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Embolism during PregnancyEmbolism during Pregnancy



Maternal Morbidity and MortalityMaternal Morbidity and Mortality

Since 1985, embolism (ie. thrombotic, air, andSince 1985, embolism (ie. thrombotic, air, andamniotic fluid ) has been the predominant causeamniotic fluid ) has been the predominant cause

of maternal deaths (20 %) in the USof maternal deaths (20 %) in the US The CDC define maternal deaths as those that The CDC define maternal deaths as those that

occur within 1 year of delivery and that areoccur within 1 year of delivery and that arerelated to the pregnancyrelated to the pregnancy

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



Causes of PregnancyCauses of Pregnancy--related Deathrelated Death

During Live Birth in the US (1991During Live Birth in the US (1991--970)970)

Embolism 21.4%Embolism 21.4%

Hypertensive disorders 19.4%Hypertensive disorders 19.4%

Hemorrhage 13.4%Hemorrhage 13.4%

Infection 12.6%Infection 12.6%

Cardiomyopathy 9.7%Cardiomyopathy 9.7%

CVA 5.3%CVA 5.3% Anesthesia Anesthesia



Venous Thromboembolism (VTE): Venous Thromboembolism (VTE):Incidence and Risk FactorsIncidence and Risk Factors

Pregnancy is associated w/ a 5 to 10 fold increase inPregnancy is associated w/ a 5 to 10 fold increase inthe risk of VTEthe risk of VTE

This risk is further increased during the last 3 monthsThis risk is further increased during the last 3 months

of pregnancyof pregnancy When untreated, up to 24% of pregnant women w/When untreated, up to 24% of pregnant women w/

deep venous thrombosis (DVT) will develop pulmonarydeep venous thrombosis (DVT) will develop pulmonaryembolism (PE) w/ a subsequent mortality of 15%embolism (PE) w/ a subsequent mortality of 15%

The increased susceptibility during pregnancy is due toThe increased susceptibility during pregnancy is due to

various physiological adaptations that result in thevarious physiological adaptations that result in thepresence of all components of Virchows triad: venouspresence of all components of Virchows triad: venousstasis (aortocaval compression) , hypercoagulabilitystasis (aortocaval compression) , hypercoagulability(increased levels of factors II, VII, VIII, and X) , and(increased levels of factors II, VII, VIII, and X) , anddamage to the vessel wall (during vaginal anddamage to the vessel wall (during vaginal and

operative delivery)operative delivery)



Risk Factors for ThromboembolismRisk Factors for Thromboembolismduring Pregnancy:during Pregnancy:

Maternal age > 35 yoMaternal age > 35 yo

Higher parityHigher parity

ObesityObesity Prolonged immobilizationProlonged immobilization

Surgery during pregnancy (including C/S)Surgery during pregnancy (including C/S)

Family or personal Hx of VTEFamily or personal Hx of VTE

PrePre--eclampsiaeclampsia

Pelvic traumaPelvic trauma

Hereditary Thrombophilia (ie. Protein C,SHereditary Thrombophilia (ie. Protein C,S

deficiency)deficiency)



Clinical ManifestationsClinical Manifestations

The most common symptoms of PE are the suddenThe most common symptoms of PE are the suddenonset of dyspnea and tachypneaonset of dyspnea and tachypnea

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

documented PEdocumented PE Clinical signs that suggest PE are tachypnea,Clinical signs that suggest PE are tachypnea,

tachycardia, and arterial oxygen desaturationtachycardia, and arterial oxygen desaturation

Lab findings include hypoxemia, resp alkalosis, and oftenLab findings include hypoxemia, resp alkalosis, and oftena normal CXRa normal CXR

EKG findings are nonspecific and may show R ventricularEKG findings are nonspecific and may show R ventricularstrain (R axis shift) , ST segment abnormalities, Tstrain (R axis shift) , ST segment abnormalities, T--wavewaveinversion and supraventricular arrhythmiasinversion and supraventricular arrhythmias



