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Intramural Left Atrial Hematoma After Aortocoronary Artery Surgery

Musat, Iulian MD*; Hieber, Cornelia MD*; Kepka, Anton MD*; Novotny, Petrus MD*; Poslussny, Peter MD; Schwarz, Sylvia MD*‡; Fitzgerald, Robert D. MD*‡

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doi: 10.1213/01.ANE.0000085641.90506.70
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A rare complication of coronary artery bypass grafting (CABG) is the development of an intramural atrial hematoma. Clinically, such hematomas can lead to hemodynamic obstruction of the efferent and afferent blood flow, causing low-cardiac output and cardiogenic shock (1). We describe the first reported case of an intraoperative left atrial hematoma during CABG and the beneficial role of echocardiography in detecting and monitoring this event.

Case Report

Three-vessel coronary artery disease was detected by coronary angiography in a 76-yr-old male (70 kg, 168 cm) with a history of hyperlipidemia, effort angina pectoris, and palpitations for approximately 2 mo. Preoperative transthoracic echocardiography showed no pathology except slight enlargement of the left atrium (41 mm), minimal mitral regurgitation with a narrow central jet, and abnormal diastolic relaxation as assessed by mitral diastolic inflow patterns. Preoperative drug treatment included metoprolol, molsidomin, and enoxaparin (2 × 40 mg/d). The patient had no surgical history.

Induction of anesthesia was unproblematic and was achieved by administration of midazolam, etomidate, and sufentanil. Pancuronium was administered for neuromuscular blockade. Anesthesia was maintained by continuous infusion of sufentanil and propofol; the patient exhibited cardiopulmonary stability before extracorporeal circulation. Precardiopulmonary bypass transesophageal echocardiography (TEE) examination included the midesophageal four-chamber view, midesophageal two-chamber view, and long-axis view, which revealed no regional wall motion abnormalities and abnormal relaxation of the left ventricle. Color Doppler examination showed minimal mitral valve regurgitation. Transgastric mid- and basal-short axis view showed a good left ventricular systolic function. Examination of the heart by the surgeon did not reveal any abnormalities.

Extracorporeal circulation was initiated after heparinization with 400 IU/kg body weight and uncomplicated cannulation of the ascending aorta, the inferior caval vein, and the sinus venosus with an introducer (RC014T, Edwards Lifesciences, Irvine CA). Heparinization was assessed by activated clotting time and remained above 500 s throughout cardiopulmonary bypass. Antegrade cold blood cardioplegia was followed by retrograde cardioplegia. Perfusion pressure during cardioplegia showed no abnormal increases (maximum, 19 mm Hg). Two grafts were performed without any difficulties: one vein to the posterior descending branch, and the internal mammary artery to the left anterior descending artery. The weaning from cardiopulmonary bypass was successful and supported by 0.4 μg · kg−1 · min−1 milrinone and 0.12 μg · kg−1 · min−1 noradrenaline. All cannulae were removed without complication and heparinization was reversed with protamine in a ratio of 1:1.

Before closing the thorax, a left atrial mass was detected by TEE (Fig. 1). The patient was again heparinized (400 IU/kg) and cardiopulmonary bypass was re-initiated. The left atrium was found to be empty, with the posterolateral wall protruding into the left atrium; no lesion of the endocardium was detected. An incision in this structure allowed for fluid blood to be emptied.

Figure 1
Figure 1:
Intraoperative midesophageal view of the left atrium. H: Echolucent mass filling the left atrium. LV = left ventricle; RV = right ventricle; LVOT = left ventricular outflow tract; AR = aortic root.

The atrium was closed and the patient weaned from bypass with unchanged inotropic and vasopressor support. However, TEE showed a new multilobed and echolucent chamber protruding into the left atrium, occupying the posterolateral two thirds of the left atrium. Color Doppler detected no communication with the left atrium. Pulse wave Doppler analysis showed no significant hemodynamic obstruction of the mitral valve and pulmonary veins or any sign of pulmonary hypertension. Left atrial and ventricular pressure were increased according to the criteria listed by Boussuges et al. (2) (E-wave: 0.85 m/s; A-wave: 0.34 m/s; E/A ratio = 2.5; systolic fraction of pulmonary venous forward flow <0.4; Pressure half time: 44 ms; duration of pulmonary venous reversal flow exceeding the duration of mitral A-wave). Another surgical intervention was not undertaken and the patient was transferred to the intensive care unit (ICU).

On the first ICU day the patient developed a systemic inflammatory response syndrome (SIRS) with a pronounced vasoplegia and increased vascular permeability; his condition deteriorated progressively. He required large amounts of IV crystalloids and large doses of vasopressors to maintain perfusion pressure. His electrocardiogram showed sinus tachycardia without any signs of myocardial infarction. During his second day in the ICU, the patient’s situation stabilized and requirements for intravascular volume replacement and pharmacological support decreased. The further course of his condition was complicated by paroxysmal atrial fibrillation, which was treated with amiodarone. However, we proceeded with ventilatory weaning and the patient’s trachea was extubated on postoperative day seven.

