Synopsis
Identify medicine-related pulmonary injury through a precise exposure timeline, stop dangerous triggers safely and exclude infection, cancer, oedema and underlying disease progression.
- Drug-induced lung disease is a causal diagnosis built from phenotype, timing, exclusion of alternatives and response to withdrawal; there is no universal confirmatory test.
- Pulmonary toxicity may appear within hours or only after years, and can worsen after stopping a medicine with a long tissue half-life.
- Obtain all prescription, hospital, oncology, infusion, over-the-counter, herbal and recreational exposures with start, dose-change and stop dates.
- Common patterns include interstitial pneumonitis, organising pneumonia, eosinophilic pneumonia, diffuse alveolar damage, pulmonary oedema, haemorrhage, pleural disease and pulmonary hypertension.
- Amiodarone can cause serious, potentially life-threatening lung toxicity with insidious onset; CT is useful when it is suspected.
- Nitrofurantoin can cause acute or chronic pulmonary reactions, and MHRA advises immediate discontinuation when pulmonary damage symptoms occur.
- Methotrexate pneumonitis is different from rheumatoid-arthritis associated ILD; infection and the underlying inflammatory disease remain important competing explanations.
- Checkpoint-inhibitor and targeted-therapy pneumonitis follows agent-specific grading and stop rules; contact oncology before unsupervised rechallenge or steroid taper.
- Improvement after withdrawal supports causality, but corticosteroids, concurrent antibiotics and the natural disease course can confound the apparent dechallenge.
- Record the suspected reaction clearly, communicate it to primary and specialist care, and submit an MHRA Yellow Card when appropriate.
Key red flags
Fever, cough, dyspnoea, hypoxaemia, diffuse opacity and sometimes eosinophilia begin soon after exposure, as can occur with acute nitrofurantoin or daptomycin reactions.
New cough, hypoxaemia or ground-glass and organising opacities during immune checkpoint, antibody-drug conjugate or targeted therapy must enter the medicine-specific oncology pathway quickly.
Falling haemoglobin, haemoptysis that may be absent, diffuse opacities and hypoxaemia during anticoagulant, cytotoxic or immune therapy requires emergency assessment and reversal or treatment planning.
Rash, fever, eosinophilia, liver injury, renal dysfunction or mucosal involvement alongside lung disease raises a multisystem drug reaction and increases urgency.
Investigation priorities
Identify plausible agents, latency, cumulative exposure and rechallenge.
Management branches
New respiratory symptoms or imaging abnormalities occur during or after a potentially pneumotoxic medicine.
- Assess severity and withhold the suspected medicine if clinically safe, seeking immediate prescribing-specialty advice when withdrawal could destabilise arrhythmia, cancer or another serious disease.
- Build a dated exposure table and define the respiratory phenotype with HRCT, physiology and laboratory tests rather than matching one drug to one image.
- Investigate infection, oedema, embolism, malignancy progression and the underlying inflammatory disease in parallel; use bronchoscopy when it changes treatment safety.
- Document causality confidence, communicate across care settings and report a serious or medically significant suspicion through the MHRA Yellow Card scheme.