Impact of Noninvasive Conservative Medical Treatment for Symptomatic Isolated Celiac Artery Dissection

Abstract

Background: There is no definite consensus regarding the management of symptomatic isolated celiac artery dissection (ICAD), and the effect of conservative medical treatment has never been evaluated.

Methods and Results: We enrolled 13 consecutive symptomatic ICAD patients without signs of arterial rupture between 2006 and 2015. All patients received noninvasive conservative medical treatment. The epidemiology, radiological findings and prognostic effect of conservative medical treatment on outcomes were retrospectively assessed. ICAD usually developed in middle-aged men around 50 years old who had a history of smoking. The patients typically presented with acute continuous epigastric pain at rest and with abdominal tenderness on physical examination. On enhanced computed tomography at presentation, the false lumen was found to be double-barreled in 2 patients (15.4%), partially thrombosed in 1 (7.7%), and completely thrombosed in 10 (76.9%). Dissection of associated branches was found in the left gastric artery in 1 patient (7.7%), common hepatic artery in 5 (38.5%), and splenic artery in 7 patients (53.8%). Malperfusion was not found in the stomach or liver but was found in the spleen in 4 patients (30.8%). During a median follow-up period of 376 (165–602) days, all patients were alive without any antiplatelet, anticoagulant, endovascular or surgical treatment.

Conclusions: Symptomatic ICAD without arterial rupture can be safely treated with conservative medical therapy over the short term. (Circ J 2016; 80: 1445–1451)

Arterial dissection is a serious medical condition, typically presenting with severe pain that can lead to impairment or absence of blood flow to peripheral vessels.¹ The thoracic and abdominal aorta is the most commonly involved artery, and strategies to prevent fatal conditions have been reported.^2,3 Although it is relatively rare, arterial dissection can also occur in other peripheral arteries, such as the cervical, coronary, celiac and superior mesenteric arteries.^4–8 Superior mesenteric artery dissection is the most frequent type of digestive artery dissection.^7,8

Symptomatic isolated celiac artery dissection (ICAD) presenting with acute abdominal pain is a very rare medical condition.^9–16 There have been several case reports and reports of small case series, but most of those studies included less than 5 patients, and there is no definite consensus on the management of symptomatic ICAD.^9–16 Some authors have recommended medical treatment with an antiplatelet and an anticoagulant to prevent organ ischemia.^9,17 Others have recommended endovascular or surgical treatment to prevent arterial aneurysm rupture.^10,18,19 On the other hand, we have previously treated these patients medically without any antiplatelet, anticoagulant, endovascular or surgical treatment. The purpose of this study was to investigate and summarize our experience retrospectively with a focus on the epidemiology of symptomatic ICAD, computed tomography (CT) findings and other radiological findings, and to determine the prognostic effect of noninvasive conservative medical treatment on outcomes in patients with symptomatic ICAD.

Methods

Study Population

We retrospectively enrolled 13 consecutive patients with ICAD presenting with acute abdominal pain at the Emergency Department of Hiroshima City Hospital during the period from December 2006 to December 2015, the largest study population so far.^6,9–19 They underwent both unenhanced and contrast-enhanced CT to evaluate the acute abdominal pain, and symptomatic ICAD with or without dissection of its main branches was confirmed by an emergency physician, cardiologist and radiologist. Patients with asymptomatic ICAD, patients with coexisting aortic dissection and patients with visceral artery dissection other than main branches of the celiac artery were excluded. (Radiological findings of all cases have been previously reported as a case report and will be updated in another journal, and we obtained reprint permission for the use of these images from the journal as stated in Figures 1–3). The study protocol complied with the Helsinki Declaration and was approved by the Ethical Committee of Hiroshima City Hospital. The requirement of written informed consent was waived because retrospective data from hospital records were used in this study and there were no interventions involving the study patients. The authors had full access to the data and take responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.

Figure 1.

Computed tomography (CT) findings of celiac artery dissection and 3 major branch dissections. Contrast-enhanced CT at presentation show celiac artery (CA) dissection of the double-barreled (A), partially thrombosed (B), and completely thrombosed (C) types, left gastric artery (LGA) dissection (D), common hepatic artery (CHA) dissection (E), and splenic artery (SA) dissection (F). Reproduced with permission from Ichiba T. J Typ Med Images Video 2016: Case ID 89, 93, 95 and 96 (http://thejtmiv.com, accessed March 5, 2016).

Figure 2.

