Avoid overaggressively correctinghypernatremia as this can put your patient at risk for cerebral edema, convulsions, coma, and death
Avoid overaggressively correctinghypernatremia as this can put your patient at risk for cerebral edema, convulsions, coma, and death: Excerpt from Avoiding Common Pediatric Errors
Author:
Craig DeWolfe, MD
What to Do - Make a Decision
The principles of correcting hypernatremia are similar to those for correcting hyponatremia. Sodium is a functionally impermeable solute, and
thus, it is the main contributor to cellular osmolarity and causes shifts of
water across cell membranes. These fluid shifts may cause cells to expand
or shrink more rapidly than the body can withstand. Rapid decreases in
brain cell size caused by hypernatremia can lead to brain injury due to
brain tissue separation from the meninges, rupture of the bridging veins,
and venous sinus thromboses. Rapid correction of severe hypernatremia
can also lead to significant brain injury from increased intracranial pressure and herniation, caused by rapid cellular expansion within the fixed
capacity of the intracranial vault. Often, rapid iatrogenic corrections of hypernatremia cause more serious complications than the original disorder.
Studies suggest that a patient with chronic hypernatremia is at a high risk
for cerebral edema when the sodium drops >0.5 mEq/L/hr. To manage
the rate of sodium decline, the practitioner needs to be aware of the general
fluid status of the patient, select the appropriate initial fluid concentration, and be prepared to frequently alter its rate and concentration based
on frequent checks of the serum sodium concentration and ongoing fluid
losses.
Hypernatremia is defined as a serum sodium concentration >145
mEq/L.Itrepresentsadeficitofwaterinrelationtothebody'ssodiumstores
and occurs as a result of a net water loss, or less commonly, a net sodium
gain. It should be considered in patients who present with anorexia, restlessness, weakness, a high-pitched cry, hyperpnea, nausea, and vomiting. The
greater and more rapidthe water andsaltdisruption, themoresignificantthe
patient's clinical manifestations. Patients with sodium concentrations >170
mEq/L may have severe neurologic symptoms, including stupor or coma.
Practitioners should have a high index of suspicion for hypernatremia when
evaluating infants and other patients who have an impaired ability to control
their free water intake.
Hypernatremia invariably denotes hypertonic hyperosmolality and results in cellular dehydration, at least transiently. Cell shrinkage in the brain
can result in vascular rupture, with cerebral bleeding or subarachnoid hemorrhages. Brain shrinkage is countered within hours as water moves from
the cerebrospinal fluid into brain cells and electrolytes enter the brain cells.
Normalization of the brain volume is complete within days as organic osmolytes(e.g., myoinositol) complete the osmotic restoration.Althoughbrain
water may be restored, the hyperosmolality of the brain persists. During rehydration, the brain can rapidly release the accumulated electrolytes but the
loss of osmolytes occurs much more slowly, a phenomenon that acts to hold
water within the cells. Therefore, slow correction of hypernatremia allows
the brain to release accumulated osmolytes and prevent cerebral edema. In
the case of overly aggressive treatment with hypotonic fluids, cerebral edema
may lead to coma, seizures, and death.
To treat hypernatremia, the practitioner should consider the underlying cause and hydration status of the patient before determining the appropriate fluid resuscitation. Hypernatremic patients may be dehydrated
from vomiting, diarrhea, or excessive sweating in addition to diuresis from
medications, relief of a urinary tract obstruction, chronic renal disease, or
hyperglycemia-induced diuresis. In each of the cases, attention to ongoing
losses is paramount to treating the hypernatremia. Conversely, a hypernatremic patient may be hypervolemic from the use of hypertonic saline,
tube feedings, or high sodium-containing antibiotics in addition to hyperaldosteronism. Finally, in the euvolemic patient one should consider fever,
hyperventilation, and mechanical ventilation as well as diabetes insipidus if
the patient has had unrestrained access to free water.
The goal of treatment is to safely but expeditiously correct fluid losses
and re-establish sodium concentrations to 145 mEq/L. Practitioners can
treat hypernatremia that develops over hours, for example, after emergent
sodium bicarbonate loads during resuscitation procedures, by dropping the
plasma sodium content by 1 mEq/L as it improves the patient's prognosis without putting him or her at risk for cerebral edema and convulsions.
If the hypernatremia developed more chronically or if the time course of
developing hypernatremia is unknown, then the hypernatremia should be
corrected more judiciously at a rate of <0.5 mEq/L/hr or 10 mEq/day.
Administering salt and water orally or by feeding tube is the preferred route
of rehydration and as a result, the practitioner should be aware of the common salt and sugar contents of commercially available rehydration products
(e.g., Pedialyte has the salt content of 25% normal saline [NS]). Emergent management of vascular compromise should be treated with boluses
of NS (generally limited to 2–3), but once hemodynamics are restored, it
is best to treat with D51/4% to D51/2% NS to replace fluid losses, provide
maintenance fluid needs, and manage the sodium disruption. Useful formulas for treating hypernatremia in the pediatric population are listed below.
The formulas estimate the effect of 1 L of infusate (where NS consists of
154 mEq of Na per liter of fluid) on the calculated serum sodium.
Change in serum Na = (infusate Na - serum Na)/(0.6 × wt in kg) + 1
Change in serum Na = (infusate Na + infusate K) - serum Na/(0.6 × wt in kg) + 1
where K = potassium, NA = sodium, and wt = weight.
Frequent early checks of the electrolyte concentrations cannot be
overemphasized as the corrections do not take into account continued water
and salt losses.
In summary, the practitioner should judiciously treat hypernatremia,
maintenance fluid needs, and ongoing losses to ensure that sodium concentrations do not fall >0.5 mEq/L/hr and to prevent cerebral edema, seizures,
coma, or death.
Suggested Readings
Adrogu´e HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342:1493–1499.
Moritz ML, Ayus JC. Preventing neurological complications from dysnatremias in children.
Pediatr Nephrol. 2005;20:1687–1700.
Reynolds RM, Padfield PL, Seckl JR. Disorders of sodium balance. BMJ. 2006;332:702–705.
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Book Source Details
- Book Title: Avoiding Common Pediatric Errors
- Author(s): Anthony D Slonim MD, DrPH; Lisa Marcucci MD
- Year of Publication: 2008
- Copyright Details: Avoiding Common Pediatric Errors, Copyright © 2008 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Avoiding Common Pediatric Errors
Authors: Anthony D Slonim MD, DrPH; Lisa Marcucci MD
Publisher: Lippincott Williams & Wilkins
Copyright: 2008
ISBN: 0-7817-7489-6
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