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PubMedDate not supplied

Diabetic ketoacidosis and pregnancy.

This paper describes the clinical course of a young diabetic primigravida who presented to her physician with vomiting and abdominal pain. Despite the conventional doses of intravenous fluid and insulin that were used to treat her suspected diabetic ketoacidosis, she remained severely acidotic and developed increasing abdominal pain. Two hundred twenty units of regular insulin over a 5-hour period were required to reverse the lipolysis, acidemia, and abdominal pain, which characterized her severe episode of diabetic ketoacidosis. This discussion emphasizes the importance of insulin in the reversal of the hyperglycemia and acidosis that accompany a diabetic crisis. The roles of bicarbonate, phosphorous, magnesium, insulin, potassium, and fluids are discussed along with conditions such as pregnancy, infection, pancreatitis, and abdominal pain, which can complicate the management of diabetic ketoacidosis.

Adolescent↗
PubMed1983

Glucose and orthophosphate incorporation and lactate release in the perfused hind limb of the rat during lactic acidemia.

A perfused preparation of the hind limb of normal and diabetic rats was used to study the effects of lactic acidosis, alone or associated with hypoinsulinemic diabetes, on the incorporation of glucose and inorganic orthophosphate (Pi) into the skeletal muscle. A well oxygenated perfusate was recirculated for ninety minutes during which the lactic acid accumulated into the medium with the ensuing pH drop. The perfusions were practiced in the hind limb of alloxanized diabetic rats, in the hind limb of diabetic rats with perfusate containing 200 microU of insulin/ml, in the hind limb of 24 hour fasted rats, and on the hind limb of fed rats, and they were compared to similar groups with normalized pH perfusate with a sodium bicarbonate infusion. In the diabetic perfusions with lactic acidemia, it was observed that the addition of insulin increased the uptake of Pi and of glucose, and reduced the release of Pi by the muscular tissues. A smaller release of Pi by the preparations obtained from fed rats was observed when compared to the hind limb preparations of fasted rats. The diabetic preparations showed an increased glucose uptake when the pH was normalized, and a decrease of Pi released by the muscles, even in the absence of insulin, and at the same time, the administration of insulin associated with the normalization of pH increased the uptake of Pi and of glucose, and decreased the Pi released by the muscles. In all the groups, the administration of sodium bicarbonate significantly increased the lactate release into the medium. It was also found that the lactic acidosis reduced the uptake of Pi by the preparations inducing hyperphosphatemia. According to these results, muscular tissue plays a role in the hypophosphatemia that has been reported in the insulin treated diabetic ketoacidosis by increasing the incorporation of Pi and reducing its release by the same tissue.

Acidosis↗
PubMed1978

[The risk of lacticate acidosis: a comparison of the 3 biguanides in treatment of diabetics (authors' transl)].

Hyperlactaemia was induced by means of a standard exercise test in 10 diabetics receiving normal treatment with biguanides (either buformin, metformin, or phenformin) in combination with either a sulfonylurea or insulin. The treatment regimen was then continued without biguanides for 3 weeks and the exercise test was repeated at the end of this period. All 3 biguanide preparations induce hyperlactaemia in diabetics. Physical stress leads to an additional increase in lactate, which reaches pathological proportions. Discontinuation of biguanide treatment leads to a significant decrease in resting and stress values. In a comparison of the 3 biguanide products, phenformin induced significantly higher lactate values in response to exercise than buformin. Of the biguanides, phenformin appears to carry the greatest risk of causing hyperlactaemia in susceptible patients, induced by concurrent circumstances, with progression to severe lacticate acidosis. The special pharmacokinetic properties of phenformin and the 8-fold higher incidence of lacticate acidosis than under buformin or metformin therapy support this observation.

Acidosis↗
PubMed2000

Distal tubule bicarbonate reabsorption in intact and remnant diabetic kidneys.

BACKGROUND: In the diabetic patient, hyperkalemia and hyperchloremic metabolic acidosis has been attributed to one or more of the following factors associated with diabetic nephropathy: hypoaldosteronism, altered potassium homeostasis, or a distal tubular (DT) defect in hydrogen ion secretion. To evaluate maximal in vivo DT acidification in streptozotocin (STZ) diabetes, unidirectional bicarbonate reabsorption (JHCO3) was measured in DTs after acid loading and in surviving DT after 2/3 nephrectomy (Nx). METHODS: Acid gavage induced hyperchloremic metabolic acidosis in four groups of rats: diabetic rats with hyperglycemia two (a) and (b) eight weeks after STZ injection, (c) diabetic rats with tight glucose control two weeks after STZ injection and insulin pump implantation; and (d) control nondiabetic rats. Another group of diabetic rats underwent (e) Nx one week after STZ injection; these rats were neither acid loaded nor pump implanted. RESULTS: In the acidotic rats, the plasma potassium concentration, the plasma and urine acid-base parameters in the three STZ diabetic groups was not different from control rats, whereas JHCO3 fluxes were brisk without important differences between groups. In Nx rats, although the plasma potassium concentration and acid-base status were normal, surviving JHCO3 fluxes were still brisk and not different from the acid-loaded rats. CONCLUSIONS: These in vivo measurements indicate there is no impairment in DT unidirectional bicarbonate reabsorption in the intact or remnant STZ diabetic kidney.

