction chain becomes apparent (Table 2).
Again, and again, Julia goes back to her experience, and thus shame and guilt gradually become apparent as further emotions associated with this situation. By working in the Emotional Field, Julia understands better why it is so difficult for her to stand up for her needs in everyday life. Because not only her fear but also shame and guilt slow her down in anger. She has a strong trio of stopper feelings (secondary emotions), which ensure that she behaves in accordance with her survival strategy.
In the first contact with her anger Julia was not even able to recognize or name it. She also felt the power that was connected with the anger and this awaked her interest. The special thing about this kind of guided confrontation is that Julia is first enabled to learn about the emotional basis for her new behaviors and this bottom-up. So, she learns not only from her mind that it would be important to assert herself, but she feels her anger and so the associated power enables her to assert herself. It is her primary emotion that becomes palpable to her as a new sensory input from the combination of her needs and conditions prevailing in environment:namely, her unyielding father. Experiencing the secondary emotion of fear makes it clear to her how strongly her existing internal model has a grip on her. Consistently directing attention to bodily sensations is the key here, as it spatially separating reflection from experience during therapeutic work. Julia understands and feels how her survival strategy prevents problem solving in present. She can experience at the same time that everything she needs emotionally for a solution is already present within her. The central experience is the tipping into each other of primary and secondary emotions. These are the best prerequisites for successfully mastering later behavioral experiments. Julia will not only be able to rationally comprehend them as an external suggestion of an expert, but also experience them as an authentic impulse from herself. And this despite the fact that it is diametrically opposed to her existing model of survival strategy.
The method rules listed in Table 3 help to adapt therapeutic behavior to the two different settings, in particular to strengthen the relationship and trust in body sensations as early warning signals.
The FEP perspective refers to testing new situations as "active learning," where uncertainties in the internal model are reduced by observations and true attributions.
This is done using directed exploration guided by the contents of the survival strategy. This selection of targets restricts the client to behaviorally relevant trajectories, reducing for the moment the variety of data a model must consider. Using FEP, it can be shown that efficient action-oriented models can be learned by now combining goal-oriented and exploratory (information-seeking) behavior.
Concrete action is designed to provide corrective experiences. "Providing corrective emotional experiences" is considered one of the recognized common factors of psychotherapy.
The focus in this respect is on developing and testing behavioral alternatives that may be more adaptive in terms of need satisfaction. In this respect, regarding the balance aspect in Figure 1, the following applies: preserve the good and dare the new. Exploitation and exploration are thus placed in a dialectical relationship to each other. This dialectical attitude is also found in modern CBT, where it is referred to as the acceptance principle. As described above, the minimization of free energy depends on the ability to control directed exploration and exploitation in such a way that the perceived stress can still be well tolerated. In constructing and executing alternative approaches, the client can take familiar and proven elements of her previous exploitative strategies and combine them with the novelty of her directed exploration. The mutually determined mixture ratio is oriented to the fact that the client can still well bear the possibly occurring fear. Thus, the goal-achievement alliance conveys an essential moment of control. Directed exploration contains, depending on the intention, a certain degree of uncertainty that cannot be avoided. Experimentation can involve more or less risky events that create a massive prediction error and thus a lot of free energy. The goal attainment alliance can provide a key skill here, which we will refer to in this context as "competence in dealing with uncertainty." This requires that failures be realistically calculated in. This is not looking through rose-colored glasses, because here the expectation of success is contrasted with possible problems in achieving the goal. That such a view:one could call it functional optimism:is more conducive to goal realization has been empirically proven by. According to this, the frequently praised positive thinking is not very promising. It only contributes efficiently to goal realization if it is simultaneously compared with a possible negative reality. This more problem-oriented view has an attention-diverting effect and, in contrast to blue-eyed positive views, provides clues as to what needs to be paid closer attention to and what may also need to be avoided; the feasible is separated from the unfeasible. In a further step, therefore, the behavior plan is still examined for possible failures using a strategy of mental contrasting and then supplemented. The practice of such competencies leads to more and more priors about appropriate policies, so that the client will minimize the free energy in the future by an appropriate policy selection process.
The client may drop out of the goal-achievement alliance, become involved only in a very non-committal way, and instead of directed exploration, just experiment aimlessly (Figure 1, 4). She may have reached a point where she is confronted with a difficult issue that she wants to avoid and distracts herself with activism, but also wants to please the therapist somehow. Stress and free energy rise again, and she may find herself trapped in old patterns again (Figure 1, 5).
Case (Continuation): Directed exploration in practice means that client and therapist work together on a goal and the plan to achieve it. This involves a successful mixture of old and successful safety regulation from the known traces of the survival strategy as well as a targeted testing of new behaviors. After working on survival strategy and reaction chain, Julia knew her own old patterns very well. As she worked on her anger and the strength that came with it, Julia learned more about the motor for her new behaviors. One evening, Julia left the therapy session full of energy and drive after a successful anger confrontation. She had apparently ignored the therapist's recommendation to think more carefully in the coming week about how she could use this anger to help solve her issues without giving up everything that is important to her. The therapist's goal was to keep the client on the path of directed exploration so that she could concretely choose the goal with her in the upcoming session and plan a suitable strategy for achieving it. However, following her anger impulse, Julia drove to the bakery on the same evening, where her father was busy preparing for the next day. With this impulsive action, she left the path of directed exploration (Figure 1, 3) and landed at the point of undirected exploration (Figure 1, 5). Without thinking about the consequences, Julia unloaded all her anger and yelled at her father. She accused him of wrecking her with his bossy manner. But her father did not put up with Julia's behavior. He also yelled at her and accused her of being ungrateful. It was only because of his hard work that she could study at all and have the life she was currently leading. As usual, he appealed to her guilty conscience. It worked well again. Julia could not counter her father's accusations and was suddenly struck by feelings of fear, guilt and shame. She fell right back into the other extreme of overly exploitation (Figure 1, 1). She apologized and backed down.
In the next therapy session, she reported the incident to her therapist, who reminded her again of her recommendation at the end of the last session. This time, Julia acquiesced and set her goal: She would like to help out at the bakery only 2x a week instead of 5x in order to have more time for her studies and her relationship. The therapist also worked out a conversation guide with Julia on how she could talk to her father in peace and also prepared her for possible difficulties in the conversation with role-playing. She wanted to talk to him after lunch on Sunday and planned 30 min for it. In this way, a good mixture between well-tried paths and new behaviors emerged, which enables Julia to achieve her goals without generating too much free energy and thus stress.
In social situations, successful communication depends on people aligning their mental states with those of their interaction partners. We speak of cooperative communication when the participants succeed in aligning their mental states about events in their shared environment. This concept of alignment is found in developmental psychology and behavioral biology. The therapeutic relationship is just that: developing and establishing a cooperative relationship through affective and goal attainment alliance. Active Inference assumes that a person uses a predictive model of what they would expect from a social interaction in terms of emotional content, what alternative emotional content would predict in the auditory or visual domain, and what a change in those expectations would do. This is echoed by and presented in the Free Energy framework. According to this, humans are endowed with an adaptive prior that controls this alignment. Accordingly, the selection of action strategies depends on providing sensory evidence that one's mental states match or are at least similar to those of the interaction partner. This adaptive prior guides actions and inferences. Specifically, the directing of attention occurs in such a way as to gather evidence for this mental match. Cooperative communication in this respect emerges in a process of convergence to shared internal models. This ideal typical progression of the process of agreement occurs in healthy interaction partners in the best-case scenario and may not be fully realized in the client-therapist relationship until the end of psychotherapy. Clients who enter the psychotherapeutic relationship with a better-safe-than-sorry strategy are certainly concerned with alignment. They strive to produce sensory evidence that conforms to their model, priors, the imperatives and prohibitions of their survival strategy, respectively. That is, their interactive world is a priori confined to a limited sensory field. However, this usually has little to do with the real person of the therapist and is, after all, primarily oriented to the prior for safety. If the therapist develops empathy for the cognitive-affective state of this safety-oriented strategy, she is able to provide signals that fit into this narrow sensory field. This has the effect of minimizing the amount of PE and lowering the free energy. This is consistent with the complementary relationship design discussed earlier. As therapy progresses, however, the goal is to expand this sensory field with the help of new experiences and the development of alternative priors. A particularly efficient way is represented by the work with the therapeutic relationship. However, since this touches the previous "secure basis" of the relationship formation, this developmental step is only indicated in the last third of the therapy. The previous secure basis was created by the therapist largely serving the client's priors. Here an emancipation of the client can be achieved by making the real therapeutic relationship visible and exploring it together. This begins with a frustration.
Case (Continuation): In the last part of therapy, it is often useful to include the therapeutic relationship in the learning process. The goal is to achieve a transfer of what has been learned so far to this particular relationship as well. Julia was making good progress in therapy and so it seemed appropriate to also explore the current state of the therapeutic relationship together. So far, Julia was used to her therapist appreciating her dutiful nature, encouraging her, and meeting her needs for appreciation and attachment. From now on, the therapist took back more and more her complementary relationship design, in which she took the lead in this "duet." She presented herself in the next therapy session as a factual rather questioning counterpart and reacted less understandingly than usual. The client had just told that she had helped her sister move. Julia was visibly irritated and seemed unsettled by the therapist's questions, whether it was really okay for Julia to let her sister help her move while she was still suffering from back pain and had been helping out so much at the bakery. Julia didn't quite know what hit her. She felt an unusual lack of understanding in her relationship and that caused stress. She didn't know how to deal with it, seemed irritated and kept silent. The therapist suggested to use this as an opportunity to take a closer look at the therapeutic relationship and to present it with Julia in the room.
For this purpose, the therapeutic alliance is represented in space. By positioning the bodies in relation to each other, the different aspects of the relationship become visible and can be felt very quickly. Using a technique that utilizes insights into the embodiment of power and psychological closeness, the client is encouraged to represent the therapeutic relationship in space. Such a representation quickly gets to the heart of the quality of the relationship while not being too confrontational. Abstract concepts of power and psychological closeness/distance are made visible in space with the help of horizontal and vertical distances. The corresponding sensory input is of high precision and may be in competition with the priors of the internal model. In this respect, the previous dysfunctional interaction style, which is also evident outside of therapy, usually becomes very apparent. At this point, the relational work can leave behind the exploitative style and become somewhat more exploratory. Exploration is supported here by the therapist resisting the implicit invitation that arises from the patient's habitual priors. The resulting interaction with the therapist is therefore contrary to the client's expectations and creates uncertainty. Uncertainty increases because the therapist has consciously created:at first gradually:a situation that resists the previous dysfunctional mechanisms of alignment.
Case (Continuation): Julia began, guided by the therapist, to present the relationship from her point of view. Julia feels inferior to her therapist:she therefore makes herself much smaller and squats down while asking the therapist to stand on the stool. She also feels dependent on her goodwill and is very afraid of doing something that could endanger it. She therefore kneels directly in front of her and looks at her from below, so that she is able to follow her reactions in gestures and facial expressions. Asked about how she feels, Julia says, that her position on her knees feels uncomfortable but also familar.
The therapist asks Julia to try something new out. Julia agrees. The therapist gets off the stool and increases the distance between Julia and her. She takes a rope which she had deposited within reach and offers Julia to grab the other end. Julia grabs it. The therapist shortens the rope so that Julia has to stand up to stay in contact with the therapist. Both are now standing in front of each other with a distance of about 1.5 m. This was how the therapist experienced the first half of their therapy together. Her primary goal was to strengthen Julia and, in the meantime, she sees her at eye level with all her new abilities. But then the following happened: The therapist reaches into the neighboring bookshelf and hands the client one book after another. The client stumbles while trying to keep five books in under her arm. The therapist asks Julia how she feels: Julia states that it felt unusual but good for her to get on eye level with the therapist with the help of the rope. But now she feels overwhelmed and frustrated. The books are hard to hold, she says, and her shoulders are already aching. She has known this feeling for so long. All the burdens and obligations are just too heavy, she says. The therapist explains to Julia that this is exactly what she wanted to achieve with her critical questioning, namely that Julia directs her attention to the burden of her duties:here represented by the burden of too many books. Julia begins to understand how important critical inquiries are for her. Since she falls into old patterns again. Julia and her therapist start talking about what alternative actions she could try out right now. Julia puts down the rope to be able to carry more books. But without the connection, she feels uncomfortable and the load is still too heavy for her. The therapist asks Julia what else she could do to lighten her load without taking off the rope. Julia hesitantly begins to understand: There are just too many heavy books. Julia feels a distinct increase in tension at the thought of putting down books she has accepted. The therapist encourages her to try it out. One book after the other moves to the floor. A first positive experience for Julia in breaking her survival strategy in the therapeutic relationship. She successfully shed burden when pointed out without having to give up connection to a significant other. On the contrary, Julia's therapist gives her a lot of credit for choosing to put down the book load. Julia feels a definite relief, and the pain in her shoulders slowly disappears. The foundation for the next level in therapeutic work is prepared, in which Julia learns to deal with frustrations within the therapeutic relationship as well.
During therapy, the client's survival strategy starts interacting with the therapist's one. This can unintentionally lead to a permanently frustrating duet. Therefore, regular supervision is an important factor for high quality in therapy. Using the already familiar case example, we would like to briefly outline this point and also embed it in the concept of free energy.
Security in therapeutic relationship is of utmost importance in order to update the client's priors, reduce her uncertainty (Figure 1, 1 and 5) and to help her more and more to achieve a balance (Figure 1, 3). However, this is only possible if the therapist is also able to her own priors during the therapy that she can be like a rock for the client. Usually it depends on the survival strategy of the therapist in which way this can become a challenge at different points of the therapeutic process. This challenge arose for the Julia's therapist toward the end of therapy:
Case (Continuation): Julia's therapist herself comes from a family with self-employed parents. Her father works as a country doctor and her mother supports him as a physician's assistant. The family climate was also characterized by a lot of pressure to perform and hardship. The father hoped that her twin brother would 1 day take over the practice and always demanded top grades from him in school. Her brother, on the other hand, was very musical and preferred to become a pianist. This led to strong conflicts in the family, in which she often took on the role of a mediator and tried to appease her father.
Survival Strategy of Julia's Therapist:
-Only if I always do my best, anticipate the needs of others, and act diplomatically
-and if I never make mistakes or show weakness
-then I maintain security by being seen and appreciation,
-and avoid being rejected.
The therapist therefore found it very easy to meet Julia's needs in terms of complementary relationship building and thus quickly establish a safe climate that reduced "free energy." However, it became much more difficult in the last third of treatment, in which it was a matter of pointing out Julia's maladaptive relationship management a bit more clearly.
Here the therapist sensed a real inner blockade to frustrate Julia in her needs. Because of her own life story, she could empathize all too well with Julia's stress and suffering. So, she went to supervision with the following question: How do I manage to get into a good directed exploration with my client despite my own patterns?
In supervision, the first step is to visualize the interaction of the two survival strategies. The emerging mutual expectations and fears, could be represented as follows:
In this (Figure 3) it becomes visible at a glance at which point it becomes difficult for Julia's therapist to keep her own free energy low: Namely, when she realizes that the therapeutic process now expects her to actively frustrate her client. Her own survival strategy immediately anticipates the occurrence of the central anxiety. She fears Julia might drop out of therapy or not open up to her anymore. If the therapist remains faithful to her survival strategy due to her own high stress (Figure 1, 1), she would simply continue to meet the client's needs in a kind of anticipatory obedience. This is exactly where supervision intervenes, because this approach would prevent the client's developmental process in the sense of directed exploration and jeopardize therapeutic progress. Through the trusting relationship with the supervisor, the therapist can update her priors and work with her not to avoid the client's frustration but to actively enter into the clarification of the therapeutic relationship and thus begin the directed exploration. To do this, the therapist risks confronting her own anxiety and learns to endure it in favor of her therapeutic role. In this way, the circle of successful therapeutic work is closed by supervision, which also enables the therapist to repeatedly establish a balance between exploration and exploitation with his or her own patterns in daily work. | active inference, cognitive behavioral therapy, embodied cognition, emotional survival, exploration-exploitation-dilemma, free energy, safety regulation, therapeutic relationship | Not supported with pagination yet | null |
PMC10149671_01 | Male | 10 | A 10-year-old male consulted our ophthalmology department due to bilateral blurred vision for one week. He had experienced a 1-week episode of flu-like symptoms, including fever and general malaise, 1 month before the ocular presentation. The best-corrected visual acuity (BCVA) was 0.025 (both eyes, BE). The intraocular pressure was within the normal range. Slit lamp examinations revealed 0.5+ anterior chamber cells (BE) with otherwise normal anterior segment structures. Indirect ophthalmoscopy revealed bilateral diffuse perivascular sheathing of the arteries and veins, Purtscher fleckens, and mild optic papillitis. Necrotizing retinitis was not observed (Figures 1A, B). OCT revealed profound macular edema with intraretinal fluid, subretinal fluid, and inner to middle retinal layer hyperreflectiveness (Figure 2A). Ultrawide-field fluorescein angiography revealed bilateral segmental phlebitis, occlusive arteritis, and retinal non-perfusion with macular ischemia. Due to previous systemic prodromes, a pediatrician was consulted for multidisciplinary care.
Physical examination results aside from the ocular findings were unremarkable. Abdominal ultrasonography revealed mild hepatomegaly. Initial hematology and serology investigations revealed an elevated erythrocyte sedimentation rate at 58 mm/h, alanine aminotransferase at 160 U/L, and positive antinuclear antibody (1:640). A systemic infection survey targeting retinal vasculitis and hepatitis revealed negative results for HSV-1, CMV, VZV, EBV, HTLV, HBV, HCV, Quantiferon-TB Gold, syphilis, and toxoplasma serology. However, a highly positive titer of HSV 2 IgM (5.10) was noted. An aqueous tap was not performed because of its invasiveness considering the age of the patient. In addition, the associated autoimmune profiles were positive for anti-smooth muscle antibody (Ab), but negative for anti-dsDNA, anti-mitochondria Ab, or anti-liver kidney microsome Ab (anti-LKM Ab). Therefore, this patient was diagnosed with post-HSV-2 infection-related FBA, PuR, and concurrent autoimmune hepatitis. The patient was initially prescribed prednisolone (40 mg/day), valaciclovir (500 mg every 12 h), and acetylsalicylic acid (100 mg every other day) (Figure 3).
Although the bilateral FBA and macular edema gradually alleviated (Figures 1C, 2B) after several weeks of medical treatment, the BCVA improvement was minimal (0.05, right eye; counting finger, left eye) (Table 1). Persistent macular ischemia, with clinical presentations of profound PuR and compatible ischemic hyperreflective changes on OCT (Figures 1C, 2C), was identified to be the main cause of poor vision. Therefore, HBOT was initiated with 2.0 atmosphere absolute (ATA) for 75 min per session, 1 session per day, 5 days per week. After a total of 39 sessions of HBOT, the visual acuity steadily improved to 0.16 (RE) and 0.2 (LE), with gradual resolution of Purtscher fleckens (Table 1). Subsequent immunosuppressive medications, including methotrexate (10 mg/week) and cyclosporine (50 mg/day), were also initiated for FBA treatment and corticosteroid tapering (Figure 3). Follow-up fundus photograph and fluorescein angiography performed 21 weeks after the initial visit and 8 weeks following HBOT revealed almost completely resolution of FBA and decrease in size of PuR, but extensive macular and mid-peripheral retinal ischemia (Figures 1D, E). Therefore, retinal photocoagulation on the non-perfusion area was performed 13 weeks after the initiation of HBOT to prevent further neovascular complications, such as vitreous hemorrhage, tractional retinal detachment, and neovascular glaucoma (Figure 1F). | purtscher-like retinopathy, atmosphere absolute, best-corrected visual acuity, frosted branch angiitis, hyperbaric oxygen therapy, optical coherence tomography, positive antinuclear antibody | Not supported with pagination yet | null |
PMC4845404_01 | Male | 27 | A 27 -years old male sustained transverse fracture of the patella with gross displacement while playing football. The fracture was subsequently stabilized with tension band wiring with two Kirschner wires (K-wire) & figure of eight stainless steel wire. The immediate post operative period was uneventful. He was discharged after stitch removal with knee support and was advised partial weight bearing with knee bending exercises in between. However, he indulged in heavy manual work including bicycling after 15 days of surgery. This led to loosening of implants and failure of reduction. He reported after 2 months of failure with pain, swelling and stiffness of the knee joint. X-rays revealed wide displacement of the fragments with loose implants (Fig. 1).
The options for such a case were either patellectomy or apposing the fragments by some means. Patellectomy would lead to difficulty in apposing the ligaments as there were gross displacements of the fragments leading to contracture of soft tissues on either side of the patella. Apposing the fragments would require extensive soft tissue dissection and lengthening of the quadriceps tendon resulting in extensive scarring and stiffness. As we were accumulating experience by using Ilizarov in various situations, we opted for it to mend the difficult situation in this case. We felt gradual docking with slow stretching of the soft tissue without any dissection would be the perfect choice for the case. After removing the implants, the fracture margins were cleared of fibrous tissue taking care not to remove any bone. As acute docking was not possible, sub-acute docking was contemplated on the table. Opposing olive wires, 2 in number on either fragments (total 4 in number), attached to traction units were passed through the fragments which were mounted on two full rings on either side (joining two half rings). The rings were fixed to distal femur and proximal tibia by wires and interconnected with threaded rods. The fragments were brought together as close as possible on the table by turning the nuts on the traction units (sub-acute docking); subsequently gradual docking was done with the help of traction units till X-ray showed complete contact. The traction unit consisted of slotted threaded rod with mounted K-wire which was held in place by nuts. These units were mounted on the ring by male post. After docking, as confirmed by X-Ray, compression was applied across the fracture site at the rate of 1/4th turn every 3rd day till one millimeter of compression was achieved (Fig. 2). Full weight bearing was allowed as pain permitted. Patient was followed up every 2 weeks looking for pin site infections and loosening of the compression achieved. Assembly was removed when X-ray showed complete healing. | difficult, fracture, modified ilizarov, patella | Not supported with pagination yet | null |
PMC9538506_01 | Male | 69 | A 69-year-old non-smoker man was admitted to Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (Wuhan, China) on 11 April 2022 and complained of cough and expectoration with bloody sputum for 2 weeks. In March 2022, he visited a local hospital due to cough and expectoration with bloody sputum, but there were no chills, fever, fatigue, or gastrointestinal complaints. A chest computed tomography (CT) scan in the local hospital on 1 April showed a patchy shadow in the right lower lobe. Physicians at the local hospital recommended that the patient should be transferred to the higher-level hospital for further diagnosis and treatment. The patient had a history of kidney calculi disease and denied the history of malignant tumor, other diseases, and surgery. Physical examination at admission showed no obvious positive signs. On 13 April, the lung-enhanced CT scan in Tongji Hospital showed a massive soft tissue shadow, about 46 x 35 mm in the lower lobe of the right lung ( Figure 1A ). To further confirm the diagnosis, the neoplasm samples in the lower lobe of the right lung were obtained using CT-guided fine-needle aspiration (FNA).
Immunohistochemical assays showed that the tumor was positive for CK7, CDX-2, C-MET, and villin; focally positive for P40, CD10, MUC6, ROS1, and mesothelin; and negative for thyroid transcription factor-1 (TTF-1), ALK, SATB2(-), MUC2(-), MUC5AC(-), PAX8(-), GATA3(-), PSA(-), NKX3.1(-), napsin A, and CK20 ( Figure 2 ). Further pathological examination resulted in a diagnosis of intestinal-type adenocarcinoma of the right lung.
The laboratory data showed that cytokeratin-19 fragment antigen21-1 (CYFRA21-1, 9.57 mug/L) and carbohydrate antigen 19-9 (CA19-9, 106.60 U/ml) levels were increased compared with normal levels. To exclude a diagnosis of colorectal adenocarcinoma, gastroscopy and rectal colonoscopy had been performed respectively. Gastroscopy showed chronic hemorrhagic gastritis and gastric body polyp. Histological examination of the gastric body polyp showed gastric fundus gland polyp. Rectal colonoscopy showed multiple polyps of the sigmoid colon, which was determined as tubular adenoma by histological examination. These pathological and immunohistochemical findings excluded lung metastases of intestinal adenocarcinoma, and the patient was finally diagnosed with pulmonary intestinal adenocarcinoma.
In order to investigate the mutation profile of the neoplasm samples, we obtained the permission of patients to use NGS for gene analysis, which is designed to identify somatic variations of 32 cancer-related genes, including EGFR, KRAS, NRAS, BRAF, RET, PIK3CA, and TP53. Gene analysis of the neoplasm samples was undertaken by GREENIKON Medical Laboratory Co., Ltd (Shanghai, China) using Illumina NovaSeq 6000 platform (Illumina, San Diego, CA). Among the 32 genes examined by this assay, only the EGFR, KRAS, and TP53 genes were mutated. EGFR showed a missense mutation (c.2257C>T, p.P753S) of exon 19. KRAS showed a missense mutation (c.35G>T, p.G12V) of exon 2. TP53 showed a missense mutation (c.401T>C, p.F134S) of exon 5 ( Table 1 ). In addition, the expression level of PD-L1 in tumor tissues of patients was detected, and IHC staining results of tissue sections showed that the tumor proportion score (TPS) of PD-L1 was 0%, indicating negative expression. From 30 April, the patient received four cycles of chemotherapy (pemetrexed + cisplatin) combined with immunotherapy (penpulimab). On 4 July, the lung-enhanced CT scan showed that the tumor was smaller than that on 13 April ( Figure 1 ). | egfr mutation, kras, tp53, case report, pulmonary enteric adenocarcinoma | Not supported with pagination yet | null |
PMC10183654_01 | Male | 48 | A 48-year-old male patient was admitted to the hospital for paroxysmal distention and pain in the middle and upper abdomen for 1 week. One week before admission, the patient experienced sudden distension and pain in the middle and upper abdomen. The specific abdominal pain site was not constant. The attack was paroxysmal, and the degree was not severe. Each attack lasted approximately 2-3 min. There was spontaneous remission without radiation pain in the shoulder and back. Changes in body position did not relieve the pain. Moreover, the pain aggravated after eating. The patient felt slightly relieved after defecation but was exhausted. He used to wake up at night because of pain. The pain was not related to fatigue and satiety. There were no symptoms of paroxysmal aggravation. Acid reflux was noted. Before the onset of the disease, the patient had consumed crab food and drank white wine. The patient had previously developed hepatitis A. He had a history of smoking and drinking for some decades, with consumption of 100 ml white wine daily.
Physical examination at admission revealed the following findings: clear mind, no apparent dry and wet rales in both lungs, uniform heart rhythm, no murmur, soft abdomen, tenderness in the right lower abdomen, no rebound tenderness, active bowel sounds, and no swelling of both lower limbs.
After admission, the relevant examination of the digestive system was performed. Abdominal ultrasound showed a rough surface of the gallbladder wall and multiple cholesterol crystals in the gallbladder. Gastroscopy revealed chronic superficial gastritis and duodenitis. Colonoscopy showed swelling and bulge of mucosa of the descending colon. Blood routine examination showed that the white blood cell count was 11.7 x 10 9/L, and the eosinophil ratio was 14.3%. Considering the patient's abdominal pain, symptomatic treatment such as esomeprazole magnesium enteric-coated tablets for protecting the stomach and pinaverium bromide tablets for relieving spasms were given. Four days later, the patient developed cough, expectorating white phlegm, and mild asthma. In the physical examination, a few wet rales could be heard in both lower lungs. The white blood cell and the levels of CRP and PCT increased. Combined with chest radiographs, lung infection was considered, and cefodizime combined with azithromycin was given for treatment. Chest CT showed the following findings: (1) Multiple patch dense shadow and nodular shadow in both lungs, with a high possibility of inflammation. It was recommended to re-examine after anti-inflammatory treatment, by excluding tumors; (2) Partial atelectasis in the lower lobe of both lungs; (3) Multiple slightly larger lymph nodes in the mediastinum and hilum of both lungs; and (4) local thickening of the pleura on both sides. After transfer to the respiratory department, the patient was given piperacillin-tazobactam combined with levofloxacin for anti-infection treatment. C-reactive protein and procalcitonin showed a downward trend. Re-examination of the blood routine showed that T lymphocytes increased while B lymphocytes and NK cells decreased. Bronchoscopy showed that all bronchial lumens were unobstructed, and the mucosa was smooth. No new organisms were found, and no special findings were found in the related pathogen examination. TBLB showed chronic inflammation and interstitial mucus degeneration (bronchial mucosa of right BII, right BIX, and left BIII). The pathological examination with colonoscopy showed that chronic inflammation in the descending colon accompanied with submucosal inflammatory granulation tissue formation and necrosis. The results of the delivery examination showed that paragonimiasis was positive, and Cryptococcus latex qualitative test was negative. The definite diagnosis was paragonimiasis. | classification, diagnosis, medical history, paragonimiasis, serological antibodies, treatment | Not supported with pagination yet | null |
PMC6507253_01 | Female | 11 | An 11-year-old, 6.6 kg, female spayed Maltese, presented comatose to the University of Queensland Veterinary Teaching Hospital within 30 minutes of blunt force trauma after being hit by a car. The dog was previously well with no current medications. Initial physical examination revealed the dog to be laterally recumbent and comatose, with bilateral pin-point pupils and an absent menace response. The oral mucous membranes were cyanotic and the dog rapidly progressed to respiratory arrest. The heart rate was initially 60 beats per minute (bpm). Unfortunately, a blood pressure reading was not recorded at this time. There was haemorrhage from the mouth with trauma evident to the oral mucosa.
A venous blood gas performed at presentation showed a mixed acidosis (pH 6.97 [reference interval: 7.35-7.44], lactate 12.4 mmol/L [reference: <2 mmol/L], pCO2 44 mmHg [reference interval: 33.6-41.2 mmHg]), and hyperglycaemia of 24.8 mmol/L [reference interval: 3.3-6.8 mmnol/L]. The sNa was in the normal range at 138 mmol/L [reference interval: 135-153 mmol/L].
An intravenous (IV) catheter was placed and 3 mg alphaxalone was given IV to permit intubation and manual intermittent positive pressure ventilation with 100% oxygen. A 20 ml/kg IV bolus of lactated Ringer's solution (LRS) was administered, followed by a 4 ml/kg bolus of 7% hypertonic saline (HTS) and an infusion of 0.5g/kg of mannitol over 20 minutes. LRS was subsequently continued at approximately 10 ml/kg/hr for one hour and then reduced to 5 ml/kg/hr. Analgesia was provided with fentanyl at 2 ug/kg IV bolus for three sequential boluses, followed by a constant rate infusion (CRI) at 4 ug/kg/hr.
Once spontaneous ventilation was noted, extubation was achieved and treatment continued in an oxygen cage. Neurological status at this time was improving, however, the dog was still obtunded with ongoing bilaterally miotic pupils and an absent menace response. The heart rate had increased to 116 bpm with strong femoral pulses and a systolic blood pressure of 180 mm Hg as measured by doppler. The respiratory rate was 60 breaths per minute with bilaterally harsh lung sounds in all fields. Chest radiographs were performed which demonstrated changes consistent with pulmonary contusions in the right cranial and left caudal lung fields. The dog was assessed as having a TBI with pulmonary contusions.
Approximately two hours after presentation and following initial treatment, a repeat venous blood gas showed the lactate had decreased to near normal at 2.8 mmol/L, with a pH of 7.34, and the hyperglycaemia had resolved (glucose 6.4 mmol/L). The dog's neurological status improved slightly, though some agitation was subsequently noted. A 0.01 mg/kg IV bolus of acepromazine was administered to address this. Five and a half hours after presentation, a venous gas showed a markedly increased sNa of 159 mmol/L (Figure 1). Other blood work remained unremarkable.
The following morning, fourteen hours following presentation the sNa was measured to be 162 mmol/L. A free water deficit of 480 ml was calculated, and her IV fluids were changed to five percent dextrose in water (D5W) at 40 ml/hr, concurrently with LRS at 25 ml/hr. The goal was to replace the free water deficit over 12 to 24 hours with a decrease of sNa of 0.5 mmol/L/hour. Despite this, 24 hours after presentation and 12 hours following free water commencement, the sNa had only decreased by 4 mmol/L to 158 mmol/L. The urine specific gravity (USG) was 1.012 concomitantly (Figure 1).
The dog was noted to have improved consciousness, but was intermittently vocalising. A head tilt to the right and rolling to the left when handled was also noted. The menace response remained bilaterally absent and there was absent conscious proprioception in both forelimbs and delayed in the hindlimbs. Withdrawal was present in all limbs. The dog was noted to be urinating large volumes frequently and refused to eat or drink. Harsh lung sounds were evident bilaterally, with an SpO2 of 94% on room air and 98% whilst receiving cage oxygen. Due to ongoing vocalisation, phenobarbitone at 2 mg/kg slow IV was commenced every 12 hours for sedation.
Approximately forty hours after presentation, the dog's mentation had markedly improved as evidenced by reduced anxiety and vocalisation. The dog was responsive to sound and was able to ambulate with assistance. Oxygen supplementation was discontinued as pulmonary function had normalised, and the fentanyl CRI was reduced to 2 ug/kg/hr. Nutritional support was initiated at this time in the form of Hills a/d slurry via syringe with a total volume of 10 ml given on this day.
Despite ongoing parenteral free water supplementation, the sNa remained elevated at 157 mmol/L, with a USG of 1.005. This poor response to free water supplementation prompted desmopressin (DDAVP) administration, one drop of 4 mug/ml solution into the conjunctival sac. Free water administration continued unaltered. Measurement of sNa 12 hours later revealed no change, remaining steady at 157 mmol/L. Therefore, a second dose of one drop DDAVP was administered conjunctivally. Almost no effect was noted as six hours later; the sNa was 156 mmol/L. At this time the desmopressin dose was increased to two drops every 12 hours. Three hours later, sNa was 151 mmol/L with concurrent D5W at 40 ml/hr and LRS at 25 ml/hr.
The dog's neurological status continued to improve. By the third day the menace response had returned in the left eye; there was reduced rolling and circling, and return of conscious proprioception in both forelimbs was noted. Despite the improvement in neurological status the dog developed intermittent head pressing, displayed ongoing subjective polyuria, and was also noted to be lame in the left foreleg, which continued throughout her hospital stay. A transient increase in rectal temperature was also noted (40.2 C); however, this normalised following active cooling with a fan and was thought most likely secondary to anxiety. Maropitant was administered at 1 mg/kg subcutaneously every 24 hours for suspected nausea (ptyalism) and ongoing inappetence. The dog subsequently began to eat 20 mls of Hills a/d slurry every four to six hours. Water was offered every four hours. LRS and fentanyl were discontinued, and D5W was increased to 50 ml/hr. She was continued on two drops of DDAVP in the conjunctival sac every 12 hours.
Despite this increase in D5W and DDAVP, during the fourth day the dog's sNa had increased again to 156 mmol/L and DDAVP was subsequently increased to three drops every 12 hours. Urine specific gravity was recorded to be 1.010 at the commencement of day 4. A mild hypokalaemia of 3.3 mmol/L (reference range: 3.4-4.9 mmol/L) was noted and LRS with 40 mmol/L KCl was recommenced at 10 ml/hr and the D5W was reduced to 40mls/hr. Four hours after the increase in DDAVP the sNa dropped to 151 mmol/L.
By the fifth day the sNa was between 151 and 153 mmol/L and frequent urination continued. The DDAVP was decreased to two drops every 12 hours, and the fluids remained unchanged.
On the sixth day sNa was 148 mmol/L. The dog became more alert and aggressive, which was consistent with her temperament prior to the TBI. She was starting to lick slurry from a bowl in addition to the syringe feeding commenced earlier. Over the following two days, her sNa remained between 148 and 150 mmol/L with a K of 4.4-4.8 mmol/L and a USG of 1.008. The clinical status remained unchanged and treatment was continued with 2 drops of DDAVP every 12 hours, and the D5W was reduced to 10 ml/hr. The USG increased slightly to 1.012 by day 8.
In the morning of day 9, the dog was ambulatory, although bumping into objects. The sNa was 144 mmol/L, and the DDAVP was therefore discontinued. The following day, the sNa was 140 mmol/L with a K of 6.2 mmol/L. The blood pH was 7.21, bicarbonate 11.2 mmol/L, pCO2 28 mm Hg, and base excess -15.2 mmol/L. The urea was 12.40 (reference interval: 3.40-10.80 mmol/L). She was given sodium bicarbonate (8.4%), 10 mmol, diluted in 50 ml of saline IV over three hours. A urine sample collected by cystocentesis showed cocci on sediment exam and amoxicillin clavulanic acid (12.5 mg/kg) was initiated subcutaneously once daily. The sNa for that day was 146 mmol/L and the K dropped to 5.1 mmol/L.
The dog had improved mentation with no head pressing or circling. Although she was ambulatory without ataxia, she would follow walls when walking. Her vision appeared reduced. The USG was 1.022 with a sNa of 148 mmol/L. She was discharged home on day 13 with oral amoxicillin clavulanic acid.
The dog returned two days later for a recheck, at which time her owner reported almost normal mentation. A repeat sNa was 152 mmol/L with a K of 4.8 mmol/L. She had an ongoing lameness of 4/5 in her left foreleg with no distinct foci of pain on palpation of the limb. Her aggressive behaviour limited the musculoskeletal examination.
During a final recheck 10 days later, the owner reported that her personality and behaviour had returned to what they had been before the accident. Given her ongoing left forelimb lameness, she was anaesthetised the following day after a preanaesthetic blood screen, in which her sNa was 143 mmol/L. Radiographs were taken of both forelimbs and showed bilateral severe osteoarthritis of her elbows, with the left being more severe than the right. The persistent lameness was likely from osteoarthritis exacerbated by trauma. | null | Not supported with pagination yet | null |
PMC7525287_01 | Female | 56 | A 56-year-old Iranian woman presented with a one-month history of low-grade fever with generalized malaise, loss of weight, and loss of appetite, and she had noticed swelling of neck glands for the similar duration. She denied any joint pains, increased hair loss, or oral ulcers. She did not have chronic cough, sore throat, or ear discharge. The patient denied any alteration of bowel habits or melena. She denied any past history and contact history of tuberculosis or any high-risk sex behaviours. Her past medical history was significant for hypertension and dyslipidemia. One month prior to this presentation, she was seen by a rheumatologist with inflammatory bilateral knee joint arthritis. Her investigations were significant for thrombocytopenia of 109 x 109/L (150-400 x 109/L). There was no involvement of other cell lines. In the workup for the ANA, rheumatoid factor and anti-CCP were negative.
On examination, she was febrile. She was neither pale nor icteric. She had firm, tender discrete lymphadenopathy, the largest measuring 2 cm, in the right upper cervical region. Respiratory and cardiovascular system examinations were normal. Abdominal examination was normal without evidence of organomegaly.
Neck ultrasonography revealed multiple cervical lymph nodes in the cervical region, the largest of which was 24 mm in size in the right submandibular, as well as numerous lymphadenopathies were seen in the right axillary region. Her blood investigations are summarized in Table 1.
The patient was treated with a course of oral antibiotics considering the possibility of bacterial lymphadenopathy (co-amoxiclav and metronidazole). No improvement in symptomatology was observed over 7-day course of antibiotics, and in addition, she was noted to have a generalized urticarial skin rash.
She underwent excision biopsy of the cervical lymph node. Histopathology revealed areas of necrosis, infiltrated with nuclear dust, paucity of granulocytes, and surrounding tissue showing mononuclear cells and reported as "benign acute necrotizing lymphadenitis" which was compatible with Kikuchi's disease. She made an uneventful recovery with normalization of hematological and biochemical parameters without a specific treatment over a period of few weeks.
One year later, she was seen in the hospital with low-grade fever, malaise, loss of appetite, and loss of weight with cervical lymphadenopathy, and repeat biopsy of the cervical lymph nodes revealed similar histopathology compatible with Kikuchi's disease. She was managed conservatively, and the patient made a full recovery. Currently, she is asymptomatic and under follow-up. | null | Not supported with pagination yet | null |
PMC5750514_01 | Female | 4 | A 4-year-old female presented to the Pediatric Emergency Department at Royal University Hospital in Saskatoon, SK, Canada, with 4 days of worsening cough and increased work of breathing and one day of anuria. Her initial vital signs showed a temperature of 37.5 degrees Celsius, pulse rate of 125 beats per minutes, blood pressure of 114/58 mmHg, respiratory rate of 70 breaths per minute, and oxygen saturation of 95% on 30 litres of high flow oxygen with 21% FiO2. On exam, she had bilateral periorbital edema, crusted nasal discharge, and pallor. Rash and purpura were absent. She had nasal flaring, intercostal retractions, and coarse crackles bilaterally although more prominent on the right.
She had cough, sore throat, and rhinorrhea at a walk-in clinic approximately one-week prior and was given a prescription for amoxicillin. She also had iron deficiency anemia six months prior and started oral iron supplementation. She otherwise had no significant past medical history, significant travel history, or recent infectious contacts. Her mother, however, did have a history of treated tuberculosis (TB). Her immunizations were up to date.
Initial laboratory investigations revealed white blood cell count 9.08 x 109/L, decreased hemoglobin 60 g/L, and normal platelet count of 349 x 109/L. Her urea (16.9 mmol/L) and creatinine (46 umol/L) were elevated. She had a slightly elevated CRP (34.5 mg/L), normal glucose (6.7 mmol/L), normal sodium (142 mmol/L), high potassium (5.9 mmol/L), mildly elevated chloride (112 mmol/L), and a low bicarbonate (15 mmol/L). Her D-dimer was 929 ug/L, APTT was low-normal (22 seconds), and fibrinogen was normal (3.42 g/L). Her urinalysis demonstrated leukocyte esterase 500 WBC/uL, protein 1.5 g/L, and blood 250 RBC/uL, with negative nitrites. Urine microscopy revealed leukocytes 20-50 WBC/HPF, erythrocytes 11-20 RBC/HPF, and granular casts 3-5/LPF.
She was transferred to the Pediatric Intensive Care Unit (PICU) after over 250 mL of hemoptysis. Her initial arterial gas showed a normal anion gap metabolic acidosis with concomitant respiratory acidosis (pH 7.25, carbon dioxide 43 mmHg, bicarbonate 18 mmol/L, and corrected anion gap 13.5). Her first chest X-ray showed bilateral consolidations with air bronchograms, consistent with diffuse pulmonary hemorrhage (Figure 1). She was initiated on bilevel positive airway pressure, but she continued to deteriorate with worsening respiratory acidosis (arterial pH 7.01, carbon dioxide 73 mmHg, and bicarbonate 18 mmol/L). She was intubated and shortly thereafter required high frequency oscillation ventilation (HFOV).
