Avoid overaggressive correction of hyponatremia as this can put your patient at risk for cerebraldemyelination
Avoid overaggressive correction of hyponatremia as this can put your patient at risk for cerebraldemyelination: Excerpt from Avoiding Common Pediatric Errors
Author:
Craig DeWolfe, MD
What to Do - Make a Decision
Hyponatremia may present in many medical conditions and requires careful assessment, treatment, and monitoring in order to prevent consequences
of rapid fluid shifts in the brain. Sodium (Na) concentrations are maintained physiologically between 135 to 145 mEq/L by a balance of salt and
water intake and excretion. Cells throughout the body respond to different serum concentrations of sodium by shifting water through an osmotic
process, but nowhere in the body are the shifts as delicate as in the cells
of the brain. If a patient has had an acute manifestations of hyponatremia,
often seen during a course ofintravenoushydration and demonstrates symptoms of hyponatremic encephalopathy, he or she would most benefit from
a rapid correction of the serum sodium level. However, if a patient has developed hyponatremia slowly, he or she could be relatively asymptomatic
but be at risk for cerebral demyelination (i.e., central pontine myelinolysis) related to sudden corrections in serum sodium levels. Taking a good
history and having an understanding of the acuity of hyponatremia will
help protect the patient from any devastating consequences of overly rapid
correction.
Patients who are dehydrated, have had a recent operation, or have a
contributing pulmonary or central nervous system disorder and have been
treated with hypotonic fluids are at risk of developing hyponatremic encephalopathy from rapid fluid shifts resulting in cerebral edema. They often
present acutely with lethargy, restlessness, seizure, respiratory arrest, or
coma. In these circumstances, rapid treatment with 3% saline under the
guidance of a specialist is beneficial. The treatment should be directed at
increasing the serum sodium by 1 mEq/L/hr until the patient is alert and
free of seizures, the serum sodium has increased by 20 mEq/L or a serum
sodium level of 125 mEq/L has been achieved. One mL/kg of 3% sodium
chloride will raise the serum sodium by approximately 1 mEq/L. Hypertonic (3% saline) should not be used in asymptomatic hyponatremia due to
the risk of rapid fluid shifts.
Patients who develop hyponatremia over a period of 24 to 48 hours or
more should have their sodium levels corrected slowly. Animal and retrospective clinical data suggest a slow correction of sodium levels by no more
than 0.5 mEq of Na per hour, with a goal correction of 15 to 20 mEq in
48 hours will limit the risk of cerebral demyelination. Cerebral demyelination, when isolated to the pontine region is called central pontine myelinolysis and is characterized by a 2-to 7-day delay in symptoms. Patients may
exhibit dysarthria, dysphagia, spastic paraparesis, and a pseudocoma with a
"locked-in stare." Lesions outside of the pontine region tend to present in a
more variable manner, with movement disorders such as ataxia and altered
mental status, including coma. In either region, serious disruptions can lead
to death. Careful calculation of sodium and water needs and ongoing losses
in addition to regular electrolyte checks, as often as every hour at the start of
treatment, will help protect the patient from these neurologic syndromes. In
addition, fluid restriction may help in certain cases of chronic hyponatremia
associated with hyper or euvolemia.
The hydration status of the patient and urine spot sodium concentrations are helpful components in the diagnostic and treatment process. If a
patientisdehydratedandhasadiluteurine(Na<30mEq/L),thedifferential
diagnosis includes dermal losses through sweating or burns or gastrointestinal losses such as vomiting and diarrhea. If the hypovolemic patient has
high urine sodium levels (urine Na >30 mEq/L), the practitioner should
consider diuretics, cerebral or nephrogenic salt wasting, or mineralocorticoid deficiency as the etiology. In patients with hypovolemia, restore the
intravascular volume with 1 to 3 normal saline boluses prior to adjusting the
concentration of sodium in the fluids. In the hypervolemic patient with a
low urine sodium, consider congestive heart failure or nephrotic syndrome
in the differential, whereas a high urine sodium should lead the practitioner
to consider chronic renal failure. In each of these cases, the practitioner
should treat the underlying cause and use fluid restriction. Finally, in the
euvolemic patient, the practitioner should consider syndrome of inappropriate secretion of antidiuretic hormone, hypopituitarism, hypothyroidism,
or water intoxication through primary polydipsia or iatrogenic administration of hypotonic fluid as the cause. In these patients, fluid restriction is the
mainstay of treatment.
The cause and acuity of the hyponatremia can effectively and safely
dictate the rate of sodium correction. If the patient is acutely symptomatic, one should treat rapidly until the symptoms have resolved or
until a 20 mEq/L increase in serum sodium concentration or concentrations of 120 to 125 mEq/dL have been achieved, whichever comes first.
Thereafter, proceed cautiously with the sodium correction, ensuring that
sodium levels are not altered >0.5 mEq/L/hr. This will help protect the
patient from any devastating consequences of the initial insult and the
correction.
Suggested Readings
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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