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Spontaneous splanchnic dissection: Application and timing of therapeutic options
From the Southern Association for Vascular Surgery
Spontaneous splanchnic dissection: Application and timing of therapeutic options Thomas J. Takach, MD, Jeko M. Madjarov, MD, Jeremiah H. Holleman, MD, Francis Robicsek, MD, and Timothy S. Roush, MD, Charlotte, NC Background: Spontaneous splanchnic dissection (SSD) occurs infrequently and has a poorly defined natural history. Few studies address the application, timing, and consequences of therapeutic options. Our goal was to apply conservative (non-operative) management in the care of each patient, reserving interventions for specific indications that may be predictive of adverse outcomes. Methods: Between 2003 and 2008, 10 consecutive patients (mean age 54.7-years-old, 70.0% male) presented with 11 SSDs involving either the celiac artery (n ⴝ 6), superior mesenteric artery (n ⴝ 3), or both (n ⴝ 1). Each patient had acute, spontaneous onset of persistent abdominal pain and was diagnosed with SSD following multidetector row computed tomographic angiography (CTA). Non-operative management (anticoagulation, anti-impulse therapy, analgesics, and serial CTA examinations) was initially used in 9 patients. Endovascular (n ⴝ 2) or operative (n ⴝ 2) intervention was performed either immediately (n ⴝ 1) or following failed medical management (n ⴝ 3) in 4 patients for specific indications that included persistent symptoms (n ⴝ 3), expansion of false lumen (n ⴝ 3), and/or radiologic malperfusion (n ⴝ 3). Results: All patients were asymptomatic after successful non-operative management or following intervention. No morbidity occurred. Upon complete follow-up (mean 13.4 months, range, 2 to 36 months), all patients remained asymptomatic. Preservation of distal perfusion with either thrombosis or ongoing regression of false lumen was achieved in 5 patients who received only non-operative management and in 4 patients following intervention. A stable chronic dissection was present in 1 patient who had only non-operative management. Conclusion: Successful outcomes following SSD may be achieved with either non-operative therapy alone or intervention if persistent symptoms, expansion of false lumen, and/or malperfusion occur. The unpredictable response of the false lumen to conservative management mandates close, long-term follow-up. Endovascular and operative interventions produced similar outcomes in a small number of patients with limited follow-up. Although SSD is currently perceived as rare, the increasing use of CTA may prove that the true incidence has been underestimated. ( J Vasc Surg 2009;50:557-63.)
Spontaneous splanchnic dissection (SSD) is uncommon and few studies address the application, timing, and consequences of therapeutic options. The natural history of this problem is ill defined. Selective cases have been known to undergo spontaneous resolution with thrombosis of false lumen and preservation of distal flow. However, other cases have been associated with both significant morbidity and mortality. In this small study, our goal was to apply conservative (non-operative) management in the care of each patient, reserving the use of interventions for specific indications that may be predictive of adverse outcomes. METHODS Between 2003 and 2008, 10 consecutive patients (mean age 54.7 years, 70.0% male) presented to our institution with 11 SSDs involving either the celiac artery (n ⫽ 6), superior mesenteric artery (n ⫽ 3), or both (n ⫽ 1). The From the Department of Cardiothoracic and Vascular Surgery, Carolinas Heart Institute, Carolinas Health Care System. Competition of interest: none. Presented in part at the Thirty-third Annual Meeting of the Southern Association for Vascular Surgery, Tucson, Ariz, January 14-17, 2009. Reprint requests: Thomas J. Takach, MD, Department of Cardiothoracic and Vascular Surgery, Carolinas Heart Institute, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232-2861 (e-mail: tjtakach@ netscape.net). 0741-5214/$36.00 Copyright © 2009 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. doi:10.1016/j.jvs.2009.02.244
demographic data and risk factors for these patients are summarized in Table I. Although 4 patients had a history of well-controlled hypertension, all patients were normotensive upon initial evaluation. Each patient had acute spontaneous onset of persistent abdominal pain and was diagnosed with SSD following multidetector row computed tomographic angiography (CTA). Each initial CTA examination was performed within 24 hours following onset of symptoms. No patient had concomitant aortic disease, including dissection, aneurysm, or significant atherosclerosis. One patient had significant atherosclerosis involving the major, concomitant (non-dissected) mesenteric vessel. On the basis of anatomic findings at initial diagnostic imaging, each patient received either immediate intervention or non-operative therapy (anticoagulation, anti-impulse therapy, analgesics, and serial CTA examinations) (Table II). The primary anatomic determinant regarding decisionmaking at this point was the presence or absence of malperfusion. Malperfusion was defined as greater than 80% compromise of the true lumen, comparing the smallest true lumen diameter with a reference diameter of contiguous, parallel, non-dissected vessel. Malperfusion syndrome was defined as the morbid consequences of either diminished or absent flow due to dissection. In the absence of malperfusion, non-operative (conservative) management was initially used in 9 patients. The patients receiving conservative management were discharged following initial diagnosis upon resolution of symptoms. Staged 557
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Table I. Patient demographics, risk factors, and management Management
Patients Mean age (range) Gender Male Female Hypertension Tobacco use Diabetes mellitus Coronary artery disease Peripheral vascular occlusive disease Dyslipidemia Chronic obstructive pulmonary disease
Intervention (open/endovascular)
Conservative (non-operative)
10 (100%) 54.7 years (42-75 years)
4 (40.0%)
6 (60.0%)
7 (70.0%) 3 (30.0%) 4 (40.0%) 4 (40,0%) 0 (0) 3 (30.0%) 1 (10.0%) 2 (20.0%) 1 (10.0%)
4 (40.0%) 0 2 (20.0%) 2 (20.0%) 0 1 (10.0%) 1 (10.0%) 1 (10.0%) 0
3 (30.0%) 3 (30.0%) 2 (20.0%) 2 (20.0%) 0 2 (20.0%) 0 1 (10.0%) 1 (10.0%)
Table II. Dissection characteristics and outcomesa Dissections Vessel of origin Celiac artery Superior mesenteric artery Extent Localized Diffuse Branch vessel involvement Present Absent False lumen natural history* Regression or thrombosis* Expansion* No change* Mean follow-up (range) (10 patients) Outcome (by patienta) Spontaneous regression Chronic dissection Intervention Type Endovascular stent Laparotomy Laparotomy/bypass Timing Immediate Delayed Mean time (range) Indication Persistent symptoms False lumen expansion Malperfusion
11 (100%) 7 (63.6%) 4 (36.4%) 4 (36.4%) 7 (63.6%) 8 (72.7%) 3 (27.3%) 6 (60.0%) 3 (30.0%) 1 (10.0%) 13.4 months (2-36 months) 5 (50.0%) 1 (10.0%) 4 (40.0%) 2 (20.0%) 1 (10.0%) 1 (10.0%) 1 (10.0%) 3 (30.0%) 20 days (2-30 days) 3 (30.0%) 3 (30.0%) 3 (30.0%)
*Excludes dissection in patient treated with immediate intervention. a Includes 11 dissections in 10 patients.
follow-up CTA examinations were performed in each patient at 30 days, then every 3 months until complete regression (thrombosis) of false lumen. Anticoagulation was continued empirically until follow-up CTA examination demonstrated either regression or unchanged diameter of false lumen. Antiimpulse therapy included continuation of antihypertensive therapy in those patients previously receiving such medication and the addition of beta-blockade therapy until CTA documentation of false lumen thrombosis.
