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Chapter 3: Acute respiratory distress syndrome (ARDS) 119

Clinical features Management
Fever, malaise, cough and shortness of breath, some- 1 Avoidance is the most important factor in manage-

times with limb pains, develops several hours after ex- ment, mainly by changing working practice.
posure to the antigen and may last up to 2–3 days. On 2 High-dose prednisolone is used to cause regression of
examination there may be tachypnoea and cyanosis, the early stages of the disease, later stages where there
with widespread fine end-inspiratory crackles and is fibrosis are not amenable to treatment.
mild wheeze.
Chronic exposure leads to a chronic disease charac- Prognosis

terised by weight loss, effort dyspnoea, cough and Recurrent exposure leads to irreversible damage and ul-
signs similar to idiopathic pulmonary fibrosis (per- timately respiratory failure, and it is particularly difficult
sisting cyanosis, fine crackles and cor pulmonale). to stop bird fanciers from pursuing their hobby. Farmer’s
lung is an occupational disease in the United Kingdom
with sufferers being entitled to compensation.
Microscopy
Infiltration with neutrophils, lymphocytes and macro-
phages. In chronic exposure non-caseating granulo- Acute respiratory distress
mas are seen comprising multinucleated giant cells, syndrome (ARDS)
within which the antigenic material may be demons-
trated.
Definition
An acute form of respiratory failure caused by diffuse
pulmonary infiltrates and alveolar damage occurring
Complications
hours to days after a pulmonary or systemic insult. Pre-
Diffuse fibrosis and formation of honeycomb lung in
viously called adult respiratory distress syndrome it has
about 5%.
been renamed as it also occurs in children.
Investigations Incidence
Chest X-ray shows a diffuse haze initially, which de-
Occurs in 20–40% of patients with severe sepsis.
velopsintomicronodularshadowing.Theupperlobes
are predominantly affected. Advanced cases may show Aetiology
features of honeycomb lung (cystic appearance). CT Many conditions are recognised as precipitants, most
chest shows ground glass appearance in acute forms commonly systemic sepsis.
due to alveolitis and extensive lung fibrosis with nod- Lung-related causes include aspiration and smoke in-
ule formation in chronic cases. halation, pneumonia, near drowning and lung contu-
There is a raised white count with a neutrophilia fol-
sion.
lowing acute exposure. There is no eosinophilia (this Other systemic causes include shock from any cause,
would suggest asthma). major trauma/burns, disseminated intravascular co-
Precipitating antibodies are present in the serum;
agulation (DIC), air, fat or amniotic fluid embolism
however, these are markers of exposure and not of and heroin overdose. It is also well reported following
the disease. cardiopulmonary bypass and pancreatitis.
Respiratory function tests shows a restrictive pattern

with reduced lung volumes, FEV 1 and FVC are low Pathophysiology
but the ratio of the two is normal/high, and gas trans- 1 Acute exudative phase:
fer is reduced. This is reversible initially, but becomes Increasedvascularpermeabilityandepithelialdam-
permanent with chronic disease. age due to neutrophil-derived toxins, mechan-
Bronchoalveolar lavage shows an increase in lympho- ical damage, cytokines and possibly abnormal

cytes and macrophages. clotting mechanisms lead to pulmonary oedema