Revisiting Pulmonary embolism Guidelines

Pulmonary Embolism
REVISITING
Edited by:
Emad M. Qasem
Clinical Scholar
Harvard Medical School
Cardiology Resident
Sohag Heart Center
GUIDELINES

Resources
• 2019 ESC GUIDELINES FOR THE DIAGNOSIS AND MANAGEMENT OF ACUTE
PULMONARY EMBOLISM.
• 2018 CARDIOLOGY IN THE ER, A PRACTICAL GUIDE.
• PASSMEDICINE Q BANK. 2019
• CLINICAL CARDIOLOGY - CURRENT PRACTICE GUIDELINES – UPDATED EDITION
2016.

A 58-year-old man is reviewed on the surgical wards 7
days after having an anterior resection for a rectal
carcinoma.
He developed a cough 2 days ago and had a chest x-ray
which showed consolidation of the right lower lobe.
A diagnosis of post-op pneumonia was made and he
was started on broad spectrum intravenous antibiotics.
Before we go …

Over the past 24 hours he has become progressively
more short-of-breath.
On examination his respiratory rate is 30/min, heart
rate 102/min, temperature of 37.2ºC and oxygen
saturations of 92% on an oxygen concentration of 35%.
Bilateral basal crackles are noted on lung auscultation.
An ECG show sinus rhythm and no acute changes.
A chest x-ray shows bilateral infiltrates in both bases.
Before we go …

Before we go …
• Bilateral lobar pneumonia
• Heart failure secondary to a myocardial infarction
• Acute respiratory distress syndrome
• Atelectasis
• Massive pulmonary embolism
What is the most likely diagnosis?

most often arise from the deep
veins of the lower extremities
and pelvis and, very rarely, from
subclavian or arm veins.
Their consequences become
apparent when >30–50% of the
pulmonary arterial bed is
occluded.

General Considerations: Pathophysiology
▪ Acute PE interferes with both Circulation and Gas Exchange.
▪ primary cause of death in severe PE:
▪ Right ventricular (RV) failure due to acute pressure overload.

▪ PE-induced vasoconstriction, mediated by the release of
thromboxane A2 and serotonin Leading to increased pulmonary
vascular resistance and RV afterload.
▪ This leads to Inotropic and chronotropic stimulation. Together with
systemic vasoconstriction (Neurohormonal Stimulation), these
compensatory mechanisms increase PAP improving flow through The
obstructed pulmonary artery.
Temporarily stabilizing systemic blood pressure (BP).

▪ The abrupt increase in PVR results in RV dilation, which alters the
contractile properties of the RV myocardium and tricuspid
regurgitation.
▪ RV pressure overload can also lead to interventricular septal
flattening and deviation toward the left ventricle in diastole, thereby
impairing LV filling.
▪ The subsequent reduction in coronary artery perfusion pressure, in
the context of the increased wall stress, leads to RV ischemia and
subsequent failure.

RV
Coronary
Perfusion
pressure

▪ LV filling is impeded in early diastole, and this may lead to a
reduction in the cardiac output (CO) leading to hemodynamic
instability.
▪ Secondary hemodynamic destabilization that sometimes occurs 24-
48 h after acute PE.

▪ the association between
elevated circulating levels of
biomarkers of myocardial
injury and an adverse early
outcome indicates that RV
ischemia is of
pathophysiological
significance in the acute
phase of PE
▪ Theories behind secondary
destabilization:
1. Recurrence of PE.
2. PE induced myocarditis.

▪ Zones of reduced flow in
obstructed pulmonary arteries.
▪ zones of overflow in the capillary
bed served by non-obstructed
pulmonary vessels

The Key point
▪ High-risk PE is defined by hemodynamic instability and encompasses the forms
of clinical presentation.

Question 1
▪A 70-year-old retired office worker is admitted to the
medical unit with a 2 day history of shortness of breath
and chest pain on inspiration.
▪He has had a normal chest x-ray and ECG. Full blood
count, C-reactive protein, urea and electrolytes are
unremarkable. Observations are within normal levels.
▪Which scoring system should be used to determine
which investigation to perform next?

