PULMONARY EMBOLISM

(P.E.)
BY:

PROFESSOR SALIH BIN SALIH

Chairman, Department of Medicine
King Abdulaziz Medical City
Professor of Medicine, College of Medicine
King Saud Bin Abdulaziz University for Health Sciences (KSAU-HS)
OUTLINE OF PRESENTATION:
Definition (Embolism, P.E., Massive P.E.)

Prevalence

Risk Factors

Pathophysiology

Clinical Features (including massive P.E.)

Diagnostic work-up

Treatment

Prevention
Definitions:
An embolism: is any detached solid, liquid or gaseous mass carried by
the blood to a site distant from its origin, the vast majority are part of a
dislodged thrombus.

Pulmonary embolism: (venous thrombo embolism that is occlusing the

pulmonary artery or some of its branches due to a dislodged thrombus in
the vast majority.

Venous thomboembolism (VTE): describes both P.E. and DVT.

Massive P.E.: Obstruction of the pulmonary arterial tree by more than

50% of the cross-sectional area, causing acute and severe cardio
pulmonary failure from right ventricular overload. It may result in death
within few hours and discovered with autopsy only.
Prevalence and Extent of the Problem of P.E.
About 20-25/100,000 of hospitalized patients may develop P.E. leading to about
200,000 deaths every year in USA.

It is the 3rd leading cause of death among hospitalized patients, and most cases are not
recognized ante-mortem.

Less than 10% of patients with fatal emboli have received specific treatment for the
condition.

More than 95% of P.E. cases source originates from deep leg veins: above the knee
such as iliofemal DVT (the most common), as well as pelvic or calf veins.

Other veins also: superficial femoral, renal, uterine and right cardiac chamber.

It is life threatening, preventable, and a significant cause of morbidity and impair
quality of life (post-thrombotic syndrome).
Risk Factors for P.E.
Same risk factors for DVT (Virchow Triad)
1. Venous Stasis
2. Injury to the vessel wall
3. Hypercoagulability state
1.) Venous Stasis: increases with immobility:
Obesity
Stroke
Bed rest – especially post-op
Hyperviscosity (polycythemia)
Increased Central Venous (low cardiac output state,
pregnancy)

2.) Injury to the vessel wall:

Prior episode of thrombosis
Orthopedic surgery
Trauma
3.) Hypercoagulability State:
Medications (oral contraceptives, Hormonal replacement
Therapy – HRT)

Disease Condition (Malignancy, Surgery)

Inherited gene defects:

 Resistance to activated Protein C (Factor V Leiden)
 Deficiency or dysfunction of Protein C, Protein S and anti-thrombin.

 Prothrombin gene mutation

Presence of Antiphospholipid antibodies (Lupus

Anticoagulants, and Anticardiolipin Antibodies)
Pathophysiology of P.E.
Blocking portion of pulmonary vasculature leads to :
pulmonary vascular resistance and PAP  RV pressure.

  Filling of LV  CO  Hypoxemia  stimulates

vasoconstriction  in PAP.

  blood flow in some areas of lung  Hyperventilation  Dead

space created in the lung (low perfusion & high ventilation)

Note: If recurrence happens, this  pulmonary HTN and chronic cor

pulmonale

 Severe (Large P.E.)  Acute Cor Pulmonale

Clinical Features
Most often, P.E. is clinically silent.
I. Symptoms:
 Dyspnea (on rest or exertion)
 Pleuritic chest pain
 Cough
 Leg pain
 Hemoptysis
 Palpitations
 Wheezing

II. Signs:
 Increased R.R. (tachypnea)
 Crackles (Rales)
 Tachycardia
 Accentuated P2 (Pulmonary Component of Second HS)
 Pleural friction Rub
 Cyanosis
 Syncopal episodes
 Systolic hypotension or shocked
 Raised JVP – prominent A waves, Right V heave
 Gallop rhythm (S3, S4, or both)

Note: P.E. may present without an associated DVT

 30 % of DVT may have silent P.E., and 70% of patients with P.E, have an associated DVT which is sypmtomatic in 25% of cases
Massive P.E.
Massive thrombus may cause RV failure.

Vascular obstruction increases physiologic dead space

(wasted ventilation) and leads to hypoxemia through
right-to-left shunting, decreased cardiac output, and
surfactant depletion causing atelectasis reflex broncho
constriction promotes wheezing and increased work of
breathing.

About 50% of P.E cases have massive P.E., 70% of them

die within the first hour after onset of symptoms
Differential Diagnosis:
Pneumonia
Asthma
Pneumothorax
C.H.F.
Acute Coronary Syndrome
Costochondritis
Musculoskeletal pain or rib fracture (Post – traumatic)
Aortic dissection
Pericardial tamponade
Lung Cancer
Primary Pulmonary hypertension
Anxiety hyperventilation
Diagnosis:
Differential diagnosis is very wide.

