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SMALL INTESTINE 411
S u g g e S t e d R e a d i n g
Avalos-González J, Portilla-deBuen E, Leal-Cortés CA, etal. Reduction of the
closure time of postoperative enterocutaneous stulas with brin sealant.
World J Gastroenterol. 2010;16(22):2793–2800.
Berry SM, Fischer JE. Enterocutaneous stulas. Curr Probl Surg.
1994;31(6):469–566.
Coughlin S, Roth L, Lurati G, Faulhaber M. Somatostatin analogues for the
treatment of enterocutaneous stulas: a systematic review and meta-analysis. World J Surg. 2012;36(5):1016–1029.
Davis KG, Johnson EK. Controversies in the care of the enterocutaneous s-
tula. Surg Clin North Am. 2013;93(1):231–250.
Draus JM Jr, Huss SA, Harty NJ, etal. Enterocutaneous stula: are treatments
improving? Surgery. 2006;140(4):570–576.
Edmunds H, Williams GH, Welch CE. External stulas arising from the gas-
trointestinal tract. Ann Surg. 2007;143(8):793–796.
Evenson AR, Fischer JE. Current management of enterocutaneous stula.
JGastrointest Surg. 2006;10(3):455–464.
Kuvshino BW, Brodish RJ, McFadden DW, Fischer JE. Serum transferrin as
a prognostic indicator of spontaneous closure and mortality in gastrointestinal cutaneous stulas. Ann Surg. 1993;217(6):615–622.
Lloyd DA, Gabe SM, Windsor AC. Nutrition and management of enterocuta-
neous stula. Br J Surg. 2006;93(9):1045–1055.
Mullen JL, Buzby GP, Matthews DC, et al. Reduction of operative morbid-
ity and mortality by combined preoperative and postoperative nutritional
support. Ann Surg. 1980;192(5):604.
Polk TM, Schwab CW. Metabolic and nutritional support of the enterocutane-
ous stula patient: a three-phase approach. World J Surg. 2012;36(3):524–
533.
Schecter WP. Management of enterocutaneous stulas. Surg Clin North Am.
2011;91(3):481–491.
Slade DA, Carlson GL. Takedown of enterocutaneous stula and complex ab-
dominal wall reconstruction. Surg Clin North Am. 2013;93(5):1163–1183.
Soeters PE, Ebeid AM, Fischer JE. Review of 404 patients with gastrointestinal
stulas: impact of parenteral nutrition. Ann Surg. 1979;190(2):189–202.
A C
M I
Susan Galandiuk, Jeffrey R. Jorden, Jonathan Rice, and Peter G. Deveaux
INTRODUCTION
Mesenteric ischemia can be either acute or chronic. e acute variant
is a life-threatening disease of sudden onset and has several distinctly
dierent causes. Most patients who are diagnosed with acute visceral
ischemia have progressed to the point of bowel necrosis. Early recognition of acute ischemia is essential to permit timely intervention
prior to bowel necrosis, irreversible multisystem organ failure, and
death. It occurs in the aging population in most developed countries with increasing frequency and is associated with many low ow
states, some of which are induced in the hospital, and may occur in
visceral arteries or veins.
Chronic visceral ischemia, on the other hand, is a manifestation of
systemic atherosclerosis and is not immediately life threatening. e
quality of life for patients with chronic ischemia can be signicantly
improved by surgical revascularization of one or more visceral arteries.
ACUTE MESENTERIC ISCHEMIA
Acute mesenteric ischemia is now encountered with increasing frequency. e consequences of unrecognized ischemia and infarction
of the viscera are devastating; in many patients, multisystem organ
failure and death are unavoidable. e causes of acute mesenteric
ischemia are listed in Table 79-1. e most frequent causes are
embolization to the superior mesenteric artery (SMA) and thrombosis of the SMA, accounting for roughly 50% and 25% of cases,
respectively. Arterial emboli, which occur most commonly in the
SMA, usually lodge 3 to 10 cm distal to the vessel origin, particularly where the vessel begins to narrow at the origin of the middle
colic artery. SMA thrombosis, on the other hand, generally occurs
at its origin. Patients who present with thrombosis oen have had
chronic mesenteric ischemia, which predisposes them to sudden
occlusion of an already stenotic vessel.
Nonocclusive mesenteric ischemia (NOMI), which accounts for
25% of cases of intestinal ischemia, results from hypovolemia, cardiac failure, sepsis, digitalis therapy, and alpha-adrenergic drugs.
e increasing use of vasopressors that diminish bowel blood ow
is responsible. Not surprisingly, the need for and use of vasopressors
of any kind, when linked with a variety of hypotensive states, sets
any patient up for mesenteric arterial or venous occlusions. Digitalis
may cause abnormal mesenteric vasospasm and is at least partially
involved with the majority of cases of NOMI. Mortality rates from
NOMI are as high as 70% because of the diculty of early diagnosis. Patients undergoing hemodialysis who experience periods of
hypotension during dialysis are at risk for NOMI. ese patients classically present with an occluded dialysis shunt that is an indicator
of the hypotensive episode. NOMI typically involves the watershed
areas of the splenic exure and le colon, except in rare instances
of hypotension related to trauma, which more oen produces right
colon ischemia.
