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Introduction: Isolated Hyperosmolar Hyperglycaemic Syndrome (HHS) is a life-threatening condition characterized by elevated serum glucose concentrations and hyperosmolality without significant ketosis. It is often described in obese adults with unknown Type 2 Diabetes (T2D), rarely in youth. In childhood the most common cause of metabolic glucose related derangement is Diabetic Ketoacidosis (DKA) in Type 1 Diabetes (T1D). Interestingly, both components can be combined with each other, thus the prevalent condition needs to be recognised implying a different therapeutic approach., Case Presentation: In this case, we report a prepubertal Caucasian obese girl admitted for two episodes of combined HHS/DKA in order to elucidate her clinical course taking into account the current pediatric recommendations based on adult guidelines for HHS., Conclusions: The treatment of HHS and even more of HHS/DKA in youth is still controversial as no specific guidelines for children are available especially during the prepubertal age. The description of our case might be helpful and offer relevant points for future consensus.

For patients presenting with suspected diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) understanding of the etiology and pathophysiology will ensure optimal emergency management. Morbidity and mortality is most often due to the underlying precipitating cause, which may include infection, infarction/ischemia, noncompliance with insulin therapy, pregnancy, and dietary indiscretion. Current guidelines are based primarily on expert opinion and consensus statements, but more recent evidence suggests that recommendations related to arterial blood gas, insulin bolus, and IV fluid replacement should be re-evaluated. This issue presents an approach to DKA and HHS management based on current evidence, with a simplified pathway for emergency department management.

Objectives: Insulin infusion therapy is commonly used in the hospital setting to manage diabetic ketoacidosis and hyperosmolar hyperglycemic state. Clinical evidence suggests both hypoglycemia and glycemic variability negatively impact patient outcomes. The hypothesis of this study was that moderate-intensity insulin therapy decreases hospital length of stay and prevalence of hypoglycemia in patients with diabetic ketoacidosis and hyperosmolar hyperglycemic state., Design: Pre-post study., Setting: Large academic medical center in the United States., Patients: Two-hundred one consecutive, nonpregnant, adult patients admitted for diabetic ketoacidosis and hyperosmolar hyperglycemic state between October 2010 and December 2014., Interventions: High-intensity insulin therapy versus moderate-intensity insulin therapy. High-intensity insulin therapy was designed to rapidly normalize blood glucose levels with bolus doses of insulin and rapid insulin titration. Moderate-intensity insulin therapy was designed to mitigate glycemic variability and hypoglycemia through avoidance of bolus dosing, a liberalized blood glucose target, and gradual insulin titration., Measurements and Main Results: Hospital and ICU length of stay were reduced by 23.6% and 38%, respectively. The relative risk of remaining in the hospital at day 7 (0.51; p = 0.022) and day 14 (0.28; p = 0.044) were significantly reduced by the moderate-intensity insulin therapy strategy. The relative risk of remaining in the ICU at 48 hours was significantly lower in the moderate-intensity insulin therapy cohort (0.34; p = 0.0048). The prevalence (35% vs 1%; p = 0.0003) and relative risk (0.028; p = 0.0004) of hypoglycemia were significantly lower in the moderate-intensity insulin therapy cohort. Glycemic variability decreased by 28.6% (p < 0.0001). There was no difference in the time to anion gap closure (p = 0.123)., Conclusions: Moderate-intensity insulin therapy for diabetic ketoacidosis and hyperosmolar hyperglycemic state resulted in improvements in hospital and ICU length of stay, which appeared to be associated with decreased glycemic variability.

