Pediatric Pulmonology 13:184-188 (1992)
Lipoid Pneumonia in Association With Gastroesophageal Reflux Lawrence E. Kurlandsky, MD,‘ Vernon Vaandrager, MD,’ Carmel L. Davy, BAD,* and Fred S. Stockinger, M D ~
INTRODUCTION
Lipoid pneumonia may be of exogenous or endogenous origin. Exogenous lipoid pneumonia was initially described in children who aspirated or inhaled milk, mineral oil, cod liver oil, and oily nose drops’; more recently, excessive use of lip gloss3 and nasogastric lipid feedings in an infant with known gastroesophageal reflux (GER)4 have also been reported as causes. Endogenous lipoid pneumonia, in which lipid originates from the lung, may be primarily or secondarily related to localized pulmonary disease, such as bronchiectasis, abscess, tuberculosis, or neoplasm .5. Lipid-laden macrophages are the pathognomonic finding in both types of lipoid pneumonia. In the exogenous type, macrophages contain lipid vacuoles of heterogeneous size and distribution, whereas in the endogenous type, macrophages contain small homogeneous lipid vacuoles imparting a histologic appearance of “foam cells.”’ We report the case of a 12 year old child with lipoid pneumonia and bronchiectasis associated with GER. The clinical and pathological features were consistent with both types of lipoid pneumonia. Distinguishing features and the differential diagnosis are presented.
’
’
CASE REPORT A 12-year-old Caucasian girl came to medical attention when she was involved in a motor vehicle accident and sustained a “whiplash” injury. A radiograph of the cervical spine was normal except for the presence of an abnormal density in the upper right chest seen on the oversized film. Subsequent radiographs and computed tomography of the chest are shown in Figures 1 and 2, respectively. The patient had been in her usual state of excellent health until 2 months before presentation when a nonproductive cough had been noted along with frequent episodes of easily controlled epistaxis, increasing fatigue, decline in school performance, and recurrent episodes of brief, sharp retrosternal chest pain, which were not associated with body position, activity, or respiration. The cough and epistaxis were attributed to the winter season and the dry air in the family’s home. There was no history of fever, hemoptysis, sputum production, chills, night 0 1992 Wiley-Liss, Inc.
sweats, weight loss, nausea, vomiting, diarrhea, or change in appetite. The history was also negative for past neonatal problems, pneumonia, wheezing, cough, heart disease, exposure to tuberculosis, or travel outside of Michigan. As an infant, she was described as “spitty” and had recurrent otitis media. She had no known allergies except for having experienced respiratory difficulty following a bee sting 2 years prior to presentation. Her tonsils were removed at 2 years of age. Immunizations were current. She engaged in no activities or hobbies that involved toxic inhalants, and did not use mineral oil, nasal sprays, or lip gloss. Family history was positive for maternal allergic rhinitis due to molds and a paternal grandfather with emphysema. The child lived in a house surrounded by pine trees and heated by gas heat. The father was a cigarette smoker. Physical examination revealed a thin, well-nourished, afebrile Caucasian girl who was in no respiratory distress. Except for decreased breath sounds over the apex of the right lung with no adventitial sounds and mild clubbing, no abnormalities were found. Laboratory evaluation yielded a white blood cell count of 10,300 cells/pL with a normal differential, and 1% eosinophils; sedimentation rate, 19 mtdhr; IgE, 5 p M / mL; serum antibodies to Aspergillus fumigcitus and A . niger negative by immunodiffusion; alpha- 1-antitrypsin, 200 mg/dL; and normal quantitative immunoglobulins, quantitative iontophoretic sweat test, echocardiography, electrocardiogram, and cardiac catheterization. Spirometry and lung volumes measured by plethysmography revealed: forced vital capacity (FVC), 68% of predicted, forced expiratory volume in 1 second (FEV,), 63%; FEV I /FVC, 851 100; forced expiratory flow between 25 From the Departments of Pediatrics’ and Pathology’ and Section of Thoracic and Cardiovascular Surgery,’ Butterworth Hospital, Michigan State University College of Human Mcdicine. Grand Rapids. Michigan. Rcccivcd Dcccrnber 28. 1991: (revision) accepted for publication April 4. 1992.
