1. PE and DVT

2. Pathogenesis of VT Virchow’s triad: Damage to vessel wall
Venous stasis
Hypercoagulability

3. Source
Most PE’s originate from thrombi in the deep venous system of the legs, although they may also originate in the pelvic, renal or upper extremity veins.
HOWEVER, less than 30% of pts will have symptoms in their legs at the time of diagnosis of PE
20% of calf vein thrombi propagate above the popliteal fossa.
20% of lower extremity venous emboli begin in the proximal veins without prior calf involvement.

4. Acquired Risk Factors Age Previous thrombosis Immobilization
Major surgery – especially Ortho
Estrogen – OCP, HRT, SERMs
Antiphospholipid Ab syndrome
Malignancy
Nephrotic syndrome
Inflammatory bowel disease
Myeloproliferative d/o – esp p. vera and ET
PNH
Long distance air travel
HIT

5. Inherited Risk Factors
Factor V Leiden mutation
G20210A prothrombin gene mutation
Antithrombin deficiency
Protein C or S deficiency
Dysfibrinogenemia
Hyperhomocysteinemia

6. Presentation Dyspnea Pleuritic chest pain Cough +/- hemoptysis
On exam may have
Tachypnea
Tachycardia S4
Loud P2
May have fever – rarely >102
In massive PE can have hypotension and shock
Look at legs for swelling and Homan’s sign – but only helpful if positive.

7. Homan’s Sign
Passive dorsiflexion of the foot with the knee straight may give pain in the calf and back of the knee when there is a deep venous thrombosis.
Some concern that vigorous dorsiflexion of the foot can expel clot from the veins and so this test may have its dangers.
The sign is not specific for DVT

8. DDX swollen calf DVT Bakers Cyst Cellulitis
Gout – if really bad it can sometimes look like a cellulitis
If bilateral think about CHF, Nephrotic syndrome, liver failure, venous insufficiency, pregnancy or pelvic mass, vasodilators esp nifedipine

9. ABG Usually shows hypoxia, hypocapnia, respiratory alkalosis
A-a gradient:
Normal 7-14 depending on age
Increases with age, FiO2 and supine posture
Estimate of normal for age:
Age/4 +4
A-a gradient = (FiO2 x713 – pCO2/0.8) – PaO2
If A-a gradient normal, PaO2 <80, Pa CO2 >45 then hypoventilation accounts for hypoxia
Increased A-a gradient occurs in V/Q mismatch, shunting and any kind of barrier to diffusion (e.g. pulmonary edema)
BUT can be normal and still have PE!

10. Labs Troponin, LDH, AST and BNP may all be elevated
Check baseline CBC, PT/PTT/INR, Cr
D-dimer
Normal D-dimer excludes PE, but positive D-Dimer is not helpful (as it can be positive in many conditions including sepsis, immobility, post Sx and CAP)

13. EKG May have non specific ST and T wave changes
“Typical” SI, QIII, TIII - rare.
Sinus tachycardia
T wave inversions in right to mid chest leads
Poor R wave progression (acute RV dilation)
P pulmonale
RV conduction delays
Right axis shift

14. CXR May have area of atelectasis
May have wedge shaped infarct peripherally
Pleural effusion occurs in about 40%

16. V/Q scanning Look for evidence of ventilation perfusion mismatch
Can only really be done if pt has normal CXR
Normal scan virtually excludes PE even if pretest clinical probability was felt to be high.
If a patient with intermediate clinical probability of PE has an intermediate scan then need further testing

17. A 60-year-old man with asthma is evaluated in the emergency department because of the acute onset of chest pain while lifting a heavy object. The pain is sharp and accentuated by deep breathing and by movement of the upper extremities. It is located over the left precordium.
The physical examination and chest x-ray are normal. A ventilation-perfusion lung scan shows matched areas of perfusion and ventilation.
Which one of the following is the correct interpretation of the ventilation-perfusion lung scan?
( A ) Normal ( B ) Low probability ( C ) Indeterminate ( D ) High probability

18. Correct Answer = A
The lung scan is normal, with matched perfusion and ventilation. This lung scan rules out a pulmonary embolism, and another source for the chest pain should be sought. Often asthma does complicate the interpretation of the lung scan, but the problem relates to matched defects in which the airway obstruction decreases the ventilation to an area of the lung. The consequent hypoxia in that area leads to reduction in blood flow in the same area. These areas are rarely segmental.

19. Doppler US of lower extremities
If high clinical suspicion should be repeated 7-10 days after initial scan as below knee DVT can propagate
Also remember that some pt develop DVT’s elsewhere – so you may not find a DVT in their legs if the source was their arm!

20. Spiral CT/CT angiogram
Used if CXR not normal
Picks up large central emboli but is less sensitive for the smaller peripheral emboli.
True pulmonary angiography rarely used now, though can do direct thrombolysis in massive PE.

22. Echo
More than 80% of pts with PE will have abnormalities of RV size or function, or TR.
McConnells sign – regional wall motion abnormalities that spare the R ventricular apex are very suggestive of PE
BUT echo is only really used for Dx of massive lifethreatening PE’s when rapid diagnosis is needed to determine whether thrombolysis should be given.

23. Treatment
Identify any contraindications to anticoagulations – if yes then IVC filter
Inquire about h/o HIT
If yes, then use direct thrombin inhibitor
Assess need for hospitalization
Extensive iliofemoral DVT with circ compromise
Increased risk of bleeding
Limited cardioresp reserve
Poor compliance
CI to LMW heparin

24. Treatment Administer LMW heparin or unfractionated heparin
Goal x PTT in first 24 hours
Check platelet count on day 3-5
Treat at least five days and until patient’s INR is >2 on coumadin for two consecutive days
Start coumadin on day 1

25. Treatment Duration 3-6 months in most patients Indefinite treatment:
>1 spontaneous event
One spontaneous life threatening event
Antiphospholipid syndrome
Antithrombin deficiency
>1 genetic allelic abnormality
Homozygote for Factor V Leiden or prothrombin gene mutation
Heterozygote for both
Protein C/S deficiency
Continuing RF especially active advanced CA

26. Contraindications to Anticoagulation
Absolute
Active bleeding
Severe bleeding diathesis
Platelet count <20
Neurosurgery, ocular surgery or intracranial bleeding within the past 10 days

27. Contraindications to Anticoagulation
Relative
Mild/moderate bleeding diathesis or thrombocytopenia
Brain mets
Major abdominal surgery within 2 days
GI or GU bleeding within 14 days
Endocarditis
Severe HTN (SBP >200, DBP > 120)

28. Inferior Vena Cava Filter
Reduce risk of PE but carry increased risk of DVT
Use in pts with DVT who cannot take anticoagulation e.g. due to bleeding risk
Also used with or without anticoagulation in patients with high risk of death should further PE occur.

29. Hypercoagulation Workup
Test all patients for unprovoked VT for antiphospholipid ab syndrome and hyperhomocysteinemia

30. Hypercoagulation Workup
Test for Factor V Leiden, prothrombin gene mutation and deficiencies of antithrombin, protein C/S in the following patients:
Family h/o VT
VT before the age of 50
Recurrent VT
Thrombosis in an unusual site (mesenteric, renal, cerebral, hepatic)
Heparin resistance (antithrombin deficiency)
Warfarin induced skin necrosis (protein C/S def)
Neonatal purpura fulminans

31. Hypercoagulation Workup
Wait to check for deficiency in antithrombin, protein C or S until 2 weeks after anticoagulation rx is completed