Question 1
▪A 70-year-old ,2 day history of shortness of breath and
chest pain on inspiration. Which scoring system should
be used to determine which investigation to perform
next?
1. CHA2DS2-VASC score
2. Two level Wells score
3. CURB-65 score
4. Rockall score
5. PERC score

Assessment of clinical (pre-test) probability
Predisposing
factors for
VTE
Clinical Signs
Patient
Symptoms

Clinical Presentation - Symptoms
84%
74%
59%
53%
30%
27%
14%
13%
Frequency of symptoms among patients Diagnosed as PE
* According to frequency of clinical manifestations, The PIOPED 2 study 1

Clinical Presentation
92
58
53
44
43
36
34
32
24
Signs of patients diagnosed as PE
* According to frequency of clinical manifestations, The PIOPED 2 study 1

▪Hypoxemia is frequent, but <40% of patients have
normal arterial oxygen saturation (SaO2
).
▪chest pain.
▪Pre-syncope.
▪Syncope.
▪Hemoptysis.
acute PE may be a frequent finding in
patients presenting with syncope (17%)

▪ Pulmonary embolism should be suspected in all patients who
present with:
▪ new or worsening dyspnea.
▪ chest pain.
▪ or sustained hypotension without an alternative obvious cause.
▪ but the diagnosis is confirmed by objective testing in only about
20% of patients.

Assessment of clinical (pre-test) probability
▪the most frequently used prediction rules are:
▪the revised Geneva rule.
▪the Wells rule.

ECG findings
▪RV strain— such as:
▪inversion of T waves in leads V1 V4,
▪a QR pattern in V1,
▪A S1Q3T3 pattern
▪incomplete or complete right bundle branch block
▪atrial arrhythmias, most frequently atrial fibrillation.

Echocardiography
▪ is insensitive for diagnosis.
▪ the detection of RV dysfunction is an ominous prognostic
factor.
▪ Regional RV dysfunction with free wall hypokinesia sparing
the apex (McConnel sign) is specific for PE but seen with
massive emboli.

D-dimer ELISA
▪ can be used to exclude PE in patients with a low suspicion of
PE.
▪ D-dimer is a degradation product of fibrin that is also
produced in a wide variety of conditions, such as cancer,
inflammation and dissection of the aorta, and pregnancy.
▪ The test is therefore of limited value in high probability of PE
because co-morbid conditions may have already raised the D-
dimer levels.

D-dimer ELISA
▪ The usually accepted threshold level is 500 ng/ml.
▪ but an age-adjusted D-dimer cut-off, defined as age ×
10 in patients 50 years or older, appears to be more
appropriate.

Chest CT with a multidetector scanner (MCT)
▪ MSCT chest with IV contrast is the principal diagnostic
imaging modality, with a negative predictive value of 95–
99%.
▪ MCT is considered at least as accurate as invasive pulmonary
angiography.
▪ In patients with a high clinical probability of PE and negative
findings on MCT, the value of additional testing is
controversial.
▪ Magnetic resonance imaging is less sensitive.

Ventilation perfusion (V/Q) scans
▪ are reserved for patients with:
1. renal failure.
2. allergy to contrast dye.
3. When a multidetector CT scanner is not available.
▪ A normal scan rules out a PE but is diagnostic in 20–50% of
patients with suspected PE (Good negative test).
▪ Single photon emission tomography ventilation perfusion (SPECT V/Q)
is a promising new modality with better sensitivity than planar V/Q.

Venous ultrasonography
▪ (compression ultrasonography), which has now replaced
venography, should precede imaging tests in pregnant
women and in patients with contraindication to CT scanning.
▪ Confirmed DVT in patients with suspected PE is an indication
for anticoagulation therapy.