Address correspondence and reprint requests to Dr. L.E. Kurlandsky. Butterworth Hospital, 100 Michigan N . E . , Grand Rapids. MI 49503.
Lipoid Pneumonia in Gastroesophageal Reflux
185
Fig. 1. Chest radiograph shows linear, lobulated masses extending from the hilum to the chest wall in the lower portion of a hyperinflated right upper lobe. Bronchiectatic changes are seen in the right middle lobe.
Fig. 2. Computed tomography shows round densities, 3-4 cm in diameter, in the right upper and middle lobes.
and 75% VC (FEF2s-,s,G,), 56%; total lung capacity (TLC), 75%; residual volume (RV), 88%; and RV/TLC, 26/ 100. No improvement was noted following nebulized albuterol. Delayed hypersensitivity skin testing demonstrated positive reactions to candida and mumps, but no reaction to purified protein derivative (PPD). Serum cholesterol was 198 mg/dL. Because of the densities noted on computed tomography (Fig. 2), a neoplasm was suspected and this led to a thoracotomy with resection of the right upper and right middle lobes.
On gross visual examination of the right upper lobe mass a partly necrotic, soft, well-marginated nodule of pinkish tan color that exuded a reddish exudate was observed. The bronchus was of normal diameter at the hilum, but close to it cystic dilatation was found, and it contained bloody fluid. The parenchyma adjacent to the bronchus was bright yellow with multiple cavities averaging 1 cm in diameter and containing a thick, green, purulent exudate. Microscopic examination showed dense bluish material within the bronchial lumina. The bronchi were generally lined by columnar epithelium that exhibited areas of necrosis and concentric lymphoid infiltrates. There was neither histiocytic palisading nor granulomatous inflammation within the bronchial walls (Fig. 3). The surrounding parenchyma was atelectatic, containing focal areas of large numbers of foamy lipid histiocytes within the alveolar spaces (Fig. 4). Surrounding the alveolar spaces and septa1 walls was a chronic inflammatory infiltrate consisting predominantly of lymphocytes. Microscopic sections were stained with Gomori’s silver methenamine, Gram stain and acid-fast stains. No fungi, bacteria, or acid-fast organisms were identified. A mucicarmine stain showed no positivity of the intra-alveolar material. Following the operation, the patient continued to experience retrosternal pain and shortness of breath with physical exercise. Subsequent evaluation was as follows. A barium swallow demonstrated a dilated lower esophagus but not GER; continuous esophageal pH monitoring over 23 hours was abnormal, demonstrating 126 episodes of reflux defined as a pH < 4.Five of these episodes lasted
186
Kurlandsky et al.
Fig. 3. Distal bronchi show a circumferential chronic inflammatory cell infiltrate of mainly lymphocytes. The lumina contain a bluish material. The surrounding parenchyma is atelectatic. No granulomas are seen. Hematoxylin and eosin, x40.
over 5 minutes, the longest being 14 minutes. Overall, there was a total of 114 minutes of reflux, or 8% of the monitoring time. Clinical correlation during this study indicated that two of three episodes of chest pain were associated with reflux as were three of four meals and 5 of 12 episodes of cough. An evaluation of her elevated serum cholesterol showed the following lipid profile compared to (normal values): cholesterol, 187 mg/dL (120-1 80); high-density lipoprotein, 43 mg/dL (45-60); low-density lipoprotein, 1 18 mg/dL (7C120); triglycerides, 129 mg/dL (30-120). Pulmonary function studies 2 years after her operation resulted in: FVC, 7 I % of predicted; FEV, 62%; FEV,/FVC, 83/100; and FEF2s-7s,A, 56%. Following an albuterol inhalation, FEV, and FEF,, 7s% improved by 13% and 26%. respectively. Lung volumes by plethysmography were: TLC 85% of predicted; RV, 133%; and RV/TLC, 33/100. These results were interpreted as signs of restrictive disease resulting from lung resection, and reversible airway obstruction with hyperinflation consistent with the diagnosis of asthma. Subsequent treatment has consisted of albuterol and ipratropium bromide metered-dose inhalation, ranitidine,
and antacids with simethicone. She has received an annual influenza vaccine and experienced three episodes of bronchitis in which no chest x-ray changes or abnormalities on physical examination were noted. However, sputum cultures were positive for Branhamella catarrhalis, and Staphylococcus aureus in addition to normal flora. These microorganisms have responded to appropriate antibiotic therapy. Exercise tolerance has improved and symptoms of retrosternal chest pain have markedly diminished. The patient’s growth accelerated, so that by 14 years of age she was at the 30th percentile for height compared to the 5th, and at the 10th percentile for weight compared to less than the 5th, at the time of her initial presentation. DISCUSSION
This 12 year old girl came to medical attention in a fortuitous manner. Although she had experienced increasing fatigue and fleeting substernal chest pain for 2 months, neither of these complaints were of a sufficient degree to bring her physicians to suspect GER. History, physical examination, and initial laboratory evaluation
Lipoid Pneumonia in Gastroesophageal Reflux
187
Fig. 4. Large numbers of foamy lipid histiocytes are present in the alveolar spaces. Hematoxylin and eosin, x4QQ.
