Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although old or recent infarcts of a cerebellar hemisphere in the territories of the posterior inferior (PICA), superior, or anterior inferior cerebellar arteries are commonplace autopsy findings, in no case have corresponding clinical symptoms been clearly identified. We have studied three cases, two clinocaopthologically and one clinicosurgically, in which an acute infarct involving only the cerebellum lay in the PICA territory distal to the branches to the medulla oblongata. The clinical manifestations consisted of rotatory dizziness intensified by motion, nausea, vomiting, imbalance, and nystagmus. In two cases, the clinical diagnosis had been a benign labyrinthine disorder. Recognition of a syndrome corresponding to cerebellar infarction in the PICA territory is important insofar as it assists in the differential diagnosis of dizziness. It becomes of crucial importance when cerebellar infarction is the prelude to cerebellar swelling and brain stem conpression leading to coma and death unless surgically relieved.
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PMID:Acute cerebellar infarction in the PICA territory. 113 Oct 70

Eight patients were seen within 15 min of intranasal self-administration of large amounts of pure D-lysergic acid diethylamide (LSD) tartrate powder. Emesis and collapse occurred along with sign of sympathetic overactivity, hyperthermia, coma, and respiratory arrest. Mild generalized bleeding occurred in several patients and evidence of platelet dysfunction was present in all. Serum and gastric concentrations of LSD tartrate ranged from 2.1 to 26 ng/ml and 1000 to 7000 mug/100 ml, respectively. With supportive care, all patients recovered. Massive LSD overdose in humans is life-threatening and produces striking and distinctive manifestations.
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PMID:Coma, hyperthermia, and bleeding associated with massive LSD overdose, a report of eight cases. 114 10

In seven patients with chronic renal failure in an advanced stage 17 episodes of upper abdominal pain, hypertension, vomiting and (in some of them) coma occurred during peritoneal dialysis with sorbitol-containing dialysate. The signs recurred in some of the patients but did not when glucose-containing dialysate of otherwise identical composition was used. Very high levels of sorbitol in CSF and serum were measured in the comatose patients. The precipitating factor is probably a reduced metabolic breakdown of sorbitol in renal failure with preferential intracellular deposition of sorbitol and subsequent cellular oedema. To avoid this dangerous reaction it is necessary to use glucose instead of sorbitol in peritoneal dialysates, despite the technical problems of sterilisation. Where this is not possible, glucose should be added in order to reduce the sorbitol concentration in the dialysate to less than 15g/l.
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PMID:[Severe side-effects during peritoneal dialysis caused by sorbitol-containing dialysate (author's transl)]. 114 25

Hyperthermia has recently been recognized as a manifestation of hypoglycemia. We describe two episodes of hypoglycemia associated with nausea, vomiting, chills, and impaired consciousness which were followed by marked hyperthermia. We suggest that the hyperthermia may result from excessive reaction to preceding hypothermia caused by the hypoglycemia. We would like to alert the clinician to the possibility of a previous, severe hypoglycemic episode in any diabetic patient with hyperthermia and coma.
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PMID:Marked hyperthermia as a manifestation of hypoglycemia in long-standing diabetes mellitus. 115 46

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.
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PMID:Acute encephalopathy in siblings. Reye syndrome vs salicylate intoxication. 125 38

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.
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PMID:Reye's syndrome without fatty liver. 127 Mar 22

Intussusception is the most frequent cause of intestinal occlusion in children aged 3-5 years. Diagnosis is easy to perform in cases with typical clinical presentation. However diagnosis may be difficult in rare cases with atypical symptoms characterized by SNC involvement, that could delay a convenient treatment. We report 4 cases of intussusception presenting initially with consciousness abnormalities, hypotonia and vomiting. In these cases differential diagnosis with other conditions associated with comatose states has to be performed. Some hypothesis may be considered to explain these clinical pictures: 1. increased endorphins excretion during abdominal pain; 2. neurotoxins of bacterial origin released and absorbed by altered bowel; 3. intestinal hormones abnormally produced during the disease. As recommended by Rachmel, the condition should be suspected in all children presenting with the association of vomiting and lethargy and a radiological or tomographic study of abdomen should be performed also in cases without intussusception typical symptoms.
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PMID:[Changes in the consciousness state as a symptom of intestinal invagination onset]. 129 38

