Hyperosmolar Non-ketotic Diabetic Coma Research Articles

Promotive effect of comprehensive management on achieving blood glucose control in senile type 2 diabetics.

The aim of this study was to evaluate the control of blood glucose and glycosylated hemoglobin A1c (HbA1c) and its influencing factors, in elderly type 2 diabetic mellitus (T2DM) patients undergoing comprehensive management. After years of comprehensive prevention of and control measures for diabetes, elderly T2DM patients who were receiving long-term health care were comprehensively evaluated through an annual physical examination. In addition to routine health examination, the patients were required to undergo HbA1c measurement. Among 688 patients, 652 were men and 36 were women, with a mean age of 78.2 ± 9.1 years. The average HbA1c was 6.6 ± 0.9%. A total of 50.6% of the patients had HbA1c <6.5%, whereas 76.3% had HbA1c <7.0%. Among all patients, 77.1, 46.4, 66.1, 67.8, 36.3, and 57.4% achieved the target total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride (TG), blood pressure, and body mass index (BMI) levels, respectively. The duration of disease and type of treatment, as well as the LDL, HDL, TG, BMI, and blood pressure levels, were significantly associated with HbA1c control. No patient was admitted because of ketoacidosis or hyperosmolar nonketotic diabetic coma in 10 years. Approximately half of the T2DM patients achieved the target HbA1c level. The more effective blood glucose control observed in our study compared with previous studies can be attributed to the effective monitoring of medical conditions and comprehensive management of patients.

Nursing care of patients with upper gastrointestinal hemorrhage with hyperosmolar nonketotic diabetic coma

Nursing care of patients with upper gastrointestinal hemorrhage with hyperosmolar nonketotic diabetic coma

Hyperosmolar Nonketotic Diabetic Comaの1治験例

Hyperosmolar Nonketotic Diabetic Comaの1治験例

Analysis in related factors of deep vein thrombosis formation in diabetic patients and the nursing strategy

Objective To study the related factors in diabetic patients with lOwer extremital deep vein thrombosis(DVT) and the nursing strategy. Methods 58 diabetic cases underwent lower limbs 99mTc-MAA veins imaging and/or ultrasunography. The related laboratory data such as fasting plasma glucose(FPG),blood cholesterol, blood triglycerides and clinic informations such as age, disease courses, lower limbs symptoms (swelling, erooted veins and diabetic foot) and acute complication (diabetic ketoacidosis and hyperosmolar non ketotic diabetic coma) were collected simultaneously. The relationship of each factors with DVT incidence were analyzed. Results 28 patients (48.3%) complicated with lower limbs DVT. The DVT incidence was signifi-cantly different among patients with different age, disease courses, FPG, blood cholesterol, blood triglycerides, lower limbs symptoms and acute complication, respectively. No significant difference was seen in patients with different blood pressure, body weight index, diabetes type. Conclusions Various dangerous factors accumu-lating in DM such as old age, long disease courses, high FPG, high blood cholesterol and high blood triglyc-erides contribute to the high incidence of lower limbs DVT. Early intervention, comprehensive treatment and in-tensive nursing should be applied to reduce the incidence of DVT. Key words: Diabetes mellitns; Deep vein thrombosis; Related factors; Nursing strategy

Endokrine Krisen

Pituitary apoplexy, diabetes insipidus, thyroid storm, myxedema coma, parathyrotoxic crisis, hypocalcemia tetany, pheochromocytoma and Addison crisis, diabetic ketoacidosis, diabetic hyperosmolar nonketotic coma, hypoglycemia and carcinoid crisis are the most important endocrine crises. Some of them are common, others very rare. All physicians nevertheless need to have at least a basic knowledge of all of them, since symptoms and signs of endocrine crises overlap with those of other severe disease states, and the failure to recognise endocrine crises as such and to begin rapidly the specific therapy can have fatal consequences.

Fatality from Olanzapine Induced Hyperglycemia

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.

Diabetic hyperosmolar non-ketotic coma, a different approach to fluid replacement

Diabetic hyperosmolar non-ketotic coma, a different approach to fluid replacement

A Case of Diabetic Hyperosmolar Nonketotic Coma with Rhabdomyolysis Accompanied by Alzheimer's Disease

A Case of Diabetic Hyperosmolar Nonketotic Coma with Rhabdomyolysis Accompanied by Alzheimer's Disease

