Acute Pulmonary Embolism Overview lecture.ppt

B
Acute Pulmonary
Embolism:
Diagnosis and
Management
Why care?
 PE is the most common
preventable cause of death in
hospitalized patients
 ~600,000 deaths/year
 80% of pulmonary emboli occur
without prior warning signs or
symptoms
 2/3 of deaths due to pulmonary
emboli occur within 30 minutes of
embolization
 Death due to massive PE is often
immediate
 Diagnosis can be difficult
 Early treatment is highly effective
Pathology
At least 90% of pulmonary emboli
originate from major leg veins.
Acute Pulmonary Embolism Overview lecture.ppt
 https://www.youtube.com/watch?v=MUW2
FTg-5h4
Natural History of VTE
 40-50% of patients with DVT develop PE, often
“silent”
 PE presents 3-7 days after DVT
 Fatal within 1 hour after onset of respiratory
symptoms in 10%
 Shock/persistent hypotension in 5-10% (up to 50% of
patients with RV dysfunction)
 Most fatalities occur in untreated patients
 Perfusion defects completely resolve in 75% of
all patients (who survive)
Diagnosis: Clinical Presentation
 Dyspnea, tachypnea, or pleuritic chest pain most
common
 Pleuritic pain = distal emboli pulmonary infarction
and pleural irritation
 Isolated dyspnea of rapid onset= central PE with
hemodynamic sequlea
 Retrosternal angina like symptoms = RV ischemia
 Syncope=rare presentation, but indicates
severely reduced hemodynamic reserve
 symptoms can develop over weeks
 In patients with pre-existing CHF or COPD,
worsening dyspnea may indicate PE
Non-Specific!!
Diagnosis: Chest X-Ray
 Usually abnormal, but non-specific
 Study of 2,322 patients with PE:
 Cardiac enlargement (27%)
 Normal (24%)
 Pleural effusion (23%)
 Elevated hemidiaphragm (20%)
 Pulmonary artery enlargement (19%)
 Atelectasis (18%)
 Parenchymal pulmonary infiltrates (17%)
Chest Radiographs in Acute Pulmonary Embolism: Results From the International Cooperative
Pulmonary Embolism Registry. Chest July 2000 118:3338; 10.1378/chest.118.1.33
Diagnosis: ECG
 Usually non-specific ST/T waves changes
and tachycardia
 RV strain patterns suggest severe PE
Diagnosis:Other tests
 Most patients with PE have a normal pulse
oximetry
Clinical Diagnosis of PE
 In summary, clinical signs, symptoms and
routine tests do not allow for the exclusion
or confirmation of acute PE but may
increase the index of its suspicion
 Consider PE in cases of unexplained
tachycardia or syncope
Diagnosis-Probability Assessment
 Implicit clinical judgement is fairly
accurate: “Do you think this patient has a
PE?”
 Validated prediction rules standardize
clinical judgement
 Wells
 Geneva
Proportion with PE
65%
30
10%
Acute Pulmonary Embolism Overview lecture.ppt
Diagnosis
 D-Dimer
Fibrin degradation product
Non specific (~40%): cancer, sepsis,
inflammation increase d-dimer levels
Spiral CT
• Direct visualization of emboli.
• Both parenchymal and mediastinal
structures can be evaluated.
• Offers differential diagnosis in 2/3 of cases
with a negative scan.
BUT…
•Dye load and large radiation dose
•Optimally used when incorporated into a
validated diagnostic decision tree
Acute Pulmonary Embolism Overview lecture.ppt
Acute Pulmonary Embolism Overview lecture.ppt
3 month
VTE rate 0.5% (all non fatal) 1.3%
This algorithm allowed for a management decision in 98% of
patients presenting with symptoms suggestive of PE
Diagnosis- Summary
 History and physical examination
 Then 1,2,3 approach:
1. Clinical decision score
2. D-Dimer test
3. Chest CT
3’. (V/Q scan remains a valid option for patients
with contraindication to CT)
Clinical Presentation
After disembarking from a 10 hour airline
flight, a 69 year old man w/o past medical
hx presents to the ER with acute dyspnea.
BP is 120/80 (baseline) and pulse is 120
BPM. Wells score = 5 (intermediate), D-
Dimer is positive.
Spiral CT shows bilateral pulmonary emboli
in >50% of arterial tree.
Poor Prognostic Signs
 Hypotension (not caused by arrhythmia,
sepsis, or hypovolemia)
SBP <90 mm Hg = 53% 90-day all cause
mortality
SBP drop of 40 mm Hg for at least 15 minutes
= 15% in–hospital mortality
 Syncope= bad
 Shock= really bad
Transverse contrast-enhanced CT scan shows maximum minor axis measurements of the
right ventricle (A) and left ventricle (B).
van der Meer R W et al. Radiology 2005;235:798-803
©2005 by Radiological Society of North America
Echocardiograms before and after Thrombolysis
Echocardiography-RV Dilation
Treatment
 Pulseless patient with suspected PE: Start ACLS and consider
administration of thrombolytics
 Stabilize the patient and provide supportive care
 Oxygen supplementation in patients with SpO2 < 90%
 For patients with respiratory failure: airway management and/or
mechanical ventilation
 (IV fluids, gentle bolus normal saline ≤ 500 mL). Avoid volume
overload, which may be harmful in cases of right ventricular strain
 Analgesics: for patients with pain, Morphine. Avoid NSAIDs if patient
receiving anticoagulation or thrombolytics
 Assess bleeding risk
 Initiate therapy based on risk stratification
and bleeding risk.