Hyperglycaemic hyperosmolar state (HHS) may occur in young patients with type 1 and type 2 diabetes and in infants with hyperglycaemia. Hyperglycaemic hyperosmolar state is characterised by extremely high glucose concentration, which, by increasing osmotic diuresis, intensifies dehydration. Hyperglycaemic hyperosmolar state criteria include the following: plasma glucose > 600 mg/dl, venous pH > 7.25, sodium bicarbonate > 15 mmol/l, slight ketonuria, plasma osmolality > 320 mOsm/kg, and impairment of consciousness (aggression, unconsciousness, convulsions). We describe the case of a 13-year-old patient with severe obesity (at presentation body mass > 120 kg, BMI > 40 kg/m2), who developed HHS (glycaemia 647 mg/dl, pH 7.18, pCO2 96.5 mmHg, BE - 5.0 mmol/l, HCO3 35.2 mmol/l; Na 167 mmol/l, plasma osmolarity 370 mOsm/kg) in the course of pneumonia and newly diagnosed type 2 diabetes (HbA1c 15.5%, C-peptide 2.63 ng/ml). In the follow-up, due to the hypoglycaemia, insulin was discontinued, metformin was administered at a dose of 2 g/day, with a further reduction to 500 mg/day, together with physical rehabilitation and a low-calorie diet. Weight reduction during 6 months of observation was approximately 37 kg. Due to breathing disorders occurring at night, the girl still needs breathing assistance (CPAP).

We report the case of a 77-year-old woman with diabetic chorea, which presented as hemiballism of the right limbs. Initial blood examination revealed that sugar and hemoglobin A1c levels were 732 mg/dl and 12.2%, respectively. Thus, a diagnosis of hyperglycemic hyperosmolar syndrome was made at a previous hospital. Ballism of the right limbs developed after 10 days and progressively worsened. After a month, the patient was admitted to our hospital. Brain MRI (axial T 1 -weighted imaging) revealed a high-signal-intensity area in the left striatum. Dopamine transporter SPECT demonstrated reduced 123 I-ioflupane binding in the bilateral striatum with left side predominance. Although haloperidol and risperidone were ineffective for her involuntary movement, chlorpromazine had a little effect. Levodopa and gabapentin combination treatments were effective in decreasing the symptoms. It was considered that dopamine antagonist was the medical treatment for diabetic chorea and that levodopa could worsen neurological symptoms such as chorea-ballism. However, in our case, levodopa treatment was effective.

Atypical antipsychotics are very widely used for various psychiatric ailments because of their less extrapyramidal side effects. Various reports of disturbances in glucose metabolism in the form of new onset diabetes mellitus, exacerbation of preexisting diabetes mellitus, diabetic ketoacidosis, hyperosmolar nonketotic coma, acute pancreatitis, and increased adiposity have been reported. We present a case of new onset diabetic ketoacidosis in a patient without a history of glucose intolerance who was being treated with olanzapine for bipolar disorder. He presented in hyperglycemic, hyperosmolar, hyperketotic state with hyperkalemia, and peaked T waves on electrocardiogram. He was treated with vigorous intravenous hydration, insulin, and kaexylate which stabilized his metabolic profile. He was discontinued off of his olanzapine and started on resperidol for his bipolar disorder. Over the course of 6 months, the patient was discontinued off of his insulin and has been doing well on his follow-up appointments. This case highlights the necessity of close blood glucose monitoring of patient on atypical antipsychotic medications irrespective of their diabetic status.

Decompensated hypothyroidism is a rare endocrine emergency but a differential that should be considered in patients presenting critically unwell with systemic illness. We report a case of myxoedema coma in a woman presenting with respiratory failure, hypotension, hypothermia and a reduced level of consciousness, all of which are poor prognostic features in decompensated hypothyroidism. The patient was admitted to critical care for mechanical ventilation and cardiovascular support and treated with a combination of insulin, liothyronine and levothyroxine, making a good recovery. We wanted to highlight this case of myxoedema coma occurring in the context of a hyperglycaemic hyperosmolar state (HHS), as the former condition is normally associated with hypoglycaemia, hyponatraemia and hypo-osmolality. Decompensated hypothyroidism should be considered in presentations of HHS as well as with other metabolic derangements, as delays in thyroid hormone replacement are associated with poorer outcomes. It has multisystem effects challenging its recognition and we discuss potential complications and their management., (2016 BMJ Publishing Group Ltd.)

