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

Alcoholic ketoacidosis (AKA) is an important and probably underdiagnosed differential diagnosis for metabolic acidosis with an increased anion gap. It occurs in patients with prolonged ethanol intake. After a brief period of starvation induced by alcoholic gastritis patients typically present with vomiting, abdominal pain and Kussmaul breathing. Routine testing for urine or serum ketones with ketostix may be negative, since they do not detect beta-hydroxybutyrate and this is characteristically elevated in AKA. We present three cases of AKA and discuss diagnosis, pathophysiology and management of this disorder.
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PMID:[Alcoholic ketoacidosis]. 825 74

A description of 1074 high school students' alcohol and other drug (AOD) use along with the consequences of such use was supplemented with comparisons of grade level and gender differences and analyses of the relationships between AOD use and incidence of adverse consequences with grade point average, attendance at religious services, frequency of dating, frequency of driving a car and frequency of having trouble at school. Alcohol was clearly the drug of choice and produced a variety of adverse consequences. Most frequently reported were arguments, trouble with parents and at school and nausea or vomiting. Grade level differences were found, but few significant gender differences emerged. Significant relationships between AOD use and consequences with all other independent variables were found.
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PMID:Drug use in a small midwestern community and relationships to selected characteristics. 826 69

AKA is an acute metabolic disorder that occurs in ethanol abusers who have usually had a recent binge and who, because of gastritis or another intercurrent illness, stop eating and drinking and often vomit repeatedly. This causes dehydration and ketoacidosis which, unlike in diabetics, is usually associated with little or no hyperglycemia or glucosuria. Despite the ketoacidosis, blood pH findings are variable, depending on the severity of coexisting metabolic alkalosis (owing to vomiting) and respiratory alkalosis (owing to pain or delirium tremens). The metabolic disorders respond rapidly and gratifyingly to parenteral rehydration and administration of glucose, potassium salts, and thiamine. Insulin is usually not necessary, except in patients known or suspected to have diabetes. Because some patients have serious coexisting acute illnesses (which may even have precipitated the acute metabolic disorder), assiduous search for those and the appropriate treatment are essential. The prognosis for the acute metabolic disorder per se is excellent, that for coexisting illness depends on the illness, and that for the ethanol abuse is still often problematic.
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PMID:Alcoholic ketoacidosis. 832 83

The concentrations of thiamin and thiamin phosphate esters were determined by high performance liquid chromatography in four patients with clinical Wernicke encephalopathy. Three were alcohol abusers, and one had prolonged vomiting and anorexia. Thiamin and thiamin monophosphate were assessed in plasma and whole blood (four patients) and in cerebrospinal fluid (two patients) before and during thiamin treatment. Thiamin diphosphate was also assessed in whole blood in the four patients. Before treatment, thiamin monophosphate was significantly decreased in all patients, and thiamin diphosphate in three. A poor increase in thiamin mono- and diphosphate was paralleled by a slow clinical improvement in one patient, while an increase in all thiamin compounds was observed in two patients with a rapid recovery. Thiamin monophosphate was a more sensitive marker of deficiency than thiamin diphosphate and unphosphorylated thiamin.
Alcohol Clin Exp Res 1993 Jun
PMID:Thiamin and thiamin phosphate ester deficiency assessed by high performance liquid chromatography in four clinical cases of Wernicke encephalopathy. 833 5

Outcome in terms of progression of Korsakoff's psychosis is known to be unlikely when the preceding thiamin deficiency syndrome, Wernicke's encephalopathy, does not follow heavy alcohol use. There is evidence that alcohol potentiates thiamin-related brain damage. It is argued here that in heavy drinkers, if vomiting precedes the onset of the encephalopathy, then the latter might develop at a time when tissue alcohol levels are close to zero. Any progression to Korsakoff's psychosis could then be associated with less or even no impairment. This outcome would not be expected if ingestion of alcohol continued during the vomiting stage. In a follow-up study of 61 cases of alcoholic Wernicke's encephalopathy, these concepts are given some support by the results obtained.
Alcohol Alcohol 1993 May
PMID:A feature of alcoholic Wernicke's encephalopathy favourable to the maintenance of memory function: vomiting. 835 45

