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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reye syndrome (RS) is an acute illness that occurs almost exclusively in children; it is characterized clinically by profuse vomiting and neurologic dysfunction, sometimes progressing to delirium, coma, and death. Continuous national surveillance for RS was established in December 1976. This report summarizes RS cases for the 1989 surveillance year (December 1, 1988-November 20, 1989).
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PMID:Reye syndrome surveillance--United States, 1989. 189 29

These studies were undertaken to investigate the relationship between medium-chain fatty acid availability, medium-chain fatty acid oxidation, and central nervous system toxicity during infusion of medium-chain triglycerides in dogs. Six dogs received a sequential, stepwise infusion of trioctanoin at three different rates for 80 min each, providing calories below and equal to resting energy expenditure in the species. Ketone body production rates (using a 14C beta-hydroxybutyrate tracer) and plasma concentrations of lactate and octanoate were monitored. Three animals were infused with saline to serve as controls. Blood-brain barrier integrity was assessed with Evans blue dye, and brain samples were taken at the end of the study to quantify brain water. Three animals were studied under anesthesia to obtain good quality EEG and intracranial pressure measurements. Results were (1) plasma octanoate increased to 0.37 +/- 0.13, 0.78 +/- 0.2, and 1.44 +/- 0.41 mmol/liter during the three infusion intervals; (2) emesis, somnolence, and coma were observed at the two highest trioctanoin rates; (3) ketone body concentrations and production increased from 102 +/- 15 to 859 +/- 54 mumol/liter and 3.6 +/- 0.43 to 18.5 +/- 1.7 mumol/kg/min, respectively, at the highest trioctanoin infusion rate; and (4) plasma lactate also increased from 1.3 +/- 0.1 to 4.3 +/- 0.9 mmol/liter at the highest infusion rate. EEG changes were also observed, consisting of high amplitude slowing and reduction in amplitude of faster components. There was no extravasation of Evans blue dye, nor change in brain water or intracranial pressure. The conclusion--medium-chain triglycerides have significant dose-related central nervous system toxicity in dogs. Therefore, caution should be exercised in clinical studies with MCTs, including careful measurement of medium-chain fatty acid concentrations.
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PMID:Metabolic and neurologic effects of an intravenous medium-chain triglyceride emulsion. 190 Nov 6

The major use of N-acetylcysteine in clinical toxicology is in the treatment of acetaminophen (paracetamol) overdosage. The hepatorenal toxicity of acetaminophen is mediated by a reactive metabolite normally detoxified by reduced glutathione. If glutathione is depleted, covalent binding to macromolecules and/or oxidation of thiol enzymes can lead to cell death. Oral or intravenous N-acetylcysteine or oral D,L-methionine mitigates acetaminophen-induced hepatorenal damage if given within 10 hours, but becomes less effective thereafter. In vivo, N-acetylcysteine forms L-cysteine, cystine, L-methionine, glutathione, and mixed disulfides; L-methionine also forms cysteine, thus giving rise to glutathione and other products. Oral therapy with N-acetylcysteine or methionine for acetaminophen poisoning is contraindicated in the presence of coma or vomiting, or if activated charcoal has been given by mouth. Nausea, vomiting, and diarrhea may also occur as a result of oral N-acetylcysteine administration. Anaphylactoid reactions including angioedema, bronchospasm, flushing, hypotension, nausea/vomiting, rash, tachycardia, and respiratory distress may occur 15-60 minutes into N-acetylcysteine infusion (20 hours intravenous regimen) in up to 10% of patients. Following accidental intravenous overdosage, the adverse reactions of N-acetylcysteine are similar but more severe; fatalities have occurred. A reduction in the loading dose of N-acetylcysteine may reduce the risk of adverse reactions while maintaining efficacy. Administration of N-acetylcysteine for a longer period might provide enhanced protection for patients in whom acetaminophen absorption or elimination is delayed. N-acetylcysteine may also have a role in the treatment of toxicity from carbon tetrachloride, chloroform, 1,2-dichloropropane, and other compounds. The possible use of N-acetylcysteine and other agents in the prevention of the neuropsychiatric sequelae of acute carbon monoxide poisoning is an important area for future research.
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PMID:Use of N-acetylcysteine in clinical toxicology. 192 4

