Conservative Treatment of Spontaneous and Isolated Dissection of Mesenteric Arteries
Article Outline
Background
Isolated and spontaneous dissection of mesenteric arteries is a rare entity; a little more than 50 cases have been reported in medical literature. There is no therapeutic consensus concerning this type of lesion.
Methods
In this study, we report the results of our treatment based on a conservative approach. This retrospective study concerns eight patients with dissection of the celiac trunk and/or of the upper mesenteric artery (UMA) who were treated between 2002 and 2006. Because these patients were not presenting with acute intestinal ischemia diagnosed by clinical examination or paraclinical tests (medical imaging/biology) or with vital complications, they were treated with an efficient anticoagulation (heparin followed by anti-vitamin K) for 3 to 6 months. Endovascular or surgical treatment was used as the first option in patients with obvious intestinal ischemia or likely to have an arterial rupture, and also when medical treatment had failed. Clinical and radiological follow-up was at 1 month, 3 months, 6 months, and 1 year and then every year. Seven men and one woman (mean age, 48.2; age range, 38-53 years) were treated. Six patients presented with isolated dissection (celiac trunk=4, UMA=2). One patient had a celiac trunk and a UMA dissection and one had a celiac trunk and a UMA dissection along with a dissection of his two renal arteries. On entering the hospital, a patient was operated on for mesenteric ischemia related to a stenosis of the upper mesenteric artery (upper aortomesenteric bypass); a covered stent was implanted in the celiac trunk of another patient presenting with a contained rupture.
Results
Both patients were successfully treated. Six patients were medically treated. One of them required an aortohepatic bypass to treat an aneurysmal evolution of the celiac trunk revealed by a computed tomography scan obtained 1 month after the symptoms had begun. In one patient, the dissection remained stable on imaging. Four patients were cured, with a mean 20.1-month follow-up.
Conclusion
Conservative treatment of spontaneous dissections of mesenteric arteries is possible when there are no complications, and it gives satisfactory results provided regular clinical and radiological checking is performed.
Introduction
Spontaneous and isolated dissection of mesenteric arteries (SDMA) is rare. Since 1947, about 55 cases have been reported in the medical literature.1 It is difficult to clinically diagnose SDMA since the symptoms are not very specific. Dissection itself generates violent and isolated abdominal pain, whereas clinical examination and biological tests are, most of the time, normal. This disease becomes all the more serious as hemorrhagic3, 4 or ischemic complications (mainly mesenteric)2 may appear and require urgent treatment.5, 6 Therefore, early SDMA diagnosis is essential since it enables therapeutic actions to prevent these complications.
Noncomplicated SDMA treatment is not properly codified mainly because the common history of this disease is not well known: during the follow-up,7 about 30% of the patients experience complications that are, unfortunately, unpredictable.
For a long time, surgical treatment has been the gold standard. Its main advantage is to propose a final treatment of the dissection. However, it can sometimes be technically difficult to perform and is uselessly invasive for 70% of the patients who will never have any complications.
Medical treatment is simpler. As with carotid dissection, usually anticoagulants are used, but they can only prevent ischemic complications.8 Moreover, some have successfully reported mere supervision without the use of anticoagulants.9, 10
Finally, more recently, many publications have shown that, because of endovascular techniques, it is possible to treat SDMA with stents and coils. 11, 12, 13 These techniques enable the treatment of any type of complication since lesions are short, while keeping in mind that the final decision will depend on the results of the anatomical analysis of the dissection. The main limit of endovascular treatment concerns its durability, for which, in this case, hindsight is lacking. Up to now, no studies have demonstrated that one treatment is better than the other.
During these past years, we have treated eight patients with SDMA, and we found that the incidence of this disease is certainly higher than supposed. Therefore, the aim of this study is to report our experience with conservative treatment at the acute stage, with a focus on clinical and imaging follow-up.
Methods
Between March 2002 and June 2006, eight patients have been treated in our cepartment for SDMA: seven men and one woman (mean age, 48.2 years; age range, 38-53 years).
