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

During a 12-month prospective study there were 125 visits to the Harlem Hospital Emergency Room for symptomatic hypoglycemia. Sixty-five patients had obtundation, stupor, or coma; 38 had confusion or bizarre behavior; 10 were dizzy or tremulous; 9 had had seizures; and 3 had suffered sudden hemiparesis. Diabetes mellitus, alcoholism, and sepsis, alone or in combination, accounted for 90% of predisposing conditions; others included fasting, terminal cancer, gastroenteritis, insulin abuse, and myxedema. Average blood glucose levels were lower among comatose than among obtunded patients, but overlap was considerable, and overall there was little correlation among cause, blood glucose levels, and symptoms. Although mortality was 11%, only one death was attributable to hypoglycemia per se, and only four survivors had focal neurological residua.
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PMID:Hypoglycemia: causes, neurological manifestations, and outcome. 400 66

Two West Indian men with no previous history of diabetes mellitus developed hyperosmolar non-ketotic diabetic coma. Intra-abdominal catastrophes secondary to mesenteric thrombosis played a major part in the death of these patients, in both of whom control of the hyperosmolar state had been achieved. Both patients had evidence of infarction of intestine at necropsy. Vascular thromboses are a major complication of this form of coma and must be considered when such patients develop signs of an acute abdomen.
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PMID:Hyperosmolar non-ketotic diabetic coma: with particular reference to vascular complications. 531 81

The pathogenesis of the abnormal metabolic state in patients with non-insulin-dependent diabetes (NIDDM) is controversial. Even the term NIDDM stirs controversy because of the easily drawn inference that individuals with this form of diabetes do not need insulin treatment. Yet many patients with NIDDM are treated with insulin; some even develop hyperosmolar coma if not given insulin. Ketoacidosis, however, is very infrequent in this syndrome, implying that these patients are not dependent on insulin treatment to prevent mass mobilization of fatty acids and ketone bodies. The phrase noninsulin-dependent is therefore appropriate when used in this restricted fashion but inappropriate when used to imply adequacy of insulin secretion. The evaluation of the adequacy of islet function in this syndrome has been complex, since there is no standard of insulin output that can be defined for normal islets without specifying the physiologic setting under which the assessment has been made. For example, individuals with normal glucose levels but variable degrees of obesity have widely varying insulin secretion rates. Thus, the choice of controls is critical when comparing islet function in NIDDM to normal. In addition, the efficiency of the B-cell response to a challenge (e.g., oral glucose tolerance test) can markedly influence the magnitude of the stimulatory glucose level during the period of testing. For example, a subject with some impairment of insulin output will tend to become more hyperglycemic during the test. The hyperglycemia may then stimulate more insulin secretion so that the overall insulin output may appear equal to or even greater than that of a normal individual. In such a closed-loop system, strict control of input variables is necessary to evaluate whether or not insulin secretion is normal. As will be discussed, control of glucose level and other variables is seldom accomplished in dynamic glucose tolerance tests. As will be presented in this review, the development of appropriately controlled studies of islet function has provided convincing evidence that islet B-cell function is abnormal in patients with NIDDM. Since these studies are based on an understanding of normal islet function, normal islet B-cell physiology is discussed before pathophysiology. Finally, the implications of this analysis for the treatment of NIDDM with diet, hypoglycemic sulfonylureas, and insulin will be discussed.
Diabetes Care
PMID:Pathophysiology of insulin secretion in non-insulin-dependent diabetes mellitus. 609 29

A 32-year-old man was admitted semi-comatose with digestive troubles to the hospital. A diabetic keto-acidosis was discovered. The diabetes was known by the patient for one year and a half, but it was not treated. Furthermore the laboratory studies showed a hyperlipidemia (type V) and an increase in pancreatic enzymes. The hyperlipidemia disappeared with insulin therapy. The chronology of the facts was probably: a hyperlipidemia associated with the diabetes, responsible of an acute pancreatitis, which induced a keto-acidosis.
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PMID:[Association of hyperlipidemia, acute pancreatitis and diabetic keto-acidosis. A case report (author's transl)]. 625 16

Chronic pancreatitis appears to be increasing likely because increase in alcohol consumption and improved diagnostic tools. So the diabetes due to chronic pancreatitis is gaining importance. In order to obtain a better understanding of that particular secondary diabetes, 179 patients with chronic pancreatitis were studied from 1970 to 1981. 154 patients were male and 25 female. Average admission age was 45, ranging from 25 to 86. All the patients underwent medical therapy, based on diet, pancreatic enzymes, pain control. 99 of them underwent even to surgery. The follow-up is ranging from 6 months to 10 years: during this period 18 patients died, 41 went lost. 120 patients are still under observation. Diabetes was found in the family history of 27 patients (15%). At hospital admission 41 patients (23%) had high fasting glycemia, 23 of them even glycosuria. Other 74 showed diabetic oral glucose tolerance test. During the follow-up time 27 became clinically diabetic, 3 died because hyperosmolar coma and 8 had to be readmitted more than once because diabetic metabolic decompensation. Among the 120 patients at the moment under control, 66 (55%) show abnormal fasting glycemia, 10 developed high blood pressure, 12 inferior limbs vasculopathy with paresthesias and intermittent claudication, 2 myocardiosclerosis and atrial fibrillation, 1 myocardial infarction, 2 chronic nephropathy, 1 diabetic retinopathy. Whereas surgery or medic therapy may relieve chronic pancreatitis typical symptoms, they appear to be useless remedy against the under lying diabetes. As the time goes on more and more patients develop glucose intolerance, quite early became insulin-dependent, are disposed to severe diabetic metabolic decompensation and can show vascular, cardiac or renal complication.
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PMID:[Chronic pancreatitis and diabetes]. 633 49

