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DVT PE INTRO Powered By Docstoc
					                               DVT/PE - INTRO

    Venous ThromboEmbolic (VTE) disease = combination of DVT, PE, superficial vein
     thrombosis, chronic venous insufficiency (spectrum of same disease)
    3rd MCC of death in USA
    2nd MCC of unexpected death (MI #1)
    Undiagnosed more common than diagnosed
    Autopsy series shows huge incidence, mostly undiagnosed
    Incidence very hard to study: true incidence unknown
    Medical pt on bed rest X 1 week: 15%
    ICU pt on bed rest X 3 days: 30%
    Post MI or CABG in CCU: 45%
    Prophylactic heparin decreases mortality in 31%
    10% of deaths occur w/i 1hr of initial symptoms
    PEA as initial arrest rhythm: 36% with PE as cause
    ALL DVTs embolize to some extent
    Severity of PE not related to severity of symptoms of DVT (can be asymptomatic)
    Incidence of PE increases from 4% to 24% within 24hrs of no anticoagulation

    DVT/PE very common
    Most DVTs are asymptomatic
    Most with DVTs will have PE
    Most PE are asymptomatic
    Most go clinically unrecgonized
    Many do not have classical signs/symptoms
    NO unifying sign, symptom, or non-invasive diagnostic tool
    Many DVTs and PE are not detectable by non-invasive imaging
    Many missed diagnoses: worry about 2% missed MI, what about 30% missed PE
    Many have poor prognosis
                   1/10 die within 10 min of acute PE
                     3/10 are diagnosed and treated: 10% of these will die in future
                     6/10 are undiagnosed and untreated: 30% of these will die in future


VIRCHOW’S TRIAD: Risk Factors for DVT/PE (Box 107-2)
     Venous injury
                     Surgery
                     Smoking
                     HTN (not DM or hyperlipidemia)
                     Trauma/Injury
                     Fractures
                     Venous catheters
                     Venous pacemakers
                     Venography
                     Vericose veins
                     Chronic Venous Insufficiency
                     IVDA
                     Previous DVT
                     Burns
     Venous stasis
                     Surgery
                     Trauma
                     Hospitalization
                     Long trips (>4hrs by Ontario Thoracic Society)
                     Inactivity
                     Pregnancy
                     Debilatation
                     Institutionalization
                     AMI
    Hypercoagulability
                     Congenital
                             -      3 deficiencies: protein C, protein S, antithrombin III
                             -      2 excesses: hyperhomocysteinemia, polymorphic prothrombin
                             -      1 weirdo: factor V leidein (APC resistance)
                     Acquired
                             -      Systemic illness: cancer, chemotherapy, pregnancy, post-
                                    partum, obesity, lupus anticoagulant, anti-cardiolipan Ab,
                                    nephrotic syndrome, PNH, hyperhomocysteinemia acquired
                                    due to B12/folate/B6 deficiency, AIDS, lupus, CHF,
                                    hemolytic anemias, hyperlipidemia, polycythemia,
                                    thrombocytosis, ulcerative colitis, IVDA, burns
                             -      Medications: oral contraceptives, hormone replacement Rx,
                                    phenothiazines, warfarin (first few days), testosterone (ask
                                    young athletic males)

    Hx of DVT/PE
    Cancer
    Immobilized limb
    Recent surgery
    Pregnancy
    Lack of Natural anticoagulants: Protein C, Protein S, Antithrombin III
    Deficiency of natural fibrinolytic system: abnormal or lack of tissue plasminogen activators
     (occurs in endothelial cells normally) or u-plasminogen activator (produced in renal cells;
     aka urokinase); can also have lack of or abnormal plasminogen (converted into plasmin by
     plasminogen activators)
    DVT hx: 25Xs more like to have DVT; 30% recurrence rate in 5yrs
    Vericose veins: 50% will get DVT with risk factor like surgery
    Hypercoagulable state: rule out in ALL even with identifiable risk factors b/c of mortality
    Cancer: look for cancer in unexplained DVT/PE; colon and ovarian are MCC
    Chemotherapy: independent risk on top of risk from Ca b/c of reduction in Prot C, S, AIII
    IBD: increases fibrinogen, decreases AIII
    Estrogen: OCP and HRT are risks
    Blood type A: decreased AIII and increased factor VIII
    Obesity: ? due to immobility or estrogen from fat (not proven)
    Peuiperum and Pregnancy
                   MC nontraumatic cause of death in pregnancy
                   3/4 cases before delivery, 1/4 after
                   Pelvic thrombophlebitis: serious complication of endometritis and universally
                    treated with anticoagulation b/c of high risk of DVT/PE
    Ovarian Vein Thrombosis
                   Severe pain in adnexa, flank, abdomen
                   Occurs in prenancy usually
                   Fever common
                   U/S, CT, MR, or laparoscopic dx

