Acute Pulmonary Embolism

2008-Apr.-11

Outline
__________________________________________

1.
2.
3.
4.
5.
6.
7.

Introduction
Epidemiology & Pathophysiology
Risk Factors
Diagnostic Approaches
Treatment
Pregnancy & APE
Conclusions

Introduction-1
most commonly originating from

deep venous thrombosis ( DVT ) of

the legs
Asymptomatic
incidentally discovered emboli
massive embolism causing
immediate death

Introduction-2
Chronic sequelae of venous

thromboembolism(VTE) (DVT & PE)

post-thrombotic syndrome
chronic thromboembolic pulmonary
H/T

Introduction-3
Acute pulmonary embolism ( APE )
may occur rapidly & unpredictably
may be difficult to diagnose

Introduction-4
Treatment can reduce the risk of death
appropriate primary prophylaxis :

effective
rate of death in the next year: 1.5% vs.
0.4%
Patients treated for APE appear to die of
recurrent thromboembolism (1.5% )
patients treated for DVT (0.4% )

Epidemiology &
Pathophysiology

Epidemiology &
Pathophysiology-1

Thrombi commonly form in deep

veins in the calf

propagate into the proximal veins,
including & above the popliteal veins
from which they are more likely to
embolize

Epidemiology &
Pathophysiology-2

About 79% of patients with PE have

evidence of DVT in their legs
PE occurs in up to 50% of patients
with proximal DVT
Dual pulmonary circulation
( pulmonary & bronchial arteries ),
pulmonary infarction : not usually
present

Epidemiology &
Pathophysiology-3

APE, anatomical obstruction is the

most important cause of

compromised physiology
release of vasoactive &
bronchoactive agents (serotonin from
platelets )---- deleterious ventilation
perfusion matching

Epidemiology &
Pathophysiology-4

As RV afterload increases, tension in

RV wall rises
dilatation, dysfunction, & ischemia of
RV
Death results from RV failure.

Epidemiology &
Pathophysiology-5
VTE is a worldwide problem, esp. in people

with known risk factors

Less common in certain regions, eg. Asia
Average annual incidence in US : 1 episode
per 1000 registered patients
US :300,000 people/year die from APE
Dx is often not made until autopsy
Hospitalized pts are at particularly high risk

Risk Factors

Acquired Risk Factors

Certain risk factors increase the likelihood
Overall, acute medical illness may be the

most common setting

Prolonged air or ground travel increases
the risk
eThrombosis:extended periods of sitting
at a computer terminal
Advancing age is another clear risk factor,
with the risk increasing after age 40

Genetic Disorders & Thromboembolic

Risk

Risk Factors for VTE

Virchow's classic triad of

risk
Hypercoagulability
Stasis
Venous injury

Diagnostic Approaches

Clinical Manifestations -1
Recognition of the symptoms & signs

of VTE may reduce diagnostic delays

Symptoms of cough, palpitations, &
dizziness & signs of fever, wheezing, &
crackles : PE or concomitant illnesses
Tachypnea & tachycardia : common
but nonspecific findings

Clinical Manifestations -2
Signs of pulm. HTN : elevated neck veins,

loud P2, right-sided gallop, & RV lift

Signs & symps. of VTE : highly suggestive but
neither sensitive nor specific
extent of symptoms depends on the
thromboembolic burden
massive PE:sudden onset of near syncope or
syncope,hypotension,severe hypoxemia, EM
dissociation, or cardiac arrest.

Clinical Manifestations -3
Leg pain, warmth, or swelling:DVT
dyspnea or chest pain, either sudden
onset or evolving over a period of
days to weeks:APE
Pleuritic chest pain , a pleural rub
(more peripheral emboli ) &
hemoptysis: pulmonary infarction

Preliminary Lab. Testing & Pretest Probability

-1

Hx., PE, & known risk factors

EKG, CXR, & ABG analysis

Preliminary Lab. Testing & Pretest Probability

-2

EKG:unexplained tachycardia:common in
APE but nonspecific
acute cor pulmonale: S1, Q3, T3 pattern,
RBBB , P-wave pulmonale, or RAD : more
common with massive embolism
---nonspecific
CXR: generally nondiagnostic
arterial oxygen tension may be normal
Aa oxygen difference may be normal

Preliminary Lab. Testing & Pretest Probability

-3

D-dimer test (+): VTE are possible

diagnoses
this test is nonspecific
infection,other inflammatory states,
cancer, & trauma
D-dimer testing is best considered
together with clinical probability

Clinical Prediction Scores for Suspected

APE-1

Clinical Prediction Scores for Suspected

APE-2

Clinical Prediction Scores for Suspected

APE-3

Preliminary Lab. Testing & Pretest Probability

-4

D-dimer test (-):with a low or moderate

pretest probability, likelihood of VTE is low

precludes the need for specific imaging
studies
high pretest probability: imaging should
be performed instead of D-dimer testing
Other biomarkers: cardiac troponin levels,
plasma levels of brain natriuretic peptide

Imaging Studies -1
Contrast-enhanced CT arteriography
the greatest sensitivity & specificity for
detecting emboli in the main, lobar, or
segmental pulmonary arteries
false (+) CT arteriography : unusual
sensitivity of spiral CT arteriography
alone = 83%, combination of this & CT
venography ,up to 90%

