Acute Lung Oedema in Severe Pre-eclampsia: Advanced Management and Anesthetic Interventions

Introduction: Acute Lung Oedema (ALO) during pregnancy is an uncommon but potentially life-threatening condition, particularly when associated with severe pre-eclampsia. This critical obstetric emergency requires prompt recognition and comprehensive management to prevent adverse maternal and fetal outcomes. Objective: This report aims to highlights the management of a complex case of ALO in a pregnant patient with severe pre-eclampsia, underscoring the essential role of multidisciplinary collaboration, evidence-based protocols, and individualized care in achieving favorable outcomes. Case Report: A 30-year-old woman at 29–30 weeks gestation presented with significantly reduced consciousness and severe shortness of breath. Clinical examination revealed hypertension, tachycardia, and profound hypoxemia, with radiological evidence of pulmonary oedema. The diagnosis included severe-feature pre-eclampsia complicated by acute respiratory distress syndrome (ARDS) secondary to ALO. Endotracheal intubation was used to protect the mother's airway, mechanical ventilation was used to help her get enough oxygen, and her blood pressure and heart rate were stabilized right away. Fluid therapy was carefully monitored to avoid exacerbating pulmonary oedema. Obstetric management prioritized delaying delivery until maternal stabilization was achieved. A surgical intervention under general anesthesia resulted in the delivery of a moderately distressed neonate. Postoperative care in the intensive care unit included continued mechanical ventilation, sedation, and meticulous fluid management. Gradual stabilization allowed for successful weaning off ventilatory support, extubation, and transfer to a general hospital ward. Discussion: Management strategies were guided by the ABCDE principle, targeting reductions in left ventricular preload and afterload, adequate oxygenation, and infection prevention. The case emphasizes the value of early diagnosis, prompt intervention, and interdisciplinary collaboration involving obstetricians, intensivists, and anesthetists. Conclusion: This case illustrates the importance of early recognition, swift intervention, and tailored care in managing ALO associated with severe pre-eclampsia. Comprehensive, team-based approaches are critical for optimizing maternal and neonatal outcomes in such high-risk scenarios.

INTRODUCTION

Acute lung oedema (ALO) in pregnancy is a rare but life-threatening condition with high maternal and perinatal morbidity and mortality and is one of the complications of pre-eclampsia with an incidence ranging from 0.08% to 1.5% (¹,²) The definitive treatment for pre-eclampsia is delivery (³). We report a case of severe pre-eclampsia complicated by pulmonary edema, in which delivery was delayed for maternal stabilization before a caesarean section under general anesthesia was performed.

The objective of this case report is to discuss the management of ALO in pregnancy complicated by severe pre-eclampsia, highlighting how important it is to use evidence-based multidisciplinary approaches to improve outcomes for both the mother and the baby.

CASE REPORT

A 30-year-old pregnant female with a decrease in consciousness for the past hour was referred to the anesthesiology department due to termination of pregnancy. The patient complained of severe shortness of breath, followed by a gradual decline in consciousness, and was unresponsive when examined. The patient was on her 7th pregnancy of 29-30 gestational weeks, had a bad obstetric history due to 5 abortions, and had no children. The fetal movement was within normal limits with a fetal heart rate of 158 bpm. The patient had a history of hypertension for the past week and has been taking methyldopa 3 x 500 mg and nifedipine 3 x 10 mg. History of other problems was denied.

Figure 1.Chest X-ray

The physical examination revealed consciousness was stupor (GCS E1M2V1), blood pressure was 175/111 mmHg, heart rate was 156 bpm, respiratory rate was 36 bpm, SpO₂was 63% with NRM 15 lpm. Body mass index was 29.77 kg/m²(overweight), with vesicular breathing sounds accompanied by crackles in both lungs and dullness to percussion of the lungs. The laboratory result was within normal limit with hemoglobin 9.8 g/dL, and urine protein +1. The thoracic x-ray revealed cardiomegaly with pulmonary oedema. The blood gas analysis showed pH was 6.97, pCO₂was 109.7 mmHg, pO₂was 70 mmHg, HCO₃was 25.4 mmol/L, BE was -6, SO 2 C was 80%, and lactate was 4.60 mmol/L.

