A 26-year-old woman with respiratory decompensation in the immediate postpartum period at Mount Sinai Medical Center in New York City

Abstract

A 26-year-old previously healthy woman developed sudden-onset hypoxaemic respiratory failure 3 days post partum. During pregnancy, the patient had displayed haematuria (26–50 red blood cells/high-power field on urine dipstick) and proteinuria (30 mg/dL on urine dipstick), which at the time was not further investigated. The pregnancy and vaginal delivery were otherwise uncomplicated. On the morning of planned discharge from the maternity ward, the patient developed sudden dyspnoea, tachypnoea, tachycardia and severe hypoxaemia (PaO2 of 48 mm Hg on room air) accompanied by 5 mL of bright red haemoptysis. Chest auscultation was normal. ECG showed sinus tachycardia with an S1Q3T3 pattern and urgent bedside echocardiogram showed evidence of right heart strain. Respiratory insufficiency in the peripartum period has many potential causes, including PE, amniotic fluid embolism, pulmonary oedema due to tocolytic therapy and peripartum cardiomyopathy. Venous thromboembolism (VTE) is approximately 80 times more common in the first week post partum when compared with the general population1 and PE is a leading cause of maternal mortality in the developed world (whereas postpartum haemorrhage is the most common cause of death in the developing world2). Haemoptysis in the setting of PE occurs in about 5% of patients, and represents pulmonary infarction.3 Given the acute onset of symptoms and echocardiographic findings, PE is the initial concern for this patient. Unfractionated heparin infusion was started. Shortly thereafter, the patient endorsed worsening dyspnoea and coughed up approximately 100 mL of bright red blood. Her heparin infusion was discontinued, and she was emergently intubated for hypoxaemia. Adequate oxygenation on the mechanical ventilator was difficult to maintain despite frequent endotracheal suctioning, use of high positive end-expiratory pressure and fraction of inspired oxygen (FiO2), initiation of neuromuscular blockade and frequent manual recruitment manoeuvres. Chest X-ray (CXR) showed diffuse, predominantly central opacities (figure 1 …