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Query: UMLS:C0017160 (gastroenteritis)
11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of severe iron overdose in two children is described, and the pathophysiology of iron toxicity and management of acute iron poisonings are reviewed. An 11-month-old boy was comatose and in shock several hours after ingesting approximately 50 ferrous sulfate tablets (elemental iron 390 mg/kg). He had hyperglycemia and leukocytosis. Lavage was performed with a solution containing deferoxamine and sodium bicarbonate, and deferoxamine was given by continuous i.v. infusion for 48 hours. The initial serum iron (SI) concentration of 14,250 micrograms/dL decreased to 657 micrograms/dL nine hours after i.v. deferoxamine therapy was initiated. A roentgenogram showed tablets in the stomach and small bowel. Packed red blood cells were administered to treat apparent necrotizing gastroenteritis. SI concentration returned to normal by day three [corrected], and the child recovered. A 2.5-year-old boy was examined 1.25 hr after ingesting an estimated 55 tablets of ferrous gluconate 325 mg (elemental iron 130 mg/kg). Initial SI concentration was 134 micrograms/dL, and total iron-binding capacity (TIBC) was 219 micrograms/dL. A roentgenogram indicated iron concretion in the stomach and iron tablets in the small bowel. He underwent lavage with solution containing sodium bicarbonate. An i.m. dose of deferoxamine was administered, followed by i.v. deferoxamine therapy. SI concentration eight hours after the ingestion was 290 micrograms/dL, and whole-bowel irrigation was begun with polyethylene glycol-electrolyte solution. The irrigation and deferoxamine therapy were discontinued 20 hours after the ingestion, when SI concentration was 73 micrograms/dL, and the child recovered. Acute iron ingestions of more than 60 mg/kg are potentially serious. Patient 1 had severe iron intoxication, while aggressive treatment prevented severe toxicity in patient 2. Acute iron toxicity includes effects on the GI tract and the cardiovascular, metabolic, hepatic, and central nervous systems. Guidelines for assessing the severity of an overdose and selecting the most appropriate therapy are provided. The indications for chelation therapy with deferoxamine, gastric decontamination procedures including use of lavage solutions and whole-bowel irrigation, and adjunctive measures are described. Management of acute iron overdose includes supportive care, GI decontamination, and chelation therapy.
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PMID:Management of acute iron overdose. 266 31

Five hundred million attacks of diarrhoea occur each year in children under 5 years of age, throughout the world, and acute gastroenteritis remains a frequent cause of admission to hospital in the United Kingdom. Current practice in the treatment of diarrhoeal dehydration in the UK is focused upon intravenous rehydration. Drugs (eg antibiotics, anti-emetics, anti-diarrhoeal agents and absorbents) are commonly prescribed, and 'therapeutic' starvation, followed by cautious reintroduction of diet, is recommended. Studies conducted by health workers in developing countries have challenged these dogma. Whilst intravenous rehydration is occasionally required (eg. in shock, ileus or coma) the majority of episodes of dehydration can be treated orally. Oral rehydration is less unpleasant than intravenous infusion, safer, quicker, cheaper and readily administered by parents with nursing supervision. Recovery may be hastened by continuing to breast feed and offer normal diet, and weight loss is minimized. These principles are being applied in pilot studies at The Children's Hospital, Birmingham. Outpatient treatment is largely supervised by trained paediatric nurses, after initial medical assessment of the child. Nurses are becoming more confident in the technique of oral rehydration, coupled with early reintroduction of food. This is reflected in less discomfort and weight loss for the child, less parental anxiety, decreased length of hospital stay, and financial savings.
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PMID:Recent advances in the care of children with acute diarrhoea: giving responsibility to the nurse and parents. 364 45

