o
o
HO bufotalin
I
digoxin
C'8H31~ FIGURE 2. Chemical structures of bufotalin and digoxin.
is not ~lear; a creatinine level of 1.5 mEqIL ,,:as very high for this 90-year-old person and could contnbute to the digitalis toxicity if the metabolism ofthis Chinese medication is similar to digoxin. The pauses seen during early hospitalization resolved as the serum digoxin level returned to zero after the medication was discontinued. We strongly believe that this medication not only caused a digitalis-like substance, but also was responsible for digitalis toxicity in our patient. Although the clinical toxicity of toad venom has been described,.·· to our knowledge, this is the first case report in the Western literature. The use of nonprescription Chinese medication among the Chinese population in the United States is quite common. We believe the reason for this, especially in the elderly Chinese and the new immigrants, is their strong cultural belief in Chinese medicine and their lack of confidence in modern western medicine. Drugs such as Yixin Wan, are easily obtained in the United States, often in ethnic grocery stores and pharmacies. With a rapidly growing nonwestern immigrant population in the United States, physicians must be alert for the potential toxicity of nonstandard therapies these patients may be taking. REFERENCES
1 Smith nv, Haber E. Medical progress: digitalis. N Eng) J Med 1973; 289:945-54, 1010-15, 1063-72, 1125-29 2 Chen KK, Henderson FG. Comparative activity of bufadienolides. J Med Pharm Chern 1961;3:111 3 Lin CS, Lin MC, Chen KS, Liu CB. Effect of a Chinese medication "kyushin" on serum digoxin concentration measurement in dogs. Jap Cire J 1989; 53:108-12 4 Lin CS, Lin MC, Chen KS, Ho CC, Tsai SR, Ho CS, et al. A digoxin-like immunoreactive substance and atrioventricular block induced by a Chinese medicine "kyushin." Jap Cire J 1989; 53:1077-80 5 Fushimi R, Thchi J, Amino N, Miyai K. Chinese medicine interfering with digOXin immunoassays. Lanet 1989;1:339 6 Flier JS. Ouabain-like activity in toad skin and its implications for endogenous regulation of ion transport. Nature 1978; 274: 285-86
7 Lichstein D, Kachalsky S, Deutch J. Identification of a ouabainlike compound in toad skin and plasma as a bufudienolide derivative. Life Sci 1986; 38:1261-70 8 Chern MS, Ray CY, Wu D. Biologic intoxication due to digitalislike substance after ingestion of cooked toad soup. Am J Cardiol 1991; 67:443-44 9 Chen KK, Kovarikova A. Pharamacology and toxicology of toad venom. J Pharmaceut Sci 1967; 56:1535-41 10 Smith nv, Antman EM, Friedman PL, Blatt CM, Marsh JD. Digitalis glycosides: mechanisms and manifestations of toxicity. Prog Cardiovasc Dise 1984; 26:413-95
950
Pulmonary Venous Infarction se d Sq con ary to uamous cell Carcinoma
WarTl1n A. WiU/amson, M.D., F.C.C.P.; Bruce S. Tronic, M.D.; Nathan Levitan, M.D.; David C. ~bb-]ohnson, M.D.; David M. Shah/an, M.D.; and F. Henry Ellis, Jr., M.D., Ph.D.t
This type of pulmonary venous infarction bas not been previously reported, namely: pulmonary vein obstruction from squamous cell carcinoma. Furthermore, this case is unique in that the characteristic pathologic vascular changes observed with pulmonary venous infarction were contrasted with a noninfarcted upper lobe that was removed from the same patient one year later. (Chnt 1992; 102:950-52) ulmonary venous infarction is a rare clinical condition P that is most commonly caused by sclerosing mediastinitis. Although other known causes exist, pulmonary venous infarction has not been reported secondary to carcinoma. We recently treated a patient with lobar pulmonary venous infarction secondary to extrinsic compression of the inferior pulmonary vein from a squamous cell carinoma. CASE REPORT
A 47-yellMJld man presented with a ten-day history of intermittent chills, pleUritic chest pain, dry cough, fever to 38.8"C, and an episode of hemoptysis. Three years previously, lvor Lewis esophagogastrectomy was performed lOr squamous cell carcinoma of the esophagus (stage IlA). I Physical examination of the chest disclosed decreased breath sounds at the base of the left lung. Results of sputum Gram stain and culture were consistent with normal flora, and results of acidfast bacilli stain were negative. Roentgenography of the thorax revealed consolidation in tbe left lower lobe with an air bronchogram and a left pleural effusion (Fig 1). No endobronchial lesions were seen bronchoscopically; however, lavage of the anteromedial basal segment of the left lower lobe resulted in the return of bloody flUid. Transbronchial biopsy revealed parenchymal necrosis. Computed tomography of the thorax revealed an extensive infiltrative process of the left lower lobe with an air bronchogram
