|Year : 2018 | Volume
| Issue : 4 | Page : 202-207
Oral feeds with or without dextrose half normal saline for treatment of hypernatremia in breastfed late preterm and term neonates: A comparison study
Ramesh Srinivasan1, Suvetha Kannappan2
1 Department of Pediatrics, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India
2 Department of Community Medicine, PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India
|Date of Web Publication||15-Oct-2018|
Dr. Ramesh Srinivasan
108-A, 4th Street, Meenakshi Garden, GN Mills Post, Coimbatore - 641 029, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Aim: The aim of this study was to compare the effect of treatment with oral feeds alone or oral feeds and 5% dextrose in 0.45% normal saline (½ dextrose normal saline [DNS]) on the rate of decline in serum sodium in breastfed late preterm and term neonates with hypernatremia. Materials and Methods: The study was conducted using retrospective data from July 2013 to June 2016. Babies with gestational age ≥ 34 weeks, birth weight ≥2000 g, age at diagnosis ≤5 days, and serum sodium 150–160 mEq/L were included in the study. Babies with congenital anomalies, sepsis, prior intravenous (IV) fluid therapy, or diseases-causing dyselectrolytemias were excluded from the study. Oral feeds group (Group 1) received breastfeeds, and formula feeds liberally. Oral feeds and IV fluid group (Group 2) received ½ DNS in addition to liberal oral feeds. Decline in serum sodium ≤0.5 mEq/L/h was considered as safe. Results: The study population consisted of 77 babies in Group 1 and 78 in Group 2. Baseline characteristics and serum sodium at admission were comparable. Group 1 had slower decline in serum sodium (P = 0.002), more babies with safe decline in serum sodium (P = 0.02), and lesser weight gain (P = 0.000). A similar result was observed in babies with serum sodium 150–155 mEq/L. No difference in treatment outcome was seen in babies with serum sodium 156–160 mEq/L. No complications or death were seen. About three fourth of cases came for follow-up, and one baby in Group 1 had a developmental delay with seizure disorder. Conclusion: In hypernatremic breastfed neonates with serum sodium 150–155 mEq/L, more babies are likely to have a safe decline in serum sodium on treatment with liberal oral feeds alone.
Keywords: Breastfeeding, hypernatremia, intravenous fluids, oral feeds, rate of decline in serum sodium
|How to cite this article:|
Srinivasan R, Kannappan S. Oral feeds with or without dextrose half normal saline for treatment of hypernatremia in breastfed late preterm and term neonates: A comparison study. J Clin Neonatol 2018;7:202-7
|How to cite this URL:|
Srinivasan R, Kannappan S. Oral feeds with or without dextrose half normal saline for treatment of hypernatremia in breastfed late preterm and term neonates: A comparison study. J Clin Neonatol [serial online] 2018 [cited 2019 Jan 20];7:202-7. Available from: http://www.jcnonweb.com/text.asp?2018/7/4/202/243343
| Introduction|| |
Exclusive breastfeeding for the first 6 months of life is recommended for optimal growth and development of infants. However, neonates who receive inadequate milk from their mother, are likely to develop hypernatremic dehydration and malnutrition. Hypernatremic dehydration is a medical emergency and is considered as a dangerous type of dehydration due to the complications associated with disease evolution and its therapy. Until date, there is no consensus on the treatment of hypernatremic dehydration in breastfed neonates. A systematic review of breastfeeding-associated hypernatremia has found that the available data about the management of this condition is inadequate.
