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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four cases of diabetic ketoacidosis presenting with abdominal pain are reported. Case 1: a 14-year-old boy suffered from sudden onset of mid-abdominal pain, then migrating to the right lower quadrant. Nausea and vomiting occurred subsequently. Appendectomy was performed under the impression of acute appendicitis in an outside surgical clinic. The patient became comatose the next day and then was transferred to our hospital. Diabetic ketoacidosis was diagnosed after the detection of hyperglycemia, glycosuria, and ketonuria on the day of admission. Unfortunately, he expired on the same day in spite of vigorous resuscitation. Case 2: a 9-year-old boy complained of abdominal pain for 10 days. There was no specific finding in the physical examination. Diabetic ketoacidosis was confirmed four days later when conscious disturbance, dehydration, and tachypnea were noticed. Case 3: a 10-year-old girl presented with a history of intermittent abdominal pain for one month. The character of the abdominal pain was nonspecific. Glycosuria was detected in a pediatric clinic. Diabetic ketoacidosis was confirmed after her referral to our hospital. Case 4: a 5-year-old girl suffered from acute abdominal pain for four hours. She was found to have tachypnea, lethargy, and ill-looking. Diabetic ketoacidosis was diagnosed after serial examinations. The abdominal pain in diabetic ketoacidosis may lead the pediatrician into diagnostic error. Therefore, when a child presented with non-specific abdominal pain, a routine urine sugar should be checked in order not to miss the possibility of diabetic ketoacidosis.
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PMID:[Abdominal pain in diabetic ketoacidosis: report of four cases]. 212 98

A 15-year-old male was admitted to the hospital because of a disturbance of consciousness. He was in good mental and physical condition until the previous day, when he vomited and experienced a reduction of consciousness. He was brought to the hospital the day following the onset of symptoms. On admission the patient was stuporous. Neurological focal signs were not demonstrated. Computed tomographic (CT) scanning on admission showed no definite abnormality. Cerebrosprinal fluid had no pleocytosis. At this time, Reye's syndrome was suspected because of the acute change of consciousness and the presence of hyperammonemia. The disturbance of consciousness progressed and he became comatose on the day following admission. CT scanning showed that the suprasellar, ambient and quadrigeminal cisterns could almost not be detected and the bilateral ventricles were narrowed. The plasma aminogram demonstrated an elevation of alanine, lysine, glutamine, glutamic acid, aspartate and proline. Ketonuria was negative, but the urinary excretion of orotic acid was markedly increased. This data was indicative of the existence of an ornithine transcarbamylase (OTC) deficiency. The patient was died on the third day after hospitalization. The OTC activity in the liver was 10% of normal. Activities of other enzymes in the urea cycle were within normal limits. It is unusual that the symptoms of the enzyme deficiency occurred, both acutely and late at an adult age, as in this case. This case demonstrates that OTC deficiency should be considered in the differential diagnosis of hyperammonemia of adult onset.
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PMID:A case of ornithine transcarbamylase deficiency with acute and late onset simulating Reye's syndrome in an adult male. 225 72

A patient with a history of diabetes mellitus and congestive heart failure was taking furosemide and metolazone as diuretics. Diabetic ketoacidosis developed, and the patient became lethargic and confused. Initial biochemical determinations showed an alkalemic pH, serum and urine ketones with an anion gap, and hyperventilation. The hyperventilation was appropriate for the degree of ketoacidosis but it was grossly inappropriate for the alkalemia. This could be explained by a direct effect of ketones on the respiratory center or a sudden increase in hydrogen ion concentration superimposed on previously chronic alkalemic pH due to the potent combination of furosemide and metolazone.
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PMID:Alkalemia in diabetic ketoacidosis. 643 81

By means of gas chromatographic methods substantial amounts of the C6-C10-dicarboxylic acids, i.e. adipic, suberic and sebacic acids, have been found in the urine from children with unexplained attacks of lethargy and hypotonia, presumably related to episodes of fever and/or insufficient food intake. The course have once been fatal and is often characterized by severe hypoglycemia without ketonuria. Systematic gas chromatographic/mass spectrometric determinations of selected organic acid metabolites in the urine, together with enzymatic measurements in fibroblasts and clinical data from 4 patients of this category, have shown that the biochemical basis of this syndrome can be inborn errors of the beta-oxidation of fatty acids, localized to the medium-chain acyl-CoA dehydrogenation system. The biosynthesis of adipic, suberic and sebacic acids was studied using ketotic rats as the model, since ketosis in rats and humans is accompanied by excessive urinary excretion of adipic and suberic acids. A probable pathway for the production of the three dicarboxylic acids was found to be an initial omega-oxidation of the medium-chain C10-C14-monocarboxylic acids followed by beta-oxidation of the resulting medium-chain dicarboxylic acids. It is argued that the source of the omega-oxidizable monocarboxylic acids in ketosis most probably is the fat deposites, and it is speculated that the patients with beta-oxidation defects supplement this source with beta-oxidation intermediate medium-chain monocarboxylic acids, accumulated as a result of the defect. The ratio between the excreted amounts of adipic acid and sebacic acid in the urine from the patients with beta-oxidation defects is less than 50. This is in contrast to the ratio in urine from ketotic patients, where it is greater than 100. Adipic acid/sebacic acid ratio-measured by means of a gas chromatographic analysis-is therefore suggested as a tool in the diagnosis of dicarboxylic acidurias. Based on the clinical picture and the pattern of a series of organic acids in the urinary metabolic profile our four patients can be divided in two types of dicarboxylic aciduria. The two types have different therapeutic implications.
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PMID:C6-C10-dicarboxylic aciduria: biochemical considerations in relation to diagnosis of beta-oxidation defects. 695 31