                  DEEP VENOUS THROMBOSIS

    Anatomy: superficial leg veins pass through fascia by perforating connector veins to enter
     the deep system
    Virtually all DVT involve calf veins except pelvic surgery and major trauma
    Progression is from distal to proximal
    Fragment breaks loose and embolizes to ivc, RA, RV, PA, lung
    70% of PE have detectable DVT with ultrasound; remainder there but not detectable
    Isolated calf DVT: 40% get PE
    Popliteal DVT: 60% get PE
    Femoral DVT: 80% get PE
    Ileofemoral DVT: 100% get PE
    Calf DVTs
                   Is there less significance from an isolated calf DVT?-------> NO, patients
                    can die from embolization of calf DVT or from embolization of propagated
                    larger DVTs; 30% of lethal or “serious” PE come from calf
                     80% propagate and become proximal DVTs
                     Large autopsy study: 25% of lethal PE and 33% of massive PE arise from
                      isolated calf DVTs
                     Older thought: treat if high risk of propagation or decompensation with PE
                     Newer thought: treat all calf DVTs
    Other sites
                     Neck, renal, vena cava
                     Heart: right sided, usu associated w/ hypokinesis related to MI
                     Upper extremity: usu associated w/ central line but can be spontaneous or
                      from chemotherapy or TPN (subclavian is most common site)
                     ANY SITE can embolize and lead to deatha

    Symptoms
                     Leg swelling, pain, usually with No hx of trauma
                     DVT risk factors as per PE but emphasis on leg immobilization, etc
    Signs
                     Entire leg swollen
                     Calf swelling > 3cm at tibial tuberosity (c/p to other side)
                     Pitting edema greater in the symptomatic leg
                     Collateral superficial venous dilatation
                     Localized tenderness over deep venous system
                     Homan’s sign: true Homan’s sign is resting plantarflexion in a relaxed foot
                     Pseudohoman’s sign: pain on passive dorsiflexion
                     Both are totally useless
                     Note: clinical examination 25% sensitive

    Skin: cellulitis, erysipelas
    Fascia: necrotizing fascitis
    Muscle: myositis, muscle strain, muscle tumor
      Tendon: tendinitis, tendon sprain
      Bone: osteomyelitis, arthritis, bone tumor
      Veins: DVT, superficial phlebitis, post-phlebitic syndrome
      Arteries: embolism, thrombosis, ischemia, vasculitis, Phelgmesia Cerula Dohlens
      Nerves: peripheral neuropathy, sciatica
      Lymph: lymphedema, lymphangitis
      Compartment syndrome
      Baker’s cyst

      Clinical Scoring Systems
                     Well’s DVT criteria
                     JAMA 1998 Scoring system
      B Mode Duplex Ultrasonography
                     Sensitivity 95% if DVT above the knee (proximal DVT)
                     Sensitivity 50% if DVT below the knee (calf DVT)
                     Sensitivity decreases for non-occlusive clots
                     Sensitivity decreases in pregnancy (60 - 70% sensitive for proximal DVT)
                     Acute vs chronic can be difficult distinction
                     NOT as good as venography
                     Normal or abnormal doesn’t neccessarily rule in or out :. consider
                      venography in low PTP and abnormal U/S, or high PTP and normal U/S
                     Previous DVT
                              -       New DVT: new non-compresible segment or marked increase
                                      in venous diameter with compression (> 4 mm)
                              -       R/O DVT: fully compressible veins or diameter increased >
                                      1mm from size on previous ultrasound

    IPGs (Plethysmography) - Maximum Venous Outflow (MVO)
                    Measures changes in lower extremity volume as function of venous outflow
                    Sensitivity with one test 50% but is 90% with serial testing (= U/S)
                    Many false positives: post-phlebitic syndrome, abdominal tumor, pregnancy
                    Day 1,4,710 after normal U/S on day 0
                    Basically replaced by ultrasound
                    May have role in pregnant patient
                    Will not detect nonobstructing flow
    Venography
                    GOLD STANDARD but interpreter dependant
                    10% done inadequately, 5% develop phlebitis, anaphylactoid rxns with dye
                    CAN determine new vs old
                    Indicated for ? upper extremity DVT and normal U/S
    Other
                    Nuclear Venogram:Inject dye into foot vein
                    CT venography or MR venography

    Degredation product of cross - linked fibrin released by fibrinolysis
    Short t1/2 but an acute clot will keep levels elevated for 1 week
    KEY POINTS on D-dimers and DVT
                    Only useful when applied to pre-test probability
                    Useful in low or moderate pre-test probatility
                    Does NOT rule out DVT in high pre-test probability
                    Good sensitivity; poor specificity
                    Latex Agglutination assay
                    Cheaper
                    Lower sensitivity; higher specificity
    ELISA
                       Enzyme Linked Immuno Assay
                       More expensive
        Anderson Hematology 2000
                       Compared overall accuracy