Acute mesenteric venous thrombosis is caused by hypercoagulable states and results in massive influxes of fluid into the
bowel wall and lumen. Conditions associated with visceral venous
thrombosis include any of the inherited hypercoagulable states
(Box 79-1), cirrhosis, inflammatory bowel disease, trauma, pancreatitis, and cancer. The mortality rate with mesenteric venous
thrombosis is greater than 80%; those figures may change because
venous thromboses are now often seen on abdominal CT scans in
relatively well patients. Such patients must be watched carefully
even in the absence of acidosis and leukocytosis.
Other, more unusual causes of acute mesenteric ischemia include
aortic dissection, cardiopulmonary bypass, and median arcuate ligament compression. Visceral artery occlusion will develop in some
patients with aortic dissection and is an absolute indication for
repair of the dissection. Mesenteric ischemia has been described in
patients aer cardiopulmonary bypass and appears to be a type of
NOMI. Patients in whom NOMI develops aer cardiopulmonary
bypass oen, but not always, are those subjected to intraaortic balloon pumps or vasopressor support for cardiac dysfunction. Median
arcuate ligament compression of the SMA or celiac axis is another
unusual cause of mesenteric ischemia that may require surgery to
release the ligament and revascularize the involved vessels. Although
familial variants of both arterial and venous occlusion exist, fortunately, they are rare.
Clinical Presentation
Patients with acute mesenteric ischemia have sudden onset of
abdominal pain that is often “far out of proportion” to the findings
on physical examination. Patients may have nausea, vomiting,
and either frank or occult gastrointestinal bleeding. Obtaining
a thorough patient history is crucial in the early differentiation
of the various forms of mesenteric ischemia. Specific history taking should include cardiac arrhythmias, pain with weight loss,
malignancy, and hematologic abnormalities. Presentation may
follow an episode of hypotension or the recent institution of digitalis therapy (both suggestive of NOMI). Acidosis and profound
leukocytosis are the most frequently recognized laboratory test
results.
Acute ischemia has three phases of presentation:
1. e initial phase is extremely painful and may consist of
abdominal pain, vomiting, diarrhea, and gastrointestinal
hemorrhage.
2. e intermediate phase is more vague and nonspecic.
3. e nal phase signies that bowel necrosis has occurred, and
pain may temporarily disappear.
412
TABLE 79-1: Causes of Acute Mesenteric Ischemia
Approximate
Cause Source
SMA embolus Cardiac 50
Incidence (%)
SMALL INTESTINE 413
SMA thrombosis Underlying
25
atherosclerosis
NOMI Low ow states,
20
medication
Mesenteric venous
thrombosis
NOMI, Nonocclusive mesenteric ischemia; SMA, superior mesenteric artery.
Hypercoagulable
states
5
BOX 79-1: Hypercoagulable states
Protein C and S deciency
Antithrombin III deciency
Dysbrinogenemia
Abnormal plasminogen
Polycythemia vera
Factor V Leiden mutation
rombocytosis
Sickle cell disease
Evaluation
Patients with acute mesenteric ischemia may have substantial
leukocytosis, fever, metabolic acidosis, and peritonitis, but these
signs often occur late, when bowel necrosis has already occurred.
Serum amylase and lactate levels are often elevated. Lactate may
be the most useful laboratory test, because it is often elevated in
the early stages of ischemia, when other tests are less informative.
Elevated D-dimer levels may aid in diagnosis but are not specific
to ischemia. Other diagnostic assays including D-lactate, intestinal fatty acid binding protein, and the isoenzyme of glutathione
S-transferase have been reported, but none has reached routine
clinical practice. Diagnostic peritoneal lavage has been used but
may only demonstrate white blood cells when frank bowel necrosis or perforation is present. Diagnostic laparoscopy can confirm
the diagnosis.
Plain radiographs are generally nonspecific but are useful to
exclude other intra-abdominal processes. Radiographic signs that
suggest visceral ischemia include bowel wall thickening, intestinal pneumatosis, and portal vein gas, with the last being a sign of
advanced disease. Use of intraluminal contrast medium is contraindicated because it can interfere with later angiography.
