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PE and DVT PE and DVT

PE and DVT

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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. - PowerPoint PPT Presentation

Text of PE and DVT

  • PE and DVT

  • Pathogenesis of VTVirchows triad:Damage to vessel wallVenous stasisHypercoagulability

  • SourceMost PEs 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 PE20% 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 FactorsAgePrevious thrombosisImmobilizationMajor surgery especially OrthoEstrogen OCP, HRT, SERMsAntiphospholipid Ab syndromeMalignancyNephrotic syndromeInflammatory bowel diseaseMyeloproliferative d/o esp p. vera and ETPNHLong distance air travelHIT

  • Inherited Risk FactorsFactor V Leiden mutationG20210A prothrombin gene mutationAntithrombin deficiencyProtein C or S deficiencyDysfibrinogenemiaHyperhomocysteinemia

  • PresentationDyspneaPleuritic chest painCough +/- hemoptysisOn exam may have TachypneaTachycardiaS4Loud P2May have fever rarely >102In massive PE can have hypotension and shockLook at legs for swelling and Homans sign but only helpful if positive.

  • Homans SignPassive 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 calfDVTBakers CystCellulitisGout if really bad it can sometimes look like a cellulitisIf bilateral think about CHF, Nephrotic syndrome, liver failure, venous insufficiency, pregnancy or pelvic mass, vasodilators esp nifedipine

  • ABGUsually shows hypoxia, hypocapnia, respiratory alkalosisA-a gradient:Normal 7-14 depending on ageIncreases with age, FiO2 and supine postureEstimate of normal for age: Age/4 +4A-a gradient = (FiO2 x713 pCO2/0.8) PaO2If A-a gradient normal, PaO2 45 then hypoventilation accounts for hypoxiaIncreased 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!

  • LabsTroponin, LDH, AST and BNP may all be elevatedCheck baseline CBC, PT/PTT/INR, CrD-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)

  • EKGMay have non specific ST and T wave changesTypical SI, QIII, TIII - rare. Sinus tachycardiaT wave inversions in right to mid chest leadsPoor R wave progression (acute RV dilation)P pulmonaleRV conduction delaysRight axis shift

  • CXRMay have area of atelectasisMay have wedge shaped infarct peripherallyPleural effusion occurs in about 40%

  • V/Q scanningLook for evidence of ventilation perfusion mismatchCan only really be done if pt has normal CXRNormal 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 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

  • 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 extremitiesIf high clinical suspicion should be repeated 7-10 days after initial scan as below knee DVT can propagateAlso remember that some pt develop DVTs elsewhere so you may not find a DVT in their legs if the source was their arm!

  • Spiral CT/CT angiogramUsed if CXR not normalPicks 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.

  • EchoMore 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 PEBUT echo is only really used for Dx of massive lifethreatening PEs when rapid diagnosis is needed to determine whether thrombolysis should be given.

  • TreatmentIdentify any contraindications to anticoagulations if yes then IVC filterInquire about h/o HITIf yes, then use direct thrombin inhibitorAssess need for hospitalizationExtensive iliofemoral DVT with circ compromiseIncreased risk of bleedingLimited cardioresp reservePoor complianceCI to LMW heparin

  • TreatmentAdminister LMW heparin or unfractionated heparinGoal 1.5-2.5 x PTT in first 24 hoursCheck platelet count on day 3-5Treat at least five days and until patients INR is >2 on coumadin for two consecutive daysStart coumadin on day 1

  • Treatment Duration3-6 months in most patientsIndefinite treatment:>1 spontaneous eventOne spontaneous life threatening eventAntiphospholipid syndromeAntithrombin deficiency>1 genetic allelic abnormalityHomozygote for Factor V Leiden or prothrombin gene mutationHeterozygote for bothProtein C/S deficiencyContinuing RF especially active advanced CA

  • Contraindications to AnticoagulationAbsoluteActive bleedingSevere bleeding diathesisPlatelet count
  • Contraindications to AnticoagulationRelativeMild/moderate bleeding diathesis or thrombocytopeniaBrain metsMajor abdominal surgery within 2 daysGI or GU bleeding within 14 daysEndocarditisSevere HTN (SBP >200, DBP > 120)

  • Inferior Vena Cava FilterReduce risk of PE but carry increased risk of DVTUse in pts with DVT who cannot take anticoagulation e.g. due to bleeding riskAlso used with or without anticoagulation in patients with high risk of death should further PE occur.

  • Hypercoagulation WorkupTest all patients for unprovoked VT for antiphospholipid ab syndrome and hyperhomocysteinemia

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

  • Hypercoagulation WorkupWait to check for deficiency in antithrombin, protein C or S until 2 weeks after anticoagulation rx is completed