Blood Supply of small intestine:

Arterial Supply:

Celiac Artery Branches:

 Common hepatic artery

 Gastroduodenal artery
 Superior pancreaticoduodenal artery: to
duodenum proximal to bile duct
 Anastomoses with inferior pancreaticoduodenal

Superior Mesenteric Artery Branches:

 Inferior pancreaticoduodenal artery (duodenum distal to bile duct); anastomoses with

superior pancreaticoduodenal
 Jejunal branches
 Ileal branches
 Ileocolic artery (with appendiceal branch)
 Arcades link adjoining jejunal and ileal branches.
 Vasa rectae connect from arcades to bowel walls.

Marginal Artery

 Connects superior and inferior mesenteric arteries

Venous Drainage

 Duodenal veins empty into splenic vein, superior mesenteric vein, and portal vein (which lies
posterior to the first part).
 Superior mesenteric vein (right portal drainage) receives jejunal, ileal, and ileocolic veins
that run alongside of arterial counterparts.

Blood supply of large intestine:

Appendicular (Appendiceal) Artery

 Branch of the ileocolic artery or of the ileal or

colic branch of the ileocolic (branches from the

superior mesenteric artery)

 Base of the appendix may be supplied by the

anterior or posterior caecal artery.

 Appendiceal artery typically passes behind the

terminal ileum, within the mesoappendix.

Appendicular (Appendiceal) Vein

 Joins ileocolic vein, which joins superior mesenteric vein (portal vein drainage)

Blood supply of rectum:

Arterial Supply

 Inferior mesenteric branches

 Superior rectal (hemorrhoidal) artery provides blood to upper rectum
 Internal iliac branches
 Middle and inferior rectal (hemorrhoidal) arteries provide blood to middle and lower
rectum.
 Inferior vesical artery branches can contribute to rectal anastomoses.

Venous Drainage

 Submucosal venous plexus connects with external rectal venous plexus running in adventitia.
 Rectal venous plexuses have connections to portal and cavel venous drainage systems and
are basis for formation of haemorrhoid’s (e.g., with portal hypertension in liver disease).
 Portal venous system tributaries (left side)
 Inferior mesenteric branches: rectal (hemorrhoidal) venous plexus drainage, down to
dentate line
 Internal iliac vein tributaries
 External rectal (hemorrhoidal) venous plexuses, below dentate line

Mesenteric ischemia

Mesenteric ischemia occurs when narrowed or blocked arteries restrict blood flow to your small
intestine. Decreased blood flow can permanently damage the small intestine. Sudden loss of blood
flow to the small intestine (acute mesenteric ischemia) from a blood clot requires immediate
surgery. Mesenteric ischemia that develops over time (chronic) is treated with angioplasty or open
surgery.
Symptoms
Acute mesenteric ischemia

Signs and symptoms of the acute form of mesenteric ischemia include:

 Abrupt, severe abdominal pain

 Urgent need to have a bowel movement

 Fever

 Nausea and vomiting

Causes

Both acute and chronic mesenteric ischemia are caused by a decrease in blood flow to
the small intestine. Acute mesenteric ischemia is most commonly caused by a blood clot
in the main mesenteric artery. The blood clot often originates in the heart. The chronic
form is most commonly caused by a buildup of plaque that narrows the arteries.

Complications

If not treated promptly, acute mesenteric ischemia can lead to:

 Sepsis. This potentially life-threatening condition is caused by the body

releasing chemicals into the bloodstream to fight infection. In sepsis, the
body overreacts to the chemicals, triggering changes that can lead to
multiple organ failure.

 Irreversible bowel damage. Insufficient blood flow to the bowel can cause

parts of the bowel to die.

 Death. Both above complications can lead to death.

Diagnosis

Your doctor might suspect that you have chronic mesenteric ischemia if you have pain
after eating that causes you to limit food and lose weight. A narrowing of the major
arteries to the small intestine can help confirm the diagnosis.

Tests might include:

  Angiography. Your doctor might recommend a CT scan, MRI or X-ray of
your abdomen to determine if the arteries to your small intestine have
narrowed. Adding a contrast dye (mesenteric angiogram, CT angiography or
magnetic resonance angiography) can help pinpoint the narrowing.

