A 50-year-old woman has complained of shortness of breath for 3 months

A 50-year-old woman has complained of shortness of breath for 3 months. It has steadily
become more severe and is associated with an occasional cough. Otherwise she has been
well. She smokes 15 cigarettes per day and drinks about 14 units of alcohol each week.
Her 20-year-old son has asthma and she has tried his salbutamol inhaler on two or three
occasions but found it to be of no real benefit. She has tested herself on her son’s peak
flow meter at home and she has obtained values of about 100 L/min. On direct questioning she says that the shortness of breath tends to be worse on lying down but there are no
other particular precipitating factors or variations through the day. She works as an office
cleaner and has no significant previous medical history.
Examination
Her respiratory rate is 18 per minute. Pulse rate is 72/min and blood pressure 138/84mmHg.
The heart sounds are normal. There is a generalized wheeze heard all over the chest but no
other abnormalities.
The chest X-ray is normal and respiratory function tests are performed (Figs 99.1 and
99.2). Results are as follows:
Actual Post-bronchodilator Predicted
FEV1 (L) 1.20 1.20 3.5–4.3
FVC (L) 4.10 4.1 4.6–5.4
FER (FEV1/FVC) (%) 29 29 72–80
PEF (L/min) 80 80 440–540
Residual volume (L) 1.8 1.8 1.6–2.8
Total lung capacity (L) 5.9 5.9 5.1–7.0
FEV1: forced expiratory volume in 1 s; FVC, forced vital capacity; FER, forced expiratory
ratio; PEF, peak expiratory flow.

EXPLANATION:

The flow–volume curve shows the same low flow throughout the whole volume of the vital
capacity. It is similar in both inspiration and expiration as shown in the flow volume loop
(Fig. 99.2). This situation is typical of a rigid large-airway obstruction. It is not reversible
with bronchodilator therapy. The spirometry trace of volume against time in such cases
shows a straight line of the same reduced flow right up to the vital capacity. These findings
are typical of a narrowing in a larger airway. On examination, this airway narrowing
is likely to produce a single monophonic wheeze which may be heard over a wide area of
the chest.
Differential diagnosis of rigid large-airway obstruction
The fixed flow in inspiration and expiration in this case suggest a rigid large-airway narrowing. If the narrowing can vary a little with pressure changes, then the pattern will
depend on the site of the narrowing (Figs 99.3 and 99.4). If it is outside the thoracic cage,
as in a laryngeal lesion, it will be more evident on inspiration. If the site is intrathoracic,
the flow limitation will be greater in expiration. Large-airway narrowing can be caused
by inflammatory conditions such as tuberculosis or Wegener’s granulomatosis, damage
from prolonged endotracheal intubation or by extrinsic pressure such as a retrosternal
goitre. However, the commonest cause is a carcinoma of a large airway
Some further investigation of the large airways is required. The great majority of symptomatic lung tumours are visible on plain chest X-ray but central lesions in large airways
may not be seen. Further investigation could be a bronchoscopy or a computed tomography (CT) scan. A bronchoscopy to see and biopsy any lesion would be best. In this case,
fibre-optic bronchoscopy showed a carcinoma in the lower trachea reducing the lumen to
a small orifice. Treatment was by radiotherapy with oral steroids to cover any initial
swelling of the tumour which might increase the degree of obstruction in the trachea.