Splenic ischemia (A–C) and splenic infarction (D–F) associated with extended splenic artery dissection. (A–C) Contrast-enhanced computed tomography (CT) at presentation show the entire spleen has insufficient contrast enhancement and that the lateral side has an enhancement defect in both the arterial (A) and venous (B) phases. However, enhanced CT on day 3 shows the spleen as fully enhanced in the arterial phase (C). (D–F) Contrast-enhanced CT at presentation shows an enhancement defect in the middle of the spleen in both in the arterial (D) and venous phases (E) without improvement on follow-up CT on day 13 (F). Reproduced with permission from Ichiba T. J Typ Med Images Video 2016: Case ID 93 and 95 (http://thejtmiv.com, accessed March 5, 2016).

Figure 3.

Angiographic (A,B) and ultrasonographic (C,D) findings of celiac artery dissection complicated by splenic artery dissection. Angiography shows 99% delayed stenosis in the splenic artery (A) in the early phase with rich collaterals around the spleen (B) in the late phase. Ultrasound shows the celiac artery and superior mesenteric artery but does not show the intimal flap of the celiac artery even after diagnosis of celiac artery dissection by computed tomography (C,D). CA, celiac artery; SA, splenic artery; SMA, superior mesenteric artery. Reproduced with permission from Ichiba T. J Typ Med Images Video 2016: Case ID 92 (http://thejtmiv.com, accessed March 5, 2016).

CT Scanning and Interpretation

CT scanning was performed using an 8-row scanner (BrightSpeed Edge, GE Healthcare) with the following parameters: 360 mA, 120 kV, pitch of 2.5–5.0 mm, and 1.25-mm collimation. Each scanning session began with unenhanced imaging from the upper abdomen to the pelvis. Contrast-enhanced CT scanning was subsequently performed over the same area. Contrast material (iopamidol, 300 mg/ml of iodine; total volume, 100 ml) was injected at a rate of 1.5–2.0 ml/s through a vein using an automated injector. The scan delay of the early arterial phase was 40–50s, and that of the delayed venous phase was 120–150s. Contrast-enhanced CT scans were reconstructed using an Advantage Workstation (GE Healthcare). Diagnosis of ICAD was confirmed by the presence of a true lumen and false lumen separated by an intimal flap on contrast-enhanced CT (Figure 1). According to the type of false lumen, ICAD was classified into 3 categories depending on the findings of the delayed venous phase: double-barreled (false lumen being completely patent), partially thrombosed and completely thrombosed (Figure 1).²⁰ Extended dissection of the main branches of the celiac artery was confirmed in the same way. Malperfusion of the stomach, liver, spleen, and intestine was confirmed by a defect of contrast medium in each organ during the delayed venous phase. The organ was considered to have ischemia if it had a complete or incomplete enhancement defect in the arterial and venous phases on initial CT but had enhancement improvement on follow-up CT. The organ was considered to have infarction if it had a complete enhancement defect on initial CT without any improvement on follow-up CT (Figure 2). The presence or absence of new false lumen enhancement and the celiac artery diameter were also evaluated on follow-up CT scans. The change in celiac artery diameter was classified as expansion or regression compared with the previous CT findings.

Treatment Strategy

Our therapeutic strategy for ICAD was noninvasive conservative medical treatment without any endovascular or surgical treatment. Patients with symptomatic ICAD were usually admitted to the hospital. The baseline initial medical treatment included administration of antihypertensive and analgesic drugs, mainly nonsteroidal anti-inflammatory drugs. No antiplatelet or anticoagulant drugs for preventing organ ischemia were prescribed. Diet was started after a 1- or 2-day period of fasting. The timing of discharge and the timing of follow-up CTs were decided by the attending physician. The rationale for this conservative medical treatment of ICAD is discussed later.

Endpoints and Statistical Analysis

We set the primary endpoint as in-hospital and out-of-hospital death. Categorical variables are shown as percentages (%) and continuous variables are shown as medians (25–75 percentile). Because this study was a retrospective case series study with a small number of patients, we did not perform any hypothetical testing and just report the summary statistics. We obtained information on the following variables from patient records for assessment of epidemiological data: age, sex, body mass index, atherosclerotic risk factors (smoking, hypertension, diabetes and dyslipidemia), onset situation, physical examination findings (pain location, tenderness and rebound), laboratory data (total bilirubin, aspartate aminotransferase, alanine aminotransferase, lactase dehydrogenase, D-dimer and lactate), CT findings, and outcome findings. Statistical analyses were performed using R software package (version 3.1.1, R Development Core Team; https://www.r-project.org/).

