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Extensive Idiopathic Benign Bilateral Asynchronous Pleural Fibrosis
Extensive Idiopathic Benign Bilateral Asynchronous Pleural Fibrosis* Teofilo L. Lee-Chiang, Jr., MD; and Janet Hilbert, MD, FCCP
We describe a young man who had been healthy until he developed extensive benign left pleural fibrosis. He subsequently developed disabling right pleural thickening a year later. No clear cause was discovered. (CHEST 1996;109:564-65) Key words: decortication; fibrosis; pleura; pleuritis
P
leural fibrosis is most commonly encountered in patients who have been exposed to asbestos. Occasionally, it may develop following significant pleural inflammation associated with collagen vascular diseases, chronic infectious processes, or medications. We present a case of rapidly progressive, extensive, disabling idiopathic benign pleural fibrosis. CASE REPORT
A 39-year-old man was well until 1 year prior to admission when he presented with dyspnea and vague left-sided chest discomfort associated with a left exudative pleural effusion and pleural thickening (Fig 1). He worked in highway construction but denied any significant occupational exposure to any respiratory irritants or carcinogens. He had no personal or family history of collagen vascular diseases, neoplasms, or chronic infection. He had smoked cigarettes since his late teens. He denied taking any medications. A left pleural decortication was subsequently performed for this extensive pleural peel. Pathologic examination revealed multiple sheets of dense mature pleura with foci of chronic, nonspecific inflammation. No tumor cells were recognized, and there was no evidence of fungal, tuberculous, or bacterial infection. Six months later, he developed right pleuritic chest pain and diminished exercise tolerance associated with right pleural thickening. No parenchymal involvement was observed on a Cf scan of the chest (Fig 2). A severe restrictive ventilatory impairment was demonstrated on pulmonary function testing. He underwent thoracoscopic p el ural biopsy. Again, pathologic studies revealed only bland fibrosis with no evidence of malignancy or infection. Because of progressive dyspnea, he underwent a right decortication. He was noted to have extensive visceral and parietal pleural thickening. The visceral pleura was approximately 4 to 5 mm thick and encased the entire right ul ng. The parietal pleura was 15 mm thick. Pathologic fmdings were identical to those found in the thoracoscopic b oi psy specimens obtained a month earlier.
F IGURE l. Initial CT scan of the chest demonstrating left pleural thickening and effusion.
the pleura presumably where dust fibers accumulate. 1 Other less common causes of pleural fibrosis include drugs (methysergide maleate, bromocriptine, ergotamine), collagen vascular diseases (rheumatoid pleuritis, systemic lupus erythematosus), and infectious diseases (tuberculosis).2·3 Fibrosis also can develop in any prolonged exudative or hemorrhagic pleural effusion such as in empyema. 4 Not all cases of pleural fibrosis, however, have a recognized cause. Buchanan and associates 3 reported four patients with diffuse pleural thickening developing in the aftermath of bilateral effusions. The patients presented with complaints of chest pain, dyspnea, cough, or malaise. Histologically, both pleural layers were thickened and covered by organizing fibrin. Three patients were successfully managed by pleural decortication. The role of corticosteroids was conflicting. They suggested the descriptive term cryptogenic bilateral fibrosing pleuritis to convey the absence of an infectious, embolic, or occupational cause. The pathogenesis of pleural fibrosis is poorly understood.
DISCUSSION
Most cases of pleural fibrosis are related to asbestos exposure. The distinctive pleural plaques consist mainly of acellular collagen covered by a layer of mesothelium. They invariably form along the pathways oflymphatic drainage of *From Yale Medical School, New Haven, Con n (Dr. Lee-Chiong); and St. Mary's Hospital, Waterb'!fY, Conn (Dr. Hilbert). Reprint requests: Dr. Hilbert, Pulrrwnary and Critical Care, St. Mary's Hospital, 56 Franklin Street, Waterburg, CT 06706 564
FIGURE 2. CT scan of the chest obtained after left pleural decortication which reveals right pleural thickening. Selected Reports