*From the Departments of Thoracic and Cardiovascular Surgery and Anatomic Pathology and the Sections of Medical Oncology and Pulmonary and Critical Care Medicine, Lahey Clinic MediC81 Center, Burlington, Mass. tCurrentlyat the Division of Thoracic and Cardiovascular Surgery, New England Deaconess Hospital, Boston. Reprint requests: Dr. WiUiamson, Lahey Clinic Hospital. 41 Mall Road. Burlington. MA 01805 Pulmonary Venous Inlardloo (WIH1am8otI et aI)
1. Roentgenography of the chest showing left lower lobe consolidation. FIGURE
(Fig 2). Pulmonary angiography with selective injection revealed no evidence of pulmonary emboli. The patient continued to he febrile despite treatment with aminoglycosides and erythromycin. Exploratory left thoracotomy revealed a serosanguineous pleural effusion and a consolidated hemorrhagic left lower lobe that had liverliJce consistency. It contained a 3-cm mass that displaced the inferior pulmonary vein anterioriy and cephalad. A frozen section biopsy specimen of this mass revealed squamous cell carcinoma, a diagnosis that was later confirmed on examination of permanent sections. Left lower lobectomy was performed from which the patient recovered uneventfully. The final pathologic report was squamous cell carcinoma and hemorrhagic infarction of the lung with fibrotic vascular changes consistent with venous infarction. It was not possible to determine whether this tumor represented a primary lung carcinoma or a metastatic lesion from previous esophageal carcinoma. The hilar lymph nodes removed with the specimen were free of tumor.
FIGURE 2. Computed tomography of the thorax demonstrating consolidation of left lower lobe with air bronchogram.
FIGURE 3. Focal hemorrhagic infarction juxtaposed with nonnal lung at the interlobular septum (original magnification, x 250). One year later, a persistent cough developed, and bronchoscopy revealed a recurrent tumor in the bronchial stump of the left lower lobe. At the time of thoracotomy, the tumor involved the left main stem bronchus, and completion pneumonectomy was required. Microscopic sections of the excised upper lobe showed viable lung without evidence of infarction or pulmonary venous hypertension. The pulmonary arterioles did not show any intimal changes, and the lymphatic channels were not dilated. DISCUSSION
Pulmonary venous infarction is an elusive diagnosis because of the nonspecific symptoms and the nonspecific diagnostic findings with conventional radiologic tests. The late or venous phase of pulmonary angiography has been demonstrated'" to be the most useful diagnostic test. Unfortunately, a venous phase on arteriography was not obtained in our patient, and the diagnosis was made by exploratory thoracotomy, as is often the case. Microscopic sections demonstrated characteristic changes seen with pulmonary infarction (Fig 3 and 4). Areas of hemorrhagic infarction were centered on and extended away from interlobular septae, encroaching on intervening viable parenchyma ofthe lung. The viable tissue ofthe lung showed a loose myxoid and fibroblastic interstitial thickening of the alveolar septal walls. The small pulmonary arterioles showed loose intimal thickening and fibrosis and considerable dilation of the pulmonary lymphatic channels. Pulmonary arteriolar changes and lymphatic dilation were not found in the upper lobe, which was removed one year later and which confirmed that these changes in the lower lobe were secondary to venous obstruction. Pulmonary venous infarction has been reported in the IiteratureJ- 17 in 21 patients. Sclerosing mediastinitis was the most common cause in 15 patients. Other causes included atrial myxoma, congenital pulmonary venous narrowing, postlobectomy thrombosis of the pulmonary vein, and obCHEST 1102 I 3 I SEPTEMBER, 1992
951
A
n.
