As a possible disease I would consider Brucellosis, typical of cattle (milk, abortion, genital secretions...). It presents with a pseudo-flu-like symptomatology (headache, arthralgias, myalgias, fever...) and other symptoms depending on the route of entry. In our case, when attending animal births, the entry is through the respiratory route, so the pulmonary infiltrates and chest pain are due to the bacteria. The treatment varies according to the affectation and mortality is very low, almost null. Morbidity and involvement in pregnant women are of greater concern. Important: it is very frequent in livestock workers (veterinarians, farmers, slaughterhouses...) if you read something like "attends births of livestock animals", "works on a farm", "is a veterinarian" suspect Brucellosis.

A 38-year-old woman of veterinary profession, in charge of monitoring wild animals and assisting in the delivery of domestic livestock. She starts with a high fever with chills, headache, myalgia and non-productive cough that she interprets as a flu-like process. She presented with chest pain. Chest X-ray showed bilateral pulmonary infiltrates in lower fields. A serologic test was performed with elevated titers of antibodies against phase II antigens. Which of the following statements is TRUE?

Both doxycycline and hydroxychloroquine are effective in treating acute forms of this disease.

In the acute form, the patient also generally has elevated antibodies to phase I antigens.

Mortality in acute forms is almost nonexistent.

Importance of clinical history in the diagnosis of psittacosis: A case report.

Psittacosis, caused by the bacteria Chlamydia psittaci, is primarily a disease of birds that can be transmitted to humans. The clinical manifestations of the disease are wide, ranging from asymptomatic illness to fulminant psittacosis with multi-organ failure. The organism gets attached to the upper respiratory mucosa after inhalation and the majority remain asymptomatic. However, some people may develop symptoms of atypical pneumonia. Psittacosis usually presents with sudden onset fever with chills and rigor, headache, and myalgia. Here we present a case of a 35 years old female with a history of close contact with parrots who presented to the ER with complaints of high-grade fever and headache for 2 weeks which started 2 days after her parrots died. The disease usually manifests as flu-like symptoms or pneumonia and is included in the differential diagnosis of community-acquired pneumonia. Investigations reveal neutrophilia, raised erythrocyte sedimentation rate, C-reactive protein, and elevated liver enzymes which were consistent with the findings of our patient. Chest X-ray showed ill-defined consolidation in the right middle and lower lobes which were inconclusive. Hence, a CT chest was done which revealed patchy ground glass opacities with surrounding consolidation giving a reverse halo sign. Due to her contact with birds and CT findings which were suggestive of psittacosis, she was started on doxycycline and her condition improved thereafter. We highlight the importance of proper history taking and awareness on zoonotic diseases to the general public to prevent, diagnose and treat the disease effectively.

[Familial outbreak of psittacosis].

Three familial cases of psittacosis are reported. The first case was a 46-year-old woman, the second case, her 18-year-old daughter. Both of them often visited the house of the third case, a 49-year-old women, who was the elder sister of case 1 and who took care of the chick of a budgerigar which she kept in the house. Case 1 came to our hospital with abrupt onset of fever, headache, nausea and general malaise. Because she was suspected to have meningitis, she was admitted to the Department of Neurology. On admission, her chest X-ray film showed bilateral ground glass shadows. She also had hypoxemia and liver dysfunction. On learning of her history of contact with the chick, psittacosis was suspected. Case 2 suffered from fever and headache. Her chest X-ray film revealed opaque infiltration in the right lower lung field. Case 3 complained of fever, headache and vomiting. Her chest X-ray film showed fan-shaped faint shadows in the left upper, middle and lower lung fields. We interpreted these findings as showing psittacosis based on anamnesis. The result of the complement fixation (CF) antibody titer against chlamydia was 1:32 in cases 2 and 3, enabling a serological diagnosis of psittacosis. The corresponding result was 1:16 in case 1. Although the CF antibody titer showed no increase, we diagnosed the case clinically as psittacosis. It is difficult to correctly diagnose psittacosis only from the physical findings and chest X-ray films. Detailed anamnesis, in particular taking a history of exposure to birds, is an important clue for diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Q fever--still a query and underestimated infectious disease.

Coxiella burnetii (C.b.) is a strictly intracellular, Gram-negative bacterium. It causes Q fever in humans and animals worldwide. The animal Q fever is sometimes designated "coxiellosis". This infection has many different reservoirs including arthropods, birds and mammals. Domestic animals and pets, are the most frequent source of human infections. Q fever may appear basically in two forms, acute and chronic (persistent). The latter form of Q fever in animals is characteristic by shedding C.b. into the environment during parturition or abortion. Human Q fever results usually from inhalation of contaminated aerosols originating mostly from tissue and body fluids of infected animals. Q fever may appear in humans either in an acute form accompanied mainly by fever (pneumonia, flu-like disease, hepatitis) or in a chronic form (mainly endocarditis). Diagnosis of Q fever is based on isolation of the agent in cell culture, its direct detection, namely by PCR, and serology. Detection of high phase II antibodies titers 1-3 weeks after the onset of symptoms and identification of IgM antibodies are indicative to acute infection. High phase I IgG antibody titers >800 as revealed by microimmunofluorescence offer evidence of chronic C.b. infection. For acute Q fever, a two-weeks-treatment with doxycycline is recommended as the first-line therapy. In the case of Q fever endocarditis a long-term combined antibiotic therapy is necessary to prevent relapses. Application of Q fever vaccines containing or prepared from phase I C.b. corpuscles should be considered at least for professionally exposed groups of the population. Infections caused by C.b. are spread worldwide and may pose serious and often underestimated health problems in human but also in veterinary medicine. Though during the last decades substantial progress in investigation of C.b. has been achieved and many data concerning this pathogen has been accumulated, some questions, namely those related to the pathogenesis of the disease, remain open.

[Two cases of acute hepatitis associated with Q fever].

Q fever which is caused by Coxiella burnetii, is a worldwide zoonosis. Many species of wild and domestic mammals, birds, and arthropods, are reservoirs of C.burnetii in nature, however farm animals are the most frequent sources of human infection. The most frequent way of transmission is by inhalation of contaminated aerosols. The clinical presentation of Q fever is polymorphic and nonspecific. Q fever may present as acute or chronic disease. In acute cases, the most common clinical syndromes are selflimited febrile illness, granulomatous hepatitis, and pneumonia, but it can also be asymptomatic. Fever with hepatitis associated with Q fever has rarely been described in the literature. Herein we report two cases of C.burnetii hepatitis presented with jaundice. In May 2011, two male cases, who inhabited in Malkara village of Tekirdag province (located at Trace region of Turkey), were admitted to the hospital with the complaints of persistent high grade fever, chills and sweats, icterus, disseminated myalgia and headache. Physical examination revealed fever, icterus and the patient appeared to be mildly ill but had no localizing signs of infection. Radiological findings of the patients were in normal limits. Laboratory findings revealed leukocytosis, increased hepatic and cholestatic enzyme levels, and moderate hyperbilirubinemia- mainly direct bilirubin, whereas serum C-reactive protein and erythrocyte sedimentation rate were found normal. Blood and urine cultures of the patients yielded no bacterial growth. Serological markers for acute viral hepatitis, citomegalovirus and Epstein-Barr virus infections, brucellosis, salmonellosis, toxoplasmosis and leptospirosis were found negative. Acute Q fever diagnosis of the cases were based on the positive results obtained by C.burnetii Phase II IgM and IgG ELISA (Vircell SL, Spain) test, and the serological diagnosis were confirmed by Phase I and II immunofluorescence (Vircell SL, Spain) method. Both cases were treated with doxycycline for 14 days and became afebrile within four days. These cases were presented to emphasize that C.burnetii infection should be considered in the differential diagnosis of patients with fever and elevated serum transaminase levels, irrespective of the presence of abdominal pain and exposure to potentially infected animals.

Pulmonary inflammatory pseudotumor due to Coxiella burnetii. Case report and literature review.

A 58-year-old man was admitted because of respiratory failure, episodic fever with chilling, cough, malaise, fatigue, myalgia and weight loss lasting for at least one month. Chest x-rays and CT scan of the chest showed bilateral pulmonary consolidations in upper lobes, the left lower lobe, and mediastinal lymphadenopathy. Bronchoscopy with cytology was unremarkable. A needle CT-guided lung biopsy documented an inflammatory pseudotumor, lymphoplasmacytic type. Serology showed high titer antibodies to phase II Coxiella burnetii infection. Therapy with doxycycline and hydroxychloroquine for three months led to a complete resolution of symptoms and radiological findings, and a marked decrease in titers to Q fever.

Q Fever: an old but still a poorly understood disease.

Q fever is a bacterial infection affecting mainly the lungs, liver, and heart. It is found around the world and is caused by the bacteria Coxiella burnetii. The bacteria affects sheep, goats, cattle, dogs, cats, birds, rodents, and ticks. Infected animals shed this bacteria in birth products, feces, milk, and urine. Humans usually get Q fever by breathing in contaminated droplets released by infected animals and drinking raw milk. People at highest risk for this infection are farmers, laboratory workers, sheep and dairy workers, and veterinarians. Chronic Q fever develops in people who have been infected for more than 6 months. It usually takes about 20 days after exposure to the bacteria for symptoms to occur. Most cases are mild, yet some severe cases have been reported. Symptoms of acute Q fever may include: chest pain with breathing, cough, fever, headache, jaundice, muscle pains, and shortness of breath. Symptoms of chronic Q fever may include chills, fatigue, night sweats, prolonged fever, and shortness of breath. Q fever is diagnosed with a blood antibody test. The main treatment for the disease is with antibiotics. For acute Q fever, doxycycline is recommended. For chronic Q fever, a combination of doxycycline and hydroxychloroquine is often used long term. Complications are cirrhosis, hepatitis, encephalitis, endocarditis, pericarditis, myocarditis, interstitial pulmonary fibrosis, meningitis, and pneumonia. People at risk should always: carefully dispose of animal products that may be infected, disinfect any contaminated areas, and thoroughly wash their hands. Pasteurizing milk can also help prevent Q fever.