Ultrasonography, which is used to demonstrate ow in the SMA
or celiac axis, is frequently obscured by dilated, gas-lled bowel
loops. A computed tomographic (CT) scan of the abdomen and pelvis can show bowel wall thickening, pneumatosis in the bowel wall,
or portal vein gas, and it is currently the study of choice. In fact, the
latest multidetector CT angiography has high sensitivity and speci-
but the gold standard in the diagnosis of acute mesenteric ischemia
remains biplanar mesenteric arteriography. Both anteroposterior and
lateral views of the visceral vessels are necessary to fully visualize all
three visceral vessels. Angiography can usually dierentiate emboli
from thrombosis, and the vasospasm of NOMI is readily apparent in
A
BB
FIGURE 79-1 Computed tomographic angiograms. A, Sagittal
maximum-intensity projection. A clot is extending from the aortic
lumen into the proximal superior mesenteric artery (arrow). The
superior mesenteric artery is reconstituted approximately 2.8 cm
beyond the origin. B, A clot centrally in the abdominal aorta extends
into and occludes the proximal inferior mesenteric artery (IMA).
smaller, branching arterioles, which may not be as well characterized
on CT angiography (Fig. 79-2).
Treatment
Initial treatment of acute mesenteric ischemia, which begins during patient evaluation, includes prompt fluid resuscitation, correction of acidosis, broad-spectrum antibiotics, and systemic
anticoagulation with heparin to prevent clot propagation. Patients
with peritoneal signs should be operated on without delay because
Acute And chronic Mesenteric ischeMiA414
FIGURE 79-2 A superior mesenteric arteriogram in a patient with
nonocclusive mesenteric ischemia, typified by tapering of distal arterial
branches. (From Allen KB, Salam AA, Lundsen AB. Acute mesenteric ischemia
after cardiopulmonary bypass. J Vasc Surg. 1992;16:393. Reprinted with
permission from Journal of Vascular Surgery and the American Association
for Vascular Surgery.)
they will all have some degree of bowel necrosis. In patients without peritonitis or other evidence of bowel necrosis, some authors
have advocated endovascular techniques. Most patients, however,
have significant abdominal symptoms that require assessment of
bowel viability and therefore a laparotomy.
SMA Embolus
At laparotomy, the SMA can be palpated at the base of the transverse mesocolon. When it is impaired or no flow is again assessed,
this site is convenient for an initial and quickly performed arteriotomy. The most common site for an embolus is just distal to the
middle colic artery. A Fogarty catheter often encounters emboli,
which can be extracted. The arteriotomy can be closed primarily
or with a patch. Bowel viability can then be assessed, and nonviable bowel can be resected. Time is of the essence for these fragile
patients, and the anesthetist should be alerted to systemic effects
of “wash out” from the previously ischemic small bowel.
SMA Thrombus
A collar-button stenotic arteriosclerotic lesion in the aorta is
the most common underlying cause of thrombotic SMA occlusion. Control of the aorta and the method of repair are complex.
Choices of reconstruction include antegrade bypasses from the
supraceliac aorta or retrograde bypasses from the iliac arteries.
The latter may be limited by distal arteriosclerotic disease. Both
autologous vein or prosthetic conduits can be used; however, in
the setting of a concomitant bowel resection, vein should be used
if possible. In some cases, an endarterectomy of the SMA can be
performed.
If an experienced clinical surgeon concurs, as with so many surgical illnesses today, a skilled angiographer can be helpful beyond
conrming the diagnosis. Approaching the aortic plaque stenosis in
the SMA is very dicult and bears the possibility of lower extremity embolism from the oen grumous aortic material. A conrming
angiogram with tiny amounts of contrast material must show
patency.
Mesenteric Venous Thrombosis
Treatment of mesenteric venous thrombosis has been primarily
systemic anticoagulation with resection of any necrotic bowel.
Venous thrombectomy has been of rare benefit because of delayed
diagnosis and the fact that the thrombus typically extends into
small veins.
Nonocclusive Mesenteric Ischemia
NOMI is treated via resection of necrotic bowel, continuous infusion of papaverine through a catheter in the SMA (both intraoperatively and postoperatively), and discontinuation of digitalis and
other vasoconstrictors. Papaverine is a vasodilator that reverses
mesenteric vasoconstriction. Heparin should never be administered through the same line as papaverine because precipitation
results when the two agents are combined. Papaverine infusion
should continue until the patient is asymptomatic and when repeat
arteriography no longer shows vasospasm. Figure 79-3 presents an
algorithm for evaluation and treatment of patients with acute mesenteric ischemia.
Long-term anticoagulation aer acute mesenteric ischemia is
controversial. Some persons advocate anticoagulation with warfarin
for venous thrombosis or arterial embolism and use of platelet inhibitors for arterial thrombosis or NOMI.
Bowel Viability
Determining bowel viability in the early ischemic period can be
difficult. The best criteria for determining viability include color,
palpable mesenteric pulses, and visible peristalsis. These combined
criteria are better indicators of bowel viability than intraoperative
Doppler, although Doppler also can be useful. Active bleeding
from adjacent mesenteric fat also can be an indicator of adequate
perfusion. Merely cutting a small segment of the adjacent fat will
allow visualization of adequate or inadequate bleeding. Another
technique for determining viability is fluorescein administration.