 Doppler ultrasound. This non-invasive test uses sound waves to estimate

blood flow, which can determine narrowing of the arteries.

 Treatment
 If a blood clot causes a sudden loss of blood flow to the small intestine, you might
require immediate surgery to treat your mesenteric ischemia. Mesenteric
ischemia that develops over time might be treated with a procedure that uses a
balloon to open the narrowed area.
 A mesh tube (stent) might be placed in the narrowed area. Mesenteric ischemia
can also be treated via open surgery through an incision.

Hemorrhoids

Haemorrhoids, also called piles, are swollen veins in your anus and lower rectum,
similar to varicose veins. Haemorrhoids can develop inside the rectum (internal
haemorrhoids) or under the skin around the anus (external haemorrhoids). Nearly
three out of four adults will have haemorrhoids from time to time. Haemorrhoids have
several causes, but often the cause is unknown. Fortunately, effective options are
available to treat haemorrhoids. Many people get relief with home treatments and
lifestyle changes.

Symptoms

Signs and symptoms of hemorrhoids usually depend on the type of hemorrhoid.

External hemorrhoids

These are under the skin around your anus. Signs and symptoms might include:
  Itching or irritation in your anal region

 Pain or discomfort

 Swelling around your anus

 Bleeding

Internal hemorrhoids

Internal hemorrhoids lie inside the rectum. You usually can't see or feel them, and
they rarely cause discomfort. But straining or irritation when passing stool can cause:

 Painless bleeding during bowel movements. You might notice small

amounts of bright red blood on your toilet tissue or in the toilet.

 A hemorrhoid to push through the anal opening (prolapsed or protruding

hemorrhoid), resulting in pain and irritation.

Thrombosed hemorrhoids

If blood pools in an external hemorrhoid and forms a clot (thrombus), it can result in:

 Severe pain

 Swelling

 Inflammation

 A hard lump near your anus

Causes

The veins around your anus tend to stretch under pressure and may bulge or swell.
Hemorrhoids can develop from increased pressure in the lower rectum due to:

 Straining during bowel movements

 Sitting for long periods of time on the toilet

 Having chronic diarrhea or constipation

 Being obese

 Being pregnant

 Having anal intercourse

  Eating a low-fiber diet

 Regular heavy lifting

Risk factors

As you age, your risk of hemorrhoids increases. That's because the tissues that
support the veins in your rectum and anus can weaken and stretch. This can also
happen when you're pregnant, because the baby's weight puts pressure on the anal
region.

Complications

Complications of hemorrhoids are rare but include:

 Anemia. Rarely, chronic blood loss from hemorrhoids may cause

anemia, in which you don't have enough healthy red blood cells to carry
oxygen to your cells.

 Strangulated hemorrhoid. If the blood supply to an internal hemorrhoid

is cut off, the hemorrhoid may be "strangulated," which can cause
extreme pain.

 Blood clot. Occasionally, a clot can form in a hemorrhoid (thrombosed

hemorrhoid). Although not dangerous, it can be extremely painful and
sometimes needs to be lanced and drained.

Prevention

The best way to prevent hemorrhoids is to keep your stools soft, so they pass easily.
To prevent hemorrhoids and reduce symptoms of hemorrhoids, follow these tips:

 Eat high-fiber foods. Eat more fruits, vegetables and whole grains.

Doing so softens the stool and increases its bulk, which will help you
avoid the straining that can cause hemorrhoids. Add fiber to your diet
slowly to avoid problems with gas.

 Drink plenty of fluids. Drink six to eight glasses of water and other

liquids (not alcohol) each day to help keep stools soft.

 Consider fiber supplements. Most people don't get enough of the

recommended amount of fiber — 20 to 30 grams a day — in their diet.
 Studies have shown that over-the-counter fiber supplements, such as
psyllium (Metamucil) or methylcellulose (Citrucel), improve overall
symptoms and bleeding from hemorrhoids.

If you use fiber supplements, be sure to drink at least eight glasses of

water or other fluids every day. Otherwise, the supplements can cause or
worsen constipation.

 Don't strain. Straining and holding your breath when trying to pass a

stool creates greater pressure in the veins in the lower rectum.

