Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 57

Maternal Collapse

PowerPoint
due to Embolism
Template
Dr Unnikrishnan P
P.G.Student
Medical College, Trivandrum
IMPORTANT CAUSES

THROMBOEMBOLISM

AMNIOTIC FLUID EMBOLISM

VENOUS AIR EMBOLISM

Anaestesiologist is often involved in the


resuscitation of patients with embolic
disorders
VENOUS
•.

THROMBO EMBOLISM
•.
VENOUS THROMBOEMBOLISM
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

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


AETIOLOGY
Changes in coagulation

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


AETIOLOGY

Venous stasis

Vascular damage: caesarean > vaginal

Obstetric conditions:
PIH
Multiple pregnancy

VIRCHOW’S TRIAD : HYPERCOAGULABILITY, STASIS, ENDOTHELIAL INJURY


RISK FACTORS

Increasing age

Prolonged immobilization

Obesity

Thrombophilia

Previous thromboembolism

Cesarean delivery

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


PATHOPHYSIOLOGY

↓BP ↓CORONARY
OCCLUSION PERFUSION
PRESSURE

↓LV VOLUME RV ISCHEMIA


↑PVR,PAP
↓COMPLIANCE RV FAILURE

RV OVERLOAD IV SEPTUMLV
PATHOPHYSIOLOGY

↓PaO₂
↑P(A-a)O₂
IMPAIRED GAS EXCHANGE
[↑DEAD SPACE,SHUNT,HYPOXEMIA,DECREASED DIFFUSION]
V/Q MISMATCH
ALVEOLAR HYPER VENTILATION
↑AIRWAY RESISTANCE
↓COMPLIANCE
[EDEMA, HEMORRHAGE,LOSS OF SURFACTANT]
ATELECTASIS
CLINICAL FEATURES: SYMPTOMS
DYSPNOEA
PALPITATION
ANXIETY
CHEST PAIN [PLEURITIC]
COUGH
HEMOPTYSIS
SYNCOPE
COLLAPSE
CLINICAL FEATURES: SIGNS

TACHYPNOEA
CREPITATION
↓ED BREATH SOUNDS
FEVER
TACHYCARDIA
ACCENTUATED S₂
JUGULAR VENOUS DISTENSION
LEFT PARASTERNAL HEAVE
HEPATIC ENLARGEMENT
THROMBOPHLEBITIS/ 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.
DIAGNOSTIC EVALUATION

ECG

RV STRAIN PATTERN
RIGHT AXIS DEVIATION
P-PULMONALE
T INVERSION IN V₁-V₄
SUPRAVENTRICULAR ARRHYTHMIAS
S₁Q₃T₃ PATTERN:
DEEP S IN L₁ DEEP Q IN L₃ T INVERSION IN L₃
DIAGNOSTIC EVALUATION

CHEST X-RAY

BLANCHING / OLIGEMIC AREA


WESTERMARK’S SIGN
HAMPTONS HUMP
ELEVATED HEMIDIAPHRAGM
FOCAL INFILTRATES
PLEURAL EFFUSION
ATELECTASIS
HAMPTON’S HUMP
DIAGNOSTIC EVALUATION

INVASIVE HEMODYNAMIC MONITORING


NORMAL TO LOW PULMONARY ARTERY OCCLUSSION
PRESSURE
INCREASED MEAN PULMONARY ARTERY PRESSURE
INCREASED CVP

ARTERIAL BLOOD GAS ANALYSIS


WIDENED P(A-a)O₂
REDUCED PaO₂
REDUCED PaCO₂

ELISA FOR D-DIMER


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

VENTILATION PERFUSION SCAN


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

HIGH PROBABILITY • START


SCAN & HIGH ANTICOAGULATION
CLINICAL SUSPICION

INDETERMINATE • SPIRAL CT
SCAN & HIGH • PULMONARY
CLINICAL SUSPICION ANGIOGRAPHY
DIAGNOSTIC EVALUATION

SPIRAL CT
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
INVASIVE
INTRALUMINAL FILLING DEFECT

MAGNETIC RESONANCE VENOGRAPHY


DIAGNOSTIC EVALUATION

ECHOCARDIOGRAPHY

SENSITIVITY AND NEGATIVE PREDICTIVE


VALUE HIGH WHEN COMBINED WITH A
LOWER LIMB USG
CAN DETECT A CLOT OR CONSEQUENT RV
DYSFUNCTION
OBVIATE NEED FOR INVASIVE PROCEDURES
HASTEN START OF ANTICOAGULATION

