maternal collapse due to embolism

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PowerPoint Template Dr Unnikrishnan P P.G.Student Medical College, Trivandrum Maternal Collapse due to Embolism

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Highlights the predisposition of the pregnant patient to embolic disorders and about the management guidelines of such disorders.

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TemplateDr Unnikrishnan PP.G.StudentMedical College, Trivandrum

Maternal Collapse due to Embolism

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THROMBOEMBOLISM

AMNIOTIC FLUID EMBOLISM

VENOUS AIR EMBOLISM

Anaestesiologist is often involved in the resuscitation of patients with embolic disorders

IMPORTANT CAUSES

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VENOUS• .

THROMBO EMBOLISM• .

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Deep Vein Thrombosis [DVT] & Pulmonary Thrombo Embolism [PTE] are the important manifestations

DVT is the most common etiology for Pulmonary Thrombo Embolism

15-24% of women with untreated DVT experience a pulmonary embolus

PTE accounts for 15% of direct maternal mortality

VENOUS THROMBOEMBOLISM

CHESTNT’S OBSTETRIC ANESTHESIA, 4/e[2009],p:837,838

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Changes in coagulation

AETIOLOGY

20% DECREASE IN PLATELET COUNT

PLATELET FUNCTION INCREASED

INCREASED FACTORS I,V,VII,VIII,IX,X,XII

INCREASED THROMBIN GENERATION

FIBRINOLYSIS NORMAL / DECREASED

SHNIDER AND LEVINSONS ANESTHESIA FOR OBSTETRICS,4/e

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Venous stasis

Vascular damage: caesarean > vaginal

Obstetric conditions: PIHMultiple pregnancy

AETIOLOGY

VIRCHOW’S TRIAD : HYPERCOAGULABILITY, STASIS, ENDOTHELIAL INJURY

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Increasing age

Prolonged immobilization

Obesity

Thrombophilia

Previous thromboembolism

Cesarean delivery

RISK FACTORS

ASRA GUIDELINES [THIRD EDITION];Reg Anesth Pain Med 2010

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PATHOPHYSIOLOGY

OCCLUSION

↑PVR,PAP

RV OVERLOAD IV SEPTUMLV

↓LV VOLUME↓COMPLIANCE

↓BP ↓CORONARY PERFUSION PRESSURE

RV ISCHEMIA RV FAILURE

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PATHOPHYSIOLOGY

↓PaO₂↑P(A-a)O₂IMPAIRED GAS EXCHANGE [↑DEAD SPACE,SHUNT,HYPOXEMIA,DECREASED DIFFUSION]V/Q MISMATCHALVEOLAR HYPER VENTILATION↑AIRWAY RESISTANCE↓COMPLIANCE[EDEMA, HEMORRHAGE,LOSS OF SURFACTANT]ATELECTASIS

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CLINICAL FEATURES: SYMPTOMS

DYSPNOEAPALPITATIONANXIETYCHEST PAIN [PLEURITIC]COUGHHEMOPTYSISSYNCOPECOLLAPSE

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CLINICAL FEATURES: SIGNS

TACHYPNOEACREPITATION↓ED BREATH SOUNDSFEVERTACHYCARDIAACCENTUATED S₂JUGULAR VENOUS DISTENSIONLEFT PARASTERNAL HEAVEHEPATIC ENLARGEMENTTHROMBOPHLEBITIS/ FEATURES OF DVT

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The Wells score • clinically suspected DVT - 3.0 points • alternative diagnosis is less likely than PE - 3.0 points • Tachycardia - 1.5 points • immobilization/surgery in previous four weeks - 1.5 points • history of DVT or PE - 1.5 points • hemoptysis - 1.0 points • malignancy (treatment for within 6 months, palliative) - 1.0 points Traditional interpretation• Score >6.0 - High • Score 2.0 to 6.0 - Moderate • Score <2.0 - Low

Alternate interpretation• Score > 4 - PE likely. Consider diagnostic imaging. • Score 4 or less - PE unlikely. Consider D-dimer to rule out PE.

