SlideShare a Scribd company logo

Pulmonary embolism

Etiology,pathophysiology,investigation and tretment of pulmonary embolism

1 of 65
Download to read offline
PULMONARY
EMBOLISM
PRESENTED BY
Dr. RAHUL GUPTA
DEFINITION
 It is an obstruction of the pulmonary artery or one of
its branches by a thrombus that originates
somewhere in the venous system or in the right
side of heart
It is most common preventable cause of death
among hospitalized patient
EPIDEMOLOGY (INDIAN SCENARIO)
 Overall, the annual incidence of PE
ranges between 23 and 69 cases per
100,000 population
 Responsible for up to 15% of all inhospital
deaths
EPIDEMOLOGY (GLOBAL SCENARIO)
The incidence of venous thromboembolism(VTE), which includes PE and
deep
venous thrombosis (DVT), has remained relatively constant, with age- and
sexadjusted rates of 117 cases per 100 000 person-years.
VTE incidence rises sharply after age 60 in both men and women, with
PE accounting for the majority of the increase.
The mortality rate associated with PE is underappreciated; it exceeds
15% in the first 3 months after diagnosis.
In nearly 25% of patients with PE, the initial clinical manifestation is
sudden death.
VIRCHOW’S
TRIAD
PREDISPOSING FACTORS
PATHOPHYSIOLOGY
Virchow’s triad of
inflammation
Recruitment of
activated platelets
releasing micro
particle
Microparticle
containing
proinflammatory
mediator binds
neutrophils
Neutrophil releases
nuclear material
forming web like
extra cellular
network
Aggregation of
platelet and
platelet dependent
thrombin
generation
PATHOPHYSIOLOGY
HEREDITARY FACTORS
 Antithrombin III deficiency
 Protein C deficiency
 Protein S deficiency
 Factor V Leiden
 Plasminogen abnormality
 Fibrinogen abnormality
CLINICAL FEATURES
SYMPTOM LIST
 73% Dyspnea
 66% Pleuritc Pain
 43% Cough
 33% Leg Swelling
 30% Leg Pain
 15% Hemoptysis
 12% Palpitations
 10% Wheezing
 5% Angina-Like pain
DIAGNOSIS
 Dr. Wells demonstrated the utility of his scoring system
for determining the pre-test probability for PEs, known
now as the Wells Criteria. This study evaluated 946
patients, and based on the criteria, divided them into
low, moderate and high probability of having a PE.
These criteria included: clinical signs and symptoms of
DVT (3 points), PE as the most likely diagnosis (3
points), tachycardia (1.5 points), immobilization for at
least 3 days or surgery within the previous 4 weeks (1.5
points), previous objectively diagnosed PE or DVT (1.5
points), hemoptysis (1 point), and malignancy (1 point).
Risk score interpretation (probability of PE) was the
following: >6 points: high risk (78.4%); 2 to 6 points:
moderate risk (27.8%);
Annals Intern Med 2001;135:98-107
Pulmonary embolism
ORIGINAL GENEVA CRITERIA
REVISED GENEVA CRITERIA
PERC RULE
 In 2004, Kline conducted a prospective study looking at eight
variables to rule out pulmonary embolism.
 The rule-out test (with poor specificity of 27% in low-risk
patients and 15% in very-low-risk patients)
 Pulmonary Embolism Rule out Criteria
(PERC) are as follows:
1. Age greater than or equal to 50 years
2. Heart rate greater than or equal to 100 beats per minute
3. Arterial oxygen saturation (SaO 2) on room air less than 95%
4. Venous thromboembolism
5. Recent (<28 days) trauma or surgery
6. Unilateral leg swelling
7. Hemoptysis
8. Oral hormone use
 Pulmonary embolism workup can be ruled out if
1. None of the above eight variables is positive.
2. A PERC evaluation is considered positive if any
one of the eight criteria are met.
 In 2015, pulmonary embolism guidelines were released by
the American College of Physicians and are summarized as
follows .
1. Use either the Wells or Geneva rules to choose tests based on a patient's risk for
pulmonary embolism.
2. If the patient is at low risk, clinicians should use the eight PERC; if a patient does
not meet all eight criteria, the risks of testing are greater than the risk for
embolism, and no testing is needed.
3. For patients at intermediate risk, or for those at low risk who do not meet all of
the rule-out criteria, use a high-sensitivity plasma D-dimer test as the initial test.
4. In patients older than 50 years, use an age-adjusted threshold (age × 10 ng/mL,
rather than a blanket 500 ng/mL), because normal D-dimer levels increase with
age.
5. Patients with a D-dimer level below the age-adjusted cutoff should not receive
any imaging studies.
6. Patients with elevated D-dimer levels should then receive imaging.
7. Patients at high risk should skip the D-dimer test and proceed to CT pulmonary
angiography, because a negative D-dimer test will not eliminate the need for
imaging in these patients.
8. Clinicians should only obtain ventilation-perfusion scans in patients with a
contraindication to CT pulmonary angiography or if CT pulmonary angiography is
unavailable.
Skwarecki B. Pulmonary embolism guidelines
released by ACP. Medscape Medical News. WebMD
Inc. Sept 28, 2015.
Pulmonary embolism
Pulmonary embolism
CHEST X-RAY
 Fleishner sign
 Hampton hump
 Westermark sign
FLEISHNER SIGN
Pulmonary embolism
Pulmonary embolism
ECG
D - DIMER
 D-dimer ELISA is an excellent screening test for
suspected PE
 A negative D-Dimer assay in low clinical probability
case rules out PE
 D-dimer ELISA was often elevated in the absence
of PE like sepsis,cancer,acute medical illness
 Low specificity and poor positive predictive value
 Sensitivity >80% for DVT and >95% for PE
ECHO
 Right ventricular enlargement or hypokinesis, especially free
wall hypokinesis, with sparing of the apex (the McConnell
sign)
 Interventricular septal flattening and paradoxical motion
toward the left ventricle, resulting in a D-shaped left ventricle
in cross section
 Tricuspid regurgitation
 Direct visualization of thrombus (more likely with
transesophageal echocardiography
CT PULMONARY ANGIOGRAPHY
 It is investigation of choice
CT PULMONARY ANGIOGRAPHY
VENOUS ULTRASONOGRAPHY
 Relies on loss of vein compressibility as the primary
criterion
 About 1/3 of pts will have no imaging evidence of DVT
 Clot may have already embolized
 Clot present in the pelvic veins (U/S usually inadequate)
 Workup for PE should continue even if dopplers (-) in a pt
in which you have a high clinical suspicion
Pulmonary embolism
LUNG SCAN
 As many as 40% of pts with high clinical suspicion for
PE and low probability scans have a PE on angiogram
 It has become second line diagnostic test for patients
who cannot tolerate intravenous contrast
 Small particulate aggregates of albumin labelled with
gamma emitting radio nucleid is injected
 Ventilation can be obtained by radio labelled inhaled gas
such as xenon, krypton
 A high probability scan is defined as two or more
segmental perfusion defects in presence of normal
ventilation scan
 The diagnosis of PE is very unlikely in pt with normal or
near normal scan.
Pulmonary embolism
Pulmonary embolism
PULMONARY ANGIOGRAM
 Most specific test available for diagnosis of PE
 Can detect emboli as small as 1-2 mm
 Most useful when the clinical likelihood of PE differs
substantially from the lung scan result or when the
lung scan is intermediate probability
 Definitive diagnosis is visualization of an
intraluminal filling defect .
 Secondary sign is abrupt occlusion of vessel,
segmental oligemia,prolonged arterial phase with
slow filling .
Pulmonary embolism
Pulmonary embolism
MANAGEMENT
Pulmonary embolism
HEPARIN
 Choices include either intravenous unfractionated heparin (UFH) or
subcutaneous low-molecular-weight heparin (LMWH) preparations
 Initial intravenous bolus of 80 units of heparin per kilogram followed
by a continuous infusion initiated at 18 units per kilogram per hour.
 The heparin drip is adjusted based on monitoring of the activated
partial thromboplastin time (aPPT), drawn 6 hours after initial bolus
dose, thn 6 hours after each dose adjustment , with a target aPPT
ratio of 2.0 to 3.5
 More recently, an approach using a fixed dose of subcutaneous
unfractionated heparin , administered as an initial dose of 333 U/kg
