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INTERNATIONAL PEDIATRIC NEPHROLOGY ASSOCIATION
3RD ANNUAL PEDIATRIC KIDNEY MEET
NEONATAL HYPERNATREMIA SECONDARY TO

LACTATIONAL FAILURE:
A PRE-AZOTEMIC CAUSE OF AKI
PRESENTER- Dr. ASHISH AGARWAL (Resident doctor)

Under the guidance of Dr. LAKHAN POSWAL
RNT MEDICAL COLLEGE, UDAIPUR
INTRODUCTION
 Hypernatremic dehydration (HND), defined as serum sodium concentration > 145 mmol/L
[mEq/L], is a potential lethal condition for neonates.
 Dehydration in newborns presents in three forms: hyponatremic, normonatremic, and
hypernatremic depending on the serum osmolality. This hyperosmolar state if not treated
immediately can lead to brain shrinkage, subdural capillary hemorrhage, venous thrombosis,
gangrene, and death.The causes of HND are either decreased fluid intake, excessive fluid loss, or
excessive sodium intake; a study by Oddie et al. has concluded that the sole cause of HND is
unsuccessful breastfeeding (lactation failure or sometimes referred as “BreastFeeding
Malnutrition”).
 It is normal for neonates to lose as much as 7% of their birth weight on the first week of their life
through normal dieresis. Thereafter, neonates should start to regain their weight by the 10th day of
their life. The first sign of neonatal hypernatremic dehydrations is weight loss (>7% of birth
weight) combined with failure to have bowel movement or the presence of urate crystals.
However, pediatricians and attending physicians in low-income countries with inadequate facility
for early diagnosis are facing difficulties at management of this uncommon but easily preventable
complication.
 CASE REPORT- An 11-day-old male baby was admitted to the Neonatal Intensive Care Unit,
Paediatric Department, in Bal Chikitsalaya, RNT Medical College, on October 8, 2023, at 9 : 20 pm. The
baby was a product of a term gestation, 39 weeks and 6 days by date, born to a 29-year-old multiparity
mother whose pregnancy was uneventful, and having previous positive feeding experience. Delivery
was via normal spontaneous vaginal with a birth weight of 3.4 kg at a health station in a village, about
12 km from Udaipur and was discharged home after 6 hrs of delivery.
 On admission, he was in a moribund state with a history of poor sucking for 4 days, absent urine-output
for 2 days, fever for the last 2 days, and hyperextended neck and extremities for 1 day. According to the
mother, the baby was doing fine soon after birth and before the onset of the illness. The mother reported
that the baby was exclusively breastfed 5-6 times/24 hrs, and she considered him to be a quiet baby who
was easily satisfied.
 By 6-7 days of age, the mother noticed that he was not well as before. He started to experience
irritability, poor sucking, and reduced urination that eventually got worse until the mother sought
medical attention. There had been no vomiting and diarrhea.
 Physical examination revealed that sick baby weighed 2.26 kg. Vital signs were PR-175 p/m, RR-
irregular 38 bp/m, T-38.3° C, SPO2-20%, and cold extremities with capillary refill time (CRT) >
3seconds. The baby was lethargic with opisthotonus posturing, labored deep breathing with marked
chest retractions, icteric sclera, dry lips, and doughy abdominal skin. Findings during the remainder of
the physical examination were unremarkable.
Picture of 11 -day neonate on admission with
hyperextended neck.
 Laboratory investigations: on day of admission were limited only to the following:

