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

The purpose of the present study was to examine the presentation and outcomes associated with diabetic ketoacidosis (DKA) in pregnancies complicated by diabetes. Eleven episodes (2%) of DKA were diagnosed during the 10-year study period. All patients were under close observation by the Diabetes-in-Pregnancy Service. Plasma glucose levels of less than 200 mg/dL were present in 4 of the 11 patients (36%), 10 (90%) of whom presented with nausea, vomiting, and decreased caloric intake. Two subsequently had fetal distress necessitating cesarean section. One fetal death occurred in a patient treated with subcutaneous insulin. Despite contemporary methods of diabetes care, near-normal plasma glucose levels are not enough to preclude diabetic ketoacidosis. Nausea, vomiting, and decreased caloric intake in an otherwise normal pregnant, diabetic woman requires evaluation to exclude ketosis.
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PMID:The changing presentations of diabetic ketoacidosis during pregnancy. 896 Jun 16

Based on case reports pathogenesis and treatment of the following diabetic emergencies were discussed: 1. The hyperosmolar non-ketotic coma without or with only modest ketosis occurring mainly in type II diabetics and the severe ketoacidosis with or without disturbed consciousness occurring mainly in type I diabetics are the two forms of severe metabolic decompensation of diabetes mellitus. 2. Severe hypoglycaemia may be caused by treatment with sulfonylureas and insulin. 3. The most dangerous life threatening adverse effect of biguanides is lactic acidosis. The incidence of ketoacidosis is about 1-5% in type I diabetics with a mortality of 3-9%. Mortality rates of hyperosmolar non-ketotic comas are much higher, approaching 20-40%, and are explained by severe concomitant complications and older age. The most important triggering factors of diabetic coma are infections, insulin dispensing errors and non-compliance. Carefully instructing patients about the risks of loosing appetite and vomiting as early signs of ketoacidosis is essential. Adequate replacement of fluid, electrolyte and water are the most important therapeutical aspects of ketoacidosis and hyperosmolar non-ketotic coma. Early diagnosis and appropriate treatment of infection by antibiotics are important. Complication of therapy (hypokalemia, hypovolemia and rapid full of oncotic pressure) should be avoided by clinical and laboratory monitoring. Treatment of acidosis with bicarbonate has been found more dangerous than useful. Severe hypoglycaemia is the most important and most dangerous side effect of sulfonylurea and insulin. The incidence of severe hypoglycaemia under glibenclamide ist 3-5 fold higher than under treatment with tolbutamide or glibornurid. Glibenclamide should not be recommended anymore. Longterm experience of the therapeutic security of new sulfonylurea derivates like glimepirid is lacking. Blood-glucose-measurements in the afternoon are important for recognizing disposition to sulfonylurea hypoglycaemia, because at this time the blood-glucose-values tend to be lower than in the morning fasting state. Under insulin treatment the following risk factors for severe hypoglycaemia need to be considered: metabolic control in the near normal range, intensified treatment with rapidly decreasing HbA1c-levels, impaired renal function, unawareness o hypoglycaemia. When the renal function is impaired, biguanide treatment is not indicated because of the risk of lactic acidosis. Most of the diabetic emergency situations are avoidable by proper education of the patients.
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PMID:[Diabetic emergencies]. 914 92

Forty-three cases of diabetic ketosis were analysed to determine the mode of presentation, treatment modalities and outcome. Among these cases 62.8% were non-insulin dependent diabetes mellitus (NIDDM) patients and 37.2% belonged to the insulin dependent diabetes mellitus (IDDM) group. Six patients had blood glucose levels of more than 250 mg/dl but less than 300 mg/dl who were grouped separately for analysis under the term "euglycaemic diabetic ketoacidosis (EGDK)". Infection was the commonest precipitating factor in diabetic ketosis in all groups. Abdominal pain and vomiting occurred with NIDDM and EGDK cases. Drowsiness was common and coma was rare. Acute myocardial infarction (MI) and pulmonary oedema occurred with NIDDM cases. Shock, acidosis, acquired respiratory distress syndrome (ARDS) and mucor mycosis were seen with IDDM cases. Mortality was 7 out of 43(16.3%). Saline requirement was lower in NIDDM and EGDK cases. Intensive insulin therapy with hourly intravenous doses were needed for IDDM cases while majority of NIDDM cases could be managed with 6 hourly doses of insulin given subcutaneously or intramuscularly.
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PMID:Changing profile of diabetic ketosis. 956 97

