Hyperosmolar Non-ketotic Diabetic Coma Research Articles

Plasma amino acid levels in hyperosmolar nonketotic diabetic coma.

The plasma amino acid levels in five patients with hyperosmolar nonketotic diabetic coma and in seven normal subjects were analysed. In the patients with hyperosmolar nonketotic diabetic coma, total amino acids were generally low, especially, the concentrations and the molar ratios of arginine, taurine and serine were significantly low, and ornithine decreased only at the concentration. The level of phenylalanine increased both at the concentration and the molar ratio, and tyrosine did only at the molar ratio. The significance of such changes in the plasma is discussed in relation to diabetic ketoacidosis or lactic acidosis.

Epidemiological studies on renal papillary necrosis with diabetes mellitus in Japan.

Eighty-six cases of renal papillary necrosis (RPN) published in Japan over the years 1949-1980 were studied. While several hundreds cases of RPN were reported in certain European countries and the USA, only 5 cases were published in Japan up until 1960. However, the number of case reports has increased to 28 over the 5 year period of 1976-1980. The ratio of diabetics (62 cases) to nondiabetics (24 cases) is about 2.6:1 and is the same as that reported by Lauer in the USA. In diabetics, RPN was more frequently seen in females (3.4:1) and at more advanced age. Frequency of bilateral occurrence was high (47.5%). The prevalence of the association of glomerulosclerosis (75.0%) was higher than that reported by Silverman et al. in the USA (47.1%). The Incidence of the association of disturbances of consciousness (29.5%) was similar to that reported by Edmondson et al.. It was concluded that the number of cases of RPN with diabetes mellitus in Japan started to increase about 20 years later than in the USA, and that the frequency of the association between RPN and diabetic glomerulosclerosis in Japan seems to be higher than in the USA. Furthermore, it was noted that RPN was frequently associated with hyperosmolar nonketotic diabetic coma.

Hyperosmolar Non-Ketotic Diabetic Coma — Less Sodium in Therapy?

Eighteen patients with hyperosmolar non-ketotic diabetic coma were studied retrospectively to identify factors affecting prognosis and to review treatment. This condition affected older women two-thirds of whom were unrecognised diabetics. Eight (44%) died. Mortality correlated with age above 60, uraemia and hyperosmolarity, but not with the degree or rate of fall of hyperglycaemia. Hyperglycaemia responded to rehydration and insulin, but in all patients serum osmolarity remained high for several days. In 14 patients (78%) the serum sodium concentration initially increased and in four (22%) serum osmolarity increased. This persistence or worsening of the hyperosmolar state can be avoided without the risk of cerebral oedema by replacing the fluid and electrolyte deficits over 48 hours and using 5% dextrose for the water deficit.

Low-Dose Insulin for Diabetic Nonketotic Hyperosmolar Coma

To the Editor.— The use of low-dose insulin for the treatment of diabetic ketoacidosis is becoming widespread. Much less is published about its use for diabetic hyperosmolar nonketotic coma. 1,2 Recently, we had the opportunity to treat a patient with diabetic hyperosmolar nonketotic coma, using low-dose insulin with gratifying results. Report of a Case.— 75-year-old woman came to an emergency room in coma. She was known to have adult-onset diabetes and had taken 40 U of NPH insulin a day for five years. She also took 50 mg of hydrochlorothiazide and 0.125 mg of reserpine daily for essential hypertension and 5 mg of prednisone every other day for asthma. She had not seen a physician for two years. On admission, she was breathing spontaneously but would respond only to deep pain by withdrawal. There were no focal or lateralizing neurological signs. Her blood pressure was 130/80 mm Hg; pulse rate,

Correction of ketosis by suppression of lipolysis with 5-methylpyrazole-3-carboxylic acid in rats with established diabetic ketoacidosis.

Because the presence of an elevated plasma free fatty acid (FFA) concentration is not always sufficient to promote ketogenesis, we examined the contribution of circulating FFAs to ketogenesis in established diabetic ketoacidosis. We studied the effects of suppression of lipolysis on ketogenesis in rats with established streptozotocininduced diabetic ketoacidosis using 5-methylpyrazole-3-carboxylic acid (5-methylpyrazole) as an antilipolytic agent. In response to this substance, plasma FFA fell from 2.42 ± 0.15 meq/L to 0.56 ± 0.06 meq/L in four hours. There was a concomitant fall in total plasma ketone from 12.17 ± 0.60 mM to 2.62 ± 0.54 mM. The fall in total plasma ketone was due predominantly to a fall in the beta-hydroxybutyrate concentration but also to a fall in the acetoacetate concentration. Although the agent slowed the rise of plasma glucose in these diabetic animals, the concentration was markedly elevated (573 ± 22 mg/dl) at four hours. Studies were performed in comparable rats with diabetic ketoacidosis to exclude the possibility that 5-methylpyrazole interferes with hepatic ketogenesis. When the plasma FFA concentration was raised by administration of a lipid emulsion and heparin (after plasma FFA and total plasma ketone had fallen in response to 5-methylpyrazole), total plasma ketone also rose despite the presence of 5-methylpyrazole. When the plasma FFA concentration was maintained at a high level by administration of a lipid emulsion and heparin from the start of the experiment, 5-methylpyrazole failed to affect the total plasma ketone concentration. Thus, availability of substrate (plasma FFAs) reversed or prevented the correction of ketosis by 5-methylpyrazole. These findings indicate that circulating FFAs are rate limiting for the maintenance of the ketotic state in established diabetic ketoacidosis and support the view that the absence of ketosis in the usual patient with hyperosmolar nonketotic diabetic coma is a result of inadequate availability of plasma FFAs for ketogenesis. 5-Methylpyrazole converts an experimental model of diabetic ketoacidosis into one resembling hyperosmolar nonketotic diabetic coma.