 Go as soon as you feel the urge. If you wait to pass a bowel movement
and the urge goes away, your stool could dry out and be harder to pass.

 Exercise. Stay active to help prevent constipation and to reduce

pressure on veins, which can occur with long periods of standing or
sitting. Exercise can also help you lose excess weight that might be
contributing to your hemorrhoids.

 Avoid long periods of sitting. Sitting too long, particularly on the toilet,

can increase the pressure on the veins in the anus.

Diagnosis

Your doctor might be able to see external hemorrhoids. Diagnosing internal

hemorrhoids might include examination of your anal canal and rectum.

 Digital examination. Your doctor inserts a gloved, lubricated finger into

your rectum. He or she feels for anything unusual, such as growths.

 Visual inspection. Because internal hemorrhoids are often too soft to be

felt during a rectal exam, your doctor might examine the lower portion of
your colon and rectum with an anoscope, proctoscope or sigmoidoscope.

Your doctor might want to examine your entire colon using colonoscopy if:

 Your signs and symptoms suggest you might have another digestive
system disease

 You have risk factors for colorectal cancer

 You are middle-aged and haven't had a recent colonoscopy

Medications
If your hemorrhoids produce only mild discomfort, your doctor might suggest over-
the-counter creams, ointments, suppositories or pads. These products contain
ingredients such as witch hazel, or hydrocortisone and lidocaine, which can
temporarily relieve pain and itching.

Don't use an over-the-counter steroid cream for more than a week unless directed by
your doctor because it can thin your skin.

External hemorrhoid thrombectomy

If a painful blood clot (thrombosis) has formed within an external hemorrhoid, your
doctor can remove the hemorrhoid, which can provide prompt relief. This procedure,
done under local anesthesia, is most effective if done within 72 hours of developing a
clot.

Minimally invasive procedures

Rubber band ligation of hemorrhoidOpen pop-up dialog box

For persistent bleeding or painful hemorrhoids, your doctor might recommend one of
the other minimally invasive procedures available. These treatments can be done in
your doctor's office or other outpatient setting and don't usually require anesthesia.
  Rubber band ligation. Your doctor places one or two tiny rubber bands
around the base of an internal hemorrhoid to cut off its circulation. The
hemorrhoid withers and falls off within a week.

Hemorrhoid banding can be uncomfortable and cause bleeding, which

might begin two to four days after the procedure but is rarely severe.
Occasionally, more-serious complications can occur.

 Injection (sclerotherapy). Your doctor injects a chemical solution into

the hemorrhoid tissue to shrink it. While the injection causes little or no
pain, it might be less effective than rubber band ligation.

 Coagulation (infrared, laser or bipolar). Coagulation techniques use

laser or infrared light or heat. They cause small, bleeding internal
hemorrhoids to harden and shrivel. Coagulation has few side effects and
usually causes little discomfort.

Surgical procedures

Only a small percentage of people with hemorrhoids require surgery. However, if

other procedures haven't been successful or you have large hemorrhoids, your
doctor might recommend one of the following:

 Hemorrhoid removal (hemorrhoidectomy). Choosing one of various

techniques, your surgeon removes excessive tissue that causes
bleeding. The surgery can be done with local anesthesia combined with
sedation, spinal anesthesia or general anesthesia.

Hemorrhoidectomy is the most effective and complete way to treat

severe or recurring hemorrhoids. Complications can include temporary
difficulty emptying your bladder, which can result in urinary tract
infections. This complication occurs mainly after spinal anesthesia.

Most people have some pain after the procedure, which medications can
relieve. Soaking in a warm bath also might help.

 Hemorrhoid stapling. This procedure, called stapled hemorrhoidopexy,

blocks blood flow to hemorrhoidal tissue. It is typically used only for
internal hemorrhoids.

Stapling generally involves less pain than hemorrhoidectomy and allows

for earlier return to regular activities. Compared with hemorrhoidectomy,
 however, stapling has been associated with a greater risk of recurrence
and rectal prolapse, in which part of the rectum protrudes from the anus.

Complications can also include bleeding, urinary retention and pain, as

well as, rarely, a life-threatening blood infection (sepsis). Talk with your
doctor about the best option for you.

