1. Dr. M. A. Sofi MD; FRCP; FRCPEdin; FRCSEdin
PULMONARY EMBOLISM
Dr. M. A. Sofi MD; FRCP; FRCPEdin; FRCSEdin

2. Pulmonary Embolism
PE is the most common preventable cause of death in hospitalized patients
600,000 deaths/year
80% of pulmonary emboli occur without prior warning signs or symptoms
2/3 of deaths due to pulmonary emboli occur within 30 minutes of embolization
Death due to massive PE is often immediate
Diagnosis can be difficult
Early treatment is highly effective

3. Natural History of VTE
40-50% of pts with DVT develop PE, often “silent”
PE presents 3-7 days after DVT
Fatal within 1 hour after onset of respiratory symptoms in 10%
Shock/persistent hypotension in 5-10% (up to 50% of patients with RV dysfunction)
Most fatalities occur in untreated pts
Perfusion defects completely resolve in 75% of all patients (who survive)

5. RISK FACTORS Acquired Risk factors (III) Inherited Risk Factors (2)
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Protein C resistance (Factor V Leiden)
Hyperhomocystinemia
Abnormal fibrinogen
Abnormal fibrinolytic system
Inherited Risk Factors
Family History (+)
Acquired risk factor (+)
Prior deep venous thrombosis
Acquired Risk factors (III)
Prior DVT
Nephrotic Syndrome
Antiphospholipid Syndrome
PNH
Waldenström Macroglobinemia

6. Risk Factors: Major risk factors: relative risk of 5-20 Surgery:
Major abdominal/pelvic surgery or hip/knee replacement (risk lower if prophylaxis used).
Postoperative intensive care.
Obstetrics:
Late pregnancy.
Puerperium.
Caesarean section
Lower limb problems:
Fracture.
Varicose veins - previous varicose vein surgery; superficial thrombophlebitis; varicose veins per se are not a risk factor
Minor risk factors: relative risk of 2-4
Cardiovascular:
Congenital heart disease.
Congestive cardiac failure.
Hypertension.
Paralytic stroke.
Oestrogens:
Pregnancy (but see major risk factors for late pregnancy and puerperium).
Combined oral contraceptive.
Hormone replacement therapy.
Renal:
Nephrotic syndrome.
Chronic dialysis.
Paroxysmal nocturnal haemoglobinuria

7. Risk Factors: Major risk factors: relative risk of Malignancy:
Abdominal/pelvic.
Advanced/metastatic.
Reduced mobility:
Hospitalization.
Institutional care.
Previous proven VTE:
Intravenous (IV) drug use (could be major or minor risk factor: no data on relative risk).
Other:
Major trauma.
Spinal cord injury.
Central venous lines.
Minor risk factors: relative risk of
Hematological:
Thrombotic disorders Consider this in cases of PE aged <40 years, recurrent VTE or a positive family history.
Myeloproliferative disorders
Miscellaneous:
Chronic obstructive pulmonary disease (COPD).
Neurological disability.
Occult malignancy.
Long-distance sedentary travel.
Obesity.
Other chronic diseases: inflammatory bowel disease, Behçet's disease.

8. Presentation:
The classic presentation of PE is the abrupt onset of pleuritic chest pain.
Shortness of breath.
Hypoxia.
Most patients with PE have no obvious symptoms at presentation.
Symptoms may vary from sudden catastrophic hemodynamic collapse to gradually progressive dyspnea.
The diagnosis of pulmonary embolism should be suspected in patients with respiratory symptoms unexplained by an alternative diagnosis
Patients with PE may present with atypical symptoms, such as the following:
Seizures
Syncope
Abdominal pain
Fever
Productive cough
Wheezing
Decreasing level of consciousness
New onset of atrial fibrillation
Hemoptysis
Flank pain
Delirium (in elderly patients)

