Case 3 A woman with chest pain
Brenda was 40 when she consulted Dr Marks with a cough and right submammary pain. Two weeks previously she had recently returned from a month’s holiday in Brazil where she had been treated for a chest infection with two courses of antibiotics. Dr Marks noted that Brenda felt slightly short of breath. She was taking the combined oral contraceptive (COCP), was a nonsmoker, and had a body mass index of 24.1. Her blood pressure was 159/95 and there were some crepitations at the right base. Dr Marks made a diagnosis of ‘pleurisy’ without recording any further detail about the pain.
What other information would you obtain?
Brenda told Dr Marks that she had had chest radiographs in Brazil that showed a lung infection. There was no observable calf or thigh swelling.
What would be your differential diagnosis and how would you discriminate between them?
A few days later Brenda became increasingly troubled by her chest pain and shortness of breath and went to A&E. She was admitted to hospital. Both the junior doctors who initially saw her suspected a pulmonary embolus. Brenda told them her pain had first occurred shortly after her flight to Brazil, and that her leg had swelled up at the same time. The diagnosis was confirmed by CT pulmonary angiogram, which showed widespread multiple pulmonary emboli.
Brenda sued Dr Marks for failing to consider the possibility of a pulmonary embolus.
Do you think her claim will succeed?
Expert opinion
Chest pain and complaints of breathlessness are both common in general practice. In this case the pain was unilateral and pleuritic in nature (sharp, well localized in time and position and worse on inspiration). It was associated with breathlessness. The differential diagnosis in this case included:
- pneumonia
- pulmonary infarction (a consequence of pulmonary embolus)
- lung abscess
- bronchiectasis
- malignancy, e.g. bronchogenic carcinoma
- pneumpthorax
- asbestos pleural disease, including mesothelioma.
The reason Dr Marks made the diagnosis of ‘pleurisy’ (presumably infective) was probably Brenda’s own account of having been diagnosed with a chest infection on holiday. Possibly because of this, Dr Marks did not record a thorough history of the timing and onset of the symptoms some 6 weeks earlier. He does not appear to have enquired about associated features such as haemoptysis. He prematurely fixed on the diagnosis of ‘pleurisy’ and did not consider a wide differential diagnosis to explain what the underlying cause of Brenda’s chest pain was.
Pulmonary emboli are relatively rare in general practice. The quoted incidence of pulmonary emboli is 25 per 100 000 per year. Thus a general practitioner with a list of 2000 will see one case every two years. According to Dalen and Master (2002):
It is well-recognized that the signs and symptoms of pulmonary embolism are nonspecific and that, as a result, the clinical recognition of pulmonary embolism is notoriously inaccurate. The lack of sensitivity of the clinical diagnosis of pulmonary embolism is evident from postmortem studies demonstrating that the majority of cases of pulmonary embolism detected postmortem were not diagnosed (or treated) prior to death.
It is estimated in the USA that only 26% of pulmonary emboli are diagnosed and treated. 74% of cases are undiagnosed or diagnosed only after death (Dalen and Master, 2002).
In the Prospective Investigation of Pulmonary Embolism Diagnosis study (PIOPED) of the patients who survived long enough to have their pulmonary emboli diagnosed by pulmonary angiography (Stein & Henry, 1997):
- 65% presented with ‘classical’ symptoms of pulmonary infarction (death of lung tissue due to the clot). These probably represent the smallest volume emboli that fragment and impact in the distal bronchial tree (Ryu et al., 1998).
- 22% presented with isolated breathlessness and no other features. Angiographic studies suggest that these are due to intermediate sized emboli that lodge in the pulmonary tree without producing infarction but significantly affect gas exchange and cause some degree of, possibly transitory, pulmonary hypertension (Ryu et al., 1998).
- 8% presented with circulatory collapse. These are the large emboli that break off from the deep pelvic veins and impact at the principle trunks of the pulmonary artery. They present with the features described by Virchow: severe acute breathlessness, poorly localized chest pain and distress (probably from right ventricular distension and ischaemia), syncope or pre syncope, followed by recovery (if the patient survives) (Ryu et al., 1998).