Colon Ischemia
Colon ischemia (CI) is an underrecognized entity associated with high
morbidity and mortality. Establishing the diagnosis and initiating appropriate
and timely treatment is critical for improving outcomes. Colon ischemia is a
disease spectrum that requires a full understanding for recognition and
treatment. This review outlines the full spectrum of CI management from
initial presentation to medical and surgical treatment.

Colon ischemia (CI), as opposed to acute mesenteric ischemia (AMI) that

affects the small bowel, is the most common type of mesenteric ischemia.

Etiology and Risk Factors

The 3 main mechanisms responsible for CI include nonocclusive CI, embolic and
thrombotic arterial occlusion, and mesenteric venous thrombosis (MVT). Nonocclusive
CI, caused by hypoperfusion of the mesenteric microvasculature, is by far the most
common mechanism, occurring in 95% of patients.3 This type of ischemia is usually
most prominent at the “watershed” areas (ie, splenic flexure and rectosigmoid junction)8;
however, any segment of the colon can be affected.5 The rectum is uncommonly
involved because of a dual blood supply from both splanchnic and systemic arterial
systems.9 Typically, nonocclusive CI is transient; however, prolonged severe ischemia
causes necrosis of the mucosal layer with potential for transmural infarction.10 Colonic
injury is related to both the hypoxic component during the episode of decreased blood
flow and the sequelae of reperfusion, which is mainly seen after partial ischemia. Here,
reperfusion results in the release of oxygen free radicals and other toxic by-products.11
Less commonly, CI can result from arterial thromboemboli or from MVT, which almost
always involves the proximal colon.12

Colon ischemia typically occurs in well-defined clinical settings, particularly in patients

with vascular risk factors. These include diabetes mellitus, coronary artery disease, and
peripheral vascular disease.4, 13 However, it can also occur without identifiable risk
factors. The heterogeneous risk factors for CI support a multifactorial pathogenesis and
emphasize the importance of a careful assessment of the medical, surgical, and
medication/drug use history in every patient with CI. Irritable bowel syndrome (IBS),
constipation, and surgical procedures such as abdominal aortic aneurysm repair are
known risk factors.14, 15, 16 Interestingly, patients with IBS exhibited increased
ischemic hypersensitivity as compared with the general population, which may account
for the disproportionate number of patients with IBS presenting for medical evaluation of
CI.17 Eliciting a thorough medication history is important, especially focused on
constipation-inducing medications (eg, opioids), immunomodulators (eg, azathioprine
and type I interferons), and illicit drugs (eg, cocaine).18, 19, 20 In addition,
neuromodulating and vasoconstricting medications, such as quetiapine and rizatriptan,
are recognized precipitants of CI.21, 22

Evaluation of thrombophilia as a cause of CI should be considered in young patients and

all patients with recurrent CI.23, 24 The degree to which acquired or hereditary
hypercoagulable states contribute to the pathogenesis of CI is not well understood.
However, the prevalence of antiphospholipid antibodies, plasminogen activator
inhibitors, and factor V Leiden sequence variations are increased in patients with CI.24

Clinical Manifestations
The clinical manifestations of CI vary depending on the extent and duration of ischemia.
Most patients have self-limiting, nongangrenous ischemia, which typically resolves
completely.
25

 However, approximately 10% of patients develop colonic necrosis and gangrene, which can
be life-threatening.
26

 These patients have a more protracted hospital course and tend to develop long-term
complications, such as chronic ischemic colitis or strictures.
Patients with CI typically present with abrupt, cramping abdominal pain of mild to moderate
severity that often affects the left side of the abdomen. This is often accompanied by an
urgent desire to defecate and the subsequent passage of bloody diarrhea within 24 hours.
5

 
, 

 Colon ischemia should be considered when the presenting symptoms are abdominal pain and
bloody diarrhea.
5

 
, 

6
 Compared with ischemia affecting the small intestine, the cramping pain that accompanies
CI is less severe and is felt laterally rather than periumbilically.
5

