Pulmonary Embolism

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Pulmonary embolism (PE) is a common and potentially lethal condition. Most patients
who succumb to pulmonary embolism do so within the first few hours of the event. In
patients who survive, recurrent embolism and death can be prevented with prompt
diagnosis and therapy. Unfortunately, the diagnosis is often missed because patients
with pulmonary embolism present with nonspecific signs and symptoms. If left
untreated, approximately one third of patients who survive an initial pulmonary embolism
die from a subsequent embolic episode.
The most important conceptual advance regarding pulmonary embolism over the last
several decades has been the realization that pulmonary embolism is not a disease;
rather, pulmonary embolism is a complication of venous thromboembolism, most
commonly deep venous thrombosis (DVT). Virtually every physician who is involved in
patient care (eg, internist, family physician, orthopedic surgeon, gynecologic surgeon,
urologic surgeon, pulmonary subspecialist, cardiologist) encounters patients who are at
risk for venous thromboembolism, and therefore at risk for pulmonary embolism.

DEFINITION:
PE is
the obstruction of the pulmonary artery or one of
its branches by a thrombus (or thrombi) that originates
somewhere in the venous system or in the right side of
the heart .
Definition for Massive PE
Acute PE with with at least 1 of the following:
1.

Sustained hypotension
SBP <90 mmHg for at least 15 minutes or requiring
inotropic support, not due to a cause other than PE,
such as arrhythmia, hypovolemia, sepsis, or LV
dysfunction, drugs,etc.

2.

Pulselessness

3.

Persistent profound bradycardia

Heart rate <40 bpm with signs or symptoms of shock
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Definition for Submassive PE

Acute PE without systemic hypotension (SBP >90 mm
Hg) but with either RV dysfunction or myocardial
necrosis.
RV dysfunction means the presence of at least 1 of
the following:
Echo: RV dilation (apical 4-chamber RV diameter
divided by LV diameter >0.9), or RV systolic
dysfunction

CT: RV dilation (4-chamber RV diameter divided

by LV diameter > 0.9)
BNP > 90 pg/mL or N-terminal pro-BNP > 500
pg/mL
ECG changes: New complete or incomplete RBBB,
anteroseptal ST elevation or depression, or
anteroseptal T-wave inversion
Myocardial necrosis is defined as either of the
following:
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 Troponin I > 0.4 ng/mL, or Troponin T > 0.1 ng/mL

Definition for Low-Risk PE
Acute PE and the absence of the clinical markers of
adverse prognosis that define massive or submassive
PE.

PREVALENCE
PE is estimated to cause 200,000 deaths each year in
the United States .
The 2nd leading cause of death among hospitalized
patients, unexpected, nontraumatic death.
Most cases are not recognized antemortem, and LESS
THAN 10% of patients with fatal emboli have received
specific treatment for the condition.
Management demands a vigilant systematic approach
to diagnosis and an understanding of risk factors so
that appropriate preventive therapy can be given .
The incidence of PE in USA is 650-900,000 per year.
AETIOLOGY
Many substances can embolize to the pulmonary
circulation, including
1. AIR (during neurosurgery, from central venous
catheters)
2. AMNIOTIC FLUID(during active labor), fat (long bone
fractures)
3. FOREIGN BODIES (talc in injection drug users)
4. PARASITE EGGS (schistosomiasis)
5. SEPTIC EMBOLI (acute infectious endocarditis)
6. TUMOR CELLS(renal cell carcinoma).
7. RED EMBOLUS (DVT, atrial fibrillation)
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The most common embolus is thrombus, which may arise

anywhere in the venous circulation or heart but most
often originates in the deep veins of the lower
extremities. Thrombi confined to the calf rarely embolize
to the pulmonary circulation. However, about 20% of calf
vein thrombi propagate proximally to the popliteal and
ileofemoral veins, at which point they may break off and
embolize to the pulmonary circulation.((50%asymptomatic
DVT)).
Pulmonary emboli will develop in 5060% of patients with
proximal deep venous thrombosis (DVT); half of these
embolic events will be asymptomatic.
DEEP VEIN THROMBOSIS:
50% of all patients with venous thrombosis of the lower extremities
have no symptoms. Approximately 5070% of patients who

