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Dr. Muhanad Majeed
Emergency Physician
Burjeel Emergency Medicine Seminar
Pulmonary Thrombo-embolism Management in
Emergency Department
Objectives
 Pretest Probability in PE
 Clinical prediction rules
 D-dimer sensitivity
 Excluding PE in Primary care setup
Definition
PE results from a clot that formed hours, days, or
weeks earlier in the deep veins that dislodges, travels
through the venous system, traverses the right
ventricle, and lodges in the pulmonary vasculature.
Primary Causes
 Three primary influences predispose a patient
to thrombus formation; these form the so-
called Virchow triad, which consists of the
following
 Endothelial injury
 Stasis or turbulence of blood flow
 Blood hypercoagulability
Pathophysiology of Pulmonary
Vascular Occlusion
• Rest dyspnea seems to be the clinical manifestation
of distorted and irregular blood flow within the lung,
referred to as ventilation-perfusion inequality.
• venous admixture: A lodged clot can redistribute
blood flow to areas of the lung with already high
perfusion relative to ventilation and as such cause
more blue blood to pass through the lung without
being fully oxygenated
Gross Anatomy
Venous Thromboembolic Risk Factors
Inherited predisposing factors include the following:
• Increased coagulation factor activity/function
 Activated protein C resistance
 Factor V Leiden mutation
 Prothrombin gene mutation
 Elevated factor VIII levels
• Defects of coagulation factor inhibitors
 Antithrombin
 Protein C
 Protein S
• Defects in fibrinolysis
• Hyperhomocysteinemia
• Altered platelet function
Venous Thromboembolic Risk Factors
Acquired predisposing factors include the following:
Advancing age (particularly > 60 years)
Previous episode of venous thromboembolism
Obesity
Malignancy
Surgery
Trauma
Hormone replacement therapy
Pregnancy
Heparin-induced thrombocytopenia
Autoimmune associated hypercoagulability (ie, lupus
anticoagulant)
Clinical Presentation
Prehospital Care
 stabilization of the patient’s airway, breathing, and circulation
 If present, chest pain should be treated
 Caution should be used before treating patients with possible PE
with vasodilating agents (such as nitroglycerin), as patients with
PE may be preload dependent.
 hypotension may be treated with normal saline bolus infusion
History, Physical Examination, And Risk
Stratification
 Risk stratification is key to the emergency medicine
approach to diagnosing PE. Factors from the history and
physical examination are used to determine how likely the
diagnosis of PE is in an individual patient
 Clinical gestalt The first study describing the use of clinical
gestalt in predicting PE is the original PIOPED (Prospective
Investigation Of Pulmonary Embolism Diagnosis) study
Risk stratification
Clinical gestalt
• It is the implicit, unstructured estimate of the pretest
probability of disease and is based on the clinician’s
education, clinical experience, and, ultimately, overall
• The first study describing the use of clinical gestalt in
predicting PE is the original PIOPED (Prospective
Investigation Of Pulmonary Embolism Diagnosis) study
Risk stratification
Wells score
The most commonly used method to predict clinical
probability, the Wells score, is a clinical prediction rule,
whose use is complicated by multiple versions being
available
Although the Wells score is the most studied, it continues to be
criticized for the lack of true objectivity. Most notably, the “an
alternative diagnosis is less likely than PE” criterion is weighted
heavily and, alone, can move someone from “no risk” to
“moderate risk.”
Risk stratification
Wells score
Risk stratification
Wells score
Risk stratification
Simplified Revised Geneva Score
Risk stratification
Simplified Revised Geneva Score
Low risk: ≤ 2 points;
high risk: ≥ 3 points.
Risk stratification
Pulmonary Embolism Rule-Out Criteria (PERC)
The PERC rule was developed by Kline et al with the specific
objective of identifying patients who have more than trivial risk
of PE but can be safely discharged without any ancillary testing.
The PERC rule requires that the clinician already have a clinical
impression of risk for PE < 15% (“very low risk”). It then asks a
series of 8 yes/no questions If the answer to all 8 questions is
“no,” then the risk of having a PE is considered to be minimal.
Risk stratification
Pulmonary Embolism Rule-Out Criteria (PERC)
1. Is the patient > 49 years of age?
2. Is the pulse rate > 99 beats per minute?
3. Is the pulse oximetry reading < 95% while the patient
breathes room air?
