Jump to comment:

• Dehydration and hypoglycaemia in term breast fed infants
  Roslyn M Thomas
  Published on: 22 March 2016

• Published on: 22 March 2016

  Dehydration and hypoglycaemia in term breast fed infants

  • Roslyn M Thomas, Consultant Paediatrician
  • Other Contributors:
    • Fernando Isaza, Warren Hyer

  Dear Editor

  We have read with interest the article by Oddie et al [1] and subsequent correspondence from Williams [2], Harding et al [3] about weighing breast fed babies. With the ongoing shortage of midwives throughout the UK, staffing levels on postnatal wards are low. We are increasingly worried about the decline in support available to mothers trying to establish lactation in the days immediately after delivery...

  Show More

  Dear Editor

  We have read with interest the article by Oddie et al [1] and subsequent correspondence from Williams [2], Harding et al [3] about weighing breast fed babies. With the ongoing shortage of midwives throughout the UK, staffing levels on postnatal wards are low. We are increasingly worried about the decline in support available to mothers trying to establish lactation in the days immediately after delivery. Early postnatal discharge from maternity units is now the norm, usually within 24 hours of delivery, and by 48-72 hours after LSCS in our hospital. We report 3 breast fed term infants who have presented within the past 6 months with profound hypoglycaemia, neonatal convulsions and significant dehydration which we attribute to undernutrition in the first 3 days after birth.

  All 3 infants have abnormal MRI changes compatible with white matter infarction secondary to hypoglycaemia and all are showing signs of significant neurodevelopmental delay within 6 months of birth. Neither the mothers nor midwives recognised any worrying signs in the infants' pattern of suckling, tone or state of alertness until the onset of convulsions (2 infants), and repeated cyanotic episodes (1 infant).

  Case 1
  A 4 day old infant (birth weight 4320g, OFC 37 cm) presented with a 48 hour history of poor feeding and jitteriness.The baby was severely dehydrated with a weight loss of 18% since birth. Convulsions commenced soon after presentation. Laboratory blood sugar was unrecordable, Hb 19.2 g/dl, Na 154 mmol/l, creatinine 116 umol/l, urea 27.8 umol/l. The baby had been discharged from hospital at 7 hours of age after a spontaneous, uncomplictaed vaginal delivery at term, and the baby was breast fed. Emergency resuscitation was required and intensive care for 4 days. No underlying infective or metabolic cause was identified, although insulin levels were not measured at the time of presentation when the infant was hypoglycaemic. Thrombophilia screen was normal. MRI scan of brain at 13 days of age revealed a widespread abnormal signal intensity throughout the white matter consistent with parasagittal infarction, a pattern recognised in hypoglycaemic brain injury. EEG at 3 weeks of age was abnormal and the infant has required ongoing anti-convulsants for clinical seizures. OFC has fallen from 90th to 25th centile by 2 months of age.

  Case 2
  An infant (birth weight 2550gm, OFC 33.5 cm) was transferred to NICU at 70 hours of age after a cyanotic episode on the postnatal ward. The baby had been delivered by semi-emergency LSCS because of growth restriction and CTG signs consistent with placental insufficency at 39 weeks gestation, but was in good condition at birth (Apgar scores 8 @ 1;10 @ 5 mins). Laboratory blood glucose was unrecordable on admission to NICU. Normoglycaemia was restored with an intravenous infusion of 10 % dextrose (7 mg/kg/min). Weight loss of 12% since birth was documented on admission to NICU. At 80 hours of age, a left sided focal convulsion occurred. No infective or metabolic cause was identified apart from hypoglycaemia. The baby had been breast fed. Cranial ultrasound on day 4 revealed a bright echodensity in the caudothalamic notch. MRI scan of brain on day 5 showed multiple haemorrhagic lesions in the white matter consistent with hypoglycaemic brain injury. In addition there was a small infarct in the right lentiform nucleus extending into the internal capsule. The aetiology of the infarct is uncertain and the results of the thrombophilia screen are awaited.

