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PubMedDate not supplied

A valid experimental brain death organ donor model.

BACKGROUND: This study was designed to establish a validated canine brain death model. Ten consecutive dogs were studied to investigate the effects of brain death on hemodynamic, metabolic, and hormonal function. METHODS: Brain death was induced by inflation of a subdurally placed balloon and was validated neuropathologically. Functional data and blood samples were collected before and 15, 45, 90, 240, 360, and 420 minutes after the induction of brain death. No inotropic or vasoactive support was given. The results are expressed as mean +/- standard error of the mean. RESULTS: The Cushing reflex occurred in all animals and lasted 13.3 +/- 1.5 minutes. Raised catecholamine levels were documented at 15 minutes, whereas the pituitary gland hormones vasopressin and adrenocorticotrophic hormone decreased significantly after 15 and 45 minutes, respectively. Triiodothyronine, thyroxine, and glucagon decreased significantly from 0.58 +/- 0.05 ng/ml, 2.20 +/- 0.15 micrograms/dl, and 49.7 +/- 9.1 pg/ml to 0.34 +/- 0.03 ng/ml (p < 0.05 versus baseline; paired two-tailed t-test), 1.14 +/- 1.14 micrograms/dl (p < 0.05), and 6.9 +/- 1.4 pg/ml (p < 0.05). Insulin and lactate dehydrogenase showed a moderate increase after brain death. Diabetes insipidus occurred after 45 minutes in nine animals (urine output 13.5 +/- 1.8 ml/kg/hour). Left and right ventricular end-diastolic pressure increased significantly toward the end of all experiments. Cardiac output increased and systemic and pulmonary vascular resistance decreased, but heart rate remained unchanged. CONCLUSION: This simple, reproducible, moderately invasive, and reliable model of brain death in animals assesses donor organ function and preservation. Cushing reflex, hyperdynamic state, catecholamine storm, vasopressin and adrenocorticotropic hormone cessation, total cerebral necrosis, and diabetes insipidus were consistent findings.

Acidosis↗
PubMed2002

[Diabetic ketoacidosis].

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called noninsulin-dependent diabetes mellitus) is not as rare as was once thought. This article reviews data about precipitating events, pathogenesis, carbohydrate, lipid and ketone, water and electrolyte metabolism in this hyperglycemic crisis. The review discusses diagnostic procedures, laboratory evaluation, differential diagnosis and treatment: replacement of fluid and electrolytes, low-dose insulin therapy and recommendations for use of bicarbonate. A discussion of complications management of diabetic ketoacidosis (hypoglycemia, hypokalemia, cerebral edema, hyperchloremic metabolic acidosis, pulmonary edema, adult respiratory distress syndrome), mortality rate and prevention are included in this review.

Adult↗
PubMed1998

Review of management of type 2 diabetes mellitus.

BACKGROUND: Commonly used drugs for type 2 diabetes are not ideal. The sulphonylureas, especially potent and long-acting agents such as glibenclamide, can induce hypoglycaemia, while metformin carries the risk of lactic acidosis. AIM: To review the management of type 2 diabetes at the major teaching hospital in Tasmania, Australia, principally to determine the extent of use of glibenclamide and metformin in the elderly and patients where published contraindications are present. METHODS: A retrospective review of the medical records for 150 consecutive patients with type 2 diabetes admitted to the hospital in mid-1997, was performed. An extensive range of demographic and clinical variables was recorded for each patient. These included the duration of type 2 diabetes, the presence of other medical conditions, medication history, presence of any contraindications to the use of metformin or sulphonylureas, biochemical measures of diabetic control, and the presence of any diabetic complications. RESULTS: The mean (+/-SD) age of the 150 patients included in the study was 70.1+/-11.8 years. The mean body mass index was 28.7+/-6.2 kg/m2 and the mean recent HbA1c level was 86+/-21%; only 24.7% of patients had a HbA1c level of 7% or lower. Of the 45 patients using glibenclamide, 40 (88.9%) had one or more risk factors for hypoglycaemia: over 65 years of age, renal impairment, or cognitive impairment and living alone. The study also found an extensive use of metformin in patients with contraindications and at highest risk of developing lactic acidosis. Sixty-six out of 70 patients (94%) using metformin had at least one contraindication according to the manufacturer's prescribing information, 57% of patients had two or three contraindications and 14% of patients had more than three contraindications. More than 20% of the patients had a renal function below published exclusion criteria. CONCLUSIONS: There was evidence of over-utilization of metformin and glibenclamide in type 2 diabetes patients most at risk of adverse reactions. Insulin therapy could be a safer and more effective management strategy in many of these patients.

Aged↗
PubMed1981

Insulin-dependent diabetes mellitus with early onset in blacks and Indians.

Insulin-dependent diabetes mellitus (IDDM) with onset below 35 years of age was studied in 52 Black and 38 Indian patients. IDDM accounted for approximately 10.4% and 1.1% of diabetes in the respective racial groups. The mean age and body weight in the Black and Indian diabetics were 27.6 years and 24.7 years, and 60.2 kg and 54.7 kg, respectively. The duration of diabetes in the majority of Blacks was 1-4 years, and that in Indians 5-9 years. The initial presentation in more than 80% of the patients was acute, with severe keto-acidosis in 15%. A positive family history of diabetes was obtained in more than 50% of Indians and in less than 6% of Blacks. Complications were present in 33% of Indian patients and were related to the duration of illness and dose of insulin required. Basal growth hormone, cortisol, cholesterol and triglyceride concentrations in serum were higher in Indians than in Blacks, but the differences were not significant. The disease was unrelated to excess alcohol intake or to pancreatic calcification.

