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Recurrent Massive Pleural Effusion Due to Pleural, Pericardial, and Epicardial Fibrosis in Histoplasmosis
selected reports Recurrent Massive Pleural Effusion Due to Pleural, Pericardial, and Epicardial Fibrosis in Histoplasmosis* Cindy D. Kilburn, M.D.; and David S. McKinsey, M.D.
Acute histoplasmosis is generally a benign, self-limited pulmonary infection. Although Histoplasma capsulatum pneumonitis is common, pleural effusions associated with histoplasmosis are quite rare, and massive pleural effusions have not been reported. There have been several reports of pericardial fibrosis secondary to histoplasmosis, but epicardial fibrosis has not been described. We report a biopsy-proven case of histoplasmosis initially associated with recurrent massive pleural effusions and excessive pleural fibrosis causing a trapped lung. The patient later developed constrictive pericarditis. Despite pericardiectomy, severe cor pulmonale occurred, and the patient died. Necropsy demonstrated fibrosis of the epicardium. (Chest 1991; 100:1715-17)
A cute histoplasmosis is usually a benign. self-limited 1"- pulmonary infection.' However, when a granuloma
containing Histoplasma capsulatum organisms ruptures into the mediastinum, an excessive fibrotic response to H capsulatum antigens can produce sclerosing mediastinitis.' Similarly, rupture of a granuloma into the pericardial space can cause constrictive pericarditis.'" Epicardial fibrosis has not been described. Although H capsulatum pneumonitis often abuts the pleural space, pleural effusions associated with histoplasmosis are uncommon. Marshall et aI" and Swinburne et al6 recently have reviewed the literature on pleural effusions associated with histoplasmosis. Pleural effusions have been observed in 1 to 5.7 percent of patients with acute histopiasmosiss- IO and also occur rarely in the setting of disseminated histoplasmosis or subpleural histoplasmosis. 6 Pleural effusions associated with histoplasmosis are generally small and self-limited and do not require specific treatment, although pleural fibrosis has been described in a few cases. 6 •1I -" Massive recurrent pleural effusions secondary to pulmonary histoplasmosis have not been reported previously. We report a case of acute histoplasmosis complicated by recurrent massive right pleural effusions, severe pleural fibrosis, constrictive pericarditis, and epicardial fibrosis.
FIGURE 1. Computerized tomographic scan of the chest. Right pleural effusion, right lower lobe atelectasis, pericardialthickening, and a right pericardial effusion are present. medication with temporary improvement. One day prior to admission, she developed a fever, anterior chest pain, and a cough with purulent sputum production and a small amount of hemoptysis. Physical examination showed a temperature of 38°C (IOOAOF), a ri~ht pleural friction rub, and a pericardial friction rub. Leukocyte count was 16,SOO/mm 3 with 89 percent neutrophils, 2 percent band cells, 7 percent lymphocytes, and 2 percent monocytes. The results of a chemistry panel, serum C3 and C, levels, serum and pleural antinuclear antibody screens, rheumatoid factor, and erythrocyte sedimentation rate were all within normal limits. Human immunodefiCiency virus antibody was ne~tive. Chest roentgenowam revealed a moderate-sized right pleural effusion, small left pleural effusion, and cardiac enlargement. Computerized tomography scan of the chest showed a right pleural effusion, thickenin~ of the pericardium with a large pericardial effusion, and a few mediastinal lymph nodes (Fig I). Echocardiogram showed a large pericardial
CASE REPORT
A 24-year-old white woman was admitted for evaluation of a large right pleural effusion. Two months earlier, she had developed acute pericarditis and was treated with a nonsteroidal antiinflammatory *From the University of Missouri-Kansas City School of Medicine, and the Department of Epidemiology and Infectious Disease, Research Medical Center, Kansas City, MO. Reprint requests: Dr. McKinsey, 2316 East Meyer Blvd, Kansas City, M064132
FIGURE 2. Chest roentgenogram obtained three months after first admission. A massive right pleural effusion is present. CHEST I 100 I 6 I DECEMBER, 1991
1715
was (~)mplicated by cardiogenic shock refractory to medical therapy and intraaortic balloon pump replacement, and on the tenth postoperative day, the patient died. Necropsy revealed extensive right pleural fibrosis, and epicardial fibrosis was observed throughout the right ventricle and in portions of the left ventricle (Fig 4). DISCUSSION
FIGURE 3. Postthoracentesis /lim demonstrates a trapped right and right hydropneumothorax.