did not support a congenital or infectious process; there- of elevated serum concentrations of cholesterol and trigfore neoplasm was suspected. The diagnoses of bron- lycerides in the presence of bronchiectasis was consistent chiectasis and lipoid pneumonia were established follow- with an animal model of endogenous lipoid pneumonia. ing surgical lung resection. The diagnosis of GER was Lipemic rabbits that had bacteria instilled into the airmade in connection with the evaluation of bronchiectasis. ways developed endogenous-type lipoid pneumonia, GER has been associated with chronic respiratory dis- while the instillation of fat did not produce the pneumoease, bronchiectasis, and lipoid pne~monia.~.'I I Pulmo- nia. 13.14 After the finding of GER, an exogenous etiology of the nary function studies in patients with GER have usually demonstrated airway obstruction, maldistribution of ven- lipoid pneumonia seemed more compelling. The radiotilation, and increased airway reactivity. I * Our patient logic patterns of exogenous lipoid pneumonia are highly subsequently developed clinical exercise- and cold air- varied but include alveolar consolidation, cavitation, ininduced asthma. Pulmonary function studies demon- terstitial disease, atelectasis, nodular and masslike leThe findstrated reversible airway obstruction and the patient has sions, or combinations of these patterns. ings in our patient are consistent with the pattern and clinically responded to bronchodilator therapy. Before the finding of GER, the lipoid pneumonia was location of these descriptions. Lung biopsy is often rehistologically consistent with an endogenous origin. This quired to establish the diagnosis. I n summury,this case report illustrates the subtle cliniwas supported by the presence of ycllow lung tissue, infiltration of the alveoli and interstitium with macro- cal manifestation of lipoid pneumonia associated with phages containing small homogeneous lipid vacuoles, GER, disguised by the dramatic radiologic presentation. enlargement of proximal lymph nodes, and involvement It suggests that in a similar case, even if no history of There was no aspiration is apparent, a search for GER should be part of of the right upper and middle lobes. I*'-' granuloma formation that would have been characteristic the initial diagnostic evaluation, before surgical biopsy or of exogenous lipoid pneumonia. In addition, the presence resection is undertaken.
".''
188
Kurlandsky et al.
ACKNOWLEDGMENTS
We are grateful to Drs. Thomas Colby, Henry Tazelaar, and Jeffrey Meyers at the Mayo Clinic in Rochester, Minnesota, for their review of pathology material. REFERENCES I . Bartlett JG. Lipoid pneumonia. In: Baum GL, Wolinsky E, eds. Textbook of Pulmonary Disease, Vol. 1 , Boston/Toronto: Little, Brown and Company, 1989. 2. Pinkerton H. Oils and fats. Their entrance into and fate in the lungs of infants and children: A clinical and pathologic report. Am J Dis Child. 1927; 33:259-285. 3. Becton DL, Lowe JE, Falletta JM. Lipoid pneumonia in an adolescent girl secondary to use of lip gloss. J Pediatr. 1984; l05:42 1-423. 4 . Wolfson BJ, Allen JL, Panitch HB, Karmazin N. Lipid aspiration pneumonia due to gastrocsophageal reflux. A complication of nasogastric lipid fcedings. Pediatr Radiol. 1989; I9:545-547. 5. McDonald JR. Harrington SW, Clagett OT. Obstructive pncumonitis of neoplastic origin. J Thorac Surg. 1949; 18:97-122. 6. Waddell WR, Sniffen RC, Sweet RH. Chronic pneumonitis: Its clinical and pathologic importance. Report of ten causes showing interstitial pneurnonitis and unusual cholesterol deposits. J Thorac Surg. 1949; 18:707-737.
