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...
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Chapter 046. Sodium and Water (Part 9) Chapter 046. Sodium and Water (Part 9) The source of free water loss is either renal or extrarenal. Nonrenal loss ofwater may be due to evaporation from the skin and respiratory tract (insensiblelosses) or loss from the gastrointestinal tract. Insensible losses are increased withfever, exercise, heat exposure, and severe burns and in mechanically ventilatedpatients. Furthermore, the Na+ concentration of sweat decreases with profuseperspiration, thereby increasing solute-free water loss. Diarrhea is the mostcommon gastrointestinal cause of hypernatremia. Specifically, osmotic diarrheas(induced by lactulose, sorbitol, or malabsorption of carbohydrate) and viralgastroenteritides 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 andpresent with ECF volume contraction and a normal plasma Na+ concentration orhyponatremia. Renal water loss is the most common cause of hypernatremia and is due todrug-induced or osmotic diuresis or diabetes insipidus (Chap. 334). Loop diureticsinterfere with the countercurrent mechanism and produce an isoosmotic solutediuresis. This results in a decreased medullary interstitial tonicity and impairedrenal concentrating ability. The presence of non-reabsorbed organic solutes in thetubule lumen impairs the osmotic reabsorption of water. This leads to water loss inexcess of Na+ and K+, known as an osmotic diuresis. The most frequent cause ofan osmotic diuresis is hyperglycemia and glucosuria in poorly controlled diabetesmellitus. Intravenous administration of mannitol and increased endogenousproduction of urea (high-protein diet) can also result in an osmotic diuresis. Hypernatremia secondary to nonosmotic urinary water loss is usually dueto: (1) Central diabetes insipidus (CDI) characterized by impaired AVP secretion,or (2) NDI resulting from end-organ (renal) resistance to the actions of AVP. Themost common cause of CDI is destruction of the neurohypophysis. This may occuras a result of trauma, neurosurgery, granulomatous disease, neoplasms, vascularaccidents, or infection. In many cases, CDI is idiopathic and may occasionally behereditary. The familial form of the disease is inherited in an autosomal dominantfashion and has been attributed to mutations in the propressophysin (AVPprecursor) gene. Nephrogenic diabetes insipidus (NDI) may be either inherited oracquired. Congenital NDI is an X-linked recessive trait due to mutations in the V2receptor gene. Mutations in the autosomal aquaporin-2 gene may also result inNDI. The aquaporin-2 gene encodes the water channel protein whose membraneinsertion is stimulated by AVP. The causes of sporadic NDI are numerous andinclude drugs (especially lithium), hypercalcemia, hypokalemia, and conditionsthat impair medullary hypertonicity (e.g., papillary necrosis or osmotic diuresis).Pregnant women, in the second or third trimester, may develop NDI as a result ofexcessive 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 orreplacing sugar with salt in infant formula can produce this complication. Clinical Features As a consequence of hypertonicity, water shifts out of cells, leading to acontracted ICF volume. A decreased brain cell volume is associated with anincreased risk of subarachnoid or intracerebral hemorrhage. Hence, the majorsymptoms of hypernatremia are neurologic and include altered mental status,weakness, neuromuscular irritability, focal neurologic deficits, and occasionallycoma or seizures. Patients may also complain of polyuria or thirst. For unknownreasons, patients with polydipsia from CDI tend to prefer ice-cold water. The signsand symptoms of volume depletion are often present in patients with a history ofexcessive sweating, diarrhea, or an osmotic diuresis. As with hyponatremia, theseverity of the clinical manifestations is related to the acuity and magnitude of therise in plasma Na+ concentration. Chronic hypernatremia is generally lesssymptomatic as a result of adaptive mechanisms designed to defend cell volume.Brain cells initially take up Na+ and K+ salts, later followed by accumulation oforganic osmolytes such as inositol. This serves to restore the brain ICF volumetoward normal. Diagnosis (Fig. 46-2) A complete history and physical examination will often provideclues as to the underlying cause of hypernatremia. Relevant symptoms and signsinclude the absence or presence of thirst, diaphoresis, diarrhea, polyuria, and the ...