1/21. Marked hyperthermia as a manifestation of hypoglycemia in long-standing diabetes mellitus.Hyperthermia has recently been recognized as a manifestation of hypoglycemia. We describe two episodes of hypoglycemia associated with nausea, vomiting, chills, and impaired consciousness which were followed by marked hyperthermia. We suggest that the hyperthermia may result from excessive reaction to preceding hypothermia caused by the hypoglycemia. We would like to alert the clinician to the possibility of a previous, severe hypoglycemic episode in any diabetic patient with hyperthermia and coma.- - - - - - - - - - ranking = 1keywords = consciousness (Clic here for more details about this article) |
2/21. Repeated hypoglycemia and cognitive decline. A case report.OBJECTIVE: diabetes mellitus has a high incidence in general population and goes by high morbidity by specific micro vascular pathology in the retina, renal glomerul and peripheral nerves. In type 1 DM, intensive therapy can prevent or delay the development of long-term complications associated with DM but hypoglycaemia especially severe hypoglycaemia defined, as a low blood glucose resulting in stupor, seizure, or unconsciousness that precludes self-treatment is a serious threat. Hypoglycaemia that may preferentially harm neurons in the medial temporal region, specifically the hippocampus, is a potential danger for the brain cognitive function which several studies failed to detect any significant effects, whereas others indicated an influence on it. A young diabetic case presented here with severe cognitive defect. Great number of severe hypoglycaemic or hyperglycaemic attacks and convulsion episodes were described in his medical history. RESULTS and CONCLUSION: Neuroradiologic findings on CT and MRI, pointed that global cerebral atrophy that is incompatible with his age. brain perfusion studies (SPECT, (99m)Tc-labeled HMPAO) also showed that there were severe perfusion defects at superior temporal region and less perfusion defects at gyrus cingulum in frontal region. These regions are related with memory processing. Severe cognitive defect in this patient seems to be closely related these changes and no another reason was found to explain except the repeated severe hypoglycaemic episodes.- - - - - - - - - - ranking = 370.81731868924keywords = unconsciousness, consciousness (Clic here for more details about this article) |
3/21. Profound hypokalemia in diabetic ketoacidosis: a therapeutic challenge.OBJECTIVE: To describe profound hypokalemia in a comatose patient with diabetic ketoacidosis. methods: We present a case report, review the mechanisms for the occurrence of hypokalemia in diabetic ketoacidosis, and discuss its management in the setting of hyperglycemia and hyperosmolality. RESULTS: A 22-year-old woman with a history of type 1 diabetes mellitus was admitted in a comatose state. Laboratory tests revealed a blood glucose level of 747 mg/dL, serum potassium of 1.9 mEq/L, pH of 6.8, and calculated effective serum osmolality of 320 mOsm/kg. She was intubated and resuscitated with intravenously administered fluids. Intravenous administration of vasopressors was necessary for stabilization of the blood pressure. Intravenous infusion of insulin was initiated to control the hyperglycemia, and repletion of total body potassium stores was undertaken. A total of 660 mEq of potassium was administered intravenously during the first 12.5 hours. Despite such aggressive initial repletion of potassium, the patient required 40 to 80 mEq of potassium daily for the next 8 days to increase the serum potassium concentration to normal. CONCLUSION: Profound hypokalemia, an uncommon initial manifestation in patients with diabetic ketoacidosis, is indicative of severe total body potassium deficiency. Under such circumstances, aggressive potassium repletion in a comatose patient must be undertaken during correction of other metabolic abnormalities, including hyperglycemia and hyperosmolality. Intravenously administered insulin should be withheld until the serum potassium concentration is (3)3.3 mEq/L.- - - - - - - - - - ranking = 0.088873449022486keywords = state (Clic here for more details about this article) |
4/21. Rapid onset of glycogen storage hepatomegaly in a type-2 diabetic patient after a massive dose of long-acting insulin and large doses of glucose.We present a case of rapid onset of glycogen storage hepatomegaly, caused by a massive dose of long-acting insulin and large doses of glucose, in a type-2 diabetic patient. A 41-year-old man was admitted to our hospital because of hypoglycemia and unconsciousness following subcutaneous administration of 180 units of insulin glargine in a suicide attempt. Despite continuous hypercaloric infusion with additional intravenous glucose injections, hypoglycemia persisted for 36 hours. Although the hepatic function was normal and no hepatomegaly was detected on admission, the liver function tests became abnormal and hepatomegaly