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Exogenous lipid pneumonia is an uncommon condition resulting from the aspiration or inhalation of fat or oil material. The prognosis in this entity is usually good and complications are rare. We report an unusual case of chronic lipid pneumonia complicated with massive haemoptysis who responded to steroid therapy after arterial embolization.
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Exogenous lipid pneumonia (ELP) is caused by the aspiration of animal, vegetal or, more often, mineral oils. Even though it may also be acute, ELP is most frequently a chronic disease, affecting people with predisposing factors, such as neuromuscular disorders, structural abnormalities and so on; very often exogenous lipid pneumonia is found in tracheotomized patients. The pathology of lipid pneumonia is a chronic inflammatory process evolving in foreign-body-like reaction, and eventually in "end-stage lung" condition. Clinically, most patients are asymptomatic; few cases only present with cough, dyspnea and chest pain. Eight cases of ELP, studied over the past 3 years, are described in this paper. All the patients were examined by chest radiographs and standard tomograms; 3 patients underwent CT. X-ray features were mono/bilateral consolidation of the lower zones, with air bronchogram and variable reduction in volume. CT density was not specific for fat tissue. In all cases the diagnosis was confirmed at biopsy. In 5 patients, followed for at least one year, clinical-radiological features showed no change. Thus, complications of ELP (especially malignant evolution) could be excluded. The authors conclude that lipid pneumonia must be considered in differential diagnosis of patients with history of usage of oils and compatible X-ray findings. The usefulness of an accurate follow-up is stressed.
Lipid analyses were carried out on the lungs of female B6C3F1 mice treated with methylnaphthalene. Cholesteryl ester, which could not be detected in lungs of control animals, was present in lungs of treated animals. Cholesterol and dipalmitoylglycerophosphocholine (DPPC) content was increased about five times in lungs of treated mice compared with control mice, and the content of a minor phospholipid was increased six times. The latter phospholipid was purified by high performance liquid chromatography and identified as phosphatidylglycerol by thin layer chromatography and by fast atom bombardment-mass spectrometry. Both DPPC and phosphatidylglycerol are known to be pneumonal surfactants produced from type II pneumocytes. Therefore, the accumulation of these lipids in lung tissue was assumed to be caused by the proliferation of type II cells induced by the administration of methylnaphthalene. The results provide important information concerning the underlying mechanism of endogenous lipid pneumonia in mice.
Endogenous lipid pneumonia has previously been diagnosed in dogs only once. This report describes a case in a dog with a persistent cough, in which the histological diagnosis was based on the presence of numerous foamy macrophages that filled the alveoli and contained small sudanophilic vacuoles. The appearance of endogenous lipid pneumonia in this animal was accompanied by Dirofilaria immitis infection and chronic bronchitis.
Endogenous lipid pneumonia was present in 19 of 27 opossums (Didelphis virginiana) trapped in the vicinity of Baton Rouge, Louisiana. The severity of lesions varied from small pleural and subpleural aggregates of foamy macrophages with minimal disruption of pulmonary architecture to large nodular accumulations of foam cells with cholesterol clefts and localized emphysema. The cause of the lipid pneumonia may be related to pulmonary nematode parasite infections, which were evident in 13 of the affected animals.
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Explore the source record for details and available documents.
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Exogenous lipid pneumonia following bronchography occurred in a woman with allergic bronchopulmonary aspergillosis (ABPA) whose bronchi had been colonized with Mycobacterium chelonei chelonei for the previous year. The lung biopsy specimen disclosed organisms within lipid vacuoles in the areas of lipid pneumonia, while caseating granulomas, the usual tissue reaction to pathogenic mycobacteria, were absent. These pathologic findings suggested that the infection with M chelonei was noninvasive, and we were able to continue the corticosteroid therapy that was necessary for control of the underlying ABPA.
A nationwide retrospective study of exogenous lipid pneumonia (ELP) was carried out to update the data on this disease, with emphasis on thoracic computed tomography (CT) scan and bronchoalveolar lavage (BAL) findings. The inclusion criteria were: 1) presence of abnormal imaging features compatible with the diagnosis of ELP; 2) presence of intrapulmonary lipids; and 3) exogenous origin of the lipid pneumonia. Forty four cases were included (20 males and 24 females; mean age 62 +/- 11 yrs), of which four were occupational (chronic inhalation of cutting mist or oily vapour in an industrial environment). Thirty of the 40 nonoccupational cases were related to aspiration of liquid paraffin used for the treatment of constipation. A condition possibly favouring oil aspiration or inhalation was present in 34 patients (77%), most commonly gastro-oesophageal reflux (n = 20) and neurological or psychiatric illness (n = 14). Fever (39%), weight loss (34%), cough (64%), dyspnoea (50%) and crepitations (45%) were the most frequent symptoms. BAL was performed in 39 cases: 23% had a lymphocytic alveolitis; 14% neutrophilic alveolitis; and 31% a mixed alveolitis (lymphocytic and neutrophilic). Alveolar consolidations (57%), ground glass opacities (39%), and alveolar nodules (23%) were the most common radiological abnormalities. The changes were bilateral (79%), predominant in the posterior and lower zones of the lobes concerned (74%), hypodense (71%), and spared the subpleural zones (52%). In 13 cases, hypodensity was retrospectively established on CT scan by the presence of a "positive angiogram". This sign may be of diagnostic value when the density measurement is either not possible or not reliable. In conclusion, this study provides an update of the clinical, biological and radiological profile of exogenous lipid pneumonia and, in particular, confirms the diagnostic benefit of computed tomography scan, which revealed bilateral and hypodense changes in a large majority of cases.
A modern concept of so-called exogenous lipid pneumonia, basing on experimental findings is given. The time course shows 3 different stages of disease with different morphological pictures. In the early stage a toxic disturbation of capillary endothelium is seen with secondary exsudation of blood plasma in alveoli. In the intermedium stage activation of alveolar and interstitial macrophages exists. The inhaled mineral oil is phagocytozed and degradated by alveolar macrophages, but interstitial macrophages are only capable for phagocytosis but not for degradation. This leads to a granulomatous and fibrous interstitial reaction, typical for the late stage of the disease.
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