SDMA was diagnosed by exploration of acute abdominal pains: three patients underwent abdominal ultrasound associated with duplex scan of the mesenteric arteries and five patients underwent abdominal duplex scan. For the three patients who underwent abdominal ultrasound, the diagnosis was confirmed with an angioscanner. Arterial dissection was confirmed when the following criteria were found14:
Every patient underwent a thorough clinical examination, abdominal scan, and a biological check-up including at least complete blood count, ionogram, hepatic and pancreatic tests, and creatinine and lactate levels. From the results of this evaluation, patients were divided into two groups:
Patients (presenting) with no complications were medically treated. Medical treatment consisted of anticoagulation with continuous intravenous administration of sodium heparin (IV bolus of 50 IU/kg, then 500 IU/kg/day) with adjustment of the dose every 4 hours until aPTT is twice or three times the reference level. This treatment was applied for about 7 days and then an angio-computed tomography (CT) scan was performed. If clinical and radiological stability were reached, heparin was replaced by a vitamin K antagonist (VKA) (fluindione, INR of 2-3). This treatment was adapted according to the clinical and CT evolution.
In case of intestinal ischemia, rupture, or suspicion of rupture, surgery was proposed. Every time, when lesions were not too extensive and/or when anatomical condition allowed the use of stents, endovascular treatment was first suggested. As for stents, we are in favor of self-expandable ones. Should ischemia occurs, they have the possibility of reopening the arterial lumen without the absolute necessity of performing balloon angioplasty, which may generate parietal trauma (extension of the dissection, rupture). Moreover, the upper mesenteric artery is an artery with a curved initial portion and is mobile in its intramesenteric part; in this case, we think that nitinol stents are more comfortable and therefore a better choice than balloon expandable stents that are very rigid. In case of rupture, we use a covered self-expandable nitinol stent (Fluency; Bard, Tempe, AZ).
Surgical treatment was the alternative choice when endovascular treatment was not technically possible. Every possible technique of repair was considered, and the final choice was made according to the patient's data (anatomy, extension of the dissection, etc.) and the surgeon's preferences.
Long-term follow-up was the same for every patient. Clinical and radiological follow-up was performed at 1, 3, and 6 months and 1 year and then once a year. Radiological checking was performed with angio-CT with the same operator.
Results
Eight patients were treated for SDMA: they were mainly men and relatively young (mean age, 48.2 years; age range, 38-53 years). Four patients were active smokers, two had arterial hypertension, one had hypercholesterolemia, and one had ankylosing spondylitis treated with an anti-tumor necrosis factor-alpha. On the average, symptoms started 10.7 days (1-21 days) before the diagnosis was made. Functionally, all the patients had sudden abdominal pain, located in the epigastric (n=7) or hypogastric (n=1) regions.
A single patient was experiencing pain when eating, which suggested intestinal ischemia. There were no cases of intestinal transit disorders, such as ileus or bloody diarrhea. In three cases, pains were so acute that patients had to be taken to the emergency department, where abdominal scan was performed to help establish a diagnosis. In five cases, after several days of failure to establish a diagnosis, a diagnosis was finally possible because of abdominal ultrasound (n=3) or CT (n=2).
The eight dissected arteries that generated symptoms were the celiac trunk in four cases and the superior mesenteric artery (SMA) in four cases. In two cases, SMA dissection was associated to other asymptomatic arterial dissections:
In these last two cases, we deemed that the symptomatic artery was the upper mesenteric artery because one patient was presenting with symptoms of mesenteric ischemia. In the other case, this diagnosis was confirmed because the pain was strictly abdominal, with an intimal flap that was thin without thrombotic material in the SMA compared with the celiac trunk and the renal arteries. In six cases, the anatomical aspect of the symptomatic dissected arteries was an intramural hematoma (IMH) and, in two cases, a dissection with two lumens.
On the biological level, a patient with pancreatitis was the only one to present with unequivocal disorders: increasing levels of lipase (435 IU/L) and amylase (567 IU/L) 24 hours after hospital admission and hyperleukocytosis (11.9 g/L).