    ASSAY              SENSITIVIY         SPECIFICITY          NPV                  PPV

    SIMPLIRED          80 (66-90)         94 (83-99)           82 (70-90)           93 (81-99)

    VIDAS (ELISA)      100 (93-100)       41 (27-56)           100 (83-100)         63 (52-74)

        General
                       Heparin if testing delayed > 2hrs
                       UFH largely replaced by LMWH
                       Bedrest INCREASE risk of PE b/c of thrombus propagation
        LMWH
                       Tinzaparin 175 Units/kg/day sc (decrease dose with RENAL FAILURE)
                       Inhibits Xa > II a thus no PTT monitoring, less platelet aggregation
                        inhibition, fewer hemorrhagic complications, freater bioavailability and more
                        predictable therapeutic levels, lower incidence of thrombocytopenia, partially
                        reversible with protamine
                       Continue for 4 - 5 days until INR therapeutic
                       Safety of home administration well established
        Warfarin
                  Start in emerg once dx made; INR goal of 2 - 3
                  General Rx for 3 months
                  Overlap with LMWH re theoretical risk of increased coagulation with first
                   doses (inhibits Protein C and S first)
   Thrombolysis
                  Clot resolution and prevention of chronic complications
                  Can be delivered right at clot by catheter delivery
                  Indicated for Phlegmasia Dolens
                  Ileofemoral clots: talk to vascular about ? catheter delivered thrombolysis
                  Streptokinase only lytic approved
   Specific Management Details
                  Superficial phlebitis: benign, tx with NSAIDs and superficial compression
                   bandages, 30% will have co-existing deep venous involvement :. ALL should
                   be followed to watch for DVT (serial U/S or IPG)
                  Calf DVT: generally treat all calf DVTS; recommendation in chest is to treat
                  Upper extremity: anticoagulation, catheter - directed thrombolysis,
                   thrombectomy or SVC filter if contraindicated to above
                  Contraindication to anticoagulation ---------> IVC filter
                  Heparin and U/S in am shown to be safe: J Emerg Med 1999: 17; 11 - 15
                  Active internal bleeding (even if minor)
                  Active external bleeding
                  Severe Prior H.I.T. (For unfractionated heparin)
                  Major truama but no active bleeding
                  Neurosurgery w/i 8 weeks
                  Hepatic or renal bx w/i 8 weeks
                  Ocular surgery within 8 weeks
                  Immediately post partum
                  Recent GI bleeding
                  Uncontrolled THN
                  Prolonged CPR
                  Diabetic retinopathy with recent hemorrhage
                    Mild HIT
                    CNS cancer
                    Recent surgery
                    Recent major vessel puncture
                    Pregnancy
                    Endocarditis

    Extensive obstruction of superficial and deep venous systems
    Leads to massively swollen leg that is white, painful, edematous, cold, and pulseless
    May just be unable to detect pulse or may be true lack of pulse due to pressure
    Indication for thrombolysis
    Amputation necessary if lysis doesn’t work

    Thrombophlebitis of subcutaneous veins from breast —> axilla
    Painful and difuguring to breast

    Superficial Thrombophlebitis usually benign
    Deep thrombophlebitis has high risk of DVT/PE
    Clinical exam cannot distinguish superficial vs deep
    Chronic venous insufficiency, post-phlebitic syndrome, and PE are complications
    Management
                    NSAIDs, graded compression stockings (not TED hose), ultrasound leg
                    No anticoagulation if NO risk factor for DVT, no history of DVT, no
                     immobility, no involvement of greater saphenous vein above the knee
                    Repeat U/S in one week to r/o propagaton
                    Abx if infected
    Isolated Thrombus
                    Ex: Peroneal or soleal thrombus
                    NSAID, hose, ambulation, repeat u/s in 1 week
    Recanalization of DVT leads to valveless channel with chronic increases pressure
    This leads to chronic edema, pain, hyperpigmentation, ulceration, and recurrent DVT/PE
    Clinical post - phlebitic syndrome in 25% of calf thrombophlebitis
    Varicose veins: incompetent venous valves leading to visible, dilated, tortuous veins
    Symptoms: chronic burning, throbbing, fatigue, cramping, pain that is BETTER with walking
     (distinguishes from arterial insuff)
    Mx: leg elevation, stockings

    PE
    Chronic Venous Insufficiency
    Postphlebitic syndrome: chronic pain, ulceration, dermatitis
    Recurrent DVT/PE
    Phlegmasia dolens

