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.

[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 ketoacidosis and hyperosmolar coma.

DKA-hyperosmolar coma is a readily diagnosed and easily treated, potentially catastrophic emergency that regularly occurs in both Type I and Type II diabetics. This review emphasized that diabetic ketoacidosis and hyperosmolar coma can, and very frequently do, occur concurrently, but it is the hyperosmolar state rather than the DKA that is the primary cause of coma and death in this condition. One must therefore vigorously treat the hyperosmolarity and resulting dehydration, especially when total calculated osmolarity exceeds 230 to 240 mOsm/L. The major aim of treatment is to rapidly replace the major water loss that is responsible for this clinical condition and to stimulate glucose metabolism with insulin. The diagnosis of this dangerous condition is relatively simple. The therapy, in most regards, is equally apparent. There are good data demonstrating that the prompt recognition of DKA-hyperosmolar coma and the simple institution of rapid rehydration have continued to reduce the mortality and complications of this potentially disastrous complication of diabetes mellitus.

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.

Necrotizing fasciitis precipitating diabetic ketoacidotic coma.

Necrotizing fasciitis is a rapidly spreading infection of the subcutaneous tissue and fascia; diabetes mellitus appears to be the most frequent underlying disease. Early diagnosis and immediate aggressive surgical therapy are paramount to curtail morbidity and mortality, but diagnosis is often difficult and unnecessarily delayed. We describe a case of necrotizing fasciitis precipitating diabetic ketoacidotic coma where correct diagnosis was not made until the 14th hospital day. We stress the fact that physicians caring for critically ill patients should be keenly aware of the possibility of necrotizing fasciitis when tending diabetic patients with unexplained fever; failure to recognize the disease can have devastating results. Finally, we believe this to be the first reported case of diabetic ketoacidotic coma precipitated by necrotizing fasciitis.

The diagnostic value of postmortem blood glucose determinations in cases of diabetes mellitus.

In 24 cases of death in diabetic coma the peripheral venous blood showed glucose levels exceeding 3.5 mg/ml (mean value 7.76 mg/ml). In a control material of deaths of other causes the blood glucose was usually low and often zero, and all values were well below the lower limit of the diabetic concentrations. The acetone contents of the diabetic blood varied widely and were of limited diagnostic value. We conclude that glucose concentrations above 3.5 mg/ml in the peripheral blood indicate that death occurred in diabetic coma.

Coma induced by intoxication.

Clinicians in the emergency department are often confronted with coma patients due to poisoning. A systematic general approach involving early consultation with a neurologist is of paramount importance. A high index of suspicion, a systematic first assessment already in the prehospital phase and early stabilisation of vital functions are the essential first steps. Specific antidotes like hypertonic glucose and thiamine are part of a "coma cocktail". The opiate antagonist naloxone should be used only when clinically indicated and in a titrated way. Flumazenil should only be used with caution and in restricted cases. Clinical neurological evaluation and technical investigations like CT-scan and laboratory tests should make part of a careful diagnostic plan. Toxicological tests deserve their place in the diagnostic work up of a coma patient with suspected poisoning. Knowledge of the possibilities of the toxicology lab and optimal communication with the clinical toxicologist is important for optimal patient care.

Hyperosmolar hyperglycemic nonketotic coma.

HHNC is a syndrome of abnormally high serum glucose and osmolality coupled with depressed consciousness and an absence of ketoacidosis. It represents as many as 20 per cent of all cases of severe hyperglycemia and constitutes a life-threatening medical emergency; however, the absence of acidosis and the insidious presentation of the disorder frequently mislead clinicians into dangerously inadequate therapeutic interventions. Aggressive therapy with intravenous fluids and potassium and the judicious use of insulin, in conjunction with careful monitoring of central venous pressure and urine output, form the mainstays of treatment. There is a strong association of HHNC with other underlying serious diseases, the detection and treatment of which are imperative to the adequate resolution of the syndrome.

[Hyperglycemic, hyperosmolar nonketotic diabetic coma in the pediatric age]. / Coma diabetico iperglicemico-iperosmolare non chetosico in età pediatrica

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.

[Nonketotic hyperosmolar coma. Clinical aspects and treatment in 12 cases]. / Il coma iperosmolare non chetosico. Aspetti clinici e trattamento in 12 casi.

Non-ketotic hyperosmolar diabetic coma is a complication of diabetes characterised by extreme dehydration, plasmatic hyperosmolarity and the absence of ketosis. The mortality rate is very high, especially in elderly subjects with type II diabetes. A personal series of 12 cases is reported with an assessment of general features, triggering factors, biochemical parameters at onset and treatment given. The data confirm reports in the literature and the results show the therapeutic superiority of continuous endovenous infusions of insulin at 3-10 mu/hour over other treatment protocols.

Diabetic ketoacidosis. Reassessment of therapeutic "truths".

The diagnosis of diabetic ketoacidosis remains, as always, a bedside clinical exercise. Rapid consideration and exclusion of other conditions associated with altered consciousness that may occur in diabetics, such as lactic acidosis, hyperosmolar states, hypoglycemia, alcohol-related ketosis, and infections, should be routine. Although recent reassessment of therapy has meant more rational and specific action, close attention to the physical and laboratory responses to treatment is equally essential for a successful outcome.

[Coma in type 2 diabete mellitus on metformin treatment]. / Coma chez un diabétique de type 2 traité par la metformine.

Non traumatic coma in diabete mellitus has two origins : hypo- or hyperglycemia. Coma with hyperglycemia can be due to ketoacidosis, hyperosmolar state or lactic acidosis. The present observation reports on a type 2 diabete mellitus patient presenting with a coma while the patient was on metformin and glibenclamide treatment. On admission, biologicals tests showed major acidosis, hyperglycemia and hyperosmolarity. No metformine accumulation was demonstrated by analytical measure. In this case, the association of hyperosmolar state and metabolic acidosis prove the difficulty of the differential diagnosis.

[Hyperosmolar hyperglycemic coma in a 10-year-old patient]. / Hyperosmolárna hyperglykemická kóma u desat'rocného pacienta.

A ten-year-old patient referred to a child ambulatory for preoperative examination suddenly falls unconscious. The physical finding and laboratory results suggest hyperosmolar hyperglycaemic coma. The authors describe the clinical course and therapeutic procedure. They draw attention to adequate fluid and ion repletion, to the importance of their balancing and to possible complications of treatment.

[Reversible long-term tachycardia and hypertension as a symptom of autonomic neuropathy in combination with sensorimotor polyneuropathy in a patient with newly discovered type 1 diabetic mellitus]. / Reverzibilní dlouhodobá tachykardie a hypertenze jako projev autonomní neuropatie v kombinaci se senzorickomotorickou polyneuropatií u nemocné s cerstvým záchytem diabetes mellitus 1. typu.

The case of 22 years old woman admitted with ketoacidotic coma and newly diagnosed insulin dependent diabetes mellitus is described. The signs of mixed sensoromotoric polyneuropathia in this patient have been discovered. After the correction of ketoacidotic hyperglycemic coma the significant tachycardia and hypertension with the abnormalities of diurnal rhythm with necessity of the intensive treatment persisted for the period of the several monthes. These changes we attributed to the significant dysfunction of the autonomic system. In the course of 1 year of good diabetes compensation the above mentionned hemodynamic changes subsided completely. In the same time the signs of mixed polyneuropatia and the incipient retinopathia disappeared. The causes of the described changes are discussed, mainly the importance of reversible microvascular changes.