Chapter 046. Sodium and Water (Part 8)

The rate of correction of hyponatremia depends on the absence or presence of neurologic dysfunction. This, in turn, is related to the rapidity of onset and magnitude of the fall in plasma Na+ concentration. In asymptomatic patients, the plasma Na+ concentration should be raised by no more than 0.5–1.0 mmol/L per h and by less than 10–12 mmol/L over the first 24 h.
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Chapter 046. Sodium and Water (Part 8) Chapter 046. Sodium and Water (Part 8) The rate of correction of hyponatremia depends on the absence or presenceof neurologic dysfunction. This, in turn, is related to the rapidity of onset andmagnitude of the fall in plasma Na+ concentration. In asymptomatic patients, theplasma Na+ concentration should be raised by no more than 0.5–1.0 mmol/L per hand by less than 10–12 mmol/L over the first 24 h. Acute or severe hyponatremia(plasma Na+ concentration be estimated by multiplying the deficit in plasma Na+ concentration by the totalbody water. Under normal conditions, total body water is 50 or 60% of lean bodyweight in women or men, respectively. Therefore, to raise the plasma Na +concentration from 105 to 115 mmol/L in a 70-kg man requires 420 mmol [(115 –105) x 70 x 0.6] of Na+. The risk of correcting hyponatremia too rapidly is thedevelopment of the osmotic demyelination syndrome (ODS). This is a neurologicdisorder characterized by flaccid paralysis, dysarthria, and dysphagia. Thediagnosis is usually suspected clinically and can be confirmed by appropriateneuroimaging studies. There is no specific treatment for the disorder, which isassociated with significant morbidity and mortality. Patients with chronichyponatremia are most susceptible to the development of ODS, since their braincell volume has returned to near normal as a result of the osmotic adaptivemechanisms described above. Therefore, administration of hypertonic saline tothese individuals can cause sudden osmotic shrinkage of brain cells. In addition torapid or overcorrection of hyponatremia, risk factors for ODS include priorcerebral anoxic injury, hypokalemia, and malnutrition, especially secondary toalcoholism. Water restriction in primary polydipsia and intravenous saline therapyin ECF volume–contracted patients may also lead to overly rapid correction ofhyponatremia as a result of AVP suppression and a brisk water diuresis. This canbe prevented by administration of water or use of an AVP analogue to slow downthe rate of free water excretion. For further discussion, see Chap. 334. Hypernatremia Etiology Hypernatremia is defined as a plasma Na+ concentration >145 mmol/L.Since Na+ and its accompanying anions are the major effective ECF osmoles,hypernatremia is a state of hyperosmolality. As a result of the fixed number of ICFparticles, maintenance of osmotic equilibrium in hypernatremia results in ICFvolume contraction. Hypernatremia may be due to primary Na + gain or waterdeficit. The two components of an appropriate response to hypernatremia areincreased water intake stimulated by thirst and the excretion of the minimumvolume of maximally concentrated urine reflecting AVP secretion in response toan osmotic stimulus. In practice, the majority of cases of hypernatremia result from the loss ofwater. Since water is distributed between the ICF and the ECF in a 2:1 ratio, agiven amount of solute-free water loss will result in a twofold greater reduction inthe ICF compartment than the ECF compartment. For example, consider threescenarios: the loss of 1 L of water, isotonic NaCl, or half-isotonic NaCl. If 1 L ofwater is lost, the ICF volume will decrease by 667 mL, whereas the ECF volumewill fall by only 333 mL. Due to the fact that Na + is largely restricted to the ECF,this compartment will decrease by 1 L if the fluid lost is isoosmotic. One liter ofhalf-isotonic NaCl is equivalent to 500 mL of water (one-third ECF, two-thirdsICF) plus 500 mL of isotonic saline (all ECF). Therefore, the loss of 1 L of half-isotonic saline decreases the ECF and ICF volumes by 667 mL and 333 mL,respectively. The degree of hyperosmolality is typically mild unless the thirst mechanismis abnormal or access to water is limited. The latter occurs in infants, thephysically handicapped, and patients with impaired mental status; in thepostoperative state; and in intubated patients in the intensive care unit. On rareoccasions, impaired thirst may be due to primary hypodipsia. This usually occursas a result of damage to the hypothalamic osmoreceptors that control thirst andtends to be associated with abnormal osmotic regulation of AVP secretion.Primary hypodipsia may be due to a variety of pathologic changes, includinggranulomatous disease, vascular occlusion, and tumors. A subset of hypodipsichypernatremia, referred to as essential hypernatremia, does not respond to forcedwater intake. This appears to be due to a specific osmoreceptor defect resulting innonosmotic regulation of AVP release. Thus, the hemodynamic effects of waterloading lead to AVP suppression and excretion of dilute urine.