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Results for “ACIDOSIS, DIABETIC”

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At least 757 records · Page 42Linked to original sources
PubMed1997

Hyperglycaemic emergencies are a common problem.

OBJECTIVE: To determine the number, type, precipitating factors and mortality associated with diabetic emergencies admitted to Groote Schuur Hospital. DESIGN: Administered questionnaire survey. SETTING: Groote Schuur Hospital, Cape Town. METHODS: All patients admitted from September 1991 to January 1992 with elevated blood glucose concentrations who required intravenous insulin and fluids were evaluated by an administered questionnaire prior to discharge from hospital. Patients were divided into four groups according to presence of ketosis, standard bicarbonate level and serum osmolality: (i) mild diabetic keto-acidosis (DKA); (ii) severe DKA; (iii) hyperosmolar state; and (iv) hyperglycaemia. RESULTS: There were 131 admissions in 122 patients. Sixty-five occurred in non-insulin-dependent diabetics, 45 in insulin-dependent diabetics and 12 in pancreatic diabetics. There were similar numbers of admissions in the four groups of hyperglycaemic emergencies. The mortality rate was 3% in the mild DKA and hyperglycaemic groups, significantly lower (P < 0.05) than in the hyperosmolar group (19%). The mortality rate was 11% in the severe DKA group (P > 0.05 v. other groups). Sixty-two per cent of participants had achieved Standard 4 to Standard 8 education. Only 39% were employed at the time of interview. Diabetic knowledge and general compliance were assessed as poor. Infections and poor compliance with hypoglycaemic therapy were the dominant precipitating factors. CONCLUSION: Hyperglycaemic emergencies precipitated largely by infections and poor compliance and associated with considerable morbidity and mortality commonly require admission to hospital. Improvement in diabetic education is required to reverse the current situation.

Adolescent↗
PubMed1998

[Lactate metabolism and lactic acidosis].

Lactate can be viewed as a metabolic dead end in that it can only be produced or utilized via pyruvate. Lactate production is determined primarily by pyruvate concentration and to a lesser extend by the redox state. Increased lactate production may result from tissue hypoxia, alkalosis, catecholamine and alanine transamination to pyruvate. Hyperlactatemia is observed in many pathological conditions. Current diagnostic criteria for lactic acidosis are a pH less than 7.35 and lactate concentration greater than 5 to 6 mmol/l. In our study series, malignancy was the most common underlying disease accompanied by lactic acidosis. Organ failure, cardiovascular disease and diabetes mellitus were also common. The prognosis of patients with these diseases were grave. In cases of lactic acidosis associated with diabetes mellitus, alcoholic liver disease, rhabdomyolysis and diabetic comas were noticeable as complications. Alcohol abuse was the most common cause of lactic acidosis associated with diabetes mellitus. In these cases, laboratory data showed prominent hyperlactatemia, hyperglycemia and acidemia and elevated anion gap. The mortality rate in these cases was 36% and higher in cases with organ failure. Treatment of lactic acidosis consists of alkalization by sodium bicarbonate with carbicarb, insulin-glucose-infusion, dichloroacetate therapy, tham administration, bicarbonate-buffered peritoneal dialysis and high bicarbonate-containing dialysis.

Acidosis, Lactic↗
PubMed1997

Complications and concurrent disease associated with diabetes mellitus.

Many animals with diabetes mellitus are severely ill on clinical presentation. The spectrum of disease is quite variable and includes diabetic ketoacidosis (DKA), ketosis without acidosis, hyperosmolar nonketotic syndrome (HNKS), and other nonketotic variants (negative urine ketones, serum osmolality < 340 mOsm/kg with or without acidosis). These more severe forms of diabetes are often precipitated by concurrent diseases such as pyelonephritis, pancreatitis, pyometra, hyperadrenocorticism, renal failure, and heart failure. To make matters worse, in-hospital treatment of diabetic dogs and cats is commonly associated with serious complications, including hypoglycemia, hypokalemia, and hypophosphatemia.

Animals↗
PubMed1989

Fluid therapy in the critically ill patient.