followed by a dose of 250 U/kg every 12 hours, has been
demonstrated to be as safe and effective as LMWH.
 Situations in which the use of UFH is
appropriate
1. Renal insufficiency.
2. Extremes of body weight.
3. Hypertensive crisis,
o Rapid adjustment of anticoagulation is
needed, such as…
A. Women in the late pregnancy who may need
caesarian sections,
B. Patients with recent surgery or
C. Recent history of bleeding
LMWH
 Advantages of LMWH compared with UFH include:
1. Longer half-life and ease of use
2. Ability to consistently achieve early therapeutic anticoagulation
3. No need to monitor anticoagulant effects
4. Reduced incidence of major bleeding complications
 In general, therapeutic monitoring is not needed with LMWH, but
there are situations where the therapeutic effetcts may be less
predictable and monitoring with ant-Xa levels is indicated
 Typical examples include:
1. Patients with antiphospholipid antibodies or other circulating
anticoagulants who have elevated baseline a PPT
2. Extremes of body weight(<40kgs and >50kgs)
3. Significant renal disease(creatinine clearance <30 ml/min)
4. Pregnancy
5. Unexplained bleeding or recurrent thrombosis during therapy
FONDAPARINUX
 A synthetic pentasaccharide, selective for factoe
Xa
 By binding rapidly and strongly to antithrombin,
fondaparinux catalyzes specifically the inhibition
of factor Xa, which results in inhibition of
thrombin generation
 Half-life of approx 17 hours, and is exctreted
almost completely by the kidneys
 It does not cause heparin induced
thrombocytopenia
THROMBOLYTIC THERAPY
1. Streptokinase
2. Urokinase
3. rt PA
 these agents convert circulating plasminogen to plasmin.
 The preferred fibronolytic regimen is 100mg rt PA over 2
hour.
Contraindication :
 Intracranial disease
 Recent surgery
 Trauma
 The exact role of thrombolytic agents in acute pulmonary
embolim remains controversial. While thrombolytic
therapy does appear to accelerate the rate of
thrombolysis, there is no convincing evidence to suggest
that
1.
2. It decreaes mortality,
3. Increases the ultimate extent of embolic resolution when measured
at 7 days,
4. Reduces thromboembolic recurrence rates,
5. improves symptomatic outcomes,
6. Decreases the incidence of thromboembolic pulmonary
hypertension
 Catheter- directed techniques have been successfully employed in
the setting of acute ileo- femoral DVT using doses of urokinase
ranging from 1.4 to 16 million units delivered over an average of 30
hours.
INTERVENTIONAL RADIOLOGIC
TECHNIQUES
 Interventional thrombus fragmentation.
 The devices use either pressured saline or a
rotating impeller to fragment central thrombi.
 The fragments are either aspirated through a
separate port on the catheter or allowed to migrate
distally.
 There limitations, including a risk of paradoxical
embolism from the clot fragments
PULMONARY EMBOLECTOMY
 It is reasonable to consider surgical
embolectomy in patients with
1. Persistent hypotension.
2. Shock.
3. Cardiac arrest.
4. Failed thrombolysis.
5. Contraindications to thrombolytics.
ORAL ANTICOAGULANTS
 Warfarin inhibits gamma carboxylation activation of
coagulation factors II, VII, IX, and X as well as
proteins C and S
Use of Warfarin without heparin is
strongly discouraged
1. It generally takes 3 to 5 days of warfarin to
achieve full therapeutic eficacy.
2. In patients with protein C deficiency, skin necrosis
or paradoxical thrombosis may occur.
WARFARIN
 INR range between 2 and 3 is recommended for most
patients
 Another rare complication of warfarin use is cholesterol
microembolism (“purple toes” syndrome), which is
thought to be due to cholesterol crystal release from
ulcerated intravascular plaques
 an initial daily dose of 5 or 10 mg with use of an
standardized nomogram to dose adjust based on INR
values obtained on days 3 and 5
 patients should receive atleast 5 days of combined
heparin and warfaein therapy, including atleast 2 days in
which the INR is in a therapeutic range prior to stopping
heparin
 Because of the teratogenic potential of warfarin, UFH or
LMWH should be used in pregnant women who
developed VTE in the first trimesters
DURATION OF THERAPY
 The risk of recurrent disease after 3 months of anticoagulation
is still in the region of 10%; therefore, the patients should be
treated with warfarin for 3 to 6 months
 Patients with idiopathic thromboembolism have higher rate of
recurrence therefore treated for atleast 6 to 12 months
 Patients with antiphospholipid antibody syndrome have
considerable risk of recurrence, therefore treated for minimum
12 months with consideration of life-long therapy
 In patients with >2 episodes of recurrence life-long
anticoagulation given
DEEP VEIN THROMBOSIS
 Thrombolysis
 Anticoagulation
 Vena cava filter
VENA CAVA FILTER
 Used in patients with contraindication to anticoagulation or patients
with recurrent embolism while on adequate anticoagulation
 Long term IVC filter increases risk of thromboembolism
 This observation lead to recent development of retrievable filters
 Four types of retrievable filters:
1. Gunther tulip filter
2. ALN filter
3. Recovery filter
4. OptEase filter
VENA CAVA FILTER
PROPHYLAXIS
INTERMITTENT PNEUMATIC COMPRESSION
 The sleeves are inflated
for a few seconds, one
leg at a time, to
compress the veins in
the legs every minute or
so.
 By causing contraction
of the leg muscles, the
sleeves mimic the
process of walking in
immobilized patients.
This ensures blood is
pushed around the
system, rather than
pooling in the legs
GRADUATED COMPRESSION STOCKING
 Compression stockings are
made of a special elastic
fabric. They are very tight at
the ankle and are less tight
as the stocking moves up the
leg. This graduated tightness
helps the leg muscles
squeeze fluid up the leg,
which improves blood flow
from the leg back to the heart
and decreases leg swelling
and pain.
Pulmonary embolism
TYPE OF EMBOLISM
1. Fat embolism
2. Venous air embolism
3. Amniotic fluid embolism
4. Septic embolism
5. Tumour embolism
6. Sickle cell disease
FAT EMBOLISM
 Due to entry of neutral at in vascular system
 Leads to dysnea, hypoxemia, petechiae, mental confusion
 Lag time of 24 to 72 hours in the onset of syndrome following the
inciting event
 Most common inciting event, fracture of long bones
 Pathophysiology :
1. Actual vascular obstruction by neutral particle of fat
2. Injurious effect of free fatty acids released by the action of lipases on
the neutral fat
 Supportive treatment advised
 Other suggested treatment intravenous ethanol, albumin, dextran,
heparin
VENOUS AIR EMBOLISM
 Due to indwelling central venous catheter, positive pressure
ventilation, trauma to thorax
 Physiological consequence due to abrupt rise in pulmonary artery
pressure
 Treatment is prevention and early detection
 Patient positioning (Trendelenburg position with left side down)
 Removal of air through central venous catheter
 Direct needle aspiration
 Closed chest cardiac massage
 Increase absorption with use of 100% oxygen
AMNIOTIC FLUID EMBOLISM
 Third leading cause of maternal mortality
 Amniotic fluid contains particulate material that can cause pulmonary
vascular obstruction
 Amniotic fluid has thromboplastic activity that leads to extensive fibrin
deposition in lung vasculature that leads to consumptive
coagulopathy leading to hypofibrinogenemia and thrombocytopenia
 Presence of squamous cell in pulmonary arterial blood once
considered pathognomonic.
SEPTIC EMBOLISM
 Microscopically septic phlebitis consist of purulent material mixed
with fibrin thrombus
 Chest X-ray display pulmonary infiltrates
 Treatment consists of anti microbial agents
TUMOUR EMBOLISM
 Most common site of origin breast, lungs, prostate, stomach and liver
 Clinical feature is typically subacute and involves progressive dysnea
, techypnea, techycardia
 Pulmonary angiographic findings reveal delapyed vascular filling,
pruning and tortuosity
Pulmonary embolism

