Lipoid Pneumonia

Lipoid pneumonia is an inflammatory lung reaction to lipid in the alveoli. It is exogenous when oil or fat is inhaled or aspirated, and endogenous when lipid accumulates from the lung itself, typically distal to an obstructing lesion, in alveolar proteinosis or with certain drugs.

Common exogenous sources are mineral oil (liquid paraffin used as a laxative or for dry mouth, or oil based nasal drops), vegetable and animal oils, petroleum jelly, oil pulling, ghee or oil given by mouth to infants in some communities, fire eating and occupational mists. Groups at risk are infants, older adults, and people with swallowing disorders, neurological disease or reflux.

Pathophysiology. Aspirated oil is emulsified and taken up by alveolar macrophages, which become lipid laden. Mineral oil is not hydrolysed so provokes a chronic foreign body reaction and fibrosis. Animal fats are hydrolysed to free fatty acids that are more inflammatory and cause acute injury. Vegetable oils lie between.

Many people have no symptoms and are found by radiograph. Others have chronic cough, dyspnoea, low grade fever, weight loss and chest pain. Acute aspiration causes fever, cough and respiratory distress within hours. Examination may be normal or show crackles.

Respiratory distress, haemoptysis or sepsis after aspiration of oil needs urgent assessment.

• History of oil use, aspiration risk or a lipid producing condition is the key to diagnosis.
• Chest radiograph: patchy or lobar consolidation, usually in the dependent segments (right middle lobe, lower lobes), sometimes a mass.
• High resolution CT: consolidation with areas of low attenuation, with fat density (about minus 30 to minus 150 Hounsfield units) in the lesion; crazy paving, ground glass and fibrosis in chronic disease.
• Bronchoalveolar lavage or sputum with lipid laden macrophages (oil red O stain), and cytology showing foamy macrophages, with a milky lavage fluid.
• Biopsy only if the diagnosis is uncertain (a fat density lesion with no clear history, or concern about cancer). Foamy macrophages in biopsy samples with vacuoles.
• Culture for bacteria and mycobacteria, since superinfection with rapidly growing nontuberculous mycobacteria (for example Mycobacterium fortuitum) is common.
• Look for the cause: swallowing assessment, reflux, drug and product history, and a CT of the chest for proximal obstruction when endogenous.

Differential diagnosis.

• Bacterial and aspiration pneumonia
• Organising pneumonia
• Lung cancer (including mucinous adenocarcinoma)
• Pulmonary alveolar proteinosis
• Hamartoma and other fat containing lesion
• Tuberculosis and fungal infection
• Vaping associated lung injury

• Stop the source of oil: withdraw mineral oil laxatives and nasal oil drops, replace with other agents (for example macrogol), and treat swallowing disorder, reflux or obstructing lesion.
• Asymptomatic or mild disease: observation with follow up imaging in 3 to 6 months.
• Symptomatic disease: supportive care (oxygen, physiotherapy), with antibiotics for superinfection (amoxicillin-clavulanate 625 mg three times daily for 7 days), and treatment of mycobacterial infection when present.
• Corticosteroid: evidence is limited. Prednisolone 0.5 mg/kg daily (30 to 40 mg) for 2 to 4 weeks, then taper over 4 to 8 weeks, is used in acute severe or progressive disease, with a response judged by imaging.
• Whole lung lavage with warm saline in selected patients with severe or progressive disease and hypoxaemia, which removes lipid laden macrophages and has been reported to produce improvement.
• Surgical resection for a localised persistent mass or complications such as abscess or bleeding.
• Prevention: educate against use of oil based preparations by mouth or nose in at risk patients, and against oil given to infants. Safe feeding strategies in infants with swallowing disorders.

Complications and prognosis. Most patients recover when exposure ceases. Chronic disease can lead to fibrosis, and infection with nontuberculous mycobacteria and lung cancer are complications.

Monitoring. Review at 4 to 6 weeks and 3 months with symptoms and chest radiograph, CT at 3 to 6 months to confirm resolution, and spirometry in chronic disease.

Referral and escalation. Refer to a respiratory physician for persisting disease, to ENT or speech therapy for swallowing assessment, and to a lavage centre for severe hypoxaemia.