Viable bowel will absorb fluorescein dye, which will fluoresce
when viewed under an ultraviolet light (Wood lamp). Fluorescein
diffuses into all tissues that contain fat with time and is useless as
a viability marker if it is not assessed early after administration.
When all else fails to clarify viability, one can warm the patient,
“refill the tank (resuscitate the patient),” go to the recovery room,
and plan a repeat exploration empirically in 8 to 12 hours.
Matsui and colleagues have used indocyanine near-infrared angiography to assist with the assessment of bowel viability in both rats
and pigs. Presumably, this concept will assist with determination
of bowel status in humans, and in some scenarios, it may actually
help determine the need for laparotomy and/or repeat laparotomy.
Figure79-4 shows this technique being used to identify a segment
of bowel with decreased perfusion at repeat laparotomy in a patient
aer an anastomotic leak and peritonitis.
The stability of the patient and the pattern of ischemia of the
intestine determine whether primary reanastomosis is performed
after resection of necrotic bowel. If the margins of the ischemia
are not clearly defined, as may occur in NOMI, then reanastomosis should not be performed. The bowel ends are stapled and a
second-look laparotomy is performed at 24 to 48 hours. If clearly
viable margins are found, anastomosis or enterostomy may be
performed in stable patients. The threshold for a second-look
laparotomy must be low. If a second-look laparotomy is planned
Suspected acute mesenteric ischemia
Fluid resuscitation
Correction of acidosis
Broad-spectrum antibiotics
Consider anticoagulation
Discontinue digitalis
SMALL INTESTINE 415
Peritoneal signs or other indicator of
necrotic or perforated bowel
Operating room for resection of
necrotic bowel
24 to 48 hours later, assess viability of
remaining bowel:
• Clinical appearance
• Mesenteric fat bleeding
• Fluorescein/UV light
• Indocyanin angiography
Normal SMA
Consider
alternate
diagnosis
Embolus
Embolectomy
and
anticoagulation
SMA
Thrombosis
Antegrade or
retrograde SMA
bypass
No peritoneal signs or
evidence of perforation
CT or MR angiography
or biplanar mesenteric
angiography
Mesenteric
venous
thrombosis
Anticoagulation
heroic efforts will be attempted; the ethical dilemmas involved in
such decision making are significant. The increasing availability
of small bowel transplants, with recent reports of 5-year graft
survival rates of slightly more than 50% and the availability of
pharmacologic agents such as teduglutide to increase small bowel
absorption, may well change our surgical approach to patients
with very limited amounts of remaining small bowel.
Nonocclusive
mesenteric ischemia
(NOMI)
Intraarterial
papaverine infusion
until asymptomatic
and angiogram
normal
FIGURE 79-3 Algorithm for the
treatment of acute mesenteric
ischemia. C T, Computed tomography;
MR, magnetic resonance; SMA,
superior mesenteric artery; UV,
ultraviolet.
FIGURE 79-4 Indocyanine near-infrared angiography demonstrating
an area of underperfused bowel in the mid portion of the image (arrow)
denoted by a darker color. The surgeon is marking the transition point
of good perfusion with a suture.
at the time of surgery, then this plan should not be changed simply
because the patient appears to be doing well in the postoperative
period. Many surgeons do not perform any resection if the entire
small bowel is necrotic, because it would relegate the patient to
lifelong parenteral nutrition. In younger patients, however, more
Laparoscopy
Laparoscopy has been applied to selected patients with acute mesenteric ischemia. Some medically unt patients with acute occlusion of
the SMA are said to have successfully undergone intra-arterial brinolytic therapy followed by laparoscopy. Diagnostic laparoscopy has
been used to verify that all bowel is viable. Fluorescein coupled with
laparoscopy has been used to assess bowel viability and is as accurate
as open laparotomy for detecting nonviable bowel, but an argon beam
laser must be used instead of a Wood lamp. Indocyanine near-infrared
angiography can also be applied laparoscopically using special imaging
equipment.
CHRONIC MESENTERIC ISCHEMIA
Chronic mesenteric ischemia is caused by atherosclerotic disease that involves two or more visceral arteries. e large number of collateral vessels in the mesenteric circulation explains the
rarity of symptomatic ischemia with only single-vessel disease.
Acute And chronic Mesenteric ischeMiA416
SMA vein graft
Celiac
FIGURE 79-5 An aortogram in a patient with severe infrarenal ath-
erosclerotic disease and occlusion of the superior mesenteric artery.
(Courtesy Tom Bergamini, MD, Louisville, Ky.)
e percentage of patients with chronic mesenteric ischemia who
will progress to bowel infarction is not known, but the symptoms
of chronic ischemia are so debilitating that treatment is desirable in
many cases. In general, two of the three visceral arterial branches
must be occluded (i.e., celiac, SMA, or inferior mesenteric artery)
for abdominal angina to develop.
Presentation
Symptoms typically include postprandial abdominal pain and weight loss.
