[Diabetic coma. Pathophysiology and treatment of diabetic coma].
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Diabetic Coma↗
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Hypophosphatemia associated coma following treatment of diabetic coma.
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Aged↗
[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↗
[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↗
[Diabetic coma--an unnecessary death].
Diabetic ketoacidosis remains a significant cause of death in cases of insulin-dependent diabetes mellitus (IDDM). Among patients hospitalised for diabetic ketoacidosis, the death rate is 5-10 per cent, cardiovascular disease, infection, and ARDS (adult respiratory distress syndrome) being major contributory factors, whereas the degree of acidosis does not differ from that among survivors. Ketoacidosis is a major determinant of the two-fold higher mortality among the youngest age-groups of IDDM patients. The age-specific incidence of ketoacidosis among patients under 20 years of age is several time higher than that among patients over 50. Intensified insulin treatment, using multiple injections or insulin pumps, probably results in an increased risk of insulin deficiency owing to the smaller insulin depots. Thus, there is a need of intensified testing for ketonuria and improved education of patients, physicians and other health care personnel, in order to promote the prevention or rapid, effective treatment of diabetic ketoacidosis.
Adolescent↗
Treatment of diabetic coma with low-dose injections of insulin.
Twenty-one patients in severe diabetic coma were treated with small doses of insulin at a rate of 4.1 units per hour (total dose about 100 units per 24 hours). Using single doses of 4 to 10 units by the intravenous or intramuscular routes the fall of blood glucose was steady in all cases. In the treatment of diabetic coma this regimen of insulin administration has proved simple, safe and effective since 1946. Main dangers during recompensation of diabetic coma are: hypovolaemia with oliguria -- anuria, dysequilibrium syndrome with cerebral edema and hypokalaemia. Therefore early intensive and adequate intravenous fluid and electrolyte replacement is the most important part of treatment. Most of the cases in this study were undiagnosed diabetics (14) and elderly patients (9). Three patients older than 65 years and a 56-year old diabetic died. In this context the most important aspects of treatment to avoid death are: prevention of diabetic coma and adequate fluid and electrolyte replacement especially in geriatric patients.
Adolescent↗
[Hyperosmotic diabetic coma as a 1st sign of diabetes].
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Age Factors↗
Hyperglycemia and diabetic coma: possible relationship to diuretic-propranolol therapy.
Two patients developed diabetic coma when taking a combination of a thiazide diuretic and propranolol. On subsequent follow-up one patient is taking no insulin and has been maintained on hydrochlorothiazide; the other patient required insulin on two occasions when challenged with a propranolol-thiazide combination, but not when the thiazide was discontinued or replaced with furosemide. These reports suggest the possibility that the risk of developing hyperglycemia and diabetic coma with this combination may be greater than when taking diuretics alone. The mechanism is probably multifactorial.
Diabetic Coma↗
[Diabetic ketoacidosis and hyperosmolar diabetic coma in childhood. Low-dose continuous intravenous infusion of insulin (author's transl)].
Continuous intravenous infusion of low doses of insulin has been successfully used since 1972 in the treatment of "diabetic coma". The achieved levels of plasma insulin satisfy the transport of glucose and the inhibition of lipolysis. We are to report upon 8 children (mean age: 8.5 years), 6 with diabetic ketoacidosis and 2 with hyperosmolar diabetic coma. Blood sugar levels of 300 mg/dl or less were reached after averagely 8 hours of therapy and an average consumption of 0.8 U insulin/kg. Sodium and potassium levels, osmolality and acid base parameters for the first 24 hours are described. Low-dose continuous intravenous insulin infusion was effective, simple and safe in all cases. The presently recommended dosage of 0.1 insulin/kg x hour is to be used flexibly (range: 0.05--0.2 U/kg x hour). The administration of bicarbonate should be cautiously used for patients with severe acidosis. Infusion of hypotonic solutions as part of the treatment of the hyperosmolar diabetic coma can be dangerous. A new therapeutic regime based on our results is proposed.
Adolescent↗
[Diabetic coma as a task for intensive therapy].
On the basis of 763 cases with diabetic coma from 1960 to 1973 is referred to the advantages of the foundation of a coma ward as department of intensive observation. It is reported on some successful changes of therapy in recent years. The introduction of methods of intensive therapy has led to a significant decrease of lethality. A sufficient administration of potassium (not less than 200 mval/die) and the prevention of a cerebral oedema are actual demands for the improvement of the prognosis of diabetic coma.
