Hypernatremic dehydration in neonates is a common condition in an exclusively breastfed infant but often underdiagnosed. Any newborn who has lost more than 10% of birthweight should be carefully evaluated and monitored for clinical features of dehydration. Efforts such as frequent follow-up for weight check, and formula supplementation, if needed, should be provided to a neonate at risk of developing complications of dehydration. Adequate lactation consultation, both inpatient and outpatient, should also be provided, especially to the primigravida mother. Here, we present a case of a neonate with severe hypernatremic dehydration caused by inadequate lactation in a primigravida mother, which resulted in cerebral venous sinus thrombosis leading to significant intracerebral hemorrhage. The infant suffered permanent neurologic damage and was sent home on technological devices (tracheostomy and gastrostomy tubes). Further, we provide a brief review of hypernatremic dehydration and sinus venous thrombosis in neonates.
A 7-day-old female infant was brought to the emergency department with decreased responsiveness and poor feeding. She was born at 384/7 weeks’ gestation, with a birthweight of 2770 g (10th–25th percentile) to a 38-year-old primiparous woman with adequate prenatal care. The pregnancy was complicated by gestational thrombocytopenia diagnosed in the third trimester, which required treatment with hydrocortisone. Her prenatal laboratory findings, including syphilis rapid plasma reagin, hepatitis Bs antigen, HIV, gonorrhea, and chlamydia, were negative. The result of her group B
On day 6, the infant became increasingly lethargic and uninterested in feeding. She was taken to the emergency department (ED) where it was recorded that she had an average of 3 wet diapers/day and less than 1 stool/day over the past 2 days. In addition, the mother endorsed a history of right-sided gaze and head deviation for a few seconds while the infant was being placed in the car seat on the way to the ED. On initial physical examination at the ED, the infant was lethargic and minimally responsive, with a prolonged capillary refill time and appeared grossly dehydrated with standing skinfolds. Her vital signs were as follows: temperature, 34.2°C (93.5°F); heart rate, 184 beats/min; respiratory rate, 64 breaths/min; and oxygen saturation, 100% in room air. Her weight was 2,220 g (∼20% below birthweight). Multiple short self-limiting brief episodes of right gaze deviation and left arm tonic-clonic movements were also noted. Laboratory testing in the ED revealed the following.
Sodium 173 mEq/L (reference range 135–145 mEq/L) Potassium 6.8 mEq/L (reference range 3.8–6.0 mEq/L) Chloride 130 mEq/L (reference range 95–110 mEq/L) BUN 165 mg/dL (reference range 7–25 mg/dL) Creatinine 1.92 mg/dL (reference range 0.2–0.4 mg/dL) Bicarbonate 10 mEq/L (reference range 18–24 mEq/L) Glucose 111 mg/dL (reference range 75–105 mg/dl)
Capillary pH 7.29 (reference range 7.35–7.45) PaCO2 32 mm Hg (reference range 35–45 mm·Hg) Base excess −10 mEq/L
White blood cells (WBC) of 18,700/ Hemoglobin of 16.7 g/dL (167 g/L) (reference 14.3–24.5 g/dl) Hematocrit of 53%, (reference 44–64%) Platelet count of 74,000/
There was no left shift on the CBC. In the ED, the infant received 2 normal saline boluses and was started on intravenous fluids and antibiotics and was transferred to a level IV neonatal intensive care unit for further care, where her vital signs improved. On examination, the infant was hypoactive but responsive to stimulation. She continued to have intermittent episodes of seizures (tonic-clonic seizures of both upper and lower extremity and right gaze deviation) on admission. Respirations were not labored, and heart sounds were normal on auscultation. Rest of the examination findings were within normal limits. Serum sodium concentration was 174 mEq/L, potassium 6.5 mEq/L, chloride 134 mEq/L, blood urea nitrogen 158 mg/dL, creatinine 1.61 mg/dL, and bicarbonate 15 mEq/L. Another normal saline bolus was given, and intravenous fluids continued. The WBC count was 11,800/
Hyperdense blood in both ventricles (left greater than right). Arrow shows left intraventricular bleeding extending into the surrounding brain parenchyma including the thalamus.
Computed tomography scan of the brain showing intraventricular hemorrhage involving the lateral third and fourth ventricles as well as the basal cistern with mild to moderate enlargement of the lateral ventricles.
The infant’s neurologic state continued to deteriorate with the cessation of spontaneous movements, absent reaction to painful stimuli, and fixed and dilated pupils. She became apneic and was intubated to support respiration. Further brain imaging with magnetic resonance imaging, including venous and arterial angiography, showed stable IVH within the lateral, third, and fourth ventricles. It also showed previously known parenchymal hemorrhages in the bilateral thalami and basal ganglia, which was more prominent on the left side. Arterial angiography showed no flow in the intracranial arteries, and venous angiography showed no flow in dural venous sinuses suggestive of cerebral venous sinus thrombosis (Figures
Magnetic resonance imaging of the brain showing intraventricular hemorrhage within the lateral third and fourth ventricles with hydrocephalus. Bilateral thalami and basal ganglia hemorrhage can be noted, primarily on the left side. Diffuse diffusion signal abnormality can be noted in the cerebral hemisphere, likely representing ischemic/necrotic changes.
Magnetic resonance imaging of the brain showing intraventricular hemorrhage within the lateral third and fourth ventricles with hydrocephalus. Bilateral thalami and basal ganglia hemorrhage can be noted, primarily on the left side. Diffuse diffusion signal abnormality can be noted in the cerebral hemisphere, likely representing ischemic/necrotic changes.
Arterial and venous magnetic resonance angiography scans of the brain showing no intracranial arterial flow. No flow signal was identified in the dural venous sinuses, likely representing underlying sinus thrombosis.
Breastfeeding is considered a normative feeding standard for all infants because of its extensive benefits to both the infant and mother. The American Academy of Pediatrics recommends exclusive breastfeeding for all infants until the age of 6 months, when complementary food can be added while continuing breastfeeding until 1 year of age [
In neonates, hypernatremia is usually defined as serum sodium levels greater than 145 mEq/L (145 mmol/L) [
In the current case, severe hypernatremia resulted in cerebral venous sinus thrombosis, which caused significant intraventricular and intracranial hemorrhage. Severe thrombocytopenia occurred due to sinus thrombosis, which further contributed to worsening of hemorrhage. Dehydration leading to hypernatremia is one of the most common causes of cerebral venous sinus thrombosis. Other risk factors include infection, maternal chorioamnionitis, hypoxic-ischemic encephalitis, and thrombophilia [
Physicians should be aware of the possibility of hypernatremic dehydration in an exclusively breastfed infant. Hypernatremic dehydration in a neonate may be associated with a devastating outcome. It should be recognized early and prevented before the emergence of complications. Lactation support should be provided to ensure successful breastfeeding. Hypervigilance is key and when a newborn infant has lost more than 10% of birthweight, frequent/daily follow-up for weight checks, lactation consultation, and temporary supplementation of formula feeds may be necessary to avoid complications.
The data used to support the study are available within the article.
The authors declare that they have no conflicts of interest.