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Retrograde Type A Aortic Dissection After Thoracoabdominal Aneurysm Repair: Early Diagnosis with Intraoperative Transesophageal Echocardiography

Rajan, Shobana MD; Sonny, Abraham MD; Sale, Shiva MD

doi: 10.1213/XAA.0000000000000125
Case Reports: Case Report

Retrograde type A aortic dissection that arises immediately after open replacement of the thoracoabdominal aorta is a rare and potentially lethal complication that has only been reported twice previously. A 74-year-old man with a history of expanding Crawford type I thoracoabdominal aortic aneurysm presented for open surgical repair. The intraoperative course was unremarkable. However, intraoperative transesophageal echocardiography after the repair revealed type A aortic dissection extending up to the sinotubular junction. Subsequently, emergent aortic arch repair was performed under deep hypothermic circulatory arrest. Early diagnosis with transesophageal echocardiography and optimal cerebral protection were instrumental in the successful outcome of this repair.

From the *Department of Anesthesiology, Albany Medical Center, Albany, New York; and Cardiothoracic Anesthesiology, Anesthesiology Institute, Cleveland Clinic, Cleveland, Ohio.

Accepted for publication September 17, 2014.

Funding: No funding.

The authors declare no conflicts of interest.

This report was previously presented, in part, at the Ohio Society of Anesthesiologists (OSA) in September 2013 and Midwest Anesthesia Residents Conference (MARC) in April 2014.

Address correspondence to Abraham Sonny, MD, General Anesthesiology, Anesthesiology Institute, Cleveland Clinic, 9500 Euclid Ave., E30, Cleveland, OH 44195. Address e-mail to

Iatrogenic type A aortic dissection (TAAD) is a rare but potentially lethal complication of cardiac or aortic surgery. Prompt diagnosis and treatment are essential for a successful outcome. We present a case of iatrogenic retrograde TAAD that occurred after open repair of a thoracoabdominal aneurysm.

Written consent was obtained from the patient for the publication of this case report.

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A 74-year-old man with a history of Crawford type I thoracoabdominal aortic aneurysm presented for open surgical repair. The aneurysm had been monitored closely by serial imaging for 5 years. However, recently, a substantial increase in the size of the aneurysm was noted, to a largest diameter of 5.4 × 5.3 cm; thus, surgical repair was advised. The medical history of the patient was otherwise significant for hypertension, hyperlipidemia, hypothyroidism, and obstructive sleep apnea. Transthoracic echocardiography revealed preserved biventricular function and mild mitral and aortic valve regurgitation.

Once the patient was brought to the operating room, standard monitors were attached. A right radial arterial line was placed preoperatively for arterial blood pressure monitoring during induction of anesthesia. In addition, a subarachnoid drain was placed to protect the spinal cord. General anesthesia was induced with etomidate and fentanyl, and neuromuscular blockade was achieved with rocuronium. The trachea was intubated with a 41F left-sided double-lumen tube whose correct position was confirmed by auscultation and fiberoptic bronchoscopy. For additional vascular access, a right internal jugular introducer sheath and a right femoral vein central venous catheter were inserted under ultrasonographic guidance. A Swan-Ganz catheter was floated through the right internal jugular sheath to monitor pulmonary artery pressures and to guide postoperative care in the intensive care unit. A right femoral arterial line also was placed to monitor arterial pressure distal to the aortic clamp.

A transesophageal echocardiography (TEE) probe was inserted for intraoperative monitoring. An initial comprehensive evaluation was performed according to the American Society of Echocardiography and Society of Cardiovascular Anesthesiologists guidelines for intraoperative TEE.1 The preoperative echocardiographic findings were confirmed. In addition, an upper esophageal short-axis view showed Katz grade 3 atherosclerotic changes in the aortic arch.

After the patient was placed in the right lateral decubitus position, a left-sided thoracoabdominal surgical incision was made. One-lung ventilation was initiated to facilitate surgical exposure. Once adequate exposure was achieved, 120 U/kg heparin was administered and aortofemoral bypass was initiated. The patient was cooled to 32°C with the help of a bypass pump. Aortic cross-clamps were applied distal to the take-off of the left subclavian artery and at the level of the celiac trunk. The proximal descending aorta was transected, and an interposition tube graft was sewn into position without difficulty. Rewarming was initiated after the aortic graft was deaired and flushed carefully. Meanwhile, the patient received an infusion of sodium nitroprusside to facilitate uniform rewarming. The cross-clamps were released uneventfully, and the patient was easily separated from aortofemoral bypass without need for any vasopressor or inotropic support.

Postoperative TEE, however, revealed significant thickening of the anterior ascending aortic wall in midesophageal aortic valve long-axis view, suggesting the presence of intramural hematoma (Fig. 1). This new ascending aortic dissection appeared to extend up to the sinotubular junction. Color Doppler interrogation also revealed worsening of aortic insufficiency (Fig. 2). A comprehensive TEE evaluation with all aortic views was performed, but the intimal entry point could not be located. Biventricular systolic function remained normal, without any new regional wall motion abnormalities, and no pericardial effusion was noted.

