1/22. Acute encephalopathy in siblings. reye syndrome vs salicylate intoxication.siblings, aged 9 and 7 years, had simultaneous onset of vomiting, disorientation, ataxia, and coma. Both children had prodromal symptoms of upper respiratory tract infections, and had been treated with large doses of aspirin. Laboratory data showed evidence of hepatocellular dysfunction, with an elevated serum ammonia level in one patient; salicylate levels were 50 and 44 mg/100 ml. The child who died had autopsy evidence of cerebral edema and fatty liver. The difficulty in clinically differentiating reye syndrome from salicylate intoxication is discussed.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/22. Reye's syndrome without fatty liver.A 2 1/2-year-old child died after an illness of three days duration, characterized by a sudden onset, vomiting, coma and a striking hyperammonemia. At autopsy, the liver was practically normal. This is a further example of Reye's syndrome with only minimal fatty infiltration of the liver. It appears that the classical massive and diffuse fatty degeneration of the liver is not an essential feature of the syndrome. The evidence for this is discussed.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
3/22. Reye's syndrome. A diagnosis occasionally first made at medicolegal autopsy.Reye's syndrome, a condition characterized pathologically by cerebral edema and fatty change of the liver, has been described extensively in the medical literature as a disease manifested clinically by encephalopathy and coma. This is a report of five cases of Reye's syndrome occurring as sudden, unexpected deaths outside of the hospital. In each of these cases, there is a vague history of a previous viral illness. A history of aspirin intake is inconstant. Each child either had no significant past illnesses or there was a history of repeated upper respiratory infections. The classic progression of signs and symptoms usually described for Reye's syndrome, where vomiting usually precedes encephalopathy and coma, was not present in any of the cases. Results of autopsies showed the characteristic findings for Reye's syndrome, and additional tests showed no other explanation for the deaths. This manifestation of the disease is seldom described in medical literature, but it may be encountered occasionally by the medical examiner.- - - - - - - - - - ranking = 2keywords = coma (Clic here for more details about this article) |
4/22. The thalamus and midbrain in reye syndrome.A previously healthy 5 1/2-year-old male had reye syndrome. He presented in coma with apnea 1 week after a viral infection and following 2 days of vomiting and progressive obtundation. He was in coma with dystonic posturing and intact brainstem function. Laboratory evaluation revealed initial hypoglycemia, and markedly elevated liver enzymes, prolonged clotting times, and elevated ammonia levels. No underlying metabolic disorder was present, and the patient completely recovered. On a modified diffusion-weighted image magnetic resonance imaging scan, restriction of diffusion in the thalamus and midbrain was observed. While abnormalities of the thalamus and midbrain have previously been reported, this is the first report of diffusion-weighted imaging indicating early impairment of water diffusion, a finding more commonly observed with stroke.- - - - - - - - - - ranking = 2keywords = coma (Clic here for more details about this article) |
5/22. Extrapulmonary manifestations of adenovirus type 7 pneumonia simulating reye syndrome and the possible role of an adenovirus toxin.Three children developed extensive extrapulmonary disease in the course of fatal adenovirus type 7 pneumonia. Several clinical features, including the unexpected onset of coma, suggested the development of reye syndrome, but biochemical and histopathologic findings were inconsistent with this diagnosis. Virologic and pathologic studies did not reveal evidence of extrapulmonary adenovirus infection, despite clinical involvement of the liver, skeletal muscle, and central nervous system. The detection in premortem sera from all three patients of adenovirus penton antigen, known to be cytotoxic in vitro, suggests a possible mechanism for the production of extrapulmonary pathology in the absence of extrapulmonary virus infection.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