Diabetic ketoacidosis and hyperosmolar hyperglycaemic syndrome are important hyperglycaemic emergencies seen in patients with diabetes. Occasionally, differentiation between the two conditions can be difficult. We present the case of a patient whose hyperglycaemic emergency was managed in a way that could have adversely influenced the outcome. We also discuss important aspects of the new Joint British Diabetes Societies Guidelines on the management of hyperglycaemic emergencies.

The hyperglycemic emergencies, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are potentially fatal complications of uncontrolled diabetes mellitus. The incidence of DKA and the economic burden of its treatment continue to rise, but its associated mortality rate which was uniformly high has diminished remarkably over the years. This Improvement in outcome is largely due to better understanding of the pathogenesis of hyperglycemic emergencies and the application of evidence-based guidelines in the treatment of patients. In this article, we present a critical review of the evidence behind the recommendations that have resulted in the improved prognosis of patients with hyperglycemic crises. A succinct discussion of the pathophysiology and important etiological factors in DKA and HHS are provided as a prerequisite for understanding the rationale for the effective therapeutic maneuvers employed in these acute severe metabolic conditions. The evidence for the role of preventive measures in DKA and HHS is also discussed. The unanswered questions and future research needs are also highlighted., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Context: Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) cause major morbidity and significant mortality in patients with diabetes mellitus. For more than 30 yr, our group, in a series of prospective, randomized clinical studies, has investigated the pathogenesis and evolving strategies of the treatment of hyperglycemic crises. This paper summarizes the results of these prospective studies on the management and pathophysiology of DKA., Setting: Our earliest studies evaluated the comparative efficacy of low-dose vs. pharmacological amounts of insulin and the use of low-dose therapy by various routes in adults and later in children. Subsequent studies evaluated phosphate and bicarbonate therapy, lipid metabolism, ketosis-prone type 2 patients, and use of rapid-acting insulin analogs as well as leptin status, cardiac risk factors, proinflammatory cytokines, and the mechanism of activation of T lymphocytes in hyperglycemic crises., Main Outcome: The information garnered from these studies resulted in the creation of the 2001 American Diabetes Association (ADA) technical review on DKA and HHS as well as the ADA Position and Consensus Paper on the therapy for hyperglycemic crises., Conclusions: Areas of future research include prospective randomized studies to do the following: 1) establish the efficacy of bicarbonate therapy in DKA for a pH less than 6.9; 2) establish the need for a bolus insulin dose in the initial therapy of DKA; 3) determine the pathophysiological mechanisms for the absence of ketosis in HHS; 4) investigate the reasons for elevated proinflammatory cytokines and cardiovascular risk factors; and 5) evaluate the efficacy and cost benefit of using sc regular insulin vs. more expensive insulin analogs on the general ward for the treatment of DKA.

Diabetic ketoacidosis (DKA) is the main hyperglycemic complication in type 1 Diabetes Mellitus (DM1). The basic principles in treatment have to be followed carefully. The patient with DKA has a very deep volume depletion. To restore the circulatory capacity is the first step. From this point on, the restoration of the lost fluids is slow, around 1% per hour, aiming at the correction of the metabolic disturbance already on and avoiding great fluctuations in osmolality, which increases the risk of having complications. Attention to the development of cerebral edema, which, once suspected, deserves an urgent treatment plan, trying to avoid neurologic sequelae or even death. Subcutaneous ultra-rapid insulin has been demonstrated to be efficient and easier to use. As the perfusion gets improved and the levels of insulin increase, the lipolysis is blocked, as well as the generation of ketones and so the acidemia tends to be solved. DKA is still a high-mortality condition. And to be in a hurry frequently leads to neurologic sequelae and even to a fatal outcome.

