A lecture on Pulmonary Embolism in Emergency Department, presented at Burjeel Hospital Emergency department Seminar, by Dr Muhanad Majeed

1. Dr. Muhanad Majeed
Emergency Physician
Burjeel Emergency Medicine Seminar
Pulmonary Thrombo-embolism Management in
Emergency Department

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

7. Gross Anatomy

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)

10. Clinical Presentation

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.”

15. Risk stratification
Wells score

16. Risk stratification
Wells score

17. Risk stratification
Simplified Revised Geneva Score

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

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

29. pulmonary infarct

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

34. D-dimer

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%.

41. Spiral CT

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

53. Probability of PE

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

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

67. Thank You.