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

Chronic alcoholism is a frequently unrecognized cause of ketoacidosis in nondiabetic patients. Seven episodes of alcoholic ketoacidosis were observed in three patients. No consciousness disturbances were present. Semi-quantitative tests for ketones were strongly positive in urine, weakly positive in serum. The anion gap was between 25 and 41 mEq/l; serum lactate was between 0.9 and 9.0 mEq/l, and, in all cases, below the anion excess. Blood glucose ammonia was increased. Massive fatty liver was documented in all patients. All ketosis episodes followed an increase of alcohol ingestion associated with one to four week-starvation and vomiting; however, at the time of admission, alcohol was weakly increased in blood. In the four episodes where diagnosis was correct, ketoacidosis was rapidly corrected without insulin administration. In conclusion, in some nondiabetic subjects, the occurence of alcohol prolongated ingestion together with starvation and vomiting is responsible for ketoacidosis; because alcoholic ketoacidosis has often a mild clinical expression, its true prevalence is underestimated; insulin administration is not required.
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PMID:[Alcoholic ketoacidosis (author's transl)]. 53 15

3 episodes of alcoholic ketoacidosis were observed in one female patient over a period of 19 months. The clinical picture consisted of vomiting, dehydration, hyperventilation and abdominal pain. Predominant laboratory findings were acidosis (pH less than 7) and hyperglycaemia, with blood glucose values of 354, 330 and 147 mg/dl. This disorder is an important cause of metabolic acidosis, but especially in the German literature there are only rare reports on this issue. The picture of ketoacidosis in mostly chronically malnourished alcoholics reflects not only the complex abnormalities of acid-base balance caused by excessive cumulation of ketoacids, but also the related severe depletion of electrolytes and extracellular volume. Adequate acute therapy (as for diabetic ketoacidosis) and thorough follow-up treatment of any concurrent conditions result in rapid reversal of the syndrome in most cases. Since there are few reports of repeated episodes in one patient, an overview of this disorder is presented concerning management and differential diagnosis of the basis of our case report.
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PMID:[Alcoholic ketoacidosis--3 episodes in one patient]. 150 41

A 37-year-old chronic alcoholic female was admitted with epigastric pain, complete anorexia, vomiting and diarrhoea. She was dehydrated, and had polypnoea. Laboratory investigations revealed severe metabolic acidosis (pH 7.14) with a major anion gap (37.4 mmol.l-1), and ketone bodies in blood and urine. Blood glucose concentration was 6.1 mmol.l-1, there was no glycosuria. Rehydration (2 l.day-1 of 5% glucose) together with sodium bicarbonate (500 ml of 1.4% sodium bicarbonate over the first four hours) normalized the pH (7.37). The ketone bodies disappeared on the following day. During the acute illness, were found high blood levels of glucagon and low levels of insulin. The diagnosis of alcoholic ketoacidosis, the pathogenesis of which remains unknown, is discussed.
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PMID:[Acidoketosis in a chronic alcoholic woman]. 192 62

Alcoholic ketoacidosis is characterized by a metabolic acidosis with an elevated anion gap. It generally is seen in the chronic alcoholic patient who has recently gone on a "binge" that was terminated because of complaints such as nausea, vomiting or abdominal pain. Caloric intake is diminished. Treatment includes volume repletion and glucose administration. Morbidity and mortality usually result from intercurrent illness.
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PMID:Alcoholic ketoacidosis. 222 84

Alcoholic ketoacidosis is a frequently encountered metabolic disturbance that follows a prolonged intake of ethanol. Following a brief duration of abstinence, patients typically present with vomiting, abdominal pain, and shortness of breath. Examination reveals Kussmaul breathing, variable volume loss, and coincident manifestations of chronic alcohol usage. Characteristic laboratory findings include anion-gap metabolic ketoacidosis, normal serum glucose, and zero ethanol levels. Phosphate measurements may be depressed, particularly after institution of therapy. Intravascular volume restitution, delivery of dextrose, attention to electrolytes, and discovery of alcohol-related illnesses are the mainstays of therapy.
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PMID:Alcoholic ketoacidosis--a review. 331 91

On the basis of one case, the authors review the symptoms and signs of alcoholic ketoacidosis. This occurs in general in a middle aged woman during the abundant ingestion of alcohol. It presents as drowsiness, headache and vomiting. Laboratory examinations reveal slight hyperglycaemia, hypokalaemia and a metabolic acidosis with the presence of ketones in the blood and urine. Blood alcohol level is nil. No other cause of ketoacidosis is found. The course is rapidly favourable. The biochemical mechanism is poorly understood.
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PMID:[A story about water]. 610 93

Alcoholic ketoacidosis is a common condition which occurs predominantly in chronic alcoholics. The usual picture is an interval of increased ethanol intake followed by one or more days of abdominal pain, vomiting, dehydration and a marked decrease in caloric intake. Acidosis is frequently as severe as in diabetic ketoacidosis, but the serum Acetest measurement of ketones may be negative or only slightly positive because of the predominance of beta-hydroxybutyrate compared with acetoacetate. Treatment with intravenous glucose and saline are the essentials of management. Insulin, bicarbonate and phosphate are usually not needed. The major cause of morbidity and mortality is not the acidosis but rather failure to adequately treat concurrent medical or surgical conditions.
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PMID:Alcoholic ketoacidosis: clinical and laboratory presentation, pathophysiology and treatment. 634 51

To evaluate the toxic effect of ethanol on erythropoiesis in alcoholic ketoacidosis (AK), 6 male patients were studied in the acute and remittent phase of AK. Episodes of metabolic acidosis in nondiabetic chronic alcoholics were associated with protracted vomiting and prolonged intestinal symptoms. AK was associated with elevated beta-hydroxybutyrate, acetoacetate and lactate/pyruvate plasma levels. Analysis of plasma lipids showed raised HDL cholesterol, fatty acids and phospholipids resulting in a concomitant disorder of lipid metabolism in red cell ghosts. A red cell metabolic disorder with reduced ATP and glutathione levels was also observed in patients suffering from mild hemolytic anemia. On admission, miscellaneous toxic effects on erythropoiesis were detected when bone marrow was aspirated. This study lends further support to the hypothesis that there is a linkage of different factors producing serious but transient hematologic and oncologic implications of ethanol in patients with AK.
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PMID:[Disorders of erythropoiesis in alcoholic ketoacidosis in patients with chronic liver diseases]. 745 61

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

1. A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2. The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a beta-hydroxybutyrate dominated ketoacidosis. 3. Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4. The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5. The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6. The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7. It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recommended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication.
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PMID:Severe metabolic acidosis in the alcoholic: differential diagnosis and management. 879 30


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