Pulmonary embolism (PE) occurs when venous thrombi dislodge and block pulmonary arterial circulation, leading to various clinical syndromes. The incidence is about 69 cases per 100,000 annually, with multiple risk factors including advanced age, obesity, and certain medical conditions. Diagnosis involves a clinical likelihood assessment and imaging tests, while treatment typically includes anticoagulation and may require thrombolysis or embolectomy for high-risk patients.

1. Pulmonary Embolism
Dr.Makhoba

2. Definition
• A condition in which venous thrombi dislodge from their
site of formation and embolize to the pulmonary arterial
circulation
• Clinical syndromes
– Massive pulmonary thromboembolism (PE)
• Systemic arterial hypotension and anatomically widespread
thromboembolism
– Moderate to large PE
• Right ventricular (RV) hypokinesis, but normal systemic arterial
pressure
– Small to moderate PE
• Normal right-heart function and normal systemic arterial pressure

3. Epidemiology
• PE
• Incidence
• 69 cases per 100,000 persons annually
• Age
• More common with advancing age
• Sex
• More common in women than in men; ratio, 1.3:1
• Venous thromboembolism (VTE): encompasses deep venous
thrombosis (DVT) and PE
• VTE-related deaths in the U.S. are estimated at 300,000 annually.
• 7% diagnosed with VTE and treated
• 34% sudden fatal PE
• 59% as undetected PE

4. Epidemiology cont’d
• Symptomatic VTE events
• Approximately two-thirds are hospital acquired.
• One-third are community acquired.
• Residents of nursing facilities are especially vulnerable.
• Estimated hospitalized patients at risk for VTE in
the U.S.
• 13.4 million patients annually
• 5.8 million surgical patients at moderate–high risk
• 7.6 million medical patients with comorbidities such as heart
failure, cancer, and stroke

5. Risk Factors (for DVT)
 Virchow’s Triad:
 Alterations in blood flow (stasis):
 Injury to endothelium (endothelial injury):
 Thrombophilia (Hypercoagulability):

6.  Stasis: mainly caused by heart failure,
prolonged immobility
 Endothelial injury: mainly caused by either
direct trauma (severed vein) or local
irritation (by chemotherapy, past DVT,
phlebitis)
 Hypercoagulability: inherited (AT III def.,
protein C, S deficiency) or acquired
(malignancy, pregnancy, AT III def., protein
C, S deficiency as in nephrotic syndrome,
DIC and liver failure.

7. Risk Factors
• Acquired risk factors
• Long-haul air travel
• Obesity
• Cigarette smoking
• Oral contraceptive use
• Pregnancy
• Postmenopausal hormone replacement
• Surgery
• Trauma
• Antiphospholipid antibody syndrome
• Cancer
• Greater risk of fatal PE
• Systemic arterial hypertension
• Chronic obstructive pulmonary disease

8. Risk factors cont’d
• Genetic risk factors
• Factor V Leiden
• Prothrombin gene mutation
• Antithrombin III deficiency
• Protein C deficiency
• Protein S deficiency
• Homocysteinemia
• Family or personal history of VTE
• Iatrogenic (upper-extremity DVT)
• Long-term indwelling central venous catheters
• Permanent pacemakers
• Internal cardiac defibrillators

9. Risk factors cont’d
• Other risk factors
• Varicose veins
• Oral corticosteroids
• Inflammatory bowel disease
• PE (not DVT specific) risk factors
• Ischemic heart disease
• Heart failure
• Cerebrovascular disease
• Greater risk of fatal PE

10. Etiology
• Caused by dislodgement of venous thrombi traveling to
pulmonary arterial circulation
• About half of patients with pelvic vein thrombosis or proximal leg DVT
have PE.
• Isolated calf vein thrombi pose a lower risk of PE.
• Upper-extremity DVTs are becoming a more common problem with
increased use of:
• Long-term indwelling central venous catheters for hyperalimentation and
chemotherapy
• Frequent insertion of permanent pacemakers and internal cardiac defibrillators
• Thrombi occur due to:
• Blood vessel wall injury
• Blood stasis/venous stasis
• Hypercoagulability

11. Symptoms & Signs
• Dyspnea (most frequent symptom)
• Tachycardia (most frequent sign)
• Chest pain
• In massive PE, pain may resemble pain of myocardial infarction.
• Pleuritic pain in PE patients with pleural involvement
• Tachypnea
• Low-grade fever
• Neck vein distention
• Accentuated pulmonic component of the second heart sound
(P2)