Recommended

Pulmonary edema & Management
Pulmonary edema & ManagementPulmonary edema & Management
Pulmonary edema & Managementhaseeb tariq
 
Pulmonary embolism
Pulmonary embolism Pulmonary embolism
Pulmonary embolism Zahra Khan
 
Pulmonary hypertension
Pulmonary hypertensionPulmonary hypertension
Pulmonary hypertensionAbhay Mange
 
Pulmonary Oedema - Pathophysiology - Approach & Management
Pulmonary Oedema  - Pathophysiology - Approach & ManagementPulmonary Oedema  - Pathophysiology - Approach & Management
Pulmonary Oedema - Pathophysiology - Approach & ManagementArun Vasireddy
 
ARDS - Diagnosis and Management
ARDS - Diagnosis and ManagementARDS - Diagnosis and Management
ARDS - Diagnosis and ManagementVitrag Shah
 
pulmonary embolism
pulmonary embolismpulmonary embolism
pulmonary embolismaravazhi
 
Pulmonary hypertension (2014) dr.tinku joseph
Pulmonary hypertension (2014) dr.tinku josephPulmonary hypertension (2014) dr.tinku joseph
Pulmonary hypertension (2014) dr.tinku josephDr.Tinku Joseph
 

More Related Content

What's hot

Pulmonary embolism
Pulmonary embolismPulmonary embolism
Pulmonary embolismAmir Mahmoud
 
Pulmonary artery Hypertension
Pulmonary artery HypertensionPulmonary artery Hypertension
Pulmonary artery HypertensionRikin Hasnani
 
Pulmonary thromboembolism
Pulmonary thromboembolismPulmonary thromboembolism
Pulmonary thromboembolismRikin Hasnani
 
Pulmonary edema
Pulmonary edemaPulmonary edema
Pulmonary edemaAmna Akram
 
Pulmonary hypertension
Pulmonary hypertensionPulmonary hypertension
Pulmonary hypertensionDoha Rasheedy
 
Acute respiratory distress syndrome (ards)
Acute respiratory distress syndrome (ards)Acute respiratory distress syndrome (ards)
Acute respiratory distress syndrome (ards)Sarath Menon
 
ACUTE RESPIRATORY DISTRESS SYNDROME. (ARDS)
ACUTE RESPIRATORY DISTRESS SYNDROME. (ARDS) ACUTE RESPIRATORY DISTRESS SYNDROME. (ARDS)
ACUTE RESPIRATORY DISTRESS SYNDROME. (ARDS) Adel Hamada
 
Interstitial Lung Disease
Interstitial Lung DiseaseInterstitial Lung Disease
Interstitial Lung DiseaseKamal Bharathi
 
Pulmonary Arterial Hypertension (PAH) presentation
Pulmonary Arterial Hypertension (PAH) presentationPulmonary Arterial Hypertension (PAH) presentation
Pulmonary Arterial Hypertension (PAH) presentationYury Viknevich
 
Pulmonary embolism ppt
Pulmonary embolism pptPulmonary embolism ppt
Pulmonary embolism pptresmigs
 
Acute Pulmonary Embolism
Acute Pulmonary EmbolismAcute Pulmonary Embolism
Acute Pulmonary EmbolismSariu Ali
 
VALVULAR HEART DISEASE
VALVULAR HEART DISEASEVALVULAR HEART DISEASE
VALVULAR HEART DISEASEhanisahwarrior
 
Acute respiratory distress syndrome
Acute respiratory distress syndromeAcute respiratory distress syndrome
Acute respiratory distress syndromePinky Rathee
 

What's hot (20)

Pulmonary embolism
Pulmonary embolismPulmonary embolism
Pulmonary embolism
 
Pulmonary artery Hypertension
Pulmonary artery HypertensionPulmonary artery Hypertension
Pulmonary artery Hypertension
 
Pulmonary edema
Pulmonary edemaPulmonary edema
Pulmonary edema
 
Pulmonary hypertension
Pulmonary hypertensionPulmonary hypertension
Pulmonary hypertension
 
Pulmonary thromboembolism
Pulmonary thromboembolismPulmonary thromboembolism
Pulmonary thromboembolism
 
