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Pulmonary Embolism

Pulmonary embolus ( PE ) happens when thrombus migrates from the venous circulation to the pulmonary vasculature and lodges in the pulmonary arterial system ( Jan Belohlavek et al 2013 )
PE is the most dangerous form of venous thromboembolism ( VTE ) Venous thromboembolism ( includes DVT & PE ) affects 5 % of the population in their lifetime Seen worldwide but papers quote a lower incidence in Asians and Native Americans in comparison to Whites and African-Americans PE is the third most common cause of CV death ( after CAD and stroke ) but has lacked behind in public awareness for e.g in comparison to other health conditions as ACS and stroke European guidelines report annual incidence rates of 0.5 to 1.0 per 1000 inhabitants It is thought that the actual figures may be higher as 40 % to 50 % of patients with DVT can develop silent PEs Incidence increases with age and is highest among individuals 70-80 yrs of age ( possibly due to reduced mobility and increased comorbidity ) It is estimated that most deaths from VTE happen in hospital setting ( for e.g post-operative , maternal ) and in people in long term care settings
PE represents a major post-operative complication and surgery increases the risk of PE five-fold Seen more in men in comparison to women but this varies according to age ( estrogen and pregnancy related risk factors )
NICE says the PE can be provoked (For e.g following trauma or from a transient risk factor such as surgery ) or unprovoked (No known cause or occurs spontaneously – this has a higher rate of recurrence )
Major risk factors Post-operative states for e.g major abdominal / pelvic surgery , hip / knee jt replacement
 Obstetrics : late pregnancy , C sec , puerperium
 Lower limb affections : fractures , extensive varicosities

Malignancies : abdominal / pelvic , advanced / metastatic stage
 Limited mobility : hospitalization , geriatric care
 H/O previous thromboembolism
Minor Cardiac – congenital heart disease , heart failure , hypertension , superficial venous thrombosis , central venous catheter Humoral -oestrogen use Others
- neurological impairment
- latent malignancy
- thrombotic defects
- long distance travel in sitting position
- obesity
- inflammatory bowel disease
- nephrotic syndrome
- chronic dialysis
- myeloproliferative disease
- paroxysmal nocturnal hemoglobinuria
All VTE risk factors reflect one of the three triad of reasons that contribute to thrombosis as identified by Rudolph Virchow namely (1 ) stasis of blood flow (2 vascular endothelial damage (3 ) hypercoagulability

