- Email: [email protected]
Encroachment Upon the Lungs of Large Chronic Pericardial Effusion
mesothelioma of the pleura. Cancer 1982; 49:2431-35 13 Chahinian AP, Pajak JF, Holland TF, Norton L, Ambinder RM, Mandel EM. Diffuse malignant mesothelioma. Ann Intern Med 1982; 96:746-55 14 Roberts GH. Distant visceral metastases in pleural mesothelioma. Br J Dis Chest 1976; 70:246-50 15 Castleman B, McNeely BV. Weekly clinicopathological eJ:ercises. N Eng) J Moo 1971; 284:778-86 16 Adams VI, Unni Diffuse malignant mesothelioma of pleura: diagnostic criteria based on an autopsy study. Am J Coo Pathol 1984; 82:15-23 17 Oels HC, Harrison EG, Carr Bematz PE . Diffuse malignant mesothelioma of the pleura: a review of 37 cases. Chest 1971; 60:564-70
n.
01:
FIGURE 2. Photomicrograph of a section of the open-lung biopsy specimen showing infiltration of the pulmonary parenchyma by mesothelioma in an epithelioid pattern with predominantly papillary morphology (H and E, original magnification 4000 x),
fered. Some reports do not distinguish between ipsilateral and contralateral lung involvement,IO,I1.I3 thereby failing to separate cases of direct tumor extension from those with actual hematogenous spread. Most others simply fail to offer well-correlated radiologic and pathologic descriptions of the parenchymal involvement. 8,IO,12-Ill Clearly, not all patients with mesothelioma and parenchymal changes on their chest roentgenograms have tumor metastases; some have concurrent asbestosts'<" or other processes. An important feature of the case reported here is the histologic confirmation of the radiographic findings, demonstrating the presence of mesothelioma in the contralaterallung. The diffuse nature of the parenchymal process illustrates a very unusual presentation of this tumor. Metastatic disease should be considered in the differential diagnosis when such a presentation occurs. REFERENCES 1 Antman KH, Corson JM , Benign and malignant pleural mesothelioma. Clin Chest Med 1985; 6:127-40 2 Becklake MR. Asbestos-related diseases of the lung and other organs : their epidemiology and implications for clinical practice. Am Rev Respir Dis 1976; 114:187-227 3 Wechsler RJ, Rao VM, Steiner RM. The radiology of thoracic malignant mesothelioma. CRC Crit Rev Diagn Imaging 1984;
20:283-310
4 Solomon A. The radiology of asbestos-related diseases with special reference to diffuse mesothelioma. Semin Oncol 1981; 8:290-301 5 Antman KH. Clinical presentation and natural history of benign and malignant mesothelioma. Semin Oncoll981; 8:313-20 6 Kay jA, Wang A, Joachim CL, Seltzer SE, Cibas E, Skarin A, et al. Malignant mesothelioma with brain metastases. Am J Med 1986; 80:95-7 7 Manfredi F, Rosenbaum D, Childress RH. Diffuse malignant mesothelioma of the pleura. Am RevRespir Dis 1965; 92:269-79 8 Urschel HC, Paulson DL. Mesotheliomas of the pleura. Ann Thorac Surg 1965; 1:559-74 9 Solomon A. Radiological features of diffuse mesothelioma. Environ Res 1970; 3:330-38 10 Elmes PC, Simpson MJC . The clinical aspects of mesothelioma. Quart J Med 1976; 15:427-49 11 Kreel L. Computed tomography in mesothelioma. Semin Oncol 1981; 8:302-13 12 Brenner J, Sordillo Pp, Magill GB, Golbey RB. Malignant
434
Encroachment Upon the Lungs of Large Chronic Perlcardlal Effuslon* Pulmonary Tamponade? Gregory C. Kane, M.D.; and William G. Figueroa, M.D., EC .C.P.
