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M L Halperin

Publications and source records attributed to M L Halperin.

257 records · Page 15Linked to original sources
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Quantitative analysis of glucose loss during acute therapy for hyperglycemic hyperosmolar syndrome.

Four patients with severe hyperglycemia and hyperosmolality were studied to quantitate the major mechanisms responsible for the fall in blood glucose concentration. Insulin was not administered to any of these patients during the first 15 h of therapy. In each case, there was a fall in glucose concentration due to dilution; this was quantitated by chloride space analysis and accounted for 24-34% of the fall in concentration. The size of the glucose pool decreased for two reasons. Glucosuria accounted for the majority of the reduction in the size of the glucose pool in the patients with the smallest decrease in extracellular fluid (ECF) volume [and hence the best preserved glomerular filtration rate (GFR)]. In contrast, glucosuria was a less important factor in causing glucose loss in the patients with very low GFR values. The size of the glucose pool also decreased due to glucose metabolism that did not require exogenous insulin. Thus the fall in glucose concentration in the initial therapy in patients with the hyperglycemic hyperosmolar syndrome is multifactorial and is not absolutely dependent on exogenous insulin. Furthermore, the patients grouped in this diagnostic category represent a heterogeneous population with the common features of severe hyperglycemia, hyperosmolality, and a negative or weakly reactive test for serum ketones.

Adult↗
PubMedDate not supplied

A physiological analysis of hyponatremia: implications for patients on peritoneal dialysis.

The basis for hyponatremia is a negative balance for sodium (Na+) plus potassium (K+) and/or a positive balance for water. In patients with normal renal function, vasopressin is needed to prevent the excretion of electrolyte-free water. Vasopressin is not important when there is little residual renal function. If hyponatremia is accompanied by a quantitatively appropriate gain in weight, this implies that a gain of electrolyte-free water was the basis for hyponatremia. In the absence of this weight gain, a loss of salts is to be suspected. If the extracellular fluid (ECF) volume is obviously low, hyponatremia is due to a deficit of NaCl, unless there is a deficit of K+. With a KCl deficit and a contracted ECF volume, there should also be a large shift of Na+ into cells, so metabolic alkalosis would not be an expected finding. In contrast, those patients with no change in weight who have a normal or expanded ECF volume are subdivided into those with a gain of solutes restricted to the ECF compartment (glucose, mannitol), or those with a deficit of solutes of intracellular fluid origin, which implies that a catabolic state (malnutrition) may be present.

Extracellular Space↗
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Hyponatremia in patients undergoing CAPD: role of water gain and/or malnutrition.

BACKGROUND: Hyponatremia has a number of different causes; some may have serious untoward implications for patients undergoing chronic ambulatory peritoneal dialysis (CAPD). OBJECTIVE: To determine the pathophysiology of hyponatremia in patients on CAPD. METHODS: A retrospective analysis was carried out on 210 patients on CAPD. We selected patients with 2-4 consecutive periods when the plasma sodium concentration was < or =130 mmol/L and again when it was > 133 mmol/L. Exclusion criteria included hyperglycemia, orthostatic hypotension, edema, and inadequate records. RESULTS: An electrolyte-free water gain appeared to be the main cause of hyponatremia in only 1 of 5 patients because this was the only patient with a significant increase in body weight. In 1 patient, there was weight loss in the hyponatremic period, suggesting tissue catabolism was present. In 3 patients, there was neither weight gain nor evidence for a contracted extracellular fluid volume in the hyponatremic period, suggesting that intracellular potassium and phosphate loss could be the major mechanism for their hyponatremia. CONCLUSION: When hyponatremia is due to a catabolic state, its management should aim to restore intracellular fluid composition (i.e., to correct malnutrition).

Female↗
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An improved approach to the patient with metabolic acidosis: a need for four amendments.

Clinicians should identify life-threatening issues in patients with metabolic acidosis. These threats may be present before therapy begins and/or anticipated after therapy commences. By adding four amendments, short-comings in the commonly used clinical approaches for the diagnosis of metabolic acidosis can be overcome. First, a definition of metabolic acidosis should consider not only the concentration of bicarbonate but also the content of bicarbonate in the extra cellular fluid compartment. The latter requires a quantitative estimate of the ECF volume, which can be obtained using the hematocrit and/or the total protein concentration in plasma. Second, to determine if the basis for metabolic acidosis was the addition of acids or the loss of NaHCO 3 , one must hunt for new anions, not only in plasma, but also in the urine. Third, it is important to measure the venous as well as the arterial PCO2 to assess the capacity to buffer H+ while minimizing H + binding to intracellular proteins. Fourth, to assess the role of the kidney in a patient with metabolic acidosis, the urine osmolal gap and the concentration of creatinine in the urine should be measured to provide an estimate of the rate of excretion of ammonium.

Acid-Base Equilibrium↗