Fll;l 4 . 1nlimal h~'pcrpla 'in of pulmonM) nrleriol (ori,ltil al magnification. 11 and E 650). B pulmon;~ arteriole flank d b~ di!. I d I mphntic chnnn I (on,ltinal ma~nificnlion. 11 (lod E x 650). structin~
f th 21 patient, 12 (57 p rent) di d of thi nditi n. Pulmonar} rt'~ tion wa posible in Ii e puti nt. and n di d po toperatively of hemorrhage. Four other patients were treated conservatively with antibiotics and survived. Experimental data'.... support the observation that survival is possible with antibiotic therapy after pulmonary venous ligation. However, when the cause ofvenous obstruction is unclear, exploratory thoracotomy and biopsy are indicated. With sclerosing mediastinitis, resection is often not possible, although resection was successful in three of the 15 reported3 .•.• cases. With a localized process causing pulmonary venous infarction, such as atrial myxoma, left atrial clot, congenital venous narrowing, or carcinoma, as in our patient, pulmonary resection is the preferred treatment.
len atrial clot au d b} mitral t nosi
10
11
12 13
14
REFERENCES 1 Beahrs OH. Henson DE. Hutter RVp, Myers MH. American joint committee on cancer: Manual for staging cancer. 3rd ed. Philadelphia: JB Lippincott Company. 1988:63-68 2 Kittredge RD, Nash AD. The many facets of sclerosing 6brosis. AJR 1974: 122:288-98 3 Dye TE. Saab SB, Almond CH. Watson L. Sclerosing mediastinitis with occlusion of pulmonary veins: manifestations and management. J Thorne Cardiovasc Surg 1977: 74:137-41 4 Bindelg\ass IL. Trubowitz S. Pulmonary vein obstruction: an uncommon sequel to chronic 6brous mediastinitis. Ann Intern Med 1958: 48:876-91 5 Yacoub MH, Thompson VC. Chronic idiopathic pulmonary hiIar 6brosis: a clinicopathological entity. Thorax 1971; 26:365-75 6 Nasser WK. Feigenbaum H, Fisch C. Clinical and hemodynamic diagnosis of pulmonary venous obstruction due to sclerosing mediastinitis. Am J Cardioll967; 20:725-29 7 Botticelli]T, Schlueter Dp, Lange RL. Pulmonary venous and arterial hypertension due to chronic 6brous mediastinitis: hemodynamics and pulmonary function. Circulation 1966: 33:86271
952
15
16 17
18
19
20 21
Katz nsl in Mazur IT. PI.11m nary infur I: an unu uru manif< wHon of fibro.lIlf;\ III -dinstinitis. liesI 1 : 77:521-24 M nd I on B. 1Hz r • lIidv g DF. \' no-occlusiv pulmonnt: infarcI: an unusual complicali n of fibro ing III eli linitis. AJR 1983; 141:175-76 Andrews EC Jr. Five cases of an undescribed form of pulmonary interstitial6brosis caused by obstruction of the pulmonary veins. Bull Johns Hopldns Hasp 1957: 100:28-42 Edwards JE, Burchell HB. Multilobar pulmonary venous 0bstruction with pulmonary hypertension: protective arterial lesions in the involved lobes. Arch Intern Med 1951: 87:372-78 Davis F\v, Andrus EC. Mitral stenosis in facsimile. N Engl J Med 1954; 251:297-302 Leech TR, Meckstroth cv, Klassen KP. Exploratory thoracotomy in chronic lymphadenitis of the mediastinum. Arch Surg 1955: 71:383-91 Hegglin R. Zollinger HU. A case of pulmonary sclerosis of particular etiology (scar tissue of the mediastinum). Cardiologia 1954; 24:92-95 Stevens LH. Hormuth DA, Schmidt PE. Atkins S, Fehrenbacher JW Left atrial myxoma: pulmonary infarction caused by pul· monary venous occlusion. Ann Thorne Surg 1987: 43:215-17 Hovaguimian H, Morris JF, Gately HL, Floten HS. Pulmonary vein thrombosis following bilobectomy. Chest 1991; 99:1515-16 Venter Cp' Dannheimer IP. Pulmonary venous thrombosis complicating lobectomy. S Afr Med J 1973; 47:2339-42 (cited by Swan and Mulliganll) Hurwitz A, Calabresi M, Cooke RW, Liebow AA. An experimental study of the venous collateral circulation of the lung: anatomical observations. Am J Patholl954: 30:1085-1115 Hurwitz A, Calabresi M, Cooke RW, Liebow AA. Experimental study of the venous collateral circulation of the lung: functional observations. J Thorne Surg 1954: 28:241-46 Hanlon CR, Sabiston DC Jr, Burke DR. Experimental pulmonary venous occlusion. J Thorne Surg 1952: 24:190-200 Swan H, Mulligan RM. An experimental study of the effect of ligation of pulmonary veins in the dog. J Thorne Surg 1948: 17:44-56 Pulmonary Venous
Infarction (WIlliamson et aJ)
o
HO bufotalin
I
digoxin
C'8H31~ FIGURE 2. Chemical structures of bufotalin and digoxin.
