Perinatal/Neonatal Case Presentation

Hypomagnesemia secondary to cerebrospinal fluid losses in a patient with congenital hydrocephalus


We describe a newborn infant with massive congenital hydrocephalus, presenting with hypomagnesemia secondary to magnesium losses through cerebrospinal fluid (CSF) aspirations. Hypomagnesemia due to CSF losses has not been described in pediatric literature.


A male infant was transferred to our neonatal intensive care unit on the first day of life with a prenatal diagnosis of congenital hydrocephalus. The baby was born at 35 weeks and 6 days of gestation to a 35-year-old gravida 1 mother by cesarean section. Pregnancy history was unremarkable until the third trimester when fetal ultrasonography showed hydrocephalus with markedly enlarged 4th ventricle exerting mass effect on the brainstem and cerebellum. There was also splaying of the spinal cord at the level of the fourth and fifth vertebrae. Fetal magnetic resonance imaging (MRI) at 32 weeks gestation showed massive enlargement of 3rd, 4th and lateral ventricles. The infant was born by cesarean section. Birth weight was 6470g, length 55 cm and head circumference 68 cm; all measurements were large for gestational age.

On examination the patient was stable on room air. He was megencephalic with prominent nasal and frontal vasculature and widely split sutures and tense anterior fontanel. Eye examination showed proptosis, lid retraction and sunset sign. He had a soft cry and moved arms and legs upon stimulation. MRI of the brain showed findings consistent with fetal MRI, and did not identify any specific cause for the massive hydrocephalus. The neural tissue had become thinner when compared to the fetal MRI, indicating worsening of hydrocephalus. Neurosurgical consult was obtained and a cerebrospinal fluid (CSF) reservoir was placed on the second day of life with plans for a ventriculoperitoneal shunt after reducing the head circumference. The CSF reservoir was tapped twice every day to relieve pressure due to hydrocephalus and to possibly reduce the head circumference. In the subsequent days, the patient developed fluid and electrolyte imbalance most likely due to the massive amount of CSF drainage (800 to 1000 ml a day). The weight estimation for fluid and caloric management was challenging because of the massive hydrocephalus. Hence head weight was estimated daily using geometric estimation (considering head a sphere (4/3πxr3)) and taken into account while calculating the daily weight for assessing fluid and nutrient intake and growth. Shoulder-to-heel length was followed as an indicator of linear growth.

The baby received enteral feeding with expressed breast milk or 20 calories/ounce formula and replacement of CSF losses with half-normal saline. Within 10 days the baby appeared malnourished despite apparently adequate nutrient intake for expected body weight for age (160 ml kg–1 per day breast milk) and normal stools. Caloric density was increased by fortifying breast milk to 22 and later 24 calories per ounce. Work-up on the 12th day of life disclosed normal electrolytes, mild hypocalcemia (total calcium 0.42 mM l–1 or 7.6 mg dl–1; ionized calcium 1.11 mM l–1), normal phosphate level (0.32 mM l–1 or 5.8 mg dl–1), severe hypomagnesemia (0.027 mM/l or 0.5 mg/dl) and normal alkaline phosphatase level (212 IU l–1). Renal losses of magnesium were ruled out by a low fractional excretion of magnesium (1%). We found no evidence for liver or renal disease. Hand radiograms showed normal bone density and no fraying of the metastases. Serum magnesium level improved progressively with intravenous administration. We suspected that hypomagnesemia resulted from refeeding and from magnesium deficit from CSF loss. On day of life 23, the CSF magnesium level was 0.15 mM l–1 (2.8 mg dl–1), compared with a serum value of 0.07 mM l–1 (1.2 mg dl–1). We found no evidence of any other deficiency, including trace elements. Oral magnesium supplementation resulted in diarrhea, which required intravenous rehydration. Therefore, magnesium depletion and ongoing CSF losses were treated with intravenous magnesium therapy. Weight gain, linear growth and nutritional status substantially improved with fortified breast milk, providing 128 calories per day per kg of expected body weight for age.

Massive CSF drainage required for reducing head size suggested increased CSF production. MRI at 4 weeks of age disclosed a mass in the posterior fossa, predominantly within the fourth ventricle (Figure 1). Complete surgical removal of the mass led to a decrease in CSF production. The pathological diagnosis was choroid plexus papilloma (World Health Organization grade I; Figure 2). Serum magnesium levels remained stable after surgery without supplementation, and subsequent growth followed the expected curve. The patient received a ventriculoperitoneal shunt at 8 weeks of age.

Figure 1

Magnetic resonance images of the choroid plexus papilloma. The images are post gadolinium T1 weighted images and the tumor intensely enhances. Choroid plexus papilloma (arrow) seen in the posterior fossa on axial view (a) and sagittal view (b). (c) Shows a sagittal view after tumor resection.

Figure 2

Tumor histology. Papillary structures with fine fibrovascular cores (x40 magnification, a); bland cytology of the cuboidal cells lining the tumor core (x200 magnification, b).


We describe a patient with hydrocephalus and massive amounts of daily CSF production and drainage due to a choroid plexus papilloma. Hypomagnesemia resulted from magnesium depletion via CSF loss. Most magnesium after birth is contained in the skeleton and soft tissue, with less than 1% in circulation.1 The estimated cumulative magnesium deficit in our patient (196 mg) at the time of confirmation accounted for 43% of the total magnesium content (456 mg) of a normal 35-week fetus.2 Intravenous magnesium administration normalized serum magnesium level and eventually corrected the magnesium depletion. We did not find any previous description of CSF loss as a cause of hypomagnesemia.

Hypomagnesemia is defined as a serum magnesium level <1.8 mg dl–1 (0.74 mmoll–1).3 Hypomagnesemia may result from inadequate intake, intracellular shift (treatment of diabetic ketoacidosis, refeeding syndrome, hungry bone syndrome), increased gastrointestinal loss (chronic diarrhea, malabsorption syndrome, steatorrhea, vomiting and nasogastric suction), or most commonly, increased loss in urine demonstrated by a fractional excretion of magnesium greater than 2–4%.4,5

Magnesium level in CSF is 25–40% higher than serum level.6 One study suggested that the CSF magnesium concentration in patients with hydrocephalus is higher than in patients with no hydrocephalus.7 This could be due to an increase in permeability of the blood–brain barrier or to increased release of magnesium from necrotic cells.7 The normative levels for CSF magnesium are 2.5±0.4 mg dl–1 or 0.13±0.02 mM l–1 (mean±s.d.) for premature and full-term infants between 12 and 24 h of postnatal age.8

Based on our findings, we recommend that magnesium levels be closely monitored in cases with high CSF losses. As oral magnesium sulfate acts as a laxative causing diarrhea, intravenous magnesium intake is necessary to correct severe magnesium deficit.


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Correspondence to L P Brion.

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Lal, C., Mir, I., Kelley, E. et al. Hypomagnesemia secondary to cerebrospinal fluid losses in a patient with congenital hydrocephalus. J Perinatol 34, 640–641 (2014).

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