Keywords
chronic mesenteric ischemia - reperfusion bowel injury - endovascular recanalization
Introduction
Patients with chronic mesenteric ischemia (CMI) typically present with insidious onset
of postprandial abdominal pain associated with significant weight loss. The association
of pain with food intake often leads to food aversion. It is commonly seen in elderly
patients with risk factors for atherosclerosis. Smoking, diabetes mellitus, and hypertension
are most common risk factor.[1] Because of the extensive collateral network, usually at least two of the three visceral
vessels are affected before patients develop symptoms.[2] However, given the spectrum of gastrointestinal disturbances associated with abdominal
pain and weight loss, the diagnosis is often made late.[3]
Most patients present with occlusion or stenosis of superior mesenteric artery (SMA)
and at least one other mesenteric vessel, most commonly the celiac trunk. Endovascular
therapy is the first line of treatment.[4] Procedure-related complications such as hematoma at the access site, dissection,
thrombosis, distal embolism, and contrast-induced nephropathy are the most commonly
described complications after endovascular therapy.[5] Intestinal ischemic reperfusion injury (RI) is a life-threatening condition with
high morbidity and mortality and is almost always seen in the setting of acute mesenteric
ischemia. Contrary to the expectation, restoration of blood flow to the ischemic bowel
further exaggerates cell injury. We present a case in which recanalization of SMA
and celiac artery in single sitting for CMI was accompanied by the typical manifestation
of reperfusion bowel injury.
Case Presentation
The patient is a 50-year-old male who had insidious onset severe postprandial abdominal
pain associated with weight loss of 6 to 7 kg in 2 to 3 months. He had aversion to
solid food and was on liquid diet. The patient was a chronic smoker and had smoked
about 2 packs of cigarettes daily for 25 years. There was no history of diabetes or
hypertension. On computed tomography (CT) angiography, there was complete atherosclerotic
occlusion of SMA (15 mm length) and inferior mesenteric artery (IMA) for a length
of 60 mm. There was also 90% stenosis involving the celiac trunk for a length of 4 mm
([Fig. 1A]).
Fig. 1 (A) Computed tomography sagittal section showing 90% stenosis of celiac trunk (yellow
arrow) with complete occlusion of superior mesenteric artery (SMA) and inferior mesenteric
artery (red arrow). (B) Digital subtraction angiography lateral view showing 90% stenosis of celiac trunk
(black arrow) with complete occlusion of SMA (red arrow).
The patient was referred to interventional radiology department for endovascular recanalization
from gastroenterology department.
Through right brachial approach, aortography performed in lateral view confirmed complete
atherosclerotic occlusion of the SMA and IMA with a critical stenosis of 90% involving
the celiac trunk ([Fig. 1B]). An intravenous heparin bolus (5000 IU) was administered. A 6F 90cm guiding sheath
(Destination; Terumo, Tokyo, Japan) was placed in the abdominal aorta and SMA ostium
was engaged with a 6F multipurpose angiographic guide catheter. The lesion in SMA
was crossed with a 0.014-inch microwire (Command ES; Abbott vascular, Illinois, United
States) and angioplasty was performed with 5 × 40 mm balloon ([Fig. 2A]). The SMA was stented with an 8 × 27 mm balloon expandable stent (EXPRESS LD, Boston
Scientific, Massachusetts, United States; [Fig. 2B]). Similarly, the celiac trunk was cannulated, the lesion was crossed with a 0.014-inch
microwire, and balloon angioplasty was performed with a 5 × 40-mm balloon ([Fig. 2C]). The celiac trunk was stented with an expandable 8 × 29 balloon stent (OMNILINK
ELITE; Abbott vascular, Illinois, United States). Complete recanalization of SMA and
celiac trunk was achieved ([Fig. 2D]).
Fig. 2 (A) Digital subtraction angiography (DSA) lateral view showing representative image
of superior mesenteric artery (SMA) balloon angioplasty. (B) DSA lateral view showing angiographic run post-SMA stenting. (C) DSA lateral view showing representative image of celiac trunk balloon angioplasty.