Serum Sodium Concentrations and Renal Complications in Hyperosmolar Non-Ketotic Diabetic Coma

Serum Sodium Concentrations and Renal Complications in Hyperosmolar Non-Ketotic Diabetic Coma

Hyperosmolar nonketotic diabetic coma: vascular complications.

ABSTRACT: Serious vascular complications can be readily overlooked in cases of hyperosmolar nonketotic diabetic coma. They were found by the authors in 3 of 5 autopsy cases. Such a high proportion attests to the importance of early recognition, not only of the type of coma but the presence of life‐threatening vascular complications.

54 Cases of Hyperosmolar Nonketotic Diabetic Coma Repoted in Japan

54 Cases of Hyperosmolar Nonketotic Diabetic Coma Repoted in Japan

Hyperosmolar hyperglycaemic non-ketotic diabetic coma complicating open heart surgery.

Hyperosmolar hyperglycaemic non-ketotic diabetic coma complicating open heart surgery.

Hyperosmolar non-ketotic diabetic coma: with particular reference to vascular complications.

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.

Pathophysiology and Surgical Implications of Hyperosmolar Non-Ketotic Diabetic Coma

Pathophysiology and Surgical Implications of Hyperosmolar Non-Ketotic Diabetic Coma

Serum lipid levels in hyperosmolar non-ketotic diabetic coma.

Levels of serum lipids were measured in two patients with hyperosmolar non-ketotic diabetic coma. Each lipid fraction was raised in a patient with severe hyperglycaemia and the degree of disturbance was less in a patient with moderate hyperglycaemia. The studies suggest that a block in the hepatic uptake of free fatty acids is not the explanation for the lack of ketosis.

On a Young Patient with Hyperosmolar Nonketotic Diabetic Coma

On a Young Patient with Hyperosmolar Nonketotic Diabetic Coma

Plasma 11-hydroxycorticosteroid and growth hormone levels in acute medical illnesses.

Adrenal cortical response in acute medical illness has been studied by measuring the plasma 11-hydroxycorticosteroid (11-OHCS) concentration in 178 patients. Those with unbalanced diabetes, acute infections, and severe myocardial infarction had high levels. The results obtained suggest that in a patient with a severe infection and hypotension a plasma 11-OHCS level of less than 15 mug./100 ml. indicates an inadequate adrenal cortical response, and one patient with septicaemia and temporary adrenal cortical insufficiency is described. Growth hormone levels were increased in patients with severe diabetic ketosis but not in those with hyperosmolar non-ketotic diabetic coma.

94 Effect of Hypertonicity on the Metabolism of Brain in Vitro

Hypertonicity of body fluids whatever the cause—hypernatremia, uremia, hyperglycemia—alters CNS function with alteration of sensorium, coma and death. Also, hypdtonicity induces acidosis (SOTOS et al.: Pediatrics 26: 925; 30: 180). The mechanism of the alterations is unclear. Rat brain slices where incubated in Krebs-Ringer phosphate buffer containing glucose-UL-C-14 or pyruvic acid-2-C-14 as substrates in 100 % O2 atmosphere (ADDANKI et al.: Ann. Biochem. 13: 458 [1965]). Using glucose as substrate, increases in tonicity due to NaCl, sucrose or glucose (340 to 1000 mOsm/kg H2O) caused decreases in O2 consumption (97 to 100%). The same hypertonic media did not change O2 consumption of rat brain homogenate. Urea up to 1000 mOsmhad no effect on O2 uptake of slices. The C14O2 evolved decreased to 80 and 10 % of control with hypertonic media containing 450 and 900 mOsm of either NaCl or sucrose with glucose as substrate. These changes were due to decreased Krebs cycle activity, since similar values were obtained when pyruvic acid-2-C-14 was used as substrate. No effect was seen with urea solutions at 450 mOsm, decreasing to 81 % of control at 900 mOsm. Studies conducted with glucose l-C-14 or 6-C-14 did not show any significant change on the activity of the hexomonophosphate shunt. The different values can be accounted for by the different osmotic effect of the solutions. The lactic acid production increased 160 % of the control with NaCl hypertonic media. These observations bear on the pathogenesis of (acidosis and) CNS alterations observed in clinical conditions with hypernatremia, hyperosmolar non-ketotic diabetic coma and experimental uremia. This investigation was supported by USPHS grants NB 05114 and FR-78. (SPR)