Left Atrial Compression by a Pericardial Hematoma Presenting as an Obstructing Intracavitary Mass: A Difficult Differential Diagnosis Edward Gologorsky, MD*, Angela Gologorsky, and Abraham Wolfenson, MD‡
MD*,
David L. Galbut,
MD†,
*Division of Cardiac Anesthesia and †Departments of Cardiac and Thoracic Surgery and ‡Cardiology, Miami Heart Institute, Miami Beach, Florida
C
ardiac sonography has been used increasingly in the diagnosis and follow-up of intracavitary and pericardial pathology. We present a case in which the transesophageal echocardiogram (TEE) was accurate in defining the pathophysiology of flow restriction but was misleading in suggesting intracavitary pathology. The importance of echocardiographic data interpretation in relation to the clinical setting is emphasized.
Case Report A 78-yr-old man with a history of smoking, hypertension, severe peripheral vascular disease, left subclavian artery stenosis, and recurrent transient ischemic attacks was evaluated for a carotid endarterectomy. A history of coronary bypass surgery 17 yr ago and several recent episodes of chest pain prompted a preoperative cardiac catheterization. The findings included a high-grade stenotic lesion in a tortuous dominant right coronary artery. There was no patent saphenous graft to this vessel. During the percutaneous angioplasty (PTCA) of the looped right coronary artery, a dissection and an occlusion occurred in the native vessel. A stent could not be placed. A ventriculogram was not performed. Hemodynamic stability in the catheterization laboratory, the patient’s reoperative status with patent left coronary system grafts, and his advanced age favored conservative management of the evolving infarct. The next morning (approximately 12 h after PTCA), the patient complained of continuing chest pressure and an upper back discomfort. An acute aortic dissection was suspected, and a computed tomography scan and transthoracic echocardiogram (TTE) were performed. Both modalities excluded an aortic dissection and suggested the presence of a Accepted for publication May 10, 2002. Address correspondence to Edward Gologorsky, MD, Anesthesia Department, Memorial Regional Hospital, 3501 Johnson St, Hollywood, FL 33021. Address e-mail to
[email protected]. AQ: 1. DOI: 10.1213/01.ANE.0000023205.91292.8F ©2002 by the International Anesthesia Research Society 0003-2999/02
large left atrial (LA) mass. A radiologist interpreted a computed tomography to show a well-circumscribed round softtissue hypodensity measuring approximately 6 cm in diameter, occupying the region of LA, and apparently intraluminal. An extracardiac origin of the mass was deemed unlikely by the radiologist. TTE, examined by several cardiologists, demonstrated a fairly large LA mass, which was possibly interfering with left ventricular (LV) inflow. Later in the day, approximately 24 h after PTCA, the patient started to be slightly short of breath. By the morning of the next day, his respiratory rate reached 24 breaths/min, Spo2 decreased to 90% despite the use of face mask oxygen supplementation, he developed bilateral rales, and the chest radiograph showed worsening of pulmonary congestion. He became diaphoretic, tachycardic to 130 per min, and had blood pressure swings from 70/50 to 150/90 mm Hg. IV furosemide was administered, and a small-dose Dopamine infusion was started. A pulmonary artery catheter was placed showing pulmonary hypertension (50/22 mm Hg), and a repeat TTE indicated the presence of a large and slightly mobile LA mass and preserved LV systolic function (ejection fraction was an estimated 0.50). Obstruction of pulmonary venous and transmitral flows was suspected. The patient was emergently brought to the operating room. After an uneventful induction of general anesthesia with fentanyl, midazolam, and vecuronium, and initiation of mechanical ventilation, an intraoperative TEE examination revealed a heterogeneous round LA mass with smooth edges that occupied most of the LA. It seemed to be attached to the posterior and lateral walls of the LA and interfered with both the transmitral and pulmonary venous flows (Figs. 1– 4). LV contractility was moderately impaired, the right ventricle (RV) seemed to be hypokinetic and dilated, and a mild tricuspid insufficiency was noted. Cardiopulmonary bypass was initiated through femoral cannulation, and reoperative sternotomy was performed without any inadvertent injury to the patent left coronary grafts or mediastinal structures. Lysis of cardiac adhesions was limited to the ascending aorta, right atrium, right anterior surface of the heart, superior and inferior venae cavae, and LA. The aorta was cross-clamped, retrograde cardioplegia given, and LA posteriorly opened to the right interatrial groove. No interatrial mass was found. Instead, an extrinsic compression of the posterior wall was responsible for obliteration of the LA
Anesth Analg 2002;95:567–9
567
568
CASE REPORTS
Figure 1. A five-chambers view. A gigantic heterogeneous roundshaped mass is seen in the left atrium (LA).
