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PubMed1978

[Differences in plasma aminograms in hepatic and diabetic coma].

In hepatic coma as well as diabetic coma severe disturbances occur in the amino acid metabolism. The defect lies in completely different levels which result two different plasma aminograms (PAG). In 24 patients with hepatic encephalopathy stage III-IV (7 patients with acute and 17 with chronic liver failure) the PAG were evaluated. The determination of the plasma amino acids (PAA) was carried out on Multichrom B (Beckmann, Munich). In hepatic coma high concentrations of Met, Tyr, Ala, Lys and Arg are found. The deviations of PAA from normal controls show between acute and chronic hepatic failure no qualitative but only quantitative differences. In diabetic coma the three branches chain AA (Val, Leu and Ile) were elevated upon 3--5 times of normal. Near normal concentrations are found for the AA Thr, Ser, Gly, Ala, Met and the aromatic AA (Phe and Tyr). The quotient between the branched chain and aromatic AA lies for hepatic coma at a mean of 1.18 and by diabetic coma at 7.18 (p less than 0.001). In hepatic coma a correlation exists between the level of the AA-quotient improvement and the decrease with a deterioriation of the metabolic encephalopathy. The high level of the AA-quotient in the patients of diabetic "coma" gives therefore a good explanation for the rare unconscious state of these patients.

Adult↗
PubMed1977

[Hyperosmolar nonketotic diabetic coma in children].

Nonketotic hyperosmolar diabetic coma is a rare manifestation of juvenile diabetes, in contrast to adult onset diabetes. To date only 20 cases have been published, the majority of them infants and toddlers. This type of diabetic coma is seen with unusual frequency in children with Down's syndrome and psychomotor retardation. The clinical picture is characterised by severe dehydration, hyperglycemia with often extremely high blood sugar levels, hyperosmolarity and glucosuria without ketonuria. Mortality in children has been high (24%). This paper reports the case of a 14-month-old girl with Down's syndrome. Clinical and therapeutic as well as pathogenetic aspects are discussed.

Diabetic Coma↗
PubMed2003

Accumulation of triglycerides in the proximal tubule of the kidney in diabetic coma.

AIMS: The present study was initiated by a very recent histochemical observation of lipid accumulation in the renal cortex of a woman who died in a diabetic coma. Two older reports of lipid accumulation in the kidneys of patients who died, most likely in a state of non-regulated diabetes, supported this observation. We have examined whether lipid accumulation in the renal cortex is characteristic of diabetic coma and, if so, which type of lipid accumulates. METHODS: Three groups were studied. Ten subjects who died in a diabetic coma, eight diabetics who died of known causes unrelated to diabetes, and seven normal control subjects without any diagnosed diabetes who died of known causes. All were subjected to histological examination for lipid accumulation in the renal cortex. Detailed analysis of cortex lipids was performed for two of the subjects who died in a diabetic coma and all diabetic controls as well as non-diabetic control subjects. RESULTS: All subjects who died in a diabetic coma showed vacuolar lesions staining strongly for lipid in the proximal tubules. Neither normal controls nor non-coma diabetics showed these lesions. Compared with normal controls, renal cortex lipid was about tripled in the two analysed diabetic coma subjects due to 60-100-fold increases of triglycerides. The non-coma diabetics did not differ from the other controls with respect to triglycerides or other types of lipid, except that cholesteryl esters were elevated, though still a quantitatively minor component. CONCLUSION: Our findings strongly indicate that vacuolar lesions in the proximal tubules are characteristic of diabetic coma and that they are caused by accumulated triglycerides. Therefore, histological examination of renal cortex using a lipid stain may be a useful forensic tool in establishing diabetic coma as the cause of death.

Adult↗
PubMed1993

[Diabetic coma and bases of proper treatment].

Hyperglycaemic, hyperosmolar coma developing in diabetes mellitus-with or without ketoacidosis-is a perilous metabolic catastrophe, preserving its clinical importance even nowadays. The features of the two basic forms of diabetic coma, the development and characteristics of clinical symptoms and laboratory alterations caused by absolute or relative lack of insulin are reported by the author. The importance of early diagnosis and up-to-date intensive treatment is emphasized, regarding the need of decreasing of the still now considerable mortality rate. Fundamental principles of the therapeutic interventions are the following: improvement of the microcirculation through appropriate compensation of fluid and elektrolytes, intravenous or intramuscular administration of low-dose insulin, prevention of hypokalemic condition, and correction of acidosis under pH 7,1 value. Moreover, the well-planned supportive treatment is also essential: prevention of thromboembolism, averting the occasional development of shock caused usually by infections, and prophylaxis of the often fatal cerebral oedema. The estimation and follow-up of osmolality and the prevention of rapid changes in serum glucose and electrolyte levels are of particular importance in every cases. Careful observation of the patients regarding the cardiorespiratory and renal functions is of great significance in both (first and second) phases of the treatment. Improvement of patients' education, controlled care of diabetic patients, reduction of the number of recidive cases and increasing knowledge regarding diabetes among the general practitioners are determined by the author as the future possibilities for the prevention of this severe metabolic disorder.

Adolescent↗
PubMed1986

Clinical features of hyperosmolar hyperglycemic nonketotic diabetic coma associated with cardiac operations.

Hyperosmolar hyperglycemic nonketotic diabetic coma after cardiac operations was reviewed in a total of 12 patients from the literature and from my experience in an attempt to determine the clinical features of this condition. Among the unique features of this disease were the following: The mortality is high (42%). The morbidity and mortality are higher in patients with no previous history of diabetes mellitus (67% and 50%) than in those with such a history (33% and 25%). Polyuria is usually a heralding symptom. There is an average time lag of 6 days between the onset of polyuria and the established diagnosis of hyperosmolar hyperglycemic nonketotic diabetic coma. The time lag in patients who died was 7.5 +/- 0.8 days (mean +/- standard error of the mean), significantly longer than in survivors (4.5 +/- 0.8 days). Polyuria usually emerges after the stormy immediate postoperative days have passed (on postoperative day 5.3 on the average). Polyuria is generally regarded as a favorable sign not suggestive of complicating hyperosmolar hyperglycemic nonketotic diabetic coma. Therapies known to precipitate this disorder are continued even after development of polyuria. Gastrointestinal bleeding can be a precipitating factor. Hyperalimentation or elemental diet may cause dehydration and trigger hyperosmolar hyperglycemic nonketotic diabetic coma. A high or rising serum sodium concentration and/or blood urea nitrogen level with polyuria may be a warning sign of this complication. Too hasty correction of the hyperosmolar state can be dangerous. Pulmonary dysfunction may be involved in the symptoms of hyperosmolar hyperglycemic nonketotic diabetic coma.

Adult↗