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Hypernatremia


Hypernatremia

Article Author:
Bhavin Sonani
Article Author:
Srividya Naganathan
Article Editor:
Mohammed Al-Dhahir
Updated:
8/26/2020 1:08:26 PM
For CME on this topic:
Hypernatremia CME
PubMed Link:
Hypernatremia

Introduction

Sodium is a dominant cation in extracellular fluid and necessary for the maintenance of intravascular volume. The human body maintains sodium and water homeostasis by concentrating the urine secondary to the action of antidiuretic hormone (ADH) and increased fluid intake by a powerful thirst response. These mechanisms to protect against developing hypernatremia are impaired in certain vulnerable populations, vasopressin deficiency, or unresponsiveness at the renal tubular level. Hypernatremia is defined as a serum sodium concentration of greater than 145 meq/L.[1][2][3][4]

Etiology

The basic mechanisms of hypernatremia are water deficit and excess solute. Total body water loss relative to solute loss is the most common reason for developing hypernatremia. Hypernatremia is usually associated with hypovolemia, which can occur in conditions that cause combined water and solute loss, where water loss is greater than sodium loss, or free water loss. Combined loss can be seen in extra-renal conditions such as gastroenteritis, vomiting, prolonged nasogastric drainage, burns, and excessive sweating. Excessive sweating can occur due to exercise, fever, or high heat exposure. Renal losses can be seen in intrinsic renal disease, post-obstructive diuresis, and with the use of osmotic or loop diuretics. Hyperglycemia and mannitol are common causes of osmotic diuresis. Free water loss is seen with central or nephrogenic diabetes insipidus (DI) and also in conditions with increased insensible loss. Central DI can occur due to inadequate production of ADH. Common causes of central DI are idiopathic, head trauma, cranial neoplasm, and pituitary infiltrative diseases, such as sarcoidosis and histiocytosis. Nephrogenic DI occurs due to tubular unresponsiveness to the action of ADH and can be inherited in an X-linked pattern or secondary to certain medications including lithium, foscarnet, and demeclocycline. Rarely, hypernatremia with inadequate fluid intake can be seen in breastfed babies, child or elder abuse, and patients with an impaired thirst response. Excess sodium usually is iatrogenic and seen in the hospital setting but can be associated with improper formula mixing, excess sodium bicarbonate ingestion, salt tablet poisoning, hyperaldosteronism, and seawater drowning.[5][6][7][8]

Epidemiology

Hypernatremia is primarily seen in infants and the elderly population. Infants receiving inadequate water replacement in the setting of gastroenteritis or ineffective breastfeeding are common scenarios. Premature infants are at higher risk due to their relatively small mass to surface area and their dependency on the caretaker to administer fluids. Patients with neurologic impairment also are at risk due to impaired thirst mechanism and lack of water availability. Hypernatremia can occur in the hospital setting due to hypertonic fluid infusions, especially when combined with the patient's inability for adequate water intake.[9]

Pathophysiology

Sodium is important to maintain extracellular fluid (ECF) volume. Changes in the ECF volume provide feedback to maintain total sodium content by increasing or decreasing sodium excretion in the urine. Sodium excretion also involves regulatory mechanisms such as the renin-angiotensin-aldosterone systems. When serum sodium increases, the plasma osmolality increases which triggers the thirst response and ADH secretion, leading to renal water conservation and concentrated urine.[10]

History and Physical

Most patients present with symptoms suggestive of fluid loss and clinical signs of dehydration. Symptoms and signs of hypernatremia are secondary from central nervous system dysfunction and are seen when serum sodium rises rapidly or is greater than 160 meq/L. Infants and Children present with irritability and agitation, which can progress to lethargy, somnolence, and coma. Other symptoms include increased thirst response in alert patients and high-pitched cry in infants. Patients with diabetes insipidus present with polyuria and polydipsia. The skin can feel doughy or velvety due to intracellular water loss. Orthostatic hypotension and tachycardia are usually present in hypovolemic hypernatremia. The patient may have increased tone with brisk reflexes and myoclonus. It is important to remember that the degree of dehydration can be underestimated in children with hypernatremia due to a shift of water from the intracellular space to the extravascular space. Polyuria is one of the common symptoms of diabetes insipidus. [11][12]

