THE CORRELATION BETWEEN

DEEP VEIN THROMBOSIS

AND PULMONARY EMBOLISM

Written by:
Putri Mulyati
030.07.208
FACULTY OF MEDICINE
TRISAKTI UNIVERSITY
JAKARTA
2010

Abstract
In the 19th century, Virchow identified a triad of factors that lead to venous
thrombosis: venous stasis, injury to the intima, and enhanced coagulation properties of the
blood. Thrombosis usually originates as a platelet nidus on valves in the veins of the lower
extremities. Further growth occurs by accretion of platelets and fibrin and progression to red
fibrin thrombus, which may either break off and embolize or result in total occlusion of the
vein. The endogenous thrombolytic system leads to partial dissolution; then, the thrombus
becomes organized and is incorporated into the venous wall.
Pulmonary embolism is present in 60-80% of patients with DVT; even though more
than half these patients are asymptomatic.

(2)

Pulmonary embolism is the third most common

cause of death in hospitalized patients, with at least 650,000 cases occurring annually.
Autopsy studies have shown that approximately 60% of patients who died in the hospital had
pulmonary embolism, and the diagnosis was missed in up to 70% of the cases.

Key words
Deep vein thrombosis, deep venous thrombosis, pulmonary embolism

(2)

Introduction
Pulmonary embolism (PE) is a common and potentially lethal condition. 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 related to venous
thromboembolism, most commonly deep venous thrombosis (DVT). Virtually every
physician who is involved in patient care encounters patients who are at risk for venous
thromboembolism, and therefore at risk for pulmonary embolism.
DVTs occur in about 1 per 1000 persons per year. It is estimated that approximately
350,000 to 600,000 Americans each year suffer from DVT and pulmonary embolism and at
least 100,000 deaths may be directly or indirectly related to these diseases. (5)
Studies of patients with proven acute pulmonary embolism have reported a high
prevalence (i.e., up to 61%) of concomitant DVT. The current results have at least two
clinical implications, First, because patients with pulmonary embolism who have concomitant
DVT have an increased risk of recurrent venous thromboembolism and pulmonary embolismrelated death compared to those without concomitant DVT, they may potentially benefit from
more intensive surveillance and treatment such as thrombolysis.(2)
Second, because patients without concomitant DVT have a relatively low rate of
venous thromboembolism recurrence and mortality, these patients may be more optimal
candidates for partial or full outpatient pulmonary embolism therapy compared to those with
concomitant DVT.

Chapter I
Deep Vein Thrombosis
Deep vein thrombosis (also known as deep-vein thrombosis or deep venous
thrombosis and usually abbreviated as DVT) is the formation of a blood clot (thrombus) in a
deep vein. It is a form of thrombophlebitis, the inflammation condition of a vein with clot
formation.
DVT is a medical emergency situation. Deep vein thrombosis commonly affects the
leg veins, such as the femoral vein, the popliteal vein, or the deep veins of the pelvis.
Occasionally the veins of the arm are affected and if its happen spontaneously, it will be
known as Paget-Schrtter disease. A DVT can occur without symptoms, but in many cases
the affected extremity will be painful, swollen, red, warm and the superficial veins may be
engorged. The most serious complication of a DVT is that the clot could dislodge and travel
to the lungs, which is called a pulmonary embolism (PE).
According to Virchow's triad, venous thrombosis occurs via three mechanisms:
decreased flow rate of the blood, damage to the blood vessel wall and an increased tendency
of the blood to clot (hypercoagulability). Several medical conditions can lead to DVT, such as
physical trauma, cancer, infections, and specific conditions such as stroke, heart failure or
nephrotic syndrome. There are several factors which can increase a person's risk for DVT,
including surgery, hospitalization, immobilization (such as when orthopedic casts are used, or
during long-haul flights, leading to economy class syndrome), smoking, obesity, age, certain
drugs (such as estrogen or erythropoietin) and inborn tendencies to form clots known as
thrombophilia (for example, in carriers of factor V Leiden). Women have an increased risk
during pregnancy and in the postnatal period.
The most commonly used tests for the diagnosis of DVT are a blood test called Ddimers and Doppler ultrasound of the affected veins.