7. Robbins LL, Sniffcn RC. Correlation between the roentgenologic and pathologic findings in chronic pneumonitis of the cholesterol type. Radiology. 1949; 53:187-201. 8. Kennedy JH. “Silent” gastroesophageal reflux: An important but little known cause of pulmonary complications. Dis Chest. 1962; 42:42-45. 9. Hughes RL, Freilich RA, Bytell DE, et al. Aspiration and occult esophageal disorders. Chest. 1981 ; 80:489-495. 10. Malfroot A, Vandenplas Y,Verlinden M,et al. Gastroesophageal reflux and unexplained chronic respiratory disease in infants and children. Pediatr Pulmonol. 1987; 3:208-213. I I . Allen CJ, Newhouse MT. Gastroesophageal reflux and chronic respiratory disease. Am Rev Respir Dis. 1984; 129:645447. 12. Allen JL, Wohl EB. Pulmonary function in older children and young adults with gastroesophageal reflux. Clin Pediatr. 1986: 25:541-546. 13. Waddell WR, Sniffen RC. Whytehead LL. The etiology of chronic interstitial pneumonitis associated with lipid deposition. J Thorac Surg. 1954; 28:134-142. 14. Waddell WR, Sniffen RC, Whytehead LL. Influence of blood lipid levels on inflammatory response in lung and muscle. A m J Pathol. 1954; 30:757-769. 15. Lipinski K, Weisbrod GL, Sanders DE. Exogenous lipoid pneumonitis: Pulmonary patterns. AJR 1981; 136:931-934. 16. Kennedy JD, Costello P, Balikian JP, Herman PG. Exogenous lipoid pneumonia. AJR 1981; 136:1145-1149.
Lipoid Pneumonia in Association With Gastroesophageal Reflux Lawrence E. Kurlandsky, MD,‘ Vernon Vaandrager, MD,’ Carmel L. Davy, BAD,* and Fred S. Stockinger, M D ~
INTRODUCTION
Lipoid pneumonia may be of exogenous or endogenous origin. Exogenous lipoid pneumonia was initially described in children who aspirated or inhaled milk, mineral oil, cod liver oil, and oily nose drops’; more recently, excessive use of lip gloss3 and nasogastric lipid feedings in an infant with known gastroesophageal reflux (GER)4 have also been reported as causes. Endogenous lipoid pneumonia, in which lipid originates from the lung, may be primarily or secondarily related to localized pulmonary disease, such as bronchiectasis, abscess, tuberculosis, or neoplasm .5. Lipid-laden macrophages are the pathognomonic finding in both types of lipoid pneumonia. In the exogenous type, macrophages contain lipid vacuoles of heterogeneous size and distribution, whereas in the endogenous type, macrophages contain small homogeneous lipid vacuoles imparting a histologic appearance of “foam cells.”’ We report the case of a 12 year old child with lipoid pneumonia and bronchiectasis associated with GER. The clinical and pathological features were consistent with both types of lipoid pneumonia. Distinguishing features and the differential diagnosis are presented.
’
’
CASE REPORT A 12-year-old Caucasian girl came to medical attention when she was involved in a motor vehicle accident and sustained a “whiplash” injury. A radiograph of the cervical spine was normal except for the presence of an abnormal density in the upper right chest seen on the oversized film. Subsequent radiographs and computed tomography of the chest are shown in Figures 1 and 2, respectively. The patient had been in her usual state of excellent health until 2 months before presentation when a nonproductive cough had been noted along with frequent episodes of easily controlled epistaxis, increasing fatigue, decline in school performance, and recurrent episodes of brief, sharp retrosternal chest pain, which were not associated with body position, activity, or respiration. The cough and epistaxis were attributed to the winter season and the dry air in the family’s home. There was no history of fever, hemoptysis, sputum production, chills, night 0 1992 Wiley-Liss, Inc.