PathophysiologyPathophysiology

Once a PE occurs, resp failure may result from eitherOnce a PE occurs, resp failure may result from eitherextensive occlusion of the pulmonary vasculature orextensive occlusion of the pulmonary vasculature orpulm edemapulm edema

Pulmonary hypertension may result from direct vascularPulmonary hypertension may result from direct vascularobstruction by a large embolus; a small embolus mayobstruction by a large embolus; a small embolus mayalso be assoc w/ severe pulm hypertension , esp. if therealso be assoc w/ severe pulm hypertension , esp. if thereis underlying cardiac or pulm disease or recurrent PEsis underlying cardiac or pulm disease or recurrent PEs

This may result in R ventricular overloadThis may result in R ventricular overload Pulmonary edema may occur from increased hydrostaticPulmonary edema may occur from increased hydrostatic

forces and the disruption of normal capillary integrityforces and the disruption of normal capillary integrity




The ensuing obstruction of the pulm vasculatureThe ensuing obstruction of the pulm vasculatureleads to an acute ventilation/perfusion (V/Q)leads to an acute ventilation/perfusion (V/Q)

mismatch and a decrease in the amount andmismatch and a decrease in the amount andquality of oxygenated blood reaching the left quality of oxygenated blood reaching the left side of the heart side of the heart

Invasive monitoring typically reveals normal toInvasive monitoring typically reveals normal to

low PA occlusion pressures, increased mean PAlow PA occlusion pressures, increased mean PApressure, and increased CVPpressure, and increased CVP



Diagnosis of PEDiagnosis of PE

Specific diagnostic tests used are V/Q scans, MRA, spiralSpecific diagnostic tests used are V/Q scans, MRA, spiralCT , or pulm angiographyCT , or pulm angiography

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

Pulm angiography is required either in patients who havePulm angiography is required either in patients who havenegative V/Q scans but strong clinical suspicion of PE ornegative V/Q scans but strong clinical suspicion of PE orin severe cases for confirmation of PE before selectivein severe cases for confirmation of PE before selectivethrombolysisthrombolysis

The radiation dose to the fetus is small and has beenThe radiation dose to the fetus is small and has been

estimated to be 0.5 rad w/ combination CXR, V/Q scan,estimated to be 0.5 rad w/ combination CXR, V/Q scan,and pulm angiography ( > 5 rads is significant enough toand pulm angiography ( > 5 rads is significant enough tocause teratogenesis)cause teratogenesis)



TherapyTherapy

Treatment of VTE can be divided into supportiveTreatment of VTE can be divided into supportivemeasures and specific therapymeasures and specific therapy

Supportive measures are aimed at improving adequateSupportive measures are aimed at improving adequateoxygenation and circulation; oxygen administration andoxygenation and circulation; oxygen administration andcardiorespiratory support w/ fluids, inotropes, andcardiorespiratory support w/ fluids, inotropes, andvasopressors are the mainstay of initial treatment vasopressors are the mainstay of initial treatment

Right atrial filling pressures should be maintained at aRight atrial filling pressures should be maintained at a

high level to maintain output from the failing Right high level to maintain output from the failing Right ventricleventricle

Specific measures include anticoagulation andSpecific measures include anticoagulation andthrombolysisthrombolysis



TherapyTherapy

Anticoagulation w/ unfractionated heparin remains the Anticoagulation w/ unfractionated heparin remains thespecific therapy of choicespecific therapy of choice

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

This is followed by subcutaneous injections of 5,000 toThis is followed by subcutaneous injections of 5,000 to10,000 IU Q 810,000 IU Q 8--12 hrs throughout pregnancy12 hrs throughout pregnancy

Heparin is discontinued shortly before delivery, andHeparin is discontinued shortly before delivery, andrestarted in conjunction w/ warfarin; Heparin is D/Cdrestarted in conjunction w/ warfarin; Heparin is D/Cdwhen the INR is between 2when the INR is between 2 --33



