Pulmonary Embolism

Original Editor Uchechukwu Chukwuemeka

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Introduction

Pulmonary embolism (PE) is responsible for most mortality as it's diverse range of clinical presentation and sometimes asymptomic presentation creates room for challenges in the diagnoses. It is medical emergence and prompt diagnosis and treatment are vital in reducing mortality and associated morbidity.

Causal Factors

  • The main cause of PE is thrombosis dislodge and circulating in the blood stream to occlude the pulmonary artery. Blood clot can occur due to serious limb injury, surgery, prolonged bed rest and static lower limb posture for more than 6 hours.
  • Cancer or cancer treatments such as chemotherapy and radiotherapy could lead to possible thrombosis formation
  • Other factors are overweight and hypercholesterolaemia as it could lead to fat embolism; pregnancy as there an increase rick of PE to in the first few weeks postpartum; smoking; some hormone replacement therapy (HRT).
  • PE can also arise from the right side of the heart
  • Non-thrombotic materials such as amniotic fluid, fat, air, bone and organ fragments.

Mechanism of Injury / Pathological Process

The initial cardiorepiratory state and size and number of emboli affects the severity of the of the change in pulmonary blood flow and respiration. a small blockage of the pulmonary artery may not be symptomatic but a large emboli can lead to several events which are deleterious the the individual. Thrombosis formation occur due to stasis in the deep veins especially the vein at the calf. Blood stasis leads to thrombosis been formed and it's dislodge makes it to circulate freely in the blood as an embolus and can occlude blood vessels; most especially the pulmonary artery. The occlusion can also be as a result of other emboli like air bolus , fat e.t.c. Pulmonary embolism causes wasted ventilation as it increases the alveoli dead space thus resulting in ventilation perfusion mismatch[1] and an increase in pulmonary artery pressures and right ventricular work.[2] Consequently, there is eventual right heart failure, accompanied by the left side of the heart due to decrease in blood volume and coronary perfusion to the left ventricle. Cardiac muscle dysfunction ensues; thus, the heart ceases to pump blood.

Prevalence/Incidence of PE

After myocardial infarction (MI) and cerebrovascular accidents (CVA), PE follows as the third leading cause of cardiovascular death.[3] Some persons with PE are umsymptomatic with incidence of 2.6%[4] and upto 71.4% in patient with distal DVT.[5] The European guidelines for the diagnosis and management of PE report annual incidence rates of venous thrombosis and PE of approximately 0.5 to 1.0 per 1000 inhabitants. A national incidence of 0.6/1000/year was reported by a study done by swedish in 2005[6]

Clinical Presentation[1]

Pyrexia

Dyspnea and/or Tachypnea

Crackle lung sound on chest auscultation

Prounced second heart sound

Pleuritic chest pain

Profuse sweating

Cough with hemoptysis

Tachycardia with rapid feeble pulse, arrhythmia

Hypotension, lightheadedness, dizziness (occasionally induced

by exercise only)

Syncope

Cyanosis

Diagnostic Procedures

PE is difficult to diagnose clinically[7] as only few cases show the triad of chest pain, dyspnoea and haemoptysis [8] and some are even umsymptomatic with incidence of 2.6%[4] and upto 71.4% in patient with distal DVT.[5]

A test such as D-dimer and Doppler Ultrasound.to for thrombosis as more than 70% of patients with PE also has DVT[9][5] with sensitivity of 86% and a specificity of 96% with a diagnostic accuracy of 95%.[10]

Chest X-ray may show a small pleural effusion or a peripheral wedge-shaped shadow indicating infarcted lung[11].[12]

Ventilation/perfusion (V/Q) scan and 50% accurate

Pulmonary angiography[7]

Computed tomographic angiography (CTA) which is a spiral CT with intravenous contrast medium is the best diagnostic tool as it is 90% conclusive.

MRI is another option used if there fear of harm from other procedures especially in pregnant women.

A PE Rule-out Criteria can be used in out patient emergency[13] as a clinical decision rule.

Outcome Measures

Duke Anticoagulation Satisfaction Scale (DASS) [14][15]

Perception of Anticoagulation Treatment Questionnaire (PACT-Q).[14]

Management / Interventions

Anticoagulant Therapy

A fast acting fibrinolytic agent such as heparin should be administered. Heparin prevents blood clot progression.