 Massive PE: thrombolytic therapy or
thrombectomy.
 Submassive and nonmassive PE:
anticoagulation or IVC filter
Thrombolytic therapy
Fibrinolytic therapy, Thrombolysis
 The pharmacologic breakdown of blood
clots formed in vessels. Indications include
STEMI, stroke, massive pulmonary
embolism, severe deep vein thrombosis,
and acute limb ischemia. Agents used
include streptokinase and alteplase.
Alteplase
 Tissue plasminogen activator
 Abbreviation: tPA, PLAT, rtPA
 A serine protease found on endothelial
cells of the blood vessels. Catalyzes the
conversion of plasminogen to plasmin,
which is the main enzyme responsible for
clot breakdown.
Approved thrombolytic regimens for
pulmonary embolism
 Streptokinase 250 000 IU as a loading dose
over 30 min, followed by 100 000 IU/h over 12–
24 h
 Accelerated regimen: 1.5 million IU over 2 h
 Urokinase 4400 IU/kg as a loading dose over 10
min, followed by 4400 IU/kg/h over 12–24 h
 Accelerated regimen: 3 million IU over 2 h
 rtPA (Alteplase)100 mg over 2 h or 0.6 mg/kg
over 15 min (maximum dose 50 mg)
Catheter Embolectomy & Fragmentation
An alternative in high-risk PE patients when thrombolysis
is absolutely contraindicated or has failed
Kucher N Chest 2007;132:657-663
Bottom line
 The decision to use thrombolytic therapy
in the intermediate risk PE group should
be made on a case-by-case basis after
carefully weighing the strength of the
indication, the potential benefits, the
contraindications, and potential adverse
effects.
IVC Filters
•May provide lifelong protection against PE
•Unclear effect on overall survival
• Complications:
•DVT (20%)
•Post thrombotic syndrome (40%)
•IVC thrombosis (30%)
•Risk/benefit ratio difficult to determine since no
randomized control evidence
•Use when there are absolute contraindications to
anticoagulation and a high risk of Venous
thromboembolism recurrence
•Consider in pregnant women with extensive
thrombosis
•Optimal duration of retrievable filters is unclear
The key is prevention
 DVT prophylaxis in at-risk patients is quite
effective
1 de 34

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Acute Pulmonary Embolism Overview lecture.ppt

  • 2. Why care?  PE is the most common preventable cause of death in hospitalized patients  ~600,000 deaths/year  80% of pulmonary emboli occur without prior warning signs or symptoms  2/3 of deaths due to pulmonary emboli occur within 30 minutes of embolization  Death due to massive PE is often immediate  Diagnosis can be difficult  Early treatment is highly effective
  • 3. Pathology At least 90% of pulmonary emboli originate from major leg veins.
  • 6. Natural History of VTE  40-50% of patients with DVT develop PE, often “silent”  PE presents 3-7 days after DVT  Fatal within 1 hour after onset of respiratory symptoms in 10%  Shock/persistent hypotension in 5-10% (up to 50% of patients with RV dysfunction)  Most fatalities occur in untreated patients  Perfusion defects completely resolve in 75% of all patients (who survive)
  • 7. Diagnosis: Clinical Presentation  Dyspnea, tachypnea, or pleuritic chest pain most common  Pleuritic pain = distal emboli pulmonary infarction and pleural irritation  Isolated dyspnea of rapid onset= central PE with hemodynamic sequlea  Retrosternal angina like symptoms = RV ischemia  Syncope=rare presentation, but indicates severely reduced hemodynamic reserve  symptoms can develop over weeks  In patients with pre-existing CHF or COPD, worsening dyspnea may indicate PE
  • 9. Diagnosis: Chest X-Ray  Usually abnormal, but non-specific  Study of 2,322 patients with PE:  Cardiac enlargement (27%)  Normal (24%)  Pleural effusion (23%)  Elevated hemidiaphragm (20%)  Pulmonary artery enlargement (19%)  Atelectasis (18%)  Parenchymal pulmonary infiltrates (17%) Chest Radiographs in Acute Pulmonary Embolism: Results From the International Cooperative Pulmonary Embolism Registry. Chest July 2000 118:3338; 10.1378/chest.118.1.33
  • 10. Diagnosis: ECG  Usually non-specific ST/T waves changes and tachycardia  RV strain patterns suggest severe PE
  • 11. Diagnosis:Other tests  Most patients with PE have a normal pulse oximetry
  • 12. Clinical Diagnosis of PE  In summary, clinical signs, symptoms and routine tests do not allow for the exclusion or confirmation of acute PE but may increase the index of its suspicion  Consider PE in cases of unexplained tachycardia or syncope
  • 13. Diagnosis-Probability Assessment  Implicit clinical judgement is fairly accurate: “Do you think this patient has a PE?”  Validated prediction rules standardize clinical judgement  Wells  Geneva
