Anesthetic management of a case of severe pre-eclampsia with antepartum hemorrhage with pulmonary edema for caesarean section.

Pulmonary edema is a rare complication of pre-eclampsia. We report a case of severe pre-eclampsia with abruptio placentae with intra-uterine fetal demise, complicated by pulmonary edema, managed under general anesthesia for caesarean section.

INTRODUCTION

Pulmonary edema rarely occurs in normal pregnancy.[1] Its incidence increases with the presence of obstetric complications like pre-eclampsia (2.9% to 3.4%)[23] or during the treatment of preterm labor (as high as 5%).[4] We report a case of severe pre-eclampsia with antepartum hemorrhage complicated with pulmonary edema, managed under general anesthesia for caesarean section.

CASE REPORT

A 20-year-old primigravida at 28 weeks gestation with severe pre-eclampsia on treatment, presented with abdominal pain since 1 day with bleeding per vagina. She was diagnosed to have abruptio placentae with IUD. In the labor room, she developed respiratory distress. On examination, heart rate was 130/min, blood pressure was 180/110 mm Hg, respiratory rate was 36/min, and auscultation revealed bilateral crepitations. Patient was diagnosed to have pulmonary edema. Arterial blood gases showed metabolic acidosis with hypoxia. Patient was given intravenous (IV) furosemide 20 mg and noninvasive ventilation on a portable ventilator with positive end-expiratory pressure (PEEP) 6 and pressure support 12. IV labetalol 20 mg was given slowly. Her condition did not improve; SPO2 started dropping below 80%. In view of worsening condition, it was decided to perform an emergency caesarean section.

Preoperative SPO2 was 82% it increased to 92% with 100% O2. Rapid sequence induction was done with IV thiopentone sodium 3 mg/kg and IV suxamethonium 1.5 mg/kg. Pt was intubated with a 7.5 number cuffed endotracheal tube. Anesthesia was maintained with O2 + air + sevoflurane 0.6-0.8%. A central venous catheter was passed in the right internal jugular vein to guide fluid management. Following delivery of the fetus, IV oxytocin infusion was started. Patient was given IV vecuronium 5 mg, and IV buprenorphine 180 mcg for analgesia. Patient received 50 mL of HES and 50 mL of Ringer's lactate intra operatively.

At the end of surgery, patient was shifted to the ICU unreversed and put on a ventilator on pressure control mode, curarised with IV vecuronium. Chest radiograph showed bilateral pulmonary infiltrates. ABG revealed metabolic acidosis. Blood pressure was 192/110 mm Hg. A propofol 1 mg/kg/h + fentanyl 1 mcg/kg/h infusion was started. Blood pressure was not controlled, so patient also was started on IV labetalol infusion @ 10 mg/h. Serial ABGs showed improvement in the acid–base status. Over the course of 2 days patients’ vitals stabilized, and the infusions were gradually tapered and stopped. Patient was put on SIMV mode the third postoperative day, and gradually weaned; extubated on the fifth postoperative day and transferred to the general ward.

DISCUSSION

Pulmonary edema is rare in the general obstetric population, occurring in around 0.05% of pregnancies. However, this incidence increases substantially with the presence of conditions such as multiple gestation, pre eclampsia, and tocolytic treatment.

Pulmonary edema may rarely occur in association with preeclampsia (i.e., perhaps 3% of pre-eclamptic patients). The pre-eclamptic patient is usually volume depleted, and pulmonary edema most commonly occurs in the early postpartum period and is often associated with aggressive, intrapartum fluid replacement. Other factors that may contribute to the pathogenesis include reduced serum albumin, elevated left ventricular afterload, and systolic and diastolic myocardial dysfunction. Increased capillary permeability may also occur, aggravated by concomitant conditions such as sepsis, abruptio placentae, or massive hemorrhage.

If pulmonary edema develops, its treatment includes oxygen, diuretics, fluid restriction to achieve reduction of preload and after load, and intermittent positive pressure ventilation.[56] As maternal oxygen reserve is decreased in pregnancy, significant arterial desaturation will occur if the patient becomes apneic for even a short time. Such episodeincreases the hypoxic risk to the fetus as well. Mechanical ventilator should be adjusted to maintain the PCO2 in the range of 30 to 32 torr. Available data on permissive hypercapnic ventilation in pregnant patients is limited, although maternal PCO2 up to 60 torr has not been shown to be detrimental to the fetus.

A multi modal treatment that ensures an optimal oxygenation and stable hemodynamics with the lowest amount of fluid seemed to be justifiable. In the absence of complete understanding of the pathogenesis of the pulmonary edema, to reduce maternal and fetal complications, management is based mainly on the treatment of symptoms and signs of the secondary effects of pre eclampsia. The management of these patients should ideally be multidisciplinary and the anesthetist should be involved in the care of patients from the early stage.[7]