Weight loss occurs because the postprandial pain causes development of
a “food phobia.” An abdominal bruit occasionally can be detected upon
physical examination. Most patients with chronic mesenteric ischemia
are women, and, as with other forms of atherosclerotic disease, smoking
and hypertension are contributing factors in these patients.
Evaluation
e diagnostic study of choice for mesenteric ischemia is biplanar
arteriography. Mesenteric arteriography may cause visceral infarction and therefore should be performed only in centers capable of
addressing this complication. Figures 79-5 and 79-6 demonstrate
some typical arteriographic ndings in patients with stenosis or
occlusion of one or more visceral arteries.
Operative Treatment
No single surgical technique is best for all cases of chronic mesenteric ischemia. e two most favored techniques are antegrade bypass
with one or more vessels and retrograde bypass. Antegrade bypass
Lateral ABD.AO.
FIGURE 79-6 An aortogram in a patient with a previous patent ante-
grade bypass to the superior mesenteric artery (SMA). Very tight celiac
stenosis can be seen just below the origin of the saphenous vein bypass.
ABD.AO., Abdominal aorta. (Courtesy Seyhan Senler, MD, New Albany, Ind.)
originates from the supraceliac aorta and, whenever possible, should
revascularize multiple visceral arteries. e supraceliac aorta is dicult
to expose but is less oen diseased than other areas of the aorta. e
benets of antegrade bypass include reduction in kinking and turbulent ow, along with greater ease of multivessel revascularization. Antegrade bypass requires at least brief cross-clamping of the aorta above
the renal vessels and therefore has a risk of renal ischemic injury.
Retrograde bypass originates from either the infrarenal aorta or
the iliac arteries and usually revascularizes only the SMA. Technically
it is easier to expose the infrarenal aorta, and cross-clamping above
the renal arteries is not required. Either type of bypass may be performed with an autogenous vein or prosthetic gra; kinking of such
gras is an obvious problem.
ree-year survival rates vary between 75% and 86% aer bypass,
but symptomatic gra failures occur in about 15% of patients. Primary patency does not appear to dier between antegrade and retrograde bypasses, with both having greater than 85% patency 6 years
aer the operation. Primary patency may be overestimated, however,
because many studies evaluate only symptomatic patients, and many
asymptomatic patients may have undetected failed bypasses.
Angioplasty
Percutaneous angioplasty with stent placement in visceral arteries is
technically more dicult than in iliac or other lower extremity arteries. Brachial access allows more technical degrees of freedom than the
femoral approach. Success has been reported with angioplasty of the
celiac artery, SMA, and inferior mesenteric artery, but limited followup periods have yielded restenosis rates as high as 50%.
SMALL INTESTINE 417
CONCLUSION
Acute mesenteric ischemia is a cause of signicant morbidity and carries a very high mortality rate, most likely because of the diculty
in early diagnosis. Because the consequences of missed or delayed
diagnosis are so devastating, clinicians who encounter patients with
typical, or even suggestive, symptoms should immediately pursue a
diagnosis of acute visceral ischemia until this diagnosis can be condently excluded.
Chronic mesenteric ischemia, although not in and of itself a lifethreatening condition, is oen dicult to diagnose. Patients without
signicant weight loss either do not have chronic visceral ischemia
or do not have ischemia severe enough to warrant an attempt at
revascularization. Patients with uncertain diagnoses but no weight
loss, however, should receive close follow-up to assess for other intraabdominal disorders, along with the possibility that chronic ischemia
will worsen and require revascularization.
S u g g e S t e d R e a d i n g S
Ando M, Ito M, Nihei Z, Sugihara K. Assessment of intestinal viability using
a non-contact laser tissue blood owmeter. Am J Surg. 2000;180:176–180.
Cooperman M, Martin Jr EW, Keith LM, Carey LC. Use of Doppler ultra-
sound in intestinal surgery. Am J Surg. 1979;138:856–859.
Karliczek A, Harlaar NJ, Zeebrechts CJ, et al. Surgeons lacks predictive
accuracy for anastomotic leakage in gastrointestinal surgery. Int J Colorec-
tal Dis. 2009;24:569–576.
Klempnauer J, Grothues F, Bektas H, Pichlmayr R. Long-term results aer
surgery for acute mesenteric ischemia. Surgery. 1996;121:239–243.
Kudszus S, Roesel C, Schachtrupp A, Höer JJ. Intraoperative laser uorescence
angiography in colorectal surgery: a noninvasive analysis to reduce the
rate of anastomotic leakage. Langenbecks Arch Surg. 2010;395:1025–1030.
Matsui A, Winer JH, Laurence RG, Frangioni JV. Predicting the survival of
experimental ischaemic small bowel using intraoperative near-infrared
uorescence angiography. Br J Surg. 2011;98:1725–1734.
Stoney RJ, Cunningham CG. Acute mesenteric ischemia. Surgery. 1993;114:
489–490.