Pulmonary encroachment by a large chronic pericardial effusion is reported in a woman with pericardiocentesis whom we recently treated. A restrictive pulmonary imp~ ment is documented with pulmonary function data obtained before and after drainage of the effusion and the patient's dyspnea improved. for pulmonary encroachment as a result of T helargepotential chronic pericardial effusion has been described theoretically in reviews of pericardial disease. U However, we
have not discovered documented evidence of this phe-
nomenon. We recently treated a patient with massive chronic pericardial effusion who demonstrated, on pulmonary function testing, restrictive pulmonary impairment which improved dramatically after drainage of the effusion. CASE REPORT
A 59-year-old black woman with a history of chronic pericardial effusion, chronic obstructive pulmonary disease, interstitial lung disease, and coronary artery disease presented with one week of progressive dyspnea on exertion . The chronic pericardial effusion was first diagnosed six years prior to admission byechocardiography; at that time, there was reluctance to undertake pericardiocentesis because it was felt the effusion was stable. Pulmonary function studies performed then showed a mixed abnormality with restrictive and obstructive components. The patient was taldng theophylline (Theodur) 300 mg twice daily and had a 40 pack-year smoking history. The patient was in mild respiratory distress, afebrile, with blood pressure 110/84 mm Hg, pulse 80 him, without pulsus paradoxus. There was jugular venous distention to 9 em. Diminished breath sounds and dullness were present at the left lung base and there was mild eJ:Piratory wheeze. The chest was otherwise clear. The abdomen was unremarkable. Extremities showed no edema. There were no neurologic deficits. Initial chest roentgenogram (Fig 1) demonstrated a massive
*From the Lankenau Hospital, Philadelphia. Reprint requests: Dr. Kane, LAnkenau Hoapltal, Philadelphia 19151
FIGURE 1. Admission chest roentgenogram demonstrates massive
FIGURE 2. Chest roentgenogram following pericardiocentesis demonstrates reduced cardiac silhouette (drainage catheter remains in place).
cardiac silhouette and discoid atelectasis bilaterally, but no interval change, Electrocardiogram showed low voltage QRS. An echocardiogram showed a massive pericardial effusion which had increased
tesis revealed marked improvement as compared to data obtained one month prior to the patients admission ('Dible2). Fluid examination revealed the effusion to be an exudate, and cytologic and Inicrobiologic euminations, including acid-fast bacilli, were negative. A decision was made to perform pericardiectomy which the patient tolerated well. Pathologic sections demonstrated diffuse fibrosis and focal chronic inflammation consistent with chronic pericarditis. Amyloid stains were negative . A diagnosis of idiopathic pericardial effusion was confirmed. The patient was discharged improved.
cardiac silhouette.
in size since one year earlier. The white blood cell count was normal. Pulmonary function studies conducted one month prior to admission are included in 'Iable 1. Arterial blood levels showed pH of7.427, Pea. of38.0 mm Hg, HC03 of25.8 mEq/L, Po. of82. 7 mm Hg with 0. saturation of 94.8 percent on room air. Physical examination was not consistent with tamponade-there was no pulsus paradoxus or hypotension. However, there was a question as to whether the pericardial effusion was causing the patient's dyspnea. We considered pulmonary encroachment by the effusion as a cause of the dyspnea and suspected the patient's pulmonary function was being compromised because of an interval increase in the size of the effusion. We performed pericardiocentesis (subxiphoid) with simultaneous right heart catheterization to monitor pressures. The data from these measurements are included in 1llble 1. Pericardiocentesis yielded 2.5 L of serosanguinous fluid, although there was no appreciable changes in right heart pressures. The patient improved subjectively and tolerated the procedure well. The next day, the chest roentgenogram showed a greatly reduced cardiac silhouette (Fig 2) and only a small amount of fluid was detected on echocardiogram. Pulmonary function testing on the second day after pericardiocen-
