Diagnosis and Treatment of Pulmonary Embolism Flashcards

1
Q

Why do emboli end up in the lungs?

A

All blood goes through the lungs
Lungs act as a protective filter - better able to deal with emboli than areas in systemic circulation such as the brain.

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2
Q

Why are the lungs an adapted organ to be the site of emboli/thrombi?

A

Immune organ - increased B and T cell response
Anti-inflammatory in highly oxidative environment
Have a high capacity to cope with some damage to lungs - shown by good survival after pneuomonectomy.

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3
Q

What are the different types of embolism?

A

Mycotic (infective)
Fat
Air
Thrombotic

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4
Q

Where to thrombotic pulomonary embolisms normally arise from?

A

Mostly from deep veins of the legs (iliac, femoral and popliteal)
Also be from IV lines or upper limb

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5
Q

What is Paget Schroetter related to upper limb thrombosis?

A

When the upper limb has an increased risk of a DVT in the axillary or subclavian veins due to extrinisic compression or repetitive injury
Often from the subclavian vein being pressed against the junction of the first rib and the clavicle
May be termed effort thrombosis.

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6
Q

What is a mycotic embolus?

A

A transfer of infective pathogens to lungs from a distant source

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7
Q

What are the common causes of a mycotic embolus?

A

Intravenous drug use - iatrogenic drug infusion, blood transfusions or illicit drug use.
Infective endocarditis.

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8
Q

What signs can indicate a mycotic emboli?

A

Oslers nodes, Janeway lesions, roth spots and splinter haemorrhages Indicates systemic emboli often from infective endocarditis.
Oslers nodes - digits, pink with pale centre, painful
Janeway lesions - non-painful, patches on palm of hands
Splinter haemorrhages - red/purple lines under nail bed following direction of nail growth.
Roth spots - small haemorrhages on eyes

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9
Q

How might infective endocarditis by indentified in the heart?

A

Ultrasound - greyscale (growth around the valve)

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10
Q

What imaging technique is commonly used to visualise a potential embolus/thrombus in the lungs?

A

Chest CT
Chest angiogram.

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11
Q

What causes a fat embolus?

A

Normally a fracture in a long bone - where large amounts of fat-containing bone marrow can be released.
Causes multifocal inflammation in the lungs.

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12
Q

What causes an air embolus?

A

Occurs from incorrect canulation that then allows gas into the veins
In most scenarios the lungs act as a filter and are able to deal with the air embolus
However, in certain scenarios such as (Osler-Weber-Rendu) can be fatal and care should be taken not to inject certain patients unnecessarily

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13
Q

What is Osler-Weber-Rendu syndrome?
How does this link to pulmonary embolus?

A

Is a genetic autosomal dominant condition
Causes the formation of AV anatamosis in the skin, mucosa, GIT and lungs etc.
These anastomosis already cause respiratory problems for the patient - hypoxemia, haemorrhage
Also allow passage of an emboli from pulmonary to systemic circulation (without return to the heart) this is known as a paradoxical emboli
May predispose the patient for a cerebral abscess or stroke.

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14
Q

How do patients with Osler-Weber-renu syndrome often present?

A

Most to least common symptoms
Nose bleeds
Skin, lips and mouth telangescesica
Pulomonary, hepatic AVMs
GIT bleeds
Cerebral AVMs
Spinal AVMs.

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15
Q

What is the consequence of a large air emboli in the heart?

A

Heart chamber does not fill with blood as is airlocked
Heart contracts around air
Causes sudden cardiocirculatory collapse and sudden death.

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16
Q

What is cardiocirculatory collapse?

A

Severe hypotension resulting in cerebral hypoperfusion and loss of consciousness
Decreased blood flow to organs can be fatal.
Cause of sudden death.

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17
Q

What is the dual circulation to the lungs?
How is this beneficial?

A

The pulomonary arteries supply deoxygenated blood to the lungs, which is them oxygenated and returned to the heart via the pulmonary veins

The bronchial arteries provide high pressure oxygenated blood to the lungs to supply the parenchyma, then drain back via the bronchial veins into systemic circulation.

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18
Q

Why are the lungs less sensitive to damage from emboli than other areas?

A

Dual circulation - pulmonary obstruction, bronchial arteries can oxygenate the tissue.
Abundant collateral circulation to different areas of the lungs.
Alveoli are full of air so simple diffusion will supply the cells to a degree.
Tissues are less sensitive to anoxia
Because of the extensive collateral circulation and the efficiency of gas transfer there is minimal impact on O2 saturation assuming the emboli are small and not continuously arriving.

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19
Q

How does the rate of thrombus/air emboli absorption vary from the lungs to other tissue?

A

The lungs absorbed all emboli faster than other tissue
However, thrombotic emboli always take longer to absorb than air in all tissue
The more sensitive to anoxia a tissue is the longer it will likely take to absorb an emboli.

