Saudi Journal of Kidney Diseases and Transplantation

CASE REPORT
Year
: 2012  |  Volume : 23  |  Issue : 1  |  Page : 125--128

Hypernatremic dehydration due to lactation failure in an exclusively breastfed neonate


Syed Ahmed Zaki1, Jayashree Mondkar2, Preeti Shanbag1, Rahul Verma2,  
1 Department of Pediatrics, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai, India
2 Department of Neonatology, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai, India

Correspondence Address:
Syed Ahmed Zaki
Department of Pediatrics, Lokmanya Tilak Municipal Medical College and General Hospital, Sion, Mumbai
India

Abstract

We report a 13-day-old exclusively breastfed neonate, admitted with a history of fever, poor feeding, lethargy and decreased urine output. The mother had history of lactation failure. The neonate had severe hypernatremia, acute renal failure and metabolic acidosis. Renal ultrasound was normal, but the sodium level in mother«SQ»s milk was 96 mEq/L (normal 7 ± 2 mEq/L). The neonate required peritoneal dialysis on the second day of admission. The biochemical investigations gradually returned to normal and the neonate was discharged on day 12 of admission. We highlight the importance of lactation management and supportive counseling to prevent complications like hypernatremic dehydration due to lactation failure.



How to cite this article:
Zaki SA, Mondkar J, Shanbag P, Verma R. Hypernatremic dehydration due to lactation failure in an exclusively breastfed neonate.Saudi J Kidney Dis Transpl 2012;23:125-128


How to cite this URL:
Zaki SA, Mondkar J, Shanbag P, Verma R. Hypernatremic dehydration due to lactation failure in an exclusively breastfed neonate. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2020 Dec 5 ];23:125-128
Available from: https://www.sjkdt.org/text.asp?2012/23/1/125/91317


Full Text

 Introduction



Human breast milk is undoubtedly the best source of nourishment for human infants. It prevents diseases, promotes health and reduces health care costs. Though breastfeeding is natural, some mothers need help initially for lactation to be established successfully. Breast feeding counseling and support is essential to prevent life-threatening complications of lactation failure in such cases. Hypernatremic dehydration is one such complication which, if not treated promptly, can lead to acute renal failure and may even require peritoneal dialysis (PD). [1] Our case highlights this uncommon but easily preventable complication that is associated with mortality and significant morbidity.

 Case Report



A 13-day-old female neonate was admitted with a history of fever, poor feeding and lethargy for three days and decreased urine output for one day. There was no history of diarrhea or convulsions and the baby was only on exclusive breast feeding. She was born to a multi-gravida mother at term, had a birth weight of 3100 g and was discharged on day three of life on breastfeeds. On enquiry, the mother gave history of poor milk output for which she did not take any medical advice.

Examination revealed a sick baby who was irritable and lethargic with moderate dehydration and sclerema. Her weight was 2200 g, indicating a weight loss of 29%. She had a respiratory rate of 30/min and was acidotic. Heart rate was 110/min and pulses were weakly felt. Capillary refill time was 5 seconds and mean blood pressure was 28 mmHg. Systemic examination was otherwise normal. A provisional diagnosis of sepsis with severe dehydration was made and the child was admitted to the neo-natal intensive care unit.

Fluid resuscitation was started immediately and the baseline investigations were done. The baby had two episodes of convulsions an hour after admission and was started on intravenous phenolbarbitone. Investigations showed hemoglobin of 18.1 g/dL, total leukocyte count of 36,500/mm3 with a differential count showing polymorphs 90% and lymphocytes 10% and a platelet count of 206,000/mm3 . Biochemical investigations revealed severe hypernatremia with renal failure. Other serum electrolytes were also deranged. Liver function tests, and serum calcium and phosphorous were normal. Arterial blood gas (ABG) analysis showed metabolic acidosis [Table 1]. The baby was started on intravenous fluid correction for hypernatremic dehydration at 220 mL/kg, initially given as 0.9% (normal) saline and subsequently as 0.45% (half-normal saline. Intravenous piperacillin/tazobactum as per creatinine clearance and dopamine was started at 10μg/kg/min. However, the serum electrolytes and the renal function tests worsened with the baby being still anuric. The baby had to be ventilated in view of shallow respiration and depressed sensorium. PD was initiated on the second day of admission for renal failure with severe hypernatremia and metabolic acidosis. The serum electrolytes, creatinine and ABG were monitored every six hours and showed improvement [Table 1]. At the end of four days, the baby was passing urine at 1.5 mL/kg/hour. PD was discontinued after completing 72 cycles. Blood culture, urine culture and fungal culture showed no growth. The serum sodium levels and renal parameters gradually returned to normal by day eight of admission [Table 1]. Urine routine showed a pH of 6.0 and specific gravity of 1005, and albumin and sugar were reported nil.{Table 1}

Ultrasonography of abdomen was done which showed mild ascites and grade 1 increased echogenicity of both kidneys. The mother's breast milk sodium was 96 mEq/L (normal 7 mEq/L).