9. Presentation:
Evidence-based literature supports the practice of using clinical scoring systems to determine the clinical probability of pulmonary embolism before proceeding with testing.
Validated clinical prediction rules should be used to estimate pretest probability of pulmonary embolism and to interpret test results
Physical signs of pulmonary embolism include the following:
Tachypnea (respiratory rate >16/min): 96%
Rales: 58%
Accentuated second heart sound: 53%
Tachycardia (heart rate >100/min): 44%
Fever (temperature >37.8°C): 43%
Diaphoresis: 36%
S3 or S4 gallop: 34%
Clinical signs and symptoms suggesting thrombophlebitis: 32%
Lower extremity edema: 24%
Cardiac murmur: 23%
Cyanosis: 19%

10. Testing:
Perform diagnostic testing on symptomatic patients with suspected Pet o confirm or exclude the diagnosis or until an alternative diagnosis is found.
Routine laboratory findings are nonspecific and are not helpful in pulmonary embolism.
A hypercoagulation workup should be performed if no obvious cause for embolic disease is apparent, including screening for conditions such as the following:
Antithrombin III deficiency
Protein C or
Protein S deficiency
Lupus anticoagulant
Homocystinuria
Occult neoplasm
Connective tissue disorders
Potentially useful laboratory tests in patients with suspected pulmonary embolism include the following:
D-dimer testing
Ischemia-modified albumin level
White blood cell count
Arterial blood gases:
Serum troponin levels
Brain natriuretic peptide

11. Imaging:
Imaging studies that aid in the diagnosis of pulmonary embolism include the following:
Computed tomography angiography (CTA): Multidetector- row CTA (MDCTA) is the criterion standard for diagnosing pulmonary embolism
Pulmonary angiography: Criterion standard for diagnosing pulmonary embolism when MDCTA is not available
Chest radiography: Abnormal in most cases of pulmonary embolism, but nonspecific
V/Q scanning: When CT scanning is not available or is contraindicated
ECG: Most common abnormalities are tachycardia and nonspecific ST- T wave abnormalities
MRI: Using standard or gated spin- echo techniques, pulmonary emboli demonstrate increased signal intensity within the pulmonary artery
Echocardiography: Transesophageal echocardiography may identify central pulmonary embolism
Venography: Criterion standard for diagnosing DVT
Duplex ultrasonography: Noninvasive diagnosis of pulmonary embolism by demonstrating the presence of a DVT at any site

12. Chest Radiography (II) Laboratory Tests
Atelectasis
Elevation of the hemidiaphragm
Pleural efusion
Dilatation of the main branches of PA
Paranchymal densities (in the lower lung fields, pleural based)
Zones of oligemia
Laboratory Tests
Chest Radiography
Usually nonspesific
Not sensitive or specific
Proximal, large segmental artery
Multiple small segmental artery

13. S1 Q3 T3 and T WAVE CHANGES

14. An immediate computed tomography pulmonary angiogram (CTPA) or
Assessment
NB: treatment may precede investigations if the patient is very ill
If PE is suspected, use the two-level PE Wells' score to estimate the clinical probability of PE
Offer patients in whom PE is suspected and with a likely two-level PE Wells' score either
An immediate computed tomography pulmonary angiogram (CTPA) or
Immediate interim parenteral anticoagulant therapy followed by a CTPA,
If a CTPA cannot be carried out immediately.
Consider a proximal leg vein ultrasound scan if the CTPA is negative and DVT is suspected.

15. D-dimer test if the result is positive:
Assessment
NB: treatment may precede investigations if the patient is very ill
D-dimer test if the result is positive:
Immediate CTPA or immediate interim parenteral anticoagulant therapy followed by a CTPA, if a CTPA cannot be carried out immediately.
For patients who have an allergy to contrast media, or who have renal impairment, or whose risk from irradiation is high:
Assess the suitability of a ventilation/perfusion single- photon emission computed tomography (V/Q SPECT)
If offering a V/Q SPECT or planar scan that will not be available immediately, offer immediate interim parenteral anticoagulant therapy.

16. Wells' Two-level PE Score
Clinical feature Point
Clinically suspected DVT (minimum leg swelling and pain on palpation of deep veins).
3.0
Alternative diagnosis less likely than PE.
Tachycardia (heart rate above 100 beats per minute).
1.5
Immobilization for more than three days or surgery in the previous four weeks
History of DVT or PE.
Haemoptysis.
1.0
Malignancy (on treatment in the preceding six months or palliative stage).
Clinical probability
4 points or less = PE unlikely.
More than 4 points = PE likely.