DISCUSSION
Hemodynamic decompensation on the basis of pericardial effusion has been well documented.U Such decompensation can result from cardiac tamponade, constrictive pericarditis, or effusive constrictive pericarditis. Pericardial effusions developing quickly are clearly linked to cardiac tamponade. However, pericardial effusions developing slowly may become quite large before cardiovascular compromise develOpS.7 In exceptional circumstances such as hypovolemia" and Table 2-Pulmonta,." .Function DtJta (AB Pre-bronchodilator Vmue.) Postpericardiocentesis
Table I-Hemodynamic DtJta (pruaura in mm Hg) PostPericardiocentesis Pre-Pericardiocentesis post tap after 24 hr R atrium R ventricle Pulmonary artery Capillary wedge Arterial blood pressure
10
26110 26110 10 108182
16
6-15
27/5
1518
120176
120182
Prepericardiocentesis post tap
Forced vital capacity (L) Forced expiratory volume (L) Diffusing capacity (% predicted) Forced expiratory volume! Forced vital capacity (%)
after 4 months
1.08
1.55
2.31
0.80
1.24
1.69
44
45
50
74
80
73
CHEST I 93 I 2 I FEBRUARY, 1988
435
ventricular hypertrophy," tamponade may occur without pulsus paradoxus. This patient did not demonstrate clinical clues indicating cardiac tamponade; however, there was some concern about early tamponade perhaps on the basis of a recent increase in the effusion volume, with a slight narrowing of the pulse pressure. Moreover, right heart catheterization demonstrated equalization of right and left heart diastolic pressures. Impending tamponade was avoided after pericardiocentesis and recurrence by pericardiectomy. We conclude that this patient's restrictive lung impairment was on the basis of encroachment by the large effusion, as indicated by the pulmonary function data in 'Iable 2. Pre- and post-pericardiocentesis studies indicated 44 percent improvement in vital capacity and 56 percent improvement in forced expiratory volume at one second, while diffusing capacity remained unchanged. While pulmonary encroachment has been described previously, 1.1 documented improvement in pulmonary function has not been reported. It remains to be seen whether pulmonary encroachment will be found to be important only when there is other underlying pulmonary impairment as in this case, or if it will be of clinical significance in patients with normal lungs. REFERENCES
1 Spodick DU. Pericardial diseases. Philadelphia: RA. Davis, 1976:4,181,312 2 Spodick DU. Chronic and constrictive pericarditis. New York: Grone and Stratton, 1964:149 3 Spodick DU. The normal and diseased pericardium: Current concepts of pericardial physiology, diagnosis and treatment. Am J Cardioll983; 1:240-51 4 Shabetai R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 1970; 26:480-89 5 Spodick DU. Acute cardiac tamponade: pathologic, physiology, diagnosis, and management. Frog Cardiovasc Dis 1967; 10:64-96 6 Hancock EW Subacute effusive-eonstrictive pericarditis. Circulation 1971; 43:183-92 7 Hancock EW Cardiac tamponade. Med Clin N America 1979; 63:223-37 8 Boltwood CM, Shah PM. The pericardium in health and disease. Curr Frob Cardioll984:1-70 9 Antman EM, Girgill ~ Grossman W Low pressure cardiac tamponade. Ann Intern Med 1979; 91:403-06
Saccular Aneurysm of the Transverse Thoracic Aorta Detected by Transesophageal Echocardlography* M. A Taams, M.D.; W J. Gwsenhoven, M.D.; E. Bas, M.D.; and Roelandt, M. D.
J.
*From the Thoraxcenter, Erasmus University, Academic Hospital Rotterdam-Dijkzigt, and the Interuniversity Cardiology Institute, Rotterdam, the Netherlands. ReJ?nnt requests: Dr. Taams, Thoraxcenter; PIO BD 156, Dr. Molewaterplein 40, 3015 GD Rotterdam, Netherlands
438
A patient with a saccular aneurysm of the thoracic aortic arch presented with severe right ventricular failure due to pulmonary artery compression. Contradictory data were derived from computed tomography, pulmonary isotope perfusion scan and cardiac catheterization. 'Iransesophageal echocardiography revealed a saccular aneurysm which compressed the main pulmonary artery and gave access to a 6stulous connection to the left pulmonary artery. Surgery confirmed these 6ndings.