R E
P
Sandy H. Fang and Jonathan E. Efron
BACKGROUND
Radiation was rst used as a treatment modality for breast cancer in
1896, and a year later Dr. David Walsh, a physician at the Western
Skin Hospital, London, described the rst case of radiation enteritis. A “practical worker” had “gastric symptoms, such as pain, tenderness on pressure, atulency, colic, and diarrhea” aer 2 hours of
daily exposure to radiation. e symptoms resolved aer the worker
started using an abdominal lead shield.
Today, radiation therapy is a common treatment for gynecologic,
urologic, and rectal malignancies. Exclusion of “innocent” bowel
from the radiation eld during radiotherapy can be dicult, and
when adjacent bowel gets in the way, radiation enteritis can result.
e incidence of radiation enteritis and proctocolitis varies according
to cancer type because treatment regimens vary between the dierent
types of pelvic malignancies.
PATHOPHYSIOLOGY
When the electromagnetic waves of radiation hit normal tissue,
they cause the release of electrons, which form hydroxyl or free
radicals. The hydroxyl radical induces apoptosis. Rapidly proliferating cells in the G2 and M phases of mitosis, such as cancer
cells, or stem cells in intestinal crypts, are most affected by radiation. Regulator genes involved in this process include CRADDD,
APAF1, p53, BCL2, XRCC1, XRCC3, and BCL2. Ionizing radiation also activates the translation of transforming growth
factor–β.
Radiation enteritis is categorized as acute and chronic. Acute
injury occurs during radiotherapy and may last up to 6 months,
whereas chronic injury occurs aer 3 months and may even present
50 years aer radiation was administered. Radiation is “the gi that
keeps on giving.”
In the acute process, radiation prevents epithelial cell mitosis
deep within the mucosal crypts; however, it does not inhibit cell
migration out of the crypts onto villi, which leads to denuding of
the mucosal protective barrier. Bacteria and other antigens can
violate the mucosa, causing an inflammatory response and bacteremia. Histologic findings include inflammatory infiltrates,
reduced crypt mitoses, crypt microabscesses, and epithelial ulceration. Progressive collagen deposition, an obliterative vasculitis
and submucosal fibrosis, lymphatic dilation, and tissue ischemia
and necrosis also occur.
Secondary colorectal malignancies occur in up to 20% of patients
aer radiotherapy, and the time between irradiation to the emergence
of a solid tumor averages 10 years. Eight percent have been linked to
previous radiation therapy, and two thirds were found to be rectosigmoid malignancies.
PREDISPOSING RISK FACTORS
e major risk factors for the development of radiation enteritis are
the volume of bowel exposure to the radiation eld and radiation
dosage (Table 80-1). Other risk factors include adhesions that pre-
vent the bowel from being excluded from the eld, radiation delivery
techniques, and the use of radiosensitizing chemotherapeutic agents,
such as uorouracil and mitomycin.
Patients who experience extreme symptoms of acute radiation
injury have a higher risk of the development of chronic radiation
enteritis, which is called consequential late eect.
Comorbid factors that increase the risk of radiation bowel injury
include collagen vascular diseases, inammatory bowel disease,
human immunodeciency virus infection, and a history of vascular
occlusive disease, such as hypertension, diabetes, smoking, atherosclerosis, and cardiovascular disease. It is hypothesized that thinner
patients with a smaller anterior-posterior diameter have an increased
risk of intestinal toxicity.
GRADING SYSTEMS
Toxicity grading systems have been proposed but have limited clinical utility. e most common toxicity grading systems are those
proposed by the Radiation erapy Oncology Group (RTOG;
Table 80-2) and the European Oncology Radiation erapy Group
(EORTG). e RTOG criteria assess short-term eects of radiation,
whereas RTOG and EORTG criteria assess long-term eects. Other
systems are the Late Eects on Normal Tissues Subjective, Objective,
Management and Analytic grading system and the Common Terminology Criteria for Adverse Events.
DIAGNOSTIC WORKUP
Symptoms of radiation enteritis are nonspecic, and the dierential diagnosis is broad (see Box 80-1). e timing of the symptoms
suggests the diagnosis. Acute enteritis is generally an abrupt illness
with nausea, vomiting, diarrhea, and bleeding. Chronic enteritis is
more gradual onset of initially vague abdominal pain or discomfort,
constipation, and nausea. Patients with acute enteritis usually have
tenderness upon abdominal palpation as a result of the active inammation, whereas persons with chronic enteritis usually do not have
tenderness.
Laboratory testing, including tumor markers to rule out recurrence or a secondary malignancy, should be performed. Computed
tomography (CT) scanning or magnetic resonance imaging (MRI)
and upper or lower endoscopy are useful imaging procedures to make
the diagnosis and establish the location and extent of the disease.
