Chapter 046. Sodium and Water (Part 9) docx

Chapter 046. Sodium and Water (Part 9) The source of free water loss is either renal or extrarenal. Nonrenal loss of water may be due to evaporation from the skin and respiratory tract (insensible losses) or loss from the gastrointestinal tract. Insensible losses are increased with fever, exercise, heat exposure, and severe burns and in mechanically ventilated patients. Furthermore, the Na + concentration of sweat decreases with profuse perspiration, thereby increasing solute-free water loss. Diarrhea is the most common gastrointestinal cause of hypernatremia. Specifically, osmotic diarrheas (induced by lactulose, sorbitol, or malabsorption of carbohydrate) and viral gastroenteritides result in water loss exceeding that of Na + and K + . In contrast, secretory diarrheas (e.g., cholera, carcinoid, VIPoma) have a fecal osmolality (twice the sum of the concentrations of Na + and K + ) similar to that of plasma and present with ECF volume contraction and a normal plasma Na + concentration or hyponatremia. Renal water loss is the most common cause of hypernatremia and is due to drug-induced or osmotic diuresis or diabetes insipidus (Chap. 334). Loop diuretics interfere with the countercurrent mechanism and produce an isoosmotic solute diuresis. This results in a decreased medullary interstitial tonicity and impaired renal concentrating ability. The presence of non-reabsorbed organic solutes in the tubule lumen impairs the osmotic reabsorption of water. This leads to water loss in excess of Na + and K + , known as an osmotic diuresis. The most frequent cause of an osmotic diuresis is hyperglycemia and glucosuria in poorly controlled diabetes mellitus. Intravenous administration of mannitol and increased endogenous production of urea (high-protein diet) can also result in an osmotic diuresis. Hypernatremia secondary to nonosmotic urinary water loss is usually due to: (1) Central diabetes insipidus (CDI) characterized by impaired AVP secretion, or (2) NDI resulting from end-organ (renal) resistance to the actions of AVP. The most common cause of CDI is destruction of the neurohypophysis. This may occur as a result of trauma, neurosurgery, granulomatous disease, neoplasms, vascular accidents, or infection. In many cases, CDI is idiopathic and may occasionally be hereditary. The familial form of the disease is inherited in an autosomal dominant fashion and has been attributed to mutations in the propressophysin (AVP precursor) gene. Nephrogenic diabetes insipidus (NDI) may be either inherited or acquired. Congenital NDI is an X-linked recessive trait due to mutations in the V 2 receptor gene. Mutations in the autosomal aquaporin-2 gene may also result in NDI. The aquaporin-2 gene encodes the water channel protein whose membrane insertion is stimulated by AVP. The causes of sporadic NDI are numerous and include drugs (especially lithium), hypercalcemia, hypokalemia, and conditions that impair medullary hypertonicity (e.g., papillary necrosis or osmotic diuresis). Pregnant women, in the second or third trimester, may develop NDI as a result of excessive elaboration of vasopressinase by the placenta. Finally, although infrequent, a primary Na + gain may cause hypernatremia. For example, inadvertent administration of hypertonic NaCl or NaHCO 3 or replacing sugar with salt in infant formula can produce this complication. Clinical Features As a consequence of hypertonicity, water shifts out of cells, leading to a contracted ICF volume. A decreased brain cell volume is associated with an increased risk of subarachnoid or intracerebral hemorrhage. Hence, the major symptoms of hypernatremia are neurologic and include altered mental status, weakness, neuromuscular irritability, focal neurologic deficits, and occasionally coma or seizures. Patients may also complain of polyuria or thirst. For unknown reasons, patients with polydipsia from CDI tend to prefer ice-cold water. The signs and symptoms of volume depletion are often present in patients with a history of excessive sweating, diarrhea, or an osmotic diuresis. As with hyponatremia, the severity of the clinical manifestations is related to the acuity and magnitude of the rise in plasma Na + concentration. Chronic hypernatremia is generally less symptomatic as a result of adaptive mechanisms designed to defend cell volume. Brain cells initially take up Na + and K + salts, later followed by accumulation of organic osmolytes such as inositol. This serves to restore the brain ICF volume toward normal. Diagnosis (Fig. 46-2) A complete history and physical examination will often provide clues as to the underlying cause of hypernatremia. Relevant symptoms and signs include the absence or presence of thirst, diaphoresis, diarrhea, polyuria, and the features of ECF volume contraction. The history should include a list of current and recent medications, and the physical examination is incomplete without a thorough mental status and neurologic assessment. Measurement of urine volume and osmolality are essential in the evaluation of hyperosmolality. The appropriate renal response to hypernatremia is the excretion of the minimum volume (500 mL/d) of maximally concentrated urine (urine osmolality >800 mosmol/kg). These findings suggest extrarenal or remote renal water loss or administration of hypertonic Na + salt solutions. The presence of a primary Na + excess can be confirmed by the presence of ECF volume expansion and natriuresis (urine Na + concentration usually >100 mmol/L). . Chapter 046. Sodium and Water (Part 9) The source of free water loss is either renal or extrarenal. Nonrenal loss of water may be due to evaporation from the skin and respiratory. concentrations of Na + and K + ) similar to that of plasma and present with ECF volume contraction and a normal plasma Na + concentration or hyponatremia. Renal water loss is the most common. by lactulose, sorbitol, or malabsorption of carbohydrate) and viral gastroenteritides result in water loss exceeding that of Na + and K + . In contrast, secretory diarrheas (e.g., cholera,