The diagnosis was G7P1A5, gravida 29 -30 weeks with severe feature pre-eclampsia, and acute respiratory distress syndrome (ARDS) due to ALO. Early management was endotracheal intubation with ETT No. 7.0, oxygenation, transport of the patient to the ICU, and ventilator mode AC PC Pi 19 RR 16 PEEP 8 FiO2 100% for the first hour and then tapering of the FiO₂. The patient was in head up position of 30˚, given IVFD Ringer lactate 20 cc/hour, fentanyl 10 mcg/hour, propofol 100 mg/hour, rocuronium 20 mg/hour, omeprazole 2 x 40 mg IV, furosemide 40 mg IV loading dose followed by 5 mg/hour IV, nebulized combivent and Pulmicort / 8 hours.

In the next 8 hours, the patient's blood pressure was 125/87 mmHg, HR 105 bpm, RR 16 bpm, peripheral saturation was 98 % (AC PC Pi 19 RR 16 PEEP 8 FiO₂60%). The P/F ratio was 245. The blood gas analysis showed pH 7.33, pCO₂39.2 mmHg, pO₂147 mmHg, HCO₃22 mmol/L, BE was -5, and SaO₂99%. Urine output was 2.63 cc/kg/hour, with a balance was (-) 1558 cc. We tried to wean off the ventilator and sedation drugs. Four hours later, the patient's consciousness was E4M6Vett, blood pressure 137/94 was mmHg, HR was 95 bpm, RR was 22 bpm, SpO₂was 98% (SIMV PC Pi 19 RR 10 PS 12 PEEP 8 FiO₂40%). Echocardiography showed EF 49%, global normocinetic, valve within normal limits, TAPSE 20, and IVC 18. We planned to terminate the pregnancy.

Caesarea section was performed under general anesthesia, induction with propofol 100mg, fentanyl 100 mcg, and relaxant using rocuronium 20 mg, all intravenously. The procedure lasted approximately 2 hours and the baby was born with an APGAR SCORE of 4/6 with a birth weight of 1100 grams. Postoperatively the patient was sedated in the ICU with ETT retention. Breathing was fully controlled with a ventilator until 6 hours postoperatively with ventilator mode AC VC Pi 18 RR 14 PEEP 8 FiO₂50%. Furosemide still administered of 5 mg/hour with six hours postoperatively, the ventilator and sedation were weaned. The patient was fully conscious and extubated one day postoperatively.

Figure 2.Chest X-ray Post Intubation

DISCUSSION

Pulmonary edema is defined as the abnormal accumulation of extravascular fluid in the lung parenchyma (⁴,⁵). Pulmonary edema can be characterized as either cardiogenic or non-cardiogenic. Pregnancy causes physiological changes that increase the risk of developing pulmonary edema (⁵,⁶). ALO in pregnant women is an uncommon yet life-threatening occurrence.

During a normal pregnancy, both pulmonary and systemic vascular resistance drop dramatically. The gradient between colloid osmotic pressure and pulmonary capillary wedge pressure lowered by around 30%, increasing the susceptibility of pregnant women pulmonary oedema. Pulmonary oedema is caused by either an increase in cardiac preload (such as fluid infusion) or increased pulmonary capillary permeability (such as in pre-eclampsia), or both (⁶,⁸,⁹).

Figure 3.Management Pathway of Acute Pulmonary Oedema in Pregnancy (¹⁰)

Preeclampsia is a frequent cause for obstetric patients to be admitted to the intensive care unit (ICU), and ALO can pose a life-threatening risk for those with preeclampsia (¹¹,¹²) In

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