Bui duy icu

Stop That Clot! Management of Massive

Pulmonary Embolism

Mai Bui-Duy, MD

“Doc, I have…”

• Chest pain: central, “crushing,” pleuritic

• Shortness of breath

• Syncope

QuickTime and aª decompressor

are needed to see this picture.

What Makes a “Massive” PE So Massive?

http://www.hindawi.com/journals/crim/2010/862028/fig1/



What Makes a “Massive” PE So Massive?



• Patients with PE & subsequent RV dysfunction can be roughly divided in 2 categories– high-risk individuals w/ ‘massive’ PE with SBP</=90 or

pressure drop of >40 mmHg x 15 min– and lower-risk patients with ‘submassive’ PE, whose BP is

preserved but whose RV function is impaired

• Massive PE is <5% of all PEs, but high mortality– Management Strategies and Prognosis of Pulmonary

Embolism Trial-3 (MAPPET-3): • PE-related mortality in those with cardiac arrest: 60%• PE-related mortality in those with cardiogenic shock: 23%• PE-related mortality in those with arterial hypotension: 14%

Risk Stratification

• Studied in hemodynamically stable patients• Meta-analysis: elevated BNP & pro-BNP had

increased risk of adverse in-hospital outcome • Meta-analysis: PE and elevated troponin had

increase in:– short-term risk of death by factor of 5.2 &– increase in risk of death from PE by factor of 9.4

Klok et al. Am J Respir Crit Care Med 2008;178:425-30Becattini et al. Circulation. 2007; 116: 427-433

Making The Diagnosis: CT• Multidetector CT: used

to diagnose or r/o PE• Can also show RV size,

which can be used for prognosis

• In one restrospective study, value <1.0 of RV/LV diameter had 100% negative predictive value for uneventful outcome



Van der Meer Radiology. 2005 Jun;235(3):798-803

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Making The Diagnosis: TTE



• Typical findings: RV hypokinesis, RV dilatation, intraventricular septal flattening w/ paradoxical motion toward LV, TR, pulmonary HTN, loss of inspiratory collapse of IVC

Making The Diagnosis: TTE

• McConnell’s sign: distinct regional pattern of right ventricular dysfunction, with akinesia of the mid free wall but normal motion at the apex– 94% specificity for acute PE

• RV hypokinesis & dilatation found to be independent predictors of 30-day mortality (in hemodynamically stable)

• Ventricular septal bowing predictor of death related to PEMcConnell et al. Am J Cardiol. 1996 Aug 15;78(4):469-73Kucher et al. Arch Intern Med 2005;165:1777-81.Sanchez et al. Eur Heart J 2008:29:1569-77.Araoz et al. Radiology 2007;242:889-97.

Initial Supportive Treatment

• Provide oxygen & pain control

• Be judicious with IVF since volume overload can worsen RV failure; maintain CVP 15–20 cm H2O

• May need pressors: consider dopamine, Levophed or epinephrine for inotropic and vasopressor effects





Treatment: Medicine

Wan et al. Circulation 2004;110, 744-749.Kucher et al. Circulation 2006;113, 577-582.



• Heparin and/or systemic thrombolysis?• 1st RCT: streptokinase+heparin vs heparin alone

(n=8); survival greater in streptokinase arm• 2hr infusion regimens of streptokinase (1.5 million

units), urokinase and rt-PA (100 mg) followed by a heparin infusion have similar efficacy & safety

• Meta-analysis: in trials including massive PE & cardiac shock, thrombolysis a/w significant reduction in death and recurrent PE compared w/ heparin

• ICOPER: of those w/ masive PE (n=108): no difference in mortality or PE recurrence @ 90 days between thrombolysis vs heparin

Treatment: Medicine

• Risk of bleeding!• Contraindications: intracranial mass, h/o ICH, CVA

or neurosurgical procedure within past 2 months, recent major trauma, severe uncontrolled HTN, ongoing suspicion for aortic dissection, active or recent respiratory/GI/GU bleeding…

• ICOPER: risk of ICH up to 3%

Kucher et al. Circulation 2006;113, 577-582.



Treatment: IR• Consider if contraindications

against systemic thrombolysis or it has already failed

• Catheter-assisted embolectomy: low-dose ‘local’ fibrinolysis and thrombus fragmentation or aspiration

• Mechanical disruption of clot brings more surface area of clot in contact with thrombolytic agent

• Systematic review (15 trials, n=594): clinical success rate 86.5% w/ low rates of complications

Kuo et al. J Vasc Interv Radiol 2009;20, 1431-1440.

Treatment: IR

Uflacker et al. J Vasc Interv Radiol 1996;7: 519-528.Lohan et al. Emerg Radiol 2007;13:161-169.

• Grade 1: fresh clot recently embolized, usually responds well to mechanical thrombectomy w/ increased flow & Oxygenation

• Grade 2: older, more organized clot; more residual clot likely to remain but still good chance of significant improvement in pulmonary flow

• Grade 3: old, organized chronic PE w/ recent worsening of acute-on-chronic PE; do not respond well to mechanical thrombectomy (need device that can scrape clot from vessel wall)



Treatment: Surgical Embolectomy

• Consider after failed fibrinolysis; effective with large centrally located thrombi

• Invasive: requires median sternotomy and cardiopulmonary bypass

• 1994 case series: surgical success 85% w/ 23% mortality vs medical therapy success rate of 75% & 33% mortality

Gulba et al. Lancet 1994;343, 576-577.

Summary: Massive PE

• Suspected PE w/ cardiogenic shock and/or persistent arterial hypotension: weight-based UFH bolus first as continue workup

• If PE confirmed on imaging (CT/TTE), give thrombolytics

• If failed or contraindication to thrombolytics, consult IR/CT Surg for catheter-based thrombolysis or surgical embolectomy

Konstantinides. N Engl J Med 2008;359:2804-13.

“Doc, I have renal failure!”

• If renal failure or contrast allergy, V/Q scans are alternative imaging mode

• Helpful if normal: negative predictive value of 97%

“Doc, I have renal failure!”• If high-probability scan: positive predictive

value of 85-90%• Often inconclusive: diagnostic in only 30-50%

of suspected PE



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