Stimulated mesothelial cells may, following pleural damage, propagate a self-sustaining reaction that culminates in the development of pleural fibrosis. 5-9 REFERENCES
1 Rom WN, Travis WD, Brody AR. Cellular and molecular basis of the asbestos-related diseases. Am Rev Respir Dis 1991; 143:408-22 2 Light RW. Pleural diseases. 2nd ed. Philadelphia: Lea & Febiger, 1990; 291 3 Buchanan DR, Johnston ID, Kerr IH, et al. Cryptogenic bilateral fibrosing pleuritis. Br J Dis Chest 1988; 82:186-93 4 Herbert A. Pathogenesis of pleurisy, pleural fibrosis and mesothelial proliferation. Thorax 1986; 41:176-89 5 Davila RM, Crouch EC. Role of mesothelial and submesothelial stromal cells in matrix remodelling following pleural injury. Am J Pathol1933; 142:547-55 6 Baumann MH, Henrich K, Sahn SA, et al. Pleural macrophages differentially·alter mesothelial cell growth and collagen production. Inflammation 1993; 17:1-12 7 Owens MW, Grimes SR. Pleural mesothelial cell response to inflammation: tumor necrosis factor-induced mitogenesis and collagen synthesis. Am J Physiol 1993; 265:L382-88 8 Kuwahara M, Kuwahara M, Bijwaard KE, et al. Mesothelial cells produce a chemoattractant for lung fibroblasts: role of fibronectin. Am J Respir Cell Mol Bioi 1991;5:256-64 9 Antony VB, Rothfuss KJ, Godbey SW, et al. Mechanism of tetracycline-hydrochloride-induced pleurodesis: tetracycline-hydrochloride-stimulated mesothelial cells produce a growth-factorlike activity for fibroblasts. Am Rev Respir Dis 1992; 146:1009-13
Subacute Rupture of the Left Ventricular Free Wall After Acute Myocardial Infarction* Three Cases of Long-term Survival Without Emergency Surgical Repair Ales Blinc, MD; Marko Noc, MD; Bojan Pohar, MD; Natasa Cemic, MD; and Matija Horvat, MD
oped sudden hypotension accompanied by a new pericardial effusion. They were initially managed with hemodynamic support. Two patients had elective openheart surgery 2 to 3 months after AMI, whereas one patient did not require surgery. All three survived 1lh to 8lh years after AMI. This report indicates that a small subset of patients with subacute ventricular free wall rupture has a benign course that may allow for prolonged survival without having to have emergency surgical repair. (CHEST 1996; 109:565-67)
AMI=acute myocardial infarction
Key words: acute myocardial infarction; subacute rupture of left ventricle; survival
myocardial infarction (AMI) is complicated by A cute rupture of the myocardial free wall in about 6% of cas-
es.1 Several distinct clinical forms of ventricular free wall rupture have been identified. 2 Sudden rupture with massive hemorrhage into the pericardium is the most common. In about one third of cases, the course is subacute with slow and sometimes repetitive hemorrhage into the pericardia! cavity.l There is general agreement that prolonged survival is possible only with prompt surgical repair, except in rare cases when rupture may go unnoticed, because it occurs in a space already confined by pericardia! adhesions.l·3•4 However, we report on three long-term survivors of subacute ventricular free-wall rupture who were treated without emergency surgical repair in our ICU during the last 8lh years. Admittedly, these patients received treatment that may be considered as unusual and nonstandard. However, since emergency surgical repair of ruptured myocardium was not available in our hospital in the past, conservative management was the only therapeutic option. CASE REPORTS CASE
Rupture of the left ventricular free wall after acute myocardial infarction (AMI) has been regarded as uniformly fatal unless emergency surgical repair is performed. Among 2,862 patients admitted with AMI to our ICU during the last 8 years, 107 patients developed rupture of the left ventricular free wall. Twentynine patients had a subacute course and three of them survived for prolonged periods without having to have emergency surgical repair. At the onset of rupture on day 1 through 7 after AMI, the three survivors devel*From the Trnovo Hospital of Internal Medicine (Dr. Blinc) and Center for Intensive Internal Medicine (Drs. Noc, Pohar, and Horvat), University Clinical Center Ljubljana, Ljubljana, Slovenia; and the DepartmeJlt of Internal Meaicine, Iwla General Hospital, Slovenia (Dr. Cernic). Reprint requests: Dr. Blinc, Trnovo Hospital of Internal Medicine, University Clinical Center Ljubljana, Riharjew 24, Ljubljana 61000, S{ovenia.
