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Query: UMLS:C0162275 (ketonuria)
553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four patients from a larger group of 18 patients receiving dextrose-free isotonic (3%) amino acid solution as nutritional support, form the basis of this report. An additional seven patients received intravenous isotonic (5%) dextrose as their sole support in the postoperative period following major elective surgery (average nitrogen balance = -12.3 +/- 2.7 g). All patients were well-nourished as determined by anthropometric measurements. The nonseptic patients receiving infusions of isotonic amino acids demonstrated an improvement in nitrogen balance (= delta 8.5 +2, P less than 0.001) when compared to the postoperative use of 100 to 150 g of glucose. However, sepsis produced a decreased net utilization of the infused crystalline amino acids such that nitrogen balance was similar to the intravenous glucose group (- 10.6 +/- 2.1). This septic response was associated with decreased plasma free fatty acid concentrations and the absence of starvation ketosis and ketonuria. While the nitrogen balance was not different in the septic and the dextrose control groups, deficiencies in plasma amino acid concentrations were observed in the group receiving intravenous infusion of glucose.
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PMID:Effect of deep surgical sepsis on protein-sparing therapies and nitrogen balance. 40 78

A review if presented of the use of low-dose insulin infusion in the management of 58 episodes of severe diabetic hyperglycaemia. Neutral insulin in a dosage of 2-4 units per hour is infused via a paediatric giving set to achieve a sustained physiological elevation of insulin levels. This method is safe, simple and rapidly effective in lowering the blood glucose level, the mean rate of fall (62 mg/100 ml/hr, or 11% per hour) being unaffected by prior insulin therapy, acidosis or ketonuria. Classification of the hyperglycaemia as ketoacidotic or hyperosmolar is unnecessary before insulin therapy is instituted, as the relative decline in glucose level is the same in the hyperosmolar non-ketotic group as in the others. Proven infection significantly lowers the rate of fall of glucose level. Hypoglycaemia and hypokalaemia are rare during low-dose infusion. Early and adequate replacement with potassium phosphate is recommended, oral potassium supplements being continued for several days. Bicarbonate therapy is rarely indicated in the management of acidosis. No patient had cerebral oedema during treatment, and one elderly patient with extensive pneumonia and empyema died during the infusion. It is suggested that continuation of low-dose insulin infusion, together with 5% dextrose solution, after the plasma glucose level reaches 200 mg/100 ml, may hasten the clearance of ketones, preventing relapse.
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PMID:Routine use of low-dose intravenous insulin infusion in severe hyperglycaemia. 99 52

This is a case of a 15-month-old child suffering from Fanconi-Bickel syndrome, characterized with Fanconi syndrome manifestations (glycosuria, amino aciduria and phosphaturia), and the build-up of glycogen in the liver in a similar manner as seen in cases of glycogenesis type Ia. Due to the presence of liver glycogenosis, the patient also has a tendency towards hypoglycemia, ketonuria, hypercholesterolemia and hypertriglyceridemia. The glycogenosis seen in the patients with the Fanconi-Bickel syndrome, does not depend on a defect in the activity of the glucose-6-phosphatase enzyme, but in fact is due to a defect in the transporter which mobilizes glucose and galactose in the liver and in the basolateral membrane of the proximal tubule of the kidney.
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PMID:[The Fanconi-Bickel syndrome]. 186 46