                            PULMONARY EMBOLI

    Pulmonary artery obstruction, release of vasoconstrictors, elevated pulmn vasc resistance
     resulting in decreased blood flow to that spot and creates “dead space”. This is probably
     less important than initially thought.
    Bronchial arterioles anastamose with pulmonary arteries thus fully obstructive PE will usually
     NOT cause pulmonary infarction even when subsegmental arteries are completely blocked
    Also, the lung shunts blood and alters ventilation which creates significant V/Q mismatch
     which is probably more important than the reduced blood flow to one particular segment
    Chronic PE, chronic pulmonary HTN, cor-pulmonale
    Hemodynamic collapse with large occlusion of pulmonary vascular tree
    Effects of PE on RV function
                    Increased right ventricular afterload may lead to dilation, dysfunction, and
                    ischemia of the RV
                   > 50% of pulmonary vascular tree occlusion causes significant pulmonary
                    HTN and acute cor-pulmonale
                   Tricuspid regurgitation will occur if pulmonary arterial pressure > 40 mmHg
                   RV hypokinesis has been found by echo in 40% of pts w/ normal systolic
                    blood pressure.
                   Hypotension responsive to fluids is characteristic of RV involvement b/c the
                    RV is very dependant on preload for its cardiac output. Nitroglycerin is

    Decreased perfusion to a segment :. ventilatory alveolar dead space
    Slight hypoxia/hypercapnia :. tacchypnea: easily compensates with small PI
    Chronic PE: V/Q mismatch, pulmn HTN, increased PAP, cor - pulmonale, right heart failure
     which may present like CHF, COPD, asthma, and is a commonly missed dx
    Pseudoshunting
                   ABG in PE behaves as though a portion of blood has been shunted through
                    unventilated segment
                   Small volume of blood through blocked segment: low flow with normal
                    ventilation thus V/Q > 1 ----> normal of slight increase Pa02 and normal
                    or slight decreased PC02
                   Large volume of blood through non-blocked areas: high flow with normal
                    ventililation thus V/Q < ------> poor exchange because of too much
                    volume thus low Pa02 and high PC02
                   In effect, the majority of the blood has become “shunted” through an
                    unventilated lung
    Other cause of altered gas exchange
                   Hyperventilation
                   Atelectasis secondary to surfactant loss
                   Transudation of alveolar fluid :. rales, rubs
                   Mediator release thus pulmn VC and bronchospasm (wheezing)
                      Pulmonary infarction, pain, splinting with resultant hypoventilation
    End Result
                      Small PE: no changes
                      Large PE: decrease Pa02, normal/decreased/increased PC02
    Chronic PE is an important cause
    Pulmonary arterial endothelium doesn’t release enough fibrinolytics to break down PE well
    Most of embolus is there permanently
    Re-canalization and new venous channels form
    Vessels are now stiff and can’t increase volume
    Decreased capacitance and increased resistance
    Increase right heart pressure and right heart failure

    Pure syndromes rarely exist; wide variety/range of presentations
    Pulmonary infarction/hemorrhage (MILD)
                      Pleurititc CP, cough, hemoptysis
                      Ddx ? pneumonia
    Submassive embolism (MODERATE)
                      Acute, unexplained SOB on exertion or rest with or without CP
                      Defined as loss of area less than two lobar arteries
                      Ddx ? pneumonia, CHF, asthma, hyperventilation
    Massive embolism (SEVERE)
                      Syncope, hypotension, cyanosis, acute cor-pulmonale
                      Defined as loss of area more than two lobar arteries
                      Ddx ? MI, hypovolemic shock, septic shock, intracranial event, arrythmia

    No unifying sign or symptom: none make or r/o dx
    History
              Dyspnea                 84%
              CP, pleuritic           74
            Apprehension              59               Dyspnea is MOST COMMON
            Cough                     53               symptom
            Hemoptysis                30
            Diaphroesis               27
            CP, non-pleuritic         14
            Syncope                   13
    Physical
            Tachypnea>16                   92%
            Tachypnea > 20            70%
            Crackles                  58
            Loud P2                   53
                                                                Tachypnea is MOST
            HR > 100                  44
            Fever > 37.8              43                       COMMON physical exam

            Diaphoresis               36                       finding
            S3/4                      34
            Thrombophelbitis          32
            LE edema                  24
            Murmur          23
            Cyanosis                  14
            Other: palpable P2, RV heave, RV lift
    Other
        Pmhx DVT/PE
        Risk factors
        May be non-thrombotic: fat, tumor, air, hair, talc, cotton, amniotic
    Ddx
        MI, aortic dissection, unstable angina, pneumonia, bronchitis, COPD exacerbation, CHF,
         asthma, pericarditis, primary pulmn HTN, rib #, pneumothorax, costochondritis, MSK
         pain, anxiety, other emboli
        Chest pain and unstable: PE, MI, aortic dissection
        SOB and unstable: PE, COPD, asthma, pthrx, pulmn edema, pneumonia, sepsis

