1/5. Nonketotic hyperglycemic hyperosmolar coma. Report of neurosurgical cases with a review of mechanisms and treatment.Seventy-eight critically ill patients who died while on the neurosurgical service were studied retrospectively to establish the prevalence of nonketotic hyperglycemic hyperosmolar coma (NHHC). All the patients had been comatose before death, and all underwent necropsy. Criteria for the diagnosis of NHHC included moderate-to-severe hyperglycemia with glucosuria, absence of significant acetonuria, hyperosmolarity with dehydration, and neurological dysfunction. This study revealed seven cases of unequivocal NHHC (9%), and six of hyperosmolarity but with incomplete records. Five of the seven confirmed cases of NHHC demonstrated no evidence of cerebral edema transtentorial herniation, or brain-stem damage, and showed central nervous system (CNS) lesions compatible with survival. Fatal complications of this syndrome, such as acute renal failure, terminal arrhythmias, and vascular accidents, both cerebral and systemic, were common in this series. The mechanism of coma in NHHC is believed related to shifts of free water from the cerebral extravascular space to the hypertonic intravascular space, with subsequent intracellular dehydration, accumulation of metabolic products of glucose, and brain shrinkage. It is uncertain whether injury to specific areas in the CNS is a predisposing factor to the development of NHHC. Factors documented to be significant in its development include nonspecific stress to primary illnesses, hyperosmolar tube feedings, dehydration, diabetes and mannitol, Dilantin, or steroid administration.- - - - - - - - - - ranking = 1keywords = water (Clic here for more details about this article) |
2/5. Cerebral oedema complicating diabetic ketoacidosis.Four children presented with cerebral oedema secondary to diabetic ketoacidosis, each of whom had a different clinical picture and time of onset of neurological deterioration. No single factor emerged as the cause of the cerebral oedema, but disturbances in brain water balance appeared to be already operative at the time of presentation with ketoacidosis. Irregularities in treatment may exacerbate these disturbances, leading to frank cerebral oedema. diagnosis of this dangerous complication of diabetic ketoacidosis depends on clinical awareness; the diagnosis may be confirmed by CT scan. Management remains empirical.- - - - - - - - - - ranking = 1keywords = water (Clic here for more details about this article) |
3/5. fructose-induced hyperlactemia in hyperosmolar syndromes.Severe hyperlactemia of 8.7, 8.6 and 7.9 mmol/l, respectively, developed in three patients with hyperosmolar syndromes (two hypernatremic, 417 and 415 mosmol/kg H2O; one hyperglycemic 437 mosmol/kg H2O) during rehydration treatment with 5% fructose in water (fructose dosage 0.5 g/kg body wt. per hour). After resolution of the electrolyte disturbances, the infusion of fructose at the same dosage increased the plasma lactate concentration in two of the patients to 4.9 and 4.0 mmol/l, indicating near normalization of hepatic lactate utilization. Thus, in addition to peripheral insulin resistance and decreased muscular glucose utilization, the hyperosmolar state is associated with a reduced tolerance to fructose. This is most likely due to an osmolality-dependent impairment of hepatic gluconeogenesis. In rehydration therapy for hyperosmolar syndromes, fructose-containing infusion solutions should no longer be used.- - - - - - - - - - ranking = 1keywords = water (Clic here for more details about this article) |
4/5. Hyperosmolar coma treated with intravenous sterile water. A study of three cases.Three patients with hyperosmolar coma were treated with intravenous isotonic saline, dextrose, and hypotonic saline solutions. The development of pulmonary edema and increasing hypernatremia precluded the further use of sodium solutions, and the presence of severe hyperglycemia made the further use of dextrose solutions undesirable. To provide further solute-free fluid, intravenous sterile water was administered through a central venous catheter. The hyperosmolar state improved, and all patients survived without biochemical evidence of hemolysis or clinical evidence of cerebral edema.- - - - - - - - - - ranking = 5keywords = water (Clic here for more details about this article) |
5/5. Physiopathology and management of hyperosmolar hyperglycemic nonketotic dehydration.Results of a review of the clinical course of five patients in whom hyperosmotic hyperglycemic nonketotic dehydration developed suggests that a treatment regimen of a high dosage of insulin and free water administration may not be effective. Analysis of the physiopathology of the syndrome points to sodium and water deficits as the principal cause of symptoms. A rapid lowering of the blood glucose level may be detrimental, since this leads to an osmotic gradient between the central nervous system and the intravascular space. Treatment should be directed at the rapid replacement of sodium and water with minimal administration of insulin. This treatment plan allows restoration of membrane potentials by an adequate supply of sodium and maintains osmotic equilibrium by providing diffusable sodium to compensate for the osmotic gradient associated with a gradual lowering of the blood glucose level.- - - - - - - - - - ranking = 3keywords = water (Clic here for more details about this article) |