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At least 55 records · Page 3Linked to original sources
PubMed1992

[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↗
PubMed1976

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↗
PubMed1987

Hyperosmolar nonketotic diabetic coma: diagnosis and management.

Hyperosmolar nonketotic diabetic coma (HHNC) is a syndrome of acute decompensation of diabetes mellitus, occurring mainly in the elderly and characterized by marked hyperglycemia, hyperosmolarity, severe dehydration, occasional neurological signs, obtunded sensorium, and absence of ketonemia or acidosis. The mortality is high. Early aggressive therapy with large amounts of normal or half normal saline, insulin, and potassium is of prime importance. Since associated diseases cause most fatalities the importance of managing these problems effectively cannot be overemphasized. Complications of therapy can be congestive heart failure secondary to excessive fluid administration, hypoglycemia if too much insulin is given, and hypokalemia if potassium is inadequately replaced.

Aged↗
PubMed1994

Armanni-Ebstein lesions of the kidney: diagnostic of death in diabetic coma?

In the period from January 1986 through April 1993, 47 cases with diabetes mellitus were autopsied at the Institute of Forensic Medicine, Odense University. In 26 cases, the diabetes had been treated with insulin, in 21 cases with oral medication or diet only. In eight insulin-dependent cases, tubular vacuolation was found in the kidneys, the so-called Armanni-Ebstein lesions. The circumstances of death and postmortem analyses of blood, urine and/or vitreous humor supported a presumed diabetic coma as the cause of death in these eight cases. Of the remaining 39 cases, six were too putrefied for histologic examination. In the remaining 33 cases and in a series of 20 non-diabetics, the cause of death was ascertained as illness (other than diabetes), traffic accidents, drowning or intoxication. In none of these cases was a diabetic coma suspected, and none of these cases showed tubular vacuolation in the kidneys. The authors conclude that tubular vacuolation of the kidneys strongly indicates death in diabetic coma.

Adult↗
PubMed1996

Fulminant malignant hyperthermia associated with ketoacidotic diabetic coma.

Malignant hyperthermia (MH) in humans is usually triggered by volatile anaesthetics and depolarizing muscle relaxants. However, other factors or drugs (e.g. cresol) are thought to induce MH. We report a case of fulminant MH associated with a ketoacidotic diabetic coma. After therapy for diabetic coma with insulin (containing the preservative cresol) and electrolyte solutions was started, the patient complained of increasing myalgia, developed a high fever and respiratory and metabolic acidosis and lost consciousness. MH was treated immediately with dantrolene; the patient recovered within 14 days. Five months later the patient was diagnosed as MH-susceptible by the in vitro caffeine and halothane contracture test. This case supports the assessment that MH and diabetes are associated diseases and that cresol could possibly trigger MH. Furthermore, therapy with dantrolene has been demonstrated to be beneficial in the treatment of MH associated with diabetic coma.

Adult↗
PubMedDate not supplied

[Biochemical analysis of the vitreous body of the eye in post-mortem diagnosis of diabetic coma].

The biochemical test of the vitreous body (VB) may be used in post-mortem diagnosis of diabetes mellitus and diabetic coma. Concentrations of glucose, lactate, keton bodies in the VB of the eye do not depend on duration of post-mortem period. Methods of diagnosis of hyperglycemic, hypoglycemic and ketoacidotic comas in the postmortem period are proposed. VB glucose over 17 mmol/l is a specific marker indicating death due to diabetic coma with hyperglycemia. Blood lactate under 16 mmol/l and glucose absence in the VB specifically mark death of hypoglycemic coma. In death of diabetic coma with ketoacidosis, a sharp rise in the level of VB ketonic bodies was observed.

Biochemistry↗
PubMed2004

[Diabetic coma and hypoglycemia in children. What to do when in an emergency].

With a few very rare exceptions, hypoglycemia and diabetic coma almost always occur in patients with diabetes mellitus, and are among the most common emergencies in children. For the emergency physician, it is important, on the basis of a specific history-taking and information from, for example, family members, supplemented by a clinical examination done in the light of knowledge of the typical symptoms of each of the entities, to determine whether hypoglycemia or diabetic coma is presenting. The most important technical examination is the measurement of blood glucose. In the event of hypoglycemia, the first therapeutic measure is the administration of sugar--in the case of a comatose patient via a venous line. The s.c. or i.m. administration of glucagon to achieve short-term improvement might be considered. In the event of a diabetic coma, abundant electrolyte solution is initially needed, followed by i.v. insulin. Referral to hospital is mandatory.

Age Factors↗
PubMed1992

Treatment of diabetic ketoacidosis and non-ketotic hyperosmolar diabetic coma.

Although mortality of diabetic ketoacidosis (KA) has decreased during the past 20 yr to 1-2%, hyperosmolar non-ketotic coma (HNC) is still lethal in 20-30% of cases due to severe underlying conditions or to complications. The most frequent causes of death are infections and thromboembolic disorders. The strategies of initial treatment of KA and HNC are similar; in KA, insulin, fluid and electrolyte replacement have first priority. In HNC, rehydration and electrolyte administration are of primary importance. It is now generally recognized that insulin therapy is best performed using low doses (4-8 units/h); after institution of insulin treatment and rehydration there are rapid changes of fluid and electrolytes from the extra- into the intravascular space. In this situation it is a major therapeutic challenge to avoid complications due to hypokalaemia, hypophosphataemia, hypomagnesaemia and hypovolaemia. These complications should be avoided by adequate replacement, and particularly by regular clinical and laboratory monitoring. When blood glucose concentrations decrease below 14 mmols/l, blood glucose concentrations should initially be maintained at this level because rapid lowering below this level may increase the risk of brain oedema. Too-vigorous fluid replacement with crystalline solutions also increases the risk that brain oedema or complications like the adult respiratory distress syndrome will develop. If hypovolaemia persists in spite of adequate crystalloid solutions, colloid-containing fluids such as albumin should be administered. It is not established whether replacements of phosphate and magnesium have clinical benefits. Nevertheless, it is probably justified to administer phosphate and magnesium when their serum concentrations are below the normal range, particularly if the clinical situation is critical. Mortality from diabetic coma in industrialized countries may only be decreased by prophylaxis, i.e. by education of all diabetic patients and physicians to detect metabolic decompensation early.

Diabetic Coma↗