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At least 1,099 records · Page 61Linked to original sources
PubMed1985

Severe hyperkalaemia and ketoacidosis during routine treatment with an insulin pump.

During a feasibility study of the use of insulin pumps to treat diabetes ketoacidosis occurred at a rate of 0.14 episodes/patient/year in the first year but was lower in subsequent years. A case of cardiac arrest secondary to hyperkalaemia during ketoacidosis occurred in a patient treated with a pump. The mean (SD) serum potassium concentration on presentation to hospital with ketoacidosis was significantly higher in patients treated with a pump (5.7 (1.1) mmol(mEq)/l) than those treated with conventional injections of insulin (4.9(0.9) mmol/l; p less than 0.01). The high rate of ketoacidosis and raised serum potassium concentrations during treatment with the pump creates doubt about the use of this treatment as an alternative regimen for large numbers of patients in a busy diabetic clinic.

Acidosis↗
PubMed2005

Effect of hypoxemia and hyperglycemia on pH in the intact cat retina.

OBJECTIVE: To examine the effects of acute hypoxemia and hyperglycemia on retinal pH to understand hyperglycemia-induced changes in the normal intact cat retina. METHODS: Spatial profiles of extracellular hydrogen ion (H+) concentration were obtained from the cat retina, in vivo, using pH-sensitive microelectrodes during normoxia (arterial partial pressure of oxygen [PaO2] = 114.5 +/- 7.9 mm Hg), normoglycemia (plasma glucose concentration, 117 +/- 19 mg/dL), acute hypoxemia (PaO2 = 29.5 +/- 2.2 mm Hg), and acute hyperglycemia (plasma glucose concentration, 303 +/- 67 mg/dL). An H+ diffusion model was fitted to the outer retinal data to quantify photoreceptor H+ production. The inner retinal pH was also examined. RESULTS: Hypoxemia induced a mean acute panretinal acidification of 0.16 pH units that originated from a 2.55-fold increase in net photoreceptor H+ production. Hyperglycemia induced an acute panretinal acidification of 0.12 pH units; however, photoreceptor H+ production levels remained unchanged. Retinal pH changes followed the course of arterial PaO2 and blood glucose changes. CONCLUSIONS: The increase in photoreceptor H+ production during hypoxemia confirms the importance of glycolysis in the retina. Hyperglycemia-induced pH changes resulted from either increased inner retinal H+ production or decreased H+ clearance/neutralization. Clinical Relevance The hyperglycemia-induced acidification that originates in the inner retina suggests that retinal acidosis may contribute to the development of diabetic retinal disease.

Acidosis↗
PubMed1992

Biguanide related lactic acidosis: incidence and risk factors.

The objective of this study was to evaluate in an open population the incidence and risk factors of biguanide related lactic acidosis. All patients currently treated in the Department of Diabetes and Lipid Metabolism of the Instituto Nacional de la Nutrición and their records were reviewed for the present use or history of administration of biguanides. The study was complemented with a revision of all admissions of diabetic patients to the emergency room during 1987-1990. In the outpatient study, 235 cases were included. No case of lactic acidosis was found. A high percentage of the biguanide treated patients had one or more lactic acidosis related risk factors. In the emergency study, 609 admissions of 273 patients were included. In 17 patients a metabolic non-ketotic acidosis was diagnosed. The frequency of non-ketotic acidosis for the different treatments was: 29.4 cases x 1000 emergency admissions for sulphonylurea treated group, 32 for sulphonylurea plus phenformin treated and 47.94 for type II insulin treated patients. All cases had severe precipitant diseases that can cause lactic acidosis with or without associated biguanide administration. No metformin related cases were found. The conclusions of this study are that biguanides in general and metformin in particular are not associated with a high risk of lactic acidosis. Severe systemic dysfunction associated with intercurrent diseases, frequently observed in diabetic patients, is the main determinant for the appearance of lactic acidosis.

Acidosis, Lactic↗
PubMed1979

Alcoholic ketoacidosis in a pregnant woman.

