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

A case of diabetic ketoacidosis presenting with alkalemia (pH, 7.61) instead of acidemia (pH less than 7.35) is discussed. Severe vomiting results in electrolyte depletion and hypovolemia, which in turn results in bicarbonate reabsorption and an alkalemia state despite the presence of ketoacids. Severe respiratory alkalosis can also result in alkalemia. Recognition of the alkalemia and its cause will lead to the institution of appropriate therapy.
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PMID:Diabetic ketoacidosis with alkalemia. 251 52

High levels of the serum free fatty acids (FFA) are found in Reye's syndrome (RS). While this is attributed to enhanced adipose tissue lipolysis, the possibility that intravascular lipolysis could augment this process was investigated by measuring lipase activity in sera from RS and other subjects. Ordinarily, lipolytic activity is not detectable in serum from unheparinized subjects. Significant lipolytic activities ranging from 1-3 mumol/ml serum per hour were detected in sera from 5 of the 7 RS patients studied. Similar activities were also found in sera from two other subjects one of whom was a long-term survivor of RS and the other who had recurrent bouts of biliary obstruction and encephalopathy. Lipase activity was negligible in the serum from 2 other RS patients, 4 other long-term survivors of RS, 2 siblings, one RS parent and in 20 disease controls including patients with influenza, diabetic ketoacidosis and cerebral edema, meningitis and febrile infections with diarrhea and vomiting. None of these individuals had received heparin. An inverse relationship was found between LPL and hepatic lipase (HL) activities. Glucose levels tended to correlate directly with LPL and inversely with HL activity. The basis for the presence of LPL activity in RS sera is not known but the presence of serum lipase activity in unheparinized patients supports the notion that the TG in the circulating lipoprotein particles probably also serve as another source of FFA in the sera of RS patients.
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PMID:Serum lipolytic activity in Reye's syndrome. 259 64

A 41-year-old male with a 25-year history of diabetes mellitus requiring 25 to 30 units of neutral protamine hagedorn (NPH) insulin daily was found dead at home. Recent history revealed that he was well until the last four days of life when he had the onset of nausea, vomiting, and anorexia coinciding with procurement of a new bottle of insulin from his pharmacist. Pertinent autopsy findings included coronary and aortic atherosclerosis, a peptic ulcer, and diabetic glomerulopathy. Chemical analysis of the vitreous humor, including glucose (813 mg/dL) and acetone (40 mg/dL), revealed that he died of diabetic ketoacidosis. Further investigation revealed that the pharmacist had accidentally substituted regular insulin, with a duration of action of up to 6 h as opposed to 24 to 28 h, for NPH. Cultures of blood and of the regular insulin yielded no growth. Analysis of this case emphasizes the importance of obtaining a careful medical and medication history and the usefulness of vitreous electrolytes when investigating a sudden death in a diabetic.
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PMID:Pharmaceutical error resulting in fatal diabetic ketoacidosis. 308 89

The plasma concentration of arginine vasopressin (AVP) is increased in diabetic ketoacidosis (DKA) in man and the rat. Although haemodynamic changes and nausea/emesis may account for the increased secretion of AVP in severe human DKA, they appear not to be responsible in moderate DKA. Streptozotocin-treated rats were studied to investigate other factors possibly involved in the secretion of AVP in DKA. Wistar rats were injected i.p. with streptozotocin (150 mg/kg body weight). Diabetic rats were maintained on 3-4 units protamine-zinc insulin (PZI)/day for 11 days, after which PZI was withdrawn for 3 days in half the rats. The plasma concentration of AVP was greater in rats with DKA than in normal controls (mean 11.4 pmol/l compared with 1.6 pmol/l; P less than 0.05). Rats with DKA had higher plasma osmolality and concentrations of blood glucose, beta-hydroxybutyrate and acetoacetate, but lower plasma carbon dioxide content than diabetic and normal controls (P less than 0.05). There were no differences in plasma levels of sodium, urea or haematocrit between rats with DKA and controls. In a separate study involving the same procedures, daily systolic blood pressure was measured using a tail cuff to occlude arterial inflow to the tail, and subsequent detection of the cuff pressure at which the first arterial pulsation appeared. No significant differences were detected between normal and diabetic rats and rats with DKA. Exponential relationships between plasma osmolality and plasma AVP (correlation coefficient, r = + 0.75; P less than 0.01), and plasma ketone bodies and plasma AVP (r = +0.60; P less than 0.05) were obtained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible mechanisms responsible for the rise in plasma vasopressin associated with diabetic ketoacidosis in the rat. 312 19

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

The evaluation of gastrointestinal symptoms in patients with diabetic acidosis frequently challenges the physician's clinical acumen. Faced with a seriously ill patient, he must judge whether the abdominal pain, nausea, or vomiting are a consequence of the metabolic decompensation, and hence likely to resolve with correction of the ketoacidosis, or if these symptoms signal a serious underlying intra-abdominal process (e.g., cholecystitis, appendicitis, etc.) which may have precipitated the development of ketoacidosis. The pathogenesis of the reversible gastrointestinal symptoms which frequently accompany diabetic acidosis has not been rigorously defined and may be multifactorial, involving metabolic, humoral, and neural processes. Careful attention to the medical history and abdominal examination greatly facilitates distinguishing patients with intra-abdominal pathology from those with reversible symptoms secondary to ketoacidosis. Similarly, the judicious use of laboratory tests (electrocardiography, blood counts, urinalysis, serum enzyme profile, and abdominal roentgenograms) materially aids in differential diagnosis. Finally, clinical suspicion of an acute abdominal process should prompt early surgical consultation and, if required, surgical intervention as the acidosis is being brought under control.
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PMID:Gastrointestinal manifestations of diabetic ketoacidosis. 641 81

