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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term micro- and macrovascular complications cause major morbidity and mortality in patients with type 2 diabetes mellitus. Up to the present it is not clear whether intensified or conventional insulin treatment is more effective to keep blood glucose concentrations close to the normal range. In the present trial 90% (n = 117) of all insulin-treated type 2 diabetic patients aged 16 to 60 years and living in the city of Jena (100,247 inhabitants), Thuringia, Germany were examined. Fourty patients (34%) were on intensive insulin therapy (ICT, > or = 2 injections of normal- and > or = 1 injection of NPH-/mixed-insulin/day, > or = 1 insulin-dose adjustments/week, > or = 2 blood-glucose self-tests/day) and 77 patients (66%) were on conventional insulin therapy (CIT). Patients with ICT had more injections/d (4.3 +/- 0.7 vs CIT 2.4 +/- 0.7, p < 0.001), more insulin-dose adjustments/week < or = 11.5 +/- 8.2 vs 2.2 +/- 5.2, p < 0.001) and more blood-glucose self-tests/week (25.2 +/- 5.7 vs 9.6 +/- 8.8, p < 0.001). Patients with ICT had higher insulin doses (0.71 +/- 0.32 vs 0.47 +/- 0.2 IU/kg body wt/d, p < 0.001), were younger (50.5 +/-6.7 vs 54.0 +/- 5.9 years, p = 0.004) and they had a non-significant tendency to a better HbAlc (8.7 +/- 2.2 vs 9.2 +/- 2.0%, p = 0.23, HPLC, Diamat, normal range 4.4-5,9%). There was a negative correlation between HbAlc and the frequency of blood-glucose self-tests/week (r = -0.23, p = 0.019) and the number of insulin-dose adjustments/week (r = -0.33, p < 0.001). There were no differences between the groups as regards body-mass index (29.7 +/-4.9 vs 28.0 +/- 4.5 kg/m2, p = 0.06), diabetes duration (12.3 +/- 6.9 vs 12.2 +/- 7.5 years, p = 0.96), duration of insulin therapy (4.2 +/-3.5 versus 4.5 +/- 4.8 years, p = 0.67), incidence of acute complications (severe hypoglycaemia, diabetic coma), prevalence of retino-, nephro- and neuropathy (assessed according to Young et al.) and education or socio-economic factors. Also, in respect of quality of life and treatment satisfaction, assessed with standardized questionnaires according to Bradley et al. and Lewis et al., there were no differences between the two groups. In conclusion, in type 2 diabetic patients, ICT seems to be indicated in a second step in "problem-patients" with bad metabolic control under CIT and/or individual's need for more flexibility. Perhaps, in these patients ICT leads to an improvement in the quality of metabolic control.
Exp Clin Endocrinol Diabetes 1999
PMID:Intensive or conventional insulin therapy in type 2 diabetic patients? A population-based study on metabolic control and quality of life (The JEVIN-trial). 1061 81

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.
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PMID:Reversal of foetal hydrops and foetal tachyarrhythmia associated with maternal diabetic coma. 1100 May

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.
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PMID:Lipids in the proximal tubules of the kidney in diabetic coma. 1111 9

A case history of a 31-year-old male schizophrenic patient is presented. The man was treated with olanzapine for three weeks before he died. After one week on a 10 mg daily dose of olanzapine, his fasting blood glucose was elevated to 11.3 mmol/L (203 mg/dL). In order to treat more aggressively his psychosis, the olanzapine dose was raised to 20 mg daily resulting in his fasting blood glucose climbing to 15.8 mmol/l (284 mg/dL). On the days preceding his death, he became progressively weaker, and developed polydipsia with polyuria. He had no personal or family history of diabetes mellitus and he was on no other medication at the time of his death. Postmortem blood, vitreous humor, and urine glucose concentrations were 53 mmol/L (954 mg/dL), 49 mmol/L (882 mg/dL), and 329 mmol/L (5922 mg/dL), respectively. Drug screen on urine and blood indicated only a small amount or olanzapine and no alcohols. Peripheral blood olanzapine concentration was within therapeutic limits, 45 ng/mL. Analysis of vitreous humor and urine revealed severe dehydration with small amounts of ketones. Death was attributed to hyperosmolar nonketotic diabetic coma, and olanzapine was felt most likely to be the cause. Another atypical neuroleptic, clozapine, has also been associated with the development and exacerbation of diabetes mellitus or diabetic ketoacidosis. We recommend including vitreous glucose and beta-hydroxybutyrate analysis as part of postmortem toxicology work up when the drug screen reveals the presence of either olanzapine or clozapine.
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PMID:Fatality from olanzapine induced hyperglycemia. 1213 3

