Pulmonary embolism

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See Pulmonary Embolism in Pregnancy for pregnancy specific information.[1]

Background

Clinical Spectrum of Venous thromboembolism

Only 40% of ambulatory ED patients with PE have concomitant DVT[2][3]

PE Types

Massive

  • Sustained hypotension (sys BP <90 for at least 15min or requiring inotropic support)
  • Pulselessness
  • Persistent profound bradycardia (HR <40 with signs of shock)

Submassive

  • Sys BP >90 but with either RV dysfunction or myocardial necrosis
  • RV dysfunction
    • RV dilation or dysfunction on TTE
    • RV dilation on CT
    • Elevation of BNP (>90)
    • ECG: new complete or incomplete RBBB, anteroseptal ST elevation/depression or TWI[4]
    • Myocardial necrosis: Troponin I >0.4

Non-Massive

  • No hemodynamic compromise and no RV strain

Sub-Segmental

  • Limited to the subsegmental pulmonary arteries

Clinical Features

Signs

  • Dyspnea
  • Pleurisy
  • Cough
  • Leg pain
  • Wheezing
  • Hempotysis

Symptoms

  • Tachypnea ~73% of the time
  • Leg swelling
  • Rales
  • Wheeze
  • Tachycardia
  • JVD

Differential Diagnosis

Chest pain

Critical

Emergent

Nonemergent

Shortness of breath

Emergent

Non-Emergent

Evaluation

  • ECG
    • Abnormal in 70% of PE patients[5]
    • Sinus tachycardia is most common finding
    • TWI in ant/sept leads + inf leads[6]
    • Nonspecific ST changes, S1Q3T3 (develops due to strain on RV)
    • RBBB or new incomplete RBBB.[7]
    • New right axis deviation
    • Atrial fibrillation
  • CXR
    • Abnormal in 70%
    • Atelectasis is most common (esp >24 hrs after onset of symptoms)
    • Pleural effusion
    • Hampton's Hump
    • Westermark's sign[8]
  • TTE
    • Eval R heart strain (bowing of septum into LV)
    • McConnel's sign (akinesis of RV base/free wall with sparing of apex)
    • Lateral right ventricular wall diameter of <5mm is suggestive of acute pulmonary hypertension while >5mm is suggestive of chronic pulmonary hypertension[9]
Hampton's Hump

Wells Criteria

Clinical Features Points
Symptoms of DVT (leg swelling and pain with palpation) 3.0
PE as likely as or more likely than an alternative diagnosis 3.0
HR >100 bpm 1.5
Immobilization for >3 consecutive days or surgery in the previous 4 weeks 1.5
Previous DVTor PE 1.5
Hemoptysis 1.0
Malignancy (receiving treatment, treatment stopped within 6 mon, palliative care) 1.0

Wells Score

Pre-test Probability Total Points
Low < 2.0
Moderate 2.0-6.0
High > 6.0

Less common risks

  • HIV (protein wasting nephropathy)
  • Nephrotic Syndrome
  • SLE with anti-cardiolipan Ab
  • Exogenous hormones (specifically estrogen)
  • Factor V Leiden
  • Antithrombin III deficiency
  • Protein C deficiency
  • Protein S deficiency
  • Hyperhomocysteinemia

Workup by Pretest Probability

  • Objective criteria (Geneva, Wells, etc.) is equal to gestalt in assessing pre-test probability[10] (ACEP Level B)

Low Probability

  • D-dimer NPV is 99.5%[11]
  • If low prob and PERC Rule negative, then no workup[12] (ACEP Level B)
  • If low prob and PERC Rule positive, then d-dimer[13] (ACEP Level B)
  • Avoid CT pulmonary angiography in low pretest probability patients that are either PERC rule negative or have a negative d-dimer
  • Age-adjusted D-Dimer in patients >50 yrs old (Age x 10 in FEU or Age x 5 in D-DU) has increased specificity without changing sensitivity[14][15]
    • Check your hospital's reference units (500 ng/L FEU = 250 ng/L D-DU)
Pretest - LR Posttest
Wells < 4 + PERC 12% 0.12 1.6%
Wells < 4 + Neg Dimer 12% 0.01 0.14%
Wells < 4 + AA Dimer 12% 0.06 0.81%
Wells < 2 + PERC 2% 0.01 0.24%
Wells < 2 + Neg Dimer 2% 0.06 0.02%
Wells < 2 + AA Dimer 2% 0.12 0.12