Pulmonary oedema
Pulmonary oedemaPulmonary oedema
Pulmonary oedema
 
Pulmonary Embolism
Pulmonary EmbolismPulmonary Embolism
Pulmonary Embolism
 
Pulmonary edema
Pulmonary edemaPulmonary edema
Pulmonary edema
 
Pulmonary embolism
Pulmonary embolismPulmonary embolism
Pulmonary embolism
 
Ards new
Ards newArds new
Ards new
 
Pulmonary hypertension
Pulmonary hypertensionPulmonary hypertension
Pulmonary hypertension
 
Acute respiratory distress syndrome (ards)
Acute respiratory distress syndrome (ards)Acute respiratory distress syndrome (ards)
Acute respiratory distress syndrome (ards)
 
ACUTE RESPIRATORY DISTRESS SYNDROME. (ARDS)
ACUTE RESPIRATORY DISTRESS SYNDROME. (ARDS) ACUTE RESPIRATORY DISTRESS SYNDROME. (ARDS)
ACUTE RESPIRATORY DISTRESS SYNDROME. (ARDS)
 
Interstitial Lung Disease
Interstitial Lung DiseaseInterstitial Lung Disease
Interstitial Lung Disease
 
Pulmonary Arterial Hypertension (PAH) presentation
Pulmonary Arterial Hypertension (PAH) presentationPulmonary Arterial Hypertension (PAH) presentation
Pulmonary Arterial Hypertension (PAH) presentation
 
Pulmonary embolism ppt
Pulmonary embolism pptPulmonary embolism ppt
Pulmonary embolism ppt
 
Acute Pulmonary Embolism
Acute Pulmonary EmbolismAcute Pulmonary Embolism
Acute Pulmonary Embolism
 
Pulmonary hypertension
Pulmonary hypertensionPulmonary hypertension
Pulmonary hypertension
 
VALVULAR HEART DISEASE
VALVULAR HEART DISEASEVALVULAR HEART DISEASE
VALVULAR HEART DISEASE
 
Acute respiratory distress syndrome
Acute respiratory distress syndromeAcute respiratory distress syndrome
Acute respiratory distress syndrome
 

Similar to Pulmonary embolism

Pulmonary Embolism lecture 2022
Pulmonary Embolism lecture 2022Pulmonary Embolism lecture 2022
Pulmonary Embolism lecture 2022Dr.Marwan Sneymeh
 
Principles of diagnosis &amp; management of acute pulmonary
Principles of diagnosis &amp; management of acute pulmonaryPrinciples of diagnosis &amp; management of acute pulmonary
Principles of diagnosis &amp; management of acute pulmonaryVijay Yadav
 
escpe1-191229130329.pptx
escpe1-191229130329.pptxescpe1-191229130329.pptx
escpe1-191229130329.pptxEastmaMeili1
 
2019 ESC guidelines on pulmonary embolism
2019 ESC guidelines on pulmonary embolism2019 ESC guidelines on pulmonary embolism
2019 ESC guidelines on pulmonary embolismSaitej Reddy
 
Acute Pulmonary Embolism Overview lecture.ppt
Acute Pulmonary Embolism Overview lecture.pptAcute Pulmonary Embolism Overview lecture.ppt
Acute Pulmonary Embolism Overview lecture.pptBasilQuran
 
pulmonary embolism (1).pptx
pulmonary embolism (1).pptxpulmonary embolism (1).pptx
pulmonary embolism (1).pptxambujkumar90
 
pulmonary embolism.pptx
pulmonary embolism.pptxpulmonary embolism.pptx
pulmonary embolism.pptxghadeereideh
 
Venous thromboembolism, THROMBOPROPHYLAXIS and management
Venous thromboembolism, THROMBOPROPHYLAXIS and managementVenous thromboembolism, THROMBOPROPHYLAXIS and management
Venous thromboembolism, THROMBOPROPHYLAXIS and managementmauryaramgopal
 
PULMONARY EMBOLISM.pptx
PULMONARY EMBOLISM.pptxPULMONARY EMBOLISM.pptx
PULMONARY EMBOLISM.pptxGurudaspundpal
 
catheter based management of pulmonary embolism
catheter based management of pulmonary embolismcatheter based management of pulmonary embolism
catheter based management of pulmonary embolismAmit Verma
 
Pulmonary embolism 2
Pulmonary embolism 2Pulmonary embolism 2
Pulmonary embolism 2samirelansary
 
Pneumothorax.pptx
Pneumothorax.pptxPneumothorax.pptx
Pneumothorax.pptxMISSCOM1
 
Revisiting Pulmonary embolism Guidelines
Revisiting Pulmonary embolism GuidelinesRevisiting Pulmonary embolism Guidelines
Revisiting Pulmonary embolism GuidelinesEmad Qasem
 

Similar to Pulmonary embolism (20)

Pulmonary Embolism lecture 2022
Pulmonary Embolism lecture 2022Pulmonary Embolism lecture 2022
Pulmonary Embolism lecture 2022
 
Pulmonary embolism
Pulmonary embolismPulmonary embolism
Pulmonary embolism
 
Principles of diagnosis &amp; management of acute pulmonary
Principles of diagnosis &amp; management of acute pulmonaryPrinciples of diagnosis &amp; management of acute pulmonary
Principles of diagnosis &amp; management of acute pulmonary
 
escpe1-191229130329.pptx
escpe1-191229130329.pptxescpe1-191229130329.pptx
escpe1-191229130329.pptx
 
2019 ESC guidelines on pulmonary embolism
2019 ESC guidelines on pulmonary embolism2019 ESC guidelines on pulmonary embolism
2019 ESC guidelines on pulmonary embolism
 
Acute Pulmonary Embolism Overview lecture.ppt
Acute Pulmonary Embolism Overview lecture.pptAcute Pulmonary Embolism Overview lecture.ppt
Acute Pulmonary Embolism Overview lecture.ppt
 
pulmonary embolism (1).pptx
pulmonary embolism (1).pptxpulmonary embolism (1).pptx
pulmonary embolism (1).pptx
 
Dr.cazaam
Dr.cazaamDr.cazaam
Dr.cazaam
 
pulmonary embolism.pptx
pulmonary embolism.pptxpulmonary embolism.pptx
pulmonary embolism.pptx
 
Venous thromboembolism, THROMBOPROPHYLAXIS and management
Venous thromboembolism, THROMBOPROPHYLAXIS and managementVenous thromboembolism, THROMBOPROPHYLAXIS and management
Venous thromboembolism, THROMBOPROPHYLAXIS and management
 
PULMONARY EMBOLISM.pptx
PULMONARY EMBOLISM.pptxPULMONARY EMBOLISM.pptx
PULMONARY EMBOLISM.pptx
 
catheter based management of pulmonary embolism
catheter based management of pulmonary embolismcatheter based management of pulmonary embolism
catheter based management of pulmonary embolism
 
Pulmonary embolism 2
Pulmonary embolism 2Pulmonary embolism 2
Pulmonary embolism 2
 