418
SMALL INTESTINE 419
TABLE 80-1: Predisposing Risk Factors for Radiation
Toxicity to Bowel
Volume of bowel
exposure to radiation
Consequential late eect Patients who experienced extreme
Comorbid factors Adhesive disease aer abdominal or
Radiation eld
Radiation dosage
Radiation delivery techniques
Patient positioning
Radiosensitizing chemotherapeutic
agents
Fluorouracil
Mitomycin
symptoms of acute radiation injury
pelvic surgery
Combined modality therapy
Collagen vascular disease
Inammatory bowel disease
Human immunodeciency virus
inner patients
History of vascular occlusive disease
Hypertension
Diabetes
Smoking
Atherosclerosis
Cardiovascular disease
TABLE 80-2: Radiation Therapy Oncology Group
Acute Radiation Morbidity Scoring Criteria: Lower
Gastrointestinal, Including Pelvis
Grade 0 No change
Grade 1 Increased frequency or change in quality of bowel
habits not requiring medication
Rectal discomfort not requiring analgesics
Grade 2 Diarrhea requiring parasympatholytic drugs (e.g.,
diphenoxylate/atropine [Lomotil])
Mucous discharge not necessitating sanitary pads
Rectal or abdominal pain requiring analgesic drugs
BOX 80-1: Differential Diagnosis of Gastrointestinal
Symptoms after Radiation Therapy
New or recurrent neoplasia
Intestinal stricture
Intestinal stula
Small bowel bacterial overgrowth
Bile salt, fat, or carbohydrate malabsorption
New diagnosis of inammatory bowel disease
Pancreatic insuciency
Irritable bowel syndrome
PREVENTION
Careful planning can minimize exposure to radiation. Physical
maneuvers have been attempted, such as prone positioning, use
of a “belly board,” and distension of the bladder to displace the
small bowel out of the pelvis. In addition, tissue expanders, biodegradable mesh slings, and intrapelvic breast prostheses have
been shown to minimize pelvic radiation exposure by up to 50%.
CT scanning simulation techniques, intensity-modulated radiation therapy, and brachytherapy targeting radiation to the cancer
decrease extraneous exposure compared with nonspecific external
beam radiation.
MANAGEMENT OF RADIATION ENTERITIS
Multiple options exist for topical and medical therapy, but evidence of
success is limited. Endoscopy and surgery are reserved for the more
extreme cases that are very symptomatic and refractory to medical
management. e risk of morbidity is high. If surgery is performed,
preoperative nutritional support may be important. Resection of the
aected bowel is the best option with an anastomosis in nonirradiated bowel (i.e., transverse colon and nonirradiated small bowel).
Sometimes bypass of a radiated terminal ileum that is trapped in the
pelvis and causing an obstruction is safer than trying to mobilize the
aected loop for resection.
Management of Radiation Injury to the Small Bowel
Grade 3 Diarrhea requiring parenteral support
Severe mucous or blood discharge necessitating use
of sanitary pads
Abdominal distention (a at plate radiograph
demonstrates distended bowel loops)
Grade 4 Acute or subacute obstruction, stula, or
perforation
Gastrointestinal bleeding requiring transfusion
Abdominal pain or tenesmus requiring tube
decompression or bowel diversion
Grade 5 Death
Enteroscopy or capsule endoscopy also may be helpful, but in patients
with chronic enteritis, strictures may exclude their use. Biopsies are
usually nonspecic but can rule out other causes of inammation.
Biopsies of chronic radiation enteritis oen show evidence of ischemia because of the stenosing vasculitis that is a feature of the disease.
Acute Radiation Enteritis
Acute radiation enteritis occurs within 3 months aer radiotherapy.
Its severity is directly related to the dose, treatment eld size, intestinal volume irradiated, and frequency of radiation administered.
Acute radiation enteritis aects up to 70% of patients. Radiotherapy
also causes bowel dysmotility, and symptoms such as nausea, emesis,
diarrhea, abdominal pain, and tenesmus are common. Aected persons oen have water, protein, and electrolyte imbalances.
No specic treatment exists for acute radiation enteritis. Management is supportive with the use of antiemetic agents, antidiarrheal
drugs, a low-residue diet, antispasmodic agents, and anticholinergic
medications (Fig. 80-1). Symptoms are self-limited and last 2 to 6
weeks aer the cessation of radiotherapy.
Chronic Radiation Enteritis
Chronic radiation injury may manifest itself between 3 months and 50
years aer radiation is administered. e incidence has been reported to
be as high as 55%. Sequelae include stricturing with obstruction, malabsorption, abscess, perforation, and stulae. Symptoms include abdominal
Radiation EntERitis and PRoctocolitis420
Radiation injury to small bowel
Acute
(<3 months)
Versus
Chronic
(>3 months)
Symptoms self-limited
supportive management
Antiemetics
Antidiarrheals
Low-residue diet
Antispasmodics
Anticholinergics
Drain
Elemental or specific exclusion diets
FIGURE 80-1 Management of radiation enteritis.
