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You are the medical house officer on-call and have been asked by the registrar to see a 31-year-old woman, who was referred by her GP complaining of chest pain. Your history-taking reveals that the pain is located in the centre of her chest and that it came on suddenly at rest the day before. It is sharp in character and non-radiating. It is associated with some shortness of breath and a non-productive cough. Deep inspiration exacerbates the pain and it is not relieved by simple analgesia. Upon eliciting her past medical history, you learn that she had recently been in hospital with a fracture of her right femoral shaft. Exploration of her social history reveals that she has smoked 10 cigarettes a day for the past 10 years. Her observations are as follows: temperature 37.2, BP 129/72 mmHg, heart rate 106 regular, respiratory rate 24 and she is saturating at 97% on room air. On examination, she is comfortable at rest and talking in complete sentences. Her hands are warm and well-perfused, and her jugular venous pressure (JVP) is not elevated. Auscultation of her heart reveals normal heart sounds and her chest is clear. An ECG shows sinus tachycardia and her chest X-ray is unremarkable.
1. Based on the history and your examination, what is the most likely diagnosis?
In a patient with this presentation, you must exclude pulmonary embolism (PE), because this is potentially life-threatening. The nature of this lady’s pain – worse on inspiration (i.e. pleuritic) – is typical of PE. The shortness of breath is also in keeping with this diagnosis. This patient has a significant risk factor for a PE: her recent hospitalization (and therefore immobility) with a fracture. Her examination findings (or rather lack thereof) are typical for PE. The most common ECG tracing in PE is sinus tachycardia. In large PEs, signs of right ventricular strain may be present on the ECG. The classic sign of right ventricular strain (and favoured by some finals examiners!) is an S wave in lead I, and a Q wave and T wave inversion in lead III (the so-called S1Q3T3 pattern), but this is rare. There may be some right axis deviation and right bundle branch block.
2. What is this patient’s pack year history?
Number of pack years=packs smoked per day multiplied by number of years. One pack year=20 cigarettes/day for 1 year. She has smoked 10 cigarettes/day for 10 years so her pack year history is 0.5x10=5 pack years.
3. Which investigation would you like to do next?
An arterial blood gas sample should be taken from the radial artery. This indicates whether or not the patient is hy-poxaemic (pO2 <8 kPa) or hypocapnic (pCO2 <4.5 kPa). In high-risk settings such as postoperative patients, a low pO2 in combination with dyspnoea, in the absence of other explanations, has a strong positive predictive value for PE.
4.Would a D-dimer be a useful investigation in this patient?
D-dimer is a fibrin degradation product that is released by the body’s fibrinolytic system in the process of dissolving the fibrin matrix of a fresh venous thromboembolism. In the investigation of suspected PE, D-dimer has a strong negative predictive value, but a weak positive predictive value. This means in patients with a low clinical probability of PE, a normal D-dimer strongly suggests the absence of a clot but a raised D-dimer warrants further investigation. Other pathologies can also cause a raised D-dimer. However, a raised D-dimer is not helpful in patients in whom PE is the most likely diagnosis from the history and examination, as a normal D-dimer does not exclude a PE in a high-risk patient. Therefore, a D-dimer level would not be a useful investigation in this patient.
5.What imaging would you like to do?
Imaging of the pulmonary vasculature is the gold standard means of diagnosing PE. A CT pulmonary angiogram (CTPA) is performed at the earliest opportunity.
6.How would you treat this patient?
Treatment of PE initially consists of anticoagulation with subcutaneous injections of low molecular weight heparin (e.g. tinzaparin or dalteparin). Most hospitalized patients are given venous thromboembolism prophylaxis with reduced dose heparin. If PE is suspected or diagnosed, the patient receives the treatment dose of low molecular weight heparin, which is much higher and is calculated according to body weight. After PE is confirmed on CTPA, the patient is started on 6 months’ treatment with warfarin to achieve an international normalized ratio (INR) of 2–3.