 
, 

 In addition, gastrointestinal hemorrhage is an unusual presentation of AMI. In severe forms

of CI, transmural infarction occurs with resultant gangrenous colitis, which is characterized
by increasing abdominal tenderness, peritoneal signs, fever, and ileus. The sudden onset of a
toxic colitis with signs of peritonitis and a rapidly progressive course are hallmarks of
universal fulminant colitis, a rare variant of CI.
Colon ischemia tends to be a segmental process that is explained by the colon being perfused
by 3 vessels: the superior mesenteric artery, the inferior mesenteric artery, and the internal
iliac artery.
5

 Although CI is often segmental and involves the left colon, it is recognized that isolated right
colon ischemia (IRCI) has a different clinical presentation and worse outcomes than does CI
affecting any other region of the colon.
5

 
, 

27

 In addition, CI may have a pancolonic distribution that carries a poor prognosis similar to
that of IRCI, with a mortality rate of up to 21%.
5

Diagnosis
A diagnosis of CI is usually suspected on the basis of history, physical examination, and
clinical setting. The differential diagnosis in patients presenting with abdominal pain and
bloody diarrhea is broad and includes inflammatory bowel disease, infectious colitis, and
colonic adenocarcinoma. Initial laboratory studies should include complete blood count,
metabolic panel, serum lactate level, lactate dehydrogenase (LDH) level, creatine kinase
level, and amylase level. White blood cell count is useful for prognostic purposes,
hemoglobin level evaluates blood loss, and acid/base status can be assessed from bicarbonate,
lactate, and LDH levels. Elevated amylase levels are associated with acute bowel ischemia.
28

 Although these laboratory tests are not diagnostic for CI, obtaining them during the initial
work-up helps in risk stratification. Synchronous stool studies should be ordered to rule out
an infectious etiology of bloody diarrhea, including stool culture, ova and parasite testing,
and Clostridium difficile toxin assay. Although C difficile infection rarely presents with
bloody diarrhea, given its increasing incidence and severity, testing for it should be part of
the initial assessment.
Computed tomography (CT) with intravenous and oral contrast is recommended as the first
imaging modality for patients with suspected CI to assess the distribution and phase of colitis.
29

 
, 

30

 The diagnosis of CI can be suggested on the basis of CT findings (eg, edema, bowel wall
thickening, and thumbprinting).
29

 
, 

30

 Initial CT scans may be nonspecific with segmental wall thickening which also may be seen
with infectious and Crohn colitis.
Formal vascular imaging studies are usually not indicated in patients with suspected CI
because at the time of the presentation, blood flow has usually returned to normal levels in
the most common nonocclusive type of CI. The subsequent pathological changes reflect the
ischemic insult to the colonic mucosa with reperfusion injury, rather than from ongoing
ischemia. Multiphasic CT angiography (CTA) should be performed on any patient with IRCI,
as the ischemic episode may be the heralding event of a focal occlusion by embolus or
thrombus of the superior mesenteric artery with impending AMI. Furthermore, CTA should
be pursued in any patient in whom the possibility of AMI cannot be excluded.
30

 Severe pain that is “out of proportion” to physical examination without bleeding is

characteristic of AMI. Computed tomographic or magnetic resonance imaging findings of
colonic pneumatosis and portomesenteric venous gas suggest transmural colonic infarction
complicating CI, which mandates urgent exploratory laparotomy.
31

 In a patient in whom the presentation of CI may be a heralding sign of AMI and who has a
negative finding on multiphasic CTA, traditional splanchnic angiography should be
considered.
30

 The role of other types of imaging is limited. A plain abdominal radiograph is frequently
nonspecific with bowel distension or pneumatosis observed only in advanced ischemia with
infarction. Barium enema has been superseded by CT and colonoscopy. Magnetic resonance
imaging has been studied in only a small number of patients with CI, with findings being
similar to those of CT.
32

 Overall, imaging can suggest or support the diagnosis of CI, but none of the imaging
findings are specific enough to make a diagnosis, except when infarction has occurred.
Colonoscopy is the principal modality used to diagnose CI, usually after CT reveals
nonspecific thickening of a colon segment. Colonoscopy allows tissue sample acquisition and
direct visualization of the colonic mucosa. Common findings in transient CI are edematous
and fragile mucosa, segmental erythema, scattered erosions, longitudinal ulcerations,
petechial hemorrhages interspersed with pale areas, purple hemorrhagic nodules, and a
sharply defined segmental involvement.
33

