1/11. Reversible tetraplegia due to polyneuropathy in a diabetic patient with hyperosmolar non-ketotic coma.critical illness polyneuromypathy has not previously been reported as a complication of diabetic coma. We describe a patient with hyperosmolar non-ketotic coma (HONK) complicating gram-negative sepsis in whom persistent coma and profound tetraplegia caused considerable concern. Although, initially, it was feared that the patient had suffered a central neurological complication such as stroke or cerebral oedema, a diagnosis of critical illness motor syndrome (CIMS) was subsequently confirmed neurophysiologically. Profound limb weakness associated with HONK is not necessarily due to a catastrophic cerebral event, rather it may be a result of CIMS, which has an excellent prognosis for full neurological recovery.- - - - - - - - - - ranking = 1keywords = cerebral (Clic here for more details about this article) |
2/11. Bilateral putaminal hemorrhage with cerebral edema in hyperglycemic hyperosmolar syndrome.Bilateral putaminal hemorrhages rarely occur simultaneously in hypertensive patients. The association of intracerebral hemorrhage with cerebral edema (CE) has been rarely reported in diabetic patients. We present a patient with bilateral putaminal hemorrhage (BPH) and CE during the course of hyperglycemic hyperosmolar syndrome (HHS). A 40-year-old man with a history of diabetes mellitus and chronic alcoholism was admitted with acute impaired mentality. His blood pressure was within the normal range on admission. Laboratory results revealed hyperglycemia and severe metabolic acidosis without ketonuria. After aggressive treatment, plasma sugar fell to 217 mg/dl, but brain CT showed BPH and diffuse CE. Our case demonstrated that HHS should be considered as a cause of BPH with CE. Initial brain imaging study may be recommended for patients with diabetic coma.- - - - - - - - - - ranking = 1558.3014304138keywords = cerebral edema, cerebral (Clic here for more details about this article) |
3/11. A new challenge in pediatric obesity: pediatric hyperglycemic hyperosmolar syndrome.OBJECTIVES: To describe four adolescents with hyperglycemic hyperosmolar syndrome, an uncommon presentation of type 2 diabetes in pediatric patients. DESIGN: Case report. SETTING: Two tertiary pediatric intensive care units in university teaching hospitals. patients: Four obese adolescents with hyperglycemic hyperosmolar syndrome associated with type 2 diabetes mellitus. INTERVENTIONS: Isotonic fluid resuscitation and insulin. MEASUREMENTS AND MAIN RESULTS: Two of the four patients died. The first patient died within the first 24 hrs of hyperglycemic hyperosmolar syndrome presumably due to hypovolemic shock. The second patient, who died, developed rhabdomyolysis and multiple-system organ failure after a prolonged intensive care unit stay. The third and fourth patients were discharged from the hospital in good health. None of the patients had cerebral edema on head computed tomography, despite differences in fluid and insulin management. CONCLUSIONS: Pediatric patients with hyperglycemic hyperosmolar syndrome have a high mortality rate and may experience multiple complications such as rhabdomyolysis and hypovolemic shock. Treatment strategies to reduce mortality are unclear and warrant further investigation.- - - - - - - - - - ranking = 311.56028608275keywords = cerebral edema, cerebral (Clic here for more details about this article) |
4/11. Childhood diabetes presenting with hyperosmolar dehydration but without ketoacidosis: a report of three cases.BACKGROUND: diabetic ketoacidosis (DKA) is a common mode of presentation of diabetes mellitus in children, accounting for 26% of new cases. Rarely, children with diabetes may develop other forms of metabolic decompensation associated with hyperglycaemia and hyperosmolality. Hyperglycaemia and hyperosmolality without ketoacidosis has high mortality in adults, although there is no data on mortality in children. case reports: We describe three children who presented to Birmingham Children's Hospital and were initially suspected to have DKA. Each child was severely hyperglycaemic and hyperosmolar but without significant ketosis or acidosis. In two of the three children, the hyperosmolar state was associated with the ingestion of large volumes of high calorie fluids preceding the presentation. These children were exquisitely sensitive to insulin and may be at a significantly higher risk of cerebral oedema in view of their hyperosmolar state. CONCLUSIONS: Hyperosmolar hyperglycaemia is a serious and rare complication at presentation of diabetes in children, and should be distinguished from DKA. These children are at an increased risk of cerebral oedema compared with DKA, and one should have a low threshold for suspicion of this complication.- - - - - - - - - - ranking = 1keywords = cerebral (Clic here for more details about this article) |