Results

We enrolled 13 consecutive patients with symptomatic ICAD from December 2006 to December 2015. Patient characteristics including initial manifestation and laboratory data are summarized in Table 1. ICAD usually developed in middle-aged men around 50 years of age who had a history of smoking. The patients typically presented with acute continuous epigastric pain at rest and with abdominal tenderness on physical examination. Approximately 60% of the patients visited the hospital within 1 day of onset; 11 (84.6%) of the patients were admitted to hospital, and the other 2 were treated as outpatients.

Table 1. Characteristics of Patients With Symptomatic ICAD

	Total (n=13)	Missing
Age (years)	53 (46–58)	0
Male (%)	12 (92.3)	0
Body mass index (kg/m2)	25.6 (23.3–28.1)	0
Atherosclerotic risk factors
Smoking (%)	9 (69.2)	0
Current (%)	4 (30.8)	0
Past (%)	5 (38.5)	0
Never (%)	4 (30.8)	0
Hypertension (%)	4 (30.8)	0
Diabetes (%)	0 (0)	0
Dyslipidemia (%)	4 (30.8)	0
Onset
Acute (%)	13 (100)	0
Rest (%)	11 (84.6)	0
Meal (%)	2 (15.4)	0
Exercise (%)	0 (0)	0
Location and duration of pain
Epigastric (%)	12 (92.3)	0
Left side (%)	5 (38.5)	0
Back (%)	2 (15.4)	0
Continuous (%)	13 (100)	0
Intermittent (%)	0 (0)	0
Physical examination
Tenderness (%)	13 (100)	0
Rebound (%)	0 (0)	0
Systolic BP (mmHg)	154 (149–168)	0
Diastolic BP (mmHg)	90 (94–109)	0
Laboratory data
Total bilirubin (mg/dl)	0.8 (0.7–1.0)	0
Aspartate aminotransferase (IU/L)	25 (24–27)	0
Alanine aminotransferase (IU/L)	23 (22–30)	0
Lactase dehydrogenase (IU/L)	208 (189–237)	1
D-dimer (μg/ml)	0.55 (0.50–1.43)	3
Lactate (mmol/L)	1.6 (1.35–2.5)	2
Visit within 24 h (%)	8 (61.5)	0
Admission at 1 st visit (%)	7 (53.8)	0
Total admission (%)	11 (84.6)	0

Categorical variables are shown as number (%) and continuous variables are shown as median (25–75th percentile). BP, blood pressure on admission; ICAD, isolated celiac artery dissection.

CT findings at initial presentation are summarized in Figure 1 and Table 2. On CT imaging, the false lumen was found to be double-barreled in 2 patients (15.4%), partially thrombosed in 1 patient (7.7%), and completely thrombosed in 10 patients (76.9%). Extended dissection of the main branches of the celiac artery was found in the left gastric artery in 1 patient (7.7%), common hepatic artery in 5 patients (38.5%), and splenic artery in 7 patients (53.8%). Malperfusion associated with dissection of 3 branches was not found in the stomach or liver but was found in the spleen in 4 patients (30.8%). There were 2 cases of splenic ischemia and 2 of splenic infarction. No patients experienced persistent abdominal pain or any complications during the follow-up period. The initial CT of the patient shown in Figure 2 revealed a diffuse defect of the contrast medium in both the arterial and venous phases, but follow-up CT on day 2 revealed full enhancement of the contrast medium in both phases. Moreover, angiography in the patient shown in Figure 3 revealed a 99% delay of the proximal splenic artery, but the spleen and splenic vein were well enhanced.

Table 2. CT Findings on Presentation of Patients With Symptomatic ICAD

	Total (n=13)	Missing
Abdominal aorta
Max. diameter (mm)	18.4 (16.6–19.1)	0
Spotty calcification (%)	11 (84.6)	0
Other atherosclerotic findings (%)	11 (84.6)	0
Celiac artery
Dissection (%)	13 (100)	0
Rupture (%)	0 (0)	0
Max. diameter (mm)	11.6 (10.6–12.6)	0
Min. lumen diameter (mm)	3.6 (3.0–4.7)*	2
False lumen
Completely thrombosed (%)	10 (76.9)	0
Partially thrombosed (%)	1 (7.7)	0
Double-barreled (%)	2 (15.4)	0
Left gastric artery
Dissection (%)	1 (7.7)	0
Malperfusion findings of the stomach (%)	0 (0)	0
Common hepatic artery**
Dissection (%)	5 (38.5)	0
Malperfusion of the liver (%)	0 (0)	0
Splenic artery
Dissection (%)	7 (53.8)	0
Malperfusion of the spleen (%)	4 (30.8)	0
Splenic ischemia (%)	2 (15.4)	0
Splenic infarction (%)	2 (15.4)	0
Intestinal ischemia (%)	0 (0)	0

Categorical variables are shown as number (%) and continuous variables are shown as median (25–75th percentile). *Two patients had double-barrel-type false lumen status, and we therefore could not differentiate the true and false lumens. **One patient showed a common hepatic artery anomaly variant. The right hepatic artery branched directly from the celiac artery and had a dissection. CT, computed tomography; ICAD, isolated celiac artery dissection.