Imported brucellosis and Q-fever coinfection in Croatia: a case report.

The brucellosis and Q-fever coinfection is very rarely reported. To our knowledge, this is the first case report of concomitant brucellosis and Q-fever, most likely imported in Croatia. A 30-year-old male agricultural worker was hospitalized on 22 April 2017 after a ten days fever up to 40°C with chills, shivering, excessive sweating, general weakness, loss of appetite and headache. A month and a half prior to the hospitalization he lost 18 kg of body weight. Three weeks before hospitalization the patient returned from Kupres (Bosnia and Herzegovina) where he was working for the past year on a sheep farm and consumed unpasteurized dairy products of sheep origin. At admission, his condition was moderately severe due to pronounced dehydration. Routine laboratory tests showed slightly elevated erythrocyte sedimentation rate, anemia, thrombocytopenia and elevated liver transaminases. The chest X-ray showed an inhomogeneous infiltrate of the lower right lung. Three sets of blood culture were cultivated. After 48 hours incubation, bacterial growth was detected in aerobic bottles. Gram-stained smear revealed small, gram-negative coccobacilli. Specimens were subcultured on blood and chocolate agar plates. Using a Vitek GN identification card, the isolated organism was identified as Brucella melitensis. 16S rRNA gene sequencing of the isolate confirmed it as a Brucella sp. Rose-Bengal test was positive, while Wright agglutination test showed a significant increase in antibody titer from 80 to 640 in paired sera. Using indirect immunofluorescence assay (IFA), Coxiella burnetii phase II IgM/IgG titers were 50 and 1024, respectively indicating acute Q-fever. The patient was treated with doxycycline and rifampicin. So far, there has been no relapse or signs of chronic infection.

Acute chest syndrome

Diagnosis The diagnosis of acute chest syndrome is made difficult by its similarity in presentation with pneumonia. Both may present with a new opacification of the lung on chest x-ray. The presence of fevers, low oxygen levels in the blood, increased respiratory rate, chest pain, and cough are also common in acute chest syndrome. Diagnostic workup includes chest x-ray, complete cell count, reticulocyte count, ECG, and blood and sputum cultures. Patients may also require additional blood tests or imaging (e.g. a CT scan) to exclude a heart attack or other pulmonary pathology. Prevention Hydroxyurea is a medication that can help to prevent acute chest syndrome. It may cause a low white blood cell count, which can predispose the person to some types of infection. Treatment Broad spectrum antibiotics to cover common infections such as Streptococcus pneumoniae and mycoplasma, pain control, and blood transfusion. Acute chest syndrome is an indication for exchange transfusion.

Hantavirus pulmonary syndrome

Signs and symptoms Initially, HPS has an incubation phase of 2–4 weeks, in which patients remain asymptomatic. Subsequently, patients can experience 3–5 days of flu-like prodromal phase symptoms, including fever, cough, muscle pain, headache, lethargy, shortness of breath, nausea, vomiting and diarrhea. In the following 5–7 day cardiopulmonary phase, the patient's condition rapidly deteriorates into acute respiratory failure, characterized by the sudden onset of shortness of breath with rapidly evolving pulmonary edema, as well as cardiac failure, with hypotension, tachycardia and shock. In this phase, patients may develop acute respiratory distress syndrome. It is often fatal despite mechanical ventilation and intervention with diuretics. After the cardiopulmonary phase, patients can enter a diuretic phase of 2–3 days characterized by symptom improvement and diuresis. Subsequent convalescence can last months to years. As of 2017, patient mortality in the USA from HPS is 36%.

Pulmonary involvement in brucellosis.

Brucellosis is a zoonotic disease caused by a Gram-negative bacillus of the Brucella genus with multisystem involvement, primarily affecting the reticuloendothelial system, joints, heart and kidneys. Although the disease can be spread by inhalation, pulmonary involvement is rare. To report a case of brucellosis with pulmonary involvement. CASE PRESENTAION: A previously healthy 36-year-old woman was admitted with complaints of fever, weakness, night sweats, dry cough and bilateral chest pain. She hed been diagnosed with pneumonia 20 days previously and was started on a course of ampicillin for 14 days, with no response. Her chest auscultation revealed diminished breath sounds and scattered crackles and rhonchi over the inferior zone of the right hemithorax. Wright and Coombs testing resulted in titres of 1:1280 and 1:640, respectively. Chest radiography revealed an area of confluent lobar consolidation in the right lower lobe. Treatment was started with a six-week course of oral doxycycline 200 mg/day and rifampicin 600 mg/day. This treatment regimen rapidly improved the patient's condition. Follow-up after one year showed no residual effects from the infection. Pulmonary involvement is a rare event in the course of brucellosis, but the rate could be higher than currently estimated. In endemic regions, brucellosis should be considered as a causative agent in patients with pulmonary symptoms. Brucellosis is a zoonotic disease caused by a Gram-negative bacillus of the <iBrucella</i genus with multisystem involvement, primarily affecting the reticuloendothelial system, joints, heart and kidneys. Although the disease can be spread by inhalation, pulmonary involvement is rare. To report a case of brucellosis with pulmonary involvement. A previously healthy 36-year-old woman was admitted with complaints of fever, weakness, night sweats, dry cough and bilateral chest pain. She hed been diagnosed with pneumonia 20 days previously and was started on a course of ampicillin for 14 days, with no response. Her chest auscultation revealed diminished breath sounds and scattered crackles and rhonchi over the inferior zone of the right hemithorax. Wright and Coombs testing resulted in titres of 1:1280 and 1:640, respectively. Chest radiography revealed an area of confluent lobar consolidation in the right lower lobe. Treatment was started with a six-week course of oral doxycycline 200 mg/day and rifampicin 600 mg/day. This treatment regimen rapidly improved the patient’s condition. Follow-up after one year showed no residual effects from the infection. Pulmonary involvement is a rare event in the course of brucellosis, but the rate could be higher than currently estimated. In endemic regions, brucellosis should be considered as a causative agent in patients with pulmonary symptoms.

[Diffuse panbronchiolitis with myeloperoxidase-specific antineutrophil cytoplasmic antibody-related vasculitis].

A 46-year-old woman was referred to our department in July 1996 with complaints of fever and myalgia in her calves. She had a 20-year history of purulent sputum; diffuse panbronchiolitis had been diagnosed in 1983. Physical examination revealed low-pithed rhonchi over the lung fieldis and hypesthesia of the right leg. She had a white blood cell count of 16,100/mm3, including 4% eosinophils, and a platelet count of 80.0 x 10(4)/mm3. The serum IgE level was 2,200 U/ml, and the cold hemagglutinin titer was high. Pulmonary-function tests showed mixed ventilatory dysfunction, and arterial blood gas analysis revealed a PaO2 of 55.8 Torr on room air. Pseudomonas aeruginosa was cultured from her sputum. A chest X-ray film and CT scan showed diffuse nodular shadows and bronchiectatic changes with mild hyperinflation. An infiltrative lesion in right S6 area could also be seen. Administration of broad-spectrum antibiotics did not alleviate her symptoms. The level of myeloperoxidase-specific antineutrophil cytoplasmic antibody (MPO-ANCA) in serum was 245 EU/ml, and 67Ga scintigraphy showed marked accumulation in the abdomen. Abdominal angiography demonstrated a bead-like appearance and irregularities in the peripheral branches of the hapatic artery, the splenic artery, the cystic artery, and the superior mesenteric artery. Because of the high MPO-ANCA level and the angiographic abnormalities, MPO-ANCA-related vasculitis was diagnosed. She was treated with 1 g of methylprednisolone daily for 3 days, followed by 60 mg of prednisolone and 50 mg of cyclophosphamide daily. Her condition improved dramatically, and the MPO-ANCA level became almost normal. During treatment, her blood pressure rose markedly with a normal serum creatinine level and normal urinalysis. Plasma renin activity was 13.3 ng/ml/hr. Renal angiography showed stenoses and irregularities in the peripheral branches of renal arteries bilaterally. These findings led to a diagnosis of renovascular hypertension due to vasculitis. Her blood pressure was controlled with an angiotensin-converting enzyme inhibitor and a calcium antagonist. Vasculitis associated with chronic supportive lung disease has occasionally been reported, which suggests a casual relation between chronic respiratory infection and ANCA-related vasculitis. Systemic vasculitis should be taken into account as a potential complication of chronic suppurative lung disease.

Histoplasmosis -- History and Physical -- Acute Pulmonary Histoplasmosis

Primary infections are frequently asymptomatic, or the patients tend to ignore mild flu-like symptoms. The major determinant of symptoms is the inoculum size. The typical incubation period is seven to 21 days. High fever, headache, nonproductive cough, and chest pain are the main symptoms. This chest pain is not pleuritic and is in the anterior chest and is believed to be due to enlargement of mediastinal or hilar lymph nodes. Most of the symptoms resolve in 10 days. Rheumatologic manifestations can occur such as arthralgias, erythema nodosum or erythema multiforme in a small number of patients (6%, mostly women). This syndrome appears to be less frequent in histoplasmosis when compared to coccidioidomycosis. Imaging shows patchy diffuse pneumonitis and hilar lymphadenopathy. There is no granulomatous inflammation as cellular immunity matures by two weeks in primary infection. During the acute pulmonary infections, a skin test may be positive in more than 90% of cases, antibody to H. capsulatum may be present in 25% to 85% of cases, the urinary antigen may be positive in 20% of cases, and sputum culture from lungs may be positive in less than 25% of cases.

