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When severe asthma persists it raises the possibility of a steroid unresponsive co-morbid condition or other underlying causes ­ Dr Curig Prys-Picard and Dr Robert Niven share three such cases from their clinic

Case study 1 Food allergy

Ken, a 33-year-old hospital porter, was referred in 2002 with poor asthma control and morning dips with a peak expiratory flow rate of 300-350L/min. He was taking budesonide/formoterol, montelukast and Uniphyllin, and required frequent oral steroid courses. His referral letter suggested the possibility of irritable bowel syndrome and abdominal discomfort after drinking wine.

Ken started on a hypoallergenic diet of two weeks of fresh fruit and vegetables only ­ no eggs, dairy or wheat products. Salicylate-containing fruits (grapes and rhubarb) and citrus fruits (including tomatoes) were also excluded. On this diet he noticed a significant improvement in his asthma control. After two weeks the excluded food groups were gradually reintroduced into his diet. His symptoms returned and peak flows dropped after ingesting either dairy products or garlic.

Ken now sticks rigidly to a dairy- and garlic-free diet. Morning peak flow has risen to 550-600L/min, he has reduced his combination inhaler from three to one puff twice daily and stopped all his other asthma medications. He has required only one course of prednisolone in two years.


Food allergies that trigger asthma often go unrecognised. Constant exposure results in chronic poor asthma control rather than anaphylactic reactions.

The 'hidden' nature of foodstuffs in pre-prepared food and the time lapse between eating and reaction prevents patients from making the association between exposure and symptoms.

Case study 2 Bronchiectasis

A 17-year-old called Alison came to see us after an acute asthma exacerbation. She had had asthma since childhood and was atopic with positive skin-prick tests to grass, housedust mite and cat. She was on high-dose fluticasone, and eformoterol and montelukast.

The next two years were characterised by frequent exacerbations, usually requiring oral steroids and sometimes admission. Ten months ago the physiotherapist identified that sputum production was a significant part of her symptomatology ­ a fact Alison had kept hidden from us all. This illustrates the significant social stigma of chronic sputum production. High-resolution CT showed widespread bronchial wall thickening and left lower-lobe bronchiectasis.

The treatment started was sputum clearance exercises with hypertonic (7 per cent) saline nebulisers. This draws water into the airway and aids sputum clearance. It has the advantage of allowing chest clearance to occur at home, in the morning and in privacy. At initiation of therapy her FEV1 rose from 2.1 to 3.1L. Alison continues to have exacerbations, but lives a normal life and stays out of hospital.


Primary bronchiectasis can result in a degree of airway hyper-responsiveness and chronic severe asthma is complicated by bronchiectatic changes in the airways in some 40 per cent of cases. Despite this, exacerbations are not routinely treated with antibiotics unless there is a chronic excessive mucus production or recurrent positive sputum microbiology.

Chronic sputum production can often be traced back into childhood and warrants specialist referral. Early aggressive mucus clearance techniques may prevent the development of bronchiectasis.

Case study 3 Hyperventilation

George was diagnosed definitively with asthma in 1994. He worked as a nursing auxiliary in a care home. In 1992 he was admitted to A&E with chest pain that was unrelated to activity, episodic, shortlived and associated dyspnoea with finger paraesthesia.

An admission in 1993 to ICU saw him intubated, but with a low partial pressure for carbon dioxide, and he was easy to ventilate with inflation pressures that were normal from the outset. He was subsequently rapidly extubated. Both these admissions had features of hyerventilation.

He was still able to continue his labour-intensive profession at this stage.

In May 1995 he was admitted to intensive care and ventilated for two days following an exacerbation precipitated by exposure to his neighbour's yacht varnish. He had a further four intensive care/high dependency admissions over the next five years, though none required prolonged intubation and there was objective evidence of hyperventilation.

Between attacks he remained well with scant use of beta2-agonists.

The year 2003 saw the gradual onset of tremor, which developed into disabling shaking during breathless attacks. Lung function at this time showed a mildly obstructive pattern. His psychological well-being suffered with frequent shaking and breathless episodes. He was unable to continue working, which further added to the psychological stress and depression.

At the time of referral to the severe asthma service the assessment

confirmed hyperventilation and investigation showed him to have poor co-ordination of his respiratory muscles such that his chest is breathing in when his abdomen is breathing out (thoraco-abdominal asynchrony).

Since June 2003 he has been treated with physiotherapy, psychotherapy and antidepressants and has had no further admissions.


Dysfunctional breathing is poorly characterised and poorly understood. The benefits of breathing retraining are disputed, though selected cases may benefit most.

Curig Prys-Picard

research fellow

Robert Niven

senior lecturer in respiratory medicine, North West Lung Centre, Wythenshawe Hospital, Manchester

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