ANESTH ANALG 2002;95:567–9
Figure 3. The transmitral flow is impeded by the mass. Fivechambers view.
Figure 2. The same left atrial (LA) mass is seen in the two-chambers view.
cavity. Anterior and inferior surfaces of the RV were completely freed from pericardial adhesions. The RV seemed hemorrhagic, and a significant intramural dissecting hematoma was noted. Inferiorly, the hematoma tracked to the coronary sinus where it may have ruptured into the adhesed and septated pericardium, producing a severe extrinsic compression of the LA posterior wall. The hematoma was evacuated and the LA closed. The patient was separated from the cardiopulmonary bypass without difficulty. TEE documented the restoration of transmitral and pulmonary venous flow with no further evidence of intracardiac pathology. However, the patient developed a severe coagulopathy, required massive blood products transfusion, re-exploration on the next day, and succumbed to multiorgan system failure on the third postoperative day. The family refused an autopsy.
Discussion The differential diagnosis between intracardiac and extracardiac pathology is often difficult and frequently made during surgery. Various cardiac and mediastinal structures, such as subdivided LA (1) and
Figure 4. The transmitral flow is impeded by the mass. Twochambers view.
inverted LA appendage (2– 4), have been misdiagnosed echocardiographically as LA masses, and a benign pericardial lipid envelope has been mistaken for pericardial tamponade by TEE (5). Localized pericardial and intramural hematomas have been described to compress various myocardial structures (6 –9). They are associated with trauma, cardiac surgery, mitral annular calcification, acute myocardial infarction, aortic valve disease, and aortic dissections. Adhesions between cardiac tissues and pericardium tend to contain hematomas and direct their spread along the paths of least resistance. TEE remains the diagnostic tool of choice, and TEE has been recommended when clinical impression of loculated pericardial tamponade is not supported by TTE (6,7,10). However, TEE is not infallible. An echographic misdiagnosis of a spontaneous intramural LA hematoma as a large LA oval-shaped mass has resulted in a surgical exploration (11). In another patient, an intramural LA hematoma secondary to heavy
ANESTH ANALG 2002;95:567–9
mitral annular calcification with abscess formation was mistaken on TEE as a large LA heterogeneous ovoid mass with smooth borders (12). A correct diagnosis was established at autopsy. In a number of hemodynamically unstable patients after open-heart surgery, postoperative echocardiography has misdiagnosed pericardial and intramural cardiac hematomas as intracavitary atrial masses (13–15). LA dissections can also masquerade as intracavitary masses or thrombi (16,17). The anterior displacement of the posterior wall of the LA with resultant obliteration of the LA cavity was responsible for the echocardiographic image suggestive of intracavitary pathology, a mechanism similar to the presented case. A dissecting hematoma may result from an unrecognized coronary artery perforation during PTCA and develop as a consequence of a RV infarction (18 –20). As in our patient, it can spontaneously drain into the pericardial space (19) and has been mistaken for LA and LV intracavitary mass (20,21). The presented case and literature review examine the role of echocardiography in the diagnosis of pericardial and intramural versus intracavitary pathology. The precise differential diagnosis may not be always possible. The collection of partially clotted blood in a restricted dissecting plane behind compliant and easily displaced atrial walls may interfere with pulmonary venous and transmitral flows. The importance of close temporal relationships to the myocardial injury or a traumatic intervention and acute development of hemodynamic and respiratory instability is emphasized. Brighter echo reflectance of a partially solidified hematoma behind the thin displaced atrial walls may create a TEE image suggestive of an intracavitary mass; however, a high level of suspicion should be maintained because a large heterogeneous mass with smooth edges broadly attached to posterior and/or lateral atrial walls may be associated with extracavitary pathology. In our case, TEE facilitated the recognition of the pathophysiology of flow obstruction analogous to that of mitral stenosis. The patient required urgent surgical restoration of transmitral and pulmonary venous flows regardless of the nature of obstruction; however, we believe that in some patients, such diagnostic distinctions may have important clinical and surgical management implications.