lun~
effusion with evidence of strandin~ of material within the effusion. Thoracentesis yielded 20 ml of exudative serosan~inous Ruid. Pleural biopsy specimen showed nonspecific inRammation with no granulomas or microorganisms. Cultures of pleural Ruid and pleural tissue were negative for bacteria, fungi, and Mycobacteria. Intermediate strength PPD skin test was negative. Acute complement fixation titer for Histoplasma yeast antibody was 1:32, and convalescent titer obtained three weeks later was 1:64; acute and chronic complement fixation tests for Histoplasma mycelial antibody were negative. Immunodiffusion was positive for the Histoplasma "M" band. Histoplasma IgM antibody by latex agglutination was negative. Complement fixation antibody titers were negative for Coccidioides, Aspergillus, and Blastomyces. Indomethacin therapy was started, and the patient's symptoms improved promptly. Three months later, the patient was found to have a massive right pleural effusion. One and a half liters of pleural Ruid were removed by thoracentesis, but after another month, follow-up chest roentgenogram showed opacification of three-quarters of the right hemithorax (Fi~ 2). A chest tube drained another 3 L of pleural Ruid; however, the right lung failed to reexpand, and pleural adhesions and a hydropneumothorax were noted (Fig 3). Thora(:otomy was performed with lysis of dense adhesions between the lung apex and anterior mediastinum with subsequent partial reexpansion of the lung. Histopathologic studies of lung nodules revealed old caseating granulomas without visible or~anisms. Cultures of lun~ tissue and pleura were negative. The patient received a regimen of naproxen and did well. Follow-up chest roent~eno~ram five months later revealed partial reexpansion of the lun~ with residual hydropneumothorax . One month later, the patient developed severe ascites. Ascitic Ruid chemistries were consistent with an exudate. Cytology and cultures were negative. Echocardiogram revealed pericardial thickening without effusion, and cardiac catheterization showed hemodynamic findings consistent with constrictive pericarditis. Pericardiectomy was performed, and the pericardium was noted to be 1 cm thick. Histopathologic studies demonstrated necrotizin~ granulomatous inRammation with caseation necrosis, diffuse fibrosis, and microorganisms morphologically (:onsistent with H capsulatum. No acid-fast organisms were observed. Fungal cultures of pericardium and pericardial Ruid were negative. Her postoperative course 1716
This previously healthy patient developed acute pulmonary and pericardial histoplasmosis and subsequently had recurrent massive right pleural effusions, as well as pleural fibrosis causing a trapped lung. Ultimately, she developed right-sided congestive heart failure and was found to have pericardial and epicardial fibrosis. The diagnosis of histoplasmosis was confirmed by observation of organisms in pericardial tissue and by significantly elevated Histoplasma yeast antibody titers. The findings in this case demonstrate that acute histoplasmosis can cause massive pleural effusions, can be associated with extensive pleural fibrosis leading to a trapped lung, and can cause fatal epicardial fibrosis. Usually, acute H capsulatum infection resolves after cellular immunity develops, causing an intense inflammatory reaction at the initial sites of infection with subsequent caseous necrosis and calcification. However, in some individuals who are presumably hypersensitive, an excessive fibrotic host response occurs when a caseous lymph node or a parenchymal focus ruptures. Fibroblasts from surrounding normal tissue promote encapsulation and subsequent fibrosis. Mediastinal fibrosis due to histoplasmosis has been welldocumented and has been associated with superior vena cava syndrome, pulmonary hypertension, bronchial stenosis, and other complications? Pleural fibrosis in histoplasmosis has been reported previously in only six cases,"·JH3 and in those cases, it was not as severe as that which occurred in
