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Pulmonary
Thromboembolism
Pulmonary Thromboembolism
• Migration of a clot (or clots) from systemic veins
(venous thrombosis) to the pulmonary vascular bed
• Incidence: Approx. 500,000/year in USA (about 10% of
5 million venous thrombosis episodes)
Approx. 10% (i.e. 50,000) are fatal
Characteristics of P.E.
Source: Deep veins of legs
Pelvic veins (women)
Upper extremity
Type: Bland
Septic
Nature: Blood, Air
Others: Tissue, fibres, liquid droplets, fat, amniotic fluid,
parasites
Venous Thrombosis
Virchow’s Triad
• Stasis
• Hypercoagulability
• Vessel wall injury
Deposition of
platelets, fibrin and
red cells on venous
valves/ sinuses
Thromboembolic Risk Factors
A. Hereditary Thrombophilias
- Protein C deficiency
- Protein S deficiency
- Antithrombin III deficiency
- Factor V Leiden mutation
- Prothrombin 20210 G/A variation
- Hyperhomocysteinaemia
- Dysfibrinogenaemia
- Familial plasminogen deficiency
B. Acquired Predispositions
Medical
• Prior VTE
• Advanced age
• Malignancy
• CHF, CCR
• Stroke, Neph. syn
• Oestrogen therapy
• Obesity, IBD
• Immobilization
• APLA syndrome
• Lupus anticoagulant
• Behcet’s syndrome
Surgical
• Major abdominal or N.S.
procedures under GA for >30
minutes
• Hip, knee arthroplasty
• Knee arthroscopy
• Hip fracture
• Major trauma
• Spinal cord injury
• Open prostatectomy
• Pregnancy and post partum period
Air Embolism
Accidental introduction during
• I.V. injections
• Haemodialysis
• C.V.P. lines
• Artificial pneumothorax or
pneumomediastinum
Factors influencing effects
1. Emboli related:
• Size of vessel
• Nature of emboli
• Extent of pulm vasc bed occlusion
2. Patient related: Preexisting cardiopulm status
3. Secondary effects:
• Hypoxaemia
• Release of neuro humoral mediators
• Reflex stimulation
Physiological Effects
1. Respiratory
• Increased dead space
• Hyperventilation
• Bronchiolar narrowing
2. Circulatory
• Systemic hypotension
• Pulmonary hypertension
• Pulmonary infarction
3. V/Q imbalances
• Venous admixture
Diagnosis of DVT
1. Clinical features
2. Contrast venography
3. Impedance plethysmography
4. Real time ultrasonography
5. M.R. venography
6. Radio labeled antibody imaging
Diagnosis of PTE
1. Clinical S & S
2. Lab. data : TLC, S. enzymes, D-dimer
3. ECG, Echocardiography
4. Art. blood gases: Dead space & A-a DO2
5. Chest radiography
6. V/Q scanning (Nuclear)
7. CT, spiral CT, MRI, Angiography (conventional angiography)
Signs and Symptoms (P.E.)
Massive
(%)
Submassive
(%)
No
cardiac/pulm
disease (%)
Dyspnoea 85 82 73
Chest pain 64 85 66
Cough 53 52 37
Haemoptysis 23 40 13
Tachypnoea 95 87 70
Tachycardia
(>100/min) 48 38 30
Loud P2 58 45 23
Rales 57 60 51
Phlebitis 36 26 11
Electrocardiography
• Sinus tachycardia
• T wave inversion in leads V1-4
• S1Q3T3 pattern
• New RBBB
• New onset atrial flutter
Radiological signs of PE
Common
•Atelectasis
•Raised hemidiaphragm
•Focal infiltrate
•Small pleural effusion
Rare
•Focal oligemia (Westermark’s sign)
CT Angiography
D-Dimer Assay
• Follows fibrinolysis of clot – may rise within 1 hour of
PTE, circulating half life about 4-6 hours
• Method: ELISA (takes 2-4 hours)
Rapid methods – Need standardization