(i) CBC-, WBC-17.7, RBC-5.71, HGB-20.8, HCT-62.9, PLT-40
(ii) RBS-51 mg/dl
(iii) Total serum Bil.–19.5 mg/dl
 With the above mentioned clinical manifestations, the baby was diagnosed as HND with
shock as the major diagnosis.
 MANAGEMENT-The baby was treated with the initial boluses of 20 ml/kg of N/S, repeated 3 times (each over 20
minutes), that is, a total of 204 ml was given over 1 hr, until the vital signs were normalized to PR-145, RR-45, T-37.2°
C, SPO2- 100%, and CRT < 3 seconds, and the baby began to void urine.
 Then, free water deficit and sodium excess were managed by gradual and slow correction over 72 hours to prevent
cerebral oedema and neurologic sequelae. The baby required reconstituted solutions of 5% D/W + 1/2 N/S at a rate of 27
ml/hr for 72 hrs.
 In view of the sick appearance, fever, and low platelet count, sepsis was considered, and therefore, antibiotics were
administered. Hyperbilirubinemia was reduced to normal with one-day exposure to phototherapy.
 By day 3, the serum sodium level was 158 mmol/L so the fluid was shifted to 10% D/W + 1/4 N/S. The serum sodium
levels returned to normal by day 5 of admission. Blood urea nitrogen and creatinine reached the normal range by day 7 of
admission, and their values were 16 mg/dL and 0.5 mg/dL, respectively.
 The baby started to feed completely orally by day 4 of admission. Daily weight monitoring indicated that the baby started
to gain rapidly and gained his original birth weight by the 6th day after he started feeding, i.e., by the 10th day after
admission; then, the rate of increment slowed down to reach 3.9 kg on discharge.
 The baby was discharged on day 14 after admission, one week after complete stabilization without any complication;
during that time, extensive training on breastfeeding was conducted and proper breastfeeding was ensured.
 Babies with severe HND in our setup are usually referred to a high-risk clinic for further follow-up to detect early
neurological sequelae after discharge from the hospital. Monthly follow-up revealed that there was no evidence of
neurological sequelae nor was any delay in developmental milestones in the first year and 2-3 months follow-up in the
second year of life.
 Discussion: HND was considered to occur in those babies who were fed with artificial feeds, powdered milk with high
sodium concentration, especially when the mother failed to add enough water in the mixture . The second plausible
explanation is that HND might have been unrecognized or misdiagnosed, as associated clinical manifestations in most
cases resemble sepsis or are associated with sepsis, and treatment of sepsis was taken as major management for this
condition . Another important clinical manifestation associated with HND is jaundice, and because hypernatremia can
cause impairment in the blood brain barrier function, which may enhance the diffusion of bilirubin across the blood-
brain barrier and thereby may enhance the risk of bilirubin encephalopathy.
 Management-Fluid therapy
Step 1: emergency phase- Restore vascular volume with boluses 20 ml/kg of N/S 20 ml × 3:4 kg = 68 ml over 20 minutes
repeated 3 times = 204 ml.
Step 2: rehydration phase Aim to correct water deficit and sodium excess within 72 hours.
-Maintenance during 3 days: 100 ml/kg/d × 3:4 kg × 3 days = 1020 ml
- Maintenance deficit = 1020 ml + 1140 ml = 2160 ml, and take initial hydration fluid out of this. 2160 ml − 204 ml = 1956
ml
-1956 ml/72 hr≒27 ml/hr of 5% dextrose + 1/2 normal saline

CONCLUSION
 HND is a serious, life-threatening disorder with high rates of mortality and morbidity. Early
diagnosis and prompt management of HND due to lactation failure by identifying simple clinical
predictors is critically important to prevent deaths of neonates, especially in resource-limited
countries. In countries with limited resources, to improve parental knowledge on breastfeeding and
monitor the inadequate fluid intake that leads to HND, the health personnel at any level of health
facility should educate mothers about adequate breast-feeding methods, to search for the early signs
of dehydration in infants.
THANK YOU!

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INTERNATIONAL PEDIATRIC NEPHROLOGY ASSOCIATION

3RD ANNUAL PEDIATRIC KIDNEY MEET

NEONATAL HYPERNATREMIA SECONDARY TO

PRESENTER- Dr. ASHISH AGARWAL (Resident doctor)

 Laboratory investigations: on day of admission were limited only to the following:

-Maintenance during 3 days: 100 ml/kg/d × 3:4 kg × 3 days = 1020 ml

-1956 ml/72 hr≒27 ml/hr of 5% dextrose + 1/2 normal saline

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