Pulmonary Embolus

Exam Cram

• Pulmonary embolus is a blood clot in the pulmonary artery

• Presentation: pleuritic chest pain (worse with breathing), sob, haemoptysis

• Diagnosis: CTPA 

• Management: anticoagulation (stratification based upon affect on heart)

Outline

Background 

Pulmonary embolus (PE) is clot in the pulmonary artery. This clot is thought to have come from a deep vein thrombosis (DVT) in the venous circulation, travelling through the right side of the heart to arrive at the lung. Therefore PEs fall under venous thrombo-embolus (VTE) bracket with DVTs. Although they are located in a artery (pulmonary artery) they are considered a venous clot, due the likely source being venous!

PEs are associated with significant mortality and morbidity through their affect on the heart. Acutely death occurs from acute pulmonary hypertension, hypotension, inadequate perfusion and cardiac arrest. Chronically, PEs can cause pulmonary HTN, right heart failure leading to left heart failure and death. This has parallels with COPD and pneumothorax morbidity. 

They can be notoriously difficult to diagnose due to their non specific presentation and are a common differential for most acutely unwell patients. 

The lung's pleura are the only source of pain fibres in the respiratory system, hence lung clots present with pleurisy. 

Assessment

History:

• Chest pain- pleuritic (worse with breathing), sudden onset

• Short of breath

• Risk Factors

  • Recent immobility for three days (illness, holiday)

  • Recent surgery within 4 weeks

  • Previous VTE, poor compliance with anticoagulation

Examination:

• Tachypnoea, tachycardia

• Concerning if hypotensive, hypoxia

• Unilateral calf pain

Investigations

• Raised d-dimer

• Normal CXR

• ECG: sinus tachycardia (rarely S1Q3T3), ECHO: right heart strain

• CTPA/ VQ scan- confirm or exclude PE

Scores

• PERC Rule- rules out PE in under 50 year olds

• Well's score- risk stratifies PE

Diagnosis 

Diagnostic criteria: CT Pulmonary angiogram- 99% sensitivity & specificity

• Can be made clinically and treatment started if too unwell for CT scanner or long delays with CT

• VQ scan option particularly in severe CKD due to the risk of contrast nephropathy

Differentials

• Pleurisy: pneumonia, pneumothorax, MSK rib pain, lung cancer

• Acutely sob/ unwell: myocardial infarction, aortic dissection

• Anxiety attack: can present similarly with acute tachypnoea, tachycardia however won't be hypoxic and may be young

Acute Management

Post Diagnosis Work up 

• Troponin & ECHO

• Bilateral USS - check for DVT to allow for comparison if represents in 3 months with right calf pain

• Rpt history & examination ?malignancy risk factors- consider OP breast USS, PSA and rarely a CTCAP or thrombophilia screen

Stratification

Severity is stratified based on affect on heart

• Massive PE: hypotensive- BP < 90/60 (once euvolaemic)

• Sub-massive PE: signs of heart strain on ECHO, CTPA or raised troponin

• Non-massive PE: nil heart strain- normal ECHO, troponin

PESI- PE severity index predicts 30d mortality

Massive PEs

PE's cause death through cardiac stress. Hypotension is a risk factor for arrest, therefore immediate intervention is required:

• Diagnosis: bedside echo can be used to start thrombolysis prior to CTPA

• Management: thrombolysis stat (alteplase) [after BP not responded to IVF]

• Disposition: admit HDU vs ICU

Sub-massive PEs

• Management: enoxaparin 1mg /kg BD whilst in hospital, DOACs PO: 2w high dose, then  3-6m lower dose

• Disposition: variation seen in clinical practice- can discharge or admit for observation for 24hrs

Non-massive PEs

• Management: DOACs PO: 2w high dose, then  3-6m lower dose

• Disposition: home

Analgesia

Typically have significant analgesia requirements

• Regular paracetamol QID PO

• Regular Ibuprofen (unless cxind) TDS PO +/- PPI cover

• PRN opioids

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Discharge planning & follow up

Follow up: Haematologist > Respiratory > GP

Decisions: 

1. Assess duration of anticoagulation

2. Weigh up cause: considering investigating for thrombophilia, malignancy, etc..

Med Reg Notes

Disposition

The majority of pulmonary emboli (PE) can be managed at a ward level, therefore signs of severe hypoxia and hypotension are very concerning signs. Hypotension requires emergency thrombolysis (which is rare). 

