Ann Thorac Surg 2007;84:e8-e9
© 2007 The Society of Thoracic Surgeons
Case Reports
Intestinal Ischemia Complicating Ascending Aortic Dissection: First Things First
Michael S. Firstenberg, MD*,
Chittoor B. Sai-Sudhakar, MBBS,
John H. Sirak, MD,
Juan A. Crestanello, MD,
Benjamin Sun, MD
Department of Cardiothoracic Surgery, The Ohio State University, Columbus, Ohio
Accepted for publication April 13, 2007.
* Address correspondence to Dr Firstenberg, Department of Cardiothoracic Surgery, North Doan Hall, 8th Floor, The Ohio State University, Columbus, OH 43210 (Email: michael.firstenberg{at}osumc.edu).
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Abstract
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Typically acute dissections of the ascending aorta are considered operative emergencies with delays in treatment potentially resulting in considerable morbidity and mortality. However, occasionally associated unstable or poorly defined problems (such as neurologic impairment or end-organ ischemia) may warrant further investigation and possible treatment to facilitate safe aortic repair. We present a case of acute ascending aortic dissection associated with an intra-abdominal vascular and enteric catastrophe that was successfully managed prior to aortic repair.
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Introduction
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Acute dissections of the ascending aorta are operative emergencies with a primary goal of intervention being to minimize the morbidity and mortality associated with end-organ malperfusion. On occasion the operative intervention on the aortic pathology is pursued in the face of malperfusion syndromes, such as neurologic complications, renal failure, or extremity ischemia, with anticipation of either improvement or stabilization of these concomitant problems. However, in some situations, such as associated mesenteric ischemia, the conventional strategy of initially addressing the aortic pathology may result in intestinal necrosis and septic complication. In such scenarios, alternative management approaches should be considered.
Our patient is a 35-year-old man who was previously healthy with no known medical problems, no significant family or social history problems, and no obvious physical characteristics suggestive of a genetic syndrome. He presented to an outside hospital with severe abdominal pain, hematemesis, and obvious bright red blood from the rectum. A computed tomographic scan of the abdomen was performed; the scan showed a dissection of the abdominal aorta in which the imaging was continued to the chest, based on the findings, which included a dissection of the ascending aorta that continued to the iliac bifurcation and an obstruction of the superior mesenteric artery.
The patient was transferred to our institution for further management. On arrival he was hemodynamically stable, but his abdomen was grossly distended, tender, and rigid. Initial laboratory data on admission included a room air arterial blood gas (pH level, 7.31; PCO
2 of 38 mm Hg; PO
2 of 64.8; a base excess of –7.7 mmol/L; HCO
3 of 19.0 mmol/L; and a lactate of 3.5 mmol/L), a complete blood count (white blood cell count, 19.0 K/uL; Hemotracrat, 45.1%; platelets, 185 K/uL), and chemistry and coagulation profiles that were both grossly normal. Attempted fenestration and stenting of the superior mesenteric artery was unsuccessful (Fig 1). In light of the stable hemodynamics and lack of neurologic impairment, but ongoing mesenteric ischemia and gastrointestinal bleeding, it was believed that heparinization and ascending repair would be catastrophic. He was taken to the operating room for planned staged repair. Intraoperative transesophageal echocardiography confirmed the ascending aortic dissection, but no pericardial effusion or aortic insufficiency was seen. The entire chest, abdomen, and full-length bilateral lower extremities were prepped and marked. A laparotomy was performed, and a left common iliac artery to superior mesenteric artery bypass was performed with a 6-mm Hemashield graft. In addition, the right colon seemed ischemic with focal areas of necrosis. Hence a right hemicolectomy and end ileostomy was performed. Large drains were placed to minimize hemoperitoneum during cardiopulmonary bypass. The fascia was closed, but the skin was left open. Transesophageal echocardiography monitoring allowed for ongoing evaluation of the ascending aorta and cardiopulmonary bypass, and the entire surgical team was available in case clinical deterioration were to occur necessitating standard emergent femoral cannulation and sternotomy. Furthermore, it was decided in advance that if emergent cardiopulmonary bypass was required, the abdomen would be simultaneously packed and loosely closed until the patient could be stabilized with control of the aortic pathology. Once the abdominal portion was complete, attention was given to the chest. At this point, echocardiography demonstrated further dilatation of the aorta and development of mild aortic insufficiency suggestive of disease progression. After routine axillary cannulation, median sternotomy, and initiation of cardiopulmonary bypass, the aorta was opened to reveal a proximal tear at the level of the sinotubular junction with a normal-appearing aortic valve and coronary ostia. The ascending aorta was replaced up to the level of the arch. The patient was successfully weaned from bypass. The remainder of the operation was performed in an uncomplicated manner. His postoperative course was unremarkable other than the postoperative development of heparin-induced thrombocytopenia, requiring management initially with argatroban, which was then converted to warfarin (Coumadin; Bristol-Myers Squibb, Princeton, NJ), and the discovery of an asymptomatic extension of his dissection to his bilateral carotid arteries. Six months later he returned for an ostomy takedown and restoration of bowel continuity. Computed tomography of the aorta 15 months post-dissection revealed a stable chronic dissection, and the patient is doing well. Pathologic evaluation of the resected aorta was unremarkable.
