Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute respiratory distress syndrome (ARDS) is the result of severe injuries of different etiologies of the capillary system in patients with previously healthy lungs, resulting in noncardiogenic pulmonary edema. The authors studied 42 infants in whom the histopathologic aspects were suggestive for ARDS. The etiologic factors of this syndrome were: severe gastroenteritis with hypovolemic or endotoxic shock (13 cases), sepsis (9 cases), fulminans purpura (2 cases), severe neurological disorders (13 cases), pulmonary infections (5 cases). In such conditions, if the infant presents hyperpnea followed by generalised cyanosis, refractory to oxygen therapy, and if there are clinical and radiologic signs of acute pulmonary edema, the diagnosis of ARDS must be considered and a complete intensive care therapy is compulsory in order to alleviate the severe prognosis of this syndrome.
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PMID:Etiological, clinical and pathomorphological aspects of acute respiratory distress syndrome in children. 1075 53

The risk factors and modes of death following acute diarrhoeal illness in children admitted to University Hospital, Kuala Lumpur between 1982 and 1997 were studied retrospectively. Among 4,689 cases of acute gastroenteritis admitted, ten deaths were noted. The case mortality rate was 2.1/1000 admissions. All deaths were infants below one year, with eight females and two males. Acute renal failure and acute pulmonary oedema were common preceding events. Female sex, infants less than twelve months, the presence of hyper or hyponatraemia and moderate to severe dehydration on admission were risk factors for deaths.
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PMID:Deaths following acute diarrhoeal diseases among hospitalised infants in Kuala Lumpur. 1104 55

GlySH-surfactant herbicide (GlySH), one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The US Environmental Protection Agency (EPA) states that 'GlySH' is of relatively low oral and acute dermal toxicity. It does not have anticholinesterase effect and no organophosphate-like central nervous system (CNS) effects. The clinical features range from skin and throat irritation to hypotension and death. Severe GlySH-surfactant poisoning is manifested by gastroenteritis, respiratory disturbances, altered mental status, hypotension refractory to the treatment, renal failure, and shock.[1] GlySH intoxication has a case fatality rate 3.2-29.3%. Pulmonary toxicity and renal toxicity seem to be responsible for mortality. Metabolic acidosis, abnormal chest X-ray, arrhythmias, and elevated serum creatinine levels are useful prognostic factors for predicting GlySH mortality.[2] There is no antidote and the mainstay of treatment for systemic toxicity is decontamination and aggressive supportive therapy. We report a case of acute pulmonary edema, which is a rare but severe manifestation of oral GlySH poisoning, where patient survived with aggressive supportive therapy.
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PMID:Glyphosate poisoning with acute pulmonary edema. 2594 77