Presence of a major risk factor conveys a 5-20 times increased risk of PE while minor factor conveys a 2-3 times increased risk
Lisa Duffett et at al ( BMJ 2020 ) report that
 50 % of VTE events are associated with a transient risk factor as recent 
surgery or hospital admission 20 % are associated with cancer Rest are associated with minor or no risk factors and thus are unprovoked.
Thrombus breaks off from deep veins or from within the right heart and lodges within large or small vessels of the pulmonary vasculature
 in up to 50 % ( or higher ) of cases PE are due to proximal DVT of the legs involving the popliteal and / or more proximal veins and less likely when confined to calf veins Thrombosis of iliac and renal veins and inferior vena cava are also responsible for a large number of PEs Non-thrombotic causes include air or fat embolism.
Pulmonary vascular occlusion leads to 
impairment of gas exchange and circulation.
A complex interplay of several factors as
 size of clot ( clot volume ) area of the pulmonary vasculature where the obstruction happens and the extent to which the pulmonary circulation is obstructed release of vasoconstrictive substances the duration over which that obstruction happens pre-existing heart/ lung disease.
Rise in pulmonary vasculature resistance – it is believed that in people with no previous lung or heart disease a pulmonary bed obstruction of 30 % to 50 % is required before pulmonary hypertension develops.
Based on haemodynamic compromise the PE can be massive (imminent risk of death and high mortality ) , non-massive and submassive.
Death happens due to right ventricular failure mainly due to sudden increase in afterload
 rt ventricle has to pump against a significantly increased afterload –> it becomes dilated and hypokinetic with a large embolus burden
 at a critical point the clot burden overwhelms the Rt ventricle’s capacity to generate enough force to achieve enough cardiac output and it fails
Hypotension and cardiac arrest which
 shows as pulseless electrical activity ( previously called as electromechanical dissociation 
or asystole.
Presentation-Diagnosing PE is a challenging task- consider the following points diagnostic accuracy decreases with increasing age presentation can be varied if PE is suspected clinical assessment alone cannot confirm or exclude the diagnosis presence of comorbidities as bronchopneumonia , COPD , asthma or chronic fibrotizing pulmonary disease pose additional diagnostic challenges presentation can vary from minimal symptoms to massive emboli which can cause sudden death or progression to right ventricular failure.
Early diagnosis is critical as acute untreated PE has a high mortality rate of up to 30 % whereas the death rate of diagnosed and treated PE is 8 %. The high early mortality rate of PE has not changed despite better diagnosis / Rx in the last 30 yrs
Presenting symptoms can include Sudden onset or worsening resting dyspnoea Progressive exercise induced dyspnoea / rapidly progressive dyspnoea Chest pain ( due to rt ventricular ischaemia ) Calf or thigh pain / swelling Cough ( non -specific and may or may not be due to PE ) Hemoptysis ( due to lung infarction ) Pleuritic chest pain ( caused by smaller peripheral emboli that cause pulmonary infarction ) Low grade fever Syncope / light headedness – suggests more extensive embolism
Clinical findings ( can be variable ) but can include
 Tachypnea Tachycardia Atrial fibrillation Hypotension Pleural rub Signs of DVT Low grade fever Hypoxia JVP elevated + other signs of rt HF Split 2nd HS Gallop rhythm
Acute massive PE most serious form with high mortality of up to 20 % 
( usually within 1st hour )
Acute submassive PE -HD stable with tachycardia , tachypnoea but evidence
 of RV dysfunction
Acute small PE -can be asymptomatic or with tachypnoea and 
tachycardia or mild pyrexia
Pulmonary infarction -small distally embolising PE with no haemodynamic compromise , can present with pleural pain , irritated cough , fever , hemoptysis , signs of consolidation ( can be difficult to distinguish from pneumonia )
Subacute massive PE-takes longer to develop due to numerous small emboli & may present with increasing exertional dyspnoe and fatigue
Suspect PE in patients with
 sudden collapse with raised JVP ( faintness or hypotension ) pulmonary haemorrhage syndrome ( pleuritic pain & or haemoptysis ) isolated dyspnoea ( no cough/ sputum / chest pain )
 Refer all suspected PE cases urgently to hospital – urgency based on clinical suspicion and stability of the patient
Various risk stratification tools are available to help predict probability of PE in secondary care A few examples of risk stratification tools are
 Well’s criteria British Thoracic Society risk stratification Revised Geneva Score or simplified revised Geneva Score Pulmonary Embolus Rule Out Criteria
Diagnosis- estimation of pre-test probability is important in result interpretation A combination of history , physical examination findings , clinical probability scores and investigations as bloods / imaging aid in diagnosis. 
A full discussion of all test modalities is not possible here , commonly accessible tests in primary care may include
ECGright heart strain ( for e.g rt axis deviation ) T wave inversion in V1- V4 ( ± the inferior leads II , III , avF ) New RBBB ( complete or incomplete ) sinus tachycardia ( most common finding ) Dominant R in V1 ( acute RV dilatation ) AF can be seen in up to 20 % of cases Oft quoted classical S1Q3T3 indicates rt heart strain and can only be seen in about 10 % cases important to remember that any condition which causes acute pulmonary hypertension may show similar ecg changes ( for e.g pneumothorax , acute bronchospasm ) The value of ECG in acute PE is primarily to r/o other life threatening conditions as MI and findings are neither specific nor sensitive to diagnose PE
D-dimer degradation product of fibrinolysis in acute clot the activation of coagulation system is associated with simultaneous fibrinolysis activation – hence D-dimer is elevated D-dimer is a sensitive but not specific test ( thus it is an unsuitable marker for PE to be confirmed ) Hence a negative D-dimer test can reliably exclude PE in patients with low pre-test probability of PE It should be noted that raised levels do not infer the presence of VTE as it is raised in hospitalised patients , sepsis , post surgery , pregnancy and many inflammatory conditions and with increasing age Hence this test should only be considered by experienced clinicians following pre-test clinical probability assessment & a careful clinical evaluation

D-Dimer should not be used as a screening tool in patients in whom venous thromboembolism is not clinically suspected( BMJ )
Oxygen saturation oxygen saturation does not measure pCO2 a patient with acute PE may be working hard to maintain normal O2 ( ABG is required for PCO2 ) oxygen saturation cannot be relied solely in the diagnostic evaluation.
CXR can be abnormal in acute PE but it may also be normal or minimally abnormal CTPA is the first line gold standard investigation for PE Treatment leads to a 20 % reduction in mortality.

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    GUIDELINES Yeovil District Hospital *Pulmonary Embolism Management Guidelines (
  4. Bĕlohlávek, Jan et al. “Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism.” Experimental and clinical cardiology vol. 18,2 (2013): 129-38.
  5. Duffett LisaCastellucci Lana AForgie Melissa APulmonary embolism: update on management and controversies 
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    Embolia pulmonar: epidemiologia e diagnóstico. Thiago Domingos Corrêa
    , Alexandre Biasi Cavalcanti , Antonio Cláudio do Amaral Baruzzi einstein. 2007; 5(3):288-293
  9. Pathophysiology of acute pulmonary embolism Dieuwertje Ruigrok

     and Anton Vonk Noordegraaf ESC CardioMed (3 end) Edited by A. John Camm, Thomas F. Lüscher, Gerald Maurer, and Patrick W. Serruys Previous Edition (2 ed.)

    Health Technology Appraisal
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  11. Turetz, Meredith et al. “Epidemiology, Pathophysiology, and Natural History of Pulmonary Embolism.” Seminars in interventional radiology vol. 35,2 (2018): 92-98. doi:10.1055/s-0038-1642036
  12. Levis, Joel T. “ECG Diagnosis: Pulmonary Embolism.” The Permanente journal vol. 15,4 (2011): 75. doi:10.7812/tpp/11-112
  13. ECG changes in Pulmonary Embolism Ed Burns Nov 3, 2020 Life in the Fast  Lane

  14. Morrone, Doralisa, and Vincenzo Morrone. “Acute Pulmonary Embolism: Focus on the Clinical Picture.” Korean circulation journal vol. 48,5 (2018): 365-381. doi:10.4070/kcj.2017.0314
  15. Pulmonary embolism Simon McRae Australian Family Physician Vol. 39, No. 7, July 2010
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