Radionucleide Scanning
• Simple and safe, if available
• Technetium99m labelled microspheres (3-4 mCi of Tc99m)
• Intravenous injection – supine position
• Counting on gamma camera
• Different projections
• Matching with freshly obtained CXR; ventilation scanning
(if mismatched)
Ventilation – Perfusion Scan
1. More useful if read along with clinical probability of
PTE
2. High probability scan highly predictive of PTE
3. Normal or near normal scan virtually rules out PTE
4. Low, indeterminate or intermediate probability scans
(30% have PTE) need further tests
Management
A. Prophylaxis
B. Anticoagulation
• Heparin, Warfarin, LMWH
• Others: Hirudins, Synthetic thrombin inhibitors
A. Thrombolysis
B. Interventional radiological techniques: Clot lysis,
disruption, removal
C. Surgical methods
Thrombolytic agents
•Streptokinase
•Urokinase
•Recombinant tissue plasminogen activator (rtPA)
Thrombolytic therapy -Contraindications
Absolute: - Hemorrhagic stroke or stroke at anytime
- Ischemic stroke in preceding six months
- Central nervous system damage or neoplasm
- Recent major trauma/surgery/head injury
- Gastrointestinal bleeding within the last month; Known active bleeding
Relative: - Transient ischemic attack in preceding six months
- Oral anticoagulant therapy
- Pregnancy or within one week postpartum
- Traumatic resuscitation
- Refractory hypertension (systolic blood pressure > 180 mmHg)
-Advanced liver disease, Active peptic ulcer
- Infective endocarditis
Anti-coagulation
• Heparin: Low mol wt heparin. Reduces progression of clot
and risk of further embolization. Subcutaneous administration
Given for 5 days.
• Oral agents: Warfarin
Fondapernux
Other agents
Monitor INR
Recommendations for duration of anti-coagulation
Thromboembolism Duration
PE secondary to a transient (reversible) risk factor 3 months
Unprovoked PE At least 3 months
First episode of unprovoked PE and low risk of bleeding, and
in whom stable
Anticoagulation can be achieved
May be considered for long term anti-coagulation
Second episode of unprovoked PE Long term anti-coagulation
PE and cancer LMWH should be considered for the first 3 to 6 months.
After this period, anti-coagulant therapy with VKA or LMWH should
be continued indefinitely or until the cancer is cured.
Prevention of VTE
• Risk identification
• Low dose unfractionated heparin
(5000 U, 8 or 12 hrs)
• Low molecular weight heparin
• Pneumatic compressive devices
• Sodium warfarin
THANK YOU

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Pulmonary Thromboembolism | Jindal Chest Clinic

  • 2. Pulmonary Thromboembolism • Migration of a clot (or clots) from systemic veins (venous thrombosis) to the pulmonary vascular bed • Incidence: Approx. 500,000/year in USA (about 10% of 5 million venous thrombosis episodes) Approx. 10% (i.e. 50,000) are fatal
  • 3. Characteristics of P.E. Source: Deep veins of legs Pelvic veins (women) Upper extremity Type: Bland Septic Nature: Blood, Air Others: Tissue, fibres, liquid droplets, fat, amniotic fluid, parasites
  • 4. Venous Thrombosis Virchow’s Triad • Stasis • Hypercoagulability • Vessel wall injury Deposition of platelets, fibrin and red cells on venous valves/ sinuses
  • 5.
