Approach to fluid and electrolyte disorders and acid-base problems

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Prim Care Clin Office Pract 35 (2008) 195–213

Approach to Fluid and Electrolyte Disorders and Acid-Base Problems
Biff F. Palmer, MD
Department of Internal Medicine, Division of Nephrology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA

Employing a systematic approach to the interpretation of serum chemistries is the most effective way toensure abnormalities are detected and correctly interpreted. This article reviews a series of steps that can be used in both the outpatient and inpatient settings. These steps will help to ensure the clinician not only identifies overt abnormalities but also subtle disturbances that may lay hidden in a routine set of serum chemistry values. Steps to interpreting a set of chemistry values  Step 1:First check serum sodium [Na] and work up tonicity disorders if abnormal  Step 2: Check serum chloride [Cl]  Step 3: Calculate anion gap  Step 4: If anion gap [, determine whether measured serum bicarbonate [HCO3] is equal to predicted [HCO3]  Step 5: Analyze arterial blood gas  Step 6: Check potassium First step: examine the serum sodium concentration Hyponatremia Is the hyponatremiarepresentative of a hypoosmolar state? There are two general causes of hyponatremia in which it is not associated with a hypoosmolar state. The first of these is pseudohyponatremia, which involves an abnormal measurement of the serum sodium (Na). This

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occurs in patients with hyperglobulinemia or hypertriglyceridemia, in whom plasma water relative to plasma solids is decreased in blood, leading to less sodium in a given volume of blood. In general, hyperglobulinemia sufficient to cause pseudohyponatremia is rare and occurs only in Waldenstrom’s macroglobulinemia. Triglycerides must be in the thousandsto cause this condition and are most commonly seen in diabetics. In general, this problem is becoming less prevalent, as many laboratories are using sodium electrodes without diluting the blood such that the plasma sodium measurement becomes independent of plasma water and solid contents. The other cause of hyponatremia in the absence of a hypoosmolar state involves true hyponatremia, but withelevations in the concentration of another osmole. Clinical examples include hyperglycemia as seen in uncontrolled diabetes or, rarely, hypertonic infusion of mannitol used in the treatment of cerebral edema. The increases in plasma glucose raise serum osmolality, which pulls water out of cells and dilutes the serum Na. For every 100 mg/dL rise in glucose or mannitol, the serum Na will quickly fallby 1.6 mEq/L. The increased tonicity will also stimulate thirst and arginine vasopressin (AVP) secretion, both of which contribute to further water retention. As the plasma osmolality returns toward normal, the decline in serum Na will be 2.8 mEq/L for every 100 mg/dL rise in glucose. The net result is a normal plasma osmolality but a low serum sodium. Is the kidney’s ability to dilute the urineintact? The presence of hypotonic hyponatremia implies that water intake exceeds the ability of the kidney to excrete water. In unusual circumstances, this can occur when the kidney’s ability to excrete free water is intact. However, because a normal kidney can excrete 20 L to 30 L of water per day, the presence of hyponatremia with normal renal water excretion implies that the patient is drinkingmore than 20 L to 30 L of water per day. This condition is referred to as primary polydipsia. These patients should have a urine osmolality less than 100 mOsm/L. While primary polydipsia is a common condition that leads to polyuria and polydipsia, it is uncommon as a sole cause of hyponatremia. In the absence of primary polydipsia, hyponatremia is associated with decreased renal water excretion...
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