Pneumothorax.pptx
Pneumothorax.pptxPneumothorax.pptx
Pneumothorax.pptx
 
Pulmonary embolism
Pulmonary embolismPulmonary embolism
Pulmonary embolism
 
Pulmonaryembolism
PulmonaryembolismPulmonaryembolism
Pulmonaryembolism
 
Revisiting Pulmonary embolism Guidelines
Revisiting Pulmonary embolism GuidelinesRevisiting Pulmonary embolism Guidelines
Revisiting Pulmonary embolism Guidelines
 
Pulmonary Embolism.pptx
Pulmonary Embolism.pptxPulmonary Embolism.pptx
Pulmonary Embolism.pptx
 
Pulmonary embolism
Pulmonary embolismPulmonary embolism
Pulmonary embolism
 
Pulmonary embolism
Pulmonary embolismPulmonary embolism
Pulmonary embolism
 

Recently uploaded

World Hearing Day 2024 : The Sound of Life
World Hearing Day 2024 : The Sound of LifeWorld Hearing Day 2024 : The Sound of Life
World Hearing Day 2024 : The Sound of LifeEar solutions
 
Nerve Resources ESSER March2024. YouTube videos and Hnad SUrgery Education Mo...
Nerve Resources ESSER March2024. YouTube videos and Hnad SUrgery Education Mo...Nerve Resources ESSER March2024. YouTube videos and Hnad SUrgery Education Mo...
Nerve Resources ESSER March2024. YouTube videos and Hnad SUrgery Education Mo...Vaikunthan Rajaratnam
 
Yantra used in Rasashastra: Equipments and Machineries
Yantra used in Rasashastra: Equipments and MachineriesYantra used in Rasashastra: Equipments and Machineries
Yantra used in Rasashastra: Equipments and MachineriesAparnaNandakumar12
 
STUDY OF BASIC FUNDAMENTALS OF URINE FORMATION PHYSIOLOGY.pptx
STUDY OF BASIC FUNDAMENTALS OF URINE FORMATION PHYSIOLOGY.pptxSTUDY OF BASIC FUNDAMENTALS OF URINE FORMATION PHYSIOLOGY.pptx
STUDY OF BASIC FUNDAMENTALS OF URINE FORMATION PHYSIOLOGY.pptxDr. Aniket Shilwant
 
Hydrocele and tumors of testis Introduction.pptx
Hydrocele and tumors of testis Introduction.pptxHydrocele and tumors of testis Introduction.pptx
Hydrocele and tumors of testis Introduction.pptxSizan Thapa
 
SNORING AND OBSTRUCTIVE SLEEP APNEA.pdf ENT BY QUICKMEDTALK
SNORING AND OBSTRUCTIVE SLEEP APNEA.pdf ENT BY QUICKMEDTALKSNORING AND OBSTRUCTIVE SLEEP APNEA.pdf ENT BY QUICKMEDTALK
SNORING AND OBSTRUCTIVE SLEEP APNEA.pdf ENT BY QUICKMEDTALKQuick MedTalk
 
Guía síndrome coronario agudo.pdf Guía síndrome coronario agudo.pdf
Guía síndrome coronario agudo.pdf Guía síndrome coronario agudo.pdfGuía síndrome coronario agudo.pdf Guía síndrome coronario agudo.pdf
Guía síndrome coronario agudo.pdf Guía síndrome coronario agudo.pdfJuniorAlexanderCasti
 
Fetal and Neonatal Physiology - Dr Faiza.pdf
Fetal and Neonatal Physiology - Dr Faiza.pdfFetal and Neonatal Physiology - Dr Faiza.pdf
Fetal and Neonatal Physiology - Dr Faiza.pdfMedicoseAcademics
 
Let's Talk About It: Ovarian Cancer (Shifting Focus: The Relationship with Yo...
Let's Talk About It: Ovarian Cancer (Shifting Focus: The Relationship with Yo...Let's Talk About It: Ovarian Cancer (Shifting Focus: The Relationship with Yo...
Let's Talk About It: Ovarian Cancer (Shifting Focus: The Relationship with Yo...bkling
 
Physiology of Growth hormone and applied aspects 4.pptx
Physiology of Growth hormone and applied aspects 4.pptxPhysiology of Growth hormone and applied aspects 4.pptx
Physiology of Growth hormone and applied aspects 4.pptxSai Sailesh Kumar Goothy
 
Gallstones (Cholelithiasis) Lifestyle, Risk factors, preventions.pdf
Gallstones (Cholelithiasis) Lifestyle, Risk factors, preventions.pdfGallstones (Cholelithiasis) Lifestyle, Risk factors, preventions.pdf
Gallstones (Cholelithiasis) Lifestyle, Risk factors, preventions.pdfSudeb Ganguly
 
Clinical validation of an Artificial Intelligence algorithm for the detection...
Clinical validation of an Artificial Intelligence algorithm for the detection...Clinical validation of an Artificial Intelligence algorithm for the detection...
Clinical validation of an Artificial Intelligence algorithm for the detection...Josep Vidal-Alaball
 
Best neurologist in jalandhar Punjab India
Best neurologist in jalandhar Punjab IndiaBest neurologist in jalandhar Punjab India
Best neurologist in jalandhar Punjab IndiaNHS Hospital
 
Materials for Spectacle Lenses​ UG STUDENTS.pptx
Materials for Spectacle Lenses​ UG STUDENTS.pptxMaterials for Spectacle Lenses​ UG STUDENTS.pptx
Materials for Spectacle Lenses​ UG STUDENTS.pptxKAUSAR NAHID
 
Anatomy and Histology of Skin(Dermis & Epidermis).pptx
Anatomy and Histology  of Skin(Dermis & Epidermis).pptxAnatomy and Histology  of Skin(Dermis & Epidermis).pptx
Anatomy and Histology of Skin(Dermis & Epidermis).pptxMathew Joseph
 
Death or Thantology.pptx death ppt useful ppt
Death or Thantology.pptx death ppt useful pptDeath or Thantology.pptx death ppt useful ppt
Death or Thantology.pptx death ppt useful pptDrSathishMS1
 
USE OF DRAINS IN SURGERY very good to have-1.pptx
USE OF DRAINS IN SURGERY very good to have-1.pptxUSE OF DRAINS IN SURGERY very good to have-1.pptx
USE OF DRAINS IN SURGERY very good to have-1.pptxKojoDanquah4
 
gynae pcd pharma franchise - Solace Biotech Limited
gynae pcd pharma franchise -  Solace Biotech Limitedgynae pcd pharma franchise -  Solace Biotech Limited
gynae pcd pharma franchise - Solace Biotech LimitedSBL DIGITAL
 

Recently uploaded (20)

World Hearing Day 2024 : The Sound of Life
World Hearing Day 2024 : The Sound of LifeWorld Hearing Day 2024 : The Sound of Life
World Hearing Day 2024 : The Sound of Life
 
Nerve Resources ESSER March2024. YouTube videos and Hnad SUrgery Education Mo...
Nerve Resources ESSER March2024. YouTube videos and Hnad SUrgery Education Mo...Nerve Resources ESSER March2024. YouTube videos and Hnad SUrgery Education Mo...
Nerve Resources ESSER March2024. YouTube videos and Hnad SUrgery Education Mo...
 
