CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 5, September/October 2022 AFRICA 273 Fatal pulmonary oedema associated with severe pre-eclampsia: challenges and lessons Nnabuike Chibuoke Ngene, Jagidesa Moodley Abstract Pre-eclampsia complicated by pulmonary oedema, severe hypertension, tachycardia and desaturation is a devastating condition. A comprehensive understanding of the aetio-pathogenesis during such an emergency is challenging in the absence of functional and responsive point-of-care imaging, and laboratory and other critical-care services. An unbooked 26-yearold gravida 3 para 1+1 presented to a primary healthcare clinic with features of pre-eclampsia, severe hypertension and pulmonary oedema. The only available antihypertensive drug, methyldopa, was administered. The patient was transferred to a district hospital and subsequently referred to a tertiary hospital. On arrival, she was booked for caesarean delivery and in the maternity ward a central venous pressure (CVP) line was inserted. The patient developed pneumo-thorax and died in the intensive care unit undelivered. This case highlights many lessons, which are discussed. If CVP monitoring is indicated before caesarean delivery, consideration must be given to line insertion in the operating room to facilitate rapid delivery should the patient’s condition deteriorate. Keywords: central venous pressure, dyspnoea in pregnancy, maternal distress, pre-eclampsia with severe features, pulmonary oedema, sympathetic crashing acute pulmonary oedema Submitted 9/3/21, accepted 13/12/21 Published online 17/2/22 Cardiovasc J Afr 2022; 33: 273–276 www.cvja.co.za DOI: 10.5830/CVJA-2021-064 Pulmonary oedema (PulmE) is a severe complication of pre-eclampsia (PE) and can result in fatal pregnancy outcomes.1 The South African Saving Mother’s Report (2014–2016) indicated that PulmE accounted for 30% of all maternal deaths due to hypertensive disorders of pregnancy.2 Increased vascular permeability due to endothelial damage, decreased intravascular oncotic pressure, lymphatic insufficiency and high capillary hydrostatic pressure from conditions such as hypertension are possible pathophysiological mechanisms of PulmE in PE.3,4 The occurrence of PulmE indicates dysfunction in one or many organ systems, such as respiratory, haematological, cardiovascular, hepatobiliary and renal systems. It interferes with gas exchange, causing hypoxaemia and hypercapnia, which may affect other organ systems. Therefore, the cause and potential sequence of events are difficult to discern, particularly if there is a lack of information about the proceeding clinical condition, and the inability to perform special investigations, such as pointof-care imaging. The management is therefore challenging and judicious therapy is required to prevent further complications.5 In such circumstances, delivery must be expedited to avert poor perinatal and maternal outcomes. We present a case of severe PE complicated by PulmE and hypokalaemia, which resulted in maternal mortality. Learning points are discussed, which will assist clinicians in the clinical management of PE with severe features such as PulmE. Case report A 26-year-old gravida 3 para 1 with one previous miscarriage, who had not commenced antenatal care, presented to a primary healthcare clinic at 34 gestational weeks with cough of five months’ duration, a history of severe headache and difficulty in breathing for a day. On examination, she had respiratory distress, bilateral pedal oedema, blood pressure (BP) of 155/118 mmHg and a fundal height measurement of 29 cm. The patient was given the only available antihypertensive drug, oral alpha methyldopa 1 g, and referred to a district hospital. Two hours later, the patient arrived at the district hospital, where she was found to have dizziness, persistent headache, mild respiratory distress, body temperature of 36.2°C, pulse of 76 beats per minute (bpm), BP of 154/114 mmHg, proteinuria of 1+, deterioration in oxygen saturation from 98 to 86%, bilateral respiratory wheezes and subsequently bilateral chest crepitations. Obstetric examination revealed a singleton live foetus at 34 gestational weeks, which was confirmed on ultrasonography. The diagnosis was PE complicated by PulmE. An indwelling urinary Foley catheter was inserted and she received co-amoxiclav, intravenous furosemide6 and nebulised salbutamol. The oxygen saturation improved from 86 to 94% following the administration of furosemide. She was placed on supplemental oxygen nasally. Magnesium sulphate (MgSO4) 4-g infusion and 5 g in each buttock intramuscularly7 were administered and the patient was referred to a tertiary hospital. In the next five hours, the patient arrived at the tertiary hospital still dyspnoeic with the Foley catheter draining clear urine. Her pulse was 119 bpm, BP was 81/50 mmHg, mean arterial pressure was 60 mmHg, respiratory rate was 44 breaths/ Department of Obstetrics and Gynaecology, School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg; and Department of Obstetrics and Gynecology, Leratong Hospital, Krugersdorp, South Africa Nnabuike Chibuoke Ngene, MB BS, Dip Obst (SA), Dip HIV Man (SA), MMed (Fam Med), FCOG (SA), MMed (O&G), PhD, ngenenc@gmail.com Women’s Health and HIV Research Group, Department of Obstetrics and Gynecology, School of Clinical Medicine, Faculty of Health Sciences, University of Kwa Zulu-Natal, Durban, South Africa Jagidesa Moodley, MB ChB, FCOG (SA), FRCOG, MD
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