17. Echocardiography Laboratory Tests
Shows emboli in main pulmonary arteries, but not in lober and segmentaL arteries
Dilated hypokinetic RV
Distorsion of the interventricular septum in diastole
Tricuspid regurgitation associated with increase in systolic pressure in pulmonary artery
Laboratory Tests
Arterial Blood Gases
Acute
PaCO2 decreases
Massive
PaO2 decreases
Submassive
Normal / Near normal

18. Ventilation-Perfusion Lung Scan
It remains the first line investigation of possible PE. It should be performed in all clinically stable patients.
A Ventilation Perfusion scan is most useful when the result category is one of normal , low or high probability.
Perfusion (-) and Ventilation (+) PE
Perfusion (N) and Clinical sym and signs (N) PE excluded
Low probability PVLS and low probability of
clinical sym and signs PE excluded
High probability PVLS and high probability of
clinical symp and signs Anticoagulation

19. Deep Vein Thrombosis

20. PERFUSION/VENTILATION LUNG SCAN

21. PERFUSION/VENTILATION LUNG SCAN

22. This algorithm allowed for a management decision in 98% of patients presenting with symptoms suggestive of PE

23. Management: Anticoagulation medications include the following:
Unfractionated heparin
Low-molecular-weight heparin
Factor Xa Inhibitors
Fondaparinux
Warfarin
Thrombolytic agents used in managing pulmonary embolism include the following:
Alteplase
Reteplase
Urokinase
Streptokinase
Surgical options
Surgical management options include the following:
Catheter embolectomy and fragmentation or surgical embolectomy
Placement of vena cava filters

24. Management: Anticoagulation and thrombolysis
Immediate full anticoagulation is mandatory for all patients suspected of having DVT or pulmonary embolism.
Diagnostic investigations should not delay empirical anticoagulant therapy.
Thrombolytic therapy should be used in patients with acute pulmonary embolism who have hypotension (systolic blood pressure< 90 mm Hg)
who do not have a high bleeding risk.
In selected patients with acute pulmonary embolism not associated with hypotension who have a low bleeding risk and whose initial clinical presentation or clinical course suggests a high risk of developing hypotension.

25. Spiral CT Direct visualization of emboli.
Both parenchymal and mediastinal structures can be evaluated.
Offers differential diagnosis in 2/3 of cases with a negative scan.
BUT…
Dye load and large radiation dose
Optimally used when incorporated into a validated
diagnostic decision tree

26. Clinical Probability of acute PE
High Probability (80-100%)
Risk factors (+) Dyspnea
Tachypnea Chest pain
Radiology (+) PaO2 decreases
P (A-a)O2 increases
Intermediate Probability (20-79%)
Low Probability (1-19%)
Risk Factors (-)
Clinical and laboratory findings can be explained
Treatment
To prevent death
To reduce morbidity
To prevent pulmonary hypertension
Progresing due to thromboemboli

27. TREATMENT Prognosis Mortality rate – 30%
Depends on associated pathology
Resolution – 5 days %
2 weeks 52%
3 months 73%
Pulmonary hypertension
recurrent microemboli (rare)
Anticoagulation
Unfractioned heparin
LMWH
Thrombolysis
Embolectomy

28. TREATMENT long acting less binding to plasma protein
Unfractioned Heparin IV 5000 U bolus U/kg aPTT- twice the control value Thrombocytopenia Early: thrombocyte aggregation slight, reveresible, no need to stop Late: antibodies against thrombocytes arterial and venous thromboemboli Osteopenia
LMWH
long acting
less binding to plasma protein
greater bioavailibity
no need monitoring

29. TREATMENT Thrombolysis
Massive pulmonery emboli with hemodynamic instability
Streptokinase
Urokinase
t-PA
**serious bleeding
Secondary prevention
UFH + oral anticoagulan (6 months)
LMWH SC + oral anticoagulan (6 months )
LMWH (pregnancy)
Recurrance / unknown origin / permanantly increased risk (throughout life)

30. Catheter Embolectomy & Fragmentation
An alternative in high-risk PE patients when thrombolysis is absolutely contraindicated or has failed