1/23. Pseudo myocardial infarct--electrocardiographic pattern in a patient with diabetic ketoacidosis.diabetic ketoacidosis is an extremely serious complication of diabetes mellitus. It arises because of a complex disturbance in glucose metabolism. There is usually a precipitating cause such as sepsis or myocardial infarction. If not recognised and appropriately treated, it can have devastating consequences. This is a case report of a patient with severe diabetic ketoacidosis and interesting electrocardiographic findings. The initial electrocardiographic (ECG) findings were suggestive of an acute myocardial infarction. The ECG changes normalised remarkably following initial management of the diabetic ketoacidosis. There have been only occasional reports of hyperkalemia causing electrocardiographic changes, closely resembling those of acute myocardial infarction.- - - - - - - - - - ranking = 1keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
2/23. syncope caused by nonsteroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors.A 85-year-old woman with diabetes mellitus and prior myocardial infarction was transferred to the emergency room with loss of consciousness due to marked bradycardia caused by hyperkalemia. The T wave during right ventricular pacing was tall and tent-shaped while the concentration of serum potassium was high, and its amplitude during pacing was decreased after correction of the serum potassium level. Simultaneously with the correction, normal sinus rhythm was restored. The cause of hyperkalemia was considered to be several doses of loxoprofen, a nonsteroidal anti-inflammatory drug (NSAID), prescribed for her lumbago by an orthopedic specialist, in addition to the long-term intake of imidapril, an angiotensin-converting enzyme inhibitor (ACEI), prescribed for her hypertension by a cardiologist. This case warns physicians that the combination of NSAID and ACEI can produce serious side effects in aged patients who frequently suffer from hypertension, diabetes mellitus, ischemic heart disease, and degenerative joint disease.- - - - - - - - - - ranking = 2keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
3/23. Hyperosmolar diabetic non-ketotic coma, hyperkalaemia and an unusual near death experience.Generally, cardiac arrest due to pulseless electrical activity has a poor outcome, except when reversible factors such as acute hyperkalaemia are identified and managed early. Hyperosmolar diabetic non-ketotic coma may lead to acute hyperkalaemia. Hyperosmolar diabetic non-ketotic coma is a metabolic emergency usually seen in elderly non-insulin dependent diabetics, characterized by severe hyperglycaemia, volume depletion, altered consciousness, confusion and less frequently neurological deficit. Cerebrovascular accident or transient ischaemic attack may be mistakenly diagnosed, particularly if the patient has no history of diabetes mellitus. Delays in diagnosis and management of glycaemic emergencies presenting as a constellation of neurological abnormalities can be avoided by routine early measurement of blood glucose. Hyperosmolar diabetic non-ketotic coma should be considered in any patient with altered consciousness or neurologic deficit in conjunction with hyperglycaemia. As hyperosmolar diabetic non-ketotic coma results in severe fluid depletion, electrolyte disturbance, profound hyperglycaemia and an altered mental state, the guiding principles of therapy include aggressive rehydration, insulin therapy, correction of electrolyte abnormalities and treatment of any underlying illnesses. Treatment of acute hyperkalaemia includes calcium ions, insulin with dextrose, salbutamol and haemodialysis.- - - - - - - - - - ranking = 1keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
4/23. Severe hyperkalemia in two patients with diabetes after cosyntropin administration.Some patients with diabetes mellitus are at increased risk for the development of hyperkalemia. Included in this group are patients with glucose-induced hyperkalemia who may have renal insufficiency, hyporeninemic hypoaldosteronism, or other impediments to the release or action of aldosterone. In an unusual demonstration of this abnormality, two patients with diabetes, who form the basis of our report, became markedly hyperglycemic and hyperkalemic after cosyntropin administration. To our knowledge, this complication of adrenocorticotropic hormone (ACTH) stimulation testing has not been previously reported. It should therefore be emphasized that the use of cosyntropin as a diagnostic agent can provoke severe hyperglycemia and hyperkalemia in a susceptible subgroup of patients with diabetes mellitus.- - - - - - - - - - ranking = 2.5970045742478keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
5/23. Persistent hyperkalemia in a patient with diabetes mellitus: a reversible defect in kaliuresis during bicarbonaturia.The purpose of this report is to apply recent advances in the understanding of the physiology of the excretion of potassium to a patient who had hyperkalemia due to a low rate of excretion of potassium. The defect was first suspected during therapy for diabetic ketoacidosis, when the concentration of potassium in plasma was unusually high (7.3 mmol/l) on admission and the deficit of potassium, as judged from the quantity of potassium infused to maintain normokalemia (40 mmol/24 h), was much less than expected. After recovery from diabetic ketoacidosis, hyperkalemia persisted despite near-normal values for creatinine and glucose in plasma. Excretion of potassium was low, considering the stimulus of hyperkalemia, and did not rise appreciably after the acute or chronic administration of a mineralocorticoid. The transtubular potassium concentration gradient (TTKG) did not exceed 6 after a large dose of fludrocortisone (200 micrograms) was administered. Notwithstanding, the TTKG rose to 14.4 following the intake of acetazolamide. We speculate that the basis for the hyperkalemia was type II hypoaldosteronism.- - - - - - - - - - ranking = 4keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
