Pulmonary embolism

Pulmonary Embolism:
⇨ Early deaths in PE are usually the result of
acute right ventricular (RV) failure and
cardiogenic shock.
⇨ After the first few days, mortality is less
common and mostly determined by
recurrent thromboembolic events and the
underlying disease state
2

Etiology
⇨ DVT and PE are components of a single disease
termed venous thromboembolism (VTE).
⇨ Embolisation of DVT to the pulmonary arteries
leads to PE.
⇨ Incidence of VTE: 1 in 1000 per year
4

VTE: Predisposing Risk Factors
1. Venous Stasis
2. Vein wall injury
3. Hypercoagulability of blood
4. Others: Immobility, Surgery, Trauma,
Malignancy, Pregnancy, Thrombophilia
5

Thrombophilia:
⇨ Any abnormality of blood coagulation that
increases the risk of thrombosis
⇨ Can be heritable or acquired.
6

“As most people with thrombophilia do
not develop DVT or PE, and diagnosis
of thrombophilia does not affect
immediate and in most cases long-
term management of these patients
7

Heritable thrombophilias:
⇨ Present in 5 percentage of the population
⇨ Most common: activated protein C
resistance, which is mediated by the factor
V Leiden mutation
8

Higher Risk Factors for DVT than PE:
1. Factor V leiden mutation
2. Oral Contraceptive use
3. Pregnancy
4. Puerperium
5. Obesity
6. Minor leg injuies
9

Higher Risk Factors for PE than DVT:
1. COPD
2. Sickle cell disease
3. Pneumonia
10

Etiology:
⇨ Most PE results from DVT in the lower limbs,
pelvic veins or IVC, although thrombi can
develop in the right atrium, right ventricle and
upper limbs.
⇨ Up to 40 percentage of patients with DVT
develop PE, although if the DVT is isolated to
below the knee, then clinically obvious PE is rare.
11

Pathophysiology:
⇨ Pulmonary arterial obstruction and the
subsequent release of vasoactive
substances such as serotonin and
thromboxane A2 from platelets lead to
elevated pulmonary vascular resistance
and acute pulmonary hypertension
13

Pathophysiology
⇨ Acute pulmonary hypertension increases
RV afterload and RV wall tension which
leads to RV dilatation and dysfunction
with coronary ischaemia being a major
contributing mechanism.
14

Factors causing LV dysfunction
and obstructive shock in PE:
1. Coronary Ischemia
2. RV systolic failure
3. Paradoxical interventricular septal shift
4. Pericardial constraint
15

Clinical Presentation:
⇨ relatively uncommon in critically ill
patients despite the frequent presence of
risk factors for VTE
⇨ Up to one in six patients have the
diagnosis made more than 10 days after
symptom onset.
17

Clinical Decision Rules:
⇨ Based on Objective Parameters (Signs,
Symptoms, Risk Factors):
1. Geneva (Accepted)
2. Pisa
3. Charlotte
4. Pulmonary Embolism Rule-out Criteria
18

⇨ Requiring Clinician Judgement:
1. Wells Score (Accepted)
19

⇨ With either strategy, patients can have their
probability determined as:
1. Unlikely: in whom PE can be safely ruled out
with a negative D-dimer result
2. Likely: in whom an imaging test is required and
in whom prompt anticoagulant therapy should
be considered
20

Symptoms:
⇨ Classic Symptoms:
1. Dyspnea
2. Pleuritic chest pain
3. Hemoptysis
⇨ Most patients will have at least one of
these symptoms, with dyspnoea being the
most common
21

Symptoms:
⇨ The combination of pleuritic chest pain
and haemoptysis reflects a late
presentation where pulmonary infarction
has occurred.
⇨ If syncope occurs, and there is no other
obvious cause, it is likely that this is a
massive PE.
22

Physical Signs:
⇨ Most frequent sign: Tachypnea
⇨ Others:
1. Tachycardia
2. Fever
3. RV dysfunction (Raised JVP, Parasternal
heave, Loud pulmonary component of
second heart sound)
23

Investigations:
⇨ Imaging test of first choice: CTPA scanning
⇨ D dimer
⇨ Biomarkers
⇨ Arterial Blood Gases
⇨ Electrocardiograph
⇨ Chest X-Ray
25

