Cardiac 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.
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 large left atrial (LA) mass. A radiologist interpreted a computed tomography to show a well-circumscribed round soft-tissue 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 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.
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 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 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.
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