Mortality/Morbidity

-Massive PE is one of the most common causes of unexpected

death, being second only to coronary artery disease as a
cause of sudden unexpected natural death at any age.
-Although PE often is fatal, prompt diagnosis and treatment
can reduce the mortality rate dramatically.
-Approximately 10% of patients in whom acute PE is
diagnosed die within the first 60 minutes. Of the remainder,
the condition eventually is diagnosed and treated in 30%
and remains undiagnosed in 60%
-. The diagnosis of PE is missed more than 400,000 patients in
the US each year, and approximately 100,000 patients die
who would have survived with the proper diagnosis and
treatment.
-Patients who survive an acute PE are at high risk for recurrent
PE and for the development of pulmonary hypertension and
chronic cor pulmonale.
Race
The incidence is high in all racial groups but differences may
exist in the incidence of DVT.
Sex
PE is common in all trimesters of pregnancy and the
puerperium.
The incidence of PE is increased in women receiving oral
contraceptive or hormone replacement therapy.
Age
Although the frequency of PE increases with age, age is not an
independent risk factor. Rather, the accumulation of other risk
factors, such as underlying illness and decreased mobility,
causes the increased frequency of PE in older patients.
Unfortunately, the diagnosis of PE is especially likely to be
missed in older patients.
 Predisposing Factors

Primary risk factors Minor risk factors

Surgery Obesity
Major Trauma Bed Rest
Cancer Estrogen therapy
CHF Myocardial infarction
Immobilization
 Causes

Hypercoagulable states Risk markers

Hypercoagulable states:

-Prolonged venous stasis or significant injury to the veins can

provoke DVT and PE in any person, Other identified "causes"
most likely serve only as triggers for a system that is already
out of balance.
-Hypercoagulable states may be acquired or congenital.
1-Congenital : resistance to activated protein C is the most
common congenital risk factor for DVT that has been identified
to date due to a genetic mutation in factor V known as "factor V
Leyden,"
2-Acquired : deficiencies in protein C, protein S, or antithrombin
III are also common underlying causes of DVT and PE
Risk markers:
The most important clinically identifiable risk markers for DVT and PE are a
prior history of DVT or PE, recent surgery or pregnancy, prolonged
immobilization, or underlying malignancy.
Many other recognized markers of risk for venous thromboembolic disease
are listed here.
AIDS (lupus anticoagulant)
Antithrombin III deficiency
Behcet Disease
Blood type A
Burns
Catheters (indwelling venous infusion catheters)
Chemotherapy
Congestive Heart Failure ( CHF )
Drug abuse (intravenous [IV] drugs)
Drug-induced lupus anticoagulant
DVT in the past
Estrogen replacements (high dose only)
Fibrinogen abnormality
Fractures
Hemolytic anemias (SCD)
Heparin-associated thrombocytopenia
Pathophysiology (Venous thrombosis)

-Most commonly it arises from the calf veins. The venous thrombi
predominately originate in venous valve pockets (inset) and at
other sites of presumed venous stasis. To reach the lungs,
thromboemboli travel through the right side of the heart. RA,
right atrium; RV, right ventricle.

-Pulmonary thromboembolism is not a disease in and of itself.

Rather, it is an often fatal complication of underlying
venous thrombosis. Under normal conditions, microthrombi
(tiny aggregates of red cells, platelets, and fibrin) are formed
and lysed continually within the venous circulatory system. This
dynamic equilibrium ensures local hemostasis in response to
injury without permitting uncontrolled propagation of clot. Under
pathological conditions, microthrombi may escape the normal
fibrinolytic system to grow and propagate. PE occurs when
these propagating clots break loose and embolize to block
pulmonary blood vessels.
Pathophysiology
-Thrombosis in the veins is triggered by venostasis,
hypercoagulability, and vessel wall inflammation. These 3
underlying causes are known as the Virchow triad. All known
clinical risk factors for DVT and PE have their basis in one or
more elements of the triad.
-Patients who have undergone gynecologic surgery, those with
major trauma, and those with indwelling venous catheters may
have DVTs that start at any location. For other patients, venous
thrombosis most often involves the lower extremities and nearly
always starts in the calf veins, which are involved in virtually
100% of all cases of symptomatic spontaneous lower extremity
DVT. Although DVT starts in the calf veins, it already has
propagated above the knee in 87% of symptomatic patients
before the diagnosis is made.
-Studies suggest that nearly every patient with thrombus in the
upper leg or thigh will have a PE if a sensitive enough test is
used !!!!!!
Signs and symptoms
Dyspnea 73%
Pleuritc Pain 66%
Cough 43%
Leg Swelling 33%
Leg Pain 30%
Hemoptysis 15%
Palpitations 12%
Wheezing 10%
Angina-Like pain 5%

