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TABLE 8.2. Causes of Mechanical Intestinal Obstruction
Small Intestine Colon
Luminal
Gallstone ileus Fecal impaction
Foreign body Foreign body
Worms
Bowel wall lesions
Tumor Tumor
Strictures Strictures
Intussusception Diverticular disease
Radiation enteritis
Extrinsic compression
Adhesions Volvulus
Hernias Extrinsic tumor
Extrinsic tumor
Extrinsic
inflammation
obstruction. If the obstruction is more distal, however,
abdominal distension occurs, and abdominal x-rays
will demonstrate typical air fluid levels and ladder formation. In the latter case, vomiting occurs late, following
onset of obstruction and pain. The obstruction may be
partial or complete; when partial, less distension is likely
and the x-ray will demonstrate gas distal to the point of
obstruction.
Pain The pain in simple bowel obstruction is colicky
and periumbilical in location; it comes in waves and may
be accompanied with audible bowel sounds. The pain is
visceral in origin and does not localize to the region
affected by the pathology, as happens when the parietal
peritoneum is involved.
FIGURE 8.11. Consequences of simple and closed-loop obstruction by an adhesive band.
malities. The higher the level of obstruction, the more
severe these changes become. The electrolyte imbalance
at its worst will lead to hypokalemic, hypochloremic
metabolic alkalosis similar to that seen in gastric outlet
obstruction. Metabolic alkalosis will not occur, however, if
significant amounts of pancreatic juice and bile are lost.
Indeed, occasionally, a degree of metabolic acidosis may
accompany severe dehydration. In low small bowel
obstruction, fluid lost into the gut lumen and peritoneal
cavity is iso-osmotic. Hence, while contraction of the
extracellular space occurs, electrolyte imbalance is rare and
appears late when it does occur.
Fluid and Electrolyte Abnormalities High small bowel
obstruction leads to early and severe vomiting, contraction
of the extracellular fluid volume, and electrolyte abnor-
TABLE 8.3. Cardinal Features of Small Bowel Obstruction
Simple
䊏
Colicky midabdominal pain
䊏
Nausea and vomiting
䊏
Distension
䊏
Obstipation
䊏
High-pitched bowel sounds with crescendo
䊏
X-ray:
➢ Distended small bowel
➢ Air-fluid level
Strangulated
䊏
Constant abdominal pain
䊏
Tenderness and rebound tenderness
䊏
Fever, leucocytosis
䊏
X-ray:
➢ Thumbprinting
➢ Air in bowel wall
➢ Air in portal vein radicles
➢ Free air if perforated
TRANGULATED OBSTRUCTION When the bowel is
S
obstructed at two sites, the segment in between is referred
to as the closed segment. This condition is much more
serious than simple obstruction because of the risk of
volvulus of the obstructed segment and vascular compromise leading to strangulated obstruction. It should always
be remembered that proximal to closed-loop obstruction
is a simple obstruction (Figure 8.11).
The closed-loop segment undergoes a series of pathophysiological changes leading to vascular compromise. As
the closed segment distends, its luminal pressure rises
because the serosa is relatively nondistensible. As the
luminal pressure increases, first the lymphatic, then the
venous drainage of the bowel wall become impaired. In
addition, the mesentery of the closed-loop segment is
compressed to a variable degree by the adhesive band,
leading to edema and thickening of the bowel wall as
lymphatic and venous drainage become progressively
compromised.
If the obstruction is not relieved, these processes can
lead to arterial compromise of the closed-loop segment.
Arterial compromise occurs more rapidly and with
more catastrophic consequences if the fluid-filled, heavy
P athophysiology ................................................................................................................................. 249
obstructed segment undergoes rotation or volvulus. The
obstruction then becomes a strangulated obstruction.
When strangulated obstruction develops, transmural
inflammation leads to peritonitis, and the symptoms
and signs change. The pain, instead of intermittent and
colicky, becomes constant and more severe. The findings
on abdominal examination include tenderness and
rebound tenderness, indicating that peritonitis has set in.
At times, the obstructed bowel may be palpable. Bowel
sounds tend to disappear. Parallel changes may also be
seen on abdominal x-ray.
The most significant radiological signal that bowel
necrosis has occurred is the presence of air within the
bowel wall itself (Figure 8.12). The presence of air within
the portal vein is a late sign. Another late development,
which must be avoided at all costs, is perforation of the
strangulated bowel. If perforation occurs, free air and
fluid may accumulate in the peritoneal cavity. The patient
develops peritonitis and becomes septic. Septic shock
and death will ensue unless the problem is promptly
corrected surgically. It is important to note that perforation is not necessary in order for severe sepsis and septic
shock to develop.
