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1. Venous Thromboembolism (VTE).

2. • Deep venous thrombosis and pulmonary
embolism (PE) can be considered as venous
thromboembolism (VTE).
• Exogenous or endogenous material that
travels to the lungs through the pulmonary
circulation,
• Causes a potential spectrum of consequences.

3. • The majority (75%) of pulmonary emboli arise
from the propagation of lower limb DVT.
• Amniotic fluid, placenta, air, fat, tumour
(especially choriocarcinoma), and
• septic emboli (from endocarditis ) are rare.

4. • PE occurs in around 1% of all patients
admitted to hospital
• Accounts for around 5% of in-hospital deaths.
• Common mode of death in patients with
cancer and stroke
• Common cause of death in pregnancy.

5. RISK FACTORS FOR VENOUS
THROMBOEMBOLISM
Surgery
• Major abdominal/pelvic surgery
• Hip/knee surgery
• Post-operative intensive care
Obstetrics
• Pregnancy/puerperium

6. Cardiorespiratory disease
• COPD
• Congestive cardiac failure
• Other disabling disease
Lower limb problems
• Fracture
• Varicose veins
• Stroke/spinal cord injury

7. • Malignant disease
• Miscellaneous
• Increasing age
• Previous proven VTE
• Immobility
• Thrombotic disorders
• Trauma

8. Pathophysiology
• The obstruction of blood flow creates alveolar
dead space
• High ventilation perfusion ratios as well as
shunting due to perfusion of atelectatic areas.
• This imbalance appears to be the principal
explanation for hypoxemia in acute PE.

9. Clinical Manifestations
• The history and physical examination are
insensitive and nonspecific for both DVT and
PE
Lower extremity venous thrombosis
• Erythema, warmth, pain, swelling, or
tenderness
• Homans' sign : pain with dorsiflexion of the
foot

10. CATEGORIES OF PULMONARY
THROMBOEMBOLI
• Acute small/medium PE
• Occlusion of segmental pulmonary artery →
infarction ± effusion
• Pleuritic chest pain, dyspnea, haemoptysis
• Tachycardia ,pleural rub, crackles, effusion
(often blood-stained)
• Low-grade fever

11. • Chest X-ray

13. Chronic PE
• Chronic occlusion of pulmonary
microvasculature, right heart failure
• Exertional dyspnoea, late symptoms of
pulmonary hypertension or right heart failure
• RV heave, loud, split P2
terminal-right heart failure
• Chest X –ray. Enlarged pulmonary artery
trunk, enlarged heart, prominent RV

14. Acute massive PE
• Major haemodynamic effects: ↓ cardiac
output; acute right heart failure
• Faintness or collapse, central chest pain,
apprehension, severe dyspnoea
• Major circulatory collapse: tachycardia,
hypotension, ↑ JVP, right ventricular gallop
rhythm, split P2 Severe cyanosis ↓ Urinary
output

15. • Usually normal, may be subtle oligaemia

16. Approch
• Is the clinical presentation consistent with PE?
• Does the patient have risk factors for PE?
• Is there any alternative diagnosis that can
explain the patient's presentation?

17. Investigations
• Chest radiography : non specific
• Important to exclude other differential
diagnosis

19. Electrocardiography
• ECG changes in PE are common but are
usually non-specific
• Useful to rule out other possible causes
D-dimer is a specific degradation product
released when fibrin undergoes endogenous
fibrinolysis
• Has a high negative predictive value and
provides a useful screening test

20. Management
• Prompt recognition and treatment is
potentially life-saving
• Supportive measures (oxygen)
Anticoagulation
• Low molecular weight heparin until INR 2-3
(five days)
• Warfarin started together with heparin
Caval filters

21. Duration of treatment
• Underlying prothrombotic risk or a history of
previous emboli
• Identifiable and reversible risk factor require
• Idiopathic VTE