# 10 - 340 Mesenteric Vascular Insufficiency

### 340 Mesenteric Vascular Insufficiency

maintains the tract patency and reduces the likelihood of recurrent 
infection and inflammation. Once the inflammation is reduced 
(4–6 weeks), the exact relationship of the fistula tract to the anal 
sphincters can be ascertained. Two general approaches are com­
mon: sphincter-cutting procedures and sphincter-sparing proce­
dures. A simple fistulotomy or fistulectomy is a sphincter-cutting 
procedure and is usually performed for intersphincteric and low 
(less than one-third of the muscle) transsphincteric fistulas. In a 
systematic review, sphincter-cutting procedures were associated 
with a 94% success rate and a 13% rate of mild fecal incontinence. 
Sphincter-sparing surgery is usually performed for a higher trans­
sphincteric fistula. These procedures include an anorectal advance­
ment flap, ligation of the internal fistula tract (LIFT procedure), 
or insertion of fibrin or cyanoacrylate glue. Sphincter-preserving 
procedures are associated with up to 78% success rates with no 
incidence of fecal incontinence.

Fistulizing disease of the anus is common in Crohn’s disease, 
and the use of mesenchymal stem cell therapy may improve heal­
ing rates of fistula associated with Crohn’s disease. The ADMIRE 
study examined the use of allogeneic expanded adipose-derived 
mesenchymal stem cells in the treatment of complex perianal fistula 
in Crohn’s disease. The study included 212 patients randomized to 
stem cell therapy or placebo. Fistula remission rates at 52 weeks 
were significantly higher with the use of stem cell therapy over pla­
cebo (59 vs 42%, respectively). Further studies are currently being 
performed to elucidate the benefits of stem cell therapy in perianal 
fistula. As with any stem cell therapy, the cost can be prohibitive to 
its standard use.
PART 10
Disorders of the Gastrointestinal System
■
■ANAL FISSURE
Incidence and Epidemiology 
Anal fissures occur at all ages but 
are more common in the third through the fifth decades. The preva­
lence is equal in males and females. It is associated with constipation, 
diarrhea, infectious etiologies, perianal trauma, and Crohn’s disease.
Anatomy and Pathophysiology 
Trauma to the anal canal occurs 
following defecation. This injury occurs in the anterior or, more com­
monly, posterior anal canal. Irritation caused by the trauma to the anal 
canal results in an increased resting pressure of the internal sphincter. 
The blood supply to the sphincter and anal mucosa enters laterally. 
Therefore, increased anal sphincter tone results in a relative ischemia 
in the region of the fissure and leads to poor healing of the anal injury. 
A fissure that is not in the posterior or anterior position should raise 
suspicion for other causes, including tuberculosis, syphilis, Crohn’s 
disease, and malignancy.
Presentation and Evaluation 
A fissure can be easily diagnosed 
on history alone. The classic complaint is pain, which is strongly asso­
ciated with defecation and is relentless. The bright red bleeding that 
can be associated with a fissure is less extensive than that associated 
with hemorrhoids and is usually only noted on wiping. On examina­
tion, most fissures are located in either the posterior or anterior posi­
tion. A lateral fissure is worrisome because it may have a less benign 
nature, and systemic disorders should be ruled out. A chronic fissure is 
indicated by the presence of a hypertrophied anal papilla at the proxi­
mal end of the fissure and a sentinel pile or skin tag at the distal end. 
Often the circular fibers of the hypertrophied internal sphincter are 
visible within the base of the fissure.
TREATMENT
Anal Fissure
The management of the acute fissure is conservative. Stool softeners 
for those with constipation, increased dietary fiber, topical anes­
thetics, glucocorticoids, and sitz baths are prescribed and will heal 
60–90% of fissures. Chronic fissures are those present for >6 weeks. 
These can be treated with modalities aimed at decreasing the anal 
canal resting pressure including nifedipine ointment applied three 