Following obstruction, bacteria proliferate in the
gut lumen. With vascular compromise of the intestinal
wall, bacteria and endotoxin invade the peritoneal
cavity transmurally, a process referred to as bacterial
dislocation.
Adynamic Ileus
When intestinal peristalsis is lost, air and fluid accumulate
within the gut lumen. In contrast to mechanical obstruction, air may be present within the entire small and large
intestine. Abdominal distension develops, but colicky
abdominal pain does not. Any abdominal pain that may
be present is likely to be due to the primary pathological
process that has caused paralytic ileus.
The causes of adynamic ileus may be abdominal or
extra-abdominal. The most frequent abdominal cause is
an inflammatory process of the gastrointestinal tract,
the pancreas, or the biliary tree (e.g., perforated ulcer,
acute appendicitis, acute pancreatitis, acute cholecystitis,
ascending cholangitis). Retroperitoneal processes (e.g.,
acute pyelonephritis, ureteral colic, retroperitoneal
hematoma, spinal injury) are also important causes. Extraabdominal causes include severe systemic sepsis, diabetic
ketoacidosis, major burn, severe head injury, and severe
inferior myocardial infarction.
Key issues for the clinician are to distinguish adynamic
ileus from mesenteric ischemia and to identify the primary
cause.
Mesenteric Ischemia
Mesenteric ischemia occurs in acute or chronic forms; it is
the acute form that causes acute intestinal obstruction.
The causes of mesenteric ischemia (Table 8.4) are most
commonly mesenteric arterial embolism and mesenteric
artery thrombosis (Figure 8.13). Frequent causes of
mesenteric arterial embolism include atrial fibrillation,
postmyocardial infarction mural thrombus, embolism following the use of pump oxygenator during heart-lung
bypass, and dislodged atheromas or thrombi during
angiography when a catheter is threaded up the aorta into
or beyond the mesenteric vessels. Mesenteric artery
thrombosis follows atherosclerotic stenosis, usually of the
superior mesenteric artery (SMA). Often, the patient may
give an antecedent history of intestinal angina. Nonocclusive mesenteric ischemia develops in low-flow states, particularly in patients with low cardiac output and especially
when digoxin and/or vasopressors are used. In nonocclusive ischemic states, it is believed that, by mechanisms
as yet unknown, a critical drop in mesenteric blood
flow causes segmental spasm in secondary and tertiary
branches of the SMA.
Although changes are discernible by electron microscope within 10 minutes and by light microscope within
60 minutes of the onset of ischemia, full-thickness infarction of the bowel wall takes about 6h and sometimes
longer to set in. Ischemia causes rapid bacterial proliferation within the lumen. As necrosis occurs, the intestinal
wall becomes permeable to luminal bacteria and endotoxin, allowing their entry into the peritoneal cavity. Septicemia and gram-negative bacteremia ensue. Hemorrhage
occurs into the lumen, and bloody fluid accumulates in the
peritoneal cavity. Massive fluid shifts into the gut lumen
and peritoneum cause hemoconcentration, oliguria, and
hypotension. Necrosis of the intestinal muscle wall releases
creatine phosphokinase (CPK), lactate dehydrogenase
(LDH), and glutamic pyruvic transaminase (GPT). These
enzymes frequently become elevated in the serum. Also,
inorganic phosphate levels rise in the serum and in peritoneal fluid.
Mesenteric venous thrombosis occurs in the setting of
portal hypertension, hypercoagulable states, use of contraceptive pills, trauma, or abdominal sepsis. A characteristic feature is the accumulation of large amounts of fluid
within the gut wall, within the mesentery, and in the peritoneal cavity (Figure 8.14).
Colonic Obstruction
Mechanical Obstruction
SIMPLE OBSTRUCTION Colon cancer and diverticulitis
account for nearly 90% of cases of large intestinal obstruction, with colon cancer alone responsible for 65% to 70%
of these.
1
The most frequent site of obstruction from either
disease is the sigmoid. Other causes of colon obstruction
include inflammatory bowel disease, postanastomotic
strictures, benign tumors, and fecal impaction. Simple
colonic obstruction occurs only when the ileocecal valve is
250 ................................................................................................................ Small and L arge Intestine
A
B
FIGURE 8.12. Air within the bowel. (A) The supine abdominal x-ray illustrates the presence of streaks
of air (arrows) within the wall of small bowel segments that are ischemic as a result of a strangulated
small bowel obstruction. Notice the dilated small bowel. (B) The abdominal CT scan in the same
patient demonstrates the ischemic segment of bowel with air in the wall (arrows) and contrast material in the lumen. CT is often performed to detect ischemic, strangulated bowel and has a much higher
sensitivity than plain x-ray. (Courtesy of Henry I. Goldman, MD.)