With our suspected diffuse alveolar hemorrhage, an upper gastrointestinal bleed (GI) was considered in the differential diagnosis. We elected not to pursue investigations of the GI tract, because her initial management in the PICU after intubation was revealing. A nasogastric tube was promptly inserted which did not indicate any evidence of gastric blood. More importantly, initial tracheal aspirates from closed inline suctioning revealed bright red blood, with subsequent aspirates suggesting a mixture of bright red and congealed blood. With her microcuffed endotracheal tube inflated and routinely monitored (q12 hrs) for minimum inflation pressures, risks for significant aspiration should have been mitigated.
She received two transfusions of packed red blood cells to correct the anemia. Given her worsening clinical status and anuria, CRRT was initiated. This led to a rapid improvement in her electrolyte abnormalities. Further investigations revealed positive perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) with anti-myeloperoxidase antibody IgG 30, and negative cytoplasmic ANCA (c-ANCA) anti-proteinase 3 antibody IgG 2. Both complements C3 (0.18 g/L) and C4 (0.10 g/L) were low. Anti-glomerular basement membrane (GBM), anti-phospholipid, and antinuclear antibodies were negative.
Although vasculitis was strongly suspected due to the constellation of pulmonary and renal findings, infectious causes were also considered. Nasopharyngeal swab for rhinovirus was positive. Blood, urine, and lower respiratory cultures were negative. Mycobacterium tuberculosis polymerase chain reaction (PCR), acid fast bacilli stain, Bordetella, Mycoplasma pneumoniae, and Hantavirus PCR were also negative.
A renal biopsy was performed which demonstrated enlarged glomeruli with diffuse endocapillary hypercellularity with numerous neutrophils and closure of glomerular capillaries (Figure 2). There was endothelial cell swelling but no areas of glomerular capillary wall necrosis or cellular crescents. On immunofluorescent histology, C3 stain showed glomeruli with finely granular 3+, irregular diffuse staining of capillary walls, and mesangium (Starry sky pattern) and IgG demonstrated 1-2+ focal segmental, granular capillary wall staining. There was no immunopositivity with IgA antibody. Electron microscopy confirmed the increased numbers of endocapillary and infiltrative inflammatory cells in the glomerular tuft as well as swelling of endothelial cells. Scattered mesangial, subendothelial deposits were present. However, the classical subepithelial "hump like" deposits were rare. The case was also reviewed by pediatric nephropathologist to confirm the diagnosis of PIGN and to rule out C3 nephropathy. Following the biopsy, a streptozyme test was done which was positive with a titre of 1 : 100.
High dose methylprednisolone therapy was initiated under the suspicion of vasculitis following renal biopsy. Upon receiving the results of the biopsy 3 days after admission, corticosteroid was stopped and emphasis was given to supportive treatment. Her chest X-ray improved greatly by day 5 in hospital (Figure 3) and she was successfully weaned off HFOV and CRRT. She subsequently developed systemic hypertension, which was managed with captopril and amlodipine. At the age of 4 years she was too young for pulmonary function tests at our institution, and a CT chest did not seem warranted given her clinical improvement.
She was evaluated in pulmonary and nephrology follow-up clinics 3 months after discharge. There was no further history of cough, shortness of breath, or anemia and the CXR completely cleared. Her C3 and C4 normalized and her blood pressure remained normotensive. She will receive long-term monitoring for respiratory and renal impairment, but she is expected to have a complete recovery. | null | Not supported with pagination yet | null |
PMC8226409_01 | Female | 31 | A 31-year-old healthy woman presented with complaint of reduced hearing in her left ear for four months which was associated with tinnitus in her left ear. There was no ear pain, discharge, or fever. She denied any nasal symptoms, chronic cough, or weight loss, and any previous contact with TB patients. She was previously treated for otitis media with multiple courses of oral antibiotics prescribed by a general practitioner, but the symptoms persisted.
Clinically, she was well. Otoscopy showed a normal external auditory canal with dull left tympanic membrane. The right ear was normal.
Nasoendoscopy revealed yellowish slough covering the left Eustachian tube opening (Figure 1). The slough was biopsied and the specimen was sent for histopathological examination (HPE) and acid-fast bacilli (AFB) staining. No cervical lymph node was palpable. Tympanometry showed type B tympanogram pattern in the left and type A tympanogram pattern in the right ear. Pure tone audiometry (PTA) was consistent with moderate mixed hearing loss in her left ear.
Chest radiograph was normal. The staining for AFB was positive and the HPE of the slough was reported as nonspecific inflammation. An early-morning sputum test for AFB performed for three consecutive days and Mycobacterium tuberculosis culture were negative.
She was diagnosed with nasopharyngeal TB. The intensive phase anti-TB treatment consisting of isoniazid, rifampicin, pyrazinamide, and ethambutol was started for 84 doses followed by a maintenance treatment with rifampicin and isoniazid for 120 doses. Nasal endoscopy showed a complete resolution of slough near the Eustachian tube opening after three months of treatment (Figure 2). Repeated PTA showed normal hearing in both ears and tympanometry type A tympanogram in both sides. Subsequently she completed six months of anti-TB therapy.
A follow-up for one year after the completion of the anti-TB treatment showed no ear or nasal symptoms. A nasal endoscopy revealed normal nasopharynx and Eustachian tube. Her hearing was also normalised. | eustachian tube, tuberculosis, unilateral hearing loss | Not supported with pagination yet | null |
PMC9358455_01 | Male | 75 | A 75-year-old man visited the Department of General Medicine, Aichi Medical University Hospital, with a complaint of dyspnea on exertion of the modified Medical Research Council dyspnea scale (mMRC) 1. He had hypertension and type 2 diabetes mellitus but no previous history of smoking or respiratory diseases. Because his chest CT showed multiple micronodules with surrounding GGOs in both lungs (Fig. 1A) and slight enlargement of mediastinal lymph nodes, he was referred to the Department of Respiratory Medicine and Allergology. Peripheral oxygen saturation (SpO2) was 98%. There was no microscopic hematuria. Serum tumor markers, carcinoembryonic antigen (0.8 ng/mL), squamous cell carcinoma antigen (1.8 ng/mL), and CYFRA (2.1 ng/mL), were not elevated. The levels of serum IgG (2284 mg/dL) and IgG4 (779 mg/dL) were high. The results of a sputum smear for acid-fast bacilli, sputum PCR for Mycobacterium tuberculosis, and serum interferon gamma release assay were all negative. His pulmonary function, including vital capacity (101.6% of the predicted value), forced vital capacity (105.1%), forced expiratory volume in 1 s (124.9%), and diffusing capacity of the lungs for carbon monoxide (112.6%), were preserved. The following diagnostic possibilities were considered: pulmonary infection including tuberculosis and mycosis, interstitial lung disease, and malignancy.
Two weeks after his first visit, bronchoalveolar lavage (BAL) and trans-bronchial needle aspiration from a mediastinal lymph node were performed using a flexible bronchoscope. The results of BAL fluid obtained from the B5 right middle lobe showed elevation of lymphocytes (13%) and eosinophils (10%). However, a definitive diagnosis could not be made by bronchoscopy results. A pulmonary manifestation of IgG4-related disease was suspected, and prednisolone 20 mg per day was initiated two weeks after the bronchoscopy. However, the steroid treatment was not effective. He was admitted to the Department of Respiratory Medicine and Allergology due to worsening dyspnea to mMRC 4. On admission, his SpO2 level had dropped to 90% in room air. Transthoracic echocardiography showed a normal left ventricular ejection fraction (70%) and a tricuspid regurgitation pressure gradient of 11 mmHg with no evidence of pulmonary hypertension. His chest CT showed increases in the areas of micronodules and GGOs (Fig. 1B) compared with those at the initial visit (Fig. 1A).
After admission, the dose of prednisolone was increased to 50 mg per day, but partial pressure of oxygen in arterial blood dropped to 55.4 mmHg with 1 L/min supplemental oxygen via nasal cannula and further radiological deterioration was confirmed on chest CT (Fig. 1C). Surgical lung biopsy for confirming the histopathological diagnosis was considered but challenging because of his age and respiratory failure. After informed consent was obtained from the patient and his family, surgical lung biopsy of the right middle lobe of the lung using a video-assisted thoracoscope for the purpose of differential diagnosis was performed two weeks after the admission. The lung biopsy revealed embolization of tumor cells into nearly all small pulmonary arterioles associated with extensive dilation. (Fig. 2A and B). Renal cell carcinoma was morphologically suspected. The tumor cells were positive for PAX8 (Fig. 2C) but negative for thyroid transcription factor-1, which finding supported renal cell carcinoma origin. A whole-body contrast-enhanced CT to identify the primary lesion showed a heterogeneous mass invading the left renal vein in the left kidney (Fig. 3A), but no massive embolus in the main pulmonary arteries (Fig. 3B). He was finally diagnosed with renal cell carcinoma of clinical T3aN0M1 stage IV. He elected not to receive systemic chemotherapy but to receive palliative care and supplemental oxygen therapy. One month after the surgery, he received a transfusion of red blood cells for severe anemia due to appearance of gross hematuria. He died four months after the surgical lung biopsy at another hospital for hospice care. | ggo, ground glass opacities, micronodules, pte, pulmonary tumor embolism, pulmonary tumor embolism, renal cell carcinoma, respiratory failure, spo2, peripheral oxygen saturation, surgical lung biopsy, mmrc, modified medical research council dyspnea scale | Not supported with pagination yet | null |
PMC3336233_01 | Male | 62 | A 62-year-old man presented with a 3-year history of recurrent episodes of high fever up to 40 C accompanied by rigors, sweating, flu-like sensation, and malaise. These episodes occurred roughly 3-4 times a year and would last between 2 to 3 days. A markedly elevated C-reactive protein of up to 64 mg/L but without a leucocytosis or elevation of the ESR was evident with the most closely monitored of the episodes. Risk factors for brucellosis, endocarditis, tuberculosis, travel to tropical countries, and retrovirus infection were negative. The patient denied anorexia and weight loss, and there was no family history of fevers, lymphoproliferative disease, or cancer. A complete physical examination was normal and without lymphadenopathy, heart murmurs, clubbing of the nails, skin rashes, joint effusions, and synovitis.
A CT scan of the chest and abdomen was completely normal as was a barium enema performed 2 years earlier. Urine cultures were negative for growth. Numerous blood tests were returned as normal or negative. These included full blood count and blood film analysis, several blood cultures, creatine kinase, and lymphocyte subset analysis, as well as tests of organ-specific autoimmunity on a liver, kidney, stomach tissue block. There was also no evidence of antinuclear antibodies, rheumatoid factor, and antineutrophil cytoplasmic antibodies. Serum immunoglobulins were normal, and there was no abnormality on serum immunoelectrophoresis. The kappa and lambda free light chain estimation by Freelite (Binding Site, UK), serum-angiotensin-converting enzyme, quantiFERON for mycobacterial infection and tests of liver and renal function as well as lactate dehydrogenase were also either normal or negative.
Following a routine positive faecal occult blood analysis, the patient underwent colonoscopy and an adenocarcinoma of the sigmoid colon was discovered. This was recorded as a stage 1 sigmoid adenocarcinoma without lymph node involvement and without abscess formation or necrosis (T1N0M0, Dukes A). The patient made an uneventful recovery and has remained free of further bouts of fever for the previous 2 years. | null | Not supported with pagination yet | null |
PMC7332175_01 | Male | 53 | A 53-year-old Caucasian man with no previous neuropsychiatric history was admitted to our local psychiatric intensive care unit (PICU) on 10 September 2017 following almost a 2-month deterioration of his mental health, physically aggressive, elevated in mood, paranoid-persecutory and grandiose delusions. Prior to his admission, he assaulted one of his neighbours. He presented with pressured speech and flights of ideas. He believed he had contact with politicians, including heads of states and powerful individuals. No cognitive deficit, no neurological symptoms. No significant medical history reported; no family history of mental disorders, no history of alcohol or substances reported as well as no previous forensic history reported. He was separated, lived on his own and worked until 2 weeks prior to his admission as a labourer. Initial routine investigations, including full blood count, renal, hepatic tests and inflammatory markers, were negative. Electroencephalography (EEG) and brain CT were normal. Psychosis was effectively treated with zuclopenthixol deaconate (600 mg/weekly) due to non-compliance with oral medication; as the psychotic symptoms improved, his aggressive behaviour also improved and on 25 October, after a month in the PICU, he was transferred to our open psychiatric ward with diagnosis of a persistent delusional disorder.
At the end of October and in the first week of November, the patient was observed to be having some twitching facial movements, thought to be anxiety-related and described as 'mini panic attacks'. On 10 November 2017, a 4 min grand mal seizure was observed. On further assessment, cognitive decline and severe short-term memory were noted; Addenbrooke's Cognitive 55/100. CT, EEG and lumbar puncture were normal; however, MRI on 29 November 2017 demonstrated bilateral high signal around the temporal horn and diffusion abnormality, suggestive of encephalitis. Consequently, the patient was transferred to medical ward and zuclopenthixol decanoate was stopped. On further investigations, anti-VGKC complex antibodies were detected in his serum. The patient was effectively treated with levetiracetam and prednisolone, and after 52 days of admission in the medical ward he was discharged to the community on 19 January 2018. His psychiatric symptoms had resolved and he did not require further psychiatric treatment. However, he continued to receive treatment under the care of a neuropsychologist for his residual cognitive deficit.
At the last follow-up, in January 2020, he lives independently, performs his normal activities of daily living and works in his previous job. He, however, complained of mild cognitive deficit.
The limbic system is composed of a group of tightly interconnected brain areas that include the cingulate gyrus, the anterior thalamus, the hypothalamus and mammillary bodies; the hippocampus, and the amygdala. The functions of the limbic system are complex and include the establishment of baseline emotional state, addiction and motivation, appetite and eating behaviours, sleep and dreams, memory, sexual behaviours and social cognition. Disruption of limbic structures has huge clinical implications and is presented with a variety of neuropsychiatric disorders including epilepsy, dementia, anxiety and mood disorders, schizophrenia as well as attention deficit and hyperactivity disorder.
VGKCs are located on the membrane of neurons in both the central nervous system (CNS) and peripheral nervous system. They play an important role in a variety of cellular processes, including the functioning of excitable cells, regulation of apoptosis, cell growth and differentiation, the release of neurotransmitters and hormones, maintenance of cardiac activity and so on.
A wide variety of clinical syndromes have been linked with antibodies to VGKCs. It has, however, been determined that patients do not have antibodies to potassium channels, nonetheless, to associated proteins, such as leucine-rich glioma-inactivated 1 (LGI1) and contactin-associated protein 2.
LGI1 is a secreted protein, mainly present in the hippocampus and the temporal cortex. It is capable of binding to a disintegrin and metalloproteinase (ADAM) family of proteins. LGI1 connects presynaptic ADAM23 to postsynaptic ADAM22, which is essential for inhibitory signal transmission from the presynaptic potassium channels to the postsynaptic anti-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor. Antibodies to LGI1 neutralise the LGI1-ADAM22 interaction and reduce postsynaptic AMPA receptors.
Anti-LGI1 antibody-associated limbic accounts for most cases of anti-VGKC complex-associated encephalitis, affecting mainly men with a male:female ratio of 2:1. This form of limbic encephalitis is characterised by subacute onset of psychiatric symptoms such as short-term memory impairment, affective symptoms and psychosis. Myoclonus, hyponatraemia and faciobrachial dystonic seizures as well as headache are common. Moreover, most patients develop faciobrachial dystonic seizures before the onset of amnestic syndrome. Respiratory failure and critical illnesses are less common in anti-LGI1-limbic encephalitis than in anti-N-methyl-D-aspartate (NMDA) antibody-associated encephalitis. Furthermore, the anti-LGI1-limbic encephalitis has better response to immunotherapy and better prognosis compared with anti-NMDA antibody-associated encephalitis. In addition, patients suffering from anti-LGI1-limbic encephalitis tend to be older men with a median age of 60. Anti-NMDA antibody-associated encephalitis predominantly affects young women under the age of 50.
Contactins are a group of cell adhesion molecules that are mainly expressed in the brain. They play pivotal roles in neurogenesis, neuronal development, synapse formation and plasticity, axo-glial interactions and neural regeneration. Contactin-associated protein-like 2 (CASPR2) is found in the central and peripheral nervous system, where it is highly expressed throughout the brain and spinal cord, particularly in the frontal and temporal lobes, striatum, dorsal thalamus and the cortex. In humans, alterations in the CASPR2 gene are associated with a variety of neurological disorders, including epilepsy, schizophrenia, autism spectrum disorders, intellectual disability and language delay, but also obesity. In addition, in humans, autoantibodies that target the extracellular domain of CASPR2 are linked to autoimmune epilepsies, cerebellar ataxia and autoimmune encephalitis.
Anti-CASPR2 antibody-associated limbic encephalitis is characterised with three main syndromes: Morvan's syndrome, Isaac's syndrome and encephalitis. The most common phenotype is Morvan's syndrome, a condition that was first described by Augustine Marie Morvan, a French physician, politician and writer, in 1890. Morvan's 'la choree fibrillaire' is characterised by neuromyotonia, pain, hyperhidrosis, weight loss, severe insomnia and hallucinations. Neuromyotonia is a rare neurological condition, which is characterised by peripheral nerve hyperexcitability. Likewise, patients with Morvan's syndrome quite often present with confusion, memory problems, fluctuations in blood pressure, painful cramps and myoclonus.
The Isaac's syndrome was a peripheral nerve hyperexcitability syndrome that presents as continuous motor activity. Clinical findings include cramps, fasciculations and myokymia. Some of these patients also present with symptoms such as hyperhidrosis and/or CNS symptoms similar to those from Morvan's syndrome.
Antibody status is not needed to consider limbic encephalitis as having a definite autoimmune origin because immune-mediated limbic encephalitis can occur without detectable autoantibodies. Measurements of autoantibodies, however, remain important because the diagnosis of autoimmune limbic encephalitis could be confirmed by their presence in cerebrospinal fluid (CSF) and/or serum. Moreover, their presence clarifies the immunological subgroup of autoimmune encephalitis, with comorbidities, tumour association and prognosis that might differ.
Analysis of CSF plays a central part in diagnosis of all cases of encephalitis. Most patients with autoimmune encephalitis have CSF antibodies and relevant antibodies are found in their CSF. Moreover, the types of antibodies in the CSF can determine the clinical picture as well as correlate with the progress of the illness. CSF analysis of patients suffering from autoimmune limbic encephalitis shows mild-to-moderate lymphocytic pleocytosis (usually less than 100 white blood cells/mm3) in 60% to 80% of patients, and elevated IgG index or oligoclonal bands in approximately 50% of cases. However, patients with LGI1 antibodies present with much lower frequency (about 40%) of CSF pleocytosis.
Brain MRI in patients with autoimmune encephalitis may be normal or bilateral abnormalities in the medial temporal lobes on T2 signal. On other hand, similar MRI findings are found in almost 95% of patients with herpes simplex virus encephalitis, as well as in individuals suffering from tuberculosis and syphilis.
EEG findings in limbic encephalitis can be normal or non-specific or showing slow-wave activities involving the temporal lobes. EEG is in particular useful for excluding subclinical seizures, as well as for prognosis and differential diagnosis. It has been suggested that normal EEG correlates with good prognosis, independent of other prognostic factors. Conversely, periodic or rhythmic patterns, seizures and new-onset refractory status epilepticus are associated with poor prognosis. Anti-LGI1 receptor-mediated limbic encephalitis is associated with faciobrachial dystonic seizures, with characteristic rapid jerking of one side of the face and/or upper extremity. EEG may show multifocal onset seizures or other abnormalities. The delta brush pattern is observed typically in patients with anti-NMDA-receptor-medicated encephalitis.
There are no established guidelines for treatment of autoimmune encephalitis, and diverse regimens are currently being used based on the patient's clinical status and the clinicians' opinion. Corticosteroids, intravenous immunoglobulin and plasma exchange are the first-line treatments. Corticosteroids are frequently the first choice, followed by intravenous immunoglobulin and plasma exchange. Corticosteroids with either intravenous immunoglobulin or plasma exchange represent the usual choice when a combination of first-line agents is administered. When first-line immunotherapy is insufficient, secondary immunomodulatory agents such as rituximab and cyclophosphamide are the most common medications. | anxiety, delusions, neuropsychiatry, psychosis | Not supported with pagination yet | null |
PMC7305717_01 | Male | 83 | An 83-year-old man presented to our department with one-day history of increasingly severe, continuous lower abdominal pain, without hyperpirexia, nausea or vomit. At this time, an increasing but still limited number of newly diagnosed COVID-19 patients were admitted on another floor of the same hospital. Patient's comorbidities included chronic obstructive pulmonary disease (COPD), arterial hypertension chronic and ischemic heart disease, previously treated by coronary angioplasty. At physical examination, the patient was eupnoic, blood pressure was 140/85 mmHg and heart rate 100 beats/minute, the abdomen was bloated and presented diffuse rebound tenderness. Blood tests showed hyperleucocytosis (WBC count: 20 x 103/muL) with neutrophilia (90%), and increased CRP (264 mg/L), without any other relevant alteration. Abdominal CT-scan showed free air, liquid collections, and severe inflammatory thickening of the sigmoid colon, presenting multiple diverticula (Fig. 1).
Laparotomy confirmed acute sigmoiditis associated with diffuse purulent peritonitis, and Hartmann's procedure (sigmoid resection and descending colon terminal stoma) was carried out. An otherwise uneventful postoperative course (first flatus on postoperative day (POD) 3, solid food resumption on POD 4, was marked by a persistent hyperleukocytosis, as WBC count ranged between 17 x 103/muL and 20 x 103/muL through POD 8, despite antibiotic therapy (piperacillin/tazobactam and metronidazole).
On POD 8 afternoon, the patient suddenly presented dry cough, sore throat, dyspnea and hyperpirexia (temperature: 38.5 C) and hypoxemia (SaO2: 88-90%) under ambient air. As he was transferred to the ICU for ongoing acute respiratory failure, further imaging examinations were planned for the differential diagnosis, being lobar pneumonitis and/or COPD exacerbation the most likely etiologies suspected. Later that day, the patient reported that his 70-year-old partner, one week before (on patient's POD 2), presented cough and mild hyperpyrexia (T: 37.8 C), was admitted to another hospital and underwent oropharyngeal swab, which later (on POD 7) resulted positive for SARS-CoV-2. Our patient's oropharyngeal swab, by real-time reverse-transcriptase-polymerase-chain-reaction (rRT-PCR), was then collected in accordance with WHO guidelines for the management of the current COVID-19 outbreak. A high-resolution computed tomography (HRCT) scan identified extensive bilateral unusual interstitial pneumonitis (Fig. 2). Owing to rapidly deteriorating respiratory function, on POD 9, the patient underwent intubation and mechanical ventilation, initially in supine position and later in prone position. On POD 10, oropharyngeal swab test resulted positive for SARS-CoV-2. Few hours later, the patient died by respiratory failure refractory to any treatment.
Shortly after SARS-CoV-2 infection was suspected, on POD 9, a retrospective investigation of patient's person-to-person contacts with medical and non-medical personnel was undertaken, in order to identify any possible further contagion. Three days after patient's death, patient's partner died by COVID-19-related respiratory failure, too. One week later, the oropharyngeal swab test of two members of our team resulted positive and three negative; the results of five more are expected. | covid-19, emergency surgery, fatal outcome, pandemic outbreak, sars cov-2 | High-resolution computed tomography scan of lung showing extensive bilateral interstitial pneumonitis. |
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PMC5958587_01 | Male | 53 | A 53-year-old farmer known to have diabetes mellitus with well-controlled blood sugars presented with intermittent episodes of high grade fever for more than a year. He had occasional dull aching pain in the left subcostal region. There was no history of reduction of weight or appetite. He never consumed ethanol. In the beginning, he received a course of antitubercular drugs for 6 months duration for a diagnosis of extrapulmonary TB in spleen, despite which his symptoms persisted.
On examination, he had normal vital signs and insignificant axillary lymphadenopathy. He had mild hepatosplenomegaly and a dull Traube's space. Rest of his systemic examination was unremarkable. The differentials considered for hypoechoic lesions in the spleen with pyrexia of unknown origin were extrapulmonary TB, sarcoidosis, infective endocarditis, splenic marginal zone lymphoma, B. pseudomallei abscess, histoplasmosis, and hematological malignancy.
His routine blood investigations were normal except for an elevated C-reactive protein (CRP) of 9.8 mg/L (ref range: <6 mg/L) and erythrocyte sedimentation rate of 60 mm/h (ref range: 3-10 mm/h). At admission, his glycated hemoglobin was 6.7%. Sonography of the abdomen revealed multiple hypoechoic lesions in the spleen with peripheral calcification which was suggestive of multiple granulomas. These findings were confirmed on computed tomography scan of the abdomen [Figures 1-3]. Serial blood cultures showed no growth. Blood-borne virus screen, angiotensin-converting enzyme levels, chest X-ray, echocardiography, and bone marrow examination were normal. Ultrasound-guided fine-needle aspiration cytology of the splenic lesion was negative for X-pert TB polymerase chain reaction and for malignant cells. Axillary lymph node biopsy did not yield any positive results. Diagnostic splenectomy was being considered when bacterial culture from the splenic aspirate grew B. pseudomellei and he was initiated on intravenous ceftazidime.
Three days later, he was noted to have icterus. Liver function tests revealed indirect hyperbilirubinemia (total bilirubin 2.2 mg/dL [ref range: 0.5-1 mg/dL]) and direct bilirubin 1.7 mg/dL with normal liver enzymes. His platelet counts dropped to <15,000/cumm3. He had mucosal bleeding and melaena necessitating platelet transfusions. The differentials considered for his thrombocytopenia were DIC, TTP, and drug-induced thrombocytopenia. However, his fibrinogen level was normal, schistocytes were absent, and coagulation parameters were normal. It was found that he was on diclofenac for pain relief after lymph node biopsy and it was stopped. Thrombocytopenia persisted despite stopping diclofenac, and ceftazidime-induced immune thrombocytopenia was considered. His antibiotic therapy was changed to meropenem along with 4 days of dexamethasone. He received 4 weeks of intravenous antibiotics and was discharged with an advice to continue co-trimoxazole and doxycycline for a period of 3 months. His platelet counts improved, and he was well at the time of discharge. During the follow-up visits, his CRP showed declining trend, and he was found to be well. | drug-induced thrombocytopenia, melioidosis, splenic granuloma, tuberculosis | Not supported with pagination yet | null |
PMC6458909_01 | Male | 69 | A 69-year-old man presented on May 1, 2018, to a hospital with fevers and diarrhea. The patient had a complicated history, with cardiovascular problems including an abdominal aortic aneurysm, atrial septal defect status after Amplatzer occluder device placed in 2008, and sick sinus syndrome status post dual-chamber pacemaker placement in 2015.
The patient was diagnosed with primary myelofibrosis with JAK2 mutation in April 2015, treated with lenalidomide and prednisone which were tapered off, and his treatment was switched to ruxolitinib. In November 2016, his disease transformed to secondary acute myelogenous leukemia. He was treated initially with induction chemotherapy with 7 + 3 cytarabine and daunorubicin, and follow-up bone marrow biopsies showed no evidence of leukemia. He was subsequently treated with one course of consolidation chemotherapy with high-dose cytarabine. He ultimately underwent HLA-matched related hematopoietic stem cell transplant from his brother in February 2017. His conditioning regimen was reduced-intensity fludarabine and melphalan. His transplant course was complicated by culture-negative neutropenic fevers and neurotoxicity due to tacrolimus, so he was switched to mycophenolate for graft-versus-host disease (GVHD) prophylaxis. Follow-up bone marrow biopsy showed persistence of fibrosis, but was negative for leukemia, and DNA testing proved that he had over 99% donor DNA in the cell population.
His posttransplant course was complicated by mild GVHD involving the skin and colon diagnosed by sigmoidoscopy. He was treated with high-dose steroids, budesonide, and sirolimus, which were ultimately tapered off by the end of July 2017. However, he developed chronic GVHD involving his mouth in September 2017, which was treated with prednisone, sirolimus, and dexamethasone swish and spit. His prednisone dose was tapered to 30 mg daily by November 2017, and by January 2018, he was only taking prednisone 10 mg daily. By March 2018, it was decreased to 10 mg every other day.
In March 2018, he developed an acute right lower extremity deep vein thrombosis involving his common femoral, profunda, femoral popliteal, posterior tibial, and peroneal veins. He was treated with tissue plasminogen activator, heparin, and thereafter apixaban.
He was admitted in early May 2018 for a week at an outside facility with abdominal pain, diarrhea, and septic shock requiring admission to the intensive care unit, necessitating the use of pressors and stress-dose steroids. He also developed acute renal failure but never required hemodialysis. Both blood and stool cultures were positive for S. enterica serotype Mbandaka. This was believed to be associated with the multistate outbreak of infections linked to cereal. The patient reported that he ate an entire box of cereal within one week prior to becoming ill. Blood culture susceptibilities demonstrated that the organism was susceptible to ampicillin, ceftriaxone, ciprofloxacin, tetracycline, tigecycline, and trimethoprim/sulfamethoxazole.
He was treated with IV ceftriaxone and discharged on amoxicillin/clavulanic acid, completing a total of three weeks of antibiotics. However, about a week after stopping antibiotics, at the end of May 2018, he was readmitted with fevers and diarrhea. Blood cultures were negative, but stool cultures were again positive for S. enterica serotype Mbandaka. He was treated initially with intravenous antibiotics and was discharged on 28 days of trimethoprim/sulfamethoxazole 1 DS tab twice per day. While on antibiotics, his abdominal pain, fevers, and diarrhea resolved.
Approximately seven days after stopping his antibiotics, in early July 2018, he developed a third recurrence of fevers and diarrhea. Blood cultures returned negative, but stool cultures were again positive. He was admitted to the hospital for the third time, treated with intravenous antibiotics for 3 days and discharged home with a second 28-day course of trimethoprim/sulfamethoxazole. Stool studies were also positive for Clostridium difficile, so he received oral vancomycin for treatment. His diarrhea and abdominal pain again resolved. Soon after his discharge, his prednisone dose was decreased to 5 mg every other day, and he was maintained on sirolimus 1 mg daily.
After his third admission, he was evaluated by infectious diseases for his recurrent infections with salmonellosis. A transesophageal echocardiogram was performed, which showed a 0.9-1 centimeter mitral valvular vegetation (Figure 1). This appeared very mobile and was associated with mild eccentric mitral regurgitation. The Amplatz closure device showed no evidence of infection, and his pacemaker leads showed no vegetation.
The patient also had a CT scan of his abdomen which showed a mild increase in the degree of mural thrombus associated with the 2.9 x 2.7 cm calcified abdominal aorta in the lower abdomen, now measuring 10 mm compared to 7 mm on the prior exam from 14 months prior. An indium-111 white blood cell scan was negative.
The patient's antibiotics were converted from oral trimethoprim/sulfamethoxazole to ceftriaxone 2 grams intravenously daily for six weeks. He was maintained on oral vancomycin for his Clostridium difficile infection. Four weeks into intravenous therapy, however, he was rehospitalized again with fevers and diarrhea. Blood and stool cultures were negative, and stool for Clostridium difficile was negative. His fevers and diarrhea ultimately resolved, and he was discharged home.
A follow-up transesophageal echocardiogram prior to discontinuation of intravenous antibiotics showed a smaller linear echodensity, now 0.5 cm, attached to the anterior leaflet of the mitral valve. There continued to be mild mitral regurgitation. Again, both the Amplatz closure device and pacemaker leads showed no vegetation.
Upon completion of six weeks of intravenous antibiotics for endocarditis, the patient restarted trimethoprim/sulfamethoxazole. He was ultimately tapered off oral vancomycin for his infection with Clostridium difficile. Length of therapy for his salmonellosis is to be determined based on follow-up stool testing and immunosuppressive course. | null | Not supported with pagination yet | null |
PMC6080867_01 | Female | 18 | An 18-year-old female who studied abroad in Australia and recently returned presented at our inpatient department with numbness and weakness in all four limbs, disturbance of orientation, and memory impairment for 5 days. She also presented with abnormal sensation in the lower limbs, difficulty walking, trouble speaking, and irritation. She was found lying on the ground in her house in Sydney and was unable to identify her brother. They also found thousands of steel bulbs (each of which contained 10 mL of pressurized N2O) in the house. She admitted that she had used N2O bulbs recreationally for >5 months. She used at least 50 bulbs during the past 5 months, one bulb every other day. During the last 4 days, she used more frequently than before, but she could not remember the exact number of bulbs she used.
Vital signs (temperature [T] 36.6 C, pulse [P] 80/min, respiratory rate [R] 20/min, and blood pressure [BP] 112/62 mmHg) were normal, and the physical examination was notable for a weakly positive Babinski sign, enhanced sensation in all four limbs, and ataxia. The upper limbs exhibited stage 4 muscle strength, while the lower limbs exhibited stage 3 muscle strength. The patient's past history of medical and psychiatric diseases were unremarkable, and there was no family history of psychiatric disorders. A full blood examination showed hemoglobin (Hb) 112 g/L, platelet count 174x109/L, white cell count 7.95x109/L, and mean corpuscular volume (MCV) 93.2 fL. Vitamin B12 was <1,500 pmol/L. The results of a urine toxicology screen were all negative, including methylam-phetamine, heroin, morphine, ketamine, and methylene-dioxyphenethylamine. Blood gas (arterial blood) analysis showed partial pressure of oxygen in the alveolar (PAO2) 97.5 mmHg, partial pressure of oxygen in the artery (PaO2) 80.0 mmHg, PCO2 37.0 mmHg, pH 7.48, and base excess (BE) 3.4 mmol/L. Liver function, renal function, and electrolyte tests showed total bilirubin (TBIL) 4.2 mumol/L, direct bilirubin (DBIL) 2.4 mumol/L, indirect bilirubin (IBIL) 1.8 mumol/L, alanine aminotransferase (ALT) 21 IU/L, aspartate aminotransferase (AST) 20 IU/L, AST/ALT 0.95, total protein (TP) 66.0 g/L, albumin (ALB) 41.8 g/L, glucose (GLU) 4.96 mmol/L, alkaline phosphatase (ALP) 40 IU/L, lactate dehydrogenase (LDH) 380 IU/L, amylase (AMY) 83 IU/L, lipase (LIP) 36 IU/L, creatinine (CREA) 46.0 mumol/L, sodium (Na) 142.7 mmol/L, potassium (K) 4.43 mmol/L, and chlorine (Cl) 104.0 mmol/L. Due to concerns regarding a potential spinal cord compromise and cerebral disease, an enhanced spinal and cerebral magnetic resonance imaging (MRI) was implemented. Figure 1A shows gyrus atrophy and broadened anfractuosity compared to the normal state on a T1-weighted image. Table 1 (before the treatment) shows the results of motor nerve conduction velocity (MCV). The motor conduction amplitude of bilateral tibial nerves, peroneal nerves, median nerves, and ulnar nerves decreased, and motor conduction velocity of bilateral median nerves and ulnar nerves similarly slowed down. Table 2 (before the treatment) shows the result of sensory nerve conduction velocity (SCV). Sensory conduction amplitude of bilateral peroneal nerves decreased, and sensory conduction velocity of bilateral median nerves, ulnar nerves, and peroneal nerves slowed down. Bilateral anterior tibial muscles showed a large amount of spontaneous potential (positive sharp wave and fibrillation wave), and the right abductor hallucis brevis showed multiple spontaneous potential (positive sharp wave and fibrillation wave), small contraction, and huge motor unit action potentials (MUAPs) in a quiet state. The patient was unable to complete the Montreal Cognitive Assessment (MoCA) and the Mini-Mental State Examination (MMSE) due to the poor medical condition.
The patient did not use N2O recreationally again, and we prescribed vitamin B12 to improve neurological symptoms and an atypical antipsychotic drug, quetiapine, to help control irritation. The patient also received HBOT with a treatment pressure of 2 atm in an air-pressurized chamber and was given 100% oxygen for a period of 90-120 minutes at a time, a procedure that was repeated three times a session for 20 sessions. The dysfunction in sensory ataxia, numbness, and impaired cognitive functioning gradually improved with treatment by hyperbaric oxygenation. The MoCA and MMSE scores after treatment were in the normal range. A subsequent MRI to re-examine the cranium showed (Figure 1B) improvement in the encephalatrophy compared with the previous MRI. The results of motor (Table 1, after the treatment) and sensory (Table 2, after the treatment) NCV showed peripheral nerve impairment improved, as indicated by increased NCV values.
Written informed consent for the publication of her clinical details and clinical images was obtained from the patient. A copy of the consent from is available for review from the editor of this journal. | n2o, cognitive dysfunction, encephalatrophy, hyperbaric oxygen therapy, recreational use | Not supported with pagination yet | null |
PMC3204624_01 | Female | 31 | We identified a novel ceftriaxone-resistant N. gonorrhoeae isolated from a 31-year-old female commercial sex worker; MIC of ceftriaxone for this isolate was high (2 microg/mL). The woman visited a clinic in Kyoto for a routine examination for sexually transmitted infections in January 2009. Although she had no obvious symptoms or signs, a throat sample collected on her first visit yielded a positive result for N. gonorrhoeae by the strand displacement amplification test (ProbeTec ET, Becton Dickinson, Franklin Lakes, NJ, USA), but a vaginal sample taken at the same time was negative. After 2 weeks, another throat sample was positive for N. gonorrhoeae when cultured on Thayer-Martin medium, and the patient subsequently received 1 g ceftriaxone intravenously. Her pharyngeal sample was also N. gonorrhoeae positive by strand displacement amplification test on the third visit 2 weeks later, and further ceftriaxone treatment was prescribed. However, a culture for test of cure was not conducted because reinfection was considered. A negative result was finally obtained in April 2009.
The culture showed positive reactions in oxidase and catalase tests. Gram staining showed gram-negative diplococci. The ID-test HN-20 Rapid system (Nissui, Tokyo, Japan) classified the bacterium as N. gonorrhoeae. Susceptibility was determined by the agar dilution method. For this strain, named H041, MIC of ceftriaxone was high (2 microg/mL), and the strain was highly resistant to penicillin G (4 microg/mL), cefixime (8 microg/mL), and levofloxacin (32 microg/mL). However, it demonstrated susceptibility to spectinomycin (16 microg/mL) and reduced susceptibility to azithromycin (0.5 microg/mL).
To characterize the ceftriaxone-resistant N. gonorrhoeae H041, multilocus sequence typing characterized the strain as ST7363, which is the predominant sequence type (ST) among cefixime-resistant clones. N. gonorrhoea multiantigen sequence typing (NG-MAST) was also performed. The NG-MAST strategy uses 2 genes, por and tbpB, for porin and a transferrin-binding protein, respectively. NG-MAST indicated that the strain H041 was ST4220 and contained the por2594 allele and the tbpB10 allele. NG-MAST 4220 is a novel ST. However, the tbpB10 allele is the most frequently observed allele (76.5%) among multilocus sequence typing-ST7363 N. gonorrhoeae strains (n = 81) (M. Ohnishi, unpub. data).
Molecular typing suggested that the novel ceftriaxone-resistant N. gonorrhoeae, H041, is closely related to the ST7363 cefixime-resistant N. gonorrhoeae. Therefore, we compared SpeI-digested genomic DNA banding patterns of strain H041 with those of other N. gonorrhoeae strains by using pulsed-field gel electrophoresis as described. Four ST7363 strains, including N. gonorrhoeae H041, and 4 ST1901 strains (another major ST among cefixime-resistant N. gonorrhoeae strains) were analyzed. The banding pattern of SpeI digested H041 genomic DNA was similar to that of other ST7363 strains and indistinguishable from that of cefixime-resistant but ceftriaxone-susceptible NG0207 (Figure).
We describe the emergence of ceftriaxone-resistant N. gonorrhoeae, isolated from a pharyngeal specimen from a female commercial sex worker. At 2 microg/mL, the MIC was 4-fold higher than that of the previously reported ceftriaxone nonsusceptible strain. Our susceptibility testing suggests that only azithromycin and spectinomycin are effective drugs for treating this strain. In this case, eradication was successful, although N. gonorrhoeae colonization of the pharynx may just be tempory because the pharynx is not an ideal site for N. gonorrhoeae growth. From the routine examinations of commercial sex workers during January-March 2009, 40 N. gonorrhoeae were isolated in the clinic, but no other ceftriaxone-resistant strains were isolated. There is no evidence of dissemination of this strain in Kyoto.
Three independent molecular subtyping methods indicated that the ceftriaxone-resistant H041 strain was N. gonorrhoeae, and it might originate from an ST7363 cefixime-resistant N. gonorrhoeae clone. There are several possible mechanisms for the acquisition of resistance, including formation of a new mosaic type penA allele as penA-X cefixime resistance and acquisition of an extended-spectrum beta-lactamase gene. The H041 strain did not produce beta-lactamase in a nitrocephin test. Further molecular analysis is needed to elucidate the precise mechanism of the ceftriaxone resistance of the H041 strain.