The initial CTA finding of malperfusion or follow-up CTA findings of delayed-onset malperfusion, distal propagation of dissection, or expansion of false lumen were specific indications for intervention. The presence of persistent, worsening, or recurrent pain at any time following initial diagnosis prompted a full investigation including repeat CTA examination in order to determine cause. In patients requiring intervention, less invasive endovascular techniques were used preferentially. Open operative procedures were used when assessment of bowel viability was mandated by the individual case. Following endovascular intervention, patients were discharged on dual (aspirin and clopidogrel) anti-platelet therapy after radiologic imaging confirmed elimination of false lumen flow, unimpeded true lumen flow, and patency of branch vessels. RESULTS Dissection characteristics and outcomes are summarized in Table II. The dissections were characterized by anatomic variability (vessel of origin, localized vs diffuse extent, presence or absence of branch vessel involvement) and an unpredictable response of the false lumen (expansion vs regression [thrombosis] vs no change, rate of change) to conservative management. Successful responses to conservative management occurred in both localized (Fig 1) and diffuse (Fig 2) disease either with (Fig 2) or without (Fig 1) branch vessel involvement. The false lumen(s) in those patients, in general, would gradually regress in size over (several months) time until complete obliteration of the false lumen with unimpeded distal patency was achieved (Fig 1, c). This group also included 2 patients with recently diagnosed SSD and limited follow-up (mean 2.0 months). These 2 patients remained asymptomatic and had ongoing regression of false lumen size but had not yet achieved complete obliteration of the false lumen while receiving conservative management. Endovascular stent placement (n ⫽ 2) or laparotomy/ mesenteric bypass (n ⫽ 2) was performed either at initial diagnostic imaging (n ⫽ 1) or following failed medical management (n ⫽ 3) in 4 patients for specific indications
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Fig 2. Computed tomographic scan three-dimensional (3D) reconstruction of a 55-year-old female with a diffuse celiac artery dissection extending to and involving the origins of all major branch vessels.
Fig 1. Computed tomographic scan cross-section (a) and threedimensional (3D) reconstruction (b and c) views of a 43-year-old female treated with conservative management only demonstrating (a) classic “double-lumen” sign (arrow) on initial study, (b) localized celiac artery dissection at time of initial diagnosis, and (c) complete resolution of dissection with thrombosis of false lumen and unimpeded distal flow at 9-month follow-up. Interval staged examinations (not depicted) had demonstrated gradual reduction in size of false lumen.
that included persistent symptoms (n ⫽ 3), expansion of false lumen (n ⫽ 3), and/or radiologic malperfusion (n ⫽ 3). In this study, our patients with a radiologic diagnosis of malperfusion had near-occlusion of true lumen flow, exceeding our diagnostic criteria of 80% compromise of true lumen flow in each case. Failure of conservative management occurred in 3 patients who required intervention. The first patient had worsening pain at 2 days and distal propagation of dissection, occurring in two separate mesenteric vessels. The second patient had recurrent pain at 30 days with CTA documentation of both false lumen expansion and malperfusion. The third patient remained normotensive and asymptomatic following hospital discharge. However, routine follow-up CTA at 30 days demonstrated the presence of malperfusion (Fig 3, a, b) and expansion of false lumen (Fig 3, b, c). The patient was treated with endovascular stent placement (Fig 3, d). In the 2 remaining patients, 1 had malperfusion (near occlusion of true lumen) (Fig 4) at time of initial diagnosis, requiring immediate intervention (endovascular stent placement) and the other had a complex distal perfusion pattern in which major branch vessel perfusion originated from both the true and false lumens (Fig 5). In that patient with a superior mesenteric artery (SMA) dissection, the true lumen supplied one proximal colic branch and the false lumen supplied a replaced right hepatic artery and all remaining colic branches. The false lumen in this patient has remained patent and unchanged in size at 36-month follow-up and is considered a stable, chronic dissection. Open operative procedures were used in 1 patient with concomitant celiac artery dissection and SMA stenosis that required concomitant revascularization, and in 1 patient with concomitant celiac and SMA dissections. The remaining 2 patients who required intervention were treated with endovascular stent placement using either self-expanding (Wallstent; Boston Scientific, Natick, Mass) or balloon-expandable (Genesis; Cordis Corp, Warren, NJ) bare metal devices.
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Fig 3. Computed tomographic scan cross-section (a) and three-dimensional (3D) reconstructions (b, c, and d) of a hemodynamically stable, asymptomatic 53-year-old male with a celiac artery dissection undergoing conservative management at 30 days follow-up demonstrating (a) malperfusion (near occlusion of true lumen), see arrow; (a, b) false lumen expansion (16.3 ⫻ 9.4 mm vs 9.0 ⫻ 5.0 mm at initial diagnosis), note mechanical compression of true lumen by the expanded false lumen, see arrow; (c) key pre-intervention anatomy notable for false lumen/dissection origin at distal celiac artery with uninvolved origins of major branch vessels; and (d) completion study following endovascular stent placement confirming complete regression with thrombosis of false lumen and unimpeded patency of major branch vessels (left gastric, splenic, and common hepatic arteries).
All patients were asymptomatic after successful nonoperative management or following intervention. No morbidity occurred. Upon complete follow-up (mean 13.4 months, range, 2 to 36 months), all patients remained asymptomatic. Preservation of distal perfusion with either thrombosis or ongoing regression of false lumen was achieved in 5 patients treated with only non-operative management and in 4 patients following intervention. In those patients, limited follow-up (mean 2.0 months) in two recent cases treated with conservative management only accounted for the finding of ongoing regression without thrombosis. In contrast, extended follow-up in the remaining patients demonstrated either immediate thrombosis of false lumen after intervention or delayed thrombosis after several months in patients receiving conservative management only. Endovascular and operative interventions produced similar outcomes in a small number of patients with limited follow-up. A stable, chronic dissection was present in 1 patient who had only non-operative management.