Q Fever -- Differential Diagnosis

Patients with acute viral infections, such as Epstein-Barr virus, cytomegalovirus, influenza, hepatitis A, B, or C virus, have similar presenting complaints, such as febrile illness, hepatitis, and myalgia. Serological tests and PCR assays are used to identify these infections. Atypical pneumonia caused by Legionella and Mycoplasma needs to be considered. They can be ruled out by detecting urine antigen or serum antibody titers. Tick-borne illnesses such as Lyme disease, relapsing fever, and Rocky Mountain spotted fever manifest with fever and headache with or without a rash. Anaplasmosis and ehrlichiosis present with fever, headache, and hepatitis, with a lesser incidence of rash. Tick-borne diseases are detected via PCR and/or serology. Zoonotic diseases such as brucellosis and leptospirosis can manifest as an acute flu-like illness with a history of exposure to animals or animal products.

An outbreak of cat-associated Q fever in the United States.

Q fever is usually acquired by contact with aerosols generated during parturition of domestic ungulates (e.g., sheep, cows, goats). In the maritime provinces of Canada, parturient cats have also been implicated in its transmission. A 66-year-old woman from eastern Maine developed high fever, rigors, headache, myalgias, pulmonary infiltrates, and elevated hepatocellular enzymes, and the diagnosis of acute Q fever was confirmed serologically. She and 14 other family members had attended a family reunion in Maine 2 weeks earlier, when they were exposed to a parturient cat. All 11 adults and older children attending the reunion developed symptoms consistent with acute Q fever. Serum samples were obtained from 10 who attended the reunion and 8 who did not attend. Titers greater than or equal to 1:64 to Coxiella burnetii were present in all who attended the reunion but in none of those who did not. Cat-associated Q fever should be considered when sporadic cases of the disease occur in the United States.

Farmer's lung

Signs and symptoms Acute Stage: After four to eight hours symptoms such as headache, irritating cough, and shortness of breath upon physical exertion, appear. Subacute Stage: Symptoms persist without further exposure, and increase in severity. Symptoms include: shortness of breath upon exertion, chronic coughing, physical weakness, occasional fever and sweating, decrease in appetite, aches and pains. Chronic Stage: Debilitating effects are now considered long-term. Symptoms include: severe shortness of breath, chronic coughing, physical weakness, occasional fever and sweating at night, decrease in appetite, and general aches and pains. These symptoms develop between four and eight hours after exposure to the antigens. In acute attacks, the symptoms mimic pneumonia or flu. In chronic attacks, there is a possibility of the victim going into shock and dying from the attack.

[A case of psittacosis with wandering infiltrates developing to acute respiratory distress syndrome].

A 52-year-old woman visited a local hospital with a high fever, non-productive cough and general fatigue. Her chest X-ray showed infiltrate in the right middle lung field. Computed tomography scans revealed ground-glass opacity and surrounding ring-shaped air-space consolidation, the "reversed halo sign". Cefpirom was administered, but her symptoms persisted and the infiltrate migrated to the left upper lobe. As cryptogenic organizing pneumonia was suspected, she was then treated with intravenously pulsed methylprednisolone followed by prednisolone. Despite these therapies, acute respiratory failure occurred and she was therefore transferred to our hospital. On admission, severe hypoxemia and diffuse bilateral infiltrates on chest images suggested acute respiratory distress syndrome. As we obtained information that a parakeet had recently died at her home, minocycline was administered, resulting in prompt improvement of the symptoms, respiratory insufficiency and pulmonary infiltrates. Finally, elevated antibody titers against Chlamydophila psittasi confirmed a diagnosis of Psittacosis. Sequential chest computed tomography scans in this case indicate that absorption of marginal air-space consolidation with extended central ground glass attenuation in concordance with a new infiltrate on another lung field appeared to create wandering infiltrate. Wandering infiltrate on chest X-ray in psittacosis may be a sign of disease progression.

Blastomycosis

a flu-like illness with fever, chills, arthralgia (joint pain), myalgia (muscle pain), headache, and a nonproductive cough which resolves within days. an acute illness resembling bacterial pneumonia, with symptoms of high fever, chills, a productive cough, and pleuritic chest pain. a chronic illness that mimics tuberculosis or lung cancer, with symptoms of low-grade fever, a productive cough, night sweats, and weight loss. a fast, progressive, and severe disease that manifests as ARDS, with fever, shortness of breath, tachypnea, hypoxemia, and diffuse pulmonary infiltrates. skin lesions, usually asymptomatic, can be verrucous (wart-like) or ulcerated with small pustules at the margins. bone lytic lesions can cause bone or joint pain. prostatitis may be asymptomatic or may cause pain on urinating. laryngeal involvement causes hoarseness. 40% immunocompromised individuals have CNS involvement and present as brain abscess, epidural abscess or meningitis.

Diagnosis and treatment of Q fever: attempts to clarify current problems in Japan.

"Q fever" is a generic term for infection caused, mostly in the form of pneumonia or bronchitis, by Coxiella burnetii (Q-fever Coxiella), a pathogen closely related to Rickettsia and Legionella. Q fever is an influenza-like, transient febrile infectious disease that is common to humans and animals; it develops after the transmission of the infectious agent from livestock or pet animals, but person-to-person transmission is rare. In Europe and the United States, it is ranked fourth or fifth as an underlying cause of community-acquired pneumonia. Many patients with Q fever have a good prognosis, and their mortality is about 1%-2% when left untreated. However, because some patients may take a long time to be cured or may have a chronic condition with poor prognosis, patients with definitely diagnosed Q fever or those strongly suspected of having Q fever are strongly recommended to receive treatment. The definite diagnosis of Q fever is made based on a significant increase in serum antibody titers, the determination of which often requires considerable time, and therefore patients must be monitored for a certain period. Q-fever Coxiella, an obligate intracellular parasite, is basically not susceptible to beta-lactam antibiotics, which barely permeate into the cells, but the parasite is susceptible to tetracyclines, macrolides, and quinolones, with these agents being sufficiently permeable into the cells. However, there are many cases of spontaneous cure, and it is likely that beta-lactam treatment may have been involved in these cases. Vaccination against Q fever is not common in Japan.

SARS-CoV-2 Infection and COVID-19 in 5 Patients in Ecuador After Prior Treatment with Hydroxychloroquine for Systemic Lupus Erythematosus.

BACKGROUND This case series describes 5 patients with SARS-CoV-2 infection and COVID-19 in Ecuador who had been treated with hydroxychloroquine for systemic lupus erythematosus (SLE) prior to their COVID-19 illness. CASE REPORT Case #1 reports a 29-year-old woman who had been treated with 200 mg of hydroxychloroquine per day for 1 year and presented with flu-like symptoms, chest pain, fever, odynophagia, asthenia, dry cough, and chills. Case #2 was a 34-year-old woman whose treatment for SLE included 200 mg of hydroxychloroquine per day since 2017. She arrived at the clinic with a dry cough, asthenia, and myalgias. Case #3 was a 24-year-old woman who had been using 200 mg of hydroxychloroquine per day since 2010. She presented with asthenia, myalgias, headaches, hypogeusia, and anosmia. Case #4 was a 39-year-old woman taking 200 mg of hydroxychloroquine every day for SLE who presented with dyspnea, chest pain, odynophagia, hypogeusia, anosmia, diarrhea, and fever. Case #5 was a 46-year-old woman who had been taking 200 mg of hydroxychloroquine since 2019. She came to our hospital complaining of chest pain, fever, and dyspnea. In all 5 patients, SARS-CoV-2 infection was confirmed with a nasopharyngeal SARS-CoV-2 reverse transcription-polymerase chain reaction (RT-PCR) test using the Cepheid/GeneXpert system. CONCLUSIONS All 5 of our patients with SLE who were taking hydroxychloroquine presented with SARS-CoV-2 infection and symptoms of COVID-19. This case series provides support for a lack of prevention of COVID-19 by hydroxychloroquine.

[Investigation of Coxiella burnetii and Brucella seropositivities in patients presenting with acute fever].