The emergence of ceftriaxone-resistant N. gonorrhoeae raises concerns for controlling gonorrhea because ceftriaxone is widely recommended and the first-line treatment for gonorrhea around the world. N. gonorrhoeae has a potential to gain an extraordinarily high MIC to ceftriaxone. Surveillance for ceftriaxone-resistant N. gonorrhoeae should be strengthened. | null | Not supported with pagination yet | null |
PMC4862298_01 | Male | 17 | A 17-year-old Indian man presented with a 1-month history of low-grade fever with anorexia followed by a 5-day history of acute sensorimotor paraparesis. There was no preceding or concurrent history of any gastroenteritis or other illness. There was no past history of any previous similar illness. The patient was well-built and nourished. Both legs had three-fifth power, absent of tendon reflexes and anesthesia below D9 spinal level. There was no palpable lymphadenopathy. Spinal magnetic resonance imaging (MRI) revealed a multi-segment confluent patchy nonmass-like granulomatous central intramedullary T1-weighted isointense and T2-weighted hyperintense signal abnormality from D7 to conus medullaris without cord expansion suggestive of granulomatous myelitis [Figure 1]. There was a marked postgadolinium enhancement on cord surface, extramedullary epidural and subdural abscesses along the cervical and dorsal cord, abnormal clumping, and contrast enhancement of cauda equina roots [Figure 2]. Vertebrae, intervertebral discs, and brain MRI were normal. Cerebrospinal fluid (CSF) analysis showed a normal opening pressure, with 230 cells/cumm (98% lymphocytes), 236 mg/dL proteins, and glucose 27 mg/dL (matching serum glucose 92 mg/dL). Antinuclear antibody and antiaquaporin-4 antibodies (AQP4-IgG) (by indirect immunofluorescence using transfected HEK2 cells and primate optic nerve as substrate) were negative, and acetylcholine esterase level was normal. Mycobacterium TB-polymerase chain reaction (PCR) in CSF was positive. HIV-ELISA was negative. The patient was neither immunosuppressed due to any illness nor was there any history of iatrogenic immunosuppression by any drugs. His chest X-ray (CXR) was normal [Figure 3], and sputum was negative for acid-fast Bacilli. Chest and abdomen computed tomography (CT) showed three soft tissue nodules in the right upper lobe, one in the right lower lobe and multiple peribronchial nodules, some with central cavitation and a 3 cm x 3.5 cm necrotic subcarinal lymph node [Figure 4]. CT was thus suggestive of endobronchial TB with tuberculous lymphadenitis. The patient did not consent for a bronchoscopic lymph node biopsy. Thus, a final diagnosis of tuberculous longitudinally extensive myeloradiculopathy was made. The patient was given dexamethasone in tapering dose with 4-drug antitubercular therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months, followed by isoniazid and rifampicin for 10 more months. Our patient was ambulatory without support within 2 weeks of treatment initiation and attained full power by the 5th week. He continues to be under our follow-up since last 18 months with no residual deficits. The patient refused for a repeat MRI scan due to severe claustrophobia in the first imaging and as he had improved. | distal myelitis, longitudinally extensive transverse myelitis, neuromyelitis optica spectrum disorders, tuberculosis | Not supported with pagination yet | null |
PMC4807951_01 | Male | 50 | A 50-year-old male electrical engineer was referred to the glaucoma unit at St. Michael's Hospital on October 20, 2010, for left uncontrolled low-tension glaucoma on maximum medical therapy. His past ocular history included a right eye trabeculectomy, followed by a right Ahmed valve placement and right cataract extraction with lens implantation in 2006. In the left eye, a left Ahmed valve was placed in 2007. A diagnosis of low-tension glaucoma had been previously established by the referring glaucoma specialist. The patient had progressive visual field loss despite IOP in the teens, with multiple failed filtration surgeries. He was highly myopic at -14.00 D in each eye. His family history was negative for glaucoma, and he had a history of remote inhaled steroid use of several months duration. Past medical history included a resolved tuberculosis infection 16 years earlier.
At the time of his visit, he was using brinzolamide 1% tid OU, brimonidine bid OU, timolol 0.5% once am OU, and bimatoprost 0.01% at hs OU. On examination, hand vitiligo was noted. Best corrected visual acuity was 20/30 OD and 20/40 OS and IOPs were 12 mmHg OD and 16 mmHg OS at 12:35 pm. Ocular motility was full, and pupils were equally reactive to light with no afferent pupillary defect. There was marked injection of the inferior lid margins and conjunctiva. Corneal thicknesses were 574 and 576 microm in the right and left eyes, respectively. The right anterior chamber showed a tube entering at the 11 o'clock position and the left anterior chamber showed a tube entering at the 4 o'clock position in the presence of iridotomies superiorly. Angles were wide open, and right posterior chamber intraocular lens was in good position. Early nuclear sclerosis was seen in the left eye. Right optic nerve head revealed severe cupping, and the left optic nerve revealed a 0.8 cup with superonasal neuroretinal rim remaining. Shallow excavation was noted in both eyes. Large temporal zones of beta parapapillary atrophy were also noted. Visual field tests showed right superior hemifield loss splitting fixation and left superior arcuate changes approaching fixation. Left visual field progression over 2 years was documented (Figure 1A and B).
In view of uncontrolled, end-stage, low-tension glaucoma with advanced progressive field loss and IOP in high teens on maximal medical therapy, the options of trabeculectomy with or without cataract extraction and intraocular lens implantation were discussed in detail with the patient. After discussing the benefits and risks of the procedure, the patient elected to proceed with combined left trabeculectomy, cataract extraction, and intraocular lens implantation with mitomycin C. The surgery was performed on November 30, 2010. Several weeks after the surgery, he underwent bleb needling due to rapid scarring and remained uncontrolled despite reinstituting maximal medical therapy. The option of gold shunt surgery was discussed to bypass conjunctival scarring issues, including the benefits and risks, and the patient elected to proceed with gold shunt surgery.
On February 22, 2011, left uncomplicated gold shunt surgery was performed. On the first day after the surgery, best corrected visual acuity was 20/200 OS, IOP measured 6 mmHg OS at 4:20 pm, with trace anterior chamber reaction. He was treated with ofloxacin qid and prednisolone 1% qh for 5 weeks. Left eye visual acuity improved, and IOP remained low over the first 3 months. On July 13, 2011, best corrected visual acuity was 20/20 OD and 20/30+2 OS. Intraocular pressures remained mostly in the low teens, using two glaucoma medications in the right eye only. The gold shunt remained in good position and glaucoma appeared stable (Figure 2A and B). Over a 5-year follow-up period, visual acuity (VA), IOPs, and glaucoma remained stable. On May 27, 2015, best corrected visual acuity was 20/30+2 OD, 20/25-2 OS, and IOP measured 14 mmHg OU at 11:35 am, with no changes in medication. The gold shunt continued to be in good position, and glaucomatous optic neuropathy remained stable (Figure 3A and B). Visual fields remained stable throughout the period of follow-up (Figure 4A-D). At his last visit on October 26, 2015, IOP measured 10 mmHg OU and 12 mmHg OS, with no changes in medication. St. Michael's Hospital Research Ethics Board approval was obtained for this case report, and the patient provided written informed consent. | glaucoma surgery, gold shunt, refractory glaucoma, suprachoroidal space, trabeculectomy, tube shunt | Not supported with pagination yet | null |
PMC7666689_01 | Female | 22 | A 22-year-old woman, without any formerly diagnosed diseases, presented to the emergency department with a 3 day history of dyspnea, fatigue and central chest pain. She reported increasing dyspnea that developed in the previous month. She also had intermittent pain in the small joints for several months. There was no family history of SLE. On examination, she had a temperature of 38.2 C, a heart rate of 115 beats/minute, blood pressure of 90/60mmHg, respiratory rate of 25 breaths/minute, muffled heart sounds and jugular distention. The electrocardiogram showed sinus tachycardia and low voltage. The chest radiograph showed an enlargement of the cardiac silhouette with a right-sided pulmonary effusion (Figure 1). The echocardiography revealed a large circumferential pericardial effusion (Figure 2), with diastolic collapse of the right atrium, dilated inferior vena cava and 30% respiratory variation of the Doppler mitral valve, confirming the diagnosis of cardiac tamponade. Initial workup showed normochromic normocytic anemia with hemoglobin at 8.5 g/dl, CRP: 75 mg/L, renal and liver function tests were normal.
Emergency pericardiocentesis was indicated but could not be performed because of the incapability to place the guidewire into the pericardial cavity. So, urgent surgical pericardiectomy with window procedure was realized, 1200 of clear fluid was evacuated. The pericardial fluid contained 2900 white blood cells/mm3, 100 red blood cells/mm3, bacteriological culture and cytologic examinations yielded negative results. The pericardial biopsy showed features of nonspecific inflammation, malignancy and tuberculosis were ruled out. Further investigations were accomplished to determine the etiology. Immunological workup revealed antinuclear antibodies titer of 1: 1280, positive anti-SSA and anti-SM antibodies and hypocomplementemia. The coombs test was positive. The diagnosis of systemic lupus erythematosus was established based on hemolytic anemia, serositis, arthralgia, positive anti nuclear and anti-SM antibodies and low complement. The patient was started on intravenous therapy with methylprednisolone followed by prednisone 60mg by mouth daily with hydroxychloroquine. She had a good clinical response and control echocardiography showed complete resolution of the pericardial effusion without recurrence. | systemic lupus erythematosus, pericardial effusion, tamponade | Not supported with pagination yet | null |
PMC4861862_01 | Male | 34 | A 34-year-old man presented to our institution with complaints of cough, low-grade fevers, abdominal pain, nausea/vomiting, and a 2-week history of weight loss. His past medical history included rheumatoid arthritis with concomitant long-term use of infliximab and a PPD conversion, during which the patient underwent 11 months of isoniazid therapy. Physical examination was unremarkable. Laboratory tests showed a mild leukocytosis of 12.5 x 103 cells/mL (normal 3.8-10.6). ESR was elevated at 108 mm/hr (normal, 0-20). CRP was 16.6 mg/dL (normal 0-0.9). A chest x-ray showed a left pleural effusion and a cluster of nodular opacities in the right upper lobe. A 7-day course of moxifloxacin resulted only in mild symptom relief.
A later CT scan with contrast showed diffuse thickening and nodularity of the omentum, infiltration of the mesentery, and a small amount of hemoperitoneum. Additionally, there were multiple prominent mesenteric lymph nodes and diffuse thickening of the small bowel. In the pelvis, there was a small volume of ascites in the rectovesicle space and enhancement of the peritoneal reflections due to peritonitis (Fig. 1). During a laparascopic biopsy done two days after the CT, extensive adhesions and infiltration of the peritoneum with thickened adhesions were noted between the omentum, bowel, and abdominal wall. The small bowel was covered with micronodular inflammatory nodules typical of a miliary spread of infection (Fig 1D). An omental biopsy showed omental fat with caseating and noncaseating granulomatous inflammation with acidfast organisms, consistent with tuberculosis. Treatment began with a multidrug protocol: rifampin, ethambutol, and moxifloxacin. The patient was discharged to home after two weeks of continued medical therapy. A CXR and CT of the chest of this patient demonstrating right-upper-lobe airspace opacities can be seen in Figure 2. | null | CT showing a subtle cluster of airspace opacities in the right upper lobe (arrow). |
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PMC8131010_01 | Female | 37 | A 37-year-old Chinese woman suffering from end-stage renal disease underwent a cadaveric kidney transplantation in November 2018. Postoperative recovery was uneventful and the serum creatinine level of the patient returned to normal three days after the transplantation. On postoperative day 8, the patient experienced acute rejection, which was treated with high-dose prednisone and plasma exchange, and after treatment, her renal function became normal. The patient developed CRKP infection one month after the kidney transplantation. The CRKP could be detected in incision secretion, urine, blood and anal swab cultures of the patient, and resulted in impaired surgical incision healing. Multi-locus sequence typing (MLST) of seven sets of DNA fragments derived from housekeeping genes was performed to examine the genetic diversity of CRKP strains isolated from the incision, urine, and fecal samples of the patient, and the results revealed that all the three strains were exclusively grouped into ST11 (Table S1 and Figure S1). The hypermucoviscous and hypervirulent nature of the Klebsiella pneumoniae were also checked using the "string test" and qRT-PCR, respectively. The results showed that the CRKP isolate exhibited a positive string test (Figure S2), and expressed virulence-associated genes (rmpA2, ybtS, iucA, rmpA and peg344; Table S2 and Figure S3), indicating its hypermucoviscous and hypervirulent phenotype. Since the CRKP isolated from the patient was resistant against most antibiotics except tigecycline, fosfomycin and polymyxin (Table S3), the combination treatment of with tigecycline (50 mg/12 hours), fosfomycin (4 g/8 hours) and meropenem (1~2 g/8 hours) and was utilized for treating the infection. The detailed treatment timeline for the CRKP infection is shown in Figure 1. After 46 days of antibiotic treatment, the incision of the patient could still not heal. The CRKP converted to be negative in the patient blood cultures, but positive in the purulent incision secretion, urine and anal swab cultures. The patient had normal body temperature and white blood cell (WBC) count (4.6x109/L), but the C-reactive protein (CRP) level was elevated (24.79 mg/L). Symptoms of urinary tract infection such as frequent and urgent urination, and pelvic pain could also be observed. Under this condition, FMT was performed, and antibiotics were stopped one day before FMT. Preoperatively, the patient took proton pump inhibitor, and polyethylene glycol electrolyte solution was given for bowel preparation. Washed microbiota suspensions from a healthy volunteer (screening protocol was shown in Table S4) obtained from fmtBank.org were used for FMT. The preparation of the washed microbiota suspensions was conducted as described previously. Briefly, 10 cm3 (about 1.0x1013 bacteria) of the final precipitated microbiota is the basic unit dose for clinical use, and the volume ratio of the final precipitation/vector solution for making suspensions is 1:2. In this study, 10.3 basic units of the washed microbiota suspensions (about 1.03x1014 bacteria) were given to the patient via nasogastric tube. The patient was not given any antimicrobial agent postoperatively. One week after FMT, the patient's urine and anal swab cultures returned negative for CRKP. The patient's incision began to heal three days after FMT, and showed complete healing 17 days after FMT (Figure 2A). The patient tolerated the FMT procedure without complications including abdominal pain, diarrhea and fever. Moreover, there was no obvious increase in serum creatinine and blood urea nitrogen (BUN) after FMT (Figure 2B), suggesting FMT did not have adverse effect on the patient's renal function. The patient had no symptoms of infection two months after FMT, indicating a positive clinical outcome.
We performed a microbiota analysis of the fecal samples from the donor and the patient. Alpha diversity analyses showed that before FMT, the patient was associated with obviously lower species richness (Chao1 index, Figure 3A) and diversity (Shannon index, Figure 3B) than the donor, which significantly increased at one week, three weeks and two months after FMT (Figure 3A and B), indicating that FMT could lead to an increase in the richness and diversity of the patient fecal microbiota. Next, beta diversity analysis was calculated using weighted and unweighted UniFrac distances, and visualized via principle coordinate analyses (PCoA) to compare microbial communities between samples. Both the weighted (Figure 3C) and unweighted (Figure 3D) UniFrac methods revealed significant divergence of the microbial communities between the donor and the patient before FMT. It should be noted that though the patient microbial community post-FMT still differed from the donor one, their distances visibly decreased, especially at one week and three weeks after FMT (Figure 3C and D).
Furthermore, we analyzed the microbial compositions in detail, and the results were visualized as cumulative histograms (Figure 4A). At genus level, Prevotella_9 (relative abundance 35.9%), Ruminococcaceae_NK4A214_group (relative abundance 12.9%) and Faecalibacterium (relative abundance 10.0%) accounted for the major bulk of the donor microbiota, while Bacteroides (relative abundance 60.6%) and Klebsiella (relative abundance 38.9%) were predominant in the recipient's sample, which accounted for nearly 90% of the total taxa. At one and three weeks after FMT, Phascolarctobacterium increased significantly in relative abundance (28.8% and 26.1%), and became the most dominant taxon. Besides Phascolarctobacterium, the proportions of [Ruminococcus]_gnavus_group, Alistipes, and Lachnoclostridium were also observed to increase after FMT. Meanwhile, at two months after FMT, Bacteroides, Lachnoclostridium and Phascolarctobacterium were the predominant populations in the fecal samples of the patient. Results of the cluster analysis showed that the fecal microbial composition of the patient following FMT was more similar to the donor microbial composition than that of the patient collected prior to FMT (Figure 4A). It should be noted that the relative abundance of Klebsiella significantly decreased at one week after FMT (61.15% vs 1.5%), and remained low at three weeks (1.4%) and two months (6.0%) after FMT (Figure 4B). Moreover, the relative abundances of Ruminococcus, Coprococcus, and Clostridium were negatively correlated with that of Klebsiella, indicating that these genera may competitively interact with Klebsiella (Figure 4C). | carbapenem-resistant klebsiella pneumoniae, fecal microbiota transplantation, gut microbiota, infection | Not supported with pagination yet | null |
PMC2892693_01 | Female | 25 | A 25-year-old woman was admitted to our hospital with an 8-month history of abdominal pain, distension, intermittent nausea, vomiting, and low-grade fever. She had undergone abdominal surgery due to an accidental gunshot injury 10 years earlier. She had ascites on physical examination. Laboratory examinations were unremarkable and the upright abdominal X-ray was normal. Abdominal ultrasound (US) showed multiloculated ascites. A computerized tomographic (CT) scan showed ascites with thin intraascitic septations. The serum-ascites albumin gradient was 0.4 g/dL and the adenosine deaminase level of ascites was 49 U/l (upper limit of normal: 40 U/l). Moreover, the ascitic fluid was straw colored with protein >3 g/dL and total cell count of 550 /muL, consisting predominantly of lymphocytes (>70%). Tumor markers were with the normal range in serum but the ascitic CA-125 level was 336 U/mL (upper limit of normal: 16 U/mL). Cultures of the ascitic fluid and blood were negative for mycobacterial colonies. She refused to undergo laparoscopy, most likely due to her busy schedule. The findings were compatible with peritoneal tuberculosis and conventional antitubercular therapy was started. She returned to the hospital six months later. At the time of her second admission, she was well but her abdominal dullness and ascites were persisting. She had not taken any kind of medication for four months. Levels of serum electrolytes, lactate dehydrogenase, creatine kinase, albumin, and total protein and results of renal- and liver-function tests were normal. Repeated abdominal and pelvic CT scanning with contrast medium showed a large MC (Figure 1). Exploratory laparotomy revealed a multiloculated thin-walled cyst arising from the colonic mesentery, adherent to the bowel loops and adjacent structures. During dissection of adhesions some of the locules ruptured, and about 5 liters of hemorrhagic fluid were suctioned. Histological examination of the biopsy specimen revealed an MC (Figure 2). The postoperative course was very good and the patient was discharged. | null | Not supported with pagination yet | null |
PMC4198265_01 | Female | 32 | A 32 years-old female, HIV positive who defaulted using Atripla for over a period of one year with current CD4 of 86/microL was referred to a tertiary hospital with chest x-ray showing a lesion suspicious of a lung tumour. She had presented at local hospital three (3) months earlier with non-productive cough, associated with left sided stabbing chest pains and fevers, and treated as a case of community acquired pneumonia. The cough and fevers subsided. Past medical history is remarkable for Pulmonary Tuberculosis in 2004. The patienthas been afebrile throughout her six weeks hospital stay. General examination revealed no respiratory distress, mild pallor and moderate finger clubbing with temperature of 36.70C. Other vitals were within the normal range. Respiratory rate of 19breaths/minute, decreased air entry in the left lower zone posteriorly, left basal coarse crepitations, left upper zone dullness on percussion with bronchial breath sounds. The rest of systemic examination was not remarkable. Full blood count showed normal WBC = 6.12K/ul and Neutrophil = 4.9K/ul, moderate anemia with Hb = 7.4g/dl, MCV = 70.1fl and Platelet = 283X 109/l. Pus results did not reveal any organisms on culture; Ziehl-Nelson for AFB was negative. Cytology results showed acute and chronic inflammatory cells, with no evidence of malignancy. Computerized tomography of the chest revealed multiple left lung abscesses, Bronchiectasis and fibrosed left middle hemithorax. In view of multiple lung abscesses complicated with bronchiectasis, the cardiothoracic surgeon has planned an elective surgical intervention to drain the abscesses and a pneumonectomy. | lung abscess, apical mass, lung tumour | Not supported with pagination yet | null |
PMC5968297_01 | Female | 78 | A 78-year-old woman was diagnosed with advanced gastric cancer with multiple lymph node metastases in January 2017. She received second-line chemotherapy with ramucirumab plus paclitaxel starting in August 2017 after failure of first-line chemotherapy. Because of complications with gastrointestinal hemorrhage due to primary gastric tumor, weekly paclitaxel monotherapy was continued from October 2017, which achieved stable disease. Four months after the beginning of second-line chemotherapy and 1 week before hospitalization, she was febrile with a temperature of 38.0 C and consulted the outpatient department. She presented with no accompanying symptoms other than fever and showed no abnormalities in physical examinations. Moreover, her complete blood count tests, serum chemistry, urinalysis, and blood culture revealed no significant findings; therefore, she was discharged home with oral antipyretics. However, 4 days later, she was febrile again with a temperature of 39.8 C along with drowsiness and was admitted to our hospital. After admission, she almost returned to full consciousness without headache and meningeal irritation signs. A computed tomography (CT) scan did not identify a significant abnormality in the brain but revealed an emerging small infiltration in the right upper lung lobe as a possible cause of the fever. She was empirically treated with piperacillin/tazobactam for possible bacterial pneumonia. Her fever gradually improved up to the 7th day of hospitalization; however, thereafter, her mild disturbance of consciousness in the form of delirium was worsening and a fever of 38-39 C was once again observed around the 10th day of hospitalization. Her disturbance of consciousness finally progressed to drowsiness by the 14th day of hospitalization. A brain CT scan on the 14th day revealed apparent ventricular enlargement and periventricular edematous changes compared with that on admission (Fig. 1). Cerebrospinal fluid was collected through a lumbar puncture, which showed a significant increase in the number of mononuclear cells (Table 1). Due to her accompanying advanced gastric cancer, meningitis carcinomatosis was first suspected, for which dexamethasone (6.6 mg/day) treatment was initiated while waiting for cytology results. However, her disturbance of consciousness persisted and deteriorated further, and another cerebrospinal fluid test was performed on the 19th day of hospitalization because of negative cytology results in the first investigation. A significant increase in polynuclear cell numbers and overall cell counts as well as a decrease in the glucose content of the cerebrospinal fluid was noted (Table 1). The cerebrospinal fluid samples were submitted for bacterial, mycobacterial, and fungal cultures. An acid-fast bacilli test of the cerebrospinal fluid was negative, but we initiated empirical anti-tuberculosis treatment since tuberculous meningitis could not be excluded with subacute onset of symptoms. On the 22nd day of hospitalization, positive tuberculosis-polymerase chain reaction (TB-PCR) of the cerebrospinal fluid confirmed the diagnosis of tuberculous meningitis. Her sputum tested was also positive on TB-PCR. Because oral medication was not possible, a triple-drug combination therapy consisting of isoniazid, levofloxacin, and streptomycin was initiated. She continued to receive anti-tuberculosis treatment, and her state of consciousness temporarily improved. Unfortunately, she died on the 37th day of hospitalization due to gastrointestinal bleeding from the gastric cancer. | chemotherapy, gastric cancer, paclitaxel, tuberculous meningitis | Not supported with pagination yet | null |
PMC9684727_01 | Male | 53 | The patient was a 53-year-old Chinese male with no history of cancer in his immediate family. The patient underwent small intestinal stromal tumor surgery in June 2020 and was treated with oral imatinib after surgery. The patient complained that on April 30, 2021, he had cough and sputum, yellow purulent sputum, with fever, up to 38.8 C, accompanied by chest tightness, no obvious chest pain, and no hemoptysis. After 3 days of infusion in the clinic, he went to a local hospital for treatment. Chest CT showed cavity changes in the left lung, left pleural fluid, and nodules in both lungs. The hospital was given piperacillin + etimicin + levofloxacin anti-infective treatment for 12 days. The cough and sputum were better than before, but there was still fever, and bloodshot sputum appeared. For further diagnosis and treatment, he came to the respiratory department of our hospital on May 14, 2021. Physical examination: thick breath sounds in both lungs, and weak breath sounds in the left lung. Blood routine: C-reaction protein (CRP)158 mg/L, white blood cell (WBC)3.38x10^12/L, red blood cell (RBC)3.36x10^12/L, hemoglobin (HGB)99 g/L, lymphocyte (LYM)0.39x10^9/L, mononuclear cell (MONO)0.74x10^9/L. Hemoglobin A1C (HbA1c) Test: 7.9%. There is no special abnormality in liver and kidney function and electrolyte examination. General bacterial, fungal sputum examination, tuberculosis and other sputum pathogenic examinations were negative. Tumor markers AFP, CEA, CA199, and PSA, were all negative. Electronic bronchoscopy showed mucosal congestion and edema in the basal segment of the left lower lobe, the lumen was narrow, and lung lavage was performed. Chest CT examination was performed on May 16, 2021 ( Figures 1A-C ). On May 17, 2021, a lung biopsy was performed for pathological examination. Symptomatic treatment was given, and a thoracic surgery consultation was recommended to recommend surgery. On June 19, 2021, the left lower lung mass and left lower lung were resected under thoracoscopy, and the left upper lung nodule was wedge-shaped. The surgical specimens were sent for pathological examination. They were then sent to the Department of Pathology, Beijing Friendship Hospital, for genetic testing of T-cell clone analysis using BIOMED-2 PCR protocols. A CHOP chemotherapy regimen (ECOG score 0 points, body surface area 1.52 m2, cyclophosphamide 1.1 g1day, pyridoxine 70 mg1day, vinorelbine 40 mg1day, prednisone 100 mg1-5day) was given on August 23, September 16, October 7, October 27, November 18, December 7, 2021, at the Department of Hematology of our hospital, and the CT scan was repeated on October 27, showing that the patient's condition improved ( Figure 1D ). Radiation therapy was performed in the oncology department of our hospital from January 4 to January 29, 2022. The patient is still under follow-up.
Pathological diagnosis on left lung biopsy on May 17, 2021, showed lymphomatoid granulomatosis, tending to grade 3.
The macroscopic examination of the surgical specimen from June 19, 2021 ( Figure 2 ) revealed a 4x1.4x1 cm piece of lung tissue in the left upper lung and a 0.8x0.8x0.7 cm tumor seen in the lung tissue at a distance of 0.6 cm from the lung resection margin. There were many irregular tissues in the left lower lung, totaling 14x12x4 cm, of which a 9x8x4 cm gray-white, gray-yellow slightly hard area could be seen. Microscopic findings: lymphoid cells infiltrated the blood vessel wall in the tumor tissue, scattered B lymphocytes in the rich T lymphocytes background, T lymphocytes heteroplasia, mitotic figures were easy to see, and large necrosis was seen in the center of the tumor. Immunohistochemistry showed tumor tissue Vim(+), CD43, CD2, CD3, CD5, CD7, CD4, CD8 lymphocytes (+); CD56 scattered(+), TiA(+), GrB(+), CD20, CD79a and PAX5 scattered lymphocytes (+); CD10(-), bcl-6(-), Bcl-2(-), Mum(-), C-myc(-), CD21(-), CK23(-), CD30(-), CD15(-), CK(-), S-100(-), CD1a(-), langerin(-), CD68, CD163 histiocytes (+); and Ki-67 dysplastic T lymphocytes were approximately 60% (+). In situ hybridization: EBER focal, scattered (+). Pathological diagnosis: (left upper lung nodule) and (left lower lung) T lymphocytes heteroplasia, lymphoma cannot be excluded; genetic testing is recommended to exclude T-cell lymphoma. The 2 lymph nodes of Group 9 submitted for examination showed reactive hyperplasia.
Gene detection results: TCRbetavbeta+Jbeta2 and DB+Jbeta1/2 showed monoclonal rearrangement. Pathological diagnosis: pulmonary non-Hodgkin CD8-positive cytotoxic T-cell lymphoma with Epstein-Barr virus infection in some cells. | case report, gastrointestinal stromal tumors, imatinib, primary pulmonary t-cell lymphoma, primary pulmonary lymphoma | Not supported with pagination yet | null |
PMC3889001_01 | Male | 20 | A 20-year-old male patient presented to our outpatient department with complaints of colicky type of pain in right lower abdomen, associated with vomiting and fever since 5 days. On examination, patient was febrile and his vitals were normal. The physical examination showed marked tenderness in right iliac fossa. On initial work up, patients leukocyte count was 17,600/mm3. Since these symptoms were consistent with appendicitis, patient was taken for emergency surgery. On laparotomy, a diffuse inflammatory mass and abscess of the appendix [Figure 1] was found and appendectomy was done. Exploration of the bowel and mesentery, through the grid iron incision showed normal ileum, cecum, and mesentery. In post-operative period, he had wound infection, which was managed by regular dressing. Histopathological examination of the appendix revealed caseating epitheliod granulomas and lumen filled with neutrophilic infiltrates [Figures 2 and 3]. Patient was later evaluated for primary source of TB else where in the body. Computed tomography (CT) abdomen and pelvis showed normal bowel loops and mesentery [Figure 4]. Chest X-ray and colonoscopy [Figures 5 and 6] were normal. Three consecutive early morning sputum sample were negative for acid fast bacilli. Tuberculin skin test was negative and erythrocyte sedimentation rate (ESR) was 80 mm/h. Patient was started on standard anti-TB drugs, course similar to pulmonary TB. | appendix, granuloma, tuberculosis | Not supported with pagination yet | null |
PMC6346858_01 | Female | 33 | We present the case of a 33-year-old Caucasian woman with a diagnosis of Behcet's syndrome with severe eye disease with left optic neuropathy and bilateral retinal vaso-occlusive vasculitis. The patient had been taking subcutaneous adalimumab 40 mg every 2 weeks (for the last 6 months), cyclosporine 150 mg twice daily (for the last 12 months) and prednisolone 10 mg once daily (for the last 14 months). Before the treatment with adalimumab was initiated, she was evaluated to exclude latent or active tuberculosis: she had no suggestive symptoms or signs, chest x-ray was normal, and an interferon-gamma release assay (IGRA) and two-step tuberculin skin test were both negative. The patient also had arterial hypertension (treated with losartan 50 mg once daily) and a history of migraine.
The patient complained of odynophagia and fever for the last 2 weeks. She had already been treated with several broad-spectrum antibiotics without resolution of her symptoms. The physical examination was unremarkable except for a hypertrophied ulcerated left tonsil (Fig. 1), cervical adenopathy and fever (38oC). The patient was admitted for further investigation. | tuberculous tonsillitis, adalimumab | Not supported with pagination yet | null |
PMC4961796_01 | Female | 41 | A 41-year-old Korean woman complained of a slight cough without dyspnea or a fever. She was referred to our department by her primary care physician. She was affected by tuberculosis when she was 34 years of age in Korea and treated with unspecified chemotherapy; no signs of relapses occurred until 41 years of age. The precise data regarding her past clinical history in Korea were unavailable. Her hearing ability was lost completely due to unknown reasons. She had no history of diabetes mellitus or other immunosuppressive diseases. Physical examinations at the initial visit showed a height of 162.0 cm, body weight of 58.0 kg, arterial blood pressure of 102/58 mmHg, pulse rate of 74/min, and body temperature of 36.5 C. The breath sounds were decreased in the left lung. No lymphadenopathy was found. Her laboratory examinations are shown in Table 1. The white blood cell count was within the normal range and C-reactive protein (CRP) level was increased to 2.91 mg/dL. The carcinoembryonic antigen (CEA) value was normal, however, the soluble interleukin-2 receptor (sIL-2R) value was increased to 1094 U/mL. The blood glucose level was normal and HIV antibody was negative. The serum immunoglobulin levels were normal. Both CD4+ and CD8+ lymphocyte counts were in the normal ranges. An interferon-gamma release assay (Cellestis Company, QuantiFERON TB Gold) was negative. The antigens for urine Streptococcus pneumoniae and Legionella pneumophila were negative. The bacterial culture, acid-fast bacilli smear and culture, and polymerase chain reaction (PCR) tests for Mycobacterium tuberculosis, M. avium, and Mycobacterium intracellulare of the sputum were all negative. A chest X-ray and CT scan showed a broad consolidation with an angiogram sign throughout the upper-lobe of left lung, however, other imaging findings such as cavity lesions, small nodules, and bronchiectasis were not observed (Fig. 1A-C). Lymph nodes around the arch of the aorta and under the carina of the trachea were slightly enlarged. PET/CT showed a high SUVmax of 26.9 on the consolidation shadow (Fig. 1D). Transbronchial aspiration cytology (TBAC) could not obtain adequate specimens from the consolidation due to stenosis of the left upper lobe bronchus. The cytodiagnosis, common bacterium culture, acid-fast bacilli smear and the PCR tests for M. tuberculosis, M. avium, and M. intracellulare of the lavage fluid were all negative. Furthermore, the acid-fast bacilli culture of the lavage fluid was negative. Thus, a CT-guided percutaneous needle lung biopsy was performed and the biopsy specimens showed caseous granulomas without atypical cells by hematoxylin and eosin (H&E) staining (Fig. 2), but no bacteria by Kinyoun staining. The bacterial culture, acid-fast bacilli smear, acid-fast bacilli culture and PCR tests for M. tuberculosis, M. avium, and M. intracellulare of the biopsy specimens were negative. The consolidation of the left lung enlarged and left pleural effusion developed one week following the lung biopsy (Fig. 1E). Thus, we performed a diagnostic puncture in the left thorax. The pleural effusion was lymphocyte predominant and serological tests showed a total protein (TP) concentration of 5.0 g/dL, albumin of 2.5 g/dL, lactate dehydrogenase (LD) of 223 IU/L, glucose of 95 mg/dL, immunoglobulin G (IgG) of 1216 mg/dL, and adenosine deaminase (ADA) of 84.3 U/L. Effusion specimens were negative for antinuclear antibody (ANA) and rheumatoid factor (RF). The acid-fast bacilli smear and PCR tests for M. tuberculosis, M. avium, and M. intracellulare of the effusion were all negative Finally, M. avium was cultured from the left pleural effusion and we diagnosed the patient with M. avium infection.
Because ethambutol (EB) was thought to be unsuitable due to her complete hearing loss, combination chemotherapy with rifampicin (RFP) 450 mg, clarithromycin (CAM) 800 mg, and levofloxacin (LVFX) 500 mg were administered. The chest image significantly improved after two years of this chemotherapy (Fig. 1F). | angiogram sign, maximum standardized uptake value (suvmax), mycobacterium avium, positron emission tomography (pet)/computed tomography (ct) | CT. scan at the initial visit revealed broad consolidation with a positive angiogram sign (arrow) throughout the upper-lobe of the left lung. |
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PMC4961796_01 | Female | 41 | A 41-year-old Korean woman complained of a slight cough without dyspnea or a fever. She was referred to our department by her primary care physician. She was affected by tuberculosis when she was 34 years of age in Korea and treated with unspecified chemotherapy; no signs of relapses occurred until 41 years of age. The precise data regarding her past clinical history in Korea were unavailable. Her hearing ability was lost completely due to unknown reasons. She had no history of diabetes mellitus or other immunosuppressive diseases. Physical examinations at the initial visit showed a height of 162.0 cm, body weight of 58.0 kg, arterial blood pressure of 102/58 mmHg, pulse rate of 74/min, and body temperature of 36.5 C. The breath sounds were decreased in the left lung. No lymphadenopathy was found. Her laboratory examinations are shown in Table 1. The white blood cell count was within the normal range and C-reactive protein (CRP) level was increased to 2.91 mg/dL. The carcinoembryonic antigen (CEA) value was normal, however, the soluble interleukin-2 receptor (sIL-2R) value was increased to 1094 U/mL. The blood glucose level was normal and HIV antibody was negative. The serum immunoglobulin levels were normal. Both CD4+ and CD8+ lymphocyte counts were in the normal ranges. An interferon-gamma release assay (Cellestis Company, QuantiFERON TB Gold) was negative. The antigens for urine Streptococcus pneumoniae and Legionella pneumophila were negative. The bacterial culture, acid-fast bacilli smear and culture, and polymerase chain reaction (PCR) tests for Mycobacterium tuberculosis, M. avium, and Mycobacterium intracellulare of the sputum were all negative. A chest X-ray and CT scan showed a broad consolidation with an angiogram sign throughout the upper-lobe of left lung, however, other imaging findings such as cavity lesions, small nodules, and bronchiectasis were not observed (Fig. 1A-C). Lymph nodes around the arch of the aorta and under the carina of the trachea were slightly enlarged. PET/CT showed a high SUVmax of 26.9 on the consolidation shadow (Fig. 1D). Transbronchial aspiration cytology (TBAC) could not obtain adequate specimens from the consolidation due to stenosis of the left upper lobe bronchus. The cytodiagnosis, common bacterium culture, acid-fast bacilli smear and the PCR tests for M. tuberculosis, M. avium, and M. intracellulare of the lavage fluid were all negative. Furthermore, the acid-fast bacilli culture of the lavage fluid was negative. Thus, a CT-guided percutaneous needle lung biopsy was performed and the biopsy specimens showed caseous granulomas without atypical cells by hematoxylin and eosin (H&E) staining (Fig. 2), but no bacteria by Kinyoun staining. The bacterial culture, acid-fast bacilli smear, acid-fast bacilli culture and PCR tests for M. tuberculosis, M. avium, and M. intracellulare of the biopsy specimens were negative. The consolidation of the left lung enlarged and left pleural effusion developed one week following the lung biopsy (Fig. 1E). Thus, we performed a diagnostic puncture in the left thorax. The pleural effusion was lymphocyte predominant and serological tests showed a total protein (TP) concentration of 5.0 g/dL, albumin of 2.5 g/dL, lactate dehydrogenase (LD) of 223 IU/L, glucose of 95 mg/dL, immunoglobulin G (IgG) of 1216 mg/dL, and adenosine deaminase (ADA) of 84.3 U/L. Effusion specimens were negative for antinuclear antibody (ANA) and rheumatoid factor (RF). The acid-fast bacilli smear and PCR tests for M. tuberculosis, M. avium, and M. intracellulare of the effusion were all negative Finally, M. avium was cultured from the left pleural effusion and we diagnosed the patient with M. avium infection.
Because ethambutol (EB) was thought to be unsuitable due to her complete hearing loss, combination chemotherapy with rifampicin (RFP) 450 mg, clarithromycin (CAM) 800 mg, and levofloxacin (LVFX) 500 mg were administered. The chest image significantly improved after two years of this chemotherapy (Fig. 1F). | angiogram sign, maximum standardized uptake value (suvmax), mycobacterium avium, positron emission tomography (pet)/computed tomography (ct) | CT. scan at the initial visit revealed broad consolidation with a positive angiogram sign (arrow) throughout the upper-lobe of the left lung. |
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PMC9410991_01 | Male | 36 | A 36-year-old man was admitted to our department for bilateral symmetric polyarthralgia touching large and small joints for two months. He also complained of bone pain in the forearm and legs, shortness of breath, and dry cough without dyspnea. He was not a smoker or alcoholic. His medical history was without specialties, including lung and liver diseases.
On physical examination, vital signs, including body mass index, were normal. A musculoskeletal examination revealed a digital clubbing with Schamroth's sign (Figure 1), bilateral and symmetric swelling of the elbow, wrist, and ankles. Palpation of the bony reliefs of the forearms and legs is also painful. The rest of the somatic examinations were normal including the lungs, heart, liver, and skin.
Laboratory findings revealed elevated acute phase reactants with erythrocyte sedimentation rate (ESR) at 90 mm and C-reactive protein (CRP) at 98.1 mg/L. Immunological examinations were negative (antinuclear antibodies (ANAs), anticitrullinated protein antibodies (ACPAs), rheumatoid factors (RFs), antinuclear antibodies (ANAs), and anti-ds DNA antibodies). Serum thyroid-stimulating hormone (TSH) and free thyroid hormones (FT3 and FT4) were normal. Renal and hepatic functions were within the normal range. Acid-fast Bacillus(AFB) smear microscopy in sputum samples of 3 successive days was negative. A sputum culture was negative for Mycobacterium tuberculosis. Bronchoscopy was normal and cultures from bronchoalveolar lavage (BAL) samples were negative for Mycobacteria and Aspergillus. Hydatid and Aspergillus serologies were negative. The human immunodeficiency virus antibody test was negative.
A chest X-ray and computed tomography (CT) showed an apical pulmonary cavity in the right lung with bronchiolitis and hilar lymphadenopathy (Figure 2(a)). Plain X-ray revealed a monolayer periosteal reaction along the bones of the forearm and legs without acro-osteolysis. Bone scintigraphy showed longitudinally radiotracer uptake along all long bones of the upper and lower extremities confirm periostosis of the tubular bones (Figure 3(a)).
In front of digital clubbing, we discussed acromegaly, thyroid acropachy, and HOA. However, the absence of prognathism and the presence of periostosis quickly excluded acromegaly. Thyroid acropachy is a manifestation of Graves' disease, in our patient, eliminated by the absence of Graves' ophthalmopathy and pretibial myxedema with TSH normal. The negativity of immunological examinations excluded inflammatory arthritis. The diagnosis of HOA was made based on the association of digital clubbing, periostosis of the tubular bones, and seronegative arthritis. Given the negativity of the AFS smear microscopy and the presence of an apical pulmonary cavity in the right lung, in our epidemiological context of tuberculosis, the diagnosis of SNPT was presumed. Indeed, our patient was treated with broad-spectrum antibiotics for 15 days but without clinical improvement. The second series of 3 AFS smear microscopy in sputum samples was done but returned negative. Finally, the diagnosis retained was the association of HOA and SNPT.
He was treated with antitubercular therapy for six months according to the national program for the fight against tuberculosis (isoniazid, rifampin, ethambutol, and pyrazinamide for two months (intensive phase), followed by isoniazid and rifampin for four months (continuation phase)).
HOA symptoms had remitted after three months of treatment. Chest CT performed two months after stopping treatment showed regression of the lung cavity (Figure 2(b)). Bone scintigraphy performed six months later showed improvement in scintigraphic abnormalities (Figure 3(b)).