Absorption↗
PubMed1983

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.

Amino Acids↗
PubMed1978

Alcoholic ketoacidosis in pregnancy.

The presence of severe ketoacidosis in the absence of hyperglycemia and glucosuria is reported in a young pregnant chronic alcohol abuser. The clinical presentation included an arterial pH of 7.15, a base deficit of 23 mEq/liter, a bicarbonate of less than 10 m Eq/liter, larger serum and urinary ketone levels, and hyperpnea with Kussmual-type respiration. Corrective therapy consisted of rapid fluid, electrolyte, bicarbonate, and glucose replacement with insulin supplementation. The ability of the fetus to tolerate the maternal metabolic derangements of "alcoholic ketoacidosis" as well as the stress of uterine contractions is discussed and contrasted with diabetic ketoacidosis.

Acidosis↗
PubMed1976

Lactic acidosis: an experimental model.

A model of spontaneous lactic acidosis was developed in alloxan diabetic rabbits by infusing intravenously beta-hydroxybutyric acid followed by a continuous infusion of NaHCO3. In half of the animals, the arterial lactate/pyruvate ratio rose from 2.5 mM/0.19mM to 20.4 mM/0.28 mM, and arterial pH fell to 7.16. In animals with lactic acidosis, the calculated ratio in blood of NAD/NADH was 1437 +/- 230, versus a normal value of 6754 +/- 1250. Both arterial PO2 and blood pressure were normal. Continued infusion of NaHCO3 led to increased blood lactate levels, with cardiorespiratory arrest in 36% of animals. Lactic acidosis did not develop in normal rabbits who were similarly treated. It is concluded that spontaneous lactic acidosis can be produced in diabetic, but not in normal, rabbits by infusion of beta-hydroxybutric acid followed by infusion of NaHCO3.

Acidosis↗
PubMed1993

Bicarbonate in the treatment of metabolic acidosis: effects on hepatic intracellular pH, gluconeogenesis, and lactate disposal in rats.

The effects of agents used in the treatment of metabolic acidosis could depend on the induced changes in intracellular pH (pHi). To determine the effect of sodium bicarbonate on hepatic pHi and function, this agent was infused into anesthetized rats with acute metabolic acidosis due to either diabetic ketoacidosis (DKA) or HCl infusion. Hepatic pHi was measured by 31P-magnetic resonance spectroscopy (MRS). A substantial increase in pHi occurred (from 7.13 +/- 0.08 to 7.32 +/- 0.08, P < .05) despite an increase in mixed venous PCO2. Isolated livers from normal rats or those with DKA were perfused at pH 6.8 and normal PCO2. With infusion of sodium bicarbonate, there was again an increase in pHi (delta pHi, + 0.27 +/- 0.06, P < .02) despite increases in both portal and hepatic venous PCO2. Lactate uptake was increased twofold to threefold (P < .001) by bicarbonate infusion in perfusions from both types of animals. Glucose output was increased twofold (P < .001) only in livers from normal animals.

Acidosis↗
PubMed1976

Studies in the renal handling of insulin in juvenile diabetics.

A technique is described for the accurate radioimmunoassay of insulin in serum and urine. This method was applied to study of renal clearance and excretion of endogenous and exogenous insulin in untreated juvenile diabetics and healthy young adults. There was good agreement between our results for normal adults and previously reported values. In six non-obese juvenile diabetics, urinary insulin clearance values, both basal (fasting) and following glucose loading (entire range 0.03 ml/min to 1.23 ml/min) were similar to those obtained for the adults (entire range 0.17 ml/min to 2.35 ml/min). The basal urinary excretion in these diabetics was generally of the same order of magnitude as that in the normals. The clearance of exogenous insulin, administered for the first time, was also of the same order as that for endogenous insulin. Markedly elevated urinary clearance and excretion of insulin during fasting and non-fasting states was demonstrated in four non-obese juvenile diabetics with no clinical evidence of abnormal proteinuria, though they demonstrated slight to mild clinical dehydration and acidosis compared with the other diabetics studied. Clearance and excretion of exogenous insulin was similarly elevated. This finding could reflect renal tubular dysfunction in these diabetics, and this dysfunction could relate to even the mild degree of dehydration and acidosis found in this study. Endogenous and exogenous insulin clearance in an obese diabetic child was similar to that for the control group.

Child↗