Total daily intake was calculated and the baby was fed on breast milk from the mother and from the milk bank and monitored for signs of dehydration. The baby was on complete oral feeds by day ten of admission. Mother's milk output gradually increased and the baby was discharged on day 12 of admission on breast milk along with diluted cow's milk. The final diagnosis was hypernatremic dehydration resulting in acute renal failure secondary to inadequate breast feeding and high breast milk sodium due to lactation failure.

 Discussion



The daily requirement of sodium for growth is 0.5 mEq/kg/day between birth and three months. To cover dermal losses, an additional 0.4-0.7 mEq/kg/day is needed, with a little more to be added for urine and stool losses. Infants fed on mature human breast milk receive enough sodium to meet their needs for growth, dermal losses and urine losses. [2] The concentration of sodium in breast milk varies as the lactation period progresses and is independent of the mother's diet. Studies of lactating women performed by Neville et al, report that a significant fall in sodium, chloride and protein and a rise in lactose precede the major increase in milk volume during early lactogenesis. [3]

Studies of the electrolyte composition of breast milk have shown a mean sodium value of 64.8 ± 4.4 mEq/L after delivery, dropping to a mean of 21.4 ± 2.3 mEq/L by the third postpartum day (colostrum) and leveling off to a value of 7 ± 2 mEq/L by two weeks (mature milk). [4] Various hypotheses, like diminished breast milk production or delayed maturation of breast milk, have been put forward to explain the mechanism of elevated concentration of breast milk sodium.

Sodium chloride and lactose concentrations combine reciprocally to maintain the milk's osmolality at a level similar to that of blood. Any fall in lactose concentration due to lactation failure could cause a rise in the sodium content of the milk. [5] Lactation failure could in turn be secondary to neonatal factors, such as primary suckling deficiency or poor suckling as a result of infection, or to maternal factors, such as stress, mastitis, or sore/retracted nipples. This can lead to a vicious circle in which when breast milk production is reduced, the neonate becomes weak and sucks poorly, and the drive for lactation drops further and dehydration occurs. Thus, hypernatremic dehydration in the breastfed neonate should suggest an abnormal concentration of sodium in the mother's breast milk, a sign of lactation failure.

The sodium load excreted by newborn infants is less than that excreted by older infants and children, so newborns are particularly sensitive to the effects of high serum sodium concentration. The relatively higher levels of insensible water loss per kilogram of body weight in infants, and less efficient conservation of water due to renal immaturity at this age, predisposes this group to dehydration. Thus, a high sodium intake in the presence of inadequate feeding can lead to hypernatremic dehydration in the newborn, as seen in our case. The source of extra sodium in our patient was from high sodium in the breast milk due to lactation failure, thus leading to hypernatremic dehydration. [6]

Hypernatremic dehydration due to inadequate breast feeding presents clinically between first and third weeks of life. Hypernatremic dehydration can occur in the first-born or even in babies whose mothers have previously breastfed successfully. [7] The spectrum of signs and symptoms includes irritability, acute CNS dysfunction and pre-renal failure. [4] A review of literature done revealed that most cases of hypernatremic dehydration due to inadequate breast feeding were managed with fluid rehydration alone. [1] Our case was different as the baby required PD and it was not possible to manage the patient conservatively as the patient's general condition was deteriorating. This could have been prevented if the child was brought to the hospital early, thereby preventing the pre-renal failure progressing to intrinsic renal failure.

Hypernatremic dehydration can be prevented by education of mothers regarding breastfeeding techniques, beginning in the antenatal period.

Those with identifiable problems should be referred promptly for lactation management and supportive counseling. Also, close follow-up of infants should be done within the first week after hospital discharge for checking weight gain and adequate hydration. [8] This will help in preventing the devastating short- and long-term consequences of hypernatremic dehydration.

 Acknowledgment



We would like to thank Dr. Sandhya Kamath, Dean, Lokmanya Tilak Municipal Medical College and General Hospital, for permitting us to publish this manuscript.

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