Editing Pulmonary embolus

Partial or complete occlusion of the pulmonary arteries

== Pathophysiology ==

* Haemodynamic consequences are determined by the size and location of the embolus, pre-existing cardiopulmonary disease, and severity of ventilation and oxygenation compromise
* Physical obstruction of pulmonary arteries is accompanied by hypoxaemic vasoconstriction and release of potent pulmonary arterial vasoconstrictors, which further increases pulmonary vascular resistance and RV afterload
* Increasing RV afterload causes RV hypokinesis and dilation, tricuspid regurgitation, and ultimately RV failure
* Once RV begins to fail, there is life-threatening reduction in coronary perfusion and downstream cardiac output
* In most patients, pulmonary clots will gradually reabsorb. In some patients, they organise into fibrotic deposits which permanently occlude the pulmonary arteries, leading to chronic pulmonary hypertension and RV dysfunction

== Aetiology ==

* Primary
* Secondary
** Majority of patients with PE have secondary PE from DVT in lower extremity/pelvis

== Clinical presentation ==

* Spectrum of asymptomatic to fatal
* Classically, sudden onset of symptoms
* Dyspnoea - if severe, indicates lobar or main vessel
* Pleuritic chest pain - pleural irritation due to distal emboli causing pulmonary infarction
** In central PE, chest pain has a typical angina character, possibly reflecting RV ischaemia
* Presyncope/syncope - can be independent of haemodynamic status
* Haemoptysis - occurs with pulmonary infarction
* Tachypnoea, tachycardia, rales/decreased breath sounds, increased JVP, fever (rare)
* Half of patients will also have symptoms of DVT

== Diagnosis ==

* High index of suspicion required
* Clinical impression has a sensitivity and specificity of 85% and 51% respectively
* Blood tests are non-specific
** D-dimer <10microg/L * age has good sensitivity
** Troponin and BNP are recommended for stratification of patients with confirmed PE
* ECG changes are unreliable
** Similar to all other causes of pulmonary hypertension
** S1Q3T3 (prominent S wave in lead I, Q wave and inverted T wave in lead III) reflects RV strain, but is seen in less than 20% of diagnosed PEs
* CXR is not sensitive or specific and all signs are rare
** Generally normal CXR
** Fleischner sign - enlarged pulmonary artery
** Hampton hump - peripheral wedge of airspace opacity - lung infarction
** Westermarck sign - regional oligaemia
** Knuckle sign - abrupt tapering or cut-off of a pulmonary artery
* CTPA
** Sensitivity 83% specificity 96%
* Echocardiogram
** Can diagnose RV dysfunction but not PE
** Not recommended routinely, but can be used to justify emergency reperfusion treatment for PA
* V/Q scan
** Primarily used in renal failure and pregnancy
** Highly sensitive but non-specific

== Approach: ==

* Wells score
** Unlikely: D-dimer +/- imaging
** Likely: imaging




== Risk stratification ==

* '''Low''' (approx 40% of PEs): normotensive patients without imaging evidence of RV dysfunction or elevated cardiac biomarkers. Mortality rate 1-2%.
* '''Intermediate''' (55% of PEs): normotensive patients with either imaging evidence of RV dysfunction or elevated cardiac biomarkers or both. Mortality rate 3-15%.
** Should try to quantify risk further by looking at RV
* '''High''' (5% of all PEs): haemodynamically unstable patients with sustained shock or hypotension <90mmHg or cardiac arrest. In-hospital mortality 15-30%.
* Can also use the '''PESI''' score to quantify risk.

== Treatment ==

* Goals
** Prevent mortality
* Initial supportive therapy (especially for intermediate or high risk patients)
** Resuscitate, being mindful of already stretched RV
** If fluid challenge fails, vasopressors will be required (noradrenaline is best because it is less likely to cause tachycardia and exacerbate hypotension)
** Systemic anticoagulation unless contraindicated - standard duration three months
*** Therapeutic clexane in most cases followed by warfarin/DOAC
** IVC filter if absolute contraindication to anticoagulation
* Thrombolysis
** Greatest benefit when done within 48 hours of symptom onset, for high-risk and selected intermediate-risk PE
** Can be done up to 14 days
** Systemic thrombolysis
*** Universally recommended for high-risk PE in absence of contraindications
*** 100mg alteplase over 2 hours
*** Demonstrated all-cause (47 vs 15%) and PE-specific (42 vs 8.4%) mortality benefit in high-risk PE
** Catheter-directed interventions
*** Useful when systemic thrombolysis is contraindicated, but not much data at this stage
*** When available, may be safer for patients who don't have a contraindication to systemic thrombolysis too
*** Controversy over how high to run the heparin infusion while doing catheter-directed interventions - some say use a lower rate like 60-80 APTT
* Surgical thrombectomy
** Traditionally done for patients with documented central PE and refractory cardiogenic shock despite maximal supportive therapy, and who have absolute contraindications/have failed thrombolytic therapy
** Best performed through a median sternotomy using a normothermic cardiopulmonary bypass

== Special populations ==

* Asymptomatic subsegmental PE
** Controversial treatment strategy
** Favour anticoagulation if: 
*** Risk factors for recurrent or progressive VTE
*** Hospitalised or have reduced mobility for another reason
*** Active cancer
*** Low cardiopulmonary reserve
*** Marked symptoms
** Favour no anticoagulation is high bleeding risk
* Thrombus in transit
** Floating right heart thrombus
** Most commonly seen with clots moving towards the pulmonary vasculature from the periphery
** Mortality rate up to 40%
** No distinct guidelines
** Surgery favoured if PFO present
* Pregnancy
** In one study, no patient with an original Wells score <6 had a PE
** Questionable utility of D-dimer since physiological levels are higher in pregnancy
** Adjusted dose LMWH is the favoured treatment
* Cancer
** First-line therapy should be LMWH for 3-6 months, or as long as the cancer or its treatment continues
* Non-thrombotic PE
** Fat embolism
*** Usually after long bone fracture or orthopaedic surgery
*** Triad of pulmonary distress, altered GCS, and petechial rash
*** Treat with supportive measures and possibly steroids
** Amniotic fluid embolism
** Tumour cell embolisation
** Septic embolisation
** Air embolisation
*** Lethal volume 100-500mL
*** Supportive - high-flow oxygen, place patient in left lateral decubitus to prevent RV outflow obstruction by airlock
*** Can attempt aspiration by central catheter

== Prognosis ==

* 10% mortality within 3 months of diagnosis
* Mortality exceeds 60% for those requiring CPR.



[[Category:Respiratory]]