Although the hourly intramuscular insulin regimen has been used in the management of diabetic ketoacidosis (DKA) in Ethiopia for over 7 years, continuous intravenous (IV) insulin infusion has never been previously used. In Tikur Anbessa Hospital, Addis Abeba, in 198788, we used the ordinary IV plastic bag and tubings alone to concurrently infuse the low-dose insulin and hydration solution in the management of 15 episodes of DKA in 13 patients, 5 males and 8 females. Initial blood glucose was over 400 mg/dl and urine ketones 4+ in all, and the level of consciousness ranged from drowsy to coma. Initially, 5 to 10 units of crystalline zinc insulin (CZI) was given IV directly to all but 2 patients. Then CZI was added to the normal saline IV bag and the dose of insulin was adjusted according to fluid requirements while at the same time maintaining the insulin rate at 5 to 10 units/hour until the blood glucose dropped to 250 mg/dl or lower. At this point the IV fluid was changed to 5% dextrose and the insulin infusion was reduced to 2 to 4 units/hour. The mean insulin requirement until the dextrose infusion was initiated was 33.2 +/- 7.3 units, IV fluid requirement was 3.5 +/- 0.8 litres and mean duration of treatment 4.4 +/- 1.6 hours. There was one death which was not due to insulin resistance, while all other patients fully recovered. The study demonstrates that insulin infusion using the ordinary IV plastic bag and tubings is safe, simple, and convenient in the management of DKA and hence should be used whenever indicated and feasible.
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PMID:The management of diabetic ketoacidosis by continuous infusion of low-dose insulin using the ordinary intravenous plastic bag and tubing. 190 Apr 69

The classic presentation of DKA, consisting of hyperglycemia, anion gap acidosis, and ketonuria, is readily recognized. The diagnosis may be missed, however, in the patient who is euglycemic, has a negative nitroprusside test for ketones, or has a nonanion gap metabolic acidosis. Treatment includes replacement of fluid and electrolytes lost through osmotic diuresis. Failure to recognize the magnitude of total-body potassium depletion and to begin replacement despite an initially normal serum potassium level may lead to fatal cardiac arrhythmia. Serum glucose must be monitored closely to avoid hypoglycemia; dextrose should be added to the infusion once the serum glucose falls to 250 mg per dl. Insulin is required to reverse ketoacid production by the liver; low-dose therapy is recommended. Ketogenesis may be reversed inadequately unless insulin treatment is continued until the anion gap has normalized. Failure to recognize precipitating causes may result in increased morbidity and mortality from underlying infection or myocardial infarction as well as rapid relapse of ketoacidosis.
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PMID:Diabetic ketoacidosis. 250 98

Forty women in whom ketonuria was detected during the first stage of labour were allocated randomly to intravenous treatment with one litre of either normal saline, Hartmann's solution, 5% dextrose or 10% dextrose. The solutions were administered over 1 h and blood was taken immediately beforehand and thereafter at 30-min intervals for 90 min to assess their effect on intermediary metabolism, plasma osmolality and acid-base status. Although both the 5 and 10% dextrose infusions caused a rapid decline in whole blood D-3-hydroxybutyrate concentrations, they also produced pathological degrees of maternal hyperglycaemia and hyperinsulinaemia and a marked elevation in the mean blood lactate and pyruvate concentrations. Administration of 10% dextrose was also associated with a significant increase in serum osmolality. Hartmann's solution produced significantly higher mean whole blood lactate and pyruvate concentrations than did normal saline. There was a significant increase in the venous base deficit in the group infused with 10% dextrose, indicating that the buffering capacity of the blood had been exceeded. It is concluded that rapid infusions of dextrose or Hartmann's solution should not be administered during labour. Normal saline should be used for rehydration and if dextrose therapy is deemed necessary the dose administered should not exceed physiological requirements.
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PMID:A comparison of the effects of four intravenous solutions for the treatment of ketonuria during labour. 399 29

A means for providing total nutrition is described in which 10% soybean oil-eggyolk phosphatide-glycerol emulsion (Intralipid) and a solution of 5% dextrose in 5% protein hydrolysate are given simultaneously into a peripheral vein, utilizing two giving sets united by a Y-connector at the needle. No ketonuria occurred, and there were no side effects from the lipid emulsion. Advantages of this system include absence of significant peripheral phlebitis, avoidance of the hazards of caval catheters, and absence of the complications of hypertonic solutions. Disadvantages include restricted forearm movement and frequent regulation of flow-rates.This system was used in 23 patients for periods of 4 to 78 days (mean 16.3 days). Weight gain and healing occurred, and all survived but one patient who died of myocardial infarction following successful surgical closure of an enterocolocutaneous fistula. The lipid system adds another method to the measures available for the management of major nutritional problems.
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PMID:Total nutrition by peripheral vein--the lipid system. 421 Mar 95

