Cases reported "Pneumonia, Lipid"

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1/14. kerosene-induced severe acute respiratory failure in near drowning: reports on four cases and review of the literature.

    OBJECTIVE: The purpose of this study is to present an unusual respiratory and cardiovascular course after intoxication and near drowning in a river contaminated with kerosene. DESIGN: case reports and review of the literature. SETTING: intensive care unit of a university-affiliated hospital. patients: Four patients after near drowning. INTERVENTION: Supportive only. RESULTS: The four patients developed acute respiratory failure. Cardiomyopathy was present in three patients and a persistent hypokalemia in two patients. The onset of the symptoms was delayed, which led to underestimation of the severity of their illness. Two of the four patients died. The diagnosis of hydrocarbon intoxication was based on bronchoalveolar lavage results, neutrophilic alveolitis with the presence of lipid-laden macrophages, and evidence of lipoid pneumonia from the autopsy performed on one victim. One patient who clinically deteriorated and another who developed a severe restrictive pulmonary disorder were treated with corticosteroids, which were effective only in the latter patient. CONCLUSIONS: Acute kerosene intoxication in a near-drowning event often results in severe respiratory and cardiac failure, with a high fatality rate. Treatment with corticosteroids may lead to a rapid improvement in lung function.
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2/14. Endogenous lipoid pneumonia associated with undifferentiated connective tissue disease (UCTD).

    BACKGROUND: Lipoid pneumonia is a rare pulmonary disease, a form of pneumonia that has no classical radiological appearance, thus it can imitate other lung diseases. Lipoid pneumonia is usually classified into two major groups, depending on whether the source of oil/fat in the respiratory tract is from an exogenous or endogenous source. Undifferentiated connective tissue disease is a term used by rheumatologists to define a group of diffuse connective tissue disorders that lack definitive characteristics of any particular well-defined disorder. MATERIAL AND methods: A case study is reported of concomitant undifferentiated connective tissue disease and endogenous lipoid pneumonia. RESULTS: Histologically the macrophages appeared filled with lipid and were similar to atherosclerotic foam cell macrophages. Antibiotic and antimycotic treatments were ineffective. However, with concomitant steroid treatment, the patient exhibited absence of lung infiltration as well as other symptoms and was discharged. Therefore it is concluded that the lipoid pneumonia was steroid dependent. CONCLUSION: Since the patient's condition responded to steroid treatment, and it is clear that steroids inhibit phospholipase activity, the authors speculate that the subsequent decreased endoperoxide production may diminish lipid uptake by macrophages via decreasing modification of LDL or other lipid sources.
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3/14. Exogenous lipoid pneumonia following ingestion of liquid paraffin.

    An asymptomatic patient with exogenous lipoid pneumonia (ELP) due to silent aspiration of liquid paraffin ingested as a lubricant was diagnosed by bronchoalveolar lavage (BAL). BAL fluid separated into oily upper phase and lower aqueous phase spontaneously. Microscopic analysis of BAL cells revealed the presence of lipid-laden alveolar macrophages. Classic histochemical staining and electron microscope examination indicated that neutral lipid was dominant but phospholipid was also present in the lipid-laden macrophages. Together with the history of ingestion of liquid paraffin, we identified that the ingested liquid paraffin was the origin of the neutral lipid in the lipid-laden macrophages observed in the BAL fluid.
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4/14. Fatal lipoid pneumonia due to bronco-aspiration of isoparaffin after ingestion of an organophosphate insecticide.

    A 66-year-old-male patient with a history of depression voluntarily ingested around 400 ml of an insecticide composed of 5% methylparathion, 75% isoparaffin, 8% etoxylated oleic acid, 4% 1,2,4-trimethylbenzene, 6% naphtha, 1% 1,3,5- trimethylbenzene, 0.4% propylbenzene and 0.3% xylene. The patient was conscious and alert at admission. gastric lavage was performed and activated charcoal administered. There were no clinical symptoms of organophospate ingestion despite reduced concentrations of erythrocyte and plasma cholinesterase. Chest X-ray showed pulmonary infiltrate compatible with bronco-aspiration. The patient evolved to respiratory failure refractory to treatment and died from multiorganic failure 23 days after ingesting the insecticide. The pathological findings included a pulmonary fibrosis in the alveolar spaces which caused enlargement of the intra-alveolar septa. Abundant lipin-laden macrophages were observed within the alveolar spaces. We review the most relevant aspects of cases of fatal lipoid pneumonia and point out that on occasion severe or fatal intoxication is due to the substances accompanying the active ingredients.
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5/14. Ultrastructural changes in animal fat associated lipoid pneumonia: report of two cases.