P athophysiology ................................................................................................................................. 251
TABLE 8.4. Causes of Mesenteric Ischemia
Superior mesenteric artery embolism: 30%
Superior mesenteric artery thrombosis: 25%
Nonocclusive mesenteria ischemia: 5%
Acute mesenteric vein thrombosis: 20%
Miscellaneous: 20%
䊏
Dissecting aortic occlusion
䊏
Trauma
䊏
Collagen vascular disease
FIGURE 8.13. Mesenteric arterial
embolism. The CT scan demonstrates an
embolus lodged in the superior mesenteric artery (SMA; arrow) in a patient
with atrial fibrillation. CT is the recommended technique to demonstrate SMA
embolus or thrombosis. (Courtesy of
Henry I. Goldman, MD.)
FIGURE 8.14. Recurrent mesenteric venous infarction
following previous resection. Notice that the previous
anastomosis is one of the demarcation lines. Typically,
in venous infarction, both the bowel and the mesentery are edematous. (Courtesy of Theodore Schrock,
MD.)
252 ................................................................................................................ Small and L arge Intestine
incompetent and coloileal reflux can occur. When the
ileocecal valve is competent (see following discussion), a
closed-loop obstruction results between the obstructing
lesion and the ileocecal valve.
Consequences of simple obstruction of the colon
include:
1. Abdominal distension. Distension is usually prominent and involves the lateral aspects of the abdomen. Even
in the colon, most of the gas distending the obstructed
bowel is derived from swallowed air, although gas produced by bacteria-induced fermentation does contribute.
2. Abdominal pain. Colicky abdominal pain is referred
to the suprapubic area (hypogastrium) and is mediated by
the T-12 and L-1 nerves.
3. Obstipation. Failure to pass feces and flatus develops
with complete colonic obstruction.
4. Vomiting. Vomiting occurs late and is typically feculent. By the time vomiting occurs, distension of the small
intestine has also occurred.
LOSED-LOOP OBSTRUCTION Closed-loop obstruc-
C
tion occurs under three conditions: when complete colonic
obstruction occurs in conjunction with a competent ileocecal valve, in sigmoid volvulus, and in cecal volvulus.
Rarely, volvulus of the transverse colon or splenic flexure
may occur.
Competent Ileocecal Valve A competent ileocecal valve
does not permit colon obstruction to decompress by reflux
into the small intestine. As a result, the cecum progressively
enlarges from its normal diameter of 10 cm or less. An
increase in cecal diameter to 12cm or more may portend
imminent cecal perforation and requires urgent or emergent decompression (Figure 8.15).
Sigmoid Volvulus Three conditions promote sigmoid
volvulus: a redundant sigmoid, long sigmoid mesentery
with a narrow base, and fecal loading due to chronic constipation. The condition tends to occur in the elderly, in
those who are bedridden, and in those receiving psychotropic medication for a psychiatric disorder.
The bowel twists counterclockwise about its long
mesentery. A complete twist of 360° leads to occlusion of
not only the bowel lumen but also of the vascular pedicle
in the mesentery. If the obstruction is not reversed
promptly, sigmoid gangrene and perforation ensue.
Usually, abdominal distension is very prominent, and
colicky suprapubic pain develops. Abdominal films show
a single large loop of bowel arising from the pelvis and
sometimes reaching the diaphragm (Figure 8.16).
FIGURE 8.15. Large bowel obstruction with cecal dilatation. The
x-ray demonstrates a huge cecum (arrows), the result of sigmoid
obstruction. The patient noted increasing distention over many
hours, and comparison to earlier abdominal films showed that
the cecum had increased from 7 cm to 12 cm in diameter. (Courtesy of Henry I. Goldman, MD.)
FIGURE 8.16. Sigmoid volvulus. The abdominal x-ray shows a
large sigmoid volvulus (arrows) occupying much of the abdomen
and pelvis, with distended colon proximally. The volvulus has
two limbs, the distal limb (arrows) and the proximal limb (S),
forming an inverted U-shape. (Courtesy of Henry I. Goldman,
MD.)