The physiopathology and clinical picture of hyperosmolar diabetic coma are described, and four personal cases are presented. This form of coma is a rare, but particularly serious complication of diabetes mellitus. Since its prognosis is poor, even when suitable treatment is provided, the greatest possible care should be devoted to preventing its main cause, namely dehydration.
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PMID:[Hyperosmolar diabetic coma. Case reports and review of the literature]. 633 18

A 12-month epidemiologic study in 1979 and 1980 of all diabetic acidosis admissions to all acute care hospitals in Rhode Island detected 152 episodes occurring in 137 persons. Eleven per cent of diabetic acidosis admissions presented in coma and the overall death-to-case ratio was 9%. Newly diagnosed diabetes accounted for 20% of these episodes, while persons having multiple episodes during the year accounted for 15% of the admissions. The annual rate of diabetic acidosis was 46 per 10,000 diabetics. Highest rates of diabetic acidosis were found for the elderly, those admitted from nursing homes and those residing in one geographic area of the state. For known diabetics with an admission for acidosis, 87% were on insulin prior to admission and 81% were nonobese. Patients seldom contacted physicians prior to admission. Insulin dose or frequency was often (40%) changed in the two weeks prior to admission. Most of the known diabetic cases of acidosis had emergency admissions for diabetes in the three-year period prior to admission and few had any structured diabetic outpatient education. Infection and noncompliance were the most frequently identified precipitants of diabetic acidosis occurring in known diabetics.
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PMID:The epidemiology of diabetic acidosis: a population-based study. 640 12

Deaths due to diabetes with acidosis or coma (DAC) in the United States from 1970 through 1978 were analyzed to determine epidemiologic characteristics associated with mortality likely to be due to diabetic ketoacidosis (DKA), a complication of diabetes mellitus considered largely preventable. Annual age-adjusted rates for DAC deaths decreased during the study period, and the secular trend was significant in all regional, race, and sex groups examined. General population-based mortality rates increased linearly with age, were higher in non-Whites than in Whites among persons aged greater than 14, were higher in females, and increased significantly with age in both races and both sexes. By region, rates were lowest in the West. DAC mortality rates specific to estimated diabetic populations decreased annually from 1970 to 1978 in all race and sex groups, and were highest at age greater than or equal to 65, but did not show significant linear increases with age, except in non-Whites. These results indicate declining secular trends, as well as age, race, sex, and regional differences in the risk of such deaths. Further studies are warranted to determine factors contributing to these differences.
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PMID:Epidemiologic characteristics of mortality from diabetes with acidosis or coma, United States, 1970-78. 641 75

A number of changes in therapy of uncontrolled diabetes have occurred in recent years. These include low-dose insulin regimens, often routine phosphate repletion, more cautious bicarbonate replacement, infusion of larger fluid volumes, the use of hypotonic solutions in hyperosmolar states, and recently magnesium repletion. These modalities (with the exception of routine magnesium repletion) have been employed at North Central Bronx Hospital since its opening in 1976. Through this retrospective analysis of 275 cases of uncontrolled diabetes we have tried to answer the following questions: What is the outcome of all episodes of uncontrolled diabetes in a municipal hospital population with a uniform treatment protocol? What are the results of treatment with new modalities in various age groups? Are the causes of death different from those tabulated in previous reports? Our results indicate a good outcome in those under the age of 50 yr regardless of the diagnosis of hyperosmolar nonketotic coma (HNC) or diabetic ketoacidosis (DKA). Mortality from DKA was 2% in those under age 50 yr and 26% in the older age group. Surprising was the low mortality in the hyperosmolar group with 0% mortality under age 50 yr and 14% in patients over this age. The major categories of causes of death in the series included sepsis, adult respiratory distress syndrome (ARDS), metabolic, cardiovascular, and shock. With the exception of ARDS, these categories were not different from other reported series. There were few thromboembolic events in this series.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Care
PMID:Uncontrolled diabetes mellitus in adults: experience in treating diabetic ketoacidosis and hyperosmolar nonketotic coma with low-dose insulin and a uniform treatment regimen. 641 94

Blacks and Indians with early-onset insulin-dependent diabetes mellitus (IDDM) were studied in order to assess the prevalence of acute and chronic complications. Of the 92 Blacks almost 70% developed ketoacidotic coma on one or more occasions, whereas 50% of the 41 Indians manifested this complication. Most of the chronic complications were related to duration of IDDM. Retinopathy was found in 14% of the Black and 22% of the Indian patients, nephropathy in 3% and 7% and neuropathy in 22% and 32% respectively. Compared with findings in other studies, IDDM in these population groups is not associated with a particularly high prevalence of chronic complications.
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PMID:Complications of early-onset insulin-dependent diabetes mellitus in Blacks and Indians. 642 Sep


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