(1)

Sometimes, further testing is required

to find the cause of the DVT. In specific cases, an attempt can be made to break down the clot
(using thrombolytic agents). To prevent further accrual and formation of new clots with a risk
of pulmonary embolism, anticoagulation is advised. Prevention of DVT is advised in many
medical and surgical inpatients using anticoagulants, graduated compression stockings (also
known as thromboembolic deterrent stockings) or intermittent pneumatic compression (IPC)
devices.

Diagnosis and Clinical Manifestation

Diagnosis
Several techniques during physical examination are needed to increase the detection
of DVT, such as measuring the circumference of the affected and the contralateral limb at a
fixed point (to objectivate edema), and palpating the venous tract, which is often tender.
Physical examination is usually unreliable for excluding the diagnosis of DVT.(3)
1.

Homans sign: Dorsiflexion of foot elicits pain in posterior calf.

2.

Pratt's sign: Squeezing of posterior calf elicits pain.

However, these medical signs do not perform well and are not included in clinical
prediction rules that combine best findings in order to diagnose DVT.(3)
The gold standard is intravenous venography, which involves injecting a peripheral
vein of the affected limb with a contrast agent and taking X-rays, to reveal whether the
venous supply has been obstructed. Because of its invasiveness, this test is rarely performed.
Probability scoring
In 2006, Scarvelis and Wells overviewed a set of clinical prediction rules for DVT, on
the heels of a widely adopted set of clinical criteria for pulmonary embolism.(7)
Wells score or criteria: (Possible score -2 to 8)
1.

Active cancer (treatment within last 6 months or palliative) -- 1 point

2.

Calf swelling >3 cm compared to other calf (measured 10 cm below tibial

tuberosity) -- 1 point
3.

Collateral superficial veins (non-varicose) -- 1 point

4.

Pitting edema (confined to symptomatic leg) -- 1 point

5.

Swelling of entire leg - 1 point

6.

Localized pain along distribution of deep venous system1 point

7.

Paralysis, paresis, or recent cast immobilization of lower extremities1 point

8.

Recently bedridden > 3 days, or major surgery requiring regional or general

anesthetic in past 4 weeks1 point

9.

Previous documented DVT-1 point.

10.

Alternative diagnosis at least as likelySubtract 2 points

Interpretation:
Score of 2 or higher - deep vein thrombosis is likely. Consider imaging the leg veins.
Score of less than 2 - deep vein thrombosis is unlikely. Consider blood test such as ddimer test to further rule out deep vein thrombosis.

Blood tests
D-dimer
In a low-probability situation, current practice is to commence investigations by
testing for D-dimer levels. This cross-linked fibrin degradation product is an indication that
thrombosis is occurring, and that the blood clot is being dissolved by plasmin. A low D-dimer
level should prompt other possible diagnoses (such as a ruptured Baker's cyst, if the patient is
at sufficiently low clinical probability of DVT). (3)
Other blood tests
Other blood tests usually performed at this point are:

complete blood count

Primary coagulation studies: PT, aPTT, Fibrinogen

liver enzymes

renal function and electrolytes

Imaging the leg veins

Impedance plethysmography, Doppler ultrasonography, compression ultrasound
scanning of the leg veins, combined with duplex measurements (to determine blood flow),
can reveal a blood clot and its extent (i.e. whether it is below or above the knee). Duplex
Ultrasonography, due to its high sensitivity, specificity and reproducibility, has replaced
venography as the most widely used test in the evaluation of the disease. (5) This test involves
both a B mode image and Doppler flow analysis. It is most sensitive and specific for
detecting proximal thrombi (in the popliteal and femoral veins), but substantially less so for
distal thrombi (in the calf veins).
It is vital that the possibility of pulmonary embolism be included in the history, as this
may warrant further investigation.A careful history has to be taken considering risk factors
including the use of estrogen-containing methods of hormonal contraception, recent longhaul flying, intravenous drug use and a history of miscarriage (which is a feature of several
disorders that can also cause thrombosis). In the case of long-haul flying, recent studies have
shown that risk of DVT is higher in travellers who smoke, are obese, or are currently taking
contraceptive pills.(2) A family history can reveal a hereditary factor in the development of
DVT. Approximately 35 percent of DVT patients have at least one hereditary thrombophilia,
including deficiencies in the anticoagulation factors protein C, protein S, antithrombin, or
mutations in the factor V and prothrombin genes.(5)