DISCUSSION Over the last 3 decades, the development and application of diagnostic methods, the evolving clarification of natural history, and the development and application of therapeutic techniques for spontaneous splanchnic dissections have been directly influenced by technological advances. Prior to 1975, all known cases of SSD were reported following either general necropsy series or the demise of the individual patient.1,2 Although angiography alone was used to diagnose several initial cases after 1975, the development and use of first generation computed tomography scanners proved to be a more effective screening tool than any other existing technique in patients with this problem.3-6 In contrast to a 100% mortality rate in 11 reported cases before 1975, only two deaths have been reported since that time.2,7,8 Between 1975 and 2008, 31 cases of spontaneous celiac artery dissection and 74 cases of spontaneous SMA dissection have been reported.2,8-14 The
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Fig 5. Computed tomographic scan sagittal view of superior mesenteric artery dissection in a 54-year-old male with the true lumen providing perfusion of first major colic branch and false lumen providing perfusion of a replaced right hepatic artery and all remaining colic branches. The false lumen remained patent and unchanged in size on follow-up, constituting a stable, chronic dissection.
Fig 4. Computed tomographic scan sagittal view (a) and three-dimensional (3D) reconstruction (b) of superior mesenteric artery dissection in a 49-year-old male demonstrating distal malperfusion due to mechanical compression of true lumen by false lumen (see arrows) at time of initial diagnosis that required placement of endovascular stent.
disparity in outcomes between the two time periods is not believed to reflect a changing pattern but rather the lack of an effective diagnostic screening method prior to 1975 and the hesitancy of investigators to report adverse outcomes or bad results in the small number of patients with this problem since 1975.15 Although mortality has been less frequently documented, SSD has been reported to have caused splenic infarction,16,17 obstructive jaundice,18 bowel infarction,7,19-22 and diffuse obliteration of small mesenteric vessels that required bowel transplantation.2 Although the 11 SSDs in this report may reflect an unusual clustering of infrequent events, the introduction of multi-slice CTA and its aggressive use in patients with abdominal pain of uncertain origin may account for the number of cases, suggesting that the true incidence of this problem has been underestimated. This hypothesis is further supported by a recent series from Japan with 19 patients that used similar diagnostic screening protocols.11 Treatment regimens have also evolved over time, having been influenced separately by an increased understanding of
the natural history of the problem and advances in technology. Initial cases were treated successfully with open resection and either bypass or transposition of the distal artery.3,4 In 1994, Ambo et al23 reported the successful, non-operative (conservative) management of an SMA dissection with subsequent thrombosis of the false lumen and preservation of distal flow. However, this approach has not proven to be universally successful. Following the initial success of Ambo and associates, 10 consecutive patients with SSD in separate case reports over a span of 7 years were initially treated with non-operative therapy.24-31 Of those patients, 3 (30.0%) required late (mean 6.7 months) conversion to an open or endovascular intervention.28-30 Over that same time period, an additional 5 patients in separate case reports were treated immediately with either an open or endovascular intervention.32-36 Endovascular stent placement was introduced as follow-up therapy for failed medical management in 200028 and as primary therapy in 2004.15 Short-term follow-up has not documented any morbidity. However, the use of endovascular stents for treatment of iatrogenic splanchnic dissections has been associated with infrequent vessel restenosis.37,38 Despite a limited number of patients in this study, variability was found with respect to extent of dissection (localized vs diffuse), involvement of branch vessels, false lumen natural history (expansion vs regression vs no change), and rate of change. Furthermore, absence of either clinical symptoms or hemodynamic instability did not preclude the delayed occurrence of either radiologic malperfusion or false lumen expansion. The small number of patients in this study precluded an effective identification of prognostic risk factors. The general absence of concomitant aortic disease, mesenteric atherosclerosis, and a history of connective tissue disorders in such patients in both this and other reports have led others to suggest alternative etiologic factors including segmental arterial mediolysis, adventitial inflammation, and disruption of the
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internal elastic lamina.8,39 The presence of a localized dissection process as described here and in other reports may represent part of a pathologic continuum that also includes penetrating ulcer, pseudoaneurysm, and aneurysm.40 While etiology and natural history remain poorly-defined in these patients, the radiologic findings of “double-lumen” sign on sagittal (Figs 4, a and 5, a) and cross-section (Fig 1, a) CTA views; false lumen expansion and subsequent compression of true lumen flow in the absence of extrinsic compression due to contiguous, extravascular tissue (Fig 3, a, b, c, and Fig 4); narrow false lumen orifice; and the ability to effectively treat this problem with bare-metal stents (Fig 3, d and Fig 4, a) have separated this problem from other vascular pathology. A major concern regarding management of these patients is identification of a “trigger” that would initiate either operative or endovascular intervention in order to preclude adverse sequelae. Our management decisions were guided by two major influences, natural history behavior in a limited number of previously reported patients with the problem, and physiologic principles derived from surgical management of dissections in other locations. Non-operative (conservative) therapy is warranted in hemodynamically stable patients with either acute SSD without anatomic malperfusion or chronic SSD without recurrent symptoms, expanding false lumen, or malperfusion. This is justified on the basis of known spontaneous regression of certain SSDs,23 the infrequent occurrence (one reported case) of rupture,8 and the documented tendency of chronic descending aorta and descending aortic branch dissections to demonstrate slow rather than abrupt or rapid change, permitting effective serial imaging in followup.41,42 In contrast, immediate operative or endovascular intervention is warranted if any of the previously documented adverse sequelae of SSD are believed to be imminent. Anatomic (vascular) malperfusion may generate thromboemboli or produce direct end-organ ischemia, resulting in a morbid outcome.16,17,19-22 Persistent symptoms, primarily pain, may be indicative of either undetected propagation of dissection, expansion of false lumen, or ischemia.42,43 Froment et al15 reported that patients with symptomatic lesions at presentation are more likely to fail conservative management, having identified a 50% failure rate in patients with such lesions. Expansion of false lumen may cause either rupture or, as demonstrated in this study, malperfusion secondary to mechanical compression of true lumen flow (Fig 3, a, b).8 Svensson et al41 reviewed dissection physiology and reported that “growth begets faster growth,” suggesting that any growth will exponentially increase over time and mandating close follow-up if immediate intervention is not undertaken. The inability to predict either regression or expansion for any specific SSD false lumen, the onset of late malperfusion and false lumen expansion in the absence of either symptoms or hemodynamic instability in this study, and literature documentation of several cases requiring late conversion of non-operative management to direct intervention mandates life-long serial imaging as part of follow-up in patients with a chronic dissection.6,29,30,44,45
This study summarizes our framework and justification for management of patients with such problems. In this small study, we experienced a conservative management failure rate of 33% and a chronic dissection rate of 10%. Our conservative management failure rate was similar to the 38.5% overall failure rate in 13 patients analyzed by Froment et al15 in a comprehensive literature review of management outcomes in patients with spontaneous SMA dissections. In contrast to those findings, Takayama et al11 in a recent study reported that only 1 (5.2%) of their 19 patients required either operative or endovascular intervention. Furthermore, 13 (68.4%) of their patients had patent and unchanged size of the dissection false lumens on follow-up imaging, constituting chronic dissections. The presence of such dissections are of special concern and necessitate close follow-up, having been associated with the late conversion of non-operative management to either operative or endovascular intervention in several cases.6,29,30,44,45 Studies of dissections at other locations have reported that a patent false lumen increases the risk of an adverse outcome.46-48 Although all patients in this study were symptomatic at presentation, 63.2% of the 19 patients studied by Takayama et al11 were asymptomatic and found incidentally after radiologic evaluation for other reasons. This may account for the larger number of chronic dissections and fewer patients requiring intervention in that study. We conclude that successful outcomes following SSD may be achieved with either non-operative therapy alone or intervention if persistent symptoms, expansion of false lumen, and/or radiologic malperfusion occur. Dissection is a dynamic and unpredictable process. In the absence of hypertension, change may occur less rapidly in this location than in the proximal aorta. However, the unpredictable response of the false lumen to conservative management mandates close, lifelong follow-up. In this study, endovascular and operative interventions had similar outcomes in a small number of patients with limited follow-up. The specific application of either interventional technique should be tailored to the needs of the individual patient since each technique offers different advantages and disadvantages. Although SSD is currently perceived as rare, the increasing use of CTA may prove that the true incidence of SSD has been underestimated. AUTHOR CONTRIBUTIONS Conception and design: TT, JM, JH, FR, TR Analysis and interpretation: TT, JM, JH, FR, TR Data collection: TT, JM, JH, TR Writing the article: TT, JM Critical revision of the article: TT, JM, JH, FR, TR Final approval of the article: TT, JM, JH, FR, TR Statistical analysis: TT, JM, JH, FR, TR Obtained funding: TT, JM, JH, FR, TR Overall responsibility: TT, JM, JH, FR, TR REFERENCES 1. Foord AG, Lewis RD. Primary dissecting aneurysms of peripheral and pulmonary arteries: dissecting hemorrhage of media. Arch Pathol 1959;68:553-77.