The clinical and biochemical data obtained in 85 patients with diabetic ketoacidosis (DKA) are presented. DKA is an acute exacerbation of diabetes, a characteristic clinico-biochemical syndrome including increasing thirst, polyuria, adynamia, dryness of the skin and mucous membranes, anorexia, nausea, vomiting, occasionally abdominal pain, Kussmaul's breath, acetone odour in the exhaled air, circulatory collapse, prerenal azotemia, stupor, coma. Glycemia level exceeds 19 mmol/l, blood pH over 7.3. The disease is marked by neutrophilic leukocytosis, blood count shift to the left, elevated blood content of creatinine and urea. It was established that the degree of consciousness abnormality does not always correlate with the degree of the clinico-biochemical manifestations of DKA. During DKA, coma occurs relatively seldom (5.9%). It is suggested to use the term "diabetic ketoacidosis", incipient or marked, indicating the degree of consciousness abnormality (stupor, coma).
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PMID:[Diabetic ketoacidosis (causes, clinico-biochemical correlations and terminology problems)]. 644 Dec 97

1. Several investigators have found that the development of post-exercise ketosis is not counteracted by glucose ingestion. Post-exercise ketosis might therefore have more in common with diabetic ketoacidosis than with starvation ketosis. 2. The effects of ingesting 100 g of glucose, alanine or starch were therefore studied in subjects rendered hyperketonaemic by prolonged running on a low carbohydrate diet, or by 65 h of starvation. These substances were also ingested by normal post-prandial subjects. 3. The runners developed post-exercise ketosis (1.81 +/- S.D. 0.81 mmol/l), which was counteracted by alanine and glucose, but only minimally by starch. 4. Fasting caused a variable ketosis (2.19 +/- S.D. 1.63 mmol/l), also counteracted by glucose and less by starch, but alanine caused vomiting. 5. Glucose and alanine lowered the blood ketone body levels of the post-prandial subjects. 6. The rising ketone body levels in starvation and after exercise were accompanied by simultaneous increases in the plasma insulin/glucagon ratios; in both, glucose ingestion increased the ratio further, while alanine decreased it. 7. It is concluded that there is no essential difference between established post-exercise and starvation ketosis, and that the blood fuel-hormone changes do not correlate with the changes in blood ketone body concentrations.
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PMID:The effects of alanine, glucose and starch ingestion on the ketosis produced by exercise and by starvation. 705 Mar 44

Zygomycosis is an uncommon, but frequently fatal, fungal infection caused by members of the class Zygomycetes. The risk factors include diabetes mellitus, uremia, leukemia and use of deferoxamine as an iron-chelating agent; healthy persons also are occasionally infected. Those fungi, spread by their ubiquitous spores, most frequently involve the respiratory system. Rhinocerebral zygomycosis occurs predominantly in patients with uncontrolled diabetic ketoacidosis. Pulmonary zygomycosis most frequently is observed in granulocytopenic and corticosteroid-treated patients. Other clinical manifestations are gastrointestinal, cutaneous, disseminated and miscellaneous. This report concerns a previously robust farmer who suffered from left upper lung abscess caused by Rhizopus spp.-one member of the order Mucorales. Initially, it was intended to administer amphotericin B to a total dose of 2,000 mg; however, the patient could not tolerate such side effects as nausea, vomiting and refused further management when the cumulative dose was 948 mg. However, he did recover without further fever and cough. Chest X-ray, followed every three months, disclosed satisfactory improvement.
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PMID:Zygomycotic lung abscess: a case report. 755 21

A 19-year-old woman with insulin-dependent diabetes mellitus (IDDM) of 3.5 years duration had been suffering from recurrent episodes of diabetic ketoacidosis (DKA), dizziness, and weight loss (16 kg, 29%) for 6 months. History and physical examination gave evidence of severe peripheral and autonomic neuropathy. Radionuclide retention on gastric emptying test at 60 min was greater than 90% (normal < 60%). On autonomic cardiovascular testing there was evidence of both parasympathetic and sympathetic damage. There was no evidence of nephropathy or retinopathy. Optimal diabetic control using 4 insulin injections (2 u/kg/day) and high-dose cisapride terminated the vomiting, and she regained the weight lost within 5 months. This case is unique in that severe diabetic neuropathy followed relatively soon after onset of disease, without other microvascular complications. The correct diagnosis of gastroparesis as the cause of the recurrent DKA and weight loss, and the specific prokinetic therapy and nearly normoglycemic control of the diabetes led to dramatic clinical and functional improvement. Specific prokinetic therapy and the nearly normoglycemic control of the diabetes led to dramatic clinical and functional improvement. Gastroparesis can cause recurrent DKA even in young patients with IDDM of short duration.
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PMID:[Severe neuropathy in a young diabetic]. 784 56


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