T
he incidence of aneurysmal involvement of the transverse thoracic aorta equals that of the ascending aorta. Life-threatening complications of aneurysm of the thoracic aorta include compression of adjacent vascular structures, rupture and fistula formation.' Angiography and computed tomography are established diagnostic methods." We present a patient in whom transesophageal echocardiography correctly established a complicated saccular aneurysm of the aortic arch. CASE REPORT
A60-year-oldpatient developed hoarseness and a 100kg increase in weight in two weeks and was admitted to a community hospital with intractable right heart failure. He had been treated for 15 years for systemic hypertension, but his medical history was otherwise uneventful. On admission, he was orthopneic and had upper right abdominal pain. There was edema of the legs, scrotum, ascites and a 5 cm enlarged, painful liver. Blood pressure and pulse rate were normal. The jugular venous pressure was extremely elevated. The left vocal cord and hemidiaphragm were paralyzed. A grade 3/6 systolic murmur existed, radiating to the carotid arteries and back. On the electrocardiogram, signs of right ventricular overload and a right axis were present. Chest x-ray film showed right-sided pleural effusion and a mediastinal mass underneath the aortic arch suggestive of an aortic aneurysm or a tumor. No diagnostic information from the aortic arch could be obtained fro~ precordial echocardiography. The CT-scan of the thorax showed a main pulmonary artery aneurysm. A pulmonary isotope perfusion scan showed no apparent abnormality. Aortography revealed a saccular aneurysm with its origin proximal to the left subclavian artery compressing the pulmonary artery. Right heart catheterization showed pulmonary hypertension (60/20mm Hg) and an elevated right atrial pressure (10 mm Hg), The patient was transferred to our unit for surgery. As the above findings were conflicting, the surgeon demanded further investigation. lhmsesophageal echocardiography was scheduled. A 3.7 MUz phased-array transducer was used mounted at the tip of a gastroscope and interfaced with a Hewlett-Packard ultrasonograph (HP 77020 AC). A pulsed Doppler study was concurrently performed using the same transducer switched to a Toshiba ultrasonograph (SSH 6OA). The patient fasted for 8 hours and antihypertensive drugs as premedication were given. As a local anesthetic, topical lidocaine was administered to the patient's hypopharynx. A large saccular aneurysm was visualized underneath the aortic arch. Neither dissection nor thrombus formation was present. Pulsed Doppler tracings showed bloodflow from the aneurysm into the left pulmonary artery indicating a fistula (Fig 1). The main pulmonary artery was compressed by the aneurysm. Numerous atherosclerotic lesions were noted in the thoracic aorta. Planned selective left cardiac catheterization was no longer felt mandatory. Within 24 hours after transesophageal echocardiography, the patient underwent surgery. Epicardial echocardiography after sternotomy confirmed the transesophageal findings. Deep hypothersaccularAneurysm or Transverse Thoracic Aorta (Teams et 8/)
n.
01:
FIGURE 2. Photomicrograph of a section of the open-lung biopsy specimen showing infiltration of the pulmonary parenchyma by mesothelioma in an epithelioid pattern with predominantly papillary morphology (H and E, original magnification 4000 x),
fered. Some reports do not distinguish between ipsilateral and contralateral lung involvement,IO,I1.I3 thereby failing to separate cases of direct tumor extension from those with actual hematogenous spread. Most others simply fail to offer well-correlated radiologic and pathologic descriptions of the parenchymal involvement. 8,IO,12-Ill Clearly, not all patients with mesothelioma and parenchymal changes on their chest roentgenograms have tumor metastases; some have concurrent asbestosts'<" or other processes. An important feature of the case reported here is the histologic confirmation of the radiographic findings, demonstrating the presence of mesothelioma in the contralaterallung. The diffuse nature of the parenchymal process illustrates a very unusual presentation of this tumor. Metastatic disease should be considered in the differential diagnosis when such a presentation occurs. REFERENCES 1 Antman KH, Corson JM , Benign and malignant pleural mesothelioma. Clin Chest Med 1985; 6:127-40 2 Becklake MR. Asbestos-related diseases of the lung and other organs : their epidemiology and implications for clinical practice. Am Rev Respir Dis 1976; 114:187-227 3 Wechsler RJ, Rao VM, Steiner RM. The radiology of thoracic malignant mesothelioma. CRC Crit Rev Diagn Imaging 1984;