Various metabolic studies were performed in a patient with the idiopathic Fanconi syndrome in whom constant ketonuria suggested that organic acidemia might contribute to the metabolic acidosis. Glucose intolerance with a diminished insulin release was found after PO or IV glucose loads and after glucagon administratio. An insulinopenic "diabetes-like" state has not previously been described in such patients. The patient had impaired galactose-glucose interconversion, elevated blood lactate levels, reduced pyruvate levels, and an increased lactate:pyruvate ratio. Hepatomegaly and hypoglycemia were not present, and liver and muscle biopsies revealed no enzymatic evidence of glycogenosis. The erythrocyte UDP galactose transferase activity was normal. The patient failed to convert fructose to glucose and had a rise in blood lactate after ethanol administration. Further studies revealed no production of glucose after alanine or glycerol administraion, each test being associated with elevated blood lactate levels and, after alanine, an increased lactate:pyruvate ratio. The lactate:pyruvate ratio was elevated after glucagon administration with increased lactate and reduced pyruvate concentrations.
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PMID:Abnormalities of carbohydrate metabolism in idiopathic Fanconi syndrome. 738 41

An alpaca and a llama in late stages of gestation were evaluated for lethargy, anorexia, and recumbency. Both camelids had cloudy, white, turbid serum, elevated serum triglyceride (1564, 5658 mg/dL, respectively) and cholesterol (158, 297 mg/dL, respectively) concentrations, and ketonuria. Signs of fetal stress were evident ultrasonographically in the alpaca, and a live cria was delivered by Cesarean section performed under general anesthesia. The alpaca developed severe metabolic acidosis, hepatic lipidosis, and acute renal failure secondary to renal lipidosis and died 36 hours after admission despite medical therapy. Histopathology revealed renal and hepatic lipidosis and neutrophilic pancreatitis. The cria died 72 hours after birth. The llama responded to IV electrolyte, dextrose, and regular crystalline insulin therapy. The pregnancy was maintained, and the llama was discharged from the hospital 20 days after admission. Two months after discharge, the llama gave birth to a live, 5 kg cria. Findings of hypertriglyceridemia, hypercholesterolemia, elevated sorbitol dehydrogenase activity, metabolic acidosis, azotemia, and ketonuria occurred in these two camelids. Based on this report, camelids appear to be similar to both horses and cattle in their response to severe energy imbalances in late gestation.
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PMID:Hyperlipemia and ketonuria in an alpaca and a llama. 806 56

A 1-year-old boy had severe anoxic brain injury owing to a cardiorespiratory arrest. He had an initial metabolic acidosis, but this largely resolved by hospital day 2. He then had a persistent, profound metabolic acidosis. Evaluation on hospital day 6 found that the patient had ketonemia, ketonuria, and a normal serum glucose level; he had received no intravenous dextrose during his hospitalization. The dextrose-free fluids were given initially to protect his brain from the deleterious effects of hyperglycemia after brain injury. Continuation beyond 24 hours was inadvertent. The initiation of dextrose-containing intravenous fluids produced a rapid resolution of his metabolic acidosis. Starvation usually produces a mild metabolic acidosis, but when combined with physiologic stress, starvation may cause a severe metabolic acidosis. Among the few reports of severe starvation ketoacidosis, our case is unique because the patient was monitored closely in an intensive care unit, allowing us to describe the time course of the acidosis in detail.
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PMID:Severe acidosis caused by starvation and stress. 1458 74


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