The management of hypernatremia in breastfed neonates is clouded with controversies. Although intravenous (IV) fluids were commonly used for hypernatremia correction, the volume of fluid needed and sodium content of the IV fluid was not well defined.,,, Oral rehydration for correcting hypernatremic dehydration in breastfed babies was also reported. Oral feeds were given either alone or along with IV fluids for correction. However, irrespective of the nature of treatment, all authors uniformly recommend frequent monitoring of serum sodium during correction as the rapid fall in serum sodium is associated with complications., The usual recommended rate of fall in serum sodium during correction is not to exceed 0.5 mEq/L/h.,
In our neonatal unit, oral feeding is allowed liberally to all hypernatremic babies along with 5% dextrose in 0.45% normal saline (½ Dextrose Normal Saline [DNS]). Some babies had received only oral feeds for correction due to the refusal of consent for IV fluid therapy by the parents. This study was planned to compare the outcome among babies treated with oral feeds alone or oral feeds and ½ DNS. The primary objective of this study was to compare the effect of treatment with oral feeds alone or with oral feeds and ½ DNS on the rate of decline in serum sodium in otherwise healthy breastfed late preterm and term neonates with hypernatremia. The secondary objectives were to compare serum sodium at the end of treatment, percentage of weight gain at the end of treatment, complications during therapy, duration of hospital stay, and neurodevelopmental impairment at follow-up.
| Materials and Methods|| |
The study was conducted at a tertiary care teaching hospital in Tamil Nadu state of India. The institution has a policy of exclusive breastfeeding for all healthy babies. As per the unit protocol, all babies were weighed daily and any baby with total weight loss of more than 10% from birth weight or weight loss per day of more than 5% were considered to have excess weight loss, and their serum sodium was measured. Serum sodium ≥150 mEq/L was considered as hypernatremia.
All babies with hypernatremia were encouraged to take liberal oral feeds. This consists of counseling and supporting the mothers to adequately breastfeed their babies and to give top up formula feeds (sodium content-7 mEq/L) only if the baby does not get satisfied after completing breastfeeds. Breast milk sodium was not checked in any mother. ½ DNS was used for IV fluid therapy. The volume of IV fluid was based on the severity of dehydration and is usually administered at half of the daily maintenance fluid requirement. The treatment target was to reduce serum sodium below 150 mEq/L.
This comparative study was conducted using the retrospective data collected from July 2013 to June 2016. The Institutional Ethics Committee approved the study. Babies with hypernatremia during the study period, were identified from the hospital database, and their case records scrutinized. Since the response to treatment and complications depends on the severity and duration of hypernatremia, only babies with similar serum sodium level and age at diagnosis were considered for comparison. The inclusion criteria consist of (1) gestational age ≥ 34 weeks, (2) birth weight ≥ 2000 g, (3) age at diagnosis ≤ 5 days, (4) serum sodium 150–160 mEq/L, and (5) treated with oral feeds alone or with oral feeds and ½ DNS. A subgroup analysis for babies with serum sodium of 150–155 mEq/L and 156–160 mEq/L was also planned. The babies, with major congenital anomalies, culture-positive sepsis, received IV fluid within 48 h before the diagnosis of hypernatremia, suspected endocrine disorders or any other significant illness which may affect adequate oral feeding or fluid and electrolyte balance, were excluded from the study.
The following details were noted: maternal age, parity, mode of delivery, gender, gestational age as completed weeks, age at diagnosis as completed days of life, birth weight, weight at diagnosis, feeding problem reported by mother, nature of feed, clinical features, infusion rate of ½ DNS, serum sodium level during treatment, duration of hospital stay, condition of the baby at discharge, and condition at follow-up. The complications such as seizures, acute kidney injury, intracranial bleed, vascular thrombosis, apnea, and bradycardia, were noted.
The total weight loss, weight loss per day, and weight gain after treatment were calculated as a percentage of birth weight. The rate of decline in sodium was calculated with the serum sodium at the beginning and end of the treatment and the time taken to attain it. The rate of decline in serum sodium ≤ 0.5 mEq/L/h was considered as safe decline, and > 0.5 mEq/L/h was considered as nonsafe decline. Acute kidney injury was defined as an increase in serum creatinine by more than 0.3 mg/dl in 24 h or serum creatinine more than 1.5 mg/dl with normal maternal serum creatinine levels. Babies were said to be normal at the time of discharge if their serum sodium was < 150 mEq/L and were taking feeds well. At follow-up, the neurodevelopment of these babies was screened with Trivandrum development screening chart (TDSC), as per the unit protocol. The babies were said to be normal neurologically, if they have attained age-appropriate developmental milestones as per TDSC and had no other neurological problem.