ThrombolysisThrombolysis

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

Streptokinase (or urokinase) and rStreptokinase (or urokinase) and r--tPA has been usedtPA has been usedduring pregnancyduring pregnancy

Urokinase is less antigenic and should have fewer sideUrokinase is less antigenic and should have fewer sideeffectseffects

Recombinant tissue plasminogen activator (rt Recombinant tissue plasminogen activator (rt--PA) doesPA) doesnot induce systemic fibrinolysis but , rather, rt not induce systemic fibrinolysis but , rather, rt--PA isPA isactive when bound to thrombin so is clot specificactive when bound to thrombin so is clot specific

Antepartum and intrapartum complications include Antepartum and intrapartum complications includematernal hemorrhage and placental abruptionmaternal hemorrhage and placental abruption



Low Molecular Weight HeparinLow Molecular Weight Heparin

(LMWH)(LMWH) Use of LMWH is controversial during pregnancy forUse of LMWH is controversial during pregnancy for

thromboprophylaxisthromboprophylaxis

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

The smaller structure of LMWH gives it advantages overThe smaller structure of LMWH gives it advantages overUH: prolonged serum half life, decreased daily dosing,UH: prolonged serum half life, decreased daily dosing,lower protein binding, lower risk of bleeding, and lowerlower protein binding, lower risk of bleeding, and lowerrisk of platelet activation and thrombocytopeniarisk of platelet activation and thrombocytopenia



Venous Air Embolism (VAE) Venous Air Embolism (VAE)

VAE is possibly the most common embolic event during VAE is possibly the most common embolic event duringthe intraoperative period and air can be demonstrated bythe intraoperative period and air can be demonstrated byprecordial Doppler auscultation in up to 50% of C/Ssprecordial Doppler auscultation in up to 50% of C/Ss

Even so, VAE is responsible for only about 1% of Even so, VAE is responsible for only about 1% of maternal deaths for a rate of approximately one deathmaternal deaths for a rate of approximately one deathper 100,000 live birthsper 100,000 live births



Risk Factors for VAERisk Factors for VAE

A gradient of A gradient of --5 cm H2O between the periphery and the5 cm H2O between the periphery and theheart would allow significant entry of air into venousheart would allow significant entry of air into venous

circulationcirculation Trendelenburg position and exteriorizing the uterusTrendelenburg position and exteriorizing the uterus

during C/S increase this gradient during C/S increase this gradient

Uterine exteriorization is thought to predispose to VAEUterine exteriorization is thought to predispose to VAEby: 1) increasing the hydrostatic gradient by raising theby: 1) increasing the hydrostatic gradient by raising theincisional area above the level of the heart ; 2) by theincisional area above the level of the heart ; 2) by thesimultaneous enlargement of the uterine sinusessimultaneous enlargement of the uterine sinusesproviding more exposure to airproviding more exposure to air




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

5 ml/ kg of air may be lethal by formation of an air5 ml/ kg of air may be lethal by formation of an airlock in the right ventricle or in the pulmonary arteriallock in the right ventricle or in the pulmonary arterialcirculation ; this can result in cardiogenic shockcirculation ; this can result in cardiogenic shock

In combination w/ PA vasoconstriction , thisIn combination w/ PA vasoconstriction , thisphenomenon can result in acute cor pulmonalephenomenon can result in acute cor pulmonale

Increased capillary permeability, platelet activation, andIncreased capillary permeability, platelet activation, andcoagulopathy may result from the effect of air oncoagulopathy may result from the effect of air onendothelial surfacesendothelial surfaces




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

Typically, the clinical picture is much lessTypically, the clinical picture is much lessdramaticdramatic

Significant hemodynamic compromise at deliverySignificant hemodynamic compromise at deliveryis only seen about 0.7% to 2% of the timeis only seen about 0.7% to 2% of the time

