Pediatric Annals

Special Issue Article 

Neonatal Hypernatremic Dehydration

Arjun Sarin, MD; Andrew Thill, MD; Clay W. Yaklin, MD

Abstract

Hypernatremic dehydration in exclusively breast-fed neonates is associated with a free water deficit secondary to inadequate fluid intake. It is a common but underrecognized problem in the primary care setting, as the degree of dehydration can be underestimated due to fluid shifts. Neonates of primiparous mothers and those who experience greater weight loss in the first week of life are at higher risk of developing hypernatremic dehydration and most often present for care between 6 and 10 days of life. No consensus treatment guidelines exist, but most experts recommend a goal reduction rate of serum sodium levels of 0.5 mEq/L per hour with correction over 48 hours. Serum sodium level greater than 160 mEq/L is a risk factor for morbidity and mortality. Complications of hypernatremic dehydration, with seizure being most common, usually occur during improper correction. Several small studies have documented varying degrees of neurodevelopmental delay on long-term follow-up of patients admitted for hypernatremic dehydration treatment as a neonate. [Pediatr Ann. 2019;48(5):e197–e200.]

Abstract

Hypernatremic dehydration in exclusively breast-fed neonates is associated with a free water deficit secondary to inadequate fluid intake. It is a common but underrecognized problem in the primary care setting, as the degree of dehydration can be underestimated due to fluid shifts. Neonates of primiparous mothers and those who experience greater weight loss in the first week of life are at higher risk of developing hypernatremic dehydration and most often present for care between 6 and 10 days of life. No consensus treatment guidelines exist, but most experts recommend a goal reduction rate of serum sodium levels of 0.5 mEq/L per hour with correction over 48 hours. Serum sodium level greater than 160 mEq/L is a risk factor for morbidity and mortality. Complications of hypernatremic dehydration, with seizure being most common, usually occur during improper correction. Several small studies have documented varying degrees of neurodevelopmental delay on long-term follow-up of patients admitted for hypernatremic dehydration treatment as a neonate. [Pediatr Ann. 2019;48(5):e197–e200.]

A healthy boy was born to a primigravida mother at 39 weeks gestation via uncomplicated spontaneous vaginal delivery. He weighed 3,760 g at birth and 3,530 g at the time of discharge 48 hours later (∼6% weight loss). He presents to clinic for his 1-week well-child check. The mother reports he is exclusively breast-fed every 3 hours for approximately 5 minutes on each breast. She reports some difficulty with latching and pain with breast-feeding. She is not sure how much milk she has been producing. On average, he has two stools and three wet diapers per day. He weighs 3,275 g (∼13% weight loss) at this visit. Parents report increasing fussiness and yellowing of his skin and sclera. On examination, he is alert but fussy with a sunken anterior fontanel, tacky mucous membranes, and distal capillary refill less than 2 seconds. Skin is soft and doughy and jaundiced to the upper thighs. Laboratory studies reveal the following: sodium 159 mEq/L; potassium 3.5 mEq/L; chloride 125 mEq/L; bicarbonate 17 mEq/L; anion gap 18; blood urea nitrogen (BUN) 48 mg/dL; and creatinine 0.7 mg/dL. Total bilirubin level was 16.7 mg/dL. A urine dipstick showed specific gravity of 1.028, 1+ protein, and 1+ ketones. He was subsequently admitted for parenteral rehydration and correction of his hypernatremia.

Background

The World Health Organization1 recommends all infants should be exclusively breast-fed for the first 6 months of life, and breast-feeding should be maintained until age 2 years along with complementary foods. However, if breast-feeding is not sufficient, dramatic weight loss and dehydration along with an increase in serum sodium concentration related to the insufficient breast milk intake may be observed early in infancy. Nutritional problems and hypernatremic dehydration are the most common causes of newborn hospitalization in developing countries.2

Hypernatremia is classically defined as a serum sodium concentration greater than 145 mEq/L (mmol/L); however, some authors use a cut-off value of 150 mEq/L to define hypernatremia.2,3 Dehydration/excessive weight loss is defined as a loss of more than 10% of birth weight prior to the end of the first week of life, and is thought to occur in up to 15% of exclusively breast-fed infants. Up to one-third of these infants will also be hypernatremic, and the reported incidence of hypernatremic dehydration in term neonates requiring admission ranges from 1% to 5%, with higher rates reported in developing countries.3–7

Despite published statistics, the true incidence of hypernatremic dehydration is difficult to define, as some retrospective studies have included only term neonates, whereas others have included late preterm (>35 weeks gestation) neonates. None have included neonates with predispositions to feeding problems, such as cleft palate, Trisomy 21, neurodevelopmental, or craniofacial disorders.3,6,7

Several risk factors have been associated with hypernatremic dehydration. In a retrospective study of exclusively breast-fed term neonates admitted for hypernatremic dehydration in Italy, a higher incidence of hypernatremia in neonates born via cesarean delivery and to mothers with lower education levels and previous negative breast-feeding experiences was observed.8 However, another retrospective review found no correlation to delivery method, but noted neonates with greater weight loss in the first week of life and those born to primiparous mothers were significantly more likely to develop hypernatremic dehydration.5 This positive correlation between percent weight loss and primiparous status with serum sodium levels has been noted in numerous other studies as well.2,8–10