4. Is there a present history of hemoptysis?
5. Is the patient receiving exogenous estrogen?
6. Does the patient have a prior diagnosis of venous
thromboembolism?
7. Has the patient had recent surgery or trauma requiring
endotracheal intubation or hospitalization in the previous 4
weeks?
8. Does the patient have unilateral leg swelling (visual
observation of asymmetry of the calves)?
Risk stratification
Sensitivity And Specificity Of Clinical Gestalt,
Wells Score, And Revised Geneva Score
Diagnostic Studies
• Chest radiography (chest x-ray)
• Electrocardiogram (ECG)
• Arterial blood gas analysis
• Quantitative D-dimer
• Computerized tomographic pulmonary
angiography (CTPA) of the chest
• Ventilation/perfusion (V/Q) lung scan
• Cardiac echocardiography
• Venous compression ultrasonography
Chest X-ray
• Chest X ray – most common finding with a PE is a
normal x-ray
• But they are useful as X-rays help to rule out
pneumonia and pneumothorax as causes of
dyspnoea etc
• Possible signs indicating a PE are as follows
Chest X-ray
Hamptons Hump
• Not always seen
• Wedged shaped pleural
based lesion
• PE in one area (Bottom
arrow) and everywhere
else is infarct
• Causes pleurisy,
irritation
Westermark Sign
• On this X-ray PE is in
Left lung
• Increase in blood flow
to right side.
• Minimal blood flow
seen to Left lung
• So the side that looks
clearer is the side with
reduced blood flow,
therefore the clot
pulmonary infarct
ECG
• A normal ECG can be seen in 30% of patients with PE.
• The classic S1Q3T3 has a sensitivity and specificity of 54%
and 62%, respectively, and was found to occur in only 20% of
patients with angiographically proven PE.
• Sinus tachycardia was found in only 36% .
• T-wave inversion in the precordial leads V1 thru V4 may also
be a sign of acute or chronic right ventricular strain,
particularly acute pulmonary embolism, 19% in non-massive
pulmonary embolism and in 85% in massive pulmonary
embolism, and is the most sensitive and specific
electrocardiographic finding in massive pulmonary
embolism.
ECG
S1Q3T3
Lead I
Exaggerated S wave
Lead III
Exaggerated Q wave
T Wave inversion
Not specific to PE, but gets you to possibly think of the diagnosis
Can be seen in any cor-pulmonale syndrome where pulmonary artery
systolic pressure is elevated
ECG
Sinus tachycardia, with an S1Q3T3 pattern noted by the circles and
anterior-inferior T-wave inversions noted by the triangles.
Electrocardiogram Of Patient With Massive Pulmonary Embolism
D-dimer
D-dimer
D-dimer testing is of clinical use when there is a suspicion of
• deep venous thrombosis (DVT)
• pulmonary embolism (PE)
• disseminated intravascular coagulation (DIC).
• It is under investigation in the diagnosis of aortic dissection.
D-dimer
• For a very high score, or pretest probability, a D-dimer will make little
difference and anticoagulant therapy will be initiated regardless of test
results, and additional testing for DVT or pulmonary embolism may be
performed.
• For a moderate or low score, or pretest probability:
• A negative D-dimer test will virtually rule out thromboembolism: the degree
to which the D-dimer reduces the probability of thrombotic disease is
dependent on the test properties of the specific test used in the clinical
setting: most available D-dimer tests with a negative result will reduce the
probability of thromboembolic disease to less than 1% if the pretest
probability is less than 15-20%.
• If the D-dimer reads high, then further testing (ultrasound of the leg veins
or lung scintigraphy or CT scanning) is required to confirm the presence of
thrombus. Anticoagulant therapy may be started at this point or withheld
until further tests confirm the diagnosis, depending on the clinical situation.
D-dimer
• Age-Adjusted D-Dimer Cutoff Levels to Rule Out
Pulmonary Embolism The ADJUST-PE Study
D-dimer
• Age adjustment of the D-dimer cut-off value
increases the specificity for the exclusion of
venous thromboembolism in higher age groups
without overly affecting sensitivity. Thus, the
proportion of elderly patients, in whom a
thromboembolic event can be ruled out,
increases
PE in Primary Care
• Qualitative point-of-care (POC) D-dimer
• Quantitative laboratory-based D-dimer
Combined with the Wells PE rule, both tests are safe to use in
excluding PE. The quantitative test seemed to be safer than
the POC test, albeit not statistically significant. The specificity
of the POC test was higher, resulting in more patients in
whom PE could be excluded.