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ECG

DIAGNOSTIC EVALUATION

RV STRAIN PATTERNRIGHT AXIS DEVIATIONP-PULMONALET INVERSION IN V₁-V₄SUPRAVENTRICULAR ARRHYTHMIASS₁Q₃T₃ PATTERN: DEEP S IN L₁ DEEP Q IN L₃ T INVERSION IN L₃

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CHEST X-RAY

DIAGNOSTIC EVALUATION

BLANCHING / OLIGEMIC AREAWESTERMARK’S SIGNHAMPTONS HUMPELEVATED HEMIDIAPHRAGMFOCAL INFILTRATESPLEURAL EFFUSIONATELECTASIS

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HAMPTON’S HUMP

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INVASIVE HEMODYNAMIC MONITORING

ARTERIAL BLOOD GAS ANALYSIS

ELISA FOR D-DIMER

DIAGNOSTIC EVALUATION

NORMAL TO LOW PULMONARY ARTERY OCCLUSSION PRESSUREINCREASED MEAN PULMONARY ARTERY PRESSUREINCREASED CVP

WIDENED P(A-a)O₂REDUCED PaO₂REDUCED PaCO₂

HIGH SENSITIVITY ESPECIALLY WHEN COMBINED WITH A USG OF LEGLOW SPECIFICITY, SINCE D-DIMER APPEARS IN NORMAL PREGNANCY SINCE SECOND TRIMESTER

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VENTILATION PERFUSION SCAN

DIAGNOSTIC EVALUATION

HIGH PROBABILITY SCAN:> 2 MODERATE TO LARGE PERFUSION DEFECTS INVOLVING >25% OF LUNG SEGMENT WITH INTACT VENTILATION

• START ANTICOAGULATIONHIGH PROBABILITY

SCAN & HIGH CLINICAL SUSPICION

• SPIRAL CT• PULMONARY ANGIOGRAPHYINDETERMINATE

SCAN & HIGH CLINICAL SUSPICION

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SPIRAL CT

DIAGNOSTIC EVALUATION

HIGH SENSITIVITY AND SPECIFICITY

↓SED REQUIREMENTS FOR FURTHER TESTING

HENCE MOST COST EFFECTIVE

LESSER RADIATION TO FOETUS THAN V/P SCAN

HIGHER MATERNAL BREAST TISSUE EXPOSURE

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DIAGNOSTIC EVALUATION

PULMONARY ANGIOGRAPHY

INVASIVEINTRALUMINAL FILLING DEFECT

MAGNETIC RESONANCE VENOGRAPHY

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ECHOCARDIOGRAPHY

COMPRESSION USG

DIAGNOSTIC EVALUATION

SENSITIVITY AND NEGATIVE PREDICTIVE VALUE HIGH WHEN COMBINED WITH A LOWER LIMB USGCAN DETECT A CLOT OR CONSEQUENT RV DYSFUNCTIONOBVIATE NEED FOR INVASIVE PROCEDURESHASTEN START OF ANTICOAGULATION

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Decreases the risk 10 fold

Begun when the high risk period begins and continued for 5-10 days

UFH : 5000 U subcutaneously Q12H

Enoxaparin : 40 mg subcutaneously Q24H

Ensure availability of FFP at the time of delivery

PROPHYLAXIS PHARMACOLOGICALINTERMITTENT PNEUMATIC COMPRESSIONELASTIC STOCKINGS

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UNFRACTIONATED HEPARIN [UFH]#

THERAPY - DVT

5000 U [80-100 U / KG] IV LOADING DOSE FOLLOWED BY 15-20 U / KG / HOUR IV INFUSIONaPTT KEPT AT 1.5 TO 2.5 TIMES NORMALIV INFUSION X 5-7 DAYS S/C HEPARINDOSE MAY HAVE TO BE ↑ED BY 50% IN 2 ND AND 3 RD TRIMESTERSDISCONTINUED WHEN PATIENT BEGINS ACTIVE LABOR / 24 HOURS BEFORE CSWARFARIN CAN BE STARTED; WHEN INR 2-3, HEPARIN CAN BE STOPPEDANTICOAGULATION CONTINUED 6 WEEKS POSTPARTUM