Berlin↗
[Hyperglycemic, hyperosmolar nonketotic diabetic coma in the pediatric age].
A case of non-ketotic hyperglycaemic-hyperosmolar diabetic coma in a 8 yr. old boy after a severe mental trauma is reported. This joins the 18 similar cases of paediatric age published up to now. On the basis of the results of virological and immunological investigations, insulinogenic function and psychodiagnosis, the diagnosis, aetiopathogenesis and therapy of this unusual event are discussed. The desirability of measuring plasma osmolarity in children diabetic coma is stressed.
Age Factors↗
Advantage in management of diabetic coma by intensive care.
A brief review of some therapy results in 763 episodes of diabetic coma from 1960 to 1973 reveals a significant decrease in lethality after institution of an intensive care unit. Present aspects of management are: intensification of shock therapy, potassium substitution and treatment of cerebral edema. The possibly dangerous role of hypotonic solutions is discussed. The lowering of the as yet high lethality of diabetic coma is an urgent necessity.
Berlin↗
[Blood lactate semiautomatic estimation during acidotic diabetic coma (author's transl)].
Blood lactate levels were determined by Lactate Analyzer 640 Kontron during the course of 7 cases of hyperglycemic hyperosmolar diabetic coma, with severe acidosis and more or less marked ketosis. In 5 cases lactate values were found in normal range; slight increases around 2 mmol/l were rapidly corrected following standard coma treatment. One of these cases presented with extreme acidosis and relatively mild hyperglycemia, with differential problems in regard to lactic acidosis. In 2 cases, the former with alcoholic cirrhosis, the latter with myocardial infarction, blood lactate was markedly increased; in the second case, full clinical recovery was accompanied by normalization of lactate levels. A previous biguanide treatment could be ruled out as a cause of lactic acidosis. Thus the association of lactic acidosis and diabetic ketoacidosis seems to be unusual in the absence of concurrent serious conditions. The semiautomatic determination of blood lactate, because of its remarkable prognostic importance, should be included among the routine procedures for the emergency treatment of diabetic coma.
Adult↗
Treatment of diabetic coma with small intravenous insulin boluses.
The clinical efficacy of small intravenous boluses of insulin in treating diabetic decompensation was tested in 23 patients presenting in either a ketoacidotic or a nonketotic diabetic coma. In addition to the usual ionic and fluid replacement, the patients received hourly intravenous injections of insulin 5 IU. This dose lowered blood glucose levels in all but two patients. In the patients who responded the percentage decrease in glycaemia was similar whatever the initial glucose concentration and averaged (+/-SE of mean) 50+/-3% in five hours. Close monitoring of insulin and glucose concentrations after intravenous insulin in three patients showed that despite the short half life of insulin the effect of the intravenous bolus lasted for about 60 minutes. The overall clinical effectiveness of this type of treatment is comparable to that of the other low-dose regimens. Owing to its simplicity, this technique of insulin administration seems most suitable for the routine treatment of diabetic coma.
Blood Glucose↗
Peritoneal dialysis in hypernatraemic, ketoacidotic diabetic coma.
Hypertonic dehydration in a 13-year-old boy with ketoacidotic diabetic coma has been treated successfully with peritoneal dialysis and isotonic fluids. Modes of treatment with either hypotonic or isotonic fluids are discussed, as is the feasibility of peritoneal dialysis. We recommend isotonic solutions composed of equal parts of 5.5% glucose and 0.9% sodium chloride combined with peritoneal dialysis in order to secure a relatively slow correction of the hypertonic state.
Adolescent↗
Neuroleptic malignant syndrome presenting as hyperosmolar non-ketotic diabetic coma.
A 50-year-old man presented with hyperosmolar non-ketotic diabetic coma associated with the neuroleptic malignant syndrome (NMS) after intramuscular treatment with haloperidol. It is suggested that NMS may occur as a complication of uncontrolled diabetes mellitus with dehydration. Conversely, NMS might precipitate diabetic coma in patients with previously well controlled blood glucose.
Body Temperature Regulation↗
Modern methods of management of diabetic coma and precoma.
Recent understanding of mechanisms concerned in the production of the diabetic comas has improved, and this has led to important changes in general concepts and practice of management. We attempt to outline these and to present a didactic scheme for therapy, as in general use at Groote Schuur Hospital.
Bicarbonates↗
[Hyperosmolar non-ketoacidotic diabetic coma].
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Diabetic Coma↗