Moderate Probability

  • D-dimer
    • However, it is unclear whether d-dimer alone is sufficient to rule-out PE[16] (ACEP Level C)

High Probability

  • Consider anticoagulation before imaging!
  • Imaging
    • CTA if GFR >60
    • V/Q if GFR <60
      • Will be nondiagnostic if patient has effusion, pneumonia, or other airspace disease
  • If imaging negative, perform additional diagnostic testing (eg, D-dimer, LE vasc US, VQ, traditional pulmonary arteriography) prior to exclusion ofVTE disease[17] (ACEP Level C)
    • A negative d-dimer in combination with a negative CTA theoretically provides a posttest probability of VTE less than 1%

Bedside Ultrasound

  • Ultrasound can help diagnosis in equivocal cases
  • Assess for right ventricular strain (RVS) and McConnell's sign
  • RVS is associated with statistically significant worse outcome[18]

Other Modalities

  • SPECT
    • Combination of noncontrast CT chest with V/Q scan
    • Avoidance of contrast for patients with renal injury
    • As sensitive as CTPA and more sensitive than planar V/Q scanning[19]

Management

Supportive care

  • Give IVF as necessary to increase preload while frequently assessing volume status

Anticoagulation

  • Treatment options include any of the following anticoagulations which are indicated for all patients with confirmed PE or high clinical suspicion (do not wait for imaging).
  • The Feb. 2016 CHEST Guideline recommends clinical surveillance over anticoagultation for subsegmental PE with no proximal DVTat low risk for recurrent VTE based on level 2C evidence[20]
  • LMWH SC
    • 1st line for most hemodynamically stable patients
    • Contraindicated in renal failure
    • Enoxaparin 1mg/kg SC q12h
    • Dalteparin 200 IU/kg SC q24h, max 18,000 IU
  • Unfractionated Heparin
    • 80 units/kg bolus; then 18 units/kg/hr
    • Check PTT after 6hr; adjust infusion to maintain PTT at 1.5-2.5x control
    • Benefit of Heparin is the short half life and easy ability to turn off the infusion. Consider
    • Patients with morbid obesity or anasarca may have poor sc absorption with LMWH
    • No need for renal dosing
    • The prefered anticoagulation if thrombolysis is being considered or if there is a bleeding risk or trauma and anticoagulation will need to be emergently discontinued
  • Dabigatran
    • A direct thrombin inhibitor
    • Approved by the FDA in 2014 for the treatment of DVTand PE
    • Dabigatran was noninferior to warfarin in reducing DVTand PE[21][22]
  • Rivaroxaban
    • Factor Xa inhibitors
    • Approved by the FDA in November 2012 for the treatment of DVTor PE
    • Associated with less bleeding, particularly in elderly patients and those with moderate renal impairment compared to standard treatments[23][24]
  • Apixaban
    • Factor Xa inhibitor
    • Approved for treatment of PE in August 2014
    • Studies show 16% reduction in VTE related death compared to standard therapy[25][26]
  • Vit K antagonist - Coumadin
    • 3-6 mo if time limited risk factor (post-op, trauma, estrogen use)
    • 6 mo - life if idiopathic etiology or recurrent
    • INR target 2.5
    • Temporary hypercoagulable state for approx 5 days
    • Initial dose is 5 mg PO

Thrombolysis

  • Major controversy exists regarding thrombolytic therapy in submassive PE. Therapy should be individualized to patients.[27][28][29] 'The mortality benefit may be greatest in patients with right ventricular dysfunction. [30]
  • Bleeding risk is increased with increasing age especially in the group ≥ 65 yo[31]

Indications

  • Patients with massive PE and acceptable risk of bleeding complications
  • Patient with submassive PE with evidence adverse prognosis + low risk of bleeding complications
    • Hemodynamic instability
    • Worsening respiratory insufficiency
    • Severe Right Ventricular dysfunction
    • Major myocardial necrosis

Thrombolytic Instructions

  • Review contraindications
  • Ongoing CPR from 2010 AHA Guidelines is not an absolute contraindication, and some studies suggest permiting 15 min of CPR to allow thrombolysis to work[32]
  • Discontinue heparin during infusion
  • Administration regimens differ widely in the literature, options not in any particular order, include:
    • Alteplase 0.6 - 1 mg/kg or 100 mg with any of the three possibilities
      • Two 50 mg boluses, 30 min apart[33][34]
      • 15 mg bolus, followed by 85 mg over 90 min[35]
      • 100 mg over 15 min[36]
    • Tenecteplase in cardiac arrest at 50 mg bolus or 0.5 mg/kg bolus in cardiac arrest[37][38][39]
  • After infusion complete measure serial aPTTs
    • Almost all studies of thrombolysis administration included heparin anticoagulation
    • Once value is <2x upper limit restart anticoagulation

