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Permanent Brain Damage From Hypernatremic Dehydration in Breastfed Infants: Patient Reports

Posted on: Friday, 17 December 2004, 03:00 CST

Introduction

Successful breastfeeding confers important physical and psychological advantages and can have lifelong health benefits,1 but inadequacy of breastfeeding may result in malnutrition, hypernatremic dehydration, and catastrophic outcomes.2-10 The increasing popularity of breastfeeding has resulted in increased frequency of this problem since it was first recognized 25 years ago.2,4 This report, based on complete emergency service, hospital, nursery hotline, and long-term outpatient records, is of 2 infants with breastfeeding malnutrition with hypernatremic dehydration (BFMHD) causing permanent brain damage, in 1 complicated by durai sinus thrombosis, and in the other accompanied by severe hypoglycemia.

Patient Reports

Patient 1

This 4,073 g term infant was the first-born child of a 34-year- old mother, delivered with outlet vacuum assistance after 10 hours of active labor. Except for a weight gain of 72 1b, the pregnancy was uncomplicated. The newborn had a weak cry and was floppy but responded readily to resuscitation with blow-by oxygen. Bedside fingerstick glucose measurements during the first 10 hours were 35, 45, 56, 37, and 33 but remained above 40 mg/dL thereafter. The mother was seen by a lactation consultant, but at the time of discharge, on day 2 of life, the baby was described as having trouble staying latched on. On day 4 of life he was noted by the nurse practitioner to have a normal feeding pattern according to the log kept by the mother and to have lost 10% of birth weight. By day 7 of life, when he was seen by the nurse practitioner, he had lost 14% of birth weight. On day 8, the mother became concerned when he did not feed at all after approximately 6 P.M.; she called the advice line and a physician advised her that she did not need to bring the baby to the emergency room, because it would not be a problem if he did not wake up to eat during the night. When the physician saw the baby the next morning, she noted severe dehydration and lethargy. On admission to hospital the infant was described as thin, emaciated, and lethargic, with dry mucous membranes, chapped lips, sunken eyes, and absent tears. Weight was 3,345 g, an 18% weight loss from birth. Blood studies included hematocrit 61%, and serum sodium 164 mEq/L, urea nitrogen 17.5 mmol/ L (49 mg/dL), and creatinine 56.6 mol/L (0.8 mg/dL).

Rehydration was begun with 30 m L of normal saline over 2 hours, to be followed by deficit replacement of 300 m L normal saline over 1 day together with maintenance fluids. Twelve hours after admission he had an episode of bradycardia for approximately 1 minute followed by perioral cyanosis, flickering of his eyes, and 20 minutes of multiple brief episodes of tonic clonic upper extremity movement. Computerized tomography (CT) scan done 2 hours later showed prominent vascular structures including the internal cerebral veins, the straight sinus, the superior sagittal sinus, and choroid plexus, considered likely due to slow flow from the dehydration. Magnetic resonance imaging (MRI) 3 hours later demonstrated complete thrombosis of the superior sagittal sinus and straight sinus. When the patient was 13 months old, MRI showed periventricular leukomalacia, ex vacua hydrocephalus of the lateral and third ventricles, and patent sagittal sinus with small venous vascular flow-void.

Neurologic status at age 4 years included controlled seizure disorder, delayed language development, spastic diplegia with inability to walk or stand, and right hand weakness.

Patient 2

The infant was born at term to a 28-year-old primagravida by emergency section for fetal distress and acidosis. Weighing 2,914 g, he appeared normal at birth, breathed spontaneously, and had a 5- minute Apgar score of 9; he was placed in the normal newborn nursery. He did not nurse well. On day 2 of life, the nurse recorded tremors of his upper extremities. He was discharged home with his mother on day 3. Late that evening the mother called 911 because the baby appeared blue, but by the time his father came on the scene, only moments later, the infant had recovered and the emergency team found his vital signs to be normal. On clay 4, the mother called the hotline at the nursery because the baby was lethargic, not feeding, and sleeping all the time; she was advised about nursing technique and reassured. Following a series of calls to the doctor's office, beginning on day 5, the parents were able to get the baby seen in the early afternoon on day 6, when it was recognized that he was severely dehydrated, and he was rushed to the pediatric intensive care unit. There he was found to be severely hypoglycemic (serum glucose 0.06 mmol/L [1 mg/dL]) as well as severely dehydrated and hypernatremic (sodium 158 mEq/L, urea nitrogen 10.96 mmol/L [86 mg/ dL]. Following fluid resuscitation including 10% dextrose, he had no further hypoglycemia. A computed tomography (CT) scan soon after admission demonstrated encephalomalacia.