have symptomatic pulmonary emboli will have lower

extremity DVT when evaluated.
Obstruction of the deep veins of the legs produces edema and
swelling of the extremity because the outflow of venous blood is
inhibited. The amount of swelling can be determined by measuring
extremity circumference at various levels with a tape measure. The
skin over the affected leg may become warmer, and superficial veins
may become more prominent. Tenderness, which usually occurs
later, is produced by inflammation of the vein wall and can be
detected by gentle palpation by the extremity. Homans Signs, pain
in the calf after sharp dorsiflexion of the foot, is not specific for
deep venous thrombosis because it can be elicited in any painful
condition of the calf. In some cases, signs of a pulmonary embolus
are the first indication of a deep venous thrombosis. - Thrombosis of
superficial veins produces pain or tenderness, redness, and warmth
of the involved area. The risk of dislodgment and embolization of
superficial venous thrombi is very low because the majority of them
undergo spontaneous lysis; thus, condition can be treated at home
with rest, extremity elevation, analgesics, and possibly antiinflammatory agents.

CAUSES:
1. Thrombus

2. Embolism
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3.
5.
7.
8.

Trauma
4. Surgery
Hypercoaguability
6. Heart failure
Pregnancy (increase coaguability of BLOOD)
Older than 50 years
9. Arial fibrillation

RISK FACTORS:

PE
are two manifestations of
disease.
((DVT))
It commonly affects
the leg
veins, such
as the
femoral vein
or the
popliteal
vein or the
deep veins
of the
pelvis.
SIGNS AND
SYMPTOMS

and DVT
the same

Pain,
Swelling
Redness
of the leg
and
dilatation
of the
surface
veins
Shinning
skin with
redness
Hotness and
tenderness
Pedal edema may occur.
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Pathogenesis:
The risk factors for PE are the risk factors for thrombus
formation within the venous circulation.

1. Venous stasis OR turbulence(Venous flow

disturbance):
o Immobility leads to local venous stasis by
accumulation of clotting factors and fibrin,
resulting in thrombus formation.
o The risk of pulmonary embolism increases with
prolonged bed rest or immobilization of a limb in
a cast.
o Paralysis increases the risk of DVT.

V. stasis leads to accumulation of platelets and

thrombin in veins
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Bed restespecially postoperative, Hip replacement,

knee replacement, caesarian operation, post delivery,
comatose patient in ICU, Fracture of long bones,
sitting for hours in work or long trip by car or airplane
or bus with out activity, CCU admission, obesity,
stroke, comatose patient).
Intra-pelvic or intra-abdominal mass impairing
venous return from the lower limbs ( ovarian mass,
cervix cancer , uterine tumors , prostate cancer ,
sigmoid cancer).

2. Hypercoagulable state(hyperviscosity)

a. The complex and delicate balance between

coagulation and anticoagulation is altered by
many diseases, by obesity, after surgery, or by
trauma.
b. Concomitant hypercoagulability may be present
in disease states where prolonged venous stasis
or injury to veins occurs.
Congenital ((inherited gene defects-Protein
defects))

Factor (V) Leiden ( 20-40%)

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G to A mutation at base pair 1691 results in amino acid

506,Glu instead of Arg
Prothrombin 20210 (6%)(G to A)
Defect or deficiency of protein C (4%) (outozomal
dominant)
Defect or deficiency of Protein S (3-4%) ( outozomal
dominant) pregnancy and estrogens reduced protein
S
Dysfibrinogenemia ( 3% )
Antithrombin deficiency ( 1% ) (outozomal dominant )
acquired deficiency of it happened in sever obesity ,
liver disease , chronic renal failer , using oral
contraceptive ,immature neonates
Dysplasminogenemia ( <1% )
Reduced Heparin cofactor II
Elevation of PAI-1
Elevation of Coagulation factors VII,VIII,IX,X,XI and II
Reduction of protein Z
Acquired Hematologic diseases :
DIC(disseminated intravascular
thrombocytopenia),thrombocytosis
HIT(heparin induced thrombocytopenia), leukemia
Anti phospholipid syndrome
TTP(thrombocytopenic thrombotic purpura)
HUS(hemolytic uremic syndrome)
Thrombocytosis, leukemia , nephrotic syndrome, Oral
contraceptives and estrogen replacement,
antiphospholipid syndrome, Homocysteinemia .

o Malignancy has been identified in 17% of patients

with venous thromboembolism.
o The neoplasms most commonly associated with
pulmonary embolism, in descending order of
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frequency, are pancreatic carcinoma;

bronchogenic carcinoma; and carcinomas of the
genitourinary tract, colon, stomach, and breast.