6/22. A case of ornithine transcarbamylase deficiency with acute and late onset simulating Reye's syndrome in an adult male.A 15-year-old male was admitted to the hospital because of a disturbance of consciousness. He was in good mental and physical condition until the previous day, when he vomited and experienced a reduction of consciousness. He was brought to the hospital the day following the onset of symptoms. On admission the patient was stuporous. Neurological focal signs were not demonstrated. Computed tomographic (CT) scanning on admission showed no definite abnormality. Cerebrosprinal fluid had no pleocytosis. At this time, Reye's syndrome was suspected because of the acute change of consciousness and the presence of hyperammonemia. The disturbance of consciousness progressed and he became comatose on the day following admission. CT scanning showed that the suprasellar, ambient and quadrigeminal cisterns could almost not be detected and the bilateral ventricles were narrowed. The plasma aminogram demonstrated an elevation of alanine, lysine, glutamine, glutamic acid, aspartate and proline. Ketonuria was negative, but the urinary excretion of orotic acid was markedly increased. This data was indicative of the existence of an ornithine transcarbamylase (OTC) deficiency. The patient was died on the third day after hospitalization. The OTC activity in the liver was 10% of normal. Activities of other enzymes in the urea cycle were within normal limits. It is unusual that the symptoms of the enzyme deficiency occurred, both acutely and late at an adult age, as in this case. This case demonstrates that OTC deficiency should be considered in the differential diagnosis of hyperammonemia of adult onset.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
7/22. Reye's syndrome in an adult.There have been over 3,500 cases of Reye's syndrome reported to the CDC since 1973. The temporal use of aspirin with a prodromal viral illness has been statistically associated with the etiology of the syndrome. Reye's syndrome presents as an acute progressive encephalopathy with varying levels of coma and normal cerebrospinal fluid (CSF). Hepatic transaminases are elevated, and the serum aspartate aminotransaminase (AST) is usually elevated three to 30 times normal. Histological changes on liver biopsy are characterized by microvesicular intrahepatocyte lipid deposition, which is rarely found in other diseases. The syndrome has rarely been reported to occur in adults over 18 years old. We report the 25th case of Reye's syndrome occurring in an adult, which initially presented as acetominophen toxicity but was shown to be Reye's syndrome on histological examination of the liver.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
8/22. Reye-like syndrome following treatment with the pantothenic acid antagonist, calcium hopantenate.Three senile patients developed fatal acute encephalopathy while receiving calcium hopantenate. The clinical, biochemical, and pathological picture was similar to Reye's syndrome. calcium hopantenate is a pantothenic acid antagonist. The serum levels of calcium hopantenate were high in coma, and that of pantothenic acid examined in one patient was lowered. Evidence obtained indicated that the Reye-like syndrome might be caused by calcium hopantenate possibly due to the induction of pantothenic acid deficiency.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
9/22. Familial Reye-like syndrome: a presentation of medium-chain acyl-coenzyme a dehydrogenase deficiency.A 20-month-old girl with a family history of two siblings who died of an encephalopathy diagnosed as reye syndrome presented to an emergency room in hypoglycemic coma and was found to have medium-chain acyl-coenzyme a dehydrogenase deficiency. The salient clinical and biochemical features of this newly described inborn error of fatty acid metabolism are described and contrasted to those of classical reye syndrome. Important clues that should lead the clinician to suspect this disorder, methods of diagnosis, and appropriate acute and long-term therapy are also discussed.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
10/22. battered child syndrome in a four year old with previous diagnosis of Reye's syndrome.A 4-year-old Black child was admitted to hospital in coma and with retinal hemorrhages. He was diagnosed as having Reye's Syndrome and remained hospitalized for 1 month. At discharge, he was neurologically compromised with spasticity of the right arm and leg, and could not walk or sit unsupported. Three weeks later he was again seen in the emergency room with a swollen right arm and leg and was subsequently readmitted. Healing fracture of the right femur and probable healing fracture of the right humerus were diagnosed. These were thought to be due to a fall from a stroller. Almost 4 months later, the child died at his home in the care of his mother's boyfriend. autopsy findings were consistent with a severely chronically battered child.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
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