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2. Morris JT, Guerriero J, Sage JG, Mansour MA. Three isolated superior mesenteric artery dissections: update of previous case reports, diagnostics, and treatment options. J Vasc Surg 2008;47:649-53. 3. Sisteron A, Vieville C. Aneurysmes des arteres a desstinee digestive. Observations personnelles. In: Courbier R (editor); Chirurgie des arteriopathies digestives. Expansion Scientifique Francaise. Paris; 1975 p. 197-202. 4. Rignault D, Pailler JL, Molinie C, Brillac J, Pagliano G. Un cas d’aneurysme dissequant de l’origine de la mesenterique superieure. Angiologie 1976;28:29-34. 5. Krupski WC, Effeney DJ, Ehrenfeld WK. Spontaneous dissection of the superior mesenteric artery. J Vasc Surg 1985;2:731-4. 6. Takahara Y, Takahashi M, Fukaya T, Kaneko M, Koyano K, Sakaguchi S. Computed tomography of isolated dissecting aneurysm of superior mesenteric artery. J Comput Assist Tomogr 1988;12:678-80. 7. Sartelet H, Fedaoui-Delalou D, Capovilla M, Marmonier MJ, Pinteaux A, Lallement PY. Fatal hemorrhage due to an isolated dissection of the superior mesenteric artery. Intensive Care Med 2003;29:505-6. 8. Kobayashi M, Mellen PF. A gastric artery aneurysm complicated by a dissection of gastric and hepatic arteries: possible role of adventitial inflammation and disruption of internal elastic lamina in splanchnic artery dissection. Am J Forensic Med Pathol 2008;29:191-5. 9. Poylin V, Hile C, Campbell D. Medical management of spontaneous celiac artery dissection: case report and literature review. Vasc Endovascular Surg 2008;42:62-4. 10. Glehen O, Feugier P, Aleksic Y, Delannoy P, Chevalier JM. Spontaneous dissection of the celiac artery. Ann Vasc Surg 2001;15:687-92. 11. Takayama T, Miyata T, Shirakawa M, Nagawa H. Isolated spontaneous dissection of the splanchnic arteries. J Vasc Surg 2008;48:329-33. 12. Casella IB, Bosch MA, Sousa WO Jr. Isolated spontaneous dissection of the superior mesenteric artery treated by percutaneous stent placement: case report. J Vasc Surg 2008;47:197-200. 13. Watring NJ, Smith CM, Stokes GK, Counselman FL. Spontaneous superior mesenteric artery (SMA) dissection: an unusual cause of abdominal pain. J Emerg Med 2008 Jan 2. [Epub ahead of print]. 14. Tsai JL, Wu YL, Lin HJ. Spontaneous superior mesenteric artery (SMA) dissection. J Emerg Med 2008;35:81-2. 15. Froment P, Alerci M, Vandoni RE, Bogen M, Gertsch P, Galeazzi G. Stenting of a spontaneous dissection of the superior mesenteric artery: a new therapeutic approach? Cardiovasc Intervent Radiol 2004;27:529-32. 16. Matsuo R, Ohta Y, Ohya Y, Kitazono T, Irie H, Shikata T, et al. Isolated dissection of the celiac artery–a case report. Angiology 2000;51:603-7. 17. Woolard JD, Ammar AD. Spontaneous dissection of the celiac artery: a case report. J Vasc Surg 2007;45:1256-8. 18. Bret PM, Partensky C, Bretagnolle M, Paliard P, Burke M. Obstructive jaundice by a dissecting aneurysm of celiac axis and hepatic artery. Dig Dis Sci 1987;32:1431-4. 19. Murata N, Yamada M, Takaba T, Suzuki K, Hashimoto T, Lee M. Surgical treatment for dissection of superior mesenteric artery. Jpn J Vasc Surg 1997;6:827-33. 20. Javerliat I, Becquemin JP, d’Audiffret A. Spontaneous isolated dissection of the superior mesenteric artery. Eur J Vasc Endovasc Surg 2003;25:180-4. 21. Oda N, Furihata T, Nagata H, Mikami H, Sakuma A, Kabota K. A case of bowel necrosis due to dissection of the superior mesenteric artery with portal gas. Nihon Rinsho Geka Gakkai Zasshi 2003;64:361-5. 22. Suzuki S, Furui S, Kohtake H, Sakamoto T, Yamasaki M, Furukawa A, et al. Isolated dissection of the superior mesenteric artery: CT findings in six cases. Abdom Imaging 2004;29:153-7. 23. Ambo T, Noguchi Y, Iwasaki H, Kondo J, Matsumoto A, Suzuki H, Takamura Y. An isolated dissecting aneurysm of the superior mesenteric artery: report of a case. Surg Today 1994;24:933-6. 24. Hyodoh H, Hyodoh K, Takahashi K, Yamagata M, Kanazawa K. Three dimensional CT imaging of an isolated dissecting aneurysm of the superior mesenteric artery. Abdom Imaging 1996;21:515-6. 25. Nakamura K, Nozue M, Sakakibara Y, Kuramoto K, Satoh M, Kobayashi S, et al. Natural history of a spontaneous dissecting aneurysm of the proximal superior mesenteric artery: report of a case. Surg Today 1997;27:272-4. 26. Dushnitsky T, Peer A, Katzenelson L, Strauss S. Dissecting aneurysm of the superior mesenteric artery: flow dynamics by color Doppler sonography. J Ultrasound Med 1998;17:781-3.
