Pulmonary Embolism Flashcards
What is an embolism? what is a pulmonary embolism? Give examples of what it can be made from
Obstruction of a BV by a foreign substance or a blood clot that travels through the bloodstream lodging in a BV, plugging the vessel
Thrombus Tumour Air Fat (90% long bone fractures) Amniotic fluid Bullet
Pulmonary embolism - the material passes through the right side ❤️ and lodges in the pulmonary arteries
What are the signs on a CXR of a fat embolism? What are the clinical signs? What about clinical signs? What is FES?
Donut sign - peribronchial cuffing
Diffuse air space opacities/ Infiltrates bilaterally
Slide 3
Petechial rash, tachycardia, fever, hypoxaemia, CNS effects
FES - fat embolism syndrome, triad lung, brain and skin emboli e.g. patent form and ovale allows embolism to reach left ❤️ -> blood to brain
What does a cerebral air embolism look like on a CT brain scan? What about after 12hrs? How can air emboli enter the body?
Midline mass effect (pushes one half over) and black lines of air seen
After 12 hrs: infarct half of brain (looks pale)
Usually iatrogenic ICU
Air entry through central venous cannulae, pulmonary artery catheters or haemodialysis catheters
How are pulmonary emboli usually formed?
90% arise from deep vein thrombosis in legs, particularly popliteal vein & more proximal veins including pelvic veins
Only 25% PE patients have symptoms or signs of DVT
Risk factors for thromboemboli
Virchow triad:
- endothelial injury
- stasis Or turbulence of blood flow
- blood hypercoagulability
- pregnancy
- Immobilisation
- previous venous thrombosis
- contraceptive pill
- long haul travel >4hrs
- cancer
- ❤️failure
- obesity
- surgery >30mins
- HRT
- thrombophilia
Risk factors for pulmonary emboli
Same as for DVT:
- overweight
- smoking
- pregnant/ postpartum period
- COCP
- HRT
- stroke
- hypertension
- CVS disease
- Immobile for long periods
- blood clotting disorders
- factor V Leiden (most common risk factor for DVT/ PE in younger ppl)
- surgery/ broken bone
- cancer
- severe injury/ burns
- > 60yrs
25% have no identifiable risks factor
What are some hypercoagulable conditions which may explain PEs?
Hypercoagulation workup should be performed if no obvious cause for emboli disease is apparent - screen for:
- antithrombin 3 deficiency
- protein C or protein S deficiency/ resistance (Factor V Leiden mutation causes resistance to activated protein C)
- lupus anticoagulant
- homocystinuria
- occult neoplasm
- CT disorders like rheumatoid arthritis
Explain how a person with a PE May get acute right ventricular overload and how this might kill them
> 30% Of total cross section of pulmonary arterial bed occluded -> Pulmonary artery pressure increases -> acute right ventricular dilation/ strain. Inotropes released to try to maintain systemic BP -> pulmonary artery vasoconstriction -> exacerbates problem
Main cause of PE death: acute right sided heart failure -> cardiogenic shock with circulatory failure or cardiac arrest secondary to arrhythmias
What can people with PE and a patent foramen ovale get?
1/3 of patients right to left shunting through PFO is present -> May severe hypoxaemia and increased risk paradoxical embolization and stroke
How can PE lead to respiratory failure?
Areas of ventilation perfusion mismatch
low right ventricle output
shunt with patent foramen ovale
How can PE lead to pulmonary infarction?
Small distal emboli May create areas of alveolar haemorrhage
-> haemoptysis, pleuritis, small pleural effusion = pulmonary infarction
10-20% cases
CXR wedge shape
Symptoms of PE
Dyspnoea 70%
Pleuritic chest pain 50%
Substernal chest pain
Cough
Haemoptysis
Syncope
Unilateral leg pain
Fever <39d, >39.5 typically not from PE
Chest wall tenderness palpating, history trauma
Signs of PE
Tachypnea RR>16/min 93%
Rales/ decreased breath sounds 50%
Accentuated second ❤️ sound (loud P2)
Tachycardia >100/min
Fever >37.8d
Diaphoresis
Low extremity oedema
Cardiac murmur
Cyanosis
Differential diagnosis for PE
Pneumothorax
Pneumonia
Myocardial infarction
Pericarditis
Pleurisy
MSK chest pain
Investigations for PE
if evidence of hypoxia requiring O2 -> blood gas: May hypoxaemia/ hypocapnia due to hyperventilation
Done to exclude other diagnosis -> CXR, most often normal
ECG: May show signs of right ventricular strain (T wave inversion right precordial leads V1-V4 and inferior leads 2,3, aVF), classic finding S1/ Q3/ T3 deep S wave lead 1, Q wave in 3, inverted T in 3 - 20%), prone supraventricular tachyarrhythmias
If normal rules out PE in those at low risk -> D- dimer - fibrin degradation product, released into blood thrombus degraded. If high likelihood (wells’ criteria score >4) but negative test: Ct pulmonary angiography
Treatment of PE in both high and low risk patients, how does it work, risks of it
Immediate heparinisation - now use subcutaneous low molecular weight heparin
- Stops thrombus propagation in pulmonary arteries and allows body’s fibrinolytic system to lyse thrombus
- Stops thrombus propagation at emboli source and reduces frequency of further PE
❌Heparin-induced thrombocytopenia: body produces antibodies to a portion of heparin that also recognise heparin-platelet complexes - binding of antibody to platelets activates them -> platelet clumps -> thombi -> DVT, PE, MI, stroke, occlusion limbs arteries
✅immediate cessation all formulations of heparin - need to use non-heparin based anticoagulants
After initial heparinisation: oral anticoagulants e.g. warfarin or rivaroxaban 3months if identifiable temporal risk factor or indefinitely if cancer or no identifiable risk factor if anti-coagulation therapy can be used
Treatment of PE in high risk patients
Haemodynamic support
Respiratory support
Exogenous fibrinolytics (streptokinase/ tPA)
- peripheral IV
- delivered directly via percutaneous catheter into pulmonary arteries
percutaneous catheter directed thrombetomy
Surgical pulmonary embolectomy (if severe)
How do you treat patients of low and high risk after initial heparinisation if no form of anti-coagulation therapy can be used?
Inferior vena cava filter - umbrella stops clots temporarily
How to prevent PE/ DVT?
- outpatient recognise and address risk factors e.g. if high risk shouldn’t be placed on OCP or HRT, advice for ppl with thrombophilia who travel >4hrs (wear stockings, walk, drink, don’t sleep)
- impatient DVT prophylaxis post-surgery/ with malignancy
Balance risks of DVT with risks of bleeding