During a 12-month prospective study there were 125 visits to the Harlem Hospital Emergency Room for symptomatic hypoglycemia. Sixty-five patients had obtundation, stupor, or coma; 38 had confusion or bizarre behavior; 10 were dizzy or tremulous; 9 had had seizures; and 3 had suffered sudden hemiparesis. Diabetes mellitus, alcoholism, and sepsis, alone or in combination, accounted for 90% of predisposing conditions; others included fasting, terminal cancer, gastroenteritis, insulin abuse, and myxedema. Average blood glucose levels were lower among comatose than among obtunded patients, but overlap was considerable, and overall there was little correlation among cause, blood glucose levels, and symptoms. Although mortality was 11%, only one death was attributable to hypoglycemia per se, and only four survivors had focal neurological residua.
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PMID:Hypoglycemia: causes, neurological manifestations, and outcome. 400 66

The main purpose of this study was to evaluate the effectiveness of an oral fluid therapy alone or combined with parenteral administration of a 5% dextrose solution to attenuate the clinical signs and the pathophysiological consequences of transmissible gastroenteritis in neonatal piglets. Eighteen two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as controls (Group 1). At the onset of diarrhea, infected piglets were divided into three groups of six (Groups 2, 3 and 4). Piglets in group 2 were not treated and were fed a milk replacer ad libitum. Piglets in group 3 were removed from the milk replacer and placed on an oral glucose-glycine-electrolyte solution ad libitum. Those in group 4 were placed on oral fluid therapy and received a 5% dextrose solution intraperitoneally at the rate of 25 mL/kg of body weight once a day. Blood samples were collected in heparin within minutes after the infected piglets became comatose and from the controls at four or five days of age. The following variables were measured: packed red cell volume, blood pH, total plasma protein and bicarbonate, blood urea nitrogen, and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets. There was a sudden and rapid progression into a comatose and moribund state one or two days later whether the infected piglets were treated or not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fluid therapy trials in neonatal piglets infected with transmissible gastroenteritis virus. 407 36

The main purpose of this work was to study changes in the balance of fluids, electrolytes and blood metabolites in neonatal piglets with severe transmissible gastroenteritis. Six two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as normal controls. Blood samples were collected in heparin when the infected piglets were moribund. The following variables were measured: packed red cell volume, total plasma protein and bicarbonate, blood pH, blood urea nitrogen and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets and they were moribund one or two days later. Before becoming moribund, most of the piglets fell rapidly into a lethargic and comatose state. The most evident changes in their blood variables were an increase in packed cell volume, total protein, blood urea nitrogen, phosphorus and magnesium levels and a decrease in pH and bicarbonate concentration as well as a severe hypoglycemia. The results suggest that severe hypoglycemia coupled with metabolic acidosis and dehydration might be an important factor contributing to the high mortality rates caused by transmissible gastroenteritis in neonatal piglets. The hypoglycemia results from a combination of the inadequate glucose metabolism inherent to neonatal piglets and the acute maldigestion and malabsorption resulting from the diffuse and severe villous atrophy induced by the virus.
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PMID:Hypoglycemia: a factor associated with low survival rate of neonatal piglets infected with transmissible gastroenteritis virus. 647 97

In the fall of 1981 the San Francisco Bay Area Regional Poison Control Center received more than 100 calls regarding wild mushroom ingestion. Ten cases, including three fatalities, had all the features of Amanita phalloides poisoning. Encephalopathy, coma and renal insufficiency occurred in all three patients who died, but did not occur in those who survived. Two of the three patients who died arrived at the hospital late in the course of their illness, and severe gastroenteritis with accompanying dehydration probably contributed to their deaths. The poison control center promoted public awareness of the mushroom hazard through newspaper and television stories and by notifying local health departments. It also has devised a simple form to improve the quality of data collection and to assist in later verification of suspected A phalloides poisoning.
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PMID:Amanita phalloides-type mushroom poisoning. 717 45

