This study described the clinical presentation, follow-up and outcomes of both endovascular and conservative treatments of SICAD. The angle between celiac trunk and the aorta was not significantly different between symptomatic and asymptomatic patients. A total of 76 patients were treated, with 27 receiving endovascular intervention, and all stents remained patent during a median follow up of 27.1 months. 49 patients received conservative treatment, except for one patient whose symptoms recurred 1 year after initial hospitalization, the symptoms of other patients have resolved.
The etiology of SICAD is unknown, with risk factors including hypertension, smoking, atherosclerosis, connective tissue diseases, vasculitis, and congenital disorders causing arterial wall weakening (e.g., Ehlers-Danlos Syndrome) 8–10. Abdominal pain is the most common symptom of SICAD. In our study, the patients exhibited similar characteristics, with approximately half having a history of hypertension and being smokers. Especially, 61 (80.3%) patients presented with symptoms. This emphasizes that although SICAD is rare, after ruling out diseases that can cause abdominal pain, it is necessary to consider whether the patient has SICAD 13. CTA for patients with abdominal pain may allow for the early diagnosis of SICAD.
The anatomic characteristics of SICAD have been previously described, including the mean diameter of celiac artery, intimal flap, extension into distal branches, and hypoperfusion 14, 15. Consistent with previous studies, our cohort showed that the dissection mostly extended to the celiac trunk, with 19.7% of patients also having simultaneous SMA dissection. Additionally, we measured the angle between the celiac trunk and the aorta. The average angle was 58.17 ± 16.04°, and there was no significant difference in the angle between symptomatic and asymptomatic patients. The symptoms of SICAD may not be influenced by the angle between the celiac trunk and the aorta.
The management option depends on the clinical features and hemodynamic status of the patients. Currently, there is no consensus on the treatment of SICAD because of the variability in clinical presentation and the course of the disease. Conservative treatment involves hydration, bowel rest, blood pressure control with antihypertensive agents (beta blockers or non-beta blockers), antithrombotic therapy (anticoagulation or antiplatelets), and antilipidemic therapy 16, 17. Li Cheng et al. 18 suggested that complete remodeling of symptomatic SICAD can be achieved in most patients with conservative treatment within 2 years of diagnosis. However, the comorbidities of SICAD may be complex, and the use of antithrombotic agents should be based on multiple considerations 17. In our study, the symptoms of patients who underwent antithrombotic therapy mostly improved without the need for secondary intervention, and half of the patients showed partial regression on CT follow-up. Only 1 patient without aneurysmal dilation experienced a recurrence of abdominal pain 1 year after initial hospitalization, and CT demonstrated that the celiac trunk dissection was slightly more dilatable than before. After rehospitalization and conservative treatment, symptoms improved and have not recurred since discharge. Regarding the treatment of patients after the recurrence of symptoms, the treatment strategies still need to be determined according on the patients’ conditions.
There is a lack of criterion of endovascular therapy in SICAD. The aims of endovascular treatment are to seal off the false lumen and re-establish blood flow 19. Endovascular treatment options include stent placement, thrombolytic therapy, embolectomy, and balloon angioplasty 20. Indications for endovascular treatment may include persistence or progression of symptoms despite conservative treatment, refractory pain, aneurysmal dilation (especially ≥ 2 cm), extension of dissection, rupture, and suspected bowel ischemia 3, 15, 21, 22. In our study, 20 (26.3%) patients met the criteria for dissection aneurysms (aneurysm diameter 1.5 times that of the celiac trunk), but only 11 patients received endovascular treatment, and none had a diameter ≥ 2 cm. Additionally, a study on spontaneous isolated celiac or superior mesenteric artery dissection showed no ruptures and only one artery greater than 2 cm in 39 patients over a follow-up period of nearly 5 years 23.
A previous retrospective study suggested that endovascular intervention may be necessary in over 50% of symptomatic SICAD patients and showed good long-term patency with rapid symptom resolution 15. In our cohort, 27 (35.5%) patients underwent endovascular intervention. Follow up CT scanning of these 27 patients showed that SICAD exhibited complete or partial regression, and none of the patients needed secondary endovascular intervention. In contrast, follow-up CT scans of patients who underwent conservative treatment showed that SICAD mostly exhibited partial regression or no change. Endovascular treatment had more favorable outcomes in terms of complete remodeling compared to conservative treatment. However, symptoms resolved in all patients in our study regardless of treatment modality.
The current study has some limitations. Firstly, it was a retrospective analysis, which comes with inherent limitations, such as selection bias. Secondly, the sample size was relatively small, and there were some losses during follow-up, potentially impacting the interpretability of the results. Thus, further studies with larger sample sizes and longer follow-up periods are necessary. Thirdly, only a few patients underwent CT rather than CTA during follow-up, and the results of the follow-up CT for these patients might be biased. Finally, the data were obtained from a single center, which may limit the generalizability of the findings.