IBM SPSS statistics for Windows- Version 24.0. (Released in 2016. IBM Corp., Armonk, N.Y., USA) was used for analysis. Numerical data were presented as mean ± standard deviation or median ± interquartile range as appropriate. Categorical data were presented as percentages and analyzed using the Chi-square test. Ordinal data were analyzed with Mann–Whitney U-test or Student's t-test. P <0.05 was considered as statistically significant.
| Results|| |
During the study period, there were 155 babies satisfying the inclusion and exclusion criteria. Among them, 77 babies were treated with oral feeds alone (Group 1), and 78 babies were treated with oral feeds and ½ DNS (Group 2) [Figure 1]. The baseline characteristics between the two groups were comparable [Table 1]. Serum sodium at diagnosis was comparable between the two groups in analysis of both the whole study population and the subgroups.
|Figure 1: Flow of cases in the study. *½ DNS - 5% dextrose in 0.45% normal saline; IV fluid – Intravenous fluid; LAMA – Left against medical advice|
Click here to view
In the whole study population, the median rate of sodium decline was significantly slower and within the safer limits in Group 1 babies. About 68% of babies had a safer decline in serum sodium in Group 1 compared to 49% in Group 2, and this difference was statistically significant. Although the median serum sodium at the end of treatment in Group 1 was slightly higher than Group 2, this was not statistically significant. The median weight gain percentage after treatment was significantly less in Group 1 [Table 2].
In babies with serum sodium 150–155 mEq/L, the median rate of sodium decline was within the safer limits in both the groups; however, Group 1 babies had a significantly slower decline compared to Group 2 babies. Babies, with safer decline in serum sodium, were significantly more in Group 1 (73%) than in Group 2 (52%). Median serum sodium at the end of treatment was slightly more in Group 1 compared to Group 2, and this was not statistically significant. The median weight gain percentage was significantly less in Group 1 [Table 3]. Eight (10%) babies in Group 1 left against medical advice due to personal reasons, before achieving targeted serum sodium.
|Table 3: Comparison of treatment outcome of babies with serum sodium 150-155 mEq/L|
Click here to view
In babies with serum sodium 156–160 mEq/L, there was no difference between the two groups in serum sodium at the end of treatment, number of babies with safer decline in serum sodium, and median weight gain percentage. Although the median rate of sodium decline was significantly higher in Group 1 compared to Group 2, it was in the nonsafe limits in both the groups.
Complications during treatment, were not seen in any baby. The median duration of hospital stay was similar in both the groups. There was no death in the study population. The number of babies followed up was similar in both the groups across the whole study population and in the subgroups. On follow-up, only one female baby in Group 1 had developmental delay, nystagmus, and seizure disorder. This baby's serum sodium at admission was 150 mEq/L, and the rate of sodium decline was 0.32 mEq/L/h. She also had prolonged jaundice requiring phototherapy for 9 days in the neonatal period.
| Discussion|| |
In this study, we have found that significantly more number of hypernatremic babies treated with oral feeds had safer fall in serum sodium compared to babies treated with oral feeds and ½ DNS. In one of the early reports on oral rehydration, Ng et al. have successfully treated four out of five babies with serum sodium of 151–154 mEq/L using only oral feeds. The authors have commented that their infants were less symptomatic, and oral therapy with breast milk and formula milk have corrected the dehydration in most of their cases. Cagler et al. recommend using breast milk or formula milk or both, as the first-line therapy in well-appearing hypernatremic neonates. Greenbaum suggests oral rehydration for mild-to-moderate hypernatremia but cautions that infant formulas, if given with IV fluids, may cause a rapid fall in serum sodium because of their low sodium content.