    Atypical presentations common: may have cc of fever, cough, reactive AW disease, Afib,
     back pain, abdominal pain, flank pain
    Classic triad SOB, CP, hemoptysis in < 20%
    Chest pain
                   Wide variety from sudden onset, slow onset, sharp, pressure and may have
                    chest wall tenderness
                   Young, healthy people with no PE risk factors and pleuritic CP: clinical
                    variables cannot r/o PE
                   Study of 200 consecutive presentations of pleuritic CP
                             -      20% found to have PE
                             -      80% found to have viral pleuritis, pneumonia, etc
                             -      Predictive of PE: pleural effusion, Pmhx DVT/PE, s/s of
                                    phlebitis, recent immobilizaiton
                             -      Do NOT diagnose viral pleuritis without -ve PE work up
    Pneumonia
                   Can be similar presentation, can be co-existent
                   Pneumonia > PE: purulent sputum, shaking chills, +ve cultures, high fever
                   PE > pneumonia: bloody nonpurulent sputum, no improvement with abx, -ve
                    cultures, minimal or no fever
                   V/Q more difficult to interpret
    Asthma
                   PE can have bronchospasm: think PE with no hx of asthma
                   Hemodynamic instablitiy and NO hx of asthma suggest PE
                   V/Q difficult to interpret with co-existence
    Other
                   Pleurisy: pain from pleural inflammation in absence of dx (viral?); some
                    don’t think this dx exists as other causes are found in majority
                   Angina/MI: commonly confused w/ PE
                   Paradoxical embolism via PFO (27%) may present with arterial emboli
                   Ca
                   Abcess

    See Virchow’s Triad
    Children: can happen in young, same Rfs
    Obesity: not known why
    Central lines: even with anticoagulation, also fat embolism
    Cancer: should look for underlying Ca
    Hypercoagulable state: look for in ALL even with other Rfs
    Antithrombin III deficiency: heparin doesn’t work
    Most important risk factors: previous DVT/PE is most important, recent surgery, Recent
     immobilization, Recent pregnancy, Underlying Ca

    Laboratory
                   INR/PTT: normal (think Lupus Anti Coagulant with long PTT)
                   Hb: normal (look for polycythemia)
                   WBC: normal or increased (doesn’t help ddx)
                   ESR: normal but increased with underlying dz
                   Plt: watch for HIT
                   LE: increased but non-specific
                   RF screen
                   D-Dimer
                            -       Utility unknown
                            -       Degredation product of cross-linked fibrin
                            -       NPV 90%: misses 10% of PE (NPV EXCELLENT)
                            -       PPV 30%: only 30% have PE (PPV POOR)
                            -       False +ves: MI, pneumonia, CHF, active cancer, post op,
                                    pregnancy, recent trauma, hemorrhage

            TEST                    SENSITIVITY             SPECIFICITY
            SimpliRED               80 - 85%                70 - 90%
            Whole Bld Aggn          90 - 95%                40 - 90%
            ELISA                   95 - 100%               30 - 60%
   ABG
             May be normal
             Pa02 may be normal or decreased
             PC02 may be normal, decreased, or increased
             Many have normal Pa02: angio proven PE 20% have > 80 mmHg, 5%
              have > 100 mmHg Pa02 on room air
             A - a gradient
                     -         Widening of the A-a gradient but normal ABG does NOT
                               R/O PE and should not be used to determine who work up
                     -         A = Fi02 X (Pb - 47) - PaC02/0.8
                     -         Normal A-a: imperfect gas Xchange, bronchial arteries
                     -         Normal is 10 + (1/10 X age)
                     -         Nonspecific, Nonsensitive
                     -         Does NOT dx or r/o PE
                     -         PIOPED: Normal A-a gradient + PC02 > 36 has 98% NPV
                               for pulmonary embolism with normal underlying lungs
                     -         Compensation can increase Pa02 :. gradient not seen
   ECG
             Sinus tacch and NSST changes are most common
             25% with unchanged ECG
             55% with non-specific fingdings: sinus tach, NSST changes
             20% with classical findings
                     -         P pulmonale: tall P in lead II
                     -         Afib
                     -         RAD
                     -         RBBB
                     -         S1 - Q3 - T3 (10% of massive)
                     -         S1 - S2 - S3
    Chest XR
                  Normal or nonspecific is most common
                  Elevated hemidiaphragm
                  Pleural effusion
                  Cardiac enlargement
                  Atelectasis
                  Hampton’s Hump = peripheral wedge shaped (apex toward hilum) infiltrate
                   corresponding to peripheral pulmonary infarction
                  Fleishner’s Sign = large, dilated, sausage - shaped pulmonary artery
                  Westermark’s sign = focal oligemia distal to dilate pulmonary artery
                  Palla’s sign: enlarged right descending pulmn artery
    Venous U/S
                  1/3 w/ PE have no evidence of DVT
                  Normal US does not R/O PE
                  Findings of DVT is indication for anticoagulation even if PE is not detected
                  Clinical detection of DVT is very poor
    Echocardiography
                  Rapid triage of acutely ill patients to define PE, MI, pericardial tamponade,
                   aortic dissection
                  Look for RV hypokinesia. McConnell sign of PE is a pattern of regional RV
                   dysfunction in which apical wall motion remains normal despite hypokinesis
                   of the free wall
                  Also: increased RV size, increased PA pressures, septal shift to left, TR,
                   increased right sided pressures, RV motion abnormalities ---------------->
                   combination 93% sensitive and 81% specific
                  TEE >> TTE but both are useful
                  Good test for consideration of ddx
                  May be used for decision for lysis re right heart strain

