PE

Question 1

definition of PE

Answer 1

Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the vascular system from another site.

Question 2

aetiology of PE

Answer 2

thrombus (>95% from DVT in lower limbs and rarely from RA in pts with AF)

clots break off and pass through the veins and the R side of the heart before lodging in pul circ

other agents: amniotic fluid embolus, air embolus, fat emboli, tumour emboli and mycotic emboli from right-sided endocarditis, RV thrombus post MI

Question 3

RF for PE

Answer 3

recent travel

recent surgery - esp abvdo, pelvic, hip, knee

hypercoagulation med

FH

previous DVT/PE

phospholipid syndrome

immobility

obesity

OCP

HF

malignancy

Thrombophilia, eg antiphospholipid syndrome

leg fracture

pregnancy/post-partum

HRT

Question 4

epidemiology of PE

Answer 4

Relatively common, especially in hospitalized patients, they occur in10–20% of those with a confirmed proximal DVT.

Question 5

sx of PE

Answer 5

depends on size and site of PE

small - may be asymptomatic

moderate - Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain.

large (or prox) - All of the above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death.

Multiple small recurrent: Symptoms of pulmonary hypertension.

can be in resp failure

dizzyness

syncope

Question 6

signs of PE

Answer 6

clinical probability assessment - Wells score >4 high probability // Revised Geneva Score (>11 high probability, 4–10 intermediate probability,<3 low probability)

pyrexia

hypotension

pleural effusion

Question 7

severity of PE

Answer 7

assessed based on associated signs:

small

• no signs
• tachycardia/tachypnoea

moderate

• tachycardia/tachypnoea
• pleural rub
• low sat - despite ox supplementation

massive

• shock
• cyanosis
• signs of R heart strain - raised JVP, L parasternal heave, accentuated S2 heart sound

multiple recurrent PE - signs of pul hypertension and RHF

Question 8

Ix for PE

Answer 8

FBC, UE, baseline clotting

low probability

• d-dimer blood test (cross-linked fibrin degradation products, highly sensitive but poor specificity).
• (high if thrombosis, inflammation, post-op, infection, malignancy)

A -ve D-dimer in a low-probability patient effective excludes PE

high probability - imaging

ECG

CXR

spiral CTPA

V/Q scan

pul angiography - gold standard, but invasive - rarely needed

US doppler of the lower limb - examine for venous thrombosis

echo - R heart strain

Question 9

Well’s score

Answer 9

if >4 - CTPA or treat with LMWH

if <4 - d-dimer

if d-dimer +ve - CTPA or LMWG

if -ve consider alternative ddx

Question 10

primary prevention for PE

Answer 10

graduated pressure stockings (TEDs) and heparin prophylaxis in at risk

early mobilisation and adequate hydration post-op

Question 11

haemodynamically stable mx of pe

Answer 11

O2

anticoag - heparin/LMWH for 5 days changing to DOAC or oral warfarin therapy (for warfarin stop heparin when INR 2-3, due to initial prothrombotic effect of warfarin) for min of 3mo

analgesics

Question 12

haemodynamically unstable - massive PE mx

Answer 12

resus

ox

IV fluid resus

thrombolysis with tPA can be considered on clinical grounds alone if cardiac arrest is imminent (50mg bolus)

• (alteplase 10mg IV over 1min, then 90mg IVI over 2h; max 1 . 5mg/kg if <65kg)

Question 13

surgical/radiological PE mx

Answer 13

Embolectomy (when thrombolysis is contraindicated).

IVC filters (Greenfield filter) may be inserted for recurrent pulmonary emboli despite adequate anticoagulation or when anticoagulation is contraindicated.

Question 14

length of PE mx

Answer 14

•Provoked: 3 months and then reassess risk to benefit profile (depends on whether risk factor persists)

Unprovoked: treatment is usually continued for >3 months (people with no identifiable risk factor)

Malignancy: continue treatment with LMWH for 6 months or until cure of cancer

Pregnancy: LMWH is continued until delivery/end of pregnancy

Question 15

DOAC for PE

Answer 15

oral alternatives to warfarin (dabigatran, rivaroxaban, apixaban, edoxaban) have been available for treatment of PE since NICE approval in 2012. They have a rapid onset of action (without the need for LMWH overlap) and can be administered in fi xed doses without the need for continuous monitoring. Monitoring is required to assess compliance, side eff ects (eg bleeding), and presence of VTE. Antidotes for DOACS are becoming available and in the USA idarucizumab is already licensed

Question 16

complications of PE

Answer 16

Death, pulmonary infarction, pulmonary hypertension, right heartfailure.

Question 17

Px of PE `

Answer 17

thirty percent untreated mortality, 8% with treatment (due to recurrent emboli or underlying disease). Patients have increased risk of future thromboembolic disease.