Imaging Studies -2
Ventilationperfusion scan : diagnostic in
the absence of cardiopulmonary disease
A normal perfusion lung scan effectively
rules out APE
high probability scan:APE should be
considered diagnostic , unless clinical
suspicion is low or Hx. of PE with an
identical previous scan

Imaging Studies -3
if the clinical story strongly suggests

PE,with a nondiagnostic VP scan, Dx.

should be rigorously pursued
nondiagnostic VP scan : with low
probability or with moderate
probability but negative D-dimer test
, no additional testing or therapy is
indicated

Imaging Studies -4
a recent study of 221 patients with

susp. APE, MRI of the lung followed by

MR venography ---successfully search
for both DVT & PE
Echocardiography may reveal findings
that strongly support hemodynamically
significant PE, offering the potential to
guide treatment

Treatment

Anticoagulation-1
Bed rest is not recommended for DVT
unless substantial pain & swelling
PE diagnosed, inpatient therapy with
initial bed rest for 24 to 48 hrs : often
recommended

Anticoagulation-2
APE (+):IV anticoagulation with LMW

heparin , or standard, UF heparin should

be initiated unless contraindicated
Not thrombolytic, but decreasing the
thromboembolic burden
If the suspicion of PE is high, parenteral
anticoagulation should be considered
even before imaging

Anticoagulation-3
Warfarin can be initiated on day 1 of

therapy
SC LMWH or weight-based UFH IV should
be administered for at least 5 days until
INR=2.0 to 3.0 for 2 consecutive days
With standard heparin,aPTT checked Q6h
until it is =1.5 to 2.5 X control
Achieving a therapeutic aPTT within 24
hours ,reduce the risk of recurrence

Anticoagulation-4
LMWHs have advantages over UFH :

greater bioavailability, more predictable

dosing, SC delivery, & a lower risk of
heparin-induced thrombocytopenia ( HIT )
Monitoring LMWH by antifactor Xa :
morbidly obese (weighing >150 kg) or
very small (<40 kg), pregnant, & very
severe renal insufficiency or rapidly
changing renal function

Anticoagulation-5
VTE require long-term anticoagulation to

prevent extension & recurrence

Documented VTE with transient risk factors
should treat 3 to 6 months, but more
extended treatment is appropriate when
significant risk factors persist, idiopathic or
previous episodes of VTE
D-dimer levels may help guide decisions
about the duration of therapy

Anticoagulation-6
Tx. with a direct thrombin inhibitor (e.g.,

argatroban or lepirudin) for HIT with

thrombosis
Tx. with warfarin should not be initiated
until disease process has been controlled
& platelet count has returned to the
normal range---potential for worsening
thrombotic complications :venous limb
gangrene & warfarin-induced skin necrosis

Placement of a Vena Caval

Filter
contraindications to anticoagulation
major bleeding during anticoagulation
recurrent embolism under adequate
therapy
filters are effective in reducing the
incidence of PE, they increase the
subsequent incidence of DVT,but do
not increase overall survival

Treatment of Massive PE
PE causing hemodynamic instability
resulting RV failure---compromised LV

preload
If saline is infused for hypotension, it
should be done with caution
Vasopressor therapy (e.g., dopamine)
should be considered if BP is not
rapidly restored

Complications of Thrombolytic Therapy1

most widely accepted indication for

thrombolytic therapy :proven PE with

cardiogenic shock
frequently considered : systemic
hypotension without shock
may be considered : severely
compromised oxygenation or a massive
embolic burden identified by image

Complications of Thrombolytic Therapy2

The most devastating complication :ICH

retroperitoneal & GI bleeding & bleeding

from surgical wounds or sites of recent

invasive procedures
Contraindications : intracranial, spinal, or
ocular surgery or disease, recent major
surgery or other invasive procedures,
active or recent major bleeding, pregnancy,
& clinically obvious risks of bleeding

Prognosis
The 3-month overall mortality :15 - 18%
Shock at presentation : increase in
mortality by a factor of 3 to 7
post-thrombotic syndrome (chronic leg
pain & swelling) & chronic
thromboembolic pulmonary
hypertension :possible long-term
sequelae of APE

Prevention-1
Without prophylaxis, risk of VTE among
acutely ill, hospitalized medical patients :
as high as 15%
Unfortunately, prophylaxis is grossly
underused ( U.S. & international studies )
Anticoagulant prophylaxis is more
effective than lower-limb mechanical
prophylaxis

Prevention-2
After total hip or knee replacement,

the risk of venous thrombosis : 50%

or higher without prophylaxis
Trauma & spinal cord injury :also
very-high-risk scenarios
Every hospitalized patient should be
assessed for the need for prophylaxis

Pregnancy & Acute

Pulmonary Embolism

Pregnancy & APE-1

increased risk for VTE : pregnancy ,

postpartum period ,& hormone therapy

Risk of a first episode of VTE= 5-fold as
high in the postpartum period as during
pregnancy
Risk of PE = 15-fold as high during the
postpartum period as during pregnancy

Pregnancy & APE-2

Low-dose oral contraceptives increase

the risk of VTE : a factor of 2 to 5

HRT increases the risk of VTE : a factor of
2 to 4
Pregnant patients with acute VTE require
the same initial approach as other
patients with regard to the need for
parenteral anticoagulation, placement of
an IVC filter, or embolectomy

Conclusions

Conclusions
Untreated PE is associated with high

mortality
Suspected PE demands prompt
diagnostic testing & assessment of
risk factors & clinical probability, with
empirical clinical assessment & a
validated clinical prediction score
when possible