Pulmonary embolism Flashcards
Define pulmonary embolism
Pulmonary embolism (PE) is a consequence of thrombus formation within a deep vein of the body –> occluding the pulmonary vasculature
Thrombus formation in the venous system occurs as a result of:
- venous stasis
- trauma
- hypercoagulability
What are the 3 factors:
- venous stasis
- trauma
- hypercoagulability
collectively known as?
Virchow’s triad
Approx what % of deep venous thrombi will embolise to the pulmonary vasculature, resulting in a PE?
Approx. 51%
Where is the most common site of venous thrombus formation?
lower extremities.
What is venous thromboembolic disease?
The preferred term to describe the spectrum of disease
- beginning with the risk factors of Virchow’s triad
- progressing to deep venous thrombosis
- resulting in life-threatening PE
What may be the consequences of a PE if it is not aggresively treated?
- RHF
- cardiac arrest
What is the aetiology of pulmonary embolism
Virchow’s triad:
- venous stasis
- trauma (vessel wall damage)
- hypercoagability
Venous stasis:
- poor blood flow and stasis promote the formation of thrombi.
- Venous stasis and congestion result in valvular damage, further promoting thrombus formation.
Vessel wall damage:
- endothelial cell damage promotes thrombus formation, usually at the venous valves.
Hypercoagulability:
- a number of other conditions (both inherited and acquired) increase the risk of PE.
Which factors/conditions are associated with venous stasis?
- age >40 years
- immobility
- general anaesthesia
- paralysis
- spinal cord injury
- MI
- prior stroke
- varicose veins
- advanced congestive heart failure
- advanced COPD.
What are the insults that can cause venous vessel wall damage?
- trauma
- previous DVT
- surgery
- venous harvest
- central venous catheterisation
Do venous thrombi occur de novo in the pulmonary vasculature?
rarely
- Clots usually form in the deep venous system of the lower extremities and embolise.
Why might a PE cause RHF?
- PE occurs when a thrombus dislodges and becomes trapped in the pulmonary vasculature.
- This obstruction increases pulmonary vascular resistance (PVR), increasing the work of the right ventricle.
- The right ventricle compensates by increasing heart rate using the Frank-Starling preload reserve via dilation.
- Further increases in PVR overcome the right ventricular (RV) compensatory mechanisms, leading to over-distension of the right ventricle, increased RV end-diastolic pressure, and decreased RV cardiac output.
- Decreased RV output leads to decreased left ventricular (LV) preload.
- As left ventricle filling and cardiac output decrease, lowered mean arterial pressure progresses to hypotension and shock. In previously healthy individuals, this can occur when as little as 50% of the pulmonary vasculature is occluded.
What do DVTs consist of?
DVTs are composed mainly of fibrin and entrapped erythrocytes (red clots)
- Unlike platelet-rich arterial thrombi
Hence endothelial damage appears to be less important in DVT than in arterial thrombosis.
Although platelet aggregation is seen, it is not evident at the site of thrombus attachment, suggesting that activation of the coagulation cascade precedes platelet activation
Recall the coagulation cascade
Recall how platelets are activated
Which conditions (both inherited and acquired) increase the risk of hypercoagulability?
- cancer
- high-oestrogen states (oral contraceptives, hormone replacement, obesity, pregnancy)
- IBD
- nephrotic syndrome
- sepsis
- blood transfusion
- inherited thrombophilia (factor V Leiden mutation, prothrombin gene mutation, protein C and S deficiency, antithrombin deficiency, and antiphospholipid antibody syndrome).
What are the strong risk factors of pulmonary embolism?
PMH
-
cancer
- multiple myeloma, brain and pancreatic cancer = highest RR
- lung, colon, and prostate cancer = most episodes
-
Recent surgery or hospitalisation
- Lower limb fractures and joint replacements = strongest provoking factors
-
Previous or current DVT
- present in 25% pts with PE
-
Pregnancy and 6 weeks postpartum
- = 4x risk of thrombosis during pregnancy
- = 60x risk after pregnany vs non-pregnant women
SH
- History of immobilisation
What are the weak risk factors for a PE?