- 5% had no symptoms at all and were diagnosed on the basis of clinical suspicion after an abnormal chest X-ray (Ryu et al., 1998).
Most clinicians (and all clinical prediction rules) rely significantly on the presence of risk factors to alert the doctor to the possibility of pulmonary embolism in clinically unobvious cases.
The British Thoracic Guideline for the management of suspected pulmonary embolism (June 2003) gives a list of risk factors and divides them into major risk factors (increasing the risk by a factor of 5 to 20) and minor risk factors (increasing risk by a factor of 2 to 4) (British Thoracic Society, 2003). This is reproduced as Case Table 3.1.
Major risk factors (relative risk 5–20) | |
Surgerya |
|
Obstetrics |
|
Lower limb problems |
|
Malignancy |
|
Reduced mobility |
|
Miscellaneous |
|
Minor risk factors (relative risk 2–4) | |
Cardiovascular |
|
Oestrogens |
|
Miscellaneous |
|
aWhere appropriate prophlaxis is used, relative risk is much lower. bInflammatory bowel disease, nephrotic syndrome, chronic dialysis, myeloproliferative disorders, paroxysmal nocturnal haemoglobinuria, Behçet’s disease. |
A recent history of long-haul air travel is widely considered to increase the risk of venous thromboembolism. The evidence is effectively reviewed in the NHS Clinical knowledge summaries (NHS, 2011). In reality only a small proportion (about 1 in 4000–5000 flights) of air travellers have a deep vein thrombosis as a result. However, use of the combined oral contraceptive, obesity, Factor V Leiden mutation and extreme height increase this risk. The World Health Organization data estimated the odds ratio for the use of the COCP when flying to be 40. Therefore the prior probability of Brenda having a PE could have been as high as 1%.
The difficulty arises when patients do not present with the ‘classical symptoms’ of pulmonary embolism result from pulmonary infarction:
- pleuritic chest pain (sharp, well localized chest pain occurring on breathing in)
- cough
- haemoptysis
- tachycardia
- tachypnoea.
In this case Brenda does not seem to have had haempotysis, although it may not have been recorded. However the persistence of symptoms of chest pain and shortness of breath over a six-week period was rather atypical for a previous diagnosis of chest infection. While pulmonary embolus is an uncommon diagnosis in general practice it should have been considered because of this combination of symptoms.
Thromboembolic disease is one of the top three medical causes of litigation against GPs. Cases tend to involve important disputes of fact about what history was given by the patient, or ought to have been elicited by a competent GP. It is also common for there to be an allegation that the GP simply failed to think of the possibility of thromboembolic disease. Both of these criticisms potentially apply in this case.
Should scoring systems be used to define risk? The Wells Rule (Wells et al., 2000) is quite well known and may even be adopted for local care pathways between primary and secondary care. However it should be borne in mind that these scoring systems have been derived from populations presenting in secondary care in whom pulmonary embolus (or deep vein thrombosis as the case may be) have already been considered as a diagnosis. They have therefore not been validated for use in primary care. The AMUSE study has validated a Clinical Prediction Rule for use in primary care but relies heavily upon and requires a D Dimer result (Buller et al., 2009).
Legal comment
It is suggested by the legal expert that Dr Marks failed in his duty because he did not elicit an adequate history. If he had elicited information that Brenda’s pain came on shortly after her flight to Brazil and that her leg had swelled up at the same time, then he would have surely been alerted to the potential diagnosis of pulmonary embolism.
The number of potential diagnoses for chest pain and breathlessness make it incumbent on a GP to explore the patient’s history carefully. It would therefore be difficult for a lawyer to obtain a contrary expert opinion.
We are not told what the outcome was for Brenda. Assuming successful treatment, she will have a claim for any pain or suffering before her problem was correctly diagnosed and treated. Since this was only a few days after the consultation, it would seem that this is a relatively small claim against Dr Marks, perhaps £2000–£3000.