A 79-year old woman was admitted with disturbed consciousness (JCS II-30). She had been given a diagnosis of type 2 diabetes 7 years previously, and was being treated with oral hypoglycemic agents. She also suffered Alzheimer's disease and Parkinson's disease. Plasma glucose and HbA1c upon admission was 676mg/dl and 9.7%, respectively. Serum Na was 153mEq/l. Urine ketone body test was negative and metabolic acidosis was not observed. Hyperglycemic hyperosmolar non-ketotic coma (HHNC) was diagnosed, and treatment was started immediately with normal saline infusion. Continuous infusion of regular insulin was needed to lower blood glucose. Disturbed consciousness and dehydration improved by the third hospital day. However, she became bedridden afterwards and received tube feeding. Up to 46 units of insulin was needed daily to control blood glucose. Urine C-peptide secretion was very low (10microg/day), suggesting that insulin therapy was essential for glycemic control long before admission. It is thought that a number of elderly diabetic patients who need insulin therapy do not receive or continue it for various reasons. Discussion is necessary to grasp the actual situation and defensive actions that can be taken.

Introduction: The article summarises the experience of the authors in the administration of insulin using an infusion dispenser at a metabolic intensive care unit (MICU) both to patients with decompensated diabetes mellitus and to patients admitted with a sepsis or other life-threatening condition of internal nature., Patients and Results: Insulin was administered with the use of a dispenser to a total of 50 patients during 6 months of 2005. 13 of those patients showed signs of ketoacidotic or hyperosmolar coma in the course of diabetes mellitus. All of these patients were compensated within 24 hours and transferred to a standard ward for further treatment within 48 hours. 37 patients were admitted in a critical condition, the cause ofwhich was sepsis and a serious internal disease in 29 and 8 patients, respectively. 12 of the patients died during their hospitalisation at MICU, of which 8 in the first 3 days after admission. No significant correlation between the age, diabetes mellitus diagnosis or an associated cardiovascular morbidity and the death at MICU was discovered, but there was a very close ling between the mortality at the intensive care unit and the baseline blood level of C-reactive protein (160 mg/l; 32-352 in the patients who died, and 111 mg/l 15-168 in the patients who survived), p < 0.01. Glycaemia at admission did not differ significantly for the patients who dies and those who survived, but average glycaemia for all three measurements at MICU was significantly higher in the patients who died (10.4 mmol/l; 6.2-22.4) as compared with those who survived (7.8 mmol/l; 5.8-16.6), p < 0.01. The time of insulin administration was significantly shorter in patients who died (3.3 days; 1-6) as compared with those who survived (5.2 days; 3-10), p < 0.01. There was no significant difference between hourly insulin dose in the patients who died (2.8 j/hour; 0.6-8.6) and in those who survived (2.6 j/hour; 0.8-7.6). A trend towards lower mortality was recorded for the group of patients with average glycaemia below 8 mmol/l and/or those in whom glycaemia mostly ranged between 4.4 and 8.0 mmol/l, but the difference was not statistically significant. A significantly lower consumption of insulin was recorded for the patients with average glycaemia below 8 mmol/l and/or those whose glycaemia measurements mostly ranged between 4.4 and 8.0 mmol/l. Hypoglycaemia defined as glycaemia below 4.4 mmol/l was present in 2% of all measurements, in 11 patients on the total, and their results were not significantly associated with mortality at MICU., Conclusion: Mortality of patients admitted with sepsis or other life-threatening condition of internal nature was significantly higher in the group of patients with higher average glycaemia among all the measurements performed at MICU. In patients who died, the total time of insulin administration was significantly shorter, but there was no difference between the average hourly insulin dose in the group of the patients who died and those who survived.

We report a case of extensive venous thrombosis of the upper extremity in a patient with a hyperosmolar hyperglycemic state (HHS). Thrombosis of the upper extremities is generally found in 4% of cases with deep venous thrombosis. Extensive, symptomatic venous thrombosis of the upper extremity, as seen in this patient, is rare except with catheter-related thrombosis. Recent studies have supported the safety and efficacy of catheter-directed thrombolysis in patients with no contraindication to thrombolytic therapy, and have recommended early catheter-directed thrombolysis. Therefore, our patient was treated with early catheter-directed thrombolysis followed by anticoagulation.