Right after a diagnosis was made, two patients required emergency treatment. The first patient presented with sudden abdominal pain 15 days before the dissection diagnosis. At first, this abdominal pain was constant but it became progressively linked to food intake, with acute abdominal pain appearing 30 minutes after the meals. Angio-CT revealed an old celiac trunk dissection with a minor aneurysmal evolution and, more important, widespread dissection of the SMA including its origin that was responsible for a reduced perfusion of the digestive track. This patient underwent an upper aortomesenteric venous bypass that suppressed intestinal ischemia symptoms. Thirty-six months after surgery, this patient is still asymptomatic (Fig. 1). The second patient rushed to hospital as he was experiencing a sudden epigastric pain. CT scan showed an IMH of the celiac trunk in association with a voluminous parietal ulceration and a periarterial hematoma that suggested a contained rupture (Fig. 2A). A covered stent was implanted in the celiac trunk (Fig. 2B). Ten months later, this patient is still asymptomatic.
Fig. 1
A. Extensive dissection of the superior mesenteric artery with intestinal ischemia. B. Angiographic control after aortomesenteric venous bypass.
Fig. 2
A. Transverse CT scan of an intramural hematomahematoma of the celiac trunk, with an ulceration (<) a periarterial hematoma leading to the diagnosis of contained rupture (∗). B. Angiographic control after implantation of a stent-graft in the celiac trunk.
Six patients had a conservative treatment with a mean 20.1-month follow-up (range, 4-36 months). Four patients were cured (two celiac trunk and two SMA). Each of these four patients had an IMH dissection (Fig. 3). At a mean 6.5-month follow-up (range, 4-12 months), they were all cured. One of these patients, who was presenting with an ulcerated IMH, is still showing ulcerations on CT scan examination but IMH has disappeared. A patient with a probable diagnosis of segmental arterial mediolysis remains stable on CT scan. A patient with a celiac trunk dissection and ischemic pancreatitis had a rapid aneurysmal evolution after a 1-month evolution. This patient underwent surgical treatment with aneurysmectomy and aortohepatic bypass. Despite early postoperative thrombosis, at present this patient is asymptomatic.
Fig. 3
Angio-CT of the superior mesenteric artery (<) A. Intramural hematoma. B. After a 6-month anticoagulant treatment, no hematoma is visible.
Discussion
SDMA is a rare but not unusual disease that is now more frequently detected because of improvement in imaging techniques and, more specifically, CT scan examination, which is widely used to explore painful acute abdominal syndromes. This can explain why more than half of the SDMA cases have been published after 2000. The treatment for noncomplicated SDMA cases with an acute stage is still debated. For a long time, surgical treatment has been the gold standard,5, 6 but it has progressively given way to anticoagulation treatment and, more recently, to endovascular treatment.11, 12, 13 Unfortunately, medical literature does not provide any data that can assess the superiority of one treatment over the other.
In our study, we have demonstrated that in the acute stage, 75% of SDMA cases can be treated with a conservative medical treatment. In two patients, emergency treatment was necessary because potentially serious complications occurred along with intestinal ischemia and possibility of arterial rupture detected on CT scan.
The diagnosis of noncomplicated SDMA is hard to reach because the main symptom that is represented by pain is common to all the possible SDMA complications, among which acute intestinal ischemia ranks first. Therefore, to choose the appropriate treatment, the surgeon will have to make sure there are no complications that would require emergency treatment. To do so, he or she conducts precise questioning as well as clinical, biological, and imaging examinations. In the case of noncomplicated SDMA, medical treatment is most often chosen. It is an empiric treatment that uses anticoagulants by analogy with the treatment of carotid artery dissections. In these diseases, 90% of ischemic complications originate from embolic rather than hemodynamic causes.15
In our study, the only thrombotic phenomenon we observed was necrosis of the pancreatic tail and of the spleen due to dissection of the splenic artery with a mechanism that a posteriori is difficult to identify.
Five of the six patients who were treated with anticoagulants were presenting with an IMH-type dissection and, in two cases, with ulceration within the hematoma. Inflammatory parietal phenomena linked to the hematoma and subendothelium exposure at the ulceration level can cause local thrombus. Therefore, anticoagulant treatment is all the more likely to be suggested because reduction of arterial lumen caliber caused by IMH may be an added factor that can generate thrombosis by reducing the arterial flow. In our study, we have not noticed any complication related to this treatment, which is in accordance with the literature. As far as the nature of the anticoagulant treatment is concerned, no consensus has been reached yet.