Yantra used in Rasashastra: Equipments and Machineries
Yantra used in Rasashastra: Equipments and MachineriesYantra used in Rasashastra: Equipments and Machineries
Yantra used in Rasashastra: Equipments and Machineries
 
STUDY OF BASIC FUNDAMENTALS OF URINE FORMATION PHYSIOLOGY.pptx
STUDY OF BASIC FUNDAMENTALS OF URINE FORMATION PHYSIOLOGY.pptxSTUDY OF BASIC FUNDAMENTALS OF URINE FORMATION PHYSIOLOGY.pptx
STUDY OF BASIC FUNDAMENTALS OF URINE FORMATION PHYSIOLOGY.pptx
 
Hydrocele and tumors of testis Introduction.pptx
Hydrocele and tumors of testis Introduction.pptxHydrocele and tumors of testis Introduction.pptx
Hydrocele and tumors of testis Introduction.pptx
 
SNORING AND OBSTRUCTIVE SLEEP APNEA.pdf ENT BY QUICKMEDTALK
SNORING AND OBSTRUCTIVE SLEEP APNEA.pdf ENT BY QUICKMEDTALKSNORING AND OBSTRUCTIVE SLEEP APNEA.pdf ENT BY QUICKMEDTALK
SNORING AND OBSTRUCTIVE SLEEP APNEA.pdf ENT BY QUICKMEDTALK
 
Guía síndrome coronario agudo.pdf Guía síndrome coronario agudo.pdf
Guía síndrome coronario agudo.pdf Guía síndrome coronario agudo.pdfGuía síndrome coronario agudo.pdf Guía síndrome coronario agudo.pdf
Guía síndrome coronario agudo.pdf Guía síndrome coronario agudo.pdf
 
Fetal and Neonatal Physiology - Dr Faiza.pdf
Fetal and Neonatal Physiology - Dr Faiza.pdfFetal and Neonatal Physiology - Dr Faiza.pdf
Fetal and Neonatal Physiology - Dr Faiza.pdf
 
Let's Talk About It: Ovarian Cancer (Shifting Focus: The Relationship with Yo...
Let's Talk About It: Ovarian Cancer (Shifting Focus: The Relationship with Yo...Let's Talk About It: Ovarian Cancer (Shifting Focus: The Relationship with Yo...
Let's Talk About It: Ovarian Cancer (Shifting Focus: The Relationship with Yo...
 
Physiology of Growth hormone and applied aspects 4.pptx
Physiology of Growth hormone and applied aspects 4.pptxPhysiology of Growth hormone and applied aspects 4.pptx
Physiology of Growth hormone and applied aspects 4.pptx
 
Gallstones (Cholelithiasis) Lifestyle, Risk factors, preventions.pdf
Gallstones (Cholelithiasis) Lifestyle, Risk factors, preventions.pdfGallstones (Cholelithiasis) Lifestyle, Risk factors, preventions.pdf
Gallstones (Cholelithiasis) Lifestyle, Risk factors, preventions.pdf
 
Clinical validation of an Artificial Intelligence algorithm for the detection...
Clinical validation of an Artificial Intelligence algorithm for the detection...Clinical validation of an Artificial Intelligence algorithm for the detection...
Clinical validation of an Artificial Intelligence algorithm for the detection...
 
A Comprehensive Fatty Liver Program .pptx
A Comprehensive Fatty Liver Program .pptxA Comprehensive Fatty Liver Program .pptx
A Comprehensive Fatty Liver Program .pptx
 
Best neurologist in jalandhar Punjab India
Best neurologist in jalandhar Punjab IndiaBest neurologist in jalandhar Punjab India
Best neurologist in jalandhar Punjab India
 
Materials for Spectacle Lenses​ UG STUDENTS.pptx
Materials for Spectacle Lenses​ UG STUDENTS.pptxMaterials for Spectacle Lenses​ UG STUDENTS.pptx
Materials for Spectacle Lenses​ UG STUDENTS.pptx
 
Anatomy and Histology of Skin(Dermis & Epidermis).pptx
Anatomy and Histology  of Skin(Dermis & Epidermis).pptxAnatomy and Histology  of Skin(Dermis & Epidermis).pptx
Anatomy and Histology of Skin(Dermis & Epidermis).pptx
 
Death or Thantology.pptx death ppt useful ppt
Death or Thantology.pptx death ppt useful pptDeath or Thantology.pptx death ppt useful ppt
Death or Thantology.pptx death ppt useful ppt
 
USE OF DRAINS IN SURGERY very good to have-1.pptx
USE OF DRAINS IN SURGERY very good to have-1.pptxUSE OF DRAINS IN SURGERY very good to have-1.pptx
USE OF DRAINS IN SURGERY very good to have-1.pptx
 
gynae pcd pharma franchise - Solace Biotech Limited
gynae pcd pharma franchise -  Solace Biotech Limitedgynae pcd pharma franchise -  Solace Biotech Limited
gynae pcd pharma franchise - Solace Biotech Limited
 