Methadone overdoses are increasing in parallel with the increased frequency of opiate substitution therapy in adults. Although unintentional methadone intoxication in children is rare, it is becoming more frequently recognized. We report 3 cases of unintentional methadone overdose in toddlers who initially displayed central nervous system depression associated with severe nonketotic hyperglycemia and discuss the possible pathophysiologic mechanisms of an underrecognized symptom of opiate intoxication in young children.

The geriatric population is at particular risk for developing hyperglycemic crises with the development of diabetes. With increasing age, insulin secretory reserve, insulin sensitivity, and thirst mechanisms decrease. The elderly are particularly vulnerable to hyperglycemia and dehydration, the key components of hyperglycemic emergencies. If recognized early, hyperglycemia can frequently be treated in the outpatient setting even with moderate or large ketonuria, provided patients can take fluids, monitor blood glucose frequently, and follow standard "sick day rules." With increased diabetes surveillance and aggressive early treatment of hyperglycemia and its complications, morbidity and mortality from acute diabetic crises in the geriatric population can be greatly reduced.

Objective: This report describes a new fatal syndrome observed in adolescent males at the initial presentation of diabetes mellitus. The features include hyperglycemic hyperosmolar coma complicated by a malignant hyperthermia-like picture with fever, rhabdomyolysis, and severe cardiovascular instability., Design: Case series., Setting: Pediatric intensive care units of 3 tertiary care facilities in the United States., Patients: Six adolescent males, 5/6 obese with acanthosis nigricans, 4/6 black., Results: Four of 6 patients died. Four of 6 patients did not have significant ketosis. Six of 6 patients had increased temperature after the administration of insulin., Conclusions: The underlying etiology of this syndrome remains unclear. Possibilities include an underlying metabolic disorder such as a fatty acid oxidation defect, an unrecognized infection, exposure to an unknown toxin, or a genetic predisposition to malignant hyperthermia. Evaluation for all these possibilities and empiric treatment with dantrolene should be considered for this type of patient until this syndrome is better characterized.

Diabetes mellitus is one of the most commonly associated diseases of patients suffering an acute myocardial infarction. Although the coexistence of acute myocardial infarction with other clinical manifestations of diabetes have been well described, extremely few data exists about the concomitant occurrence of hyperosmolar hyperglycaemic nonketotic coma and myocardial infarctions. This article presents three patients with this association and aimed to discuss the clinical course and treatment strategies of this rare condition.

We describe a case of non-ketotic hyperglycemia (NKH), heralded by complex partial seizures and aphasia of epileptic origin, besides versive and partial motor seizures. This clinical picture was accompanied by left fronto-temporal spikes in the EEG. The seizures were controlled by carbamazepine only after the control of the diabetes. A month later, carbamazepine was discontinued. The patient remained without seizures, with normal language, using only glybenclamide. Complex partial seizures, opposed to simple partial seizures, are rarely described in association to NKH. Epileptic activity localized over language regions can manifest as aphasia.

Impairment of the catabolism of glycine caused by "failure" of the glycine cleavage enzyme complex results in an inability to oxidatively decarboxylate this amino acid. As a result of this inability, the alpha carbon of glycine does not enter the one-carbon pool, leading to its reduction or depletion, and toxic accumulation of this amino acid neurotransmitter occurs. Strategies for the treatment of the clinical condition known as nonketotic hyperglycinemia, an autosomal recessive disorder associated with absent or diminished glycine cleavage enzyme activity, include reduction of the glycine burden, replenishment of the one-carbon pool, and antagonism of the neurotransmitter effects of glycine. Until recently, antagonism focused on interference with the glycine-associated chloride ionophore that is enriched in the brain stem and spinal cord, using strychnine as a specific intervention. However, the recent recognition of a "strychnine-insensitive" binding site for glycine on the N-methyl-D-aspartic acid (NMDA) receptor complex, a glutamate-gated cationic channel, has led to some newer approaches. Also, the recognition of milder, atypical variants of classic nonketotic hyperglycinemia has stimulated efforts to evaluate the therapeutic efficacy of these strategies to antagonize the NMDA receptor complex.