Furthermore, the patient did not present any adverse and unanticipated events during the treatment period. | null | Not supported with pagination yet | null |
PMC9838795_01 | Male | 27 | A 27-year-old male patient from Cameroon presented with precordial pleuritic chest pain of 1-month duration. The pain was associated with intermittent dry cough, low-grade fever, weight loss, and gradually worsening dyspnoea on exertion. The worsening of dyspnoea with the occurrence of paroxysmal nocturnal dyspnoea prompted consultation. He had significant medical history. He was a former inmate who had spent 10 months in prison. The symptoms started while he was in prison. The blood pressure was 100/76 mmHg and the heart rate of 130/min. The heart sounds were regular, rapid, and muffled. There was pericardial friction rub best heard along the left sternal edge. There was jugular venous distension and tender hepatomegaly. There was no lower extremity oedema. The lung examination was normal. The diagnosis of pericarditis complicated with effusion and right heart failure was made. A chest x-ray showed marked symmetric cardiomegaly (Figure 1). The lung parenchyma was normal. The electrocardiogram (ECG) showed sinus tachycardia with a complete left bundle branch block. The White cell count was 8500/mm3, haemoglobin at 9.8 g/dL, mean corpuscular volume (MCV) = 67 fl. The C-reactive protein (CRP) was 48 mg/L and the erythrocyte sedimentation rate (ESR) was 100 mm. The HIV serology was negative. A transthoracic echocardiogram showed a circumferential pericardial effusion measuring 21 mm over the inferior wall and 19 mm over the anterior wall, with a lot of fibrin. There was marked respiratory variation in mitral and tricuspid inflow. There was collapse of the right ventricular free wall. The inferior vena cava (IVC) was dilated with an absent respiratory variation. The left ventricular systolic function was normal. The diagnosis of a large fibrinous pericardial effusion with signs of hemodynamic compromise was made (Figure 2). There was no impairment of global or segmental left ventricular systolic function. He was started on empirical treatment for pericardial TB. An emergency pericardiocentesis was performed draining about 150 cc of straw-coloured fluid which was sent to the laboratory for analysis. A simple wet mount preparation of the fluid revealed motile (coiling) round worms (with slender anterior ends) identified as T. spiralis (Figure 3). An additional movie file shows this in more detail (see Additional files S2 and S3). Total protein of the pericardial fluid was 75.6 g/L which was compartible with an exudate. The anti-TB medications were stopped and the patient was started on albendazole 400 mg twice a day in association with corticosteroids. His clinical condition improved after 5 days with the improvement of dyspnoea and blood pressure. A repeat echocardiogram showed a significant regression of the effusion after 10 days of treatment. The patient was discharged but he never showed up for a follow-up visit. | africa, pericarditis, trichinella spiralis, case report, tamponade | Not supported with pagination yet | null |
PMC3833587_01 | Female | 40 | A 40-year-old Ghanaian female farmer presented to her internist with an exacerbation of asthma. She has lived all of her life in Tamale, Ghana, and she and her physician were accustomed to asthmatics having increased symptoms at this time, during the dry season when the Harmattan, dry desert winds carrying sand off of the Sahara, blanket northern Ghana. Her baseline medication was only an albuterol inhaler, which was used rarely on an as-needed basis. In prior years, she would increase her albuterol to two puffs four times a day, and that would typically control her bronchospasm. For the previous 5 weeks, her medications were albuterol inhaler two puffs four times a day, budesonide 400 mug two puffs two times a day, montelukast 10 mg per day, and fluticasone 250 mug/salmeterol 50 mug one puff two times a day. Her respiratory symptoms did not abate, so she was put on two courses of prednisone 20 mg per day for 5 days, the last course ending 2 weeks previously, without relief.
She presented to an outpatient medical clinic in Tamale, a city with limited access to x-rays or blood tests. The patient complained of mild shortness of breath at rest but severe dyspnea on exertion for 1 month that had increased over the past 2 weeks despite the additional medications ordered by her internist. She denied experiencing orthopnea, chest pain, cough, fever, chills, abdominal pain, heartburn, dyspepsia, leg trauma, or swelling. The symptoms did not alter at any time of the day. She had a history of hypertension diagnosed many years ago but never took antihypertensive medication due to financial constraints. She also has had many episodes of malaria, with the last episode 5 months earlier, which was treated with artemether/lumefantrine. Her family history is significant for a mother who has had asthma since she was a teenager. The patient is poor, lives in Tamale, has never had a chest x-ray, and has had no blood tests for 15 years. Controlling her asthma is crucial as she is a farmer who works in the field 7 days a week performing manual labor.
The patient is a thin, muscular woman who appeared with mild dyspnea at rest. She was able to speak in full sentences without distress but had a mild increase in shortness of breath when asked to climb onto the exam table. She had a blood pressure of 106/70, heart rate of 98, respiratory rate of 22, and temperature of 37 C (98.6 F). Examination of the nose and throat were normal. Auscultation of the lungs was remarkable for bilateral wheezing in mid-late expiration in all lung fields with prolonged expiration and 1+ bibasilar inspiratory crackles. There were no areas of dullness to percussion. Cardiac exam revealed a regular rate and rhythm without murmurs, and heart sounds were not muffled. Neck veins were unable to be visualized. Abdominal exam revealed a scaphoid abdomen with normal bowel sounds, no masses or organomegaly, and no tenderness. There was no calf tenderness and no lower-extremity edema. She had 2+ carotid, dorsalis pedis, femoral, and radial pulses bilaterally.
The clinic did not have radiographic capabilities. However, a physician from the United States was visiting and teaching ultrasonography to the Ghanaian clinicians. He used a portable bedside ultrasound that had been previously donated to evaluate the patient. Subcostal and 4-chamber apical views revealed a swinging heart within a large pericardial effusion with diastolic collapse of the right ventricle. A diagnosis of pericardial tamponade was made, and an emergency pericardiocentesis was performed via a parasternal approach in the left third intercostal space. After 100 cc of straw-colored fluid were removed, the patient was significantly improved. A total of 750 cc was aspirated, and a repeat ultrasound now revealed a trivial effusion with normal ventricular function. The patient then stated that her breathing was normal. Post-procedure, the patient had clear lungs, a blood pressure of 180/100, a heart rate of 72, and a respiratory rate of 12. She was referred to Accra, the capital of Ghana, for blood tests that were performed 10 days later. Her creatinine was 8.2 and blood urea nitrogen (BUN) was 92. She had a normal chest x-ray and after an extensive evaluation by a nephrology consultant was diagnosed with renal failure due to hypertensive nephropathy. She received dialysis and 1 year later had no recurrence of cardiac tamponade but still required albuterol inhaler as needed that was increased to every 6 hours during the Harmattan to control her bronchospasm. | bronchospasm, asthma, atypical asthma, bedside ultra-sound, cardiac asthma, cardiac tamponade, case report | Not supported with pagination yet | null |
PMC3638494_01 | Male | 32 | A 32-year-old man form the Indian subcontinent presented to the emergency department 2 days after having been kicked in the scrotum during a football match with increasing pain and swelling of the right hemiscrotum. A firm discrete mass was noted at the lower pole of the right epididymis that was clinically inseparable from the otherwise unremarkable testicle. The right testicle was nontender and sat in a normal position with no signs of scrotal skin ecchymosis. The history suggested that the scrotal mass had been present for approximately 12 months, and a preliminary diagnosis of a haemorrhagic cyst caused by trauma was made. Initial management included scrotal support, analgesia, and a follow-up magnetic resonance imaging (MRI) scan. The MRI confirmed a 2.3 cm irregular lesion arising posterior to the lower pole of the right testis that enhanced peripherally with central necrosis and therefore could not rule out a potentially malignant lesion (Figure 1(a)). After informed consent, a scrotal exploration and epididymectomy was performed. Grossly, the specimen measured 25 mm in maximum diameter. Sectioning revealed a 20 mm yellow, partly necrotic tumour mass (Figure 1(b)).
Histological examination (H+E) showed a central area of coagulative necrosis with surrounding reactive fibroblastic tissue and inflammation (Figure 2). Irregular clusters and solid nests of viable epithelioid cells were present, partly obscured by the fibroblastic tissue reaction (Figure 3).
On immunohistochemical staining, these epithelioid cells were positive for CAM5.2 and CK7 and also expressed the mesothelial markers calretinin and WT1 (Figure 4). The H+E appearances and immunoprofile were consistent with a partly necrotic/infarcted adenomatoid tumour. No evidence of malignancy was seen. The tumour was well circumscribed and completely excised at all margins. The patient was informed of the results, reassured, and discharged from further followup. | null | Not supported with pagination yet | null |
PMC8651557_01 | Female | 43 | A 43-year-old female, whose height was 160 cm and weight 46 kg [body mass index (BMI) 18.0], was admitted due to 2 months of repeated fever and space-occupying lesions in the liver on May 15, 2020 (day-1). The highest body temperature appeared at night but returned to normal in the morning, with dry cough, shortness of breath, and dull pain in the liver area. The physical examination of the whole body showed no obvious positive signs, there were no abdominal tenderness and percussion pain, and no enlarged superficial lymph nodes were palpated. So, the patient still could live and work properly. She lived in Chongqing city, whose economic situation is medium as a furniture sales staff. She visited Guangzhou province 6 months ago on business for 2 days. She denied any contact with livestock and eating wild vegetables, raw fish, shrimp, and so on, but drank tap water every day. The local hospital prescribed empirical antimicrobial therapy with azithromycin and Chinese herbal medicines; however, the treatment failed to relieve the symptoms of the patient. Thus, the patient was transferred to our hospital for further evaluation. An outline of the episodes is described in Figure 1. Chest CT scan showed no infection in the lungs, while mass-like shadows in the liver were observed on the abdominal CT scan. Routine blood parameters revealed elevated white blood cell and eosinophil count (Figure 2).
Enhanced MRI of the upper abdomen showed the increased liver volume, uneven liver parenchyma signal, liver interstitial edema, and accumulated fluid in the abdominal cavity on hospital day 2 (Figure 3A). Laboratory tests showed elevated IgE (333 ng/mL), white blood cell, and eosinophil count on hospital day 5. Microbial tests, including blood cultures, stool examination, and stool precipitation, did not detect any pathogens. Eggs were not detected by direct fecal smear and fecal washing precipitation. Due to excessive pharyngeal reflex during gastroduodenal tube placement, two attempts failed to obtain the bile of the patient. The diagnosis of tuberculosis was excluded for the negative results of the chest CT scan, tuberculin skin test, tuberculosis IgG and IgM antibody screening, and T-Spot examination. Meanwhile, ovarian tumors, liver tumors, gastrointestinal tumors, and hematological tumors were also excluded temporarily as the negative results of abdominal enhanced CT and tumor marker detection such as AFP, CA-50, CEA, TAP, CA-125, CA-199, CA-242, and CA-724 and so on. The serum parasite IgG antibody, including schistosome, paragonimiasis, cysticercosis, trichinella spiralis, liver fluke, sparganosis, and hydatid IgG antibody detected by ELISA were negative on hospital day 12. Piperacillin-sulbactam was used as an antibacterial treatment for 10 days from hospital days 4-13.
However, the body temperature of the patient fluctuated several times, and the eosinophil count was not significantly reduced (Figure 2). So, an enhanced CT of the lower abdomen was performed on hospital day 13, which showed multiple shadows of abnormal density in the liver and a small amount of effusion, suggesting the possibility of infectious and neoplastic lesions (Figure 3B). Because of the high fever, biapenem was adjusted to be used to cover drug-resistant bacteria for more than 2 weeks from hospital day-14 to day-32.
To further confirm the diagnosis, an ultrasound-guided percutaneous liver biopsy was conducted on hospital day-14. The hepatic histopathology reported mild inflammation in the portal area and eosinophil infiltration in the inflammatory necrotic area, with no evidence of malignancy, liver abscess, and parasitic infection on hospital day 20 (Figure 1).
As treatment with antibiotics was ineffective (long-term fever, significantly elevated eosinophils count, intrahepatic lesions), the enhanced MRI of the upper abdominal was re-examined on hospital day 33, which indicated no absorption of intrahepatic lesions (Figure 3C). Meanwhile, combined with Chongqing epidemiological studies of Clonorchis sinensis, parasite infection was suspected and praziquantel was used as treatment. The body temperature decreased, and the patient was discharged on day 36.
During the period of hospital days 33 and 67, the patient still had repeated fever with a maximum temperature of 39 C (Figure 2). An enhanced MRI of the upper abdominal showed that the liver shadow had less absorption (Figure 3D). So, albendazole was adjusted as the treatment on the follow-up day. Albendazole was orally taken 0.8 g once a day for half a month. As the body temperature of the patient decreased, the dose of albendazole was decreased to 0.6 g for half a month after drug withdraw. On the follow-up day, the dose of albendazole was not adjusted and the patient was prescribed to take albendazole according to taking half a month and stopping for half a month. Firstly, the peak temperature of the body decreased significantly. Secondly, the eosinophil count decreased and ultimately returned to normal. However, there was still a high fever up to 40 C (Figure 2), occasionally. Meanwhile, the enhanced MRI of the upper abdominal reexamined on follow-up day 137 showed that there was no significant absorption of the lesions compared with the previous (Figure 3E). So far, after a total of 106 days of empirical anti-parasitic treatment, the body temperature and eosinophil count decreased significantly, but the imaging manifestations did not improve significantly.
To identify the pathogen, liver tissue collected on hospital day 14 and peripheral blood on follow-up day 137 were sent for mNGS with the written consent of the patient. The total reads of the liver tissue and blood were 6.93 and 30,379 Mb, respectively. Meanwhile, the reads mapped to microbes in the liver tissue and blood were 934,425, and 29,009. The number of species-specific reads aligning to the Fasciola hepatica genome in the liver biopsy and blood was 3 and 51, respectively (Figure 4). Finally, the disease was diagnosed with fascioliasis hepatica with triclabendazole as the first-line drug. However, for the sake of the unavailability of triclabendazole under the epidemic of COVID-19 in China and other countries, and the partial effectiveness of albendazole on the fascioliasis hepatica which significantly decreased the body temperature and eosinophil count of the patient, albendazole was used with a prolonged treatment time following the previous way.
Eventually, after receiving treatment of albendazole for more than 7 months, the body temperature and eosinophil count of the patient normalized with no obvious clinical manifestations. So, albendazole was discontinued on day-300. After more than 3 months after drug withdrawal on follow-up day 148, the enhanced MRI of the upper abdominal showed that the intrahepatic low-density shadow was smaller (Figure 3F), and the blood mNGS was negative (Table 1), suggesting the albendazole treatment was effective. | albendazole, case report, fascioliasis hepatica, metagenomic next-generation sequencing (mngs), precision treatment | Not supported with pagination yet | null |
PMC3481907_01 | Male | 40 | A 40-year-old man presented with large plaques of 30 years duration over right upper limb, right side of the chest and back, and right lower limb. The lesion started as a small papule over right upper limb near the elbow when he was 10 years old. Since then it steadily grew in size to involve whole of the limb and also the right side of the chest and back. He developed similar lesions, one over the right thigh after about 2 years of the first lesion that gradually enlarged to involve most of the thigh circumferentially and one more lesion over the left side of the back since one year [Figure 1]. The lesions were asymptomatic except for mild itching. There was no history of trauma prior to the onset of the lesions or the past history suggestive of tuberculosis of any part of the body. There was no family history of tuberculosis or contact with a tuberculosis patient. He consulted many doctors and applied various creams but of no help.
On examination, there were three plaques, two large and one small, with well-defined borders and irregular margins:
Plaque no. 1: involving right upper limb, right side of the chest and back measuring about 60 x 45 cm.
Plaque no. 2: about 6 x 3 cm over the left side of the back.
Plaque no. 3: over right thigh, involving circumferentially, measuring about 40 cm longitudinally and 50 cm circumferentially.
Within the plaque, there were areas of thick hyperkeratosis and large, thick adherent crusts on an erythematous base. Ulceration at some places and areas of scarring and atrophy in between the areas of hyperkeratosis were present. There was no regional or generalized lymphadenopathy. The patient could not extend the shoulder and elbow completely because of contracture. Systemic examination was normal.
Hematological investigations revealed anemia (Hb: 10.1 g%), raised erythrocyte sedimentation rate (67 mm/first hour). The Mantoux test was strongly positive with a reading of 22 x 20 mm at 72 h. Chest X-ray was normal. X-ray of the involved parts showed no evidence of underlying tissue infiltration. Sputum was negative for acid fast bacillus (AFB). Scrapings from crusts were negative for fungus. Culture for M. tuberculosis and fungus were negative. ELISA for HIV was nonreactive. Histopathologic examination of the biopsy specimen revealed hyperplastic epidermis, upper and mid-dermis showing numerous noncaseating epitheloid granulomas with Langhan's type of giant cells [Figure 2]. No fungal elements or AFB were seen on tissue section.
Based on clinical features and investigations, a diagnosis of lupus vulgaris was made and the patient was started on antitubercular treatment cat-I. There was dramatic improvement in skin lesions within 3 weeks and after 6 weeks the lesions showed 70-80% of improvement. After 12 weeks, there was almost total healing of the lesions [Figure 3]. | cutaneous tuberculosis, giant plaque, lupus vulgaris | Not supported with pagination yet | null |
PMC7876933_01 | Male | 65 | A 65-year-old male with hypertension and diabetes mellitus complained of sudden thoraco-abdominal pain. At history he referred to be in treatment with antiplatelet and anti-hypertensive drugs. Patient denied any previous family history of similar pathology. CT-scan showed an ATBAD, from left subclavian artery (LSA) to the superior mesenteric artery (SMA), and a 72 mm large infrarenal AAA. CT-angiography showed a significant true lumen compression from an expanding false lumen (Fig. 1, Fig. 2, Fig. 3). No malperfusions symptoms or signs were evident. Uncontrollable systemic hypertension and pain (thoracic and abdominal) were the indications to treatment. To reduce the invasiveness of the procedures and address simultaneously both ATBAD and AAA a totally endovascular approach was chosen.
Intervention was conducted without placement of spinal drain.
In our vascular operating room, under general anesthesia and systemic heparinization (ACT > 250 s), a bilateral surgical common femoral artery (CFA) and a bilateral percutaneous brachial artery (BA) accesses were gained. A through and through wire from the right CFA to the right BA (bodyfloss technique) was constructed in consideration of the arch anatomy and to create a stable platform for the thoracic stent-graft advancement and deployment by applying adequate tension to the bodyfloss wire.
An adequate proximal landing zone was identified in zone 2 Hishimaru aortic arch. To maintain LSA perfusion a chimney was planned. From the left BA access a 10 x 31 mm Silene covered stent (InSitu Technologies Inc, St. Paul, MN, USA) was advanced and parked at the origin of the LSA so that half of the length was positioned inside the aortic arch and the remaining into the LSA. A 40 x 223 mm Valiant Navion (Medtronic, Inc., Minneapolis, MN, USA) was placed and deployed in zone 2 aortic arch through the bodyfloss wire. At this stage, the Silene covered stent (InSitu Technologies Inc) was deployed. A kissing ballooning of both the Valiant Navion (Medtronic, Inc.) thoracic stent-graft and the LSA chimney was performed. Sizing of the thoracic and LSA devices were performed according to the current understandings. The control angiography confirmed the adequate proximal sealing, the absence of leakages and the maintained LAS patency.
The second step consisted of endovascular aneurysm repair (EVAR) carried with a 32 mm bifurcated ENDURANT II (Medtronic, Inc.) stent-graft from the infrarenal aorta to both common iliacs carried with the use of the speed cannulation gate technique. The control angiography confirmed the adequate proximal and distal sealing, the absence of leakages and the maintained internal iliacs patency.
The third step was performed with the placement of a 36 x 180 mm Zenith endovascular dissection stent (Cook Medical, Bloomington, IN, USA) between the thoracic and the abdominal stent-graft. This bare metal stent is intended to supports the collapsed true lumen without covering the reno-visceral branches as reported in the PETTICOAT (provisional extension to induce complete attachment) technique (Fig. 4). The final angiographic control confirmed the above mentioned partial findings and the maintained patency of reno-visceral arteries and a reduced refueling of the false lumen.
After procedure the patient was transferred in the intensive care unit (ICU) for monotoring of vital functions where the extubation was carried after 12 h with no complications or signs of spinal cord ischemia (SCI). On the second postoperative day the patient was transferred from ICU and discharged at home after seven days.
The one year CT angiogarphy showed good placement of thoracic and abdominal graft with good remodeling of false lumen in absence of symptoms and complete exclusion of AAA. | case report, complicated aortic b dissection, petticoat | Not supported with pagination yet | null |
PMC2799331_01 | Male | 45 | A 45 year old white American male of Italian descent presented with a life-long history of occult gastrointestinal blood loss, chronic anemia, iron deficiency, and frequent bouts of abdominal pain as a child and young adult. Repeated episodes of acute gross gastrointestinal bleeding late in his fourth decade and multiple episodes of small bowel perforation required five surgical interventions between 38-45 years of age. Surgical exploration of the small intestine and intra-operative endoscopy revealed multiple recurrent small intestinal ulcerations. Histologic specimens of the ileum and jejunum revealed multiple small, well-demarcated ulcers with minimal surrounding inflammation. Stenotic ileal web formations were also described proximal to several ulcers. Misoprostol (800 mcg daily), an oral prostaglandin E1 analog, had been initiated with subsequent resolution of anemia for a period of 27 months until GI bleeding recurred again.
Colonoscopy and esophagogastroduodenoscopy had been performed on multiple occasions and always had been normal. Mesenteric arteriograms, gastrin secretion and laboratory and histologic evaluation for celiac sprue and inflammatory bowel disease were all normal. He denied having had diarrhea, nausea, vomiting or constipation. He had no history of bruising or non-gastrointestinal bleeding symptoms or severe or recurrent infections.
A clear cell renal carcinoma (Furman Grade II) was resected at age 40. A brief period of mild wheezing in early childhood was reported without subsequent respiratory complaints. A shellfish allergy causing urticaria was reported. Medications included iron sulfate and a multivitamin in addition to misoprostol. Use of nonsteroidal anti-inflammatory and corticosteroid medications was specifically denied.
The patient's father had died with multiple myeloma, and varying malignancies were reported in second and third degree relatives. No renal malignancy was reported in family members. There was no family history of ulcers.
Physical examination revealed a well-developed male. Blood pressure was normal. A 2/6 systolic murmur was heard at the left sternal border. His abdomen was notable for multiple well-healed surgical scars. Physical exam was otherwise unremarkable.
An electrocardiogram and an echocardiogram were normal. Ultrasonography demonstrated normal kidneys with evidence of prior partial resection. Blood cell counts, electrolytes, renal and liver function values were normal.
Quantification of the patient's urinary prostanoid metabolites demonstrated reduced levels compared with reference values (Table 1). The patient's mother and sister did not have reduced urinary prostanoid metabolite levels.
The finding that 11d-TxB2 excretion was reduced by 84.1% led to the hypothesis that TxA2 biosynthesis by the platelet was impaired. This was assessed by measurement of TxB2 released into the serum during blood clotting, which is derived almost entirely from platelets. The patient's mean serum TxB2 was reduced by 95.9% (Table 2). This could reflect pharmacologic inhibition of platelet COX-1, COX-1 deficiency or lack of the COX-1 substrate, AA (Figure 1). A genetic deficiency of thromboxane synthase seemed unlikely due to the depressed biosynthesis of other prostanoids. To distinguish between these possibilities, the product of the platelet 12-lipoxygenase, 12-HETE, was measured in serum; 12-HETE should be unchanged or increased with pharmacologic or genetic impairment of COX-1 catalytic activity. The level of 12-HETE in the patient's serum was decreased by 97.8% (Table 2), a finding consistent with an almost complete absence of the release of AA during platelet activation. The patient's mother and sister exhibited intermediate values for platelet-derived TxB2 and 12-HETE that were below or at the lower end of the normal range.
LTE4 was below the limit of detection of 1 pg/ml in the patient's urine whereas the range of normal values was 19-60 pg/ml.
LTB4 produced by whole blood activated by calcium ionophore from the patient measured 7.2 +- 3.3 ng/ml whereas whole blood from healthy volunteers produced 243.7 +- 22.6 ng/ml LTB4 (Table 2).
COX-1 activity was assessed by measuring production of thromboxane A2 by washed platelets after incubation with [2H8] AA. Both deuterated and non-deuterated TxB2 were quantified, reflecting conversion by COX-1 of exogenous and endogenous substrate, respectively. [2H8] TxB2 levels were similar between the patient and controls, reflecting normal COX-1 activity in the patient's platelets. Platelet activation by exogenous agonists, including arachidonic acid, induces release of endogenous arachidonic acid from cellular storage pools. Notably, non-deuterated TxB2 levels from the patient's platelets were much lower than controls (0.04 vs. 0.51 ng/103 platelets; n=1), indicating an impaired release of endogenous AA.
Platelet function was assessed by monitoring platelet aggregation and dense granule secretion in response to stimulation by ADP or collagen. ADP 5muM and collagen 2 mug/ml were the lowest doses of these reagents inducing granule secretion in all controls. ADP 5 muM induced a diminished aggregation of the patient's platelets compared with controls (n=6), mean 73.0 +- 8.29 vs. 92.67 +- 11.91 maximum % aggregation (p<0.005). Collagen 2 mug/ml also induced less aggregation in the patient, inducing a mean % maximal aggregation of 61.0 +- 14.8 vs. 95.33 +- 15.2 in controls (p<0.005). Notably, ATP release, which is a measure of dense granule secretion, in response to ADP was completely absent in the patient's platelets as opposed to controls which released a mean 0.88 +- 0.33 nmol ATP (p=0.001). ATP release in response to collagen 2mug/ml also was decreased significantly in the patient vs. controls, mean 0.16 +- 0.032 vs. 1.1 +- 0.34 nmol (p=0.002). Normal aggregation and ATP release were observed in the patient's PRP with addition of AA 250 muM.
Immunobloting for cPLA2alpha in the patient's platelets detected protein of expected molecular weight but in diminished quantity (approximately 38% of control). COX-1 was detected in equal amounts in the patient and controls.
The patient's mean total PLA2 activity in sonicated platelets represented 27.2 % of the activity in controls, with mean activity 0.77 +- 0.32 vs. 2.83 +- 0.47 pmol/min/50mug protein (p<0.0005) in controls.
Three transitions encoding non-synonymous codons in the patient's cPLA2alpha alleles were found by sequencing cPLA2alpha cDNA. These included a T to C transition (c.[331T>C]) resulting in a TCT to CCT substitution encoding a Ser to Pro change at residue 111 (p.[S111P]), a G to A transition (c.[ 1454G>A]) resulting in a CGT to CAT substitution encoding an Arg to His change at residue 485 (p.[R485H]) and an A to G transition (c.[ 1952A>G]) resulting in an AAG to AGG substitution encoding a Lys to Arg change at residue 651 (p.[K651R]). The patient was heterozygous for all three transitions and no changes were found in the 3' or 5' untranslated regions. Sequencing of cPLA2alpha cDNA from the patient's mother and sister showed that the mother was heterozygous for the p.[S111P] variant but was homozygous for the p.[R485] and p.[K651] alleles. The sister was heterozygous for both the p.[R485H] and p.[K651R] variants but was homozygous for p.[S111] alleles. This inheritance pattern demonstrates that the patient was compound heterozygous with the p.[S111P] transition on one allele and both the p.[R4885H] and p.[K651R] transitions on the other allele. All of the variants detected in cDNA products were confirmed by direct sequencing of the corresponding segments of genomic DNA. | null | Not supported with pagination yet | null |
PMC9447446_01 | Male | 25 | A 25-year-old Chinese man presented with the edema of the lower limbs and kidney dysfunction two years ago. The patient was then diagnosed as IgA nephropathy, based on the pathologic result of renal biopsy. The serum creatinine level was 222 mumol/L at that time. One year ago, the serum creatinine was increased to more than 600 mumol/L and regular hemodialysis was initiated. The patient was admitted to our hospital in August 2020 for kidney transplantation. On admission, physical examination revealed that multiple lymph nodes were palpable on both sides of the neck, which were painless and mobile. The maximal one with a size of 5 cm x3 cm was on the right supraclavicular fossa of the neck. The tremor of the arteriovenous fistula for hemodialysis on the left forearm was well. The results of a routine peripheral blood test at the time of admission were as follows: hemoglobin 89 g/L, white blood cells 10.80 x 109/L, neutrophil percentage 83.4%, and platelets 490 x 109/L. The serum creatinine was 1429 mumol/L. The computed tomography (CT) scan of the chest and abdomen revealed two inflammatory small nodules of 0.3 cm in the lower lobes of both lungs and reduced sizes of both kidneys. Regular hemodialysis (three times per week) was performed. On the 3rd day after admission, the patient suffered from fever, with a temperature of 38.8 C. The repeated blood test results were as follows: hemoglobin 86 g/L, white blood cells 12.35 x 109/L, neutrophil percentage 77.9%, and platelets 474 x 109/L. The PCT level was 5.73 ng/mL and cefmetazole was prescribed. PCT was measured using the electrochemical luminescence method (VIDAS Brahms PCT, Mannheim, Germany) according to the manufacturer's instructions. On the 10th day after admission, the symptom of fever was not well controlled and the patient still suffered from intermittent fever, with a maximal body temperature of 39.9 C. The PCT increased to 26.7 ng/mL. Antibiotic was upgraded to meropenem accordingly. On the 12th day after admission, although the temperature dropped to below 38 C after adjusting the antibiotic, the PCT increased to 63.10 ng/mL, and the level of C-reactive protein (CRP) was 186.00 mg/L (normal range <5 mg/L). Vancomycin was added. On the 14th day after admission, the biopsy of the lymph node on the right supraclavicular fossa of the neck was performed. On the 17th day after admission, the body temperature dropped to the normal range and remained normal in the remaining duration of the hospital stay. The histopathology result of lymph node biopsy revealed as inflammatory necrosis with granulomatous formation (Figure 1). The acid-fast staining was positive and a small number of DNA fragments of Mycobacterium tuberculosis was detected by Tuberculosis (TB)-qPCR monitoring. On the 21st day after admission, an antituberculosis regimen consisting of isoniazid, rifapentine, ethambutol, and levofloxacin was started and the surgery for kidney transplantation was canceled. The PCT declined gradually to 4.18 ng/mL on the same day and the antibiotics were downgraded to Piperacillin-tazobactam. On the 24th day after admission, the PCT level, dropped to the lowest point in admission monitoring, at 2.9 ng/mL. After that, the PCT increased gradually to 39.4 ng/mL on the 41st day after admission. There was no fever, cough, diarrhea, abdominal pain, frequent urination, and painful urination et al. The count of white blood cells was 4.58x109/L. The level of IL-6 was 8.55 pg/mL (normal range 0-7 pg/mL) and the level of CRP was 11.1 mg/L. The antibiotics were upgraded to meropenem and vancomycin again with the antituberculosis regimen continued. However, there was no marked decline of serum PCT levels. On the 51st day after admission, the PCT level was 94.9 ng/mL. The count of white blood cells was 3.8x109/L. Twice blood cultures were performed and the results were negative. The parasite antigen test was negative. The echocardiography test showed no obvious abnormalities in cardiac structure or blood flow. The thyroid function was normal. The patient was present with no complaint and in good spirit. After another 21 days course of treatment with both meropenem and vancomycin, On the 61st day after admission, the PCT level was 42.6 ng/mL. The count of white blood cells was 3.91x109/L. The levels of IL-6 and CRP were in the normal range (3.02 pg/mL and 4.27 mg/L, respectively). Without the obvious clinical manifestation of sepsis, the antibiotics meropenem and vancomycin were stopped and the patient was discharged from the hospital (Figure 2). However, the antituberculosis regimen was still going on. One month after the discharge, the patient was in a good state and complained no discomfort. He was retested with the PCT of 2.941 ng/mL and the metagenomic Next-Generation Sequencing of pathogenic microorganisms was negative. | bacterial infection, dialysis, procalcitonin, tuberculosis | Not supported with pagination yet | null |
PMC8532220_01 | Male | 10 | A previously healthy 10-year-old Indian boy developed acute onset of weakness and numbness of both lower limbs 7 days before admission. The weakness reached nadir over a period of approximately two days. On the fourth day of the illness, he developed a difficulty in micturition leading to urinary retention while bowel passage was normal. There was a history of fever, vomiting, and headache 2 weeks before admission.
General physical examination was unremarkable. On neurological examination, the child was fully alert, there were no cranial nerve palsies or meningeal signs. Biceps, triceps, and brachioradialis reflexes were normal while knee and ankle reflexes were brisk. Muscle tone was normal, muscle power (MRC scale) for both lower limbs was 1/5. Upper limbs were unaffected. Touch, position, temperature sensations were decreased more in the left lower limb compared to the right, but a clearly defined sensory level could not be identified.
An outside cerebrospinal fluid (CSF) report showed white blood cells (WBC) 258/microL, with lymphocyte 93.4%. A repeat CSF on the following day showed a WBC of 268/microL. CSF PCR for Mycobacterium tuberculosis, Escherichia coli, Haemophilus influenzae, Listeria monocytogenes, Neisseria meningitidis, Streptococcus agalactiae, Streptococcus pneumonia, cytomegalovirus, enterovirus, HSV 1 and 2, human herpesvirus 6, human parechovirus, varicella zoster virus, and Cryptococcus neoformans/gatti were negative. Cerebrospinal fluid PCR for EBV was positive, serum IgG for EBV capsid antigen was positive while IgM was negative. Cerebrospinal fungal stain and culture, oligoclonal bands, anti-aquaporin-4, and anti-MOG tests were negative. Whole spine contrast MRI showed a mild diffuse increase in cord bulk with an intramedullary hyperintense signal on T2 weight images involving the entire length of the spinal cord and conus medullaris, indicating a longitudinally extensive transverse myelitis (Figure 1). Contrast MRI of the brain revealed leptomeningeal enhancement involving the brain and pial surface of the spinal cord (Figure 2).
The patient was treated with a high dose (1 g/day) of intravenous methylprednisolone for 5 days, after which he began to show clinical improvement. It was then continued with oral prednisone (60 mg/day) for 4 weeks and then was tapered off. Ceftriaxone, clindamycin, and azithromycin were also given. He underwent physiotherapy that was continued after discharge. A follow-up CSF examination performed on the seventh day of admission showed a reduction of WBC count to 59/microL and negative EBV PCR.
At the time of discharge, muscle power improved to grade 4/5 on both lower limbs. He started walking a few steps without support. There was no numbness in the lower limbs, bowel passage and micturition were normal. Sensations of touch, position, temperature were normal. He was discharged on oral prednisolone and physiotherapy after nine days of hospitalization (16 days after initial onset). Two weeks after discharge patient regained almost complete mobility. Three months after discharge the child was completely normal and his spine and brain MRIs showed complete resolution of lesions and disappearance of contrast enhancement. | acute transverse myelitis, case report, children, epstein-barr virus | Not supported with pagination yet | null |
PMC6377617_01 | Female | 58 | The patient's course is outlined in Fig. 1a.
A 58-year-old, previously healthy, white female presented to her primary care provider (PCP) with the desire to remove a right posterior scalp cyst for cosmesis. This non-inflamed, non-draining, painless, 1-2 cm cyst had been present for close to 10 years without change in size or fluctuance. The cyst was initially drained by the PCP, but, when it recurred 6 months later, the PCP excised the cyst and sent the specimen for routine pathology. The initial read of the tissue sample was high-grade invasive carcinoma with squamous features and arising in association with a PTT. Based on the pathology, the PCP referred the patient to a plastic surgeon for a more definitive excision of the lesion and repair of the defect. The lesion was excised with negative margins and pathology read as invasive high-grade squamous cell carcinoma (SCC). Eight months post resection, the lesion recurred locally along with a palpable right posterior cervical lymph node (LN). A positron emission tomography (PET) scan at that time demonstrated hypermetabolic activity in the posterior occiput and in a posterior neck LN. Fine needle aspiration (FNA) of both the primary scalp lesion and LN were completed, and pathology was reported as SCC, similar to the primary lesion.
With a working diagnosis of locally advanced SCC, the patient's care was referred to a tertiary care center. There, a dermatopathologist re-evaluated the previous biopsy specimens and altered the diagnosis from SCC to MPTT (Fig. 1b). Subsequently, the patient was referred to a head and neck surgeon for modified radical posterior neck and lymph node dissection. Intraoperative findings uncovered the presence of nodal metastases to the posterior neck with extranodal extension, extensive perineural invasion of the spinal accessory nerve, and jugular venous invasion of the MPTT. After surgery, the case was discussed at a multi-disciplinary tumor board, and a common head and neck cancer protocol of adjuvant chemotherapy (weekly carboplatin plus paclitaxel) with concurrent radiation was recommended. The patient tolerated the adjuvant chemoradiotherapy with expected toxicities including nausea and fatigue.
Fifteen months after her neck dissection (1 year after completing chemoradiotherapy), FNA of a suspicious right paraspinal LN at C5 documented disease recurrence. The patient underwent a revision neck dissection (extending from the sternocleidomastoid, anteriorly, to halfway down the trapezius, posteriorly) with final pathology specimens consistent with metastatic MPTT. A subsequent PET scan demonstrated hypermetabolic activity in a right supraclavicular LN, multiple mediastinal LNs, and in a 0.8 x 1.1 cm right lower lung lobe parenchymal nodule. An endobronchial ultrasound (EBUS) and transbronchial needle aspiration (TBNA) showed involvement of level 4 and 7 mediastinal LN by carcinoma. Molecular profiling of the tissue using a multiplexed PCR assay (SNaPshot) identified a PIK3CA c.G3140A (p.H1047R) mutation. Given the paucity of evidence for this mutation in this cancer, the patient was treated with a standard regimen for metastatic SCC (consisting of docetaxel and cisplatin every three weeks). At the same time, the patient was put on the waitlist for NCT01219699, a phase I study of oral BYL719 (alpelisib, a PI3Kalpha-selective inhibitor) in adult patients with advanced solid malignancies, whose tumors have an alteration of the PIK3CA gene.
Seven months after completion of her second chemotherapy regimen, the patient was found to have progressive metastatic pulmonary disease on routine computerized tomography (CT) scan (she was asymptomatic at this time). The patient then enrolled in the trial of alpelisib at 450 mg daily. Her only suspected adverse effects related to the study drug were nausea and weight loss. After 3 months of treatment, she demonstrated a partial response per RECIST (Fig. 1c and S1). Additionally, an on-treatment research biopsy, obtained 3 months after the start of alpelisib, demonstrated a significant reduction in proliferation as assessed by Ki67 staining (Fig. 1d, e).
Four months after starting the study drug, the patient developed a community acquired pneumonia (CAP), and the treatment was suspended. Although the CAP resolved both clinically and radiographically, the patient was started on 2 L/min oxygen due to a persistent cough that was not responsive to therapy. It was unclear if the patient had progressive disease or a drug-related pneumonitis at this time (although this is not a known adverse effect of alpelisib). Two months after stopping alpelisib, a surveillance CT scan demonstrated peritoneal carcinomatosis. Within days of this CT scan, the patient was admitted to the hospital with increased work of breathing requiring 4 L/min oxygen. The patient opted for no aggressive measures and was symptomatically treated until her death a week later.
Prior to her passing, the patient consented to a rapid autopsy, which revealed the suspected cause of death to be widely metastatic MPTT. There were innumerable metastases in the lungs, the largest being 3.0 x 3.0 x 2.2 cm in dimension (Fig. S2a). Another heavily involved site was the liver, which contained multiple metastases, the largest being 3.5 x 2.5 x 0.6 cm in dimension (Fig. S2b). The cancer also was found to involve a papillary muscle of the heart, the pericardium, fundus of the stomach, ileum, colon, omentum, right ovary, soft tissues of the neck, both adrenal glands, and the pelvic peritoneum. Interestingly, many of the lesions identified at autopsy were not visualized on the CT scan taken two weeks prior to the patient's death. Neuropathology demonstrated no evidence of CNS metastases. No microbiological evidence of pneumonia was found in the lungs, and cultures did not grow any causative pathogenic bacteria or fungi. | null | Not supported with pagination yet | null |
PMC3465890_01 | Male | 41 | On initial outpatient presentation to our community mental health center patient was a 41-year old, college-educated single male, with a twenty-four-year history of severe OCD and depressive symptoms. Other than his former outpatient psychiatrist continuing his monthly prescription for Zoloft he had had no consistent psychiatric followup in the community for over ten years before coming to us. The patient's chief initial complaint was worsening depression in the context of the recent termination of a romantic relationship:the 19-year-old escort he had been seeing on a monthly basis for six months had since refused to take his calls, to respond to his texts, or to see him anymore. The patient had been attending a monthly OCD support group at our center for several months before this and learned of the possibility of individual psychiatric care via Internet search.
The patient had no history of inpatient hospitalization, no history of suicide attempt or other violence. Suffering from obsessive-compulsive symptoms since age 17, he has been receiving state and federal assistance for disability secondary to the disorder since age 28. The patient breaks down his current OCD behavior into four categories: (1) a poking sensation in the jaw as if with a hanger, (2) skin and hair, especially his beard, so obsessed with thoughts of trimming his beard that he often appears thought-blocked during conversation, (3) preoccupations w/scratches on glass surfaces or other surfaces with a sheen, and (4) obsessions with women and ideas of physical perfection.
The patient also has significant hoarding behaviors. Unable to live in his state-subsidized apartment any longer secondary to clutter, he splits his time between his divorced parents' homes. Currently it takes the patient several hours to groom daily; he showers two times per week secondary to the length of time required, moves his bowels every three days for the same reason. He eats one meal a day, never wears a coat, and never exercises. He no longer brushes his teeth due to the time it takes:has monthly cleanings. He no longer masturbates secondary to the lengthy cleaning afterward. He does see an escort about once per month. Though he denies ever having experienced sexual side effects from Zoloft, he takes a med holiday four days before planned sexual activity to maximize the experience. Extremely well read on OCD, the patient often contributes to newsletters; he quotes studies, papers, and authorities frequently.
The patient's depressive symptoms vary with the intensity of particular OCD symptoms, overall well managed on Zoloft. The suggestion of atypical antipsychotics as medication augmentation had previously been met with pleasant but firm resistance. Pt has rituals around medication taking, and this has limited pharmacotherapeutic interventions.
The patient was first diagnosed with OCD at age 17. He reports the onset was sudden, that he was sitting in his high school gym during a film session for football practice when his attention was drawn to a wire coat hanger hanging on the back of a door. He became suddenly and powerfully obsessed with the thought of the hanger uncoiled and poking him in the jaw from the inside out. So vivid was this thought that he reports actually feeling the pain of this. From that point on his obsessions grew and flourished with accompanying, evolving compulsions. The one constant in his history is this poking sensation that has never remitted. The patient, who prides himself on an outstanding memory, has much difficulty recalling the events of his history between ages 17 and 18. He does recall, however, worsening symptoms during his freshman year of college at a top-tier university; he saw therapists and behavioral specialists at two of the top such facilities in the world during his undergraduate years and had multiple med trials at that time, all with modest success.
The patient also reports another especially noteworthy episode during his junior year of college in which he initiated electrolysis treatment in order to manage his facial grooming better. He adamantly denies this was part of any exposure therapy. He reports that during the first minute of his very first treatment he panicked at the sight of redness on his face, a temporary effect of which he had been well warned. He ran from the facility, hyperventilated in his car, and reports that this incident opened the floodgates of anxiety with which he has been struggling since. He has not shaved since.
The patient next saw a psychoanalyst for several years after college, who also placed him on the Zoloft he still currently takes. He intermittently worked in professional capacities in Boston and New York, returning to his parents' home in between jobs, seeing different clinicians in each location. He never sustained employment for longer than a year and never was promoted beyond entry level. He did become involved in romantic relationships as a younger man, none lasting longer than several months. He has seen exclusively escorts since 2005. After the patient was awarded public assistance in 1999, he was unable to afford further treatment, and as he put it, "I was free to explore my obsessions and compulsions to their logical conclusions." The intensity and length of rituals increased substantially. The only therapeutic interaction at this time was his attending various support groups in his region, groups at which he enjoyed taking on a senior role to those with "OCD-light."