Indications for HDU/  ICU: 

1. Hypoxia- requiring NIV or intubation

2. Haemodynamic instability- hypotension requiring vasopressors

Indications for emergency thrombolysis: 

• Haemodynamic instability

  1. 1. SBP < 90

     2. Requiring inotropic support

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Chronic Management

The likely cause of the PE dictates there risk of re-occurance and long term management. 

Risk of PE: 

4% lifetime risk: Average person [1]

< 3% per year: First provoked PE- e.g. major surgery, trauma or bed rest > 4d [3]

8% per year Active cancer,  APS or at least one PE without a transient provoked RF [3]

Provoked PEs

PEs with a clear cause can be labelled as provoked. If the provoked risk factor is avoidable, these have the lowest rates of re-occurrence. If the risk factor is persistent, these have the highest rates of reoccurring. Examples of clear causes:

Transient provoked PEs

• Surgery or trauma within 4 weeks

• Immobilization of 3d or more in last two weeks

• Recent flight

Persistent provoked PEs

• Cancer- particularly Haematological

• Chronic infection- i.e. osteomyelitis

• Thrombophilia

Unprovoked PEs

PEs without a clear cause have a far higher risk of re-occurance and hence PO DOACs often given for 6 months. If this is a second PE, then the risk of reoccurance is high enough to justify 'lifelong' anticoagulation, until the risks outweigh the benefits (in old age). 

Thrombophilia screen (6)

1. Protein C deficiency

2. Protein S deficiency

3. Antithrombin deficiency (previously thrombin III)

4. Factor V Leiden (controversial)

5. Homocystinuria

6. Prothrombin gene mutation

7. Antiphospholipid syndrome (APS): anti B2 glycoprotein-1, anti-cardiolipin

Factor V Leiden is the commonest cause of thrombophilia. Although its autosomal dominant it has a variable penetrance. Therefore a positive result is difficult to interpret as firstly, it may not be responsible for the clot and secondly, even if it was responsible it won't change the type of long term anti-coagulant advised. For this reason some haematologists don't include it in their thrombophilia screening panel. 

Long Term Management Summary

• First episode of a transient provoked PE can be managed with 3m DOAC PO, usually apixaban.

• 2nd PE usually requires lifelong anticoagulation

• Cancer  and pregnancy related PEs treated with LWMH

• Provoked PEs do not require CTCAP ?malignancy or thrombophilia screen as standard

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ECG Changes in PE

Sinus tachycardia is commonest rhythm for a PE. 

There can be signs of right heart strain- right axis deviation, RBBB, p wave pulmonale (increase pressure in right atrium). 

S1Q3T3 is poorly sensitive or specific but a popular exam question. In summary if there is TWI in V3, consider it. 

Thrombolysis

BTS recommend Alteplase as standard

Pulmonary Embolus in Pregnancy

Assessment

• History, examination, obs- tachycardia can be normal for pregnancy.

• D-dimer, well's and PERC scores not validated in pregnancy.

• Basic work up: ECG, troponin and chest XR.

• CXR usually justifiable as very low radiation and may find causes of pleurisy.

• USS can be considered prior to CTPA- if shows DVT, CTPA could be avoided- as treatment is same. 

Radiation [3]

CXR: 0.1mSv, 10 day equivalent

CTPA: 5mSv, 500 days, risk of maternal breast cancer

 VQ Scan: 2mSv, 200 days-  however can be inconclusive, requiring CTPA

Plan

1. CTPA > VQ Scan

2. Management: LMWH 

There appears to be debate within the online guidelines, MRCP and clinical practice. My experience is that due to the risk of a VQ scan being indeterminate, a CTPA is preferred; both are justified as being safer than an undiagnosed PE. 

Lay Summary

Pulmonary embolus. Pulmonary means lung and embolus means clot, particularly a clot that started in one location and causing blocks a vessel in another location. Pulmonary embolus typically form in the calf and then travel through the blood into the lung. A pulmonary embolus is commonly referred to as a PE. This clot in the lung can produce its typical symptoms of shortness of breath, chest pain worse with breathing in and coughing up blood (haemoptysis). Diseases with similar presentations include- pneumonia, a muscle or rib injury to the chest wall or a pneumothorax (where the lung has tear, leaking air into the chest). A pulmonary embolus is usually managed by the emergency doctors and most GPs would refer their patients into emergency if they were concerned about one. 