Erdemir et al. have compared oral feeds and IV fluids for correcting hypernatremia in breastfed neonates. Babies with no feeding difficulties, were given breast milk/formula, and those with poor feeding or vomiting received only IV fluids. At 24 h of therapy, 80% of oral feeds group had a safe decline in serum sodium compared to only 36% in IV fluid group. In this study, a safe decline in serum sodium was seen in 68% of babies on oral feeds alone and in 49% of babies on IV fluids + oral feeds. In Erdemir et al. study, among babies with serum sodium 156–168 mEq/L, 69% had a safe decline in serum sodium with oral feeds, and none had safe decline with IV fluids. Whereas in our study, among babies with serum sodium 156–160 mEq/L, the safe decline in serum sodium was seen in about 30% of babies in both the groups. In this study, ½ DNS was used for correction along with oral feeds whereas Erdemir et al. have used 1/5 normal saline along with daily maintenance fluids. It was also observed in our study that the percentage of babies with rate of decline in serum sodium ≤ 1 mEq/L/h was almost the same in both groups across all serum sodium ranges.
Oral therapy for hypernatremia correction may be complicated by feed intolerance, necrotizing enterocolitis, and spontaneous intestinal perforation., However, all babies in this study tolerated the feeds well. Bolat et al., in their study, on the treatment of hypernatremia using IV fluids, have concluded that serum sodium correction rate more than 0.5 mEq/l/h is an independent risk factor for death or convulsion. However, in this study, no death or therapy-related complications were seen in babies with both safe and unsafe decline in serum sodium. Bilgin et al. have treated 149 babies with oral feeds or IV fluids depending on the severity, and no death was reported. Similarly, Ozdogan et al. have treated 29 babies with oral feeds or IV fluids. There was no death, and all babies were neurologically normal at follow-up. Yaseen et al. have treated 27 babies with oral feeds or IV fluids or both. Only one baby on IV fluids had seizures due to fast rehydration and had abnormal neurological examination at follow-up.
On long-term follow up of our study population, only one baby in oral feeds alone group had neurodevelopmental impairment. This baby had safe decline in serum sodium but had a prolonged period of jaundice. It has been found in animal studies that hyperosmolar conditions can disrupt the blood–brain barrier and potentiate the neurotoxic effect of bilirubin. Ergenekon et al. have shown that there is no correlation between serum sodium at admission and neurodevelopmental test scores at follow-up. Bolat et al. have found no significant difference in neurodevelopmental outcome by the rate of correction of serum sodium.
A recent systematic review by Bischoff et al. has found only two retrospective studies reporting the outcome of various therapies for hypernatremia in breastfed neonates, of which one has compared exclusive oral feeds with exclusive IV fluids. We have tried to feed all the babies irrespective of IV fluid administration as babies with breastfeeding-associated hypernatremia are not only dehydrated but also starving. We have shown that oral feeds can be safely given to all clinically stable babies with less severe hypernatremia.
This study has the following limitations. The volume of feeds ingested by the babies was not measured. Although all babies could have been fed with measured volume of expressed breast milk, this was not done since it may interfere with the assessment of breastfeeding and may affect the bonding between the mother and baby. Weighing the baby before and after direct breastfeed might have helped in roughly estimating the volume of milk ingested by the baby. There is a chance for attrition bias in the study due to eight babies in Group 1 leaving the hospital before their serum sodium normalized. Follow-up details were not available for all cases and for one baby with developmental delay identified through TDSC, the diagnosis could not be refined using a confirmatory test such as Bayley scale of infant development. A randomized controlled trial comparing oral feeds with and without IV fluids administration may help to find the correct strategy for managing hypernatremia in otherwise healthy breastfed neonates.
| Conclusion|| |
In hypernatremic breastfed neonates with serum sodium 150–155 mEq/L, the treatment with liberal oral feeds alone using breastfeeds and/or formula feeds can cause safe decline in serum sodium in more number of babies compared to babies receiving IV fluids in addition. However, careful monitoring of the serum sodium is needed during hypernatremia correction irrespective of the nature of treatment given. A randomized control trial comparing oral feeds alone with oral feeds and IV fluids are needed to provide concrete evidence.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Kramer MS, Kakuma R. The Optimal Duration of Exclusive Breastfeeding-A Systematic Review. Geneva: World Health Organization; 2002.
