Chapter 046. Sodium and Water (Part 7) potx

Chapter 046. Sodium and Water (Part 7) Diagnosis (Fig. 46-1) Hyponatremia is not a disease but a manifestation of a variety of disorders. The underlying cause can often be ascertained from an accurate history and physical examination, including an assessment of ECF volume status and effective circulating arterial volume. The differential diagnosis of hyponatremia, an expanded ECF volume, and decreased effective circulating volume includes congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome. Hypothyroidism and adrenal insufficiency tend to present with a near-normal ECF volume and decreased effective circulating arterial volume. All of these diseases have characteristic signs and symptoms. Patients with SIADH are usually euvolemic. Figure 46-1 Algorithm depicting clinical approach to hyponatremia. ECF, extracellular fluid; SIADH, syndrome of inappropriate antidiuretic hormone secretion. Four laboratory findings often provide useful information and can narrow the differential diagnosis of hyponatremia: (1) the plasma osmolality, (2) the urine osmolality, (3) the urine Na + concentration, and (4) the urine K + concentration. Since ECF tonicity is determined primarily by the Na + concentration, most patients with hyponatremia have a decreased plasma osmolality. The appropriate renal response to hypoosmolality is to excrete the maximum volume of dilute urine, i.e., urine osmolality and specific gravity of <100 mosmol/kg and 1.003, respectively. This occurs in patients with primary polydipsia. If this is not present, it suggests impaired free-water excretion due to the action of AVP on the kidney. The secretion of AVP may be a physiologic response to hemodynamic stimuli or it may be inappropriate in the presence of hyponatremia and euvolemia. Since Na + is the major ECF cation and is largely restricted to this compartment, ECF volume contraction represents a deficit in total body Na + content. Therefore, volume depletion in patients with normal underlying renal function results in enhanced tubule Na + reabsorption and a urine Na + concentration <20 mmol/L. The finding of a urine Na + concentration >20 mmol/L in hypovolemic hyponatremia implies a salt-wasting nephropathy, diuretic therapy, hypoaldosteronism, or occasionally vomiting. Both the urine osmolality and the urine Na + concentration can be followed serially when assessing response to therapy. SIADH is characterized by hypoosmotic hyponatremia in the setting of an inappropriately concentrated urine (urine osmolality >100 mosmol/kg). Patients are typically normovolemic and have normal Na + balance. They tend to be mildly volume-expanded secondary to water retention and have a urine Na + excretion rate equal to intake (urine Na + concentration usually >40 mmol/L). By definition, they have normal renal, adrenal, and thyroid function and usually have normal K + and acid-base balance. SIADH is often associated with hypouricemia due to the uricosuric state induced by volume expansion. In contrast, hypovolemic patients tend to be hyperuricemic secondary to increased proximal urate reabsorption. Hyponatremia: Treatment The goals of therapy are twofold: (1) to raise the plasma Na + concentration by restricting water intake and promoting water loss and (2) to correct the underlying disorder. Mild asymptomatic hyponatremia is generally of little clinical significance and requires no treatment. The management of asymptomatic hyponatremia associated with ECF volume contraction should include Na + repletion, generally in the form of isotonic saline. The direct effect of the administered NaCl on the plasma Na + concentration is trivial. However, restoration of euvolemia removes the hemodynamic stimulus for AVP release, allowing the excess free water to be excreted. The hyponatremia associated with edematous states tends to reflect the severity of the underlying disease and is usually asymptomatic. These patients have increased total body water that exceeds the increase in total body Na + content. Treatment should include restriction of Na + and water intake, correction of hypokalemia, and promotion of water loss in excess of Na + . The latter may require the use of loop diuretics with replacement of a proportion of the urinary Na + loss to ensure net free-water excretion. Dietary water restriction should be less than the urine output. Correction of the K + deficit may raise the plasma Na + concentration by favoring a shift of Na + out of cells as K + moves in. Water restriction is also a component of the therapeutic approach to hyponatremia associated with primary polydipsia, renal failure, and SIADH (Chap. 334). The recent development of nonpeptide vasopressin antagonists has introduced a new selective treatment for euvolemic and hypervolemic hyponatremia. . Chapter 046. Sodium and Water (Part 7) Diagnosis (Fig. 46-1) Hyponatremia is not a disease but a manifestation. by restricting water intake and promoting water loss and (2) to correct the underlying disorder. Mild asymptomatic hyponatremia is generally of little clinical significance and requires no. total body water that exceeds the increase in total body Na + content. Treatment should include restriction of Na + and water intake, correction of hypokalemia, and promotion of water loss