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Embolism during Pregnancy. Maternal Morbidity and Mortality. Since 1985, embolism (ie. thrombotic, air, and amniotic fluid ) has been the predominant cause of maternal deaths (20 %) in the US

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Embolism during Pregnancy

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Embolism during Pregnancy


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Maternal Morbidity and Mortality

  • Since 1985, embolism (ie. thrombotic, air, and amniotic fluid ) has been the predominant cause of maternal deaths (20 %) in the US

  • The CDC define maternal deaths as those that occur within 1 year of delivery and that are related to the pregnancy

  • Among women who died after a live birth, the leading causes of death were embolism and PIH


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Causes of Pregnancy-related Death During Live Birth in the US (1991-970)

  • Embolism 21.4%

  • Hypertensive disorders 19.4%

  • Hemorrhage 13.4%

  • Infection 12.6%

  • Cardiomyopathy 9.7%

  • CVA 5.3%

  • Anesthesia 1.8%


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Venous Thromboembolism (VTE): Incidence and Risk Factors

  • Pregnancy is associated w/ a 5 to 10 fold increase in the risk of VTE

  • This risk is further increased during the last 3 months of pregnancy

  • When untreated, up to 24% of pregnant women w/ deep venous thrombosis (DVT) will develop pulmonary embolism (PE) w/ a subsequent mortality of 15%

  • The increased susceptibility during pregnancy is due to various physiological adaptations that result in the presence of all components of Virchow’s triad: venous stasis (aortocaval compression) , hypercoagulability (increased levels of factors II, VII, VIII, and X) , and damage to the vessel wall (during vaginal and operative delivery)


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Risk Factors for Thromboembolism during Pregnancy:

  • Maternal age > 35 yo

  • Higher parity

  • Obesity

  • Prolonged immobilization

  • Surgery during pregnancy (including C/S)

  • Family or personal Hx of VTE

  • Pre-eclampsia

  • Pelvic trauma

  • Hereditary Thrombophilia (ie. Protein C,S deficiency)


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Clinical Manifestations

  • The most common symptoms of PE are the sudden onset of dyspnea and tachypnea

  • Symptoms may be absent in up to 70% of patients w/ documented PE

  • Clinical signs that suggest PE are tachypnea, tachycardia, and arterial oxygen desaturation

  • Lab findings include hypoxemia, resp alkalosis, and often a normal CXR

  • EKG findings are nonspecific and may show R ventricular strain (R axis shift) , ST segment abnormalities, T-wave inversion and supraventricular arrhythmias


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Pathophysiology

  • Once a PE occurs, resp failure may result from either extensive occlusion of the pulmonary vasculature or pulm edema

  • Pulmonary hypertension may result from direct vascular obstruction by a large embolus; a small embolus may also be assoc w/ severe pulm hypertension , esp. if there is underlying cardiac or pulm disease or recurrent PEs

  • This may result in R ventricular overload

  • Pulmonary edema may occur from increased hydrostatic forces and the disruption of normal capillary integrity


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Pathophysiology

  • The ensuing obstruction of the pulm vasculature leads to an acute ventilation/perfusion (V/Q) mismatch and a decrease in the amount and quality of oxygenated blood reaching the left side of the heart

  • Invasive monitoring typically reveals normal to low PA occlusion pressures, increased mean PA pressure, and increased CVP


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Diagnosis of PE

  • Specific diagnostic tests used are V/Q scans, MRA, spiral CT , or pulm angiography

  • V/Q scans are indeterminate or intermediate 60% of the time and the risk of PE is 20% in this situation

  • Pulm angiography is required either in patients who have negative V/Q scans but strong clinical suspicion of PE or in severe cases for confirmation of PE before selective thrombolysis

  • The radiation dose to the fetus is small and has been estimated to be 0.5 rad w/ combination CXR, V/Q scan, and pulm angiography ( > 5 rads is significant enough to cause teratogenesis)