is not ~lear; a creatinine level of 1.5 mEqIL ,,:as very high for this 90-year-old person and could contnbute to the digitalis toxicity if the metabolism ofthis Chinese medication is similar to digoxin. The pauses seen during early hospitalization resolved as the serum digoxin level returned to zero after the medication was discontinued. We strongly believe that this medication not only caused a digitalis-like substance, but also was responsible for digitalis toxicity in our patient. Although the clinical toxicity of toad venom has been described,.·· to our knowledge, this is the first case report in the Western literature. The use of nonprescription Chinese medication among the Chinese population in the United States is quite common. We believe the reason for this, especially in the elderly Chinese and the new immigrants, is their strong cultural belief in Chinese medicine and their lack of confidence in modern western medicine. Drugs such as Yixin Wan, are easily obtained in the United States, often in ethnic grocery stores and pharmacies. With a rapidly growing nonwestern immigrant population in the United States, physicians must be alert for the potential toxicity of nonstandard therapies these patients may be taking. REFERENCES
1 Smith nv, Haber E. Medical progress: digitalis. N Eng) J Med 1973; 289:945-54, 1010-15, 1063-72, 1125-29 2 Chen KK, Henderson FG. Comparative activity of bufadienolides. J Med Pharm Chern 1961;3:111 3 Lin CS, Lin MC, Chen KS, Liu CB. Effect of a Chinese medication "kyushin" on serum digoxin concentration measurement in dogs. Jap Cire J 1989; 53:108-12 4 Lin CS, Lin MC, Chen KS, Ho CC, Tsai SR, Ho CS, et al. A digoxin-like immunoreactive substance and atrioventricular block induced by a Chinese medicine "kyushin." Jap Cire J 1989; 53:1077-80 5 Fushimi R, Thchi J, Amino N, Miyai K. Chinese medicine interfering with digOXin immunoassays. Lanet 1989;1:339 6 Flier JS. Ouabain-like activity in toad skin and its implications for endogenous regulation of ion transport. Nature 1978; 274: 285-86
7 Lichstein D, Kachalsky S, Deutch J. Identification of a ouabainlike compound in toad skin and plasma as a bufudienolide derivative. Life Sci 1986; 38:1261-70 8 Chern MS, Ray CY, Wu D. Biologic intoxication due to digitalislike substance after ingestion of cooked toad soup. Am J Cardiol 1991; 67:443-44 9 Chen KK, Kovarikova A. Pharamacology and toxicology of toad venom. J Pharmaceut Sci 1967; 56:1535-41 10 Smith nv, Antman EM, Friedman PL, Blatt CM, Marsh JD. Digitalis glycosides: mechanisms and manifestations of toxicity. Prog Cardiovasc Dise 1984; 26:413-95
950
Pulmonary Venous Infarction se d Sq con ary to uamous cell Carcinoma
WarTl1n A. WiU/amson, M.D., F.C.C.P.; Bruce S. Tronic, M.D.; Nathan Levitan, M.D.; David C. ~bb-]ohnson, M.D.; David M. Shah/an, M.D.; and F. Henry Ellis, Jr., M.D., Ph.D.t
This type of pulmonary venous infarction bas not been previously reported, namely: pulmonary vein obstruction from squamous cell carcinoma. Furthermore, this case is unique in that the characteristic pathologic vascular changes observed with pulmonary venous infarction were contrasted with a noninfarcted upper lobe that was removed from the same patient one year later. (Chnt 1992; 102:950-52) ulmonary venous infarction is a rare clinical condition P that is most commonly caused by sclerosing mediastinitis. Although other known causes exist, pulmonary venous infarction has not been reported secondary to carcinoma. We recently treated a patient with lobar pulmonary venous infarction secondary to extrinsic compression of the inferior pulmonary vein from a squamous cell carinoma. CASE REPORT
A 47-yellMJld man presented with a ten-day history of intermittent chills, pleUritic chest pain, dry cough, fever to 38.8"C, and an episode of hemoptysis. Three years previously, lvor Lewis esophagogastrectomy was performed lOr squamous cell carcinoma of the esophagus (stage IlA). I Physical examination of the chest disclosed decreased breath sounds at the base of the left lung. Results of sputum Gram stain and culture were consistent with normal flora, and results of acidfast bacilli stain were negative. Roentgenography of the thorax revealed consolidation in tbe left lower lobe with an air bronchogram and a left pleural effusion (Fig 1). No endobronchial lesions were seen bronchoscopically; however, lavage of the anteromedial basal segment of the left lower lobe resulted in the return of bloody flUid. Transbronchial biopsy revealed parenchymal necrosis. Computed tomography of the thorax revealed an extensive infiltrative process of the left lower lobe with an air bronchogram