#Sipes SL,Venous thromboembolic disease in pregnancy ;Semin Perinatol 1990#American College of Obst & Gyn Comm. on practice;ACOG Practice bulletin no:19,AUG2000

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THERAPY - DVT

GREATER ANTITHROMBOTIC ACTIVITY [ANTIFACTOR Xa]THAN ANTICOAGULANT ACTIVITY [ANTIFACTOR IIa]DON’T AFFECT aPTT

#Sipes SL,Venous thromboembolic disease in pregnancy ;Semin Perinatol 1990#American College of Obst & Gyn Comm. on practice;ACOG Practice bulletin no:19,AUG2000

LOW MOLECULAR WEIGHT HEPARIN [LMWH]

Enoxaparin 40 MG OD-BD [1 MG = 100 U] PROPHYLAXIS 30-80 MG BD THERAPEUTIC ANTICOAGULATION

Dalteparin 2500-5000 U OD-BD THROMBOPROPHYLAXIS100 U/KG BD THERAPEUTIC ANTICOAGULATION

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PULMONARY EMBOLISM-TREATMENT: GOALS

SUPPORT MATERNAL CIRCULATION

PROVIDE ADEQUATE MATERNAL AND FOETAL OXYGENATION

PREVENT RECURRENCE

MINIMIZE LONG TERM MORBIDITY

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PULMONARY EMBOLISM-TREATMENT #

Standard UFH; 80-150U/kg followed by continuous infusion of 15-25 U/kg/hour to keep aPTT at twice normal values

#American College of Obst & Gyn Comm. on practice;ACOG Practice bulletin no:19,AUG2000#Weiner CP et al; management of thromboembolic disease during pregnancy; Clinical Obstet Gynecol 1985

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ABSOLUTEINTRACRANIAL BLEEDSERIOUS ACTIVE BLEEDINGRECENT BRAIN/EYE/SPINAL SURGERYSEVERE THROMBOCYTOPENIARELATIVEHEMORRHAGIC DIATHESISRECENT STROKERECENT MAJOR SURGERYSEVERE UNCONTROLLED HYPERTENSION [DBP>110 MM OF HG]BACTERIAL ENDOCARDITIS

CONTRA INDICATIONS- ANTICOAGULATION

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Transvenous implantation of an IVC filter

INFERIOR VENACAVAL INTERRUPTION

ANTICOAGULATION CONTRAINDICATED ANTICOAGULATION FAILED PROXIMAL DVT RECURRENT EMBOLI

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THROMBOLYSIS

MASSIVE EMBOLISM WITH HEMODYNAMIC INSTABILITY

ECHO EVIDENCE OF RV HYPOFUNCTIONEXTENSIVE ILEOFEMORAL THROMBOSIS40% OBSTRUCTION ON PULMONARY

ANGIOGRAPHY

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Monitoring of coagulation: Thrombin time [Most sensitive]aPTTFDP

Complications:Maternal hemorrhage, Placental abruption

THROMBOLYSIS

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STREPTOKINASE

UROKINASE

RECOMBINANT TISSUE PLASMINOGEN ACTIVATOR [ rt- PA ]

THROMBOLYSIS

2,50,000 IU OVER 30 TO 60 MINUTES FOLLOWED BY 1,00,000 IU/HOUR FOR 24 HOURS

LESS ANTIGENICINITIAL DOSE 4400 IU FOLLOWED BY 4400 IU / KG /HOUR

CLOT SPECIFICDOES NOT INTRODUCE SYSTEMIC FIBRINOLYSIS10 MG IV BOLUS ; FOLLOWED BY 90 MG IN 2 HOURS

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SURGICAL EMBOLECTOMY

THROMBOLYSIS CONTRAINDICATED THROMBOLYSIS FAILEDRAPIDLY DETERIORATING PATIENT

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ANAESTHETIC IMPLICATIONS- ANTICOAGULATED PATIENT

ANTICIPATE AIRWAY BLEEDING

ARRANGE BLOOD PRODUCTS

ANTICOAGULATION & NEURAXIAL BLOCKADE

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AMNIOTIC FLUID

EMBOLISM

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INCIDENCE 1 IN 8000- 1 IN 30,00025-80% MATERNAL MORTALITY50% FOETAL DEATH

AMNIOTIC FLUID EMBOLISM

DEVASTATING EMERGENCY

HIGH MORTALITY

NEUROLOGICAL DYSFUNCTION

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HOW DOES IT STARTS?