•
FIGURE 4. Photomicrograph shows cross-section of markedly thickened and fibrotic epicardium (arrows) (original magnification, x 30). Recurrent Massive Pleural Effusion (Kilburn, McKinsey)
our patient. Constrictive pericarditis has been reported rarely,3.4 and epicardial fibrosis has not been described previousl~ to our knowledge. The occurrence of severe pleural, pericardial, and epicardial fibro~~~~.. oQUr ~ti~nt was remarkable and suggests an underlying immunologic disorder, although we were unable to define a specific immunologic defect. This patient demonstrates that excessive fibrosis from H capsulatum infection can occur not only in the mediastinum, pericardium, and pleura, but also in the epicardium. Recurrent massive pleural effusions may occur. Histoplasmosis is not currently listed as a possible etiology for pleural effusions,14 but it should be included in the differential diagnosis in view of our findings. Congestive heart failure refractory to medical or surgical therapy can occur as a result of epicardial fibrosis. ACKNOWLEDGMENTS: The authors thank Drs. William Eubank, Douglas Paone, and David Wilt for allowing us to participate in the care ofthis patient and Dr. Michael Caughron for providing necropsy results. REFERENCES
1 Goodwin RA, Des Prez RM. State of the art: histoplasmosis. Am Rev Respir Dis 1978; 117:929-56 2 Dunn EJ, Ulicny KS, Wright CB, Gottesman L. Surgical implications of sclerosing mediastinitis. Chest 1990; 97:338-46 3 Wooley CF, Hosier OM. Constrictive pericarditis due to Histoplasma capsulatum. N Eng) J Moo 1961; 264:1230-32 4 Saslaw S, Norfleet RG, Dapra OJ. Acute histoplasma pericarditis. Arch Intern Moo 1968; 122:162-66 5 Marshall BC, Cox JK, Carroll KC, Morrison RE. Case report: histoplasmosis as a cause of pleural effusion in the acquired immunode6ciency syndrome. Am J Moo Sci 1990; 300:98-101 6 Swinburne AJ, FOOullo AJ, Wahl G~ Fornand B. Histoplasma, pleural 6brosis, and slowly enlarging pleural effusion in an asymptomatic patient. Am Rev Respir Dis 1987; 135:502-03 7 Ward JI, Weeks M, Allen 0, Hutcheson RH, Anderson R, Fraser D~ et ale Acute histoplasmosis: clinical, epidemiologic, and serologic 6ndings of an outbreak associated with exposure to a fallen tree. Am J Moo 1979; 66:587-95 8 Straus SE, Jacobsen ES. The spectrum of histoplasmosis in a general hospital: a review of 55 cases diagnosed at Barnes hospital between 1966 and 1977. Am J Med Sci 1980; 297:14758 9 Wheat LJ, Slama TG, Eitzen HE, Kohler RB, French ML, Biesecker JL. A large urban outbreak of histoplasmosis. Ann Int Moo 1981; 94:331-37 10 Gustafson TL, Kaufman L, Weeks R, Ajello L, Hutcheson RH, Wilber SL, et al. Outbreak of acute pulmonary histoplasmosis in members of a wagon train. Am J Moo 1981; 71:759-65 11 Schub 8M, Spivey CG, Baird GO. Pleural involvement in histoplasmosis. Am Rev Respir Dis 1966; 94:225-32 12 Brewer PL, Himmelwrigbt IE Pleural effusion due to infection with HiBtoplasma capsulatum. Chest 1970; 58:76-79 13 Stead ww, Eichenholz A, Stauss HK. Operative and pathologic 6ndings in twenty-four patients with syndrome of idiopathic pleurisy with effusion, presumably tuberculous. Am Rev Tuberc 1955; 71:473-501 14 Kinasewitz GT, Fishman AI! Pulmonary effusions. In: Fishman ~ 00. Pulmonary diseases and disorders, 2nd 00. New York: McGraw- Hill Book Co, 1988:2134-35
Combined Laser Phototherapy and Growth Factor Treatment of EJQ)o~hial Obstruction after Lung transplantatlon* MarshaU I. Hertz, M.D.;t Kftth R. Harmon, M.D.; David R. Knighton" M.D.; Barbara C. Cahill" M.D.; Arndt J. Duvall Ill" M.D.; Sara']. Shumway, M.D.; and R. Morton Bolman Ill" M.D." FoC.C.1!