Most authors recommend continuous intravenous administration of heparin (aPPT between 2 and 3) followed by a VKA treatment; however, low-molecular-weight heparin have been recently used with success.1 Some authors also add antiplatelet agents.1, 8 This practice can be justified during the acute stage since the subendothelium exposure is likely to trigger primary hemostasis. But in the long run, this prescription does not appear to be justified because, in these young patients, SDMA does not usually have an arteriosclerosis origin.7 The treatment duration is also empiric. The anticoagulant treatment with VKAs is planned for 3 to 6 months according to clinical evolution and imaging data. For example, patients cured after a 4-month follow-up were no longer given VKA as soon as recovery without any further complications was confirmed.
Two-thirds of our patients who were medically treated were cured within a mean 6.5-month time. All these patients had a dissection with IMH that disappeared progressively, which allowed the artery to be completely restored; a parietal ulceration persisted in one single case. Therefore, we deem that intramural-type SDMA is the best indication for medical treatment. A patient presenting with a typical two-lumen dissection remained stable at imaging follow-up while clinical symptoms had disappeared within a few days. This certainly can be explained by the presence of large entry and exit tear sites at intimal flap level with a fast running flow in the false channel, which prevents thrombosis and perpetuates the lesion.
Finally, in this series, only one patient who had been medically treated required an early surgical treatment for an aneurysmal evolution of the celiac trunk dissection that occurred during the month following the beginning of the symptoms. This dissection with IMH presented with an acute pancreatitis. Therefore, the aneurysmal evolution may have been triggered by local pancreatic enzyme increase, especially elastase, because these enzymes can experimentally generate aneurysms.16
All in all, in our series, the unfavorable rate of medically treated patients is twice smaller than the given reports in the literature in which 30% of the patients require a surgical adjuvant treatment. 7 Of course, these results must be read keeping in mind the small number of patients who were taken in consideration in our study. Should all the patients in the series be brought together, three of eight patients, which represents 37.5%, required a surgical treatment during the month following the beginning of the symptoms.
These results show that patients presenting with SDMA have to be, both clinically and paraclinically, regularly checked especially at the first stage of the disease. We are suggesting performing imaging 1 week after the beginning of the symptoms, at 1, 3, and 6 months, and then every year. The elected technique of imaging is CT scan with contrast injection. It enables a satisfactory spatial resolution to study the dissected vessel and its collateral branches as well as the abdominal viscera irrigated by the pathologic artery. Duplex scan is also an important examination that enables us to evaluate hemodynamic consequences of the dissection but we have not used it for follow-up.
Except for anticoagulant treatment, there is no etiologic SDMA treatment; also, apart from very specific clinical circumstances, etiologic diagnosis is rarely made.7 Because our patients were young and had very little chance of having atheromatosus risk factors, atheromatosus origin is very improbable.
Among our eight patients, one certainly had segmental arterial mediolysis because the lesions were pluripedicular, in the mesenteric and the renal arteries and associated with an aneurysmal jejunal branch of the SMA, but histological confirmation would be needed to make this diagnosis. Except for this patient, no other patients are presenting with clinical or paraclinical signs that could point to a specific diagnosis, even if this notion has most often been reported in the literature.
Finally, as far as the treatment of complications is concerned, all the surgical or endovascular techniques can be potentially used and no preferential treatment can be defined. Each case has to be separately debated taking into consideration the medical environment and the surgeon's habits.
Conclusion
In our study, we have suggested that, when no complications occur (intestinal ischemia, rupture), most patients presenting with SDMA can initially undergo a conservative treatment because, in over 80% of the cases, lesions can be cured or remain stable during the follow-up. This therapeutic approach requires clinical supervision and, above all, regular CT scan examination; even if complications are not frequent, they can always occur during the follow-up.
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PII: S0890-5096(09)00219-2
doi:10.1016/j.avsg.2008.01.016
© 2009 Annals of Vascular Surgery Inc. Published by Elsevier Inc All rights reserved.
