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Pulmonary embolism (PE)

Causes : PEs usually arise from a venous thrombosis in the pelvis or legs.


Rare causes include: right ventricular thrombus (post-MI): septic emboli (right-sided endocarditis); fat, air, or amniotic fluid embolism; neoplastic cells; parasites.


Risk factors: Any cause of immobility or hyper-coagulability Q:


Defective inhibition of coagulation factors

Impaired clot lysis

a.    Factors V Leiden resistance (Resistance to activated protein C)
b.    Antithrombin III deficiency
c.    Protein C deficiency
d.    Protein S deficiency
e.    Prothrombin gene mutation
f.    Antiphospholipid antibody or lupus anticoagulant

a.    Dysfibrogenemia
b.    Plasminogen deficiency
c.    tPA deficiency
d.    Uncertain Mechanism
e.    Hyperhomocysteinemia


Risk Factor

  1. Recent surgery .                      
  2. Recent stroke or MI.            
  3. Disseminated malignancy.   
  4. Pregnancy Q;                    
  5. Postpartum Q;                      
  6. Estrogen therapy
  7. Protein S deficiency                  
  8. Atrial fibrillation           
  9. Antiphospholipid syn.             
  10. Prolonged bed rest

Clinical features        

  1. These depend on the number, size, and distribution of the emboli;        
  2. Small emboli may be asymptomatic Q, whereas large emboli are often fatal Q.
  3. It is asymptomatic in 70% cases (AIPG 07)
  4. Sudden onset of breathlessness is the most common symptom.
  5. Pleuritic chest pain
  6. Hemoptysis Q; (LQ 2012)
  7. Dizziness,
  8. Syncope Q.

Signs: Pyrexia; cyanosis; tachypnoea Q; tachycardia; hypotension Q; raised JVP Q, pleural rub Q; pleural effusion Q. Paradoxical bradycardia can occur.(NQ) 


Extra Edge:
  1. “Dyspnea is the most frequent symptom of PE & tachypnea is the most frequent sign.’
  2. Chest pain is due to pulmonary infarction & usually indicated a small PE located distally near the pleura.
  3. Pulmonary embolism is the most common cause of Acute RVF (AIIMS May 2009)


CXR may be normal, or may show

  1. Focal oligemia of affected segment (Westermark sign Q)
  2. Dilated right descending pulmonary artery (Palla’s sign Q)
  3. Wedge-shaped opacities above the diaphragm (Hampton’s Hump Q)
  4. Small pleural effusion


  1. Sinus Tachycardia (Most Common)
  2. SI QIII TIII Pattern (Most characteristic)
    1. Deep S waves in lead I                    
    2. Q wave in Lead III      
    3. Inverted T wave in lead III 

Blood Test


The D-dimer assay is a very sensitive for pulmonary embolism with a sensitivity of greater than 95%.

Dimmer Assay in P.E (and DVT): 
(Ref. Hari. 18th ed., Pg- 2172)

  1. D-Dimer is a fibrin degradation product
  2. Elevation of D-Dimer thus indicates that a endogenous fibrinolytic process is taking place.
  3. Elevation indicates endogenous and often clinically ineffective thrombolysis D-Dimer assays are highly sensitive for presence of Thromboembolic Disease
  4. D-Dimer test is useful as a 'test for exclusion' or a 'rule out test' and is not a diagnostic test.
  5. D-dimers : only perform in those patients without a high probability of a PE. A negative D-dimer test excludes a PE in those with a low or intermediate clinical probability, and imaging is NOT required. However, a positive test does not prove a diagnosis of a PE, and imaging is required.

D-Dimer Assays

Highly sensitive for presence of

Thromboembolic Disease

1.   PE (Sensitivity>95%)
2.   DVT (Sensitivity>80%)
3.   DIC


Not specific for presence of

Thromboembolic Disease

Levels are also increased in

1. MI

2. Pneumonia

3. Sepsis

4. Cancer
5. Pregnancy
6. Heart failure
7. Postoperative state


CT pulmonary angiography (CTPA),

  1. Which can show clots down to 5th-order pulmonary arteries (after the 4th branching).
  2. This may also be useful for subjects with indeterminant on isotope scans.
  3. Now It is the best screening test (PNQ) (Ref. Hari. 18th ed., Pg- 2174)

Important Points:

  1. V/Q scan (look for perfusion defects with no corresponding ventilation defects). If 'normal', a PE is reliably excluded.
  2. Bilateral leg ultrasound (or rarely venograms) may also be sufficient to confirm, but not exclude, a PE in patients with a co-existing clinical DVT.
  3. Echo - Mc Connell. Sign: Hypokinesia of free RV wall with normal RV apex motion (Ref. Hari. 18th ed., pg -174) (LQ 2012)


  1. Anticoagulate with low molecular weight heparin eg dalteparin (AIIMS May 2014)
  2. Start oral warfarin.
  3. Placement of a vena caval filter Q in patients who develop emboli despite adequate anticoagulation

Fig: Acute management of pulmonary thromboembolism.


Decompression (Caisson) Disease.

  1. Encountered in deep-sea divers and underwa­ter workers.
  2. As the underwater depth and consequent atmospheric pressure increase, increasing amounts of oxygen and accompanying gases (nitrogen or helium) dissolve in the blood and tissue fluids.
  3. Once ascent begins (decompression), the dissolved gases come out of solu­tion and form minute bubbles in the bloodstream and tissues,
  4. Coalescence of these bubbles produces even larger masses capable of becoming significant emboli in the bloodstream.
  5. Peri­articular bubbles produce the bends. Bubbles formed within the lung or gaseous emboli give rise to respiratory difficulties, with severe substernal pain referred to as the chokes.
  6. CNS manifestations headache, visual disturbances behavioral disori­entation.
  7. Involvement of the inner ear may produce vertigo and the staggers.
  8. All these manifestations may appear within hours of the too rapid ascent, but skeletal manifestations caisson disease of bone-may sometimes appear days later.
  9. Foci of aseptic necrosis, typically of femoral and humeral heads, and medullary foci, particularly in the lower femur and upper tibia, attributed to embolic occlusion of the vascular supply.
  10. The rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints is responsible for the painful condition called the bends.
  11. Gas emboli may also induce focal ischemia in a number of tissues, including brain and heart (machinery murmur). In the lungs, edema, hemorrhages, and focal atelectasis or emphysema may appear, leading to respiratory distress, the so-called chokes.
  12. Treatment: placing the individual in a compression chamber where the baromet­ric pressure may be raised, thus forcing the gas bubbles back into solution.

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