D-Dimer:
⇨ Useful for exclusion of VTE, particularly when
it is normal and combined with a low-risk
clinical assessment
⇨ Negative D-dimer tests, particularly using
ELISA, ELFAs and latex quantitative assays, are
highly predictive of the absence of both DVT
and PE
26

D-Dimer:
⇨ A high D-dimer concentration is also an
independent predictive factor associated with
mortality.
⇨ D-dimer levels are often elevated in ICU patients
for reasons including infection, inflammation,
cancer, surgery and trauma, acute coronary
syndrome, stroke, peripheral artery disease or
ruptured aneurysm. 27

D-Dimer
⇨ D-dimer tests should be used with caution in
patients who are elderly (as the upper limit of
normal increases with age), who have prolonged
symptoms and who are already receiving
therapeutic anticoagulant therapy.
⇨ Reporting units and performance of the assay used
by the laboratory need to be considered when
using D-dimer cut offs to rule out PE.
28

Age Adjusted D-Dimer Cut off:
⇨ defined as age in years × 10 in patients above
50 years of age
⇨ Increases the number of low-to-intermediate
probability patients:
1. Revised Geneva score <5 or
2. Wells Score </= 4) in whom PE can be safely
ruled out.
29

Biomarkers:
⇨ Little use for confirming or excluding the
diagnosis
⇨ Assist in risk stratification of patients with
diagnosed PE
30

Biomarkers:
⇨ Admission troponin levels may be falsely
low in some patients who present early,
so the troponin level at 8 hours is a better
marker for risk stratification for these
patients
31

Heart Fatty Acid Binding Protein:
⇨ Cytoplasmic protein which appears in the
circulation as early as 90 minutes after
myocardial injury
⇨ Is an emerging biomarker for predicting
adverse outcomes after PE
32

Arterial Blood Gases:
⇨ A normal arterial blood gas profile does not
exclude the diagnosis of PE
⇨ Hypoxaemia (with a widened alveolar-arterial
oxygen gradient), hypocapnia and an increased
end-tidal CO2 gradient should raise the suspicion
of PE, even if these are common findings in
critically ill patients for other reasons.
33

Arterial Blood Gases:
⇨ Metabolic acidosis may be present if
shock from a large PE occurs
34

Electrocardiograph:
⇨ Normal ECG is found in 1/3rd of patients
⇨ ECG abnormalities and the presence of atrial
fibrillation are associated with a higher risk of
adverse outcomes.
⇨ Also useful in excluding acute myocardial
infarction and pericarditis.
35

“Presence of T-wave inversion
in both lead III and V1
increases the likelihood of PE
as compared to acute coronary
syndrome
36

Electrocardiograph:
⇨ Most frequent ECG abnormalities are:
1. Non-specific S–T depression and T-wave
inversion in leads V1–V4
2. Right bundle branch block
3. S1Q3T3 pattern (deep S-wave in lead I and a
Q-wave and inverted T-wave in lead III)
4. S-T segment elevation in lead AVR, reflecting
right heart strain
37

Chest X-Ray
⇨ often normal or only slightly abnormal
⇨ Non-specific signs:
1. Cardiac enlargement
2. Pleural effusion
3. Elevated hemidiaphragm
4. Atelectasis and localised infiltrates
38

Chest X-Ray
⇨ More specific findings are uncommon and include:
1. Focal oligaemia
2. A peripheral wedge-shaped density above the
diaphragm (Hampton hump)
3. An enlarged right descending pulmonary artery
(Palla sign)
39

Imaging:
⇨ Required in any patient with a high or likely
clinical probability
⇨ CTPA scan has the advantages:
1. Greater diagnostic accuracy
2. Ready availability at most hospitals
3. More rapid image acquisition time
4. Possibility of making an alternative diagnosis
40

CTPA:
⇨ Can be used to assess the severity of PE
⇨ Increased RV/LV ratio is the most
significant marker of severity of PE.
⇨ Can also identify the causative DVT in the
veins of the legs, pelvis and abdomen or
detect alternative or additional diagnoses
41

CTPA:
⇨ Severity stratification is further increased
by combining CTPA scanning with other
tests such as troponin, BNP or NT-Pro-
BNP
⇨ Planar and SPECT V/Q scan retain a role
when CTPA is either unavailable or
contraindicated
42