20:283-310
4 Solomon A. The radiology of asbestos-related diseases with special reference to diffuse mesothelioma. Semin Oncol 1981; 8:290-301 5 Antman KH. Clinical presentation and natural history of benign and malignant mesothelioma. Semin Oncoll981; 8:313-20 6 Kay jA, Wang A, Joachim CL, Seltzer SE, Cibas E, Skarin A, et al. Malignant mesothelioma with brain metastases. Am J Med 1986; 80:95-7 7 Manfredi F, Rosenbaum D, Childress RH. Diffuse malignant mesothelioma of the pleura. Am RevRespir Dis 1965; 92:269-79 8 Urschel HC, Paulson DL. Mesotheliomas of the pleura. Ann Thorac Surg 1965; 1:559-74 9 Solomon A. Radiological features of diffuse mesothelioma. Environ Res 1970; 3:330-38 10 Elmes PC, Simpson MJC . The clinical aspects of mesothelioma. Quart J Med 1976; 15:427-49 11 Kreel L. Computed tomography in mesothelioma. Semin Oncol 1981; 8:302-13 12 Brenner J, Sordillo Pp, Magill GB, Golbey RB. Malignant
434
Encroachment Upon the Lungs of Large Chronic Perlcardlal Effuslon* Pulmonary Tamponade? Gregory C. Kane, M.D.; and William G. Figueroa, M.D., EC .C.P.
Pulmonary encroachment by a large chronic pericardial effusion is reported in a woman with pericardiocentesis whom we recently treated. A restrictive pulmonary imp~ ment is documented with pulmonary function data obtained before and after drainage of the effusion and the patient's dyspnea improved. for pulmonary encroachment as a result of T helargepotential chronic pericardial effusion has been described theoretically in reviews of pericardial disease. U However, we
have not discovered documented evidence of this phe-
nomenon. We recently treated a patient with massive chronic pericardial effusion who demonstrated, on pulmonary function testing, restrictive pulmonary impairment which improved dramatically after drainage of the effusion. CASE REPORT
A 59-year-old black woman with a history of chronic pericardial effusion, chronic obstructive pulmonary disease, interstitial lung disease, and coronary artery disease presented with one week of progressive dyspnea on exertion . The chronic pericardial effusion was first diagnosed six years prior to admission byechocardiography; at that time, there was reluctance to undertake pericardiocentesis because it was felt the effusion was stable. Pulmonary function studies performed then showed a mixed abnormality with restrictive and obstructive components. The patient was taldng theophylline (Theodur) 300 mg twice daily and had a 40 pack-year smoking history. The patient was in mild respiratory distress, afebrile, with blood pressure 110/84 mm Hg, pulse 80 him, without pulsus paradoxus. There was jugular venous distention to 9 em. Diminished breath sounds and dullness were present at the left lung base and there was mild eJ:Piratory wheeze. The chest was otherwise clear. The abdomen was unremarkable. Extremities showed no edema. There were no neurologic deficits. Initial chest roentgenogram (Fig 1) demonstrated a massive
*From the Lankenau Hospital, Philadelphia. Reprint requests: Dr. Kane, LAnkenau Hoapltal, Philadelphia 19151
FIGURE 1. Admission chest roentgenogram demonstrates massive
FIGURE 2. Chest roentgenogram following pericardiocentesis demonstrates reduced cardiac silhouette (drainage catheter remains in place).
cardiac silhouette and discoid atelectasis bilaterally, but no interval change, Electrocardiogram showed low voltage QRS. An echocardiogram showed a massive pericardial effusion which had increased
tesis revealed marked improvement as compared to data obtained one month prior to the patients admission ('Dible2). Fluid examination revealed the effusion to be an exudate, and cytologic and Inicrobiologic euminations, including acid-fast bacilli, were negative. A decision was made to perform pericardiectomy which the patient tolerated well. Pathologic sections demonstrated diffuse fibrosis and focal chronic inflammation consistent with chronic pericarditis. Amyloid stains were negative . A diagnosis of idiopathic pericardial effusion was confirmed. The patient was discharged improved.
cardiac silhouette.
