Pulmonary embolism

DS Mulajker, Vasu Vardhan

Introduction
Pulmonary embolism (PE) and deep vein thrombosis (DVT) are the two different
manifestations of one disease – Venous thromboembolism (VTE). Pulmonary embolism
occurs most commonly due to an embolus from the deep vein thrombosis of the legs. About
79% of patients with PE will have DVT and in the rest usually the whole thrombus from the
lower limb would have embolised. Conversely PE occurs in 50% of patients with DVT. The
clinical manifestations range from an asymptomatic presentation to massive embolism
leading to death.
The occlusion of the pulmonary vasculature may lead to an acute potentially fatal but
reversible right venticular failure. The clinical features become manifest when more than 30 –
50% of pulmonary arterial bed becomes occluded. Early diagnosis is imperative as effective
therapy exists and is life-saving.

Risk Factors

Overall acute medical illness is the most common setting in which VTE occurs.
Certain surgical procedures like total hip and knee replacement, prolonged immobilization
are also important risk factors. The proportion of patients with idiopathic PE was recently
reported to be around 20%.

Odds Ratio > 10 Odds ratio 2 – 9 Odds ratio < 2

Fracture (hip or leg) Arthroscopic knee surgery Bed rest > 3 days
Hip/Knee replacement Central venous lines Prolonged car/air travel
Major general surgery Chemotherapy Increasing age
Major trauma Chronic heart/respiratory failure Laparoscopic surgery
Spinal cord injury Hormone replacement therapy Obesity
Malignancy Varicose veins
Pregnancy and post partum Polycythemia Vera
Oral contraceptive use
Thrombophilic states

Clinical manifestations
Patients with acute PE present with acute or subacute onset dyspnea or chest pain.
Pleuritic chest pain and hemoptysis occur in patients with pulmonary infarctions, which are
caused by small, peripheral emboli. Patients may also complain of cough, palpitations and
fever. Tachycardia and tachypnoea are the most common findings. Massive embolus may
cause pulmonary hypertension and right heart failure leading to elevated jugular venous
pressure, left parasternal heave and a loud P2. Leg pain, warmth and swelling suggest
presence of a deep vein thrombosis.

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Diagnosis
Routine investigations may suggest, but can never make a diagnosis of pulmonary embolism.
CXR
Majority of patients with PE have abnormal X Rays; unfortunately none of the
findings are specific for embolism and none of them are diagnostic. Infiltrates abutting the
pleura are common, and despite classical emphasis, may not be wedge shaped. Blunting of
costophrenic angles can occur in about 50%.
Westermark sign (prominent central pulmonary artery with focal area of avascularity),
the Hampton hump (wedge shaped pleural based density just above the diaphragm) , the
Fleishner sign (prominence of central pulmonary artery) and Palla’s sign ( enlargement of
right descending pulmonary artery) on Chest X Rays were once considered specific for PE,
but studies do not bear out this assumption.
ECG
Electrocardiographic findings in pulmonary embolism are diverse and nonspecific.
The most common abnormalities include sinus tachycardia, T-wave inversion, and
abnormalities of the ST segment. With more extensive occlusion, the electrocardiogram
may reveal an "S1Q3T3" pattern, a pseudo infarction pattern (Qr in V 1), a complete or
incomplete right bundle-branch block, or right axis deviation. These abnormalities are
found in < 6% of patients, though their absence does not exclude pulmonary embolism.
Rhythm disturbances other than sinus tachycardia are uncommon and usually confined to
patients with underlying cardiac disease.
ABG
Arterial hypoxemia is found in only 80% of patients with pulmonary
embolism.however an abnormal alveolar – arterial O2 gradient is more sensitive than
hypoxaemia alone in diagnosing pulmonary embolism.
Echocardiography
Unexplained right ventricular volume or pressure overload may suggest PE. A
distinct echocardiographic pattern involving akinesia of the mid-free right ventricular wall
with apical sparing has been described (Mc Connell sign). The overall sensitivity of
transthoracic echocardiography in pulmonary embolism approximates 50%
Transesophageal echocardiography has 90% sensitivity and specificity in detection
of proximal emboli involving the pulmonary trunk and the right and left main pulmonary
arteries. It may also rule out other diagnostic possibilities such as right ventricular
infarction, endocarditis, pericardial tamponade, and aortic dissection in patients with
unexplained shock and evidence of elevated central venous pressure.
Ventilation-perfusion lung scanning
The negative predictive value of this study is almost 100%, i.e., a negative study
rules out pulmonary embolism. A V/Q scan reported as highly probable (characterized by
multiple, segmental-sized, mismatched defects) is also very specific for PE. In a recent
study, of the total patients being evaluated for PE, V/Q scans were reported as normal in
14% and highly probable in 13%leaving a large number of patients with indeterminate
diagnosis.
CT arteriography
Contrast enhanced CT arteriography has the greatest sensitivity and specificity in
detecting emboli in the main, lobar and segmental arteries. The development of
multidetector CT has further reduced scanning times and improved the visualization of
subsegmental emboli.
D-dimer

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 D-dimer test measures the plasma levels of specific degradation products of cross-
linked fibrin. Studies report a high sensitivity (>95%) of D-dimer ELISA and a useful
negative predictable value( > 95%).A negative ELISA thus excludes pulmonary embolism
in patients with low or intermediate pre-test probability.
Troponins
They may be elevated in patients with massive pulmonary embolism and are
useful in risk stratification of individuals with a confirmed diagnosis of pulmonary
embolism.

