Paediatric Nephrology Journal of Bangladesh

: 2022  |  Volume : 7  |  Issue : 1  |  Page : 41--43

Hypernatremic dehydration with acute kidney injury in a neonate: A therapeutic challenge

Azmeri Sultana, Sharmin Afroze, Israt Jahan, Abdul Baten 
 Dr. M R Khan Shishu Hospital & Institute of Child Health, Dhaka, Bangladesh

Correspondence Address:
Dr. Azmeri Sultana
Dr. M R Khan Shishu Hospital & Institute of Child Health, Dhaka


Neonatal hypernatremic dehydration is not so uncommon and causes high morbidity and mortality if associated with acute kidney injury (AKI). We herein discuss a neonate who presented with serum sodium of 193 mmol/L with AKI, and we successfully treated this neonate with peritoneal dialysis.

How to cite this article:
Sultana A, Afroze S, Jahan I, Baten A. Hypernatremic dehydration with acute kidney injury in a neonate: A therapeutic challenge.Paediatr Nephrol J Bangladesh 2022;7:41-43

How to cite this URL:
Sultana A, Afroze S, Jahan I, Baten A. Hypernatremic dehydration with acute kidney injury in a neonate: A therapeutic challenge. Paediatr Nephrol J Bangladesh [serial online] 2022 [cited 2023 Jan 29 ];7:41-43
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Full Text


Hypernatremia is a frequent electrolyte disturbance in the neonatal population, and it can set off long-term morbidity and mortality when associated with acute kidney injury (AKI).[1],[2] Many factors are responsible for the development of neonatal hypernatremia, and one of the utmost important causes is hypoalimentation (hypovolemic hypernatremia).[3] Neonates with weight loss more than 10% in their initial days of life, inadequate breastfeeding, and increased extrarenal water loss due to larger surface area are susceptible to develop hypernatremia.[2] It has been reported that up to 35% of neonates may present with hypernatremic dehydration.[4]

We herein discuss an exclusively breastfed neonate presented with severe hypernatremia with AKI who was treated successfully with intravenous fluid and peritoneal dialysis (PD).

 Case Report

An 11-day-old female baby born to a 26-year-old primigravida, by lower uterine segment Cesarean section at term without any eventful postnatal period, presented to us with the complaints of reluctant to feed, less activity for 4 days, and anuria for 18 hours. Her birth weight was 3.8 kg and Appearance, Pulse, Grimace, Activity & Respiration (APGAR) scores were normal. There was no history of diarrhea or vomiting, but the mother complained of inadequate breast milk though the baby was on exclusive breastfeeding. Examination revealed an ill-looking baby, lethargic, severely dehydrated; reflex activity was moderate. Vital signs were within the normal limit. Fontanelle was open and not bulged. Air entry was equal on both sides of the lung. Heart sounds were audible in all four areas of the precordium. Her admission weight was 2.5 kg indicating a weight loss of 34% from birth weight. All other systemic examination findings were within the normal limit. Fluid resuscitation was started immediately by 0.9% NaCl at 20 mL/kg; then a repeat dose was given. Provisional diagnosis was neonatal sepsis with AKI. The baby had two episodes of convulsions an hour after admission and was started on intravenous phenobarbitone. Initial investigation revealed hypernatremia of serum Na+, 193 mmol/L, and high creatinine, 4.9 mg/dL. An initial laboratory report is listed in [Table 1]. Fluid calculation was done, and 0.45% normal saline was started. PD was started in view of anuria, high creatinine, hyperkalemia, and metabolic acidosis after 8 hours of admission. The serum electrolytes, creatinine, and arterial blood gas analysis were monitored every 12 hours and showed improvement [Table 2]. Changes in serum sodium are depicted in [Figure 1]. From day 5 onward, the baby was passing urine at 1.5 mL/kg/hour. PD was discontinued after 96 hours. No further convulsion occurred during PD or thereafter. The serum sodium levels and renal parameters gradually returned to normal by the seventh day of admission. The baby was on complete oral feeds by day 8 of admission. Mother’s milk output gradually increased, and the baby was discharged on the ninth day of admission. We advised the estimation of sodium in mother’s breast milk, but they refused to do. So, our final diagnosis was hypernatremic dehydration due to lactational failure with stage 3 AKI (kidney disease improving global outcome [KDIGO]). She was followed up after 15 days and was found clinically well, and laboratory parameters were also normal.{Table 1} {Table 2} {Figure 1}


Hypernatremic dehydration in a neonate is a medical emergency. Clinical presentations of hypernatremic dehydration due to lactation failure usually occur around 10 days, ranging from the third to the 21st day of neonatal period.[5] Our case presented at 11 days, which is consistent with these findings.

Sharma et al. showed in their study that a majority of (81%) hypernatremic neonates were born to primiparous women and were on exclusive breastfeeding.[6] Similarly present case was also born to primi and was on exclusive breastfeeding. Some other studies published the same findings, i.e., hypernatremia in exclusively breastfed babies born to primiparous females.[7],[8],[9]

Our case presented with reluctance to feed, lethargy, dehydration, oliguria, and seizure. A retrospective study of neonatal hypernatremia demonstrated 75% presented with poor feeding and convulsion. Other presenting features were fever, lethargy, dehydration, and oliguria, which is similar to our case.[7]

Breastfeeding failure is attributed to low milk production and insufficient breastfeeding, which causes a high sodium concentration in breast milk, resulting in hypernatremic dehydration in neonates.[10] Usually, sodium concentration in matured breast milk is low; furthermore, this protects against the development of hypernatremic dehydration in exclusively breastfed newborns. The electrolyte composition of breast milk showed a mean sodium of 64:8 ± 4:4 mmol/L on the first postpartum day, dropping to a mean of 21:4 ± 2:3 mmol/L by the third postpartum day (colostrum), and then decrease to a value of 7 ± 2mmol/L by 2 weeks (mature milk).[11] Hence, variation in the normal physiology and maintaining the high levels of sodium concentration in breast milk are closely associated with lactation failure.[12],[13] Our case also had history of inadequate breastfeeding and low milk production, but we could not estimate the sodium level of the mother’s breast milk as they did not give consent to do it.

The rapid correction of hypernatremia should not be done because of associated cerebral edema. The goal is to reduce serum sodium gradually by 10–12 mmol/L/day.[14] Frequent monitoring of serum sodium should be done 4–6 hourly to adjust the sodium level. In this case, we applied the general recommendations for the treatment of hypernatremic dehydration consisted of an emergency phase (restoration of vascular volume with 20 mL/kg of N/S) followed by a rehydration period (the sum of free water deficit and maintenance fluid requirement administered evenly over 48–72 hours with 0.45% normal saline).[14],[15] But after 8 hours of admission, we started PD due to anuria, high creatinine, hyperkalemia, and metabolic acidosis. In order to decrease serum sodium gradually, we did sodium profiling in PD fluid, i.e., add 3% of NaCl in PD fluid and titrate it according to blood level. Similarly, Zaki et al. managed a case of a newborn with severe hypernatremic dehydration with PD.[16] We stopped PD at day 5 and baby was discharged at day 9 with advice.


The timely diagnosis of hypernatremic dehydration with AKI among exclusive breastfeeding neonates is crucial for prompt treatment and survival of the baby. PD with sodium profiling in PD fluid can successfully treat this condition with a gradual and desired decrease of blood sodium level.

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Conflicts of interest

There are no conflicts of interest.


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