Pediatric emergency medicine trisk 2857 2857
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the serum osmolality, then central or nephrogenic diabetes insipidus should
be considered. The urine sodium concentration may also assist diagnosis.
During hypernatremic hypovolemia, the urine sodium is generally less than
25 mEq/L due to the effect of aldosterone to maintain perfusion. If
hypernatremia is due to salt excess, the appropriate renal response is to
excrete sodium, and the urine sodium concentration would be elevated.
TABLE 100.6
CAUSES OF HYPERNATREMIA BASED UPON TOTAL BODY
SODIUM CONTENT
Low total body
sodium
Normal total body
sodium
Diarrhea
Vomiting
Increased insensible losses Salt poisoning
Fever
Inappropriately mixed
formula
Prematurity
Salt water drowning
Phototherapy
NaHCO3 given with CPR
Ostomy losses
Osmotic diuresis
Immature renal
conservation
(prematurity)
High total body sodium
Radiant warmers
Tachypnea
Nephrogenic DI
Central DI
DI, diabetes insipidus; NaHCO3 , sodium bicarbonate; CPR, cardiopulmonary resuscitation.
Clinical manifestations. The clinical manifestations of hypernatremia are
primarily neurologic. The rise in the plasma osmolality causes water
movement out of the brain. The decrease in brain volume may lead to the
rupture of the blood vessels contained in the membranes that tether the
brain to the overlying skull and elsewhere. Early clinical manifestations can
include lethargy, weakness, fever, and irritability. More severe
manifestations include seizures and coma. Symptoms are more likely if the
disturbance is acute and rapid. If hypernatremia evolves slowly, there is
cerebral adaptation to protect brain cell volume. Adaptive mechanisms
include movement of cerebrospinal fluid into the brain, uptake of sodium
