Page 1373 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

946 PART 8: Renal and Metabolic Disorders

TABLE 99-2 Causes of Hypernatremia
Increased CEFW a Sweat and Insensible Losses Water Loss into Cells Increased Intake of Sodium Central Impairment of Thirst
Central diabetes insipidus Fever Severe exercise Infusions of hypertonic sodium bicarbonate Reset osmostat
Nephrogenic diabetes insipidus Tachypnea Seizures Infusions of hypertonic saline Elderly patients
Hypercalcemia Burns Hypertonic dialysate
Hypokalemia Exercise Overdose of salt tablets
Recovery from acute tubular necrosis
Postobstructive diuresis
X-linked recessive
Lithium
Demeclocycline
Osmotic diuresis
Hyperglycemia
Mannitol
Urea (catabolic state, high-protein tube feedings)
Diarrhea (osmotic)
Lactulose
Sorbitol
Malabsorption
a Note: Patients with increased electrolyte-free water losses that are able to increase water intake will maintain eunatremia. These conditions increase the demand for water, but if that demand is met they will not
cause hypernatremia.

Specific therapy should be employed to reduce ongoing water losses,
V iv × (Na + K ) − V × (Na + K ) − V × Na such as correcting hypercalcemia-induced diuresis or administering
Na = iv iv u u u s
TBW + V desmopressin (DDAVP) to patients with CDI. Beyond this, correcting
hypernatremia requires giving hypotonic fluid either enterally or paren-
Na = 0.4 × (1000 + 0) − 0.4 × 140 terally. The enteral route is preferred, as it allows the use of electrolyte-
42 + 0.4
free water rather than hypotonic or dextrose-containing fluids. Though
Na = 8.1 the optimum speed of correction has not been rigorously determined,
studies on infants and children showed no seizures when sodium was
9
FIGURE 99-1. Change in sodium following a cardiac arrest. This patient was given corrected at less than 0.5 mmol/L per hour. The sodium can be safely
4 amps of sodium bicarbonate during a code. Each amp of bicarbonate contains 100 mL and lowered by 10 mmol in the first day of therapy. Patients with acute
has a concentration of 1 mmol/mL or 1000 mmol/L. The patient is anuric so the urine volume, (<48 h) increases in sodium (eg, from hypertonic bicarbonate infu-
10
Na, and K drop out. The patient weighs 70 kg and has 60% body water so TBW = 42. See sions) can safely be corrected at 1 mmol/L per hour. The change in
caption to Eq. 99-4 for explanation of variables.
cerebral effects, hypernatremia inhibits insulin release and causes insu-
lin resistance, predisposing patients to hyperglycemia.
In response to increased serum tonicity and volume loss, cells com-
pensate by increasing the number of intracellular osmoles. Initially cells
move extracellular electrolytes into the cells, and later they transfer
amino acids and other small molecules into the cell. Increased intracel-
lular osmolality restores intracellular volume, and decreases the clinical
impact of hypernatremia.
Treatment: The goal of treating hypernatremia is to arrest any ongoing
cause of hypernatremia, and then to restore serum sodium to normal.

V × (Na + K ) − V × (Na + K ) − V × Na
Na = iv iv iv u u u s
TBW + V
Na = 8 × (0 + 0) − 18 × (8 + 15) − (−14) × 140
42 + (−14)
Na = 30.8

FIGURE 99-2. Change in sodium in a patient with central diabetes insipidus who stopped FIGURE 99-3. Increased plasma osmolality causes a shift of water out of the intracellular
his desmopressin and is ingesting an inadequate quantity of water. The patient weighs 70 kg compartment. Decreased cell volume impairs tissue function, particularly in the central
and has 60% body water so TBW = 42. See caption to Eq. 99-4 for explanation of variables. nervous system.

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