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Diagnóstico médico actual ytratamiento 2021

21 a 03: Hipernatremia

FUNDAMENTOS DEL DIAGNÓSTICO

El aumento de la sed y la ingesta de agua son la principal defensa contra la hipernatremia.

La osmolalidad de la orina ayuda a diferenciar la pérdida de agua renal de la no renal.

CONSIDERACIONES GENERALES
Hypernatremia is defined as a sodium concentration greater than 145 mEq/L. All patients with hypernatremia have hyperosmolality, unlike
hyponatremic patients who can have a low, normal, or high serum osmolality. Hypernatremia develops when there is a relative loss of water that is
inadequately compensated for by water ingestion. Rarely, excess sodium intake contributes to hypernatremia when it is associated with an increase in
extracellular volume.

The primary responses to hypernatremia are stimulation of thirst (to increase water intake) and increased secretion of ADH (to minimize water loss in
the urine). Cells in the hypothalamus are able to sense minimal changes in serum osmolarity, triggering the thirst mechanism and subsequent intake of
water. It is nearly impossible to develop hypernatremia in the context of an intact thirst mechanism with appropriate access to water.

RESULTADOS CLÍNICOS
A. Symptoms and Signs

When the patient is dehydrated, orthostatic hypotension and oliguria are typical findings. Because water shifts from the cells to the intravascular space
to protect volume status, symptoms may be delayed. Lethargy, irritability, and weakness are early signs. Hyperthermia, delirium, seizures, and coma
may be seen with severe hypernatremia (ie, sodium greater than 160 mEq/L). Symptoms in older adults may not be specific.

B. Laboratory Findings

The first steps in evaluating patients with hypernatremia are assessing the urine volume, osmolality, and the osmole excretion rate. The latter can be
calculated by multiplying the urine osmolality with urine volume. The copeptin test is discussed below.

C. Etiology

The initial step is to determine whether the patient with hypernatremia is oliguric, ie, urine flow less than 0.5 mL/min, or nonoliguric. Patients who are
nonoliguric can be further subdivided by measurement of a urine osmolality.

1. The oliguric patient (urine flow less than 0.5 mL/min)

This is found in several scenarios.

A . REDUCED WATER INTAKE

Hypernatremia will develop in patients with reduced water intake secondary to the inability to communicate and/or limited access to water.
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B . NONRENAL WATER LOSSES
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Nonrenal sites of water loss include sweat, gastrointestinal tract, and the respiratory tract. This is most commonly seen in patients with diarrhea or in
febrile patients on a ventilator.
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A . REDUCED WATER INTAKE

Hypernatremia will develop in patients with reduced water intake secondary to the inability to communicate and/or limited access to water.

B . NONRENAL WATER LOSSES

Nonrenal sites of water loss include sweat, gastrointestinal tract, and the respiratory tract. This is most commonly seen in patients with diarrhea or in
febrile patients on a ventilator.

C . SHIFT OF WATER INTO CELLS

Rarely, hypernatremia may manifest from a shift of water into cells due to the intracellular gain of an effective osmole. This may be seen with seizures
or rhabdomyolysis.

2. The nonoliguric patient (urine flow greater than 0.5 mL/min)

A . URINE OSMOLALITY LESS THAN 250 MO S M / K G

Hypernatremia in the setting of dilute urine is characteristic of diabetes insipidus (DI) or release of a vasopressinase. Central DI results from
inadequate ADH release from the pituitary (stroke, tumor, infiltration). In nephrogenic DI, ADH levels are normal or even elevated, but the kidneys are
less sensitive to the effects. Common causes include lithium therapy, post-relief of urinary obstruction, chronic interstitial nephritis, hypercalcemia,
and hypokalemia. Central and nephrogenic DI can be distinguished by the response to exogenous DDAVP administration while hypernatremic. An
innovative test to assist in the differentiation of patients with hypotonic polyuria is the measurement of copeptin, a C-terminal peptide synthesized
with vasopressin, which mirrors its concentration over a wide range of plasma osmolalities. Elevated levels of copeptin in the setting of hypernatremia
suggest the presence of vasopressin and therefore exclude a diagnosis of central DI. Vasopressin is unstable in isolated plasma, and levels are not
helpful.