Improving the outcome of ketoacidosis

Practical Diabetes InternationalVolume 13, Issue 2 p. 63-63 Letters to the EditorFree Access Improving the outcome of ketoacidosis Geoff Gill MSc MD FRCP DTM&H, Geoff Gill MSc MD FRCP DTM&H Consultant Physician and Endocrinologist Liverpool, UKSearch for more papers by this author Geoff Gill MSc MD FRCP DTM&H, Geoff Gill MSc MD FRCP DTM&H Consultant Physician and Endocrinologist Liverpool, UKSearch for more papers by this author First published: March/April 1996 https://doi.org/10.1002/pdi.1960130214Citations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Huddle KR, Gill GV. Reducing acute hyperglycaemic mortaity in African diabetic patients. Diabet Med 1989; 6: 64– 6 2 Rolfe M, Ephraim GG, Lincoln DC, Huddle KR. Hyperosmolar nonketotic diabetic coma as a cause of emergency hyperglycaemic admission to Baragwanath Hospital. South Afr Med J 1995; 85: 173– 6 Citing Literature Volume13, Issue2March/April 1996Pages 63-63 ReferencesRelatedInformation

A metabolic complication of severe burns

A 32-year-old male was referred to intensive care with possible respiratory sepsis 15 days after sustaining 73 per cent TBSA electrical burns. Investigation revealed previously undiagnosed hyperosmolar non-ketotic diabetic coma. The aetiology, pathogenesis and management of this recognized complication of major burns is discussed. An interesting feature of this case is recovery from 73 per cent burns, severe hyperosmolar non-ketotic diabetic coma and a serum osmolality of 429 mosmol/kg, each of which carry a high mortality probability.

Hyperosmolar non-ketotic diabetic coma and rhabdomyolysis

Rhabdomyolysis is a rare but potentially fatal complication of hyperosmolar states. We report a case of severe hyperosmolar non-ketotic diabetic coma causing rhabdomyolysis in a young man. Despite very high levels of creatine kinase there was no detectable myoglobinuria. Creatine kinase estimation should be a standard investigation in all patients presenting with a hyperosmolar state.

高浸透圧性非ケトン性糖尿病性昏睡に，横紋筋融解症（Ｒｈａｂｄｏｍｙｏｌｙｓｉｓ）による急性腎不全を合併した１例

高浸透圧性非ケトン性糖尿病性昏睡に，横紋筋融解症（Ｒｈａｂｄｏｍｙｏｌｙｓｉｓ）による急性腎不全を合併した１例

Neuroleptic Malignant Syndrome Presenting as Hyperosmolar Non-ketotic Diabetic Coma

A 50-year-old man presented with hyperosmolar non-ketotic diabetic coma associated with the neuroleptic malignant syndrome (NMS) after intramuscular treatment with haloperidol. It is suggested that NMS may occur as a complication of uncontrolled diabetes mellitus with dehydration. Conversely, NMS might precipitate diabetic coma in patients with previously well controlled blood glucose.

Suppressive effect of vasopressin on ketosis in diabetic rats.

In order to clarify if vasopressin (VP) plays a role in the pathophysiology of hyperosmolar nonketotic diabetic coma (HNDC), VP has been infused to diabetic rats and plasma levels of glucose (PG), ketone bodies, FFA and glucagon were determined. High-dose VP infusion (1.2 U/kg/h) caused gradual elevation of PG (60%) and glucagon levels (600%), while ketone bodies showed transient decrease (20%) at 30 min. Under the suppression of endogenous glucagon secretion by constant infusion of somatostatin (100 micrograms/kg/h), high dose VP showed 25% increase in PG levels and 30% reduction of ketone body levels for the subsequent VP infusion for 1.5 hour. Low-dose VP infusion (0.06 U/kg/h) had no hyperglycemic effect, but suppressed ketosis (20%) in the same condition. There were no changes in plasma FFA concentrations, indicating no significant effect of VP on lipolysis. The results indicate that VP often elevated in HNDC may play an important role for the pathophysiology of HNDC through suppression of hepatic ketogenesis.

A Case of Rhabdomyolysis Caused by Hyperosmolar Non-Ketotic Diabetic Coma with Prader-Willi Syndrome

A Case of Rhabdomyolysis Caused by Hyperosmolar Non-Ketotic Diabetic Coma with Prader-Willi Syndrome

A Case of Diabetic Non-Ketotic Hyperosmolar Coma with an Increase with Plasma 3-Hydroxybutyrate.

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.

A Case of Hyperosmolar Non-Ketotic Diabetic Coma Accompanied with Rhabdomyolysis Caused by Dehydration and Excess Infusion

A Case of Hyperosmolar Non-Ketotic Diabetic Coma Accompanied with Rhabdomyolysis Caused by Dehydration and Excess Infusion

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.

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.

A Case of Hyperosmolar Non-ketotic Diabetic Coma with Various Complications

A Case of Hyperosmolar Non-ketotic Diabetic Coma with Various Complications