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Therapy

  • Treatment of VTE can be divided into supportive measures and specific therapy

  • Supportive measures are aimed at improving adequate oxygenation and circulation; oxygen administration and cardiorespiratory support w/ fluids, inotropes, and vasopressors are the mainstay of initial treatment

  • Right atrial filling pressures should be maintained at a high level to maintain output from the failing Right ventricle

  • Specific measures include anticoagulation and thrombolysis


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Therapy

  • Anticoagulation w/ unfractionated heparin remains the specific therapy of choice

  • An IV bolus followed by an infusion to achieve an activated partial thromboplastin time (aPTT) of 1.5 to 2 times the upper level of control values for 10 to 14 days

  • This is followed by subcutaneous injections of 5,000 to 10,000 IU Q 8-12 hrs throughout pregnancy

  • Heparin is discontinued shortly before delivery, and restarted in conjunction w/ warfarin; Heparin is D/C’d when the INR is between 2 -3


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Thrombolysis

  • Thrombolytic therapy should be considered in patients w/ massive PE

  • Streptokinase (or urokinase) and r-tPA has been used during pregnancy

  • Urokinase is less antigenic and should have fewer side effects

  • Recombinant tissue plasminogen activator (rt-PA) does not induce systemic fibrinolysis but , rather, rt-PA is active when bound to thrombin so is clot specific

  • Antepartum and intrapartum complications include maternal hemorrhage and placental abruption


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Low Molecular Weight Heparin (LMWH)

  • Use of LMWH is controversial during pregnancy for thromboprophylaxis

  • Because LMWH has greater antithrombotic activity (anti-factor Xa) than anticoagulant activity (anti-factor IIa), it does not affect the aPTT

  • The smaller structure of LMWH gives it advantages over UH: prolonged serum half life, decreased daily dosing, lower protein binding, lower risk of bleeding, and lower risk of platelet activation and thrombocytopenia


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Venous Air Embolism (VAE)

  • VAE is possibly the most common embolic event during the intraoperative period and air can be demonstrated by precordial Doppler auscultation in up to 50% of C/S’s

  • Even so, VAE is responsible for only about 1% of maternal deaths for a rate of approximately one death per 100,000 live births


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Risk Factors for VAE

  • A gradient of -5 cm H2O between the periphery and the heart would allow significant entry of air into venous circulation

  • Trendelenburg position and exteriorizing the uterus during C/S increase this gradient

  • Uterine exteriorization is thought to predispose to VAE by: 1) increasing the hydrostatic gradient by raising the incisional area above the level of the heart ; 2) by the simultaneous enlargement of the uterine sinuses providing more exposure to air


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Pathophysiology

  • The major cause of death from VAE is circulatory arrest from air entrapped in the right ventricular outflow tract

  • 5 ml/ kg of air may be lethal by formation of an “air lock” in the right ventricle or in the pulmonary arterial circulation ; this can result in cardiogenic shock

  • In combination w/ PA vasoconstriction , this phenomenon can result in acute cor pulmonale

  • Increased capillary permeability, platelet activation, and coagulopathy may result from the effect of air on endothelial surfaces


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Clinical Manifestations

  • Massive VAE can present as a sudden and devastating event w/ hypotension, hypoxemia, and even cardiac arrest

  • Typically, the clinical picture is much less dramatic

  • Significant hemodynamic compromise at delivery is only seen about 0.7% to 2% of the time

  • Signs of air embolism include tachycardia, tachypnea, cyanosis, mottled skin, and occasionally, a wheel-mill murmur heard by stethoscope


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Resuscitation of Massive VAE

  • Discontinue nitrous oxide and give 100% O2

  • Prevent further air entrapment ( flood surgical field, change position)

  • Support ventilation as needed

  • Support circulation

  • If hemodynamic instability persists, consider placement of central line to attempt aspiration of air

  • Expedite delivery

  • If there is delayed emergence from GA, consider neurodiagnostic imaging to r/o intracerebral air ( arterial gas embolism) ; these patients may benefit from hyperbaric therapy, esp. if done w/in 5 hrs


