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Pulmonology > Clin Med Venous Thromboembolism > Flashcards

Clin Med Venous Thromboembolism Flashcards

1
Q

Define venous thromboembolism

A

Blood clot, usually from the deep veins of the leg [also air, fat, tumor, foreign body] that occludes pulmonary vasculature

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2
Q

venous thromboembolism etiology

A
  • major cause of death in the United States, with as many as 650,000 cases/yr
  • > 400,000 diagnoses of PE are missed in the United States annually.
  • most deaths from PE are due to failure to diagnose rather than failure to treat adequately
  • two thirds of patients die within 1 hour of symptom onset; this is the golden hour
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3
Q

mortality in venous thromboembolism

A
  • mortality is 15% w/i 3 mos after occurance
  • in 25% of PE, initial manifestation is death
  • 3rd leading cause of death among hospitalized pt
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4
Q

most important risk factors in venous thromboembolism

A

*Virchow’s Triad
-stasis
-venous injury/endothelial damage
-hypercoaguability
(most pts have multiple)

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5
Q

inherited risks for venous thromboembolism

A
  • factor V Leiden
  • prothrombin gene mutation
  • low protein C, S and antithrombin
  • family hx of VTE
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6
Q

acquired risk factors for venous thromboembolism

A

▪ Smoking* ▪ Obesity* ▪ Immobility* ▪ Age >40 years ▪ Malignancy ▪ Pregnancy ▪ Atherosclerosis* ▪ Trauma, surgery, hospitalization* ▪ Infection ▪ Long haul travel (plane or auto) ▪ Electronic leads, indwelling catheters ▪ Previous DVT ▪ Pelvic or long bone fractures ▪ APL antibody syndrome (venous or arterial) ▪ Hyperhomocysteinemia (venous or arterial)

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7
Q

pts in who there is a high clinical suspicion for underlying disorder

A
  • PE not associated w/ acquired risk factor
  • family hx
  • can be after 1st event
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8
Q

What is initial eval of thrombophilia directed toward?

A 
most common causes: 
▪ Factor V Leiden
▪ Prothrombin gene mutation
▪ APL Ab syndrome
▪Hyperhomocysteinemia

less common:
-protein C&S def., ATIII def.

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9
Q

gas exchange abnormalities in the pathophys of embolus

A
  • gas exchange abnormalities (R–>L shunt leads to hypoxemia and increased a-A gradient)
  • VQ mismatch
  • increased dead space
  • respiratory alkalosis
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10
Q

respiratory alkalosis as a sign of PE

A
  • often is a sign of increased dead space and impaired minute ventilation
  • may suggest massive PE
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11
Q

hemodynamic abnormalities

A

▪ Depends on clot burden/size of embolus
▪ Increased vascular resistance/RV afterload
▪ May cause RV dilation, hypokinesis, tricuspid regurgitation, FAILURE
▪ Interventricular flattening, impaired LV filling
▪ Increased wall stress and ischemia

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12
Q

symptoms of venous thromboembolism

A

▪ Dyspnea ▪ Chest pain (often pleuritic) ▪ Apprehension ▪ Cough** ▪ Hemoptysis ▪ Syncope ▪ Palpitation ▪ Wheezing ▪ Leg pain ▪ Leg swelling

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13
Q

signs of venous thromboembolism

A 
▪ Tachycardia
▪ Tachypnea
▪ Hypoxemia
▪ Accentuated S2
▪ Fever
▪ Diaphoresis
▪ Cardiac murmur
▪ JVD
▪ Cyanosis
▪ Hypotension
▪ Signs of DVT
▪ Homan’s test - not reliable
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14
Q

d-dimer as lab test for venous thromboembolism

A

▪ Non-specific measure of fibrinolysis ▪ Measured by ELISA
▪ High sensitivity (positive in present of disease)
▪ High negative predictive value (disease is absent when test is negative) in the OUTPATIENT setting

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15
Q

when to use d-dimer

A

use in outpatient setting/ER, not inpatient test for ruling out PE

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16
Q

CXR in venous thromboembolism

A
  • usually normal
  • may show collapse, consolidation, small pleural effusion, elevated diaphragm
  • uncommon findings
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17
Q

What are some examples of uncommon findings in imaging for venous thromboembolism

A
  • Westermark’s sign: dilation of vessels proximal to clot

- Hampton’s hump: pleural based opacities w/ convex medial margins

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18
Q

diagnosis w/ ECG in venous thromboembolism

A
  • may show complete or incomplete RBBB
  • T wave inversions are anteriorly S1Q3T3 ***
  • large S wave in lead 1
  • Q wave w/ T wave inversion in lead 3
  • sign of RV strain
  • not as common
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19
Q

V/Q scan in venous thromboembolism

A
  • old standard

- currently reserved for renal impairment, IV contrast allergy, pregnancy, chronic PE

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20
Q

how is V/Q can done?