Journal of Thrombosis and Haemostasis
Computerized Tomographic
Pulmonary Angiography
 CTPA has become the primary radiologic study ordered for the evaluation of
PE52,53 and is the overwhelming choice among both emergency clinicians
 The use of CTPA for the visualization of the pulmonary vasculature and the
evaluation of PE was first described in 1992 by Remy-Jardin
 Studies evaluating multidetector CT are fewer, but, as expected, they show
improved accuracy, with sensitivities between 83% and 100% and specificities
between 89% and 98%.
Spiral CT
Tomographic scan showing infarcted left lung,
large clot in right main pulmonary artery
CTPA Limitations
 A drawback to the use of CTPA is the exposure to radiation and iodinated
intravenous contrast material. A CTPA subjects the patient to an average effective
radiation dose of 15 mSv (ranges between 2 and 20 mSv), which is equivalent to
approximately 150 2-view chest x-rays
 There are 2 primary adverse reactions to iodinated intravenous contrast media:
1. development of anaphylaxis or other immediate systemic allergic reaction.
2. contrast-induced nephropathy.
Therefore, a history of allergy to intravenous contrast iodine and a history of renal
insufficiency may make V/Q scan the better choice.
Ultrasound
• Non-invasive
• Looks at lower limbs
• Doppler USS looks at
vein for flow and
compressibilty to see if
clot present
USS Results
• If +ve for DVT and patient has
respiratory distress symptoms
you can rule in a PE, since the
DVTs can embolise easily and
enter the lungs causing
respiratory problems
• If -ve for DVT, unsure whether
there is a PE or not, as a clot
from other part of body may have
embolised the lung, or a whole
DVT may have travelled to the
lung
• So a –ve result does not give a
thorough answer, whilst a +ve
result may rule it in
ECHO
• Sometimes beneficial
• The right ventricle
pumps blood to lungs
• If clot is present the
pressure at site of clot
increases and so does
the pressure in the right
ventricle
ECHO
• The severity of this Pulmonary
Artery Pressure (PAP) and the
severity of the clot, is found by
looking at the tricuspid valve and
noting how much regurge occurs
(Tricuspid jet)
• If tricuspid jet is high then PAP
differential between RA and RV is
great and the clot burden is large
• All these tests may help in the
possible diagnosis of a PE, but are
not definitive tests
VQ Scan
• Nuclear medicine scan
• Looks at perfusion and ventilation
• In pneumonia for example, you would get decreased
perfusion and decreased ventilation due to the
purulent material present this is a “Matched Deficit”
• In a PE there is decreased perfusion of the lung in
the area but ventilation remains the same this is an
“Unmatched Deficit”
• Does Not affect patient in renal failure
• Impaired view if patient has pneumonia etc
VQ Scan
• The patients ventilation is
assessed by them breathing
in Xenon
• For perfusion the patient is
injected with Technigas
(Tc99mMAA)
• Use Gamma Camera (a
glorified Geiger counter) to
measure the nuclear
material
Probability of PE
Probability of PE
• Normal - Full ventilation and perfusion seen
• Low Probability for PE – (<20%)
• Intermediate probability for PE- V and P in same area
(Matched deficit) (20-80%)
• High Probability for PE – Normal V and P (Un-Matched deficit)
(>80%)
Gold Standard
• Pulmonary Angiogram –
Most accurate test, but not
always best for patient
(most invasive)
• Catheter inserted into right
side of the heart, dye is
injected directly into
pulmonary artery, observed
under fluoroscopy
• Dangerous,
• mortality rate, especially
in patients with PE
Management approach
Empirical anticoagulation
Supportive therapies
• Respiratory support
• Intravenous fluids
• Vasopressors
• Bed rest
Initial anticoagulation
Thrombolytic therapy
Surgical intervention
Venous filters
Long-term (extended) anticoagulation
Anticoagulation
• In patients with confirmed PE, anticoagulation should continue for
at least 3 months.