*From the Departments of Thoracic and Cardiovascular Surgery and Anatomic Pathology and the Sections of Medical Oncology and Pulmonary and Critical Care Medicine, Lahey Clinic MediC81 Center, Burlington, Mass. tCurrentlyat the Division of Thoracic and Cardiovascular Surgery, New England Deaconess Hospital, Boston. Reprint requests: Dr. WiUiamson, Lahey Clinic Hospital. 41 Mall Road. Burlington. MA 01805 Pulmonary Venous Inlardloo (WIH1am8otI et aI)
1. Roentgenography of the chest showing left lower lobe consolidation. FIGURE
(Fig 2). Pulmonary angiography with selective injection revealed no evidence of pulmonary emboli. The patient continued to he febrile despite treatment with aminoglycosides and erythromycin. Exploratory left thoracotomy revealed a serosanguineous pleural effusion and a consolidated hemorrhagic left lower lobe that had liverliJce consistency. It contained a 3-cm mass that displaced the inferior pulmonary vein anterioriy and cephalad. A frozen section biopsy specimen of this mass revealed squamous cell carcinoma, a diagnosis that was later confirmed on examination of permanent sections. Left lower lobectomy was performed from which the patient recovered uneventfully. The final pathologic report was squamous cell carcinoma and hemorrhagic infarction of the lung with fibrotic vascular changes consistent with venous infarction. It was not possible to determine whether this tumor represented a primary lung carcinoma or a metastatic lesion from previous esophageal carcinoma. The hilar lymph nodes removed with the specimen were free of tumor.
FIGURE 2. Computed tomography of the thorax demonstrating consolidation of left lower lobe with air bronchogram.
FIGURE 3. Focal hemorrhagic infarction juxtaposed with nonnal lung at the interlobular septum (original magnification, x 250). One year later, a persistent cough developed, and bronchoscopy revealed a recurrent tumor in the bronchial stump of the left lower lobe. At the time of thoracotomy, the tumor involved the left main stem bronchus, and completion pneumonectomy was required. Microscopic sections of the excised upper lobe showed viable lung without evidence of infarction or pulmonary venous hypertension. The pulmonary arterioles did not show any intimal changes, and the lymphatic channels were not dilated. DISCUSSION
Pulmonary venous infarction is an elusive diagnosis because of the nonspecific symptoms and the nonspecific diagnostic findings with conventional radiologic tests. The late or venous phase of pulmonary angiography has been demonstrated'" to be the most useful diagnostic test. Unfortunately, a venous phase on arteriography was not obtained in our patient, and the diagnosis was made by exploratory thoracotomy, as is often the case. Microscopic sections demonstrated characteristic changes seen with pulmonary infarction (Fig 3 and 4). Areas of hemorrhagic infarction were centered on and extended away from interlobular septae, encroaching on intervening viable parenchyma ofthe lung. The viable tissue ofthe lung showed a loose myxoid and fibroblastic interstitial thickening of the alveolar septal walls. The small pulmonary arterioles showed loose intimal thickening and fibrosis and considerable dilation of the pulmonary lymphatic channels. Pulmonary arteriolar changes and lymphatic dilation were not found in the upper lobe, which was removed one year later and which confirmed that these changes in the lower lobe were secondary to venous obstruction. Pulmonary venous infarction has been reported in the IiteratureJ- 17 in 21 patients. Sclerosing mediastinitis was the most common cause in 15 patients. Other causes included atrial myxoma, congenital pulmonary venous narrowing, postlobectomy thrombosis of the pulmonary vein, and obCHEST 1102 I 3 I SEPTEMBER, 1992
951
A
n.
