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Hyponatraemia as a consequence of serial liquor punctures in preterm infants with a ventricular access device after posthaemorrhagic hydrocephalus
  1. K Tenbrock1,
  2. A Kribs1,
  3. B Roth1,
  4. B Speder2
  1. 1Department of Neonatology and Pediatric Intensive Care, University Children’s Hospital of Cologne, Cologne, Germany
  2. 2Neurosurgical Department, University Hospital of Cologne
  1. Correspondence to:
    Dr Tenbrock, Walter Reed Army Institute of Research, MCR, Washington DC 20307-5100, USA;
    klaus.tenbrock{at}na.amedd.army.mil

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We observed hyponatraemia in several preterm children treated with a ventricular access device (Rickham reservoir)1 after intraventricular haemorrhage (IVH)2 and serial liquor puncture to drain liquor. To rule out a connection, we retrospectively investigated the data of all preterm children (23–32 weeks of gestational age) treated at the University Children’s Hospital of Cologne with a ventricular access device during 1996–1999 (n = 16).

Sixteen of 480 preterm infants (3.3%) of less than 1500 g birth weight (430–1500 g) developed an IVH and required treatment with a ventricular access device. The mean gestational age of these children was 27 weeks (range 23–32).

Twelve of them (75%) developed hyponatraemia (< 130 mmol/l). The minimum serum sodium of all patients was 110–136 mmol/l (mean (SD) 125.8 (6.3) mmol/l). The maximum amount of liquor tapped a day was 3–34 ml (mean 15.6 ml). The resulting daily loss of sodium in the tapped liquor was 0.4–3.7 mmol/kg/day (mean (SD) 1.98 (0.94) mmol/kg/day). The extent of the hyponatraemia (minimal serum sodium) correlated significantly with the maximum daily sodium loss in liquor (r = 0.78, p < 0.001, fig 1).

Further analysis of the use of drugs—for example, thiazides—did not contribute to this correlation. Two children with hyponatraemia developed general hypotonia with poor feeding; this prompted further diagnostic measures to exclude syndrome of inappropriate antidiuretic hormone (SIADH) or excessive sodium loss in urine. The investigations were negative. Both children showed normal neurology after adequate replacement of the sodium lost. No child with hyponatraemia developed other acute neurological symptoms such as seizures.

This is the first report of hyponatraemia as a consequence of serial liquor punctures with a ventricular access device in children.3 The sodium loss was sometimes as high as the normal sodium requirement per day (3–5 mmol/kg/day).

Hyponatraemia in children caused by the use of a ventricular access device should be managed carefully and the sodium replaced promptly. Loss of sodium by serial liquor tapping must be taken into the differential diagnosis of hyponatraemia in preterm infants.

Figure 1

Relation between serum sodium concentration and maximum sodium loss in the liquor (r = 0.78, p < 0.001).

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