The patient has no history of psychiatric hospitalizations. He has no history of suicidality or homicidality, though he frequently talks philosophically/existentially of suicide. Ironically, he points to his atheism as his main protective factor against suicide, stating that he knows this is all he has, and so he would never kill himself. He has no significant substance use history. There is a diffuse history of depression and anxiety on both sides of the patient's family, with patient's mother and maternal grandmother receiving medication treatment.
The patient's medical history is significant for a concussion received while playing football a week before onset of OCD. There was no loss of consciousness or hospitalization, and patient reports no adverse effects otherwise. Otherwise there is no other significant medical history, and patient was taking no other medications.
Developmentally, the patient and his mother deny any pre or perinatal issues. Patient reports toilet training was problematic, though mother denies any issue. There is no history of physical or sexual abuse, though patient states that his father had "a terrible temper," and was "emotionally unequipped to deal with work and a family." At one time stated he "hated" his father as a child. His only sibling is a younger brother, "the picture of normalcy;" he owns his own business, is married, with two young children. Pt reports a positive relationship with his niece, nephew, and sister-in-law, as well as supportive relationships with his mother and brother as a child. His parents both are educators, and he attended public school till 8th grade. He then attended an exclusive private school for high school, repeating his freshman year secondary to "poor adjustment":mother states the patient had difficulty with the transition from public to private school. Patient admits to being keenly aware of the financial discrepancies around him at that school. He was a varsity athlete, with good academic performance after freshman year, no truancy. Despite being in treatment, patient graduated college in four years with an education degree.
The patient, unable to live in his apartment secondary to hoarding, currently lives alternate weeks between his now divorced parents' homes. He still maintains several close friendships from high school and college and entertains aspirations for a literary career. He remains politically engaged, reading up on current issues and maintaining strong opinions, and also remains engaged in the latest literature on OCD. | null | Not supported with pagination yet | null |
PMC4561093_01 | Female | 40 | A previously healthy 40-year-old woman presented with one-week history of diffuse urticarial rash to the dermatology ward which was successfully treated with systemic steroids and antihistamine medications. Three weeks prior to admission, treatment with methimazole 10 mg twice daily had been initiated due to a presumptive diagnosis of Grave's thyroiditis. The diagnosis was made in an outpatient clinic according to typical clinical picture, with low TSH level 0.01 MU/L (normal range 0.35-5.5 MU/L) and high T4 level of 59.1 Pmol/L (normal range 10-20 Pmol/L).
On admission the patient had no symptoms suggestive of hyperthyroidism; on physical examination, an extensive urticarial rash was observed on the limbs and trunk. The patient had a blood pressure of 131/60 mm/Hg, temperature of 36. C, respiration rate of 16 breaths/min, and a pulse rate of 83 beats/min. Her hands were warm and displayed resting tremor. Cardiac examination was normal, but jugular venous distention was noted. Lungs were clear to auscultation. There was no peripheral edema. Extra ocular movements were normal. There was no proptosis or periorbital edema. Thyroid gland was not tender, was slightly enlarged, and had a rubbery consistency on palpation.
Laboratory examinations revealed a white blood cell count: 15.5 x 109 cells/millilitre (normal range: 4-10 x 109 cells/millilitre) with 90% neutrophils and hemoglobin was 12.7 g/dL. On the second day of her hospitalization the patient began to complain of worsening abdominal pain. Liver function tests were taken initially on day two and showed mild abnormality in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gama-glutamil transferase (GGT) levels (86, 72, and 88 U/L, resp.). At this time point, methimazole treatment was discontinued. On the third day of the hospitalization enzyme levels were as follows: ALT 270 U/L, AST 430 U/L, and GGT 210 U/L (normal ranges 0-40 U/L for ALT, 0-35 U/L for AST, and 5-36 U/L for GGT). T4 level was 47 Pmol/L (normal range 10-20 Pmol/L) and T3 level was 5.5 Nmol/L (normal range 1.2-3 Nmol/L).
An abdominal ultrasound showed a large amount of ascites. A diagnostic tap showed fluid with a milky white appearance. Triglyceride level was 12.2 mmol/L (1080 mg/dL), and total protein and lactate dehydrogenase (LDH) levels in ascites were 3.3 g/dL and 326 U/L, respectively. Gram stain was negative for bacteria and fluid cultures were negative. Purified protein derivative (PPD) skin test, acid fast stains of peritoneal fluid, and fluid cultures for tuberculosis were all negative. Serologies for hepatitis A virus, hepatitis B virus, and hepatitis C virus were all negative. Serologies for Epstein-Barr virus and Cytomegalovirus were consistent with prior exposure. Abdominal computed tomography (CT) showed peritoneal fluid, an undefined ovarian mass on the right, and no other abnormalities. Liver size and consistency were normal. Vaginal US did not define the mass better. A lymphangiogram showed no anatomical abnormalities of abdominal lymph vessels or nodes. A gynecological exam was normal, including vaginal ultrasound (US) to define the ovarian mass found on CT scan. The ovarian mass represented a corpus luteum most probably. A follow-up abdominal US after four days showed that the peritoneal fluid had disappeared.
In parallel to this workup the patient started developing signs and symptoms of thyrotoxicosis such as rapid atrial fibrillation which was not present before the discontinuation of methimazole, worsening tremor, and moderate pulmonary hypertension diagnosed with echocardiography. Since treatment with other antithyroid drugs was considered dangerous and since treatment with iodine was expected to have influence only after 4-8 weeks, and the patient had severe symptoms, a therapeutic thyroidectomy was performed two months after admission.
After the procedure the patient was free of symptoms and a follow-up echocardiography showed marked improvement in her pulmonary hypertension. After 1 year of follow-up the patient was asymptomatic, without pulmonary hypertension and with no peritoneal fluid. | null | Not supported with pagination yet | null |
PMC7210701_01 | Female | 28 | A 28-year-old female presented to Fatmawati Hospital, Jakarta, Indonesia due to progressive tetraparesis accounting for seven months. Initially there was mild neck pain, and then she experienced numbness along with weakness of all four extremities. The symptoms were gradually worsened such that at the time of admission, she could not walk.
A series of radiographic and CT scan depicted multiple vertebral body destruction anteriorly, along with facet joint dislocation and mild retrolisthesis of C4-C5 segments (Figs. 1, 2). MR images of the cervical region was demonstrated pathologic contrast enhancement on C4 to T7 vertebrae, a total of fourteen contiguous segments, with spinal canal stenosis on the level of C4 to T4 and bilateral anterolateral paravertebral soft tissue abscess at the level of C4 to T9 (Fig. 3). Those findings were highly typical of spinal tuberculosis.
The patient was administered anti-tuberculous agents for two months before undergoing one-staged posterior-only debridement, decompression, and instrumentation. Postoperative radiographs demonstrated that the kyphosis was obviously improved (Fig. 4). After the surgery, the patient was put on a cervicothoracic brace. The patient was closely followed up, and after 12 months postoperatively, she regained neurological recovery with only mild residual neck pain. The patient demonstrated a satisfying level of functional improvement as recorded by the Neck Disability Index (NDI) and SF-36 scores of 4/100 and 94%, respectively.
Bony bridge on CT images was discovered at 18 months of follow-up, along with the normal value of erythrocyte sedimentation rate and C-reactive protein; it was the time we discontinued the anti-tuberculous therapy. | cervicothoracic spinal tuberculosis, multilevel contagious involvement | Not supported with pagination yet | null |
PMC7378631_01 | Female | 27 | A 27-year-old woman who suffered a high-energy trauma after being hit by a car presents herself to the Emergency Department of a trauma hospital level III with multiple trauma. After initial ABDCE by ATLS, she was suffering from pain in the pelvis, left arm, and both knees. On physical examination, there was deformity and edema in the left arm with functional disability, but without neurovascular changes. The pelvis presented with pain on palpation, but without instability. The knees were quite edematous without blisters and apparent varus deformity bilaterally. Varus stress was positive grade III. She had a negative anterior and posterior drawer exam. Dorsalis pedis and posterior tibial pulses were normal, as well as the neurological examination of the normal lower limb. The skin was intact for all injuries.
Left arm radiographic examination showed a distal third left diaphyseal humerus's fracture that was classified as AO/ASIF (Arbeitsgemeinschaft Osteosynthesefragen/Association for the Study of Internal Fixation) 12 B2C. Radiography of the pelvis showed right pubic branch fracture with minimal deviation (Tile/AO A1). Radiographic examination of the knees showed bilateral avulsion fractures of the fibular head associated with the arcuate signal, being classified as AO/ASIF 41 A19 (Figure 1). For a better definition of the fracture pattern, fragment size, and surgical planning, a CT (Computerized Tomography) scan of both knees was performed (Figure 1). The pelvis fracture was treated nonsurgically. The humerus fracture was initially immobilized, and surgical treatment was performed later with open anatomical reduction and fixation with a dynamic compression plate associated with an interfragmentary screw. Bilateral immobilization on the knees was performed temporarily, and surgical treatment was performed seven days after hospitalization because it was the time needed for edema regression.
The procedure was performed on a radiolucent operating table in a horizontal supine position with spinal anesthesia associated with a regional ultrasound-guided femoral nerve block (LOGIQ S8, GE Healthcare , USA) with a high-frequency linear transducer (8-15 MHz). It was performed pneumatic tourniquet with pressure 100 mmHG above the systolic pressure first on the right side. After the first procedure was finished, the pneumatic tourniquet was deflated and the contralateral side surgical procedure was begun. The posterolateral rotatory drawer maneuver and dial test were performed under anesthesia at this time, which were positive lesion of the posterolateral corner. The first knee to be operated (right knee) was placed at 70 of flexion, while the other (left knee) was in full extension on the radiolucent surgical table. A lateral curvilinear hockey stick incision was made parallel to the posterior aspect of the ITB, curving over the lateral femoral condyle towards distally to the area between Gerdy's tubercle and the anterior aspect of the fibular head. An excessively anterior incision in the skin makes access and dissection of the common fibular nerve difficult. Initially, the common fibular nerve was dissected and isolated, leaving it marked with a cardiac tape without any traction.
Fibular head's comminuted fracture with the conjoint tendon (biceps femoris long head and lateral collateral ligament) inserted without injury was identified. Also, it was observed a single large fragment of the lateral edge of the tibia with an ALL complex inserted without injury. Krackow suture was performed with No. 5 ethibond thread in the conjoint tendon together with the posterolateral ligament complex (Figure 2(a)). The tibial fragment was provisionally fixed with three 2.0 Kirschner wire and, after checking the reduction, definitively fixed with two 4.5 mm cannulated screws and two washers (Medtronic Sofamor Danek Inc., Memphis, TN, USA). Transosseous tunnels were performed in the fibular head (10 mm distal to the fracture line and were 15 mm away from each other) to fix the posterolateral ligament complex (Figure 2(b)). On the left knee, the exact same access was used. Isolation of the fibular nerve and cardiac tape marking was performed. Multifragmentary fracture of the lateral edge of the tibia with the insertion of the integral ALL complex was observed, as well as fibular head avulsion fracture with multiple microfragments with an intact conjoint tendon. Krackow suture was performed in the conjoint tendon together with the posterolateral ligament complex (PLC) and another suture, separately, in the iliotibial band (Figure 2(c)). Transosseous PLC fixation was performed on the fibular head, and the main fragments were fixed on the lateral margin of the tibia with 1.5 Kirschner wires. The ALL complex was fixed by a pull-out technique, creating a transtibial tunnel and tied to a 3.5 DCP plate (Medtronic Sofamor Danek Inc., Memphis, TN, USA) in an anterior cortex placed through anterior mini access (Figure 2(d)). Control radiography was performed intraoperatively on both knees (Figure 3).
The postoperative period was performed with a specific physiotherapy protocol similar to that used for PLC ligament injuries. In the immediate postoperative period, the knees were kept in an articulated brace with a range of motion (ROM) gradually allowed (1-2 weeks: 0 -60 ; 3-4 weeks: 0-90 ). After the 5th week, progression occurred to complete ROM in order to avoid arthrofibrosis. Isometric exercises of quadriceps, hamstrings, sural triceps, and anterior tibialis, as well as active and passive range of motion of the hip, knee, and ankle, were performed from the first postoperative day. In relation to the other lesions, she developed a slight superficial infection of the surgical wound on his left arm in the immediate postoperative period, which was treated only with serial dressings and an oral antibiotic for 5 days. Pubic branch fracture remained well throughout the follow-up, with no deviation. Weightbearing was not allowed in the first four weeks. The brace was discontinued after the first month, being used only during weight-bearing which was started after thirty days of surgery with two axillary crutches. Full weight-bearing was allowed only after two months of surgery. Outpatient returns were performed 15, 30, 60, 120, and 180 days after surgery.
The patient evolved well in the late postoperative period, showing fracture consolidation after three months of surgery. She had normal walking with a full range of motion of the hip, knee, and ankle (Figure 4). She did not present anteroposterior instability to the stress tests (Lachman, anterior drawer, posterior drawer, and pivot shift), nor valgus and varus instability. She felt no pain after 3 months. She returned to his usual sport (volleyball) after 180 days with a Lysholm functional score 15/95 points (excellent). | null | Not supported with pagination yet | null |
PMC8192798_01 | Male | 58 | A 58-year-old, asymptomatic male presented to our hospital (Lishui Municipal Hospital, Lishui, China) for a physical examination. Written informed consent was obtained from the patient for the publication of the present study. The patient had no history of cigarette smoking, hypertensive disease, diabetes mellitus, hepatitis or tuberculosis. Routine blood, liver function, renal function, blood glucose, coagulation function and serum electrolyte test results were all within the normal range. Enhanced computed tomography (CT) (Philips, Brilliance ICT CP 200063) of the chest showed a 3.5 x 3.1-cm mass in the posterior mediastinum, and no other lesions were identified in the thoracic cavity (Figure 1).
A contrast-enhanced CT scan showed an enhanced mass with homogeneous internal density and clear tumor boundaries. A preoperative diagnosis of schwannoma was considered due to the enhanced CT features. Right-side video-assisted thoracoscopic surgery (VATS) was performed under general anesthesia due to the possibility that the mass was malignant. The 4th intercostal incision in the right axillary front was ~3 cm wide and was used as the operating hole; the 7th intercostal incision in the right midaxillary line was ~2 cm wide and was used as the observation hole. Intraoperatively, the tumor had clear boundaries, no invasion of surrounding tissues, and slight toughness. There was no evidence of intraspinal extension of the tumor. The boundary of the tumor was carefully separated with an ultrasonic knife, and the tumor was completely excised. The operation time was 20 min, and the bleeding volume was 20 ml. A chest tube was placed and removed 2 days after the operation. The surgical margins of resection were microscopically negative. Pathological examination revealed the presence of angiosarcoma (Figure 2A) and schwannoma (Figure 2B) components. Immunohistochemical staining for cluster of differentiation (CD) 31 (Figure 2C), CD34, EGR, vimentin, SOX-10 (Figure 2D) and S-100 was strongly positive. The patient rapidly recovered and was eventually discharged. Two months post-surgery, the patient returned for chest CT and had no evidence of tumor metastasis or recurrence (Figure 3 and see timeline in Figure 4). | angiosarcoma, mediastinum, schwannoma, surgery, thoracoscopic | Not supported with pagination yet | null |
PMC1242218_01 | Female | 0 | A forty-year-old housewife, from a very low socio-economic status group, presented with history of gradually progressive weakness of left lower limb of 6 months duration, rapidly progressive weakness of right lower limb of 8 days duration and urinary incontinence of 6 months duration. She had been living near a very unhygienic abattoir and admitted to drinking unpasteurised goat's milk. There was history of fever on and off with night sweats. There was no history trauma or past history of tuberculosis. On examination, she was moderately built and nourished. General physical examination was normal. She was febrile with a temperature of 99 F (37.2 C). Vital parameters were normal. Neurologically she was conscious, alert and orientated. Cranial nerve examination was normal. There was no papilledema and meningeal signs were absent. She had flaccid areflexic paraplegia with power 0/5 (MRC grade). She had impaired sensations in both lower limbs with a level at T10. Perianal sensations were impaired and she had poor anal tone. Routine haematological parameters revealed a total white blood cell (WBC) count of 13,980/cu mm with neutrophil predominance. Erythrocyte sedimentation rate ESR (Westergreen) was 50 mm in 1 hour. Standard agglutination test (tube) titer was 1:320 and 2-mercaptoethanol agglutination test titer was 1:80. Plain radiograph of lumbosacral spine was normal. MRI scan of the spine showed a lesion in the spinal cord extending from lower part of T12 to L2. It was hyper-intense on T1WI and iso-intense on T2WI There was cord edema extending cranially up to T10 (figure 1).
She underwent T11 to L3 laminectomy. The lower end of the cord and the conus medullaris were swollen and the cauda equina nerve roots were pushed to the right side. Myelotomy was done at the conus level. At a depth of about 0.5 cm, purulent fluid was encountered, which was sent immediately for microbiological analysis. Under operating microscope the abscess cavity was visualized through the limited myelotomy (fig 2). The abscess was completely evacuated, after which the cord and conus had become lax and pulsating well. Dura was closed completely.
Pus revealed gram-negative bacilli. It was inoculated aerobically [Brucella agar, chocolate and MacConkey media], and anaerobically [Kanamycin-vancomycin laked sheep blood agar (KVLB) and Bacteroides bile esculin agar (BBE)]. Brucella agar and CA were incubated in CO2 jar and after 2 days minute translucent colonies were seen. Gram stain from culture showed gram-negative bacilli. Oxidase, catalase, and urease test were positive. There was no H2S production and it was resistant to dye inhibition. The organism was confirmed as Brucella melitensis . The organism isolated in blood culture taken preoperatively, also was identified as Brucella melitensis.
Postoperatively she had fever, headaches and vomiting lasting for about 1 week. It subsided once antibiotics were instituted. She was started on injection streptomycin 1 gm once a day for 1 month with oral doxycycline 100 mgm twice a day for 1 month. After one month she received oral rifampicin 450 mgm once a day with oral doxycycline 100 mgm twice a day for 1 month. Dexamethasone was given only perioperatively and was rapidly tapered and stopped in the post-operative period. Post operatively she gradually improved in neurological status. At 2-year follow up she had grade 3/5 power in both lower limbs and was mobilising on a wheel chair. The urinary symptoms did not resolve and she continues to be on Foley catheter. She refused a repeat MRI scan, as she could not afford it. | null | Not supported with pagination yet | null |
PMC5035335_01 | Male | 37 | A 37 year old male presented in a tertiary care University Hospital with the chief complaint of prolonged fever after return from a business trip to Malaysia. While in Malaysia, the patient developed an episode of diarrhea for 4 days followed by high fever, rigors and malaise. He described a self-resolved similar episode in a co-traveler that lasted for 5 days.
He returned to Greece on the fifth day of his syndrome. Five days later, due to prolonged fever, he was admitted to the department of Medicine at a tertiary care university hospital. He reported no significant medical history and was receiving no medications at the time of evaluation.
The physical exam was unremarkable, except for a temperature of 39 C, a blood pressure of 120/80 mmHg, a heart rate of 88 beats per minute and an oxygen saturation of 97%. The abdominal examination revealed no tenderness or organomegaly. There were no enlarged peripheral lymph nodes, joint findings or rash.
Laboratory work-up at admission revealed polymorphonuclear leukocytosis with 25,800 white blood cells (82% polymorphonuclear cells, 11% lymphocytes, 5% monocytes, eosinophils 2%), Hct: 35.7% and CRP: 198 mg/L (normal < than 6 mg/L). He was admitted to the hospital for investigation and treatment. During his stay he underwent an extensive evaluation including: a) repeat complete blood testing that disclosed persistent leukocytosis, a severe normocytic anemia with a hematocrit as low as 25% (that required administration of 3 packed red blood cell units), thrombocytosis (as high as 594 x 109/L) and an elevated CRP (as high as 234 mg/L) and erythrocyte sedimentation rate of 100-110 mm/hour; b) multiple blood, stool and urine culture sets were taken that were negative for any pathogen; c) repeat stool cultures that were negative for Salmonella spp., Shigella spp., Yersinia spp., Campylobacter spp. and Aeromonas spp.; d) repeat stool ova and parasite testing that was negative for parasites; e) negative stool culture for C. difficile as well as negative C. difficile toxin assay; f) negative Giardia lamblia, cryptosporidium and entamoeba antigen; g) negative interferon gamma release assay; h) negative HIV, HTLV I and II, CMV, EBV, Echinococcus granulosus, Toxoplasma gondii, Brucella melitensis, leishmania spp, syphilis, hepatitis A, B and C serologies and; i) a bone marrow aspirate examination with normal results.
The patient did not respond to several courses of antimicrobials including sequential use of ciproflocacin and metronidazole followed by piperacillin-tazobactan, followed by meropenem with vancomycin, and last a combination of docycycline and gentamycin.
A computed tomography of the abdomen revealed multiple enlarged and necrotic mesenteric lymph nodes, and edema in the wall of the distal ileum and the entire colon. A colonoscopy showed aphthous ulcerations in many parts, especially in the cecum, the ileocecal junction and the first part of the terminal ileum; histology was nonspecific. Twenty days into his course a new CT scan disclosed exacerbation of the disease with a lot of enlarged necrotic mesenteric lymph nodes and 2 focal deformities in the spleen about 1 cm in size. By this time the patient developed arthritis in the left ankle joint and an atypical bilateral rash in the shins resembling nodular panniculitis. At that point a quadruple anti-tuberculous regimen was initiated. Tissue samples obtained during an exploratory laparotomy from the abnormal mesenteric lymph nodes, showed acute purulent and focally granulomatous suppurating lymphadenitis with extension of acute inflammation into the perinodular mesenteric fat adjacent adipose tissue; PAS and Grocott stains disclosed no fungi, whereas PCR for Mycobacterium tuberculosis was negative.
The patient was diagnosed with aseptic abscesses syndrome and was treated with systemic administration of corticosteroids (40 mg of prednisone) together with methotrexate (15 mg/week). After tissue PCR results came back negative for TBc, the anti-TBc regimen was discontinued.
The patient had an excellent response to the immunosuppressive treatment with rapid clinical improvement with restoration of all his abnormal laboratory parameters during a 6 month follow-up. He is followed by a gastroenterologist for the possibility of development of inflammatory bowel disease. | diarrhea, gastroenteritis, post-travel, “septic abscess” | Not supported with pagination yet | null |
PMC3656671_01 | Male | 45 | A 45-year-old man was admitted to our hospital with a series of focal and generalized epileptic seizures. Initial clinical presentation showed a disoriented patient with left-sided tongue bite. Neurological examination disclosed paresis of the left hand. Laboratory results were normal apart from low potassium and low haemoglobin levels. ECG and thoracic X-ray were also unremarkable. Computed tomography of the brain showed a haemorrhagic partially calcified lesion in the right parietal lobe. Subsequent MRI studies revealed a haemorrhagic transformed and space-occupying lesion diagnosed as a cavernoma (fig. 1, fig. 2). According to the clinical symptoms and the anatomical correlation, the cavernoma was the underlying lesion responsible for the new onset of focal epileptic seizures.
The patient's previous medical history included intensive treatment with various chemotherapeutic agents including cytarabine/idarubicin (first cycle), cytarabine/amsacrine (second cycle) and cytarabine/etoposide (third cycle) for the treatment of acute myeloid leukaemia (AML), subtype M2, in 1999. After early bone marrow recurrence in March 2000, he received reinduction chemotherapy (S-HAM) and an allogenic HSCT in July 2000. As part of the therapy, he was treated with TBI with 12 Gy in 6 fractions. After diverse infections (sinusitis, invasive pulmonary aspergillosis and mucositis) he finally achieved complete remission. Later on, he suffered from treatment-related secondary arterial hypertension most probably due to cyclosporine-associated renal impairment. He frequently complained about headaches which led to a first cerebral MRI in 2006 to exclude secondary causes. The MRI scan was entirely normal, without evidence of vascular lesions (fig. 3). Until 2011, neither a neurological evaluation nor a further radiological evaluation was performed.
According to the well-documented history including former cerebral MRI studies, we speculate that the newly diagnosed cavernoma in 2011 was triggered by TBI. | de novo cavernoma, radiation-induced cavernoma, total body irradiation | Not supported with pagination yet | null |
PMC7597567_01 | Female | 87 | An 87-year-old Japanese woman was transferred to our emergency room with a right hip pain after she fell in her nursing home in April 2020. In Japan, up to 5000 patients were COVID-19 positive, the beginning of COVID-19 outbreak, and one-fifth of patients were from our province at the time. She had past history of controlled arrhythmia and had no dementia. She had no history of fever, fatigue, or respiratory symptoms within the 14 days before presenting to our hospital. Physical examination on admission revealed: body temperature, 36.8 C, peripheral oxygen saturation (SpO2), 94% under room air; respiratory rate, 16 breaths/min; blood pressure, 169/66 mmHg; and heart rate, 57 beats/min. Tenderness was noted in the right Scarpa's triangle and greater trochanter of the femur, accompanied by limited range of hip motion due to pain. Blood testing showed elevations in C-reactive protein (0.55 mg/dL) and white blood cell count (12,000 cells/mm2) with neutrophilia (80.3%) and lymphopenia (14.3%). Radiography showed right femoral intertrochanteric fracture (AO/OTA classification: type 31-A2.3) (Figure 1A,B), and only 2 nodular shadows in the upper lobe of the left lung (Figure 1C). Given the global COVID-19 pandemic, chest computed tomography (CT) was performed on admission and showed ground-glass opacities with consolidation in the dorsal segment of the right lower lung field. From this CT image, aspiration pneumonia was speculated as a diagnosis (Figure 1D-I). However, to confirm whether the pneumonia was due to COVID-19, qualitative real-time reverse-transcriptase-polymerase-chain-reaction (RT-PCR) assay testing for severe acute respiratory syndrome coronavirus (SARS-CoV-2) from nasopharyngeal swabs was carried out, yielding a positive result. Femoral intertrochanteric fracture with concomitant COVID-19 infection was thus diagnosed.
Because of the infection, conservative treatment was applied to the fracture and delayed operation was planned. Rehabilitation under partial weight-bearing was started after hospital admission. On day 2, temperature increased to 37.4 C, and low SpO2 (<90%) appeared, required supplemental oxygen (1 L/min) by day 5. The patient recovered from the disease and was free of oxygen by day 10, and RT-PCR testing yielded negative results on both day 14 and day 16. Full weight-bearing was permitted from day 14. At this moment, the patient was able to ride a wheelchair and she had no hope for surgical treatment. Therefore, conservative treatment was continued. No recurrence of positive RT-PCR was seen on day 28, and she was returned to her welfare facility, able to use a wheelchair as she had before. Treatment was ongoing and she showed no other complications such as infection, dementia or deep vein thromboses. Throughout the treatment period, no cross-infection from the patient was identified in our hospital.
This case report was produced in accordance with the CARE reporting guidelines. | asymptomatic covid-19, chest ct, coronavirus infection disease 2019 (covid-19), femoral intertrochanteric fracture, geriatric trauma, real-time reverse-transcriptase-polymerase-chain-reaction (rt-pcr) | Not supported with pagination yet | null |
PMC6458939_01 | Male | 25 | A 25-year-old man from Ghana was admitted to our hospital for an altered mental state, weight loss, neck pain, cough, fever, nausea, vomiting, and photophobia for 7 days. He reported a cough with greenish phlegm and blood-tinged sputum and a weight loss of ~20 lb in the last month. He reported that he could not eat because he was always nauseous and experienced nonbilious, nonprojectile vomiting. He denied chest pain, difficulty breathing and swallowing, diarrhea, dysuria, and skin rashes. His past medical history included intermittent asthma and migraines, but he was not on any medications. He did not have any significant family history or prior surgeries. He reported that he smoked 10 cigarettes a day for the past 5 years, drank alcohol occasionally, and denied illicit drug use except for marijuana. He reported that he last traveled to Ghana 6 months priorly, and he denied having contact with sick persons. He reported that he was sexually active with many partners but denied any prior sexually transmitted diseases.
Examination revealed a cachectic young male with a heart rate of 102 beats/min, a blood pressure of 108/69 mmHg, a respiratory rate of 20 breaths/min, a temperature of 98 F, and a 96% oxygen saturation in ambient air. He had a body mass index of 19.2 kg/m2 and was lethargic but oriented. He had no icterus or cervical or axillary lymphadenopathy. He had clear bilateral breath sounds, and his cardiovascular and abdominal examinations were unremarkable. He had a good pulse and no peripheral edema.
On admission, the patient tested positive for HIV with a CD4 count less than 20 and a high viral load. Pneumonia and meningitis resulting from opportunistic infections were considered, and he was treated for bacterial meningitis and tuberculosis (TB) even though the lumbar puncture was delayed because the patient was restless and uncooperative. The lumbar puncture results showed a pressure of 23 cm H2O, a white blood cell count of 2, a red blood cell count of 57, a protein level of 102 mg/dl, and a glucose level of 25 mg/dl. The Gram stain and bacterial antigen tests were negative.
There was a high suspicion of pulmonary TB and tuberculous meningitis due to recent travel to Ghana, and the initial chest X-ray showed multiple nodular opacities suggestive of miliary TB (Figure 1(a)). The micronodular appearance was confirmed by a chest CT scan without contrast (Figure 1(b)). Despite a quantiFERON negative test result, quadruple therapy for TB with isoniazid, pyrazinamide, ethambutol, and rifampin (RIPE) was continued.
On succeeding days, yeast was growing in the patient's blood cultures and a Gram stain of the patient's cerebrospinal fluid (CSF) showed presence of yeast cells. The titer of Cryptococcus in the CSF was greater than 1 : 1024 and was eventually identified as Cryptococcus neoformans. Thus, antibacterial meningitis treatment was discontinued, and the patient was started on amphotericin B and flucytosine. Anti-TB medications were continued. He underwent placement of a lumbar drain due to a persistent headache and photophobia. Antiretroviral treatment was not started, but the patient was treated with prophylaxis medications for opportunistic infections. At this time, the patient had four persistently negative acid-fast bacilli sputum smears and was negative for the sputum Mycobacterium tuberculosis PCR test.
The patient underwent FFB with BAL and TBBx. In the BAL, >100,000 CFU/mL of Staphylococcus haemolyticus grew; thus, the treatment for bacterial pneumonia was modified. Tissue culture and TBBx showed the presence of Cryptococcus neoformans. Higher magnification microscopy showed the presence of both hyphae and yeast cells (Figures 2(a) and 2(b)). The patient showed clinical improvement and was discharged on oral fluconazole. | null | Not supported with pagination yet | null |
PMC7298644_01 | Female | 77 | A 77-year-old African American female with hypertension and rheumatoid arthritis on chronic prednisone therapy presented to the hospital with fever, weakness, and unsteady gait. The patient had a history of latent tuberculosis infection reportedly treated over 15 years ago, and abdominal lymphadenopathy with granulomatous histology of unknown etiology three years ago. Laboratory testing showed normal hemoglobin, elevated leukocyte count of 35,000 cells/muL, and normal C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Her liver and kidney function were normal, and electrolytes were within normal limits. Physical examination revealed high fever and limited left hip mobility due to weakness and pain. Computed tomography of the hip joint revealed progressive destruction of her sacroiliac joint and a 10 x 8 x 7-centimeter (cm) fluid collection in front of her left iliopsoas muscle (Fig. 1, Fig. 2). A presumptive diagnosis of pyogenic sacroiliitis and psoas abscess were made and the patient was placed on broad-spectrum antimicrobials.
The patient underwent saucerization and partial excision of her left ilium and sacrum, surgical placement of antimicrobial beads, and drainage of the psoas abscess. Biopsy from the bone and drainage from the psoas abscess were also sent for further evaluation. The bone biopsy revealed ill-defined granulomas and the gram stain, AFB stain, GMS stain. and bacterial cultures of the psoas drainage were negative. Samples were sent for tuberculosis and fungal cultures. One out of four blood culture bottles grew Enterococcus faecalis sensitive to ampicillin. Given that all other testing was negative, the patient was sent to a nursing home with intravenous ampicillin therapy for a six-week course. Two days after completing treatment, the patient presented to the hospital again with recurrence of symptoms especially with nightly high fevers and weakness. Laboratory findings were only significant for an elevated WBC of 12,000 cells/muL. CT revealed healing sacroiliitis, no obvious new abscess, and post-surgical placement of antimicrobial beads (Fig. 3). Initial consideration was incomplete treatment given the timing of the symptoms after cessation of antimicrobials; however, the previous AFB culture coincidentally was found to be positive in the seventh week, and TB was confirmed by PCR from the culture positive samples. During the initial encounter,the patient underwent a CXR as a routine work up which didn't show any infiltrates; however during further work up after the AFB culture, a CXR was repeated and revealed new right upper lobe infiltrates suggestive of pulmonary tuberculosis (Fig. 4).
The patient did not present with respiratory symptoms; however, she was placed in respiratory isolation and sputum was tested for AFB. She was started on rifampin, isoniazid, pyrazinamide and ethambutol (RIPE) therapy, with the addition of moxifloxacin to also cover for multi-drug resistant tuberculosis (MDR-TB). The patient's fever subsided after one week of treatment, and after two weeks of treatment she markedly improved and had negative AFB smear and PCR on induced sputum. She was released from isolation precautions and discharged with follow up with the public health department. At the time of discharge, the patient exhibited functional decline and deconditioning due to prolonged hospital stay as well as chronic debilitating illness. She was assessed by physical therapy using Barthel Index score which is a measurement of activities of daily living and revealed a value of 45 points and partially independent. She was placed in a sub-acute rehabilitation facility after inpatient hospital discharge. | diagnostic delays, iliopsoas abscess, musculoskeletal tuberculosis | Not supported with pagination yet | null |
PMC4756250_01 | Male | 79 | A 79-year-old man with a past history of diabetes mellitus and tuberculosis presented with decreased visual acuity on the right side and was diagnosed with retrobulbar optic neuritis. Medical treatment with a steroid (prednisolone 40 mg/day) was initiated and continued for 2 months but provided no symptom relief and subsequently resulted in a recurrence of tuberculosis. The steroid was discontinued, antituberculosis therapy was initiated. As the patient's cognitive function began to decline 2 weeks later, cerebrospinal fluid (CSF) examination and MRI were performed. A CSF examination showed an elevated cell count and the protein level (cell count: 139/dL, glucose: 72 mg/dL, protein: 101 mg/dL) and was positive for the Aspergillus antigen. Fluid attenuated inversion recovery (FLAIR) imaging revealed an isointense lesion in the right side of the sphenoid sinus and a high-intensity lesion spreading at the bottom of the bilateral frontal lobes (Fig. 1A, B). Based on these findings, a diagnosis of fungal meningoencephalitis due to intracranial extension of Aspergillus sinusitis was made.
Antifungal therapy with amphotericin B was started, but it was subsequently changed to micafungin because of an adverse effect on renal function. Follow-up CSF examination and MRI performed 26 days after starting of antifungal therapy showed decreased CSF cell counts (cell count: 6/dL, glucose: 71 mg/dL, protein: 130 mg/dL), some shrinkage of the sphenoid sinus lesion, and a de novo right ICA aneurysm projecting anteriorly into the sphenoid sinus at the C3 portion (Fig. 1C). It was noted that bilateral anterior cerebral arteries (ACAs) distal to the anterior communicating artery (AcoA) were pooly visualized, suggesting the presence of arterial stenosis caused by frontal base meningoencephalitis. Because a three-dimensional computed tomography (3D-CT) angiogram taken 5 days later showed rapid growth of this fungal aneurysm (from 9 mm x 3 mm to 11 mm x 10 mm) (Fig. 1D), we planned an emergency operation to prevent the aneurysm rupturing, which might have resulted in fatal epistaxis. Pre-operative single photon emission computed tomogram (SPECT) showed presence of a hypoperfusion area in the anterior cerebral artery distribution (Fig. 1E).
Under endotracheal general anesthesia, a high-flow bypass from the external carotid artery to the M2 portion of the middle cerebral artery (MCA) was established on the right side using a radial artery graft following a superficial temporal artery (STA) - MCA assist bypass to the M4 portion distal to the anastomosis site of the high-flow bypass. Subsequently, the right ICA was trapped between its origin in the neck and the C2 portion of the ICA. A marked granulomatous change was seen in the dura mater in the frontal base. The right ophthalmic artery was involved in the trapping, as the patient's right visual acuity consisting of only light perception just before the operation. We believed that performing anterior clinoidectomy to expose the ophthalmic artery might further accelerate the intracranial invasion of Aspergillus species. Finally, we anastomosed the frontal branch of the STA to the cortical branch of the right ACA to increase perfusion in its territory.
The patient's postoperative course was uneventful. MRI taken 4 days after the operation showed patency of both the radial artery graft and the frontal branch of the right STA (Fig. 2A). There was no new cerebral infarction. The right ICA had been obliterated and the aneurysm was not visualized. Post-operative SPECT taken 2 weeks after the operation showed improved perfusion in the right anterior cerebral artery distribution (Fig. 2B). Antifungal treatment was continued with itraconazole until plasma concentrations of beta-D-glucan had decreased to within normal limits. Fifty-five days after the operation, the patient was transferred to a rehabilitation hospital because of persisting cognitive function impairment. | null | Not supported with pagination yet | null |
PMC8822337_08 | Male | 10 | A 10-year-old, male castrated domestic shorthair cat weighing 8.9 kg was presented for a 6 week duration of worsening stridor, wheezing, intermittent coughing and terminal retching exacerbated by exercise and stress. Tracheal auscultation revealed loud referred upper airway sounds. Thoracic radiographs revealed a 3 cm soft-tissue mass at the level of C3-C5 invading and occluding 85-90% of the tracheal lumen. There was a mild bronchial-unstructured interstitial pattern in all lung fields. An esophagram ruled out extraluminal compression by an esophageal mass. Cervical ultrasound showed circumferential involvement of the trachea with intraluminal invasion (Figure 1). Evaluation of fine-needle aspirate samples from the mass was suspicious for a carcinoma. The cat was discharged with directions for hospice care, including piroxicam (2.5 mg PO q24h) and was humanely euthanized 14 days later. Necropsy confirmed the presence of a circumferential tracheal mass with intraluminal invasion (Figure 2). The tumor was submitted for histopathology and subsequent immunohistochemistry (Figures 3 and 4). Samples were fixed in 10% buffered formalin for up to 48 h, trimmed, routinely processed for histology, embedded in paraffin, cut at 5 mum and stained with hematoxylin and eosin.
Immunohistochemistry required additional formalin-fixed, paraffin-embedded sections of the tracheal tumor for staining using anticytokeratin (AE1/AE3) antibodies. These slides were cut at 5 mum on charged slides, air-dried and then heated at 60oC for 15 mins. Slides were then deparaffinized with xylene and rehydrated through graded ethanols to deionized water. Antigen sites were unmasked using proteinase K (Dako) treatment at room temperature for 5 mins. Slides were then rinsed in Tris-buffered saline/Tween (TBST) at pH 7.6 for 10 mins before being loaded onto the Dako Autostainer, where all procedures are performed at room temperature and all slides are rinsed with TBST between the following steps. Endogenous blocks were performed by treating slides with 3% hydrogen peroxide for 5 mins followed by a serum-free protein block (Dako) for 5 mins. Mouse cytokeratin AE1/AE3 primary antibodies (1:800) were applied and incubated for 30 mins. A horseradish peroxidase-labeled polymer system (Dako EnVision+System) was applied for 30 mins followed by a 10 min application of 3,3'-diaminobenzidine chromogen (Dako). All slides were then taken off the Dako Autostainer, rinsed in deionized water, then counterstained with hematoxylin for 5 s. Slides were blued in ammonia water, then dehydrated through ethanol, cleared with xylene and coverslipped. Negative control slides were processed Universal Negative Control+ mouse serum instead of primary antibodies. Cytokeratin (AE1/AE3) was validated by using respiratory epithelium and the mixed tracheal glands as in internal control within the examined slide.
The neoplasm in this case was a carcinoma representative of epithelial origin with defined cellular nests but no definitive glandular structures to further categorize it as an adenocarcinoma. It is possible that this neoplasm was a poorly differentiated adenocarcinoma or may represent a malignant transformation of tracheal epithelium consistent with a primary tracheal carcinoma. The latter would represent a unique tumor described in the cat. | null | Not supported with pagination yet | null |
PMC9114638_01 | Male | 40 | A previously well 40-year-old Indonesian male presented with transient loss of consciousness following a fall-from-standing height while working as a sailor aboard a ship. He sustained traumatic brain injury (TBI) with subarachnoid and subdural hemorrhages and multiple facial fractures with raised serum creatine kinase 1014 U/L (NR <210U/L). His initial Glasgow coma scale score was 14. His injuries were managed conservatively. His initial serum sodium concentration was 140 mmol/L with normal renal panel and serum potassium 3.8 mmol/L. Full blood count and liver function test were unremarkable. Intravenous (IV) 0.9% sodium chloride (NaCl) infusion 2L/day was given for the first 3 days of admission in view of the significantly raised creatine kinase worrisome for early-onset rhabdomyolysis. However, serum sodium progressively fell to 125 mmol/L, and he was referred to the Endocrinology service on day 8 of admission (D8). His vital signs were stable with no hypotension or tachycardia (heart rate 81 beats/min, blood pressure 133/87 mmHg). He was clinically euvolemic with moist mucous membranes, clear lung fields on auscultation, and no peripheral oedema. Investigations revealed hypo-osmolar hyponatremia with markedly elevated urine sodium (144 mmol/L) and urine osmolality (1,045 mOsm/kg). His renal and thyroid function were normal and peak serum cortisol was normal (611 nmol/L) after a 1mcg ACTH-stimulation test. The clinical impression was SIADH from TBI. Intravenous sodium chloride drip was stopped, and he was restricted to 750 ml of fluid per day and given additional sodium chloride tablets (up to 272 mmol/day). Urine sodium concentration was persistently high even after saline infusion drip was discontinued (Figure 1).
