1,5-Anhydro-d-glucitol in vitreous humor and cerebrospinal fluid - A helpful tool for identification of diabetes and diabetic coma post mortem.

Since there are no characteristic morphological findings post mortem diagnosis of diabetes mellitus and identification of diabetic coma need to be confirmed by suitable biomarkers. The postmortem identification of preexisting hyperglycemia or diabetic coma can be difficult if the matrices for the determination of the established biomarkers are not available or the obtained results are close to the established cut-off values. 1,5-Anhydroglucitol (1,5-AG), the 1-deoxy form of glucose, competes with glucose for renal reabsorption. Therefore low serum concentrations of 1,5-AG, reflect hyperglycemic excursions over the prior 1-2 weeks in diabetic patients. To evaluate postmortem 1,5-AG concentrations in vitreous humor (VH) and cerebrospinal fluid (CSF), a liquid chromatographic mass spectrometric method for the quantification of 1,5-AG in VH and CSF was developed and validated according to international guidelines. In order to establish a cut-off for the identification of an ante mortem existing diabetes and the diagnosis of a diabetic coma in deceased the relationships between 1,5-AG concentrations in VH and CSF to other diabetes associated biochemical parameters of 47 non-diabetic, 86 diabetic and 9 cases of diabetic coma were examined. In 83 of these cases, both matrices could be obtained and analyzed. Comparisons of the respective HbA1c, Glucose in VH or Sum-formula of Traub to 1,5-AG concentrations in VH and CSF resulted in correlation coefficients R2≤0.2. For the application of 1,5-AG concentrations in VH against CSF, a linear regression gave a correlation coefficient of R2=0.955. Comparable linear correlations of 1,5-AG concentrations could be observed between VH and femoral venous blood (FVB) (R2=0.839) as well as between CSF and FVB (R2=0.756). Due to overlapping concentration ranges, the determination of a reliable cut-off for the differentiation of diabetic disease to diabetic coma cases was not possible. However, the 1,5-AG concentrations in VH and CSF in cases of deceased diabetics were significantly lower (p<0.05) than in non-diabetic deceased and therefore indicate a pre-existing diabetes or even a diabetic coma as the cause of death.

Esofagitis necrosante aguda asociada coma diabético hiperosmolar / Acute necrotising oesophagitis associated with hyperosmolar diabetic coma

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Detection of diabetic metabolism disorders post-mortem--forensic case reports on cause of death hyperglycaemia.

Diabetic coma is the most severe form of hyperglycaemic metabolic disorders. The post-mortem diagnosis of this disorder of glucose metabolism can be difficult and vague due to a lack of characteristic morphological findings. Six death cases caused by diabetic coma are described with special focus on biochemical (and histological) findings. The possible glycaemia markers glucose, lactate, HbA1c, fructosamine, anhydroglucitol, and ketone bodies were measured and the usefulness of these parameters is evaluated and discussed. Estimations of glucose concentrations in vitreous humour or cerebrospinal fluid and of ketone bodies in blood or other matrices are obligatory while measurements of HbA1c, fructosamine, or anhydroglucitol can only provide additional information on the long-term adjustment of diabetes in the deceased. Lactate concentrations (addition of glucose and lactate levels to form the sum formula of Traub) do not give more information than the glucose concentration itself and can be therefore omitted.

Clinical and forensic examinations of glycemic marker 1,5-anhydroglucitol by means of high performance liquid chromatography tandem mass spectrometry.

Postmortem diagnosis of diabetes and a diabetic coma can be difficult because of the lack of characteristic morphological findings. 1,5-Anhydroglucitol (1,5-AG), the 1-deoxy form of glucose, competes with glucose for reabsorption in the kidneys. Therefore, diabetics with a permanent hyperglycemia show significantly lower serum concentrations of 1,5-AG than non-diabetics. A liquid chromatography-mass spectrometric method for the determination of 1,5-AG in serum and postmortem blood was developed and validated according to international guidelines. Linearity was given between 1 µg/ml and 50 µg/ml. Recovery rates ranged between 70.8% and 89.8%, the limit of quantification of the procedure was 0.20 µg/ml, limit of quantification was 0.55 µg/ml. Serum of 199 diabetics and 116 non-diabetics and femoral blood of 31 diabetic and 27 non-diabetic deceased was measured. Average concentrations were significantly (p<0.001) higher in non-diabetics compared to diabetics ante and postmortem. Seven of the diabetics may have died because of a hyperglycemic coma indicated by a sum formula of Traub>450 mg/dl. 1,5-AG average concentrations in these deceased were not significantly different to diabetics which did not die because of a diabetic coma. Concentrations of 1,5-AG give a hint for not well controlled diabetes antemortem and postmortem and can be assumed as an additional and alternative information postmortem to the measurement of HbA1c or fructosamine.

