Perioperative Managment Of   Hypernatremia

Hypernatremia is caused by serum sodium concentration of more than 150 mEq/L. Usually, it reflects an underlying defect in water metabolism. Hyperosmolality stimulates thirst, which usually prevents the development of hypernatremia. This condition carries high morbidity and mortality, especially during treatment.

Pathophysiology: Hypernatremia occurs in the following 3 ways:

1. Pure water depletion (eg, diabetes insipidus)

2. Sodium excess (eg, salt poisoning)

3. Water depletion exceeding sodium depletion (eg, diarrhea)

These mechanisms cause hypernatremia either alone or in concert. As a result of increased extracellular sodium, plasma tonicity increases. This increase in tonicity results in removal of fluid from within the cells, resulting in cell desiccation. Extracellular volume remains normal at the expense of intracellular dehydration, which is responsible for the clinical manifestations of hypernatremia.

Infants, because of certain physiologic characteristics, are predisposed to dehydration. They have larger surface area in relation to height or weight than adults, for example, and have relatively large evaporative water losses. Although it is not clear at exactly what age infants are able to fully concentrate urine, some normal infants are unable to concentrate beyond 700 mOsm/L in the early months of life. These 2 factors are primarily responsible for higher incidence of hypernatremia in children with diarrhea.

Hypernatremia causes decreased cellular volume as a result of water efflux from the cells in order to maintain equal osmolality inside and outside the cell. Central nervous system problems occur if the cellular shrinkage goes beyond a certain limit, causing thrombosis of small arteries and veins. This results in tearing of blood vessels and ensuing intracranial bleed.

The central nervous system has special adaptive capabilities during hypernatremic episodes. Animal models with hypernatremia show water efflux from neurons occurs during acute phases. The experiments also showed increased intracellular concentration of electrolytes. This phenomenon was observed within 8 hours of onset of hypernatremia.

During chronic hypernatremia (after 2 days of onset of hypernatremia), organic osmolytes start appearing inside the neurons. Researchers postulate that some of the osmolytes move inside the cells while others are synthesized within the cell. These organic osmolytes were initially called idiogenic molecules, and the primary function of these osmolytes is to prevent cellular dehydration. Even though the presence of organic osmolytes is considered to be protective, it causes significant problems during rehydration. Rapid rehydration results in cerebral edema by relative hypotonic fluids entering the cerebral neurons.

Frequency:

• In the US: The reported incidence varies from 9-68% (average 24.5%).

• Internationally: In developing nations, the reported incidence varies from 1.5-20%.

Mortality/Morbidity:

• Several authors report severe brain damage from hypernatremia in infants.

• The reported rate of persistent neurologic abnormality is 11%-15%, consisting of intellectual deficits, seizure disorders, and spastic plegias.

• Overall mortality is about 10%.

Race: No predilection is documented.

Sex: No gender difference exists.

• Hospitalized patients on exclusive intravenous fluids

• Coma

• Newborn

• Toddler

• Diabetes insipidus

• Alkali therapy

• Diarrhea

• Fever

• Renal disorders (eg, dysplasia, medullary cystic, polycystic, tubulointerstitial disease)

• Obstructive uropathy

• Electrolyte disturbances (eg, hypokalemia, hypercalcemia)

• Heat stroke or excessive hypotonic fluid loss

• Symptoms

• Irritability

• High pitched cry or wail

• Periods of lethargy interspersed with periods of irritability

• Altered sensorium

• Seizures

• Fever

• Oligoanuria

• Excessive diuresis

Physical:

• Skin turgor

• Extracellular and plasma volume tend to be maintained in hypernatremic dehydration until dehydration is severe (greater than 10% loss of body weight).

• When the severity of dehydration results in loss of 10% of body weight, skin turgor becomes reduced and a characteristic doughy is present.

• Irritability

• High pitched cry or wail

• Altered sensorium

• Seizures

• Increased muscle tone

• Oligoanuria

• Fever

• Rhabdomyolysis

Causes:

• Hypovolemic hypernatremia

• Diarrhea

• Excessive perspiration

• Renal dysplasia

• Obstructive uropathy

• Osmotic diuresis

• Euvolemic hypernatremia

• Central diabetes insipidus causes
  • Idiopathic

  • Head trauma

  • Suprasellar or infrasellar tumors (eg, craniopharyngioma, pinealoma)

  • Granulomatous disease (sarcoid, tuberculosis, Wegener granulomatosis)

  • Histiocytosis

  • Sickle cell disease

  • Cerebral hemorrhage

  • Infection (meningitis, encephalitis)

  • Associated cleft lip and palate

• Nephrogenic diabetes insipidus causes
  • Congenital (familial)

  • Renal disease (obstructive uropathy, renal dysplasia, medullary cystic disease, reflux nephropathy, polycystic disease)

  • Systemic disease with renal involvement (sickle cell disease, sarcoidosis, amyloidosis)

  • Drugs (amphotericin, phenytoin, lithium, aminoglycosides, methoxyflurane)

• Hypervolemic hypernatremia

• Improperly mixed formula

• NaHCO₃ administration

• NaCl administration

• Primary hyperaldosteronism

• Serum osmolality

• BUN, creatinine

• Urine sodium

• In cases of hypovolemic hypernatremia, extrarenal losses show urine sodium less than 20 mEq/L and renal losses show urine sodium greater than 20 mEq/L.

• In euvolemic hypernatremia, urine sodium is variable.

