Pulmonary Embolism

An embolus is a detached intravascular mass capable of clogging capillary beds at a site far from its origin. An embolism is when this event happens. A pulmonary embolism is when this happens in the lungs and lodges in the pulmonary artery or one of its branches (Ross and Wilson 2001). Factors that predispose thrombus formation are 1. An abnormality of the smooth endothelium (lining) Damage to the blood vessel wall can cause intravascular clotting, e.g. surgery, injury 2. Abnormal blood flow in the vessel Reduced rate of blood flow from long periods of rest, prolonged low blood pressure and pressure of the veins. 3. Increased coagulability of the blood Triggers intravascular clotting (Ross and Wilson 2011). While a thrombus lodges at the site of formation, an emboli is on the move. Most emboli are made up of parts of thrombi but can also consist of Fragments of plague, fragments of heart valves, tumour fragments, amniotic fluid (from childbirth), fat, air, pus (from an abscess), clumps of platelets and nitrogen (in decompression sickness). Emboli in veins move towards the heart and lodge in the lungs (PE) or liver. The most common cause of a PE is deep vein thrombosis (Ross and Wilson 2001).

DVT (deep vein thrombosis) cannot always be avoided however prevention of predisposing factors should be taken, the Royal Marsden (2008) states that to monitor signs of DVT and PE signs we need to watch out for a) b) Complaints of calf or thigh pain Erythema, warmth, tenderness & abnormal swelling of the calf or thigh in the affected limb

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c) Numbness or tingling of the feet d) Dyspnoea, chest pains or signs of shock e) Pain in the chest, back or ribs which gets worse if the patient breathes deeply f) Coughing up blood These should be reported immediately. It is characterised by a sharp sudden pain, worse on deep inspiration, which is often relived by bending forwards. (Alexander et al 2006). A PE can mimic the symptoms of an exacerbation in COPD (Chronic obstructive pulmonary disease) by causing worsening dyspnoea. J A Wedzicha and J R Hurst (2007) said that although pulmonary embolism is not thought to predispose to exacerbation, there have been a number of reports suggesting that the prevalence of deep venous thrombosis and pulmonary embolism is increased in patients with COPD. The hypothesis that COPD exacerbations may trigger pulmonary embolic events is plausible as acute infections are known to predispose to deep venous thrombosis and pulmonary embolism. Furthermore, patients with COPD are often elderly, may be immobile, and often have systemic inflammation and comorbid conditions, all of which increase susceptibility to venous thromboembolism. They found that it is possible that in addition to airway infection, venous thromboembolism may play a part in exacerbation recurrence in people with COPD. There is prevalence, as shown in a study. It showed a 25% prevalence of PE in patients with COPD hospitalized for severe exacerbation of unknown origin, (Leblond et al 2006). However another study showed that the prevalence of unsuspected pulmonary embolism is very low in patients admitted in the emergency department for an acute exacerbation of their COPD. These results argue against a systematic examination for pulmonary embolism in this population (Wedzicha and Hurst 2007). These findings support the findings of Rutschmann et al (2007). The authors conclude that as the prevalence of pulmonary embolism is so low, systematic investigation in patients presenting with COPD exacerbations is not required.

Nice Guidelines issued in June 2010 state that when patients are referred to hospital with an exacerbation of COPD they need 1.3.3.2 In all patients with an exacerbation referred to hospital:

a chest radiograph should be obtained arterial blood gas tensions should be measured and the inspired oxygen concentration should be recorded an ECG should be recorded (to exclude comorbidities) a full blood count should be performed and urea and electrolyte concentrations should be measured a theophylline level should be measured in patients on theophylline therapy at admission if sputum is purulent, a sample should be sent for microscopy and culture

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blood cultures should be taken if the patient is pyrexial. [2004]

Hassans symptoms appear to be a result from the pulmonary embolism that has made his COPD worse. Rather than infective exacerbation of his COPD. In the case of Hassans, His Parkinsons and COPD are normally managed separately. Mark A Stacy, MD says that COPD is an "obstructive" airway disease, like asthma, which means that it is hard to move air through bronchial tubes (the pipes). PD can cause "restrictive" airway problems, which means that it is hard to generate the muscle power to pull or push air in. so they can be related a spirometry may be needed to determine whether to treat the COPD with more of these medications or to treat the restrictive problems of PD by increasing PD medications. At this point in Hassans treatment he is to unwell for a spirometry test. As I have seen these preformed and require a lot of effort by the patient. References Margret Alexander, Josephine (Tonks) N.Fawcett and Phyllis J.Runciman (2006), Nursing practise Hospital and Home the adult, China; Churchill Livingstone Elsevier Lisa Dougherty and Sara Lister, 2008, The Royal Marsden hospital Manual of clinical nursing procedures, student edition, Italy; Wiley-Blackwell Ross and Wilson 2001, Anatomy and Physiology in health and illness 9th edition, Spain; Churchill Livingstone an imprint of Elsevier science limited Nice Guidelines, Chronic obstructive pulmonary disease: Management of chronic obstructive pulmonary disease in adults in primary and secondary care (partial update) June 2010. http://publications.nice.org.uk/chronic-obstructive-pulmonary-disease-cg101/guidance assessed on the 17/03/12 Tillie-Leblond I, Marquette CH, Perez T, Scherpereel A, Zanetti C, Tonnel AB, Remy-Jardin M. 2006, Pulmonary embolism in patients with unexplained exacerbation of chronic obstructive pulmonary disease: prevalence and risk factors. Ann Intern Med. 2006 Mar 21;144(6):390-6. Rutschmann OT, Cornuz J, Poletti PA, Bridevaux PO, Hugli OW, Qanadli SD, Perrier A. 2007, Should pulmonary embolism be suspected in exacerbation of chronic obstructive pulmonary disease? Thorax. 2007 Feb;62(2):121-5. Epub 2006 Nov 13.

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J A Wedzicha and J R Hurst, 2007, Chronic obstructive pulmonary disease exacerbation and risk of pulmonary embolism, Thorax. 2007 February; 62(2): 103104. doi:10.1136/thx.2006.073098, PMCID: PMC2111243, Copyright 2007 BMJ Publishing Group Ltd and British Thoracic Society. Mark A Stacy, MD http://forums.webmd.com/3/parkinsons-disease-exchange/forum/772 assessed on the 17/03/12
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