• dabigatran, rivaroxaban, apixaban, or edoxaban, are recommended
over vitamin K antagonist (VKA) therapy (usually warfarin)
• VKA is in turn recommended over low-molecular weight heparin
(LMWH)
• Fondaparinux is generally reserved for patients with heparin-
induced thrombocytopenia (HIT)
BMJ Best Practice
Last updated Sep 12, 2016
IVC Filter
• If anticoagulation
treatment
contraindicated IVC
Filter
If clot travels it gets
caught in IVC Filter
IVC Filter
• It is possible for blood clot to be caught and
develop in IVC filter
• Cochrane Collaboration recommends IVC for
1. Recurrent PE despite use of anticoagulation, or in
absolute contra-indication to anticoagulation
2. Proximal DVT with massive pulmonary thrombosis
– next one could kill patient
3. Trauma Patient – needing operation
Prevention
• Bilateral Lower Extremity
Sequential Compression Devices
TEDs and Flowtrons
When the legs are squeezed
the veins release a factor which
thins the blood stopping clot
formation,
the rhythmic motion copies that
of leg movement
• Thromboprophylaxis
Dalteparin
Genetic Blood Tests
• 25-50% of patients with VTE have an inherited disorder
• There are genetic causes of metabolism which may be tested for
- Factor V Leiden – causes increased clotting as variant cannot be
inactivated by Factor Protein C (5% of popn and 20% of pts with thrombus)
- Factor Protein C Deficiency – results in normal cleaving of Factor Va and
Factor VIIIa
- 20210 (prothrombin) Mutation – 2-3 times risk of clot formation
- MTHMFR affects regulation of homocysteine
- Lupus anticoagulant- prothrombotic agent which can cause inappropriate
clotting
- Anti phospholipid antibody – confused autoimmune response
If any of these are positive and patient has a clot then may need
treatment for longer
Summary
 The decision to discharge a patient who presents with chest pain as the
primary complaint should be made only after careful consideration of
potential consequences.
 Evaluation and decision (with reasoning) must be well documented.
 Patients with Chest Pain Are at Risk—Use Both Liberal Consultation and
Liberal Admission Policies
 It is better to sound foolish than be unsafe
References
 American College of Chest Physicians evidence-based clinical
practice guidelines. Chest. 2012 Feb;141(2 Suppl):e419S-
94S.Cayley, W.E. Diagnosing the cause of chest pain. (2005).
American Family Physician, Vol 72 (10), 2012-21.
 Diagnostic approach to chest pain in adults. (2014). UpToDate.
 Differential diagnosis of chest pain in adults. (2014).
UpToDate.
 Evaluation of chest pain in the emergency department.
(2014). UpToDate.
Pearl
Great EKG Practice Site
http://ecg.bidmc.harvard.edu/maven/mavenmain.asp
Thank You.

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Update on Pulmonary Embolism

  • 1. Dr. Muhanad Majeed Emergency Physician Burjeel Emergency Medicine Seminar Pulmonary Thrombo-embolism Management in Emergency Department
  • 2.
  • 3. Objectives  Pretest Probability in PE  Clinical prediction rules  D-dimer sensitivity  Excluding PE in Primary care setup
  • 4. Definition PE results from a clot that formed hours, days, or weeks earlier in the deep veins that dislodges, travels through the venous system, traverses the right ventricle, and lodges in the pulmonary vasculature.
  • 5. Primary Causes  Three primary influences predispose a patient to thrombus formation; these form the so- called Virchow triad, which consists of the following  Endothelial injury  Stasis or turbulence of blood flow  Blood hypercoagulability
  • 6. Pathophysiology of Pulmonary Vascular Occlusion • Rest dyspnea seems to be the clinical manifestation of distorted and irregular blood flow within the lung, referred to as ventilation-perfusion inequality. • venous admixture: A lodged clot can redistribute blood flow to areas of the lung with already high perfusion relative to ventilation and as such cause more blue blood to pass through the lung without being fully oxygenated
  • 8. Venous Thromboembolic Risk Factors Inherited predisposing factors include the following: • Increased coagulation factor activity/function  Activated protein C resistance  Factor V Leiden mutation  Prothrombin gene mutation  Elevated factor VIII levels • Defects of coagulation factor inhibitors  Antithrombin  Protein C  Protein S • Defects in fibrinolysis • Hyperhomocysteinemia • Altered platelet function
  • 9. Venous Thromboembolic Risk Factors Acquired predisposing factors include the following: Advancing age (particularly > 60 years) Previous episode of venous thromboembolism Obesity Malignancy Surgery Trauma Hormone replacement therapy Pregnancy Heparin-induced thrombocytopenia Autoimmune associated hypercoagulability (ie, lupus anticoagulant)