 The colon single-stripe sign is a highly specific sign of CI, defined as a single inflammatory
band of erythema with erosion along the longitudinal axis of the colon.
34

 Early colonoscopy, within 48 hours of presentation, should be performed in patients with

suspected CI to confirm the diagnosis.
26

 
, 

35

 In patients with severe CI, limited colonoscopy with biopsies, stopping at the distal most
extent of disease, should be performed to confirm the nature of the CT abnormality. Biopsies
should be deferred in cases of gangrene. Colonoscopy should not be performed in patients
who have signs of acute peritonitis or evidence of irreversible ischemic damage on imaging
studies. Sigmoidoscopy is limited in its ability to reliably diagnose CI.
36

 If the diagnosis remains in question, abdominal exploration may be needed.

Clinical Management
A proposed algorithm for the management of CI (adapted from recent
guidelines
3

) is shown in the Figure. Before deciding on the appropriate management,

patients should be risk stratified into mild, moderate, or severe disease,
with tailored treatment promptly initiated.
3

 Patients with mild disease have typical symptoms of CI, with a segmental

colitis not isolated to the right colon and absence of the poor prognostic
factors observed in moderate disease.
3

 Moderate disease includes any patient with up to 3 of the following factors:

male sex, hypotension, tachycardia, abdominal pain without rectal
bleeding, blood urea nitrogen level greater than 20 mg/dL, hemoglobin
level less than 12 g/dL, LDH level greater than 350 U/L, serum sodium
level less than 136 mEq/L, white blood cell count greater than 15×109/L, or
colonoscopically identified mucosal ulceration.
3

 Severe disease is defined by more than 3 of the previously listed criteria

or any of the following: peritoneal signs on physical examination,
pneumatosis or portal venous gas on CT, gangrene on colonoscopy, or a
pancolonic distribution or IRCI on CT or colonoscopy.
3

 Finally, chronic kidney disease with dialysis or poor Eastern Cooperative

Oncology Group status has recently been shown to be an independent risk
factor for severe disease,
37

 but is not included in the American College of Gastroenterology risk-

stratifying model.
Most cases of CI resolve spontaneously and do not require specific
therapy. These patients have reversible ischemic colopathy or transient
ulcerating CI.
38

 
, 

39

 Patients with more significant disease require hospitalization to monitor for

complications and signs of irreversible disease. Initial medical management
centers on general supportive measures such as bowel rest, intravenous
hydration, and correction of precipitating conditions.
3
 Parenteral nutrition may be indicated if a protracted course is predicted.
No specific therapeutic modality has ever been tested in a clinical trial
setting. Broad-spectrum antimicrobial therapy should be considered for
patients with moderate or severe disease,
38

 
, 

39

 
, 

40

 because of the perceived increased risk of bacterial translocation in the

setting of acute ischemia and reperfusion injury. The antibiotic regimen
typically consists of an antianaerobic agent plus a fluoroquinolone.
3

 Glucocorticoids have no role, unless the CI is a complication of vasculitis.

Antithrombotic therapy is not indicated for most patients with CI as most
patients have nonocclusive ischemia. However, anticoagulant therapy is
indicated when ischemia develops owing to MVT or ischemia secondary to
cardiac thromboembolization. If a cardiac source of embolism is suspected,
an electrocardiogram, Holter monitoring, and transthoracic echocardiogram
should be obtained.
Surgical intervention should be considered in the presence of CI
accompanied by peritonitis, hemodynamic instability, IRCI, and pancolonic
CI as well as in the presence of gangrene.
26

 
, 

38

 
, 

39

 Without surgical intervention, mortality from necrotic bowel approaches

100%, and mortality after surgical intervention for CI is upward toward 50%.
41

 
, 

42

 The surgical procedure depends on the nature and extent of the CI but
most commonly includes total or subtotal colectomy, right hemicolectomy,
or segmental colectomy with either a primary anastomosis or a diverting
stoma.
Patients with CI can develop sequelae of the disease, even after
reperfusion. Therefore, close follow-up is important after an episode of CI.
The management approach to CI is outlined in the Table. Strategies for
prevention of recurrent episodes of CI should focus on blood pressure
management to ensure optimal colonic perfusion, aggressive treatment of
constipation, and education on maintaining appropriate hydration,
especially in the setting of illness or exercise. A full medication review
should occur, with attention to medications listed earlier in this review.
Moreover, in young patients (<40 years of age) with CI or those presenting
with recurrent CI without obvious risk factors, evaluation of
hypercoagulable states should be considered.
27