Despite strict fluid restriction, his serum sodium continued to downtrend to 121 mmol/L (Figure 1). Urine sodium concentration (132-164 mmol/L) and urine osmolality (569-613 mOsm/kg) remained significantly raised. Differential diagnoses for the etiology of his refractory hyponatremia included (a) mild central hypocortisolism post-TBI, (b) SIADH, and (c) CSW. Although initial peak cortisol response to 1-mcg ACTH stimulation test exceeded 500 nmol/L with normal ACTH levels, this did not rule out acute central hypocortisolism precipitated by the recent TBI due to preserved adrenal tissue to external ACTH stimulation during acute pituitary injury. Thus, an insulin tolerance test was performed to assess the hypothalamic-pituitary-adrenal axis. He received 0.35 u/kg of regular insulin and achieved symptomatic hypoglycemia (plasma glucose 2.4 mmol/L) with a peak cortisol level of 502 nmol/L. The test was stopped prior to achieving the target of plasma glucose <2.2 mmol/L because the patient could not tolerate the hypoglycemia symptoms. In view of borderline cortisol response and the declining sodium concentrations, a trial of IV hydrocortisone replacement was started, but this did not result in an improvement of hyponatremia. The hyponatremia did not fulfill the criteria for CSW because he was clinically euvolemic with normal serum urea and creatinine and he did not have polyuria. Intravenous fluid administration worsened the hyponatremia. Fractional excretion of uric acid (FeUA) performed on D22 of admission was low at 9.29% (<11%) when patient was euvolemic was suggestive although not specific for SIADH. A repeat FeUA on D27 admission was still low at 7.98%.
Despite fluid restriction, high load of sodium chloride tablets and hydrocortisone, serum sodium fell further to 119 mmol/L with persistently raised urine sodium (110 mmol/L) and urine osmolality (844 mOsm/kg) and the patient reported worsening vertiginous giddiness associated with nausea. His renal function remained normal without potassium or magnesium derangement throughout the admission. In view of symptomatic hyponatremia, he was given 150 ml of IV 3% NaCl which transiently raised serum sodium level to 122 mmol/L. However, serum sodium level decreased to 119 mmol/L the next day (D22). Sodium chloride tablets were increased to 24 tablets daily and a decision was made for trial of oral fludrocortisone 0.05 mg (D22). This led to significant improvement in serum sodium to 127 mmol/L with a mild decrease in urine sodium from 155 to 139 mmol/L (D23) although the rise may not be attributed solely to fludrocortisone, in view of the relatively minor decrease in urine sodium concentration, and the subsequent rise in urine sodium concentration (200 mmol/L on D29). The usage of sodium chloride tablets and persistence of fluid restriction also contributed to the improvement in hyponatremia. Oral fludrocortisone was served every other day (0.05 mg) with gradual improvement in serum sodium (131 mmol/L on D25). After low dose fludrocortisone was started, there was also successful tapering of oral sodium chloride tablets down to 12 tablets a day, with further tapering till it was stopped 6 weeks later. He was discharged well on D29. A week later at the Endocrine clinic, his serum sodium normalized (138 mmol/L) while on lower doses of sodium chloride tablets, low dose hydrocortisone, and fludrocortisone 0.05 mg every other day. Fludrocortisone and hydrocortisone were stopped. His sodium level remained normal (142 mmol/L) without any medications 6 weeks after discharge. During this prolonged hospital stay for hyponatremia, the patient in case 1 expressed his concern that the symptomatic dizziness from hyponatremia would persist and affect his ability to work. He was relieved that both his symptoms and hyponatremia resolved completely. He was able to resume work subsequently. | siadh literature review, case report, cerebral salt wasting (csw), hyponatremia, syndrome of inappropriate antidiuretic hormone (siadh), traumatic brain injury, urinary sodium | Not supported with pagination yet | null |
PMC7118411_01 | Female | 86 | An 86-year-old woman had been diagnosed with rheumatoid arthritis 4 years prior to this case, and was prescribed prednisolone 5 mg + salazosulfapyridine 500 mg per day. Here, she presented to the Department of Rheumatology with fatigue, non-productive cough for 7 days, and fever for 3 days. She had no hemoptysis, night sweats, weight loss, or chest pain. She also reported no recent history of exposure to illness or hospitalization. The patient's vital signs were stable on admission. Chest auscultation revealed reduced breath sounds in the right lower zones. Laboratory investigations revealed an elevated level of C-reactive protein (6.61 mg/L) without leukocytosis. Interferon-gamma release assay (T-SPOT .TB; Oxford Immunotec, Oxford, United Kingdom) results were positive. Chest radiography showed dullness of the right costophrenic angle, while computed tomography scan of the chest revealed right pleural effusion with right lower lobe compressive atelectasis (Fig. 1A and B). Pleural fluid biochemical analysis revealed that the pleural fluid protein/serum protein ratio was 0.78, with a pleural fluid lactate dehydrogenase level of 784 U/L, indicative of an exudate according to light criteria. The pleural fluid glucose level was 101 mg/dL, which was within normal range. Pleural fluid differential cell count showed predominant lymphocytosis and a high adenosine deaminase level (151.6 IU/L).
Sputum cultures demonstrated no bacterial growth and smears were negative for the presence of acid-fast bacilli. Rheumatoid pleuritis or tuberculous pleurisy was suspected and the patient was transferred to the Department of pulmonology for further examination. Before microbiological tests on pleural fluid were completed, and in an effort to attain a definitive diagnosis for early treatment, thoracoscopy was performed by semi-rigid pleuroscopy under sedation with local anesthesia.
Thoracoscopic findings showed diffuse dissemination of micronodules on the parietal pleura and fibrin adhesions between the visceral and parietal pleura (Fig. 1C). Pleural cryobiopsy was performed by using a 1.9-mm cryoprobe (ERBECRYO, ERBE, US) and the target area of the parietal pleura was frozen for 6 seconds (Fig. 1D).
Specimens obtained from the cryoprobe are shown in Fig. 2A and B: these exhibited the size of 0.9 cm; microscopic findings demonstrated 200-300-mum caseating and non-caseating epitheloid cell granulomas with Langerhans type giant cells. The Ziehl-Neelsen stain for acid-fast bacilli was positive. Based on the above results, the patient was diagnosed with TB pleurisy; due her use of immunosuppressants, anti-tuberculosis treatment was planned for 10 months. At the most recent outpatient follow-up, she had completed 6 months of treatment and was clinically in good condition. Chest radiography showed regression of the pleural effusion, and her clinical course was consistent with our diagnosis. | cryobiopsy, elderly, semi-rigid pleuroscopy, tb, tuberculous, tuberculous pleurisy | Not supported with pagination yet | null |
PMC7118411_02 | Male | 91 | A 91-year-old man was introduced to our ward for further examination due to a history of exertional dyspnea for 2 months and the finding of massive right pleural effusion in a general health examination. He had been diagnosed with pleurisy of unknown origin during childhood and had no clear history of exposure to illness.
The patient's vital signs were stable on admission. Chest auscultation revealed reduced breath sounds in the right lower zones. Laboratory investigation showed an elevated level of C-reactive protein (2.39 mg/L) without leukocytosis. Interferon-gamma release assay (T-SPOT ) results were indeterminate. Chest radiography and computed tomography scan of the chest revealed massive right pleural effusion (Fig. 3A and B).
Pleural fluid biochemical analysis revealed that the pleural fluid protein/serum protein ratio was 0.7 with a pleural fluid lactate dehydrogenase level of 180 U/L, indicative of an exudate. Lymphocyte predominance and high adenosine deaminase level (90.1 IU/L) were observed and TB pleurisy was suspected. Sputum and pleural effusion cultures demonstrated no bacterial growth and smears were negative for the presence of acid-fast bacilli. For definitive diagnosis, pleural biopsy was performed via thoracoscopic cryobiopsy (Fig. 3C and D), using a freezing time of 6 seconds. Specimens obtained from the cryoprobe are shown in Fig. 2C and D: these exhibited the size of 0.8 cm; microscopic findings demonstrated epitheloid granulomas with necrosis and many Langerhans type giant cells, highly suggestive of tuberculosis. The Ziehl-Neelsen stain for acid-fast bacilli was negative. Based on the above results, the patient was diagnosed with TB pleurisy. He completed anti-tuberculosis therapy with complete disease remission and will continue follow-up in the Department of Thoracic Medicine outpatient clinic. | cryobiopsy, elderly, semi-rigid pleuroscopy, tb, tuberculous, tuberculous pleurisy | Not supported with pagination yet | null |
PMC5477428_01 | Male | 39 | A 39-year-old male with no significant past medical history was transferred, intubated and sedated to our burn center, following a 40% TBSA deep partial thickness and full thickness burns to face, head, bilateral upper and lower extremities, perineum, scrotum, and penis. The mechanism of burn was a gasoline fire, following a gasoline container spillage and explosion near a kerosene lamp in a garage.
On admission, the patient underwent an emergent right upper extremity escarotomy with successful return of pulses. Post initial fluid resuscitation, the patient underwent staged grafting of his burns. Following debridement, he underwent xenograft application and partial skin grafting from the trunk to the right arm 32 x 30 cm, right hand size 15 x 15 cm, left hand size 15 x 15 cm, left arm size 20 x 20 cm. He also underwent xenograft application to 30 x 60 cm and to the right leg.
On postoperative day 1, the patient deteriorated into acute respiratory failure. Thick tenacious secretions, prompted an urgent bronchoscopy and bronchoalveolar lavage (BAL). Broad-spectrum antibiotics were initiated to cover for methicillin-resistant Staphylococcus aureus and Gram-negative organism based on the grams stain. The bronchoscopy showed copious secretions in multiple lung fields. The BAL culture had >100,000 CFU streptococcus pneumonia that was resistant to clindamycin. The hypoxemia continued to worsen within hours on volume control (VC) ventilation, pressure regulated volume control (PRVC), pressure control (PC), APRV and on the volumetric diffusive ventilation. A brief summary of the ventilator changes and salient clinical findings are outlined in Table 1. The patient was sedated and neuromuscular blocked once the FiO2 requirements escalated >0.8. The acutely worsening and refractory hypoxemia prompted urgent changes to ventilator management. The FiO2 requirements escalated from 0.5 immediately post-operation to 1.0 over 4 h. The positive end-expiratory pressure (PEEP) was titrated using constant-flow, pressure-volume curve (PVC) method to prescribe optimal PEEP. The PEEP on conventional modes of ventilation was 15 cm H2O before we transitioned to APRV. The peak airway pressures remained >33 cm H2O (mean airway pressures 12-16 cm H2O). The dynamic compliance was <17 ml/cm H2O.
APRV settings were P high 32, P low 0 and Time high 3.5 s, Time low 0.5 s. Mean airway pressures in APRV were 30 cm H2O. The patient continued to deteriorate on APRV with worsening hypercarbia, hypoxemic and acidemic that prompted the change to the volume diffusive respirator (VDR) or volumetric diffusive ventilation. The VDR settings I:E was 3:1, frequency was 585, VDR peak pressure control was 40 cm H2O.
Hemodynamically, the patient required four units packed cells along with intermittent vasoactive medications to maintain mean arterial pressure (MAP) > 65 mm Hg during the period of deterioration.
Given his single organ failure, a decision was made to initiate V-V ECMO. The ECMO cannulation was done under transesophageal echocardiographic guidance after a quick evaluation that ruled out significant valular dysfunction and showed a preserved left ventricular ejection fraction. V-V ECMO was initiated and managed for 4 days with no complications. Patient was successfully weaned from ECMO on day 7. The patient was ultimately discharged to a skilled care facility on day 27. | ards, burns, conventional ventilation failure, extra corporeal membrane oxygenation, rescue ventilation, veno-venous ecmo | Not supported with pagination yet | null |
PMC5477428_02 | Male | 53 | A 53-year-old reportedly healthy African American male was admitted with 25% TBSA partial and full thickness burns to his upper extremities, chest and back following a flash burn from a grease fire. After burn shock resuscitation, he underwent excision/debridement/grafting of his back, upper extremities and chest. His hands and forearms were autografted and upper arms were covered with xenograft.
His post-graft clinical course was complicated by new onset pulmonary infiltrates; fevers and vasopressor dependent septic shock 96 h post admission. His post recovery from vasopressor-dependent shock was complicated by episodes of delirium, early onset pneumonia (Gram-positive cocci) and late onset fevers (day 10-15) of ill-defined etiology (multiple microbiology cultures, fungal cultures were negative but the serum procalcitonin remained positive). His indolent clinical picture and microbiological profile were not aligned. This prompted concern that the source of infection had not cleared with the rounds of antibiotics or we were not adequate covering all pathogens. The infectious disease recommendation was that he completes a course of 14 days of broad-spectrum antibiotics. He was on broad-spectrum antibiotics up to his deterioration.
The mechanical ventilatory course was also rocky for this patient. He was ventilator dependant from day 3 to 14 on a complex trajectory of escalating and deescalating ventilator support. He was weaned to pressure support on day 12 with settings of 20 cm pressure over PEEP and PEEP of 10 cm H2O. He continued to be tachypneic with respiratory rates in the upper 20 and 30 ranges. It is worth noting that the patient was extubated for < 24 h prior to his acute deterioration on day 16.
Less than 24 h, post extubation (day 17), the patient deteriorated rapidly requiring urgent re-intubation and high degree of mechanical ventilator support. The patient was neuromuscularly blocked once we transitioned to pressure control ventilation on FiO2 1.0 early in the deterioration episode. Post intubation, he deteriorated rapidly with severely reduced pulmonary dynamic compliance < 8 ml/cm H2O (normal > 50 ml/cm H2O). Resultant peak pressure were >45 mm Hg.
We cycled through low tidal volume ventilation using VC, PC, PRVC, ARPV, and a trial of prone positioning for twelve hours. This ranged from conventional ventilation (SIMV, PC) to PRVC and APRV. High PEEP prescriptions of 12-16 cm H2O, and high FiO2 0.6 -1.0. APRV settings were P high 33, P low 0 and Time high 3.5 s, Time low 0.5 s. Mean airway pressures on APRV were 28 cm H2O. The ongoing refractory hypoxemia that was not responding to the ventilator changes precluded longer trials of prone positioning or alternate rescue modes of ventilation like VDR.
He was progressively acidemic from hypercarbia and we could not improve the PaO2 > 45 mm Hg on FiO2 1.0 during the prone position trail. He however maintained his hemodynamics and did not require vasopressors at this point in time. Given his isolated respiratory failure we decided to trial him on V-V ECMO. ECMO was successfully initiated and managed for 24 days. The patient was successfully weaned off ECMO and off mechanical ventilation post tracheostomy and was discharged to a nursing facility on hospital day 54. | ards, burns, conventional ventilation failure, extra corporeal membrane oxygenation, rescue ventilation, veno-venous ecmo | Not supported with pagination yet | null |
PMC4278095_01 | Female | 37 | A 37-year-old woman with a past medical history of bacterial endocarditis of the pulmonic, mitral, and tricuspid valves due to intravenous drug abuse, with subsequent tricuspid valve replacement and pulmonary embolism presented to our Emergency Department (ED) complaining of generalized myalgias and shortness of breath. She had no history of congenital cardiac disease. Notes in the medical record indicated that she had baseline oxygen deprivation attributed to a historical diagnosis of pulmonary hypertension. In the ED, she was tachypneic, tachycardic, and had persistent oxygen saturations around 88% on room air mandating the need for oxygen via nasal cannula at 2 l/min. Upon physical exam, she was in moderate respiratory distress and diaphoretic. Cardiovascular examination revealed a harsh, blowing holosystolic grade IV/VI murmur noted at the left upper sternal border. The rest of her physical exam was unremarkable. A complete metabolic panel (CMP) showed no abnormalities and a complete blood count (CBC) showed only mild anemia. No arterial blood gases were tested. An electrocardiogram (EKG) demonstrated a right bundle branch block, but no other marked abnormalities. Due to suspicion for pulmonary embolism, a CT scan of the chest was performed. The CT scan was negative for pulmonary embolism, but did reveal an anomalous vein connecting the left brachiocephalic vein to the left superior pulmonary vein [Figures 1 and 2 and Video 1]. The CT study demonstrated intravenously administered contrast passing from the left brachiocephalic vein through the anomalous vessel into the left superior pulmonary vein to the left atrium, indicating a right-to-left shunt via the anomalous vein. The anomalous vein measured 9 mm in maximum diameter. Subsequently, transthoracic and transesophageal echocardiography was performed. This demonstrated dilatation of the right atrium and right ventricle, severe tricuspid valve regurgitation, and elevated right ventricular pressure estimated at 30 mm Hg. The inferior vena cava was dilated without respiratory variation, also consistent with elevated right atrial pressure. A small fistula between the ascending aorta and the right ventricle was also seen likely secondary to endocarditis. In retrospect, this fistula was not visible on CT due to streak artifacts from the previous tricuspid valve prosthesis. Agitated saline injection showed appearance of bubbles in the left atrium from the left superior pulmonary vein, confirming an intrapulmonary right-to-left shunt. MRI of the anomalous vein was also performed to evaluate the flow characteristics [Figure 3]. As the patient was claustrophobic, only a limited evaluation of the anomalous vein could be performed. The study demonstrated monophasic, inferiorly directed flow within the vessel toward the left superior pulmonary vein, with the flow calculated as 20 ml per heartbeat.
Shortly after admission, treatment was started for bacterial endocarditis and subsequent blood cultures were positive for Escherichia coli. Her symptoms were attributed to bacterial endocarditis and right-heart overload secondary to the severe tricuspid valve regurgitation and the small fistula between the aortic root and the right ventricle. Right-to-left shunting through the anomalous pulmonary vessel was also believed to further exacerbate her hypoxia. No interventions were undertaken with regard to the anomalous vessel during the patient's hospital course. The patient left the hospital against medical advice before completion of therapy and was lost to follow-up. | computed tomography, levoatriocardinal vein, magnetic resonance imaging, partial anomalous pulmonary venous connection, right-to-left shunt | 37-year old female who presented with dyspnea and hypoxia with a diagnosis of levoatriocardinal vein. Axial images from contrast-enhanced CT scan of the chest demonstrate the abnormal vessel. (c) Image at the level of the left atrium shows bright undiluted contrast in the left superior pulmonary vein (arrow) draining into the left atrium (LA). Thus, the inferiorly directed flow through the anomalous vein produces an extracardiac right-to-left shunt. |
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PMC4278095_01 | Female | 37 | A 37-year-old woman with a past medical history of bacterial endocarditis of the pulmonic, mitral, and tricuspid valves due to intravenous drug abuse, with subsequent tricuspid valve replacement and pulmonary embolism presented to our Emergency Department (ED) complaining of generalized myalgias and shortness of breath. She had no history of congenital cardiac disease. Notes in the medical record indicated that she had baseline oxygen deprivation attributed to a historical diagnosis of pulmonary hypertension. In the ED, she was tachypneic, tachycardic, and had persistent oxygen saturations around 88% on room air mandating the need for oxygen via nasal cannula at 2 l/min. Upon physical exam, she was in moderate respiratory distress and diaphoretic. Cardiovascular examination revealed a harsh, blowing holosystolic grade IV/VI murmur noted at the left upper sternal border. The rest of her physical exam was unremarkable. A complete metabolic panel (CMP) showed no abnormalities and a complete blood count (CBC) showed only mild anemia. No arterial blood gases were tested. An electrocardiogram (EKG) demonstrated a right bundle branch block, but no other marked abnormalities. Due to suspicion for pulmonary embolism, a CT scan of the chest was performed. The CT scan was negative for pulmonary embolism, but did reveal an anomalous vein connecting the left brachiocephalic vein to the left superior pulmonary vein [Figures 1 and 2 and Video 1]. The CT study demonstrated intravenously administered contrast passing from the left brachiocephalic vein through the anomalous vessel into the left superior pulmonary vein to the left atrium, indicating a right-to-left shunt via the anomalous vein. The anomalous vein measured 9 mm in maximum diameter. Subsequently, transthoracic and transesophageal echocardiography was performed. This demonstrated dilatation of the right atrium and right ventricle, severe tricuspid valve regurgitation, and elevated right ventricular pressure estimated at 30 mm Hg. The inferior vena cava was dilated without respiratory variation, also consistent with elevated right atrial pressure. A small fistula between the ascending aorta and the right ventricle was also seen likely secondary to endocarditis. In retrospect, this fistula was not visible on CT due to streak artifacts from the previous tricuspid valve prosthesis. Agitated saline injection showed appearance of bubbles in the left atrium from the left superior pulmonary vein, confirming an intrapulmonary right-to-left shunt. MRI of the anomalous vein was also performed to evaluate the flow characteristics [Figure 3]. As the patient was claustrophobic, only a limited evaluation of the anomalous vein could be performed. The study demonstrated monophasic, inferiorly directed flow within the vessel toward the left superior pulmonary vein, with the flow calculated as 20 ml per heartbeat.
Shortly after admission, treatment was started for bacterial endocarditis and subsequent blood cultures were positive for Escherichia coli. Her symptoms were attributed to bacterial endocarditis and right-heart overload secondary to the severe tricuspid valve regurgitation and the small fistula between the aortic root and the right ventricle. Right-to-left shunting through the anomalous pulmonary vessel was also believed to further exacerbate her hypoxia. No interventions were undertaken with regard to the anomalous vessel during the patient's hospital course. The patient left the hospital against medical advice before completion of therapy and was lost to follow-up. | computed tomography, levoatriocardinal vein, magnetic resonance imaging, partial anomalous pulmonary venous connection, right-to-left shunt | 37-year-old female who presented with dyspnea and hypoxia with a diagnosis of levoatriocardinal vein. Reformatted images from chest CT scan demonstrate the abnormal vessel. (a) Reformatted coronal image shows flow through the levoatriocardinal cardinal vein (arrow) to the left superior pulmonary vein (arrowhead). |
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PMC4278095_01 | Female | 37 | A 37-year-old woman with a past medical history of bacterial endocarditis of the pulmonic, mitral, and tricuspid valves due to intravenous drug abuse, with subsequent tricuspid valve replacement and pulmonary embolism presented to our Emergency Department (ED) complaining of generalized myalgias and shortness of breath. She had no history of congenital cardiac disease. Notes in the medical record indicated that she had baseline oxygen deprivation attributed to a historical diagnosis of pulmonary hypertension. In the ED, she was tachypneic, tachycardic, and had persistent oxygen saturations around 88% on room air mandating the need for oxygen via nasal cannula at 2 l/min. Upon physical exam, she was in moderate respiratory distress and diaphoretic. Cardiovascular examination revealed a harsh, blowing holosystolic grade IV/VI murmur noted at the left upper sternal border. The rest of her physical exam was unremarkable. A complete metabolic panel (CMP) showed no abnormalities and a complete blood count (CBC) showed only mild anemia. No arterial blood gases were tested. An electrocardiogram (EKG) demonstrated a right bundle branch block, but no other marked abnormalities. Due to suspicion for pulmonary embolism, a CT scan of the chest was performed. The CT scan was negative for pulmonary embolism, but did reveal an anomalous vein connecting the left brachiocephalic vein to the left superior pulmonary vein [Figures 1 and 2 and Video 1]. The CT study demonstrated intravenously administered contrast passing from the left brachiocephalic vein through the anomalous vessel into the left superior pulmonary vein to the left atrium, indicating a right-to-left shunt via the anomalous vein. The anomalous vein measured 9 mm in maximum diameter. Subsequently, transthoracic and transesophageal echocardiography was performed. This demonstrated dilatation of the right atrium and right ventricle, severe tricuspid valve regurgitation, and elevated right ventricular pressure estimated at 30 mm Hg. The inferior vena cava was dilated without respiratory variation, also consistent with elevated right atrial pressure. A small fistula between the ascending aorta and the right ventricle was also seen likely secondary to endocarditis. In retrospect, this fistula was not visible on CT due to streak artifacts from the previous tricuspid valve prosthesis. Agitated saline injection showed appearance of bubbles in the left atrium from the left superior pulmonary vein, confirming an intrapulmonary right-to-left shunt. MRI of the anomalous vein was also performed to evaluate the flow characteristics [Figure 3]. As the patient was claustrophobic, only a limited evaluation of the anomalous vein could be performed. The study demonstrated monophasic, inferiorly directed flow within the vessel toward the left superior pulmonary vein, with the flow calculated as 20 ml per heartbeat.
Shortly after admission, treatment was started for bacterial endocarditis and subsequent blood cultures were positive for Escherichia coli. Her symptoms were attributed to bacterial endocarditis and right-heart overload secondary to the severe tricuspid valve regurgitation and the small fistula between the aortic root and the right ventricle. Right-to-left shunting through the anomalous pulmonary vessel was also believed to further exacerbate her hypoxia. No interventions were undertaken with regard to the anomalous vessel during the patient's hospital course. The patient left the hospital against medical advice before completion of therapy and was lost to follow-up. | computed tomography, levoatriocardinal vein, magnetic resonance imaging, partial anomalous pulmonary venous connection, right-to-left shunt | 37-year-old female who presented with dyspnea and hypoxia with a diagnosis of levoatriocardinal vein. Reformatted images from chest CT scan demonstrate the abnormal vessel. (b) Volume-rendered image from an anterior perspective shows the levoatriocardinal vein (large arrow) connecting the left brachiocephalic vein (BCV) to the left superior pulmonary vein (arrowhead). Note small pulmonary venous branches (small arrows) connecting to the anomalous vessel. SVC = Superior vena cava; LA = Left atrium. |
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PMC4278095_01 | Female | 37 | A 37-year-old woman with a past medical history of bacterial endocarditis of the pulmonic, mitral, and tricuspid valves due to intravenous drug abuse, with subsequent tricuspid valve replacement and pulmonary embolism presented to our Emergency Department (ED) complaining of generalized myalgias and shortness of breath. She had no history of congenital cardiac disease. Notes in the medical record indicated that she had baseline oxygen deprivation attributed to a historical diagnosis of pulmonary hypertension. In the ED, she was tachypneic, tachycardic, and had persistent oxygen saturations around 88% on room air mandating the need for oxygen via nasal cannula at 2 l/min. Upon physical exam, she was in moderate respiratory distress and diaphoretic. Cardiovascular examination revealed a harsh, blowing holosystolic grade IV/VI murmur noted at the left upper sternal border. The rest of her physical exam was unremarkable. A complete metabolic panel (CMP) showed no abnormalities and a complete blood count (CBC) showed only mild anemia. No arterial blood gases were tested. An electrocardiogram (EKG) demonstrated a right bundle branch block, but no other marked abnormalities. Due to suspicion for pulmonary embolism, a CT scan of the chest was performed. The CT scan was negative for pulmonary embolism, but did reveal an anomalous vein connecting the left brachiocephalic vein to the left superior pulmonary vein [Figures 1 and 2 and Video 1]. The CT study demonstrated intravenously administered contrast passing from the left brachiocephalic vein through the anomalous vessel into the left superior pulmonary vein to the left atrium, indicating a right-to-left shunt via the anomalous vein. The anomalous vein measured 9 mm in maximum diameter. Subsequently, transthoracic and transesophageal echocardiography was performed. This demonstrated dilatation of the right atrium and right ventricle, severe tricuspid valve regurgitation, and elevated right ventricular pressure estimated at 30 mm Hg. The inferior vena cava was dilated without respiratory variation, also consistent with elevated right atrial pressure. A small fistula between the ascending aorta and the right ventricle was also seen likely secondary to endocarditis. In retrospect, this fistula was not visible on CT due to streak artifacts from the previous tricuspid valve prosthesis. Agitated saline injection showed appearance of bubbles in the left atrium from the left superior pulmonary vein, confirming an intrapulmonary right-to-left shunt. MRI of the anomalous vein was also performed to evaluate the flow characteristics [Figure 3]. As the patient was claustrophobic, only a limited evaluation of the anomalous vein could be performed. The study demonstrated monophasic, inferiorly directed flow within the vessel toward the left superior pulmonary vein, with the flow calculated as 20 ml per heartbeat.
Shortly after admission, treatment was started for bacterial endocarditis and subsequent blood cultures were positive for Escherichia coli. Her symptoms were attributed to bacterial endocarditis and right-heart overload secondary to the severe tricuspid valve regurgitation and the small fistula between the aortic root and the right ventricle. Right-to-left shunting through the anomalous pulmonary vessel was also believed to further exacerbate her hypoxia. No interventions were undertaken with regard to the anomalous vessel during the patient's hospital course. The patient left the hospital against medical advice before completion of therapy and was lost to follow-up. | computed tomography, levoatriocardinal vein, magnetic resonance imaging, partial anomalous pulmonary venous connection, right-to-left shunt | 37-year year-old female who presented with dyspnea and hypoxia with a diagnosis of levoatriocardinal vein. Contiguous axial images from contrast-enhanced CT scan of the chest demonstrate the abnormal vessel. Beginning at the level of the left brachiocephalic vein, bright undiluted contrast drains inferiorly as it flows through the anomalous vessel, to the left superior pulmonary vein, and finally into the left atrium. Therefore, this flow demonstrates an extra-cardiac right-to-left shunt. |
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PMC8408892_01 | Male | 17 | A 17-year-old male patient presented at our facility with a rapidly growing anterior neck mass of about 4 weeks duration. There was no history of fever, weight loss, night sweat, or thyroid hormone related symptoms. The family history was unremarkable for malignancy or tuberculosis.
Physical examination revealed circa 4 cm x 5 cm slightly right sided, nontender, soft to firm consistency, movable, roughly demarcated anterior neck swelling. The swelling moved slightly upon swallowing but not with protrusion of the tongue. There were no associated regional lymphadenopathy and the overlying skin was unremarkable.
The laboratory findings were as follows: Haemoglobin 16.5 g/dl, Leucocytes 8275/ul, Thrombocytes 27,300/ul, Calcium 4.98 mval/l, TSH 2.89 uU/ml, FT3 3.39 pg/ml, FT4 1.24 ng/dl, INR-1.030, Creatinine 1.02 mg/dl. Tumor markers: Alpha-fetoprotein (AFP) 1.74 ng/ml, Human chorionic gonadotropin (hCG) < 1.20 U/l, Calcitonin 2.36 pg/ml, Lactate dehydrogenase (LDH)309U/l (normal range < 248), Thyroglobulin (Tg) 29.8 ng/ml, Anti-thyroid peroxidase (anti-TPO)21.9 IU/ml (normal range 1-16).
A thyroid ultrasound revealed an enlarged thyroid gland with right lobe volume of 62 ml and left lobe volume of about 14 ml. A big lesion of about 40 ml was located around the caudal part of the right lobe. It also showed multiple thyroid nodes. Thyroid scintigraphy confirmed a multinodular goiter with "cold" nodes.
Magnetic resonance imaging (MRI) of the neck revealed diffused contrast enhanced right sided neck mass of about 8.2 cm x 3.4 cm x 3.6 cm with extension to the base of the tongue. Around the sinus sphenoidalis and sinus mastoidis was found little fluid without any evidence of tumor, infiltration or lymphadenopathy. (Figure 1).
Exploration, thyroidectomy and surgical resection of the tumor was carried out on the 21.01.2019. We found an enlarged multinodular thyroid gland with diffuse tumor of the right lobe infiltrating the nearby tissues and pressing on the trachea.
Frozen section histological examination revealed a tumor most likely to be germ cell tumor and sensitive to Chemotherapy. Based on these intraoperative and the histological findings, we carried out near-total thyroidectomy aiming at tumor debulking and tracheal decompression without causing damage to the nearby organs.
The postoperative was uneventful, and the patient was discharged on the fifth postoperative day. The final histological examination revealed a teratocarcinosarcoma of the thyroid gland, an analog to the sinonasal teratocarcinosarcoma (Figures 2-4).
Immunnohistochemical staining with desmin and myogenin revealed rhabdomyoblastic differentiation of the stromal component (Figure 5). Subsequently, SALL4 staining was done to exclude immature teratoma with rhabdomyosarcomatous foci.
Staging Computed tomography (CT) of the thorax, Magnetic Resonance Imaging (MRI) of the abdomen, Head and Neck as well as Full Body Scintigraphy did not show any evidence of metastasis or primary tumor focus. The patient was given chemotherapy with Cisplatin, Etoposid, and Ifosfamid. The tumor was found to be regressive after the chemotherapy. A second staged surgical resection was carried out on the third of April 2019. This was followed with Radiochemotherapy. The Patient is currently doing well and is on surveillance. | germany, teratocarcinosarcoma, cancer, sinonasal, thyroid | Not supported with pagination yet | null |
PMC8651021_01 | Male | 70 | A 70-year-old male smoker (1 pack a day for 40 years) presented in April 2014 with painless, subacute, bilateral visual decline of 1 month's duration. His past medical history was unremarkable; however, weight loss of 17 kg in recent months as well as myalgia and fatigue were noted.
Examination revealed a bilateral best corrected visual acuity of 20/30. There was no color vision loss. The intraocular pressure values were within the normal range in both eyes. While the anterior chamber was quiet, mild to moderate vitritis was observed in both eyes. Despite the mildly hazy view, indirect ophthalmoscopy yielded no change in the posterior segments (Fig. 1 a-h). A fluorescein angiogram revealed no abnormality (Fig. 1 e, f).
Optical coherence tomography images displayed normal foveal architecture with a few hyper-reflective dots in the posterior vitreous of both eyes corresponding to the vitreous cells (Fig. 1 g, h). The initial diagnosis was bilateral intermediate uveitis.
A full systemic and laboratory work-up was performed in collaboration with a rheumatologist and pulmonologist. Lab investigations included a complete blood count; analysis of serum liver enzymes, renal function, electrolytes, inflammatory markers (erythrocyte sedimentation rate, C-reactive protein), angiotensin-converting enzyme, and rheumatological markers (antinuclear antibody, antineutrophil cytoplasmic antibodies, and rheumatoid factor); infection screening (syphilis and tuberculosis); brain magnetic resonance imaging; and chest radiography. Treatment with 40 mg oral prednisolone was initiated once an infectious etiology was excluded. Finally, positron emission tomography (PET-CT) scanning was used to explore the possibility of sarcoidosis or malignancy.
The PET-CT images revealed an increased uptake of 2-(fluorine-18)-fluoro-2-deoxy-D-glucose in area of the hilar and mediastinal lymph nodes (Fig. 2). To determine the nature of the primary tumor, a biopsy was performed during a bronchoscopy. SCLC (T2N3M0) was established the histopathological examination. The patient was then referred to an oncologist for additional treatment.
After 2 weeks of oral steroid therapy, a subsequent examination yielded a visual acuity of 20/20 and very little lingering bilateral haze (Fig. 3). The patient began a course of chemotherapy, and oral steroid treatment was tapered and terminated. The final diagnosis was bilateral paraneoplastic vitritis. No further visual symptoms were reported during follow-up. Unfortunately, the patient passed away in 2019. | paraneoplastic syndrome, small-cell lung cancer, uveitis, vitritis | Not supported with pagination yet | null |
PMC4980804_01 | Male | 44 | A 44-year-old man sustained a 55% total body surface area burn secondary to a gasoline fire. He required numerous rounds of excision and autografting and was discharged to inpatient rehabilitation on postburn day 45. Approximately 3 months postburn, he presented to clinic with a persistent area of hypertrophic granulation tissue overlying his left tibia at the site of a previous full-thickness skin excision and split-thickness skin graft. The lesion was found to be squamous cell carcinoma (SCC).
What are the predisposing factors and average time at presentation of a Marjolin's ulcer?
What are the histological findings?
How are these lesions diagnosed and treated?
What is the prognosis? | acute marjolin's ulcer, burn, nonhealing wound, skin graft, squamous cell carcinoma | Not supported with pagination yet | null |
PMC5364197_01 | Female | 75 | A 75-year-old woman was admitted to the Jikei University Hospital due to impaired consciousness and status epilepticus. She was referred to the hospital's outpatient clinic 24 days before admission to investigate a progressive mass-like lesion with a maximum diameter of 30 mm that was located on her left upper lung. Positive results from an interferon-gamma-release assay (T-spot.TB assay, Oxford Immunotec Ltd. Marlborough, MA, USA) and a tuberculosis polymerase chain reaction (PCR) led to a diagnosis of pulmonary tuberculosis 16 days before admission. A sputum culture showed that the patient was positive for tuberculosis, and the diagnosis was later confirmed. The patient was prescribed four anti-tuberculosis medications (isoniazid, rifampicin, ethambutol, and pyramide). She did not start taking full doses of the medications until two days prior to her admission due to anxiety over the side effects. Her medical history included hypertension, gastric ulcer and hyperlipidemia, but she had been healthy until admission. On the day of admission, she was found lying on the floor at her home and was transported to the hospital. At the emergency room, she developed generalized seizures five times and was admitted to the intensive care unit to undergo treatment for statue epilepticus.
On admission, the patient was unconscious (Glasgow Coma Scale, E1V1M3) with a body temperature of 37C, a heart rate of 108/min, a respiratory rate of 18 breaths/min, a saturation level of 99% on room air and a blood pressure of 160/90 mmHg. Physical examinations showed normal breath and heart sounds and no swelling of her extremities. Neurological examinations revealed an increase of muscle tonus, especially in the lower limbs. Biochemical examinations showed hyponatremia (120 mEq/L) with low serum osmolality (253 mOsm/kg), high urinary osmolality (458 mOsm/kg), and a normal urinary sodium concentration (81 mEq/L) (Table). Despite the patient's severe hyponatremia, her serum antidiuretic hormone (ADH) level was not decreased (3.3 pg/mL); it was close to the upper limit of the normal range (0.3-4.2 pg/mL). The patient's thyroid, kidney, and adrenal functions were normal. The fact that her blood urea nitrogen (BUN) to creatinine (Cr) ratio was 6.6 and the fact that she did not experience severe diarrhea or vomiting implied that she was clinically euvolemic. Based on these laboratory findings, this patient met the criteria for SIADH, which were as follows: decreased effective osmolality; urinary osmolality, >100 mOsm/kg of water; clinical euvolemia; urinary sodium concentration, >40 mmol/L; and normal thyroid and adrenal functions. Chest radiography and computed tomography (CT) showed a wedge-shaped infiltrative shadow with small tree-in-bud satellite lesions in the left upper lobe of the lung (Fig. 1). With the exception of pulmonary tuberculosis, contrast-enhanced CT of the whole body did not reveal any malignant or infectious diseases. Brain magnetic resonance imaging (MRI) revealed no abnormalities and electroencephalograms, which were taken three times, were all normal. A cerebrospinal fluid examination (CSF) showed no increase in the cell count (0 cells/uL) or the total protein level (47 mg/dL), no decrease in the glucose (102 mg/dL), and was culture-negative for tuberculosis and bacteria. Repeated blood cultures were also negative for bacteria. She was not taking any medicines that have previously been reported as a potential cause of SIADH. It was therefore concluded the patient's SIADH was caused by pulmonary tuberculosis. Among the prescribed medications, only isoniazid has the potential to lead to seizures. However, this possibility was excluded due to a lack of complications during re-administration. Accordingly, we concluded that the patient's status epilepticus could be attributed to hyponatremia, which had caused by pulmonary tuberculosis-associated SIADH.
The patient did not develop seizures after infusion of fosphenytoin sodium hydrate. Her level of consciousness improved after an infusion of saline to treat her abnormal serum sodium concentration, and she became conscious on the second day after admission (Fig. 2). Rhabdomyolysis occurred due to the patient's status epilepticus, and her creatine kinase (CK) levels increased (6,630 IU/L). SIADH did not recur after the patient resumed taking the anti-tuberculosis medicines and she was discharged from the hospital on the 22nd day after admission. The fact that she improved with treatment verified our diagnosis. | null | Not supported with pagination yet | null |
PMC4943130_01 | Female | 9 | A 9-year-old girl presented with low-grade fever for 1 month and abdominal distension for 15 days along with labored breathing. There was loss of appetite. There was no cough or contact with TB. On examination, height was 117 cm, weight was 17 kg. She had anemia with generalized insignificant lymphadenopathy. On systemic examination, she had hepatomegaly with other systems being normal. Investigations showed a hemoglobin of 8.02 g/dl, white blood cell count of 11,100/cumm (72% polymorphs and 27% lymphocytes), erythrocyte sedimentation rate of 100 mm at end of 1 h. HIV ELISA was negative. Her mantoux test was positive. Ultrasonography abdomen showed multiple upper retroperitoneal lymphadenopathy largest being 11 cm. Computed tomography (CT) chest showed left upper lobe consolidation with cavitation with patchy opacities in the right lung and necrotic mediastinal adenopathy suggestive of TB. Liver function tests were normal. She was started on four drugs ATT consisting of isoniazid (H), rifampicin (R), ethambutol (E), and pyrazinamide (Z). One month after starting ATT, she was detected to have a pericardial rub. Her echocardiography showed 1.7 cm pericardial effusion. She was continued on same ATT, and steroids were added which were then tapered after 2 months. At the end of 3 months of ATT, her ultrasound abdomen showed decrease in the size of adenopathy to 6 mm. At the end of 'hs of ATT, chest X-ray showed right pleural effusion with fissural effusion and left upper zone consolidation. At end of 5 months of ATT, she had gained 6 kg and on ophthalmological evaluation, she was found to have bilateral papilledema. Chest X-ray showed disappearance of effusion. She had no neurological manifestations. CT brain showed mild prominence of lateral and third ventricles. She was continued on same ATT. A repeat fundus examination was normal after 2 months. She was given ATT for 12 months in view of above manifestations. She had gained 9 kg in those 12 months and was alright on subsequent follow-up. | paradoxical reaction, pericardial effusion, tuberculosis | Not supported with pagination yet | null |
PMC3507031_01 | Male | 30 | A 30-year-old male patient presented to our clinic with a history of tender swelling on the dorsum of middle phalanx of left index finger. The patient noted the mass since 12 months, which gradually became larger. The mass was 13 mm in diameter [Figure 1], with mild tenderness and firm in palpation, slightly mobile and, without marked movement on interphalyngeal motion, and no obvious adhesion to adjacent skin. The sensation of the finger was normal. Flexor and extensor tendons were intact; however, finger motion was slightly limited.
There was no history of major trauma, sharp injury, infection, or constitutional symptoms such as malaise, fever, or weight loss. Laboratory tests (CBC diff, ESR, CRP, Ca, P, Alk-P) were within normal limit. Tests for tuberculosis, brucella and syphilis were negative. Chest roentgenogram was normal.
Other imaging investigations included simple x-ray and CT-scan of the index finger. Conventional posteroanterior and lateral radiography revealed a paraosteal sclerotic lesion just abutting middle phalanx with bone density similar to adjacent bone and slight periosteal reaction [Figure 2], and further evaluation with CT-scan noted that the lesion has a patchy irregular border without cortical destruction or sauccerization and there is no typical zonal pattern in the lesion [Figure 3].