Lung transplantation has resulted in dramatic functional improvement in patients with end-stage pulmonary diseases. Among the complications of lung transplantation are dehiscence and stenosis at the site of the bronchial or tracheal anastomosis. In this case report, we describe a single lung transplant reci~nt in whom partial bronchial dehiscence, followed by ~berant growth of granulation tissue, resulted in obstruction of the bronchial lumen. After mechanical dilation failed to produce lasting relief of bronchial obstruction, a novel approach to this problem was successfully employed: YAG laser phototherapy was used to remove obstructing granulation tissue, followed by application of a preparation derived from autologous blood platelets to promote epithelialization of the bronchial anastamosis. The bronchus remains patent and fully epithelialized six months after thera~ (Chat 1991; 100:1717-19)
I
PDWHF = plalelet-derived wound healing lOrmuia
I
Tung transplantation has resulted in dramatic functional
.l..J improvement in patients with end-stage pulmonary disease of diverse etiolo~ Transplantation of pulmonary tissue may be accomplished by single lung transplantation (unilateral or bilateral), double lung transplantation, or combined heart and lung transplantation. l -3 A significant problem after lung transplantation is dehiscence and stenosis at the site of the bronchial or tracheal anastomosis. These problems have been approached by excluding patients receiving corticosteroids as candidates for transplantation, and by wrapping the anastomosis with the recipient's omentum or other suitable vascularized tissues to facilitate revascularization of the anastomotic site.4.5 Despite these innovations, however, anastomotic dehiscence and stenosis continue to occur in some lung transplant recipients. In this report, we describe a single lung transplant recipient in whom partial dehiscence of the bronchial anastomosis, followed by exuberant growth of granulation tissue into the bronchial lumen, resulted in bronchial obstruction. A novel approach to this problem was successfully employed: YAG laser phototherapy was used to remove the obstructing granulation tissue, followed by application of a preparation derived from autologous blood platelets to promote epithelialization of the bronchial anastomosis. ·From the Departments of Medicine, Surgery, and Otolaryngology, and the Minnesota Heart and Lung Institute, University of Minnesota, Minneapolis. tRecipient of a Young Faculty Award from the American Lung Association of Minnesota. Reprint requests: Dr. Hertz" Box 276" University of MinneMJtIJ Hospital" 420 Delaware SE,l Minneapolis 55455 CHEST I 100 I 6 I DECEMBER, 1991
1717
Acute histoplasmosis is generally a benign, self-limited pulmonary infection. Although Histoplasma capsulatum pneumonitis is common, pleural effusions associated with histoplasmosis are quite rare, and massive pleural effusions have not been reported. There have been several reports of pericardial fibrosis secondary to histoplasmosis, but epicardial fibrosis has not been described. We report a biopsy-proven case of histoplasmosis initially associated with recurrent massive pleural effusions and excessive pleural fibrosis causing a trapped lung. The patient later developed constrictive pericarditis. Despite pericardiectomy, severe cor pulmonale occurred, and the patient died. Necropsy demonstrated fibrosis of the epicardium. (Chest 1991; 100:1715-17)
A cute histoplasmosis is usually a benign. self-limited 1"- pulmonary infection.' However, when a granuloma
containing Histoplasma capsulatum organisms ruptures into the mediastinum, an excessive fibrotic response to H capsulatum antigens can produce sclerosing mediastinitis.' Similarly, rupture of a granuloma into the pericardial space can cause constrictive pericarditis.'" Epicardial fibrosis has not been described. Although H capsulatum pneumonitis often abuts the pleural space, pleural effusions associated with histoplasmosis are uncommon. Marshall et aI" and Swinburne et al6 recently have reviewed the literature on pleural effusions associated with histoplasmosis. Pleural effusions have been observed in 1 to 5.7 percent of patients with acute histopiasmosiss- IO and also occur rarely in the setting of disseminated histoplasmosis or subpleural histoplasmosis. 6 Pleural effusions associated with histoplasmosis are generally small and self-limited and do not require specific treatment, although pleural fibrosis has been described in a few cases. 6 •1I -" Massive recurrent pleural effusions secondary to pulmonary histoplasmosis have not been reported previously. We report a case of acute histoplasmosis complicated by recurrent massive right pleural effusions, severe pleural fibrosis, constrictive pericarditis, and epicardial fibrosis.