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27. Yasuhara H, Shigematsu H, Muto T. Self-limited spontaneous dissection of the main trunk of the superior mesenteric artery. J Vasc Surg 1998;27:776-9. 28. Leung DA, Schneider E, Kubik-Huch R, Marincek B, Pfammatter T. Acute mesenteric ischemia caused by spontaneous isolated dissection of the superior mesenteric artery: treatment by percutaneous stent placement. Eur Radiol 2000;10:1916-9. 29. Sparks SR, Vasquez JC, Bergan JJ, Owens EL. Failure of nonoperative management of isolated superior mesenteric artery dissection. Ann Vasc Surg 2000;14:105-9. 30. Sheldon PJ, Esther JB, Sheldon EL, Sparks SR, Brophy DP, Oglevie SB. Spontaneous dissection of the superior mesenteric artery. Cardiovasc Intervent Radiol 2001;24:329-31. 31. Kodaira M, Fukaya T. Gastrointestinal: isolated and spontaneous dissection of the superior mesenteric artery. J Gastroenterol Hepatol 2001;16:933. 32. Ando M, Ito M, Mishima Y. Spontaneous dissecting aneurysm of the main trunk of the superior mesenteric artery: report of a case. Surg Today 1995;25:468-70. 33. Barmeir E, Halachmi S, Croitoru S, Torem S. CT angiography diagnosis of spontaneous dissection of the superior mesenteric artery. AJR Am J Roentgenol 1998;171:1429-30. 34. Iha K, Nakasone Y, Nakachi H, Horikawa Y, Gushiken M, Matsuda H. Surgical treatment of spontaneous dissection of the superior mesenteric artery: a case report. Ann Thorac Cardiovasc Surg 2000;6:65-9. 35. Wadhwani R, Modhe J, Pandey K, Gujar S, Sukthankar R. Color Doppler sonographic diagnosis of dissecting aneurysm of the superior mesenteric artery. J Clin Ultrasound 2001;29:247-9. 36. Gouëffic Y, Costargent A, Dupas B, Heymann MF, Chaillou P, Patra P. Superior mesenteric artery dissection: case report. J Vasc Surg 2002;35: 1003-5. 37. Loomer DC, Johnson SP, Diffin DC, DeMaioribus CA. Superior mesenteric artery stent placement in a patient with acute mesenteric ischemia. J Vasc Interv Radiol 1999;10:29-32. 38. Sheeran SR, Murphy TP, Khwaja A, Sussman SK, Hallisey MJ. Stent placement for treatment of mesenteric artery stenoses or occlusions. J Vasc Interv Radiol 1999;10:861-7. 39. Slavin RE. Segmental arterial mediolysis: course, sequelae, prognosis, and pathologic-radiologic correlation. Cardiovasc Pathol 2008, Nov 20. [Epub ahead of print]. 40. Attia C, Villard J, Boussel L, Farhat F, Robin J, Revel D, Douek P. Endovascular repair of localized pathological lesions of the descending thoracic aorta: midterm results. Cardiovasc Intervent Radiol 2007;30:628-37. 41. Svensson LG, Kouchoukos NT, Miller DC, Bavaria JE, Coselli JS, Curi MA, et al. Expert consensus document on the treatment of descending thoracic aortic disease using endovascular stent-grafts. Ann Thorac Surg 2008;85(1 Suppl):S1-41. 42. Pochettino A, Bavaria JE. Aortic dissection. In: Kaiser LR, Kron IL, Spray TL (editors); Mastery of cardiothoracic surgery. Lippincott Williams & Wilkins, Philadelphia, PA; 2007. p. 534-44. 43. Oda T, Ono H, Muranaka H, Takai F. The right gastroepiploic artery as an alternative inflow source in acute mesenteric ischemia. J Vasc Surg 2005;41:1061-4. 44. Cormier F, Ferry J, Artru B, Wechsler B, Cormier JM. Dissecting aneurysms of the main trunk of the superior mesenteric artery. J Vasc Surg 1992;15:424-30. 45. Fenoglio L, Allione A, Scalabrino E, Alberto G, Benedetti V, Pomero F, et al. Spontaneous dissection of the celiac artery: a pitfall in the diagnosis of acute abdominal pain. Presentation of two cases. Dig Dis Sci 2004;49:1223-7. 46. Bernard Y, Zimmermann H, Chocron S, Litzler JF, Kastler B, Etievent JP, et al. False lumen patency as a predictor of late outcome in aortic dissection. Am J Cardiol 2001;87:1378-82. 47. Szeto WY, McGarvey M, Pochettino A, Moser GW, Hoboken A, Cornelius K, et al. Results of a new surgical paradigm: endovascular repair for acute complicated type B aortic dissection. Ann Thorac Surg 2008;86:87-93; discussion 93-4. 48. Tsai TT, Evangelista A, Nienaber CA, Myrmel T, Meinhardt G, Cooper JV, et al. Partial thrombosis of the false lumen in patients with acute type B aortic dissection. N Engl J Med 2007;357:349-59. Submitted Jan 6, 2009; accepted Feb 21, 2009.
Spontaneous splanchnic dissection: Application and timing of therapeutic options Thomas J. Takach, MD, Jeko M. Madjarov, MD, Jeremiah H. Holleman, MD, Francis Robicsek, MD, and Timothy S. Roush, MD, Charlotte, NC Background: Spontaneous splanchnic dissection (SSD) occurs infrequently and has a poorly defined natural history. Few studies address the application, timing, and consequences of therapeutic options. Our goal was to apply conservative (non-operative) management in the care of each patient, reserving interventions for specific indications that may be predictive of adverse outcomes. Methods: Between 2003 and 2008, 10 consecutive patients (mean age 54.7-years-old, 70.0% male) presented with 11 SSDs involving either the celiac artery (n ⴝ 6), superior mesenteric artery (n ⴝ 3), or both (n ⴝ 1). Each patient had acute, spontaneous onset of persistent abdominal pain and was diagnosed with SSD following multidetector row computed tomographic angiography (CTA). Non-operative management (anticoagulation, anti-impulse therapy, analgesics, and serial CTA examinations) was initially used in 9 patients. Endovascular (n ⴝ 2) or operative (n ⴝ 2) intervention was performed either immediately (n ⴝ 1) or following failed medical management (n ⴝ 3) in 4 patients for specific indications that included persistent symptoms (n ⴝ 3), expansion of false lumen (n ⴝ 3), and/or radiologic malperfusion (n ⴝ 3). Results: All patients were asymptomatic after successful non-operative management or following intervention. No morbidity occurred. Upon complete follow-up (mean 13.4 months, range, 2 to 36 months), all patients remained asymptomatic. Preservation of distal perfusion with either thrombosis or ongoing regression of false lumen was achieved in 5 patients who received only non-operative management and in 4 patients following intervention. A stable chronic dissection was present in 1 patient who had only non-operative management. Conclusion: Successful outcomes following SSD may be achieved with either non-operative therapy alone or intervention if persistent symptoms, expansion of false lumen, and/or malperfusion occur. The unpredictable response of the false lumen to conservative management mandates close, long-term follow-up. Endovascular and operative interventions produced similar outcomes in a small number of patients with limited follow-up. Although SSD is currently perceived as rare, the increasing use of CTA may prove that the true incidence has been underestimated. ( J Vasc Surg 2009;50:557-63.)
