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DVT/PE - INTRO EPIDEMIOLOGY/GENERAL COMMENTS Venous ThromboEmbolic (VTE) disease = combination of DVT, PE, superficial vein thrombosis, chronic venous insufficiency (spectrum of same disease) 3 rd  MCC of death in USA 2 nd  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 KEY POINTS 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 PATHOPHYSIOLOGY 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

83 -- DVT and PE

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  • 8/12/2019 83 -- DVT and PE



    EPIDEMIOLOGY/GENERAL COMMENTS Venous ThromboEmbolic (VTE) disease = combination of DVT, PE, superficial vein

    thrombosis, chronic venous insufficiency (spectrum of same disease)

    3rdMCC of death in USA

    2ndMCC 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

    ALLDVTs 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


    VIRCHOWS 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

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    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, hyperhomocysteinemiaacquired 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


    Immobilized limb

    Recent surgery


    NOTES ON RISK FACTORS Lack of Natural anticoagulants: Protein C, Protein S, Antithrombin III

    Deficiency of natural fibrinolytic system: abnormal or lack of tissue plasminogenactivators (occurs in endothelial cells normally) or u-plasminogen activator (produced inrenal cells; aka urokinase); can also have lack of or abnormal plasminogen (convertedinto 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

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    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



    Anatomy: superficial leg veins pass through fascia by perforating connector veins toenter 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 propagatedlarger 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


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    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 Homans sign: true Homans sign is resting plantarflexion in a relaxed foot Pseudohomans 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

    Bakers cyst


    Clinical Scoring Systems Wells 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 doesnt 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 markedincrease 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)

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    Measures changes in lower extremity volume as function of venousoutflow

    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

    SIMPLIRED Latex Agglutination assay Cheaper Lower sensitivity; higher specificity

    ELISA Enzyme Linked Immuno Assay More expensive

    Anderson Hematology 2000 Compared overall accuracy


    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)

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    Diabetic retinopathy with recent hemorrhage Mild HIT CNS cancer

    NOT CONTRAINDICATIONS TO HEPARIN 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 doesnt 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 withwalking (distinguishes from arterial insuff)

    Mx: leg elevation, stockings



    Chronic Venous Insufficiency

    Postphlebitic syndrome: chronic pain, ulceration, dermatitis

    Recurrent DVT/PE

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    Phlegmasia dolens


    Pulmonary artery obstruction, release of vasoconstrictors, elevated pulmn vascresistance resulting in decreased blood flow to that spot and creates dead space. Thisis probably less important than initially thought.

    Bronchial arterioles anastamose with pulmonary arteries thus fully obstructive PE willusually NOT cause pulmonary infarction even when subsegmental arteries arecompletely blocked

    Also, the lung shunts blood and alters ventilation which creates significant V/Q mismatchwhich 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, andischemia of the RV

    > 50% of pulmonary vascular tree occlusion causes significant pulmonaryHTN and acute cor-pulmonale

    Tricuspid regurgitation will occur if pulmonary arterial pressure > 40mmHg

    RV hypokinesis has been found by echo in 40% of pts w/ normal systolicblood pressure.

    Hypotension responsive to fluidsis characteristic of RV involvementb/c the RV is very dependant on preload for its cardiac output.

    Nitroglycerin is contraindicated.


    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 heartfailure 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 normalventilation thus V/Q > 1 ----> normal of slight increase Pa02 and normal orslight decreased PC02

    Large volume of blood through non-blocked areas: high flow with normalventililation thus V/Q < ------> poor exchange because of too muchvolume thus low Pa02 and high PC02

    In effect, the majority of the blood has become shunted through anunventilated lung

    Other cause of altered gas exchange Hyperventilation Atelectasis secondary to surfactant loss Transudation of alveolar fluid :. rales, rubs

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    Thrombophelbitis 32

    LE edema 24

    Murmur 23

    Cyanosis 14 Other: palpable P2, RV heave, RV lift


    Pmhx DVT/PE

    Risk factors

    May be non-thrombotic: fat, tumor, air, hair, talc, cotton, amniotic


    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 cannotr/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


    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

    dont 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

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    See Virchows 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 doesnt work

    Most important risk factors: previous DVT/PE is most important, recent surgery, Recentimmobilization, Recent pregnancy, Underlying Ca


    Laboratory INR/PTT: normal (think Lupus Anti Coagulant with long PTT) Hb: normal (look for polycythemia) WBC: normal or increased (doesnt 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 SPECIFICITYSimpliRED 80 - 85% 70 - 90%Whole Bld Aggn 90 - 95% 40 - 90%ELISA 95 - 100% 30 - 60%

    ABG NO PREDICTIVE VALUE 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 PEand should not be used to determine whowork 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

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    PIOPED: Normal A-a gradient + PC02 > 36 has 98% NPVfor 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 Hamptons Hump = peripheral wedge shaped (apex toward hilum)

    infiltrate corresponding to peripheral pulmonary infarction Fleishners Sign = large, dilated, sausage - shaped pulmonary artery

    Westermarks sign = focal oligemia distal to dilate pulmonary artery Pallas 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 signof 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

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    DVT w/o symptoms/signs of PE Repeat evaluation before d/c anticoagulation with irreversible risk factor(s)


    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,

    bronchospasm 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 Dont overdx: low suspcion and high prob V/Q: angiogram indicated Dont underdx: high suspicion and nondiagnostic V/Q: angiogram


    Serial scan is an option if no angiogram available (look for change inperfusion)

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    LOW 2% 4% 16% 56%

    MOD 6% 16% 28% 88%

    HIGH - 40% 66% 96%




    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

    ----> 4thgeneration: sensitivity 86%

    Peripheral vessles = > 4thgeneration: 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 dont 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

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    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 3rdorder)

    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


    Monoclonal AB

    Computer assisted V/Q interpretation

    Dielectric imaging

    Pulmn capillary volume

    CT venography MR venographySUPPORTIVE MANAGEMENT OF PE

    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 volumemay really increase right sided pressure and cause septal shift and worsen hypotension(dont 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 notdecrease 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)

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    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 doesnt 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 ofHIT, 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 untilheparin 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



    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

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    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,

    cardiomyopathy) 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 aminocaproicacid (plasminogen activator inhibitor - 5 gm iv over 30 min then 1 gm/hr ivuntil bleeding stops)

    Administration UNSTABLE: rt-PA 100 mg iv over 2hrs (or 15 mg bolus then 30 mg over

    hr then 35 mg over one hour) PEA ARREST: rt-PA 50 mg iv bolus

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    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

    Birds nest is infrarenal; greenfiel is suprarenal Indications

    anticoagulation contraindicated b/c of active bleeding reccurrent venous thrombosis despite adequate

    anticoagulation recurrent PE + RHF in pts that are not candidates for

    thrombolysis prophylaxis of extremely high risk patients

    IMPORTANT NOTE*Heparinization should begin ASAP (ie; during

    diagnostic w/u) if clinical suspicion is moderate -high*Consider thrombolysis or other invasivetreatments if suspecting massive PE

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    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, 3rdtrimesters

    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: contraindicatedin pregnancy

    Lysis if necc.

    Embolectomy if necc.

    Prophylaxis is important



    Etiology: central line, iv, trauma, surgery, dialysis, vaginal insufflation, SCUBA

    Traditional teaching is that fairly substantial amount of air required but has occurred withas 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


  • 8/12/2019 83 -- DVT and PE


    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





    Bone marrow