times a day and botulinum toxin type A, up to 20 units, injected into 
the internal sphincter on each side of the fissure. Both treatments 
are associated with a fissure healing rate of >80%. Surgical manage­
ment includes anal dilatation and lateral internal sphincterotomy. 
Usually, one-third of the internal sphincter muscle is divided; it is 
easily identified because it is hypertrophied. Recurrence rates from 
medical therapy are higher, but this is offset by a risk of inconti­
nence following sphincterotomy. Lateral internal sphincterotomy 
may lead to incontinence more commonly in women.
Acknowledgment
The author thanks Cory Sandore for providing some illustrations for this 
chapter.
■
■FURTHER READING
Bharucha AE et al: Surgical interventions and the use of device-aided 
therapy for the treatment of fecal incontinence and defecatory disor­
ders. Clin Gastroenterol Hepatol 15:1844, 2017.
Daniels L et al: Randomized clinical trial of observation versus antibi­
otic treatment for a first episode of CT-proven uncomplicated acute 
diverticulitis (DIABOLO trial). BJS 104:52, 2017.
Guttenplan M: The evaluation and office management of hemor­
rhoids for the gastroenterologist. Curr Gastroenterol Rep 19:30, 2017.
Hall J et al: The American Society of Colon and Rectal Surgeons 
Clinical Practice Guidelines for the treatment of left-sided colonic 
diverticulitis. Dis Colon Rectum 63:728, 2020.
Panes J et al: Long-term efficacy and safety of stem cell therapy 
(Cx601) for complex perianal fistulas in patients with Crohn’s disease. 
Gastroenterology 154:1334, 2018.
Prichard D, Bharucha AE: Management of pelvic floor disorders: 
Biofeedback and more. Curr Treat Options Gastroenterol 12:456, 
2014.
Salfity HV et al: Minimally invasive incision and drainage technique 
in the treatment of simple subcutaneous abscess in adults. Am Surg 
83:699, 2017.
Strate LL, Morris AM: Epidemiology, pathophysiology, and treat­
ment of diverticulitis. Gastroetenterology 156:1282, 2019.
Sugrue J et al: Sphincter-sparing anal fistula repair: Are we getting 
better? Dis Colon Rectum 60:1071, 2017.
Tursi A: Dietary pattern and colonic diverticulosis. Curr Opin Clin 
Nutr Metab Care 20:409, 2017.
Daniel Willie-Permor, Mahmoud Malas

Mesenteric Vascular 

Insufficiency
INTESTINAL ISCHEMIA
■
■INCIDENCE AND EPIDEMIOLOGY
Intestinal ischemia occurs when splanchnic perfusion fails to meet the 
metabolic demands of the intestines, resulting in ischemic tissue injury. 
Mesenteric ischemia affects 2–3 people per 100,000 with an increasing 
incidence in the aging population. Mortality with acute presentation 
remains high (between 50 and 80%), and early diagnosis and prompt 
intervention are crucial in improving clinical outcomes. Intestinal isch­
emia is further classified into chronic mesenteric ischemia (CMI) and 
acute mesenteric ischemia (AMI). CMI is secondary to multiple major 
visceral arterio-occlusive disease with involvement of the superior 
mesenteric artery (SMA) most worrisome. AMI is most associated with