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Fig 1. Selective visceral angiogram indicating complete occlusion of the superior mesenteric artery approximately 3 to 4 cm distal from its origin (arrow).
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Comment
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Acute dissection of the ascending aorta is a true cardiovascular emergency with 50% mortality in the first 48 hours [1]. Death is a consequence of either frank rupture, cardiac failure (ie, ischemia or acute heart failure), or malperfusion syndromes, such as stroke or mesenteric and visceral ischemia. In one series, malperfusion syndromes with end-organ ischemia are associated with an 89% perioperative mortality, but with aggressive medical therapy and delayed intervention (
20 days), mortality was reduced to 25% [2]. Although successful delayed operative intervention has been described, it is usually in the context of a delay in diagnosis or severe comorbidities [3] with survival attributed to patient self-selection and a potentially more stable presentation. As such, this can justify a strategy of addressing concomitant problems that may complicate operative and postoperative management. With advances in aortic fenestration, end-organ malperfusion can often be addressed prior to aortic repair. However, although fenestration may restore blood flow, the metabolic complications of ischemia-reperfusion or septic sequelae of intestinal necrosis account for the considerable and potentially unsurvivable scenarios [4]. Fortunately, according to the International Registry of Acute Aortic Dissection database, mesenteric ischemia is an uncommon complication of ascending aortic dissection, occurring in less than 2.5% of patients [5], but when it does occur there is no uniform approach to successful management [6]. In our patient, a staged approach succeeded due to continuous aortic imaging with preparation for potential acute decompensation and adherence to fundamental principles of (1) restoring adequate perfusion to limit further organ damage, (2) resection of necrotic tissue to prevent septic complications, and finally (3) addressing the precipitating cause.
In conclusion, acute ascending aortic dissection is a life-threatening event. A primary goal of early surgery with graft replacement of the diseased aorta is to minimize morbidity and mortality by preventing or reserving end-organ malperfusion. However, when existing systemic or visceral malperfusion (as in our case, intestinal infarction) is already occurring and complicates repair, a strategy of addressing the abdominal complications prior to aortic repair can succeed. Nevertheless it is critical to monitor the aortic pathology and be prepared for cardiopulmonary bypass in the unpredictable event of hemodynamic instability.
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References
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- Anagnostopoulos CE, Prabhakar MJ, Kittle CF. Aortic dissections and dissecting aneurysms Am J Cardiol 1972;30:263.[Medline]
- Deeb GM, Williams DM, Bolling SF, et al. Surgical delay for acute type A dissection with malperfusion Ann Thorac Surg 1997;64:1669-1675.[Abstract/Free Full Text]
- Scholl FG, Coady MA, Davies R, et al. Interval or permanent nonoperative management of actue type A aortic dissection Arch Surg 1999;134:402-406.[Abstract/Free Full Text]
- Cambria RP, Brewster DC, Gertler J, et al. Vascular complications associated with spontaneous aortic dissection J Vasc Surg 1988;7:199-209.[Medline]
- Rampoldi V, Trimarchi S, Eagle KA, et al. International Registry of Acute Aortic Dissection (IRAD) Investigators Simple risk models to predict surgical mortality in acute type A aortic dissection: the International Registry of Acute Aortic Dissection Score Ann Thorac Surg 2007;83:55-61.[Abstract/Free Full Text]
- Okita Y, Takamoto S, Ando M, Morota T, Kawashima Y. Surgical strategies in managing organ malperfusion as a complication of aortic dissection Euro J Cardiothorac Surg 1995:242-247.
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Abstract
Introduction
