Pulmonary Embolism and Deep Vein Thrombosis

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Pulmonary Embolism and Deep Vein Thrombosis
Samuel Z. Goldhaber and Ruth B. Morrison
Circulation. 2002;106:1436-1438
doi: 10.1161/01.CIR.0000031167.64088.F6
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CARDIOLOGY PATIENT PAGE
Pulmonary Embolism and Deep Vein Thrombosis
Samuel Z. Goldhaber, MD; Ruth B. Morrison, RN, BSN, CVN
T
he heart pumps oxygenated blood through the aorta to
smaller arteries. After the blood supplies nutrients to
vital organs, it returns through veins for reoxygenation
in the lungs (Figures 1 and 2). Blood clots called deep vein
thrombi (DVT) often develop in the deep leg veins. Pulmonary embolism (PE) occurs when clots break off from vein
walls and travel through the heart to the pulmonary arteries.
The broader term venous thromboembolism (VTE) refers to
DVT, PE, or to a combination of both.
What Is the Epidemiology?
VTE poses a public health threat with an estimated incidence
in the United States of 250 000 to 2 million cases per year.
Predisposition to VTE arises from acquired conditions, inherited disorders, or both. Many of the acquired risk factors can
be modified, thus lessening the likelihood of PE or DVT.
What Are the Acquired Risk Factors?
Long-haul air travel is the most talked-about risk factor for
PE. Other acquired risk factors include obesity, cigarette
smoking, hypertension, immobilization, surgery, and trauma.
Chronic medical illnesses such as congestive heart failure,
chronic obstructive pulmonary disease, and cancer also predispose to PE. PE is also a prominent women’s health issue.
Risk factors include oral contraceptives, pregnancy, and
hormone replacement therapy.
factors is sometimes called a prothrombotic or thrombophilic
state.
How Is the Diagnosis Established?
DVT most often originates in the calf, with a persistent
cramping or “charley horse” that intensifies over several
days. Leg swelling and discoloration may accompany the
increase in discomfort. Upper-extremity DVT may cause
otherwise unexplained upper arm or neck swelling. The most
frequently used diagnostic imaging test is the noninvasive
venous ultrasound examination.
Many patients with PE have a vague sense that something
is wrong but have difficulty defining or describing the
problem. Consequently, they often delay seeking medical
attention. At times, because symptoms are so vague and
nonspecific, medical professionals will diagnose anxiety
rather than PE. To establish the diagnosis of PE, the most
frequently used noninvasive imaging test is the rapid-speed
chest computed tomography (CT) scan.
What Are the Warning Signals of PE?
●
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Unexplained shortness of breath (the most common
symptom of PE)
Chest discomfort, usually worse with a deep breath
or coughing
A general sense of anxiety or nervousness
Lightheadedness or blacking out
What Are the Inherited Disorders?
Heredity plays an important role in a patient’s susceptibility
to PE. We are just beginning to develop genetic tests (such as
factor V Leiden and the prothrombin gene mutation) that can
identify those who are predisposed. The presence of these risk
What Should I Expect at the Hospital?
Definitely Expect:
●
●
From the Cardiovascular Division, Brigham and Women’s Hospital,
Harvard Medical School, Boston, Mass.
Correspondence to Samuel Z. Goldhaber, MD, Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, 75
Francis St, Boston, MA 02115. E-mail [email protected]
(Circulation. 2002;106:1436-1438.)
© 2002 American Heart Association, Inc.
Circulation is available at http://www.Circulationaha.org
DOI: 10.1161/01.CIR.0000031167.64088.F6
●
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Questions about symptoms of chest or leg discomfort, breathing difficulties, or lightheadedness
Questions about whether you or your family members have suffered prior VTE
A check of your blood pressure, pulse rate, breathing
rate, heart, lungs, and legs
An ECG and chest x-ray
Possibly Expect:
●
A blood test (D-dimer) that screens for PE (If results
are normal, PE is extremely unlikely.)
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Goldhaber and Morrison
Pulmonary Embolism and Deep Vein Thrombosis
1437
Figure 2. Deoxygenated blood returns to the heart and lungs for
reoxygenation. SVC indicates superior vena cava; IVC, inferior
vena cava; RA, right atrium; RV, right ventricle; and PA, pulmonary artery. Adapted with permission from MediClip, Clinical
Cardiopulmonary Images 1997, CATHRHT.TIF, Williams &
Wilkins, Baltimore, Md.
Figure 1. The arterial (red) and venous systems (blue) are
depicted. The left ventricle (LV) ejects oxygenated blood into the
aorta, which circulates blood to vital organs. Deoxygenated
blood travels through the venous system to the right atrium,
right ventricle, and pulmonary artery. Adapted with permission
from MediClip, Clinical Cardiopulmonary Images 1997,
CCP01026.TIF, Williams & Wilkins, Baltimore, Md.