Absolute contraindicatimewons

  • Any prior intracranial hemorrhage,
  • Known structural intracranial cerebrovascular disease (e.g. AVM)
  • Known malignant intracranial neoplasm
  • Ischemic stroke within 3mo
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis
  • Recent surgery encroaching on the spinal canal or brain
  • Recent closed-head or facial trauma with radiographic evidence of bony fracture or brain injury

Relative contraindications

  • Age >75 years
  • Current use of anticoagulation
  • PE in Pregnancy
  • Noncompressible vascular punctures
  • Traumatic or prolonged CPR (>10min)
  • Recent internal bleeding (within 2 to 4 weeks)
  • History of chronic, severe, and poorly controlled hypertension
  • Severe uncontrolled hypertension on presentation (sys BP >180 or dia BP >110)
  • Dementia
  • Remote (>3 months) ischemic stroke
  • Major surgery within 3 weeks

IVC Filter

  • Indications
    • anticoagulation contraindicated in patient with PE
    • failure to attain adequate anticoagulation during treatment

Disposition

  • Patients with significant clot burden generally require admission for anticoagulation
  • Consider discharge in low risk patients with peripheral PE[40]

Prognosis

The Pulmonary Embolism Severity Index (PESI)[41]

Prognosis Variable Points Assigned
Demographics
Age +Age in years
Male +10
Comorbid Conditions
Cancer +30
Heart Failure +10
Chronic Lung Diseae +10
Clincal Findings
Pulse >110 b/min +20
sBP < 100 +30
RR > 30 +20
Temp <36 C +20
AMS +60
Art O2 Saturation <90% +20
Risk Class 30-Day Mortality Total Point Score
I 1.60% <65
II 3.50% 66-85
III 7.10% 86-105
IV 11.40% 106-125
V 23.90% >125