In suspected PE cases
With shock or hypotension

In suspected PE cases
Without shock or hypotension

• In stable patients, the simplified version of the Pulmonary
Embolism Severity Index (sPESI) is a practical way for risk
stratification of patients with diagnosed PE.
• The 30-day mortality risk for PE patients is 31%.
• Shock and sustained hypotension indicate an in-hospital mortality
of 58%.
• BNP and pro-BNP elevated levels, as well as troponins , also
indicate an adverse outcome, especially in the context of
echocardiographic RV dysfunction.

Acute therapy – Hemodynamically stable
▪ Initial short-term therapy with heparin (UFH or LMWH) or
fondaparinux for at least 5 days.
▪ followed by therapy with a vitamin K antagonist for at least 3
months, depending on the risk of recurrence.
▪ LMWH are at least as efficacious and safe as UFH.
What to start?

▪ Fondaparinux is also efficacious and safe, compared to UFH.
▪ may be used in heparin-induced thrombocytopenia (although not
approved for this purpose).
▪ contraindicated in creatinine clearance <20 mL/min.
What to start?

▪UFH:
▪ IV bolus 80 IU/kg (or 5000 IU).
▪ followed by continuous infusion 18 IU/kg/h (or 1000 IU/h),
▪ aiming at aPTT 1.5–2.5 control (measured 4–6 h after bolus and 3
h after each dose adjustment).
What to start?

▪ Enoxaparin:
▪ 1 mg/kg/12 h SC (or 1.5 mg/kg/24 h)
▪ Fondaparinux:
▪ 5 mg SC (body weight <50 mg)
▪ 7.5 mg SC (body weight 50–100 kg)
▪ 10 mg SC (body weight >100 kg).
What to start?

▪ In patients with a high clinical probability of pulmonary embolism,
anticoagulant treatment should be initiated while diagnostic
confirmation is awaited.
When to start?

▪ low-risk patients might be managed on an outpatient basis after
discharge ≤ 24 h after diagnosis, with instructions on self-
performed SC injections.
When to discharge?

Vitamin K antagonists
▪ started at the first day of IV/SC anticoagulation, with a target of INR
2–3.
When to start?

▪ If PE secondary to a temporary (reversible) risk factor, therapy with
vitamin K antagonists should be given for 3 months.
▪ Risk of recurrent pulmonary embolism is less than 1% per year on
anticoagulation and 2 to 10% per year after the discontinuation of
such therapy.
For how long?

The duration of long-term anticoagulation should be based on:
1. the risk of recurrence after cessation of treatment with vitamin K
antagonists.
2. the risk of bleeding during treatment.
indefinite anticoagulation with periodic reassessment of
the risk–benefit ratio.

▪ Male sex.
▪ Proximal DVT.
▪ elevated D-dimer levels after discontinuing anticoagulation.
▪ Cancer.
▪ inherited thrombophilia (factors V and II).
▪ Obesity.
▪ unprovoked PE.

▪ An INR of 2.0–3.0 is recommended during the first 3–6 months
after the acute event.
▪ After an initial course, low-intensity therapy (INR 1.5–1.9) may be
an option.

new oral anticoagulants
▪ safe alternative to warfarin without the need for monitoring.
▪ They are used either with initial treatment with heparin (dabigatran,
edoxaban) or as a single-drug but with intensified dose for the initial
1 or 3 weeks (apixaban and rivaroxaban, respectively).
When to start?

▪ dose of 150 mg twice daily has been shown not to be inferior to
warfarin in patients with PE or deep vein thrombosis.
▪ with reduced risk of bleeding in patients already having received
heparin for 5–11 days.
dabigatran

▪ 15 mg twice daily for 3 weeks.
▪ followed by 20 mg once daily without initial heparin.
▪ equal to enoxaparin followed by a vitamin K antagonist, albeit with
less bleeding risk.
rivaroxaban

▪ 10 mg twice for 7 days.
▪ followed by 5 mg twice for 6 months without initial heparin.
Apixaban

▪ 60 mg once.
▪ Or 30 mg once in patients with creatinine clearance 30–50 mL/min
or a body weight <60 kg)
▪ Both after initial treatment with heparin
Edoxaban

Statin therapy
▪ decreases the risk of recurrent PE, irrespective of VKA

Inferior vena cava filters
▪ are recommended only in patients in whom anticoagulation cannot
be used.
▪ In patients presenting with a significant bleeding risk.
▪ inferior vena cava filter insertion compared with anticoagulant
therapy was associated with a lower risk of PE-related death and a
higher risk of recurrent VTE.
▪ Retrievable vena cava filters are preferable, since permanent vena
cava filters increase the risk of DVT.