Clinical manifestation
There may be no symptoms referable to the location of the DVT, but the classical
symptoms of DVT include pain, swelling and redness of the leg and dilation of the surface
veins. In up to 25% of all hospitalized patients, there may be some form of DVT, which often
remains clinically inapparent (unless pulmonary embolism develops).(7)
In phlegmasia alba dolens, the leg becomes pale and cool with a diminished arterial
pulse caused by spasm. It is usually results from acute occlusion of the iliac and femoral
veins because of DVT.
An acute and nearly total venous occlusion of the entire extremity outflow, including
the iliac and femoral veins happens in the phlegmasia cerulea dolens . The leg can be painful,
cyanosed, and oedematous . Venous gangrene may supervene.

Chapter II
Pulmonary Embolism
Pulmonary emboli usually arise from the thrombi originating in the deep venous system of
the lower extremities; however, rarely they may originate in the pelvic, renal, or upper
extremity veins or the right heart chambers. After traveling to the lung, large thrombi can
lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause
hemodynamic compromise. Smaller thrombi typically travel more distally, occluding smaller
vessels in the lung periphery. These are more likely to produce pleuritic chest pain by
initiating an inflammatory response adjacent to the parietal pleura. Most pulmonary emboli
are multiple, and the lower lobes are involved more commonly than the upper lobes.
Respiratory consequences
Acute respiratory consequences of pulmonary embolism include increased alveolar dead
space, pneumoconstriction, hypoxemia, and hyperventilation. Later, two additional
consequences may occur: regional loss of surfactant and pulmonary infarction. Arterial
hypoxemia is a frequent but not universal finding in patients with acute embolism. The
mechanisms of hypoxemia include ventilation-perfusion mismatch, intrapulmonary shunts,
and reduced cardiac output. Pulmonary infarction is an uncommon consequence because of
the bronchial arterial collateral circulation.
Hemodynamic consequences
Pulmonary embolism reduces the cross-sectional area of the pulmonary vascular bed,
resulting in an increment in pulmonary vascular resistance, which, in turn, increases the right
ventricular afterload. If the afterload is increased severely, right ventricular failure may
ensue. In addition, the humoral and reflex mechanisms contribute to the pulmonary arterial
constriction. Prior poor cardiopulmonary status of the patient is an important factor leading to
hemodynamic collapse. Following the initiation of anticoagulant therapy, the resolution of
emboli occurs rapidly during the first 2 weeks of therapy. Significant long-term nonresolution
of emboli causing pulmonary hypertension or cardiopulmonary symptoms is uncommon.

Clinical Manifestation and Risk Factors

Patients with pulmonary embolism may present with atypical symptoms. These
symptoms include seizures, syncope, abdominal pain, fever, productive cough, wheezing,
decreasing level of consciousness, new onset of atrial fibrillation, flank pain, delirium (in
elderly patients) .(3)
Fever of less than 39C may be present in 14% of patients. Pleuritic chest pain
without other symptoms or risk factors and also chest wall tenderness upon palpation, without
a history of trauma, may be the sole physical finding in rare cases.(3)
The most common physical signs in the PIOPED (Prospective Investigation of
Pulmonary Embolism Diagnosis) study were

tachypnea (70%), rales (51%), tachycardia

(30%), fourth heart sound (24%), accentuated pulmonic component of the second heart sound
(23%).(8)
Risk Factors for Virchow's Triad and PE
This table lists risk factors for Virchow's triad(3) a set of conditions that predispose a
person for pulmonary embolism (PE).
Risk factor

Examples and mechanism

Lower blood-flow states and decreased mobility associated with age

increase the risk of clot formation.

Age-related dehydration may increase blood viscosity, potentiating

clot formation.

Certain cancers (such as pancreatic, ovarian, and lung cancer) and

chemotherapy can lead to hypercoagulability.
Women with a history of breast cancer who take tamoxifen or
raloxifene are at higher risk for blood clots.

Age

Cancer

Cardiovascular
Endovascular
Estrogen

Patients receiving chemotherapy that requires central venous access

are at higher risk for endovascular damage, which can lead to blood
clots.

Cardiovascular disease may cause low blood-flow states that disease

raise the risk of clot formation and lead to hypercoagulability.