Tokat province and Kelkit Valley located in the Black Sea region of Turkey are endemic areas for brucellosis and Crimean-Congo hemorrhagic fever. Since the risk factors are similar, the probability of Coxiella burnetii seroposititivity is assumed to be also high in this area. The aim of this study was to investigate Q fever and brucellosis seropositivity in patients with acute fever. A total of 53 patients (37 male, 16 female; age range: 18-65 years, mean age: 47.13 ± 16.40 years) who were admitted to the emergency room and infection diseases outpatient clinics of Gaziosmanpasa University hospital with acute fever between June 2011-June 2012 were included in the study. Symptoms, physical examination findings and laboratory test results of the patients were recorded. In addition, their place of residence, relationship with rural area, and history of contacts with animals were questioned. The presence of C.burnetii phase II lgM and lgG antibodies were investigated by indirect immunofluorescent antibody assay, and Brucella spp. antibodies by Rose Bengal and standard tube agglutination methods in the serum samples of patients. C.burnetii seropositivity was determined in 19 (36%) of the patients, and 2 (4%) of them were diagnosed as acute Q fever with the positivity of both lgG and lgM antibodies. Among the seropositive and seronegative patients, there was no statistically significant differences in terms of age, gender, animal contact, occupation, place of residence and relationship with rural-life (p> 0.05). Acute fever was attributed to pneumonia in 10 patients and of them five were found positive for phase II lgG antibodies. There was no significant difference between C.burnetii seropositive and seronegative patients in terms of the presence of pneumonia (p= 0.30). In two patients diagnosed as acute Q fever no signs of pneumoniae were detected in the chest X-rays; one of these cases was resided in the city and the other in the rural area while both had contact with animals. The most frequently detected symptoms in patients with acute Q fever were malaise, fatigue, chills, cough, sputum, dyspnea, nausea, abdominal pain and diarrhea. Brucella seropositivity was detected in 6 (11%) patients and four of them were diagnosed as acute brucellosis. Four of the Brucella seropositive patients were also found positive for C.burnetii. Sixteen (84%) of C.burnetii seropositive patients were male and 3 (16%) were female. Eleven of them were living in the village and eight in the city, however six out of eight urban patients had a history of relation with rural-life, resulting a total of 17 (89%) rural-contacts. In addition, 79% (15/19) of seropositive cases had the history of animal contact most commonly with cattle and sheep (11/15; 73%). When the laboratory findings were compared, serum ferritin levels were found to be significantly higher in patients with acute Q fever then those seronegative patients (874 ng/ml mean value vs. 150 ng/mL mean value; p= 0.04), however there was no significant difference between the other laboratory parameters (p> 0.05). Our data indicated that Q fever seropositivity was quite high in Tokat region and the reason may be attributed to entwined life between rural and urban areas. In conclusion in the patients presenting with acute fever, brucellosis and Q fever should be considered in differential diagnosis, since both infections are endemic in that area of Turkey.

A 15-year-old with chest pain: An unexpected etiology.

A 15-year-old female with no significant past medical history presented to the emergency department with 1 day of substernal and pleuritic chest pain, chills, cough, and hematuria. She also had swelling of the face and ankles that resolved by presentation. She was found to have elevated troponin and brain natriuretic peptide during initial workup. Electrocardiogram was normal, but there were significant pleural effusions on chest x-ray. She was strep positive and had blood pressure up to 150/90, prompting admission for cardiac monitoring and cardiology consultation. Blood pressure decreased down to 125/72 without intervention. She was afebrile with unlabored breathing and normal saturations. She was clear to auscultation bilaterally, with no abdominal distension or hepatosplenomegaly, and edema was not evident on exam. There was mild erythema to the bilateral tonsillar pillars. Initial considerations included viral myocarditis, pericarditis, and atypical nephritic syndrome. Workup revealed elevated antistreptolysin antibodies, low C3 complement, negative antineutrophil cytoplasmic antibodies, and negative flu testing. Renal sonography was unremarkable. Cardiology recommended echocardiography, which confirmed pleural effusions but revealed no cardiac abnormalities. Urinalysis revealed hematuria and mild proteinuria. Diagnosis was found to be post-streptococcal glomerulonephritis complicated by fluid overload and left ventricular strain secondary to hypertensive emergency. Post-streptococcal glomerulonephritis is the most common cause of acute glomerulonephritis in children. The mechanism of disease is a proliferation and inflammation of the renal glomeruli secondary to immunologic injury, with deposition of immune complexes, neutrophils, macrophages, and C3 after complement activation. This leads to hematuria, proteinuria, and fluid overload. Edema is present in 65%-90% of patients, progressing to pulmonary involvement in severe cases. Cardiac dysfunction secondary to fluid overload is a potentially fatal outcome in the acute setting. Physicians should consider post-streptococcal glomerulonephritis for patients presenting with hypertension, cardiac/pulmonary pathology, or symptoms of acute heart failure in the context of strep infection.

Q fever: current concepts.

Persons with Q fever usually present with severe retrobulbar headache, a fever to 104 degrees F or higher with shaking chills, general malaise, myalgia, chest pain, and sometimes pneumonia and hepatitis. Cattle, sheep, goats, and ticks are the primary reservoirs of the etiologic agent, Coxiella burnetii. Humans are usually infected by inhaling infectious aerosols. Because C. burnetii can survive for long periods in the environment, it poses a continuing health hazard once it is disseminated. Q fever usually occurs sporadically, but large outbreaks are frequently observed throughout the world, particularly among abattoir workers and personnel working in research centers. Q fever endocarditis follows a chronic course and is frequently fatal. Tests for antibodies to C. burnetii are required for confirmation of the diagnosis. Tetracyclines remain the mainstay of treatment for acute Q fever, and tetracyclines in combination with other antibiotics have been advocated for patients with Q fever endocarditis. Vaccines for Q fever have been proven effective in clinical trials.

A 47-Year Old Woman With Rapidly Progressive Hypoxemic Respiratory Failure.

A 47-year-old Hispanic woman presented to a pulmonology clinic with 2 weeks of cough productive of white sputum and worsening dyspnea on exertion, requiring increasing supplemental oxygen. In addition, she reported fatigue, night sweats, diffuse myalgias, and extremity weakness. She denied hemoptysis, fevers, chills, weight loss, or rash. Her medical history is significant for undifferentiated rapidly progressive hypoxemic respiratory failure 2 years before her current presentation. At that time, she presented to the ED with 3 weeks of progressive shortness of breath and cough. Chest CT imaging showed bilateral infiltrates concerning for infection, and she was treated empirically for community-acquired pneumonia. She developed worsening hypoxemic respiratory failure despite broadening of her antibiotics and subsequently required intubation. Her course was further complicated by pulseless electrical activity arrest with return of spontaneous circulation and development of shock requiring multiple vasopressors. Because of difficulty with oxygenation, she was referred to our center for extracorporeal membrane oxygenation evaluation and was ultimately started on venous-arterial extracorporeal membrane oxygenation. Bronchoscopy with BAL was negative for bacterial, viral, and fungal origins, and initial autoimmune evaluation (antinuclear antibody and rheumatoid factor) was negative, except an elevated creatine kinase (CK) to 3,000. Her course was complicated by heparin-induced thrombocytopenia, and as a result she suffered limb ischemia requiring amputation of her left lower extremity. Elevated CK at that time was attributed to compartment syndrome before amputation. The patient recovered clinically with supportive care and was ultimately discharged on 2 L supplemental oxygen, with a diagnosis of acute respiratory failure of unclear origin. The patient had stability in her clinical symptoms until this current presentation.

Coxiella burnetii (Q fever) pneumonia.

Pneumonia is one manifestation of acute Q fever following infection with Coxiella burnetii. Fever, headache, and myalgia dominate the clinical picture of Q fever pneumonia. Cough is nonproductive and may be absent despite the presence of pneumonia. While in most instances pneumonia results in an illness of mild-to-moderate severity, on occasion it is rapidly progressive and results in respiratory failure. Infection occurs as a result of inhalation of contaminated aerosols. Infected cattle, sheep, and goats are the usual reservoirs for this zoonosis. In some areas, infected parturient cats serve as the reservoir, and in such instances, rounded opacities are seen on the chest radiograph. The diagnosis of C. burnetii pneumonia is usually confirmed by demonstration of a fourfold or greater rise in antibody titer. Treatment is usually with a tetracycline or rifampin for 7 to 10 days.

Nitrofurantoin

Pulmonary toxicity The pulmonary toxicity caused by nitrofurantoin can be categorized into acute, subacute, and chronic pulmonary reactions. The acute and subacute reactions are thought to be due to a hypersensitivity reaction and often resolve when the drug is discontinued. Acute reactions have been estimated to occur in about one in 5000 women who take the drug. These reactions usually develop 3–8 days after the first dose of nitrofurantoin, but may occur from a few hours to a few weeks after starting the drug. Symptoms include fever, dyspnea, chills, cough, pleuritic chest pain, headache, back pain, and epigastric pain. Chest radiograph will often show unilateral or bilateral infiltrates similar to pulmonary edema. Treatment includes discontinuation of the nitrofurantoin, which should result in symptom improvement within 24 hours.

[Acute bronchiolitis due to Mycoplasma pneumoniae and successfully treated with steroids].

A high fever, coughing, stridor, and dyspnea developed in a 52-year-old woman on October 19, 1995. She went to a local clinic and was treated with oral penicillin and intravenous cefpirome. The symptoms worsened, and she was admitted to our hospital on October 26. Coarse crackles and wheezing were heard in both lung fields. The white blood cell count was 9000/mm3 and arterial blood gas analysis revealed a PaO2 of 49.8 Torr on room air. A chest roentgenogram obtained on admission showed a few small bibasilar nodular infiltrates, and a chest CT scan showed thickened bronchial walls along with small nodules having a centrilobular distribution. Of the cells in bronchoalveolar lavage fluid, 88% were neutrophils, but tests for bacteria and mycobacteria were negative. The cold-agglutinin titer was 1:512. The Mycoplasma pneumoniae antibody titer (IIIA) was 1:640 and viral serology tests were negative. Acute bronchiolitis due to M. pneumoniae was diagnosed and treatment with intravenous minocycline was started. The symptoms (coughing, fever, and stridor) resolved and the small nodules on chest CT scan disappeared, but hypoxemia remained. At the same time, an obstructive ventilatory defect (FEV1% 62.8%) and abnormal ventilation/perfusion lung scans were noted. Development into bronchiolitis obliterans was suspected, so administration of methyl prednisolone (1 g/day for 3 days) and prednisolone was started. The response to steroids was good. Pulmonary function improved and the arterial PaO2 at the time of discharge was 86 Torr (room air). Use of steroid therapy in the early phase of bronchiolitis obliterans seemed to be effective.

Acute Q fever pneumonia: a review of 80 hospitalized patients.