A
B
FIGURE 8.17. Cecal volvulus. (A) The abdominal x-ray shows a large air collection in the left upper
quadrant, with transverse colon gas present. The large air collection is actually the cecum, which has
migrated to the left upper quadrant due to a cecal volvulus. (B) The barium enema, taken 4 days later,
shows a narrowed cecum and ascending colon (arrows). While the volvulus spontaneously reduced,
ischemic changes had already occurred, leading to this appearance of the segment involved in the
volvulus. (Courtesy of Henry I. Goldman, MD.)
Cecal Volvulus Cecal volvulus is much less common
Pseudo-obstruction
than sigmoid volvulus, occurring with half the frequency.
A predisposing condition is incomplete embryologic fixation of the cecum, which results in hypermobility of the
organ. The terminal ileum is also involved in the twisting.
The cecum comes to lie in the left upper quadrant, and a
closed-loop obstruction occurs (Figure 8.17). Because no
twist of the mesentery occurs, vascular obstruction is not
a significant problem.
Cecal volvulus causes distal small bowel obstruction
proximal to the closed-loop obstruction. Distension and
colicky pain develop in the midabdomen. The patient
often has a previous medical history of similar but milder
attacks.
Pseudo-obstruction is profound ileus without evidence of
luminal obstruction. Colonic pseudo-obstruction, or
Ogilvie’s syndrome, is the best known variety, but the
disease can also affect the small intestine. Although the
cause is unknown, some have suggested sympathetic overactivity based on anecdotal evidence that epidural anesthesia ameliorates the condition. It is likely, however, that
the pathophysiology is more complicated and possibly
involves abnormalities of the peptidergic enteric nervous
system.
Ogilvie’s syndrome may follow acute illness, an opera-
tion (e.g., hysterectomy), or it might affect patients who
254 ................................................................................................................ Small and L arge Intestine
Important consequences of maldigestion include:
1. Malabsorption of fat, leading to diarrhea with greasy,
foul-smelling, and floating stools.
2. Weight loss.
3. Malabsorption of fat-soluble vitamins A, D, E, and K.
In patients with maldigestion, vitamin K deficiency
must be corrected with intravenous administration of
phytonadione (AquaMEPHYTON®) prior to surgery.
Reduced Intestinal Bile Salt
Reduced intestinal bile salt occurs in the blind-loop syndrome and when the ileum has been resected or severely
diseased (e.g., Crohn’s ileitis). In the blind-loop syndrome,
bacterial overgrowth leads to deconjugation of bile salts,
in turn leading to defective micelle formation. The consequences are several and include:
1. Malabsorption of fat and, to a lesser degree, proteins
and carbohydrates.
2. Colonic loss of water and electrolytes, due to the stimulating effect of unabsorbed fatty acids entering the
colon and leading to diarrhea.
3. Macrocytic anemia due to malabsorption of vitamin
B
12
, which binds to anaerobic bacteria.
4. Hypocalcemia due to the binding of calcium by unabsorbed fatty acids.
5. Enteric hyperoxaluria due to excessive absorption
of oxalate from the colon as a consequence of the
hypocalcemia, which interferes with formation of
insoluble calcium oxalate.
6. Weight loss.
Major resection of the ileum or severe disease in this
segment of bowel removes its important absorptive function of fat and vitamin B
12
.
Inadequate Absorptive Surface
Intestinal resection or bypass and chronic vascular
insufficiency lead to malabsorption because of critically
reduced absorptive surface. (The short bowel syndrome
will be described later.) Intestinal bypass may be performed in the treatment of morbid obesity or heterozygous familial hypercholesterolemia. In the latter, the distal
one third of the small intestine is bypassed, interrupting
the enterohepatic circulation, and resulting in increasing
amounts of cholesterol being converted to bile salts, which
are then excreted. Plasma cholesterol levels—particularly
LDL cholesterol—fall, resulting in an increased HDL
cholesterol ratio in the plasma.
Chronic mesenteric vascular insufficiency leads to
general villous atrophy in the small intestine, with loss of
absorptive surface and brush-border enzymes. The effect
is reduced absorption of all nutrients, leading to severe
weight loss.