Fluid therapy products for use in the critically ill patient are described. Various specific clinical syndromes are described in detail, including shock, hypoalbuminemia, heart failure, liver failure, diabetic keto-acidosis and pancreatitis. Pathophysiology and specific therapeutic recommendations are given for these clinical syndromes.

Animals↗
PubMed1974

Clinical phenotypes in kidney transport disorders.

Approximately 20 inherited disorders of kidney transport occurring in man have so far been defined. Most of these diseases have characteristic clinical profiles. They can be divided into four groups: 1) the amino acid transport mutations which include the cystinurias, hyperdibasicaminoaciduria, Joseph syndrome, Hartnup disease, and the methionine malabsorption syndrome: 2) the sugar transport mutations characterized by glucose (renal glucosuria), and glucose-galactose malabsorption; 3) the electrolyte and water transport disorders, among which are familial hypophosphatemic rickets, vitamin D-dependent rickets, pseudohypoparathyroidism, proximal and distal renal tubular acidosis, and nephrogenic diabetes insipidus; and 4) the "mixed" kidney transport mutations such as the "Busby", Fanconi, Lowe, Luder-Sheldon syndromes, and glucoglycinuria.

Abnormalities, Multiple↗
PubMedDate not supplied

Overwhelming strongyloidiasis in a diabetic patient following ACTH treatment and keto-acidosis.

A non insulin-dependent Zairian patient developed ketoacidosis and then overwhelming strongyloidiasis following ACTH treatment. Severe cardiovascular and respiratory failure, associated with severe acute hypoprotidemia, preceded death, which occurred within three days. Pathologic examination revealed a massive parasitic infiltration of the gastro-enteric mucosa, mesenteric lymph nodes, and the pulmonary tissue and vessels. We suggest that ACTH treatment and keto-acidosis induced immune deficiency and triggered the acute parasitic episode, in a patient originating from an endemic area. Badly controlled diabetes should be known as a risk factor of hyperinfection by Strongyloides stercoralis in latent carriers.

Adrenocorticotropic Hormone↗
PubMed2004

Diabetes mellitus in an infant.

Onset of diabetes in the first year of life is uncommon, most cases being those of transient diabetes of the newborn. We report the case of a child who presented at 10 weeks of age with diabetic keto-acidosis, and continues to be insulin dependent at 18 months.

Age of Onset↗
PubMed2002

[Metformin-associated lactic acidosis with acute renal failure in type 2 diabetes mellitus].

CASE REPORT: An 83-year-old patient was admitted to our hospital because of gastrointestinal symptoms, mental confusion and dysarthria. The patient suffered from type 2 diabetes mellitus and was taking metformin. A mild renal insufficiency was known. On admission, we found impaired consciousness, Kussmaul breathing, a body temperature of 32.1 degrees C, and hemodynamic instability. Laboratory testing revealed lactic acidosis (pH 6.71, base excess--30, standard bicarbonate 4.0 mmol/l, lactate 24.4 mmol/l) and acute renal failure with a creatinine of 10.6 mg/dl and blood urea nitrogen of 134 mg/dl. Electrolytes were not altered; the blood glucose was elevated (147 mg/dl). According to history, physical examination, and laboratory testing the diagnosis metformin-induced lactic acidosis with acute renal failure was made. This diagnosis was confirmed by an elevated level of metformin. As soon as possible a bicarbonate hemodialysis was initiated. After 8 hours of hemodialysis the acid-base metabolism was almost balanced and the vigilance of the patient normalized. No further sessions of hemodialysis were needed and insulin therapy was started. CONCLUSIONS: Metformin-induced lactic acidosis is a common side effect in patients with renal insufficiency. For an early diagnosis, clinical symptoms of intoxication should be well known by physicians and patients. First-line therapy for correction of lactic acidosis and effective elimination of metformin is bicarbonate hemodialysis. Sodium bicarbonate infusions are not able to correct the acid-base metabolism sufficiently. For prevention the renal function should be monitored closely and metaformin therapy should be stopped, if a deterioration of renal function is observed.

Acidosis, Lactic↗