A case of alcoholic ketoacidosis in a 23-year-old chronic alcoholic, gravada V, para IV, is reported. Symptoms were constant, severe, nonradiating pain with crampy exacerbations, anorexia, nausea and vomiting. The patient had a tender and irritable full-term uterus. She was treated inhospital with vigorous fluid therapy and 5% dextrose in normal saline, sodium bicarbonate, glucose and insulin and showed improvement overnight. Alcoholic ketoacidosis has not been reported in pregnant women. Metabolic derangements combine to produce ketoacidosis more readily in the pregnant alcoholic. Differentiation of alcoholic ketoacidosis and diabetic ketoacidosis is important since treatment varies. For alcoholic ketoacidosis, treatment is vigorous rehydration with dextrose-saline while diabetic ketoacidosis usually requires multiple therapeutic modalities.

Acidosis↗
PubMed1985

Acute hemolytic anemia caused by severe hypophosphatemia in diabetic ketoacidosis.

Hypophosphatemia in diabetic ketoacidosis is well recognized, but is believed to be usually of moderate severity. We describe 2 patients in whom acute hemolytic anemia secondary to severe (0.19-0.35 mmol/l) hypophosphatemia has developed 1-2 days following treatment for diabetic ketoacidosis. Our experience indicates that severe hypophosphatemia requiring phosphate supplementation does occur in diabetic patients, and calls for increased awareness for the clinical and laboratory manifestations of this complication of diabetic ketoacidosis.

Acidosis↗
PubMed1997

Acromegaly in a woman presenting with diabetic ketoacidosis and insulin resistance.

A 22-year-old Chinese woman presented with typical features of diabetic ketoacidosis. There was a family history of diabetes but she was not obese. Plasma glucose and bicarbonate levels were 27.0 mmol/l and 5 mmol/l, respectively. Significant insulin resistance was noticed: she needed up to 15 units of insulin per hour. She required up to 120 units daily for her diabetic control even after her acidosis had subsided. She was then noticed to have the clinical features of acromegaly. The diagnosis was confirmed, and a cranial CT scan confirmed the presence of a pituitary macroadenoma. She underwent uneventful trans-sphenoidal resection of the tumour and her insulin requirement gradually lessened. Acromegaly should be considered in the differential diagnosis of unexplained insulin resistance.

Acromegaly↗
PubMed1997

[Diabetic emergencies].

Based on case reports pathogenesis and treatment of the following diabetic emergencies were discussed: 1. The hyperosmolar non-ketotic coma without or with only modest ketosis occurring mainly in type II diabetics and the severe ketoacidosis with or without disturbed consciousness occurring mainly in type I diabetics are the two forms of severe metabolic decompensation of diabetes mellitus. 2. Severe hypoglycaemia may be caused by treatment with sulfonylureas and insulin. 3. The most dangerous life threatening adverse effect of biguanides is lactic acidosis. The incidence of ketoacidosis is about 1-5% in type I diabetics with a mortality of 3-9%. Mortality rates of hyperosmolar non-ketotic comas are much higher, approaching 20-40%, and are explained by severe concomitant complications and older age. The most important triggering factors of diabetic coma are infections, insulin dispensing errors and non-compliance. Carefully instructing patients about the risks of loosing appetite and vomiting as early signs of ketoacidosis is essential. Adequate replacement of fluid, electrolyte and water are the most important therapeutical aspects of ketoacidosis and hyperosmolar non-ketotic coma. Early diagnosis and appropriate treatment of infection by antibiotics are important. Complication of therapy (hypokalemia, hypovolemia and rapid full of oncotic pressure) should be avoided by clinical and laboratory monitoring. Treatment of acidosis with bicarbonate has been found more dangerous than useful. Severe hypoglycaemia is the most important and most dangerous side effect of sulfonylurea and insulin. The incidence of severe hypoglycaemia under glibenclamide ist 3-5 fold higher than under treatment with tolbutamide or glibornurid. Glibenclamide should not be recommended anymore. Longterm experience of the therapeutic security of new sulfonylurea derivates like glimepirid is lacking. Blood-glucose-measurements in the afternoon are important for recognizing disposition to sulfonylurea hypoglycaemia, because at this time the blood-glucose-values tend to be lower than in the morning fasting state. Under insulin treatment the following risk factors for severe hypoglycaemia need to be considered: metabolic control in the near normal range, intensified treatment with rapidly decreasing HbA1c-levels, impaired renal function, unawareness o hypoglycaemia. When the renal function is impaired, biguanide treatment is not indicated because of the risk of lactic acidosis. Most of the diabetic emergency situations are avoidable by proper education of the patients.

Acidosis, Lactic↗