To emphasize epidemiologic, clinical, or radiologic characteristics whose detection could lead to an early diagnosis and to enhance therapeutic efficacy. Eighty hospitalized patients from 1982 to 1996. The diagnosis of Q fever infection was serologically confirmed in all the patients (phase II Coxiella burnetii antibody) using the complement fixation test and/or the indirect immunofluorescence antibody test. Patients from rural and urban areas were noted in the same proportion; however, the usual epidemiologic factors such as contact with cats or farm animals were found in 40% of the patients. Mean age+/-SD was 49+/-20 years, and there was a higher sex ratio of male to female patients (1:3.44). We found a specific seasonal distribution since 80% of the cases occurred between February and May. Delay before referring to hospital was 8.2+/-7.8 days, while 69.3% of the patients received an antibiotic treatment that was mainly penicillin or cephalosporin. The dominant clinical features were dry cough and high fever, as the maximal temperature reached more then 40 degrees C in 58% of the patients. Digestive symptoms were rare. WBC count remained within normal range in 80% of the cases with a low proportion of lymphocytes in half of the patients, and the sedimentation rate was usually elevated (55+/-34 mm). Altered liver function consisted more frequently in an elevated level of alkaline phosphatase (70% of the cases) than transaminases, while hyponatremia was frequently mentioned (28.2% of the patients). We found radiologic evidence of unique lobar or segmental alveolar opacity involving more likely the lower lobes in 55 patients, and multiple or interstitial opacities in the others. Chest radiographs were considered normal in eight patients. The clinical response was favorable in all the patients with a reduction in fever 4.8+/-3.9 days after the start of treatment with the second antibiotic that included mainly erythromycin or quinolones, and chest radiographs returned to normal in 81% of the patients within the first month.

[Clinical manifestation of Q fever and tuberculosis, similarly caused by intracellular parasites].

Q fever is a generic term for pneumonia, bronchitis, etc. caused by infection with Coxiella burnetii, a rickettsia-related species of bacteria, in humans. Q-fever is a transient and acute febrile illness that takes a course similar to influenza, and its clinical picture greatly differs from that of tuberculosis that takes a chronic course. The reason for this is thought to be because the generation time of C. burnetii is extremely short (several tens of minutes) compared with Mycobacterium tuberculosis, though those are similar intracellular parasites. Q fever is fourth- or fifth-ranked among the community-acquired pneumonias in the United States and Europe but has a good prognosis with 1-2% of mortality even in the cases that follow a natural course without treatment. Meanwhile, there is a chronic type that follows a protracted course or has a poor prognosis. Therefore, cases definitely diagnosed with Q fever or strongly suspected of Q fever should seek aggressive treatment. Q fever is definitely diagnosed by confirming significant increase in serum antibody titer, but the patients should be followed because in many cases it takes a long time before serum antibody titer increases. Beta-lactams are ineffective against C. burnetii, an obligate intracellular parasite. Although tetracyclines, macrolides, quinolones, rifampicin, etc. are used effectively in the treatment of Q fever, many cases appear to improve by beta-lactam administration because the illness often takes a natural course.

Neurology_Adams

Q fever, unlike the other rickettsioses, is not associated with an exanthem. In the few cases with which we are familiar, the main symptoms were those of a low-grade meningitis. Rare instances of encephalitis, cerebellitis, and myelitis are also reported, possibly as postinfectious complications. There is usually a tracheobronchitis or atypical pneumonia (one in which no organism can be cultured from the sputum) and a severe prodromal headache. In these respects, the pulmonary and neurologic illnesses resemble that of the other main cause of “atypical pneumonia,” M. pneumoniae. The Q fever agent (Coxiella) should be suspected if there are concomitant respiratory and meningoencephalitic illnesses and there has been exposure to parturient animals, to livestock (including abattoir workers, who are also exposed to Brucella and anthrax), or to wild deer or rabbits. The diagnosis can be made by the finding of a severalfold increase in specific immunofixation antibodies. Patients who survive

[Symptomatic acute Q fever: a series of 87 cases in an area of Mallorca].

Q fever is a widespread zoonotic infection caused by Coxiella burnetii (C. burnetii). Acute infection varies from a self-limited flu-like illness to pneumonia or hepatitis. A retrospective case study from March 2003 to December 2011 was conducted in the Hospital Son Llàtzer in Palma de Mallorca. Acute Q-fever was diagnosed in a patient with clinical suspicion and IgM in phase ii positive (≥ 1/40), with a positive IgG (≥1/80), or when IgG seroconversion was observed during convalescence. A total of 87 cases of acute Q fever were diagnosed. The median age was 50 years (range 21-89), and 69 (79.3%) were male. Fever and headache were the most common symptoms. Pneumonia was diagnosed in 39 (44.8%) patients, febrile episode in 21 (24.1%), and acute hepatitis in 23 (25.6%). Increased serum transaminases were observed in 19 (21.8%). Doxycycline was prescribed in 29 cases (33.4%). There were 30 (34.5%) patients lost to follow up after hospital discharge. A favorable outcome was observed in all other cases. Only one new case progressed to chronic Q fever. A total of 87 cases of acute Q fever were diagnosed. The median age was 50 years (range 21-89), and 69 (79.3%) were male. Fever and headache were the most common symptoms. Pneumonia was diagnosed in 39 (44.8%) patients, febrile episode in 21 (24.1%), and acute hepatitis in 23 (25.6%). Increased serum transaminases were observed in 19 (21.8%). Doxycycline was prescribed in 29 cases (33.4%). There were 30 (34.5%) patients lost to follow up after hospital discharge. A favorable outcome was observed in all other cases. Only one new case progressed to chronic Q fever. Acute Q fever acute is common our environment. Pneumonia was the most common clinical presentation. Even although doxycycline was prescribed in a small number of patients, a favorable outcome was observed in all cases.

Q-uestioning the Diagnosis: An Educational Case Report.

Q fever is a zoonotic infection that may lead to acute or long-term renal injury. Given its rare incidence, Q fever is not often considered on the initial differential diagnosis for glomerular disease which can lead to delays in treatment. This case highlights the importance of avoiding early diagnostic closure and revisiting the differential diagnosis in the setting of an atypical clinical presentation or response to treatment. A 52-year-old female was referred for assessment of possible glomerulonephritis. She described a 3-month history of bilateral lower extremity rash, intermittent knee pain with swelling, and a 2-year history of subjective fevers. Urinalysis showed persistent microscopic hematuria, and her creatinine was elevated at 94 umol/L (baseline 59 umol/L). Her initial investigations included an elevated C-reactive protein (CRP) and rheumatoid factor with a weakly positive anti nuclear antibody (ANA). Kidney biopsy was consistent with an immune complex mesangial proliferative glomerulonephritis. Light microscopy showed diffuse global mesangial hypercellularity. Immunofluorescence was positive for trace mesangial IgG and kappa, 1+ IgM, lambda and C1q, and 2+ C3. Electron microscopy showed mesangial electron dense deposits. These findings were felt to be most in keeping with mesangial proliferative lupus nephritis; however, it was acknowledged that clinical and laboratory findings supporting this diagnosis were lacking. Following treatment with oral prednisone her symptoms resolved, and renal function improved. However, she was unable to taper off prednisone completely without her symptoms returning. Additional immunosuppressive therapies were trialed, but she remained steroid dependent with disease flares related to prednisone tapers. Her atypical response to treatment led to consideration of alternative diagnoses, and further investigation revealed positive Q fever serology (phase-I IgG 1:1892, phase II IgG 1:8192, phase-I and -II IgM < 1:16). She was diagnosed with long-term Q fever and was treated with doxycycline and hydroxychloroquine. She remained on treatment for 2 years. During this time, her symptoms resolved, hematuria disappeared, and her creatinine returned to baseline. Following cessation of therapy, her Q fever IgM titres rose, and she was restarted on doxycycline and hydroxychloroquine indefinitely. (1) Keeping a broad differential diagnosis in the setting of atypical clinical features or unexpected response to therapy is important for ensuring accurate diagnosis and appropriate treatment. (2) Clinical improvement in relation to immunosuppressive therapy does not preclude an infectious cause of glomerular disease.

[Acute and chronic Q fever; epidemiology, symptoms, diagnosis and therapy of infection caused by Coxiella burnetii].

Q fever is a zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium. Domestic ungulates and parturient cats are the primary reservoirs of infection. The animals excrete the bacterium in urine, faeces, milk and amniotic fluid. After desiccation the micro-organism spreads via aerosols. After inhalation or ingestion and an incubation period of 2-6 weeks acute Q fever may develop with atypical pneumonia and hepatitis as major clinical symptoms. The infection also may present as a flu-like illness or remain asymptomatic. Generally, the prognosis is favourable. However, endocarditis or another chronic form of Q fever occasionally develops with possibly fatal outcome. Diagnosis relies upon serologic testing with an indirect immunofluorescence method. Doxycycline is the antibiotic of choice in the treatment of Q fever. Endocarditis needs therapy for years with the addition of rifampin or hydroxychloroquine. Q fever is poorly recognised due to the variety of clinical presentations.


Hypercapnia and acidosis produce vasodilatation causing increased cerebral blood flow. According to the described examination the Glasgow is 4 (O1V1M2). Cerebral perfusion pressure is mean arterial pressure minus intracranial pressure. Cerebral edema in which cellular edema is produced by the introduction of extracellular fluid into the intracellular compartment is cytotoxic.

A 49-year-old man is admitted to the ICU for traumatic brain injury after an accident at work. In the physical examination he does not open his eyes, does not emit sounds before being intubated and presents extension of extremities to nociceptive stimulus. An intracranial pressure sensor is placed and a decompressive craniotomy must be performed due to intraparenchymal hemorrhage. Which of the following statements is correct?

On arrival she is in a Glasgow scale coma of 7.