Nausea and vomiting are both common in early pregnancy. Most cases are mild and do not require treatment. However, persistent vomiting and severe nausea can progress to hyperemesis if the woman is unable to maintain adequate hydration, and fluid and electrolyte as well as nutritional status are jeopardised. Hyperemesis gravidarum is a diagnosis of exclusion, characterised by prolonged and severe nausea and vomiting, dehydration, ketosis and bodyweight loss. Investigation may show hyponatraemia, hypokalaemia, a low serum urea level, metabolic hypochloraemic alkalosis and ketonuria. The haematocrit is raised and the specific gravity of the urine is increased. There may be associated liver function test abnormalities and abnormal thyroid function tests, with biochemical thyrotoxicosis with raised free thyroxine levels and/or suppressed thyroid-stimulating hormone levels. The pathophysiology of hyperemesis is poorly understood. Various hormonal, mechanical and psychological factors have been implicated. Studies have demonstrated a direct relationship between the severity of hyperemesis, the degree of biochemical hyperthyroidism and the levels of human chorionic gonadotrophin (hCG). Management of hyperemesis should include hospitalisation, intravenous fluid and electrolyte replacement, thiamine (vitamin B1) supplementation, use of conventional antiemetics and psychological support. Most patients improve spontaneously with the help of the above measures without long term sequelae. Conventionally, antiemetics are not usually prescribed, especially before 12 weeks gestation, except for women with hyperemesis. This reluctance relates to fears which are often unfounded concerning the teratogenic effects of antiemetics. Severe hyperemesis, refractory to conventional management with intravenous fluids and antiemetics is a rare, miserable and disabling condition, associated with multiple hospital admissions, time away from work and the family, and psychological morbidity. If inadequately or inappropriately treated, it may cause Wernicke's encephalopathy, central pontine myelinolysis and death. In extreme cases, women may request, or their obstetricians recommend, termination of the pregnancy. There are uncontrolled data supporting a beneficial effect of corticosteroids in these women, and a randomised placebo-controlled trial is currently in progress.
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PMID:Treatment of nausea and vomiting in pregnancy. When should it be treated and what can be safely taken? 970 51

Isovaleric acidemia, an autosomal recessive disorder, is due to isovaleryl-coenzyme A dehydrogenase deficiency and is one of the branched-chain aminoacidopathies. Isovaleric acidemia may present in the neonatal period with an acute episode of severe metabolic acidosis, ketosis, and vomiting and may lead to coma and death in the first 2 months of life. This report concerns an infant who presented at 10 days of age because of lethargy, poor feeding, hypothermia, cholestasis, and thrombocytopenia, leukopenia, and profound pancytopenia. Death occurred at 19 days of age. Autopsy showed mild fatty change in the liver and extramedullary hematopoiesis, generalized Escherichia coli sepsis, and myelodysplasia of the bone marrow with arrest of the myeloid series at the promyelocytic stage. The appearance resembled promyelocytic leukemia, but the diagnostic 15:17 translocation was not present. The maturation arrest in granulopoiesis in isovaleric acidemia appears to be most likely due to a direct metabolic effect on granulocyte precursor cells.
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PMID:Isovaleric acidemia with promyelocytic myeloproliferative syndrome. 1019 53

The aim of the study was to evaluate renal activity during cyclic vomiting with ketosis. The clinical material was obtained from 50 cases of children hospitalized in Department of Pediatrics Military Medical University within 1993-1999 what makes about 1% of all patients. The examined group consisted of 26 boys (52%) and 24 girls (48%). Three of the children were repeatedly hospitalized (3 to 8 times) because of acetonemic vomiting. The special attention during the laboratory studies was paid to evaluation of renal activity. Vomiting with ketosis were associated with temporary kidneys acute dysfunction in 46% of cases. In 98% of cases the parenteral hydration was necessary. Ketonemic vomiting with kidneys dysfunction was observed mainly with the children in pre-school age.
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PMID:[Cyclic vomiting with ketosis as a cause of acute kidney dysfunction: own clinical experience]. 1089 37