(1) arterio-occlusive mesenteric ischemia, (2) nonocclusive mesenteric 
ischemia, and (3) mesenteric venous thrombosis.
CMI is the failure to achieve normal postprandial hyperemic intes­
tinal blood flow. This occurs due to an imbalance between supply and 
demand of oxygen metabolites to the intestinal tract similar to cardiac 
angina. CMI occurs due to significant atherosclerotic disease leading to 
the narrowing of the SMA and/or celiac artery origins.
AMI is the occurrence of an abrupt cessation of mesenteric blood 
flow, usually embolic or thrombotic in nature. Approximately 50% 
of AMI is due to embolus to the mid to distal SMA. The embolus 
etiology includes atrial fibrillation, recent myocardial infarction, soft 
atherosclerotic plaque, infective endocarditis, valvular heart disease, 
and recent cardiac or vascular catheterization. Approximately 25–30% 
of the cases are characterized by an acute-on-chronic thrombosis 
in patients with preexisting mesenteric atherosclerosis. Thrombotic 
occlusion most commonly occurs at areas of severe atherosclerotic 
narrowing at the SMA and the celiac artery.
Nonocclusive mesenteric ischemia represents 20% of the cases and 
is secondary to intestinal ischemia when subjected to acute hemody­
namic instability. Patients above the age of 50, especially those with 
coexisting conditions like myocardial infarction, congestive heart 
failure, aortic insufficiency, and renal or liver disease, who are also 
undergoing cardiovascular surgery, face the highest risk. Hypovolemia, 
shock, and use of vasoconstrictive agents (e.g., digoxin, α-adrenergic 
agonists, cocaine) can precipitate ischemia in these patients. It is the 
most prevalent gastrointestinal disease complicating cardiovascular 
surgery. The incidence of ischemic colitis following elective aortic 
repair is 5–9%, and the incidence triples in patients following emergent 
repair.
Mesenteric venous thrombosis accounts for <10% of cases and is 
generally precipitated by a hypercoagulable state due to an underlying 
inherited disorder such as factor V Leiden, prothrombin mutation, 
protein S deficiency, protein C deficiency, antithrombin deficiency, and 
antiphospholipid syndrome. It may also occur as a result of acquired 
thrombophilia in malignancies, hematologic disorders, and use of oral 
contraceptives.
■
■ANATOMY AND PATHOPHYSIOLOGY
The blood supply to the intestines is supplied by the celiac artery, SMA, 
and inferior mesenteric artery (IMA) (Fig. 340-1). Extensive collat­
eralization occurs between major mesenteric trunks and branches of 
the mesenteric arcades. Collateral vessels within the small bowel are 
numerous and meet within the duodenum and the bed of the pancreas. 
Collateral vessels within the colon meet at the splenic flexure and 
descending/sigmoid colon. These areas, which are inherently at risk for 
decreased blood flow, are known as Griffiths’ point and Sudeck’s point, 
respectively, and are the most common locations for colonic ischemia 
(Fig. 340-1, shaded areas). The splanchnic circulation can receive up 
to 30% of the cardiac output. Protective responses to prevent intestinal 
ischemia include abundant collateralization, autoregulation of blood 
flow, and the ability to increase oxygen extraction from the blood.
Occlusive ischemia is a result of disruption of blood flow by an 
embolus or progressive thrombosis in a major artery supplying the 
intestine. In >75% of cases, emboli originate from the heart and pref­
erentially lodge in the SMA just distal to the origin of the middle colic 
artery. Progressive stenosis of typically two of the three major vessels 
supplying the intestine is required for the development of chronic 
intestinal angina. Involvement of the SMA is most worrisome. Non­
occlusive ischemia is disproportionate mesenteric vasoconstriction 
(arteriolar vasospasm) in response to a severe physiologic stress such 
as shock. If left untreated, early mucosal stress ulceration will progress 
to full-thickness injury.
■
■PRESENTATION, EVALUATION, 

AND MANAGEMENT
Patients with CMI typically present with insidious onset of symptoms 
and classically present with recurrent episodes of acute dull, crampy, 
postprandial epigastric pain, which has also been referred to as “intesti­
nal angina.” Patients also describe fear of eating resulting in weight loss. 

