Transcript Case Presentation - Calgary Emergency Medicine

Case Presentation
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45f acute CP, dyspnea, near-syncope
Pale, diaphoretic, looks unwell
Afebrile, HR 110, RR 32, BP 118/68
Sats 75% RA, 92% on NRB
JVP elevated
HS Normal
Chest clear
Portable CXR
ECG
Next?
ECHO
• Significant RV dilation
• Increased R sided pressures
• RV hypokinesis
• Clot visible in RV
CT-pulmonary angiogram
Management
• Heparin PE protocol initiated
• Colleague asks why you haven’t
thrombolysed yet
“But she’s not in shock!”
“Yeah, but she’s a submassive PE”
“…what’s a submassive PE?”
Thrombolysis of the
Submassive PE
Michael Kenney MD CCFP(EM)
Dept of Emergency Medicine
University of Calgary
Objectives
1. Define submassive PE
2. Discuss clinical significance of a
submassive PE
3. Determine an evidence-based
approach to identifying the SMPE
4. Review the literature regarding efficacy
of thrombolytics in SMPE
5. Review contraindications to
thrombolytics in PE
6. Local expert opinion on alternate
therapy
Massive PE
• Pulmonary embolism in the setting of
hemodynamic instability (SBP<90)
PE + Shock = Massive PE
• Literature supports thrombolytics
(Kearon et al, Chest 2008)
Submassive PE (SMPE)
• Pulmonary embolism in the setting of
a hemodynamically stable patient
with ECHO-proven evidence of right
ventricular dysfunction
PE + NBP + RV dysfunction = SMPE
ECHO in Submassive PE
• RV hypokinesis
• RV dilation
• Pulmonary hypertension >30mmHg
• Septal shift > RV hypokinesis > RV dilation
(Wolde et al, Arch Int Med 2004; Kline et al, Am Heart Journal,
2008)
ECG Strain  RV Dysfunction
Clinical Significance
• When compared to patients with PE and
normal RV function
– Higher mortality (8-13%)
– Higher in-hospital complications
– Higher long-term cardiopulmonary morbidity
• Pulm hypertension
• R CHF
( Kreit et al, Chest 2005)
Pathophysiology
Identifying the SMPE
1. Clinical
2. ECG
3. Cardiac biomarkers
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Troponins
BNP
4. CT Scan
Clinical Clues
• Syncope
• Significant tachycardia
• Significant hypoxia
• P/E
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JVD
Parasternal heave
Split P2
TR murmur
ECG in SMPE
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Strain pattern (T inversion V1-V4)*
S1-Q3-T3
RAD
RBBB
• Insensitive and mostly non-specific
• Strain pattern specific for RV strain  RV
dysfunction
Cardiac Markers
• Troponins
• BNP
Cardiac Markers
• Troponins
– Correlates with presence of RV
dysfunction
– Predictive of complicated in-hospital
course
– Associated with increased mortality in
setting of PE
– NPV 93-97% for 30 day mortality
(Konstantinides, Circulation 2002; La Vecchia et al Heart,
2005; Askey et al, Am J or Emer Med 2007)
Cardiac Markers
• BNP
– Correlates with RV dysfunction
– 95-99% NPV for complicated in-hospital
course
– Predictive of elevated 30 day mortality
– Significantly predicted greater dyspnea
at rest, decreased exercise tolerance
at 6 months
(Wolde et al, Circulation, 2003; Binder, Circulation 2005; Kline
et al, Am Heart Journal, 2008)
Cardiac Markers
• Negative markers = lower risk, more
favorable course
• Positive markers = ECHO
• Use clinical judgement
• Serial testing
CT Scan
• RV enlargement on the CT
angiogram defined as RV diameter
>90% LV diameter, appears to be an
independent risk factor for death
and nonfatal clinical complications
(Kucher et al, Circulation, 2006; Schoepf et al
Circulation, 2005)
ED assessment of the
Hemodynamically Stable PE
Therapy
1. Anticoagulation (heparin)
2. Thrombolytic therapy
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Efficacy
Choice of agent
Absolute Contraindications
Risk factors for Major Bleeding
3. Catheter embolectomy
4. Surgical embolectomy
Efficacy of Thrombolytics in
SMPE
The Literature
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<800 patients overall
Not all randomized controlled
Some studies lysed all PE’s
SMPE not consistently defined
UK, SK, tPA
Efficacy of Thrombolytics in
SMPE
Cardiopulmonary Physiology
– Markedly improves PAP, RV function
and pulmonary perfusion
– Only one study long-term
• benefit persists @ 7years
Efficacy of Thrombolyitics in
SMPE
Clinical Outcome Measures
– Lower inhospital complication
•Fewer recurrent PE
•Less use of vasopressors, intubation,
rescue embolectomy
– Trends toward improved mortality
– No study or meta-analysis large enough
to clearly show mortality benefit
Major Bleed
1. Intracranial Hemorrhage
2. Any bleed leading to shock
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GI and retroperitoneal most common
3. Any bleed leading to transfusion >
2U PRBCs or surgery
Contraindications
Absolute
• Hx of hemorrhagic CVA
• Active intracranial neoplasm
• Recent (<2 months) intracranial surgery or
trauma
• Recent (<2 weeks) major GI bleed or
major surgery
Tapson et al, Chest, Oct 2008
Risk Factors for ICH
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Age > 70
Female
Weight < 70kg
SBP >170 or DBP >95
PHx ischemic CVA
DM
Elevated INR
PLT < 100
RF 0-1 = 0.5-1%
2-4 = 2.5%
>5 = 4%
Thrombolytics cause
Intracranial Hemorrhage
1%
Choice of Thrombolytic
• tPA only lytic approved
• tPA 100mg
– 10mg bolus, remaining 90mg over 2 hours
– most widely studied and accepted in PE
• TNK has not been studied adequately in
PE
– 0.5mg/kg (50mg max)
– One study 22 patients, equivalent to tPA
Bottom Line of
Thrombolytics in SMPE
• tPA
• Trends but no definitive mortality
benefit in SMPE
• Case-by-case, not routine
• Benefit vs bleeding risk assessment
• Involve intensivist early
• Involve patient and family
Embolectomy
• Percutaneous Catheter Extraction
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Pigtail rotational catheter
Usually tPA in addition
May take hours
Angiojet coming
• Surgical Embolectomy
– Rare benefit over percutaneous
– If absolute contraindications and IR unable
IVC Filter Placement
• Reduces short term risk of recurrent
PE
• Consider in PE
– Little cardiac reserve
– Significant extremity clot burden
– Contraindications to lytics, or high risk
for bleeding
Summary
 Submassive PE = normal BP + RVD
 Significant morbidity and mortality
associated
 Reviewed clinical clues, ECG
findings, and cardiac markers
helpful in identifying the patient with
SMPE
 ECHO if RV dysunction suspected
Summary
 Thrombolytics
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improve cardiopulmonary
hemodynamics
lower in-hospital complications
Trends, but no clear mortality benefit
 Reviewed absolute
contraindications and risk factors
for major bleed
 Discussed non-medical therapeutic
options
Questions?