An excisional biopsy with dorsolateral incision was performed. The lesion was 1 x 1 x 1.5 cm in size, white-grayish in color, with hard consistency, and no adhesion to adjacent tendons or soft tissues. Histopathologic examination revealed proliferation of fibroblasts that are loosely arranged, a prominent myxoid matrix, and deposits of osteoid rimmed by uniform osteoblasts. Multinucleated giant cells were also existed [Figure 4]. | digit, fibro-osseous pseudotumor, heterotopic ossification, soft tissue lesion | Not supported with pagination yet | null |
PMC6558611_01 | Female | 62 | A 62-year-old otherwise healthy woman presented with three to four months of mechanical right groin pain radiating to the right buttock. She had a history of a benign soft-tissue mass in the right thigh that had been biopsied 10 years earlier, and the patient was told it was a myxoma. No other workup was done at the time, and no other lesions were clinically detectable. She had been very active and played tennis regularly. She was assessed with a hip ultrasound for her right groin pain and was prescribed physiotherapy. During physiotherapy, she felt a snap in her right groin and was no longer able to ambulate without a walker. Initial radiographs demonstrated a lucent intramedullary lesion within the subtrochanteric region:further characterized by a focally aggressive appearance with cortical destruction and lytic expansion of the lesser trochanter (Figures 1(a) and 1(b)). A ground-glass appearance, typical of fibrous dysplasia, was also noted in the mid-femoral shaft (Figure 1(c)).
Further workup included a Computed Tomography (CT) scan of the chest, abdomen, and pelvis which showed multiple hepatic and renal cysts but no evidence of a primary carcinoma or lung metastases. Bloodwork including serum protein electrophoresis was normal. A Total Body Bone Scan (TBBS) revealed increased uptake in the right proximal femur and two areas of relatively mild uptake in the mid femur. Fat-suppressed T2 Magnetic Resonance Imaging (MRI) displayed an intermediate to high signal lesion within the medullary cavity of the proximal and mid right femoral shaft (Figure 2(a)). In line with the initial radiographs in which two benign sites of fibrous dysplasia were noted, in the third proximal lesion, there was cortical destruction with an extraosseous soft-tissue mass in the region of the lesser trochanter. Additionally, in keeping with the known myxoma, a soft-tissue T2 hyperintense mass within the medial distal thigh was also present (Figure 2(b)). On further review of the MRI images, five other myxomas were seen. The imaging features were consistent with Mazabraud's Syndrome, with sarcomatous transformation of benign fibrous dysplasia in the proximal femur.
Due to the high risk of fracture, the patient was immediately placed on bedrest and a biopsy was not performed:as a preventative measure to reduce fracture risk. She was taken to the operating room and underwent wide resection of the proximal right femur with endoprosthetic reconstruction via a lateral approach. Along with bony specimens, one of the soft-tissue masses was also excised and sent to pathology for investigation (Figures 3(a) and 3(b)). Pathology later confirmed a high-grade osteosarcoma in the setting of fibrous dysplasia and a benign myxoma (Figures 4(a)-4(d)). There were no complications during the procedure.
Postoperatively, the patient stayed in the hospital for one week, with physiotherapy beginning on postoperative day one. Her postoperative course followed the normal trajectory of recovery with no major complaints or issues at her two-week follow-up. The patient declined adjuvant chemotherapy. The standard management of osteosarcoma at our center would include wide surgical excision with neoadjuvant or adjuvant chemotherapy (methotrexate- and doxorubicin-based multidrug regimens). The patient is being followed to assess for complications and local or systemic relapse every three months with radiographs of the femur and chest. At one year postoperatively, there have been no complications or evidence of disease relapse. | null | Not supported with pagination yet | null |
PMC8575374_02 | Male | 11 | At enrollment, the patient (Figure 4A) was 11 years old. After completing the trial, he entered pathfinder 8 and is currently studying at university. Prior to pathfinder 5 enrollment, the patient was receiving SHL rFVIII twice weekly but continued to experience bleeds on this PPX regimen. Of note, his estimated FVIII trough level was 2.5% at 48 hours and, as such, it was estimated that his levels would be <1% at 72 hours. According to the treating physician, during the 12 months prior to pathfinder 5 inclusion his ABR was 3, with all bleeds involving traumatic injuries to joints. Without N8-GP treatment his physician felt that he would have needed to escalate to SHL rFVIII injections three times per week, which the patient was keen to avoid.
During the 5 years that he received N8-GP in pathfinder 5, the patient had an ABR of 1 and a trough FVIII level of 2.9%. He was initially able to maintain twice-weekly injections and this supported his participation in sports. Later sports became his priority and he started to play American football and rugby. To support this lifestyle, he was escalated to three injections per week to provide higher FVIII trough levels when he transitioned to pathfinder 8 at around 16 years of age. Now at 18 years of age, he is once again less active (mainly due to COVID-19 pandemic) and has reverted back to a twice-weekly regimen. | extended half-life, factor viii, joint health, prophylaxis, surgery | Not supported with pagination yet | null |
PMC10329462_01 | Female | 70 | A 70-year-old woman (60 kg, 160 cm) was admitted to the hospital with chest and back pain, and limited mobility for five months. Five months ago, the patient felt continuous pain in the chest and back without significant cause. The pain area was fixed and accompanied by fever (the highest temperature was 39 C). There were no chills or convulsions, chest tightness or wheezing, numb lower limbs, or other symptoms. Four months before admission, thoracic magnetic resonance imaging (MRI) revealed abnormal signals in the appendages of the T9, T11, and T12 vertebrae, consistent with tuberculosis. Therefore, she was treated with isoniazid, rifampicin, ethambutol, and pyrazinamide. However, her symptoms did not improve.
Physical examination on admission was as follows: temperature 37 C, pulse rate 81 times/min, respiration rate 20 times/min, blood pressure 124/87 mmHg. A focused physical examination revealed kyphosis deformity, tenderness of the spinous process of T11-12 vertebrae, and pain to percussion. The admission diagnosis was bony destruction of the T11-12 vertebrae of unknown cause.
The patient continued to take isoniazid (0.3 g, once a day), rifampicin (0.6 g, once a day), ethambutol (0.75 g, once a day), pyrazinamide (0.5 g, three times a day) for anti-tuberculosis treatment, and tiopronin (200 mg, once a day, intravenous) was given for liver protection. On the second day of hospitalization, computed tomography (CT) of the thoracolumbar vertebrae revealed bony destruction of T11 and T12 vertebral bodies with a slight swelling of the surrounding soft tissues. MRI of the lumbar spine and hip showed presumptive infectious lesions in the T11-12 vertebral bodies and the right appendage of T12, consistent with tuberculosis. Subcutaneous fascial edema was observed in the lumbar region. A T-score of less than -2.5 indicated osteoporosis.
Laboratory tests showed a white blood cell count of 2.5x109/L, low neutrophil counts, uric acid 487 micromol/L, and positive T SPOT-TB testing. Leucogen tablets (20.0 mg, three times a day), calcitonin injection (20 U, twice a week), and calcitriol soft capsules (0.25 microg, twice a day) were added. On the fifth hospital day, a needle biopsy of the affected vertebrae revealed no evidence of tuberculosis.
On the tenth hospital day, the patient was treated with debridement, decompression, instrumentation, and fusion surgery and was given cefazolin (1.0 g every eight hours) to prevent surgical site infection. The day after surgery, body temperature increased to 39 C, and C-reactive protein (CRP) increased to 129.08 mg/L. Considering the possibility of surgical incision infection, we continued cefazolin. On the thirteenth hospital day, cefazolin was discontinued after the body temperature returned to normal.
On the sixteenth hospital day, the CRP was 21.37 mg/L, and next-generation sequencing of the vertebral body indicated the sequence number of Aspergillus tubingensis was 28. The patient was diagnosed with Aspergillus tubingensis spondylitis. Because the tuberculosis evidence of thoracic vertebral lesions was insufficient, anti-tuberculosis treatment was discontinued. The clinical pharmacist recommended caspofungin (initial loading agent 70 mg, maintaining 50 mg, intravenous injection, once a day) for anti-Aspergillus treatment, and switching it to VRZ after rifampicin discontinuation for 7-14 days, considering the continuous induction effect of rifampicin on drug-metabolizing enzymes.
On the twenty-ninth hospital day, caspofungin was discontinued due to stomach discomfort. The treatment regimen was changed to oral VRZ (200 mg every 12 hours). However, the patient complained of blurred vision, hallucinations, and sleeplessness at night after taking two doses of VRZ tablets. The clinical pharmacist suggested that VRZ tablets be adjusted to 200 mg daily and instructed the patient to stop eating grapefruit on the thirtieth hospital day.
On the thirty-third hospital day, the trough concentration of VRZ was 0.82 mg/L (effective range: 1.0-5.0 microg/mL); therefore, the clinical pharmacist suggested it should be adjusted to 150 mg every 12 hours, but this regimen was not accepted. The patient was discharged in stable condition, on VRZ tablets (200 mg every 12 hours), calcitriol soft capsules (0.25 microg twice a day), and leucogen tablets (20 mg three times per day), and the patient was instructed present for complete blood count, erythrocyte sedimentation, liver and kidney function tests, electrolytes, CRP, and VRZ levels regularly. The patient was followed up and measured VRZ concentrations at eleven days, three months, and six months after discharge. The VRZ dose was adjusted based on monitoring results. Liver functions remained normal during VRZ treatment. The timeline of the treatment process is displayed in Table 1. The dosing regimen and trough concentration changes of VRZ during the treatment are presented in Figure 1. Radiographic images, including CT scans and MRIs, are shown in Figure 2. | aspergillus tubingensis spondylitis, case report, enzyme-induction effect of rifampin, individualized pharmaceutical care, voriconazole | Not supported with pagination yet | null |
PMC9339741_01 | Female | 12 | A 12-year-old girl presented, complaining of prominent lower front teeth, protruded chin, and compromised mastication and phonation. She had very low self-esteem as she was constantly ridiculed for her unpleasant smile and facial appearance. The family history was not suggestive of any genetic predisposition. Extraoral examination revealed a bilaterally symmetrical face, a mesoprosopic facial form, a concave facial profile with midface deficiency, a retrusive upper lip, a prominent lower lip, an acute nasolabial angle, and a shallow mentolabial sulcus (Figure 1). A low lip line was evident upon smiling with almost negligible maxillary incisor display and excessive mandibular incisor display. CO-CR discrepancy was discernible with the inability to move the mandible backward with the incisors edge to edge in the retruded contact position. However, mild deviation of the mandible towards the left was noted on jaw closure from initial contact position to habitual occlusion position. The tongue was normal in size and function. In addition, the patient exhibited habitual oral breathing despite a patent nasal airway. TMJ exhibited normal functional activity.
Intraorally, she displayed bilateral Cl III molar and canine relationships with retained upper right deciduous canine and lower deciduous second molars. A long span of crossbite extending from the maxillary right deciduous canine to the left permanent first molar was observed. Incisor overbite was 5 mm, and overjet was -4 mm. The upper dental midline was shifted to the right of the facial midline by 2 mm. The lower dental midline was shifted to the left by 3mm compared to the upper dental midline (Figure 1). Both dental arches were relatively well-aligned. Model analysis revealed a transpalatal arch width of 33 mm in the first molars.
A panoramic radiograph, taken at the early permanent dentition stage of development, did not reveal any bony or periodontal abnormalities (Figure 2a). Cephalometric analysis revealed a skeletal Cl III anteroposterior relationship (ANB, -6 ; Wits appraisal, -8 mm), a retrognathic maxilla (SNA, 76 ), a prognathic mandible (SNB, 82 ), and a hypodivergent growth pattern. A large maxillomandibular discrepancy with Co-A to Co-Gn of 26 mm was noted (the normal range is 20-23 mm). The maxillary incisors were slightly proclined (U1 to SN, 105 ), whereas mandibular incisors had normal inclinations (IMPA, 89 ) (Figure 2b; Table 1). The soft tissue analysis confirmed upper lip retrusion and lower lip protrusion. The patient was in the CS3 stage of skeletal maturation, according to the CVMI method.
Based on the clinical and cephalometric examinations, the cause of this patient's malocclusion was an underdeveloped maxilla and mandibular prognathism.
The treatment goals were to (1) improve the skeletal jaw relationship by protracting the maxilla anteriorly relative to the cranium and redirecting mandibular growth, (2) correct anterior and posterior crossbites, (3) eliminate CO/CR discrepancy, (4) achieve esthetically favorable and functionally effective overjet and overbite, (5) establish canine-guided functional occlusion with anterior guidance, (6) improve frontal and profile esthetics, and (7) ensure that the patient breathed mostly through the nose.
Considering the patient's age and severity of the skeletal and occlusal disharmony, a bone-anchored maxillary protraction treatment protocol was suggested since it offers the advantages of ensuring 24-hour bone-borne force, at the same time avoiding the problems associated with dental anchorage. However, the patient and her parents declined this approach because of the underlying concerns about the associated surgical risks. Thus, a conservative two-stage treatment approach commensurate with the patient's young age and the parents' wishes was adopted. An orthopedic approach involving concurrent Alt-RAMEC and PFM therapy for effective maxillary advancement was contemplated as a stage 1 procedure, followed by fixed orthodontic mechanotherapy during phase 2 to achieve well-interdigitated buccal occlusion. However, the parents were informed of the possible need for orthognathic surgery in the future, considering the likelihood of intermaxillary sagittal relationship worsening if the craniofacial growth proved unfavorable or if the patient did not comply with the recommended duration of orthopedic treatment.
The first phase of treatment involved the Alt-RAMEC protocol performed with an 11-mm bonded Hyrax-type expander (Leone A2620, Leone Orthodontic Products, Italy), with the simultaneous use of a Petit-type facemask for protraction of the maxilla. A 7-week Alt-RAMEC protocol of alternating expansions and constrictions commenced with expansion in the first week, alternating to constriction in the second week, and completed with expansion in the seventh week (Figures 3a, 3b, and 3c). Daily activation of the expansion or constriction was 0.4 mm (0.20 mm per turn, one turn in the morning, and one turn at night). 5/16", 14 oz. Protraction elastics (600 g per side) were attached from the hooks on the maxillary expander near the maxillary canines, with a downward and forward pull of 30 from the occlusal plane (Figures 3d and 3e). The facemask was worn for 16 hours per day for nine months.
Following the removal of bonded Hyrax assembly after six months, the skeletofacial esthetics improved considerably. However, a posterior open bite of large magnitude (approximately 5 mm) was observed (Figure 4). At the beginning of phase 2 treatment, 0.022*0.028-inch slot pre-adjusted fixed appliances (MBT prescription) were placed in the maxillary and mandibular dental arches. Initial alignment and leveling were achieved with sectional archwires in the upper arch and continuous wires in the lower arch, starting with improved superelastic 0.016-inch NiTi wire, followed by 0.020*0.020-inch SS wire. A modified occlusal settling appliance,consisting of retentive pin-head clasps and lateral acrylic flanges, was used as an interim adjunct to prevent lateral tongue thrust to facilitate rapid settling of buccal segment occlusion (Figure 5).
Third molar germectomy was performed, followed by distalization of the mandibular right second molar, using compressed nickel-titanium open-coil spring on a 0.017*0.025-inch stainless steel (SS) wire to create space for mandibular right second premolar. Simultaneous use of short Cl III elastics helped counteract the mesial reactionary forces. Once adequate space had been created, the second premolar erupted spontaneously in its position in the arch (Figure 5). A normal sequence of continuous stainless-steel archwires was subsequently used to level and coordinate the arches.
While maintaining the original intercanine width in mandibular arch form, individualized first- and third-order bends were carefully incorporated in the maxillary and mandibular continuous 0.019*0.025-inch SS archwires to detail the tooth positions. Judicious use of short and light (3.5 oz.) Cl III and vertical spaghetti elastics helped improve occlusal interdigitation.
After debonding, retention consisted of maxillary and mandibular wraparound Hawley retainers worn during the daytime and a reverse twin block (RTB) appliance at night for 24 months. The patient was regularly monitored every six months to evaluate mandibular growth.
The total treatment duration was 27 months. Post-treatment final records showed the achievement of the desired treatment objectives, i.e., significant improvement in facial esthetics with the correction of the maxillary deficiency, better lip support and an improved nasolabial angle, along with the establishment of normal overjet and overbite, and well-intercuspated buccal occlusion with canine guidance (Figure 6). Dramatic improvement of the lip line and smile arc was discernible with adequate maxillary incisor display on smiling. Anterior movement of the upper lip, posterior movement of the lower lip, and soft tissue pogonion contributed to improvements in the patient profile. Nasal breathing also showed spontaneous improvements. Reverse twin block with upper and lower acrylic guided components was used as passive retention at night to prevent relapse (Figure 6).
A panoramic radiograph revealed good root parallelism with no significant apical resorption (Figure 7a). Cephalometric superimposition demonstrated improvements in the maxillomandibular relationship (Wits, -8 mm -1 mm; ANB, -6 1 ), the sagittal position of the maxilla (SNA, 76 79 ), and establishment of a harmonious soft-tissue profile along with the clockwise rotation of mandibular base (FMA, 24 ; SN-GoGn, 32 ) (Figures 7b, 7c, and 7d).
At 2.5-year and 4-year follow-up appointments, the harmonious facial balance and intermaxillary dental relationships were well-maintained (Figures 8 and 9). | adolescence, alt-ramec, cl iii malocclusion, orthopedic, protraction facemask, stability | Not supported with pagination yet | null |
PMC6080505_01 | Female | 32 | A 32-year-old HIV seronegative female patient, currently working as a research assistant in a healthcare facility presented with a second episode of massive haemoptysis within a 5-month period. She had been diagnosed with microbiologically proven PTB 6 years prior to her admission and completed 6 months of therapy. However, this was complicated by fibro-cavitatory destruction of her left lung with post-TB bronchiectasis (Fig. 1). Over the course of her follow up at the pulmonology clinic, and 2 years prior to this current presentation, she developed apical mycetoma's, which were identified on computed topographical scan of the chest (Fig. 2) and due to evident haemoptysis, she was considered for a left pneumonectomy. Her lung function test showed a restrictive lung pattern with a FEV1 of 64%, a FVC of 67% (FEV1/FVC of 95) and a DLCO of 74. Furthermore, a nuclear medicine split perfusion scan indicated no discernible perfusion to the affected lung. An electrocardiogram and echocardiogram were performed, indicating the presence of pulmonary hypertension.
On examination during this admission, she was haemodynamically stable with a blood pressure of 127/82 mmHg and a sinus tachycardia of 110 beats/min. She was afebrile, her respiratory rate measured 20 breaths/min and she was a-cyanotic on room air with an oxygen saturation of 93%. Marked digital clubbing and subconjunctival pallor were noted. On respiratory examination, evidence of left sided volume loss was present with decreased expansion of the left chest wall and compensatory hyperinflation of the right. The breath sounds on the right were vesicular in nature but the left side had breath sounds of reduced intensity with amphoric breath sounds and coarse crackles predominantly in the upper zone. No evidence of decompensated cor-pulmonale was present on cardiovascular examination, but pulmonary hypertension and mediastinal shift to the left were evident. A para-sternal heave with a palpable P2 were elicited, as was a loud pulmonary component of the second heart sound. Her apex beat was displaced to the anterior axillary line in the fifth intercostal space with tracheal deviation to the left side. Initial laboratory results showed a microcytic hypochromic anaemia with a haemoglobin of 7.7 g/dL (MCV = 73.8fl; MCHC = 31.4g/dL) and a platelet count of 487 x 109/l. Further haematological work-up demonstrated an iron-deficiency anaemia with a ferritin of 37 mug/l, percentage saturation of 5% and associated morphological features. Her renal and liver function tests were normal. Her C-Reactive Protein was 32mg/L and her INR measured 1.28. An Xpert MTB/RIF assay was performed and was reported as negative for mycobacterium tuberculosis.
She was admitted to medical high care. Transfused 1 unit of packed red blood cells and initiated on oral codeine phosphate. An emergency computed topographical pulmonary angiogram (CTPA) was performed and suggested the presence of a Rasmussen's aneurysm but formal angiography was deemed necessary for confirmation. Direct angiography indicated a pulmonary arterial blush adjacent to the left upper lung cavity confirming the presence of a Rasmussen's aneurysm (Fig. 3). Despite difficult initial ventilation due to her diseased lung, selective right bronchial intubation was performed and successful arterial embolization was achieved. Following 48 hours of post-procedural monitoring in a high care setting, she was stepped down to the general medical ward where after 6 days of remaining haemoptysis free, she was discharged home and is currently awaiting left sided pneumonectomy. | null | Not supported with pagination yet | null |
PMC5179082_01 | Unknown | 60 | The human tissues analyzed in this study (livers, lungs and kidneys) were obtained from four dengue fatal cases that occurred during a Brazilian outbreak of DENV-3 in 2002 in Rio de Janeiro. All patients died with a clinical diagnosis of severe dengue with infections confirmed by positive serum IgM antibodies. The four negative controls, from both sexes and ranging from 40 to 60 year old, were non-dengue and did not present any other infectious disease. More information about these cases can be found in a previous report of our laboratory. Briefly: | null | Not supported with pagination yet | null |
PMC9719436_01 | Female | 39 | A 39-year-old female patient presented to external consult after presenting on May 2021, a fall from her height secondary to a syncopal episode, as well as anomic aphasia, dizziness, and short-term memory loss. She presented again on August 2021, after another syncopal episode, as well as the gradual loss of sensibility and strength in all 4 extremities, and intense pain located in the cervical and thoracic regions.
During the physical examination, the patient remained alert, orientated, and cooperative, with oxygen saturation of 88%, a rhythmic heartbeat, globally diminished sensibility (1/2 ASIA), and strength (3/5 ASIA) in the upper extremities. A 3 cm diameter flyctena was documented on the medial aspect of the left heel, as well as spontaneous and involuntary movements of the left leg. A patient with a history of urinary tract infection was treated with ciprofloxacin for three weeks. Laboratories were obtained, showing chronic anemia grade 2 (WHO), platelets 515 K/muL and leucocytes 6 K/muL.
A series of X-rays and MRI were performed (Figure 1), which demonstrated multiple erosive and expansive lesions in the intervertebral discs and endplates in all segments of the spine, the most important being at the cervical region (C3-C7), with destruction and collapse of C6 and an abscess compressing the spinal cord. At the thoracic region (T6-T7), there was noted another abscess with significant compression of the spinal cord as a well as endplate and disc destruction, and at the thoracolumbar junction (T12-L1), an early process of spondylodiscitis was noted, with the erosion of the disc and endplates and an abscess in the medullary canal.
On November 2021, the patient was admitted for surgery under the diagnosis of spondylodiscitis to stop the progression of the severe neurological deficit. A staged surgical approach was preferred over a single surgical approach for two main reasons: first, the patient presented with suboptimal health status and second, it was the surgical team's choice of approach.
Based on physical exploration and neurological deficit, the first surgery was conducted in the most symptomatic region, the thoracic spine. A lateral retropleural thoracic approach was conducted, an osteotomy of the rib was performed, and selective lung intubation was needed to deflate it during the procedure. Affected levels (T6-T7) were identified and before I&D, multiple samples were obtained for cultures and histopathological study. Debridement included a corpectomy of T6, stability of the spine was achieved by placement of a titanium cage filled with allograft and matrix, and fixation was done with lateral T5-T7 screws and rod. A chest tube was placed and maintained for the next 72 hours, and broad-spectrum antibiotic therapy was initiated with vancomycin and meropenem awaiting culture results (Figure 2).
The biopsy sample demonstrated extensive fibrosis with a mixed inflammatory infiltrate and fragments of bone and cartilage with reactive-looking atypia. Under PAS and Ziehl-Neelsen stains, no microorganisms were identified. The cultures isolated Escherichia coli extended-spectrum beta-lactamases (ESBL) and Gram-positive cocci Staphylococcus aureus. Rose bengal and GeneXpert MTB/RIF (mycobacterium tuberculosis/rifampin) studies were negative for tuberculosis and brucellosis (Figure 3). The patient was discharged home after clinical improvement of pain and function, and infectology indicated a 6-week oral antibiotic course at home with ertapenem, trimethoprim/sulfamethoxazole, and doxycycline.
A second surgical intervention was scheduled on January 2022 after the patient presented with deterioration of sensibility and strength in the upper extremities. The cervical spine X-rays showed progression of the collapse and deformity noted in the previous MRI. An anterior cervical approach (Smith-Robinson) on the right side was performed, I&D of the prevertebral and medullary canal was carried out and multilevel discectomies were done in levels C3-C4 and C6-C7 and replaced with PEEK cages with matrix, and fusion and stabilization were maintained with an anterior 64 mm titanium plate and locked screws (Figure 4). After the surgical procedure, the patient reported minimal neck pain but right leg pain persisted, mobilization outside of bed with assistance was allowed, and the patient was discharged home with antibiotic and analgesic treatment with neurological rehabilitation for 3 months.
In April 2022, during follow-up, low back pain while walking and intractable pain in the right leg continued despite rehabilitation and analgesic medication. The patient was readmitted and scheduled for surgery, a direct posterior thoracolumbar approach was carried out at T12-L1 for I&D, discectomy, foraminal decompression, and fixation with transpedicular screws and rods. Evolution at 24 and 36 hours post-op showed pain decline and increased strength in the lower extremities (Figure 5). The patient was discharged home to continue with rehabilitation therapy in an ambulatory center. | null | Not supported with pagination yet | null |
PMC3951777_02 | Female | 55 | He was tested twice, 2 and 6 weeks after the present concussion. His findings were compared to a control group of 12 healthy adults (5 females), aged between 19 and 55 years old (30+-14). We looked for control subjects spanning a wide age range to minimize the potential impact of age-related effects. The age of the patient was included within this age range. Comparison of the results in our patient with a subset of the control subjects closer to his age (mean 44 years of age) did not affect any of the reported findings. The control subjects had no psychiatric or neurological conditions, normal neurological and medical exams, no history of concussions or TBI, were not taking any medications, and had no contraindications to receive TMS.
All participants tolerated the procedures, including TMS, without any side effect or complication. In particular, the patient did not have any headache either just before or at the end of each of the session. No other adverse events (pain, difficulty in concentrating, thinking, change in mood) were reported. All participants gave written informed consent for participation in the study, which had been approved by the local Institutional Review Board.
Brain MRI and DTI studies were obtained using a 3T GE scanner. Anatomical images were acquired using a T1-weighted, three-dimensional, magnetization-prepared, rapid-acquisition, gradientecho (MPRAGE) volume acquisition with a voxel resolution of 1 mm3. Diffusion images were acquired using a diffusion-weighted, single-shot, spin-echo, echo-planar imaging sequence (TE = min, TR = 17,000 ms, FOV 96 mm, voxel size = 2.2 mm 3, 30 nonlinear directions with b-value of 1,000 s/mm2). For precise quantitative measurement of changes in structural MRI, voxel-based morphometry (VBM) was done using FSL-VBM toolbox implemented in the FSL. Brain was extracted and created the study-specific template. All the images were non-linearly registered to the template and GLM using permutation testing was carried out. For diffusion tensor imaging analysis, we used Tract-Based Spatial Statistics (TBSS), which is widely used for whole-brain voxelwise comparison of white matter. First, data were preprocessed for head motion, and distortions due to eddy currents. Brain was extracted and DTI data was calculated for each voxel after fitting the diffusion tensor model to each voxel. This mean image was thresholded at an FA value of 0.2 and skeletonized to generate a white matter tract skeleton representing the center of the tracts common to all subjects. Permutation testing was used to calculate the t-statistics maps (uncorrected p<0.05).
No significantly different areas were found in VBM analysis (uncorrected p<0.05). DTI analysis revealed that changes in fractional anisotropy (FA) in the TBI patient did not differ from the findings in the controls (uncorrected p<0.05) (Fig. 1). Importantly, as part of the acute clinical evaluation after the concussion, the patient underwent a more complete clinical MRI study, including T2 weighted images that ruled out small hemorrhagic intraparenchymal lesions, intracranial hematomas and other signs of pathology.
Neuropsychological function was tested with the Immediate Postconcussion Assessment and Cognitive Test (ImPACT) and the CANTAB battery (Cambridge Cognition) and did not reveal any measurable cognitive deficits in the patient despite his subjective complaints.
Single- and paired-pulse TMS were applied using biphasic and monophasic figure-of-eight coils respectively (each wing, mean diameter 50 mm and outer diameter 70 mm) attached to a Nexstim stimulator (Nexstim Ltd, Helsinki, Finland). Continuous theta burst stimulation (cTBS) was applied using a biphasic figure-of-eight coil (each wing inner diameter 35 mm and outer diameter75 mm) attached to a MagPro stimulator (MagVenture A/S, Farum, Denmark).
Paired-pulse TMS over the left primary motor cortex (M1) was used to assess intracortical facilitation (ICF, tested with 12 ms between pulses) and short/long-interval intracortical inhibition (SICI and LICI, 3 and 100 ms between pulses respectively). The patient had significantly greater ICF at both time points. LICI was absent at week 2, but returned to normal at week 6. SICI in our patient was not different from the control group, which showed expected patterns of SICI, ICF and LICI (Fig. 2A).
Plasticity was evaluated with cTBS, expected to induce inhibition of the stimulated left M1 as indexed by a depression of motor-evoked potentials (MEPs) in contralateral hand muscles in response to subsequent single-pulse TMS. EEG was recorded simultaneously using the Nexstm eXimia TMS-compatible system. Contrary to the findings in controls, our patient had significant MEP facilitation at week 2, at 0, 5, 10 and 20 minutes after cTBS, but displayed normal inhibition of MEPs at week 6 (see Fig. 2B for the values up to 10 minutes after cTBS).
EEG raw data were high-pass filtered (1 Hz), epoched around each TMS pulse (-0.2 to 0.6 s, baseline: pre-TMS). For each subject, an Independent Component Analysis was run to identify and eliminate artifacts and remaining noisy channels were interpolated. Topographical EEG maps, 50 ms after single-pulse TMS, showed that at week 2, the patient had less intense and more widespread activation in response to single-pulse TMS over left M1 than the control group. This activation over left M1 was increased after cTBS, whereas it was decreased for the control group. At week 6, although the activation remained widespread, there was no more massive increase after cTBS (Fig. 2C).
In control subjects, the interhemispheric cross-correlation between temporal signals recorded over the two motor cortices (0 to 600 ms after the single-pulse TMS) tended to decrease 5 min after cTBS compared to baseline, whereas correlation between the stimulated M1 and the ipsilateral parietal and frontal areas tended to increase. The TBI patient significantly differed from the control subjects with a cTBS-induced increase of left M1-left parietal correlation at week 2, but not at week 6 (Fig. 2D and E). | null | Not supported with pagination yet | null |
PMC9612512_01 | Male | 0 | A 22-month-old African boy, born at full-term after normal pregnancy in Belgium, with no relevant medical history nor recent travel history and fully vaccinated according to the Belgian schedule, presented with dry cough and high fever for 3 days and respiratory distress for 24 h.
At admission, the child appeared grumpy, had tachycardia, and had a high fever (40 C). The first blood test showed mild inflammatory syndrome.
Pneumonia with pleural effusion was diagnosed clinically and on a chest X-ray. Intravenous (IV) penicillin (500,000 units/kg/day) was the first chosen antibiotic. Respiratory conditions worsened quickly, requiring a transfer to our pediatric intensive care unit (PICU) 6 h after admission.
Then, another chest X-ray showed a massive pleural effusion with tracheal deviation and a partial collapse of the left lung. At that time, the inflammatory syndrome had increased showing a discrepancy between leukocytes count (4160/mul) and C-reactive protein (CRP; 265 mg/L). IV flucloxacillin (200 mg/kg/day) and clindamycin (30 mg/kg/day) immediately replaced penicillin. The pleural effusion required a surgical drain placed by video-thoracoscopy.
Two days after thoracoscopy, the patient's general status deteriorated and he developed a septic shock requiring invasive ventilation, fluid resuscitation, and vasoactive amines. The shock remained refractory despite the adjunction of hydrocortisone, and an acute respiratory distress syndrome (ARDS) arose. Impaired cardiac function and ARDS led to venoarterial extracorporeal membrane oxygenation (ECMO) support for 9 days whereas invasive ventilation was required for 6 weeks. Acute renal insufficiency (KDIGO stage 3) was treated by continuous hemodiafiltration for 5 weeks with complete resolution of the renal insufficiency before discharge.
Because of the brutal degradation, the antibiotic therapy was transiently extended to IV ceftriaxone (100 mg/kg/day) and IV vancomycin (40 mg/kg/day continuously after a charge IV dose of 10 mg/kg) for 2 days, until obtaining the isolation of an MSSA from the pleural sample. Blood cultures remained negative. Flucloxacillin was finally administrated for 6 weeks and clindamycin for 10 days. IV human immunoglobulins (2 g/kg) were administered due to the initial suspicion of toxic shock syndrome.
Gradually, pulmonary lesions turned into bilateral pneumatoceles and necrotizing pneumonia (Figure 1). The pleural drain was left in place for several days because of persistent pneumothorax secondary to bronchopleural fistulas.
Based on the severe presentation and the unusual aggressive clinical course, we requested both spa-typing and the detection of a PVL toxin by polymerase chain reaction (PCR) on the SA recovered from the pleural sample and results came positive 13 days after admission (spa-type t021). Other exotoxins (toxic shock syndrome toxin-1 - TSST-1, exfoliatin A - eta, and exfoliatin B - etb) were negative. Enterotoxins had not been tested. The presence of PVL, TSST-1, eta, and etb genes was tested by end-point PCR using primers previously described. No contact with people having skin or soft tissue infections have been reported.
The patient showed mild short-term neurological disability (mild encephalopathy on the electroencephalogram) but gradually improved. One month after his admission, a cerebral magnetic resonance imaging (MRI) showed intraventricular, right lateral ventricle occipital horn, and right frontal white matter hemosiderin deposits, as well as ventricular dilatation. On a control 5 months later, the hemosiderin deposits remained with a significant decrease of ventricular dilatation.
At the 2-month follow-up, he presented unsteady walking, poor language for his age, and also sleep disorders. He recovered stable walking and good sleep quality at the 9-month follow-up even if his language remained underdeveloped for age.
The pneumatoceles were still seen on chest X-ray at the 2-month follow-up but without clinical impact. Chest X-ray significantly improved 1 year later. | panton-valentine leucocidin, staphylococcus aureus, children, methicillin-sensitive staphylococcus aureus, severe infections | Not supported with pagination yet | null |
PMC9612512_02 | Female | 0 | A 21-month-old African girl born in Belgium without medical history or travel history (for her and her family) and fully vaccinated, presented with a 3-day high fever to another emergency department where treatment by oral amoxicillin had been initiated. Four days later, because of persistent high fever and the onset of a one-sided cervical bulk, she came to the emergency room of our institution.
Cervical bulk was indurated, painful, and measured 3 cm on its long axis, at palpation. Initial blood analysis demonstrated a major inflammatory syndrome with a white blood cell count of 22,330/mul (with 16,190/mul absolute neutrophils) and a CRP of 180 mg/L. Indeed, a cervical MRI showed an abscess cavity measuring 10 cm long and 2 cm wide on a necrotic lymph node. This abscess extended to the anterior parapharyngeal space fusing to the middle mediastinum, next to cardiac vessels. Its massive extension reduced the size of the trachea (Figure 2).
After diagnostic imaging, IV ceftriaxone (100 mg/kg/day) associated with IV clindamycin (30 mg/kg/day) were started and the abscess was drained under ultrasound guidance. MSSA was isolated from the abscess sample but blood cultures stayed negative. After microbiological results, antibiotic therapy was changed to flucloxacillin (200 mg/kg/day) only and continued for 15 days (10 intravenously). A PVL test yielded positive in a spa-type t008 isolate. The PCR for other exotoxins (TSST-1, eta, and etb) were negative. Enterotoxins had not been investigated. She did not report any close contact with people having skin or soft tissue infections.
The total length of her hospital stay was 11 days including 5 at PICU. She had no sequelae of the infection at the 1-year follow-up. | panton-valentine leucocidin, staphylococcus aureus, children, methicillin-sensitive staphylococcus aureus, severe infections | Not supported with pagination yet | null |
PMC9612512_03 | Female | 14 | A 14-year-old fully vaccinated African girl born in Belgium, without any medical background and whose last travel with her family had been 10 years before to Congo Brazzaville. She was admitted to the Emergency Department of our institution for chest pain and dyspnea associated with deterioration of general condition for a few hours. She also had fever (around 38.7 C) and cough for 3 days.
A week before these complaints, she had a dizzy spell in the shower, which resulted in a fall. The day after she started to complain of coccygeal pain.
She presented with pulmonary infection and a major inflammatory syndrome on a blood test (CRP at 275 mg/L). She was admitted to the PICU for circulatory failure needing hemodynamic support with norepinephrine and milrinone for 2 days. The differential diagnosis between toxic shock syndrome, pediatric inflammatory multisystemic syndrome, and septic shock with pulmonary onset led to the initiation of IV broad-spectrum antibiotic therapy, ceftriaxone (100 mg/kg/day), and clindamycin (900 mg 3 times per day) combined with IV human immunoglobulins (2 g/kg).
At admission to PICU, a pancarditis with endocarditis of the mitral valve apparatus and pericardial effusion were highlighted. The extended workup showed cerebral, pulmonary, renal, and cutaneous emboli. An MRI of the pelvis, performed because of the history of coccygeal pain, revealed sacral osteomyelitis and multiple adjacent abscesses (Figure 3). Therefore, the suspected mechanism of septic shock was endocarditis with multiple emboli secondary to sacral osteomyelitis.
MSSA was found in multiple samples, namely: blood cultures (during 7 days), urine cultures, and cultures from pericardial fluid and pelvic abscesses. The liquid from ascites was negative.
From the first identification of MSSA, the second day of hospitalization, antibiotic treatment was changed for high-dose IV flucloxacillin (200 mg/kg/day) and clindamycin, held for 8 weeks and 11 days, respectively.
A test for PVL was found to be positive in a spa-type t5691 isolate. Investigations for other exotoxins (TSST-1, eta, and etb) were negative. Enterotoxins had not been tested. She had never been in contact with anyone presenting with recurrent skin or soft tissue infections.
Sustained bacteremia for 7 days despite a well-conducted antibiotic therapy and the numerous infected sites secondary to emboli required the drainage of the infected site (pelvic abscesses) to stop blood cultures to be positive.
Seven months after the beginning of this medical history, the patient started sport again with good tolerance. She had no sequelae. | panton-valentine leucocidin, staphylococcus aureus, children, methicillin-sensitive staphylococcus aureus, severe infections | Not supported with pagination yet | null |
PMC10343122_01 | Male | 70 | A 70-year-old married male presented with painful genital ulcer for 20 days. Initially, the patient developed single skin-colored elevated lesion over the shaft of the penis which gradually ruptured leaving behind a raw area associated with clear fluid discharge. The patient was admitted to surgery ward for nonhealing ulcer, was given oral antibiotic and anti-inflammatory medications but did not improve so was referred to the dermatology outpatient department for further evaluation. Reference was done to the dermatology department. No history of any drug ingestion before development of ulcer was present. On history, he denied any extramarital contact. He was not a known diabetic or hypertensive, but his HBa1c was 6.7 on admission. Cutaneous examination showed single circular ulcer of 2 cm x 3 cm in size with undermined edges, granulomatous base, and serous discharge over the ventral aspect of the penis [Figure 1]. There was no inguinal or femoral lymphadenopathy. The ulcer did not bleed on touch. Giemsa stain did not reveal bacillary or coccobacillary Donovan bodies. Gram stain prepared from the ulcer was negative. Biopsy was taken keeping donovanosis, sarcoidosis, PG, cutaneous tuberculosis, and SCC penis as differential diagnosis. Histopathologic examination from the ulcer edge showed granulation tissue with moderate to intense mixed polymorphonuclear, lymphocytic and plasmacytic inflammatory infiltrate, many congested blood vessels, and vast areas of hemorrhage and necrosis [Figure 2a and b]. The routine laboratory investigation, rapid plasma reagin, X-ray chest PA view, enzyme-linked immunosorbent assay-HIV, HBsAg, anti-HCV, urine routine, and microscopy were negative. On the basis of clinical examination and other investigations which ruled out other conditions, an alternate diagnosis of PG was made. The patient was treated with oral prednisolone 20 mg once a day and then in tapering doses, for a month and topical soframycin cream. Lesions healed within 15 days [Figure 3]. | neutrophilic dermatosis, penile, pyoderma gangrenosum | Not supported with pagination yet | null |
PMC7643780_01 | Male | 15 | A 15-year-old Caucasian boy was diagnosed with B-NHL involving lymph nodes, mediastinum and bones. The patient was treated according to B-NHL-BFM (Berlin-Frankfurt-Munster) 1997 protocol combined with Rituximab.
Seven days after the fifth chemotherapy course, the patient was hospitalized for fever (37.9 C), severe cytopenia (white blood cell count 0.15 x 109/L, neutrophils 0 x 109/L, platelet count 23 x 109/L, Hb 96 g/L), elevated C-reactive protein [C-RP] (92 mg/l), but normal procalcitonin [PCT] (0.33 ng/ml) and vital signs (blood pressure 124/69 mmHg, heart rate 79 beats per minute [bpm], peripheral oxygen saturation [Sp02] 97%). After drawing blood cultures from central line and peripheral vein, an empiric antibiotic treatment with ceftazidime, amikacin and teicoplanin was promptly initiated together with granulocyte colony stimulating factor (GCSF), while prophylaxis with cotrimoxazole and fluconazole was continued. On day 4 tachypnea, dyspnea, hypoxemia (Sp02 80%), tachycardia (heart rate 150 bpm) and left hemithorax acute pain appeared together with an increase of CRP (440 mg/l) and PCT (3.13 ng/ml). On physical examination, lung auscultation revealed diminished breath sounds and rales over the left lung. The first set of blood cultures was negative as well as the second one and the blood samples for galactomannan (GM) and beta-d-glucan (BDG) antigens. Lung computerized tomography (CT) showed a left extensive consolidation associated with pleural effusion (Figure 1).
Considering a possible fungal origin of pneumonia and the profound B-lymphocytopenia, micafungin (100 mg/day) was started and, in order to enhance the innate immunity, a 3-day course of intravenous IgM-enriched immunoglobulins was administered. On day 6 the fever disappeared while the neutrophils recovered over 0.5 x 109/L. On day 7, BDG was markedly positive (> 523 pg/ml) while GM remained negative. On day 9, high fever reappeared associated with edema and hyperemia on the left neck. A second lung CT revealed a slight increment of the left lung consolidation (Figure 2). A neck ultrasound detected a swelling lesion in left thyroid lobe (19 x 19 mm) and an abdomen ultrasound found a nodule in the middle-superior part of the right kidney (25 x 22 mm). This nodular lesions, as well as the lung one, were intensely hypermetabolic on positron emission tomography (PET)-CT scan proving to have probably the same infectious origin. We performed a needle aspiration of the thyroid lesion showing only the presence of a suppurative process. Blood cultures and serum GM were again negative whereas serum BDG value returned into normal range.