A dog treated for a pancreatic abscess inadvertently received 1800 ml of hyperosmolar solution within a two hour period. Blood glucose reached 44 mmol/litre and the plasma osmolality was estimated to be more than 334 mOsm/litre. Lipaemia was severe and persisted for several days. The dog developed nausea, vomiting, depression, severe hyperglycaemia, polyuria, glucosuria and hypokalaemia. These symptoms were consistent with a hyperosmolar hyperglycaemic syndrome. Treatment with insulin and intravenous fluid rapidly corrected the hyperglycaemia, electrolyte imbalances and water deficits. The dog recovered and no long-term sequelae were observed.

Nonketotic hyperglycinaemia (NKH) is an inborn error of the glycine cleavage system resulting in seizures and mental retardation. Two prior reports noted an anticonvulsant effect from high-dose dextromethorphan (DM) in this disorder, although the two reported patients demonstrated widely disparate DM requirements and drug levels. We report two children with NKH who also demonstrated disparate and variable DM metabolism which markedly influenced the dose-concentration-response relationship. Levels of DM and its primary metabolite dextrorphan (DX) were utilized to guide DM therapy and exhibited patterns reflective of the extensive and poor metabolizer phenotypes for CYP2D6, the cytochrome P450 isoform responsible for DM metabolism. In the patient who appeared to represent the extensive metabolizer (EM) phenotype, treatment with the non-specific cytochrome P450 inhibitor cimetidine was required to reduce biotransformation of DM to DX and, thus, to increase DM plasma concentrations. In the patient with the apparent poor metabolizer (PM) phenotype, a change in the DM preparation to a sustained-release form and increase in the dosing interval was required to lower DM plasma concentrations. These cases demonstrate the importance of CYP2D6 phenotype in providing safe and effective DM therapy to patients with NKH.

Nonketotic hyperglycemic hyperosmolar coma is an uncommon, but significant, complication of type II diabetes mellitus with a high overall mortality rate. Treatment of this entity is controversial but mandates aggressive fluid resuscitation and strict control of serum glucose levels. In the patient described, nonketotic hyperglycemic hyperosmolar coma complicated by diabetes insipidus was successfully treated with desmopressin acetate. To the authors' knowledge, this is the first reported case of nonketotic hyperglycemic hyperosmolar coma associated with partial central diabetes insipidus.

We have seen a case of "diabetic non-ketotic hyperosmolar coma" with ketosis. An 84-year-old man was brought into the hospital in a deeply comatous and dehydrated state. The initial blood glucose level was 1252 mg/dl with plasma osmolarity of 435 mOsm/l, but no ketonuria was detected by the nitroprusside method (Ketostix). However, the plasma 3-hydroxybutyrate (3-OHBA) level was 5 mM in a newly developed bedside film test. The serum ketone bodies were later found to be 5.56 and 0.82 mmol/l for 3-OHBA and acetoacetate (AcAc), respectively. A marked increase in glucagon, cortisol and ADH with renal dysfunction (creatinine 5.0 mg/dl) were noted. An abnormal electrocardiogram, occular convergence and chorea like movement disappeared after correction of metabolic disturbances. The moderate level of IRI (14 microU/ml) on admission and a good response to glucagon 2 months after admission also indicate that the present case is a typical hyperosmolar non-ketotic coma. Because of a preferential increase in 3-OHBA, ketonuria seemed to be absent in the regular nitroprusside test. Marked dehydration is thought to cause renal dysfunction, and the increase in ADH may have helped to prevent further aggravation of ketoacidosis. We propose to change the term hyperosmolar non-ketotic coma (HNC) to diabetic hyperosmolar coma (DHC), because sometimes patients with hyperosmolar non-ketotic diabetic coma are ketotic, as seen in the present case. Determination of 3-OHBA or individual ketone bodies in blood is important and essential for the differential diagnosis of diabetic coma. The diagnosis of either ketoacidotic or hyperosmolar coma should be made depending on the major expression of ketoacidosis or hyperglycemic hyperosmolarity.