References 1. Shimaya K, Kurihashi A, Tanaka N, Higashidate M. Subdivided left atrium mimicking a cardiac tumor. Int J Cardiol 1999;68: 235– 8.
CASE REPORTS
569
2. Botero M, Davies LK. An unexpected left atrial mass during cardiac surgery. J Cardiothorac Vasc Anesth 2000;14:483– 4. 3. Kanemitsu N, Okabe M, Wariishi S, et al. Inverted left atrial appendage. Jpn J Thorac Cardiovasc Surg 2000;48:597– 8. 4. Barzaghi N, Locatelli A, Maselli D, et al. A left atrial mass after cardiac surgery. J Cardiothorac Vasc Anesth 2000;14:485– 6. 5. Kuvin JT, Basu AK, Khabbaz KR, et al. Benign lipid envelope of the heart simulating a pericardial hematoma. J Am Soc Echocardiogr 2001;14:234 – 6. 6. Kochar GS, Jacobs LE, Kotler MN. Right atrial compression in postoperative cardiac patients: detection by transesophageal echocardiography. J Am Coll Cardiol 1990;16:511– 6. 7. Pepi M, Doria E, Fiorentini C. Cardiac tamponade produced by a loculated pericardial hematoma simulating a right atrial mass. Int J Cardiol 1990;29:383– 6. 8. Tardif JC, Taylor K, Pandian NG, et al. Right ventricular outflow tract and pulmonary artery obstruction by postoperative mediastinal hematoma: delineation by multiplane transesophageal echocardiography. J Am Soc Echocardiogr 1994;7:400 – 4. 9. Shehata AR, Gillam LD, Weisburst MR, Chen C. Pericardial hematoma causing saphenous vein graft compression. Am Heart J 1996;131:598 –9. 10. Hutchison SJ, Smalling RG, Albornoz M, et al. Comparison of transthoracic and transesophageal echocardiography in clinically overt or suspected pericardial heart disease. Am J Cardiol 1994;74:962–5. 11. Shaikh N, Rehman NU, Salazar MF, Grodman RS. Spontaneous intramural atrial hematoma presenting as a left atrial mass. J Am Soc Echocardogr 1999;12:1101–3. 12. Schecter SO, Fyfe B, Pou R, Goldman ME. Intramural left atrial hematoma complicating mitral annular calcification. Am Heart J 1996;132:455–7. 13. Alfonso F, Zamorano J, Castanon J, et al. Postoperative pericardial hematoma causing localized cardiac tamponade and presenting echocardiographically as a right atrial mass. Am Heart J 1991;122:252– 4. 14. Momenah TS, McElhinney DB, Brook MM, et al. Intramyocardial hematoma causing cardiac tamponade after repair of ebstein malformation: erroneous echocardiographic diagnosis as intracavitary thrombus. J Am Soc Echocardiogr 1998;11:1087–9. 15. Tsubo T, Araki I, Ishihara H, Matsuki A. Atrial septal hematoma immediately after cardiac surgery: detection using transesophageal echocardiography. Anesthesiology 1995;83:620 –1. 16. Gallego P, Oliver JM, Gonzalez A, et al. Left atrial dissection: pathogenesis, clinical course, and transesophageal echocardiographic recognition. J Am Soc Echocardogr 2001;14:813–20. 17. Schmid ER, Schmidlin D, Jenni R. Images in cardiology: left atrial dissection after mitral valve reconstruction. Heart 1997;78: 492. 18. Werner GS, Figulla HR, Grosse W, Kreuzer H. Extensive intramural hematoma as a cause of failed coronary angioplasty: diagnosis by intravascular ultrasound and treatment by stent implantation. Cathet Cardiovasc Diagn 1995;36:173– 8. 19. Harpaz D, Kriwisky M, Cohen AJ, et al. Unusual form of cardiac rupture: sealed subacute left ventricular free wall rupture, evolving to intramyocardial dissecting hematoma and to pseudoaneurism formation—a case report and review of literature. J Am Soc Echocardiogr 2001;14:219 –27. 20. Tighe DA, Raichlen JS, Paul JJ. Infarct related intramyocardial dissection: clinical course and echocardiographic recognition. Echocardiography 1995;12:613– 8. 21. Stollberger C, Finsterer J, Waldenberger FR, et al. Intramyocardial hematoma mimicking abnormal left ventricular trabeculation. J Am Soc Echocardiogr 2001;14:1030 –2.
