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Diabetic coma without ketoacidosis.
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Hyperosmolar non-ketonic diabetic coma.
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[Hyperosmolar non-ketoacidotic diabetic coma].
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[Genesis, diagnosis and treatment of diabetic coma].
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[Hyperosmotic, anacidotic diabetic coma].
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[Atypical diabetic coma].
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[Hyperosmolar diabetic coma without ketoacidosis in purulent meningitis (author's transl)].
Hyperosmolar diabetic coma without ketoacidosis was observed as a complication of purulent meningitis in 3 patients. Diagnostic difficulties arise due to slow onset of hyperosmolality and misinterpretation of organic cerebral fits and the increasing disturbance of consciousness. Therapy is complicated by the necessity of treatment with anticonvulsants and sodium containing antibiotics which affect sugar and sodium balance. Abrupt lowering of serum osmolality leads to further increase of cerebral oedema. Slow normalisation of blood sugar and sodium values over several days may lead to satisfactory outcome despite unconsciousness of long duration. These complications could be overcome with high doses of insulin and large amounts of hypotonic infusion in two patients, one female succumbed.
[Ten rules to govern the administration of insulin in diabetic coma].
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Insulin treatment of diabetic coma.
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[The ECG in the diabetic coma].
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[Medical resuscitation applied to diabetic coma].
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Serum free insulin concentrations during the treatment of diabetic coma and precoma with low dose intramuscular insulin.
Fifty patients in diabetic coma or precoma, 33 of whom had previously received insulin and had circulating insulin antibodies, were studied during treatment with a low-dose intramuscular insulin regime. In the presence of insulin antibodies, serum free insulin was separated from bound insulin by steady-state gel filtration. The initial mean serum free insulin concentration in the group of patients without insulin antibodies was 9 mU/1, 1 to 2 hours after intramuscular therapy it had risen to 22 mU/1, and after 7 to 8 hours to 73 mU/1. The corresponding concentrations for the group with insulin antibodies were 13, 23 and 74 mU/1. No relationship was found between the concentrations of serum free insulin attained and the age of the patients, their initial degree of acidosis, dehydration, and systolic blood pressure, the insulin antibody characteristics of their sera, nor the rate of decline of the blood glucose.
Hyperosmolar non-ketotic diabetic coma -- less sodium in therapy?
Eighteen patients with hyperosmolar non-ketotic diabetic coma were studied retrospectively to identify factors affecting prognosis and to review treatment. This condition affected older women two-thirds of whom were unrecognised diabetics. Eight (44%) died. Mortality correlated with age above 60, uraemia and hyperosmolarity, but not with the degree or rate of fall of hyperglycaemia. Hyperglycaemia responded to rehydration and insulin, but in all patients serum osmolarity remained high for several days. In 14 patients (78%) the serum sodium concentration initially increased and in four (22%) serum osmolarity increased. This persistence or worsening of the hyperosmolar state can be avoided without the risk of cerebral oedema by replacing the fluid and electrolyte deficits over 48 hours and using 5% dextrose for the water deficit.
The role of the ketone bodies in the etiology of diabetic coma.
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[Insulin lipodystrophy and diabetic coma].
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[Early signs of diabetic coma].
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