Spontaneous splanchnic dissection (SSD) is uncommon and few studies address the application, timing, and consequences of therapeutic options. The natural history of this problem is ill defined. Selective cases have been known to undergo spontaneous resolution with thrombosis of false lumen and preservation of distal flow. However, other cases have been associated with both significant morbidity and mortality. In this small study, our goal was to apply conservative (non-operative) management in the care of each patient, reserving the use of interventions for specific indications that may be predictive of adverse outcomes. METHODS Between 2003 and 2008, 10 consecutive patients (mean age 54.7 years, 70.0% male) presented to our institution with 11 SSDs involving either the celiac artery (n ⫽ 6), superior mesenteric artery (n ⫽ 3), or both (n ⫽ 1). The From the Department of Cardiothoracic and Vascular Surgery, Carolinas Heart Institute, Carolinas Health Care System. Competition of interest: none. Presented in part at the Thirty-third Annual Meeting of the Southern Association for Vascular Surgery, Tucson, Ariz, January 14-17, 2009. Reprint requests: Thomas J. Takach, MD, Department of Cardiothoracic and Vascular Surgery, Carolinas Heart Institute, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232-2861 (e-mail: tjtakach@ netscape.net). 0741-5214/$36.00 Copyright © 2009 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. doi:10.1016/j.jvs.2009.02.244
demographic data and risk factors for these patients are summarized in Table I. Although 4 patients had a history of well-controlled hypertension, all patients were normotensive upon initial evaluation. Each patient had acute spontaneous onset of persistent abdominal pain and was diagnosed with SSD following multidetector row computed tomographic angiography (CTA). Each initial CTA examination was performed within 24 hours following onset of symptoms. No patient had concomitant aortic disease, including dissection, aneurysm, or significant atherosclerosis. One patient had significant atherosclerosis involving the major, concomitant (non-dissected) mesenteric vessel. On the basis of anatomic findings at initial diagnostic imaging, each patient received either immediate intervention or non-operative therapy (anticoagulation, anti-impulse therapy, analgesics, and serial CTA examinations) (Table II). The primary anatomic determinant regarding decisionmaking at this point was the presence or absence of malperfusion. Malperfusion was defined as greater than 80% compromise of the true lumen, comparing the smallest true lumen diameter with a reference diameter of contiguous, parallel, non-dissected vessel. Malperfusion syndrome was defined as the morbid consequences of either diminished or absent flow due to dissection. In the absence of malperfusion, non-operative (conservative) management was initially used in 9 patients. The patients receiving conservative management were discharged following initial diagnosis upon resolution of symptoms. Staged 557
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Table I. Patient demographics, risk factors, and management Management
Patients Mean age (range) Gender Male Female Hypertension Tobacco use Diabetes mellitus Coronary artery disease Peripheral vascular occlusive disease Dyslipidemia Chronic obstructive pulmonary disease
Intervention (open/endovascular)
Conservative (non-operative)
10 (100%) 54.7 years (42-75 years)
4 (40.0%)
6 (60.0%)
7 (70.0%) 3 (30.0%) 4 (40.0%) 4 (40,0%) 0 (0) 3 (30.0%) 1 (10.0%) 2 (20.0%) 1 (10.0%)
4 (40.0%) 0 2 (20.0%) 2 (20.0%) 0 1 (10.0%) 1 (10.0%) 1 (10.0%) 0
3 (30.0%) 3 (30.0%) 2 (20.0%) 2 (20.0%) 0 2 (20.0%) 0 1 (10.0%) 1 (10.0%)
Table II. Dissection characteristics and outcomesa Dissections Vessel of origin Celiac artery Superior mesenteric artery Extent Localized Diffuse Branch vessel involvement Present Absent False lumen natural history* Regression or thrombosis* Expansion* No change* Mean follow-up (range) (10 patients) Outcome (by patienta) Spontaneous regression Chronic dissection Intervention Type Endovascular stent Laparotomy Laparotomy/bypass Timing Immediate Delayed Mean time (range) Indication Persistent symptoms False lumen expansion Malperfusion
11 (100%) 7 (63.6%) 4 (36.4%) 4 (36.4%) 7 (63.6%) 8 (72.7%) 3 (27.3%) 6 (60.0%) 3 (30.0%) 1 (10.0%) 13.4 months (2-36 months) 5 (50.0%) 1 (10.0%) 4 (40.0%) 2 (20.0%) 1 (10.0%) 1 (10.0%) 1 (10.0%) 3 (30.0%) 20 days (2-30 days) 3 (30.0%) 3 (30.0%) 3 (30.0%)
*Excludes dissection in patient treated with immediate intervention. a Includes 11 dissections in 10 patients.
follow-up CTA examinations were performed in each patient at 30 days, then every 3 months until complete regression (thrombosis) of false lumen. Anticoagulation was continued empirically until follow-up CTA examination demonstrated either regression or unchanged diameter of false lumen. Antiimpulse therapy included continuation of antihypertensive therapy in those patients previously receiving such medication and the addition of beta-blockade therapy until CTA documentation of false lumen thrombosis.
The initial CTA finding of malperfusion or follow-up CTA findings of delayed-onset malperfusion, distal propagation of dissection, or expansion of false lumen were specific indications for intervention. The presence of persistent, worsening, or recurrent pain at any time following initial diagnosis prompted a full investigation including repeat CTA examination in order to determine cause. In patients requiring intervention, less invasive endovascular techniques were used preferentially. Open operative procedures were used when assessment of bowel viability was mandated by the individual case. Following endovascular intervention, patients were discharged on dual (aspirin and clopidogrel) anti-platelet therapy after radiologic imaging confirmed elimination of false lumen flow, unimpeded true lumen flow, and patency of branch vessels. RESULTS Dissection characteristics and outcomes are summarized in Table II. The dissections were characterized by anatomic variability (vessel of origin, localized vs diffuse extent, presence or absence of branch vessel involvement) and an unpredictable response of the false lumen (expansion vs regression [thrombosis] vs no change, rate of change) to conservative management. Successful responses to conservative management occurred in both localized (Fig 1) and diffuse (Fig 2) disease either with (Fig 2) or without (Fig 1) branch vessel involvement. The false lumen(s) in those patients, in general, would gradually regress in size over (several months) time until complete obliteration of the false lumen with unimpeded distal patency was achieved (Fig 1, c). This group also included 2 patients with recently diagnosed SSD and limited follow-up (mean 2.0 months). These 2 patients remained asymptomatic and had ongoing regression of false lumen size but had not yet achieved complete obliteration of the false lumen while receiving conservative management. Endovascular stent placement (n ⫽ 2) or laparotomy/ mesenteric bypass (n ⫽ 2) was performed either at initial diagnostic imaging (n ⫽ 1) or following failed medical management (n ⫽ 3) in 4 patients for specific indications
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Fig 2. Computed tomographic scan three-dimensional (3D) reconstruction of a 55-year-old female with a diffuse celiac artery dissection extending to and involving the origins of all major branch vessels.