Procedures such as central line placement may cause damage

endovascular damage leading to inflammation and blood clots.

Estrogen in birth control pills and hormone replacement therapy can

increase clotting factors, resulting in hypercoagulability.

Family history
Immobility
Inflammation

Inherited disorders, such as sickle-cell anemia, polycythemia, and

thrombophilia, create hypercoagulability.

Bed rest and a prolonged cramped position reduce blood flow, which
increases coagulability.

Inflammation such as infection may increase the risk of blood clots.

Obesity raises the risk of blood clots due to decreased bloodflow

states that create hypercoagulopathy.

Obese women who smoke are at even higher risk.

Weight of the fetus on pelvic veins may reduce blood return from the
legs, causing blood pooling and clot formation.

Increased estrogen levels during pregnancy promote coagulability.

Elevated fibrinogen levels increase blood viscosity and

hypercoagulability, raising the risk of clots. Data suggest smoking
cessation lowers fibrinogen levels, showing a link between smoking
and increased fibrinogen.

When combined with other risk factors, smoking significantly

increases the risk of clots.

Patients with long bone fractures or who have had surgical bone repair
are at increased risk for fat emboli.

Postoperative patients are at increased risk for clots due to immobility,

decreased blood flow, and hypercoagulability.

Obesity

Pregnancy

Smoking

Surgery

Deep Vein Thrombus and Pulmonary Embolism : Is There Any

Correlation?

Pulmonary Embolism (PE) occurs when a pulmonary artery becomes blocked

usually by a blood clot that has broken free from its site of origin and embolized or migrated
to the lungs. If misdiagnosed, unrecognized, or untreated, PE can cause death quickly
within just an hour. It's fatal in up to 26% of cases. (1)
Massive PE, defined as causing 50% or more occlusion of the pulmonary capillary
bed, can result in obstructive shock with systemic hypoperfusion (low cardiac output and
acute pulmonary hypertension with right ventricular failure).

(1)

It must be remedied

immediately to save the patient's life.

Pathophysiology
The usual underlying cause of PE is deep vein thrombosis (DVT) in a lower
extremity, the pelvis, or even an upper extremity.
DVT, in turn, typically results from one or more of these conditions: venous stasis,
blood hypercoagulability (increased clotting), or endovascular damage. Known collectively
as Virchow's triad, these conditions can stem from a range of situations. For instance, venous
stasis and hypercoagulability may result from immobilization or regional states of low blood
flow caused by trauma (especially to the lower legs), burns, shock, obesity, or heart disease.
Endovascular damage may stem from central venous access or venous procedures, when
invasion and manipulation of the intimal wall of the vein increase platelet aggregation or
fibrin production, causing clot formation.
Blood flow and blood vessel
There are some procoagulant in the blood such as thrombosit, fibrinogen,
prothrombine, calcium, and so on. Anticoagulant in the blood also present, such as AT
III, S Protein , C Protein. If pro and anti coagulant lost their balance it will be known
as hypercoagulable state which the blood will be easier to becomes a clot and obstruct
the organ vessel. In the other way, increase of procoagulation factor or red blood cell,
will increase the viscosity and can cause lower blood flow (velocity). This condition
will minimize the blood flow to the target organ and trigger the coagulation so deficit
blood flow will be performed and causing the organ dysfunction.
Thrombosis
Endotel injury will attract adhesion of the thrombocyte and will agregate
procoagulan factors and finally formed a thrombus.