  • 6. Thromboembolic Risk Factors A. Hereditary Thrombophilias - Protein C deficiency - Protein S deficiency - Antithrombin III deficiency - Factor V Leiden mutation - Prothrombin 20210 G/A variation - Hyperhomocysteinaemia - Dysfibrinogenaemia - Familial plasminogen deficiency
  • 7. B. Acquired Predispositions Medical • Prior VTE • Advanced age • Malignancy • CHF, CCR • Stroke, Neph. syn • Oestrogen therapy • Obesity, IBD • Immobilization • APLA syndrome • Lupus anticoagulant • Behcet’s syndrome Surgical • Major abdominal or N.S. procedures under GA for >30 minutes • Hip, knee arthroplasty • Knee arthroscopy • Hip fracture • Major trauma • Spinal cord injury • Open prostatectomy • Pregnancy and post partum period
  • 8. Air Embolism Accidental introduction during • I.V. injections • Haemodialysis • C.V.P. lines • Artificial pneumothorax or pneumomediastinum
  • 9. Factors influencing effects 1. Emboli related: • Size of vessel • Nature of emboli • Extent of pulm vasc bed occlusion 2. Patient related: Preexisting cardiopulm status 3. Secondary effects: • Hypoxaemia • Release of neuro humoral mediators • Reflex stimulation
  • 10. Physiological Effects 1. Respiratory • Increased dead space • Hyperventilation • Bronchiolar narrowing 2. Circulatory • Systemic hypotension • Pulmonary hypertension • Pulmonary infarction 3. V/Q imbalances • Venous admixture
  • 11. Diagnosis of DVT 1. Clinical features 2. Contrast venography 3. Impedance plethysmography 4. Real time ultrasonography 5. M.R. venography 6. Radio labeled antibody imaging
  • 12. Diagnosis of PTE 1. Clinical S & S 2. Lab. data : TLC, S. enzymes, D-dimer 3. ECG, Echocardiography 4. Art. blood gases: Dead space & A-a DO2 5. Chest radiography 6. V/Q scanning (Nuclear) 7. CT, spiral CT, MRI, Angiography (conventional angiography)
  • 13. Signs and Symptoms (P.E.) Massive (%) Submassive (%) No cardiac/pulm disease (%) Dyspnoea 85 82 73 Chest pain 64 85 66 Cough 53 52 37 Haemoptysis 23 40 13 Tachypnoea 95 87 70 Tachycardia (>100/min) 48 38 30 Loud P2 58 45 23 Rales 57 60 51 Phlebitis 36 26 11
  • 14. Electrocardiography • Sinus tachycardia • T wave inversion in leads V1-4 • S1Q3T3 pattern • New RBBB • New onset atrial flutter
  • 15. Radiological signs of PE Common •Atelectasis •Raised hemidiaphragm •Focal infiltrate •Small pleural effusion Rare •Focal oligemia (Westermark’s sign)
  • 17.
  • 18.
  • 19.
  • 20. D-Dimer Assay • Follows fibrinolysis of clot – may rise within 1 hour of PTE, circulating half life about 4-6 hours • Method: ELISA (takes 2-4 hours) Rapid methods – Need standardization
  • 21. Radionucleide Scanning • Simple and safe, if available • Technetium99m labelled microspheres (3-4 mCi of Tc99m) • Intravenous injection – supine position • Counting on gamma camera • Different projections • Matching with freshly obtained CXR; ventilation scanning (if mismatched)
  • 22. Ventilation – Perfusion Scan 1. More useful if read along with clinical probability of PTE 2. High probability scan highly predictive of PTE 3. Normal or near normal scan virtually rules out PTE 4. Low, indeterminate or intermediate probability scans (30% have PTE) need further tests
  • 23. Management A. Prophylaxis B. Anticoagulation • Heparin, Warfarin, LMWH • Others: Hirudins, Synthetic thrombin inhibitors A. Thrombolysis B. Interventional radiological techniques: Clot lysis, disruption, removal C. Surgical methods
  • 25. Thrombolytic therapy -Contraindications Absolute: - Hemorrhagic stroke or stroke at anytime - Ischemic stroke in preceding six months - Central nervous system damage or neoplasm - Recent major trauma/surgery/head injury - Gastrointestinal bleeding within the last month; Known active bleeding Relative: - Transient ischemic attack in preceding six months - Oral anticoagulant therapy - Pregnancy or within one week postpartum - Traumatic resuscitation - Refractory hypertension (systolic blood pressure > 180 mmHg) -Advanced liver disease, Active peptic ulcer - Infective endocarditis
  • 26. Anti-coagulation • Heparin: Low mol wt heparin. Reduces progression of clot and risk of further embolization. Subcutaneous administration Given for 5 days. • Oral agents: Warfarin Fondapernux Other agents Monitor INR
  • 27. Recommendations for duration of anti-coagulation Thromboembolism Duration PE secondary to a transient (reversible) risk factor 3 months Unprovoked PE At least 3 months First episode of unprovoked PE and low risk of bleeding, and in whom stable Anticoagulation can be achieved May be considered for long term anti-coagulation Second episode of unprovoked PE Long term anti-coagulation PE and cancer LMWH should be considered for the first 3 to 6 months. After this period, anti-coagulant therapy with VKA or LMWH should be continued indefinitely or until the cancer is cured.
  • 28. Prevention of VTE • Risk identification • Low dose unfractionated heparin (5000 U, 8 or 12 hrs) • Low molecular weight heparin • Pneumatic compressive devices • Sodium warfarin