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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) 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 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
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

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, postpartum, 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)

MOST COMMON RISK FACTORS Hx of DVT/PE Cancer Immobilized limb Recent surgery Pregnancy NOTES ON RISK FACTORS 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


INTRODUCTION/PATHOPHYSIOLOGY 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 PRESENTATION Symptoms Signs

Leg swelling, pain, usually with No hx of trauma DVT risk factors as per PE but emphasis on leg immobilization, etc

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

DIFFERENTIAL DIAGNOSIS OF LEG PAIN 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 DIAGNOSIS OF DVT 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 marked increase in venous diameter with compression (> 4 mm) R/O DVT: fully compressible veins or diameter increased > 1mm from size on previous ultrasound

NOTHING ON HX OR PHYSICAL EXAM CAN RULE OUT A DVT


IPGs (Plethysmography) - Maximum Venous Outflow (MVO)

Venography Other

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 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 Nuclear Venogram:Inject dye into foot vein CT venography or MR venography

D-DIMER AND DVT 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

ASSAY SIMPLIRED VIDAS (ELISA)

SENSITIVIY 80 (66-90) 100 (93-100)

SPECIFICITY 94 (83-99) 41 (27-56)

NPV 82 (70-90) 100 (83-100)

PPV 93 (81-99) 63 (52-74)

MANAGEMENT General LMWH

Heparin if testing delayed > 2hrs UFH largely replaced by LMWH Bedrest INCREASE risk of PE b/c of thrombus propagation 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 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)

Warfarin

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 ABSOLUTE CONTRAINDICATIONS TO HEPARIN Active internal bleeding (even if minor) Active external bleeding Severe Prior H.I.T. (For unfractionated heparin) RELATIVE CONTRAINDICATIONS TO HEPARIN > choose UFH vs LMWH! 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 NOT CONTRAINDICATIONS TO HEPARIN Recent surgery Recent major vessel puncture Pregnancy Endocarditis

PHLEGMASIA DOLENS 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 MONDORS SYNDROME Thrombophlebitis of subcutaneous veins from breast > axilla Painful and difuguring to breast THROMBOPHLEBITIS 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 CHRONIC VENOUS INSUFFICIENCY 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 COMPLICATIONS OF DVT PE Chronic Venous Insufficiency Postphlebitic syndrome: chronic pain, ulceration, dermatitis Recurrent DVT/PE

Phlegmasia dolens

PULMONARY EMBOLI
HEMODYNAMIC RESULTS 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 contraindicated.

RESPIRATORY EFFECTS 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 COR PULMONALE Chronic PE is an important cause Pulmonary arterial endothelium doesnt 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 cant increase volume Decreased capacitance and increased resistance Increase right heart pressure and right heart failure CLINICAL SYNDROMES OF PULMONARY EMBOLI 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 SIGNS AND SYMPTOMS 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 COMMON physical exam Fever > 37.8 43 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

PRESENTATIONS 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 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

RISK FACTORS 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, Recent immobilization, Recent pregnancy, Underlying Ca

NON-IMAGING DIAGNOSTIC MODALITIES 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 SimpliRED Whole Bld Aggn ELISA 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 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 SENSITIVITY 80 - 85% 90 - 95% 95 - 100% SPECIFICITY 70 - 90% 40 - 90% 30 - 60%

ECG

PIOPED: Normal A-a gradient + PC02 > 36 has 98% NPV for pulmonary embolism with normal underlying lungs Compensation can increase Pa02 :. gradient not seen

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

NON-INVASIVE IMAGING MODALITIES 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 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 V/Q SCANNING Indications

Suspected PE w/o other proven dx

Technique

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 indicated Serial scan is an option if no angiogram available (look for change in perfusion)

POST - TEST PROBABILITY OF PE WITH COMBINATION OF PRE - TEST PROBABILITY AND V/Q SCANNING FROM PIOPED DATA PRE - TEST PROB LOW MOD HIGH NORMAL V/Q 2% 6% LOW PROB V/Q 4% 16% 40% INTERMED PROB V/Q 16% 28% 66% HIGH PROB V/Q 56% 88% 96%

POST - TEST P PROBABILITY OF PE WITH COMBINATION OF PRE - TEST PROBABILITY AND V/Q SCANNING FROM McMASTER DATA PRE - TEST PROB LOW MOD HIGH NORMAL 1.2% 0% 13% NON - HIGH 3% 12% 47% HIGH PROB 100% 100% 33%

SPIRAL CT 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 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

ANGIOGRAM 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

OTHER IMAGING Fiberoptic angioscopy Digital subtraction angio MRI Monoclonal AB Computer assisted V/Q interpretation Dielectric imaging Pulmn capillary volume CT venography MR venography SUPPORTIVE 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 volume may 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) ANTICOAGULATION FOR PE 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 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 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

CONTRAINDICATIONS TO THROMBOLYSIS AND HEPARIN 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

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

SURGICAL 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

PREVENT RECURRENCE 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 invasive treatments if suspecting massive PE

PE IN PREGNANCY
INTRODUCTION 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 CLINICAL 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
AIR EMBOLISM 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 system

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

FAT EMBOLISM Etiology: trauma Presentation: altered LOC, thrombocytopenia, resp failure Can pass lungs and go systemic Mx: No heparin, high dose steroids, o2 AMNIOTIC FLUID EMBOLISM Etiology: miscarriage, abruption, trauma, during delivery Same presentation: note DIC almost universal Supportive mx: consider aminocapric acid, DIC mx, MUST empty uterus OTHER EMBOLI Septic Fat Tumor Bone marrow Bile

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