Cerebral perfusion pressure is mean arterial pressure plus intracranial pressure.

Vasogenic cerebral edema is due to cellular edema, membrane rupture and cell death.

Cerebral vascular flow increases with hypercapnia and acidosis.

Role of decompressive craniectomy in the management of severe head injury with refractory cerebral edema and intractable intracranial pressure. Our experience with 48 cases.

The effects of decompressive craniectomy in the treatment of severe head injury remain unclear. Only very few randomized studies relating to this topic exist in the literature, including a very small number of patients with no class I evidence. We rretrospectively reviewed a series of 221 patients operated on for a head injury during a 25-month period. Of these, 48 patients underwent a decompressive craniectomy. All data available on patients' Glasgow Coma Scale score, pupil size and reaction, and intracranial pressure were collected and analyzed. The patients' outcome was evaluated by the Glasgow Outcome Scale (GOS) and the results compared with the data available in the Traumatic Coma Data Bank. Furthermore, the results were analyzed in respect of the time of surgical intervention (early or late), age, and the preoperative Glasgow Coma Score. Decompressive craniectomy reduced the midline shift in all patients with monolateral diffuse brain edema and contusions having a median value of 7 mm; in the remaining, it ameliorated the basal cisterns effacement. At a mean follow-up of 14 months, 6 (12.5%) patients died, 7 (15%) were discharged home with a GOS of 5, 18 (40%) showed a favorable outcome after rehabilitation with a GOS of 4 and 5, 6 (12.5%) had a severe disability (GOS 3), 9 (20%) were in a vegetative state (GOS 2), and 2 were lost to follow-up. The younger age, earlier surgery, and higher preoperative Glasgow Coma Scale score were related to better outcome (P < .001, P < .05, and P < .034, respectively). Our results seem to support the idea that decompressive craniectomy coupled with neurointensive care may be an effective way to reduce intractable raised intracranial pressure, and probably to improve patients outcome. However, it should be obvious that our results and those available in the literature can not be considered conclusive.

Cerebral edema

Additionally, ventilation with use of positive pressure (PEEP) can improve oxygenation with the negative effect of decreasing cerebral venous drainage and increasing intracranial pressure (ICP), and thus, must be used with caution. Fluid management and cerebral perfusion Maintenance of cerebral perfusion pressure using appropriate fluid management is essential in patients with brain injury. Dehydration, or intravascular volume loss, and the use of hypotonic fluids, such as D5W or half normal saline, should be avoided. Blood serum ion concentration, or osmolality, should be maintained in the normo to hyperosmolar range. Judicial use of hypertonic saline can be used to increase serum osmolality and decrease cerebral edema, as discussed below.

Cerebral edema

Intracranial pressure monitoring Intracranial pressure (ICP) and its management is a fundamental concept in traumatic brain injury (TBI). The Brain Trauma Foundation guidelines recommend ICP monitoring in individuals with TBI that have decreased Glasgow-Coma Scale (GCS) scores, abnormal CT scans, or additional risk factors such as older age and elevated blood pressure. However, no such guidelines exist for ICP monitoring in other brain injuries such as ischemic stroke, intracerebral hemorrhage, cerebral neoplasm.

Cerebral edema

The treatment of cerebral edema depends on the cause and includes monitoring of the person's airway and intracranial pressure, proper positioning, controlled hyperventilation, medications, fluid management, steroids. Extensive cerebral edema can also be treated surgically with a decompressive craniectomy. Cerebral edema is a major cause of brain damage and contributes significantly to the mortality of ischemic strokes and traumatic brain injuries. As cerebral edema is present with many common cerebral pathologies, the epidemiology of the disease is not easily defined. The incidence of this disorder should be considered in terms of its potential causes and is present in most cases of traumatic brain injury, central nervous system tumors, brain ischemia, and intracerebral hemorrhage. For example, malignant brain edema was present in roughly 31% of people with ischemic strokes within 30 days after onset.

Stages of death

The heart and lungs are vital organs for human life due to their ability to properly oxygenate human blood (lungs) and distribute this blood to all vital organs (heart). Hence failure of the heart to pump blood or the lungs to obtain oxygen can lead to a cardiopulmonary death where the heart stops pumping and there is no pulse. In the brain, this can be manifested by a hypoxic state which leads to cerebral edema and thus an increase in intracranial pressure. The rise in intracranial pressure can lead to further disruption in cerebral blood flow, leading to necrosis or tissue death. The aforementioned mechanism is the most common cause of brain death, however this increase in intracranial pressure does not always occur due to an arrest in cardiopulmonary function. Traumatic brain injuries and subarachnoid hemorrhages can also increase the intracranial pressure in the brain leading to a cessation of brain function and hence death. While cardiopulmonary death can be easily assessed by

Osmotherapy

An increase in cerebral water content is called cerebral edema and it usually results from traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), subdural hematoma, ischemic stroke, brain tumors, infectious disorders and intracranial surgery. Cerebral edema may result in compromised regional cerebral blood flow (CBF) and intracranial pressure (ICP) gradients which could lead to death of the affected. Increased ICP leads to increased intracranial volume. Unmonitored ICP leads to brain damage by global hypoxic ischemic injury due to reduction in cerebral perfusion pressure (CPP) which is found by subtracting the ICP from mean arterial pressure (MAP), cerebral blood flow, and mechanical compression of brain tissue due to compartmentalized ICP gradients. Cerebral edema is mainly classified into cytotoxic edema, vasogenic edema and interstitial edema.

Cerebral edema

It is important to note that prolonged hyperventilation in those with traumatic brain injuries has been shown to worsen outcomes. Barbiturates Induction of a coma via the use of barbiturates, most notably pentobarbital and thiopental, after brain injury is used for secondary treatment of refractory ICP. Yet their use is not without controversy and it is not clear whether barbiturates are favored over surgical decompression. In patients with traumatic brain injuries, barbiturates are effective in reducing ICP but have failed to show benefit to clinical outcomes. Evidence is limited for their use in cerebral disease that include tumor, intracranial hypertension, and ischemic stroke. There are several adverse effects of barbiturates that limit their use, such as lowering of systemic blood pressure and cerebral perfusion pressure, cardiodepression, immunosuppression, and systemic hypothermia.

Impact of intracranial pressure measurement on survival in patients with severe traumatic brain injury.

The aim of the study was to assess (i) a group of patients with established intracranial pressure (ICP) sensor in severe brain injuries scoring 3 points of Glasgow Coma Scale, (ii) mortality and survival of the patients within periods of 7, 30, 180 and 270 days; and (iii) predictive value of intracranial pressure and cerebral perfusion pressure for short and long-term survival of patients with traumatic brain injury. The group consisted of 61 patients with trauma brain injury scoring 3 points of Glasgow Coma Scale, continuously monitored for intracranial pressure cerebral perfusion pressure at the Intensive Care Unit setting in Nové Zámky. Follow-up period was between 7 and 270 days. Measured values and other recorded data were analysed using methods of descriptive and inferential statistics. ICP values below 20 mmHg were associated with a significantly lower risk of death of an individual patient at particular time. Accordingly, cerebral perfusion pressure values above 70 mmHg during 0-2 days were associated with a significantly higher long-term survival. Overall mortality rates within 30 days showed no peaks on survival curves. In the periods of 0-7 days, within 30 days, and between 30 and 180 days we recorded 24, 51 and 2 deaths, respectively. In the period between 180 and 270 days, mortality was zero. The survival of trauma brain injury patients depends on the speed and quality of pre-hospital care and adequate follow-up treatment at specialized intensive care units. High levels of intracranial pressure and low cerebral perfusion pressure values in the early period after brain injury are closely related to mortality of patients within 30 days. Intracranial pressure monitoring may help to avoid problems and allow intervention before they become life-threatening (Tab. 4, Fig. 4, Ref. 23). Text in PDF www.elis.sk.

Pressure reactivity index

PRx and outcome prediction A high PRx indicating disturbed pressure autoregulation predicts poor outcome in traumatic brain injury. PRx as a treatment target PRx varies with the concurrent cerebral perfusion pressure (CPP) in a U-shaped way. It has been suggested that the CPP with the lowest PRx is optimal (CPPopt) and CPP-values close to optimal have been associated with better outcome. CPP values above CPPopt are believed to cause hyperemia, i.e. to high cerebral blood flow that may cause cerebral edema and intracranial hypertension, whereas CPP values below CPPopt are believed to cause hypoperfusion and ischemia resulting in tissue damage. See also Cerebral autoregulation Intracranial pressure Cushing's triad References Intensive care medicine Neurotrauma Neurophysiology

Brain Death Criteria -- Function

Brain death occurs as a result of an acute catastrophic brain injury. Abrupt loss of cerebral perfusion occurs if a concomitant elevation of intracranial pressure is more than mean arterial pressure (cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) - intracranial pressure (ICP). This process was studied by monitoring brain tissue oxygenation in patients with brain death and can occur via two different mechanisms:

Cerebral edema

Clinical researches have recommended ICP and cerebral perfusion pressure (CPP) monitoring in any persons with cerebral injury who are at risk of elevated intracranial pressure based on clinical and neuroimaging features. Early monitoring can be used to guide medical and surgical decision making and to detect potentially life-threatening brain herniation. There was however, conflicting evidence on the threshold values of ICP that indicated the need for intervention. Researches also recommend that medical decisions should be tailored to the specific diagnosis (e.g. subarachnoid hemorrhage, TBI, encephalitis) and that ICP elevation should be used in conjunction with clinical and neuroimaging and not as an isolated prognostic marker.

[Intracranial pressure monitoring in patients with severe craniocerebral injury].