PATHOPHYSIOLOGY

AMNIOTIC FLUID ENTRY

ACTIVATES PROCOAGULANT SYSTEM DIC

PULMONARY MICROEMBOLIZATION

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FIRST PHASE[30 MIN] SECOND PHASE

BIPHASIC RESPONSE

PULMONARY VASOSPASM

PULMONARY HYPERTENSION

RIGHT HEART DYSFUNCTION

LVF, PULMONARY EDEMA

ARDS

DIC

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“ANAPHYLACTOID SYNDROME OF PREGNANCY”

?COMMON MECHANISM

AFE

SEPSIS

ANAPHYLAXIS

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CLINICAL FEATURES

A/C RESPIRATORY FAILURE, HYPOXIA

HEMODYNAMIC COLLAPSE

COAGULOPATHY

ANXIETY NAUSEA CHILLS• .

CYANOSIS COMA• .

More details: AFE Registry Criteria by Clark et al 1983-1995

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DIFFERENTIAL DIAGNOSIS

•PLACENTAL ABRUPTION

•ECLAMPSIA

•UTERINE RUPTURE

OBSTETRIC CONDITIONS

•PULMONARY EMBOLISM , VAE

•M.I., CVA, ASPIRATION PNEUMONIA

•ANAPHYLAXIS

NON OBSTETRIC CONDITIONS

•TOTAL SPINAL ANESTHESIA

•LOCAL ANESTHETIC TOXICITY

ANESTHETIC COMPLICATIONS

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DIAGNOSIS

CHEST X-RAY• NORMAL / DIFFUSE

PULMONARY OEDEMA

INVASIVE MONITORING• ↑CVP,PAP,PACWP

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DIAGNOSIS

IMMUNOSTAINING

• MONOCLONAL ANTIBODY DIRECTED AGAINST A GLYCOPROTEIN FOUND IN AMNIOTIC FLUID

DETECTION OF ZINC COPROPORPHYRIN IN MATERNAL PLASMA• A COMPONENT OF MECONIUM

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MANAGEMENT

• OXYGEN• INTUBATION• MECHANICAL VENTILATIONOXYGENATION &

VENTILATION

• LARGE BORE IVA• IV FLUIDS & BLOOD PRODUCTS• INTRA ARTERIAL / PA CATHETER• INOTROPES

HEMODYNAMIC SUPPORT

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MANAGEMENT

• CRYOPPT,FFP,PLATELETS,BLOOD• CRYOPPT REPLACES FIBRINOGEN &

FIBRONECTIN HELP IN REMOVAL OF CELLULAR DEBRIS BY RES

• ?EPIDURAL HEMATOMA

CORRECT COAGULOPATHY

• CCF,PULMONARY EDEMA,ARDS• ARF, NEUROLOGICAL SEQUELAE

TREAT SEQUELAE OF SHOCK

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MANAGEMENT

• NECESSARY TO SUCCESSFULLY PERFORM CPR IN THIRD TRIMESTERDELIVERY

FOETAL MONITORING

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VENOUS AIR EMBOLISM

• ..