  Case 3
  A 60 hour old infant (birth weight 2760g, OFC 31.7 cm) was admitted with lethargy, poor feeding and convulsions within 9 hours of discharge home from the postnatal ward. He had been born by semi-elective LSCS because of failing fetal growth and oligohydramnios. No resuscitation was required at birth. Apgar scores were 9 @ 1;10 @ 5mins. He was breast fed. Laboratory blood sugar was unrecordable on readmission. An intravenous infusion of glucose at 13 mg/kg/min restored normoglycaemia. Weight loss of 6% from birth was documented. Infection, metabolic and thrombophilia screen revealed no other abnormality. MRI scan of brain at 11 days of age showed posterior and temporal white matter infarction consistent with hypoglycaemic brain injury. OFC has fallen from 10th to well below 3rd centile by 7 months of age and he has significant neurodevelopment delay.

  These 3 infants presented with significant hypoglycaemia within 4 days of birth and all have abnormal MRI scans consistent with hypoglycaemic brain injury. Transient hyperinsulinaemia was not excluded in any of the infants as insulin levels were not measured at the time of initial presentation with hypoglycaemia.The glucose requirement to restore normoglycaemia was not particularly high, however, and as there was no recurrence of hypoglycaemia in any of the infants after commencing the infusion of glucose, transient hyperinsulinaemia seems unlikely. Two infants (cases 2 and 3) were delivered by LSCS because of signs of placental insufficiency, and therefore may have been at risk of hypoglycaemia, but as they were in good condition at birth and birthweight was not <10th centile, the mothers and infants all received "normal" postnatal care. The reason for the hypoglycaemia in case 1 is unclear. The mother showed no overt signs of gestational diabetes, and transient hyperinsulinaemia remains a possible explanation. No other underlying pathology in the infants was demonstrated. All infants are showing signs of neurodevelopmental delay and feeding problems and two have developed microcephaly. Because of the concomitant weight loss (> 12 % in cases 1 and 2), we have concluded that undernutrition whilst attempting to establish lactation is the most likely cause of the hypoglycaemia.

  We are painfully aware that there is a low midwife/ mother ratio on our postnatal ward and that mothers may not always be able to receive optimal supervision and support whilst attempting to establish lactation. The use of lay breast counsellers and appropriately trained health care assistants to support breast feeding mothers, particularly primipara and mothers who may benefit from additional support after LSCS, is being explored. We support the view of Williams that experienced midwives can assess the establishment of lactation and clinical hydration of the baby by observation of feeding pattern and other clinical signs without having to resort to early weighing. However, there is a national shortage of midwives and we believe that very few maternity units have sufficient midwives to provide optimal support for all mothers to establish successful lactation. Discussion with other paediatric colleagues suggests that they are also seeing a resurgence of dehydration and hypoglycaemia in a small number of breast fed term infants.

  Healthy term breast fed babies have been shown to tolerate asymptomatic hypoglycaemia during early lactation (4), but infants at risk of hypoglycaemia because of fetal undernutrition may require additional feeding or glucose intake in the first few days after birth. Birth weight <10th centile is commonly used to identify babies who might benefit from routine blood glucose monitoring in the first few days after birth, but it is only a crude indicator of which babies may be at risk of hypoglycaemia, particularly if postnatal nutrition is inadequate. Clear guidelines for health care workers about the clinical assessment of adequacy of breast feeds to include observation of suckling pattern, state of alertness, frequency of stools and wet nappies, particularly after 12 hours of age, may help to prevent dehydration and hypoglycaemia. We would not dismiss the potential benefit of weighing some, but not all, breast fed babies on 2nd or 3rd day after birth, as this may identify babies with significant weight loss before more serious symptoms develop. The challenge remains to prevent serious complications in a minority of potentially vulnerable infants without undermining the establishment of successful breast feeding for the majority of normal term infants.

  R Thomas
  F Isaza
  W Hyer

  References (1) Oddie S, Richmond S, Coulthard M. Hypernatraemic dehydration and breast feeding: a population study. Arch Dis Child 2001;85: 318-320.
  (2) Williams A . Weighing breast fed babies. Arch Dis Child Fetal Neonatal Ed 2001;86:F69.
  (3) Harding D, Cairns P, Gupta S, et al. Hypernatraemia: why bother weighing breast fed babies? Arch Dis Child Fetal Neonatal Ed 2000;85:145.
  (4) Hawdon J, Ward Platt M P, Aynsley-Green A. Patterns of metabolic adaptation for preterm and term infants in the first neonatal week. Arch Dis Child 1992;67:357-365.

  Show Less

  Conflict of Interest:
  None declared.

  • Back to top