Embolism during Pregnancy Robert Nichols, DO Embolism during Pregnancy

Embolism Pulmonary Embolism Venous Air Embolism Amniotic Fluid embolism

Embolism One of the leading causes of maternal mortality Non-cardiovascular diseases, 15.3%. Cardiovascular diseases, 14.7%. Infection or sepsis, 12.7%. Hemorrhage, 11.3%. Cardiomyopathy, 10.8%. Thrombotic pulmonary embolism, 9.0%. Hypertensive disorders of pregnancy, 7.6%. Cerebrovascular accidents, 6.5%. Amniotic fluid embolism, 5.7%. Anesthesia complications, 0.2%. www.cdc.gov/reproductivehealth/maternalinfanthealth/pmss.html

Pulmonary Embolism Difficult diagnosis and management 2 patients at risk Overdiagnosis results in unnecessary and often dangerous treatments to both patients Usual imaging modalities must be considered with developing fetus

Pulmonary Embolism Higher risk 2/2 Virchows triad Hypercoagulability Vascular damage Venous stasis DVT occurs approximately 3x more frequently than PE DVT occurs on left leg in 85% of cases Likely due to compression of iliac vein by iliac artery and gravid uterus Isolated pelvic DVT is also much more common in parturients

Pulmonary Embolism ACOG guidelines to diagnosis Diagnosis often difficult D-Dimer unreliable in pregnant patients Risk of radiation exposure in pregnancy must be considered

Treatment LMWH is treatment of choice in early pregnancy Can be given as outpatient Do not cross placenta and are is not secreted in breastmilk 1mg/kg q12 IV unfractionated heparin preferred near delivery and in renal failure Able to reverse urgently if needed Also does not cross placenta or go into breastmilk Bolus 80u/kg followed by 18u/kg/h, titrated to achieve therapeutic aPTT If SC initial dose is 17,500 units then titrated to aPTT Thrombolytic drugs appropriate in hemodynamically unstable or hypoxic Fetal loss vs. maternal death Warfarin teratogenic and generally contraindicated in pregnant patient

Venous Air Embolism Entrapment of air or medical gases into venous system causing symptoms and signs of pulmonary vessel obstruction 1% of maternal deaths Incidence varies WIDELY depending on the source Depends on surgical position, diagnostic tools

Pathophysiology Vascular access and gradient between injury site and right heart must be present for VAE to occur Determined by rate, volume, duration, patient position, type of gas Pulmonary vessels can filter most air emboli from venous circulation Larger emboli can cause a variety of symptoms

Risk Factors VAE Trendelenburg position Placental abruption Placenta previa Exteriorization of uterus Manual placental extraction Severe preeclampsia Antepartum hemorrhage hypovolemia

Diagnosis Know clinical signs and symptoms May manifest as chest tightness or short breath with or without hypotension or decreased oxygen saturation in conscious patients Variety of diagnositic tools

Treatment Inform Surgeon Adequate hydration Prevent further gas entry Flood surgical field Remove origin of gas entry Increase right atrial pressure and trap air in right atrium Reverse Trendelenburg when possible Left lateral recumbent position Discontinue N2O and ventilate with 100% oxygen Attempt to aspirate air through central line when appropriate Resuscitate Fluid administration Inotropes, vasopressor, pulmonary vasodilators CPR if necessary Hyperbaric oxygen when appropriate

Amniotic fluid embolism 5.7% of pregnancy related deaths in United States in 2011-12 Poorly understood Diagnosis traditionally made at autopsy when fetal squamous cells are found in pulmonary circulation Diagnosis of exclusion Mortality of AFE approaches 80% 50% die within the first hour of onset of symotoms

AFE Pathophysiology Theorized that amniotic fluid and cells enter circulation and trigger anaphylactic reaction Fetal material not always found in patients with AFE and fetal material found in patients who did not trigger anaphylaxis Currently believed that fluid or some other substance enters maternal circulation and triggers anaphylactic reaction OR activates complement cascade OR both. Occurs in 2 phases 1. pulmonary artery vasospasm with pulmonary hypertension and elevated right ventricular pressure which causes hypoxia. Hypoxia causes myocardial and pulmonary capillary damage, left heart failure and ARDS. 2. Those who survive phase 1 have hemorrhagic phase with massive hemorrhage with uterine atony and DIC; however, fatal consumptive coagulopathy may be the initial presentation

AFE risk factors Multiparity Advanced maternal age Male fetus Trauma Abruption Previa Non-Hispanic black women have more than 2x risk of AFE Women with cerebrovascular disease have 25x risk Cardiac disease have 70x risk!

Treatment Supportive Early resuscitation Pulmonary edema common – fluid input and output must be closely monitored Left heart failure treated with ionotropes Case reports show successful outcomes with hemodialysis with plasmapheresis and ECMO with intra-aortic balloon pump DIC treated with blood components. Consider activated factor VIIa for severe hemorrhage 2 cases report success with bilateral uterine artery embolization

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