P.E. diagnosis should be excluded rather than confirmed.

Clinical features are often non-specific and the majority

of P.E. cases are missed and die.

If suspected should be excluded once you think of it, and

to identify rapidly and accurately when urgent treatment is
required.
 Initial Investigations:
ECG – Sinus Tachycardia – it is more common to see
 The classical picture seen in S1Q3T3 (Prominent S in Lead 1, Prominent Q wave and inverted T wave in lead III) – and seen in minority of cases.
 RV Strain pattern & RBBB may be seen

Chest X-ray: may be normal

 May show non-specific abnormalities such as: atelectasis, parenchymal abnormalities, cardiomegaly, elevation of the hemidiaphragm or a pleural effusion.

ABG Analysis:
 Typically, blood gases show hypoxia and hypocapnia – but they are non-specific and not always present.

Bio-maker of Cardiac injury:

 BNP or Pro-BNP maybe elevated because of RV stretching
and Troponin and injury & strain – non specific findings
Imaging for P.E.
 CT pulmonary angiography (CTPA): the most common imaging technique,
widely available, and sensitive.

 Ventilation perfusion (V/Q) isotope lung scanning: +ve mismatched defects

in the perfusion scan – indicating impaired blood flow to the lungs – but
normal ventilation because air entry to the lungs is normal.

Timescale of investigation:
 Diagnostic testing for VTE should be performed within 24 hours of initial
presentation.
 When imaging is required, the first dose of anticoagulant should be given –
if it will take more than 1 hour for suspected P.E. and 4 hours for suspected
DVT.
Diagnosis of P. E.
Risk scoring (Wells score):
 4 likely
£ 4 unlikely

Measurement of D-Dimer:
If negative, VTE (DVT and or P.E.) is very unlikely especially if Wells score is
low.
But if Wells score is low, and D-Dimer is raised, then radiological imaging is
required to confirm or exclude VTE.

Imaging for DVT (if present):

Doppler Ultrasonography
 Positive in 95% of Proximal DVT
 Positive 70 of Distal DVT quicker and non-invasive

Venography: Not used nowadays, used to be the gold standard.

Initial Treatment:
Traditional:
 Parenteral
anticoagulant
 Intravenousunfractionated heparin (UFH)
 Low MW Heparin (S.C.)
 Fondaparinux (S.C.)

Oral Vitamin K antagonist (e.g. warfarin)

(Needs at least 5 days to provide therapeutic anticoagulation), and monitored by P.T and INR

Direct Oral Anticoagulants (DOACs)

 Edoxaban and Dabigatran: usually started after 5 days of parenteral anticoagulation wish Low MW Heparin
 Apixaban and Rivaroxaban: Do not need parenteral anticoagulation.

Note: In pregnancy, warfarin and DOACs are contraindicated as they cross the placenta.

In breast-feeding mother, warfarin and Low MW Heparin are safe, but DOACs safety is not
established.

Duration of therapy: at least 3 months.

Treatment of P. E.
1. Symptomatic (supportive) treatment.

2. IV unfractionated heparin (UFH)

3. Thrombolytic therapy – if indicated

4. Oral Anitcoagulants

5. Inferior Vena Caval filter (umbrella).

Prevention of VTE
Prevention is better than cure

The frequency of VTE among hospitalized patients ranges widely, 20% in medical patients
and to 80% of critical care patients and high risk surgical patients.

Padua risk assessment model is used,  4 is high risk group, and should receive prophylaxis.

High risk group: includes recent major ortho surgery, Abdominal/pelvic cancer for Surgery,
and more than 3 of the intermediate risk factors.

Intermediate risk: includes not ambulating outside the room twice/day, active infection or
malignancy, major surgery (non-ortho), previous history of VTE or stroke, central or PICC line,
IBD, Obesity (BMI  30), Age 60. HRT or contraceptive use, hyper coagulable state, burns,
cellulitis, varicose veins, COPD, and H.F.

Low Risk:
 Minor procedure and age  40 years with no other risk factor.
 Minor surgery or immobility for 24 hours
Pharmacologic Prophylaxis:
I. Parenteral
I. Enoxaparin: 30 – 40 mg subcutaneously once or twice /day
II. Dalteparin: 2500 – 5000 units subcutaneously once per day
III. Fondaparinux: - 2.5 mg subcutaneously once per day
IV. Unfractionated heparin: 5000 units subcutaneously 2-3
times/day.

II. Oral
I. Rivaroxavan: 10mg once/day
II. Apixaban: 2.5 mg twice/day
III. Dabigatran: 110 mg first day, then 220 mg once/day
IV. Warfarin: variable, once/day (INR Goal 2.5)
V. Aspirin: Variable (for hip and knee replacement.