DISCUSSION
Abdominal vascular injuries caused by blunt trauma are uncommon, with a reported incidence of 5 to 10% [
1]. Isolated CA injury, which is an injury to the CA without concomitant aortic injury, is the least common among all abdominal arterial injuries. To date, only 8 reports of isolated CA injury following blunt trauma have been reported [
2–
9]. These cases, except for 1 case without a detailed description, are summarized, along with our two cases, in
Table 1. All but one of the injuries (CA rupture managed by surgical ligation) [
3], including our two cases, were CA dissections. In this report, we focus on the clinical presentation, treatment, and outcomes of these isolated CA dissections.
All of the reported traumatic CA dissections were in male patients. Whether this is associated with the known male preponderance of spontaneous CA dissection [
10] needs to be validated. The traumatic CA dissections were associated with various blunt injuries, and not all were associated with a direct blow to the abdomen, indicating there may be other mechanisms underlying the development of CA dissection. Some authors have suggested that celiac trunk compression by an anomalous median arcuate ligament during rapid expiration may compress and injure the CA [
11], while the possible role of other predisposing factors, including hypertension, atherosclerosis, smoking history, and collagen vascular disease has also been investigated in spontaneous CA dissection, although the results so far have been inconclusive.
The clinical presentation of CA dissection varies widely, from no symptoms to severe epigastric pain. Among symptomatic patients, abdominal pain is the most common symptom, and often begins several days after the initial injury. More than half of the reported patients had elevated liver enzymes, but this is of low diagnostic value because mild elevations of the hepatic enzymes are also commonly associated with liver contusion or muscle injuries after blunt abdominal trauma. However, an acute elevation of liver enzymes in a patient with known traumatic CA dissection should warrant further evaluation, because it may be a sign of liver necrosis from hepatic artery involvement [
4]. Among all reported cases of traumatic CA dissection, 4 showed involvement of branches of the CA (splenic artery and common hepatic artery, n=3 and common hepatic artery only, n=1).
All of the reported traumatic CA dissections have been diagnosed by contrast-enhanced CT. CT has become the primary modality of radiologic evaluation for blunt trauma patients, and has been shown to be useful in detecting arterial injuries [
12,
13]. However, focal dissections of the CA can be missed by standard single-phase images with 5-mm thick sections [
5], and we recommend repeat CT angiography or three-phase abdominal CT with 3-mm sections with reconstructed multiplanar images when injuries to visceral arteries are suspected and the initial CT is nondiagnostic. Common CT findings of CA dissections are intimal flap, thrombosed false lumen, segmental fat infiltration, aneurysmal dilatation of CA, and extension of dissection into branch arteries [
14].
Because of its rarity, as well as the diverse clinical course and outcomes of the reported cases of traumatic isolated CA dissection, there are no agreed-upon recommendations for when and how to treat this injury. Some patients with traumatic CA dissections, including ours, have been managed with antiplatelet therapy (n=3; aspirin 81 mg or 100 mg), anticoagulation (n=3; enoxaparin or heparin converted to warfarin for 3 months), or endovascular stenting (n=1) in addition to blood pressure control. Recent experience with nontraumatic isolated CA dissection also supports conservative management with antiplatelet medication, anticoagulants, or no medication in patients without ischemic or hemorrhagic complications [
10,
15–
17]. Antiplatelet drugs or anticoagulants are commonly used to stabilize the injured arterial wall and prevent thrombotic occlusion of the involved arteries. However, some authors advocate that these antithrombotic drugs should not be used in acute visceral artery dissections, as it will delay thrombosis of the false lumen and possibly thereby lead to propagation of the dissection [
18]. Although there has been no direct comparison, a recent systemic review showed that outcomes of spontaneous CA dissection were good regardless of the conservative treatment chosen [
10].
As in nontraumatic CA dissection, surgical or endovascular intervention should be considered in patients with persistent symptoms, aneurysmal change, or hemorrhagic complications. Endovascular stenting or embolization is preferred over surgery because it is relatively less invasive. Surgical therapy is usually reserved only for patients who need revascularization of multiple branch arteries.
Obstruction of the celiac artery or its branches, either as a complication of CA dissection or following therapeutic ligation or embolization, rarely leads to organ ischemia because of the abundant collateral circulation. Even in the rare cases where thrombosis accompanying CA dissection has caused partial splenic infarct, pancreatitis, or liver dysfunction, the patients have been managed successfully with conservative measures [
16,
17]. However, close observation is important because two lethal ischemic complications, fulminant hepatic failure after traumatic CA dissection [
4], and multiple organ ischemia leading to septic shock after spontaneous CA dissection [
19], have been reported. Late aneurysmal change is another feared complication, and is detected in 6% of patients with conservatively managed spontaneous CA dissections [
10]. Repair is generally necessary when the aneurysm is over 2 to 3 cm in size.
Most of the aneurysmal changes after traumatic CA dissection have occurred within 2 months [
10], but they have also been detected as late as the fourth year [
20], which highlights the importance of long term follow-up for patients with CA dissection.
In summary, isolated celiac artery dissection is a rare occurrence after blunt trauma. Uncomplicated cases can be safely managed conservatively with or without antithrombotic therapy plus blood pressure control. Long term follow-up is mandatory because of the risk of late aneurysmal change.