Sildenafil Citrate Therapy for Oligohydramnios: A Randomized Controlled Trial

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We read the article by Maher et al1 with great enthusiasm. The present study has shown improvement in the amniotic fluid index after sildenafil addition to hydration therapy. This benefit has opened up a plethora of possible physiologic mechanisms, including an improvement in uteroplacental and fetal renal blood flow.
Pregnancy alters the cardiovascular hemostasis to sustain the fetus. This alteration comprises an increase in blood volume and cardiac output and a decrease in systemic vascular resistance.2 The stressed blood volume may increase during pregnancy owing to splanchnic venous compression by the pregnant uterus. A further addition of substantial intravenous saline would push the Frank-Starling curve to the extreme right, leading to inappropriate elevation in left ventricular end diastolic pressure and, thus, would put the patient at risk for pulmonary edema and tissue edema.3,4 This generalized edema has the potential to impair systemic and tissue oxygenation.
Apart from uteroplacental vasodilatation in pregnancy, the extent of systemic vasodilatation and fetal vasodilatation could not be ascertained. Nevertheless, the addition of hydration therapy definitely would prevent the fall in systemic blood pressure after sildenafil treatment. Furthermore, sildenafil increases the venous capacitance to allow more intravenous fluid without a significant increase in central venous pressure and mean capillary filling pressure. However, an exaggerated increase in central venous pressure and systemic blood pressure after hydration therapy should be anticipated in patients with preeclampsia.
The status of amniotic fluid is mainly determined by the fetal kidney excretion system. Therefore, an improvement in fetal blood pressure and renal blood flow becomes essential for the augmentation of fetal kidney function. The fetal myocardium is nonaccommodative, and, therefore, fetal cardiac output and blood pressure may not improve with an increase in venous return.5 Thus, it seems that relative blood volume deficiency and systemic vasoconstriction in the fetus could be the contributing factor for oligohydramnios.
The fetal cardiac output is mainly improved by an increase in heart rate.6 Stroke volume is almost fixed during fetal life; however, in a volume-deficient fetus, an augmentation in fetal cardiac output could be achieved by improvement in venous return through the Frank-Starling mechanism.7 Fetal renal blood flow and pressure can improve only by improvement in fetal cardiac output. Although placental transfer of sildenafil has not been quantified, owing to its chemical characteristics it is likely to cross the placenta easily. Resistivity index of umbilical and fetal renal artery has been associated with hourly urine output by the fetus.8 Therefore, it is likely that sildenafil could have lowered the resistivity index of umbilical and fetal renal artery. The systemic vasodilatation by sildenafil in the fetus could have augmented the fetal heart rate through reflex mechanism. Fetal heart rate monitoring appears reasonable during this treatment protocol. Furthermore, sildenafil may cause maternal and fetal pulmonary artery vasodilatation and physiologic shunting. The exact mechanism of oligohydramnios is still unknown, and the present study has excluded several possible etiopathogenetic factors responsible for oligohydramnios; therefore, generalization of the present finding merits reconsideration.
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