3. Endothelial injury
INJURY TO ENDOTHELIUM CAN BE CAUSED BY
1. ATHEROSCLEROSIS
2. HYPERTENSION
3. HYPERCHOLESTEROLEMIA
4. RADIATION INJURY
5. SMOKING
6. Thrombophlebitis
-Vascular disease
7. -Foreign bodies (IV/central venous catheters)

Pathophysiology
When a thrombus completely or partially obstructs a
pulmonary artery(massive embolus) or its branches in
diseased lung or heart,

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 The alveolar dead space is increased. The area,

although continuing to be ventilated, receives little or
no blood flow. Thus, gas exchange is impaired or
absent in this area.

Regional blood vessels and bronchioles constrict.

More than 50% of the vascular bed has to be occluded

before PAP becomes substantially elevated
In patients without cardiopulmonary disease,
occlusion of 25-30 % of the vascular bed .

Causes an increase in pulmonary vascular resistance.

Impaired gas exchange
A

Ventilation/perfusion mismatch

B. Release of inflammatory mediators leads to

surfactant dysfunction, atelectasis, alveolar
hemorrhage ,Intrapulmonary shunting

PVR from

1. The regional vasoconstriction

2. Reduced size of the pulmonary

vascular bed.

An increase in pulmonary arterial pressure

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 An increase in right ventricular work to maintain

pulmonary blood flow.
When obstruction approaches 75%, the RV must
generate systolic pressure in excess of 50mmHg to
preserve pulmonary circulation.

When the work requirements of the right ventricle

exceed its capacity, right ventricular failure occurs,
leading to a decrease in cardiac output followed by a
decrease in systemic blood pressure and the
development of shock.(fatigue , syncopy, dizziness).

SYMPTOMOLOGY:
Clinical clues cannot make the diagnosis of PE; their
main value lies in suggesting the diagnosis.
The symptoms are quite variable according to the
heart and lung situation whether they are healthy or
diseased and degree of damage.
Most of the cases are missed as no specific symptom
that the symptoms can be explained by other
diagnosis by most of doctors which can lead to lose of
the patients.
Signs and symptoms are highly variable, nonspecific, and common in patients without PE.
Fatal PE typically leads to death within one to two
hours of the event.

Small PE in healthy pt= asymptomatic.

Dyspnea (80%) usually acute onset

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 Pleuritic chest pain

(44%)
Calf pain/swelling
(41-44%)
Orthopnea (28%)
Wheezing (21%)
Cough (20%)
Syncope (14%)
Hemoptysis (7%)

1.Dyspnea is the most frequent symptom; all of a

SUDDEN in high risk patients , while in bed or moving
from resting state, NEVER GRADUAL, The duration
and intensity of the dyspnea depend on the extent of
embolization ,heart and lung status.
2. Chest pain is common and is usually sudden and
pleuritic. It may be substernal and misdiagnosed
with angina pectoris or a myocardial infarction. It is
severe from the first minute in high risk patient.
3. All chest symptoms may occur and all of sudden
onset in absence of other possibilities(( acute
pneumothorax , acute left ventricular failure, acute
dissection of ascending aorta)).
97% with PE have at least one of the following:
1. Dyspnea
2. Tachypnea
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3. Pleuritic pain
Presence of DVT should trigger initial suspicion.
OTHERS may present with low cardiac out put symptoms
such as dizziness, syncopy, profuse sweating, sudden
fatigability in suspected high risk patient with dyspnea
mimicking vasovagal attacks.
OTHERS may present with sudden vomiting with
epigastric pain and diarrhea with fatigue and right
hypochondrial discomfort or heaviness due to right side
congestion in massive/submassive P.E. WITH
HYPOTENSION.
Other symptoms include anxiety, fever, tachycardia,
apprehension, cough, diaphoresis, hemoptysis,
unexplained fatigue or palpitation/shivering.
SIGNS:
Tachypnea (53%)
(24%)