in size since one year earlier. The white blood cell count was normal. Pulmonary function studies conducted one month prior to admission are included in 'Iable 1. Arterial blood levels showed pH of7.427, Pea. of38.0 mm Hg, HC03 of25.8 mEq/L, Po. of82. 7 mm Hg with 0. saturation of 94.8 percent on room air. Physical examination was not consistent with tamponade-there was no pulsus paradoxus or hypotension. However, there was a question as to whether the pericardial effusion was causing the patient's dyspnea. We considered pulmonary encroachment by the effusion as a cause of the dyspnea and suspected the patient's pulmonary function was being compromised because of an interval increase in the size of the effusion. We performed pericardiocentesis (subxiphoid) with simultaneous right heart catheterization to monitor pressures. The data from these measurements are included in 1llble 1. Pericardiocentesis yielded 2.5 L of serosanguinous fluid, although there was no appreciable changes in right heart pressures. The patient improved subjectively and tolerated the procedure well. The next day, the chest roentgenogram showed a greatly reduced cardiac silhouette (Fig 2) and only a small amount of fluid was detected on echocardiogram. Pulmonary function testing on the second day after pericardiocen-
DISCUSSION
Hemodynamic decompensation on the basis of pericardial effusion has been well documented.U Such decompensation can result from cardiac tamponade, constrictive pericarditis, or effusive constrictive pericarditis. Pericardial effusions developing quickly are clearly linked to cardiac tamponade. However, pericardial effusions developing slowly may become quite large before cardiovascular compromise develOpS.7 In exceptional circumstances such as hypovolemia" and Table 2-Pulmonta,." .Function DtJta (AB Pre-bronchodilator Vmue.) Postpericardiocentesis
Table I-Hemodynamic DtJta (pruaura in mm Hg) PostPericardiocentesis Pre-Pericardiocentesis post tap after 24 hr R atrium R ventricle Pulmonary artery Capillary wedge Arterial blood pressure
10
26110 26110 10 108182
16
6-15
27/5
1518
120176
120182
Prepericardiocentesis post tap
Forced vital capacity (L) Forced expiratory volume (L) Diffusing capacity (% predicted) Forced expiratory volume! Forced vital capacity (%)
after 4 months
1.08
1.55
2.31
0.80
1.24
1.69
44
45
50
74
80
73
CHEST I 93 I 2 I FEBRUARY, 1988
435
ventricular hypertrophy," tamponade may occur without pulsus paradoxus. This patient did not demonstrate clinical clues indicating cardiac tamponade; however, there was some concern about early tamponade perhaps on the basis of a recent increase in the effusion volume, with a slight narrowing of the pulse pressure. Moreover, right heart catheterization demonstrated equalization of right and left heart diastolic pressures. Impending tamponade was avoided after pericardiocentesis and recurrence by pericardiectomy. We conclude that this patient's restrictive lung impairment was on the basis of encroachment by the large effusion, as indicated by the pulmonary function data in 'Iable 2. Pre- and post-pericardiocentesis studies indicated 44 percent improvement in vital capacity and 56 percent improvement in forced expiratory volume at one second, while diffusing capacity remained unchanged. While pulmonary encroachment has been described previously, 1.1 documented improvement in pulmonary function has not been reported. It remains to be seen whether pulmonary encroachment will be found to be important only when there is other underlying pulmonary impairment as in this case, or if it will be of clinical significance in patients with normal lungs. REFERENCES
1 Spodick DU. Pericardial diseases. Philadelphia: RA. Davis, 1976:4,181,312 2 Spodick DU. Chronic and constrictive pericarditis. New York: Grone and Stratton, 1964:149 3 Spodick DU. The normal and diseased pericardium: Current concepts of pericardial physiology, diagnosis and treatment. Am J Cardioll983; 1:240-51 4 Shabetai R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 1970; 26:480-89 5 Spodick DU. Acute cardiac tamponade: pathologic, physiology, diagnosis, and management. Frog Cardiovasc Dis 1967; 10:64-96 6 Hancock EW Subacute effusive-eonstrictive pericarditis. Circulation 1971; 43:183-92 7 Hancock EW Cardiac tamponade. Med Clin N America 1979; 63:223-37 8 Boltwood CM, Shah PM. The pericardium in health and disease. Curr Frob Cardioll984:1-70 9 Antman EM, Girgill ~ Grossman W Low pressure cardiac tamponade. Ann Intern Med 1979; 91:403-06
Saccular Aneurysm of the Transverse Thoracic Aorta Detected by Transesophageal Echocardlography* M. A Taams, M.D.; W J. Gwsenhoven, M.D.; E. Bas, M.D.; and Roelandt, M. D.