A
  1. radioactive compound inhaled into lung; normal lung will be evenly distrubuted
  2. radioactive compound injected into vein; no injected material reaches region past PE
  3. “mismatch” of inhaled and injected compounds on the lung scan images = PE
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21
Q

CT scan used as diagnosis in venous thromboembolism

A
  • new standard
  • spiral CT/multislice
  • data suggests that CT is as accurate as invasive angiography (gold standard)
  • negative predictive value of 99%
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22
Q

MRI/MR angiogram as diagnosis in venous thromboembolism

A
  • good at visualizing blood flow

- similar to invasive angiogram

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23
Q

diagnostic algorithm for venous thromboembolism

A

refer to slide 26 for flow chart

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24
Q

risk stratification

A
  • anticoagulate first!
  • hemodynamic stability
  • elevated biomarkers (troponin, BNP)
  • if BNP (brain naturetic peptide) is elevated consider ECHO
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25
Q

ECHO

A

▪ Insensitive for diagnosis but can risk stratify in pts with known PE
▪ In normotensive pts (hemodynamically stable) RV dysfunction is an independent risk factor for early death
▪ McConnell’s sign: regional RV dysfunction w/ free wall apical sparing is throughout to be specific for PE

26
Q

Tx by anticoagulation

A
  • initial anticoagulation w/ UFH or LMWH

- Unfractionated heparin (UFH)

27
Q

Unfractionated Heparin

A

▪ Maintain PTT at 60-80 seconds
▪ Preferred in pts undergoing further therapy (can be reversed)
▪ Weight based nomogram effective for initiating therapy
▪ Can be reversed:
-Preferred in pts undergoing further therapy
-Use in pts with high bleeding risk
▪ Contraindicated in patients with hx of heparin induced
▪ Pregnancy and morbidly obese patient may need factor Xa monitoring
thrombocytopenia (HIT)

28
Q

LMWH (Lovenox) Low molecular weight heparin

A

▪ More predictable response
▪ Dosed at 1mg/kg q12, given subQ
▪ Dose adjustments:
-Kidney disease – give q24 if creatinine clearance <30
-Pregnancy – usually need to monitor factor Xa; some need dose adjustment
▪ Obesity – usually will not dose over 100mg q12:
-May need factor Xa monitoring

29
Q

oral agents for tx

A

-coumadin (Warfarin)

-Non vit. K oral agents (NOACs) : 
▪ Apixaban (Eliquis) 
▪ Rivaroxaban (Xarelto) 
▪ Dabigatran (Pradaxa) 
▪ Edoxavab (Savaysa)
30
Q

Warfarin

A

▪ Vitamin K antagonist
▪ Diet can effect levels
▪ Dose response variation ▪ Dose determined by INR: therapeutic range INR is 2-3
▪ Must have concurrent therapy with UFH/LMWH for 5 days AND until INR >2 for 2 consecutive days
▪ Risk of bleeding

31
Q

Apixaban (Eliquis)

A

▪ Factor Xa inhibitor
▪ No dosing adjustment for age or
renal disease (Dosing is adjusted when used for
atrial fibrillation)
▪ Use with caution in liver disease ▪ Lower incidence of bleeding
▪ 10mg BID x7 days, then 5mg BID
complications

32
Q

Rivaroxaban (Xarelto)

A 
▪ Factor Xa inhibitor
▪ Not easily reversible
▪ Low incidence of GI bleed and  ICH
▪ Cannot use in renal disease
▪ 15mg BID for 21 days, then 20mg qHS: Must be taken with a large meal
33
Q

Dabigatran (pradaxa)

A 
▪ Direct thrombin inhibitor
▪ No dose adjustment for renal
▪ Must have 5 days of therapy with
▪ 150mg BID
disease
UFH/LMWH prior to initiation
34
Q

Edoxaban (Savaysa)

A

▪ Factor Xa inhibitor
▪ Must have 5 days of therapy with UFH/LMWH prior to initiation
▪ Dose adjustments for renal disease
▪ 60mg once daily

35
Q

Fondaparinux (Arixtra)

A

▪ ArgatrobanSynthetic pentasaccharide with anti-Xa activity
▪ No adjustments but cannot be used if CrCl <30 ▪ No risk of HIT
▪ 2.5mg subcutaneous injection once daily

36
Q

Argatroban

A

▪ Direct thrombin inhibitor

▪ Used inpatient in the form of a drip

37
Q

Thrombolytics

A

▪ Only use in case of hemodynamic instability* (rarely used)
▪ t-PA (Altepase): FDA approved for PE; 100mg infused over 2 hrs
▪ No difference in mortality or recurrent PE at 90 days when compared to UFH
▪ Remember contraindications for t-PA (active bleeding, surgery w/i last 30 days, allergy)