sweats, weight loss, nausea, vomiting, diarrhea, or change in appetite. The history was also negative for past neonatal problems, pneumonia, wheezing, cough, heart disease, exposure to tuberculosis, or travel outside of Michigan. As an infant, she was described as “spitty” and had recurrent otitis media. She had no known allergies except for having experienced respiratory difficulty following a bee sting 2 years prior to presentation. Her tonsils were removed at 2 years of age. Immunizations were current. She engaged in no activities or hobbies that involved toxic inhalants, and did not use mineral oil, nasal sprays, or lip gloss. Family history was positive for maternal allergic rhinitis due to molds and a paternal grandfather with emphysema. The child lived in a house surrounded by pine trees and heated by gas heat. The father was a cigarette smoker. Physical examination revealed a thin, well-nourished, afebrile Caucasian girl who was in no respiratory distress. Except for decreased breath sounds over the apex of the right lung with no adventitial sounds and mild clubbing, no abnormalities were found. Laboratory evaluation yielded a white blood cell count of 10,300 cells/pL with a normal differential, and 1% eosinophils; sedimentation rate, 19 mtdhr; IgE, 5 p M / mL; serum antibodies to Aspergillus fumigcitus and A . niger negative by immunodiffusion; alpha- 1-antitrypsin, 200 mg/dL; and normal quantitative immunoglobulins, quantitative iontophoretic sweat test, echocardiography, electrocardiogram, and cardiac catheterization. Spirometry and lung volumes measured by plethysmography revealed: forced vital capacity (FVC), 68% of predicted, forced expiratory volume in 1 second (FEV,), 63%; FEV I /FVC, 851 100; forced expiratory flow between 25 From the Departments of Pediatrics’ and Pathology’ and Section of Thoracic and Cardiovascular Surgery,’ Butterworth Hospital, Michigan State University College of Human Mcdicine. Grand Rapids. Michigan. Rcccivcd Dcccrnber 28. 1991: (revision) accepted for publication April 4. 1992.
Address correspondence and reprint requests to Dr. L.E. Kurlandsky. Butterworth Hospital, 100 Michigan N . E . , Grand Rapids. MI 49503.
Lipoid Pneumonia in Gastroesophageal Reflux
185
Fig. 1. Chest radiograph shows linear, lobulated masses extending from the hilum to the chest wall in the lower portion of a hyperinflated right upper lobe. Bronchiectatic changes are seen in the right middle lobe.
Fig. 2. Computed tomography shows round densities, 3-4 cm in diameter, in the right upper and middle lobes.
and 75% VC (FEF2s-,s,G,), 56%; total lung capacity (TLC), 75%; residual volume (RV), 88%; and RV/TLC, 26/ 100. No improvement was noted following nebulized albuterol. Delayed hypersensitivity skin testing demonstrated positive reactions to candida and mumps, but no reaction to purified protein derivative (PPD). Serum cholesterol was 198 mg/dL. Because of the densities noted on computed tomography (Fig. 2), a neoplasm was suspected and this led to a thoracotomy with resection of the right upper and right middle lobes.
On gross visual examination of the right upper lobe mass a partly necrotic, soft, well-marginated nodule of pinkish tan color that exuded a reddish exudate was observed. The bronchus was of normal diameter at the hilum, but close to it cystic dilatation was found, and it contained bloody fluid. The parenchyma adjacent to the bronchus was bright yellow with multiple cavities averaging 1 cm in diameter and containing a thick, green, purulent exudate. Microscopic examination showed dense bluish material within the bronchial lumina. The bronchi were generally lined by columnar epithelium that exhibited areas of necrosis and concentric lymphoid infiltrates. There was neither histiocytic palisading nor granulomatous inflammation within the bronchial walls (Fig. 3). The surrounding parenchyma was atelectatic, containing focal areas of large numbers of foamy lipid histiocytes within the alveolar spaces (Fig. 4). Surrounding the alveolar spaces and septa1 walls was a chronic inflammatory infiltrate consisting predominantly of lymphocytes. Microscopic sections were stained with Gomori’s silver methenamine, Gram stain and acid-fast stains. No fungi, bacteria, or acid-fast organisms were identified. A mucicarmine stain showed no positivity of the intra-alveolar material. Following the operation, the patient continued to experience retrosternal pain and shortness of breath with physical exercise. Subsequent evaluation was as follows. A barium swallow demonstrated a dilated lower esophagus but not GER; continuous esophageal pH monitoring over 23 hours was abnormal, demonstrating 126 episodes of reflux defined as a pH < 4.Five of these episodes lasted
186
Kurlandsky et al.
