83 -- DVT and PE

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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

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

http://www.bcltechnologies.com/easypdf/

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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)

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 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

DEEP VENOUS THROMBOSIS

INTRODUCTION/PATHOPHYSIOLOGY

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

PRESENTATION

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

Signs


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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 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

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

Baker’s cyst

DIAGNOSIS OF DVT

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 markedincrease 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)


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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

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 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)


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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

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 doesn’t work

MONDOR’S 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 withwalking (distinguishes from arterial insuff)

Mx: leg elevation, stockings

COMPLICATIONS OF DVT

PE

Chronic Venous Insufficiency

Postphlebitic syndrome: chronic pain, ulceration, dermatitis

Recurrent DVT/PE


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Phlegmasia dolens

PULMONARY EMBOLIHEMODYNAMIC RESULTS

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 fluids is characteristic of RV involvementb/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 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

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

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


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RISK FACTORS

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, Recentimmobilization, 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 (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 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 PE and 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

NON-INVASIVE IMAGING MODALITIES

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

V/Q SCANNING

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)

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,

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 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 inperfusion)


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POST - TEST PROBABILITY OF PE WITH COMBINATION OFPRE - TEST PROBABILITY AND V/Q SCANNING FROM PIOPED DATA

PRE - TESTPROB

NORMAL V/Q LOW PROBV/Q

INTERMEDPROB V/Q

HIGH PROBV/Q

LOW 2% 4% 16% 56%

MOD 6% 16% 28% 88%

HIGH - 40% 66% 96%

POST - TEST P PROBABILITY OF PE WITH COMBINATION OF

PRE - TEST PROBABILITY AND V/Q SCANNING FROM McMASTER DATA

PRE - TEST PROB NORMAL NON - HIGH HIGH PROB

LOW 1.2% 3% 100%

MOD 0% 12% 100%

HIGH 13% 47% 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 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


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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 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(don’t 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 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 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 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

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


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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 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

½ hr then 35 mg over one hour) PEA ARREST: rt-PA 50 mg iv bolus


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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

Bird’s 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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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 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

system


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

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


Documents

83 -- DVT and PE