Case 2 Making matters worse
Mrs Turnbull is a 74-year-old lady with moderate COPD having smoked 10 cigarettes per day for over 50 years. Six years ago, she had two episodes of pulmonary oedema associated with paroxysmal atrial fibrillation. When she was in sinus rhythm she had a reasonable exercise tolerance and echocardiography showed mildly impaired left ventricular function, left atrial dilatation (6.5 cm) and moderate mitral regurgitation. Both episodes of atrial fibrillation had occurred despite concurrent beta blocker therapy.
What therapeutic options were available to Mrs Turnbull’s physician six years ago?
In view of her poor tolerance of rhythm change a decision was made to commence Mrs Turnbull on amiodarone, initially at a dose of 200 mg three times a day, reducing to twice a day after a week, and after a further week coming down to 200 mg once a day as maintenance therapy. The consultant cardiologist who saw her in outpatients wrote down these instructions for Mrs Turnbull and also wrote a clear letter to her general practitioner. A one month follow-up appointment had been made but for some reason this did not occur and Mrs Turnbull was not reviewed in outpatients at all.
Over the next four years, Mrs Turnbull remained quite well but then she began to develop worsening shortness of breath and was troubled by a persistent cough. Mrs Turnbull’s GP had been treating her for what he assumed to be progressive COPD and more recently also for probable heart failure. After a particularly bad few days she is admitted on a general medical take where she is found to be short of breath at rest, apyrexial, and hypoxic with a PaO2 of 7.9KPa on room air. There are fine inspiratory crepitations to both mid zones, the JVP is not seen and there is a pan systolic murmur at the apex. Mrs Turnbull is seen by Dr Wagstaff, a core medical trainee.
What treatment should Dr Wagstaff institute?
Dr Wagstaff agrees with the likely diagnosis of heart failure and requests a chest X-ray. The chest film is consistent with heart failure but it also raises the possibility of pulmonary fibrosis. After several days treatment for heart failure with no real improvement a high resolution CT scan is performed which shows widespread mid and lower zone pulmonary fibrosis consistent with amiodarone-induced pulmonary toxicity.
The amiodarone is withdrawn and Mrs Turnbull is commenced on oral steroids but her breathlessness progresses. After a protracted and difficult few weeks in hospital, she dies. Her family ask why she was put on such a dangerous medication in the first place and why she was not warned of possible side effects. They also question why she was not monitored and ask whether the adverse impact of amiodarone could have been spotted earlier, and been reversed.
How should Dr Wagstaff reply?
Expert opinion
Paroxysmal atrial fibrillation can be difficult to control and if a patient has not responded to beta blockade and tolerates the arrhythmia poorly, then amiodarone, although associated with serious side effects, is a reasonable treatment to consider. However, close monitoring is necessary and generally one would expect to do baseline tests including: chest examination (or chest X-ray), ECG, liver and thyroid function tests. These should be repeated six monthly thereafter. If a patient achieves suppression of the paroxysmal atrial fibrillation then a dosage reduction to 100 mg a day may be justified.
Patients should be informed of the likelihood of side effects (about 50% of patients will develop side effects on long-term therapy though generally only about 20% will need to stop the amiodarone). Careful monitoring will detect significant thyroid disease and six-monthly chest examination or X-ray may alert the prescriber to the development of pulmonary disease in time to avert irreversible damage. The presence of pre-existing pulmonary pathology probably increases the risk of pulmonary fibrosis. It also may delay recognition of the true cause of any reduction in exercise capacity.
If serious pulmonary side effects do arise then withdrawal of amiodarone may be associated with improvement or cessation in progression. If a chest X-ray had been done it is likely that Mrs Turnbull’s fibrosis would have been picked up sooner allowing prompt withdrawal of the amiodarone and she might not have gone on to develop irreversible disease.
The family have asked if this might have been spotted sooner and the simple answer has to be yes. There was a clear failure of adequate communication between the cardiologist and the GP. It is commonplace for a ‘shared care protocol’ to be drawn up to cover the use of drugs like amiodarone in which the responsibilities of the specialist and the GP are clearly set out. In particular responsibility for undertaking monitoring and determining any dosage adjustments should be stipulated at the outset. No such shared care arrangement was in place for Mrs Turnbull and the GP was inexperienced in the use of amiodarone and did not appreciate the risk or the need for long term monitoring.
The following is an example of a typical shared care protocol:
Shared care assumes communication between the specialist, GP and patient. The intention to share care should be explained to the patient and accepted by them. Patients should be under regular follow-up which provides an opportunity to discuss drug therapy.
- Carry out ECG monitoring, serum potassium measurements, LFTs and TFTs prior to treatment and communicate to patient’s GP.
- Initiate treatment as per the local hospital protocol and prescribe until the dose is stable (normally first 3 weeks) and/or the GP formally agrees to shared care.
- Write to the GP requesting shared care and outline shared care protocol criteria.
- Liaise with GP regarding changes in disease management, drug dose, missed clinic appointments.
- Ensure clinical supervision of the patient is undertaken by follow-up as appropriate.
- Ensure the patient understands the nature and complications of drug therapy and their role in reporting adverse effects promptly.
- Be available to give advice to GP and patient.
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