CME Module 2: Amniotic Fluid Embolus, Obstetrics Next >


The Case


A 32 year old Para 1 Gravida 2 was admitted to hospital in active labor at 40 weeks gestation. Prior to admission she had spontaneous rupture of membranes. Six hours later she underwent an uncomplicated spontaneous vaginal delivery without any requirement for analgesia. The amniotic fluid was noted to be clear at the time of delivery. Immediately post delivery the patient complained of mild dyspnea and appeared restless and agitated. Auscultation of her chest revealed bilateral air entry with no adventitious sounds. Oxygen saturation was 90% on room air. She was treated with supplemented oxygen by face mask which resulted in an increase in oxygen saturation to 98%. In light of her rapid improvement, no further treatment or investigations were deemed necessary. However, 4 hours later the patient once again complained of shortness of breath and at this time was noted to be both tachycardic and tachypneic. Supplemental oxygen was again administered with improvement in her oxygen saturation from 84 to 90%. Her heart rate was 124 and BP was stable at 130/80. Chest examination revealed that she now had bilateral inspiratory crackles and chest x-ray confirmed extensive alveolar infiltrates. EKG was unremarkable except for sinus tachycardia. Blood gases revealed PH 7.48, PaO2 60 on 40% ventimask, and PCO2 31. At this point the etiology of her respiratory distress was unclear but included pulmonary infection, aspiration, embolism (thrombotic or amniotic fluid), acute myocardial infarction and peripartum cardiomyopathy.

The patient was transferred to the ICU where she continued to deteriorate from both a respiratory and cardiovascular standpoint. Intubation and mechanical ventilation were instituted. Abundant proteinaceous secretions were suctioned from the ETT. These were analyzed and found to have a protein content of 68 grams/liter while the simultaneous plasma level was 78 grams/liter. Hemodynamic instability required fluid therapy, vasopressors and invasive monitoring including an arterial line and Swan Ganz catheter. The initial PA pressure were 39/24 and the PCWP was 19mmHg. Transthoracic echocardiography revealed mild left atrial enlargement, global hypokinesis and decreased ejection fraction to 32%, all consistent with left ventricular failure. Following treatment with lasix and low dose dopamine infusion, the PCWP returned to normal at 10mmHg. Aspiration of blood from the pulmonary microvasculature revealed several components of amniotic fluid including squamous cells, lanugo hair, mucin strands and amorphous material.

Although initial coagulation parameters on admission to ICU revealed the presence of a consumptive coagulopathy, the patient never developed any clinical evidence of bleeding. She was gradually weaned from the ventilator and discharged from hospital 10 days later. Two months postpartum repeat pulmonary function tests and echocardiogram were completely within normal limits.


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