The antifungal therapy was enhanced adding voriconazole to micafungin, while the antibiotic therapy was modified introducing metronidazole and replacing ceftazidime and amikacin with meropenem. Despite this, the fever persisted with a CRP rising to 425.8 mg/L on day 11. On day 17 the patient underwent a bronchoalveolar lavage (BAL) that resulted negative for bacteria, fungi, Mycobacterium tuberculosis, GM and BDG antigen.
The patient continued to experience evening fever peaks and cough. On day 32 we repeated a CT scan showing unaltered the left lung consolidations and the left thyroid lobe lesion and an increase of the multiple nodules at the right kidney. These radiological findings were discussed in a multidisciplinary meeting with radiologists, infectivologists and pediatric hematologists discovering that the main lung lesion was presenting the reverse halo sign from the beginning. Given the lack of improvement and the severe clinical conditions, on day 36 the patient underwent left superior lung lobectomy. No postoperative complications were observed and the patient was discharged home 13 days later. The histopathological examination was consistent with a fungal pneumonia for the presence of hyphae. The identification of fungal DNA was performed by sequencing the internal transcribed spacer (ITS) domain of the rDNA gene and D1-D2 region of ribosomal sub-unites, according to the method described by White et al. that revealed the presence of Lichtheimia corymbifera (Figure 3). Therefore, the patient suspended voriconazole and received antifungal therapy with liposomal amphotericin B (5 mg/kg three times a week) and posaconazole (3 x 200 mg/d) for 7 weeks.
Six days after discharge home the patient developed low grade fever (37.5 C), painful increase and hyperemia of the left emithyroid (60 x 50 mm), increased of CRP 125 mg/l and PCT 0.13 ng/ml) with normal blood count. The patient underwent an urgent hemithyroidectomy with surgical drainage with rapid clinical improvement. The cultural search for bacteria, fungi and Mycobacteria resulted negative.
The patient continued a secondary prophylaxis with posaconazole (3 x 200 mg/day) for 18 months. A lung CT, performed 6 months after surgery, showed only postoperative changes whereas the renal lesion disappeared after 12 months of posaconazole treatment. | fungal infection, mucormycosis, pediatric non hodgkin lymphoma | CT lung scan showing the extensive consolidation (57 x 61 mm) at the lower lobe of the left lung associated with pleural effusion. |
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PMC7643780_01 | Male | 15 | A 15-year-old Caucasian boy was diagnosed with B-NHL involving lymph nodes, mediastinum and bones. The patient was treated according to B-NHL-BFM (Berlin-Frankfurt-Munster) 1997 protocol combined with Rituximab.
Seven days after the fifth chemotherapy course, the patient was hospitalized for fever (37.9 C), severe cytopenia (white blood cell count 0.15 x 109/L, neutrophils 0 x 109/L, platelet count 23 x 109/L, Hb 96 g/L), elevated C-reactive protein [C-RP] (92 mg/l), but normal procalcitonin [PCT] (0.33 ng/ml) and vital signs (blood pressure 124/69 mmHg, heart rate 79 beats per minute [bpm], peripheral oxygen saturation [Sp02] 97%). After drawing blood cultures from central line and peripheral vein, an empiric antibiotic treatment with ceftazidime, amikacin and teicoplanin was promptly initiated together with granulocyte colony stimulating factor (GCSF), while prophylaxis with cotrimoxazole and fluconazole was continued. On day 4 tachypnea, dyspnea, hypoxemia (Sp02 80%), tachycardia (heart rate 150 bpm) and left hemithorax acute pain appeared together with an increase of CRP (440 mg/l) and PCT (3.13 ng/ml). On physical examination, lung auscultation revealed diminished breath sounds and rales over the left lung. The first set of blood cultures was negative as well as the second one and the blood samples for galactomannan (GM) and beta-d-glucan (BDG) antigens. Lung computerized tomography (CT) showed a left extensive consolidation associated with pleural effusion (Figure 1).
Considering a possible fungal origin of pneumonia and the profound B-lymphocytopenia, micafungin (100 mg/day) was started and, in order to enhance the innate immunity, a 3-day course of intravenous IgM-enriched immunoglobulins was administered. On day 6 the fever disappeared while the neutrophils recovered over 0.5 x 109/L. On day 7, BDG was markedly positive (> 523 pg/ml) while GM remained negative. On day 9, high fever reappeared associated with edema and hyperemia on the left neck. A second lung CT revealed a slight increment of the left lung consolidation (Figure 2). A neck ultrasound detected a swelling lesion in left thyroid lobe (19 x 19 mm) and an abdomen ultrasound found a nodule in the middle-superior part of the right kidney (25 x 22 mm). This nodular lesions, as well as the lung one, were intensely hypermetabolic on positron emission tomography (PET)-CT scan proving to have probably the same infectious origin. We performed a needle aspiration of the thyroid lesion showing only the presence of a suppurative process. Blood cultures and serum GM were again negative whereas serum BDG value returned into normal range.
The antifungal therapy was enhanced adding voriconazole to micafungin, while the antibiotic therapy was modified introducing metronidazole and replacing ceftazidime and amikacin with meropenem. Despite this, the fever persisted with a CRP rising to 425.8 mg/L on day 11. On day 17 the patient underwent a bronchoalveolar lavage (BAL) that resulted negative for bacteria, fungi, Mycobacterium tuberculosis, GM and BDG antigen.
The patient continued to experience evening fever peaks and cough. On day 32 we repeated a CT scan showing unaltered the left lung consolidations and the left thyroid lobe lesion and an increase of the multiple nodules at the right kidney. These radiological findings were discussed in a multidisciplinary meeting with radiologists, infectivologists and pediatric hematologists discovering that the main lung lesion was presenting the reverse halo sign from the beginning. Given the lack of improvement and the severe clinical conditions, on day 36 the patient underwent left superior lung lobectomy. No postoperative complications were observed and the patient was discharged home 13 days later. The histopathological examination was consistent with a fungal pneumonia for the presence of hyphae. The identification of fungal DNA was performed by sequencing the internal transcribed spacer (ITS) domain of the rDNA gene and D1-D2 region of ribosomal sub-unites, according to the method described by White et al. that revealed the presence of Lichtheimia corymbifera (Figure 3). Therefore, the patient suspended voriconazole and received antifungal therapy with liposomal amphotericin B (5 mg/kg three times a week) and posaconazole (3 x 200 mg/d) for 7 weeks.
Six days after discharge home the patient developed low grade fever (37.5 C), painful increase and hyperemia of the left emithyroid (60 x 50 mm), increased of CRP 125 mg/l and PCT 0.13 ng/ml) with normal blood count. The patient underwent an urgent hemithyroidectomy with surgical drainage with rapid clinical improvement. The cultural search for bacteria, fungi and Mycobacteria resulted negative.
The patient continued a secondary prophylaxis with posaconazole (3 x 200 mg/day) for 18 months. A lung CT, performed 6 months after surgery, showed only postoperative changes whereas the renal lesion disappeared after 12 months of posaconazole treatment. | fungal infection, mucormycosis, pediatric non hodgkin lymphoma | CT lung scan showing the slight increment of the left lung consolidation (53 x 77 mm) appearing as an area of pulmonary opacity surrounded by normal parenchyma. |
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PMC4320181_01 | Female | 30 | A 30-year-old female with a fever, scleritis, and auricular pain for a duration of 3 months was examined. She was finally diagnosed with RP from her symptoms, auricle biopsy and response to corticosteroid therapy according to the proposed diagnostic criteria (McAdam et al.; Damiani and Levine). She frequently took non-steroidal anti-inflammatory drugs (NSAIDs) along with predonisolone for pain control. Subsequently, she experienced episodes of lower abdominal pain 2 months after the initial diagnosis of RP. Although her abdominal symptoms temporally subsided with steroid pulse therapy, the abdominal pain relapsed and the bloody stools as well as anemia emerged after terminating steroid pulse therapy. As a result, we started to investigate her abdomen and GI tract. Laboratory tests revealed an increased inflammatory response (white blood cells 10,300/mul; C-reactive protein, 5.4 mg/dl), hypoalbuminemia (total protein, 5.9 g/dl, albumin, 2.9 g/dl), and anemia (red blood cells, 3.20 x 106/mul, hemoglobin, 8.7 g/dl, hematocrit, 27.2%) (Table 1). Abdominal contrast-enhanced computed tomography (CT) scan revealed thickening of the ileocecal wall, and positron emission tomogaraphy (PET) revealed accumulation in the intestinal tract at the terminal ileum. Total colonoscopy (TCS) revealed oval-shaped deep ulcers on the terminal ileum with deformity and destruction of the ileocecal valve (Figure 1). In addition, reddish edematous mucosa and ulcers were detected in the oral side of the ileum. Biopsy specimens taken from the terminal ileum showed nonspecific inflammatory findings. There were no abnormal findings in her large intestinal mucosa and upper GI tracts. We highly suspected the possibility of intestinal BD from the characteristic endoscopic findings, but the case did not meet the diagnostic criteria because of lacking the major BD symptoms such as oral aphthoid ulcers, eye symptoms, skin lesions or genital ulcers. In addition, other diseases such as NSAIDs-induced enteritis were not completely denied; therefore, we selected a conservative therapy and planned a close follow-up. After restricting food and NSAIDs from the initial TCS, slight improvements were observed in her abdominal symptoms. However, no significant change was evident on colonoscopy performed 4 weeks after the initial TCS. Differential diagnoses included intestinal BD, Crohn's disease, NSAIDs-induced enteritis, malignant lymphoma, and infectious colitis such as cytomegalovirus colitis or enteric tuberculosis. However, the test results, including a biopsy, culture, and various imaging tests did not provide a definitive diagnosis. We decided to perform surgery in order to make a definite diagnosis and avoid the GI perforation because of the presence of deep and active ulcers. An ileocecal resection was performed 5 weeks after the initial TCS. Gross findings of the resected specimen showed that the ileocecal valve was highly deformed and destroyed by deep ulcers. Furthermore, large and small ulcers were diffusely-scattered on the ileal mucosa, from the ileocecal valve to 30 cm on the oral side (Figure 2). Histological examination revealed ulcer formation with destruction of muscularis propria. The ulcer base was rather flat and showing involvement of nonspecific chronic inflammation with fibrotic change. The mucosa around the ulcers remained relatively normal in structure (Figure 3). There were no specific findings such as granulomas, CMV-infected cells, vasculitis or thrombus formation; thus, we remained to believe intestinal BD as the diagnosis.
After the operation, she was in stable condition. We followed her progress on an outpatient basis while tapering her prednisolone dosage. However, RP symptoms such as fever, scleritis, and auricular pain relapsed 5 months after the operation, in addition to the recurrence of abdominal pain and watery diarrhea. This led us to perform TCS which revealed multiple deep and round ulcers developing at the anastomotic site. We also observed multiple erosions and aphthae on the oral side of the small intestine and large bowel from the ascending colon to the rectum (Figure 4). We initiated infliximab (IFX) administration, which has been reported to be effective against both RP and BD. After the administration of IFX, her cartilaginous and abdominal symptoms dramatically improved. A follow-up TCS was performed at the end of the fourth administration of IFX. We identified ulcer scars at the anastomosis site and inflammation of the large intestine improved (Figure 5). We recognized that both RP and BD were responsive to IFX administration. Currently as an outpatient, she is regularly receiving IFX treatment and continues to remain in good health. | ileocecal ulcers, intestinal behçet’s disease, magic syndrome, relapsing polychondritis | Not supported with pagination yet | null |
PMC8057857_01 | Female | 40 | The data on the risk of preterm labor in pregnant patients with COVID-19 as opposed to those without is very mixed. A systematic review of over 350 pregnant patients showed that preterm labor rates in patients >30 weeks' gestation were 15%. This rate is increased from the national average of 10% preterm birth rate in the United States. Another observational study of 55 pregnant patients with infection yielded a rate of 43% preterm labor in that specific cohort. These patients ranged in age from 23 to 40 years old, and all were infected with COVID-19 in the third trimester. There is thought that the infection and fever may increase the likelihood of preterm labor. There is also a sense of bias in the data, as many providers are more inclined to induce labor in infected patients for fear of unknown or unforeseen complications. There is insufficient data to determine the exact etiology of the cause of preterm labor and whether there is a causal relationship between COVID-19 infection and preterm labor. However, there appears to be an association of third trimester COVID-19 infections and the rate of preterm labor.
Similar to the rates of preterm labor, the rates of cesarean delivery in patients afflicted with COVID-19 are elevated due to provider preference not to deliver vaginally. An extensive systematic review of over 500 COVID-19 infected pregnant patients reported rates for delivery in 435 patients. The cesarean delivery rate in these patients was at 84.7%; only a reported 8 cases required ICU level of care. This indicates that the cesarean delivery rate was correlated to physician practice and erring on the side of caution rather than required cesarean for maternal and neonatal complications. There were no maternal deaths in this study and only one neonatal death.
Similarly, another cohort study between March and April showed increased cesarean rates from normal in COVID-19-infected patients. These patients were stratified from asymptomatic to severe disease based on WHO classification. In the severely infected patients, 52.4% were delivered via C-section instead of 92% of the critical patients delivered via C-section. There were decreased rates in asymptomatic and mild cases. This cohort study made an association between the severity of the COVID-19 infected and the mode of delivery with higher rates of cesarean in patients with more severe disease. Lastly, another systematic review in pregnant patients with greater than 90% hospitalization rates for COVID-19 pneumonia showed an increased C-section rate of 91%. This study shows the increased rate in severe COVID-19 pneumonia requiring oxygen support and hospitalization and is not representative of most of the population infected with COVID-19.
There is little data regarding the differing rates between post-partum hemorrhage (PPH) in those vaginally delivered with and without COVID-19 serologically identified infection. Due to the hypercoagulable changes associated with pregnancy and COVID-19, there is reason to believe there would be altering PPH rates in patients afflicted. However, early Chinese studies showed there was no increased risk of PPH in patients delivering with COVID-19, although in the study, there was increased usage of oxytocin during and after delivery. In the event of PPH, there has been a suggestion against the use of antifibrinolytic agents, such as tranexamic acid, due to the increased risk of thrombosis involved in severe and critical COVID-19-infected patients. Thus, practitioners may choose against this and other treatments that can cause pulmonary arterial vasoconstriction, such as methylergotamine, due to hypoxia's theoretical risk. There is limited data to support these suggestions or findings.
There was seemingly no increased rate of maternal mortality in multiple systematic reviews and cohort studies in those hospitalized with COVID-19. The mortality rate in pregnant and non-pregnant patients is relatively equal. In two systematic reviews in New York and of selected widespread databases, the mortality rate of over 250 and 350 patients, respectively, was 0.0%. In contrast to other coronavirus outbreaks such as SARS and MERS, COVD-19 shows no increased maternal mortality risk. SARS had reported 25% and MERS a 28% risk of maternal mortality. There is an increased hospitalization and ICU admissions rate with mechanical ventilation compared to a matched non-pregnant cohort. However, this is not associated with any increased rate of mortality in pregnant patients. There is no known correct number of maternal mortalities currently, but it is believed to be similar to the rate of COVID-19 infection mortality of the general population. In Florida, pregnancy mortality is assessed quarterly by the Pregnancy Associated Mortality Review (PAMR), a statewide maternal mortality review process tasked to better understand why women are dying during pregnancy, childbirth, and the year post-partum. Approximately half the states in the U.S. have a comprehensive maternal mortality review process.
As important as the effects of COVID-19 infection are on the mother, the infection may also impact the developing fetus. Due to the unknown nature of the coronavirus, infected pregnant patients will often have questions and concerns regarding the effects of coronavirus on their fetus. Most importantly, they will have concern for risk of transmission to the fetus, risk of fetal mutations and malformations, and, ultimately, risk for fetal demise. As per the currently available literature, there seems to be no clear vertical transmission of the virus to the fetus. A small observation study conducted in the U.S. of 43 newborns from infected mothers showed 0 positive results upon testing during the first day of life. In opposition, there is data showing a small positive rate in newborns. In a relatively larger systematic review of 936 positive mothers, there was a 3.2% COVID-19 PCR positive rate via nasopharyngeal swab (27/936) in neonates. This rate mirrored other studies done in China in 2020 during the outbreak. These rates were for third-trimester maternal COVID-19 infection. These rates were deemed to be similar to pathogens that cause congenital infections. Due to the limited data of first-trimester infections, it is difficult to conclude any early antepartum vertical transmission to the neonate. A lancet observational cohort study done in New York City of over 1400 deliveries, including 116 to COVID-19 positive mothers, showed that no neonates at 24 hours tested positive for coronavirus. Of the 82 neonates who followed up within 5 to 7 days, 68 roomed with their mothers, and 64 were breastfed for the 5 to 7 days of rooming. The repeat COVID-19 PCR was negative in all neonates who were breastfed and who followed up. This suggests that breastfeeding is safe, and there is limited vertical transmission of COVID-19 to neonates. There may be components of inappropriate measures taken in those with positive COVID-19 serologies at 24 hours. This conflicting data makes it difficult for physicians to educate their patients regarding vertical COVID-19 transmission.
However, it is possible to educate patients regarding the potential risks of neonatal COVID-19 infection. The overwhelming majority of data regarding neonatal COVID-19 infections shows mild respiratory distress as the most common complication. A review in the Children's Hospital of Wuhan reported on 33 patients born from COVID-19 positive mothers, three of these patients had COVID-19 infection, and the symptoms included fever with neonatal sepsis and acute hypoxic respiratory failure without cyanosis.
Current data suggests that there is no risk of teratogenic effects in developing fetuses due to COVID-19 antepartum infection. Although the data is limited due to limited reviews and small observational studies, preliminary research shows no teratogenicity.
Treatment of infectious disease in pregnant patients often presents a unique challenge due to the many known and unknown adverse effects of antimicrobials on the developing fetus. This, coupled with the evolving treatment of COVID-19, makes this challenge even more difficult.
The current understanding and treatment of COVID-19 in non-pregnant patients is often influenced by the severity of the disease, individual comorbidities, degree of immunosuppression of the patient, and various other factors. Many patients are placed on an experimental treatment that shows promising preclinical or early phase clinical trial data. Many of the current pharmaceutical drugs used to treat COVID-19 are not well studied in pregnancy, adding even more reason for hesitancy in prescribing physicians. Thus, severity indexes must be used to stratify COVID-19 positive patients. Many stratification methods used in non-pregnant patients, such as D-dimer levels, Sequential organ failure assessment (SOFA) score, and O2 saturation, differ in pregnancy due to maternal physiologic changes. Pregnant patients have a hypercoagulable state coinciding with elevated D-dimer levels at baseline. Thus, D-dimer should not be used to stratify the severity of COVID-19 infection in pregnant patients. Oxygen saturation levels also differ in pregnant patients as, at baseline, this population has a higher resting PaO2 level to increase fetal oxygenation. Thus, there is a higher threshold for dropping oxygen saturation levels. Many physicians use the cutoff of <92% or even lower in non-pregnant patients with COVID to begin supplemental oxygen. However, the WHO recommends maintaining an O2 saturation between 92-95% and a PaO2 >70 in pregnant patients to decrease the risk of fetal hypoxemia and acidosis. The threshold for mechanical ventilation in pregnancy is also reduced for the reasons mentioned previously. With increasing oxygen supplementation without response and PaO2 <70, evidence suggests early intubation decreases the morbidity and mortality rates of pregnant patients with acute hypoxemic respiratory failure.
Pregnancy is a known state of hypercoagulability - predisposing patients to venous and arterial thromboembolism. There have been many preliminary reports and observational studies that support an increased risk of thrombosis in patients with COVID-19. Current evidence supports venous thromboembolism (VTE) prophylaxis with unfractionated or low-molecular-weight heparin (LMWH) for all pregnant patients admitted with COVID-19. Five thousand units of unfractionated heparin (UFH) every 12 hours are recommended over LMWH because it is more readily reversible. However, UFH is classified as a pregnancy category C drug while LMWH falls in category B, which may sway practitioners towards the use of LMWH for anticoagulation in the inpatient setting. LMWH may also be used in cases in which delivery is not expected within days to weeks. There are reports of many hospitals using full-dose anticoagulation in patients with worsening oxygen saturation <92% on >4L of supplemental oxygen. However, there is currently minimal data to support therapeutic dose anticoagulation without diagnosed deep vein thrombosis, pulmonary embolism or clinical signs, and symptoms of the clot.
Remdesivir is the most recent antiviral studied in the treatment of COVID-19. This antiviral is used in patients with severe COVID-19 under study protocol, initially given through compassionate use and more recently approved by the FDA for more widespread administration. This is less so done in pregnant patients as this drug was developed to treat Ebola and Marburg viruses. However, recently accepted manuscript data spanning from March 21 to June 16 described the use of remdesivir in hospitalized pregnant women with confirmed COVID-19 infection and O2 saturation <94% who met the criteria to be enrolled in the compassionate use program. Of the 86 patients enrolled in this study, 19 were delivered before their first course of remdesivir and were included in the immediate post-partum group. The remaining patients, whose median gestational age was 28 weeks, were started on remdesivir with follow-up after 28 days. After the 28-day follow-up, the oxygen requirement in 96% of the pregnant patients decreased.
Furthermore, 93% of those requiring mechanical ventilation were extubated, 93% recovered, and 90% were discharged. Adverse events were experienced in 29% (22/67) of the cohort. These adverse events were described as anemia, constipation, dysphagia, worsening hypoxia, and deep vein thrombosis, among others. Other side effects shown included increasing liver function tests and serum creatinine levels with seven pregnant women discontinuing the study drug due to adverse events. Currently, remdesivir is classified as a pregnancy category B2 pharmaceutical drug - epitomizing the limited data of remdesivir in the pregnant cohort. There is little data regarding the fetal effects of remdesivir from its current usage in the treatment of COVID-19 infections or during prior clinical trials to treat Ebola. With consideration of the low molecular weight and avid protein binding, it is hypothesized that remdesivir may cross the placenta, although more clinical studies are needed to determine any adverse neonatal effects.
Corticosteroids, such as dexamethasone, are currently indicated in the treatment of severely ill non-pregnant patients who require oxygen or ventilatory support. Corticosteroids are often indicated in pregnant patients who are in or at high risk for preterm labor to promote fetal lung maturity. More recently, there has been data supporting the use of dexamethasone in patients with severe COVID-19 infection. This controlled trial demonstrated that in patients either requiring oxygen support or on mechanical ventilation, there was a decrease in 28-day mortality rates. Dexamethasone or betamethasone is the preferred agents used to induce fetal pulmonary maturation in patients between 24 and 34 weeks of gestation at increased risk for preterm labor. Other corticosteroids that have been used include methylprednisolone or hydrocortisone, as these steroids limit fetal steroid exposure. This theoretical usage has less published data for reducing maternal mortality. All corticosteroids, including dexamethasone, belong to the pregnancy category C due to the fact that these pharmaceutical drugs cross the placenta and are only partially metabolized by placental enzymes into inactive metabolites. These molecular properties, coupled with the potential teratogenicity of dexamethasone, have given physicians much trepidation. Potential side effects of dexamethasone on the developing fetus include theoretical distortions of osteogenesis in the fetus and fetal malformations such as oral clefts and intrauterine fetal growth restriction. Despite these possible adverse outcomes, the American College of Obstetricians and Gynecologists (ACOG) recommends that treatment with dexamethasone should not be withheld in pregnant patients when indicated. Thus, it is recommended to use dexamethasone in pregnant patients in the ICU or mechanically ventilated patients due to the benefits shown in the treatment of COVID-19 and for the maturing neonate.
With the recent release of the mRNA vaccines, Pfizer-BioNtech (BNT162b2) and Moderna (mRNA-1273), there is concern from pregnant patients regarding the vaccine's detrimental effects in utero. However, mRNA vaccines do not contain the live virus that causes COVID-19; therefore, COVID-19 cannot be contracted from the vaccine. Additionally, mRNA vaccines do not interact with one's DNA because the mRNA does not enter the nucleus of the cell. Cells break down the mRNA quickly after the mRNA is translated into the protein. Due to this fact, mRNA vaccines are unlikely to pose a specific risk in pregnancy. The actual risks of mRNA vaccines to the pregnant person and her fetus are unknown because these vaccines have not been adequately studied in this population. In a cohort study evaluating the immunogenicity and reactogenicity of COVID-19 mRNA vaccination (BNT162b2 and mRNA-1273) in pregnant and lactating women, the vaccines induced antibody titers equivalent in pregnant and lactating women to non-pregnant women. These mRNA COVID-19 vaccines generated robust humoral immunity in pregnant and lactating women, similar to that observed in non-pregnant women. Further, the vaccine-induced immune responses were significantly greater than the response to natural infection, and the immune transfer to neonates was also observed via placenta and breast milk.
COVID-19 vaccine (Ad26.COV2.S) functions differently:in that the vaccine is a viral vector vaccine. This uses a viral vector to deliver the COVID-19 spike protein from which immunity is developed. Viral vectors have been previously given to pregnant patients of all trimesters in large-scale Ebola vaccination trial and no adverse pregnancy-related outcomes that affect the infant, were associated with viral vector vaccination in these trials. Currently, an open-label, phase 2 study to evaluate the safety, reactogenicity, and immunogenicity of Ad26.COV2.S in healthy pregnant is ongoing. The purpose of this ongoing clinical trial is to assess the safety and reactogenicity of Ad26.COV2.S administered intramuscularly (IM) as a 2-dose schedule, in adult participants during the second and/or third trimester of pregnancy and (potentially) post-partum. This study is also going to assess the humoral immune response in peripheral blood of adult participants, to Ad26.COV2.S administered IM as a 2-dose schedule during the second and/or third trimester of pregnancy, 28 days after the first and second vaccination.
In animals, development and reproductive toxicity (DART) studies using the mRNA (BNT162b2 and mRNA-1273) and Ad26.COV2.S vaccines before or during pregnancy found no safety concerns. There were no direct or indirect harmful effects with respect to female reproduction, fetal/embryonal development, or postnatal development.
The American College of Obstetricians and Gynecologists (ACOG) recommends COVID-19 vaccines should not be withheld from pregnant individuals who meet the criteria for vaccination based on the Advisory Committee on Immunization Practices (ACIP)-recommended priority groups. | covid-19, neonatal outcomes, placenta, pregnancy, sars-cov-2, treatment, vaccine, vertical transmission | Not supported with pagination yet | null |
PMC3235990_01 | Male | 27 | A 27-year-old Peruvian male was admitted to our hospital because of fever, chills, productive cough, and chest pain. The patient had been in his usual state of general health until three months earlier when he began to notice some chest discomfort which was pleuritic in nature. The pleuritic chest pain was soon followed by the development of fever and productive cough. After a couple of weeks, the patient presented to a different hospital. At that hospital he was treated for lung abscess of the lingular lobe with clindamycin and an aminogylcoside for a period of four weeks, with little radiographic or clinical improvement. The patient was eventually discharged and presented to the emergency room several weeks later with no resolution in his symptoms.
There was no history of dyspnea, hemoptysis, seizure disorder, or alcohol or drug abuse. He denied any history of sick contacts. The patient was born and raised in Peru and had worked as a farm laborer prior to his migration to the United States five years prior to presentation. The patient had a history of contact with all domestic and farm animals while living in a farming village inland from Lima in his native Peru.
Physical examination on admission to the hospital showed a young, toxic-looking male with an oral temperature of 102 degrees Fahrenheit, a pulse rate of 120 beats per minute, respiratory rate of 20 breaths per minute, oxygen saturation of 95%, and a blood pressure of 110/70 mmHg.
Abnormal physical findings were confined to the chest, which showed bronchial breath sounds, an impaired percussion note, and few rales over the left lower chest anteriorly and laterally. There was mild clubbing of the fingers. Examination of the heart and the abdomen was unremarkable.
Initial white blood cell count was 10,900, with 60% polymorphonucleocytes, 7% band formations, 17% lymphocytes, 3% monocytes, and 13% eosinophils. A comprehensive metabolic panel, remaining complete blood count, and electrocardiogram were unremarkable. The chest radiograph (Fig. 1) showed a large thick-walled cavity involving the lingular lobe, containing an irregular wavy fluid level, suggestive of floating particulate matter ("waterlily sign"). A left lateral decubitus chest film confirmed mobility of the contents of the cavity.
Eventual gram stain of the sputum showed polymorphonucleocytes with mixed bacterial flora but the culture was negative. Computed tomography of the chest also supported the findings noted on the chest radiograph and failed to disclose any intrahepatic or abdominal abnormalities.
A fiberoptic bronchoscopic examination showed mucosal inflammation and mucopurulent secretions in the lingular and left lower lobe bronchi. The airways were patent. A fistulous communication between the accessible airways and the cavity was not identified. Bronchial washings were negative for malignant cells and for acid-fast bacilli on smear examination. An intermediate strength purified protein derivative (tuberculosis) skin test showed a 15 mm induration.
The patient was initially treated with clindamycin 600 mg intravenously every six hours for a period of ten days without a substantive clinical response. A. fumigatus had been isolated from bronchial washings. This information, coupled with a positive serum precipitin test for A. fumigatus, supported the diagnosis of an aspergilloma in a chronic abscess cavity. A Casoni test was not done. The patient underwent thoracotomy and resection of the lingular lobe.
Gross examination of the surgical specimen (Fig. 2) revealed the cavity to be a hydatid cyst that was 7.5 cm in its largest diameter. The cyst consisted of an outer shell, the ectocyst, with a glistening white inner surface. Contained within was a pearly membranous structure, the endocyst, lying in a pool of turbid brownish fluid. The surrounding lung parenchyma was compressed and firmly adherent to the outer surface of the ectocyst. Microscopic examination of the fluid sediment (Fig. 3) disclosed several hooklets and other remnants of scolices diagnostic of cystic echinococcosis. Histologic examination of the pericyst (Fig. 4) showed inflammatory changes and infiltration by numerous septate hyphae consistent with Aspergillus species. A. fumigatus was isolated on culture from the cystic fluid. Bacterial culture of the cystic fluid was negative.
Following surgical resection of the hydatid cyst, the patient recovered uneventfully and became afebrile on the sixth post-operative day. There were no postoperative complications. The patient has remained in good health and has failed to show recurrence for three years after thoracotomy. | aspergillus, aspergilloma, echinococcosis, hydatid cyst, lung abscess, lung cavity | Not supported with pagination yet | null |
PMC3738353_01 | Female | 7 | A 7-year-old Chinese girl presented to our department with a 3-week history of low-grade fever and cough. Her previous history was unremarkable. Physical examination revealed a soft abdomen with a tender liver edge 3 cm below the right costal margin and a palpable spleen tip; the chest was found to be normal. Routine laboratory tests were normal except for hemoglobin 9.9 gr/dL (nv 11.5-14.5) and erythrocyte sedimentation rate (ESR) of 79 mm/h (nv < 38). Tuberculin skin test was positive with 20 mm induration. Quantiferon-TB Gold test was 59 IU/mL (nv < 0.34). HIV test was negative. Chest X-ray showed mild thickening along the right major fissure and bilateral hilar enlargement. Abdominal ultrasound (US) performed using a 3.5 mHz convex transducer (Acuson Sequoia 512, Siemens, Mountain View, CA, USA) revealed mild hepatomegaly, multiple hypoechoic nodules up to 13 mm in diameter scattered throughout the liver and spleen (Fig. 1); slight wall thickening of the last ileal loop and ascending colon, and multiple enlarged mesenteric lymph nodes were also shown. Multidetector computed tomography (CT) of the abdomen was performed using 16-slice CT scan (LightSpeed, GE Healthcare, Milwaukee, WI, USA) with 5-mm slice thickness (reconstructed 2.5 mm) and low dose technique (80 kv, 50-90 mAs) after i.v. contrast medium administration. CT revealed multiple rounded, low-density lesions in the liver and spleen, ranging in size from 2 to 18 mm (Fig. 2); peripancreatic, periportal, para-aortic, and paracaval lymph nodes up to 15 mm in diameter with no calcification, and diffuse small bowel wall thickening were also shown. CT of the chest demonstrated small opacities in the right lower lobe and multiple enlarged lymph nodes in the hilar, paraesophageal, and paratracheal regions (Fig. 3). Direct smear microscopy for acid-fast bacilli in the sputum and gastric lavage was negative, but the culture for Mycobacterium tuberculosis was positive. Colonoscopy showed a nodular, ulcerated mass that partially obstructed the cecum. Intestinal biopsy and image-guided needle biopsy of the liver revealed granulomatous tissue with caseous necrosis. Both direct smear microscopy for acid-fast bacilli and culture for Mycobacterium tuberculosis of intestinal and liver biopsy specimens were negative.
Diagnosis of macronodular hepatosplenic TB with concomitant intestinal and lung involvement was made, and a three-drug anti-TB therapy consisting of isoniazid, rifampicin, and pyrazinamide was planned. After 9-month therapy, there was a marked improvement in the general condition, and the liver and spleen were no longer palpable. Abdominal US revealed reduction in size and peripheral calcification of the hepatosplenic lesions (Fig. 4); abdominal lymph nodal groups were normal. | tuberculosis, children, liver, spleen | Not supported with pagination yet | null |
PMC3323333_01 | Male | 54 | In August 2000, a 54-year-old comatose man was admitted to our infectious diseases department with a 10-day history of fever. He had a medical history of vertebral arthrosis (lumbar laminectomy in 1989) and insulin-dependent diabetes mellitus. Six weeks before, he had received for 3 days gluteal injections with kebusone (an intramuscular nonsteriodal antiinflammatory drug [NSAID]) for acute lower back pain. Twenty-eight days after the first injection, a gluteal abscess developed, which was surgically drained, without perioperative antimicrobial therapy. Three days later, he became febrile, and pyrexia persisted despite local wound management and treatment with oxacillin, 4 g/day for 3 days; cefuroxime, 3 g/day, and gentamicin, 160 mg/day for another 7 days.
The patient became comatose and was transferred to our department. At that time, the physical examination showed fever (40.2 C), neck stiffness, Brudzinski sign, thoracic dullness, and bilateral crackling rales. The level of C-reactive protein was 123 mg/L. Renal failure was noted with a creatinine blood level of 312 mmol/L and uncontrolled diabetes with fasting glucose of 24.75 mmol/L. Computed tomographic (CT) scan of the brain did not show brain abscesses or tumors. Examination of the cerebrospinal fluid (CSF) indicated a protein level of 2.67 g/L, decreased glucose concentration of 0.55 mmol/L, and a leukocyte count of 2.3 x 109/L with 96% neutrophils; no microbial pathogens were demonstrable under direct examination of CSF. Chest x-ray identified bronchopneumonia and bilateral pleural effusion. The pleural fluid analysis revealed a purulent exudate:protein, 4.5 g/L:containing 55% neutrophils. A urine specimen and three blood samples were obtained for cultures over the first 4 hours after admission. A bacterial invasive infection was considered and the antibiotic therapy was started with ceftriaxone, 2 g/day, and rifampin, 1,200 mg/day. Concomitantly, the patient received colloids to reestablish blood volume, intravenous dexamethasone, 6 mg four times daily, to diminish the cerebral edema; and fast-acting insulin to control hyperglycemia.
On day 3, the urine and CSF cultures were positive for E. hermanii, and the pleural fluid and all three blood cultures yielded methicillin-susceptible S. aureus. The E. hermanii strain produced a yellow pigment. The drug susceptibility was assessed by AtB Expression system (BioMerieux, Marcy l'Etoile, France). The Staphylococcus strain was susceptible to oxacillin, cotrimoxazole, tetracycline, and ciprofloxacin and resistant only to penicillin. E. hermanii is naturally resistant to aminopenicillins and carbenicillin; this strain was susceptible to third-generation cephalosporins, carbapenems, cotrimoxazole, and quinolones and resistant to aminoglycosides.
The patient's clinical central nervous system status improved, and he came out of the coma, but his temperature remained >37.5 C. He started to report lumbar pain. On day 5, the antimicrobial regimen was switched to meropenem. After 24 hours, the patient became apyretic, and glucose and creatinine levels were normal on day 8. However, on day 10, fever, inflammation of the right thumb, and intensified lower back pain developed. The abdominal CT and bone scintigraphy indicated abscess of the psoas, L4-L5 spondylitis, and thumb periostitis. Intravenous ciprofloxacin was added, 400 mg twice daily, and apyrexia occurred on day 14. On day 21, open surgery was performed, consisting of drainage of the psoas abscess and curettage of the L4-L5 disc. On day 30, clinical improvement and C-reactive protein level of 4.2 mg/L, led to a change to oral antimicrobial agents: cotrimoxazole 2 g/day and ciprofloxacin 1.5 g/day. This regimen was continued for 2 months while the patient was seen as an outpatient. The patient remained afebrile and inflammation-free for the entire 24-month followup period.
Polymicrobial invasive infections represent a major therapeutic problem. However, they are infrequent: only 3.2% of infectious endocarditis cases and 6.27% of 2,188 community-acquired bacteremia cases were polymicrobial. Polymicrobial infections and elevated bacteremia levels are more frequently associated with diabetes; 20%-35% of the skin and soft tissue infections in persons with diabetes are polymicrobial, and 15.7%-20% of the community-acquired bacteremia cases were registered in persons with diabetes. The probable entry site for S. aureus was cutaneous. Intramuscular NSAIDs are known to cause aseptic necrosis, predisposing the patient to staphylococcal abscesses. Hyperglycemia itself is a risk factor for soft-tissue infections. The role of perioperative antimicrobial therapy in preventing the dissemination of infection from a surgically drained abscess is controversial. E. hermanii usually produces wound or gastrointestinal tract infections; in our patient, E. hermanii probably originated from the skin or from the gastrointestinal tract. E. hermanii could be involved more frequently in polymicrobial invasive infections; of E. hermanii invasive infections noted in four published reports, two were polymicrobial.
Initial antimicrobial drug therapy was established empirically for probable staphylococcal meningitis. The ongoing fever and persistent metabolic disturbances led to an escalation of therapy. Some authors recommend carbapenems as the initial regimen against invasive methicillin-susceptible S. aureus infections with meningeal or bone involvement. The patient's lower back and the invasive staphylococcal infection urged us to consider septic bone involvement. The imaging studies confirmed the existence of vertebral osteomyelitis; ciprofloxacin was used based on its excellent bone diffusion and its in vitro activity on the two isolated strains. Surgical intervention eradicated of one of the septic foci and decreased risk for spinal cord injury; 27 (47%) of the 58 patients with spondylodiscitis who were treated surgically had a better outcome than the other patients with medical care only. Control of the infection allowed changing to an oral regimen after 1 month. We selected cotrimoxazole and ciprofloxacin for their in vitro effectiveness against the two pathogens. Although this agent is not usually used to treat bone infection, we used cotrimoxazole on the basis of evidence provided by several communications that indicated a superior efficiency to referential regimens.
In conclusion, the identification of all organisms involved in polymicrobial invasive infections may require cultures of specimens from all accessible septic foci. For E. hermanii, a role of "associated" pathogen in a polymicrobial invasive infection could be considered. Medical therapy alone could be insufficient, and the combined therapy allowed for a successful outcome in invasive infection with lumbar spondilodiscitis. | null | Not supported with pagination yet | null |
PMC2627818_01 | Female | 72 | A 72-year-old asymptomatic woman presented to the clinic for a checkup. She had a history of cholecystectomy, hypothyroidism, and hypertension. She had been treated with thyroid hormone (Puran T4, 75 mug), an anti-hypertensive agent (the angiotensin-converting enzyme inhibitor Enalapril , 20 mg), an antiarrhythmic drug (Diltiazem , 90 mg), and acetylsalicylic acid (200 mg). She reported use of oral contraceptives for over 30 years. She had no history of smoking, drinking, drug abuse or family history of liver disease.
On physical examination, the liver was palpable to 6.5 cm from the right costal, and 10 cm from the appendix xiphoid; it was painless, and had a rugged and hard consistency. Laboratory studies revealed the following: red blood cells, 3,690,000/mm3; hemoglobin, 11.7 g/dL; hematocrit, 35%; platelets, 278,000/mm3; cholesterol, 186 mg/dL; triglycerides, 70 mg/dL; glucose, 85 mg/dL; TSH, 2.8 U/mL; serum creatinine, 0.7 mg/dL; ALT, 47 U/L; AST, 29 U/L; GGT, 23 U/L; alkaline phosphatase, 138 U/L; TB, 0.8 mg/dL; DB, 0.4 mg/dL; PT, 12 s; INR, 1.0; PTT, 29 s; folic acid, 11 mg/mL; alpha-fetoprotein, 2.08 ng/mL; iron, 106 mug/dL; vitamin B12, 210 pg/mL; ferritin, 170 mg/L; LDH, 384 IU/L; and CEA 2.4 ng/mL.
Abdominal ultrasound revealed an enlarged and heterogeneous liver that contained an expansive and heterogeneous lesion measuring 14 x 9.4 cm with poorly defined limits, including two echogenic nodular areas, measuring 6.3 and 3.2 cm, respectively. The gallbladder was not visualized.
Computed tomography (CT) of the upper abdomen (Figure 1) showed a heterogeneous lesion - measuring 15 x 14 x 10 cm - with a partially well-defined margin and hypodense permeating areas, some with attenuation values compatible with soft parts, and others with liquefaction located in the left liver lobe. After endovenous contrast injection, the lesion showed intense and non-homogeneous impregnation in the arterial and portal phases, with hypodense permeated areas located in the left lobe, notably parts II and III; these areas determined recoil and reduced the size of vascular structures adjacent to the liver. The injury also caused bulging of the border of adjacent liver tissue, causing a compressive effect on other abdominal structures, especially the stomach and pancreas.
Magnetic resonance (MR) imaging of the upper abdomen showed different components within the lesion. T2-weighted images in the peripheral region showed a discrete heterogeneous hyperintense signal, while the central portion was hypointense. In T1-weighted images, the signal in the periphery of the mass was similar to the muscle signal and the center of the lesion showed a signal that was clearly hypointense. Although impregnation of both components began in the arterial phase, the peripheral region showed a stronger signal during the arterial and portal phases, followed by signal decay in the late phase due to relatively rapid washout, indicative of hypervascularization. The center of the mass was far more intense in the late phase, probably due to slow flow through the vascular components (Figures 2 and 3).
Surgery and pathological analysis revealed a hepatic segment measuring 17.5 x 14 x 8 cm and weighing 1200 g that contained a 15 x 9 cm brown tumor with ill-defined limits. The tumor had a gelatinous component and showed hemorrhaged, necrotic, and cystic areas. The final diagnosis was TA. The patient progressed well and she remains asymptomatic after one year of follow up. | null | Not supported with pagination yet | null |
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