Gyromitra esculenta (Pers.: Fr.) Fr. and a few other mushrooms have caused severe poisonings and even deaths in humans. Clinical data are characterized primarily by vomiting and diarrhoea, followed by jaundice, convulsions and coma. Gastrointestinal disorders distinguish this poisoning. Frequent consumption can cause hepatitis and neurological diseases. The species of concern are mainly G. esculenta and G. gigas (Kromb.) Cooke (non Phill.). Nevertheless, recent advances in chromatography, biochemistry and toxicology have established that other Ascomycetes species also may prove toxic. Gyromitrin (acetaldehyde methylformylhydrazone, G) and its homologues are toxic compounds that convert in vivo into N-methyl-N-formylhydrazine (MFH), and then into N-methylhydrazine (MH). The toxicity of these chemicals, which are chiefly hepatotoxic and even carcinogenic, has been established through in vivo and in vitro experiments using animals, cell cultures and biochemical systems. When we consider the chemical nature and the reactivity of these natural compounds, we suggest that chemical and biochemical mechanisms may explain their intrinsic biological activity.
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PMID:Poisoning by Gyromitra esculenta--a review. 193 97

During 1984-1989, 19 Bedouin children, 4-8 years old, were hospitalized because of henbane plant (Hyoscyamus reticulatus) poisoning. There were 14 cases in the autumn, 3 in the spring and 2 in the summer. The most prominent signs were altered state of consciousness (including deep coma in 3) and flushed dry, warm skin in all. Pupils were dilated in 18 of the 19 and restlessness and hallucinations were present in 17. Less common were vomiting, increased tendon reflexes, convulsions, involuntary movements, ataxia, hypertension, hyperpyrexia and tachycardia. Therapy included intravenous physostigmine in 7 and sedatives (diazepam and triclofos) in 6. All were free of symptoms within 24 hours of admission. Henbane may grow as an annual or biennial. Renewed growth of leaf rosettes occurs before the first rains and they attract attention in the fields. The parts of the plant eaten by most of the children were the roots, which are easily mistaken for the edible roots of other plants. The main alkaloids in henbane are atropine (hyoscyamine) and scopolamine (hyoscine) which explains the clinical picture of mixed stimulation and depression of the brain. Educational measures should be undertaken to prevent poisoning of Bedouin children by eating such plants.
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PMID:[Henbane (Hyoscyamus reticulatus) poisoning in children in the Negev]. 195 6

In Canada in late 1987 there was an outbreak of an acute illness characterized by gastrointestinal symptoms and unusual neurologic abnormalities among persons who had eaten cultivated mussels. Health departments in Canada solicited reports of this newly recognized illness. A case was defined as the occurrence of gastrointestinal symptoms within 24 hours or of neurologic symptoms within 48 hours of the ingestion of mussels. From the more than 250 reports received, 107 patients met the case definition. The most common symptoms were vomiting (in 76 percent of the patients), abdominal cramps (50 percent), diarrhea (42 percent), headache, often described as incapacitating (43 percent), and loss of short-term memory (25 percent). Nineteen patients were hospitalized, of whom 12 required intensive care because of seizures, coma, profuse respiratory secretions, or unstable blood pressure. Male sex and increasing age were associated independently with the risks of hospitalization and memory loss. Three patients died. Mussels associated with this illness were traced to cultivation beds in three river estuaries on the eastern coast of Prince Edward Island. Domoic acid, which can act as an excitatory neurotransmitter, was identified in mussels left uneaten by the patients and in mussels sampled from these estuaries. The source of the domoic acid appears to have been a form of marine vegetation, Nitzschia pungens, also identified in these waters in late 1987. The contaminated mussels from Prince Edward Island were removed from the market, and no new cases have occurred since December 1987. We conclude that the cause of this outbreak of a novel and severe intoxication was the ingestion of mussels contaminated by domoic acid, a potent excitatory neurotransmitter.
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PMID:An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. 207 68

A case of severe hypoglycaemia precipitated by fasting in a child is described. As a result of the hypoglycaemia, the patient became brain damaged. The mechanism causing the hypoglycaemia was a defect in the fatty acid beta-oxidation enzyme, the connecting link acyl-CoA dehydrogenase. During a prolonged fast, fatty acids are not converted to acetyl-CoA and ketone bodies which participate in Kreb's cycle for production of energy to a sufficient extent. This result in non-ketotic hypoglycaemia with excretion of organic acids in the urine. As a rule, the symptoms occur for the first time during the first to second years of life in connection with common infectious diseases, with vomiting followed by clouding of consciousness and possibly coma, but the condition may also present with sudden unexpected death. Treatment consists of intravenous glucose. The diagnosis is established by testing the urine for hexanoylglycin and other substances and is confirmed by culture of skin fibroblasts and measurement of beta-oxidation activity. The disease is an autosomally recessive inherited condition. In families where there have been cases of unexplained hypoglycaemia and clouding of consciousness and cases of unexplained death in infancy or "near misses", all of the family members should be offered examination for the above mentioned enzyme deficiency.
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PMID:[Severe hypoglycemia and clouding of consciousness caused by deficiency of the connecting link acyl CoA dehydrogenase]. 200 Jun 54