    Indications
                    Suspected PE w/o other proven dx
                    DVT w/o symptoms/signs of PE
                    Repeat evaluation before d/c anticoagulation with irreversible risk factor(s)
   Technique
                    Radioisotope labelled albumin
                    Must take all four views to see all segments
                    May not detect small or non-occlusive emboli
                    Perfusion defect with COPD, CHF, vasoconstriction and consolidation
                     complicated picture: serial V/Qs are an option
                    Perfusion scan is most useful; ventilation less useful
                    Difficult with non-cooperative patient because they have to breath in a mask
                     (unconscious, demented, aggressive)
                    Can do perfusion scan only in pregnancy
   Results
                    Old: low, intermediate, high probability
                    New: normal, non-diagnostic, high probability
                    NON - diagnostic should NOT be called low probability
                    Nondiagnostic: 43% sensitive; PPV 21%
   Perfusion Scan
                    Not sensitive or specific
                    Small infarction with severe symptoms may not be seen
                    Massive embolus may not be detected if non-occluding or asymmetric
                    Perfusion defect ddx: consolidation, atelectasis, vasoconstriction, COPD,
                     CHF, PE
   Ventilation Scan
                    Increases specificity but not sensitivity
                    Measures radioactive gas as it goes throught the lung
                    Abnormalities may show up as poor inflow or delayed washout
   Mismatch
                    Initial: decreased perfusion, normal ventilation
                    Later: some decreased ventilation due to atelectasis, splinting, edema,
                    Large ventilation defect with minimal perfusion defect: airspace dz
                            Large perfusion defect with minmal ventilation defect: PE
          Application
                            Must combine with clinical suspicion/pre-test probability
                            Know your endpoints
                            Don’t overdx: low suspcion and high prob V/Q: angiogram indicated
                            Don’t underdx: high suspicion and nondiagnostic V/Q: angiogram indicated
                            Serial scan is an option if no angiogram available (look for change in


    PRE - TEST           NORMAL V/Q            LOW PROB            INTERMED              HIGH PROB
    PROB                                       V/Q                 PROB V/Q              V/Q

    LOW                  2%                    4%                  16%                   56%

    MOD                  6%                    16%                 28%                   88%

    HIGH                 -                     40%                 66%                   96%

    PRE - TEST PROB           NORMAL                   NON - HIGH                HIGH PROB

    LOW                       1.2%                     3%                        100%

    MOD                       0%                       12%                       100%

    HIGH                      13%                      47%                       33%

          Specific PE protocol with venous contrast
          Good for large, central PE and for ddx
          Central vessels = 1st ----> 4th generation: sensitivity 86%
          Peripheral vessles = > 4th generation: sensitivity 63%
          BUT true sensitivity is UNKNOWN; difficult to study, PIOPED II is studying
          True sensitivity varies with scanner, reader, size of PE, location of PE
          May have role in underlying lung dz where V/Q is less helpful
          Role for in borderline unstable patient who you don’t want to send to nuclear med
          Wide range of published sensitivities: 53 - 100%
          Wide range of published specficities: 81 - 100%
          Recent metanalysis: sensitivity 68%
          NO study to say that CT-ve has ruled out a PE
          NO study has used CT in clinical algorithms
          CT venography ----> scan legs for ? DVT at same time (part of PIOPED II)
          CT angiography promising
    Goldstandard
    Risks: mortality 0.5%, complication 9%
    Must know technique to r/o PE: single injection and single PA view do not r/o PE
    Must have selective cannulation of each branch of main pulmonary arteries: 26 branches
    Small and peripheral PE may NOT be detected (anything smaller than 3rd order)
    Poor kappa values with subsegmental defects
    This is NOT a perfect test but is the best we have
    False -ves (10%): small, distal PE or misreading
    False +ves (1%): tumor, extrinsic compression
    Emergent if unstable or cannot anticoagulate
    May wait hours if stable and can begin anticoagulation
    Risks: anaphylactoid reaction, arrythmia, arterial rupture
    No extra risk in pregnancy

