Cases reported "diabetic coma"

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1/66. mucormycosis, a threatening opportunistic mycotic infection.

    mucormycosis is a rare and invasive mycotic opportunistic infection, occurring mostly in predisposed patients, mainly diabetics and immunocompromised individuals. The evolution of this fungal infection is frequently fatal unless aggressive treatment is started, or predisposing factors are handled. Our first patient was a known diabetic who had ketoacidotic coma at admission, complicated with pulmonary mucormycosis, and needed surgical resection followed by antimycotic therapy. The second patient did not survive his severe aplastic anemia (with neutropenia) and hemochromatosis (treated with desferrioxamine), complicated with a systemic rhizopus infection, despite treatment with amphotericin b and granulocyte-colony-stimulating factors. ( info)

2/66. Bilateral basal ganglion haemorrhage in diabetic ketoacidotic coma: case report.

    We report bilateral oedema and haemorrhagic transformation in the basal ganglia of a 59-year old woman with severe diabetic ketoacidosis. Lack of cerebral vascular autoregulation, followed by blood-brain barrier disruption due to the so-called breakthrough mechanism is presumed to be the cause. ( info)

3/66. 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. ( info)

4/66. 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. ( info)

5/66. 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. ( info)

6/66. 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. ( info)

7/66. 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. ( info)

8/66. Possible functional regression of insulinoma with prolonged octreotide.

    A 75 year old woman was treated for over three years with the somatostatin analogue, octreotide for an insulinoma. She had presented in a hypoglycaemic coma. c-peptide and insulin concentrations were both raised and an area of increased vascularity within the pancreas was shown by angiography. No lesion was found at laparotomy and no resection was performed. After over three years of octreotide treatment it was withdrawn for a week. Her insulin and c-peptide concentrations were greatly reduced at this time and remained so. ( info)

9/66. Acute rhino-orbito-cerebral mucormycosis.

    Report of the typical clinical course and pathological findings in acute rhino-orbito-cerebral mucormycosis following diabetic coma. Invasion of orbital nerves by the fungus with neural and perineural changes may contribute to the neuroophthalmological symptoms in this disease besides the predilection for blood vessels with consequent thrombosis. ( info)

10/66. 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. ( info)
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