PMH
-
Other significant medical comorbidities
- e.g. congestive heart failure, COPD, concurrent sepsis
- Obesity
- increasing age
- varicose veins
- Known thrombophilias
-
other
- Central vein catheter, Nephrotic syndrome, Chronic dialysis, Myeloproliferative disorders, Paroxysmal nocturnal haemoglobinuria, Behcet’s disease, Blood transfusion
SH
- Long-distance travel
- Smoking
DH
- Combined oral contraceptive pill
- HRT
FH
- 1st-degree relative with a history of confirmed PE or DVT
What % of PEs occur with no underlying risk factors?
30% of cases
can be spontaneous
Summarise the epidemiology of pulmonary embolism
- UK: 47,594 cases of PE were reported in the 1-year period between 2013 and 2014
- higher in older age groups
What are the symptoms of pulmonary embolism?
- dyspnoea
-
peuritic chest pain
- acute onset
- localised to one side of the chest
- unlikely to be central
- (caused by pleural irritation due to distal emboli causing pulmonary infarction)
- cough
-
pain & swelling leg
- commonly 1 leg, although both legs may be affected
uncommon
- fever
-
haemoptysis
- ensure it is true, and not originating from elsewhere
What is the nature of onset of PE symptoms?
acutely rather than gradually
What are the signs of pulmonary embolism o/e?
- tachypnoea
-
hypoxaemia
- Oxygen saturations <94%
- but only presents in 60% of cases
-
creps O/A
- explains cough
- There may also be evidence of a concurrent DVT*
- UNCOMMON: signs of shock/hypotension or severely reduced haemodynamic reserve*
What are the signs of shock/hypotension or severely reduced haemodynamic reserve?
shock:
- altered cognition
- cool extremities
- mottled or ashen skin
- slow capillary refill
- oliguria.
What score is used to assess the risk of PE?
Wells score
- used to assess the likelihood of a PE in any non-pregnant patient who is haemodynamically stable
What are the criteria for the Wells score?
And how many points does each criterion receive?
How is the Well’s score interpreted?
This will categorise the patient into either
- ‘PE likely’ (Wells score >4)
- ‘PE unlikely’ (Wells score ≤4)
- While signs of RHF may be uncommon, what are they?
- And what do they imply?
- Hypotension, syncope, tachycardia
- high-risk PE with a larger clot burden and a higher mortality rate
How does the Well’s score guide Tx and investigations?
If a patient has a ‘PE likely’ Wells (or Geneva) score:
- start anticoagulation
- arrange investigation with definitive imaging (CTPA if available)
If a patient has a ‘PE unlikely’ Wells (or Geneva) score:
- order a D-dimer unless pt fulfils all Pulmonary Embolism Rule-Out Criteria
- (in which case a PE can be effectively ruled out and no further investigations are indicated)
What is the Pulmonary Embolism Rule-Out Criteria?
Apply PERC to any patient classified as ‘PE unlikely’ based on Wells (or Geneva) score.
No further investigation is indicated if a patient meets all the PERC criteria (a PE can effectively be ruled out).
- The risk for PE is considered to be lower than the risk of testing.
Request D-dimer testing for any patient in whom the PERC criteria fail to rule out a PE (i.e., one of more criterion not fulfilled).
The PERC criteria are:
- Age <50 years
- Heart rate <100 bpm
- SaO2 on room air ≥95%
- No unilateral leg swelling
- No haemoptysis
- No recent surgery or trauma (≤4 weeks ago requiring treatment with general anaesthesia)
- No prior PE or DVT
- No hormone use (oral contraceptives, hormone replacement, or oestrogenic hormones use in male or female patients).