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Amniotic Fluid Embolism

  • It’s estimated that between 5-18 % of all maternal deaths are due to AFE

  • Reported mortality rates range from 26% to as high 86%

  • AFE constitutes the leading cause of mortality during labor and the first few postpartum hours

  • Maternal death occurs in one of three ways: 1) sudden cardiac arrest, 2) hemorrhage due to coagulopathy, 3) or initial survival w/ death due to ARDS and multiple organ failure


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Risk Factors for AFE

  • Advanced age

  • Multiparity

  • Tumultuous labor

  • Rupture of membranes

  • Fetal death

  • Trauma

  • Uterine overdistention (multiple gestation, fetal macrosomia)


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Pathophysiology of AFE

The anaphylactoid reaction to AFE breaks down to 3 phases:

  • Immediate Phase: occurs when initially exposed and can present as 1) resp distress 2) cyanosis 3)hemodynamic instability 4) cerebral hypoperfusion w/ seizures, confusion or coma

  • Second Phase: characterized by coagulopathy and hemorrhage ; this may be the first and only presentation of AFE


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Pathophysiology

  • Phase Three: the period after the acute insult is over and the tissue injury is established

  • These patients may die from the severe lung or brain injury, multi-organ failure, or because of an infection acquired during the stay at the ICU


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Clinical Manifestations

  • Signs and symptoms tend to be nonspecific and common to other forms of embolism

  • Resp distress, cyanosis, cardiovascular collapse, coma, and hemorrhage tend to be the five cardinal signs of AFE

  • Hemorrhage and fetal distress may be the initial symptoms


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Diagnosis of AFE

  • In the past, the definitive diagnosis was made only at autopsy by finding fetal squamous cells in the maternal pulmonary circulation

  • However, cells of fetal origin were only found in 73% of patients who expired and underwent autopsy

  • Conversely , some Obstetricians have found fetal squamous cells in maternal circulation w/o any evidence of AFE


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Diagnosis of AFE

  • CXR may be completely normal and the EKG may show signs of acute right ventricular strain in the early stages

  • Echocardiography at the bedside usually confirm severe left ventricular failure

  • Most patients are hemodynamically unstable so it is often difficult to do any specific testing in time to alter management


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Management of AFE

Treatment of AFE is supportive and directed toward:

  • Maintaining oxygenation

  • Maintaining cardiac output, SBP>90 mmHg

  • Acceptable peripheral organ perfusion (urine output >25 ml/hr)

  • Correcting coagulation abnormalities

  • RE-establishing uterine tone


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Management of AFE

Pharmacological treatment may include:

  • Crystalloids, vasopressors, and inotropic agents (fluids should be restricted once the initial hypotensive episode has resolved to prevent pulmonary edema w/ subsequent ARDS)

  • Corticosteroids (Hydrocortisone 500mg Q6 hr)

  • Therapeutic heparinization to limit intravascular coagulation is controversial

  • In rare instances, cardiopulmonary bypass and pulmonary thromboembolectomy have been successfully used


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Summary

  • Embolic events are a major cause of maternal mortality

  • Early recognition, diagnosis, and therapy helps reduce the incidence of maternal morbidity and mortality

  • Therapy for pulmonary embolism focuses on the prevention of recurrent PEs

  • Venous air embolism is a common occurrence during C/S but most of these are small, transient events; massive VAE during vaginal or C/S is rare but can be fatal

  • Amniotic fluid embolism may occur at any time during labor and delivery


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Summary

  • The syndrome of AFE typically presents w/ dyspnea, cyanosis, and sudden CV collapse but these signs and symptoms may be compatible w/ other embolic events


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Bibliography

  • Gei AF, Vadhera RB, Hankins GD, et al. Embolism during Pregnancy. Anesthesiology Clin N Am 21 (2003) 165 -182

  • Hawkins JL. Anesthesia-related Maternal Mortality. Clin OB and Gyn 2003; 46: 679-686

  • Ross BK. ASA Closed Claims in obstetrics: lessons learned. Anesthesiology Clin N Am 21 (2003) : 183-197


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