1
A 64-year-old man with a 10-year history of hypertension was admitted with anterolateral AMI, which was confirmed by ECG and the temporal pattern of creatine phosphokinase. Treatment with IV streptokinase was begun 3 h after the onset of chest pain. Eight hours after admission, the patient suddenly became nauseated and lost consciousness. The systolic arterial pressure fell from 125 to 70 to 90 mm Hg, and the heart rate decreased from 96 to 60 beats per minute. The central venous pressure rose from 12.5 to 19 em H20. Pressure equalization in the heart chambers documented by a Swan-Ganz catheter was consistent with cardiac tamponade. The right atrial pressure was 22118 mm Hg, the right ventricular pressure was 27/18 mm Hg and the pulmonary artery pressure was 27/22 mm Hg. Echocardiography revealed a pericardial effusion that was up to 1-cm wide and had high acoustic density echoes. The patient was treated by infusion of a colloid hydroxyethyl starch solution, followed by that of normal saline solution and lowdose dopamine (2.5 to 5 pg'kg'min). The systolic arterial pressure was stabilized at about 115 mm Hg within half an hour and the heart CHEST 11 09 I 2 I FEBRUARY, 1996
565
We describe a young man who had been healthy until he developed extensive benign left pleural fibrosis. He subsequently developed disabling right pleural thickening a year later. No clear cause was discovered. (CHEST 1996;109:564-65) Key words: decortication; fibrosis; pleura; pleuritis
P
leural fibrosis is most commonly encountered in patients who have been exposed to asbestos. Occasionally, it may develop following significant pleural inflammation associated with collagen vascular diseases, chronic infectious processes, or medications. We present a case of rapidly progressive, extensive, disabling idiopathic benign pleural fibrosis. CASE REPORT
A 39-year-old man was well until 1 year prior to admission when he presented with dyspnea and vague left-sided chest discomfort associated with a left exudative pleural effusion and pleural thickening (Fig 1). He worked in highway construction but denied any significant occupational exposure to any respiratory irritants or carcinogens. He had no personal or family history of collagen vascular diseases, neoplasms, or chronic infection. He had smoked cigarettes since his late teens. He denied taking any medications. A left pleural decortication was subsequently performed for this extensive pleural peel. Pathologic examination revealed multiple sheets of dense mature pleura with foci of chronic, nonspecific inflammation. No tumor cells were recognized, and there was no evidence of fungal, tuberculous, or bacterial infection. Six months later, he developed right pleuritic chest pain and diminished exercise tolerance associated with right pleural thickening. No parenchymal involvement was observed on a Cf scan of the chest (Fig 2). A severe restrictive ventilatory impairment was demonstrated on pulmonary function testing. He underwent thoracoscopic p el ural biopsy. Again, pathologic studies revealed only bland fibrosis with no evidence of malignancy or infection. Because of progressive dyspnea, he underwent a right decortication. He was noted to have extensive visceral and parietal pleural thickening. The visceral pleura was approximately 4 to 5 mm thick and encased the entire right ul ng. The parietal pleura was 15 mm thick. Pathologic fmdings were identical to those found in the thoracoscopic b oi psy specimens obtained a month earlier.
F IGURE l. Initial CT scan of the chest demonstrating left pleural thickening and effusion.
the pleura presumably where dust fibers accumulate. 1 Other less common causes of pleural fibrosis include drugs (methysergide maleate, bromocriptine, ergotamine), collagen vascular diseases (rheumatoid pleuritis, systemic lupus erythematosus), and infectious diseases (tuberculosis).2·3 Fibrosis also can develop in any prolonged exudative or hemorrhagic pleural effusion such as in empyema. 4 Not all cases of pleural fibrosis, however, have a recognized cause. Buchanan and associates 3 reported four patients with diffuse pleural thickening developing in the aftermath of bilateral effusions. The patients presented with complaints of chest pain, dyspnea, cough, or malaise. Histologically, both pleural layers were thickened and covered by organizing fibrin. Three patients were successfully managed by pleural decortication. The role of corticosteroids was conflicting. They suggested the descriptive term cryptogenic bilateral fibrosing pleuritis to convey the absence of an infectious, embolic, or occupational cause. The pathogenesis of pleural fibrosis is poorly understood.
DISCUSSION
Most cases of pleural fibrosis are related to asbestos exposure. The distinctive pleural plaques consist mainly of acellular collagen covered by a layer of mesothelium. They invariably form along the pathways oflymphatic drainage of *From Yale Medical School, New Haven, Con n (Dr. Lee-Chiong); and St. Mary's Hospital, Waterb'!fY, Conn (Dr. Hilbert). Reprint requests: Dr. Hilbert, Pulrrwnary and Critical Care, St. Mary's Hospital, 56 Franklin Street, Waterburg, CT 06706 564
FIGURE 2. CT scan of the chest obtained after left pleural decortication which reveals right pleural thickening. Selected Reports
Stimulated mesothelial cells may, following pleural damage, propagate a self-sustaining reaction that culminates in the development of pleural fibrosis. 5-9 REFERENCES