Fig. 3. Distal bronchi show a circumferential chronic inflammatory cell infiltrate of mainly lymphocytes. The lumina contain a bluish material. The surrounding parenchyma is atelectatic. No granulomas are seen. Hematoxylin and eosin, x40.
over 5 minutes, the longest being 14 minutes. Overall, there was a total of 114 minutes of reflux, or 8% of the monitoring time. Clinical correlation during this study indicated that two of three episodes of chest pain were associated with reflux as were three of four meals and 5 of 12 episodes of cough. An evaluation of her elevated serum cholesterol showed the following lipid profile compared to (normal values): cholesterol, 187 mg/dL (120-1 80); high-density lipoprotein, 43 mg/dL (45-60); low-density lipoprotein, 1 18 mg/dL (7C120); triglycerides, 129 mg/dL (30-120). Pulmonary function studies 2 years after her operation resulted in: FVC, 7 I % of predicted; FEV, 62%; FEV,/FVC, 83/100; and FEF2s-7s,A, 56%. Following an albuterol inhalation, FEV, and FEF,, 7s% improved by 13% and 26%. respectively. Lung volumes by plethysmography were: TLC 85% of predicted; RV, 133%; and RV/TLC, 33/100. These results were interpreted as signs of restrictive disease resulting from lung resection, and reversible airway obstruction with hyperinflation consistent with the diagnosis of asthma. Subsequent treatment has consisted of albuterol and ipratropium bromide metered-dose inhalation, ranitidine,
and antacids with simethicone. She has received an annual influenza vaccine and experienced three episodes of bronchitis in which no chest x-ray changes or abnormalities on physical examination were noted. However, sputum cultures were positive for Branhamella catarrhalis, and Staphylococcus aureus in addition to normal flora. These microorganisms have responded to appropriate antibiotic therapy. Exercise tolerance has improved and symptoms of retrosternal chest pain have markedly diminished. The patient’s growth accelerated, so that by 14 years of age she was at the 30th percentile for height compared to the 5th, and at the 10th percentile for weight compared to less than the 5th, at the time of her initial presentation. DISCUSSION
This 12 year old girl came to medical attention in a fortuitous manner. Although she had experienced increasing fatigue and fleeting substernal chest pain for 2 months, neither of these complaints were of a sufficient degree to bring her physicians to suspect GER. History, physical examination, and initial laboratory evaluation
Lipoid Pneumonia in Gastroesophageal Reflux
187
Fig. 4. Large numbers of foamy lipid histiocytes are present in the alveolar spaces. Hematoxylin and eosin, x4QQ.
did not support a congenital or infectious process; there- of elevated serum concentrations of cholesterol and trigfore neoplasm was suspected. The diagnoses of bron- lycerides in the presence of bronchiectasis was consistent chiectasis and lipoid pneumonia were established follow- with an animal model of endogenous lipoid pneumonia. ing surgical lung resection. The diagnosis of GER was Lipemic rabbits that had bacteria instilled into the airmade in connection with the evaluation of bronchiectasis. ways developed endogenous-type lipoid pneumonia, GER has been associated with chronic respiratory dis- while the instillation of fat did not produce the pneumoease, bronchiectasis, and lipoid pne~monia.~.'I I Pulmo- nia. 13.14 After the finding of GER, an exogenous etiology of the nary function studies in patients with GER have usually demonstrated airway obstruction, maldistribution of ven- lipoid pneumonia seemed more compelling. The radiotilation, and increased airway reactivity. I * Our patient logic patterns of exogenous lipoid pneumonia are highly subsequently developed clinical exercise- and cold air- varied but include alveolar consolidation, cavitation, ininduced asthma. Pulmonary function studies demon- terstitial disease, atelectasis, nodular and masslike leThe findstrated reversible airway obstruction and the patient has sions, or combinations of these patterns. ings in our patient are consistent with the pattern and clinically responded to bronchodilator therapy. Before the finding of GER, the lipoid pneumonia was location of these descriptions. Lung biopsy is often rehistologically consistent with an endogenous origin. This quired to establish the diagnosis. I n summury,this case report illustrates the subtle cliniwas supported by the presence of ycllow lung tissue, infiltration of the alveoli and interstitium with macro- cal manifestation of lipoid pneumonia associated with phages containing small homogeneous lipid vacuoles, GER, disguised by the dramatic radiologic presentation. enlargement of proximal lymph nodes, and involvement It suggests that in a similar case, even if no history of There was no aspiration is apparent, a search for GER should be part of of the right upper and middle lobes. I*'-' granuloma formation that would have been characteristic the initial diagnostic evaluation, before surgical biopsy or of exogenous lipoid pneumonia. In addition, the presence resection is undertaken.