After severe head injury intracranial pressure (ICP) must be measured continuously for management to assess and maintain the cerebral perfusion. Therefore in our hospital epidural transducers are used. To prove the efficiency of this method in a 12-month period the clinical courses of 23 patients with intracranial pressure transducers were analysed retrospectively. Eighteen patients survived, 5 of them without residuals, 13 with residuals and 2 remained in coma. In 14 patients secondary rises of intracranial pressure were observed between days 3 and 6 post injury. The mean ICP value of the survivors revealed 25 mm Hg. whereas the expired showed 60 mm Hg. In 17 patients the measurements were considered as reliable, 6 measurements were not reliable, which included 1 of the 5 patients who died. One transduce was displaced, another one showed a hemorrhage at the drill hole. There was no infection.

Traumatic brain injury

Secondary injury events include damage to the blood–brain barrier, release of factors that cause inflammation, free radical overload, excessive release of the neurotransmitter glutamate (excitotoxicity), influx of calcium and sodium ions into neurons, and dysfunction of mitochondria. Injured axons in the brain's white matter may separate from their cell bodies as a result of secondary injury, potentially killing those neurons. Other factors in secondary injury are changes in the blood flow to the brain; ischemia (insufficient blood flow); cerebral hypoxia (insufficient oxygen in the brain); cerebral edema (swelling of the brain); and raised intracranial pressure (the pressure within the skull). Intracranial pressure may rise due to swelling or a mass effect from a lesion, such as a hemorrhage. As a result, cerebral perfusion pressure (the pressure of blood flow in the brain) is reduced; ischemia results. When the pressure within the skull rises too high, it can cause brain death or

Effects of varying levels of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure.

To determine the influence of positive end-expiratory pressure (PEEP) on intracranial pressure and cerebral perfusion pressure. Neurosurgical intensive care patients requiring intracranial pressure monitoring and mechanical ventilation were studied in a randomized, controlled study. Tertiary care, neurosurgical intensive care unit. Eighteen patients were enrolled in the study. Patients had posttraumatic head injuries (n = 9), subarachnoid hemorrhage (n = 7), obstructive hydrocephalus (n = 1), and intracerebral hemorrhage of unknown cause (n = 1). Patients had PEEP levels of 5, 10, and 15 cm H2O applied to their lungs. Changes in intracranial pressure, mean arterial pressure, and cerebral perfusion pressure were measured. The results were analyzed separately for patients with normal and increased intracranial pressure (> 15 mm Hg). PEEP at 5 cm H2O had no effect on intracranial pressure in the group with normal intracranial pressure. However, PEEP at 10 and 15 cm H2O produced a significant (p < .05) increase in intracranial pressure (1.9 and 1.5 mm Hg, respectively). In the group with increased intracranial pressure, no significant change in intracranial pressure occurred at any of the PEEP levels used. In both groups, cerebral perfusion pressure was unchanged throughout. In patients with normal intracranial pressure, PEEP at 5 cm H2O did not significantly alter intracranial pressure. The clinical relevance of the intracranial pressure increase at PEEP levels of 10 and 15 cm H2O is questionable because cerebral perfusion pressure did not change and remained > 60 mm Hg. In patients with increased intracranial pressure, higher levels of PEEP did not significantly change intracranial pressure or cerebral perfusion pressure.

Blunt trauma

Most patients with more severe traumatic brain injury have of a combination of intracranial injuries, which can include diffuse axonal injury, cerebral contusions, and intracranial bleeding, including subarachnoid hemorrhage, subdural hematoma, epidural hematoma, and intraparenchymal hemorrhage. The recovery of brain function following a traumatic accident is highly variable and depends upon the specific intracranial injuries that occur, however there is significant correlation between the severity of the initial insult as well as the level of neurologic function during the initial assessment and the level of lasting neurologic deficits. Initial treatment may be targeted at reducing the intracranial pressure if there is concern for swelling or bleeding within this skull, which may require surgery such as a hemicraniectomy, in which part of the skull is removed. Blunt trauma to extremities

Cerebral edema

There are several clinical conditions in which vasogenic edema is present: CNS tumors, like glioblastoma and meningioma Infections like meningitis, abscess, and encephalitis Inflammatory central nervous system disease such as multiple sclerosis Brain hemorrhage Traumatic brain injuries can lead to increased intracranial pressure, local damage, reduced cerebral blood flow, and focal ischemia secondary to vasogenic edema. Late stage of ischemic stroke after rapid recovery from cytotoxic edema Hypertensive encephalopathy Radiation injury Ionic (Osmotic) In ionic edema, the solute concentration (osmolality) of the brain exceeds that of the plasma and the abnormal pressure gradient leads to accumulation of water intake into the brain parenchyma through the process of osmosis. The blood-brain barrier is intact and maintains the osmotic gradient. The solute concentration of the blood plasma can be diluted by several mechanisms:

[Craniocerebral injuries: initial treatment and at resuscitation units].

Head injury is the main cause of death or disability among under-45-year-olds. This review covers the main pathophysiological aspects of head injury as well as initial treatment and management in the intensive care recovery ward. The chief therapeutic aim is to maintain adequate cerebral perfusion pressure rather than to maintain normal levels of intracranial pressure. An important challenge is to avoid development of secondary lesions, and in this context arterial hypotensive events that affect prognosis and the survival of such patients merit special attention. We reject treatment based on indiscriminate use of hyperventilation and mannitol and underline the importance of providing adequate sedation and analgesia while maintaining normal flow and pressure and adequate monitoring of such patients.

Intracranial pressure

Pathophysiology Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly constant due to autoregulation, but for abnormal mean arterial pressure (MAP) or abnormal ICP the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the mean arterial pressure: CPP = MAP − ICP . One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean systemic pressure, cerebral perfusion falls. The body's response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.

Intracranial pressure and cerebral perfusion pressure in severe head injury.

Monitoring and management of intracranial pressure (ICP) are fundamental to modern neurotraumatology. Although never formally proven to independently improve outcome in prospective, randomized, placebo-controlled trials, there is such a predominance of indirect support for this modality that most neurotrauma protocols are impossible with-out its inclusion and ethical considerations virtually preclude placebo-controlled trials of its efficacy. In addition to the question of improving outcome, ICP monitoring is also useful in guiding the use of potentially harmful treatment modalities such as hyperventilation, mannitol, and barbiturates, and also provides important prognostic data. ICP monitoring provides information on the likelihood of cerebral herniation and allows calculation of the cerebral perfusion pressure (CPP). Although there is no constant threshold for herniation, the most commonly used treatment threshold is 20 to 25 mm Hg. In addition, ICP trends are indispensable in providing the earliest possible indication of critical intracranial mass effects when combined with other clinical indicators. CPP is the difference between mean arterial pressure and ICP. CPP is an important clinical indicator of cerebral blood flow (CBF). Cerebral autoregulation generally remains at least partially preserved after severe head injury, although the CPP value at which it is activated appears to be shifted upward. Therefore, maintaining adequate CBF appears to require using an elevated minimal CPP threshold when treating the injured brain. A generally accepted value of 70 mm Hg is suggested.

Cerebral edema

Increased intracranial pressure (ICP) is a life-threatening surgical emergency marked by symptoms of headache, nausea, vomiting, decreased consciousness. Symptoms are frequently accompanied by visual disturbances such as gaze paresis, reduced vision, and dizziness. Increased pressures within the skull can cause a compensatory elevation of blood pressure to maintain cerebral blood flow, which, when associated with irregular breathing and a decreased heart rate, is called the Cushing reflex. The Cushing reflex often indicates compression of the brain on brain tissue and blood vessels, leading to decreased blood flow to the brain and eventually death. Causes Cerebral edema is frequently encountered in acute brain injuries from a variety of origins, including but not limited to:

[Prognostic correlation of intracranial pressure monitoring in patients with severe craniocerebral injury].

To explore the clinical application of intracranial pressure (ICP) monitoring and its prognostic correlation in patients with severe craniocerebral injury. A total of 216 severe craniocerebral injury patients with scores of Glasgow coma scale 3-8 underwent craniotomy at Affiliated Qilu Hospital, Shandong University.And 168 cases of ICP monitoring were divided into 3 treatment groups and another 48 cases without ICP monitoring selected as the control group.According to ICP, stepwise treatment was administered to control the level of ICP and maintain the cerebral perfusion pressure to analyze the relationship between ICP monitoring and prognosis. As compared with the control group, there were significant decreases of disability and mortality rate for patients with ICP monitoring (A, B, C group). Especially group C had a better prognosis than the other groups for statistical significance.In addition, the dose and duration of mannitol of group A, B or C were significantly lower than those of the control group (P < 0.05). The application of ICP monitoring is capable of reducing mortality, improving prognosis and enhancing success rate of treating severe craniocerebral injury.

Middle cerebral artery syndrome

Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with MCA syndrome. More distal blockages tend to produce milder deficits due to more extensive branching of the artery and less ischemic response. In contrast, the most proximal occlusions result in widespread effects that can lead to significant cerebral edema, increased intracranial pressure, loss of consciousness and could even be fatal. In such occasions, mannitol (osmotic diuretic) or hypertonic saline are given to draw fluid out of the edematous cerebrum to minimise secondary injury. Hypertonic saline is better than mannitol, as mannitol being a diuretic will decrease the mean arterial pressure and since cerebral perfusion is mean arterial pressure minus intracranial pressure, mannitol will also cause a decrease in cerebral perfusion.

Intracranial monitoring in patients with head trauma.