TEE or transthoracic echocardiographic examinations were performed each day. On the first two days, no changes in structure or dimension were apparent. The protruding mass appeared to occlude the blood flow into the left ventricle; the mitral inflow velocity was normal with an increased diastolic slope (deceleration time, 152 ms). The pressure half time was decreased, indicating that no mitral stenosis was present (Fig. 2). No pulmonary venous obstruction was documented. In the next days, the atrial mass regressed and the structure appeared more solid, with a central echolucent area. On the sixth day, the control echocardiography showed a regression of the atrial mass to only one-third of the atrium area (Fig. 3).

Figure 2
Figure 2:
Fourth postoperative day: midesophageal view of the left atrium. Multiplane angle is rotated to approximately 90 degrees. LV = left ventricle; LA = left atrium; H = hematoma.
Figure 3
Figure 3:
Sixth postoperative day: midesophageal view of the left atrium. *Echolucent mass in the posterolateral wall of left atrium. LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.

The patient’s condition further improved and he was transferred to the intermediate care unit on the eighth day after the surgery, and he was discharged from the hospital on postoperative day 18.

Forty weeks after his discharge, we examined the patient. He was in excellent condition and staged New York Heart Association II. A transthoracic echocardiography was performed in parasternal long-axis view and apical four-chamber view. His left ventricular function was good, with a hypokinesis of the basal inferior wall. The abnormal diastolic relaxation persisted. There were no apparent signs of an atrial dissection, and no indications of mitral valve pathologies were detected (Fig. 4).

Figure 4
Figure 4:
Apical four-chamber view recorded 40 wk after operation. Note the normal image of the left atrium (LA). LV = left ventricle; RA = right atrium; RV = right ventricle.


Atrial dissections and hematomas are rare complications of cardiac surgery, and descriptions in the literature are uncommon. Gallego et al. (1) described 11 cases over 8 years, all of which were described as happening days and years after mitral valve surgery. Intraoperative occurrence was reported only once, for a right atrial hematoma (3). In that case, the intramural hematoma was only detected 23 days after surgery. The hematoma was attributed to a lesion acquired during the cannulation procedure. Spontaneous atrial hematomas were also reported previously, although only in connection with predisposing diseases, e.g., amyloidosis (4,5). Pathophysiologically, left atrial hematoma occurs with an atrial dissection and is described as a complication associated with mitral valve surgery (1). Predispositions to this condition are rheumatic disease, amyloidosis, myocardial infarction, and a preceding blunt trauma (1).

We can only hypothesize on the cause of the hematoma in our patient. Indeed, he showed no signs of any predisposing condition or myocardial infarction. Furthermore, we cannot exclude an unintended iatrogenic lesion, possibly by a venous rupture resulting from retrograde cardioplegic perfusion. However, perfusion pressure was monitored and did not show any abnormal increase. The surgeon’s examination of the heart during the second extracorporeal circulation did not reveal any pathology. An echocardiographic inspection of the coronary sinus was made impossible by the atrial mass, and an angiographic examination of this hypothesis was hindered by the patient’s condition in the immediate postoperative period.

Another point of discussion is the indication for reoperation. As the atrial mass reappeared after the second extracorporeal circulation, it was agreed that, in light of the patient’s relative stability, the risk posed by a third extracorporeal circulation should be avoided. Instead, a second operation was scheduled for a later time when the patient’s condition would stabilize. The decision to reexplore was guided by the patient’s clinical situation and the echocardiographic examinations. We were awaiting a decline in the hemodynamics or an increase of the atrial hematoma, and either one of these situations would have prompted surgical reexploration. However, close monitoring of the hemodynamics and frequent echocardiographic controls allowed us to postpone and finally avoid a surgical intervention.

Echocardiographic examinations are considered to be the most advanced monitoring procedure for intracardiac masses (6). In this patient, we performed daily examinations after surgery and identified an occlusion of two-thirds of the atrium during the first two days after surgery. The increase in mitral inflow velocity was attributed to the concomitant clinical picture of the SIRS. Regression of the atrial mass was closely monitored by echocardiography and showed satisfactory resolution.

Thus, we conclude that echocardiography was successful in detecting an unexpected and otherwise undetected atrial mass. Under close echocardiographic monitoring, we were able to postpone and finally determine that further surgical intervention was not required.


1. Gallego P, Oliver JM, Gonzales A, et al. Left atrial dissection: pathogenesis, clinical course, and transesophageal echocardiographic recognition. J Am Soc Echocardiogr 2001; 14: 813–20.
2. Boussuges A, Blanc P, Molenat F, et al. Evaluation of left ventricular filling pressure by transthoracic Doppler echocardiography in the intensive care unit. Crit Care Med 2002; 30: 362–7.
3. Trappe HJ, Daniel WG, Hetzer R, et al. Intramural right atrial hematoma following coronary artery bypass surgery. Am Heart J 1985; 109: 917–8.
4. Watanabe K, Miguel B, Kemeny JL, et al. Spontaneous intramural left atrial hematoma associate with systemic amyloidosis. Ann Thorac Surg 2001; 72: 2132–4.
5. Shaikh N, Rehman NU, Salazar MF, Grodman RS. Spontaneous intramural atrial hematoma presenting as a left atrial mass. J Am Soc Echocardiogr 1999; 12: 1101–3.
6. Aru GM, Falchi S, Cardu G, et al. The role of transesophageal echocardiography in the monitoring of cardiac mass removal: a review of 17 cases. J Card Surg 1993; 8: 554–7.
© 2003 International Anesthesia Research Society