FIGURE 1. Computerized tomographic scan of the chest. Right pleural effusion, right lower lobe atelectasis, pericardialthickening, and a right pericardial effusion are present. medication with temporary improvement. One day prior to admission, she developed a fever, anterior chest pain, and a cough with purulent sputum production and a small amount of hemoptysis. Physical examination showed a temperature of 38°C (IOOAOF), a ri~ht pleural friction rub, and a pericardial friction rub. Leukocyte count was 16,SOO/mm 3 with 89 percent neutrophils, 2 percent band cells, 7 percent lymphocytes, and 2 percent monocytes. The results of a chemistry panel, serum C3 and C, levels, serum and pleural antinuclear antibody screens, rheumatoid factor, and erythrocyte sedimentation rate were all within normal limits. Human immunodefiCiency virus antibody was ne~tive. Chest roentgenowam revealed a moderate-sized right pleural effusion, small left pleural effusion, and cardiac enlargement. Computerized tomography scan of the chest showed a right pleural effusion, thickenin~ of the pericardium with a large pericardial effusion, and a few mediastinal lymph nodes (Fig I). Echocardiogram showed a large pericardial
CASE REPORT
A 24-year-old white woman was admitted for evaluation of a large right pleural effusion. Two months earlier, she had developed acute pericarditis and was treated with a nonsteroidal antiinflammatory *From the University of Missouri-Kansas City School of Medicine, and the Department of Epidemiology and Infectious Disease, Research Medical Center, Kansas City, MO. Reprint requests: Dr. McKinsey, 2316 East Meyer Blvd, Kansas City, M064132
FIGURE 2. Chest roentgenogram obtained three months after first admission. A massive right pleural effusion is present. CHEST I 100 I 6 I DECEMBER, 1991
1715
was (~)mplicated by cardiogenic shock refractory to medical therapy and intraaortic balloon pump replacement, and on the tenth postoperative day, the patient died. Necropsy revealed extensive right pleural fibrosis, and epicardial fibrosis was observed throughout the right ventricle and in portions of the left ventricle (Fig 4). DISCUSSION
FIGURE 3. Postthoracentesis /lim demonstrates a trapped right and right hydropneumothorax.
lun~
effusion with evidence of strandin~ of material within the effusion. Thoracentesis yielded 20 ml of exudative serosan~inous Ruid. Pleural biopsy specimen showed nonspecific inRammation with no granulomas or microorganisms. Cultures of pleural Ruid and pleural tissue were negative for bacteria, fungi, and Mycobacteria. Intermediate strength PPD skin test was negative. Acute complement fixation titer for Histoplasma yeast antibody was 1:32, and convalescent titer obtained three weeks later was 1:64; acute and chronic complement fixation tests for Histoplasma mycelial antibody were negative. Immunodiffusion was positive for the Histoplasma "M" band. Histoplasma IgM antibody by latex agglutination was negative. Complement fixation antibody titers were negative for Coccidioides, Aspergillus, and Blastomyces. Indomethacin therapy was started, and the patient's symptoms improved promptly. Three months later, the patient was found to have a massive right pleural effusion. One and a half liters of pleural Ruid were removed by thoracentesis, but after another month, follow-up chest roentgenogram showed opacification of three-quarters of the right hemithorax (Fi~ 2). A chest tube drained another 3 L of pleural Ruid; however, the right lung failed to reexpand, and pleural adhesions and a hydropneumothorax were noted (Fig 3). Thora(:otomy was performed with lysis of dense adhesions between the lung apex and anterior mediastinum with subsequent partial reexpansion of the lung. Histopathologic studies of lung nodules revealed old caseating granulomas without visible or~anisms. Cultures of lun~ tissue and pleura were negative. The patient received a regimen of naproxen and did well. Follow-up chest roent~eno~ram five months later revealed partial reexpansion of the lun~ with residual hydropneumothorax . One month later, the patient developed severe ascites. Ascitic Ruid chemistries were consistent with an exudate. Cytology and cultures were negative. Echocardiogram revealed pericardial thickening without effusion, and cardiac catheterization showed hemodynamic findings consistent with constrictive pericarditis. Pericardiectomy was performed, and the pericardium was noted to be 1 cm thick. Histopathologic studies demonstrated necrotizin~ granulomatous inRammation with caseation necrosis, diffuse fibrosis, and microorganisms morphologically (:onsistent with H capsulatum. No acid-fast organisms were observed. Fungal cultures of pericardium and pericardial Ruid were negative. Her postoperative course 1716