The detection of neurodegenerative and neurometabolic diseases in children relies on a high index of suspicion as most will present as common paediatric problems such as recurrent vomiting, feeding problem, failure to thrive, sepsis, or developmental delay. Alternatively, children may present with an acute encephalopathy or with a chronic progressive encephalopathy. Clinical clues suggestive of neurometabolic disorders include encephalopathic features such as microcephaly, macrocephaly, developmental regression, developmental arrest, change in sensorium, seizures, hypotonia, hypertonia, abnormal eye signs; also extrapyramidal or cerebellar signs and systemic features like abnormal respiration, hepatosplenomegaly, abnormal hair, liver dysfunction, renal tubular dysfunction, cardiomyopathy, and feeding difficulties or growth problems. Initial screening include tests for acidosis, ketosis, hyperlacticemia, and hyperammonemia. Further investigations should amino acid chromatography, assays of organic acids, specific enzyme assay of white cell or fibroblast culture, and histopatholgy of cell and tissue biopsy (white blood cell, skin, muscle, conjunctiva, bone marrow, liver, rectum, or brain). The correct diagnosis holds implications for targeted therapeutic intervention, genetic counselling, and possibly, prenatal diagnosis.
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PMID:Neurodegenerative diseases in children. 1184 61

The purpose of this study was to determine time of onset of ketosis and efficacy when the classic ketogenic diet is initiated at full calories without a prior fast in children with epilepsy. A retrospective hospital and neurology clinic chart review was done of all 14 children commenced on the classic ketogenic diet at full calories without a prior fast between January 1, 1997, and May 31, 2001, to determine time to ketosis, time to good ketosis (urine ketones > or =80 mg/dL), and success of the ketogenic diet. Median age at diet initiation was 63 months (25th-75th percentile 47-149 months). There were 7 girls and 7 boys. Four had symptomatic generalized epilepsy, whereas the remainder had partial seizures +/- secondary generalization. Twelve of 14 children suffered seizures on a daily basis prior to the ketogenic diet. Six were commenced on the diet as outpatients, whereas 8 were admitted to hospital. No patients were fasted. All admitted patients were started on a 1:1 ketogenic ratio at full calories for the first 24 hours and advanced to a 3:1 or 4:1 ratio over 3 to 4 days, while outpatients were started on a 1:1 or 2:1 ratio and similarly advanced. Thirteen of 14 patients were successfully started on the diet, with 1 developing vomiting and food refusal during the initial hospitalization but after ketosis was established. One child was lost to follow-up after initial hospital discharge. Information regarding time to ketosis was determined for all inpatients. Mean time to onset of ketosis was 33 hours (range 17 to 48) and to good ketosis, 58 hours (range 40 to 84). Five of 12 children (42%) experienced success with the ketogenic diet, and all of these had their antiepileptic medications either withdrawn (n = 3) or decreased (n = 2). The ketogenic diet can be effectively initiated without a fast in children with epilepsy. Time to ketosis and diet efficacy are similar to protocols that use a fast.
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PMID:Is a fast necessary when initiating the ketogenic diet? 1202 32

Hyperemesis gravidarum is a common entity characterized by severe and protracted vomiting during pregnancy not attributed to any organic or metabolic condition other than pregnancy itself. It may lead to fluid and electrolyte imbalances as well as ketosis, and its diagnosis is made per exclusion. While the accurate etiology and pathophysiology of hyperemesis gravidarum remain largely unknown, numerous theories have been proposed in attempts to explain this peculiar phenomenon. The different therapeutic modalities aim to correct the hypovolemic state, electrolyte imbalance and ketosis. The present manuscript reviews the pertinent medical literature regarding this illness in order to refine our understanding of its pathophysiology, clinical manifestations and therapeutic modalities.
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PMID:[Hyperemesis gravidarum: an updated review]. 1264 92

Isovaleric acidemia (IVA), a recessive autosomal disorder, is caused by isovaleryl-CoA dehydrogenase deficiency. Isovaleric acidemia may present with symptoms during the acute stage of severe metabolic acidosis, ketosis, vomiting and altered mental status. This report concerns a 2-month-old female infant diagnosed as isovaleric acidemia by tandem mass spectrometry. She presented with two episodes of vomiting, poor activity and pancytopenia without obvious metabolic acidosis and hyperammonemia. She received combined therapy of L-carnitine, glycine and low protein and leucine diet. Hemogram and serum isovalerylcarnitine (IVC) were measured during the treatment. The depressed leukocyte and platelets recovered when serum isovalerylcarnitine level increased.
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PMID:Isovaleric acidemia diagnosed promptly by tandem mass spectrometry: report of one case. 1562 72


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