MATERNAL COLLAPSE DUE TO EMBOLISM
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TemplateDr Unnikrishnan PP.G.StudentMedical College, Trivandrum
Maternal Collapse due to Embolism
THROMBOEMBOLISM
AMNIOTIC FLUID EMBOLISM
VENOUS AIR EMBOLISM
Anaestesiologist is often involved in the resuscitation of patients with embolic disorders
IMPORTANT CAUSES
VENOUS• .
THROMBO EMBOLISM• .
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
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
Venous stasis
Vascular damage: caesarean > vaginal
Obstetric conditions: PIHMultiple pregnancy
AETIOLOGY
VIRCHOW’S TRIAD : HYPERCOAGULABILITY, STASIS, ENDOTHELIAL INJURY
Increasing age
Prolonged immobilization
Obesity
Thrombophilia
Previous thromboembolism
Cesarean delivery
RISK FACTORS
ASRA GUIDELINES [THIRD EDITION];Reg Anesth Pain Med 2010
PATHOPHYSIOLOGY
OCCLUSION
↑PVR,PAP
RV OVERLOAD IV SEPTUMLV
↓LV VOLUME↓COMPLIANCE
↓BP ↓CORONARY PERFUSION PRESSURE
RV ISCHEMIA RV FAILURE
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
CLINICAL FEATURES: SYMPTOMS
DYSPNOEAPALPITATIONANXIETYCHEST PAIN [PLEURITIC]COUGHHEMOPTYSISSYNCOPECOLLAPSE
CLINICAL FEATURES: SIGNS
TACHYPNOEACREPITATION↓ED BREATH SOUNDSFEVERTACHYCARDIAACCENTUATED S₂JUGULAR VENOUS DISTENSIONLEFT PARASTERNAL HEAVEHEPATIC ENLARGEMENTTHROMBOPHLEBITIS/ FEATURES OF DVT
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.
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
CHEST X-RAY
DIAGNOSTIC EVALUATION
BLANCHING / OLIGEMIC AREAWESTERMARK’S SIGNHAMPTONS HUMPELEVATED HEMIDIAPHRAGMFOCAL INFILTRATESPLEURAL EFFUSIONATELECTASIS
HAMPTON’S HUMP
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
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
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
DIAGNOSTIC EVALUATION
PULMONARY ANGIOGRAPHY
INVASIVEINTRALUMINAL FILLING DEFECT
MAGNETIC RESONANCE VENOGRAPHY
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
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
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
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
PULMONARY EMBOLISM-TREATMENT: GOALS
SUPPORT MATERNAL CIRCULATION
PROVIDE ADEQUATE MATERNAL AND FOETAL OXYGENATION
PREVENT RECURRENCE
MINIMIZE LONG TERM MORBIDITY
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
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
Transvenous implantation of an IVC filter
INFERIOR VENACAVAL INTERRUPTION
ANTICOAGULATION CONTRAINDICATED ANTICOAGULATION FAILED PROXIMAL DVT RECURRENT EMBOLI
THROMBOLYSIS
MASSIVE EMBOLISM WITH HEMODYNAMIC INSTABILITY
ECHO EVIDENCE OF RV HYPOFUNCTIONEXTENSIVE ILEOFEMORAL THROMBOSIS40% OBSTRUCTION ON PULMONARY
ANGIOGRAPHY
Monitoring of coagulation: Thrombin time [Most sensitive]aPTTFDP
Complications:Maternal hemorrhage, Placental abruption
THROMBOLYSIS
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
SURGICAL EMBOLECTOMY
THROMBOLYSIS CONTRAINDICATED THROMBOLYSIS FAILEDRAPIDLY DETERIORATING PATIENT
ANAESTHETIC IMPLICATIONS- ANTICOAGULATED PATIENT
ANTICIPATE AIRWAY BLEEDING
ARRANGE BLOOD PRODUCTS
ANTICOAGULATION & NEURAXIAL BLOCKADE
AMNIOTIC FLUID
EMBOLISM
INCIDENCE 1 IN 8000- 1 IN 30,00025-80% MATERNAL MORTALITY50% FOETAL DEATH
AMNIOTIC FLUID EMBOLISM
DEVASTATING EMERGENCY
HIGH MORTALITY
NEUROLOGICAL DYSFUNCTION
HOW DOES IT STARTS?
PATHOPHYSIOLOGY
AMNIOTIC FLUID ENTRY
ACTIVATES PROCOAGULANT SYSTEM DIC
PULMONARY MICROEMBOLIZATION
FIRST PHASE[30 MIN] SECOND PHASE
BIPHASIC RESPONSE
PULMONARY VASOSPASM
PULMONARY HYPERTENSION
RIGHT HEART DYSFUNCTION
LVF, PULMONARY EDEMA
ARDS
DIC
“ANAPHYLACTOID SYNDROME OF PREGNANCY”
?COMMON MECHANISM
AFE
SEPSIS
ANAPHYLAXIS
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
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
DIAGNOSIS
CHEST X-RAY• NORMAL / DIFFUSE
PULMONARY OEDEMA
INVASIVE MONITORING• ↑CVP,PAP,PACWP
DIAGNOSIS
IMMUNOSTAINING
• MONOCLONAL ANTIBODY DIRECTED AGAINST A GLYCOPROTEIN FOUND IN AMNIOTIC FLUID
DETECTION OF ZINC COPROPORPHYRIN IN MATERNAL PLASMA• A COMPONENT OF MECONIUM
MANAGEMENT
• OXYGEN• INTUBATION• MECHANICAL VENTILATIONOXYGENATION &
VENTILATION
• LARGE BORE IVA• IV FLUIDS & BLOOD PRODUCTS• INTRA ARTERIAL / PA CATHETER• INOTROPES
HEMODYNAMIC SUPPORT
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
MANAGEMENT
• NECESSARY TO SUCCESSFULLY PERFORM CPR IN THIRD TRIMESTERDELIVERY
FOETAL MONITORING
VENOUS AIR EMBOLISM
• ..
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
Pressure gradient as small as -5 cm of H₂O
PATHOPHYSIOLOGY
Surgical Field
Heart
RISK FACTORS
PATHOPHYSIOLOGY
LEFT UTERINE DISPLACEMENT
TRENDELENBERG POSITION
REDUCED CVP
EXTERIORISATION OF UTERUS
PATHOPHYSIOLOGY
AIR
P-HTN
V/Q MISMATCH
IMPAIRED GAS
EXCHANGE
Paradoxical Air Embolism may occur in case of intracardiac defects
PATHOPHYSIOLOGY
AIR TRAP RV-PA
PUL BLOOD FLOW STOP ↓LV FILLING
↓COCARDIAC ARREST
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
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
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
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
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
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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