Serum sodium level greater than 160 mEq/L is a risk factor for morbidity and mortality. The most commonly cited complications include seizures, bradycardia, vascular thrombosis, disseminated intravascular coagulation, renal failure, intracranial hemorrhage, pontine myelinosis, cerebral edema, and death. Seizure is the most common complication and usually occurs during correction of the hypernatremia, as do the other common complications.2,10–12

Pathophysiology

Hypernatremia represents a deficit of water in relation to the body's sodium stores, which can result from excess free water loss (gastrointestinal tract, kidneys, insensible losses), insufficient free water intake (inadequate breast-feeding), or excess influx of sodium (enteral, parenteral, mineralocorticoid axis abnormality).13 In breast-feeding neonates, this free water deficit and subsequent hypernatremic dehydration is due to insufficient intake of fluids. Mature human breast milk is normally low in sodium; however, high levels of sodium in breast milk are closely associated with lactation failure. In the past, it was postulated that this elevated sodium concentration contributed to hypernatremia in the neonate, but newer data has shown the relatively low volume of hypernatremic breast milk does not represent a large enough solute load to affect the neonate's serum sodium levels. Rather, insufficient intake of free water drives the hypernatremia. Neonatal problems such as cleft palate, borderline prematurity, and neurodevelopmental or craniofacial disorders can also result in difficulties establishing breast-feeding, but have not been evaluated as potential independent risk factors for hypernatremic dehydration.3,5,6,10,14

Hypernatremia results in hypertonic intravascular contents, which causes fluid shifts from the cells to the intravascular space. Thus, the neonate may appear less hemodynamically compromised, resulting in underestimation of the degree of dehydration by as much as 5%. This also increases the chances an affected infant will present late for medical care.15 In the acute phase, the cellular shrinkage due to cerebral cellular dehydration can cause rupture of bridging veins, leading to intracranial hemorrhage. However, cellular shrinkage in the brain is countered by an adaptive response leading to cellular uptake of other electrolytes (over hours) and organic osmolytes, termed idiogenic osmoles, (over days) to normalize brain volume. It is the presence of these organic osmolytes that can result in cerebral edema if sodium correction occurs too rapidly, as they are only slowly dissipated from brain cells over the course of days.11,16

Presentation and Evaluation

Age of presentation of an affected neonate can range from 3 to 21 days of life, with 6 to 10 days of life being most common.4–6,9 Several retrospective case reports found the most common signs and symptoms on presentation included jaundice, fever, fussiness, poor oral intake, poor/absent suck reflex, and decreased urination/defecation. In severe cases, caregivers may also report apnea, color change, or seizures as well. On examination, signs of dehydration including poor peripheral perfusion are likely to be present, as well as tachycardia, doughy skin, depressed mentation or irritability, hyperreflexia, and spasticity.4,7,9,11,17 The association of hypernatremia with severe hyperbilirubinemia might contribute to long-term neurologic sequelae, as hypernatremia can cause disruption of the blood-brain barrier, facilitating diffusion of bilirubin across the barrier, enhancing the risk of bilirubin encephalopathy.5

The differential diagnosis of hypernatremic dehydration, depending on severity of symptoms at presentation, may include sepsis, meningitis, intracranial hemorrhage, congenital heart disease, accidental or intentional salt poisoning via incorrect formula preparation (less likely if solely breast-fed), inborn error of metabolism, or mineralocorticoid axis abnormality.17

Laboratory testing is based on age and clinical presentation with ill-appearing younger infants, requiring a more comprehensive approach, akin to an evaluation for sepsis. Laboratory diagnosis of hypernatremia itself can be made with a basic metabolic profile, which will also provide evaluation of serum potassium and glucose as well as creatinine and BUN, which may also be affected by poor hydration. Bilirubin panel, liver function tests, and measurements of urine and serum osmolality can also be performed if the underlying etiology is not clear.4,5,9,11

Management

Even with a potentially large pool of infants who could be affected by hypernatremic dehydration, a Cochrane review in 2017 found no randomized clinical trials or systematic reviews focusing on treatment of hypernatremic dehydration and its outcomes, as well as no consensus about optimal treatment.3

Hypernatremia treatment is directed at treating the underlying cause and correcting the water deficit. However, there is no consensus about proper rehydration strategies in hypernatremic neonates. There are no widespread accepted guidelines to what extent hypernatremic dehydration may be corrected exclusively by increasing oral feeds (adding formula or expressed breast milk), when parenteral fluids are indicated, and which parenteral solution is most appropriate to avoid excessively rapid serum sodium correction.3

