- Количество слайдов: 31
PE and DVT
Pathogenesis of VT Virchow’s triad: – Damage to vessel wall – Venous stasis – Hypercoagulability
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.
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
Inherited Risk Factors Factor V Leiden mutation G 20210 A prothrombin gene mutation Antithrombin deficiency Protein C or S deficiency Dysfibrinogenemia Hyperhomocysteinemia
Presentation Dyspnea Pleuritic chest pain Cough +/- hemoptysis On exam may have Tachypnea Tachycardia S 4 Loud P 2 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.
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
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
ABG Usually shows hypoxia, hypocapnia, respiratory alkalosis A-a gradient: Normal 7 -14 depending on age Increases with age, Fi. O 2 and supine posture Estimate of normal for age: – Age/4 +4 A-a gradient = (Fi. O 2 x 713 – p. CO 2/0. 8) – Pa. O 2 If A-a gradient normal, Pa. O 2 <80, Pa CO 2 >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!
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)
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
CXR May have area of atelectasis May have wedge shaped infarct peripherally Pleural effusion occurs in about 40%
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
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 ventilationperfusion 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
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.
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!
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.
Echo More than 80% of pts with PE will have abnormalities of RV size or function, or TR. Mc. Connells 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.
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
Treatment Administer LMW heparin or unfractionated heparin Goal 1. 5 -2. 5 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
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
Contraindications to Anticoagulation Absolute – Active bleeding – Severe bleeding diathesis – Platelet count <20 – Neurosurgery, ocular surgery or intracranial bleeding within the past 10 days
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)
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.
Hypercoagulation Workup Test all patients for unprovoked VT for antiphospholipid ab syndrome and hyperhomocysteinemia
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
Hypercoagulation Workup Wait to check for deficiency in antithrombin, protein C or S until 2 weeks after anticoagulation rx is completed