38
Q

HIT (heparin induced thrombocytopenia)

A

▪ Formation of IgG against heparin platelet factor IV complex
▪ Both UFH and LMWH can cause this (Less with LMWH)
▪ If suspected stop all heparin containing products

39
Q

when to screen for HIT

A
  • when platelets drop by >50% within 2 weeks of therapy

- Must check serotonin release assay to conform dx

40
Q

What drug to start in the incidence of HIT

A

▪ Start direct thrombin inhibitor

  • Argatroban
  • ondaparinux (Arixtra)
  • lepirudin
41
Q

invasive procedures for embolus

A
  • surgical embolectomy
  • catheter directed embolectomy (angiovac)
  • IVC filter
42
Q

surgical embolectomy

A

▪ Only used for hemodynamic instability AND with contraindication to anticoagulation
▪ Requires a specialized center
▪ Can be effective
▪ Small published numbers

43
Q

Catheter directed embolectomy (AngioVac)

A

▪ Emerging as effective therapy with fibrinolytics cannot be used
▪ Can be performed up to 5 days after event

44
Q

IVC filter

A

-go in through femoral and place filter in IVC
▪ 5% risk of recurrent pulmonary embolus, especially after 6 months
▪ Continue anticoagulation if possible
▪ Remove after 2 months
▪ Complication of leg swelling can occur

45
Q

How to determine which anticoagulation to use?

A
  • CHEST 2016 guidelines: anticoag therapy for 3 mos* unless otherwise indicated
  • recommend using newer agents such as NOACs over Warfarin in the tx of VTE not associated w/ cancer
46
Q

In what diseases/history is a LMWH the recommended agent for tx?

A
  • cancer
  • pregnancy
  • liver disease (NOACs contraindicated)
47
Q

In what diseases/history is Warfarin the recommended agent for tx?

A
  • renal disease

- GI bleed (or Apixaban)

48
Q

In what diseases/history is a UFH the recommended agent for tx?

A

-if thrombolytics used initially

49
Q

In what diseases/history are NOACs that don’t require monitoring the recommended agent for tx?

A

in noncompliance

50
Q

if the 1st thromboembolic event in the context of a reversible risk factor, what is the duration of therapy?

A

3 mos

51
Q

Case: Idiopathic first thromboembolic event.

What is the duration of tx?

A

▪ Treat for 3 months
▪ Further therapy at discretion of clinician:
-Risk factors include age, sex, d-dimer (men have 75% increased risk of recurrence; women 15%)

52
Q

Case: recurrent VTE

What is the duration of tx?

A

▪ Treat for >3 months if bleeding risk is low to moderate

▪ May consider prolonged therapy and evaluate yearly

53
Q

In the presence of continuing risk factors, what is the duration of tx?

A

treat indefinitely

54
Q

risk stratification flow chart

A

refer to slide 43

55
Q

recommendations for using Warfarin

A

▪ Heparin therapy should be continued for at least 5 days
▪ Oral anticoagulation should be overlapped with heparin for 4-5 days
▪ Heparin and Warfarin can be initiated simultaneously: dc heparin on day 5-6 if INR has been therapeutic for 2 consecutive days
▪ Discontinue heparin on day 5-6 if INR has been therapeutic for 2 consecutive
▪ Longer periods of initial heparin therapy is considered in the case of massive PE or iliofemoral thrombosis

56
Q

recommendations for IVC filters

A

▪ No longer recommended in pt on anticoagulation: Only used when anticoagulation is contraindicated
▪ Should be removed if possible

57
Q

What to add to tx after stopping anticoagulation

A

consider adding ASA if no contraindication

58
Q

general tx in low risk PE

A

-treat at home vs early hospital discharge (3 days):
▪ Controversial
▪ Clinically stable with good cardiopulmonary reserve
▪ Pt has no contraindication to NOAC
▪ Consider the patient

59
Q

Tx when there is a recurrence of VTE while on anticoagulation

A

▪ New recommendation is to treat with Lovenox for one month
▪ Evaluate reasons for failure (compliance, new active malignancy, true recurrence)
▪ If recurrent VTE in a cancer patient, increase Lovenox dose by ¼ or 1/3

60
Q

how to prevent thromboembolism in inpatient setting

A 
▪ LMWH: 
-40mg subQ once daily
-30mg subQ once daily if CrCl <30 
-30mg subQ BID if BMI >40 
▪ UFH
▪ Graded compression stocking (TED hose) 
▪ Sequential compression devices (SCDs)
61
Q

prognosis of thromboembolism

A

▪ Depends on underlying cause rather than PE itself
▪ Good outcomes when diagnosed early and treated adequately
▪ Perfusion defects resolve in most

Pulmonology (11 decks)

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