5/11. Hyperosmolar non-ketotic hyperglycaemia.Thorough assessment of the patient and good understanding of potential complications enhance patient care and safety. Correction of volume depletion and maintenance of a strict fluid balance chart is essential to avoid complications of congestive cardiac failure, cerebral or pulmonary oedema, renal failure and further dehydration. Careful monitoring of electrolytes and administration of supplements should be undertaken to prevent instability. Regular monitoring of blood glucose levels and careful insulin administration should be undertaken to prevent fluctuations in blood glucose levels. Any possible source of infection should be identified and treated as prescribed. Good basic nursing care for the patient and support and counselling for the patient and his family are essential components of holistic care.- - - - - - - - - - ranking = 0.5keywords = cerebral (Clic here for more details about this article) |
6/11. Diabetic non-ketotic hyperglycaemia presenting as chorea--a case report.We report a patient with hyperosmolar non-ketotic hyperglycaemia who presented with chorea and septic arthritis on his knee. The chorea resolved completely and quickly with correction of the metabolic disturbance, only to return just as quickly when his metabolic disturbance subsequently deteriorated as a result of overwhelming septicaemia, suggesting coexisting cerebral ischaemia, although the basis of focal neurological sign in non-ketotic hyperglycaemia remains controversial.- - - - - - - - - - ranking = 0.5keywords = cerebral (Clic here for more details about this article) |
7/11. Asymptomatic, nonketotic, severe hyperglycemia with hyponatremia.We describe five patients with asymptomatic, nonketotic, severe hyperglycemia (serum glucose concentrations between 45.8 and 92 mmol/L) in the face of renal insufficiency are described. As opposed to most of the previously described patients with hyperglycemic, nonketotic, hyperosmolar coma, our patients were hyponatremic. The lack of symptoms in our patients may be related to the absence of cerebral cellular dehydration. Aggressive treatment of hyperglycemia in such patients is unnecessary. attention to the serum sodium level as well as to the serum glucose concentration will allow recognition of this clinical entity.- - - - - - - - - - ranking = 0.5keywords = cerebral (Clic here for more details about this article) |
8/11. Cerebral edema complicating nonketotic hyperosmolar coma.Cerebral edema as a complication of the therapy of diabetic coma has been described for over 50 years, although modern awareness dates to about 1967. Almost all cases have occurred in patients with diabetic ketoacidosis (DKA). Although a few cases of cerebral edema have been reported in patients with nonketotic hyperosmolar coma (NKHC), these are in general not well documented by either autopsy data of cat scans. Over a period of 9 years, I have encountered 5 patients who developed cerebral edema as a complication of the therapy of NKHC. The initial plasma glucose in these patients was 1,496 /- (SD) 296 mg/dl and plasma osmolality was 382 /- 29 mosm/kg. All had depression of sensorium to at least a stupor (stage I coma or greater). All were treated with intravenous insulin and either 77 or 154 mM NaCl, and plasma glucose fell at a mean rate of 38 mg/dl/h. In all patients, plasma glucose fell below 250 mg/dl (mean of 18 /- 66 mg/dl) and all patients experienced increased depression of sensorium, elevated csf pressure, and brain swelling as diagnosed by cat scanning. Therapy with various combinations of glucose, mannitol and steroids were without effect. In 1 patient, insertion of a subdural intracranial screw lowered intracranial pressure from 24 to 3 cm of H2O. Three of the 5 patients died and 2 remain in a persistent vegetative state, 1 of whom is also quadriplegic.(ABSTRACT TRUNCATED AT 250 WORDS)- - - - - - - - - - ranking = 623.12057216551keywords = cerebral edema, cerebral (Clic here for more details about this article) |
9/11. 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 = 311.56028608275keywords = cerebral edema, cerebral (Clic here for more details about this article) |
10/11. Hyperosmolar non-ketotic coma in diabetic stroke patients.Hyperosmolar non-ketotic coma in diabetes is a life-threatening condition. We describe three patients, aged 59-67 years, who developed hyperosmolar coma during the first ten days after admission for stroke. Common to all three were normal plasma osmolality and slightly elevated plasma creatinine levels on admission, treatment with diuretics, parenteral dextrose administration before and low urinary glucose output during the coma. In the five days preceding the coma, total fluid deficits were 3.8, 6.5 and 9.4 1, respectively. In one patient the rate of glucose delivery had clearly exceeded utilization during adequate insulinization, in another a marked reduction in urinary glucose output preceded extreme hyperglycaemia and coma. Two of the three patients died, both from extensive thrombus formation in cerebral arteries and multiple emboli to the lungs. We conclude that enhanced endogenous glucose production and reduced renal clearance of glucose may contribute to precipitate hyperosmolar non-ketotic coma. A close monitoring of fluid and dextrose administration seems mandatory in diabetic stroke patients, in particular if renal function is impaired or if diuretics are given. insulin treatment should be considered in all diabetic patients during the first days after a stroke.- - - - - - - - - - ranking = 0.5keywords = cerebral (Clic here for more details about this article) |
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