We present the case of a 60-year-old male who arrived at the emergency department
with acute abdominal pain and abdominal distension of 1-day duration. He had no known
comorbidities and was not on any regular medications, including antiplatelets, anticoagulants,
or nonsteroidal anti-inflammatory drugs (NSAIDs). Clinical examination revealed features
suggestive of peritonitis. An urgent contrast-enhanced computed tomography (CT) of
the abdomen along with CT angiography was performed, which revealed a gastric antral
perforation, pneumoperitoneum, and free peritoneal fluid.
Incidentally, CT angiography also revealed complete thrombosis at the origin of the
celiac trunk, attributed to chronic atherosclerotic plaque. Notably, all three major
branches of the celiac axis—the left gastric artery (LGA), common hepatic artery (CHA),
and splenic artery—were occluded. Despite this extensive thrombosis, prominent collateral
circulation was observed. A well-developed pancreaticoduodenal arterial arcade near
the pancreatic head was seen supplying the CHA and LGA. Numerous tortuous arterial
collaterals had formed, effectively replacing the function of the splenic artery.
Further evaluation revealed the right gastric artery arising normally from the CHA,
and the right gastroepiploic artery originating from the gastroduodenal artery. The
left gastroepiploic artery, however, was not visualized. Instead, multiple small arterial
branches, presumably collaterals, were seen supplying the gastric fundus. Additionally,
a significant stenosis at the origin of the superior mesenteric artery (SMA) was identified.
Compensatory vascular remodeling was evident in the form of a prominent arc of Riolan
connecting the SMA and the inferior mesenteric artery (IMA) ([Fig. 1]).
Fig. 1 Coronal maximum intensity projection (A) and volume rendered (B) computed tomography (CT) image show common hepatic artery (CHA) (white thin arrow)
and left gastric artery (LGA) (curved arrow) arising from the peripancreatic arcade.
Enlarged arc of Riolan is seen between superior mesenteric artery (SMA) and inferior
mesenteric artery (IMA) (dashed arrow). Multiple collaterals are seen replacing the
splenic artery (thick white arrow) arising from the peripancreatic arcade and arc
of Riolan. Oblique coronal volume rendered CT image (C) shows ostial stenosis in SMA (black arrow) and filling defect at the site of origin
of celiac trunk due to atherosclerotic plaque. IMA, inferior mesenteric artery.
Celiac artery (CA) thrombosis is an incidental finding seen in a notable proportion
of patients undergoing abdominal CT imaging, with reported incidence ranging from
12.5 to 49%.[1] The CA plays a crucial role in perfusing the upper abdominal viscera, including
the stomach, liver, spleen, pancreas, and proximal duodenum. In cases where the celiac
axis is occluded, the body often compensates via collateral pathways, predominantly
through the pancreaticoduodenal arcades and anastomoses between the left and right
gastric arteries and the gastroepiploic arteries—pathways that represent inter- and
intraceliac collateral networks.[2]
The present case is remarkable due to the complete thrombosis of the entire celiac
axis along with all its branches, which is rarely documented. The collateral circulation
supplying the upper abdominal organs had to be entirely rerouted through the pancreaticoduodenal
arcades—branches of the SMA. However, with a high-grade stenosis at the SMA origin,
this compensatory mechanism was further challenged. The presence of a markedly developed
arc of Riolan—a collateral connection between the IMA and SMA—underscored the extent
to which the body had adapted to preserve visceral perfusion. This unique vascular
remodeling enabled maintenance of blood supply to both the bowel and the solid upper
abdominal organs in the face of critical arterial compromise.
Although CA occlusion is sometimes asymptomatic due to such collateralization, in
this patient, the coexistence of SMA stenosis critically limited the perfusion reserve.
This compounded visceral ischemia, most notably affecting the gastric antrum, which
in turn predisposed the patient to ischemic gastric perforation. In the absence of
other identifiable risk factors—such as peptic ulcer disease, Helicobacter pylori infection, NSAID use, or malignancy—chronic gastric ischemia due to arterial insufficiency
was determined to be the most plausible cause. The patient underwent emergency surgical
repair of the gastric perforation and was started on oral dual-antiplatelet therapy
to prevent future episodes of visceral ischemia. He recovered well postoperatively
with no further ischemic complications and was discharged in stable condition after
5 days.
This case highlights several key learning points. First, complete thrombosis of the
celiac trunk and its branches is rare and can be easily overlooked if not systematically
evaluated, especially in the absence of overt symptoms. Second, the development of
dual-level compensatory collateral pathways—from the SMA to celiac territory and further
from the IMA to SMA—is a fascinating example of vascular adaptation. Third, it reinforces
the role of CT angiography with advanced reconstruction techniques such as maximum
intensity projection and volume-rendered reconstruction in clearly delineating complex
vascular anatomy and its pathological alterations.[3]
Understanding these collateral routes is not just of academic interest but has direct
clinical implications. In cases of unexplained abdominal pain or visceral ischemia,
especially in older patients with known atherosclerotic disease, a thorough evaluation
of the mesenteric and celiac vasculature is warranted. Moreover, recognition of collateral
pathways becomes crucial during surgical interventions or endovascular procedures,
where inadvertent ligation or compromise of such vessels can lead to catastrophic
outcomes.
In conclusion, this case documents a rare and severe form of chronic splanchnic arterial
insufficiency with adaptive collateralization via the IMA. It highlights the critical
role of radiologic imaging in identifying both the underlying etiology and the compensatory
mechanisms in patients presenting with acute abdominal emergencies. Early recognition
of such vascular anomalies can significantly impact patient outcomes by guiding appropriate
surgical and interventional management strategies.
