Pulmonary Venous

Thromboembolism
Pulmonary venous thromboembolism,
often referred to as pulmonary
embolism, is a common, serious, and
potentially fatal complication of
thrombus formation within the deep
venous circulation
• Majority of cases are not recognized
antemortem, and fewer 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
 Many substances can embolize to
the pulmonary circulation, including ;

• Air (during neurosurgery, from central

venous catheters)
• Amniotic fluid (during active labor)
• Fat (long bone fractures)
• Foreign bodies (talc in injection drug
users)
• Parasite eggs (schistosomiasis)
• Septic emboli (acute infectious
endocarditis)
• Tumor cells (renal cell carcinoma)
• 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 major calf muscles

• Thrombi confined to the calf rarely embolize

to the pulmonary circulation. However, calf
vein thrombi propagate proximally to the
popliteal and ileofemoral veins, at which
point they may break off and embolize to the
pulmonary circulation
 Risk factors
• Pulmonary embolism and DVT are two
manifestations of the same disease

• Venous stasis
• Venous stasis increases with immobility (bed
rest—especially postoperative—obesity, stroke),
hyperviscosity (polycythemia), and increased
central venous pressures (low cardiac output
states, pregnancy).

• Injury to the vessel wall

• Vessels may be damaged by prior episodes of
thrombosis, orthopedic surgery, or trauma
 Hypercoagulability
(Virchow's triad)
Hypercoagulability can be caused by

• Medications (oral contraceptives, hormonal replacement

therapy)

• Disease (malignancy, surgery)

• Inherited gene defects

Most common inherited cause in white populations is
resistance to activated protein C, also known as factor V
Leiden

• Other major risks for hypercoagulability include the following:

deficiencies or dysfunction of protein C, protein S, and
antithrombin III; prothrombin gene mutation; and the
presence of antiphospholipid antibodies (lupus anticoagulant
and anticardiolipin antibody).
 Clinical Findings
Symptoms and Signs
• The clinical diagnosis of pulmonary
thromboembolism is notoriously difficult for two
reasons

• First, the clinical findings depend on both the size

of the embolus and the patient's preexisting
cardiopulmonary status

• Second, common symptoms and signs of

pulmonary emboli are not specific to this disorder
 Symptoms      
• Dyspnea
• Respirophasic chest pain
• Cough
• Legpain
• Hemoptysis
• Palpitations
• Wheezing
• Anginal pain
 Signs
• Respiratory rate >16-20/min
• Crackles (rales)   
• Heart rate > 100/min
• Fourth heart sound (S4)
• Accentuated pulmonary component of
second heart sound (S2P)   
• T >37.5 °C - 38.5 °C
• Homans' sign
• Pleural friction rub
• Third heart sound (S3)
• Cyanosis
 Indeed, no single symptom
or sign or combination of
clinical findings is specific to
pulmonary thromboembolism
 Laboratory Findings
ECG

• Abnormal in 70% of patients with pulmonary

thromboembolism

• Most common abnormalities are sinus

tachycardia and nonspecific ST and T wave
changes (S1 Q3 T3)

• Few patients have P pulmonale, right ventricular

hypertrophy, right axis deviation, and right
bundle branch block
 Arterial blood gases

• Reveal acute respiratory alkalosis due to

hyperventilation

• The arterial PO2 and the alveolar-arterial oxygen

difference (A–a– DO2) are most often abnormal in
patients with pulmonary thromboembolism

• Profound hypoxia with a normal chest radiograph

in the absence of preexisting lung disease is
highly suspicious for pulmonary
thromboembolism.
 Plasma levels of D-dimer

• Plasma levels of D-dimer, a degradation

product of cross-linked fibrin, are elevated in
the presence of thrombus

• Using a D-dimer threshold between 300 and

500 ng/mL, the quantitative enzyme-linked
immunosorbent assay (ELISA) has shown a
sensitivity for venous thromboembolism
 Imaging and Special
Examinations
Chest radiography
• The chest radiograph is necessary to exclude other
common lung diseases and to permit interpretation
of the ventilation-perfusion ( V/ Q) scan, but it does
not establish the diagnosis by itself

• A prominent central pulmonary artery with local

oligemia (Westermark's sign) or pleural-based areas
of increased opacity that represent intraparenchymal
hemorrhage (Hampton's hump) are uncommon

• Paradoxically, the chest radiograph may be most

helpful when normal in the setting of hypoxemia
 Lung scanning
• A perfusion scan is performed by injecting radiolabeled
microaggregated albumin into the venous system, allowing
the particles to embolize to the pulmonary capillary bed

• To perform a ventilation scan, the patient breathes a

radioactive gas or aerosol while the distribution of
radioactivity in the lungs is recorded