A 3 1/2-year-old boy presented at three months of age with an acute episode of lethargy, somnolence, hypoglycemia, hepatomegaly, and cardiomegaly, which responded poorly to restoration of the blood sugar level to normal. The absence of ketonuria during subsequent episodes of severe hypoglycemia prompted a search for a defect in fatty acid oxidation. Plasma carnitine (2.0 to 5.0 mumol per liter), muscle carnitine (0.01 to 0.02 mumol per gram, wet weight) and liver carnitine (0.021 to 0.065 mumol per gram, wet weight) were all less than 5 per cent of the normal mean. During a 36-hour fast, ketones were barely detectable. Prolonged treatment with oral carnitine over a six-month period resulted in increased muscle strength, a dramatic reduction in cardiac size, relief of cardiomyopathy, partial repletion of carnitine levels in plasma and muscle, and complete repletion in the liver. Systemic carnitine deficiency is an easily treatable cause of recurrent Reye's-like syndrome. Its diagnosis requires measurement of carnitine levels.
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PMID:Systemic carnitine deficiency--a treatable inherited lipid-storage disease presenting as Reye's syndrome. 743 84

A 71 year old hypertensive and non insulin-dependent diabetic patients with moderate renal insufficiency taking 500 mg/d of metformin and 5 mg/d of enalapril, developed metabolic acidosis characterized by fairly elevated anion gap, hyperchloremia, severe hyperkalemia, normal plasma level of beta-hydroxybutyric acid, absence of ketonuria and high plasma level of lactic acid. This biochemical feature allowed us to ascribe the pathogenesis of metabolic acidosis both to the increased plasma level of lactic acid and to the type IV renal tubular acidosis syndrome, the precipitating factor being an infection of urinary tract (as we assumed on the basis of the urine culture). The patient was dehydrated and lethargic; the ECG revealed the presence of nonparoxysmal junctional tachycardia. The clinical evolution was favorable thanks to the treatment with the infusion of isotonic saline solutions, mild alkalinizing solutions, low-dose regular insulin and antibiotics. It is likely that metformin and enalapril, regularly assumed by the patient, could have played a iatrogenic role even if they were taken in low dosages. This event points out the importance of complying with the indications and especially the contraindications of these drugs, to avoid life threatening complications as that one occurred in this case.
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PMID:[Lactic acidosis and severe hyperkalemia in a diabetic patient treated with metformin and enalapril: influence of acute renal disease and drugs]. 775 38

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

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy]. 817 67

A 71 year old hypertensive, non insulin-dependent diabetic patient with moderate renal insufficiency taking 500 mg/d of metformin and 5 mg/d of enalapril, developed metabolic acidosis characterized by fairly elevated anion gap, hyperchloremia, severe hyperkaliemia, normal plasma level of 3-hydroxybutyric acid, absence of ketonuria and high plasma level of lactic acid. This biochemical feature allowed us to ascribe the pathogenesis of metabolic acidosis, both to the increased plasma level of lactic acid and to the type IV renal tubular acidosis syndrome, the precipitating factor being an infection of urinary tract (as we assumed on the basis of the urine culture). The patient was dehydrated and lethargic; the ECG revealed the presence of nonparoxysmal junctional tachycardia. The clinical evolution was favorable under the treatment with an infusion of isotonic saline solutions, mild alkalinizing solutions, low-dose regular insulin and antibiotics. It is likely that metformin and enalapril, regularly taken by this nephropathic patient, could have played an iatrogenic role, even if the doses were low. This case highlights the importance of complying with the contraindications of these drugs, to avoid the rare but reported life-threatening complications of metformin administration.
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PMID:Possible synergistic effect of metformin and enalapril on the development of hyperkaliemic lactic acidosis. 948 83

Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 48 mg/dL, MBG/ 8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to follow-up after 1.5, 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state.
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PMID:Transient clinical diabetes mellitus in cats: 10 cases (1989-1991). 1005 60


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