Fibrinolysis
▪ The greatest benefit is observed when treatment is initiated within
48 h of symptom onset.
▪ thrombolysis can still be useful in patients who have symptoms for
6–14 days.
Best time to give?

Fibrinolysis
Stop or continue anticoagulation when
giving thrombolysis?
▪ UFH heparin is discontinued before thrombolysis and restarted
when the aPTT is <80 s, but it can be continued with alteplase,
reteplase or Tenecteplase.

Fibrinolysis
In low risk
▪ no benefit over conventional anticoagulation in stable, low-risk patients with
PE.
▪ In case of right ventricular dysfunction, thrombolytic therapy is associated with
lower rates of all-cause mortality and increased risks of major bleeding and
intracranial hemorrhage (especially in patients >65 years of age).
In intermediate-risk
▪ normotensive patients, fibrinolysis with Tenecteplase and heparin has also
conferred a reduction in death or hemodynamic collapse at 7 days, but at a
significant excess in hemorrhagic stroke, especially in those ≥75 years old.

Fibrinolysis
Thus, intermediate-risk patients should receive fibrinolysis
only if they decompensate
An alternative strategy in normotensive patients might consist of
reducing by 50% (or even more) the dosage of the thrombolytic agent
used
Fibrinolysis is recommended in hypotensive patients (SBP <90
mmHg)

Streptokinase
There are two regimens:
▪ Accelerated regimen: 1.5 million IU over 2 h.
▪ Conventional regimen: 250 000 IU over 30 min
▪ followed by 100 000 IU/h over 12–24 h.

alteplase
▪ 100 mg over 2 h or 0.6 mg/kg over 15 min up to 50 mg

Urokinase, reteplase and tenecteplase
Could be used.
▪ urokinase (4400 IU/kg over 10 min, then 4400 IU/kg/h over 12–24 h, or 3
million IU over 2 h.

Contraindications
▪ intracranial disease.
▪ uncontrolled hypertension.
▪ ischaemic stroke in previous 6 months.
▪ major surgery or trauma within the last 3 weeks.
▪ gastrointestinal bleeding within the last month.

Hemodynamically unstable patients
▪ Anticoagulation.
▪ Urgent CCU admission.
▪ Insert Central Venous Catheter.
▪ Modest fluid challenge.
▪ Dobutamine and epinephrine.
▪ Fibrinolysis.
▪ Percutaneous mechanical thrombectomy.
▪ Surgical embolectomy.

Modest fluid challenge
▪ (500 mL dextran) may increase cardiac index.
▪ Aggressive volume expansion may worsen RV function.
▪ Nasal oxygen should be given for hypoxia.
▪ If mechanical ventilation is necessary, positive end-expiratory
pressure should be applied with caution since it may worsen RV
failure.

Fibrinolysis
▪ offers a 59% reduction in mortality and is clearly indicated in
patients with hemodynamic instability.

Extended therapy
▪ risk factors for VTE.
▪ proximal or multiple PEs.
▪ residual vein thrombosis after anticoagulation.
▪ Abnormal D-dimer after cessation of anticoagulation.
Risk factors for recurrence

Prevention of VTE
▪ Heparin, LMWH or UF, is used for thromboprophylaxis of VTE in surgical and
medical hospitalized patients.
▪ rivaroxaban (10 mg daily for 35 days) reduced the risk of venous
thromboembolism.
▪ Enoxaparin 50 mg SC once daily.
▪ Apixaban 2.5 mg twice daily for 30 days.

Revisiting Pulmonary embolism Guidelines

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