The case of a non diabetic 6-year-old boy affected by Down's syndrome, who developed hyperosmolar hyperglycemic non-ketotic coma following the infusion of hypertonic dextrose solution during general anesthesia for a surgical procedure for cryptorchidism is reported. Following surgery, the patient remained deeply comatose and generalized seizures occurred. Hyperosmolarity due to hyperglycemia and acidosis were reduced by administration of insulin at low rate, hypotonic saline and sodium-bicarbonate solutions. The patient's clinical conditions promptly improved following normalization of blood glucose levels. An oral glucose tolerance test performed three months later was normal. The authors emphasize the potential risk of hyperosmolar hyperglycemic non-ketotic coma also in non diabetic patients treated with hypertonic dextrose solutions, during surgery events.

The results of the study involving 123 patients suffering from hyperglycemic diabetic coma lead to the conclusion on ineffectiveness of high-dose insulin. Treatment of hyperglycemic coma by low-dose insulin is more preferable as warranting continuous decrease of glycemia without its transformation into hypoglycemia, ++post-hypoglycemia hyperglycemia, brain edema.

Hypoglycaemia remains a serious and much feared complication of insulin therapy. In this study, patients attending an accident and emergency department in hypoglycaemic coma were randomized to treatment with either intravenous dextrose (25g) or intramuscular glucagon (1mg), administered into the right thigh. Restoration of normal conscious level was slower after glucagon than dextrose (9.0 vs 3.0 min, P less than 0.01), although the average duration of hypoglycaemic coma was 120 min. Two patients in the glucagon-treated group, who failed to show satisfactory recovery after 15 min, required additional treatment with intravenous dextrose. On questioning following recovery, all except two patients reported loss of awareness of the onset of hypoglycaemia Intramuscular glucagon is valuable in the treatment of severe hypoglycaemia outwith hospital and, although the slightly slower and less predictable recovery may appear to make it a less attractive option than intravenous dextrose in the accident and emergency department, this must be balanced against the advantages of ease of administration and a lower incidence of serious adverse effects.

Cerebral edema as a complication of the therapy of diabetic coma has been described for over 50 years, although modern awareness dates to about 1967. Almost all cases have occurred in patients with diabetic ketoacidosis (DKA). Although a few cases of cerebral edema have been reported in patients with nonketotic hyperosmolar coma (NKHC), these are in general not well documented by either autopsy data of cat scans. Over a period of 9 years, I have encountered 5 patients who developed cerebral edema as a complication of the therapy of NKHC. The initial plasma glucose in these patients was 1,496 +/- (SD) 296 mg/dl and plasma osmolality was 382 +/- 29 mosm/kg. All had depression of sensorium to at least a stupor (stage I coma or greater). All were treated with intravenous insulin and either 77 or 154 mM NaCl, and plasma glucose fell at a mean rate of 38 mg/dl/h. In all patients, plasma glucose fell below 250 mg/dl (mean of 18 +/- 66 mg/dl) and all patients experienced increased depression of sensorium, elevated csf pressure, and brain swelling as diagnosed by cat scanning. Therapy with various combinations of glucose, mannitol and steroids were without effect. In 1 patient, insertion of a subdural intracranial screw lowered intracranial pressure from 24 to 3 cm of H2O. Three of the 5 patients died and 2 remain in a persistent vegetative state, 1 of whom is also quadriplegic.(ABSTRACT TRUNCATED AT 250 WORDS)

A 12 year old female patient presenting non ketotic hyperosmolar hyperglycemic coma as initial sign of diabetes mellitus is presented. She was successfully treated with continuous infusion of low dose of insulin and saline and glycosaline isotonic sera. Potassium was precociously added to the hydrating solutions. During convalescence she suffered a left iliofemoral thrombophlebitis which remitted with appropriate treatment. In coma stage, C-peptide was close to normal, indicating active insulin production by the pancreas.