Left phrenic a.
Aorta
Right phrenic a.
Splenic a.
Griffiths’
point
Celiac trunk
Pancreaticoduodenal a.
Arc of
Riolan
SMA
IMA
Marginal a.
IIA
Sudeck’s
point
Hemorrhoidal aa.
Superior
Middle
Inferior
CHAPTER 340
FIGURE 340-1  Blood supply to the intestines includes the celiac artery, superior 
mesenteric artery (SMA), inferior mesenteric artery (IMA), and branches of the 
internal iliac artery (IIA). Griffiths’ and Sudeck’s points, indicated by shaded areas, 
are watershed areas within the colonic blood supply and common locations for 
ischemia.
Mesenteric Vascular Insufficiency 
Chronic diarrhea may also be noted. Duration of symptoms is typically 
6–12 months. Physical examination will often reveal a malnourished 
patient with other manifestations of atherosclerosis. Prompt diagnostic 
investigation is necessary to rule out gastrointestinal malignancies 
and other possible causes, and may include accelerated evaluation 
via esophagogastroduodenoscopy, colonoscopy, abdominal computed 
tomography (CT) scan, and abdominal ultrasound examination.
Duplex ultrasound has gained popularity as a screening tool for 
evaluation of the mesenteric vessels due to high sensitivity and speci­
ficity. Mesenteric duplex scan demonstrating a high peak velocity of 
flow in the SMA is associated with an ~80% positive predictive value 
of mesenteric ischemia. More significantly, a negative duplex scan vir­
tually precludes the diagnosis of mesenteric ischemia. It is important 
to perform the test while the patient is fasting because the presence 
of increased bowel gas prevents adequate visualization of flow distur­
bances within the vessels or the lack of a vasodilation response to feed­
ing during the test. Thin-sliced CT angiography is the gold standard 
diagnostic tool in assessing the degree of atherosclerotic disease of 
the aortic and visceral vessels as well as evaluating the bowels. Venous 
phase can also help diagnose mesenteric vein thrombosis.
The management of CMI includes aggressive medical therapy of 
atherosclerotic disease including cessation of smoking and antiplatelet 
and lipid-lowering medications. A full cardiac and vascular evaluation 
should be performed before intervention on CMI.
Treatment, involving either endovascular, open surgical, or hybrid 
revascularization, should be individualized based on the patient’s 
comorbidities and anatomy. Endovascular revascularization involves 
targeted vessel treatment with visceral stents with the SMA anatomy 
being the key determinant. The revascularization of the celiac axis and 
IMA represents secondary focal points, offering potential therapeutic 
benefits. This approach becomes particularly relevant when the SMA 
is deemed unsuitable for intervention or when technical outcomes 
are deemed suboptimal. Open revascularization involves antegrade 
bypass from the supraceliac aorta or retrograde bypass typically from

the common or external iliac arteries with a synthetic or autogenous 
graft to the targeted vessels, usually the SMA and/or celiac artery. In 
patients with suitable lesions requiring revascularization, an endovas­
cular approach is recommended as the first-line therapy. It is especially 
favorable for short segment stenosis with minimal to moderate calci­
fication or thrombus. Angioplasty with endovascular stenting in the 
treatment of CMI is associated with an 80% long-term success rate. 
Open revascularization should be considered in patients with lesions 
not amenable to endovascular treatment, such as severe calcification, 
longer lesions, small vessel diameter, or failed endovascular interven­
tions, or in a specific subset of younger, healthier patients, in whom 
the potential long-term advantages may outweigh the heightened 
perioperative risks. Retrograde open mesenteric stenting (ROMS) is a 
hybrid approach, combining aspects of both traditional open surgical 
bypass and percutaneous endovascular therapy. ROMS is primarily 
indicated for treating mesenteric ischemia, both acute and chronic, 
particularly in cases where conventional endovascular or open surgical 
approaches are not feasible or have been unsuccessful. This includes 
scenarios where there is significant stenosis or occlusion in the mesen­
teric arteries that cannot be adequately addressed through less invasive 
percutaneous methods from the aorta or in situations where immediate 
direct visualization and potential resection of the bowel are necessary 
due to the presence of necrosis or perforation. The technique involves 
a laparotomy that allows for direct bowel assessment and the exposure 
and stenting of the SMA using a retrograde approach through the 
midsegment of the SMA, thus allowing for immediate revasculariza­
tion, assessment of bowel viability, and, if necessary, bowel resection. 
ROMS also offers the advantage of faster operative times compared 
to traditional bypass and avoids the placement of prosthetic material 
in potentially contaminated peritoneal cavities, which is a significant 
concern in the setting of bowel necrosis and peritonitis.

PART 10
Disorders of the Gastrointestinal System
Acute intestinal ischemia remains one of the most challenging 
diagnoses. The mortality rate of AMI is >50%. The most significant 
indicator of survival is the timeliness of diagnosis and treatment. An 
overview of diagnosis and management of each form of intestinal isch­
emia is given in Table 340-1.
AMI resulting from arterial embolus or thrombosis presentation 
is nonspecific and requires a high index of suspicion for the diag­
nosis. The most common complaint, occurring in 95% of cases, is 
severe, acute, nonremitting abdominal pain that is strikingly out of 
proportion to the physical findings. The reason behind the pain being 
TABLE 340-1  Overview of the Management of Acute Intestinal Ischemia
KEY TO EARLY 