was detected on hospitalization day 3. Plain abdominal computed tomography (CT) scanning confirmed liver enlargement, with hepatic CT attenuation markedly elevated at 83.7 HU. Liver biopsy revealed hepatocytic glycogen deposition with edematous degeneration. Based on these findings, the diagnosis was made as rapid onset glycogen storage hepatomegaly caused by administration of a massive dose of long-acting insulin and supplementation with large doses of glucose. With improved glycemic control, the liver function improved, the CT findings of hepatomegaly improved, and the hepatic CT attenuation decreased. Repeat liver biopsy also confirmed almost complete disappearance of glycogen deposits. When hepatic dysfunction or hepatomegaly is detected during treatment with insulin, the possibility of hepatic glycogen deposition should be considered. CT scanning and liver biopsy were useful in diagnosing this case.- - - - - - - - - - ranking = 370.81731868924keywords = unconsciousness, consciousness (Clic here for more details about this article) |
5/21. Glucose metabolism in a patient with insulinoma complicated by hyperosmolar non-ketotic state.A case of a patient with organic hyperinsulinism complicated by the development of hyperosmolar state is described. The hyperosmolar state was induced by vomiting and dehydration during an acute urinary tract infection. Impairment of glucose metabolism was confirmed by the finding of reduced tissue sensitivity to insulin during a euglycaemic clamp.- - - - - - - - - - ranking = 0.53324069413492keywords = state (Clic here for more details about this article) |
6/21. Lateral pontine and extrapontine myelinolysis associated with hypernatremia and hyperglycemia.Efforts to understand and prevent pontine and extrapontine myelinolysis have focused on the correction of hyponatremia, but controversy persists. We report a woman who presented in hyperosmolar diabetic coma with hypernatremia (169 mEq/l) and hyperglycemia (954 mg/dl). plasma sodium rapidly increased to 188 mEq/l before gradually returning to normal. She remained obtunded and died 21 days later. autopsy showed widespread, symmetrical demyelination involving the subcortical white matter, corpus callosum, anterior commissure, extreme, external, and internal capsules, fornix, thalamus, cerebellum, and lateral pons. The central pons and lateral geniculate nuclei were uninvolved. This case illustrates that lateral pontine and extrapontine myelinolysis can be associated with hypernatremia and hyperosmolality. In both hypo- and hypernatremic states, the significant event may be an increase in serum sodium or serum osmolality of sufficient rapidity and magnitude.- - - - - - - - - - ranking = 0.088873449022486keywords = state (Clic here for more details about this article) |
7/21. cerebrospinal fluid lactate in patients with diabetes mellitus and hypoglycaemic coma.cerebrospinal fluid (CSF) lactate and pyruvate concentrations were determined in 20 patients with diabetes mellitus but without disturbance of consciousness and five who recovered from hypoglycaemic coma. CSF lactate was slightly but significantly higher in diabetes mellitus (1.78, SEM 0.04 m mol/l) than that in 15 control subjects (1.40, SEM 0.05 m mol/l). In those who recovered from hypoglycaemic coma, CSF lactate was markedly elevated to 2.45-4.43 m mol/l. CSF glucose concentrations, however, were substantially the same between treated hypoglycaemic and diabetes mellitus groups. These findings indicate that CSF lactate levels increase with glycaemic levels in diabetes mellitus owing to enhanced glucose influx into glycolytic pathway of the brain, and also increases in treated hypoglycaemic coma probably due to mitochondrial dysfunction or damage.- - - - - - - - - - ranking = 1keywords = consciousness (Clic here for more details about this article) |
8/21. 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)- - - - - - - - - - ranking = 0.17774689804497keywords = state (Clic here for more details about this article) |
9/21. diabetes mellitus in kearns-sayre syndrome.A 20-year-old woman with kearns-sayre syndrome (KSS) suddenly experienced two episodes of diabetic coma. She was studied to determine whether diabetes mellitus (DM) resulted from insulin resistance or from an insulin secretion abnormality, using the euglycemic glucose clamp technique and the glucagon tolerance test. She had a deficiency of insulin secretion from beta cells. It is important to recognize in practice the onset of DM in patients with mitochondrial myopathy. We would suggest that a genetic linkage or mitochondrial dysfunction may be responsible for the association of both disease states.- - - - - - - - - - ranking = 0.088873449022486keywords = state (Clic here for more details about this article) |
10/21. 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 = 0.088873449022486keywords = state (Clic here for more details about this article) |
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