Hypo/hypernatremia

1. Description of the problem

What every clinician needs to know

Normal serum sodium (Na) is tightly regulated between 135 to 145 mEq/L. Hyponatremia results when serum na is below 135meq/L. Hypernatremia is present when serum Na is greater than 150mEq/L. Na disturbances are usually a problem of water balance rather than sodium balance. this is especially true of hypernatremia.

Clinical features

Hyponatremia

When serum Na decreases, there is a reduction of plasma osmotic gradient resulting in water moving into the brain. Most neurologic symptoms are attributable to cerebral overhydration. Patient can present with lethargy, apathy, vomiting, headcahe, seizures and coma. Serum Na of 125meq/L is considered the seizure threshold, below which seizures or other central nervous manifestations will result. Most patients with hyponatremia have normal muscle tone and function.

Hypernatremia

Child maybe irritable with “high-pitched” cry or wail. Periods of lethargy may be interspersed with periods of irritability. If dehydration and hypernatremia is severe, coma, increased muscle tone and seizures may be noted. Hypertonicity secondary to hypernatremia can result in brain shrinkage and tearing of cerebral vessels (especially in neonates), resulting in brain hemorrhage. Severe hypernatremia (as induced by use of hypertonic saline for traumatic brain injury) can result in acute kidney injury.

Key management points

Hyponatremia

Patient with seizures or acute decrease of serum Na below 125mEq/L may need 3% hypertonic saline to raise the serum Na. More chronic hyponatremia is managed conservatively (correct about 12-15mEq/L/day) to prevent development of central pontine myelinolysis.

Hypernatremia is usually corrected by using free water or relative hypotonic fluids. It should be corrected slowly over 48 hours to prevent development of cerebral edema.

2. Emergency Management

Stabilizing the patient

For hyponatremia: When serum Na is under 125 or for symptomatic seizures, use 5cc/Kg of 3% hypertonic saline over 5-10 minutes.

For hypernatremia: Correct dehydration/shock first followed by careful treatment of underlying condition. Use of isotonic solutions may not correct serum na and may require hypotonic solutions.

Other key points

Hyponatremia: Slow correction of about 12-15mEq/L/day unless symptomatic or with seizures on presentation.

Hypernatremia: Slow correction over 48 hours.

3. Diagnosis

Diagnostic criteria and tests

Hyponatremia and hypernatremia should be suspected in any patient with seizures, coma or altered mental status on presentation. Stat serum Na should be checked at bedside and confirmed by sending a basic metabolic panel to the laboratory. Urinary electrolytes and urine osmolality may be sent. A CT brain scan may be needed for patients with cerebral edema or brain injury. Central venous pressure monitoring may be required to assess the degree of hydration. Spot urinary Na greater than 30mEq/L is indicative of high urinary Na excretion. This is especially useful in salt wasting polyurias. A rising serum Na with urinary output above 3cc/kg/hr is highly suggestive of diabetes insipidus unless proven otherwise. A patient with hypernatremia may have decreased skin turgor and a characteristic “doughy” feel can be appreciated when the skin of the abdomen is pinched between the fingers.

Normal lab values

Serum Na normal range: 135-145 meq/L

Hyponatremia: Serum Na under 135meq/L. For hypernatremia: serum Na greater than 150mEq/L

Other possible diagnoses

Hyponatremia: Isotonic pseudohyponatremia (plasma osmolality between 280-295mOsm/kg) is seen with increase in plasma lipids and proteins, especially if serum Na is measured using flame spectrophotometry. Glucose and mannitol can cause factitious hyponatremia (plasma Osm above 295mOsm/kg). This is a true hyponatremia caused by redistribution of water from intracellular to extracellular space. For every 100mg/dl increase in blood sugar, the serum Na decreases by 1.6mEq/L.

4. Specific Treatment

First-line therapies

Hyponatremia: In addition to emergency therapy mentioned above, any underlying condition must be sought and appropiately treated. Euvolemic hyponatremia (e.g. SIADH) can be treated with fluid restriction. Patients with hypervolemic hyponatremia (such as congestive heart failure, nephrotic syndrome etc.) can be treated with water and salt restriction.