Livingstone VH, Willis CE, Abdel-Wareth LO, Thiessen P, Lockitch G. Neonatal hypernatremic dehydration associated with breast-feeding malnutrition: A retrospective survey. CMAJ 2000;162:647-52.
Greenbaum LA. Deficit therapy. In: Kliegman RM, editor. Nelson Textbook of Pediatrics. 20th
ed. Philadelphia, PA: Elsevier; 2016. p. 388-90.
Lavagno C, Camozzi P, Renzi S, Lava SA, Simonetti GD, Bianchetti MG, et al
. Breastfeeding-associated hypernatremia: A systematic review of the literature. J Hum Lact 2015;32:67-74.
Bischoff AR, Dornelles AD, Carvalho CG. Treatment of hypernatremia in breastfeeding neonates: A systematic review. Biomed Hub 2017;2:454980.
Posencheg MA, Evans JR. Acid-base, fluid and electrolyte management. In: Gleason CA, Devaskar SU, editors. Avery's Diseases of the Newborn. 9th
ed. Philadelphia, PA: Elsevier Saunders; 2012. p. 367-89.
Ng PC, Chan HB, Fok TF, Lee CH, Chan KM, Wong W, et al
. Early onset of hypernatremic dehydration and fever in exclusively breast-fed infants. J Paediatr Child Health 1999;35:585-7.
Cagler MK, Altugan FS, Ozer I. Exclusive breastfeeding and hypernatremic dehydration. Iran J Publ Health 2005;34:1-11.
Erdemir A, Kahramaner Z, Turkoglu E, Kanik A, Sutcuoglu S, Ozer EA. Comparison of oral and intravenous fluid therapy in newborns with hypernatremic dehydration. J Matern Fetal Neonatal Med 2014;27:491-4.
Parrish CR, Rosner MH. Clinical observations correcting hypernatremia: Enteral or intravenous hydration? Pract Gastroenterol 2014;137:68-72.
Huston RK, Dietz AM, Campbell BB, Dolphin NG, Sklar RS, Wu YX. Enteral water for hypernatremia and intestinal morbidity in infants less than or equal to 1000 g birth weight. J Perinatol 2007;27:32-8.
Bolat F, Oflaz MB, Guven AS, Özdemir G, Alaygut D, Doğan MT, et al
. What is the safe approach for neonatal hypernatremic dehydration? A retrospective study from a neonatal intensive care unit. Pediatr Emer Care 2013;29:808-13.
Bilgin LK, Akcay F, Altinkaynak K, Altindag H. Hypernatremia in breastfed newborns: A review of 149 cases. J Trop Pediatr 2011;58:332-4.
Ozdogan T, Iscan M, Ellikcioglu C, Yildiz E. Hypernatremic dehydration in breast-fed neonates. Arch Dis Child 2006;91:1041-7.
Yaseen H, Salem M, Darwich M. Clinical presentation of hypernatremic dehydration in exclusively breast-fed neonates. Indian J Pediatr 2004;71:1059- 62.
Wennberg RP, Johansson BB, Folbergova J, Siesjo BK. Bilirubin induced changes in brain energy metabolism after osmotic opening of the blood brain barrier. Pediatr Res 1991;30:473-8.
Ergenekon E, Unal S, Gucuyener K, Soysal SE, Koç E, Okumus N, et al
. Hypernatremic dehydration in the newborn period and long-term follow up. Pediatr Int 2007;49:19-23.
Moritz ML. Preventing breastfeeding-associated hypernatremia: An argument for supplemental feeding. Arch Dis Child Fetal Neonatal 2013;98:F378-9.
Neifert MR. Prevention of breastfeeding tragedies. Pediatr Clin North Am 2001;48:273-97.
[Table 1], [Table 2], [Table 3]