Hypernatremia


Article Author:
Navid Mahabadi
Srividya Naganathan


Article Editor:
Mohammed Al-Dhahir


Editors In Chief:
Linda Lindsay


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Kyle Blair
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
7/16/2019 2:00:11 PM

Introduction

Sodium is the 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 powerful thirst response. These mechanisms to protect against developing hypernatremia are impaired in certain vulnerable populations and conditions with 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 solute excess. Total body water loss relative to solute loss is the most common reason for developing hypernatremia. Hypernatremia usually is 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 suction, burns, and excessive sweating. Renal loss can be seen in chronic kidney disease, diabetes mellitus, post-obstructive diuresis, and with the use of osmotic diuretics. Free water loss is seen in central or nephrogenic diabetes insipidus (DI) and also in conditions with an increased insensible loss. Central DI is due to inadequate production of ADH, structural abnormalities, or acquired by autosomal dominant or recessive pattern. Nephrogenic DI is due to tubular unresponsiveness to the action of ADH and can be inherited in an X-linked pattern or secondary to a number of medications. Rarely, hypernatremia with inadequate fluid intake can be seen in breastfed babies, child or elder abuse, and in patients with an impaired thirst response. Excess sodium usually is iatrogenic and seen in the hospital setting but also can be associated with improper formula mixing, excess sodium bicarbonate ingestion, 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 lack of communication of the thirst response to the caregiver. Hypernatremia can occur in the hospital setting due to hypertonic fluid infusions, especially when combined with the patient's inability for water intake.

Pathophysiology

Sodium is important to maintain 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 and triggers an increase in thirst response and ADH secretion, leading to renal water conservation and concentrated urine.

History and Physical

Most patients present with symptoms suggesting fluid loss and clinical signs of dehydration. Symptoms and signs of hypernatremia are secondary to central nervous system dysfunction and are seen when serum sodium rises rapidly or is greater than 160 meq/L. 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. The skin can feel doughy or velvety due to intracellular water loss. Other findings include 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. The most serious complication of hypernatremia is brain hemorrhage, including subarachnoid or subdural hemorrhage due to rupture of bridging veins and dural sinus thrombosis. Hypernatremia is associated with a mortality rate as high as 15% to 20%.

Evaluation

The etiology of hypernatremia usually is evident based on the history and physical exam. 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 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.

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. 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.[9][10]

  • 0.6 (1-145/current sodium) x body weight
  • 4ml x body weight 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 the serum sodium by not more than 12 meq in a 24-hour period. 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 loss. 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.

Pearls and Other Issues

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 a multidisciplinary 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.

Healthcare workers 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 12 meq in a 24-hour period. 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 loss. 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.[11][12] (Level V)


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Hypernatremia - Questions

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Which of the following is true about hypernatremia?



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What is an early symptom in a patient with hypernatremia?



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If extracellular sodium ion concentration increases what effect does this have on membrane potential?



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Which is not a common cause of hypovolemic hypernatremia?



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Which is not an important principle in correcting hypernatremia?



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A 10-month-old has had gastroenteritis with decreased urine output for three days. The parents report that she was difficult to arouse after her nap. She weighs 10 kg but had weighed 12 kg at her nine-month well-child visit. She is not tachycardic and her blood pressure is normal. Her skin shows decreased turgor and feels doughy. Her fontanelle is sunken. Oxygen saturation is normal. Laboratories are drawn. Which fluid should be used for hydration?



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A 2-month-old infant is admitted for emesis and diarrhea for 4 days. The initial laboratories showed sodium 155 mEq/L, potassium 2.8 mEq/L, chloride 118 mEq/L, bicarbonate 15 mEq/L, creatinine 1.7 mEq/L, blood urea nitrogen 65 mEq/L, and glucose 185 mEq/L. Normal saline bolus was administered in the emergency department. Select appropriate management.



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What is the definition if hypernatremia?



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Hypernatremia - References

References

Barma MA,Soiza RL,Donnan PT,McGilchrist MM,Frost H,Witham MD, Serum sodium level variability as a prognosticator in older adults. Scandinavian journal of clinical and laboratory investigation. 2018 Nov - Dec     [PubMed]
Qian Q, Hypernatremia. Clinical journal of the American Society of Nephrology : CJASN. 2019 Feb 6     [PubMed]
Slaughter RJ,Watts M,Vale JA,Grieve JR,Schep LJ, The clinical toxicology of sodium hypochlorite. Clinical toxicology (Philadelphia, Pa.). 2019 Jan 28     [PubMed]
Rubin AN,Espiridion ED,Kattan M,Desmarais EC, Serotonin Syndrome with Atypical Hypernatremia. Cureus. 2018 Nov 19     [PubMed]
Yano T,Uchimura S,Nagahama M,Yonaha T,Taniguchi M,Tsuneyoshi I, Continuous hemodiafiltration for hypernatremia and a simple formula for stepwise regulation of the sodium concentration in a dialysate. Journal of clinical anesthesia. 2019 Aug     [PubMed]
Iraqi B,Abilkassem R,Dini N,Agadr A, A three-year-old boy with hypodipsic hypernatremia syndrome. The Pan African medical journal. 2018     [PubMed]
Das MK,Ali MA,Latif T,Islam MN,Hossain MA,Moniruzzaman MM,Oliullah M,Haque SA,Gosh AK, Comparison of Serum Electrolytes Abnormality and Renal Function Status in Asphyxiated and Normal Baby in a Tertiary Level Hospital. Mymensingh medical journal : MMJ. 2018 Oct     [PubMed]
Imai N,Shibagaki Y, The prevalence of dysnatremia in the elderly patients without CKD. The American journal of emergency medicine. 2019 Mar     [PubMed]
Baldeweg SE,Ball S,Brooke A,Gleeson HK,Levy MJ,Prentice M,Wass J, SOCIETY FOR ENDOCRINOLOGY CLINICAL GUIDANCE: Inpatient management of cranial diabetes insipidus. Endocrine connections. 2018 Jul     [PubMed]
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