Fig 1. Computed tomographic scan cross-section (a) and threedimensional (3D) reconstruction (b and c) views of a 43-year-old female treated with conservative management only demonstrating (a) classic “double-lumen” sign (arrow) on initial study, (b) localized celiac artery dissection at time of initial diagnosis, and (c) complete resolution of dissection with thrombosis of false lumen and unimpeded distal flow at 9-month follow-up. Interval staged examinations (not depicted) had demonstrated gradual reduction in size of false lumen.
that included persistent symptoms (n ⫽ 3), expansion of false lumen (n ⫽ 3), and/or radiologic malperfusion (n ⫽ 3). In this study, our patients with a radiologic diagnosis of malperfusion had near-occlusion of true lumen flow, exceeding our diagnostic criteria of 80% compromise of true lumen flow in each case. Failure of conservative management occurred in 3 patients who required intervention. The first patient had worsening pain at 2 days and distal propagation of dissection, occurring in two separate mesenteric vessels. The second patient had recurrent pain at 30 days with CTA documentation of both false lumen expansion and malperfusion. The third patient remained normotensive and asymptomatic following hospital discharge. However, routine follow-up CTA at 30 days demonstrated the presence of malperfusion (Fig 3, a, b) and expansion of false lumen (Fig 3, b, c). The patient was treated with endovascular stent placement (Fig 3, d). In the 2 remaining patients, 1 had malperfusion (near occlusion of true lumen) (Fig 4) at time of initial diagnosis, requiring immediate intervention (endovascular stent placement) and the other had a complex distal perfusion pattern in which major branch vessel perfusion originated from both the true and false lumens (Fig 5). In that patient with a superior mesenteric artery (SMA) dissection, the true lumen supplied one proximal colic branch and the false lumen supplied a replaced right hepatic artery and all remaining colic branches. The false lumen in this patient has remained patent and unchanged in size at 36-month follow-up and is considered a stable, chronic dissection. Open operative procedures were used in 1 patient with concomitant celiac artery dissection and SMA stenosis that required concomitant revascularization, and in 1 patient with concomitant celiac and SMA dissections. The remaining 2 patients who required intervention were treated with endovascular stent placement using either self-expanding (Wallstent; Boston Scientific, Natick, Mass) or balloon-expandable (Genesis; Cordis Corp, Warren, NJ) bare metal devices.
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Fig 3. Computed tomographic scan cross-section (a) and three-dimensional (3D) reconstructions (b, c, and d) of a hemodynamically stable, asymptomatic 53-year-old male with a celiac artery dissection undergoing conservative management at 30 days follow-up demonstrating (a) malperfusion (near occlusion of true lumen), see arrow; (a, b) false lumen expansion (16.3 ⫻ 9.4 mm vs 9.0 ⫻ 5.0 mm at initial diagnosis), note mechanical compression of true lumen by the expanded false lumen, see arrow; (c) key pre-intervention anatomy notable for false lumen/dissection origin at distal celiac artery with uninvolved origins of major branch vessels; and (d) completion study following endovascular stent placement confirming complete regression with thrombosis of false lumen and unimpeded patency of major branch vessels (left gastric, splenic, and common hepatic arteries).
All patients were asymptomatic after successful nonoperative management or following intervention. No morbidity occurred. Upon complete follow-up (mean 13.4 months, range, 2 to 36 months), all patients remained asymptomatic. Preservation of distal perfusion with either thrombosis or ongoing regression of false lumen was achieved in 5 patients treated with only non-operative management and in 4 patients following intervention. In those patients, limited follow-up (mean 2.0 months) in two recent cases treated with conservative management only accounted for the finding of ongoing regression without thrombosis. In contrast, extended follow-up in the remaining patients demonstrated either immediate thrombosis of false lumen after intervention or delayed thrombosis after several months in patients receiving conservative management only. Endovascular and operative interventions produced similar outcomes in a small number of patients with limited follow-up. A stable, chronic dissection was present in 1 patient who had only non-operative management.
DISCUSSION Over the last 3 decades, the development and application of diagnostic methods, the evolving clarification of natural history, and the development and application of therapeutic techniques for spontaneous splanchnic dissections have been directly influenced by technological advances. Prior to 1975, all known cases of SSD were reported following either general necropsy series or the demise of the individual patient.1,2 Although angiography alone was used to diagnose several initial cases after 1975, the development and use of first generation computed tomography scanners proved to be a more effective screening tool than any other existing technique in patients with this problem.3-6 In contrast to a 100% mortality rate in 11 reported cases before 1975, only two deaths have been reported since that time.2,7,8 Between 1975 and 2008, 31 cases of spontaneous celiac artery dissection and 74 cases of spontaneous SMA dissection have been reported.2,8-14 The
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Fig 5. Computed tomographic scan sagittal view of superior mesenteric artery dissection in a 54-year-old male with the true lumen providing perfusion of first major colic branch and false lumen providing perfusion of a replaced right hepatic artery and all remaining colic branches. The false lumen remained patent and unchanged in size on follow-up, constituting a stable, chronic dissection.
Fig 4. Computed tomographic scan sagittal view (a) and three-dimensional (3D) reconstruction (b) of superior mesenteric artery dissection in a 49-year-old male demonstrating distal malperfusion due to mechanical compression of true lumen by false lumen (see arrows) at time of initial diagnosis that required placement of endovascular stent.
