Differentials
Acute respiratory distress syndrome
SIGNS / SYMPTOMS
Seen in the setting of sepsis or trauma. No difference in signs and symptoms from aspiration pneumonitis, which can itself lead to acute respiratory distress syndrome.[43]
INVESTIGATIONS
Bilateral alveolar infiltrates can be indistinguishable from those seen in aspiration pneumonitis.
Asthma exacerbation
SIGNS / SYMPTOMS
Wheezing is paroxysmal and intermittent and usually diffuse. It decreases after bronchodilators, is polyphonic, and is characterised by many different pitches. Cough is triggered by exercise, cold, sleep, and allergens. Patient may have history and/or family history of atopy or asthma.[44]
INVESTIGATIONS
Pulmonary function tests usually show reversible obstructive ventilatory impairment.[44]
COPD exacerbation
SIGNS / SYMPTOMS
Wheezing is diffuse and associated with increased mucus production and history of progressive dyspnoea.
INVESTIGATIONS
Chest x-ray shows peribronchial cuffing and hyperinflation.
Infectious pneumonia
SIGNS / SYMPTOMS
No difference in signs and symptoms.
INVESTIGATIONS
Chest x-ray may show lobar consolidation.
Heart failure
SIGNS / SYMPTOMS
Orthopnoea, paroxysmal nocturnal dyspnoea, and right upper quadrant discomfort may be features. Sputum, if present, is usually frothy. Fever is usually absent.[45]
The third heart sound gallop rhythm has up to 50% sensitivity but 90% specificity. Pulsus alternans, characterised by evenly spaced strong and weak peripheral pulses, is pathognomonic of severe left ventricular failure.[45][46]
INVESTIGATIONS
Chest x-ray may reveal enlarged pulmonary vessels, cardiomegaly, and signs suggestive of pulmonary oedema, such as airspace shadowing in a batswing distribution, Kerly B lines and bilateral pleural effusions; the infiltrates improve quickly after diuresis.
N-terminal pro-B-type natriuretic peptide (NT-proBNP) >300 ng/L (>300 picograms [pg]/ml) or brain natriuretic peptide >100 nanograms/L (>100 pg/mL) is suggestive of heart failure, although elevated levels may be associated with a wide variety of cardiac and non-cardiac causes.
Negative pressure pulmonary oedema
SIGNS / SYMPTOMS
Characterised by the presence of stridor. Caused by partial occlusion of the airway if the patient is undergoing sedation or general anaesthesia.
INVESTIGATIONS
Chest x-ray shows signs suggestive of pulmonary oedema, such as airspace shadowing in a batswing distribution, Kerly B lines and bilateral pleural effusions.
Cystic fibrosis with exacerbation
SIGNS / SYMPTOMS
Wheezing presents early in life, with accompanying poor weight gain, diarrhoea, and recurrent sinus and pulmonary infections. Nasal examination may reveal polyps. Cough is productive and wet, suggesting a suppurative process such as bronchiectasis. Patient may have family history of bronchiectasis.[44]
INVESTIGATIONS
Sweat chloride test shows elevated level of chloride. Chest x-ray may reveal bronchiectasis, but CT scan is more sensitive.[47]
Acute interstitial pneumonitis
SIGNS / SYMPTOMS
No differentiating symptoms or signs, but they develop over a few days to several weeks. In some cases, it is idiopathic (Hamman-Rich syndrome); or it can be caused by collagen vascular disorders, cytotoxic drugs, or infectious aetiologies; or it can develop in a pre-existing idiopathic pulmonary fibrosis.[41]
INVESTIGATIONS
Bilateral alveolar infiltrates can be indistinguishable from those seen in aspiration pneumonitis.
Bronchoalveolar lavage cell count reveals >10% neutrophils, and lung biopsy shows diffuse alveolar damage.[41]
Cryptogenic organising pneumonia
SIGNS / SYMPTOMS
No differentiating symptoms or signs. Can be idiopathic or due to collagen vascular disorders, drugs, radiation, or infection.[41]
INVESTIGATIONS
Bilateral alveolar infiltrates can be indistinguishable from those seen in aspiration pneumonitis. Bronchoalveolar lavage cell count in organising pneumonia may reveal neutrophilia and sometimes lymphocytosis (but <25% lymphocytes) with eosinophilia (but <25% eosinophils).[41]
Acute eosinophilic pneumonia
SIGNS / SYMPTOMS
No differentiating symptoms or signs, but duration of illness is usually <1 week. Can be idiopathic or caused by drugs.[41]
INVESTIGATIONS
Bilateral alveolar infiltrates can be indistinguishable from those seen in aspiration pneumonitis. Bronchoalveolar lavage cell count reveals >25% eosinophils. Eosinophilic pleural effusion is rare. Eosinophilic infiltration and diffuse alveolar damage may be seen on lung biopsy.[48]
Acute hypersensitivity pneumonitis
SIGNS / SYMPTOMS
No differentiating symptoms or signs, but usually develops within 4 to 6 hours after inhalation of an organic agent. Caused by environmental and work-related antigens.[41]
INVESTIGATIONS
Bilateral alveolar infiltrates can be indistinguishable from those of aspiration pneumonitis. Granulomatous and cellular pneumonitis with diffuse alveolar damage may be seen on lung biopsy. Bronchoalveolar lavage cell count shows lymphocytosis (>25%) and sometimes neutrophilia (<10%).[41]
Diffuse alveolar haemorrhage
SIGNS / SYMPTOMS
Haemoptysis is absent in 33% of patients. Causes include vasculitis, collagen vascular disorders, anti-basement membrane antibody disease, coagulopathies, antiphospholipid antibody syndrome, and diffuse infections.[41]
INVESTIGATIONS
Bilateral alveolar infiltrates can be indistinguishable from those of aspiration pneumonitis. Pulmonary capillaritis, bland haemorrhage, and diffuse alveolar damage seen on lung biopsy.
Bronchoalveolar lavage shows progressively bloodier return. Cytology shows red blood cells and haemosiderin-laden macrophages.
Urinalysis may show proteinuria, haematuria, and red cell casts in cases of pulmonary-renal syndromes.[41]
Neurogenic pulmonary oedema
SIGNS / SYMPTOMS
No differentiating symptoms or signs. Usually develops within minutes to hours after acute central nervous system injury such as seizures, head injury, or cerebral haemorrhage. Resolves within 48 to 72 hours.[49]
INVESTIGATIONS
Bilateral alveolar infiltrates may be indistinguishable from those seen in aspiration pneumonitis.[49]
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