Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Metabolic alkalosis is regarded as the "classical" electrolyte abnormality occurring with hypertrophic pyloric stenosis (HPS) but recent experience suggests that atypical electrolyte findings frequently occur and delay establishing the correct diagnosis. The records of 65 infants with HPS treated by pyloromyotomy during the past 4 years were reviewed to determine the serum electrolytes at the initial presentation. The four study groups formed included 8 (12.3%) patients in group A with serum bicarbonate (HCO3) below 18 mEq/L (mean 15.7 +/- 0.5 mEq/L); 19 (29%) in group B with HCO3 between 18 and 25 (22.9 +/- 0.3); 22 (33.8%) in group C with HCO3 between 25 and 30 (27.0 +/- 0.3) and 16 (24.6%) in group D with HCO3 over 30 (34.0 +/- 0.9). Established values for normal HCO3 in neonates is 20.1 +/- 2.5 (mean +/- SD). The mean values in group D for HCO3, potassium (4.0 +/- 0.18 mEq/L), and chloride (88.75 +/- 2.15 mEq/L) were each significantly different (p less than 0.001) from determinations of similar electrolytes in other groups. The duration of vomiting in group D of 10.5 +/- 1.3 days is almost double the time (p less than 0.001) in group A, and was associated with more severe dehydration, predominantly acid urine (pH less than 6), and ketonuria as compared to other groups. No significant difference in other demographic characteristics including the age at presentation, the gestational age, sex distribution, or types of formula used was observed. The results of the study emphasize that serum electrolytes in early HPS may be normal, that HCO3 is significantly lower than established normals for older children, and that the effects of hydrogen-ion loss elevating the serum HCO3 precedes alterations in other serum electrolytes.
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PMID:The spectrum of serum electrolytes in hypertrophic pyloric stenosis. 662 80

Severe ketonuria developed during sedation with propofol in a 12 year old girl with brain injury. Deep sedation with propofol (5.1 mg/kg/h) was required because of agitation and severe intracranial hypertension; as a part of our management protocol, glucose intake was restricted to 5 Kcal/h. After 18 hours of propofol infusion there was intense ketonuria (8+ by Ketostix) without any evidence of metabolic acidosis (pH, HCO3- and anion gap were within normal values). At this time, indirect calorimetry (Deltatrac) confirmed that energy expenditure was principally based on fat consumption (70% of energy expenditure). Lowering the propofol infusion rate and increasing glucose intake reduced fat consumption to 39% within 8 hours: at this time, Ketostix was negative for ketone bodies. This case illustrates a potential risk of ketonuria during prolonged sedation with propofol (a 10% solution of intralipid), particularly if glucose intake is restricted. Monitoring urinary ketone bodies is recommended under these circumstances.
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PMID:Massive ketonuria during sedation with propofol in a 12 year old girl with severe head trauma. 820 21