  • 11. Prehospital Care  stabilization of the patient’s airway, breathing, and circulation  If present, chest pain should be treated  Caution should be used before treating patients with possible PE with vasodilating agents (such as nitroglycerin), as patients with PE may be preload dependent.  hypotension may be treated with normal saline bolus infusion
  • 12. History, Physical Examination, And Risk Stratification  Risk stratification is key to the emergency medicine approach to diagnosing PE. Factors from the history and physical examination are used to determine how likely the diagnosis of PE is in an individual patient  Clinical gestalt The first study describing the use of clinical gestalt in predicting PE is the original PIOPED (Prospective Investigation Of Pulmonary Embolism Diagnosis) study
  • 13. Risk stratification Clinical gestalt • It is the implicit, unstructured estimate of the pretest probability of disease and is based on the clinician’s education, clinical experience, and, ultimately, overall • The first study describing the use of clinical gestalt in predicting PE is the original PIOPED (Prospective Investigation Of Pulmonary Embolism Diagnosis) study
  • 14. Risk stratification Wells score The most commonly used method to predict clinical probability, the Wells score, is a clinical prediction rule, whose use is complicated by multiple versions being available Although the Wells score is the most studied, it continues to be criticized for the lack of true objectivity. Most notably, the “an alternative diagnosis is less likely than PE” criterion is weighted heavily and, alone, can move someone from “no risk” to “moderate risk.”
  • 18. Risk stratification Simplified Revised Geneva Score Low risk: ≤ 2 points; high risk: ≥ 3 points.
  • 19. Risk stratification Pulmonary Embolism Rule-Out Criteria (PERC) The PERC rule was developed by Kline et al with the specific objective of identifying patients who have more than trivial risk of PE but can be safely discharged without any ancillary testing. The PERC rule requires that the clinician already have a clinical impression of risk for PE < 15% (“very low risk”). It then asks a series of 8 yes/no questions If the answer to all 8 questions is “no,” then the risk of having a PE is considered to be minimal.
  • 20. Risk stratification Pulmonary Embolism Rule-Out Criteria (PERC) 1. Is the patient > 49 years of age? 2. Is the pulse rate > 99 beats per minute? 3. Is the pulse oximetry reading < 95% while the patient breathes room air? 4. Is there a present history of hemoptysis? 5. Is the patient receiving exogenous estrogen? 6. Does the patient have a prior diagnosis of venous thromboembolism? 7. Has the patient had recent surgery or trauma requiring endotracheal intubation or hospitalization in the previous 4 weeks? 8. Does the patient have unilateral leg swelling (visual observation of asymmetry of the calves)?
  • 21. Risk stratification Sensitivity And Specificity Of Clinical Gestalt, Wells Score, And Revised Geneva Score
  • 22.
  • 23.
  • 24.
  • 25. Diagnostic Studies • Chest radiography (chest x-ray) • Electrocardiogram (ECG) • Arterial blood gas analysis • Quantitative D-dimer • Computerized tomographic pulmonary angiography (CTPA) of the chest • Ventilation/perfusion (V/Q) lung scan • Cardiac echocardiography • Venous compression ultrasonography
  • 26. Chest X-ray • Chest X ray – most common finding with a PE is a normal x-ray • But they are useful as X-rays help to rule out pneumonia and pneumothorax as causes of dyspnoea etc • Possible signs indicating a PE are as follows
  • 27. Chest X-ray Hamptons Hump • Not always seen • Wedged shaped pleural based lesion • PE in one area (Bottom arrow) and everywhere else is infarct • Causes pleurisy, irritation
  • 28. Westermark Sign • On this X-ray PE is in Left lung • Increase in blood flow to right side. • Minimal blood flow seen to Left lung • So the side that looks clearer is the side with reduced blood flow, therefore the clot
  • 30. ECG • A normal ECG can be seen in 30% of patients with PE. • The classic S1Q3T3 has a sensitivity and specificity of 54% and 62%, respectively, and was found to occur in only 20% of patients with angiographically proven PE. • Sinus tachycardia was found in only 36% . • T-wave inversion in the precordial leads V1 thru V4 may also be a sign of acute or chronic right ventricular strain, particularly acute pulmonary embolism, 19% in non-massive pulmonary embolism and in 85% in massive pulmonary embolism, and is the most sensitive and specific electrocardiographic finding in massive pulmonary embolism.