(D) DSA lateral view showing angiographic run post-SMA and celiac trunk stenting.
Post-procedure next day, postprandial abdominal pain was replaced by mild generalized
abdominal discomfort. Ultrasonography of abdomen showed patent stents and mild diffuse
bowel wall edema and hyperperistaltic bowel loops. After 48 hours, abdominal discomfort
increased and was associated with bloating, abdominal distention and two episodes
of vomiting. He was afebrile. There was no guarding or tenderness in abdomen. There
was no signs of infection and hemoglobin was stable. Ultrasonography and plain CT
of abdomen revealed edematous bowel loop and mild-to-moderate free fluid in the peritoneal
cavity ([Fig. 3]). The condition was consistent with reperfusion bowel injury secondary to hyperperfusion
following mesenteric artery revascularization. Bowel rest was given, and patient was
kept nil per oral for 48 hours followed by only sips of water for next 24 hours. He
was on parenteral fluid therapy and gradually liquid diet followed by soft diet was
started for him. Ultrasonography on 6th post-procedure day showed near complete resolution
of bowel edema and ascites. Patient was discharged on seventh post-procedure day tolerating
soft diet.
Fig. 3 (A) Ultrasound image showing thickened edematous bowel wall (yellow arrow). (B) Ultrasound image showing peritoneal free fluid (yellow arrow). (C) Computed tomography (CT) image showing pelvic free fluid (asterisk). (D) CT image showing edematous bowel wall thickening (yellow arrow).
Discussion
RI is caused following the restoration of blood flow to an ischemic organ resulting
in additional cellular damage. The underlying mechanism of RI is not specific to the
intestine and is a consequence of oxidative stress following reperfusion, leading
to an increase in reactive oxygen species (ROS), and local inflammation leading to
cell death. This complex and multifactorial pathophysiological process is not yet
fully understood and has been studied in preclinical models in various organs, particularly
the heart, brain, liver, and intestine.[3]
The intestine is one of the most sensitive organs for RI. In RI injury, the barrier
function of the mucosa is destroyed, and vascular permeability is increased. The increased
vascular permeability allows inflammatory cells to activate and adhere. These inflammatory
cells release ROS, proinflammatory chemokines, and protein kinases. In addition, disruption
of the intestinal barrier allows bacterial translocation that further stimulates inflammatory
response.[6]
In the setting of RI, CT scan shows bowel wall thickening (>5mm) in association with
mucosal hyperenhancement, submucosal edema, mesenteric stranding, or free fluid. It
may also be associated with venous dilatation in the adjacent mesentery.[5]
The severity of RI varies with severity of ischemia (partial vs. complete), onset
of ischemia (acute vs. chronic), duration of time ischemia has been present, and the
bowel segment involved. This phenomenon primarily occurs when there is abrupt interruption
of blood flow in circumstances like embolic phenomenon, acute mesenteric thrombosis,
hypovolemic shock, aortic dissection, and aortic aneurysm surgery.[4]
In CMI due to gradual nature of occlusion and secondary collateralization, there is
some degree of ischemia conditioning of the bowel. Therefore, RI is uncommon in CMI.
Moreover, the degree of severity of RI in this scenario even if it develops is relatively
mild considering the chronic nature of disease where bowel is already primed to ischemia.
We could find only a single report of reperfusion bowel injury post-endovascular revascularization
in CMI. Here also both celiac trunk and SMA were revascularized in a single session.[3] Clinical and imaging findings resolved completely within a week. If this is a complication
unique to simultaneous revascularization of celiac artery and SMA, we do not have
an answer.
It is generally recommended to avoid simultaneous revascularization of both carotid
arteries in single sitting to avoid reperfusion brain injury. Deriving a corollary
from carotid circulation and considering the common pathophysiology of RI irrespective
of the organ involved, it seems reasonable to avoid simultaneous revascularization
of celiac artery and SMA.