P athophysiology ................................................................................................................................. 255
TABLE 8.5. Surgically Relevant Causes of Malabsorption
Maldigestion
䊏
Postgastrectomy steatorrhea
䊏
Pancreatic insufficiency
䊏
Zollinger–Ellison syndrome
Reduced intestinal bile salt
䊏
Blind-loop syndrome
䊏
Ileal resection or disease
Inadequate absorptive surface
䊏
Intestinal resection or bypass
䊏
Chronic mesenteric vascular insufficiency
Primary mucosal defects
䊏
Inflammatory
➢ Crohn’s disease
➢ Radiation enteritis
䊏
Endocrine/metabolic
➢ Carcinoid syndrome
➢ Hypoparathyroidism
➢ Adrenal insufficiency
➢ Diabetes mellitus
are on motility-inhibiting drugs and opiates. Pain is
usually not an important symptom, but abdominal distension can be massive and lead to cecal perforation. Cecal
dilatation of 12 cm or more should prompt either endoscopic or surgical decompression.
MALABSORPTION SYNDROME
Malabsorption syndrome is caused by a variety of
conditions, including maldigestion and as a result of
inadequate absorptive surface or primary mucosal absorptive defects, which may be inflammatory, biochemical,
genetic, endocrine, or metabolic in nature. Of the numerous causes of malabsorption, those relevant in surgical
practice are listed in Table 8.5. The list excludes several
disorders of malabsorption, not because they are unimportant, but because they are not usually encountered
in surgical practice. These include such conditions
as Whipple’s disease (due to infection with Tropheryma
whippelii), celiac sprue (gluten-sensitive enteropathy),
tropical sprue (cause unknown), and a-betalipoproteine-
mia (due to absence of ApoB, which causes defective chylomicron formation).
Maldigestion
Steatorrhea is seen following gastrectomy, in ZES, and
in exocrine pancreatic insufficiency. Postgastrectomy
steatorrhea is probably due to defective mixing of
chyme and pancreatic juice as well as increased intestinal
transit time. In ZES, the excessive acid load entering the
small intestine inactivates pancreatic lipase and other
enzymes. Exocrine pancreatic deficiency is seen primarily
in chronic pancreatitis and following major pancreatic
resection.
Primary Mucosal Defects
Malabsorption also occurs when a large segment of the
small intestine is damaged by severe Crohn’s disease or
radiation enteritis. Several endocrine/metabolic disorders
can also cause malabsorption, including the carcinoid
syndrome, hypoparathyroidism, adrenal insufficiency, and
diabetes mellitus.
DIARRHEA
The various causes of diarrhea are given in Table 8.6. Six
important categories of causes are recognized, including
inflammatory, osmotic, secretory, altered intestinal motility, factitious, and postoperative.
Inflammatory Diarrhea
Inflammatory conditions such as ulcerative colitis,Crohn’s
disease, and radiation enterocolitis damage the intestinal
mucosa and cause diarrhea. Clinical features include fever,
abdominal pain, and bloody stools.
Osmotic Diarrhea
Conditions responsible for this type of diarrhea increase
the osmotic load in the stool, creating an osmotic gap
between the fecal water and plasma. Some conditions—
including pancreatic insufficiency, bacterial overgrowth,
and short bowel syndrome—increase fatty acid and bile
acid concentrations in the stool, typically making it bulky,
greasy, and foul smelling. Nutrient deficiencies and weight
loss develop. Diarrhea improves with fasting.
Secretory Diarrhea
Secretory diarrhea is most often the result of excessive
secretion of peptides by functioning tumors (e.g., ZES,
VIPoma). The peptides cause oversecretion of water and
electrolytes. There is no osmotic gap between the plasma
and fecal water, and the diarrhea does not improve with
fasting. The cause of diarrhea in ZES is complex and
includes:
1. Large volume acid load into the intestine.
2. Increased small bowel motility because of the action of
pharmacologic levels of gastrin.
3. Jejunitis and damage to intestinal mucosa.
4. Inactivation of pancreatic enzymes due to acid pH in
the gut lumen.
The secretory products of peptide-secreting tumors
and their actions are described in Chapter 4.
Altered Intestinal Motility
Diarrhea can be caused by a number of neurologic conditions that alter intestinal motility, including the early
phase of Crohn’s disease, and fecal impaction.
Postoperative Diarrhea
Postvagotomy diarrhea and the dumping syndrome are
described in detail in Chapter 2. Subtotal colectomy with
ileoproctostomy causes diarrhea that tends to improve
with time. Approximately 20% to 30% of patients with
ileoproctostomy, however, have lifelong diarrhea.
CONSTIPATION
Frequency of defecation varies from individual to individual and may range from two to three times a day, to once
every 3 to 5 days. Constipation implies infrequent passage
of hard stools. The causes may be metabolic, endocrine,
neurologic, mechanical, or drug induced.
