Pulmonary Embolism

Question 1

Define PE.

Answer 1

A consequence of thrombus formation within a deep vein of the body, embolising to pulmonary vasculature.

Question 2

What is Virchow’s triad?

Answer 2

1. stasis
2. hypercoagulability
3. vessel wall damage

Question 3

Describe the epidemiology of PE.

Answer 3

Approximately 51% of DVTs will embolise to the pulmonary vasculature, resulting in a PE.

UK ~50,000 a year

1-1.5/1000 population per year

Question 4

What are the risk factors for PE, relative to Virchow’s triad?

Answer 4

Vessel wall damage - cell damage –> thrombus formation at venous valves. Examples:

• trauma,
• previous DVT,
• surgery,
• venous harvest,
• central venous catheterisation

Venous stasis - poor flow/stasis cause thrombi and result in valvular damage, further promoting thrombus formation. Stasis increased in:

• >40yrs
• immobility
• general anaesthesia
• paralysis
• spinal cord injury
• MI, stroke,
• varicose veins,
• advanced congestive HF,
• advanced COPD

Hypercoagulability - inherited + acquired conditions:

• cancer,
• high oestrogen,
• IBD,
• nephrotic syndrome,
• sepsis,
• blood transfusion,
• inherited thrombophilia

Question 5

Name 5 types of inherited thrombophilia –> hypercoagulability.

Answer 5

• Factor V Leiden mutation
• Prothrombin gene mutation
• Protein C and S deficiency
• Antithormbin deficiency
• Antiphospholipid antibody syndrome

Question 6

Describe the consequences of pulmonary embolism on the heart.

Answer 6

Rarely de novo. Usually DVT –> emboli. Obstruction increases pulmonary vascular resistance (PVR) increasing the WORK or RIGHT ventricle –> increased HR (Frank-Starling). Eventually PVR is so high that there is

• over-distension of the RV
• increased RV end-diastolic pressure
• decreased RV cardiac output —> decreased LV preload –> hypotension and shock

Question 7

What are the differences between the thrombi formed in arteries and deep veins?

Answer 7

DVT = fibrin and entrapped erythrocytes (red clots). Platelet aggregation is not seen at the site of thombus attachment.

Question 8

What percentage of pulmonary vasculature needs to be occluded to cause hypotension and shock?

Answer 8

In healthy individuals it can be as little as 50%

Question 9

Symptoms of pulmonary embolism.

Answer 9

• Feeling of apprehension
• Cough (+haemoptysis)
• Presyncope or syncope
• Chest pain
• Dyspnoea
• Fever (in 10%)

Question 10

What are the signs of pulmonary embolism on physical examination?

Answer 10

• Hypotension (systolic BP<90mmHg)
• Tachypnoea
• Tachycardia
• Elevated JVP (if cor pulmonale present)
• Fever
• HEAVES (sternal)
• Accentuated pulmonary component of S2 (if cor pulmonale present)
• Unilateral swelling/tenderness of calf

Question 11

What initial and later investigations would you do for a PE?

Answer 11

History and examination, followed by 2 level Wells score to estimate clinical probability of PE.

Wells >4 then PE likely so:

1. Admit
2. Arrange immediate CTPA (or V/Q)
3. Interim anticoagulation if delay

Wells 4 or less PE unlikely:

• D-dimer test within 4 hours
• Interim anticoagulation if delay
• CTPA if positive D dimer -
• Interim anticoagulation if delayed
• Stop anticoagulation if negative CTPA

Other tests to consider:

• Coagulation studies (INR, PT, aPTT to establish baseline)
• ABG - hypoxia and hypocapnia
• CXR
• ECG
• Lower limb USS
• V/Q scan
• Echo
• U&E
• Thrombophilia screen
• BNP, NT-proBNP, H-FABP.

Question 12

What are the Wells and Geneva scoring systems?

Answer 12

Question 13

Describe the results of these scans in PE:

CTPA

V/Q scan

Bloods:

Answer 13

CTPA - direct visualisation of a thrombus in pulmonary artery (partial or incomplete)

V/Q scan - an area of ventilation will not be perfused in V/Q scan

Bloods:

1. Coagulation studies - establish a baseline prior to commencing anticoagulation
2. U&E - guide anticoagulation
3. D-dimer - ELEVATED but should not be done if the likelihood of PE is already high

Question 14

What might you see in CX of pulmonary embolism? What is sometimes seen on ECG?

Answer 14

CXR:

• band atelectasis
• elevation of hemidiaphragm
• prominent central pulmonary artery (Fletcher’s sign)
• oligaemia at site of embolism

ECG: “S1Q3T3” pattern of acute cor pulmonale is classic; this is termed the McGinn-White Sign. A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain.

Question 15

Why do you give IV fluids to someone with massive PE?

Answer 15

Given if systolic BP is <90mmHg

Question 16

How do you manage a PE?

Answer 16

Emergency:

• ABCDE
• Respiratory support e.g. O2
• Anticoagulation 3-6months e.g. rivaroxaban 15mg BD 3 weeks days followed by maintenance 20mg OD

Conservative:

• Monitor anticoagulation
• Provide leaflet on anticoagulation

Medical:

• Anticoagulation 3-6 months
• Thrombolysis - systemic or catheter-directed
• Open pulmonary embolectomy

Surgical:

• IVC filter -consider in those who cannot have anticoagulation

Question 17

Why do you give these treatments in massive PE w/ shock/hypotension?

Vasopressors

IV fluids

Answer 17

IV fluids - if systolic BP is <90mmHg but aggressive volume expansion is of no benefit and may worse RV function.

Vasoactive agents (noradrenaline/dobutamine/adrenaline) - if systolic BP is less than 90mmHg then these vasopressors may be given to improve RV function and RV coronary perfusion but should be limited to hypotensive patients.

Question 18

Which anticoagulants and thrombolytic therapy would you use in PE?

Answer 18

Offer:

1st line - apixaban or rivaroxaban

If these are not suitable: LMWH for at least 5 days followed by dabigatran or edoxaban.

Length of treatment depends on whether it is provoked or unprovoked.

Question 19

What are the complications of PE and its management?

Answer 19

Complications:

• Acute bleeding during treatment
• Pulmonary infarction
• Cardiac arrest/death - due to acute RV failure
• Chronic thromboembolic pulmonary hypertension
• Heparin associated thrombocytopenia
• Recurrent venous thromboembolic events

Question 20

What is the prognosis in PE?

Answer 20

• If left untreated then prognosis is poor → chronic thromboembolic pulmonary hypertension → HF
• Mortality rate is higher if patients are over 70, have cancer, CCF, COPD, systolic arterial hypotension, tachypnoea and RV hypokinesis on echo.

Question 21

How can you manage cardiac arrest due to PE?

Answer 21

Usual CPR, adrenaline +/- defibrillation if VF/VT

Can administer thrombolysis if patient is not responding to ALS

Question 22

What is the diagnosis?

Answer 22

Saddle PE - causing a PE on both the left and right sides.