• In hypervolemic hypernatremia, urine sodium is greater than 20 mEq/L.

• Urine osmolality

Imaging Studies:

• Computed tomography scans diagnose intracranial tumors, granulomatous diseases such as sarcoid, tuberculosis, histiocytosis, and other intracranial pathologies.

• Magnetic resonance imaging further delineates the pathology.

• Ultrasound of the kidney rules out kidney diseases as a cause of nephrogenic diabetes insipidus.

Other Tests:

• Aldosterone

• Cortisol

• ADH

• ACTH

Medical Care:

• Correction of hypernatremia

• While correcting hypernatremia, do not drop sodium level rapidly because rapid decline in serum sodium can cause cerebral edema.

• Recommended duration of correction is over 48-72 hours.

• Recommended rate of correction is 0.5 mEq/h.

• This is best accomplished by giving deficit correction and maintenance fluids over 48-72 hours.

• Since hyperglycemia is a common accompaniment, glucose may be given as 2.5% dextrose solution.

• Calcium may be added, depending on the serum calcium content.

• Once the child is urinating, add 40 mEq/L KCl to fluids to aid water absorption into cells.

• If the serum sodium concentration is more than 200 mEq/L, peritoneal dialysis should be done using a high glucose, low sodium dialysate.

• Calculate total body water (TBW) deficit and replacement fluid volume.
  • Calculation of TBW deficit and replacement volume: The calculation of free water deficit is based on assumption that the product of TBW and plasma sodium concentration is always constant.
    Current TBW X Current P Na = Normal TBW X Normal P Na

    Using a normal plasma sodium concentration of 140 mEq/L and rearranging terms yields the following relationship:

    Current TBW = Normal TBW X (140/Current P Na)

  • The normal TBW usually is 60% of lean body weight in men and 50% of lean body weight in women. However, in hyponatremia associated with free water deficits, the normal TBW should be approximately 10% less than usual. Once the current TBW is calculated, the water deficit is taken as the difference between the normal TBW and the current TBW.
    TBW deficit (L) = Normal TBW – Current TBW

    Example: Assume that the child with weight of 10 kg has plasma sodium of 160 mEq/L. The normal TBW will be 0.5 X 10 = 5 L. The current TBW is 5 X 140/160 = 4.375 L. The TBW deficit is 5- 4.375 = 0.625 L.

  • Replacement of volume: The volume of replacement fluid needed to correct the water deficit is determined by the concentration of sodium in the replacement fluid. The replacement volume can be determined as follows:
    Replacement of volume (L) = TBW deficit X (1/1-x) (x = replacement fluid Na/154).

    If the replacement fluid is 0.45 normal saline, the replacement volume will be 0.625 X (1/0.5) = 1.25 L.

• If the patient is hypotensive, correct hypotension with normal saline, lactated Ringer solution, or 5% albumin, regardless of serum sodium concentration.

• Hyperglycemia may accompany hypernatremia. Insulin treatment is not recommended because it may increase brain idiogenic osmole content.

• Correction of associated conditions

Consultations:

• Critical care

• Symptomatic hypernatremia patients may need to be transferred to a pediatric intensive care unit for appropriate management and monitoring.

• Endocrinology

• Obtain consultation for patients with primary hyperaldosteronism.

• Nephrology

• Consultation is recommended in cases in cases of renal failure, obstructive uropathy, and when serum sodium level is more than 180 mEq/L for possible peritoneal dialysis.

• Consultation is also recommended for patients with renal dysplasia, medullary cystic disease, reflux nephropathy, and polycystic disease.

Diet:

• In diabetes insipidus, sodium and protein-restricted diet should be given.

The following medications are used in patients with diabetes insipidus.

• Frequent electrolyte monitoring

• Restricted sodium and protein

• Treatment of underlying disease

Further Outpatient Care:

• Treatment of underlying disease

• Restricted sodium and protein

Transfer:

• Patients with symptomatic hypernatremia should be transferred to pediatric intensive care unit for appropriate management and close monitoring.

• Patients should be transferred to a facility that has dialysis in case of renal failure or if the serum sodium is higher than 180 mEq/L.

Deterrence/Prevention:

• Avoid making oral rehydration solution at home or adding salt to any commercial infant formula.

• Treatment of underlying cause.

Complications:

• Seizures can occur because of hypernatremia per se, which is very rare. It is usually seen during treatment of hypernatremia because of rapid decline in serum sodium. So, it is very important to correct hypernatremia very slowly.

• Mental retardation

• Intracranial hemorrhage

• Intracerebral calcification

• Cerebral infarction

• Cerebral edema, especially during treatment

• Hypocalcemia

• Hyperglycemia

Prognosis:

• Patients usually recover from hypernatremia.

• Patients with recurrent hypernatremic dehydration will develop neurologic sequelae, especially infants with diabetes insipidus.

Patient Education:

• For parents

• Avoid making oral rehydration solutions at home or adding salt to any commercial infant formula.

• Watch for neonatal dehydration and perinatal care, especially for breast-feeding mothers.

• Evaluate breast-fed infant routinely during first weeks of life.

• For patients with diabetes insipidus

• Monitor weight and urine output since significant changes of sodium are associated with changes in weight.

• Restricting sodium and protein intake.

• Drinking liberal amounts of water.

• Make sure thirst develops before taking medications.

Medical/Legal Pitfalls:

• Rapid correction of sodium in patients with chronic hypernatremia