Signs of air embolism include tachycardia,Signs of air embolism include tachycardia,tachypnea, cyanosis, mottled skin, andtachypnea, cyanosis, mottled skin, andoccasionally, a wheeloccasionally, a wheel--mill murmur heard bymill murmur heard bystethoscopestethoscope



Resuscitation of Massive VAEResuscitation of Massive VAE

1.1. Discontinue nitrous oxide and give 100% O2Discontinue nitrous oxide and give 100% O2

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

3.3. Support ventilation as neededSupport ventilation as needed4.4. Support circulationSupport circulation

5.5. If hemodynamic instability persists, considerIf hemodynamic instability persists, considerplacement of central line to attempt aspiration of airplacement of central line to attempt aspiration of air

6.6. Expedite deliveryExpedite delivery7.7. If there is delayed emergence from GA, considerIf there is delayed emergence from GA, consider

neurodiagnostic imaging to r/o intracerebral air (neurodiagnostic imaging to r/o intracerebral air (arterial gas embolism) ; these patients may benefit arterial gas embolism) ; these patients may benefit from hyperbaric therapy, esp. if done w/in 5 hrsfrom hyperbaric therapy, esp. if done w/in 5 hrs



Amniotic Fluid Embolism Amniotic Fluid Embolism

Its estimated that between 5Its estimated that between 5--18 % of all maternal18 % of all maternaldeaths are due to AFEdeaths are due to AFE

Reported mortality rates range from 26% to as highReported mortality rates range from 26% to as high86%86%

AFE constitutes the leading cause of mortality during AFE constitutes the leading cause of mortality duringlabor and the first few postpartum hourslabor and the first few postpartum hours

Maternal death occurs in one of three ways: 1) suddenMaternal death occurs in one of three ways: 1) suddencardiac arrest, 2) hemorrhage due to coagulopathy, 3)cardiac arrest, 2) hemorrhage due to coagulopathy, 3)or initial survival w/ death due to ARDS and multipleor initial survival w/ death due to ARDS and multipleorgan failureorgan failure



Risk Factors for AFERisk Factors for AFE

1.1. Advanced age Advanced age

2.2. MultiparityMultiparity

3.3. Tumultuous laborTumultuous labor

4.4. Rupture of membranesRupture of membranes

5.5. Fetal deathFetal death

6.6. TraumaTrauma7.7. Uterine overdistention (multiple gestation, fetalUterine overdistention (multiple gestation, fetal

macrosomia)macrosomia)



Pathophysiology of AFEPathophysiology of AFE

The anaphylactoid reaction to AFE breaks down toThe anaphylactoid reaction to AFE breaks down to

3 phases:3 phases: Immediate Phase: occurs when initially exposedImmediate Phase: occurs when initially exposed

and can present as 1) resp distress 2) cyanosisand can present as 1) resp distress 2) cyanosis3)hemodynamic instability 4) cerebral3)hemodynamic instability 4) cerebral

hypoperfusion w/ seizures, confusion or comahypoperfusion w/ seizures, confusion or coma Second Phase: characterized by coagulopathySecond Phase: characterized by coagulopathy

and hemorrhage ; this may be the first and onlyand hemorrhage ; this may be the first and onlypresentation of AFEpresentation of AFE




Phase Three: the period after the acute insult isPhase Three: the period after the acute insult isover and the tissue injury is establishedover and the tissue injury is established

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




Signs and symptoms tend to be nonspecific andSigns and symptoms tend to be nonspecific andcommon to other forms of embolismcommon to other forms of embolism

Resp distress, cyanosis, cardiovascular collapse,Resp distress, cyanosis, cardiovascular collapse,coma, and hemorrhage tend to be the fivecoma, and hemorrhage tend to be the fivecardinal signs of AFEcardinal signs of AFE

Hemorrhage and fetal distress may be the initialHemorrhage and fetal distress may be the initialsymptomssymptoms