eye disorders .pptx
eye disorders .pptxeye disorders .pptx
eye disorders .pptx
 

Pulmonary embolism

  • 2. DEFINITION  It is an obstruction of the pulmonary artery or one of its branches by a thrombus that originates somewhere in the venous system or in the right side of heart It is most common preventable cause of death among hospitalized patient
  • 3. EPIDEMOLOGY (INDIAN SCENARIO)  Overall, the annual incidence of PE ranges between 23 and 69 cases per 100,000 population  Responsible for up to 15% of all inhospital deaths
  • 4. EPIDEMOLOGY (GLOBAL SCENARIO) The incidence of venous thromboembolism(VTE), which includes PE and deep venous thrombosis (DVT), has remained relatively constant, with age- and sexadjusted rates of 117 cases per 100 000 person-years. VTE incidence rises sharply after age 60 in both men and women, with PE accounting for the majority of the increase. The mortality rate associated with PE is underappreciated; it exceeds 15% in the first 3 months after diagnosis. In nearly 25% of patients with PE, the initial clinical manifestation is sudden death.
  • 7. PATHOPHYSIOLOGY Virchow’s triad of inflammation Recruitment of activated platelets releasing micro particle Microparticle containing proinflammatory mediator binds neutrophils Neutrophil releases nuclear material forming web like extra cellular network Aggregation of platelet and platelet dependent thrombin generation
  • 9. HEREDITARY FACTORS  Antithrombin III deficiency  Protein C deficiency  Protein S deficiency  Factor V Leiden  Plasminogen abnormality  Fibrinogen abnormality
  • 11. SYMPTOM LIST  73% Dyspnea  66% Pleuritc Pain  43% Cough  33% Leg Swelling  30% Leg Pain  15% Hemoptysis  12% Palpitations  10% Wheezing  5% Angina-Like pain
  • 13.  Dr. Wells demonstrated the utility of his scoring system for determining the pre-test probability for PEs, known now as the Wells Criteria. This study evaluated 946 patients, and based on the criteria, divided them into low, moderate and high probability of having a PE. These criteria included: clinical signs and symptoms of DVT (3 points), PE as the most likely diagnosis (3 points), tachycardia (1.5 points), immobilization for at least 3 days or surgery within the previous 4 weeks (1.5 points), previous objectively diagnosed PE or DVT (1.5 points), hemoptysis (1 point), and malignancy (1 point). Risk score interpretation (probability of PE) was the following: >6 points: high risk (78.4%); 2 to 6 points: moderate risk (27.8%); Annals Intern Med 2001;135:98-107
  • 17. PERC RULE  In 2004, Kline conducted a prospective study looking at eight variables to rule out pulmonary embolism.  The rule-out test (with poor specificity of 27% in low-risk patients and 15% in very-low-risk patients)  Pulmonary Embolism Rule out Criteria (PERC) are as follows: 1. Age greater than or equal to 50 years 2. Heart rate greater than or equal to 100 beats per minute 3. Arterial oxygen saturation (SaO 2) on room air less than 95% 4. Venous thromboembolism 5. Recent (<28 days) trauma or surgery 6. Unilateral leg swelling 7. Hemoptysis 8. Oral hormone use
  • 18.  Pulmonary embolism workup can be ruled out if 1. None of the above eight variables is positive. 2. A PERC evaluation is considered positive if any one of the eight criteria are met.
  • 19.  In 2015, pulmonary embolism guidelines were released by the American College of Physicians and are summarized as follows . 1. Use either the Wells or Geneva rules to choose tests based on a patient's risk for pulmonary embolism. 2. If the patient is at low risk, clinicians should use the eight PERC; if a patient does not meet all eight criteria, the risks of testing are greater than the risk for embolism, and no testing is needed. 3. For patients at intermediate risk, or for those at low risk who do not meet all of the rule-out criteria, use a high-sensitivity plasma D-dimer test as the initial test. 4. In patients older than 50 years, use an age-adjusted threshold (age × 10 ng/mL, rather than a blanket 500 ng/mL), because normal D-dimer levels increase with age. 5. Patients with a D-dimer level below the age-adjusted cutoff should not receive any imaging studies. 6. Patients with elevated D-dimer levels should then receive imaging. 7. Patients at high risk should skip the D-dimer test and proceed to CT pulmonary angiography, because a negative D-dimer test will not eliminate the need for imaging in these patients. 8. Clinicians should only obtain ventilation-perfusion scans in patients with a contraindication to CT pulmonary angiography or if CT pulmonary angiography is unavailable. Skwarecki B. Pulmonary embolism guidelines released by ACP. Medscape Medical News. WebMD Inc. Sept 28, 2015.
  • 22. CHEST X-RAY  Fleishner sign  Hampton hump  Westermark sign
  • 26. ECG
  • 27. D - DIMER  D-dimer ELISA is an excellent screening test for suspected PE  A negative D-Dimer assay in low clinical probability case rules out PE  D-dimer ELISA was often elevated in the absence of PE like sepsis,cancer,acute medical illness  Low specificity and poor positive predictive value  Sensitivity >80% for DVT and >95% for PE
  • 28. ECHO  Right ventricular enlargement or hypokinesis, especially free wall hypokinesis, with sparing of the apex (the McConnell sign)  Interventricular septal flattening and paradoxical motion toward the left ventricle, resulting in a D-shaped left ventricle in cross section  Tricuspid regurgitation  Direct visualization of thrombus (more likely with transesophageal echocardiography
  • 29. CT PULMONARY ANGIOGRAPHY  It is investigation of choice
  • 31. VENOUS ULTRASONOGRAPHY  Relies on loss of vein compressibility as the primary criterion  About 1/3 of pts will have no imaging evidence of DVT  Clot may have already embolized  Clot present in the pelvic veins (U/S usually inadequate)  Workup for PE should continue even if dopplers (-) in a pt in which you have a high clinical suspicion
  • 33. LUNG SCAN  As many as 40% of pts with high clinical suspicion for PE and low probability scans have a PE on angiogram  It has become second line diagnostic test for patients who cannot tolerate intravenous contrast  Small particulate aggregates of albumin labelled with gamma emitting radio nucleid is injected  Ventilation can be obtained by radio labelled inhaled gas such as xenon, krypton  A high probability scan is defined as two or more segmental perfusion defects in presence of normal ventilation scan  The diagnosis of PE is very unlikely in pt with normal or near normal scan.
  • 36. PULMONARY ANGIOGRAM  Most specific test available for diagnosis of PE  Can detect emboli as small as 1-2 mm  Most useful when the clinical likelihood of PE differs substantially from the lung scan result or when the lung scan is intermediate probability  Definitive diagnosis is visualization of an intraluminal filling defect .  Secondary sign is abrupt occlusion of vessel, segmental oligemia,prolonged arterial phase with slow filling .
  • 41. HEPARIN  Choices include either intravenous unfractionated heparin (UFH) or subcutaneous low-molecular-weight heparin (LMWH) preparations  Initial intravenous bolus of 80 units of heparin per kilogram followed by a continuous infusion initiated at 18 units per kilogram per hour.  The heparin drip is adjusted based on monitoring of the activated partial thromboplastin time (aPPT), drawn 6 hours after initial bolus dose, thn 6 hours after each dose adjustment , with a target aPPT ratio of 2.0 to 3.5  More recently, an approach using a fixed dose of subcutaneous unfractionated heparin , administered as an initial dose of 333 U/kg followed by a dose of 250 U/kg every 12 hours, has been demonstrated to be as safe and effective as LMWH.