12. • Massive PE is often indicated by:
• Dyspnea
• Syncope
• Hypotension
• Cyanosis
• Small PE located distally near the pleura is often indicated
by:
• Pleuritic pain
• Cough
• Hemoptysis
• Pulmonary infarction

13. • Young and previously healthy persons (even those with
an anatomically large PE):
• May appear anxious
• Have dyspnea on moderate exertion
• Lack classic signs
• In older patients experiencing vague chest discomfort:
• PE may not be apparent unless signs of right-heart failure are
present
• Edema
• Congestive hepatomegaly
• Systemic venous distention

14. Differential Diagnoses
• Acute coronary syndrome, including unstable angina and acute
myocardial infarction
• Pneumonia, bronchitis, exacerbation of asthma or chronic
obstructive pulmonary disease
• Congestive heart failure
• Pericarditis
• Pleurisy, including "viral syndrome"; costochondritis; other
musculoskeletal discomfort
• Rib fracture, pneumothorax
• Primary pulmonary hypertension
• Anxiety

15. Non thrombotic PE
• Fat embolism from:
• Blunt trauma
• Long-bone fracture
• Tumor embolism
• Bone marrow embolism
• Air embolism
• Amniotic fluid embolism
• Cement and bony fragment emboli can occur after total hip or knee
replacement.
• Embolism in intravenous drug users
• Hair
• Talc
• Cotton

16. Diagnostic Approach
• Diagnostic strategy for PE
• Initial task is to decide whether the clinical likelihood of PE is high (see below).
• Outpatient or emergency department setting
• Non-high-clinical likelihood: Check D-dimer level on enzyme-linked immunosorbent
assay (ELISA).
• Normal: Stop workup; negative quantitative D-dimer latex immunoassay result and a low pretest
probability of thromboembolism together are sufficient to exclude acute PE.
• Elevated: See "Imaging" for patients with high likelihood.
• Inpatient or high likelihood: Use imaging.
• Chest CT with contrast, if renal function is normal and no contrast allergy
• Lung scan, if renal insufficiency or renal contrast allergy
• Imaging non diagnostic: Check lower-extremity ultrasonography.
• Positive for DVT: Treat accordingly.
• Normal or non diagnostic: Check transesophageal echocardiography or MR or
pulmonary angiography.

17. Assessment of clinical likelihood (modified
Wells score)
• High clinical likelihood of PE if the point score
exceeds 4.
• Signs and symptoms of DVT: 3
• Alternative diagnosis less likely than PE: 3
• Heart rate >100/min: 1.5
• Immobilization >3 days; surgery within 4 weeks: 1.5
• Prior PE or DVT: 1.5
• Hemoptysis: 1
• Cancer: 1
• Non-high likelihood if score ≤ 4

18. Laboratory Tests
• Plasma D-dimer ELISA
• Elevated level (>500 ng/mL) in > 95% of patients with PE sensitive, but
nonspecific for PE
• Levels increase in patients with myocardial infarction, sepsis, or almost any
systemic illness.
• Therefore, test has no useful role for people who are already hospitalized.
• Can be used to help exclude PE: negative predictive value of up to 99.6%
• Cardiac biomarkers
• Serum troponin levels increase in RV microinfarction.
• Myocardial stretch often results in elevation of brain natriuretic peptide
(BNP) or NT-pro-brain natriuretic peptide.
• Elevated cardiac biomarkers predict an increase in major complications
and mortality from PE.

19. Imaging
• Chest radiography (CXR)
• Normal or near-normal result in a dyspneic
patient occurs in PE.
• Well-established abnormalities
• Focal oligemia (Westermark’s sign)
• Peripheral wedge-shaped density above the
diaphragm (Hampton’s hump)
• Enlarged right descending pulmonary artery
(Palla’s sign)

20. Westermark Sign
 represents a focus of oligemia (
vasoconstriction) seen distal to a
pulmonary embolism.While the
chest x-ray is normal in the
majority of PE cases, the
Westermark sign is seen in 2% of
patients.
 The sign results from a
combination of:
 The dilation of the pulmonary arteries
proximal to the embolus and
 the collapse of the distal vasculature
creating the appearance of a sharp cut
off on chest radiography.

21. Hampton Hump
Radiologic sign which
consists of a shallow
wedge-shaped opacity in
the periphery of the lung
with its base against the
pleural surface.

22. Venous ultrasonography
• Confirmed DVT is usually an adequate surrogate for
PE.
• Loss of vein compressibility is the primary criterion
for DVT.
• Half of patients with PE have no imaging evidence of
DVT, probably because the clot has already embolized
to the lung or is in the pelvic veins.
• Workup for PE should continue if there is high clinical
suspicion, despite a normal result on ultrasonography.