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20
Q

What does Virchows triad state will increase the risk of thrombus formation?

A

Venous statis - immobile patients, long flight, after surgery etc
Endothelial disruption/surgery - around cannulas, central lines or from hypertension
Hypercoagulability - obesity, smoking, cancer, antiphospholipid syndrome.

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21
Q

How common is it for a DVT to form a PE?

A

50% untreated DVT will form a PE

22
Q

What are some statistics showing why the number of pulmonary embolisms is so high?

A

80% of pelvic surgery patients develop DVT post surgery
- Common cause of adult sudden death, in patient death and all deaths.
The risk of DVT increases with age

23
Q

What are the pathological consequences of a PE?

A

The lung tissue is ventilated but not perfused, this area of lung may infarct (chest pain) but often does not due to the collateral blood supply.
Results in intra-pulmonary dead space and impaired gas exchange (resulting in shortness of breath)
Reduction in cross-sectional area of the pulmonary arterial bed
Elevation of pulmonary arterial pressure
Reduction in cardiac output as left heart filling decreases, high RA pressure can reopen the patent foramen ovale.
Potential circulatory collapse and cardiac arrest due to RVD
Alveolar collapse occurs worsening hypoxemia.

24
Q

What are the outcomes of a pulmonary embolism?

A

Untreated PE - 10% die within one hour and 30% die within 1 month
67% of deaths are not diagnosed pre-mortem
34% show rapid detrioration prior to death making them hard to treat fast enough
If PE is treated it reduces your risk of mortality by 5%
Recurrence depends on risk factors - 2 to 4% of people have reoccurences of which 5 to 7% are fatal.

25
Q

What is the use of D-dimer as a test for pulmonary embolism?

A

D-dimer indicates fibrinolysis has occurred - hence thrombus formation must have also occurred
Therefore will be elevated in a PE has occured
95% sensitivity, 50% specificity.
Low specificity means only has negative predictive value aka - if low value can rule out PE as a differential diagnosis.

26
Q

What can cause a D-dimer score to increase?

A

PE
Inflammation, infection, cancer
Also increases naturally with age.

27
Q

What is the purpose of Wells Scoring for PE?

A

NICE recommends the use of the original score Wells score for PE
A score over 4 indicates PE is likely, a score below 4 indicates a PE is unlikely.
A score of three is given for clinical signs/symptoms of DVT, alternative diagnosis is less likely.
A score of 1.5 is given for HR above 100, immobilisation, previous DVT/PE
A score of one is given for haemoptysis or active cancer.

28
Q

What is the use of a ultrasound in the diagnosis of a PE/DVT?

A

Greyscale ultrasound - vein should be compressible if not compressible indicates a thrombus
Can be done from the CFV to the diaphragm
From the PV to the ankle
Excellent specificity and good sensitivity

29
Q

What is the use of doppler ultrasound in the diagnosis of a PET/DVT?

A

Doppler showing an absence of venous flow indicates a thrombus.

30
Q

What is V/Q matching?

A

Stands for ventilation (air) perfusion (blood) mismatch
Pulmonary vessels normally constrict and dilate to ensure plentiful blood flow to alveoli that are well ventilated and vice versa

31
Q

What is a pulmonary dead space?

A

An area of the lung with ventilation but inadequate perfusion, pulmonary arteriolar vasoconstriction
Oxygen can not enter the bloodstream
This could be anatomic in cause - e.g no blood flow
Or physiological in cause - not enough blood flow.

32
Q

What is meant by a pulmonary shunt?

A

Shunt occurs when there’s adequate blood supply/perfusion but low inadequate ventilation.

33
Q

What is a V/Q scan?

A

A ventilation scan and a perfusion scan
Can be compared to identify a VQ mismatch.
Used with SPECT is more sensitive than a planar image
Only requires a low dose of contrast.
Is useful in pregnancy and post-partum
However, is highly dependent on reporter confidence and expertise
Up to 66% have a non-diagnostic result

34
Q

What is the usefulness of an echocardiography in a pulmonary embolism formation?

A

Only images the heart not the lungs
Useful for assessing hemodynamic effects of current embolic burden.
May suggest mortality by identifying RV strain or co-existent heart disease
Has a poor sensitivity and poor specificity for PE as only indicates changes in heart not why changes have occured.

35
Q

What is a CTPA?

A

A CT pulmonary angiogram
Contrast media is used to opaque the pulmonary arteries and check for occlusions
83% sensitivity and 96% specific to PE
Has a high negative predicietive power and low and intermediate risks
There are 3 generations of CT scanners meaning high spatial and temporal resolution, greater confidence/experience from reporters

36
Q

What are the drawbacks from the use of a CTPA?