• A defect on perfusion scanning represents diminished blood

flow to that region of the lung

• Defects in the perfusion scan are interpreted in conjunction

with the ventilation scan to give a high, low, or intermediate
(indeterminate) probability that pulmonary
thromboembolism is the cause of the abnormalities.
 CT
• Helical CT arteriography is rapidly
supplanting V/Q scanning as the initial
diagnostic study for suspected pulmonary
thromboembolism

• Helical CT arteriography requires

administration of intravenous
radiocontrast dye but is otherwise
noninvasive
 Venous thrombosis studies

• Seventy percent of patients with pulmonary

thromboembolism will have DVT on
evaluation, and approximately half of
patients with DVT will have pulmonary
thromboembolism on angiography

• Commonly available diagnostic techniques

include venous ultrasonography, impedance
plethysmography, and contrast venography
 Pulmonary arteriography
• Pulmonary arteriography remains the
reference standard for the diagnosis of
pulmonary thromboembolism

• An intraluminal filling defect in more than

one projection establishes a definitive
diagnosis

• Pulmonary arteriography is a safe but

invasive procedure with well-defined
morbidity and mortality data
 MRI
• The test is noninvasive and avoids
the use of potentially nephrotoxic
radiocontrast dye

• Expensive and not widely available

Integrated approach
for diagnosis of
Pulmonary embolism
 Treatment
Anticoagulation
• The standard regimen of heparin followed by 6 months of oral warfarin

• Heparin
• Heparin binds to and accelerates the ability of antithrombin
III to inactivate thrombin, factor Xa, and factor IXa. It thus
retards additional thrombus formation, allowing endogenous
fibrinolytic mechanisms to lyse existing clot

• Heparin is administered in dosages determined by body

weight

• It is necessary to monitor the activated partial

thromboplastin time (aPTT) and adjust dosing to maintain
the aPTT 1.5–2.5 times control

• Unfractionated Heparin
• Low Molecular Weight Heparin
• LMW heparins are depolymerized
preparations of heparin, they are
administered once or twice daily without
the need for coagulation monitoring, with
subcutaneous route

• Anticoagulation therapy for venous

thromboembolism is continued for a
minimum of 3 months, so oral
anticoagulant therapy with warfarin is
usually initiated concurrently with heparin
• Warfarin
• Warfarin affects hepatic synthesis of vitamin K-dependent
coagulant proteins

• It usually requires 5–7 days to become therapeutic; therefore,

heparin is generally continued for 5 days

• Adequacy of therapy must be monitored by following the

prothrombin time, The target INR is 2.5, with the acceptable
range from 2.0 to 3.0; below 2.0, there is an increased risk of
thrombosis; above 4.0, there is an increased risk of
hemorrhage

• Warfarin has interactions with many drugs

• Warfarin is a pregnancy category X medication, indicating

known fetopathic and teratogenic effects

• When oral anticoagulation with warfarin is contraindicated,

LMW heparin is a convenient alternative.
• It is reasonable to continue therapy for 6
months after a first episode when there
is a reversible risk factor, 12 months
after a first-episode idiopathic thrombus,
and 6–12 months to indefinitely in
patients with nonreversible risk factors
or recurrent disease

• The major complication of

anticoagulation is hemorrhage
 Thrombolytic Therapy
• Streptokinase, urokinase, and recombinant tissue
plasminogen activator (rt-PA; alteplase) increase
plasmin levels and thereby directly lyse
intravascular thrombi

• In patients with established pulmonary

thromboembolism, thrombolytic therapy
accelerates resolution of emboli within the first 24
hours compared with standard heparin therapy

• Current evidence supports thrombolytic therapy

for pulmonary thromboembolism in patients at
high risk for death in whom the more rapid
resolution of thrombus may be lifesaving. Such
patients are usually hemodynamically unstable
despite heparin therapy
 Additional Measures
• Inferior vena cava filter
• Interruption of the inferior vena cava may be indicated in
patients with a major contraindication to anticoagulation
who have or are at high risk for development of proximal
DVT or pulmonary embolus
• It is also recommended for recurrent thromboembolism
despite adequate anticoagulation amd for chronic recurrent
embolism with pulmonary hypertension

• Mechanical or surgical extraction of thrombus

• In rare critically ill patients for whom thrombolytic therapy is
contraindicated or unsuccessful, mechanical or surgical
extraction of thrombus may be indicated
• Pulmonary embolectomy is an emergency procedure of last
resort with a very high mortality rate.
 Prevention

• Early ambulation
• Low-dose unfractionated heparin
• Low-molecular-weight heparin
(LMWH)