Patient outcomes and follow-up CT findings are summarized in Figure 2 and Table 3. The median follow-up period was 376 (165–602) days. All patients were alive without any antiplatelet, anticoagulant, surgical or endovascular treatment during the follow-up period. A 1–2-month follow-up CT was not performed in 2 patients (15.4%) and follow-up CT after more than 1 year was not performed in 7 patients (53.8%). One patient underwent angiography on the day of presentation and 3 patients underwent an ultrasound test (Figure 3). However, ICAD was not detected by the ultrasound test in those 3 patients. There were 2 (18.2%) cases of diameter enlargement in the celiac artery at 1–2 months after presentation (Table 3); 1 patient underwent follow-up CT at 1 year, which revealed diameter regression from 13.5 mm to 10.3 mm, and the 1-year follow CT finding was not available for the other patient but that patient is planned to undergo follow-up CT at 1 year. In our study, 6 patients underwent follow-up CT examination within 1 year (Table 3). Although the diameter of the celiac artery gradually decreased over time in all 6 cases, a thrombosed false lumen was newly enhanced in 3 cases at 1 year.

Table 3. Outcomes in Patients With Symptomatic ICAD

	Total (n=13)	Missing
Patient outcomes
Duration of admission to discharge (days)	7 (6–8.5)*	0
In-hospital death (%)	0 (0)*	0
Follow-up duration (days)	376 (165–602)	0
Out-of-hospital death (%)	0 (0)	0
Open surgery (%)	0 (0)	0
Endovascular surgery (%)	0 (0)	0
Follow-up CT findings at 1–2 months		2
Diameter expansion (%)	2 (18.2)
Diameter regression (%)	9 (81.8)
New false lumen enhancement (%)	4 (36.4)
Follow-up CT findings within 1 year		7
Diameter expansion (%)	0 (0)
Diameter regression (%)	6 (100)
New false lumen enhancement (%)	3 (50.0)

Categorical variables are shown as number (%) and continuous variables are shown as medians (25–75th percentile). *Number of patients was 11 because 2 patients were followed up as outpatients. Abbreviations as in Table 2.

Discussion

We retrospectively investigated and summarized our experience of 13 cases of symptomatic ICAD with a focus on the epidemiology, radiological findings, and prognostic effect of noninvasive conservative medical treatment on outcomes. All of the patients were alive after a median follow-up period of 376 days (quartile: 165–602 days) without any significant complications and without receiving any endovascular or surgical treatment during the follow-up period. Our study is the first and the largest case series to evaluate symptomatic ICAD with standardized conservative medical treatment.^6,9–19 We therefore believe that our results provide clinically useful information on a management strategy for symptomatic ICAD and give physicians new insights into this condition.

Characteristics of ICAD Presentation

There have been several case reports and small case series of symptomatic ICAD, but most of them have included less than 5 patients, and there are no comprehensive data about the characteristics of symptomatic ICAD presentation.^9–16 The initial manifestation is usually acute continuous epigastric pain at rest and sometimes in combination with left side pain possibly caused by splenic ischemia. All of the present patients showed abdominal tenderness on physical examination without rebound pain. Blood pressure (BP) on admission was relatively high (Table 1). However, because the percentage of a history of hypertension was only 30.8%, these BP values might have been influenced by pain. The results of biochemical tests shown in Table 1 may not be helpful for diagnosing ICAD or related organ ischemia associated with dissection of celiac artery branches, although other clinical studies indicated the usefulness of D-dimer for the diagnosis of aortic dissection.²¹ Regarding the radiological findings, the diagnosis of ICAD has usually been made on the basis of contrast-enhanced CT.^22,23 In our patients, diagnosis of ICAD was based on contrast-enhanced CT. Ultrasound was performed in 3 patients (Figure 3), but we could not detect ICAD in those patients. There are 2 possible reasons for the difficulty in detecting ICAD by ultrasound: (1) detection of the celiac artery was limited by gastrointestinal gas, thick anterior abdominal wall musculature and fat, especially in obese patients and (2) an adequate ultrasound signal from the intimal flap was not obtained because the celiac artery branches vertically from the abdominal aorta. In other words, the vectors of the ultrasound signal and of the intimal flap are essentially parallel.^24,25 Thus, a contrast-enhanced CT evaluation should be performed if ICAD is suspected based on medical interview and physical examination.

