Emergency caesarean section with careful haemodynamic management and general anaesthesia can successfully manage acute pulmonary edema in a parturient with severe preeclampsia and previously unoptimized mitral valve prolapse.
Dear Editor, Hypertensive disorders in pregnancy, such as chronic hypertension, gestational hypertension and preeclampsia, cause complications in about 5%–10% of pregnancies.[1] We report a case of preoperative pulmonary oedema in a primigravida with twin gestation and severe preeclampsia diagnosed with mitral valve prolapse and moderate mitral regurgitation. A 25-year-old parturient at 36 weeks of gestation was rushed from the emergency room to the operation theatre, given active labour and foetal distress. She gave a history of a recent diagnosis of hypertension, for which she was on oral labetalol 100 mg thrice a day for the last seven days. The echocardiography revealed mitral valve prolapse, moderate mitral regurgitation and mild pulmonary artery hypertension. Given the increasing trend of blood pressure (200/120 mmHg), intravenous labetalol 20 mg, magnesium sulphate 4 g and furosemide 20 mg were administered. In the operating room, the patient had complaints of severe breathlessness, fever and productive cough with crepitations on auscultation, for which head-end elevation with oxygenation followed by intravenous furosemide 40 mg was administered. Simultaneously, all standard monitors, including a five-lead electrocardiogram (ECG), non-invasive blood pressure (NIBP), pulse oximeter and capnograph, were attached. Baseline vitals were blood pressure of 160/110 mmHg, pulse rate of 110 beats/min and oxygen saturation (SpO2) of 85% on room air with tachypnoea of 35 breaths/min. Intravenous nitroglycerine bolus 1 mg was administered. Emergency caesarean section was planned under general anaesthesia after obtaining written informed high-risk consent because of foetal distress, valvular heart disease and pulmonary oedema. Rapid sequence induction was performed with arterial and central venous cannulation for invasive blood pressure monitoring and fluid management. After tracheal intubation, pink froth was observed in the tube with increased airway pressure. Loud audible crackles could be heard. Intravenous nitroglycerine infusion (0.5–4 µg/kg/min) and bolus doses of furosemide amounting to a total of 100 mg (over an interval of 2 min) were administered to manage a significant rise in blood pressure (~190/120 mmHg). Approximately 200 ml of pink frothy fluid was suctioned endotracheally. Anaesthesia was maintained with sevoflurane (0.8%–1%) with oxygen and air mixture at 50:50 concentration. After the delivery of twins, gradual improvement in airway pressures with a reduction of blood pressure (150/100 mmHg) and crackles was noted. Midazolam 1 mg and morphine 3 mg were administered intravenously post-delivery of two healthy male babies, along with oxytocin 20 IU administered intravenously in 100 ml normal saline. Post-surgery, the patient was shifted to the intensive care unit (ICU) for elective overnight ventilation because of bilateral crepitus. The trachea was extubated uneventfully on postoperative day 1. Pulmonary oedema is a life-threatening condition associated with preeclampsia in 0.08%[2] and severe preeclampsia in 2.9% of cases.[3] Pulmonary oedema is classified into two types – cardiogenic and non-cardiogenic. Our patient had both; recently diagnosed non-optimised cardiac conditions of mitral valve prolapse with moderate mitral regurgitation and severe preeclampsia. She came to the emergency room in foetal distress, giving us no time to optimise her, making it an anaesthetic challenge. The pathogenesis of pulmonary oedema in severe preeclampsia is explained by hypervolaemia, left ventricular failure and pulmonary capillary leakage.[4] Other causes include underlying cardiac disease, fluid overload and tocolytic use of drugs like magnesium sulphate. Uncontrollable blood pressure, foetal distress, placental abruption, declining renal function, HELLP (haemolysis [H], elevated liver enzymes [EL] and low platelets [LP]) syndrome and chronic severe systemic symptoms are all conditions necessitating emergency termination of pregnancy.[5] In the present case, mitral valve prolapse leading to moderate mitral regurgitation may have increased intravascular hydrostatic pressure in the lung’s blood vessels, ultimately leading to pulmonary oedema. This article also highlights that cardiac disease becomes evident in the later stages of pregnancy, after which the patient decompensates. So, diagnostic tools like echocardiograms done earlier can be of enormous help in prevention and early management in such cases. Oxygen therapy, intravenous fluid restriction, furosemide and central haemodynamic monitoring are crucial. Control of high blood pressure with intravenous antihypertensives is recommended. Furosemide is recommended for its vasodilation and diuretic property. Sodium nitroprusside, nicardipine, nifedipine, prazosin and hydralazine can also be considered.[4-6] Urgent termination of pregnancy with tracheal intubation successfully prevented maternal and foetal morbidity and mortality in our case. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
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Shah et al. (2023) studied this question.
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