Fll;l 4 . 1nlimal h~'pcrpla 'in of pulmonM) nrleriol (ori,ltil al magnification. 11 and E 650). B pulmon;~ arteriole flank d b~ di!. I d I mphntic chnnn I (on,ltinal ma~nificnlion. 11 (lod E x 650). structin~
f th 21 patient, 12 (57 p rent) di d of thi nditi n. Pulmonar} rt'~ tion wa posible in Ii e puti nt. and n di d po toperatively of hemorrhage. Four other patients were treated conservatively with antibiotics and survived. Experimental data'.... support the observation that survival is possible with antibiotic therapy after pulmonary venous ligation. However, when the cause ofvenous obstruction is unclear, exploratory thoracotomy and biopsy are indicated. With sclerosing mediastinitis, resection is often not possible, although resection was successful in three of the 15 reported3 .•.• cases. With a localized process causing pulmonary venous infarction, such as atrial myxoma, left atrial clot, congenital venous narrowing, or carcinoma, as in our patient, pulmonary resection is the preferred treatment.
len atrial clot au d b} mitral t nosi
10
11
12 13
14
REFERENCES 1 Beahrs OH. Henson DE. Hutter RVp, Myers MH. American joint committee on cancer: Manual for staging cancer. 3rd ed. Philadelphia: JB Lippincott Company. 1988:63-68 2 Kittredge RD, Nash AD. The many facets of sclerosing 6brosis. AJR 1974: 122:288-98 3 Dye TE. Saab SB, Almond CH. Watson L. Sclerosing mediastinitis with occlusion of pulmonary veins: manifestations and management. J Thorne Cardiovasc Surg 1977: 74:137-41 4 Bindelg\ass IL. Trubowitz S. Pulmonary vein obstruction: an uncommon sequel to chronic 6brous mediastinitis. Ann Intern Med 1958: 48:876-91 5 Yacoub MH, Thompson VC. Chronic idiopathic pulmonary hiIar 6brosis: a clinicopathological entity. Thorax 1971; 26:365-75 6 Nasser WK. Feigenbaum H, Fisch C. Clinical and hemodynamic diagnosis of pulmonary venous obstruction due to sclerosing mediastinitis. Am J Cardioll967; 20:725-29 7 Botticelli]T, Schlueter Dp, Lange RL. Pulmonary venous and arterial hypertension due to chronic 6brous mediastinitis: hemodynamics and pulmonary function. Circulation 1966: 33:86271
952
15
16 17
18
19
20 21
Katz nsl in Mazur IT. PI.11m nary infur I: an unu uru manif< wHon of fibro.lIlf;\ III -dinstinitis. liesI 1 : 77:521-24 M nd I on B. 1Hz r • lIidv g DF. \' no-occlusiv pulmonnt: infarcI: an unusual complicali n of fibro ing III eli linitis. AJR 1983; 141:175-76 Andrews EC Jr. Five cases of an undescribed form of pulmonary interstitial6brosis caused by obstruction of the pulmonary veins. Bull Johns Hopldns Hasp 1957: 100:28-42 Edwards JE, Burchell HB. Multilobar pulmonary venous 0bstruction with pulmonary hypertension: protective arterial lesions in the involved lobes. Arch Intern Med 1951: 87:372-78 Davis F\v, Andrus EC. Mitral stenosis in facsimile. N Engl J Med 1954; 251:297-302 Leech TR, Meckstroth cv, Klassen KP. Exploratory thoracotomy in chronic lymphadenitis of the mediastinum. Arch Surg 1955: 71:383-91 Hegglin R. Zollinger HU. A case of pulmonary sclerosis of particular etiology (scar tissue of the mediastinum). Cardiologia 1954; 24:92-95 Stevens LH. Hormuth DA, Schmidt PE. Atkins S, Fehrenbacher JW Left atrial myxoma: pulmonary infarction caused by pul· monary venous occlusion. Ann Thorne Surg 1987: 43:215-17 Hovaguimian H, Morris JF, Gately HL, Floten HS. Pulmonary vein thrombosis following bilobectomy. Chest 1991; 99:1515-16 Venter Cp' Dannheimer IP. Pulmonary venous thrombosis complicating lobectomy. S Afr Med J 1973; 47:2339-42 (cited by Swan and Mulliganll) Hurwitz A, Calabresi M, Cooke RW, Liebow AA. An experimental study of the venous collateral circulation of the lung: anatomical observations. Am J Patholl954: 30:1085-1115 Hurwitz A, Calabresi M, Cooke RW, Liebow AA. Experimental study of the venous collateral circulation of the lung: functional observations. J Thorne Surg 1954: 28:241-46 Hanlon CR, Sabiston DC Jr, Burke DR. Experimental pulmonary venous occlusion. J Thorne Surg 1952: 24:190-200 Swan H, Mulligan RM. An experimental study of the effect of ligation of pulmonary veins in the dog. J Thorne Surg 1948: 17:44-56 Pulmonary Venous
Infarction (WIlliamson et aJ)
