SESSION TYPE: Critical Care Case Report Posters
PRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM
INTRODUCTION: Amniotic fluid embolism (AFE) is a potentially devastating clinical syndrome characterized by hypoxia, shock, disseminated intravascular coagulopathy (DIC), and altered mental status .
CASE PRESENTATION: A previously healthy primigravid 38 year old female was induced at 40 weeks + 5 days. Six hours post-induction, fetal decelerations as well as maternal hypoxia and hypotension were noted, resulting in a stat C-section. The patient demonstrated severe hypoxemia and hypoperfusion (ABG=7.24/39/50/17/-10.1, 100% FiO2) which rapidly progressed to DIC (INR=3.9, aPTT=89.5sec, fibrinogen=<40mg/dL). Upon closure of the patient's abdomen, an increase in peak inspiratory pressure and severe hypotension were recorded. Reopening of the midline incision revealed intraabdominal hemorrhage resulting in the abdominal compartment syndrome. Concurrent to surgical hemostasis, thromboelastography was used to guide massive transfusion efforts. The patient developed multiple organ dysfunction syndrome, acute respiratory distress syndrome, and shock refractory to multiple vasopressors and inotropes. A transthoracic echocardiogram demonstrated signs of pulmonary hypertension (PAP >50mmHg) and acute right ventricular failure. Inhaled nitric oxide was initiated at 40 ppm with improvements in oxygenation as well as hemodynamics. Neither the mother nor her daughter suffered any long term cognitive or other end organ impairment. Both patients were discharged home uneventfully on hospital day 24.
DISCUSSION: Amniotic fluid embolism accounts for 10% of maternal deaths in developed countries with an associated neonatal mortality rate between 20-60% . Several risk factors for AFE have been identified. These include older maternal age (≥35 years old), operative or instrumented birth, race, and medical conditions such as eclampsia. Data regarding induction of labor as a risk factor for AFE are conflicting. Entry of amniotic fluid constituents with a resulting immunologic or inflammatory response, in conjunction with physical obstruction at key sites of the maternal vasculature, are proposed mechanisms underlying the pathophysiology of AFE. Diagnosis of AFE is clinical and should be suspected in the pregnant patient who acutely presents with shock associated with respiratory failure during labor and delivery or in the immediate postpartum period. Treatment of AFE syndrome is supportive and should be directed towards cardiopulmonary stabilization, reversal of coagulopathy, and end-organ support.
CONCLUSIONS: Despite an improved understanding of AFE, maternal morbidity and mortality remain high. Early recognition and aggressive intervention remain the key to successful management of this uncommon disease.
1) Moore J, Baldisseri MR. Amniotic fluid embolism. Crit Care Med 2005; 33(10):S279-S285.
2) Conde-Agudelo A, Romero R. Amniotic fluid embolism: an evidence-based review. Am J Obstet Gynecol 2009;201:445.e1-13.
DISCLOSURE: The following authors have nothing to disclose: Dennis Kim, Vishal Bansal, Raul Coimbra
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