Sedation

A sedative to decrease the patient’s anxiety and pain;

Oxygen Therapy

Oxygen to reduces the pulmonary artery pressure and improve PAO2.

Embolectomy

Differential Diagnosis[16]

  • Acute heart failure,
  • Pneumonia
  • Chronic obstructive pulmonary disease exacerbation
  • Atrial fibrillation 
  • Acute myocardial infarction

Resources

add appropriate resources here

References

  1. 1.0 1.1 Hough, A. Physiotherapy in Respiratory Care; An evidence-based approach to respiratory and cardiac management. 3rd eds. United Kingdom: Nelson Thomes Ltd, 2001
  2. Hillegass E. Essential of Cardiopulmonary Physical Therapy. 3rd ed. Missouri,St. Louis: Saunders Elsevier. 2011
  3. Weitz JI. Pulmonary embolism. In: Goldman L, Schafer AI, editors. Goldman's Cecil Medicine. 24th efition. Philadelphia, PA: Elsevier; 2011
  4. 4.0 4.1 Dentali F, Ageno W, Becattini C, Galli L, Gianni M, Riva N et al. Prevalence and clinical history of incidental, asymptomatic pulmonary embolism: a meta-analysis.Thromb Res. 2010;125(6):518-22. doi: 10.1016/j.thromres.2010.03.016.
  5. 5.0 5.1 5.2 Krutman M, Wolosker N, Kuzniec S, de Campos Guerra JC, Tachibana A, de Almeida Mendes C. Risk of asymptomatic pulmonary embolism in patients with deep venous thrombosis. J Vasc Surg Venous Lymphat Disord. 2013;1(4):370-5. doi: 10.1016/j.jvsv.2013.04.002.
  6. Andersson T, Söderberg S. Incidence of acute pulmonary embolism, related comorbidities and survival; analysis of a Swedish national cohort. BMC Cardiovasc Disord. 2017; 17: 155. doi: 10.1186/s12872-017-0587-1
  7. 7.0 7.1 Pryor JA, Webber BA. Eds. Physiotherapy for Respiratory and Cardiac problems. 2ndedition. Churchill Livingstone, London. 1998; p47
  8. Goldstein M, Cornil A. Clinical diagnosis of pulmonary embolism.Acta Chir Belg. 1986;86(2):79-83.
  9. Edmondson, R. The causes and management of pulmonary embolism. Care Crit. Ill. 1194; 10:26-9.
  10. Kory PD, Pellecchia CM, Shiloh AL, Mayo PH, DiBello C, Koenig S. Accuracy of ultrasonography performed by critical care physicians for the diagnosis of DVT. Chest. 2011;139(3):538–42.
  11. Elliott CG, Goldhaber SZ, Visani L, DeRosa M. Chest radiographs in acute pulmonary embolism. Results from the International Cooperative Pulmonary Embolism Registry. Chest. 2000;118(1):33-8.
  12. Shawn TSH, Yan LX, Lateef F. The chest X ray in pulmonary embolism: Westermark sign, Hampton's Hump and Palla's sign. What's the difference? Journal of Acute Disease. 2018; 7(3): 99-102
  13. Kline JA, Courtney DM, Kabrhel C, Moore CL, Smithline HA, Plewa MC et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost. 2008;6(5):772–80
  14. 14.0 14.1 Essers BA, Prins MH. Methods to measure treatment satisfaction in patients with pulmonary embolism or deep venous thrombosis. Curr Opin Pulm Med. 2010;16(5):437-41.
  15. Samsa G, Matchar DB, Dolor RJ, Wiklund I. Hedner E, Wygant G et al. A new instrument for measuring anticoagulation-related quality of life: development and preliminary validation. Health Qual Life Outcomes. 2004; 2: 22. doi: 10.1186/1477-7525-2-22
  16. Squizzato A, Luciani D, Rubboli A, Di Gennaro L, Landolfi R, De Luca C et al. Differential diagnosis of pulmonary embolism in outpatients with non-specific cardiopulmonary symptoms. Intern Emerg Med. 2013;8(8):695-702.