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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute fatty liver of pregnancy is a rare, potentially fatal, complication of late pregnancy. The incidence is estimated at 1:7000-1:15000 pregnancies. Presentation is classically with malaise, nausea and vomiting, abdominal pain and rarely encephalopathy. Prolongation of laboratory clotting tests is an early feature. Ultrasound examination of the liver is performed to exclude biliary stasis. Rapid clinical deterioration may occur and urgent delivery should be organised. Anaesthetists form part of a multidisciplinary approach before, during and after delivery but there are few reports of anaesthetic involvement. One dilemma facing an anaesthetist called to assist in these cases is the potentially negative effect of general anaesthesia on hepatic encephalopathy versus the risks associated with regional anaesthesia in the presence of coagulopathy. Postoperative analgesia may also be complicated by impaired renal and hepatic function. We present three cases that occurred in our unit in a 6-month period illustrating the spectrum of disease severity and the successful use of different anaesthetic techniques to facilitate management including delivery.
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PMID:Acute fatty liver of pregnancy; three cases and discussion of analgesia and anaesthesia. 1727 81

A 40-year-old man, who had suffered from general malaise and brown urine during his stay in China, was admitted with remarkable jaundice and hepatocellular disorders soon after he returned to Japan. Because his coagulation test results worsened, he was transferred to our hospital. No evidence of hepatitis A-D virus infection, autoimmune hepatitis, or metabolic disorders was noticed. His prothrombin time was extended (18%), grade II encephalopathy appeared on the second hospital day, and fulminant hepatitis was diagnosed. Artificial liver support was introduced, and his hepatic coma and coagulation parameters gradually recovered. Genotype IV hepatitis E virus RNA was detected in his early phase sera and also both IgG and IgM type anti-hepatitis E virus antibodies were detected. Fulminant hepatitis E resulting from infection in China was diagnosed.
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PMID:[A case of fulminant hepatitis E treated with artificial liver support]. 1728 17

Cat-scratch disease is one of several diseases known to be caused by Bartonella species. Some infections due to Bartonella resolve spontaneously without treatment with antibiotics, but in other cases the disease can be fatal without treatment. This case study reports a 7-year-old male who presented with an unexplained encephalopathy and unusual retinal findings associated with evidence supporting infection by B. henselae. The 7-year-old male presented with a 2-week history of general malaise and cervical lymphadenopathy progressing onto fever, headache, vomiting, and confusion associated with meningism. Lumbar puncture revealed a raised cerebrospinal fluid protein, low glucose, and raised white cell count. Abnormal retinal findings and raised antibodies titres to B. quintana indicated a diagnosis of cat-scratch disease. He was treated with azithromycin orally for 3 weeks and made a complete recovery.
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PMID:Encephalopathy with retinitis due to cat-scratch disease. 1803 41

Lyme disease is the most common tick-borne disease in the United States. This review details the risk factors, clinical presentation, treatment, and prophylaxis for the disease. Information was obtained from a search of the PubMed and MEDLINE databases (keyword: Lyme disease) for articles published from August 31, 1997, through September 1, 2007. Approximately 20,000 cases of Lyme disease are reported annually. Residents of the coastal Northeast, northwest California, and the Great Lakes region are at highest risk. Children and those spending extended time outdoors in wooded areas are also at increased risk. The disease is transmitted to humans through the bite of the Ixodes tick (Ixodes scapularis and Ixodes pacificus). Typically, the tick must feed for at least 36 hours for transmission of the causative bacterium, Borrelia burgdorferi, to occur. Each of the 3 stages of the disease is associated with specific clinical features: early localized infection, with erythema migrans, fever, malaise, fatigue, headache, myalgias, and arthralgias; early disseminated infection (occurring days to weeks later), with neurologic, musculoskeletal, or cardiovascular symptoms and multiple erythema migrans lesions; and late disseminated infection, with intermittent swelling and pain of 1 or more joints (especially knees). Neurologic manifestations (neuropathy or encephalopathy) may occur. Diagnosis is usually made clinically. Treatment is accomplished with doxycycline or amoxicillin; cefuroxime axetil or erythromycin can be used as an alternative. Late or severe disease requires intravenous ceftriaxone or penicillin G. Single-dose doxycycline (200 mg orally) can be used as prophylaxis in selected patients. Preventive measures should be emphasized to patients to help reduce risk.
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PMID:Diagnosis and treatment of Lyme disease. 1845 88

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that may occur in people with normal liver-associated enzyme levels, despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl who had absence seizure and complained about progressive dizziness and general malaise several days after restarting valproate. Then, she presented vomiting and decreased consciousness three weeks after valproate use. Notably, her serum ammonia level was five times the upper limit of normal (184 micrommol/L), with normal liver-associated enzyme and supra-therapeutic valproate level. EEG showed continuous generalized slowing. The tandem mass analysis revealed carnitine deficiency. Consciousness improved after emergent hemodialysis. Ammonia level and EEG also returned to normal. Possible mechanisms, risk factors and the treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy treated by hemodialysis. 1879 59