disparity in outcomes between the two time periods is not believed to reflect a changing pattern but rather the lack of an effective diagnostic screening method prior to 1975 and the hesitancy of investigators to report adverse outcomes or bad results in the small number of patients with this problem since 1975.15 Although mortality has been less frequently documented, SSD has been reported to have caused splenic infarction,16,17 obstructive jaundice,18 bowel infarction,7,19-22 and diffuse obliteration of small mesenteric vessels that required bowel transplantation.2 Although the 11 SSDs in this report may reflect an unusual clustering of infrequent events, the introduction of multi-slice CTA and its aggressive use in patients with abdominal pain of uncertain origin may account for the number of cases, suggesting that the true incidence of this problem has been underestimated. This hypothesis is further supported by a recent series from Japan with 19 patients that used similar diagnostic screening protocols.11 Treatment regimens have also evolved over time, having been influenced separately by an increased understanding of
the natural history of the problem and advances in technology. Initial cases were treated successfully with open resection and either bypass or transposition of the distal artery.3,4 In 1994, Ambo et al23 reported the successful, non-operative (conservative) management of an SMA dissection with subsequent thrombosis of the false lumen and preservation of distal flow. However, this approach has not proven to be universally successful. Following the initial success of Ambo and associates, 10 consecutive patients with SSD in separate case reports over a span of 7 years were initially treated with non-operative therapy.24-31 Of those patients, 3 (30.0%) required late (mean 6.7 months) conversion to an open or endovascular intervention.28-30 Over that same time period, an additional 5 patients in separate case reports were treated immediately with either an open or endovascular intervention.32-36 Endovascular stent placement was introduced as follow-up therapy for failed medical management in 200028 and as primary therapy in 2004.15 Short-term follow-up has not documented any morbidity. However, the use of endovascular stents for treatment of iatrogenic splanchnic dissections has been associated with infrequent vessel restenosis.37,38 Despite a limited number of patients in this study, variability was found with respect to extent of dissection (localized vs diffuse), involvement of branch vessels, false lumen natural history (expansion vs regression vs no change), and rate of change. Furthermore, absence of either clinical symptoms or hemodynamic instability did not preclude the delayed occurrence of either radiologic malperfusion or false lumen expansion. The small number of patients in this study precluded an effective identification of prognostic risk factors. The general absence of concomitant aortic disease, mesenteric atherosclerosis, and a history of connective tissue disorders in such patients in both this and other reports have led others to suggest alternative etiologic factors including segmental arterial mediolysis, adventitial inflammation, and disruption of the
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internal elastic lamina.8,39 The presence of a localized dissection process as described here and in other reports may represent part of a pathologic continuum that also includes penetrating ulcer, pseudoaneurysm, and aneurysm.40 While etiology and natural history remain poorly-defined in these patients, the radiologic findings of “double-lumen” sign on sagittal (Figs 4, a and 5, a) and cross-section (Fig 1, a) CTA views; false lumen expansion and subsequent compression of true lumen flow in the absence of extrinsic compression due to contiguous, extravascular tissue (Fig 3, a, b, c, and Fig 4); narrow false lumen orifice; and the ability to effectively treat this problem with bare-metal stents (Fig 3, d and Fig 4, a) have separated this problem from other vascular pathology. A major concern regarding management of these patients is identification of a “trigger” that would initiate either operative or endovascular intervention in order to preclude adverse sequelae. Our management decisions were guided by two major influences, natural history behavior in a limited number of previously reported patients with the problem, and physiologic principles derived from surgical management of dissections in other locations. Non-operative (conservative) therapy is warranted in hemodynamically stable patients with either acute SSD without anatomic malperfusion or chronic SSD without recurrent symptoms, expanding false lumen, or malperfusion. This is justified on the basis of known spontaneous regression of certain SSDs,23 the infrequent occurrence (one reported case) of rupture,8 and the documented tendency of chronic descending aorta and descending aortic branch dissections to demonstrate slow rather than abrupt or rapid change, permitting effective serial imaging in followup.41,42 In contrast, immediate operative or endovascular intervention is warranted if any of the previously documented adverse sequelae of SSD are believed to be imminent. Anatomic (vascular) malperfusion may generate thromboemboli or produce direct end-organ ischemia, resulting in a morbid outcome.16,17,19-22 Persistent symptoms, primarily pain, may be indicative of either undetected propagation of dissection, expansion of false lumen, or ischemia.42,43 Froment et al15 reported that patients with symptomatic lesions at presentation are more likely to fail conservative management, having identified a 50% failure rate in patients with such lesions. Expansion of false lumen may cause either rupture or, as demonstrated in this study, malperfusion secondary to mechanical compression of true lumen flow (Fig 3, a, b).8 Svensson et al41 reviewed dissection physiology and reported that “growth begets faster growth,” suggesting that any growth will exponentially increase over time and mandating close follow-up if immediate intervention is not undertaken. The inability to predict either regression or expansion for any specific SSD false lumen, the onset of late malperfusion and false lumen expansion in the absence of either symptoms or hemodynamic instability in this study, and literature documentation of several cases requiring late conversion of non-operative management to direct intervention mandates life-long serial imaging as part of follow-up in patients with a chronic dissection.6,29,30,44,45
This study summarizes our framework and justification for management of patients with such problems. In this small study, we experienced a conservative management failure rate of 33% and a chronic dissection rate of 10%. Our conservative management failure rate was similar to the 38.5% overall failure rate in 13 patients analyzed by Froment et al15 in a comprehensive literature review of management outcomes in patients with spontaneous SMA dissections. In contrast to those findings, Takayama et al11 in a recent study reported that only 1 (5.2%) of their 19 patients required either operative or endovascular intervention. Furthermore, 13 (68.4%) of their patients had patent and unchanged size of the dissection false lumens on follow-up imaging, constituting chronic dissections. The presence of such dissections are of special concern and necessitate close follow-up, having been associated with the late conversion of non-operative management to either operative or endovascular intervention in several cases.6,29,30,44,45 Studies of dissections at other locations have reported that a patent false lumen increases the risk of an adverse outcome.46-48 Although all patients in this study were symptomatic at presentation, 63.2% of the 19 patients studied by Takayama et al11 were asymptomatic and found incidentally after radiologic evaluation for other reasons. This may account for the larger number of chronic dissections and fewer patients requiring intervention in that study. We conclude that successful outcomes following SSD may be achieved with either non-operative therapy alone or intervention if persistent symptoms, expansion of false lumen, and/or radiologic malperfusion occur. Dissection is a dynamic and unpredictable process. In the absence of hypertension, change may occur less rapidly in this location than in the proximal aorta. However, the unpredictable response of the false lumen to conservative management mandates close, lifelong follow-up. In this study, endovascular and operative interventions had similar outcomes in a small number of patients with limited follow-up. The specific application of either interventional technique should be tailored to the needs of the individual patient since each technique offers different advantages and disadvantages. Although SSD is currently perceived as rare, the increasing use of CTA may prove that the true incidence of SSD has been underestimated. AUTHOR CONTRIBUTIONS Conception and design: TT, JM, JH, FR, TR Analysis and interpretation: TT, JM, JH, FR, TR Data collection: TT, JM, JH, TR Writing the article: TT, JM Critical revision of the article: TT, JM, JH, FR, TR Final approval of the article: TT, JM, JH, FR, TR Statistical analysis: TT, JM, JH, FR, TR Obtained funding: TT, JM, JH, FR, TR Overall responsibility: TT, JM, JH, FR, TR REFERENCES 1. Foord AG, Lewis RD. Primary dissecting aneurysms of peripheral and pulmonary arteries: dissecting hemorrhage of media. Arch Pathol 1959;68:553-77.
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