Chapter 046. Sodium and Water (Part 8) pdf

Sodium and Water Part 8 The rate of correction of hyponatremia depends on the absence or presence of neurologic dysfunction.. be estimated by multiplying the deficit in plasma Na+ conce

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 Acute or severe hyponatremia (plasma Na+ concentration <110–115 mmol/L) tends to present with altered mental status and/or seizures and requires more rapid correction Severe symptomatic hyponatremia should be treated with hypertonic saline, and the plasma Na+ concentration should be raised by 1–2 mmol/L per hour for the first 3–

4 h or until the seizures subside Once again, the plasma Na+ concentration should probably be raised by no more than 12 mmol/L during the first 24 h The quantity

of Na+ required to increase the plasma Na+ concentration by a given amount can

be estimated by multiplying the deficit in plasma Na+ concentration by the total body water

Under normal conditions, total body water is 50 or 60% of lean body weight 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 the

development of the osmotic demyelination syndrome (ODS) This is a neurologic

disorder characterized by flaccid paralysis, dysarthria, and dysphagia The diagnosis is usually suspected clinically and can be confirmed by appropriate neuroimaging studies There is no specific treatment for the disorder, which is associated with significant morbidity and mortality Patients with chronic hyponatremia are most susceptible to the development of ODS, since their brain cell volume has returned to near normal as a result of the osmotic adaptive mechanisms described above Therefore, administration of hypertonic saline to these individuals can cause sudden osmotic shrinkage of brain cells In addition to rapid or overcorrection of hyponatremia, risk factors for ODS include prior cerebral anoxic injury, hypokalemia, and malnutrition, especially secondary to alcoholism Water restriction in primary polydipsia and intravenous saline therapy

in ECF volume–contracted patients may also lead to overly rapid correction of hyponatremia as a result of AVP suppression and a brisk water diuresis This can

be prevented by administration of water or use of an AVP analogue to slow down the 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 ICF particles, maintenance of osmotic equilibrium in hypernatremia results in ICF volume contraction Hypernatremia may be due to primary Na+ gain or water deficit The two components of an appropriate response to hypernatremia are increased water intake stimulated by thirst and the excretion of the minimum volume of maximally concentrated urine reflecting AVP secretion in response to

an osmotic stimulus

In practice, the majority of cases of hypernatremia result from the loss of water Since water is distributed between the ICF and the ECF in a 2:1 ratio, a given amount of solute-free water loss will result in a twofold greater reduction in the ICF compartment than the ECF compartment For example, consider three

scenarios: the loss of 1 L of water, isotonic NaCl, or half-isotonic NaCl If 1 L of water is lost, the ICF volume will decrease by 667 mL, whereas the ECF volume will 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 of half-isotonic NaCl is equivalent to 500 mL of water (one-third ECF, two-thirds ICF) 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 mechanism

is abnormal or access to water is limited The latter occurs in infants, the physically handicapped, and patients with impaired mental status; in the postoperative state; and in intubated patients in the intensive care unit On rare

occasions, impaired thirst may be due to primary hypodipsia This usually occurs

as a result of damage to the hypothalamic osmoreceptors that control thirst and tends to be associated with abnormal osmotic regulation of AVP secretion Primary hypodipsia may be due to a variety of pathologic changes, including granulomatous disease, vascular occlusion, and tumors A subset of hypodipsic

hypernatremia, referred to as essential hypernatremia, does not respond to forced

water intake This appears to be due to a specific osmoreceptor defect resulting in nonosmotic regulation of AVP release Thus, the hemodynamic effects of water loading lead to AVP suppression and excretion of dilute urine