23. Chest CT
• CT with intravenous contrast
• Can effectively diagnose large, central PE
• Can detect peripherally located thrombi in
sixth-order branches
• In patients without PE, lung parenchymal
images may establish alternative diagnoses not
apparent on chest radiography.

24. Bilateral PE

25. Pulmonary angiography
• Selective pulmonary angiography is the most specific
examination available for definitively diagnosing PE.
• Detects emboli as small as 1–2 mm
• Definitive diagnosis of PE depends on visualization
of intraluminal filling defect in > 1 projection.
• Secondary signs of PE
• Abrupt occlusion ("cut-off") of vessels
• Segmental oligemia or avascularity
• Prolonged arterial phase with slow filling
• Tortuous, tapering peripheral vessels

26. PE on pulmonary angiogram

27. Lung scanning: V/Q
• Second-line diagnostic test for PE
• Mostly used for patients who cannot tolerate intravenous contrast
• Perfusion scan defect indicates absent or decreased blood flow,
possibly due to PE.
• Ventilation scans, obtained with radiolabeled-inhaled gases such as
xenon or krypton, improve the specificity of the perfusion scan.
• Abnormal ventilation scans indicate an abnormal nonventilated lung, providing possible
explanations for perfusion defects other than acute PE.
• High probability of PE is defined as ≥ 2 segmental perfusion defects in the presence of
normal ventilation.
• Diagnosis of PE is very unlikely in patients with normal and near-
normal scans but is ~90% certain in patients with high-probability
scans.
• Most patients have nondiagnostic scans, and fewer than half of patients with
angiographically confirmed PE have a high-probability scan.
• As many as 40% of patients with high clinical suspicion for PE and low-probability
scans have PE confirmed by angiography.

28. V/Q Scan
 Identifies mismatches between areas that are ventilated but not
perfused
 Best initial test in patients with clear CXR
 Scan can be interpreted as High, Intermediate, or Low
probability of PE, or normal
 Normal rules out PE
 High-probability scan is diagnostic of PE if the clinical suspicion is
also high
 Low-probability scan rules out PE only in a pt with low pretest clinical
probability (because PE is found in roughly 15% of pts with low-
probability scans)
 Intermediate-probability scan requires further evaluation (16-66%
chance of PE depending on pretest probability)

29. V/Q Scan

30. CARDIAC Echocardiography
• >50% of patients with PE have normal echocardiograms.
• Helps with rapid triage of extremely ill patients (can usually reliably
differentiate among illnesses that have radically different treatment)
– Acute myocardial infarction
– Pericardial tamponade
– Dissection of the aorta
– PE complicated by right-heart failure
• Transthoracic echocardiography
– Rarely images thrombus directly
– McConnell’s sign (best known indirect sign of PE on transthoracic echo)
• RV free-wall hypokinesis with normal RV apical motion, appears to be specific for PE.
• Transesophageal echocardiography
– Should be considered when CT scanning facilities are not available or when a
patient has renal failure or severe contrast allergy that precludes administration
of contrast despite premedication with high-dose corticosteroids
– Can directly visualize large proximal PE
• Detection of RV dysfunction due to PE helps to stratify risk, delineate
prognosis, and plan optimal management.

31. EKG Findings
Classic findings may include:
•Sinus tachycardia
•New onset Atrial fibrillation or flutter
•Rt axis deviation
•S1Q3T3 sign: S wave in lead I, a Q wave in lead III, and an inverted T wave in lead
III
•T-wave inversion in leads V1 to V4: reflects RV strain

32. Treatment
General guidelines
• Primary therapy
• Treatment options
• Clot dissolution with thrombolysis or
• Removal of PE by embolectomy
• Primary therapy is reserved for patients at high risk of an adverse clinical
outcome.
• Hemodynamic instability
• RV dysfunction
• Detection of RV hypokinesis on echocardiography is the most widely used approach to risk
stratification.
• Elevation of troponin level due to RV microinfarction
• Secondary prevention of recurrent PE
• Anticoagulation with heparin and warfarin
• Placement of an inferior vena caval (IVC) filter

33. Heparin
• Heparin prevents additional thrombus formation and permits
endogenous fibrinolytic mechanisms to lyse clot that has already
formed.
• After 5–7 days of heparin, residual thrombus begins to stabilize in the
endothelium of the vein or pulmonary artery.
• Does not directly dissolve thrombus that already exists.
• UFH (Unfractionated heparin)
• IV bolus, 5000–10,000 U, then continuous infusion of 1000–1500 U/h
• Activated partial thromboplastin time (aPTT) at least twice the control
value should provide a therapeutic level.
• Nomograms based on a patient’s weight may assist in adjusting the dose.
• Weight based: initial bolus of 80 U/kg, then initial infusion rate of 18 U/kg
hourly