●
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A chest CT scan, which directly images blood clots
causing blockages in the pulmonary arteries
A lung scan, which indirectly identifies areas of
decreased blood flow in the lung tissue as a consequence of PE
Blood tests to detect a prothrombotic state, especially in relatively young and otherwise healthy
patients with PE or DVT
What Treatment Will I Receive?
PE can range from mild to severe. Mild PE is managed with
blood thinners (anticoagulation). Severe PE requires additional measures, such as clot busters (thrombolytic therapy)
or embolectomy, a procedure in which the clot is removed
with either a catheter or surgery.
Anticoagulation begins with a combination of 2 blood
thinners: (1) heparin, administered intravenously or by
injection, and (2) warfarin, an oral blood thinner. Heparin
comes in 2 principal forms. The traditional unfractionated
form ordinarily requires intravenous administration. There is
no fixed dose for this type of heparin. Instead, the dose is
titrated to a blood test called the partial thromboplastin
time. This blood test is usually performed several times daily
for the first few days and then once daily thereafter. More
recently, low-molecular-weight heparins have begun replacing unfractionated heparin. Low-molecular-weight heparins
are ordinarily prescribed in proportion to the patient’s weight,
require no blood testing, and necessitate injection once or
twice daily.
We overlap heparin treatment with warfarin until the oral
blood thinner becomes effective, usually after 5 to 10 days of
combined therapy. We determine the proper dose of warfarin
by a blood test reported as the International Normalized Ratio
(INR). The target INR range is usually between 2.0 and 3.0.
Interactions with food, alcohol, and other drugs can dramatically alter the INR. Sometimes, major fluctuations in the
INR occur for no apparent reason. Too high an INR may
result in bleeding as a side effect. Too low an INR may result
in recurrent clotting. Patients may need their INR checked
every few weeks or months, according to the stability of the
readings. It is important for patients to keep a record of their
values over time.
PE is usually treated in the hospital with intravenous
unfractionated heparin as a bridge to warfarin. In contrast,
DVT can often be managed successfully on an outpatient
basis with low-molecular-weight heparin injections as a
bridge to oral anticoagulation with warfarin. The most controversial area in VTE therapy is the optimal duration of
warfarin anticoagulation. The current recommendation is
usually at least 6 months of anticoagulation, but it can
sometimes be longer, according to individual patient
circumstances.
In patients who cannot tolerate anticoagulation or those for
whom anticoagulation fails, a permanent metal filter is
inserted into the inferior vena cava, the largest vein below the
heart, to prevent large blood clots from reaching the pulmonary arteries and causing PE. Unfortunately, the filter devices
do not halt the clotting process. Their presence predisposes to
future venous clots on or below the filter.
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1438
Circulation
September 17, 2002
Prevention
Maintaining ideal body weight with a healthy nutritional
program and exercise regimen will generally reduce the
likelihood of venous thrombosis. Specific other measures are
shown below:
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●
●
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To prevent immobility or inactivity: Walk, jog,
bicycle, or swim.
To prevent obesity: Limit caloric intake, exercise,
and avoid saturated fats.
To prevent VTE during air travel: Drink extra water,
walk if feasible, wear vascular compression stockings, and avoid alcohol.
To quit cigarette smoking: Use nicotine patch, gum,
or spray, or consider the prescription drug
bupropion.
To control hypertension: Self-check blood pressure,
and report elevated readings to primary care
provider.
To deal with a known genetic predisposition to VTE:
Alert your healthcare provider about the family
history and any abnormal blood tests related to a
clotting tendency.
To prevent VTE after trauma or surgery: Discuss
with the treating physician the implementation of
measures such as mechanical compression boots for
the legs and/or blood thinners given either intravenously or as injections.
●
●
To prevent VTE during a hospitalization precipitated
by a medical condition: Discuss with the treating
physician measures such as mechanical compression
boots for the legs and/or blood thinners given either
intravenously or as injections.
To prevent VTE when planning birth control: Discuss VTE risks, and consider alternatives to oral
contraceptives.
To prevent VTE during pregnancy: Consider daily
self-injected heparin if considered at high risk of
VTE.
To prevent VTE during hormone replacement therapy: Keep in mind that VTE risks with hormone
replacement therapy are similar to those of oral
contraceptives.
Supplemental Reading
1. Goldhaber SZ. Pulmonary embolism. N Engl J Med. 1998;339:93–104.
2. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism:
clinical outcomes in the International Cooperative Pulmonary Embolism
Registry (ICOPER). Lancet. 1999;353:1386 –1389.
3. Goldhaber SZ, ed. Frequently asked questions of the Pulmonary
Embolism Support Group, Brigham and Women’s Hospital. Available at:
http://icoper.cineca.com/faq icoper.htm. Accessed August 23, 2002.
4. Geerts WH, Heit JA, Clagett GP, et al. Prevention of venous thromboembolism. Chest. 2001;119:132S–175S.
5. Goldhaber SZ, Ridker PM. Thrombosis and Thromboembolism. New
York, NY: Marcel Dekker, Inc; 2002.
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