This previously healthy patient developed acute pulmonary and pericardial histoplasmosis and subsequently had recurrent massive right pleural effusions, as well as pleural fibrosis causing a trapped lung. Ultimately, she developed right-sided congestive heart failure and was found to have pericardial and epicardial fibrosis. The diagnosis of histoplasmosis was confirmed by observation of organisms in pericardial tissue and by significantly elevated Histoplasma yeast antibody titers. The findings in this case demonstrate that acute histoplasmosis can cause massive pleural effusions, can be associated with extensive pleural fibrosis leading to a trapped lung, and can cause fatal epicardial fibrosis. Usually, acute H capsulatum infection resolves after cellular immunity develops, causing an intense inflammatory reaction at the initial sites of infection with subsequent caseous necrosis and calcification. However, in some individuals who are presumably hypersensitive, an excessive fibrotic host response occurs when a caseous lymph node or a parenchymal focus ruptures. Fibroblasts from surrounding normal tissue promote encapsulation and subsequent fibrosis. Mediastinal fibrosis due to histoplasmosis has been welldocumented and has been associated with superior vena cava syndrome, pulmonary hypertension, bronchial stenosis, and other complications? Pleural fibrosis in histoplasmosis has been reported previously in only six cases,"·JH3 and in those cases, it was not as severe as that which occurred in
•
FIGURE 4. Photomicrograph shows cross-section of markedly thickened and fibrotic epicardium (arrows) (original magnification, x 30). Recurrent Massive Pleural Effusion (Kilburn, McKinsey)
our patient. Constrictive pericarditis has been reported rarely,3.4 and epicardial fibrosis has not been described previousl~ to our knowledge. The occurrence of severe pleural, pericardial, and epicardial fibro~~~~.. oQUr ~ti~nt was remarkable and suggests an underlying immunologic disorder, although we were unable to define a specific immunologic defect. This patient demonstrates that excessive fibrosis from H capsulatum infection can occur not only in the mediastinum, pericardium, and pleura, but also in the epicardium. Recurrent massive pleural effusions may occur. Histoplasmosis is not currently listed as a possible etiology for pleural effusions,14 but it should be included in the differential diagnosis in view of our findings. Congestive heart failure refractory to medical or surgical therapy can occur as a result of epicardial fibrosis. ACKNOWLEDGMENTS: The authors thank Drs. William Eubank, Douglas Paone, and David Wilt for allowing us to participate in the care ofthis patient and Dr. Michael Caughron for providing necropsy results. REFERENCES
1 Goodwin RA, Des Prez RM. State of the art: histoplasmosis. Am Rev Respir Dis 1978; 117:929-56 2 Dunn EJ, Ulicny KS, Wright CB, Gottesman L. Surgical implications of sclerosing mediastinitis. Chest 1990; 97:338-46 3 Wooley CF, Hosier OM. Constrictive pericarditis due to Histoplasma capsulatum. N Eng) J Moo 1961; 264:1230-32 4 Saslaw S, Norfleet RG, Dapra OJ. Acute histoplasma pericarditis. Arch Intern Moo 1968; 122:162-66 5 Marshall BC, Cox JK, Carroll KC, Morrison RE. Case report: histoplasmosis as a cause of pleural effusion in the acquired immunode6ciency syndrome. Am J Moo Sci 1990; 300:98-101 6 Swinburne AJ, FOOullo AJ, Wahl G~ Fornand B. Histoplasma, pleural 6brosis, and slowly enlarging pleural effusion in an asymptomatic patient. Am Rev Respir Dis 1987; 135:502-03 7 Ward JI, Weeks M, Allen 0, Hutcheson RH, Anderson R, Fraser D~ et ale Acute histoplasmosis: clinical, epidemiologic, and serologic 6ndings of an outbreak associated with exposure to a fallen tree. Am J Moo 1979; 66:587-95 8 Straus SE, Jacobsen ES. The spectrum of histoplasmosis in a general hospital: a review of 55 cases diagnosed at Barnes hospital between 1966 and 1977. Am J Med Sci 1980; 297:14758 9 Wheat LJ, Slama TG, Eitzen HE, Kohler RB, French ML, Biesecker JL. A large urban outbreak of histoplasmosis. Ann Int Moo 1981; 94:331-37 10 Gustafson TL, Kaufman L, Weeks R, Ajello L, Hutcheson RH, Wilber SL, et al. Outbreak of acute pulmonary histoplasmosis in members of a wagon train. Am J Moo 1981; 71:759-65 11 Schub 8M, Spivey CG, Baird GO. Pleural involvement in histoplasmosis. Am Rev Respir Dis 1966; 94:225-32 12 Brewer PL, Himmelwrigbt IE Pleural effusion due to infection with HiBtoplasma capsulatum. Chest 1970; 58:76-79 13 Stead ww, Eichenholz A, Stauss HK. Operative and pathologic 6ndings in twenty-four patients with syndrome of idiopathic pleurisy with effusion, presumably tuberculous. Am Rev Tuberc 1955; 71:473-501 14 Kinasewitz GT, Fishman AI! Pulmonary effusions. In: Fishman ~ 00. Pulmonary diseases and disorders, 2nd 00. New York: McGraw- Hill Book Co, 1988:2134-35
Combined Laser Phototherapy and Growth Factor Treatment of EJQ)o~hial Obstruction after Lung transplantatlon* MarshaU I. Hertz, M.D.;t Kftth R. Harmon, M.D.; David R. Knighton" M.D.; Barbara C. Cahill" M.D.; Arndt J. Duvall Ill" M.D.; Sara']. Shumway, M.D.; and R. Morton Bolman Ill" M.D." FoC.C.1!
Lung transplantation has resulted in dramatic functional improvement in patients with end-stage pulmonary diseases. Among the complications of lung transplantation are dehiscence and stenosis at the site of the bronchial or tracheal anastomosis. In this case report, we describe a single lung transplant reci~nt in whom partial bronchial dehiscence, followed by ~berant growth of granulation tissue, resulted in obstruction of the bronchial lumen. After mechanical dilation failed to produce lasting relief of bronchial obstruction, a novel approach to this problem was successfully employed: YAG laser phototherapy was used to remove obstructing granulation tissue, followed by application of a preparation derived from autologous blood platelets to promote epithelialization of the bronchial anastamosis. The bronchus remains patent and fully epithelialized six months after thera~ (Chat 1991; 100:1717-19)
I
PDWHF = plalelet-derived wound healing lOrmuia
I
Tung transplantation has resulted in dramatic functional
.l..J improvement in patients with end-stage pulmonary disease of diverse etiolo~ Transplantation of pulmonary tissue may be accomplished by single lung transplantation (unilateral or bilateral), double lung transplantation, or combined heart and lung transplantation. l -3 A significant problem after lung transplantation is dehiscence and stenosis at the site of the bronchial or tracheal anastomosis. These problems have been approached by excluding patients receiving corticosteroids as candidates for transplantation, and by wrapping the anastomosis with the recipient's omentum or other suitable vascularized tissues to facilitate revascularization of the anastomotic site.4.5 Despite these innovations, however, anastomotic dehiscence and stenosis continue to occur in some lung transplant recipients. In this report, we describe a single lung transplant recipient in whom partial dehiscence of the bronchial anastomosis, followed by exuberant growth of granulation tissue into the bronchial lumen, resulted in bronchial obstruction. A novel approach to this problem was successfully employed: YAG laser phototherapy was used to remove the obstructing granulation tissue, followed by application of a preparation derived from autologous blood platelets to promote epithelialization of the bronchial anastomosis. ·From the Departments of Medicine, Surgery, and Otolaryngology, and the Minnesota Heart and Lung Institute, University of Minnesota, Minneapolis. tRecipient of a Young Faculty Award from the American Lung Association of Minnesota. Reprint requests: Dr. Hertz" Box 276" University of MinneMJtIJ Hospital" 420 Delaware SE,l Minneapolis 55455 CHEST I 100 I 6 I DECEMBER, 1991
1717