with

Low blood flow in vein will make a red thrombus which has eritrocyte as the main
component, fibrinogen, and other procoagulation factors that give out its red color.
A clot on the wall of the vessel will unsmoothen the blood flow because this clot has a
potensial to get bigger than its original size and also has a tendency to broken free and
migrated along the vessel. This is known as embolus or emboli. The emboli will be a
serious problem if the diameter of the vessel that passed by the emboli smaller than
the emboli itself so it can obstruct the blood vessel spontaneously.(6)
Fibrinolysis / Thrombolysis
Fibrinolysis is a body mechanism to destroy the fibrin or thrombus in the body. The
main component is plasminogen that will be activated by tissue plasminogen
activator (t-PA) and known as plasmin. Endotel injury will activate thrombosis proses
and loading of t- PA from the endotel and the tissue, t- PA will activate the
plasminogen and convert it into plasmin form which will destroy blood clot fibrin and
lyse it and also decrease other procoagulan such as fibrinogen, factor V, factor VIII ,
and cause platelet dysfunction. T-PA and plasmin in the sirculation will be anticipated
by produce plasminogen activator inhibition (PAI-1) which will inhibit tissue
plasminogen activator or t-PA and 2- antiplasmin (2-AP) so the activity of these
substance can be stopped because these two substance can harass the coagulation
system.
Fibrinolitic activity is regionally.(6) D- dimer is the product of FDP and in the clinical,
can be used to see the activity of fibrinolysis. Activity of the plasmin can be seen with
some laboratory examination such as PT, APTT, Fibrinogen, faCtor V, and faCtor
VIII. Platelet disfuction, trouble of aggregation thrombocyte can be happen because
of the influence from FDP. Influence of the plasmin to the abnormality from von
Willenbrand faCtor-glycoprotein 1b intraction, makes trouble of thrombocyte
adhesion.

How a Pulmonary Embolism Evolves

A blood clot that has become dislodged and migrated to the lung, pulmonary
embolism (PE) typically originates from deep vein thrombosis in a lower extremity, the
pelvis, or an upper extremity. A pulmonary vessel becomes obstructed when air or a foreign
object enters the venous system.

A dislodged clot that has moved through the right side of the heart and

embolized to the lung, where it has become lodged in a smaller pulmonary vessel. Once

lodged there, the clot prevents blood from reaching that lung section, creating dead space (a
high ratio of ventilation to perfusion [V/Q]). Pulmonary capillaries distal to the occluded
vessel receive decreased or absent blood flow (low Q) and can't eliminate carbon dioxide
(CO2) from that lung region despite continuation of ventilation (normal to high V).

With sustained absence of blood flow, lung ischemia may occur, which

increases local cytokine production and regional lung edema. If lung permeability and edema
formation evolve, a low V/Q ratio develops in previously unaffected lung regions,
compromising oxygenation. During the early phase of a PE, hypoxemia may be undetectable,
with clinicians noticing only respiratory alkalosis due to tachypnea in a compensatory attempt
to reduce CO2. Later, obvious hypoxemia may develop and become refractory to
supplemental oxygen because of a worsening low V/Q ratio.

Signs and symptoms

Often, PE and DVT don't cause symptoms, making these conditions challenging to
detect. In many patients, even extensive testing fails to confirm these disorders.
When PE signs and symptoms do occur, they may be nonspecific, and include: (1)

shortness of breath

dry cough

hemoptysis

diaphoresis or sudden chest pain that worsens with deep inspiration. The chest

pain typically ccompanies lung infarction, as the pleura is the only part of the lung that can
sense pain.

More severe clinical findings may include hypotension, hypoxemia,

and loss of consciousness. Classically, these occur with a massive PE, multiple PE, or
in situ clot propagation. DVT causes signs and symptoms in only about half of those
affected. Signs and symptoms of DVT in the leg include positive Homan's sign,
Pratts sign, redness or discoloration, and increased warmth and swelling in the
affected leg. Early DVT diagnosis and management are crucial, helping to prevent
emboli from migrating to the pulmonary vasculature.

Diagnosis
Early clinical history of DVT, complete physical examination, lab finding, and also
some other test might be involved, such as:

Computed Tomography Scans

CT scans to look for blood clots in the lungs and legs. Dye is injected into a vein in patiens
arm. The dye makes the blood vessels in the lungs and legs show up on an x-ray image.
While the patien lie on a table, an x-ray tube rotates around, taking pictures from different
angles.This test allows doctors to detect most cases of PE. The test only takes a few minutes.
Results are available shortly after the scan is completed.
Lung Ventilation/Perfusion Scan
A lung ventilation or perfusion scan, or VQ scan, uses a radioactive substance to show how
well oxygen and blood are flowing to all areas of the lungs. This test can help detect PE.
Pulmonary Angiography
It is another test used to diagnose PE. It's not available at all hospitals, and a trained specialist
must perform the test. A flexible tube called a catheter is threaded through the groin (upper
thigh) or arm to the blood vessels in the lungs. Dye is injected into the blood vessels through
the catheter.
X-ray pictures are taken to show blood flowing through the blood vessels in the lungs. If a
blood clot is found, your doctor may use the catheter to extract it or deliver medicine to
dissolve it.
A scoring tool such as the Geneva score to aid PE diagnosis is very useful. (3) The simplified
Geneva score is based on nine patient risk factors and clinical variables; patients with a total
score of two points or less are considered unlikely to have PE.
For instance, where each item carries one point, suppose a patient:

has a history of a previous DVT or PE (1 point)

is age 65 or older (1 point)

has hemoptysis (1 point)