A guideline for early diagnosis of metabolic disorders affecting central nervous system during neonatal and early infancy was presented. Clinical manifestations associated with inborn errors of metabolism in the neonatal period are poor feeding, vomiting, diarrhea, abnormalities in muscle tonus, dyspnea, convulsion, coma and so on, and these are not specific to each disorder. However, such symptoms or signs as described below have often intimate relation to metabolic disorders: (1) previous children died of undetermined causes during early infancy; (2) complication of sepsis; (3) onset in the early neonatal period; (4) developmental and growth retardation. When newborns and infants have these symptoms or signs, we should start simple screening studies immediately for metabolic disorders, including CBC, hepatic function tests, blood glucose, lactate, pyruvate, ketone bodies, ammonia, blood gas analysis, urinalysis (including non-glucose reducing substance tests and FeCl3 reaction) and so on. As for CBC, we have to make our own effort to find spherocytosis and vacuoles in lymphocytes. Family history, especially the mother's personal history, is indispensable. During physical examinations, we must pay attention to facial appearance, skin color, macroglossia, hair abnormalities, peculiar odor of the urine and hepatosplenomegaly. When abnormality is found in these clinical signs or simple laboratory examinations, we should not hesitate to start dietary treatment even if special examinations for differential diagnosis are on the way.
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PMID:[CNS disorders caused by metabolic disorders]. 201 2

In this report we present aspects of the epidemiology of headache (i.e., pain in the head, face, ear, or neck) among children with brain tumors. The data are derived from the 3,291 subjects in the Childhood Brain Tumor Consortium databank. Overall, 62% of the children with brain tumors experienced chronic or frequent headaches prior to their first hospitalization: 58% of children with supratentorial tumors and 70% of children with infratentorial tumors. The relative frequency of headache increased through age 7 and then leveled off regardless of tumor location. For children under age 5, headache rarely had a duration of more than 1 year prior to hospitalization. Among children over age 4, headache duration of at least one year was significantly greater for supratentorial than for infratentorial tumors. Children with a brain tumor and headache had a different distribution of symptoms and neurologic signs than those without headache. Tumor location and headache status were interactively associated with the presence of other symptoms and neurologic signs. Children with headache had a greater number of other symptoms and neurologic signs. Regardless of tumor location among children with headache, nausea or vomiting, papilledema, and hypoactive tendon reflexes were more frequent, while upper extremity weakness, optic atrophy, and irritability were less frequent. Diplopia, coma, stiff neck, anesthesia or hypesthesia, pupillary abnormalities, and abnormalities of personality, academic performance, or speech were associated with headache in children with supratentorial tumors. No specific symptoms or neurologic signs were associated with headache in children with infratentorial tumors. Supratentorial craniopharyngioma, ependymoma, and protoplasmic astrocytoma were associated with significantly high rates of headache as was infratentorial pilocytic astrocytoma.
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PMID:The epidemiology of headache among children with brain tumor. Headache in children with brain tumors. The Childhood Brain Tumor Consortium. 202 72

A case of isovaleric acidemia appearing as diabetic ketoacidosis with acute encephalopathy and pancytopenia was reported. A three-year-old male patient, with mild psychomotor retardation, had recurrent bouts of acute encephalopathy and pancytopenia after episodes of upper respiratory infection. At admission, he had vomiting associated with dehydration, acidosis, ketonuria, coma and a pungent, rather unpleasant odor. Laboratory features included hyperglycemia, hyperammonemia, hyperamylasemia, hypocalcemia, neutropenia, thrombocytopenia and subsequent anemia. Urine organic acid profiles showed profuse amount of 3-beta-hydroxyisovaleric acid (295 mg/ml) and isovalerylglycine (616 mg/ml) by gas chromatography-mass spectrometry. Levels of amino acids in the serum and urine were normal. The patient received treatment with rehydration and insulin, with rapid improvement. After the acute illness, blood glucose levels returned to normal. The patient was doing well on a low-protein diet in recent 3 months.
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PMID:Isovaleric acidemia: report of one case. 212 76


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