  • 42.  Situations in which the use of UFH is appropriate 1. Renal insufficiency. 2. Extremes of body weight. 3. Hypertensive crisis, o Rapid adjustment of anticoagulation is needed, such as… A. Women in the late pregnancy who may need caesarian sections, B. Patients with recent surgery or C. Recent history of bleeding
  • 43. LMWH  Advantages of LMWH compared with UFH include: 1. Longer half-life and ease of use 2. Ability to consistently achieve early therapeutic anticoagulation 3. No need to monitor anticoagulant effects 4. Reduced incidence of major bleeding complications  In general, therapeutic monitoring is not needed with LMWH, but there are situations where the therapeutic effetcts may be less predictable and monitoring with ant-Xa levels is indicated  Typical examples include: 1. Patients with antiphospholipid antibodies or other circulating anticoagulants who have elevated baseline a PPT 2. Extremes of body weight(<40kgs and >50kgs) 3. Significant renal disease(creatinine clearance <30 ml/min) 4. Pregnancy 5. Unexplained bleeding or recurrent thrombosis during therapy
  • 44. FONDAPARINUX  A synthetic pentasaccharide, selective for factoe Xa  By binding rapidly and strongly to antithrombin, fondaparinux catalyzes specifically the inhibition of factor Xa, which results in inhibition of thrombin generation  Half-life of approx 17 hours, and is exctreted almost completely by the kidneys  It does not cause heparin induced thrombocytopenia
  • 45. THROMBOLYTIC THERAPY 1. Streptokinase 2. Urokinase 3. rt PA  these agents convert circulating plasminogen to plasmin.  The preferred fibronolytic regimen is 100mg rt PA over 2 hour. Contraindication :  Intracranial disease  Recent surgery  Trauma
  • 46.  The exact role of thrombolytic agents in acute pulmonary embolim remains controversial. While thrombolytic therapy does appear to accelerate the rate of thrombolysis, there is no convincing evidence to suggest that 1. 2. It decreaes mortality, 3. Increases the ultimate extent of embolic resolution when measured at 7 days, 4. Reduces thromboembolic recurrence rates, 5. improves symptomatic outcomes, 6. Decreases the incidence of thromboembolic pulmonary hypertension  Catheter- directed techniques have been successfully employed in the setting of acute ileo- femoral DVT using doses of urokinase ranging from 1.4 to 16 million units delivered over an average of 30 hours.
  • 47. INTERVENTIONAL RADIOLOGIC TECHNIQUES  Interventional thrombus fragmentation.  The devices use either pressured saline or a rotating impeller to fragment central thrombi.  The fragments are either aspirated through a separate port on the catheter or allowed to migrate distally.  There limitations, including a risk of paradoxical embolism from the clot fragments
  • 48. PULMONARY EMBOLECTOMY  It is reasonable to consider surgical embolectomy in patients with 1. Persistent hypotension. 2. Shock. 3. Cardiac arrest. 4. Failed thrombolysis. 5. Contraindications to thrombolytics.
  • 49. ORAL ANTICOAGULANTS  Warfarin inhibits gamma carboxylation activation of coagulation factors II, VII, IX, and X as well as proteins C and S Use of Warfarin without heparin is strongly discouraged 1. It generally takes 3 to 5 days of warfarin to achieve full therapeutic eficacy. 2. In patients with protein C deficiency, skin necrosis or paradoxical thrombosis may occur.
  • 50. WARFARIN  INR range between 2 and 3 is recommended for most patients  Another rare complication of warfarin use is cholesterol microembolism (“purple toes” syndrome), which is thought to be due to cholesterol crystal release from ulcerated intravascular plaques  an initial daily dose of 5 or 10 mg with use of an standardized nomogram to dose adjust based on INR values obtained on days 3 and 5  patients should receive atleast 5 days of combined heparin and warfaein therapy, including atleast 2 days in which the INR is in a therapeutic range prior to stopping heparin  Because of the teratogenic potential of warfarin, UFH or LMWH should be used in pregnant women who developed VTE in the first trimesters
  • 51. DURATION OF THERAPY  The risk of recurrent disease after 3 months of anticoagulation is still in the region of 10%; therefore, the patients should be treated with warfarin for 3 to 6 months  Patients with idiopathic thromboembolism have higher rate of recurrence therefore treated for atleast 6 to 12 months  Patients with antiphospholipid antibody syndrome have considerable risk of recurrence, therefore treated for minimum 12 months with consideration of life-long therapy  In patients with >2 episodes of recurrence life-long anticoagulation given
  • 52. DEEP VEIN THROMBOSIS  Thrombolysis  Anticoagulation  Vena cava filter
  • 53. VENA CAVA FILTER  Used in patients with contraindication to anticoagulation or patients with recurrent embolism while on adequate anticoagulation  Long term IVC filter increases risk of thromboembolism  This observation lead to recent development of retrievable filters  Four types of retrievable filters: 1. Gunther tulip filter 2. ALN filter 3. Recovery filter 4. OptEase filter
  • 56. INTERMITTENT PNEUMATIC COMPRESSION  The sleeves are inflated for a few seconds, one leg at a time, to compress the veins in the legs every minute or so.  By causing contraction of the leg muscles, the sleeves mimic the process of walking in immobilized patients. This ensures blood is pushed around the system, rather than pooling in the legs
  • 57. GRADUATED COMPRESSION STOCKING  Compression stockings are made of a special elastic fabric. They are very tight at the ankle and are less tight as the stocking moves up the leg. This graduated tightness helps the leg muscles squeeze fluid up the leg, which improves blood flow from the leg back to the heart and decreases leg swelling and pain.
  • 59. TYPE OF EMBOLISM 1. Fat embolism 2. Venous air embolism 3. Amniotic fluid embolism 4. Septic embolism 5. Tumour embolism 6. Sickle cell disease
  • 60. FAT EMBOLISM  Due to entry of neutral at in vascular system  Leads to dysnea, hypoxemia, petechiae, mental confusion  Lag time of 24 to 72 hours in the onset of syndrome following the inciting event  Most common inciting event, fracture of long bones  Pathophysiology : 1. Actual vascular obstruction by neutral particle of fat 2. Injurious effect of free fatty acids released by the action of lipases on the neutral fat  Supportive treatment advised  Other suggested treatment intravenous ethanol, albumin, dextran, heparin
  • 61. VENOUS AIR EMBOLISM  Due to indwelling central venous catheter, positive pressure ventilation, trauma to thorax  Physiological consequence due to abrupt rise in pulmonary artery pressure  Treatment is prevention and early detection  Patient positioning (Trendelenburg position with left side down)  Removal of air through central venous catheter  Direct needle aspiration  Closed chest cardiac massage  Increase absorption with use of 100% oxygen
  • 62. AMNIOTIC FLUID EMBOLISM  Third leading cause of maternal mortality  Amniotic fluid contains particulate material that can cause pulmonary vascular obstruction  Amniotic fluid has thromboplastic activity that leads to extensive fibrin deposition in lung vasculature that leads to consumptive coagulopathy leading to hypofibrinogenemia and thrombocytopenia  Presence of squamous cell in pulmonary arterial blood once considered pathognomonic.
  • 63. SEPTIC EMBOLISM  Microscopically septic phlebitis consist of purulent material mixed with fibrin thrombus  Chest X-ray display pulmonary infiltrates  Treatment consists of anti microbial agents
  • 64. TUMOUR EMBOLISM  Most common site of origin breast, lungs, prostate, stomach and liver  Clinical feature is typically subacute and involves progressive dysnea , techypnea, techycardia  Pulmonary angiographic findings reveal delapyed vascular filling, pruning and tortuosity