Tachycardia

Rales (18%)
breath sounds (17%)

Decreased

Accentuated P2 (15%)
distension (14%)

JV

Signs of DVT

Physical examination findings are quite variable in

pulmonary embolism and, for convenience, may be
grouped into 4 categories as follows:
Massive pulmonary embolism
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o The patient in SHOCK. (( systemic hypotension,

poor perfusion of the extremities, tachycardia,
and tachypnea , drowzy)).
o Additionally, signs of pulmonary hypertension
such as palpable P2 second left intercostal space,
loud P2, right ventricular S3 gallop, and
(tricuspid regurgitation) may be present.
Acute pulmonary infarction
o These patients have decreased excursion of the
involved hemithorax, palpable or audible pleural
friction rub, and even localized tenderness.
o

Signs of pleural effusion, such as dullness to

percussion and diminished breath sounds, may
be present.

Acute embolism without infarction

o These patients have nonspecific physical signs
that may easily be secondary to another disease
process.
o Tachypnea and tachycardia frequently are
detected, pleuritic pain sometimes may be
present, crackles may be heard in the area of
embolization, and local wheeze may be heard
rarely.
Multiple pulmonary emboli or thrombi
o Physical signs of pulmonary hypertension and cor
pulmonale.
o Patients may have elevated jugular venous
pressure, right ventricular heave, palpable P2 ,
right ventricular S3 gallop, TR, hepatomegaly,
ascites, and dependent pitting edema.
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These findings are not specific for pulmonary

embolism and require a high index of suspicion
for pursuing appropriate diagnostic studies.

LUNG EXAMINATION- collapse, consolidation where

there is 2ry pneumonia which may delay the
diagnosis, elevation of diaphragm, cavitating lung
cavity with missed diagnosis mimicking lung abscess,
pleural effusion , pleural rub , localized wheezing
,basal inspiratory fine crepiataion .

Assessment and Diagnostic Findings:

No single noninvasive test is sufficiently sensitive or

specific to diagnose or exclude PE in all patients.
No single test can reliably rule out PE.
Yep, that includes CT Angio (right?)
THEY ARE HELPFUL IN MASSIVE /SUBMASSIVE PE NOT
SMALL .
The clinical priorities in the investigation of patients
with suspected PE include:
1. Diagnosis of extensive PE
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2. Diagnosis of PE in patients with severe symptoms

and/or poor cardiopulmonary reserve
3. Diagnosis of any PE when associated with
symptomatic or asymptomatic proximal DVT
4. Diagnosis in patients presenting with possible
recurrent PE

1.ABG-arterial blood gases:

pO2 pCO2
Increased A-a gradient
2.D-dimer:

This blood screening test relies on the principle that

most patients with PE have ongoing endogenous
fibrinolysis that is not effective enough to prevent PE
but that does break down some of the fibrin clot to ddimers .

Although elevated plasma concentrations of d-dimers

are sensitive for the presence of PE, they are not
specific.
patients with a low clinical probability of PE who had
negative d-dimer results, additional diagnostic
testing was not necessary
Different assays have different sensitivities
PE in low-risk patients with a negative D-dimer
o Thrombus formation >72 hrs before blood draw
(circulating dimer t1/2 = 8 hrs)
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o Subsegmental PE
False-positives = age >70, pregnancy, active
malignancy, recent surgery, liver disease, RA,
infections, trauma
False-negatives = Coumadin use, symptoms >5days,
small clots or infarction, isolated calf vein thrombosis.
Therefore, the plasma d-dimer assay is ideally suited
for outpatients or emergency department patients
who have suspected PE but no coexisting acute
systemic illness OR history of venous
thromboembolism and whose symptoms are of short
duration.
This test is generally not useful for acutely ill
hospitalized inpatients because their D-dimer levels
are usually elevated. A normal d-dimer assay appears
to be as diagnostically useful as a normal lung scan to
exclude PE.
D-dimer test should not be used when the clinical
probability of pulmonary embolism is high, because
the test has low negative predictive value in such
cases.
3.Electrocardiographic Signs:
Sinus tachycardia( THE COMMENEST )
Incomplete or complete right bundle branch block
Right-axis deviation
T wave inversions in leads III and aVF or in leads V 1-V4
S wave in lead I and a Q wave and T wave inversion in
lead III (S1Q3T3)
QRS axis greater than 90 degrees or an indeterminate

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axis
Atrial fibrillation or atrial flutter

4.Chest Radiography:
A near-normal radiograph in the setting of severe
respiratory compromise is highly suggestive of
massive PE.(AHA)

Major chest radiographic abnormalities are

uncommon.
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Focal oligemia (Westermark sign) indicates massive

central embolic occlusion.

