Pulmonary embolism is a blockage in the pulmonary arteries usually caused by blood clots. It can be diagnosed based on risk factors, symptoms, and tests like a D-dimer blood test, CT scan, or lung scan. Treatment depends on severity but generally involves blood thinners like heparin or warfarin to prevent further clots. For severe cases, thrombolysis can dissolve clots while a vena cava filter may be placed for recurrent clots or if blood thinners are contraindicated.

1. DR.Bilal Natiq Nuaman, MD
C.A.B.M.,F.I.B.M.S.,D.I.M.
2018-2019 1

2. Definition
● Sudden occlusion of the pulmonary arterial vasculature,
which results in obstruction of the blood flow to the lung
parenchyma .
● Commonly blood clot 80% (thrombotic)
● Fat embolism
● Air embolism
● Amniotic fluid embolism
● Foreign body embolism (eg, talc in injection drug use)
● Parasite egg embolism (schistosomiasis)
● Septic emboli (from right sided endocarditis)
● Tumor emboli (choriocarcinoma and renal cell
carcinoma)
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3. Epidemiology
●PE is the third most common cause of death
Etiology
● Pulmonary embolism is most commonly due to a
thrombus (blood clot) originating from Deep Veins
of the lower extremities and pelvis.
● pelvis (10-15%
● leg (70-80%
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4. Pathophysiology
● Thrombus-blood clot along the wall of a normal or
slightly damaged blood vessel
● Virchow s triad gives the 3 primary influences of a
thrombus formation
● Endothelial Injury
● Stasis or turbulent flow
● Blood hypercoagulability
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6. Criteria of diagnosis
● Presence of risk factors for PE.
● Clinical presentation consistent with PE.
● Exclusion of alternative diagnoses .
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7. ● Most important clinically identifiable risk factors for
DVT and PE:
●Prior history of DVT or PE
●Recent surgery or pregnancy
●Prolonged immobilization
●Underlying malignancy.
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8. Classic Triad of pulmonary embolism
Sudden onset of unexplained dyspnea is the most
common, and often the only symptom of pulmonary
embolism. Pleuritic chest pain and Hemoptysis are
present only when infarction has occurred.
1. Dyspnea,
2.Hemoptysis
3.Pleuritic chest pain
In reality the triad occurs in
<20% of patients
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9. Classification
● Based on clinical presentation and investigations
● Treatment of Pulmonary Embolism (PE) are best
understood when classified
● Acute Massive PE
● Acute Small/Medium PE
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20. D-dimer
● Dimerized plasmin fragment D
● Fibrin degradation product
● A negative D-dimer test excludes PE if there is low
or intermediate pretest probability.
● but not specific indicator of thromboembolic
disorders
● Raised in inflammatory conditions e.g. Pneumonia
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21. Arterial Blood Gas
● Hypoxemia occurs in about 90% of patients with
PE
● The degree of hypoxemia doesn’t accurately
predict the size of the PE
●PaO2 of <90 mmHg not explained by
CXR findings strongly suggest PE
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22. Chest X-Ray
● Use to Rule out other causes
● Initial CXR normal in 1/3rd
of patients
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24. Electrocardiograph
● The most common ECG abnormalities are:
● Sinus tachycardia
● Right axis deviation
● Nonspecific ST segment abnormalities (40% of pts)
● RBBB
● These findings are not sensitive or specific enough
to aid in the diagnosis of PE
●S1Q3T3pattern is observed in only 20% of patients
● ECG pattern is normal in 1/3rd
of patients
● Exclude: Myocardial Infarction and Pericarditis
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25. Spiral CT
● Contrast material infused
● Spiral chest CT scans are excellent for detecting
pulmonary emboli in the central pulmonary arteries
● Does not detect emboli in beyond segmental vessels
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26. CT Scan
Fig 1. Spiral CT of patient showing large thrombus
(arrowed) within the left pulmonary artery
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27. Doppler Ultra sound
● Detection of thrombosis in femoral & popliteal veins
vessels
● Primarily or secondarily involved in the majority of
patients with PE
● Doppler Ultra sound has a sensitivity and specificity of
95 – 100 %
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28. Ventilation/Perfusion Scan
● It is based on identifying areas of ventilation without
perfusion (mismatched defects)
● Technetium isotope is given IV to detect areas of non-
perfusion
● Labeled xenon is inhaled to demonstrate non-aerated
lung
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29. Pulmonary Arteriography
● “Gold Standard”
● Called upon when clinical suspicion of PE is high
and other studies are inconclusive.
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32. Management
● General Measures
●ABC’s
●O2 in all PE (if hypoxemia restore to >90%)
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35. Medical
● Initiate Heparin
● Obtain baseline coagulation studies then administer
IV heparin as a bolus (5000U or 80U/kg) then as a
constant infusion (1280U/h or 18U/kg/hr
● Goal is to maintain PTT between 1.5—2.5 times the
control value (60--80sec)
● Initiate Warfarin
● Once therapeutic dose of heparin achieved, oral
warfarin is began at 5--20mg/day and the PT is
checked daily
● Dose adjusted until PT measurements show a stable
INR (between 2-3)
● Heparin and warfarin therapy should overlap for
about 5 days
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40. Medical
● Heparin should be stopped when the INR>2
● Warfarin therapy should be continued
● Minimum of 6 weeks for pts with identifiable and
reversible risk factor
● At least 3 months for pts with no identifiable risk
factor
● life for Pts with prothrombotic risk
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44. Thrombolytic therapy
Indication- Massive PE
● The preferred fibrinolytic regimen is 100 mg of
recombinant tissue plasminogen activator (tPA)
administered as a continuous peripheral
intravenous infusion over 2 hrs.
● The sooner thrombolysis is administered, the
more effective it is.
● However, this approach can be used for at least 14
days after the PE has occurred.
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45. Surgical
● Vena caval filter
● Percutaneous thrombectomy
● Pulmonary embolectomy
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46. Caval filter
● Filter inserted in IVC below
origin of renal vessels
● Indications
● Pts with recurrent PE
despite adequate
anticoagulation
(prophylacticaly)
● Pts for whom
anticoagulation is
contraindications (eg.
immediately after surgery)
● Patients with massive PE
who survived but in whom
recurrent embolism will be
invariably fatal 46

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