DIAGNOSIS
TREATMENT OF 
UNDERLYING CAUSE
TREATMENT OF SPECIFIC LESION
CONDITION
Arterio-occlusive 
mesenteric ischemia
1.  Arterial embolus
Computed tomography 
angiography (CTA)
Early laparotomy
Anticoagulation
Cardioversion
Thrombectomy
Broad-spectrum antibiotics
2.  Arterial thrombosis
Duplex ultrasound
CTA
Anticoagulation
Broad-spectrum antibiotics
Resuscitation
Mesenteric venous 
thrombosis
Venous thrombosis
CTA with venous phase
Anticoagulation
Resuscitation
Nonocclusive 
mesenteric ischemia
Vasospasm:
Hypoperfusion:
CT
Resuscitation
Support cardiac output
Avoid vasoconstrictors
Broad-spectrum antibiotics
Source: Modified from GB Bulkley, in JL Cameron (ed): Current Surgical Therapy, 2nd ed. Toronto, BC Decker, 1986.

disproportionate to the clinical findings is that ischemia initiates from 
the mucosal layer and progresses toward the serosal layer. This may be 
associated with nausea (44%), vomiting (35%), diarrhea (35%), and 
blood per rectum (16%). Later findings will demonstrate peritonitis 
and cardiovascular collapse. Specific clinical features can help differen­
tiate the underlying etiology, whether embolic or thrombotic. Patients 
with embolic ischemia are typically older adults with underlying con­
ditions that predispose to embolism such as atrial fibrillation, prior 
embolic event, or recent infective endocarditis. Thrombotic ischemia 
typically presents as an acute occlusion in patients with underlying 
atherosclerotic disease who may have been previously diagnosed with 
CMI.
AMI is a surgical emergency requiring emergent admission to 
a monitored bed or intensive care unit for resuscitation with fluids 
and broad-spectrum antibiotics in addition to further evaluation. If 
the diagnosis of intestinal ischemia is being considered, consultation 
with a surgical service is necessary. Often the decision to operate 
is made on a high index of suspicion from the history and physical 
exam despite normal laboratory findings. In patients with suspected 
AMI, a CT angiography with 1-mm or thinner cuts should be used to 
detect mesenteric arterial occlusive disease most likely from embolic 
or thrombotic etiology and is the gold standard. Additional diagnostic 
modalities that may be useful in diagnosis, but should not delay surgi­
cal therapy, include electrocardiogram (ECG) and echocardiogram. 
Patients with AMI should be given a heparin bolus immediately and 
started on a therapeutic heparin drip. Correction of electrolyte abnor­
malities and empiric broad-spectrum antibiotic therapy should also be 
initiated instantly.
If CT angiography verifies acute embolic occlusion of the SMA, sur­
gical exploration should not be delayed. The goal of operative explora­
tion is to resect compromised bowel, restore blood supply, and preserve 
all viable bowel. The entire length of the small and large bowel begin­
ning at the ligament of Treitz should be evaluated. The SMA artery 
should be localized, typically at the mesocolon of the transverse colon. 
A transverse arteriotomy of the SMA should be made with removal of 
embolus with an embolectomy Fogarty catheter passed in a retrograde 
and antegrade manner to restore blood flow. In the case of SMA occlu­
sion where the embolus usually lies just proximal to the origin of the 
middle colic artery, the proximal jejunum is often spared while the 
remainder of the small bowel up to the transverse colon may become 
ischemic. Nonviable bowel should be resected. Questionable bowel 
TREATMENT OF SYSTEMIC 
CONSEQUENCE
Laparotomy
Embolectomy
Assess viability and resect nonviable 
bowel
Anticoagulation
Resuscitation
Broad-spectrum antibiotics
Emergent surgical intervention
Assessment of bowel
Endovascular approach: thrombolysis, 
angioplasty, and stenting
Endarterectomy/thrombectomy or 
vascular bypass
Assess viability and resect nonviable 
bowel
Anticoagulation
Resuscitation
Broad-spectrum antibiotics
Emergent surgical intervention
Assessment of bowel
Anticoagulation
Hypercoagulable workup
Anticoagulation
Resuscitation
Broad-spectrum antibiotics
Support cardiac output
Avoid vasoconstrictors
Vasospasm
Intraarterial vasodilators
Hypoperfusion
Assess viability and resect dead bowel
Resuscitation
Broad-spectrum antibiotics
Support cardiac output
Avoid vasoconstrictors