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PIRNGADI MEDAN

Pulmonary Embolism
Pulmonary embolism (PE) is a blockage of the main artery of the lung or one of its
branches by a substance that has travelled from elsewhere in the body through the
bloodstream (embolism). PE most commonly results from deep vein thrombosis (a blood clot
in the deep veins of the legs or pelvis) that breaks off and migrates to the lung, a process
termed venous thromboembolism (VTE). A small proportion of cases are caused by the
embolization of air, fat, or talc in drugs of intravenous drug abusers or amniotic fluid. The
obstruction of the blood flow through the lungs and the resultant pressure on the right
ventricle of the heart lead to the symptoms and signs of PE. The risk of PE is increased in
various situations, such as cancer or prolonged bed rest 1.

Background and incidence

Pulmonary embolism (PE) occurs when venous thrombosis, usually from the deep
veins of the proximal legs, travels to the lungs causing a potential spectrum of consequences,
including dyspnea,chest pain, hypoxemia, and sometimes death. Deep venous thrombosis
(DVT) and PE known as venous thrombo embolism (VTE). PE probably accounts for
100,000 to 200,000 deaths in a year in the United States. Autopsy studies have repeatedly
documented the high frequency with which PE has gone unsuspected and undetected. VTE

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occurs worldwide and is usually, but not always, associated with specific risk factors. A
crucial point

is that DVT, therefore PE are often preventable. Although other substances such as malignant
cells, fat droplets, air bubbles, and carbon dioxide can embolize to the lung, this article
focuses on VTE. Because of the lack of specific symptoms and signs, DVT and PE are
frequently clinically unsuspected, leading to substantial diagnostic and therapeutic delays and
resulting in considerable morbidity and mortality. Furthermore, prophylaxis continues to be
dramatically under used. The incidence of VTE is high in hospitalized patients, and both
surgical as well as medical patients are at risk 1.
Signs and Symptoms
Symptoms of PE are typically sudden in onset and may include one or many of the
following: dyspnea (shortness

of

breath),tachypnea (rapid

breathing), chest

pain of

"pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More
severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and
fingers), collapse, and circulatory instability because of decreased blood flow through the
lungs and into the left side of the heart. About 15% of all cases of sudden death are
attributable to PE 2.
Diagnosis
The diagnosis of PE is based primarily on validated clinical criteria combined with
selective testing because the typical clinical presentation (shortness of breath, chest pain)
cannot be definitively differentiated from other causes of chest pain and shortness of breath.
The decision to do medical imaging is usually based on clinical grounds,such as the medical
history, symptoms and findings on physical examination, followed by an assessment of
clinical probability.
a. Blood tests
Hypoxemia is common in acute PE.
b. Electrocardiography
2

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Electrocardiographic findings, which are present in most patients with acute PE, are
non specific, but these abnormalities, including ST-segment abnormalities, T-wave changes,
and left or right axis deviation, are common.
c. Chest radiography
The chest radiograph is often abnormal inpatients with acute PE, but as with
electrocardiography, it is nearly always nonspecific. Common radiographic findings include
atelectasis, pleuraleffusion, pulmonary infiltrates, and mild elevation of a hemidiaphragm.

d. MRI
MRI has been used to evaluate clinically suspected PE, but at present the main
advantage of MRI in this disease process is the excellent sensitivity and specificity for the
diagnosis of DVT.
e. Echocardiography in acute pulmonary embolism
Echocardiography, which can often be obtained more rapidly than either lung
scanning

orpulmonary

arteriography,

may

reveal

findingsthat

strongly

support

hemodynamically significant pulmonary embolism 2.

Treatment

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Options for treatment of acute DVT and PE include anticoagulation with lowmolecular-weigh the parin or standard heparin,thrombolytic therapy, and inferior vena cava
filterplacement. Massive PE is occasionally treated with surgical embolsectomy 3.
Prognosis
Mortality from untreated PE is said to be 26%. This figure comes from a trial
published in 1960 by Barrit and Jordan, which compared anticoagulation against placebo for
the management of PE. Barritt and Jordan performed their study in the Bristol Royal
Infirmary in 1957. This study is the only placebo controlled trial ever to examine the place of
anticoagulants in the treatment of PE, the results of which were so convincing that the trial
has never been repeated as to do so would be considered unethical. That said, the reported
mortality rate of 26% in the placebo group is probably an overstatement, given that the
technology of the day may have detected only severe PEs.
Prognosis depends on the amount of lung that is affected and on the co-existence of
other medical conditions; chronic embolisation to the lung can lead to pulmonary
hypertension. After a massive PE, the embolus must be resolved somehow if the patient is to
survive. In thrombotic PE, the blood clot may be broken down by fibrinolysis, or it may be
organized and recanalized so that a new channel forms through the clot. Blood flow is
restored most rapidly in the first day or two after a PE. Improvement slows thereafter and
some deficits may be
permanent. There is controversy over whether or not small subsegmental PEs need to be
treated at all and some evidence exists that patients with subsegmental PEs may do well
without treatment. Once anticoagulation is stopped, the risk of a fatal pulmonary embolism is
0.5% per year 3.

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References
1. Bobadilla RA, Garcia-Juarez JA, Hong E, et al: Serotonergic receptors involved in the
hemodynamic changes observed during pulmonary embolism. Proc West Pharmacol Soc
1991; 34: 439-442.
2. Schmidt GA: Pulmonic embolic disorders: Thrombus, Air and Fat, in Hall JB, Schmidt
GA, Wood LDH (eds): Principles of Critical Care. McGraw-Hill 1992; pp 1476-1492.
3. Hellenic J. 2007. Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. 101-132