  • 16. Diagnosis  D-Dimer Fibrin degradation product Non specific (~40%): cancer, sepsis, inflammation increase d-dimer levels
  • 17. Spiral CT • Direct visualization of emboli. • Both parenchymal and mediastinal structures can be evaluated. • Offers differential diagnosis in 2/3 of cases with a negative scan. BUT… •Dye load and large radiation dose •Optimally used when incorporated into a validated diagnostic decision tree
  • 20. 3 month VTE rate 0.5% (all non fatal) 1.3% This algorithm allowed for a management decision in 98% of patients presenting with symptoms suggestive of PE
  • 21. Diagnosis- Summary  History and physical examination  Then 1,2,3 approach: 1. Clinical decision score 2. D-Dimer test 3. Chest CT 3’. (V/Q scan remains a valid option for patients with contraindication to CT)
  • 22. Clinical Presentation After disembarking from a 10 hour airline flight, a 69 year old man w/o past medical hx presents to the ER with acute dyspnea. BP is 120/80 (baseline) and pulse is 120 BPM. Wells score = 5 (intermediate), D- Dimer is positive. Spiral CT shows bilateral pulmonary emboli in >50% of arterial tree.
  • 23. Poor Prognostic Signs  Hypotension (not caused by arrhythmia, sepsis, or hypovolemia) SBP <90 mm Hg = 53% 90-day all cause mortality SBP drop of 40 mm Hg for at least 15 minutes = 15% in–hospital mortality  Syncope= bad  Shock= really bad
  • 24. Transverse contrast-enhanced CT scan shows maximum minor axis measurements of the right ventricle (A) and left ventricle (B). van der Meer R W et al. Radiology 2005;235:798-803 ©2005 by Radiological Society of North America
  • 25. Echocardiograms before and after Thrombolysis Echocardiography-RV Dilation
  • 26. Treatment  Pulseless patient with suspected PE: Start ACLS and consider administration of thrombolytics  Stabilize the patient and provide supportive care  Oxygen supplementation in patients with SpO2 < 90%  For patients with respiratory failure: airway management and/or mechanical ventilation  (IV fluids, gentle bolus normal saline ≤ 500 mL). Avoid volume overload, which may be harmful in cases of right ventricular strain  Analgesics: for patients with pain, Morphine. Avoid NSAIDs if patient receiving anticoagulation or thrombolytics  Assess bleeding risk
  • 27.  Initiate therapy based on risk stratification and bleeding risk.  Massive PE: thrombolytic therapy or thrombectomy.  Submassive and nonmassive PE: anticoagulation or IVC filter
  • 28. Thrombolytic therapy Fibrinolytic therapy, Thrombolysis  The pharmacologic breakdown of blood clots formed in vessels. Indications include STEMI, stroke, massive pulmonary embolism, severe deep vein thrombosis, and acute limb ischemia. Agents used include streptokinase and alteplase.
  • 29. Alteplase  Tissue plasminogen activator  Abbreviation: tPA, PLAT, rtPA  A serine protease found on endothelial cells of the blood vessels. Catalyzes the conversion of plasminogen to plasmin, which is the main enzyme responsible for clot breakdown.
  • 30. Approved thrombolytic regimens for pulmonary embolism  Streptokinase 250 000 IU as a loading dose over 30 min, followed by 100 000 IU/h over 12– 24 h  Accelerated regimen: 1.5 million IU over 2 h  Urokinase 4400 IU/kg as a loading dose over 10 min, followed by 4400 IU/kg/h over 12–24 h  Accelerated regimen: 3 million IU over 2 h  rtPA (Alteplase)100 mg over 2 h or 0.6 mg/kg over 15 min (maximum dose 50 mg)
  • 31. Catheter Embolectomy & Fragmentation An alternative in high-risk PE patients when thrombolysis is absolutely contraindicated or has failed Kucher N Chest 2007;132:657-663
  • 32. Bottom line  The decision to use thrombolytic therapy in the intermediate risk PE group should be made on a case-by-case basis after carefully weighing the strength of the indication, the potential benefits, the contraindications, and potential adverse effects.
  • 33. IVC Filters •May provide lifelong protection against PE •Unclear effect on overall survival • Complications: •DVT (20%) •Post thrombotic syndrome (40%) •IVC thrombosis (30%) •Risk/benefit ratio difficult to determine since no randomized control evidence •Use when there are absolute contraindications to anticoagulation and a high risk of Venous thromboembolism recurrence •Consider in pregnant women with extensive thrombosis •Optimal duration of retrievable filters is unclear
  • 34. The key is prevention  DVT prophylaxis in at-risk patients is quite effective