    Fiberoptic angioscopy
    Digital subtraction angio
    MRI
    Monoclonal AB
    Computer assisted V/Q interpretation
    Dielectric imaging
    Pulmn capillary volume
    CT venography
    MR venography
    General ABC approach
    Initial stabilization
    Oxygen may cause pulmonary VD and decrease pain
    Pain relief
    Fluids, pressors for hypotension
    Volume expansion ineffective b/c of obstruction: NOTE ON VOLUME; too much volume
     may really increase right sided pressure and cause septal shift and worsen hypotension
     (don’t flog)
    tPA or surgery most imp for hypotension
    Pressors: epi, norepi, dopamine (want beta and alpha)

    Mainstay of management
    Unfractionated Heparin
                   Start ASAP with suspicion, do not wait for V/Q, or angio
                   Prevents further clot formation and reduces embolization: does not decrease
                    the size of the clot (no lytic actions)
                   Subcutaneous heparin is NEVER appropriate for tx of DVT/PE
                   Risks: ineffective (most imp), hemorrhage (4%), HIT
                   Reversal with protamine sulphate 15 mg (avoid with fish allergy)
                   Targets II a and X a
                   Bolus 100 - 150 U/kg (80 U/kg is NOT enough), infusion 18 U/kg/hr to
                    achieve goal PTT > 1.5 X normal
                   Note higher doses than ACS b/c of relative hypercoagulable states
                   Only 60% will reach goal PTT with 80 units/kg bolus
                   Recurrent PE can occur while on heparin
                   Heparin doesn’t work with AIII deficiency
    LMW Heparins
                   Less bleeding, no PTT monitoring
                   LMWH equal to UFH (trends to being better with Tinzaparin: Gould 1999)
                   Outpatient treatment is safe (Kovacs 2000)
                   LMWH and return in am has not been proven safe (as with DVT): general
                    approach; healthy, normal vitals, low risk of decompensation, no history of
                    HIT, adequate pain control = safe
                   Safe in pregnancy
                   Lower risk of serious complications 0.5% (?reference)
                   Can cause minor bump in AST/ALT
                   Remember to decrease dose with renal failure (decreased clearance)
                     Tinzaparin 175 Units/kg/day sc
                     Enoxaparin 1 mg/kg sc bid
                     Dalteparin 200 units/kg sc od
                     DVT prophylaxis: Enoxaparin 30 mg sc bid
    Warfarin
                     Inhibits II, VII, IX, X, protein C, protein S, AIII
                     Initial increases coagulation due to inhibition of Protein C/S formation thus
                      risk for clot propagation and warfarin induced necrosis :. NEVER start until
                      heparin anticoagulation is therapeutic (Warfarin Skin Necrosis)
                     Start warfarin on day one; continue heparin for 5 days or until INR > 2.5
                     INR 2.5 - 3.5; risk of PE increases significantly with INR < 2.0
                     Many food, herbal, drug interactions
                     Duration ??? 3/12 -------> 6/12

    Complicated
    See table 83-4
    Age is irrelevant
    Prior NON-hemorrhagic CVA is not a C/I
    Pregnancy is not a C/I
    Heparin is not a C/I to thrombolysis
    Thrombolysis Absolute C/I
                     Active external bleeding
                     Active internal bleeding
                     Neurosurgery < 2 months
                     Ocular surgery < 2 months
                     Hepatic or renal biopsy < 2 months
                     Recent retinal hemmorrhage (diabetic) < 2 months
    Heparin
                     Active external bleeding
                     Active internal bleeding
                     HIT
    Absolute Indication = Hemodynamic Instability
                   Anticoagulation does not lyse clot, only prevents propagation
                   Immediate improvement in RV dilation, hypokinesis, TR
                   Has replaced surgery except for contraindications and failure
                   May need to use b/f dx in deteriorating pt with high suspicion
                   Good RCT evidence in the hypotensive patient
    Debatable Indications
                   Exhaustive (or poor) CVS or respiratory reserves
                             -       Hypoxemia + Hypotension
                             -       Normal 02/BP with severe resp CV dz (one lung,
                             -       Rationale: very little reserve for compensation
                   Anticipated recurrence of PE
                             -       Known irreversible coagulopathy, permanently immobilized,
                                     past medical history of PE/DVT
                             -       Rationale: extremely high risk for chronic cor pulmonale
                   Right Heart Strain on echo (no hypotension)
                             -       Consider STAT TTE to evaluate
                             -       Some evidence for but not convincing
                   Cardiac Arrest
                                    Theory: initial PEA arrest rhythm: 36% with PE as cause
                                    Unknown effectiveness
                                    Studies are very small
                                    Dose unknown
                                    BOLUS of 50 mg iv over 15 min
    Notes on thrombolysis
                   Mortality reduction from routine Lysis: UPET, USPET (quicker recovery,
                    fewer recurrence, reduced mortaltiy)
                   Severe bleeding: 4%
                   ICH: 1%
                   Management of minor bleeding: pressure to site and continue thrombolysis
                   Managment of severe bleeding: stop lysis, FFP 6 units, cryoprecipitate 10
                      units, protamine if recent heparin (look up dose), consider aminocaproic acid
                      (plasminogen activator inhibitor - 5 gm iv over 30 min then 1 gm/hr iv until
                      bleeding stops)
    Administration
                     UNSTABLE: rt-PA 100 mg iv over 2hrs (or 15 mg bolus then 30 mg over
                      ½ hr then 35 mg over one hour)
                     PEA ARREST: rt-PA 50 mg iv bolus

