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

Two patients experienced anaphylactic reaction to insect stings, with residual encephalopathy. One patient had anaphylaxis despite hyposensitization with whole-body extracts, thus supporting recent reports that reliable protection cannot be achieved unless pure venom is used. The other patient had pathologic confirmation of anoxic encephalopathy, thus supporting the concept that encephalopathy with anaphylaxis is secondary to associated circulatory collapse rather than a primary allergic response of brain disease.
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PMID:Near-fatal and fatal anaphylactic reactions to insect sting. 71 47

Hepatic dysfunction occurs in up to 10% of patients with sickle cell crisis; however, hepatic failure is quite unusual. Cocaine hepatotoxicity has recently been recognized in humans with liver biopsies showing varying patterns of necrosis. Most patients reported with cocaine intoxication have rhabdomyolysis with renal failure, and half of the cases have been fatal. A patient with concomitant sickle cell crisis and cocaine intoxication presented with hepatic failure, coagulopathy, and encephalopathy. Transjugular liver biopsy showed focal areas of confluent necrosis and large areas of collapse. Cocaine intoxication should be considered in the differential diagnosis of hepatic failure in patients with sickle cell anemia.
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PMID:Sickle cell crisis and cocaine hepatotoxicity. 144 96

Vitamin E pretreatment significantly prevented E. coli-induced Disseminated Intravascular Coagulation (DIC) in rats (1). DIC, a reduction in fibrinogen and a falling platelet count and diffuse haemorrhage are part of the clinical features of Haemorrhagic Shock Encephalopathy Syndrome (HSES), recognised as a disease entity in the 1980s (2). At the SIDS Conference 1974 Reisinger described the effect of Escherichia coli (E. coli) endotoxin on the rabbit (3). An early effect was a reduction in fibrinogen and a falling platelet count, resulting in the release of relatively large amounts of the neuro-transmitter serotonin, stored in platelets (3, 4). Fibrinogen inhibited the release of serotonin from platelets (24). Serotonin is released from platelets during platelet aggregation (14). Platelet aggregation is inhibited by vitamin E (1). Serotonin is a neuro-transmitter associated with deep sleep, respiratory movements and cardiovascular collapse (3). Death at a later stage involved vascular permeability, edema and haemorrhage. After fibrin-platelet clots had formed DIC was present in lungs, kidneys and other organs (3). Medical researchers in Australia linked almost half of SIDS victims with a poisonous strain of intestinal E. coli bacteria (5). Dietary selenium in the intestinal villous tip is considered a daily modulator of cytochrome P450-dependent metabolism of drugs and toxins absorbed by intestinal mucosa (6). Villous atrophy occurs in HSES (2).
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PMID:Sudden infant death syndrome (SIDS) and the immune response. 146 Nov 72

We report the case of a three week old newborn who developed bilateral adrenal hemorrhage. This is an extraordinary case because of the late presentation of the hemorrhage as well as the excessive amount of blood involved. The newborn was the product of a normally evolved to full-term pregnancy, with a prolonged and traumatic delivery. The child had severe neonatal hypoxia and encephalopathy which required intensive care. The child was discharged in good conditions a week later. A week after that, the child is readmitted due to circulatory collapse, extreme paleness and a hemoglobin count of 3 g/dL. The newborn was treated for hypovolemic shock and improved substantially. The bilateral intraabdominal mass was detected and using an intravenous pyelography, ultrasonography and a CAT scan, a severe bilateral adrenal hemorrhage was seen. Adrenal failure was excluded and the child's care allowed for him to be discharged a week later in excellent conditions an followed as an outpatient until the hematomas subsided. This problem should be suspected in hypoxic newborns for which they should be submitted to abdominal ultrasonography before being discharged.
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PMID:[Massive neonatal hemorrhage of the adrenal glands]. 227 50

We attempted to ascertain the mechanism of portal hypertension and ascites complicating acute hepatitis in 66 patients who underwent transvenous liver biopsy and measurement of hepatic venous pressure gradient. Increase in hepatic venous pressure gradient was related to the severity of acute hepatitis, as indicated by the significant correlation between the values for hepatic venous pressure gradient and serum bilirubin, serum albumin or coagulation factor V, and by its higher value in patients with, than in patients without, encephalopathy. Hepatic venous pressure gradient was higher in patients with, than in patients without, ascites (12.5 +/- 3.4 vs. 8.4 +/- 3.6 mmHg, respectively; p less than 0.001). No ascites was clinically detectable in the patients in whom hepatic venous pressure gradient was below 6 mmHg. We tested the hypothesis that sinusoidal collapse due to liver cell dropout was a major factor in portal hypertension. Semiautomatic determination of the fractional area of sinusoidal collapse on chromotrope-stained sections and automatic measurement of Sirius red-stained collagen fiber density were performed. Hepatic venous pressure gradient significantly correlated with fractional sinusoidal collapse area (r = 0.61, p less than 0.001) and with Sirius red-stained collagen fiber density (r = 0.43, p less than 0.01). We conclude that portal hypertension in the course of acute hepatitis is related to the severity of liver damage and is a major factor in the development of ascites. Portal hypertension is mainly determined by intrahepatic vascular space being reduced by the collapse of sinusoids.
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PMID:Portal hypertension and ascites in acute hepatitis: clinical, hemodynamic and histological correlations. 277 10