1 Rom WN, Travis WD, Brody AR. Cellular and molecular basis of the asbestos-related diseases. Am Rev Respir Dis 1991; 143:408-22 2 Light RW. Pleural diseases. 2nd ed. Philadelphia: Lea & Febiger, 1990; 291 3 Buchanan DR, Johnston ID, Kerr IH, et al. Cryptogenic bilateral fibrosing pleuritis. Br J Dis Chest 1988; 82:186-93 4 Herbert A. Pathogenesis of pleurisy, pleural fibrosis and mesothelial proliferation. Thorax 1986; 41:176-89 5 Davila RM, Crouch EC. Role of mesothelial and submesothelial stromal cells in matrix remodelling following pleural injury. Am J Pathol1933; 142:547-55 6 Baumann MH, Henrich K, Sahn SA, et al. Pleural macrophages differentially·alter mesothelial cell growth and collagen production. Inflammation 1993; 17:1-12 7 Owens MW, Grimes SR. Pleural mesothelial cell response to inflammation: tumor necrosis factor-induced mitogenesis and collagen synthesis. Am J Physiol 1993; 265:L382-88 8 Kuwahara M, Kuwahara M, Bijwaard KE, et al. Mesothelial cells produce a chemoattractant for lung fibroblasts: role of fibronectin. Am J Respir Cell Mol Bioi 1991;5:256-64 9 Antony VB, Rothfuss KJ, Godbey SW, et al. Mechanism of tetracycline-hydrochloride-induced pleurodesis: tetracycline-hydrochloride-stimulated mesothelial cells produce a growth-factorlike activity for fibroblasts. Am Rev Respir Dis 1992; 146:1009-13
Subacute Rupture of the Left Ventricular Free Wall After Acute Myocardial Infarction* Three Cases of Long-term Survival Without Emergency Surgical Repair Ales Blinc, MD; Marko Noc, MD; Bojan Pohar, MD; Natasa Cemic, MD; and Matija Horvat, MD
oped sudden hypotension accompanied by a new pericardial effusion. They were initially managed with hemodynamic support. Two patients had elective openheart surgery 2 to 3 months after AMI, whereas one patient did not require surgery. All three survived 1lh to 8lh years after AMI. This report indicates that a small subset of patients with subacute ventricular free wall rupture has a benign course that may allow for prolonged survival without having to have emergency surgical repair. (CHEST 1996; 109:565-67)
AMI=acute myocardial infarction
Key words: acute myocardial infarction; subacute rupture of left ventricle; survival
myocardial infarction (AMI) is complicated by A cute rupture of the myocardial free wall in about 6% of cas-
es.1 Several distinct clinical forms of ventricular free wall rupture have been identified. 2 Sudden rupture with massive hemorrhage into the pericardium is the most common. In about one third of cases, the course is subacute with slow and sometimes repetitive hemorrhage into the pericardia! cavity.l There is general agreement that prolonged survival is possible only with prompt surgical repair, except in rare cases when rupture may go unnoticed, because it occurs in a space already confined by pericardia! adhesions.l·3•4 However, we report on three long-term survivors of subacute ventricular free-wall rupture who were treated without emergency surgical repair in our ICU during the last 8lh years. Admittedly, these patients received treatment that may be considered as unusual and nonstandard. However, since emergency surgical repair of ruptured myocardium was not available in our hospital in the past, conservative management was the only therapeutic option. CASE REPORTS CASE
Rupture of the left ventricular free wall after acute myocardial infarction (AMI) has been regarded as uniformly fatal unless emergency surgical repair is performed. Among 2,862 patients admitted with AMI to our ICU during the last 8 years, 107 patients developed rupture of the left ventricular free wall. Twentynine patients had a subacute course and three of them survived for prolonged periods without having to have emergency surgical repair. At the onset of rupture on day 1 through 7 after AMI, the three survivors devel*From the Trnovo Hospital of Internal Medicine (Dr. Blinc) and Center for Intensive Internal Medicine (Drs. Noc, Pohar, and Horvat), University Clinical Center Ljubljana, Ljubljana, Slovenia; and the DepartmeJlt of Internal Meaicine, Iwla General Hospital, Slovenia (Dr. Cernic). Reprint requests: Dr. Blinc, Trnovo Hospital of Internal Medicine, University Clinical Center Ljubljana, Riharjew 24, Ljubljana 61000, S{ovenia.
1
A 64-year-old man with a 10-year history of hypertension was admitted with anterolateral AMI, which was confirmed by ECG and the temporal pattern of creatine phosphokinase. Treatment with IV streptokinase was begun 3 h after the onset of chest pain. Eight hours after admission, the patient suddenly became nauseated and lost consciousness. The systolic arterial pressure fell from 125 to 70 to 90 mm Hg, and the heart rate decreased from 96 to 60 beats per minute. The central venous pressure rose from 12.5 to 19 em H20. Pressure equalization in the heart chambers documented by a Swan-Ganz catheter was consistent with cardiac tamponade. The right atrial pressure was 22118 mm Hg, the right ventricular pressure was 27/18 mm Hg and the pulmonary artery pressure was 27/22 mm Hg. Echocardiography revealed a pericardial effusion that was up to 1-cm wide and had high acoustic density echoes. The patient was treated by infusion of a colloid hydroxyethyl starch solution, followed by that of normal saline solution and lowdose dopamine (2.5 to 5 pg'kg'min). The systolic arterial pressure was stabilized at about 115 mm Hg within half an hour and the heart CHEST 11 09 I 2 I FEBRUARY, 1996
565