COMPRESSION USG
PROPHYLAXIS
PHARMACOLOGICAL
INTERMITTENT PNEUMATIC COMPRESSION
ELASTIC STOCKINGS

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
THERAPY - DVT
UNFRACTIONATED HEPARIN [UFH]#
5000 U [80-100 U / KG] IV LOADING DOSE
FOLLOWED BY 15-20 U / KG / HOUR IV INFUSION
aPTT KEPT AT 1.5 TO 2.5 TIMES NORMAL
IV INFUSION X 5-7 DAYS S/C HEPARIN
DOSE MAY HAVE TO BE ↑ED BY 50% IN 2 ND AND 3
RD TRIMESTERS
DISCONTINUED WHEN PATIENT BEGINS ACTIVE
LABOR / 24 HOURS BEFORE CS
WARFARIN CAN BE STARTED; WHEN INR 2-3, HEPARIN
CAN BE STOPPED
ANTICOAGULATION 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
LOW MOLECULAR WEIGHT HEPARIN [LMWH]

GREATER ANTITHROMBOTIC ACTIVITY [ANTIFACTOR Xa]


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

Enoxaparin
40 MG OD-BD [1 MG = 100 U] PROPHYLAXIS
30-80 MG BD THERAPEUTIC ANTICOAGULATION
Dalteparin
2500-5000 U OD-BD THROMBOPROPHYLAXIS
100 U/KG BD THERAPEUTIC ANTICOAGULATION

#Sipes SL,Venous thromboembolic disease in pregnancy ;Semin Perinatol 1990


#American College of Obst & Gyn Comm. on practice;ACOG Practice bulletin no:19,AUG2000
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
CONTRA INDICATIONS-
ANTICOAGULATION

ABSOLUTE
INTRACRANIAL BLEED
SERIOUS ACTIVE BLEEDING
RECENT BRAIN/EYE/SPINAL SURGERY
SEVERE THROMBOCYTOPENIA
RELATIVE
HEMORRHAGIC DIATHESIS
RECENT STROKE
RECENT MAJOR SURGERY
SEVERE UNCONTROLLED HYPERTENSION [DBP>110 MM OF HG]
BACTERIAL ENDOCARDITIS
INFERIOR VENACAVAL
INTERRUPTION
Transvenous implantation of an IVC filter

ANTICOAGULATION CONTRAINDICATED
ANTICOAGULATION FAILED
PROXIMAL DVT
RECURRENT EMBOLI
THROMBOLYSIS
MASSIVE EMBOLISM WITH HEMODYNAMIC
INSTABILITY
ECHO EVIDENCE OF RV HYPOFUNCTION
EXTENSIVE ILEOFEMORAL THROMBOSIS
40% OBSTRUCTION ON PULMONARY
ANGIOGRAPHY
THROMBOLYSIS

Monitoring of coagulation:
Thrombin time [Most sensitive]
aPTT
FDP

Complications:
Maternal hemorrhage, Placental abruption
THROMBOLYSIS
STREPTOKINASE
2,50,000 IU OVER 30 TO 60 MINUTES FOLLOWED BY
1,00,000 IU/HOUR FOR 24 HOURS

UROKINASE
LESS ANTIGENIC
INITIAL DOSE 4400 IU FOLLOWED BY 4400 IU / KG /HOUR

RECOMBINANT TISSUE PLASMINOGEN


ACTIVATOR [ rt- PA ]
CLOT SPECIFIC
DOES NOT INTRODUCE SYSTEMIC FIBRINOLYSIS
10 MG IV BOLUS ; FOLLOWED BY 90 MG IN 2 HOURS
SURGICAL EMBOLECTOMY

THROMBOLYSIS CONTRAINDICATED
THROMBOLYSIS FAILED
RAPIDLY DETERIORATING PATIENT
ANAESTHETIC IMPLICATIONS-
ANTICOAGULATED PATIENT

ANTICIPATE AIRWAY BLEEDING

ARRANGE BLOOD PRODUCTS

ANTICOAGULATION & NEURAXIAL BLOCKADE


AMNIOTIC FLUID

EMBOLISM
AMNIOTIC FLUID EMBOLISM

DEVASTATING EMERGENCY

HIGH MORTALITY

NEUROLOGICAL DYSFUNCTION

INCIDENCE 1 IN 8000- 1 IN 30,000


25-80% MATERNAL MORTALITY
50% FOETAL DEATH
PATHOPHYSIOLOGY
HOW DOES IT STARTS?