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Malinow et al published the first study of VAE during cesarean delivery in 1987¹

Subclinical VAE occurred in 97% of patients receiving GA for cesarean delivery²

VAE occurred in approx 67% of patients receiving neuraxial anesthesia³

1.Malinow AM et al,Anesthesiology 19872.Lew TWK et al, VAE during CS,Anesth Analg 19933.Handler JS,VAE during CS Reg Anesth 1990

VENOUS AIR EMBOLISM

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Pressure gradient as small as -5 cm of H₂O

PATHOPHYSIOLOGY

Surgical Field

Heart

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RISK FACTORS

PATHOPHYSIOLOGY

LEFT UTERINE DISPLACEMENT

TRENDELENBERG POSITION

REDUCED CVP

EXTERIORISATION OF UTERUS

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PATHOPHYSIOLOGY

AIR

P-HTN

V/Q MISMATCH

IMPAIRED GAS

EXCHANGE

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Paradoxical Air Embolism may occur in case of intracardiac defects

PATHOPHYSIOLOGY

AIR TRAP RV-PA

PUL BLOOD FLOW STOP ↓LV FILLING

↓COCARDIAC ARREST

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Morbidity and mortality depends on

CLINICAL FEATURES

CLINICAL FEATURES

VOLUME OF AIRRATE OF INFUSION OF AIRSITE OF EMBOLIZATION>3 ML / KG OF AIR IS FATAL

GASPING RESPIRATIONHEAVY, NON RADIATING RETROSTERNAL CHEST PAIN

ARRHYTHMIARAISED CVPHYPOTENSIONDECREASED OXYGEN SATURATIONCHANGE IN HEART SOUNDSMILL WHEEL MURMERINCREASED AIRWAY PRESSURE

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Trans esophageal echo

Doppler Ultrasound

ETCO₂ETN₂PULMONARY ARTERY PRESSURECVPECG

MONITORING / DIAGNOSIS

DETECT <0.015 ML / KG/MIN OF AIRHIGHLY SENSITIVE

COMBINATION OF A PRECORDIAL DOPPLER & ETCO₂ HAVE HIGH SENSITIVITY & SPECIFICITY

P-WAVE CHANGES, ST-T ↓,HEART BLOCK, BRADYCARDIA

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PREVENT FURTHER AIR ENTRY

MANAGEMENT

NOTIFY SURGEONFLOOD THE SURGICAL FIELD WITH SALINEJUGULAR COMPRESSIONLOWER THE HEAD / 15⁰ HEAD DOWN TILT IN LEFT LATERAL DECUBITUS POSITION-DURANTS POSITION

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TREAT INTRAVASCULAR AIR

MANAGEMENT

ASPIRATE AIR VIA CENTRAL VENOUS CATHETER [>200ML OF FOAM OVER A PERIOD OF 3 MINUTES]DISCONTINUE NITROUS OXIDEFiO₂ :1.0PRESSORS /INOTROPESCHEST COMPRESSIONNEURODIAGNOSTIC IMAGINGHYPERBARIC O₂ THERAPY IN PARADOXICAL AIR EMBOLISM

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5-10⁰ HEAD UP TILT WHEN UTERUS IS EXTERIORIZED

PRECORDIAL DOPPLER MONITORING IN HIGH RISK CASES

ADEQUATE HYDRATION TO RAISE CVP AND LA PRESSURE

PREVENTION

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REFERENCES

•Chestnut’s Obstetric Anesthesia Principles and Practice, David H. Chestnut,[2009] 4/e•Shnider and Levinsons anesthesia for obstetrics,4/e•Why Mothers Die 2004-2005 Report; the Confidential Review of Maternal Deaths in Kerala•ASA Abstracts, Cardiac Arrest during Labor: Amniotic Fluid Embolism with Thrombus in Patent Foramen Ovale. Aparna Dalal, M.D., Mark Shulman, M.D. Anesthesiology, Caritas St. Elizabeth's Medical Center, Boston, MA, Anesthesiology 2008; 109 A1337• Martin SR, Foley MR. Intensive care in obstetrics: an evidence-based review. Am J Obstet Gynecol. 2006 Sep;195(3):673-89. • Porat S, Leibowitz D, Milwidsky A, Valsky DV, Yagel S, Anteby EY.Transient Intracardiac thrombi in Amniotic fluid embolism.BCOG. 2004 May;111(5):506-10.• Saad A, El-Husseini N, Nader GA, Gharzuddine W. Echocardiographically detected mass "in transit" in early amniotic fluid embolism. Eur J Echocardiogr. 2006 Aug;7(4):332-5. Epub 2005 Aug 10.

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