Bilateral putaminal hemorrhages rarely occur simultaneously in hypertensive patients. The association of intracerebral hemorrhage with cerebral edema (CE) has been rarely reported in diabetic patients. We present a patient with bilateral putaminal hemorrhage (BPH) and CE during the course of hyperglycemic hyperosmolar syndrome (HHS). A 40-year-old man with a history of diabetes mellitus and chronic alcoholism was admitted with acute impaired mentality. His blood pressure was within the normal range on admission. Laboratory results revealed hyperglycemia and severe metabolic acidosis without ketonuria. After aggressive treatment, plasma sugar fell to 217 mg/dl, but brain CT showed BPH and diffuse CE. Our case demonstrated that HHS should be considered as a cause of BPH with CE. Initial brain imaging study may be recommended for patients with diabetic coma.
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PMID:Bilateral putaminal hemorrhage with cerebral edema in hyperglycemic hyperosmolar syndrome. 1220 43

This review describes the current guidelines of German diabetes association for the management of diabetic coma, both of diabetic ketoacidosis and hyperosmolal coma. The outline focuses on emergency treatment and the management on the intensive care unit, in particular, volume and insulin therapy, and potassium replacement. The delineation of the concept of low insulin therapy is emphasized to avoid the incidence of disequilibrium syndrome. Also, the indications for bicarbonate therapy in diabetic ketoacidosis are critically discussed, as well as phosphate and magnesium replacement. With today's therapeutic possibilities the therapeutic goal, i.e. a low mortality, may be achieved, dependent on the underlying illness.
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PMID:[Diabetic coma. Management of diabetic ketoacidosis and nonketotic hyperosmolar coma]. 1468 88

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.
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PMID:[Diabetic coma and hypoglycemia in children. What to do when in an emergency]. 1555 20

The final diagnosis of death in hypoglycaemic or diabetic coma should always be done as a synopsis of anamnestic response, morphology, biochemical (glucose, lactate, HBA1c, ketonic bodies, insulin, and C-peptide) and toxicological findings. High glucose levels in vitreous humour (more than 13 mmol/L, 234 mg/dL) or combined values of glucose and lactate in vitreous humour or in cerebrospinal fluid over threshold values of 23.7 mmol/L (427 mg/dL) and 23.4 mmol/L (422 mg/dL) respectively, can be an indicator of the pre-mortem hyperglycaemic state with fatal outcome. The determination of glycated haemoglobin, acetone and other ketone bodies improve the diagnostic values of the whole procedure. Diabetic ketoacidosis (blood acetone >0.3 g/L) is more often the cause of death of diabetic patients than the non-ketotic hyperosmolal state. Hypoglycaemia is deemed fatal if the combined values are lower than 5.5 mmol/L (100 mg/dL) and can not be excluded if they are lower than 8.9 mmol/L (160 mg/dL). Two cases of detected hypoglycaemia are described further. A psychiatric patient with diabetes (Hba1c 8.4%) committed suicide with an insulin overdose. The combined values of glucose and lactate in vitreous humour and in cerebrospinal fluid were 3.3 and 4.1 mmol/l, respectively. In another case a low combined glucose and lactate value (8.7 mmol/L) in vitreous humour indicated, besides the high concentration of glibenclamide (0.9 mg/L) in the blood of a driver with a poorly controlled diabetic condition (Hba1c = 10.6%), a state of decreasing blood glucose in the time before the accident causing the driver to feel un-well and behave inappropriately.
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PMID:Diagnostic values of combined glucose and lactate values in cerebrospinal fluid and vitreous humour--our experiences. 1563 73

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.
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PMID:[Biochemical analysis of the vitreous body of the eye in post-mortem diagnosis of diabetic coma]. 1607 52

Hyperglycaemic hyperosmolar syndrome is a major acute complication of decompensated diabetes mellitus. It represents the second most common aetiology of diabetic coma and is associated with excess mortality. It is characterised by severe hyperglycaemia, hyperosmolality and dehydration in the absence of significant ketosis, afflicting principally middle-aged-to-elderly patients. Early clinical diagnosis and prompt treatment, consisting of fluid replacement, insulin therapy, restoration of electrolyte disturbances and management of concurrent illnesses may improve the outcome. This review provides an outline of the diagnostic approach of patients with manifestations of hyperglycaemic hyperosmolar syndrome and discusses the contemporary therapeutic recommendations.
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PMID:Therapeutic management of hyperglycaemic hyperosmolar syndrome. 1614 5


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