Initial treatment consists of fluid resuscitation with normal saline (154 mEq/L of sodium) or colloid, such as Lactated Ringer's solution (130 mEq/L of sodium), 10 to 20mL/kg boluses over 20 to 60 minutes if there are signs of hemodynamic compromise. Once this has been accomplished, the sum of the free water deficit and maintenance fluid requirements as well as any remaining fluid deficits are administered over 48 hours. If there are any other significant ongoing insensible losses, these too should be included in subsequent hydration fluids. Several formulas are available to calculate the free water deficit. One such formula, assuming a total body water of 70% of a neonate's body weight is: free water deficit (L) = 0.7 × actual weight (kg) × [(current serum Na/desired serum Na) − 1].11,15,18

A retrospective case series by Bolat et al.5 found that correction of the serum sodium by a rate greater than 0.5 mEq/L per hour was a risk factor for death and seizure in neonates being treated for hypernatremic dehydration. This has been observed in other case reviews as well, with most of the complications of hypernatremia occurring during overly rapid correction. This follows logically, as hypernatremic dehydration in breast-fed neonates develops over the course of several days. Therefore, a drop-in serum sodium levels of no greater than 10 to 12 mEq/L over a 24-hour period is desired.3

Once the free water deficit has been determined and added to the maintenance fluid needs, a fluid rate can be determined. Previous studies report 5% dextrose in 0.2% normal saline (31 mEq/L of sodium) as the generally accepted starting fluid composition. Once urine output has resumed, potassium can be added to the fluids. Electrolytes can be checked every 1 to 4 hours to ensure adequate rate of reduction in serum sodium. Generally, the rate of fluid replacement should be adjusted rather than the composition of the fluids to ensure appropriate rate of correction. This may result in a correction period exceeding 48 hours.11,15,18

One caveat to the starting fluid composition occurs in the setting of severe hypernatremic dehydration (serum sodium >175 mEq/L). In this situation, even traditionally isotonic fluids are relatively hypotonic, and multiple fluid boluses with normal saline can result in too rapid a correction. Therefore, some authors recommend rechecking serum sodium levels soon after volume correction if initial sodium is greater than 175 mEq/L, and possibly giving small volumes of 3% saline (513 mEq/L of sodium) to counteract this possible rapid drop from volume correction. In general, 1 mL/kg of 3% saline will increase the serum sodium concentration by 1 mEq/L.11,13,15,16,18

Sequelae and Prevention

Similar to treatment, few studies document long-term outcomes/complications related to hypernatremic dehydration and no guidelines exist regarding recommended length of follow up for neonates admitted for treatment. Escobar et al.19 observed 106 neonates for 5 years after treatment for hypernatremic dehydration and compared them to a control group of 168 randomly selected term healthy births without any neurodevelopmental disorders, born during the same time period within the Kaiser Permanente Medical Care Program. No significant difference was found between the case and control groups in cognitive tests and neurologic and behavior problems. However, only 6.6% of the cohort had serum sodium levels greater than 160 mEq/L.19 On the other hand, Boskabadi et al.9 observed 65 neonates admitted for treatment with mean serum sodium levels of 158 mEq/L over 2 years. Growth parameters and developmental milestones were assessed and compared at age 6, 12, 18, and 24 months. The results showed severity of hypernatremia strongly correlated with developmental delay at early ages, as 25% of the study group showed some delay at age 6 months, versus 0.3% for the control group. This delay did decrease over time, with only 12% of the study group showing delays at age 24 months. Hypernatremic neonates also exhibited lags in weight gain, which did correct by age 12 to 18 months. No differences were noted with height or head circumferences.9

Mild hypernatremia should not be considered a benign occurrence, and breast-fed infants with greater than 7% weight loss or significant jaundice should be evaluated for hypernatremic dehydration and the possible need for oral or parenteral fluid supplementation. Physicians and parents should pay particular attention for the signs and symptoms of feeding difficulties and ideally all families will have access to regular lactation services during the first 2 weeks of an infant's life to minimize the risk of hypernatremic dehydration.11,14

References

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  7. Uras N, Karadag A, Dogan G, et al. Moderate hypernatremic dehydration in newborn infants: Retrospective evaluation of 64 cases. J Matern Fetal Neonatal Med. 2007;20(6):449–452. doi:. doi:10.1080/14767050701398256 [CrossRef]
  8. Manganaro R, Mami C, Marrone T, et al. Incidence of dehydration and hypernatremia in exclusively breast-fed infants. J Pediatr. 2001;139(5):673–675. doi:10.1067/mpd.2001.118880 [CrossRef]
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Authors

Arjun Sarin, MD, is a Pediatric Emergency Medicine Fellow. Andrew Thill, MD, is a Pediatric Emergency Medicine Fellow. Clay W. Yaklin, MD, is a Pediatric Emergency Medicine Fellow. All authors are affiliated with the Division of Emergency Medicine, Children's Mercy-Kansas City.

Disclosure: The authors have no relevant financial relationships to disclose.

Address correspondence to Andrew Thill, MD, Division of Emergency Medicine, Children's Mercy-Kansas City, 2401 Gillham Road, Kansas City, MO 64108; email: arthill@cmh.edu.

10.3928/19382359-20190424-01

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