6/23. Significant hyperkalemia after discontinuation of an insulin pump.patients with diabetes and insulin pumps may need their insulin therapy modified during surgery. Often, this is done with blood glucose as the end point. Changing insulin therapy can also have profound effects on potassium homeostasis in certain patients. This case demonstrates that changes in insulin therapy warrant not only close monitoring of blood glucose, but also of serum potassium. This patient's comorbidities and treatments that could alter potassium homeostasis are also reviewed.- - - - - - - - - - ranking = 0.11940091484956keywords = diabetes (Clic here for more details about this article) |
7/23. pseudohypoaldosteronism: case report and discussion of the syndrome.A 41-year-old man, complaining of leg cramps, was found to have persistent hyperkalemia. Except for mild hypertension, his physical examination and laboratory values to exclude connective tissue diseases and diabetes mellitus were normal. Renal function testing revealed a normal glomerular filtration rate and tubular capacity to acidify and dilute, as well as near-normal ability to concentrate his urine. Hormonal evaluation revealed a normal cortisol, as well as normal resting and stimulated renin and aldosterone levels. A selective defect in tubular potassium secretion was demonstrated. In the absence of aldosterone deficiency or renal dysfunction, it was assumed that the patient had primary renal resistance to aldosterone, known as pseudohypoaldosteronism. Treatment with hydrochlorothiazide controlled his hyperkalemia and hypertension. His case emphasizes the diagnostic and therapeutic factors that should be considered in evaluating and treating a non-hospitalized patient with sustained hyperkalemia.- - - - - - - - - - ranking = 1keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
8/23. Big renin and biosynthetic defect of aldosterone in diabetes mellitus.To determine the cause of selective aldosterone deficiency in two patients with diabetes mellitus, studies of renin and of aldosterone-precursor metabolites were performed under conditions of sodium depletion and ACTH stimulation. plasma renin concentration was elevated in both patients, and stimulated plasma renin activity was low in one and normal in the other. Fractionation of plasma extracts demonstrated the presence of "big renin," a relatively inactive precursor of renin. Metabolites of aldosterone precursors were increased, suggesting deficient 18-hydroxylase in one patient and dehydrogenase in the other. The results suggest that hypoaldosteronism in diabetic patients may result from combined defects in both renin and aldosterone biosynthesis.- - - - - - - - - - ranking = 5keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
9/23. Endocrine crises. hyperkalemia.Clinical disorders causing hyperkalemia require a basic understanding of normal K homeostasis, which consists of external and internal K balances. The kidney is predominant in maintaining the external balance of K, and a number of mechanisms exist to provide a renal adaptation to defend against K excess. Likewise, several factors are known to modulate internal K balance--i.e., its distribution within the body. Some of these factors may provide defense against hyperkalemia before the kidneys have time to adapt. potassium retention by the kidney causes hyperkalemia when renal failure is advanced, or earlier in the face of impaired tubular function in a variety of disorders. hyperkalemia out of proportion to loss of renal function also occurs in the syndrome of hyporeninemic hypoaldosteronism. Drug-induced hyperkalemia is increasingly common and usually is caused by nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors, cyclosporine, or K-sparing diuretics. Clinical disorders of internal K imbalance include diabetes mellitus, systemic acidosis, and use of beta-blockers. hyperkalemia is usually asymptomatic, but the danger of cardiac arrest or arrhythmia in severe hyperkalemia forces prompt clinical attention. Available treatment choices include agents that antagonize the effect of K on membrane potentials, redistribute it internally into cells, and remove it altogether from the body. The diagnostic work-up can then proceed, first by distinguishing renal and extrarenal causes, then by examining the roles of specific factors outlined in the section on normal K homeostasis.- - - - - - - - - - ranking = 1keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
10/23. Acquired partial corticosterone methyl oxidase type II defect in diabetes mellitus. Case of hyperreninemic hypoaldosteronism.The aim of this study was to investigate the pathogenesis of hypoaldosteronism in diabetes. Endogenous elevation of plasma renin activity and exogenous corticotropin were used to study steroidogenesis. Observations were made over 12 yr on the evolution and treatment of hyperkalemia in a diabetic subject. In 1977, potassium, baseline cortisol, aldosterone, and renin activity were normal; renin activity increased normally with posture; and cortisol responded normally to ACTH infusion. Nine yr later, persistent hyperkalemia was documented. Upright renin activity was elevated to 5.26 ng.L-1.s-1, with concomitant elevation of 18-hydroxycorticosterone (18-OHB) and a low-normal aldosterone level. One hour after administration of 0.25 mg i.m. cosyntropin, cortisol increased normally, aldosterone increased from 220 to 360 pM, and 18-OHB increased from 3700 to 4800 pM. During treatment with fludrocortisone, fludrocortisone with furosemide, and furosemide alone, improvement of hyperkalemia was noted. Endogenous hyperreninemia and basal elevations of 18-OHB, accompanied by limited aldosterone responsiveness to renin and ACTH, suggest the presence of a partial corticosterone methyl oxidase type II defect. Evolution of hyperkalemia between 1977 and 1986 suggests this defect was acquired.- - - - - - - - - - ranking = 4.1194009148496keywords = diabetes mellitus, mellitus, diabetes (Clic here for more details about this article) |
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