Surgery or fracture within 1 month (1 point)

Active malignancy (1 point)

Unilateral lower limb pain (1 point)

Pain on deep vein palpation of lower limb and unilateral edema (1 point)

Heart rate 75 to 94 bpm (1 point)

Heart rate greater than 94 bpm

* +1 * Heart rates of 75 to 94 bpm receive 1 point, while heart rates higher than 94bpm receive a
further point (i.e. 2 points in total)

Management
The goal of treatment is to halt PE evolution by reducing the propagation of an
existing clot or preventing a new clot from forming and embolizing.

(1)

A patient with

confirmed PE may receive anticoagulants or thrombolytics or may undergo surgery.

Hemodynamically significant PE frequently is an indication for thrombolysis (clot
lysis) rather than just anticoagulant therapy.(1) In situ clot propagation can be treated
effectively with anticoagulation if intervention begins early and therapeutic goals are
achieved and maintained. Use of heparin nomograms may help clinicians reach these goals
and minimize failure.
Although heparin and warfarin don't lyse existing clots, they help prevent clot
propagation and allow the body to lyse the clot naturally.(1) The natural lytic process takes
several months to break down the clot and recannulize the vessel, so prolonged
anticoagulation is needed. Warfarin (Coumadin) is given orally but doesn't take effect for
several days; generally, it's given in combination with I.V. heparin until an appropriate
International Normalized Ratio (INR) is reached. The goal of anticoagulant therapy is to
achieve an INR of 2 to 2.5 for a range of 3 to 6 months. (1) Possible adverse effects of
anticoagulants include bruising and bleeding.
The Joint Commission notes that anticoagulants are more likely than other
medications to cause harm because of their complex dosing, insufficient monitoring, and
inconsistent patient adherence.(1)

Regular INR monitoring and teaching patients about

therapy are essential to helping them achieve desired outcomes.

Surgical removal of a clot is called an embolectomy. This treatment is rarely used for
PE.(2) This kind of treatment considered only for people who can not have another kinds of
treatment or those whose clot is so dangerous that they cant wait the medicine to work.
Embolectomy also may be an option for those whose condition is stable but shows of the
significant sign of reduced blood flow in the pulmonary artery.

Conclusion
Pulmonary embolism (PE) is now present in 60-80% of patients with deep vein thrombus
(DVT), even though more than half these patients are asymptomatic. . (7) This is the third most

common cause of death in hospitalized patients, with at least 650,000 cases occurring
annually. In autopsy studies have shown that approximately 60% of patients who died in the
hospital had pulmonary embolism, and the diagnosis was missed in up to 70% of the cases. (2)
This condition must be recognized immediately to save the patient's life and control the
prevalence of this case. Even PE and DVT don't cause symptoms, this condition making these
case more challenging to detect.
Although DVT starts in the calf veins, in cases of pulmonary embolism, it will usually
propagate proximally to the popliteal vessels, and from that area embolize.
The goal of treatment is to halt PE evolution by reducing the propagation of an existing clot
or preventing a new clot from forming and embolizing. (1) A patient with confirmed PE may
receive anticoagulants or thrombolytics or may undergo surgery.

References

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American College of Chest Physicians. Antithrombotic and Thrombolytic

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Anderson FA, Jr, Wheeler HB, Goldberg RJ, Hosmer DW, Patwardhan NA,

Jovanovic B, Forcier A, Dalen JE. A population-based perspective of the hospital

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Andrews, PL. Detecting, Managing, and Preventing Pulmonary Embolism:

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Kearon C, Hirsh .Venous thromboembolism. In DC Dale, DD Federman, eds.,

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Silverstein MD, Heit JA, Mohr DN, Petterson TM, O'Fallon WM, Melton

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