At age 4 months he began infantile spasms 10-15 times daily, which were significantly ameliorated by adrenocorticotropic hormone starting at age 6 months. An electroencephalogram demonstrated hypsarrythmia, and a CT scan showed cortical atrophy with slight ventricular dilatation and an infarct in the left occipital lobe. Magnetic resonance imaging of the brain at 1 year of age demonstrated watershed injury in the occipital cortex, the parasagittal cortex, and the white matter, consistent with ischemic injury. At 7 years of age, he was having a few seizures daily with anticonvulsant therapy, was able to walk with a wide-based gait, but could not feed himself or communicate. He had minimal vision and remained in diapers.

Discussion

Breastfeeding malnutrition with hypernatremic dehydration, defined as a weight loss of 10% or more, with clinical signs of dehydration, and serum sodium concentration >150 mEq/L, may occur in as many as 10% of urban 1 newborns who are followed up closely.3,4,6,9 Devastating outcomes, as in the present report, are associated with late diagnosis in those without adequate postnatal follow-up. In 1 series of 5 patients, 2 infants had multiple cerebral infarctions and another infant had an iliac artery thrombus resulting in amputation; several months after discharge, all were neurologically normal.4 Four instances of durai sinus thrombosis as seen in patient 1 have been reported, 3 with a fatal outcome,5,7 and 1 without residual.8 The single individual without residual developed signs of cerebral thrombosis 12 hours after the start of therapy, as patient 1 did.

Hyperglycemia was noted in 13 of 42 reported infants with BFMHD reviewed by van Amerongcn et al,7 whereas hypoglycemia was noted in only 4 affected infants. In contrast to patient 2, who was admitted with a serum glucose concentration near zero, the range in these 4 patients was 1.1-2.2 mmol/L (20-39 mg/dL); this range would also include patient 1.

Breastfeeding failure occurs with ~20% of primagravidas, who account for the vast majority of instances of BFMHD. Greater than normal sodium concentration of maternal milk has been noted in such cases.10 A likely contributing factor in patient 2 was hypoglycemia, suggested by the tremors observed in the nursery, which were not taken as a cue along with the poor feeding, to check blood glucose concentration, which should have been monitored in any case because of the prolonged labor and fetal distress. It is not possible to determine whether severe and prolonged hypoglycemia or the BFMHD was primarily responsible for the permanent brain damage.

These patient reports and increasing recognition of BFMHD over the past 2 decades emphasize the importance of close monitoring of weight gain and hydration in breastfed infants, with appropriate studies and intervention if weight loss exceeds 10% of birth weight. Poor feeding in the first days and weeks of life may be the only indicator of serious disease and cannot be treated perfunctorily.

REFERENCES

1. von Kries R, Koletz.ko B, Sauerwald T, et al. Breastfeeding and obesity: cross sectional study. BMJ. 1999;319:147-150.

2. Markarian M, Griswold W, Mendoza S. Hypernatremic dehydration resulting from inadequate breast-feeding. Pediatrics. 1979;63:931- 932.

3. Rowland TW, Zori RT, Lafleur WR, Reiter EO. Malnutrition and hypernatremic dehydration in breast-fed infants. JAMA. 1982;247:1016- 1017.

4. Cooper WO, Atherton HD, Kahana M, Kotagal UR. Increased incidence of severe breast-feeding malnutrition and hypernatremia in a metropolitan area. Pediatrics. 1995;96:957-960.

5. Kaplan JA, Siegler RW, Schmunk GA. Fatal hypernatremic dehydration in exclusively breast-fed newborn infants due to maternal lactation failure. Am J Forensic Med Pathol. 1998;19:19- 22.

6. Livingstone VH, Willis CE, Abdel-Wareth LO, et al. Neonatal hypernatremic dehydration associated with breast-feeding malnutrition: a retrospective survey. Can Med Assoc J. 2000;162:647- 652.

7. van Amerongen RH, Moretta AC, Gaeta TJ. Severe hypernatremic dehydration and death in a breast-fed infant. Pediatr Emerg Care. 2001;17:175-180.

8. Gebara BM, Everett KO. Dural sinus thrombosis complicating hypernatremic dehydration in a breastfed neonate. Clin Pediatr. 2001;40:45-48.

9. Manganaro R, Mami C, Marrone T, et al\. Incidence of dehydration and hypcrnatremia in exclusively breast-fed infants. J Pediatr. 2001;139:673-675.

10. Jaramillo I, Lopez G, Hernandez H. Hypernatremic dehydration and death in an infant (letter). Pediatr Emerg Care. 2001;17:179- 180.

Arlan L. Rosenbloom, MD

Clin Pediatr. 2004;43:855-857

Division of Endocrinology, Department of Pediatrics, University of Florida College of Medicine, Gainesville, Florida.

Correspondence to: Arlan L. Rosenbloom, MD, Children's Medical Services Center, 1701 SW 16th Ave., Building B, Gainesville, FL 32608-1153.

2004 Westminster Publications, Inc., 708 Glen Cove Avenue, Glen Head, MY 11545, U.S.A.

Copyright Westminster Publications, Inc. Nov/Dec 2004

Source: Clinical Pediatrics

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