A peripheral wedge-shaped density above the

diaphragm (Hampton hump) usually indicates
pulmonary infarction.

Subtle abnormalities suggestive of PE include

enlargement of the descending right pulmonary
artery, elevated diaphragm,collapse.
The vessel often tapers rapidly after the enlarged
portion. PE.

5.Echocardiographic Signs:

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 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.
Pulmonary hypertension
with a tricuspid
regurgitant jet velocity
>2.6 m/sec.

Loss of respiratoryphasic collapse of the

inferior vena cava
with inspiration.

Dilated inferior vena

cava without
physiologic
inspiratory
collapse.
Direct visualization of thrombus (more likely with
transesophageal echocardiography)
Overview of Imaging Modalities for Pulmonary
Embolism:

Lower extremity venous ultrasonography

Multidetector helical CT pulmonary angiography

MRI

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Ventilation-perfusion scintigraphy (V/Q scan)

6. Computed Tomography
1. Size, location, and extent of thrombus
2. Other diagnoses that may coexist with PE or
explain PE symptoms:
Pneumonia, Atelectasis,
Pericardial effusion, Pneumothorax, abscess,
Left ventricular enlargement
3. Pulmonary artery enlargement === pulmonary
hypertension
Age of thrombus: acute, subacute, chronic
4. Location of thrombus: pulmonary arteries , deep
leg veins,
5.Right ventricular enlargement
6.Contour of the interventricular septum: whether
it bulges toward the left ventricle, thus indicating
right ventricular pressure overload
7.Incidental masses or nodules in lung

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7. CT pulmonary Angiography

CT angiography (CTA) is the initial imaging modality of

choice for stable patients with suspected pulmonary
embolism(low risk).

Sensitivity/Specificity ~90%

withholding anticoagulation after negative pulmonary

CTA results appears to be safe.

CTPA use increased 10-fold from 1998-2006

Incidence increased 81% from 1998-2006
(112/100,000) with only 3% mortality reduction
o Increased in-hospital antigcoagulation
complications during that same time period

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8. Spiral CT- can visualize main, lobar, and segmental

pulmonary emboli with a reported sensitivity of
greater than 90%.
Spiral CT scanning can help detect emboli as small
as 2 mm that are affecting up to the seventh border
division of the pulmonary artery.
A further benefit of spiral CT scanning is that the
results may suggest an alternative diagnosis in up
to 57% of patients.
A significant limitation of spiral CT scanning is that
small subsegmental emboli may not be detected.
o The technique is as follows:

Spiral CT examination is performed immediately after infusion

of 150-200 mL of 30% contrast material.

Scanning is performed from the level of the aortic arch to

approximately 2 cm below the level of the inferior pulmonary
vein while the patient is holding his or her breath at full
inspiration.

If the patient is not able to hold his or her breath for 20-30
seconds, scanning may be performed during gentle breathing .

Positive findings on CT imaging include a central

intravascular filling defect within the vessel lumen,
eccentric tracking of contrast material around a
filling defect, and complete vascular occlusion.
Smooth filling defects making an obtuse angle with
a vessel wall may represent chronic thrombi or
recent recanalization. In the lung parenchyma,
signs of pulmonary embolism include oligemia,
pulmonary hemorrhage (ground-glass attenuation),
and pulmonary infarction (peripheral wedgeshaped pleural-based opacification.

9. Ventilation-perfusion (V/Q) scanning of the lungs:

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This is an important diagnostic modality for

establishing the diagnosis of pulmonary embolism.

However, V/Q scanning should be used only 1.when CT

scanning is not available or 2. If the patient has a
contraindication to CT scanning or intravenous
contrast material.

