A 76-year-old Caucasian female attended our pulmonology outpatient clinic with a four-week history of cough with mucous-purulent sputum and dyspnea. The patient was a nonsmoker and had worked for a few years in a cotton factory. Her past medical history was negative for any contact with substances known to be associated with lipoid pneumonia. She had not travelled recently and had no pets. She had been treated for atrial fibrillation with amiodarone (200 mg OD) for 30 years, systemic hypertension, diabetes mellitus type II and hypothyroidism. Physical examination revealed a well built and nourished patient with pulse rate 69 per minute and blood pressure 110/70 mmHg. Vital signs were within normal range with SpO2 of 95% in room air. Her physical examination revealed bibasal lung crackles, but no evidence of pallor, icterus, cyanosis, clubbing or lymphadenopathy. Her blood work-up was within normal range. Pulmonary function testing demonstrated moderate restrictive lung disease and  decreased diffusion capacity. (see Table 1).
Since chest X-ray showed bilateral infiltrates, a high resolution computed tomography (HRCT) was conducted. The latter revealed areas of ground glass appearance significantly in the lower lobes of both lungs and airspace consolidations were seen as well (Fig.1, [a], [b]). The shadows improved 2 years later (Fig. 1, [c]).
Radiologically, differential diagnosis included atypical pneumonia, interstitial lung disease and tuberculosis was ruled out. The patient underwent fiberoptic bronchoscopy for bronchial wash and bronchoalveolar lavage (BALF) was collected for immunological studies as well. The bronchial washings were sent for smear for acid fast bacilli and cytological examination. No microorganisms were isolated by 48bacteriological examination and no malignant cells were found.
The total cell count of the BALF was 287,500/ml. The cells consisted of macrophages (64%), lymphocytes (31%), neutrophils (3%), and eosinophils (2%). The evaluation of BALF with specific staining and coloration showed the presence of fat-laden macrophages (oil red O stain). Figure 2 [a], [b] Extracellular oily droplets were found on a sputum cytology examination. These findings were suggestive of lipoid pneumonia.
a
The patient had never aspirated or inhaled mineral or vegetable oils and she had never used petroleum jelly intranasally or extra-nasally as  decongestant. However, it is described in the literature that chronic use of amiodarone can cause endogenous lipoid pneumonia (phospholipidosis). Amiodarone, as an amphiphilic cationic compound, interferes with the movement of phospholipids across intracellular membranes and inhibits phospholipid catabolism through its potent inhibitory effect on lysosomal phospholipase 2. Drug-induced phospholipidosis assumes the form of a 'foamy cell 'response.
In our case, the patient had been taking amiodarone (200 mg OD) for 30 years which was considered the most likely cause. It was therefore discontinued and replaced with digoxin (0.25 mg OD) for the treatment of atrial fibrillation. She was also started on oral prednisolone (20 mg OD) which was gradually tapered over a period of six months.
Computed tomography images of a 76-year-old female with lipoid pneumonia revealed ground-glass opacities and bronchiectasis in both lungs.