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Letters to the Editor

Indian Pediatrics 2000;37: 449-450

Magnesium Sulphate for Persistent Pulmonary Hypertension in Newborns


Persistent pulmonary hypertension of the newborn (PPHN) is charaterized by increased pulmonary vascular resistance resulting in right to left shunting across the fetal channels. The resulting hypoxemia and acidosis lead to pulmonary vasoconstriction worsening the problem. A variety of treatment modalities including vasodilators have been used. Mag-nesium sulphate, though not a selective pulmo-nary vasodilator, may have potential benefits in treatment of PPHN. In this communication, we share our experience of using magnesium sulphate in PPHN.

The subjects of this study included 9 newborn babies who had persistent duskiness or frequent color changes and oxygen satura-tions less than 90% on head box oxygen, not explained adequately by their respiratory status. Clinical details like birth weight, gestational age, associated conditions like perinatal asphyxia, meconium passage in utero, polycythemia and sepsis were noted. Pulmonary artery pressure (PAP) was estimated from peak velocity of tricuspid regurgitation on a portable Doppler echocardiography machine (Esaole Biomedica SIM 5000 D plus). Magnesium sulphate was given as an infusion over 4-6 hours in a dose of 50 mg/kg/h (without a loading dose) for 3-4 days. Adrenaline was administered as an infusion 0.2 mg/kg/min to counter the possibility of hypotension caused by magnesium sulphate.

The birth weight and gestational age ranged between 2-3.4 kg and 36-40 weeks, respectively. Six babies had perinatal asphyxia (mild in 3, moderate in 1 and severe in 2). Liquor was meconium stained in 6 babies. Two babies had hematocrit more than 65. PAP ranged between 46 and 93 mmHg. No baby had structural heart defect or evidence of right-to-left shunt. All babies favorably responded to magnesium sulphate infusion in terms of improvement in oxygen saturation above 93%. Mean response time was 20 minutes and duration of treatment ranged between 3-6 days. In four babies repeat echocardiography was possible and showed decline in PAP. Two babies died. Both were severely asphyxiated and were low birth weight. Chest skiagram revealed cardiomegaly and pulmonary edema, and the other showed evidence of meconium aspiration syndrome. No baby was excessively sedated or had respiratory depression following magne-sium sulphate infusion.

Doppler echocardiography allows indirect estimation of PAP. Usefulness of PAP estima-tion from tricuspid regurgitation jet peak velocity has been adequately validated(1). However, in one study(2), in 30% of neonates with suspected PPHN, the above method failed to obtain initial measurements. Some of these neonates were found to have high PAP by other methods.

Magnesium the natural calcium blocker, antagonizes calcium ion entry into smooth muscle cells, thus promoting vasodilatation. It may also exert its favorable influence on nitric oxide synthetase, cyclic nucleotides, endo-thelins and prostaglandins(3). Abu-Osba and collea-gues successfully treated hypoxia-induced PPHN in sheep by using magnesium sulphate(4). Subsequently, they treated 9 newborns with severe PPHN. Magnesium sulphate was chosen as a therapy after the infants failed to improve with conventional treatment and other vasodilators. At 6 hours, both the PaO2, oxygen saturation and arterial pH improved significantly. Seven of the nine infants survived(5). Magnesium sulphate may have helped due to sedative, muscle relaxant, bronchodilator effects or increasing alkalosis associated with it.

In our study, right-to-left shunt was not demonstrated on echocardiography. This may be because we started magnesium sulphate without waiting for echocardiograms, since it often took 6-8 hours to organize these studies. All the babies showed prompt improvement in oxygen saturations and 7 out of 9 patients survived. It would have been ideal to assess the severity by alveolar arterial oxygen gradient. However, it was not possible since facility for blood gas analysis was not available. We used smaller dose of magnesium sulphate and avoided the bolus to avoid respiratory depression, since these babies were not mechanically ventilated. However, the results of this study need to be confirmed in controlled trials.

S.R. Daga,
B. Verma,
R.G. Lotlikar,

Pediatric Unit,
Cama and Albless Hospital,
Mumbai 400 001, India.

 References

1. Skinner JR, Stuart AG, O’Sullivan J. Heads A, Boys RJ, Hunter S. Right heart pressure determination by Doppler in infants with tricuspid regurgitation. Arch Dis Child 1993; 69: 216-220.

2. Skinner JR, Hunter S, Hey EN. Hemodynamic features at presentation in persistent pulmonary hypertension of the newborn and outcome. Arch Dis Child 1996; 74: F26-F32.

3. Patole SK, Finer NN. Experimental and clinical effects of magnesium infusion in the treatment of neonatal pulmonary hypertension. Magnesium Research 1995; 8: 373-388.

4. Abu-Osba YK, Rhydderch D, Balsundasam S, Galal O, Rajjal A, Halees Z, et al. Reduction of hypoxia induced pulmonary hypertension (HIPN) by MgSO4 in sheep. Pediatr Res 1990; 27: 351A.

5. Abu-Osba YK, Galal O, Manasra K, Rajjal A. Treatment of severe pulmonary hypertension of the newborn with magnesium sulphate. Arch Dis Child 1995; 67: 31-35.

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