Chapter 046. Sodium and Water (Part 8) pdf

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.