What are the primary investigations for ?pulmonary embolism?
imaging
-
CT pulmonary angiography (CTPA)
- = definitive
- PE is confirmed by direct visualisation of thrombus in a pulmonary artery
- might also show signs of RVH
-
echocardiogram
- for haemodynamically unstable patients who cannot have CTPA
- Do not use echocardiography routinely in haemodynamically stable patients with suspected PE
- mobile right heart thrombi can be detected by transthoracic or transoesophageal echocardiography
- will also show RVH and RVF
-
ECG
- not diagnostic of PE
- excludes other causes
- Can indicate RV strain suggestive of PE
bloods
-
D dimer
- elevated (>500 ng/mL)
-
FBC
- May indicate thrombocytopenia or anaemia. These patients are at an increased risk of complications from bleeding when taking an anticoagulant
- May also indicate thrombocythaemia or polycythaemia which increase the risk of venous thromboembolism (VTE).
-
U&Es
- Checks baseline renal function
- for prescription of some anticoagulants e.g. low molecular weight heparin, fondaparinux, apixaban, rivaroxaban, dabigatran (should be used carefully in those with renal impairment)
-
coagulation studies: PT, INR, aPTT
- needed to establish baseline values before starting anticoagulation
-
LFTs
- Abnormal LFTs can influence the choice of anticoagulation.
What is D dimer?
- fibrin degradation product
- a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis
indictes presence of a thrombus/clot
When might a CTPA be contraindicated?
- pregnant
- young
- renal impairment
- contrast allergy
–> use echo instead
What are some possible secondary investigations to be considered when suspecting a PE?
ABG
- Do not perform an ABG if the oxygen saturations are within normal range on room air
- might show hypoxaemia and hypocapnia suggestive of PE
CXR
- usually normal (hence is used to exclude other causes)
- but may show atelectasis
- pleural effusion elevation of hemidiaphragm can be suggestive of a PE
lower limb compression venous US
- to investigate patients suspected of having a concurrent DVT
- might show inability to fully compress lumen of vein using US transducer
cardiac biomarkers - high sensitivity troponin (either I or T), NT-proBNP or BNP
- not used in diagnosing PE
- But can aid prognostic assessment (higher = worse prognosis)
- Do not use routinely to risk stratify patients.
ventilation-perfusion (V/Q) scan
- can be performed in patients with an elevated D-dimer and a contraindication to CTPA
- PE likely when an area of ventilation is not perfused
Name some emerging investigations for PE
What is the management pathway of pulmonary embolism?
reperfusion therapy=
- Systemic thrombolysis is the standard treatment of choice.
- Do not allow supportive therapy to delay thrombolysis, which may quickly restore haemodynamic stability.
- Use vasoactive drugs if SBP remains <90 mmHg after thrombolysis and adequate fluid resuscitation.
What is the management pathway of pulmonary embolism in haemodynamically unstable patients?
Haemodynamically unstable patients require:
- immediate primary reperfusion (usually thrombolysis)
- anticoagulation
- supportive care
Ongoing anticoagulation therapy is indicated to reduce the risk of recurrent events or fatal PE.
Name some complications of pulmonary embolism
What is heparin induced thrombocytopenia (HIT)?
HIT is an adverse immune-mediated drug reaction that leads to the formation of IgG antibodies against heparin-platelet factor IV complexes.
The incidence of HIT (following a minimum of 4 days heparin exposure) is believed to be between 0.1% and 1% in medical patients receiving prophylactic or therapeutic doses of heparin. In patients with cancer, the incidence may be 1%.
Risk factors include (but are not limited to):
- duration and type of heparin exposure
- patient population
- severity of trauma
- gender - women have approximately twice the risk of developing HIT as men.
The incidence can be minimised by use of a low molecular weight heparin or fondaparinux.
Clinical prediction rules to assist physicians with determining the probability that a patient has HIT have been developed
What is the prognosis of pulmonary embolism?
The Pulmonary Embolism Severity Index (PESI) and simplified Pulmonary Embolism Severity Index (sPESI) classify patients with confirmed PE without shock or hypotension into categories associated with increasing 30-day mortality.
- Using sPESI, patients in the high-risk category have a short-term mortality of 10.9%
- while patients in the low-risk category have 30-day mortality of 1%.
Mortality is often due to cardiogenic shock secondary to right ventricular (RV) collapse (precipitated by RV dysfunction)