Adolescent↗
PubMed2005

Diabetic ketoacidosis in pregnancy.

OBJECTIVE: The development of diabetic ketoacidosis in pregnancy is a medical emergency, requiring treatment in an intensive care setting. Both the mother and the fetus are at risk for significant morbidity and mortality. Physiologic changes unique to pregnancy provide a background for the development of diabetic ketoacidosis. An understanding of these physiologic changes assists in the management of the two patients being treated. Treatment of the patient with diabetic ketoacidosis includes insulin therapy and careful fluid management; recommendations for management are presented. PATIENTS: Pregnant women, either with preexisting diabetes or with diabetes diagnosed during pregnancy. CONCLUSIONS: Prompt recognition of the clinical manifestations of diabetic ketoacidosis, followed by appropriate, timely treatment will optimize outcome for the pregnant woman and her fetus.

Acidosis↗
PubMed1991

Urinary catecholamine in children with diabetic ketoacidosis.

Urinary excretion of norepinephrine, epinephrine and dopamine was investigated in children with diabetic ketoacidosis. Besides pronounced hyperglycemia and metabolic acidosis, severe hypovolemia was also observed. At the onset of the study, urinary excretion of norepinephrine, epinephrine and dopamine was markedly elevated. Fluid replacement decreased urinary catecholamine excretion. Norepinephrine: 996 +/- 97 vs. 253 +/- 29; dopamine: 5,108 +/- 480 vs. 3,175 +/- 715; epinephrine: 402 +/- 81 vs. 77 +/- 200 pmol/min/1.73 m2. During ketoacidosis, there was a significant negative correlation between urinary norepinephrine excretion and endogenous creatinine clearance. Urinary output of both norepinephrine and dopamine correlated significantly with diuresis, while sodium excretion only correlated with dopamine excretion. Our data suggest that in diabetic ketoacidosis increased urinary excretion of norepinephrine may participate in renal hypoperfusion and hypofiltration. Elevated renal dopamine production contributes to sodium loss, characteristic for diabetic ketoacidosis.

Adolescent↗
PubMed1998

Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis.

STUDY OBJECTIVE: To determine whether venous blood gas values can replace arterial gas values in the initial emergency department evaluation of patients with suspected diabetic ketoacidosis. METHODS: This prospective comparison was performed in an adult university teaching hospital ED. Samples for arterial and venous blood gas analysis were obtained during initial ED evaluations. The venous gas samples were collected with samples for other blood tests at the time of intravenous line insertion. Both arterial and venous samples were obtained before the initiation of treatment. RESULT: Data from 44 episodes of diabetic ketoacidosis in 38 patients were analyzed. Laboratory findings of those patients with diabetic ketoacidosis were as follows (mean +/- SD): arterial pH, 7.20 +/- 14; venous pH, 7.17 +/- 13; serum glucose, 33.8 +/- 16 mmol/L (609 +/- 288 mg/dL); arterial HCO3-, 11.0 +/- 6.0 mmol; venous HCO3-, 12.8 +/- 5.5 mmol/L; serum CO2, 11.8 +/- 5.0 mmol/L; and anion gap, 26.7 +/- 7.6 mmol/L. The mean difference between arterial and venous pH values was 0.03 (range 0.0 to 0.11). Arterial and venous pH results (r = .9689) and arterial and venous HCO3- results (r = .9543) were highly correlated and showed a high measure of agreement. CONCLUSION: Venous blood gas measurements accurately demonstrate the degree of acidosis of adult ED patients presenting with diabetic ketoacidosis.

Adolescent↗
PubMed1976

The diabetic day-care unit. I. Development of an index to evaluate diabetes control.

In order to measure the effect of a diabetic day-care unit on diabetes control two scoring scales were constructed, one for insulin-dependent diabetics and the other for patients managed by diet or oral agents or both. Both scales were based on observations of blood and urine glucose concentrations, ketonuria, symptoms of diabetes and deviation from ideal weight. The scale for insulin-dependent diabetics also included the frequency and severity of insulin reactions and frequency of hospital admission for acidosis. Scores for 45 insulin-dependent patients and for 55 diabetics treated by diet with or without oral agents in the unit indicated significant improvement in diabetes control in both groups.

Administration, Oral↗
PubMed1976

[Lactic acidosis after administration of buformine (author's transl)].

An 85-year-old female diabetic was admitted in coma, having been on antidiabetic treatment with the biguanide derivative "Silubin retard", 600 mg/d, for one-and-a-half months. The anion deficiency was 57 mmol/l, pH 6.9, suggesting the diagnosis of lactic acidosis in the absence of other causes of metabolic acidosis. Blood lactic acid levels of more than 16.65 mmol/l (150 mg/100 ml) confirmed the diagnosis. Administration of 875 mmol sodium bicarbonate over 12 hours corrected the deficiency. On admission to hospital there had been slight pre-renal failure. Myocardial infarction developed as a result of tissue hypoxia but did not prove clinically important. On the second day there were signs of a compensated disseminated intravascular coagulopathy with upper gastro intestinal haemorrhage. The woman died suddenly 18 days later of pulmonary embolism.

Acidosis↗