Hypernatremia: Underlying cause must be sought and treated. For Diabetes insipidus (DI) an IV vasopressin drip of L-deamino-(8-D-arginine) can be used. For refractory hypernatremia with fluid overload and acute kidney injury, dialysis may be required.

5. Disease monitoring, follow-up and disposition

Expected response to treatment

With appropriate therapy prognosis is excellent, provided underlying cause can be fixed.

Incorrect diagnosis

If fluid restriction does not correct hyponatremia in SIADH, the diagnosis of SIADH must be reconsidered. SIADH is commonly chest and CNS infections (pneumonia and meningitis respectively). It is also seen in cerebral edema and brain tumors. It is a diagnosis of exclusion.

Patients serum Na must be closely followed almost q2hourly initially till stable value is obtained and with every change in IV fluids.

Pathophysiology

Hyponatremia: Decline in serum Na results in decrease in serum osmolality; the osmotic gradient that develops across the blood brain barrier causes water to move into the brain. Symptoms result from overhydration of the brain.

Hypernatremia represents a deficiency of water relative to total body sodium content and is usually a a disorder of water balance. Hypernatremia can result in cellular dehydration, resulting in tearing of cerebral blood vessels and brain hemorrhage.

Epidemiology

Causes of hyponatremia

Once hypotonic hyponatremia (plasma Osm under 280mOsm/kg) is confirmed, then based on extracellular fluid (ECF) volume we can classify hyponatremia as:

Hypovolemic hyponatremia: (a) Common causes include GI (diarrhea, vomiting), excessive sweating and third spacing (burns, pancreatitis, ascites, effusions); (b) renal causes include use of diuretics, salt wasting nephropathy, adrenal insufficiency, pseudohypoaldosteronism and metabolic alkalosis.
Euvolemic hyponatremia: SIADH, glucocorticoid deficiency, hypothyroidism and water intoxication.
Hypervolemic hyponatremia: (a) edema forming states (congestive heart failure, cirrhosis and nephrotic syndrome); and (b) kidney injury (acute/chronic).

Causes of hypernatremia

Sodium excess, such as improperly mixed formula or excessive sodium bicarbonate administration.
Water deficit: Diabetes insipidus, DKA, inadequate access to water.
Water deficit in excess of sodium deficit: diarrhea, osmotic diuretics obstructive uropathy and renal dysplasia.

The most common causes of DI seen in PICU are secondary to head trauma and and suprasellar tumors (e.g. craniopharyngioma).

Prognosis

Depends on underlying cause of hypo/hypernatremia.

Special considerations for nursing and allied health professionals.

Close monitoring of serum sodium and anticipation of changes is important. For example, the postoperative patient has multiple reasons for hyponatremia including fluid therapy given, as well as pain and medications that stimulate ADH release. It is vital to closely monitor serum Na in such patients. More recent studies are focusing on the potential ill effects of hyponatremia resulting from iatrogenic conditions such as administration of low tonicity maintenance IV fluids in hospitals.

What's the evidence?

Adrogue, H, Madias, N. “Hypernatremia”. N Eng J Med. vol. 342. 2000. pp. 1493-9.

Adrogue, H, Madias, N. “Hyponatremia”. N Engl J Med. vol. 342. 2000. pp. 1581-9.

Holliday, MA, Friedman, Al, Segar, WE. “Acute hospital-induced hyponatremia in children: A physiologic approach”. J Pediatr. vol. 145. 2004. pp. 584-7.

Oh, MS, Carroll, HJ. “Disorders of sodium metabolism: hypernatremia and hyponatremia”. Crit Care Med. vol. 20. Jan 1992. pp. 94-103.

Berry, PL, Belsha, CW. “Hyponatremia”. Pediatr Clin North America. vol. 37. 1990 Apr. pp. 351-63.

Conley, SB. “Hypernatremia”. Pediatr Clin North America. vol. 37. 1990 Apr. pp. 365-72.

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Critical Care Medicine