Because abdominal pain is very common chief complaint in the emergency department and includes differential diagnoses such as gastric ulcer, cholelithiasis and myocardial infarction, careful interview, physical examination and appropriate diagnostic tests such as ECG and CT are needed.²⁶

Etiology of ICAD

Historically, arterial dissections, especially aortic dissections, have been considered to be associated with atherosclerotic changes, such as changes related to hypertension, diabetes, smoking, dyslipidemia, obesity, and aging.² Several studies have also shown that collagen disorders, trauma, and localized arterial spasm can lead to arterial dissections.^27–29 In our study, a high percentage of the patients with ICAD had a smoking history (69.2%) and were slightly obese (Table 1). Although the prevalence of each of the other atherosclerotic risk factors was not very high, CT examination of the abdominal wall revealed spotty calcification and other atherosclerotic findings in 11 (84.6%) of the 13 patients (Table 2). Thus, we speculate that atherosclerosis has an important role in the development of ICAD.

Rationale for Conservative Treatment

The 2 major clinical problems in treating symptomatic ICAD are arterial aneurysm rupture and organ ischemia associated with dissection of the major branches: left gastric artery (stomach), common hepatic artery (liver), and splenic artery (spleen).^5,6,17 Endovascular or surgical treatment should be performed in patients with rupture of a celiac artery aneurysm.³⁰ It has been reported that control of BP by antihypertensive and analgesic medications is effective for preventing this fatal event.^1,31 However, there is no definite consensus regarding the management of organ ischemia.^9–16 The stomach and liver have rich collateral circulations anatomically. There have been no case reports of stomach or liver ischemia associated with ICAD.^9–16 So it is very difficult to describe invasive treatment strategies in such cases, considering the lack of previous evidence. In particular, the liver is strongly protected against ischemia because of the double supply of the hepatic artery and portal vein.³² Thus, patients may need bypass surgery or endovascular treatment only in very specific cases such as liver transplantation with acute portal vein thrombosis.³³ In fact, enhanced CT revealed no apparent ischemia of these 2 organs in our study (Table 2), suggesting that we do not need to be overly concerned about stomach or liver ischemia. Just to be safe, we provided patients with a 1- or 2-day period of fasting, and no patients experienced any unpleasant symptoms or complications during the treatment. As for the spleen, it seems that there are no apparent anatomical collaterals. However, we think that conservative medical treatment is sufficient in ICAD patients with splenic ischemia or infarction. The initial CT in the patient shown in Figure 2 revealed a diffuse defect of the contrast medium in both the arterial and venous phases, but follow-up CT on day 2 revealed full enhancement of the contrast medium in both phases. Moreover, angiography in the patient shown in Figure 3 revealed a 99% delay of the proximal splenic artery, but the spleen and splenic vein were well enhanced, suggesting that there was a small but rich collateral circulation around the spleen. Thus, our experience showed that the spleen has a subtle but rich microcirculation or has the potential to develop collaterals over time. The rationale for conservative treatment without antiplatelet or anticoagulant therapy is based on these results indicating rich collaterals for the 3 organs. Moreover, the risk of bleeding discourages us from using an antiplatelet drug and an anticoagulant to prevent organ ischemia.^34,35

Clinical Implications

Our study demonstrated that symptomatic ICAD without signs of arterial rupture was successfully treated with conservative medical therapy without any antiplatelet, anticoagulant, endovascular or surgical treatment for a median follow-up period of 376 (165–602) days. The next area of interest is the long-term prognosis. In general, visceral artery aneurysms with a diameter greater than 20 mm are assumed to be high risk for rupturing.³¹ For example, the diameter in a previous case report of ruptured celiac artery dissection was 23 mm; the aneurysm was bilobed and ruptured into the retroperitoneal space.³⁰ In addition to the arterial diameter, a change in false lumen thrombosis may also be important.^31,36 A thrombosed false lumen was newly enhanced in 3 cases at 1 year in our study, which indicated a risk of possible future rupture.^31,36 We therefore recommend regular follow-up CT examinations to evaluate the risk of rupture, such as false lumen enhancement and increased arterial diameter.^6,9,37,38

Study Limitations

First, it was a single-center, retrospective observational study. Second, although the number of patients enrolled in this study was the largest so far, it is still small. Third, we could not examine long-term prognosis in detail. Because of these limitations, our findings must be interpreted with caution.

Conclusions

Our study demonstrated that symptomatic ICAD without signs of arterial rupture was successfully treated with conservative medical therapy without any antiplatelet, anticoagulant, endovascular or surgical treatment.

Conflict of Interest

None declared.

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