The signs and symptoms serve only to raise the

suspicion of pulmonary embolus
Investigations
1-Laboratory : identify risk or predisposing factors for
DVT (CBC, ESR, Leukocytosis, ABG)
2-Pulmonary function tests :
A- Decrease in DLCO
B- Increase in dead space
C-ventilation-perfusion mismatch
3-Testing for PE.
-A chest radiograph
-ECG
-Ventilation-perfusion scanning (V/Q scanning).
-Angiography
-Spiral CT - D.dimer
Look for ventilation-perfusion mismatch
(i.e.) areas with poor perfusion and good ventilation
By calculating A-a O2 gradient = PaO2
(alveolar) - PaO2 (arterial) = 8
Normal A-a O2 gradient is 5-20 and increases
with age.
-Elevated in 80% to 90% in PE
-Normal in 10% to 20% in PE
PAO2 (alveolar) = 150 - 1.2(PaCO2),
assuming patient breathing room air
Testing for PE
-A chest radiograph
-ECG
-Ventilation perfusionscanning(V/Qscanning).
-Angiography
-Spiral CT
-D-dimer
Abnormalities on Chest Radiography
14% Normal
68% Atelectasis and parenchymal densities
48% Pleural Effusion
35% Pleural based opacity
24% Elevated diaphragm
15% Prominent central pulmonary artery
7% Cardiomegally
5% Pulmonary edema
 Atelectasis

Atelectasis and parenchymal densities are quite common. Most of these

densities are caused by pulmonary hemorrhage and edema
 Pleural Effusion

Pleural effusions are common and most often unilateral

occupying less than 15% of a hemithorax
 Elevated diaphragm

A diaphragm may be elevated, reflectingvolume loss in the affected lung .

ECG of Acute pulmonary embolus
-An S1Q3T3 pattern:
prominent S wave in lead I, Q wave and
inverted T wave in lead III
-Sinus tachycardia
-T wave inversion in leads V1 - V3
-Right Bundle Branch Block
-low amplitude deflections
Ventilation-perfusion scanning
It visualizes the gas exchange in the lungs
using
Xenon-133 and the perfusion of the lung
using
technetium99m-labeled albumin aggregates.
In practical terms, the test can be:
* High probability.
Intermediate probability.
Low probability.
*Normal .
 High probability V/P scan

This V/P scan demonstrates a high probability scan with multiple segmental
defects and normal ventilation in those areas
Intermediate probability V/P scan

scans with sub segmental defects or defects of any size that match
abnormalities on the chest x-ray or the ventilation scan.
Pulmonary angiogram
It is the "gold standard" test
-If you absolutely must know whether the
patient had pulmonary
-embolism there is no substitute for a well
done angiogram.
-With the angiogram you look for cut-offs
in the vascular tree or for intraluminal
filling defects.
Pulmonary angiogram showing
intraluminal filling defects.
Computed Tomography

The typical appearance of a pulmonary infarct on CT includes a pleural based

density with convex borders and a linear strand at the apex of the triangle.
The differential diagnosis for this abnormality includes infarct, hemorrhage,
pneumonia, fibrosis, neoplasia and edema.
D-dimer

-A marker for thrombosis and fibrinolysis,

can be useful in the exclusion of PE.
- Specific conditions that will give positive
Ddimer tests include trauma,
postoperative state,and malignancies.
-30% with PE will have normal D-dimer
Treatment of Pulmonary
Embolism

1- Anti shock measures: O2,monitoring,fluid

resuscitation for secondary right-sided
heart failure, Inotrops.
2-Anticoagulant : Heparin, oral anticoagulant
and LMWH.
3- Thrombolytics.
4- Caval Interruption.
2-Anticoagulant
1.A - Heparin
- Dose :loading dose of 5,000 U followed by
approximately 1,000 U/h.
OR: a bolus dose of 10,000-15,000 u for PE.
-Action :potentiate antithrombin III
-Controlled by :PTT
-Contraindications :hypertension , peptic
ulcer ,blood diseases
-Antidote :protamine sulphate
1.B - Low-molecular-weight heparin
LMWH (anti-factor Xa )

- Enoxaparin: (Clexane)

- Dalteparin.

-Nadroparin calcium. (Fraxiparine)

-Tinzaparin sodium . (Innohep)

N.B.
Only low-molecular-weight heparin and
graded compression stockings have been
shown to reduce the incidence of
pulmonary embolism.
2 -Oral anticoagulants (Warfarin)
- Action : It depletes vitamin K-dependent clotting
factors (II, VII, IX, and X).
-It is taken orally. Begin with 5 mg QHS.
-Warfarin therapy can begin on day one of heparin
therapy.
- Controlled by: ratio of treated to control PT & INR
(International normalization ratio) of 2 to 3 is
considered therapeutic.
- Monitor daily using the PT (Prothrombin time), until
a stable INR for 2 days. Then 2 to 3 times weekly for 1 to
2 weeks, and then monthly.
-Antidote : vitamin K
N.B.
1- Heparin should be continued for at least 4 days total and for at least 2
days after a therapeutic INR is obtained.
2- Continue using anticoagulation (warfarin) for at least 6 months.
3 - Thrombolysis:
(Patients still require heparin)
- Include : TPA , Streptokinase , Urokinase
- Indications :
- if PE is confirmed with angiogram or high-
probability V/Q and there is:
- Evidence of right heart failure, unresponsive to
standard therapy.
- Respiratory failure from PE, but the benefits are
less well established.
* Regimens approved by FDA:
- Streptokinase 250,000 IU over 30 minutes
followed by 100,000IU/hr for 24 to 72 hours.
-TPA 100 mg as continuous infusion over 2 hours.-
- Contraindications : early postoperative,
early postpartum
- Antidote : blood transfusion
4 - Caval Interruption:

- Indications : if anticoagulation is
contraindicated or ineffective, consider
vena cava interruption with a filter such as
the Greenfield filter.
-Vena cava filters are less effective than
anticoagulation and may lead to increased
rates of DVT and may not protect against PE
(same PE and death rates as controls).
All Credit To
My colleagues
Thank You