Hyperosmolar Hyperglycemic Nonketotic Coma Research Articles

A Case of Hyperosmolar Hyperglycemic Nonketotic Coma Caused by Severe Dehydration during Ramadan

A Case of Hyperosmolar Hyperglycemic Nonketotic Coma Caused by Severe Dehydration during Ramadan

Concepts of Fluid Therapy in Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Nonketotic Coma

Despite many advances in the overall treatment of type I diabetes mellitus during the last few years, no major advance has been made in decreasing the mortality rate of diabetic ketoacidosis or hyperosmolar hyperglycemic nonketotic coma. A major concern in both of these disease states is the development of cerebral edema during treatment. The guiding principles of therapy in both disease states are rehydration, electrolyte replacement, insulin therapy, and treatment of any underlying illnesses. If the patient is hypotensive, therapy begins with colloid or normal saline administration to support blood pressure. Fluid and electrolyte deficits should be calculated and replaced during 48 hours. Low-dose insulin therapy is employed for treatment of hyperglycemia. Neurologic function should be carefully monitored and mannitol administered if a change in neurologic function occurs.

Diabetic emergencies.

Diabetic emergencies continue to be a significant cause of premature death in patients with diabetes. They include the diabetic comas (hypoglycaemia, severe diabetic ketoacidosis, hyperosmolar hyperglycaemic non-ketotic coma, lactic acidosis), emergency surgery and myocardial infarction. There is still considerable avoidable morbidity and mortality during treatment, and as a result of misdiagnosis. Simple guidelines are thus needed for the general practitioner and admitting physician to improve management. Hypoglycaemia is far the commonest diabetic emergency, and is relatively easy to diagnose and treat. Delays in treatment are potentially damaging and largely unnecessary. Diabetic ketoacidosis is still relatively common but is often preventable. Initial treatment for this and hyperosmolar nonketotic coma is rehydration. This is followed by IM or IV infusion of moderate amounts of insulin, early potassium replacement, and alkali only if the acidaemia is severe. Lactic acidosis requires mainly rigorous alkalinisation but is very rare. The metabolic derangements in emergency surgery and myocardial infarction are best treated by combined glucose, potassium and insulin infusions. In all cases treatment is easiest and probably more successful if consistent simple guidelines are provided.

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Nonketotic Coma

Diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma are two of the most common acute complications of diabetes. The pathophysiologic changes that occur in both disease states represent an extreme example of the super-fasted state. The physiology of the fed and fasted state, evaluation, therapeutic issues, recommendations for therapy, immediate follow up care, and complications of therapy are reviewed for both syndromes.

Fluid and Electrolyte Disorders Associated with Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar Nonketotic Coma

DKA and HHNK are emergency conditions requiring quick medical care and nursing intervention. DKA can develop at any age and is most likely to occur in the insulin-dependent patient. The hallmark signs of DKA are a relative or absolute lack of insulin along with acidosis, ketosis, and hyperglycemia. Insulin and fluid and electrolyte therapy are initiated to control the hyperglycemia and prevent shock and further complications. The patient in HHNK presents with a very high serum glucose level (higher than in DKA), a high serum osmolarity, and usually no ketosis or acidosis. The patient may also experience more severe and sudden neurologic changes than those in DKA. Most patients who experience HHNK are older and may also have some other underlying disease process present. The nursing process should be used to correct the fluid and electrolyte imbalances and to prevent further complications in both DKA and HHNK. The patient needs to understand the reasons for his or her hyperglycemic crisis and how to prevent it from occurring in the future. Assessment of the patient's knowledge about diabetes is essential so that proper education can be incorporated into his or her plan of care.

Clinical Features of Hyperosmolar Hyperglycemic Nonketotic Diabetic Coma Associated with Cardiac Operations

Hyperosmolar hyperglycemic nonketotic diabetic coma after cardiac operations was reviewed in a total of 12 patients from the literature and from my experience in an attempt to determine the clinical features of this condition. Among the unique features of this disease were the following: The mortality is high (42%). The morbidity and mortality are higher in patients with no previous history of diabetes mellitus (67% and 50%) than in those with such a history (33% and 25%). Polyuria is usually a heralding symptom. There is an average time lag of 6 days between the onset of polyuria and the established diagnosis of hyperosmolar hyperglycemic nonketotic diabetic coma. The time lag in patients who died was 7.5 +/- 0.8 days (mean +/- standard error of the mean), significantly longer than in survivors (4.5 +/- 0.8 days). Polyuria usually emerges after the stormy immediate postoperative days have passed (on postoperative day 5.3 on the average). Polyuria is generally regarded as a favorable sign not suggestive of complicating hyperosmolar hyperglycemic nonketotic diabetic coma. Therapies known to precipitate this disorder are continued even after development of polyuria. Gastrointestinal bleeding can be a precipitating factor. Hyperalimentation or elemental diet may cause dehydration and trigger hyperosmolar hyperglycemic nonketotic diabetic coma. A high or rising serum sodium concentration and/or blood urea nitrogen level with polyuria may be a warning sign of this complication. Too hasty correction of the hyperosmolar state can be dangerous. Pulmonary dysfunction may be involved in the symptoms of hyperosmolar hyperglycemic nonketotic diabetic coma.

