Cranial diabetes insipidus (DI) is a rarely reported complication of severe intraventricular hemorrhage (IVH). It needs for its diagnosis in the neonatal period. One such case reported in this communication.

A male baby was born at 29 weeks of gestation to a 35-year-old mother by emergency cesarean section which was necessitated because of prolonged rupture of membrane, maternal sepsis, foetal bradycardia and breech presentation. Despite antenatal steroid the baby had a stormy initial period as he developed respiratory distress and subsequently Persistent Pulmonary Hypertension of Newborn

(PPHN) needing high ventilatory supports, inotropes and prostacyclin to stabilise. He had a further episode of severe desaturation and bradycardia along with tonic convulsion on day 2. Cranial ultrasound scan confirmed suspected intracranial bleed with a bilateral Grade (IV) IVH and midline shift.

On day 8 hypernatremia (Na = 158 meq/L) was noted which persisted despite increasing the total fluids to 180 ml/Kg/day. As he was also noted to have polyuria (5 to 7 ml/Kg/hr) and dropping body weight further bio-chemical tests were performed which revealed persistently raised serum osmolarity in comparison to urine osmolality (Table I). A central cause of DI was suspected due to significant weight loss, persistent hypernatremia, increased urinary output, low urine osmolality and grade (IV) bilateral IVH which was confirmed by intranasal Desmopressin (DDAVP) Challenge (Table I).

He was started on intranasal DDA VP the dose of which had to be adjusted frequently in accordance with his biochemical parameters. MRI scan done at corrected age of 38 weeks gestation revealed gross sequel of IVH with an intact hypothalamus and pituitary. A trial to stop DDAVP at the age of 7 months (corrected age 4.5 months) unfortunately failed. At present he is maintaining a stable biochemistry on a dose of DDAVP 3 µg (0.52 µg/kg) with steady weight gain on the 9th centile.

The main etiological factors reported in neonatal cranial DI have been asphyxia, severe infections, CNS abnormalities and rarely IVH(1). Lack of Anti-diuretic Hormone (ADH) secretion due to impairment in the functions of magnacellular neurons from supraoptic and paraventricular nuclei is postulated to be the basic pathogenesis(2).

Diagnosis of cranial DI in neonate is extremely challenging and requires high index of suspicion(2). Hypernatremia is not unusual particularly in sick preterm but persistent hypernatremia not resolving despite increased fluid intake should be an important red flag. The combination of weight loss, hypernatremia, increased urinary output and low urine osmolality compared to serum has been suggested to indicate DI in newborns(3). These were present in our baby and awareness of this lead us to a trial of DDAVP which clinched the diagnosis. A medline search of articles in English literature revealed only two surviving baby with IVH as a cause of cranial DI(4,5). This might be related to the fact that IVH resulting in cranial DI are usually life threatening as well as the degree of difficulty in diagnosing it.

Rajiv Sinha,
Peter Martin,
St Peter’s Hospital,
Chertsey, UK.

1. Wang LC, Cohen ME, Duffner PK. Aetiologies of Central diabetes insipidus in children Pediatr Neurol 1994 ; 11: 273-277.

2. Krebes VL, Damiani D, Diniz EM, et al. Central diabetes insipidus as a complication of neonatal pathology: report of three cases. Acta Paediatrica Japonica 1998; 40: 146-149.

3. Giacoia GP, Watson S, Karathanos A. Treatment of neonatal diabetes insipidus with desmopressin Southern Med J 1984; 77: 75.

4. Atasay B , Berberoglu M, Gunlemez A, et al. Management of central diabetes insipidus with oral desmopressin in a premature neonate. Journal of Pediatric Endocrinology & Metabolism 2004; 17: 227-230.

5. Yu VHY. Treatment of neonatal diabetes insipidus with desmopressin Aust Pediatr J 1980; 16: 284-286.