Figure 1

Figure 1

Figure 2

Figure 2

The decision was made to repair the dissection immediately. Heparin was reversed with protamine, and hemostasis was achieved expeditiously, followed by closure of the thoracoabdominal incision. The patient was then turned onto his back, and sternotomy was performed. After full-dose heparin was administered, arterial cannulation was achieved through a right subclavian side graft, and venous cannulation was performed through a right atrial cannula advanced from the femoral vein under echocardiographic guidance. Cardiopulmonary bypass was initiated uneventfully. The ascending aorta was then clamped and ostial and retrograde cardioplegia administered. The patient was cooled to a core temperature of 18°C during the course of 30 minutes to ensure cerebral protection. Then, deep hypothermic circulatory arrest (DHCA) was initiated, and myocardial protection was achieved by both antegrade and retrograde cardioplegia. A nasopharyngeal temperature probe was used to monitor core temperature. Ice packs were placed around his head to prevent passive warming of the brain.

The ascending aorta and arch were replaced with a tube graft, and the native aortic valve was resuspended. There was no evidence of intimal disruption in the ascending aorta, but the intimal layer of the aorta was found to be very friable. After 10 minutes of DHCA, the distal anastomosis was completed, and rewarming was initiated. Once the patient was adequately rewarmed, the aortic cross-clamp was removed, and the patient was separated from cardiopulmonary bypass without need for any vasopressor or ionotropic infusions. Nevertheless, he received 11 units of packed red blood cells for acute blood-loss anemia. In addition, he was given fresh-frozen plasma, platelets, and cryoprecipitate for coagulopathy. He remained hemodynamically stable, and TEE revealed adequate biventricular function. Once hemostasis was achieved, his chest was closed, and the patient was transferred to the intensive care unit.

On postoperative day 1, he showed fairly dense left-sided hemiparesis, mostly involving the left upper extremity. Noncontrast computed tomography of the head revealed subacute infarcts involving the right parietal and occipital lobes, suggesting a middle/posterior cerebral circulation territory watershed event, presumably due to hypoperfusion. In addition to the stroke and associated cognitive deficits, his postoperative course was complicated by malnutrition and respiratory failure that necessitated tracheostomy.

Despite these complications, he was successfully separated from the ventilator. His cognitive deficits and hemiparesis improved remarkably during the next few days. He was discharged to a long-term acute care facility on postoperative day 23 with minimal residual weakness of his left upper extremity.

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In rare instances, iatrogenic TAAD occurs during or immediately after cardiac operations. Its reported incidence ranges from 0.06% to 0.29%,2–5 and the mortality associated with it was as high as 43% in 1 series.3 Retrograde TAAD that arises immediately after open replacement of the thoracoabdominal aorta is even more rare and, to our knowledge, has only been reported twice previously in the literature.6,7 These replacement procedures differ from cardiac operations in that the ascending aorta is not visible in the surgical field; thus, abnormalities can only be detected by intraoperative imaging. In 1 reported case, TAAD was diagnosed intraoperatively and then successfully repaired,7 whereas the other case was diagnosed postmortem after the patient experienced cardiopulmonary arrest on the second postoperative day.6 In both cases, the tear was found to originate from the aortic cross-clamp site.

Although TAAD is uncommon after open aortic operations, retrograde TAAD is known to occur after endovascular stent graft placement in the descending thoracic aorta. A recent large, retrospective review of data from 1010 patients who had endovascular repair of the thoracic aorta showed the incidence of retrograde TAAD after this procedure to be 1.6%.8 The dissection usually was located at the tip of the proximal bare spring of the endovascular graft. In cases of iatrogenic TAAD after cardiac operations, the tears have been found to originate at the site of aortic cannulation, aortic cross-clamping, or anterograde cardioplegia, or at the proximal anastomosis of the bypass graft.

In addition to significant early mortality risk, iatrogenic TAAD poses a high risk of postoperative morbidity such as prolonged ventilation, renal failure, and cardiogenic shock.9 A large retrospective analysis of the Society of Thoracic Surgery database found age older than 60 years, Asian race, preoperative steroid use, peripheral vascular disease, and femoral cannulation site to be the risk factors for intraoperative aortic dissection.5

One important modifiable factor that could affect outcome in these patients is early diagnosis. Routine intraoperative TEE could be instrumental in identifying iatrogenic TAAD before it becomes a catastrophic event. In a report of their series, Hwang et al.2 point out that once his team began using intraoperative TEE routinely, the early mortality after iatrogenic TAAD decreased from 75% to 17%. When performed by an experienced operator, TEE is highly specific and sensitive in detecting thoracic aortic dissection; its sensitivity is 98%, which is comparable with the sensitivity of computed tomography (100%) and magnetic resonance imaging (98%).10 In addition to detecting the dissection, TEE also helps determine its anatomy and extent and can be useful to diagnose associated complications such as aortic insufficiency, pericardial effusion, and coronary ischemia. Apart from routine examination, TEE in a patient after repair of a thoracoabdominal aortic aneurysm should focus on identifying these complications. Meticulously obtained aortic views would help identify extension or presence of a new dissection.

Another important modifiable factor is cerebral protection. Repairing TAAD involving the arch is challenging and requires DHCA for success. Poor outcomes have been associated with suboptimal cerebral protection when arch vessels were involved or when deep hypothermia could not be achieved before circulatory arrest.2,4 Although early repair and restoration of flow to cerebral vessels is essential, providing sufficient time to achieve deep hypothermia during the repair is necessary for optimal cerebral protection. Thus, every effort should be made to achieve deep hypothermia before repair. Efficient surgical decision-making and a skilled perioperative team are essential to successful repair.

In summary, retrograde TAAD is an extremely rare but potentially lethal complication during aortic operations. Successfully treating this complication requires early diagnosis and optimal cerebral protection. Routine TEE is instrumental in early diagnosis in these cases, especially in patients with risk factors for dissection.

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