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At least 19 recordsLinked to original sources
PubMed1996

Partial central diabetes insipidus complicating nonketotic hyperglycemic hyperosmolar coma.

Nonketotic hyperglycemic hyperosmolar coma is an uncommon, but significant, complication of type II diabetes mellitus with a high overall mortality rate. Treatment of this entity is controversial but mandates aggressive fluid resuscitation and strict control of serum glucose levels. In the patient described, nonketotic hyperglycemic hyperosmolar coma complicated by diabetes insipidus was successfully treated with desmopressin acetate. To the authors' knowledge, this is the first reported case of nonketotic hyperglycemic hyperosmolar coma associated with partial central diabetes insipidus.

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PubMed1989

[Low-dose dopamine treatment of patients in nonketotic hyperosmolar hyperglycemic coma].

In the acute neurosurgical setting, nonketotic hyperosmolar hyperglycemic coma (NHC) is thought to be caused by cerebral dehydration therapy and administration of steroids, glycerol, or mannitol. The mortality of this complication is reportedly very high, and is due to acute renal and/or cardiac failure. The authors evaluated the effect of low-dose dopamine (LDD; 1 to 5 micrograms/kg/min) administration in 10 patients with this syndrome. LDD was given to five patients. In these cases, hypovolemia was treated under central venous pressure monitoring with an iso-osmolar hyponatremic lactate solution given in a volume greater than the urine output. After the hypovolemia was corrected, the fluid was administered in a volume equal to the urine output until the serum osmolarity was normalized. In the five patients not given LDD, a large quantity of hypotonic solution was rapidly administered. In all patients treated with LDD, the urinary sodium increased and the urinary output stabilized. Consequently, the excess urea-nitrogen and serum sodium were quite easily washed out. The total net intake volume for the normalization of serum osmolarity was small and the duration of treatment was much shorter than that of patients not treated with LDD. The LDD regimen was not associated with complications, such as aggravation of cerebral edema, renal failure, or cardiac failure. On the other hand, three of the five patients not given LDD died of acute renal and/or cardiac failure without normalization of laboratory data. It is emphasized that this therapy, which results in beta-effect of catecholamine, sodium diuresis, and increased renal blood flow, is a practical means of managing acute neurosurgical cases complicated by NHC.

Adult↗
PubMed1975

Closed head injury complicated by nonketotic hyperglycemic hyperosmolar coma.

A case of nonketotic hyperglycemic hyperosmolar coma occurring in a patient with closed head injury and basilar skull fracture is reported. The metabolic abnormality masqueraded as a progression of central transtentorial herniation due to cerebral edema. It is suggested that the development of this complication is related to various predisposing factors normally employed in cases of critically ill, neurologically compromised patients. The anatomic lesions found at autopsy were considered inappropriate as a cause of death; the occurrence of central transtentorial herniation three days before death had been reversed. An awareness of this syndrome is emphasized in considering patients receiving steroids, mannitol, tube feedings, Dilantin, and dehydrative measures as part of their care.

Adult↗
PubMed1988

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.

Diabetic Coma↗
PubMed1987

Hyperosmolar, hyperglycemic, nonketotic coma in a patient receiving home total parenteral nutrient therapy.

A patient who developed hyperosmolar, hyperglycemic, nonketotic coma (HHNC) while receiving home total parenteral nutrient (TPN) therapy is described, and the etiology, clinical features, and treatment of HHNC are reviewed. A 51-year-old black man diagnosed as having Dukes' stage D signet-cell carcinoma of the rectum was discharged on home TPN therapy after a prolonged hospital course and the persistence of a gastrointestinal fistula. Seventeen days after discharge, the patient developed polyuria, became febrile, and lost mental acuity. Upon hospitalization, the patient's physical condition and laboratory values were consistent with the diagnosis of HHNC. The patient was treated with intravenous fluids and small quantities of insulin. The patient's home records indicated that he had lost large volumes of fluid through his fistula, resulting in a net negative fluid balance. The patient's records also indicated that he had had mild glycosuria with a normal urine output at home. This normal urine output despite a body-fluid deficit could be explained by osmotic diuresis related to either glucose or urea. Hypotonic fluid loss resulting from fistula output and osmotic diuresis may have led to this patient's hypertonic state and critical illness. The patient died on hospital day 11 as a result of widely disseminated cancer. HHNC arises most often as a complication of non-insulin-dependent diabetes. It is also a major complication resulting from hypertonicity related to glucose intolerance or other conditions that can occur in patients receiving TPN therapy. The underlying cause of the hyperosmolar state appears to be dehydration.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetic Coma↗
PubMed1983

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.

Administration, Oral↗
PubMedDate not supplied

Optimal insulin delivery in diabetic ketoacidosis (DKA) and hyperglycemic, hyperosmolar nonketotic coma (HHNC).

Both diabetic ketoacidosis (DKA) and hyperglycemic, hyperosmolar nonketotic coma (HHNC) are stressful metabolic occurrences brought about by the orchestration of numerous events. Adequate hydration and replacement of electrolytes, along with physiologic doses of insulin, are treatment objectives for both of these conditions. Additionally, the physician must search for the factors precipitating these events and frequently evaluate the patient's overall condition.

Biological Availability↗
PubMed1990

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.

Child↗
PubMed1989

Hyperosmolar hyperglycemic nonketotic coma.

HHNC is a syndrome of abnormally high serum glucose and osmolality coupled with depressed consciousness and an absence of ketoacidosis. It represents as many as 20 per cent of all cases of severe hyperglycemia and constitutes a life-threatening medical emergency; however, the absence of acidosis and the insidious presentation of the disorder frequently mislead clinicians into dangerously inadequate therapeutic interventions. Aggressive therapy with intravenous fluids and potassium and the judicious use of insulin, in conjunction with careful monitoring of central venous pressure and urine output, form the mainstays of treatment. There is a strong association of HHNC with other underlying serious diseases, the detection and treatment of which are imperative to the adequate resolution of the syndrome.

Diabetic Coma↗
PubMed1992

Hyperosmolar hyperglycemic nonketotic coma in Waldenström's macroglobulinemia associated with type II diabetes and complicated by pulmonary tuberculosis.

In this paper we describe a successfully treated case of hyperosmolar hyperglycemic non ketotic coma (HHNC). The HHNC was observed in a patient affected by Waldenström's macroglobulinemia, associated with type II diabetes and complicated by pulmonary tuberculosis. Hyperosmolar hyperglycemic nonketotic coma is a clinical condition with a high mortality rate associated with a severe increase in blood viscosity. This increase in blood viscosity justifies several clinical manifestations of the HHNC. We believe that an increase in the blood viscosity produced by the simultaneous presence of the single diseases mentioned above may have encouraged the development of hyperosmolar coma in the case reported.

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