A doctor would usually perform a chest XR, a set of bloods and a ECG to look for other causes. A CT scan is the definitive investigation ( a CTPA- CT pulmonary arteries) and this will usually be able to rule in or out a pulmonary embolus. 

If the CTPA shows a blood clot, usually blood thinners would be started, often newer versions of warfarin such as apixaban. The dose would often be high for a few, medium for three to 6 months. If there are no signs of heart damage then a discharge can be made with follow up in the community. 

A pulmonary embolus requires community follow up from either a GP, hematologist (blood doctor) or respiratory (lung) doctor. This is because the blood clot can be a symptom of another illness. Commonly the terms provoked or unprovoked are used to state whether there was an obvious trigger. For example if there was recent surgery, this would be a provoked blood clot but if there was no obvious triggers, this would be unprovoked. Provoked blood clots are less concerns for underlying conditions because an obvious trigger is identified. Your community specialist is required to decide whether the blood clot was provoked. This will guide how long they advise the blood thinners to be continued and whether any other investigations are required. 

References

1. NHS, Thrombophilia-screen, NHS choices. Available at: https://www.southtees.nhs.uk/services/pathology/tests/thrombophilia-screen/ (Accessed: 11 October 2024).

2. Arnesen, C.A. et al. (2021) ‘Estimated lifetime risk of venous thromboembolism in men and women in a Danish nationwide cohort: Impact of competing risk of death’, European Journal of Epidemiology, 37(2), pp. 195–203. doi:10.1007/s10654-021-00813-w.

3. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Authors/Task Force Members:, Stavros V. Konstantinides, Guy Meyer, Cecilia Becattini, Héctor Bueno, Geert-Jan Geersing, Veli-Pekka Harjola, Menno V. Huisman, Marc Humbert, Catriona Sian Jennings, David Jiménez, Nils Kucher, Irene Marthe Lang, Mareike Lankeit, Roberto Lorusso, Lucia Mazzolai, Nicolas Meneveau, Fionnuala Ní Áinle, Paolo Prandoni, Piotr Pruszczyk, Marc Righini, Adam Torbicki, Eric Van Belle, José Luis Zamorano, Document Reviewers: Nazzareno Galié (CPG Review Coordinator) (Italy), J. Simon R. Gibbs (CPG Review Coordinator) (United Kingdom), Victor Aboyans (France), Walter Ageno (Italy), Stefan Agewall (Norway), Ana G. Almeida (Portugal), Felicita Andreotti (Italy), Emanuele Barbato (Italy), Johann Bauersachs (Germany), Andreas Baumbach (United Kingdom), Farzin Beygui (France), Jørn Carlsen (Denmark), Marco De Carlo (Italy), Marion Delcroix (Belgium), Victoria Delgado (Netherlands), Pilar Escribano Subias (Spain), Donna Fitzsimons (United Kingdom), Sean Gaine (Ireland), Samuel Z. Goldhaber (United States of America), Deepa Gopalan (United Kingdom), Gilbert Habib (France), Sigrun Halvorsen (Norway), David Jenkins (United Kingdom), Hugo A. Katus (Germany), Barbro Kjellström (Sweden), Mitja Lainscak (Slovenia), Patrizio Lancellotti (Belgium), Geraldine Lee (United Kingdom), Grégoire Le Gal (Canada), Emmanuel Messas (France), Joao Morais (Portugal), Steffen E. Petersen (United Kingdom), Anna Sonia Petronio (Italy), Massimo Francesco Piepoli (Italy), Susanna Price (United Kingdom), Marco Roffi (Switzerland), Aldo Salvi (Italy), Olivier Sanchez (France), Evgeny Shlyakhto (Russian Federation), Iain A. Simpson (United Kingdom), Stefan Stortecky (Switzerland), Matthias Thielmann (Germany), Anton Vonk Noordegraaf (Netherlands). European Respiratory Journal Jan 2019, 1901647; DOI: 10.1183/13993003.01647-2019

4. https://litfl.com/ecg-changes-in-pulmonary-embolism/