Methanol intoxication can be a challenge, in part because it is relatively uncommon but also because of the pharmacokinetics involved. A patient may not experience symptoms and thus may not present for treatment for several hours, or even a day or two, after exposure to the toxic substance. Yet, the interval between ingestion and treatment is one of the most important factors in determining patient outcome. Typical symptoms of methanol intoxication include lethargy, vertigo, vomiting, blurred vision, and decreased visual acuity. Treatment focuses on prevention of methanol conversion to its toxic metabolites, correction of metabolic acidosis, and elimination of the toxic substances from the system. Ethanol and bicarbonate administration and hemodialysis have been effective.
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PMID:Methanol intoxication. How to help patients who have been exposed to toxic solvents. 838 47

A 51-year-old man with no significant medical history presented to the emergency department with acute onset of confusion, nausea, and vomiting. He denied ethanol abuse and was not taking any medications.
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PMID:Confusion and nausea in a man who appeared to be drunk. 859 16

A thirty three-year-old male complaining of vomiting was diagnosed as having type 3 advanced gastric cancer of upper stomach and multiple liver metastasis, and had undergone total gastrectomy. The conclusive stage was P2H2n4se stage IVb. Intraoperatively, ethanol injection was performed for the liver metastasis under ultrasonography, and CDDP 100 mg was injected into the intra-abdominal cavity. Postoperative adjuvant therapy was added using oral fluorouracil and OK-432. Then we utilized FP chemotherapy (consisting of 5-FU and cisplatin) and radiotherapy for the bone metastasis. The patient survived 4 years and 4 months with good quality of life.
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PMID:[A case of advanced gastric cancer responding to chemotherapy and radiotherapy]. 867 4

Alcohol withdrawal syndrome (AWS) may result in nausea, vomiting, diarrhea, weakness, sweating, tremors, tachycardia, hypertension, agitation, delirium, hallucinations, seizures, and death beginning 6 hours after alcohol cessation in alcoholics. Benzodiazepines are cross-tolerant with ethanol and are considered first-line therapy for treating AWS. Chlordiazepoxide and diazepam are first metabolized by hepatic oxidation, then glucuronidation. Lorazepam and oxazepam undergo only hepatic glucuronidation. Benzodiazepine oxidation is decreased in persons with liver disease and the elderly. Accumulation with resultant excessive sedation and respiratory depression may be significant when administering chlordiazepoxide or diazepam to patients with impaired oxidative metabolism. Lorazepam and oxazepam metabolism is minimally affected by age and liver disease. Chlordiazepoxide and diazepam are erratically absorbed by the intramuscular route. Lorazepam is predictably absorbed by the intramuscular route. Oxazepam is not available in parenteral form. Lorazepam appears to be the safest empiric choice among the various benzodiazepines for treating AWS in the elderly and in patients with liver disease, or those who require therapy by the intramuscular route.
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PMID:Benzodiazepines for alcohol withdrawal in the elderly and in patients with liver disease. 870 Jul 92

We report a case of acute pancreatitis with diabetic ketoacidosis associated with increased serum myoglobin concentration, acute renal failure, and disseminated intravascular coagulation. A 49-year-old man suffering from diarrhea, vomiting, and somnolence was admitted to the hospital. He had had flu-like symptoms for 4 days prior to the onset of these symptoms. He was a habitual drinker and had been consuming 360 ml-900 ml of the drink "shochu" (distilled spirits containing 28% alcohol) daily for 30 years. Laboratory data on admission revealed elevated serum levels of pancreatic enzymes, including amylase, trypsin, lipase, pancreatic secretory trypsin inhibitor (PSTI), phospholipase A2 (PLA2), and elastase-1, as well as elevated levels of glucose (373 mg/dl), ketone bodies (3675 mumol/l), and myoglobin (229.8 ng/ml). Treatment with subcutaneous insulin and intravenous administration of electrolyte fluid and the systemic protease inhibitor, gabexate mesilate, was begun immediately. Early after the initiation of treatment, there was an increase in serum creatinine (4.9 mg/dl), and thromobocytopenia (15000/microliters) was observed. The patient completely recovered from renal failure and acute pancreatitis, but required insulin therapy. Alcohol ingestion and dehydration are thought to have played a major role in the triggering of the acute pancreatitis. We examined the relationship among acute pancreatitis, diabetic ketoacidosis, and hypermyoglobinemia in the literature.
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PMID:Acute pancreatitis with diabetic ketoacidosis associated with hypermyoglobinemia, acute renal failure, and DIC. 884 91


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