SPECT V/Q
⇨ SPECT V/Q has equivalent diagnostic yield
to CTPA, with lower radiation dose
43

Factors associated with worst
outcomes:
1. An increased RV/LV ratio
2. High thrombus load
3. Central location of the clot
44

Echocardiography:
⇨ The most common findings:
1. RV dilatation
2. RV hypokinesis
3. Paradoxical interventricular septal motion
towards the LV
4. Tricuspid regurgitation
5. Pulmonary hypertension 45

“The pattern of RV hypokinesis with
apical sparing (McConnell sign)
reflects tethering of the RV apex to
the hyperdynamic LV and was
considered pathognomonic for PE
46

Echocardiography:
⇨ Pulmonary acceleration time less than 60 ms
with maximum tricuspid regurgitate pressure of
less than 60 mmHg (60/60 sign) may be more
sensitive for diagnosing PE in patients without
underlying cardiorespiratory comorbidities
⇨ The presence of RV dysfunction correlates with
mortality
47

Transthoracic Echocardiography:
1. Allows estimation of pulmonary arterial pressure
2. Identification of intracardiac thrombi
3. Aids in differential diagnosis by raising suspicion
of aortic dissection
4. Directly identifies embolus in proximal pulmonary
arteries
48

Anticoagulation
If a leg DVT is confirmed,
anticoagulation is required
unless the DVT is entirely below
the knee where the associated
morbidity is low
49

Ultrasound:
⇨ Highly accurate in symptomatic or
proximal DVT
⇨ Best use is when a CTPA scan is
contraindicated
50

Ultrasound:
⇨ Proximal compression ultrasound (CUS)
with four-point compression (bilateral
femoral vein at the saphenofemoral
junction and bilateral popliteal veins) has
excellent specificity for diagnosis of PE in
the right clinical setting
51

Hemodynamically Stable Patient:
⇨ Preferred initial test: CTPA scan
⇨ If positive, the patient should be stratified
into high or moderate risk
⇨ The presence of clot within pulmonary
arteries confirms the diagnosis of PE.
53

⇨ If a CTPA scan is not possible
(contraindicated or unavailable), an
alternative investigation such as a V/Q
scan, MRA or ultrasound should be
considered
54

⇨ Echocardiograph: to assess RV dysfunction
for high risk patients who have:
1. Clot within proximal pulmonary arteries
2. Raised RV/LV ratio (i.e. >0.9–1.0)
3. Raised troponin (repeated at 8 hours if not
elevated on admission), BNP or NT-pro-BNP.
55

Hemodynamically Unstable Patient:
⇨ First Test: Echocardiograph perferably
Transesophageal if patient is intubated
⇨ If the patient has acute RV dilatation with
systolic dysfunction and visible embolus,
PE is confirmed.
56

⇨ If there is RV dilatation with or without systolic
dysfunction but no visible embolus, then a CTPA
scan is required depending on how unstable the
patient is
⇨ If there is no RV dilatation, the haemodynamic
instability is unlikely to be due to PE. Finding an
alternative diagnosis is the priority.
57

⇨ If echocardiography is not readily available, a
CTPA scan should be performed unless a
proximal CUS can expediently confirm a DVT
58

Management:
⇨ Once PE has been confirmed, patients at all
levels of severity should receive anticoagulation
with either unfractionated or LMWH), or newer
oral anticoagulants (NOACs), to prevent further
embolisation
⇨ To assist in planning management it is important
to grade the severity of PE
60

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Red
Is the color of blood, and
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Is the color of gold, butter
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spectrum of visible light,
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Blue
Is the colour of the clear sky
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courage
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of ebony and of
outer space
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of gold, butter and
ripe lemons
White is the color
of milk and fresh
snow
Blue is the colour
of the clear sky
and the deep sea
Yellow is the color
of gold, butter and
ripe lemons
White is the color
of milk and fresh
snow
Blue is the colour
of the clear sky
and the deep sea
danger and
courage
Black is the color
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1 3 5
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2
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clear sky and the deep
sea
danger and courage
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space
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lemons
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SWOT Analysis
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WEAKNESSES
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