Diagnosing PE

Diagnosis of PE requires the assessment of the pretest probability. The clinical

assessment of an astute assessment clinician is the most important part of the diagnostic
algorithm. The PIOPED study clearly demonstrated that the clinical assessment was the
most important factor in the diagnosis of PE. This is best accomplished by means of
Well’s score for PE.

Well’s score Point

s

Previous VTE 1.5

Heart rate > 100 beats/min 1.5

Recent surgery or 1.5

immobilization

Clinical signs of DVT 3

Alternative diagnosis less likely 3

Haemoptysis 1

Cancer 1

Clinical probability

Low 0–1

Intermediate 2–6

High >6

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 Diagnostic algorithm for PE

Recent ESC guidelines have defined ‘Confirmed PE’ as a probability of PE high

enough to indicate need for PE specific therapy and ‘Excluded PE’ as a probability of PE
low enough to justify withholding treatment.

Treatment
It has two aspects:
1. Treatment of acute PE
2. Prevention of recurrent VTE
The approach to the treatment is based on presence of risk factors and is summarised in the
following table( Table 1) and algorithm.

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Table 1. Assessment of risk factors for PE

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 Algorithmic depiction of approach to treatment of PE

1. Treatment of Acute PE
The mode of treatment depends on the hemodynamic stability of the patient.

Hemodynamically unstable patient

Acute RV failure with low systemic output is the leading cause of death.
1. Anticoagulation with unfractionated heparin should be initiated without
delay in patients with high-risk PE.
2. Systemic hypotension should be corrected to prevent progression of RV
failure and death due to PE.
3. Vasopressive drugs are recommended for hypotensive patients with PE.

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 Dobutamine and dopamine may be used in patients with PE, low cardiac
output and normal blood pressure. Aggressive fluid challenge is not
recommended
4. Oxygen should be administered in patients with hypoxaemia.
5. Thrombolytic therapy should be used in patients with high-risk PE
presenting with cardiogenic shock and/or persistent arterial hypotension.
6. Surgical pulmonary embolectomy is a recommended therapeutic alternative
in patients with high-risk PE in whom thrombolysisis is absolutely
contraindicated or has failed.
7. Catheter embolectomy or fragmentation of proximal pulmonary arterial
clots may be considered as an alternative to surgical treatment in high-risk
patients when thrombolysis is absolutely contraindicated or has failed.

Hemodynamically stable patient

1. Anticoagulation should be initiated without delay in patients with high or

intermediate clinical probability of PE while diagnostic workup is still
ongoing.
2. Use of LMWH or Fondaparinux is the recommended form of initial
treatment for most patients with non-high-risk PE. In patients at high risk
of bleeding and in those with severe renal dysfunction, unfractionated
heparin with an aPTT target range of 1.5–2.5 times normal is a
recommended form of initial treatment.
3. Initial treatment with unfractionated heparin, LMWH or Fondaparinux
should be continued for at least 5 days and may be replaced by vitamin K
antagonists only after achieving target INR levels for at least 2 consecutive
days.
4. Routine use of thrombolysis in non–high-risk PE patients is not
recommended, but it may be considered in selected patients with
intermediate-risk PE.
5. Thrombolytic therapy should be not used in patients with low-risk PE.

Anticoagulation
This is achieved by means of heparin and vitamin K antagonists. The goal is to
achieve rapid anticoagulation while minimizing risk of bleeding. The VKAs must be started
on the first day along with heparin/LMWH/Fondaparinux and the overlap continued till
therapeutic INR is achieved.
Thrombolytics
1. Streptokinase: 250000 IU as loading dose over 30 min, then 100000 IU/h for 12 –
24 hr.
2. Urokinasse: 4400 IU/Kg as a loading dose over 10 min, followed by 4400 IU/Kg
over 12 – 24 hr.
3. rtPA: 100 mg over 2 hr or 0.6 mg/kg over 15 min (max dose of 50 mg)

2. Prevention of recurrent VTE

Indication for anticoagulation Duration of therapy

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First VTE with reversible risk factor
Minimum 3 months
First idiopathic VTE Minimum 6 – 12 months; can consider
indefinite
VTE associated with malignancy LMWH for 3 – 6 months, then indefinite
or till malignancy resolves
VTE first episode with 12 months
hypercoagulable state
Two or more episodes Indefinite