A

Test is highly available may be over ordered, parituclary in specialities with little experience with PE, leading to lower hit rate and need to traige CTPA
Radiation dose can increase young patients relative lifetime risk of cancer by 5% - particularly important in peri-partum mums.
Large amount of artefacts.
Difficult to diagnose subsegmental PE
Uncertainty around safety of giving a person on warfarin (blood thinners) a CT.

37
Q

What is a PE overcall and what are the consequences of this?

A

An overcall is to diagnose a condition that does not actually exist
6% interderterminate rate in PECT diagnosis
This has consequences because of the mortality rate associated with treatment
Warfarin - 3% morbidity per year and 1% mortality per year
In STSFT 1 mortality per 18 months from overcalls.

38
Q

What are some of the potential treatments for a PET?

A

LMWH initially followed by heparin (3% mb, 1% mortality)
NOAC - similar efficacy and reduced M&M, however is overdose does occur are more difficult to reverse
Bleeding risk in patients - use a LAA occlusion device or an IVC filters .

39
Q

How long should treatment last for patients with a thromboembolism?

A

If occured due to a strong, transient risk factor considered provoked e.g after srugery so is unlikely to occur again - offer 3 months of treatment
If occurred due to ongoing strong risk factors such as cancer or unprovoked events there is an increased risk of reoccurrence and should be considered for extended treatment

40
Q

What are some major risk factors for a PE?

A

DVT
Previous DVT or PE
Active cancer
Recent surgery - particularly pelvic surgery
Lower limb trauma
Significant immobility, for example due to hospitalisation
Pregnancy, particularly 6 weeks post partum

41
Q

What are some minor risk factors for a Pulmonary embolism?

A

Use of the combined oral contraceptives or hormone replacement therapy
Known thromophilias
Long distance travel
Obesity
Increasing Age.

42
Q

What are the risks and management associated with a subsegmental PE?

A

Requires more sensitive CT scanners or can be missed
Debateable if overdiagnosis - normal lung function to catch these emboli
No proper randomised control trials to show if treatment is necessary
Majority are treated with antti-coagulation
Subsegmental PE with no proximal DVT is thought to have low clinical risk, patients are high risk once on anticoagulant therapy

43
Q

How does the British Thoracic Society calculate the pulmonary embolism severity index?

A

Factor - score
Age - age in years
Male - + 10
Cancer - + 30
Heart failure +10
Chronic lung disease +10
Pulse above 110 +20
Systolic BP above 100 +30
RR above 30 +20
Temperature below 36 +20
Altereted mental status +60
Arterial blood oxygen saturation +20.

Considers patient demographics, health status and clinical findings to calculate a score to indicate their risk of mortality from a DVT within the next 30 days

44
Q

How does the Pulmonary Embolism Severity Index score influence the clinical management of a patient?

A

Score correlates to risk lower score (below 85) are low risk and can be treated at home
Intermediate cases may need discussion but could be treated as an in or outpatient
In patient treatment should be given to all patients scoring 106 or above because these are high or very high risk of mortality in the next 30 days.

45
Q

What tends to be the outpatient treatment for patients with a pulmonary embolism?

A

Administered LMWH
CTPA as outpatient within 24hours.

46
Q

What can facotrs means a patient with a PE is not suitable to be an outpatient?

A

Considerd PESI score
Haemodynamically unstable, active bleeding, severe liver impairement, pregnancny, history of herpain induced thrombocytopenia among many more

47
Q

What are the risks and potential treatment strategies from a massive pulmonary PE?

A

High risk of cariogenic shock and cardiovascular compromises and cardiovascular collapse.
Evidence suggests that a fibrinolytic (streptokinase) should be used alongside heparin rather than just heparin alone.

48
Q

What are the risks and management associated with a submassive (intermediate) PE?

A

Fibrinolytic/anti-coagulants decrease risk of PE but increase risk of major hemorrhage and stroke
Mortality is hight and tends to be no benefit from thrombolysis, catheter directed thrombolysis or low dose may be potential options to reduce risks of treatment
Submassive show RV dysfunction
Also produce cardiac biomarkers such as BNP, NpBNP and Troponin assay.

49
Q

What is the clinical approach to deciding to treat a patient with an acute PE? (high risk)

A

If patient shows evidence of Acute PE including shock hypotension consider if high, intermediate or low risk
If high risk give systemic thrombolysis unless contraindicated then consider surgical embolectomy or catheter direct thrombolysis if contraindicated

50
Q

What is the clinical apprahc guidance for a patient with a low or intermediate risk PE?

A

Consider PESI is above 2 then test for RV dysfunction and elevated biomarkers
If present treat as high risk patient
If not present that treat with anti-coagulation
If PESI below 2 then patient is low risk and should be treated with anti-coagulation.