See Also

{{Thrombolysis Submassive PE Trials}}

External Links

References

  1. ↑ D-Dimer Concentrations in Normal Pregnancy: New Diagnostic Thresholds Are Needed. Kline et all. Clinical Chemistry May 2005 vol. 51 no. 5 825-829 http://www.clinchem.org/content/51/5/825.long
  2. ↑ Righini M, Le GG, Aujesky D, et al. Diagnosis of pulmonary embolism by multidetector CT alone or combined with venous ultrasonography of the leg: a randomised non-inferiority trial. Lancet. 2008; 371(9621):1343-1352.
  3. ↑ Daniel KR, Jackson RE, Kline JA. Utility of the lower extremity venous ultrasound in the diagnosis and exclusion of pulmonary embolism in outpatients. Ann Emerg Med. 2000; 35(6):547-554.
  4. ↑ David Da Costa. Bradycardias and atrioventricular conduction block BMJ. 2002 March 2; 324(7336): 535–538
  5. ↑ Marchick, MR et al. 12-lead ECG findings of pulmonary hypertension occur more frequently in emergency department patients with pulmonary embolism than in patients without pulmonary embolism. Ann Emerg Med. 2010 Apr;55(4):331-5.
  6. ↑ Kosuge M, Kimura K, Ishikawa T, et al. Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T waves. Am J Cardiol 2007; 99: 817–821
  7. ↑ Shopo, JD et al. Findings from 12-lead electrocardiography that predict circulatory shock in pulmonary embolism; a systematic review and meta-analysis. Acad Emerg Med. 2015 Oct;22(10):1127-37
  8. ↑ Sreenivasan S, Bennett S, Parfitt VJ. Images in cardiovascular medicine. Westermark's and Palla's signs in acute pulmonary embolism. Circulation. 2007 Feb 27;115(8):e211. full text
  9. ↑ Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010; 23(7):685-713.
  10. ↑ ACEP Clinical Policy for Pulmonary Embolism full text
  11. ↑ Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple
  12. ↑ ACEP Clinical Policy for Pulmonary Embolism full text
  13. ↑ ACEP Clinical Policy for Pulmonary Embolism full text
  14. ↑ Schouten, HJ, et al. Diagnostic accuracy of conventional or age adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis. BJM. 2013; 346:f2492.
  15. ↑ Adams, D, et al. Clinical utility of an age-adjusted D-dimer in the diagnosis of venous thromboembolism. Ann Emerg Med. 2014; 64:232-234.
  16. ↑ ACEP Clinical Policy for Pulmonary Embolismfull text
  17. ↑ ACEP Clinical Policy for Pulmonary Embolism full text
  18. ↑ Taylor, RA, et al. Point-of-care focused cardiac ultrasound for prediction of pulmonary embolism adverse outcomes. The Journal of Emergency Medicine. 2013; 45(3):392–399.
  19. ↑ Lu Y, Lorenzoni A, Fox JJ, Rademaker J, Vander Els N, Grewal RK, Strauss HW, Schöder H. Noncontrast perfusion single-photon emission CT/CT scanning: a new test for the expedited, high-accuracy diagnosis of acute pulmonary embolism. Chest. 2014 May;145(5):1079-88
  20. ↑ Kearon, Clive, et al. "Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report." Chest (2016).[fulltext]
  21. ↑ Schulman S, Kearon C, Kakkar AK, et al. Dabigatran versus warfarin in the treatment of acute venous thromboembolism. N Engl J Med. 2009; 361(24):2342-52.
  22. ↑ Schulman S, Kakkar AK, Goldhaber SZ, et al. Treatment of acute venous thromboembolism with dabigatran or warfarin and pooled analysis. Circulation. 2014; 129(7):764-72.
  23. ↑ Hughes S. Rivaroxaban Stands up to standard anticoagulation for VTE treatment. Medscape Medical News. December 13, 2012.
  24. ↑ Buller HR, on behalf of the EINSTEIN Investigators. Oral rivaroxaban for the treatment of symptomatic venous thromboembolism: a pooled analysis of the EINSTEIN DVTand EINSTEIN PE studies [abstract 20]. Presented at: 54th Annual Meeting and Exposition of the American Society of Hematology; December 8, 2012; Atlanta, Ga.
  25. ↑ Agnelli G, Buller HR, Cohen A, et al. Oral apixaban for the treatment of acute venous thromboembolism. N Engl J Med. 2013; 369(9):799-808.
  26. ↑ Agnelli G, Buller HR, Cohen A, Curto M, Gallus AS, Johnson M, et al. Apixaban for extended treatment of venous thromboembolism. N Engl J Med. 2013; 368(8):699-708.
  27. ↑ Elliott C. et al. Fibrinolysis of Pulmonary Emboli — Steer Closer to Scylla.
  28. ↑ Sharifi M et al. Moderate pulmonary embolism treated with thrombolysis (from the “MOPPETT trial). J Cardiol 2013; 111: 273-7
  29. ↑ Meyer G. Fibrinolysis for patients with intermediate-risk pulmonary embolism. NEJM 2014; 370(15): 1402-1411
  30. ↑ Chatterjee. S et al. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis. JAMA 2014; 311(23):2414-21. PubMed ID: 24938564.
  31. ↑ EBQ:Thrombolysis_in_Pulmonary_Embolism_Metanalysis#Outcomes
  32. ↑ Hayes BD. What’s the Code Dose of tPA? Updated August 2016. https://www.aliem.com/2013/whats-code-dose-of-tpa/.
  33. ↑ Kürkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med. 2000;160(10):1529-1535.
  34. ↑ Ruiz-Bailén M, Aguayo-de-Hoyos E, Serrano-Córcoles M, et al. Thrombolysis with recombinant tissue plasminogen activator during cardiopulmonary resuscitation in fulminant pulmonary embolism. A case series. Resuscitation. 2001;51(1):97-101.
  35. ↑ Kürkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med. 2000;160(10):1529-1535.
  36. ↑ Abu-Laban R, Christenson J, Innes G, et al. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med. 2002;346(20):1522-1528.
  37. ↑ Fatovich D, Dobb G, Clugston R. A pilot randomised trial of thrombolysis in cardiac arrest (The TICA trial). Resuscitation. 2004;61(3):309-313.
  38. ↑ Bozeman W, Kleiner D, Ferguson K. Empiric tenecteplase is associated with increased return of spontaneous circulation and short term survival in cardiac arrest patients unresponsive to standard interventions. Resuscitation. 2006;69(3):399-406.
  39. ↑ Böttiger B, Arntz H, Chamberlain D, et al. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008;359(25):2651-2662.
  40. ↑ Vinson DR, Zehtabchi S, Yealy DM. Can selected patients with newly diagnosed pulmonary embolism be safely treated without hospitalization? A systematic review. Ann Emerg Med. 2012; 60:651-662.
  41. ↑ Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med. 2005;172:1041-1046.
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