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 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

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

Embolism Hypertensive disorders Hemorrhage Infection Cardiomyopathy CVA Anesthesia

21.4% 19.4% 13.4% 12.6% 9.7% 5.3% 1.8%

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)

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 PrePre-eclampsia Pelvic trauma Hereditary Thrombophilia (ie. Protein C,S deficiency)

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 Tinversion and supraventricular arrhythmias

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

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

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)

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

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 8Heparin is discontinued shortly before delivery, and restarted in conjunction w/ warfarin; Heparin is D/C d when the INR is between 2 -3

Thrombolysis


Thrombolytic therapy should be considered in patients w/ massive PE Streptokinase (or urokinase) and r-tPA has been used rduring pregnancy Urokinase is less antigenic and should have fewer side effects Recombinant tissue plasminogen activator (rt-PA) does (rtnot induce systemic fibrinolysis but , rather, rt-PA is rtactive when bound to thrombin so is clot specific Antepartum and intrapartum complications include maternal hemorrhage and placental abruption

Low Molecular Weight Heparin (LMWH)



Use of LMWH is controversial during pregnancy for thromboprophylaxis Because LMWH has greater antithrombotic activity (anti(antifactor Xa) than anticoagulant activity (anti-factor IIa), it (antidoes 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

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

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

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

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 wheelstethoscope

Resuscitation of Massive VAE

1. 2.

3. 4. 5.

6. 7.

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

Amniotic Fluid Embolism



It s estimated that between 5-18 % of all maternal 5deaths 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

Risk Factors for AFE

1. 2. 3. 4. 5. 6. 7.

Advanced age Multiparity Tumultuous labor Rupture of membranes Fetal death Trauma Uterine overdistention (multiple gestation, fetal macrosomia)

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

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 multian infection acquired during the stay at the ICU

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

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

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

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  RERE-establishing uterine tone

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

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

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

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 AnesthesiaOB and Gyn 2003; 46: 679-686 679Ross BK. ASA Closed Claims in obstetrics: lessons learned. Anesthesiology Clin N Am 21 (2003) : 183-197 183-