In this paper we discuss the first five Argentinean patients presenting isovaleric acidemia (IVA), an alteration of leucine catabolism due to a genetic defect of isovaleryl-CoA dehydrogenase. Belonging to unrelated families, one from native (H. Fam.) and the other from Italian ancestry (M. Fam.); the patients presented the clinical pattern highly suggestive of the disease: they were siblings, had disease-free intervals, vomiting, ketoacidosis crises, "sweaty feet" odor and progression of the neurologic involvement from somnolence and stupor to profound coma. In the four children of H. Fam. the disease had a late but severe beginning; one of the girls died (N.H.). The boy from M. Fam. presented a neonatal form of clearly benign course. The disease was confirmed by gas-chromatography (GC) of volatile acids in serum and also by the typical urinary acid GC-profiles (Fig. 1, A and B); the isovalerylglycine quantitative evaluation in urinary samples collected during crises is shown in Table 1. The morphological findings in liver and brain of N.H. showed at the ultrastructural study, an extensive fatty degeneration and greatly marked mitochondrial alterations in the liver and edema, neuronal karyorrhexis and karyolysis in the brain (Fig. 2). The therapeutic protocol based on a low leucine or low protein diet and use of glycine is described. The evolutionary follow up, more than 10 years for the first case, showed a normal mental development in three of them and retardation in the first child of H. Fam., who had a late diagnosis. IVA is still valuable as a paradigm in the acquisition of a highly clinical suspicion and for its introduction in the study of genetic organic acidemias.
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PMID:[Phenotypic expression variation of isovaleric acidemia in Argentinian patients. A long term follow-up]. 130 4

The increased prevalence of rodents resistant to warfarin led to the development of the hydroxycoumarin anticoagulant brodifacoum. A 25-year-old man attempted suicide by consuming four boxes of d-CON Mouse-Prufe II; each box contains 42 g of bait that is 0.005% brodifacoum. He presented to a hospital nine days later with syncope, hematochezia, gross hematuria, epistaxis, anemia, and a severe coagulopathy. Radiographic studies were consistent with pleural, pericardial, and mediastinal hemorrhages. Vitamin K and fresh frozen plasma were given, and he was later discharged on oral phytonadione (vitamin K1). The patient's coagulopathy recurred, necessitating multiple plasma transfusions and prolonged treatment with oral phytonadione. Fifteen weeks after hospital discharge, he presented again with a history of additional brodifacoum ingestion. Neurologic status was initially normal, but in the emergency department he suddenly became comatose soon after emesis was induced with syrup of ipecac. Computed tomography of the brain revealed a subarachnoid hemorrhage that led to brain death less than 24 hours later. This case demonstrates the severe and prolonged coagulopathy that can result from ingestion of brodifacoum, a compound that has a toxic potency about 200-fold that of warfarin and a half-life as much as 60 times longer.
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PMID:Fatal rodenticide poisoning with brodifacoum. 134 54

Fourteen patients developed massive putaminal-thalamic hemorrhage. All patients were young black men. They were hypertensive but without chronic hypertensive vascular changes. They had been treated with antihypertensive medication for less than 3 yr. All patients presented with a prodromal headache beginning 18-30 h before the brain hemorrhage. Initial clinical signs were heralded by a change in the headache pattern and vomiting. All patients became comatose and hemiplegic within 4-12 h. CT showed a hyperdense putaminal-thalamic hemorrhage which was 60 to 86 mm in maximal diameter. There was marked mass effect with secondary intraventricular extension. All patients died within 72 h, despite rapid and adequate blood pressure control and maximal medical treatment of cerebral edema and increased intracranial pressure.
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PMID:Massive putaminal-thalamic nontraumatic hemorrhage. 139 83


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