    Traditional or cultural practices in different parts of the world where oils are used continue to produce lipoid pneumonia. We report the ultrastructural findings and observations in animal fat associated lipoid pneumonia from two children following a cultural practice of forced feeding with animal fat (ghee). Clinical findings showed an acute or chronic chest infection which failed to respond to anti-microbial therapy. X-ray and chest CT scan revealed collapse/consolidations of the right middle and left lower lobes. histology and electron microscopy revealed thickening and destruction of the alveolar septa, filling of alveolar spaces with red blood cells and macrophage which contained both primary and secondary lysosomes. The alveolar walls contained mostly type II pneumocyte with most of them surrounded by thickened basement membranes with only a small portion of their surfaces exposed directly to the alveolar space where it showed numerous microvilli.
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6/14. Coexisting endogenous lipoid pneumonia, cholesterol granulomas, and pulmonary alveolar proteinosis in a pediatric population: a clinical, radiographic, and pathologic correlation.

    Benign pulmonary diseases that have been associated with the accumulation of endogenous lipids within the alveoli, bronchioles, and interstitial tissues include endogenous lipoid pneumonia (ELP), pulmonary alveolar proteinosis (PAP), pulmonary interstitial and intra-alveolar cholesterol granulomas (PICG), various xanthomatous lesions, and malakoplakia. In ELP, fat-filled finely vacuolated macrophages fill the alveoli. In PAP, the aveoli become filled with cholesterol and periodic acid-Schiff (PAS)-positive acellular debris. In PICG, cholesterol esters are released from degenerating macrophages and, as organization occurs, the cholesterol is deposited in the form of acicular clefts within the interstitium. These morphologically distinct presentations of endogenous lipid deposition within the lung have long been thought to represent unique disease processes but several authors now postulate a possible relationship between these entities. We report here on the clinical, radiographic, and morphologic findings in eight pediatric patients with diverse primary disease processes who were subsequently found to have varying and often coexisting degrees of ELP, PAP, and PICG.
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7/14. bronchoalveolar lavage in the diagnosis of lipoid pneumonia.

    Lipoid pneumonia (LP) is an uncommon entity with the characteristic radiographic features and histologic findings of alveoli filled with vacuolated, lipid-laden histiocytes. We questioned whether bronchoalveolar lavage (BAL) could be useful in the confirmation of LP. We examined lipid stains (oil-red O) in BAL specimens from 18 cases, representing a variety of pulmonary disease states, and compared them with an index case of confirmed LP. The index case of LP had a history of chronic intranasal use of mentholated petrolatum with subsequent x-ray findings of progressive air bronchograms. Positive histochemical confirmation (oil-red O) performed on frozen sections of transbronchial lung biopsy was obtained. Eleven of the non-LP cases had no intracellular staining of BAL macrophages with oil-red O stain, whereas the index case of LP exhibited markedly positive intracytoplasmic staining of macrophages for lipid. The remaining seven cases showed minimal to mild lipid staining with only one other case having moderate staining. This study demonstrates that BAL macrophages from patients with a variety of pulmonary states and without suspected LP do not demonstrate significant staining for intracellular lipids, in contrast with the expected strong positivity of LP. Lipid staining of BAL specimens, although not entirely specific, may be a preferred method for confirming the diagnosis of LP, thereby avoiding more invasive procedures.
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8/14. Radiographic bilateral cavitary lesions in lipoid pneumonia.

    We report a case of lipoid pneumonia with pulmonary bilateral cavitated lesions. The diagnosis was based on the finding of abundant lipid-laden alveolar macrophages in bronchoalveolar lavage and the presence of histologic changes indicative of lipoid pneumonia in transbronchial lung biopsy.
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9/14. diagnosis of a case of lipoid pneumonia by bronchoalveolar lavage.

    Exogenous lipoid pneumonia (ELP) was diagnosed by bronchoalveolar lavage (BAL) in a 57-year-old woman with a long history of using oily nose drops. Since clinical and roentgenological presentations are nonspecific, BAL, along with specific staining of recovered alveolar macrophages, represents a safe alternative to more invasive diagnostic procedures whenever a diagnosis of ELP is suspected.
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10/14. Coexisting endogenous and exogenous lipoid pneumonia and pulmonary alveolar proteinosis in a patient with neurodevelopmental disease.

    We report a unique case of coexisting exogenous lipoid pneumonia, endogenous lipoid pneumonia (ELP), and pulmonary alveolar proteinosis (PAP) in a 5-year-old patient with severe neurodevelopmental disease. The patient presented with gastroesophageal reflux and presumed chronic lung disease resulting from recurrent aspiration pneumonias and succumbed to respiratory failure. The autopsy showed lipid-laden macrophages and periodic acid-Schiff-positive granular material in alveolar spaces and multilamellated structures within both alveolar macrophages and extracellular debris. These findings were similar to those in previous reports of coexisting ELP and PAP in the setting of gastroesophageal reflux. However, the present case differed by the presence of scattered large osmiophilic extracellular lipid vacuoles. Besides strengthening the association between ELP and PAP and their relationship to gastroesophageal reflux, this case suggests that they may arise together with exogenous lipoid pneumonia, through related mechanisms, in the setting of neurodevelopmental disease.
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