  • 31. ECG S1Q3T3 Lead I Exaggerated S wave Lead III Exaggerated Q wave T Wave inversion Not specific to PE, but gets you to possibly think of the diagnosis Can be seen in any cor-pulmonale syndrome where pulmonary artery systolic pressure is elevated
  • 32. ECG
  • 33. Sinus tachycardia, with an S1Q3T3 pattern noted by the circles and anterior-inferior T-wave inversions noted by the triangles. Electrocardiogram Of Patient With Massive Pulmonary Embolism
  • 35. D-dimer D-dimer testing is of clinical use when there is a suspicion of • deep venous thrombosis (DVT) • pulmonary embolism (PE) • disseminated intravascular coagulation (DIC). • It is under investigation in the diagnosis of aortic dissection.
  • 36. D-dimer • For a very high score, or pretest probability, a D-dimer will make little difference and anticoagulant therapy will be initiated regardless of test results, and additional testing for DVT or pulmonary embolism may be performed. • For a moderate or low score, or pretest probability: • A negative D-dimer test will virtually rule out thromboembolism: the degree to which the D-dimer reduces the probability of thrombotic disease is dependent on the test properties of the specific test used in the clinical setting: most available D-dimer tests with a negative result will reduce the probability of thromboembolic disease to less than 1% if the pretest probability is less than 15-20%. • If the D-dimer reads high, then further testing (ultrasound of the leg veins or lung scintigraphy or CT scanning) is required to confirm the presence of thrombus. Anticoagulant therapy may be started at this point or withheld until further tests confirm the diagnosis, depending on the clinical situation.
  • 37. D-dimer • Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism The ADJUST-PE Study
  • 38. D-dimer • Age adjustment of the D-dimer cut-off value increases the specificity for the exclusion of venous thromboembolism in higher age groups without overly affecting sensitivity. Thus, the proportion of elderly patients, in whom a thromboembolic event can be ruled out, increases
  • 39. PE in Primary Care • Qualitative point-of-care (POC) D-dimer • Quantitative laboratory-based D-dimer Combined with the Wells PE rule, both tests are safe to use in excluding PE. The quantitative test seemed to be safer than the POC test, albeit not statistically significant. The specificity of the POC test was higher, resulting in more patients in whom PE could be excluded. Journal of Thrombosis and Haemostasis
  • 40. Computerized Tomographic Pulmonary Angiography  CTPA has become the primary radiologic study ordered for the evaluation of PE52,53 and is the overwhelming choice among both emergency clinicians  The use of CTPA for the visualization of the pulmonary vasculature and the evaluation of PE was first described in 1992 by Remy-Jardin  Studies evaluating multidetector CT are fewer, but, as expected, they show improved accuracy, with sensitivities between 83% and 100% and specificities between 89% and 98%.
  • 42.
  • 43.
  • 44.
  • 45. Tomographic scan showing infarcted left lung, large clot in right main pulmonary artery
  • 46. CTPA Limitations  A drawback to the use of CTPA is the exposure to radiation and iodinated intravenous contrast material. A CTPA subjects the patient to an average effective radiation dose of 15 mSv (ranges between 2 and 20 mSv), which is equivalent to approximately 150 2-view chest x-rays  There are 2 primary adverse reactions to iodinated intravenous contrast media: 1. development of anaphylaxis or other immediate systemic allergic reaction. 2. contrast-induced nephropathy. Therefore, a history of allergy to intravenous contrast iodine and a history of renal insufficiency may make V/Q scan the better choice.