Diagnosis of AFEDiagnosis of AFE

In the past, the definitive diagnosis was made only at In the past, the definitive diagnosis was made only at autopsy by finding fetal squamous cells in the maternalautopsy by finding fetal squamous cells in the maternalpulmonary circulationpulmonary circulation

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

Conversely , some Obstetricians have found fetalConversely , some Obstetricians have found fetalsquamous cells in maternal circulation w/o any evidencesquamous cells in maternal circulation w/o any evidence

of AFEof AFE



Diagnosis of AFEDiagnosis of AFE

CXR may be completely normal and the EKGCXR may be completely normal and the EKGmay show signs of acute right ventricular strainmay show signs of acute right ventricular strain

in the early stagesin the early stages Echocardiography at the bedside usually confirmEchocardiography at the bedside usually confirm

severe left ventricular failuresevere left ventricular failure

Most patients are hemodynamically unstable soMost patients are hemodynamically unstable soit is often difficult to do any specific testing init is often difficult to do any specific testing intime to alter management time to alter management



Management of AFEManagement of AFE

Treatment of AFE is supportive and directedTreatment of AFE is supportive and directedtoward:toward:

Maintaining oxygenationMaintaining oxygenation Maintaining cardiac output, SBP>90 mmHgMaintaining cardiac output, SBP>90 mmHg

Acceptable peripheral organ perfusion (urine Acceptable peripheral organ perfusion (urine

output >25 ml/hr)output >25 ml/hr) Correcting coagulation abnormalitiesCorrecting coagulation abnormalities

RERE--establishing uterine toneestablishing uterine tone



Management of AFEManagement of AFE

Pharmacological treatment may include:Pharmacological treatment may include:

Crystalloids, vasopressors, and inotropic agents (fluidsCrystalloids, vasopressors, and inotropic agents (fluidsshould be restricted once the initial hypotensive episodeshould be restricted once the initial hypotensive episodehas resolved to prevent pulmonary edema w/ subsequent has resolved to prevent pulmonary edema w/ subsequent ARDS) ARDS)

Corticosteroids (Hydrocortisone 500mg Q6 hr)Corticosteroids (Hydrocortisone 500mg Q6 hr)

Therapeutic heparinization to limit intravascularTherapeutic heparinization to limit intravascular

coagulation is controversialcoagulation is controversial

In rare instances, cardiopulmonary bypass and pulmonaryIn rare instances, cardiopulmonary bypass and pulmonarythromboembolectomy have been successfully usedthromboembolectomy have been successfully used



SummarySummary

Embolic events are a major cause of maternal mortalityEmbolic events are a major cause of maternal mortality

Early recognition, diagnosis, and therapy helps reduceEarly recognition, diagnosis, and therapy helps reduce

the incidence of maternal morbidity and mortalitythe incidence of maternal morbidity and mortality Therapy for pulmonary embolism focuses on theTherapy for pulmonary embolism focuses on the

prevention of recurrent PEsprevention of recurrent PEs

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

Amniotic fluid embolism may occur at any time during Amniotic fluid embolism may occur at any time duringlabor and deliverylabor and delivery



BibliographyBibliography

Gei AF, Vadhera RB, Hankins GD, et al. Embolism duringGei AF, Vadhera RB, Hankins GD, et al. Embolism duringPregnancy. Anesthesiology Clin N Am 21 (2003) 165Pregnancy. Anesthesiology Clin N Am 21 (2003) 165 --182182

Hawkins JL. AnesthesiaHawkins JL. Anesthesia--related Maternal Mortality. Clinrelated Maternal Mortality. ClinOB and Gyn 2003; 46: 679OB and Gyn 2003; 46: 679--686686

Ross BK. ASA Closed Claims in obstetrics: lessonsRoss BK. ASA Closed Claims in obstetrics: lessonslearned. Anesthesiology Clin N Am 21 (2003) : 183learned. Anesthesiology Clin N Am 21 (2003) : 183--197197

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