The treatment of head-injured patients has over the past 15 years become significantly more complex and involved. The rising interest in the treatment of these patients has been driven in large part by the growing body of evidence showing that there is a definite association between elevated ICP and increased mortality and long-term morbidity. The effective treatment of intracranial hypertension with hyperventilation, osmotic agents, and barbiturate therapy has been aided by the regular use of ICP monitoring in most neurosurgical centers. A continuing and ongoing record of ICP allows for the judicial and appropriate use of modern treatment modalities.

Long-term intracranial pressure monitoring in comatose patients suffering from head injuries. A critical survey.

On the basis of a series of 75 patients, the practical use of Icp continuous long-term recording in severe head injuries without mass lesions or remaining deeply comatose after surgical procedures is critically analyzed. ICP monitoring alone seems to be not essential for prognosis. Conversely it is of much greater use as a guide to management (respirator treatment, osmotics, CSF drainage). If the pros and cons of the procedure are carefully weighed, it would appear that, for the time being, ICP long-term monitoring is justified only in comatose patients on intensive care.

Is there an upper limit of intracranial pressure in patients with severe head injury if cerebral perfusion pressure is maintained?

Authors of recent studies have championed the importance of maintaining cerebral perfusion pressure (CPP) to prevent secondary brain injury following traumatic head injury. Data from these studies have provided little information regarding outcome following severe head injury in patients with an intracranial pressure (ICP) greater than 40 mm Hg, however, in July 1997 the authors instituted a protocol for the management of severe head injury in patients with a Glasgow Coma Scale score lower than 9. The protocol was focused on resuscitation from acidosis, maintenance of a CPP greater than 60 mm Hg through whatever means necessary as well as elevation of the head of the bed, mannitol infusion, and ventriculostomy with cerebrospinal fluid drainage for control of ICP. Since the institution of this protocol, nine patients had a sustained ICP greater than 40 mm Hg for 2 or more hours, and five of these had an ICP greater than 75 mm Hg on insertion of the ICP monitor and later experienced herniation and expired within 24 hours. Because of the severe nature of the injuries demonstrated on computerized tomography scans and their physical examinations, these patients were not aggressively treated under this protocol. The authors vigorously attempted to maintain a CPP greater than 60 mm Hg with intensive fluid resuscitation and the administration of pressor agents in the four remaining patients who had developed an ICP higher than 40 mm Hg after placement of the ICP monitor. Two patients had an episodic ICP greater than 40 mm Hg for more than 36 hours, the third patient had an episodic ICP greater than of 50 mm Hg for more than 36 hours, and the fourth patient had an episodic ICP greater than 50 mm Hg for more than 48 hours. On discharge, all four patients were able to perform normal activities of daily living with minimal assistance and experience ongoing improvement. Data from this preliminary study indicate that intense, aggressive management of CPP can lead to good neurological outcomes despite extremely high ICP. Aggressive CPP therapy should be performed and maintained even though apparently lethal ICP levels may be present. Further study is needed to support these encouraging results.

Decompressive craniectomy

Other effects In addition to reducing ICP, studies have found decompressive craniectomy to improve cerebral perfusion pressure and cerebral blood flow in head injured patients. Decompressive craniectomy is also used to manage major strokes, associated with "malignant" edema and intracranial hypertension. The pooled evidence from three randomised controlled trials in Europe supports the retrospective observations that early (within 48 hours) application of decompressive craniectomy after "malignant" stroke may result in improved survival and functional outcome in patients under the age of 55, compared to conservative management alone. The procedure is recommended especially for young patients in whom ICP is not controllable by other methods. Age of greater than 50 years is associated with a poorer outcome after the surgery. Complications Infections such as meningitis or brain abscess can occur after decompressive craniectomy.

Cerebral edema

Vasogenic Extracellular brain edema, or vasogenic edema, is caused by an increase in the permeability of the blood-brain barrier. The blood-brain barrier consists of astrocytes and pericytes joined together with adhesion proteins producing tight junctions. Return of blood flow to theses cells after an ischemic stroke can cause excitotoxicity and oxidative stress leading to dysfunction of the endothelial cells and disruption of the blood-brain barrier. The breakdown of the tight endothelial junctions that make up the blood–brain barrier causes extravasation of fluid, ions, and plasma proteins, such as albumin, into the brain parenchyma. Accumulation of extracellular fluid increases brain volume and then intracranial pressure causing the symptoms of cerebral edema. There are several clinical conditions in which vasogenic edema is present:

[Intracranial pressure in severe brain injuries. 2nd Part: Therapeutic interests and prognosis].

Sixty-seven patients with severe head injury underwent intracranial pressure (ICP) monitoring (10 extradural and 57 intraventricular). All patients had Liege coma scale (LCS) score of 12 or less. Ventriculitis (E. Coli) occurred in one patient (1,8%). The intraventricular method allows C.S.F. drainage with lowering of I.C.P. even with slit ventricles. After 8 days, if an intracranial hypertension persists, we perform a ventriculo-atrial drainage. Pressure recording is a useful way of following the patient's evolution and a guide for prognosis of survival. If I.C.P. is constantly below 5 torr, then the probability of a bad outcome is great. The study also confirms the high mortality rate (93%) if I.C.P. is greater than 40 torr.

[Intracranial pressure and brain death].

Cerebral death occurs during reanimation as an isolated destruction of the entire brain. It is the result of a malignant and irreversible increase of the intracranial pressure. Continuous registration of the intracranial and systemic blood pressures which is done as a routine monitoring procedure in the majority of deep coma patients, allows to identify the moment when cerebral perfusion has come to a complete standstill, and also allows to confirm its irreversibility. At the end of an ischaemic period of 8 to 10 minutes, absolutely lethal to brain tissue, cerebral death is completed. To be on the safe side, the expiration of a 15 to 20 minute period of complete circulatory arrest within the cranial cavity is recommended before further diagnostic measures, especially cerebral arteriography, are undertaken as final proof of dissociated brain death, permitting the explantation of vital organs for grafting. At present, due to possible technical difficulties, reliance upon epidural intracranial pressure measurement alone must still be discouraged. Nevertheless, this investigation method can be most useful in the early timing of the so-called terminal angiography in order not to delay the diagnosis of brain death and its medical consequences.

Intracranial pressure

One of the most damaging aspects of brain trauma and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure. ICP is very likely to cause severe harm if it rises too high. Very high intracranial pressures are usually fatal if prolonged, but children can tolerate higher pressures for longer periods. An increase in pressure, most commonly due to head injury leading to intracranial hematoma or cerebral edema, can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause brain herniation, and restrict blood supply to the brain. It is a cause of reflex bradycardia. Low ICP

Neurointensive care

Basic life support monitoring: Electrocardiography, pulse oximetry, blood pressure, assessment of comatose patients. Neurological monitoring : Serial neurologic examination, assessment of comatose patients (Glasgow Coma Scale plus pupil or four score), ICP (subarachnoid hemorrhages, TBI, Hydrocephalus, Stroke, CNS infection, Hepatic failure), multimodality monitoring to monitor disease and prevent secondary injury in states that are insensitive to neurological exam or conditions confounded by sedation, neuromuscular blockade and coma. Intracranial pressure (ICP) management: Ventricular catheter to monitor Brain oxygen and concentrations of glucose and PH. With treatment options of Hypertonic serum, barbiturates, hypothermia and decompressive hemi-craniotomy Common neurointensive care illnesses and treatments Traumatic brain injury: Sedation, ICP monitoring and management, Decompressive Craniectomy, Hyperosmolar therapy and maintain hemodynamic stability.

Hypercapnic cerebral edema presenting in a woman with asthma: a case report.

Common causes of non-traumatic acute cerebral edema include malignant hypertension, hyponatremia, anoxia, and cerebral vascular accident. The computed tomographic images and data obtained during care of the patient described in this case report provide evidence that hypercarbia can cause increased intracranial pressure and coma without permanent brain injury. Partial pressure of carbon dioxide evaluation for coma is essential to provide faster diagnosis and therapeutic correction in certain common critical disease states. We present the case of a patient in a coma associated with cerebral edema during a typical asthma exacerbation with hypercapnic respiratory failure. An obese 63-year-old African American woman with asthma presented to our hospital with facial swelling and shortness of breath. Immediately following intubation for hypercapnic respiratory failure, she was noted to have a dilated, unresponsive right pupil. An emergent computed tomographic head scan revealed that she had increased intracranial pressure. A neurosurgeon agreed with the computed tomography interpretation and recommended no surgical intervention. The patient's respiratory acidosis was corrected with ventilatory management over several hours in the intensive care unit. Nine and one-half hours later a follow-up head computed tomographic scan was read as normal without cerebral edema. At 12 hours, the patient's right pupil was 5 mm in diameter and reactive. By 24 hours, her pupils were symmetrically equal and reactive. Her symptoms had improved, and she was extubated. A brain magnetic resonance imaging scan revealed no abnormalities. Alteration of consciousness related to hypercapnia during respiratory failure is not generally thought to be related to cerebral edema. Respiratory acidosis resulting from hypercarbia is known to produce carbon dioxide narcosis and coma, but no current treatment algorithm suggests that rapid hypercapnia correction can be critical to neurologic outcome. To the best of our knowledge, our case is a unique example of the physiological changes that may occur in relation to arterial carbon dioxide concentration in the normal brain in the setting of typical hypercapnic respiratory failure. Correction of respiratory acidosis reversed the neurologic symptoms and physiology causing cerebral edema and coma in our patient. Rare similar cases have been sporadically reported in the medical literature, typically in children. Our case is also unusual in that rapid deterioration and clinical status were directly observed on simultaneous computed tomographic scans. Had this patient been found unresponsive, or had she had brief respiratory or cardiac arrest, the scan could have been interpreted as global anoxic injury leading to a different therapeutic course.