    Embolectomy
                     Indications: (i) contraindication to thrombolytics (ii) failure of lytics (iii)
                      insufficient time to thrombolyse
                     Open (thoracotomy) versus catheter extraction
                     No evidence to compare to tPA
    Cardiopulmonary Bypass
                     Fem - Fem bypass
                     Profound hypoxemia or shock
                     NOT a contraindication to lysis b/c left in until completion
    Emergent Thoracotomy
                     Bilateral, massage PA, open cardiac massage
                     Proven or high probability PE with cardiac arrest
                     Not beneficial with cardiac arrest after lytics
    Heparin prophylaxis (subQ is NOT adequate, must be iv if unfractionated)
    Graded compression stalkings work if proper, truly graded stolkings
    Intermittent pneumatic compression effective if used properly
    IVC filters
                   Basically used if contraindication or failure of anticoagulation
                   Bird’s nest is infrarenal; greenfiel is suprarenal
                   Indications
                            -       anticoagulation contraindicated b/c of active bleeding
                            -       reccurrent venous thrombosis despite adequate
                            -       recurrent PE + RHF in pts that are not candidates for
                            -       prophylaxis of extremely high risk patients

                                       IMPORTANT NOTE
                       *Heparinization should begin ASAP (ie; during
                       diagnostic w/u) if clinical suspicion is moderate -
                       *Consider thrombolysis or other invasive
                       treatments if suspecting massive PE
                                PE IN PREGNANCY

     MC medical cause of death in pregnancy
     Antepartum and post-partum at increased risk
     75% are ante, 25% are post-partum
     Equal distribution of 1st, 2nd, 3rd trimesters
     Septic PE important complication of septic pelvic thromboplebitis
     Ovarian vein thrombosis: adnexal pain, SOB, fever
     Amniotic fluid embolus also a problem

     U/S or IPG: first test, dx if +ve (U/S poor in pregnancy, consider IPG)
     V/Q
                      Risk of V/Q less than that of PE
                      Can do perfusion scan only to decrease rads
                      Complete scan is 50 mrads which is about 5 CXRs
                      Never been ill effects recorded from 50 mrad dose
                      Recommendation for pregnant workers with radiation is 500 mrad
                      Actual toxic fetus dose is thought to be 5 rads
                      EMPTY bladder ASAP (send well hydrated) b/c risk is mostly from
                       acumulation of iv contrast in bladder which is close to uterus
                      No breast feeding X 15hrs after
     Spiral CT: relatively high dose
     Angio: safe
     Radiation: ultrasound or IPG, V/Q, CT, angiogram (least ----> most)
     Heparin: safe, usual dose, LMWH an option
     Warfarin: contraindicated in pregnancy
     Lysis if necc.
    Embolectomy if necc.
    Prophylaxis is important

                                    OTHER EMBOLI

    Etiology: central line, iv, trauma, surgery, dialysis, vaginal insufflation, SCUBA
    Traditional teaching is that fairly substantial amount of air required but has occurred with as
     little as 20 ml from iv line
    Note: can pass lungs unlike PE thus will go arterial
    Presentation: SOB, CP, hypotension, DIC, altered LOC, ARDS
    Mx
                    Turn on side, 100% oxygen
                    Left lateral decubitus: traps air in RA and prevents embolization to arterial
                    Aspirate via swan or right heart catheter
                    Thoracotomy and direct needle aspiration of intracardiac air for full arrest not
                     responding to CPR
                    ? HBOT to decrease size of bubbles

    Etiology: trauma
    Presentation: altered LOC, thrombocytopenia, resp failure
    Can pass lungs and go systemic
    Mx: No heparin, high dose steroids, o2

    Etiology: miscarriage, abruption, trauma, during delivery
    Same presentation: note DIC almost universal
    Supportive mx: consider aminocapric acid, DIC mx, MUST empty uterus
    Septic
    Fat
    Tumor
    Bone marrow
    Bile

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