A review of 15 cases of pancreas transplantation at the Presbyterian University Hospital in Pittsburgh showed that all of the neurologic complications occurred outside of the pancreas transplantation surgery itself. Major CNS complications included hypoxic encephalopathy (20 per cent), cerebral and spinal-cord infarction (7 per cent), and seizures (13 per cent). These appeared to be closely associated with cardiovascular collapse or cardiac arrest that often occurred following septic, hemorrhagic, or additional surgical-anesthetic stresses, removed in time from the transplantation. When patients who died of sudden cardiorespiratory arrest were included, the overall frequency of global cerebral ischemia was 33 per cent. The occurrence of herpes zoster neuritis (13 per cent) was contrasted with the lack of CNS infections. The possible associations of visual hallucinations with cyclosporine therapy (7 per cent), CSF pleocytosis with OKT3 therapy (7 per cent), and compressive neuropathy with operative-anesthetic monitoring (7 per cent) were discussed in relation to previous reports in the literature. Randomized controlled clinical studies were suggested to distinguish more clearly the complications due to pancreas transplantation from those due to the natural history of the underlying diabetes and to distinguish the beneficial and adverse effects of pancreas transplants from those of coexisting renal transplants.
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PMID:Neurologic complications of pancreas transplants. 304 46

The clinical, laboratory and histological features of 47 patients with what is defined as late onset hepatic failure are reviewed. Twenty-five of the patients were female and 22 male with a median age of 45 years. Hepatic dysfunction was severe as evidenced by the prolongation of prothrombin time (median = 32 sec, range = 17 to 120 sec). In only four cases was a viral etiology proven (2 hepatitis B, 2 hepatitis A) although the similarity of the clinical features to patients with fulminant viral hepatitis--apart from the longer period of illness prior to the onset of encephalopathy (median = 9 weeks, range = 8 to 24 weeks)--made non-A, non-B infection a possibility in the remainder. There were also similarities to chronic active hepatitis with low titer antibodies to smooth muscle or antinuclear factor in 17% and elevation of the serum IgG in 49%. Liver biopsy in 5 of 8 survivors more than 1 year after initial presentation showed chronic active hepatitis in three. Lobular inflammatory infiltrate, bridging necrosis and multilobular collapse were the features of the acute stage of illness in both the survivors and fatal cases. The patients given corticosteroids did not have a statistically significant improvement in survival, and overall mortality for the series was 81%. Hepatic transplantation, successfully performed in one patient, would appear to offer the best chance of survival for the majority of these patients.
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PMID:Late onset hepatic failure: clinical, serological and histological features. 308 35

An ad hoc panel of the American Medical Association prepared a report to identify severe, irreversible pertussis vaccine reactions and to establish criteria for attributing such reactions to the vaccine. Severe but reversible reactions, their likely duration and effects, and the clinical criteria for attribution were also examined. Three types of reactions which may produce residual brain damage lasting more than one year are encephalopathy, complex febrile convulsions, and afebrile convulsions. Serious pertussis vaccine reactions which are unlikely to have persistent adverse effects are simple febrile convulsions, anaphylaxis, and shock collapse. The panel also noted that there is no evidence that killed vaccine such as the pertussis vaccine can cause any insidious, delayed harmful effects.
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PMID:Pertussis vaccine injury. AMA Ad Hoc Panel on Pertussis Vaccine Injury. 405 31

Circulatory collapse and sudden death was defined retrospectively as one of the major critical problems among 23 respirator-dependent patients with amyotrophic lateral sclerosis (ALS). Six cases died from sudden cardiac arrest or anoxic encephalopathy following the circulatory collapse. In five among the six cases, sudden death or cardiac arrest occurred during sleep at night. Eight cases had had episodes of marked fluctuation of blood pressure before death, including paroxysmal elevation of blood pressure and heart rate, and successive sudden pressure fall without compensatory tachycardia. The spells of hypotension often occurred during sleep. In addition, the prospective study of diurnal variation of blood pressure, heart rate, plasma norepinephrine and plasma renin activity in nine respirator-dependent ALS patients showed continuous tachycardia and more remarkable nocturnal decrease of blood pressure compared with the control subjects. Plasma norepinephrine levels were constantly higher in the ALS patients particularly in a daytime. These indicate the continuous sympathetic hyperactivity in ALS. We discuss the cause of the circulatory collapse and sudden death in the respirator-dependent ALS patients in terms of the autonomic dysregulatory mechanism or the sympathetic hyperactivity.
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PMID:Circulatory collapse and sudden death in respirator-dependent amyotrophic lateral sclerosis. 793 21

Hypoxic encephalopathy during the late gestation and perinatal period occupies a large part as a cause of mentally and physically handicaps. An extensive study on the pathogenesis and pathophysiology of the hypoxic brain damage is, therefore, the matter of urgency to minimize the occurrence of handicapped children. The main factors and/or processes relating to hypoxic or hypoxic-ischemic brain damage are (1) structural and functional immaturity of the brain vascular system and (2) a metabolic cascade triggered by hypoxia. As the following metabolic cascade subsequent to hypoxia has been partly made clear; (a) disturbance of the energy metabolism, (b) excessive release of excitatory amino acids and subsequent activation of NMDA and K/Q receptors at the cell membrane, (c) collapse of the membrane ion pump, and (d) increase in turnover of membrane phospholipids.
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PMID:[Pathogenesis of hypoxic encephalopathy during pre- and peri-natal periods]. 813 81


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