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that can occur in people with normal liver-associated enzyme levels, and despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl suffering from absence seizures, who complained of progressive dizziness and general malaise several days after restarting valproate. She developed vomiting and decreased consciousness after 3 weeks of valproate use. She had a serum ammonia level five times higher than the upper normal limit, normal liver-associated enzymes, and a supra-therapeutic valproate level. Electroencephalography (EEG) showed continuous generalized slowing. Tandem mass spectrometry analysis revealed carnitine deficiency. Her consciousness improved after emergent hemodialysis. Her ammonia level and EEG also became normal. Possible mechanisms, risk factors and treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.
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PMID:Valproate-induced hyperammonemic encephalopathy. 1913 74

Scleroderma renal crisis (SRC) occurs in 5-10% of SSc patients, who may present with an abrupt onset of hypertension, acute renal failure, headaches, fevers, malaise, hypertensive retinopathy, encephalopathy and pulmonary oedema. Patients at greatest risk of developing SRC are those with diffuse cutaneous or rapidly progressive forms of SSc, and treatment with a recently commenced high dose of corticosteroid. Laboratory tests may demonstrate hypercreatinaemia, microangiopathic haemolytic anaemia (MAHA), thrombocytopaenia and hyperreninaemia. Renal crisis is also linked to a positive ANA speckled pattern, antibodies to RNA polymerase I and II, and an absence of anti-centromere antibodies. Early, aggressive treatment with angiotensin-converting enzyme inhibitors has improved prognosis in SRC, although 40% of the patients may require dialysis, and mortality at 5 yrs is 30-40%. Median time to recovery is 1 yr, and typically occurs within 3 yrs. Prognosis is worse for males, but may not be related to corticosteroid use, presence of MAHA or severity of renal pathology. Modification of endothelin over-activity, which is implicated in the pathogenesis of SRC, may offer a future therapeutic approach.
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PMID:Renal complications and scleroderma renal crisis. 1948 21

Legionnaires' disease is primarily a pneumonic process caused by Legionella pneumophilia, a gram-negative aerobic bacillus but also has multiple system involvement. The most common manifestation is encephalopathy suggesting a generalized brain dysfunction but focal neurological manifestations have been reported. We report a patient with Legionella pneumonia associated with cerebellar dysfunction and unilateral facial nerve weakness. 51-year-old previously healthy male presented with shortness of breath, cough, slurred speech, and unsteadiness on feet associated with malaise, fevers and myalgias. Patient's family reported facial asymmetry for 2 days. Patient had no significant medical history and was not on any medication. He denied smoking, alcohol or illicit drug use. Chest X-ray showed bilateral lower lobe infiltrates. Urinary antigen assay for Legionella pneumophilia serogroup 1 was positive. Patient was started on intravenous moxifloxacin. On day 5 the patient was discharged home and continued oral moxifloxacin for two weeks. After the two weeks, his respiratory symptoms, gait ataxia and dysarthria resolved. We report the first case of Legionnaires' disease with cerebellar dysfunction and seventh nerve palsy. Legionnaires' disease should be considered in patients with any neurological symptoms in the setting of pneumonia. Failure to recognize and treat the infection may lead to poor outcomes.
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PMID:Legionnaires' disease with facial nerve palsy. 2146 Oct 48

Acute mercury vapor poisoning is a rare but fatal toxicological emergency. People are exposed to mercury in daily life by the way of foods, vaccines, antiseptics, ointments, amalgam or occupation. We present here, the clinical picture and management of four members of the same family who were exposed to elemental mercury. Three of the family members were seen in another hospital with malaise, fever, eritematous rash and pulmonary problems. Their questioning revealed the mercury exposure. Having a suspicion of heavy metal intoxication, blood and urine mercury levels were measured and mercury intoxication was diagnosed. On admission to our hospital, two patients already had chelation therapy. In three of them we found three distinct abnormalities: encephalopathy, nephrotic syndrome and polyneuropathy. The fourth family member had minor symptoms. This family is an example for the inhalation exposure resulting from inappropriate handling of liquid mercury. During the first days, flu like illness ensues. Then, severe pulmonary, neurological, renal, hepatic, hematological and dermatological dysfunctions develop. Blood and urine mercury levels should be tested on suspicion, but it must be kept in mind that blood level is unreliable in predicting the severity of mercury toxicity. The priority in the treatment should be removing the patient from the source of exposure. Then British anti-Lewisite, edetate calcium disodium, penicillamine, Sodium 2,3-dimercaptopropane-1-sulfhonate and 2,3-dimercaptosuccinic acid can be used for binding the mercury. We conclude that since mercury-containing devices are present in daily life, physicians must be able to recognize the clinical manifestations and treatment of mercury poisoning.
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PMID:Mercury vapor inhalation and poisoning of a family. 2290 71

Hepatitis E virus genotype 3 is not rare in developed countries, and may cause chronic hepatitis in immunocompromised patients. This may not only lead to abnormalities in liver test and malaise, but to severe neurological symptoms as well. In this case, chronic hepatitis E infection caused encephalopathy, an atactic gait, Lhermitte's sign, incomplete bladder emptying and peripheral sensory neuropathy in a renal transplant recipient. The diagnosis was not performed until years after the onset of first symptoms and several months after the onset of neurological symptoms. If treated adequately, viral load can be reduced in over two-thirds of patients and neurological symptoms are often resolved. More widespread knowledge about this virus and its extrahepatic manifestations may lead to a quicker diagnosis, and may limit pathology. Serological screening should be added to standard pretransplant virological screening, so that, in the future, patients without antibodies could be vaccinated.
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PMID:Hepatitis E-associated encephalopathy in a renal transplant recipient. 2478 62


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