Acute symptomatic hyponatraemia is a life-threatening emergency which must be diagnosed and treated promptly. The initial symptoms are often dramatic, with seizures and coma, and there is therefore a risk that the diagnosis and the urgent sodium correction therapy may be delayed by procedures such as computed tomography (CT) of the brain. As the most common aetiological factors are psychotic polydipsia and different iatrogenic causes, this condition usually develops in hospitalised patients. Water intoxication alone is very unlikely to cause severe hyponatraemia in a person with normal renal function, unless for some reason the antidiuretic hormone secretion is increased. We describe a case in which dehydration due to common gastroenteritis in combination with excessive intake of water caused the death of a young, previously healthy woman. Increased awareness of this potentially fatal condition is recommended.
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PMID:Fatal hyponatraemic brain oedema due to common gastroenteritis with accidental water intoxication. 947 92

A prospective case-control study conducted on the north coast of Papua New Guinea in 1993-96 investigated the hypothesis that alpha(+)-thalassemia provides a selective advantage against endemic Plasmodium falciparum. In this geographic area, alpha(+)-thalassemia affects more than 90% of the population. 249 children admitted to Madang Hospital with one or more symptoms of severe malaria (severe anemia, coma, hypoglycemia, acidosis, and hyperlactatemia) were paired with 249 randomly selected healthy age- and sex-matched controls. Also enrolled were 233 children with infections other than malaria, primarily respiratory infections, gastroenteritis, and meningitis. Compared with healthy community controls, the risk of severe malaria was 0.40 (95% confidence interval (CI), 0.22-0.74) in alpha(+)-thalassemia homozygotes and 0.66 (95% CI, 0.37-1.20) in heterozygotes. The lowest odds ratios for alpha(+)-thalassemia homozygotes were recorded in the acidosis and hyperlactatemia subgroups--the two complications most predictive of malaria mortality. Unexpectedly, the risk of hospital admission with infections other than malaria was reduced to a similar degree in homozygous (0.36; 95% CI, 0.22-0.60) and heterozygous (0.63; 95% CI, 0.38-1.07) children. Although the relevant mechanism is unknown, these findings confirm a clear interaction between thalassemia hemoglobinopathy and both malarial and other infections. Given its high frequency and protective effect against malaria and some other infections, alpha(+)-thalassemia is likely to have a major impact on child survival in coastal Papua New Guinea.
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PMID:alpha+-Thalassemia protects children against disease caused by other infections as well as malaria. 940 82

The case of fatal course of rotaviral gastroenteritis at eight months old boy has been described. Two days history of frequent watery stools in home care, hyperosmolar dehydration grading to hypovolemic shock, cardiopulmonary resuscitation in regional hospital, transported comatose with vital functions support. In spite of temporary stabilization of the patient, there was retrogression to multiorgan failure (ischemic myocardial infliction, circulatory failure, ARDS, renal failure, DIC, enteritis, post ischemic hepatopathy). Four day later patient exits. Rotaviruses have been proved from stools specimen post mortem.
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PMID:[Lethal course of rotavirus gastroenteritis - a case history.]. 1592 23

A 75-year-old man, with a long history of recurrent lymphoplasmacytoid lymphoma, presented with diffuse large-cell lymphoma affecting adrenal glands and causing severe hypoadrenalism. The lymphoma responded to rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) chemotherapy. Seven months postcompletion of chemotherapy, he developed signs of gastroenteritis and septicaemia. He deteriorated 24 h postadmission with a significant fall in Glasgow Coma Scale Score. Polymerase chain reaction testing of cerebrospinal fluid suggested enteroviral encephalitis. He responded symptomatically to intravenous immunoglobulins. His immunoglobulin levels were monitored weekly and supplemented to maintain immunoglobulin G level at 10 g/l, but in spite of this, his neurological condition deteriorated and he died after 14 weeks. Rituximab can cause prolonged B-cell deficiency. We speculate that profound immunosuppression induced by rituximab, together with previous chemotherapy, predisposed this patient to fatal enteroviral meningoencephalitis.
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PMID:Enteroviral meningoencephalitis in a patient with non-Hodgkin's lymphoma treated previously with rituximab. 1643 Apr 65


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