J.
*From the Thoraxcenter, Erasmus University, Academic Hospital Rotterdam-Dijkzigt, and the Interuniversity Cardiology Institute, Rotterdam, the Netherlands. ReJ?nnt requests: Dr. Taams, Thoraxcenter; PIO BD 156, Dr. Molewaterplein 40, 3015 GD Rotterdam, Netherlands
438
A patient with a saccular aneurysm of the thoracic aortic arch presented with severe right ventricular failure due to pulmonary artery compression. Contradictory data were derived from computed tomography, pulmonary isotope perfusion scan and cardiac catheterization. 'Iransesophageal echocardiography revealed a saccular aneurysm which compressed the main pulmonary artery and gave access to a 6stulous connection to the left pulmonary artery. Surgery confirmed these 6ndings.
T
he incidence of aneurysmal involvement of the transverse thoracic aorta equals that of the ascending aorta. Life-threatening complications of aneurysm of the thoracic aorta include compression of adjacent vascular structures, rupture and fistula formation.' Angiography and computed tomography are established diagnostic methods." We present a patient in whom transesophageal echocardiography correctly established a complicated saccular aneurysm of the aortic arch. CASE REPORT
A60-year-oldpatient developed hoarseness and a 100kg increase in weight in two weeks and was admitted to a community hospital with intractable right heart failure. He had been treated for 15 years for systemic hypertension, but his medical history was otherwise uneventful. On admission, he was orthopneic and had upper right abdominal pain. There was edema of the legs, scrotum, ascites and a 5 cm enlarged, painful liver. Blood pressure and pulse rate were normal. The jugular venous pressure was extremely elevated. The left vocal cord and hemidiaphragm were paralyzed. A grade 3/6 systolic murmur existed, radiating to the carotid arteries and back. On the electrocardiogram, signs of right ventricular overload and a right axis were present. Chest x-ray film showed right-sided pleural effusion and a mediastinal mass underneath the aortic arch suggestive of an aortic aneurysm or a tumor. No diagnostic information from the aortic arch could be obtained fro~ precordial echocardiography. The CT-scan of the thorax showed a main pulmonary artery aneurysm. A pulmonary isotope perfusion scan showed no apparent abnormality. Aortography revealed a saccular aneurysm with its origin proximal to the left subclavian artery compressing the pulmonary artery. Right heart catheterization showed pulmonary hypertension (60/20mm Hg) and an elevated right atrial pressure (10 mm Hg), The patient was transferred to our unit for surgery. As the above findings were conflicting, the surgeon demanded further investigation. lhmsesophageal echocardiography was scheduled. A 3.7 MUz phased-array transducer was used mounted at the tip of a gastroscope and interfaced with a Hewlett-Packard ultrasonograph (HP 77020 AC). A pulsed Doppler study was concurrently performed using the same transducer switched to a Toshiba ultrasonograph (SSH 6OA). The patient fasted for 8 hours and antihypertensive drugs as premedication were given. As a local anesthetic, topical lidocaine was administered to the patient's hypopharynx. A large saccular aneurysm was visualized underneath the aortic arch. Neither dissection nor thrombus formation was present. Pulsed Doppler tracings showed bloodflow from the aneurysm into the left pulmonary artery indicating a fistula (Fig 1). The main pulmonary artery was compressed by the aneurysm. Numerous atherosclerotic lesions were noted in the thoracic aorta. Planned selective left cardiac catheterization was no longer felt mandatory. Within 24 hours after transesophageal echocardiography, the patient underwent surgery. Epicardial echocardiography after sternotomy confirmed the transesophageal findings. Deep hypothersaccularAneurysm or Transverse Thoracic Aorta (Teams et 8/)