Basic management of medical emergencies: recognizing a patient's distress.

BACKGROUND AND OVERVIEW: Medical emergencies can happen in the dental office, possibly threatening a patient's life and hindering the delivery of dental care. Early recognition of medical emergencies begins at the first sign of symptoms. The basic algorithm for management of all medical emergencies is this: position (P), airway (A), breathing (B), circulation (C) and definitive treatment, differential diagnosis, drugs, defibrillation (D). The dentist places an unconscious patient in a supine position and comfortably positions a conscious patient. The dentist then assesses airway, breathing and circulation and, when necessary, supports the patient's vital functions. Drug therapy always is secondary to basic life support (that is, PABCD). CONCLUSIONS AND CLINICAL IMPLICATIONS: Prompt recognition and efficient management of medical emergencies by a well-prepared dental team can increase the likelihood of a satisfactory outcome. The basic algorithm for managing medical emergencies is designed to ensure that the patient's brain receives a constant supply of blood containing oxygen.

Postmortem identification of hyperglycemia.

The detection of diabetic coma postmortem requires accurate biochemical analysis. Due to continuous consumption of glucose by surviving cells postmortem, blood glucose levels decrease rapidly. Therefore, vitreous fluid has been used as a substitute in forensic practice, since it has a very low cell count. It has been repeatedly reported that the sum value of vitreous glucose and lactate should be used to estimate the original antemortem blood glucose level, based on the assumption that pre-existing glucose is gradually converted to lactate under anaerobic conditions during agonal phase and the early postmortem period. In this study, we applied a strategy including consistent sampling of vitreous fluid from the centre of both eyes of deceased subjects as soon as possible after arrival at the morgue, and immediate bedside analysis using a blood gas instrument. In total, 3076 cases were included during 2004-2006. We found that, after an initial drop of vitreous glucose during the very early postmortem period, the levels stayed stable for appreciable time postmortem. Analysis of a second sample collected at autopsy 1-3 days later gave similar results (R(2)=0.90). In contrast, the vitreous lactate levels showed a steady increase. This implies that the sum value of glucose and lactate increases with postmortem time, as reflected by vitreous potassium level. In fact, a statistically significant difference in the sum value was seen between subjects with potassium below 10 mmol/L (n=1086) and above 20 mmol/L (n=531), p<.001. In addition, in this large material, we did not identify a single case with circumstantial indication of hyperglycemia that only showed high vitreous lactate. We therefore suggest that vitreous glucose alone should be used to diagnose hyperglycemia postmortem and that the limit of 10 mmol/L should have a good specificity for diabetic coma, which theoretically would equal an original blood glucose value of about 26 mmol/L. As to the methodology, we found that sonication, centrifugation and addition of fluoride to the samples are unnecessary procedures when using a blood gas instrument. The strategy resulted in a doubling of the number of diabetic coma identified at our department compared to preceding period when analysis only was performed on selected cases.

[Hypoglycaemic coma due to falsely elevated glucose values in a patient with diabetes mellitus and peritoneal dialysis]. / Hypoglykemisch coma als gevolg van foutiefverhoogde glucosewaarden bij een patiënte met diabetes mellitus en peritoneale dialyse.

A 45-year-old female diabetes-mellitus patient on peritoneal dialysis was admitted because of vertigo. During her stay in hospital she developed a comatose condition with abnormal head posture and deviation ofthe eyes to the left. Capillary blood from the fingertip showed a glucose value of 15.4 mmol/l. However, the automatically obtained glucose value delivered with a blood-gas analysis was found to be 1.2 mmol/l. The neurological state of the patient normalised fully after intravenous glucose administration. The glucose values were falsely elevated because the patient used a peritoneal dialysis fluid at night which contained icodextrin as an osmotic agent. Metabolites of icodextrin can influence blood-glucose measurements taken using analyzers that depend on the enzyme glucose dehydrogenase. To prevent potentially life-threatening situations, the use of an adequate glucose meter is of paramount importance.

[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.

[Diabetic coma and hypoglycemia in children. What to do when in an emergency]. / Diabetes-komplikationen bei Kindern. Nach dem Fussballspiel: Insulinbedarf falsch eingeschätzt.

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.

[Diabetic coma. Management of diabetic ketoacidosis and nonketotic hyperosmolar coma]. / Coma diabeticum. Management der diabetischen Ketoazidose und des nicht ketoazidotischen hyperosmolaren Komas.

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.