AMNIOTIC FLUID ENTRY

ACTIVATES PROCOAGULANT SYSTEM


 DIC

PULMONARY MICROEMBOLIZATION
BIPHASIC RESPONSE

FIRST PHASE[30 MIN] SECOND PHASE

PULMONARY LVF, PULMONARY EDEMA


VASOSPASM

PULMONARY
ARDS
HYPERTENSION

RIGHT HEART
DIC
DYSFUNCTION
“ANAPHYLACTOID SYNDROME OF
PREGNANCY”

SEPSIS

AFE ANAPHYLAXIS

?COMMON
MECHANISM
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


• TOTAL SPINAL ANESTHESIA
COMPLICATIONS
• LOCAL ANESTHETIC TOXICITY
ANESTHETIC
• PULMONARY EMBOLISM , VAE CONDITIONS
• M.I., CVA, ASPIRATION PNEUMONIA NON OBSTETRIC
• ANAPHYLAXIS
• PLACENTAL ABRUPTION CONDITIONS
• ECLAMPSIA OBSTETRIC
• UTERINE RUPTURE
DIFFERENTIAL DIAGNOSIS
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
OXYGENATION & • INTUBATION
• MECHANICAL VENTILATION
VENTILATION

• LARGE BORE IVA


HEMODYNAMIC • IV FLUIDS & BLOOD PRODUCTS
• INTRA ARTERIAL / PA CATHETER
SUPPORT • INOTROPES
MANAGEMENT

• CRYOPPT,FFP,PLATELETS,BLOOD
• CRYOPPT REPLACES FIBRINOGEN &
CORRECT FIBRONECTIN HELP IN REMOVAL
COAGULOPATHY OF CELLULAR DEBRIS BY RES
• ?EPIDURAL HEMATOMA

• CCF,PULMONARY
TREAT EDEMA,ARDS
SEQUELAE OF • ARF, NEUROLOGICAL
SHOCK SEQUELAE
MANAGEMENT

• NECESSARY TO
SUCCESSFULLY PERFORM
DELIVERY CPR IN THIRD TRIMESTER

FOETAL
MONITORING
VENOUS AIR EMBOLISM
•.
.
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 1987


2.Lew TWK et al, VAE during CS,Anesth Analg 1993
3.Handler JS,VAE during CS Reg Anesth 1990
PATHOPHYSIOLOGY

Pressure gradient as small as -5 cm of H₂O

Surgical
Field

Heart
PATHOPHYSIOLOGY
RISK FACTORS

LEFT UTERINE DISPLACEMENT

TRENDELENBERG POSITION

REDUCED CVP

EXTERIORISATION OF UTERUS
PATHOPHYSIOLOGY

V/Q
MISMATCH
IMPAIRED
P-HTN GAS
EXCHANGE

AIR
PATHOPHYSIOLOGY

AIR TRAP PUL BLOOD ↓LV


RV-PA FLOW STOP FILLING

CARDIAC
ARREST ↓CO

Paradoxical Air Embolism may occur in case


of intracardiac defects
CLINICAL FEATURES

Morbidity and mortality depends on


VOLUME OF AIR
RATE OF INFUSION OF AIR
SITE OF EMBOLIZATION
>3 ML / KG OF AIR IS FATAL

CLINICAL FEATURES
GASPING RESPIRATION
HEAVY, NON RADIATING RETROSTERNAL CHEST PAIN

ARRHYTHMIA
RAISED CVP
HYPOTENSION
DECREASED OXYGEN SATURATION
CHANGE IN HEART SOUNDS
MILL WHEEL MURMER
INCREASED AIRWAY PRESSURE
MONITORING / DIAGNOSIS

Trans esophageal echo


DETECT <0.015 ML / KG/MIN OF AIR
HIGHLY SENSITIVE

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

ETCO₂
ETN₂
PULMONARY ARTERY PRESSURE
CVP
ECG
P-WAVE CHANGES, ST-T ↓,HEART BLOCK, BRADYCARDIA
MANAGEMENT

PREVENT FURTHER AIR ENTRY


NOTIFY SURGEON
FLOOD THE SURGICAL FIELD WITH SALINE
JUGULAR COMPRESSION
LOWER THE HEAD / 15⁰ HEAD DOWN TILT
IN LEFT LATERAL DECUBITUS POSITION-
DURANTS POSITION
MANAGEMENT

TREAT INTRAVASCULAR AIR

ASPIRATE AIR VIA CENTRAL VENOUS CATHETER


[>200ML OF FOAM OVER A PERIOD OF 3
MINUTES]
DISCONTINUE NITROUS OXIDE
FiO₂ :1.0
PRESSORS /INOTROPES
CHEST COMPRESSION
NEURODIAGNOSTIC IMAGING
HYPERBARIC O₂ THERAPY IN PARADOXICAL
AIR EMBOLISM
PREVENTION

5-10⁰ HEAD UP TILT WHEN UTERUS IS


EXTERIORIZED
PRECORDIAL DOPPLER MONITORING IN HIGH RISK
CASES
ADEQUATE HYDRATION TO RAISE CVP AND LA
PRESSURE
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.
.

PowerPoint
Thanks!
Template

You might also like