".''
188
Kurlandsky et al.
ACKNOWLEDGMENTS
We are grateful to Drs. Thomas Colby, Henry Tazelaar, and Jeffrey Meyers at the Mayo Clinic in Rochester, Minnesota, for their review of pathology material. REFERENCES I . Bartlett JG. Lipoid pneumonia. In: Baum GL, Wolinsky E, eds. Textbook of Pulmonary Disease, Vol. 1 , Boston/Toronto: Little, Brown and Company, 1989. 2. Pinkerton H. Oils and fats. Their entrance into and fate in the lungs of infants and children: A clinical and pathologic report. Am J Dis Child. 1927; 33:259-285. 3. Becton DL, Lowe JE, Falletta JM. Lipoid pneumonia in an adolescent girl secondary to use of lip gloss. J Pediatr. 1984; l05:42 1-423. 4 . Wolfson BJ, Allen JL, Panitch HB, Karmazin N. Lipid aspiration pneumonia due to gastrocsophageal reflux. A complication of nasogastric lipid fcedings. Pediatr Radiol. 1989; I9:545-547. 5. McDonald JR. Harrington SW, Clagett OT. Obstructive pncumonitis of neoplastic origin. J Thorac Surg. 1949; 18:97-122. 6. Waddell WR, Sniffen RC, Sweet RH. Chronic pneumonitis: Its clinical and pathologic importance. Report of ten causes showing interstitial pneurnonitis and unusual cholesterol deposits. J Thorac Surg. 1949; 18:707-737.
7. Robbins LL, Sniffcn RC. Correlation between the roentgenologic and pathologic findings in chronic pneumonitis of the cholesterol type. Radiology. 1949; 53:187-201. 8. Kennedy JH. “Silent” gastroesophageal reflux: An important but little known cause of pulmonary complications. Dis Chest. 1962; 42:42-45. 9. Hughes RL, Freilich RA, Bytell DE, et al. Aspiration and occult esophageal disorders. Chest. 1981 ; 80:489-495. 10. Malfroot A, Vandenplas Y,Verlinden M,et al. Gastroesophageal reflux and unexplained chronic respiratory disease in infants and children. Pediatr Pulmonol. 1987; 3:208-213. I I . Allen CJ, Newhouse MT. Gastroesophageal reflux and chronic respiratory disease. Am Rev Respir Dis. 1984; 129:645447. 12. Allen JL, Wohl EB. Pulmonary function in older children and young adults with gastroesophageal reflux. Clin Pediatr. 1986: 25:541-546. 13. Waddell WR, Sniffen RC. Whytehead LL. The etiology of chronic interstitial pneumonitis associated with lipid deposition. J Thorac Surg. 1954; 28:134-142. 14. Waddell WR, Sniffen RC, Whytehead LL. Influence of blood lipid levels on inflammatory response in lung and muscle. A m J Pathol. 1954; 30:757-769. 15. Lipinski K, Weisbrod GL, Sanders DE. Exogenous lipoid pneumonitis: Pulmonary patterns. AJR 1981; 136:931-934. 16. Kennedy JD, Costello P, Balikian JP, Herman PG. Exogenous lipoid pneumonia. AJR 1981; 136:1145-1149.