Clinical features of hyperosmolar hyperglycemic nonketotic diabetic coma associated with cardiac operations

Hyperosmolar hyperglycemic nonketotic diabetic coma after cardiac operations was reviewed in a total of 12 patients from the literature and from my experience in an attempt to determine the clinical features of this condition. Among the unique features of this disease were the following: The mortality is high (42%). The morbidity and mortality are higher in patients with no previous history of diabetes mellitus (67% and 50%) than in those with such a history (33% and 25%). Polyuria is usually a heralding symptom. There is an average time lag of 6 days between the onset of polyuria and the established diagnosis of hyperosmolar hyperglycemic nonketotic diabetic coma. The time lag in patients who died was 7.5 +/- 0.8 days (mean +/- standard error of the mean), significantly longer than in survivors (4.5 +/- 0.8 days). Polyuria usually emerges after the stormy immediate postoperative days have passed (on postoperative day 5.3 on the average). Polyuria is generally regarded as a favorable sign not suggestive of complicating hyperosmolar hyperglycemic nonketotic diabetic coma. Therapies known to precipitate this disorder are continued even after development of polyuria. Gastrointestinal bleeding can be a precipitating factor. Hyperalimentation or elemental diet may cause dehydration and trigger hyperosmolar hyperglycemic nonketotic diabetic coma. A high or rising serum sodium concentration and/or blood urea nitrogen level with polyuria may be a warning sign of this complication. Too hasty correction of the hyperosmolar state can be dangerous. Pulmonary dysfunction may be involved in the symptoms of hyperosmolar hyperglycemic nonketotic diabetic coma.

Hyperosmolar Hyperglycemic Nonketotic Coma: A Complication of Short-term Systemic Corticosteroid Use

Hyperosmolar hyperglycemic nonketotic coma is a serious and often lethal clinical biochemical syndrome. We report three cases of ophthalmic problems that were treated with a short course of oral corticosteroids and which resulted in the development of hyperosmolar hyperglycemic nonketotic coma. Two of these cases concerned relatively young, previously healthy patients and had fatal outcomes. The third patient, who was elderly, survived because of early detection and initiation of therapy. All three cases demonstrate that hyperosmolar hyperglycemic nonketotic coma is a serious potential complication of systemic steroidal therapy, even in a short course of treatment such as is often used in ophthalmology.

The role of race and environment in the development of hyperosmolar hyperglycaemic non-ketotic coma.

Summary In a retrospective study of patients presenting with hyperosmolar hyperglycaemic non-ketotic coma no evidence was obtained to suggest that the condition occurs more commonly in black patients. Suspicions that poor social background rather than race predisposes patients to the condition are borne out by the fact that 10 of the 13 patients were socially isolated.

Acute hyperosmolar hyperglycemia causes axonal shrinkage and reduced nerve conduction velocity

Cats infused with hypertonic dextrose to increase plasma glucose to values at or above those found in human hyperglycemic hyperosmolar nonketotic coma developed a small but progressive reduction of conduction velocity of A alpha motor fibers during 6 h which was not prevented by the addition of myo-inositol. Axonal shirnkage, probably sufficient to cause the reduction in conduction velocity, and other morphometric features were similar to those produced by hyperosmolar fixation of normal nerve and by streptozotocin diabetes in rats.

Hyperosmolar hyperglycemic nonketotic coma, a cause of delayed recovery from anesthesia.

Hyperosmolar hyperglycemic nonketotic coma, a cause of delayed recovery from anesthesia.

Hyperosmolar hyperglycemic nonketotic coma in a patient undergoing emergency cholecystectomy.

Hyperosmolar hyperglycemic nonketotic coma in a patient undergoing emergency cholecystectomy.

Misleading Synopsis-Abstract

In the BRIEF REPORT by Curtis et al, "Chlorthalidone-Induced Hyperosmolar Hyperglycemic Nonketotic Coma," published June 19 (220:1592-1593, 1972), the first two sentences of the synopsis-abstract should have been combined to read as follows: "Hyperosmolar hyperglycemic nonketotic coma developed in a patient with diabetes mellitus<i>and</i>essential hypertension follow<i>ing</i>the addition of chlorthalidone to his usual medications." (Italics indicate changes.)

Hyperosmolar hyperglycaemic non-ketotic diabetic coma complicating open heart surgery.

Hyperosmolar hyperglycaemic non-ketotic diabetic coma complicating open heart surgery.

Chlorthalidone-Induced Hyperosmolar Hyperglycemic Nonketotic Coma

Hyperosmolar hyperglycemic nonketotic coma developed in a patient with diabetes mellitus. Essential hypertension followed the addition of chlorthalidone to his usual medication. Profound hyponatremia, sustained insulin-resistant hyperglycemia, and hyperuricemia were atypical findings attributed to the pharmacologic properties of chlorthalidone.

Hyperosmolar hyperglycemic non-ketotic coma following general anesthesia: report of a case.

Hyperosmolar hyperglycemic non-ketotic coma following general anesthesia: report of a case.

Hyperosmolar hyperglycemic nonketotic coma during peritoneal dialysis.

Hyperosmolar hyperglycemic nonketotic coma during peritoneal dialysis.