New criteria for V/Q scanning diagnosis of pulmonary

embolism, from the Prospective Investigation of
Pulmonary Embolism Diagnosis (PIOPED) II trial:
High probability criteria are as follows:
Two large (>75% of a segment) segmental
perfusion defects without corresponding
ventilation or chest x ray defects.
One large segmental perfusion defect and 2
moderate (25-75% of a segment) segmental
perfusion defects without corresponding
ventilation or radiographic abnormalities.
Four moderate segmental perfusion defects
without corresponding ventilation or chest
radiographic abnormalities

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 Intermediate probability criteria are as follows:

One moderate to fewer than 2 large
segmental perfusion defects without
corresponding ventilation or chest
radiographic abnormalities
Corresponding V/Q defects and radiographic
parenchymal opacity in lower lung zone
Single moderate matched V/Q defects with
normal chest radiographic findings
Corresponding V/Q and chest
radiography small pleural effusion
Difficult to categorize as normal, low, or high
probability
Low probability criteria are as follows:
Multiple matched V/Q defects, regardless of
size, with normal chest radiographic findings
Corresponding V/Q defects
and radiographic parenchymal opacity in
upper or middle lung zone
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 Corresponding V/Q defects and large pleural

effusion
Any perfusion defects with substantially
larger radiographic abnormality
Defects surrounded by normally perfused
lung (stripe sign)
More than 3 small (<25% of a segment)
segmental perfusion defects with normal
chest radiographic findings
Nonsegmental perfusion defects
(cardiomegaly, aortic impression, enlarged
hila)
Very low criterion is 3 small (<25% of a segment)
segmental perfusion defects with normal chest
radiograph findings.
Advantage
1. a normal V/Q scan rules out PE
>99% negative predictive value
2. the radiation dose is low
3. iodine-based contrast is not used
other investigations:
1.MRI
2.PULMONARY ANGIOGRAPHY
3. Multidetector helical CT pulmonary angiography

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0-2 = PE unlikely ,

3-7 = PE likely
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Prevention
Prevent deep venous thrombosis.
1. Active leg exercises
2. The intermittent pneumatic leg compression device
( venous stasis).
3. Use of elastic compression
stockings
4.
Anticoagulant therapy

Medical Management
General measures to improve respiratory and vascular
status
Anticoagulation therapy
Thrombolytic therapy
Surgical intervention
GENERAL MANAGEMENT
Oxygen therapy is administered to correct the
hypoxemia, relieve the pulmonary vascular
vasoconstriction, and reduce the pulmonary
hypertension.

Thrombolytics
Evidence of circulatory/respiratory insufficiency
Hypotension (SBP <90)
Hypoxia (SpO2 <95%)
Evidence of RV dysfunction
RV dilation/hypokinesis
Elevated troponin-I (>0.4) or proBNP (>900)
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 EKG changes
FDA-recommended dose: Alteplase 100mg over 2hrs

Therapeutic anticoagulation with subcutaneous

LMWH, intravenous or subcutaneous UFH with
monitoring, unmonitored weight-based
subcutaneous UFH, should be given to patients with
objectively confirmed PE and no contraindications to
anticoagulation.
UFH=Weight-based dosing (nomogram)
IV bolus 80mg/kg IV bolus, then 18mg/kg/hr
Monitor PTT (1.5-2.0 x), CBC
Continue 4-5d and therapeutic on Warfarin for 2d
(INR>2.0)
LMWH
Alternative regimen Lovenox 1mg/kg SC q12h

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 Better bioavailability, longer half-life, more

predictable effect
No monitoring of PTT (follow CBC)
Contraindications: renal failure (CrCl<30), weight
extremes
Warfarin
Start when therapeutic on Heparin
Monitor INR daily
Goal: INR 2.0-3.0 for

3-6 months

Identified precipitant 3 mos

First idiopathic episode

6 mos

Prolonged/indefinite:
2 thrombotic episodes
1 spont. life-threatening episode
Anti-phospholipid antibody
deficiency

syndrome, ATIII

Catheter embolectomy
Surgical embolectomy
Reasonable for
Massive PE if still unstable after fibrinolysis

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 Massive/Submassive PE if fibrinolysis is contraindicated or there is evidence of adverse

prognosis
o Three General Categories of Percutaneous
Intervention
Aspiration thrombectomy
Thrombus fragmentation
Rheolytic thrombectomy

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