 
, 

28

 
, 

29

 Of note, severe ischemia causes ulceration and inflammation, which may
evolve into segmental ulcerating colitis or fibrotic strictures. These lesions
may be asymptomatic, but they should be followed by repeat endoscopy to
document healing or the development of persistent colitis or stricture.
3

 Colonic strictures can usually be observed, with surgery indicated only

when symptomatic. Endoscopic dilation of an ischemic stricture is an
alternative to surgery, although this modality has not been formally
evaluated in strictures secondary to CI. Recurrent episodes of bacteremia
or sepsis in patients with unhealed areas of segmental colitis are
indications for elective segmental colon resection.
Mesenteric Vascular Disease
Mesenteric vascular disease is a condition that develops when the arteries in the
abdomen that supply the intestines with blood become narrowed due to the build-up
of plaque (a process called atherosclerosis). The result is a lack of blood supply to
the intestines. The disease can come on suddenly with severe abdominal pain or
may develop over time.

Risk factors for mesenteric vascular disease include atrial fibrillation, heart failure,

chronic renal failure, smoking, a family history of atherosclerosis, high blood
pressure, diabetes, high cholesterol, advanced age, obesity and a sedentary
lifestyle.

Symptoms
Patients with mesenteric artery disease often experience weight loss and severe
abdominal pain following meals. Other symptoms include vomiting, dizziness and
low blood pressure due to accumulation of acid in the blood.

Diagnosis
Diagnosis is typically made through ultrasound or direct imaging of the artery.
Imaging tests include CT scan, magnetic resonance angiography (MRA) or an
arteriography, which can be used to determine the location and the extent of the
disease.

Treatment Options
Patients whose symptoms are mild to moderate can often manage their disease by
making lifestyle changes that include: quitting smoking, getting regular exercise and
managing related conditions such as diabetes, high blood pressure and high
cholesterol.

Surgical Options
Endarterectomy:  Involves the surgical removal of plaque build-up on the inner
lining of the artery.

Bypass Grafting: Redirects blood flow around an area of blockage. The procedure

creates an alternate channel for blood flow, bypassing an obstructed or damaged
vessel. The graft may come from a healthy section of the patient's own vein, or from
a synthetic material such as Dacron™.

Endovascular Options
Balloon Angioplasty and Stenting: A catheter with a small balloon at the end is
inserted through an artery in the groin and guided to the narrowed segment of the
artery. When the catheter reaches the blockage, the balloon is inflated to widen the
narrowed artery (known as balloon angioplasty).
In some cases, it may be necessary to place a stent (a wire-mesh tube that expands
to hold the artery open). The stent is left permanently in the artery to provide a
reinforced channel for blood flow.

Superior mesenteric artery syndrome

Superior mesenteric artery syndrome (SMAS) is a digestive condition that occurs when the
duodenum (the first part of the small intestine) is compressed between two arteries (the aorta
and the superior mesenteric artery). This compression causes partial or complete blockage of
the duodenum.[1] Symptoms vary based on severity but can be severely debilitating.[2]
Symptoms may include abdominal pain, fullness, nausea, vomiting, and/or weight loss.[3]
SMAS typically is due to loss of the mesenteric fat pad (fatty tissue that surrounds the
superior mesenteric artery). The most common cause is significant weight loss caused by
medical disorders, psychological disorders, or surgery. In younger patients, it most
commonly occurs after corrective spinal surgery for scoliosis. Delays in diagnosis may result
in significant complications. Depending on the cause and severity, treatment options may
include addressing the underlying cause, dietary changes (small feedings or a liquid diet),
and/or surgery. Symptoms may not resolve completely after treatment.