B . URINE OSMOLALITY GREATER THAN 300 MO S M / K G

Patients with an elevated urine osmolality and a high urine volume have an osmotic diuresis. Both glucose and urea in the urine can promote polyuria
associated with an increased free water excretion.

TRATAMIENTO
Treatment of hypernatremia includes both correcting the cause of the fluid loss, and replacing the water electrolyte deficit.

A. Choice of Fluid for Replacement

In general, the treatment of patients with hypernatremia involves inducing a positive water balance by the administration of hypotonic fluids. This can
be accomplished either through the gastrointestinal tract with oral intake or boluses via a feeding tube or intravenously (or a combination of both).
Because it can be difficult to correct large water deficits via the gastrointestinal tract alone, the most common strategy is infusion of 5% dextrose in
water (distilled water is contraindicated due to the development of hemolysis). Although there appears to be little risk in the rapid correction of
hypernatremia, caution should be exercised when infusing large amount of 5% dextrose in water due to the risk of hyperglycemia and subsequent
development of an osmotic diuresis, which can aggravate hypernatremia.

In patients who are concurrently volume depleted, priority should be to restore euvolemia via the administration of isotonic fluids.

B. Calculation of Water Deficit

Fluid replacement should include correcting the free water deficit and adding maintenance fluid to replace ongoing and anticipated fluid losses.

1. Chronic hypernatremia

The water deficit is the amount of water calculated to restore the sodium concentration to normal (140 mEq/L). Total body water (TBW) (Table 21–1)
correlates with muscle mass and therefore decreases with advancing age, cachexia, and dehydration and, on average, is lower in women than in men.
Current TBW equals 40–60% current body weight.
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It should be emphasized that the water deficit represents a static period in time and a critical mistake that is often made when considering the volume
of water needed to restore sodium balance is failure to incorporate ongoing water loss via urinary output and insensible losses. Insensible losses can
1. Chronic hypernatremia
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The water deficit is the amount of water calculated to restore the sodium concentration to normal (140 mEq/L). Total body water (TBW) (Table 21–1)
correlates with muscle mass and therefore decreases with advancing age, cachexia, and dehydration and, on average, is lower in women than in men.
Current TBW equals 40–60% current body weight.

It should be emphasized that the water deficit represents a static period in time and a critical mistake that is often made when considering the volume
of water needed to restore sodium balance is failure to incorporate ongoing water loss via urinary output and insensible losses. Insensible losses can
be estimated as 500–1000 mL daily; however, they can vary significantly. The proportion of urine volume that is free water can be estimated by
calculating the electrolyte free water (EFW) clearance via the equation below.

2. Rate of sodium correction

Although it would be appealing to apply similar principles for patients with hyponatremia to patients with hypernatremia, this practice is not
supported by the literature. A slow rate of correction is usually recommended on the basis of osmotic brain adaptation that occurs with chronic
hypernatremia and corresponding theoretical risk of cerebral edema if hypernatremia is corrected too quickly. However, a relatively large
retrospective study found no evidence of morbidity or mortality with rapid correction of hypernatremia in critically ill patients with admission or
hospital-acquired hypernatremia.

3. Treatment of the underlying cause

The underlying cause of the hypernatremia should be identified and addressed. For patients who have central DI, vasopressin deficiency should be
replaced by administration of DDAVP.

CUÁNDO HACER REFERENCIA

CUÁNDO ADMITIR
Patients with symptomatic hypernatremia require hospitalization for evaluation and treatment.

Significant comorbidities or concomitant acute illnesses, especially if contributing to hypernatremia, may necessitate hospitalization.

Chauhan K et al. Rate of correction of hypernatremia and health outcomes in critically ill patients. Clin J Am Soc Nephrol. 2019 May 7;14(5):656–63.
[PubMed: 30948456]

Fenske W et al. A copeptin-based approach in the diagnosis of diabetes insipidus. N Engl J Med. 2018 Aug 2;379(5):428–39.
[PubMed: 30067922]

Seay NW et al. Diagnosis and management of disorders of body tonicity-hyponatremia and hypernatremia: Core Curriculum 2020. Am J Kidney Dis.
2020 Feb;75(2):272–86.
[PubMed: 31606238]

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