Cases reported "Diabetic Coma"

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1/24. Reversal of foetal hydrops and foetal tachyarrhythmia associated with maternal diabetic coma.

    Foetal hydrops is always a challenge for the clinician. We report a case of tachycardia associated with hydrops and hydramnios in a pregnancy complicated with diabetic coma at 28 weeks gestation. Normal foetal heart rate was recorded immediately after correction of maternal acidotic status and hydrops eventually disappeared. The woman was delivered at 32 weeks and the baby had an uncomplicated postnatal course. We hypothesise that maternal ketoacidosis has been the precipitating factor of tachycardia and congestive heart failure and that this case is conceptually similar to the "late death" phenomenon, reported in cases of poorly controlled maternal diabetes.
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2/24. lipids in the proximal tubules of the kidney in diabetic coma.

    Vacuolization of the renal tubular epithelial cells (the Armanni-Ebstein lesion) associated with diabetic hyperglycemia is usually regarded as an accumulation of glycogen. In a case of death of diabetic coma, the vacuoles were stained strongly for lipids. This observation may have both clinical and therapeutic consequences, and may increase our knowledge of the metabolism in diabetes.
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3/24. Recurrent hyperosmolar nonketotic episodes in a young diabetic.

    A 15-month-old girl was successfully treated for substantial hyperosmolarity in the absence of ketosis at the onset of permanent insulin-requiring diabetes mellitus. hypotonic solutions containing small amounts of glucose and subcutaneous administration of low doses of insulin were empolyed. Potassium was added to the hydrating solutions during the second hour of treatment. In the next three months, two recurrences of this syndrome were verified and successfully treated in a similar manner.
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4/24. 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.
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5/24. Postoperative hypoglycaemic coma associated with chlorpropamide.

    A 72-year-old male being treated with chlorpropamide for diabetes mellitus had an emergency operation for a perforated gastric ulcer. Hypoglycaemic coma occurred after the operation.
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6/24. 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.
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7/24. 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.
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8/24. Sudden and unexpected deaths after the acute onset of diabetes mellitus.

    Four cases of sudden and unexpected death caused by the acute onset of diabetes mellitus are reported. Three are examples of acute juvenile diabetes while the fourth demonstrated the aketotic form of diabetic coma. Such instances can present a diagnostic problem to the forensic pathologist. The usefulness of vitreous humor glucose analysis to diagnose such a condition is stressed.
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9/24. Interpreting survival rates for the treatment of decompensated diabetes: are we saving too many lives?

    Discussion of the case of a patient admitted to hospital with decompensated diabetes revealed a conflict in attitudes to resuscitation of the patient from that disorder and from cardiac arrest. A survey was sent to 200 diabetologists and 200 cardiologists in the United Kingdom, asking about their management of diabetes and their therapeutic approaches to cardiac arrest for 3 elderly patients admitted with severe decompensated diabetes. The response rate was poor (27%) but the answers showed that all 3 patients were more likely to be resuscitated from decompensated diabetes than from cardiac arrest. Possible reasons for a different approach to the two conditions are discussed, and suggestions are put forward for a greater involvement by patients in decisions about future resuscitation.
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10/24. 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.
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