Upload
abigail-hazel-patino-navea
View
220
Download
0
Embed Size (px)
Citation preview
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 1/31
Embolism during PregnancyEmbolism during Pregnancy
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 2/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 3/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 4/31
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)
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 5/31
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)
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 6/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 7/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 8/31
PathophysiologyPathophysiology
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 9/31
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)
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 10/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 11/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 12/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 13/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 14/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 15/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 16/31
PathophysiologyPathophysiology
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 17/31
Clinical ManifestationsClinical Manifestations
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 18/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 19/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 20/31
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)
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 21/31
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 22/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 23/31
PathophysiologyPathophysiology
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 24/31
Clinical ManifestationsClinical Manifestations
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 25/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 26/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 27/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 28/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 29/31
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
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 30/31
8/4/2019 OB Embolism
http://slidepdf.com/reader/full/ob-embolism 31/31
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