Intestinal failure
Nutritional supplementation
Total parenteral nutrition
pain, constipation, obstruction, gastrointestinal bleeding, and even peritonitis, suggestive of perforation. Strictures develop in 53% of patients,
and symptomatic intestinal obstruction occurs from 0.8% to 13% of the
time. Fistula formation is less common (in 0.6% to 17% of cases).
Intestinal failure due to radiation therapy may be a result of bowel
obstruction related to radiation strictures, short bowel syndrome,
malabsorption, dysmotility, and stulae. Elemental or specic exclusion diets are not curative, but nutritional supplementation plays a
supportive role for persons with intestinal failure or for nutritional
repletion prior to surgery. One- and 5-year survival rates for persons
with intestinal failure resulting from chronic radiation enteritis who
require total parenteral nutrition (TPN) are 76% and 64%, respectively. For patients who are not surgical candidates, TPN is palliative.
Surgery is reserved for persons who have severe symptoms that
are not relieved by medical management. e most common indication for surgery is stricturing disease that causes obstruction. Other
indications include bleeding, perforation, malabsorption, and stulae. One third of patients with chronic radiation enteritis will require
surgery, and symptoms will recur in 50% of patients. Surgical options
include fecal diversion with an ostomy, bowel resection with or without an ostomy, intestinal bypass, and adhesiolysis. Intestinal bypass
and adhesiolysis have fallen out of favor, and resection is optimal.
e goal is to resect any irradiated tissue, because the presence of
irradiated tissue may contribute to postoperative complications,
and irradiated bowel is mostly not functional. Strictureplasty may
be an option for multiple short strictures, but unlike the strictures
of Crohn disease, the antimesenteric border of the bowel in persons
with radiation strictures is diseased. Strictureplasty is not indicated
for the treatment of perforation, hemorrhage, stula, or short segments of disease in patients with adequate bowel length. In cases in
which extremely dense hostile adhesions are encountered and dissection would lead to extensive serosal tears, enterotomies, or vascular
injury, intestinal bypass may be considered.
Surgery is associated with postoperative morbidity as high as 75%
and mortality up to 30%. e anastomotic leak rate ranges from 9%
to 36% and is thought to be improved by increasing surgical experience in the management of chronic radiation enteritis. Other causes
of morbidity include intra-abdominal abscess, intestinal stula or
postoperative peritonitis, wound dehiscence, intra-abdominal hemorrhage, and short bowel syndrome. e immediate repeat operation
rate due to postoperative complications is 13.1%. Incomplete resection causing postoperative obstruction occurs in 1.9% of patients.
Short bowel syndrome is observed in 14.6% to 49.5% of patients in
some studies, with the majority requiring long-term total parenteral
nutrition with its higher mortality rate. Long-term follow-up shows
Medically refractoryAbscess
Surgery
Fecal diversion with ostomy
Bowel resection
with or without ostomy
Intestinal bypass
Adhesiolysis
that a repeat operation is required in up to 60% of patients. Risk factors for a repeat operation include emergency surgery, an anastomotic leak, and male gender.
Management of Radiation Injury to the Colon
Acute Radiation Colitis
In most patients with acute radiation colitis, the disease is self-limited
and management is supportive (Fig. 80-2). Antidiarrheal medication
and diets excluding lactose and fat are used to control diarrhea. In
persons who are refractory to antidiarrheal drugs, some studies have
demonstrated the ecacy of octreotide. Most studies have failed to
show success with 5-aminosalicylic acid (5-ASA) agents in the treatment of radiation colitis; however, a small, randomized controlled
pilot study has shown the ecacy of balsalazide in the treatment of
acute radiation-induced proctosigmoiditis. It has a unique delivery
system, in which 99% of the drug is delivered to the distal colon.
Chronic Radiation Colitis
Chronic radiation colitis may present as diarrhea (as a result of bacterial overgrowth, increased intestinal transit, and malabsorption),
obstruction due to stricturing disease, or perforation. It also serves
as a precancerous condition. Partial obstruction is initially treated
conservatively with modication of diet to a liquid–so mechanical diet. In cases in which a complete bowel obstruction is present, a
nasogastric tube and possible nutritional supplementation with TPN
are needed. However, the obstruction is likely to progress, eventually
requiring resection with a possible ostomy.
Management of Radiation Injury to the Rectum
e rectum is the organ most commonly exposed to pelvic radiation. Acute radiation injury aects 75% of patients who undergo
pelvic radiation who keep their rectum, and chronic radiation proctitis develops in 20% of patients. Symptoms include abdominal pain,
rectal pain, loose stools, urgency, bleeding, rectal pain, fecal incontinence, and tenesmus. Chronic sequelae include stulization, sepsis,
perforation, bleeding, abdominal pain, diarrhea, constipation, and
fecal incontinence. Whereas malabsorption is common in persons
with radiation enteritis, it is uncommon in persons with radiation
proctitis.