34. LMWH(Low molecular weight heparin)
• Enoxaparin
• Preferred dose: 1 mg/kg SC twice daily
• Alternate dose: 1.5 mg/kg daily
• Tinzaparin 175 units/kg once daily with normal renal function
• Greater bioavailability, more predictable dose response, few
complications, and longer half-life than UFH
• No laboratory monitoring or dose adjustment is needed unless
the patient is markedly obese or has renal dysfunction.
• Overall 29% reduction in mortality and major bleeding rates
compared with UFH
• Weight-adjusted doses must be adjusted downward in renal
insufficiency because the kidneys excrete LMWH.

35. Complications of heparins
• Hemorrhage
• If life-threatening or intracranial hemorrhage, administer
protamine sulfate 1–1.5 mg IV per 100 U heparin
• Maximum, 50 mg/dose; rate, 5 mg/min
• Monitor aPTT
• Osteopenia
• Less frequent with LMWH
• Heparin-induced thrombocytopenia (HIT)
• Thrombosis due to heparin-induced thrombocytopenia
• Elevations in aminotransferase levels

36. Alternatives to Heparin
• Fondaparinux (Anti-Xa
pentasaccharide) .Given Subcutaneously
• Rivaroxaban, Apixaban; Oral direct Factor Xa
inhibitors.
• No laboratory monitoring is required
• Have no antidotes

37. Warfarin
• Full effect of warfarin often requires 5 days.
• Overlapping with heparin for 5 days counteracts early
procoagulant effect of unopposed warfarin.
• Dose
• Usual starting dose is 5–10 mg/d.
• Most common maintenance doses
• Average-sized adult: 5 mg/d
• Obese or large young patients who are otherwise healthy: 7.5 or 10 mg/d
• Malnourished patients or after prolonged courses of antibiotics: 2.5 mg/d
• Prothrombin time is standardized with the INR to assess
anticoagulant effect.
• Target INR is usually 2.5, with a range of 2.0–3.0.

38. Complications of Warfarin
• Hemorrhage
• Cryoprecipitate or fresh-frozen plasma (usually 2 U) to
achieve immediate hemostasis
• Recombinant factor VIIa for life-threatening bleeding in the
setting of excessive warfarin
• Vitamin K for less serious bleeding or an excessively high
INR
• Skin necrosis (rare)
• Alopecia
• Contraindications
• Pregnancy

39. Monitoring
• Heparin therapy
• An aPTT at least twice the control value should provide therapeutic level.
• Monitor platelet counts to possible complications of thrombocytopenia and development of
heparin-induced thrombocytopenia.
• Warfarin therapy
• Prothrombin time is standardized with the INR to assess anticoagulant effect.
• Target INR is usually 2.5, with a range of 2.0–3.0.
• INR is monitored daily after second or third dose until in therapeutic range for 2 consecutive
days.
• Then 2–3 times weekly for first 1–2 weeks
• Then weekly for first 4 weeks
• If stable, once every 4 weeks
• More frequent monitoring is required if dosage is adjusted.
• Chronic thromboembolic pulmonary hypertension
• Patients with PE should be followed to ensure that if they have initial pulmonary
hypertension, it abates over time (usually 6 weeks).
• All patients receiving anticoagulation therapy should be monitored for bleeding
complications.

40. Duration of treatment
• Provoked PE: 3–6 months of anticoagulation
• Idiopathic: indefinite

41. Complications
• Hypoxemia
• Right-heart failure
• Hypotension
• Lung hemorrhage
• Chronic thromboembolic
pulmonary hypertension

42. Prognosis
• Progressive RV failure is the usual cause of death from
PE.
• RV dysfunction on baseline echocardiography of patients with
PE who presented with a systolic blood pressure >90 mmHg
was associated with a doubling of the 3-month mortality rate.
• Combination of RV dysfunction plus elevated biomarkers
such as troponin portends an especially ominous
prognosis.
• Elevated cardiac biomarkers predict an increase in major
complications and mortality from PE.
• Successful thrombolytic therapy rapidly reverses RV
failure and leads to a lower rate of death and recurrent PE.

43. Prevention
• Mechanical and pharmacologic measures often
succeed in preventing PE.
• Minidose UFH: 5000 U SC tid
• LMWH
• Enoxaparin: 40 mg SC qd
• Dalteparin: 2500 or 5000 U SC qd
• Graduated compression stockings (GCS): 10–18
mmHg
• Intermittent pneumatic compression devices (IPC)