Symptoms

The signs and symptoms of superior mesenteric artery syndrome vary but may

include:[3][5][1]
 Feeling full quickly when eating
 Bloating after meals
 Burping (belching)
 Nausea and vomiting of partially digested food or bile-like liquid
 Small bowel obstruction
 Weight loss
 Mid-abdominal "crampy" pain that may be relieved by the prone or knee-chest
position or by lying on the left side

Cause
SMAS typically is due to loss of the mesenteric fat pad (fatty tissue that surrounds the
superior mesenteric artery).[3] The superior mesenteric artery forms an angle with the
abdominal aorta (due in part to the mesenteric fat pad), and part of the duodenum sits within
this angled space. Anything that sharply narrows the angle between the aorta and superior
mesenteric artery can cause compression of the duodenum, resulting in SMAS.[1][3]
The most common cause of loss of the mesenteric fat pad is significant weight loss caused by
medical disorders, psychological disorders, or surgery. Anatomic abnormalities can also
contribute to SMAS. In younger patients, it most commonly occurs after corrective spinal
surgery for scoliosis.[3]

There are some reports of familial cases of SMAS, and one report of affected identical twins.
This suggests there may be a genetic predisposition to SMAS in some people.[3][6]

There are also several reported cases of SMAS associated with celiac axis compression
syndrome.[3]

Inheritance
SMAS is not considered an inherited condition. Most cases occur sporadically in people with
no family history of SMAS.[1]

There are some reports of familial cases of SMAS, and one report of affected identical twins.
This suggests there may be a genetic predisposition to SMAS in some people.

Diagnosis
Superior mesenteric artery syndrome (SMAS) may be suspected based on signs and
symptoms, although symptoms can be nonspecific. The diagnosis is often made after other
causes of symptoms have been ruled out.

Tests that may be needed to evaluate a person with symptoms of SMAS include abdominal
X-rays, upper GI series, ultrasound, arteriography, and computed tomography (CT scan).

Diagnosis is often delayed, and this may result in significant complications, including gastric
pneumatosis (gas within the walls of the GI tract), accumulation of gas in the portal vein,
formation of an obstructing duodenal bezoar (solid mass of indigestible material), or fatalities
due to electrolyte abnormalities or gastric perforation.

Treatment
Treatment for superior mesenteric artery syndrome typically focuses on addressing the
underlying cause of the condition. For example, symptoms often improve after lost weight is
restored or a body cast is removed. Nasogastric decompression (a tube passed through the
nose into the stomach) and proper positioning after eating (such as lying in the left side or
standing or sitting with a knee-to-chest position) may be recommended to alleviate
symptoms.

In severe cases, intravenous (IV) nutritional support and/or a feeding tube may be needed to
provide enough calories. Affected people can usually then be started on oral liquids, followed
by slow and gradual introduction of small and frequent soft meals as tolerated. Then, regular
solid foods may be introduced. Metoclopramide treatment to avoid vomiting may be
beneficial for some people.

Surgery may be needed if other treatment strategies do not work. However, other treatment
options should usually be tried for at least 4-6 weeks before considering surgery.

Surgery options are:

Strong’s procedure: Where the duodenum is re-positioned to the right of the superior
mesenteric artery

Gastrojejunostomy: Where the jejune (the part of the intestines that continues with the
duodenum) is joined directly to the stomach

Duodenojejunostomy with or without division or resection of the fourth part of the

duodenum.

Prognosis
Superior mesenteric artery syndrome can be severely debilitating and may require
long term management, medications, costly parenteral nutrition (intravenous
feeding) and rigorous follow-up. The long-term outlook (prognosis) can depend on
whether the condition is diagnosed and treated in a timely manner. The prognosis
may be excellent if it is diagnosed quickly and appropriate therapy is given.
[1]
 However, the condition may go unrecognized until a person experiences symptoms
for a long time. In the past, deaths have been reported due to complications including
progressive dehydration, hypokalaemia (low potassium), and oliguria (producing too
little urine). Most deaths have been reported in people in whom the diagnosis was
delayed or missed.

Other complications that may arise in people with SMAS include

 Other electrolyte imbalances
 Malnutrition
 Hypotension
 Peptic ulcer disease
 Aspiration pneumonia