  • 47. Ultrasound • Non-invasive • Looks at lower limbs • Doppler USS looks at vein for flow and compressibilty to see if clot present
  • 48. USS Results • If +ve for DVT and patient has respiratory distress symptoms you can rule in a PE, since the DVTs can embolise easily and enter the lungs causing respiratory problems • If -ve for DVT, unsure whether there is a PE or not, as a clot from other part of body may have embolised the lung, or a whole DVT may have travelled to the lung • So a –ve result does not give a thorough answer, whilst a +ve result may rule it in
  • 49. ECHO • Sometimes beneficial • The right ventricle pumps blood to lungs • If clot is present the pressure at site of clot increases and so does the pressure in the right ventricle
  • 50. ECHO • The severity of this Pulmonary Artery Pressure (PAP) and the severity of the clot, is found by looking at the tricuspid valve and noting how much regurge occurs (Tricuspid jet) • If tricuspid jet is high then PAP differential between RA and RV is great and the clot burden is large • All these tests may help in the possible diagnosis of a PE, but are not definitive tests
  • 51. VQ Scan • Nuclear medicine scan • Looks at perfusion and ventilation • In pneumonia for example, you would get decreased perfusion and decreased ventilation due to the purulent material present this is a “Matched Deficit” • In a PE there is decreased perfusion of the lung in the area but ventilation remains the same this is an “Unmatched Deficit” • Does Not affect patient in renal failure • Impaired view if patient has pneumonia etc
  • 52. VQ Scan • The patients ventilation is assessed by them breathing in Xenon • For perfusion the patient is injected with Technigas (Tc99mMAA) • Use Gamma Camera (a glorified Geiger counter) to measure the nuclear material
  • 54. Probability of PE • Normal - Full ventilation and perfusion seen • Low Probability for PE – (<20%) • Intermediate probability for PE- V and P in same area (Matched deficit) (20-80%) • High Probability for PE – Normal V and P (Un-Matched deficit) (>80%)
  • 55. Gold Standard • Pulmonary Angiogram – Most accurate test, but not always best for patient (most invasive) • Catheter inserted into right side of the heart, dye is injected directly into pulmonary artery, observed under fluoroscopy • Dangerous, • mortality rate, especially in patients with PE
  • 56. Management approach Empirical anticoagulation Supportive therapies • Respiratory support • Intravenous fluids • Vasopressors • Bed rest Initial anticoagulation Thrombolytic therapy Surgical intervention Venous filters Long-term (extended) anticoagulation
  • 57. Anticoagulation • In patients with confirmed PE, anticoagulation should continue for at least 3 months. • dabigatran, rivaroxaban, apixaban, or edoxaban, are recommended over vitamin K antagonist (VKA) therapy (usually warfarin) • VKA is in turn recommended over low-molecular weight heparin (LMWH) • Fondaparinux is generally reserved for patients with heparin- induced thrombocytopenia (HIT) BMJ Best Practice Last updated Sep 12, 2016
  • 58. IVC Filter • If anticoagulation treatment contraindicated IVC Filter If clot travels it gets caught in IVC Filter
  • 59. IVC Filter • It is possible for blood clot to be caught and develop in IVC filter • Cochrane Collaboration recommends IVC for 1. Recurrent PE despite use of anticoagulation, or in absolute contra-indication to anticoagulation 2. Proximal DVT with massive pulmonary thrombosis – next one could kill patient 3. Trauma Patient – needing operation
  • 60. Prevention • Bilateral Lower Extremity Sequential Compression Devices TEDs and Flowtrons When the legs are squeezed the veins release a factor which thins the blood stopping clot formation, the rhythmic motion copies that of leg movement • Thromboprophylaxis Dalteparin
  • 61. Genetic Blood Tests • 25-50% of patients with VTE have an inherited disorder • There are genetic causes of metabolism which may be tested for - Factor V Leiden – causes increased clotting as variant cannot be inactivated by Factor Protein C (5% of popn and 20% of pts with thrombus) - Factor Protein C Deficiency – results in normal cleaving of Factor Va and Factor VIIIa - 20210 (prothrombin) Mutation – 2-3 times risk of clot formation - MTHMFR affects regulation of homocysteine - Lupus anticoagulant- prothrombotic agent which can cause inappropriate clotting - Anti phospholipid antibody – confused autoimmune response If any of these are positive and patient has a clot then may need treatment for longer
  • 62.
  • 63. Summary  The decision to discharge a patient who presents with chest pain as the primary complaint should be made only after careful consideration of potential consequences.  Evaluation and decision (with reasoning) must be well documented.  Patients with Chest Pain Are at Risk—Use Both Liberal Consultation and Liberal Admission Policies  It is better to sound foolish than be unsafe
  • 64. References  American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012 Feb;141(2 Suppl):e419S- 94S.Cayley, W.E. Diagnosing the cause of chest pain. (2005). American Family Physician, Vol 72 (10), 2012-21.  Diagnostic approach to chest pain in adults. (2014). UpToDate.  Differential diagnosis of chest pain in adults. (2014). UpToDate.  Evaluation of chest pain in the emergency department. (2014). UpToDate.
  • 65. Pearl Great EKG Practice Site http://ecg.bidmc.harvard.edu/maven/mavenmain.asp
  • 66.