Evaluation

The etiology of hypernatremia usually is evident based on history and physical examination. Plasma volume, plasma osmolality, urine volume, concentrating ability, and osmolality can help to further differentiate between renal and extrarenal causes. In DI, the urine is inappropriately diluted with normal urine volume and urine osmolality less than the serum osmolality. When DI is suspected, a water deprivation test may be performed with the administration of desmopressin. In central DI, desmopressin administration demonstrates an increase in urine osmolality, while in the nephrogenic variety, there is no response to desmopressin. In extrarenal causes, the body tries to conserve fluids with appropriately low urine volume, high specific gravity, and urine osmolality greater than serum osmolality.[13]

Treatment / Management

Proper management of hypernatremia involves identifying the underlying condition and correcting the hypertonicity. The goal of therapy is to correct both the serum sodium and the intravascular volume. Fluids should be administered orally or via a feeding tube whenever possible. In patients with severe dehydration or shock, the initial step is fluid resuscitation with isotonic fluids before free water correction. Hypernatremia is corrected by calculating the free water deficit using one of the following formulas.[14][15]

  • Total Body Water[0.6 in men and 0.5 in women x body weight(kg)] x [(plasma sodium/140) -1]
  • 4ml x bodyweight x (desired change in serum sodium meq/L)

It is important to remember that rapid correction of hypernatremia can lead to cerebral edema because water moves from the serum into the brain cells. The goal is to decrease serum sodium by not more than 12 meq in 24 hours. Close serial monitoring of serum sodium every 2 to 4 hours is essential during the acute phase of correction. Seizures occurring during correction of hypernatremia is a sign of cerebral edema due to rapid shifts in osmolality, and the administration of hypotonic fluids should be halted. The estimated free water deficit should be corrected over 48 to 72 hours with a decrease in serum sodium not exceeding 0.5 meq per hour. Patients should be carefully monitored for the rate of correction, urine output, and ongoing losses. In cases of sodium intoxication, the free water requirement may be too large and cause volume overload, requiring the use of loop diuretics and, at times, peritoneal dialysis to remove excess sodium. Older children and adults with central DI may need desmopressin, which is available in intranasal and oral forms. Water intoxication and hyponatremia are adverse effects seen with the use of desmopressin.

Differential Diagnosis

  • Cirrhosis
  • Central diabetes insipidus
  • Diarrhea
  • Hypocalcemia
  • Hyponatremia
  • Nephrogenic diabetes insipidus
  • Thirst defect
  • Type 1 diabetes mellitus

Complications

The most serious complication of hypernatremia is subarachnoid or subdural hemorrhage due to the rupture of bridging veins and dural sinus thrombosis. It can lead to permanent brain damage or death. Rapid correction of chronic hypernatremia causes cerebral edema, seizure, and permanent brain damage.[16]

Pearls and Other Issues

  • Hypernatremia occurs due to net water loss or excess sodium intake. 
  • It is more common in infants or elderly population with neurological or physical impairment.
  • It is crucial to identify acute versus chronic onset hypernatremia before correcting the free water deficit. 
  • It is important to remember that hypernatremia should be corrected over 48 hours. Rapid correction can lead to cerebral edema and seizures.

Enhancing Healthcare Team Outcomes

Hypernatremia is best managed by an interprofessional team that includes an internist, endocrinologist, emergency department physician, nurse practitioner, and the primary care provider. The key is to identify the cause and correct the hypertonicity. The goal of therapy is to correct both the serum sodium and the intravascular volume. In patients with severe dehydration or shock, the initial step is fluid resuscitation with isotonic fluids before free water correction.

Health care providers should be cognizant of the fact that rapid correction of hypernatremia can lead to cerebral edema because water moves from the serum into the brain cells. The goal is to decrease the serum sodium by not more than 10 to 12 meq/L in 24 hours. The acute phase of sodium correction requires monitoring of serum sodium levels every 2 to 4 hours. Frequent communication between the attending physician, the nursing staff, and the pharmacist is crucial to avoid the rapid correction of sodium level. Rapid correction of sodium level can lead to a seizure, cerebral edema, or permanent neurological deficit. Special attention should be given to high-risk nursing home patients with neurological or physical impairments who are prone to develop recurrent hypernatremia. Discharge care coordination among discharging physician, primary care physician, and nursing home staff can prevent readmission due to hypernatremia. Serum sodium and drug levels should be periodically monitored in patients who are taking medications known to cause nephrogenic diabetes insipidus.[17][18] [Level 5]


References

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