256 ................................................................................................................ Small and L arge Intestine
TABLE 8.6. Causes of Chronic Diarrhea
Inflammatory
䊏
Ulcerative colitis
䊏
Crohn’s disease
䊏
Radiation enterocolitis
䊏
AIDS
Osmotic
䊏
Pancreatic insufficiency
䊏
Short bowel syndrome
䊏
Bacterial overgrowth
䊏
Celiac disease
䊏
Lactase deficiency
䊏
Whipple’s disease
Secretory
䊏
ZES
䊏
Carcinoid
䊏
VIPoma
䊏
Medullary thyroid cancer
䊏
Villous adenoma of rectum
䊏
Cholerrhetic diarrhea
Altered intestinal motility
䊏
Inflammatory bowel disease
䊏
Fecal impaction
䊏
Neurologic disease
Factitious
䊏
Laxative abuse
Postoperative
䊏
Postvagotomy
䊏
Dumping syndrome
䊏
Ileoproctostomy
Abbreviations: AIDS, acquired immunodeficiency syndrome; ZES,
Zollinger–Ellison syndrome.
Metabolic Causes
Constipation can be caused by hypokalemia, hypercalcemia, and uremia. The exact mechanisms are
unknown, but the effects appear to be intestinal smooth
muscle repolarization.
Endocrine Causes
Hypothyroidism is the prototypical endocrine cause of
constipation. Panhypopituitarism causes constipation,
due in part to hypothyroidism. Pregnant women often
suffer from constipation, the cause of which may be both
hormonal and mechanical.
Neurologic Causes
Constipation is a common feature of a variety of neurologic disorders, including multiple sclerosis and Parkinson’s disease. Paraplegic patients and those with stroke also
suffer from constipation. Their inactivity and several of
the drugs used to treat them contribute to the problem.
Patients with psychiatric disorders also suffer from constipation, perhaps for the same reasons.
Mechanical Causes
Constipation may be caused by mechanical obstruction due to tumors, hernias, strictures, and volvulus.
Pseudo-obstruction was discussed earlier as a cause
of bowel obstruction. Constipation may also be caused
by structural abnormalities such as the descending
perineum syndrome, rectal prolapse or intussusception, or
rectocele.
Drug-induced Constipation
Chronic use of a variety of drugs is associated with constipation. The most common culprits are opiates, psychotropic drugs, antidepressants, aluminum-containing
antacids, calcium-channel blockers, antihypertensives,
and iron supplements. The mechanisms of action are ill
understood.
RADIATION INJURY
The gastrointestinal epithelium, because of its rapid cell
turnover rate, is susceptible to radiation injury. When
given in weekly fractionated doses not exceeding 200 cGy,
a total dose of 4000 cGy is usually well tolerated. The risk
of radiation injury increases rapidly beyond that dose,
especially beyond 5000cGy. Radiation injury of the gastrointestinal tract may be acute or delayed.
Acute Radiation Injury
The gastrointestinal mucosa is the site of acute radiation
injury, which develops within 3 to 4 days after treatment.
Usually, with cessation of therapy, this injury resolves
rapidly. Three forms of acute radiation injury may be
emphasized:
Gastric Perforation
During or immediately following completion of radiation
therapy for large lesions of gastric lymphoma, gastric
perforation may occur. This complication occurs when
there is transmural involvement with highly radiosensitive
lymphoma.
Acute Radiation Enteritis
The rapidly proliferating mucosa of the small intestine,
particularly the jejunum, is highly radiosensitive. Symptoms include abdominal pain and diarrhea. The injury is
usually self-limited and the mucosa repairs rapidly upon
cessation of treatment.
Radiation Proctocolitis
Most commonly associated with pelvic radiation for
uterine and cervical cancer and for prostate and bladder
cancer. Proctocolitis may also follow adjuvant radiation
therapy for rectal cancer. Proctocolitis develops when
tissue doses exceed 5000 to 6000cGy. Symptoms may
develop during the course of therapy. The mucosa
becomes edematous and hyperemic, accompanied by
development of multiple ulcers. Bloody diarrhea and
tenesmus indicate more severe damage.
Late Radiation Injury
While acute radiation injury involves primarily the
mucosa, late radiation injury is due primarily to injury of
small vessels in the submucosa. The vessels undergo progressive proliferative arteritis, leading to vascular obliteration and ischemia and, ultimately, fibrosis and stricture
formation. The injury may occur months to years after
treatment. In the rectum, radiation endarteritis may
produce ischemic mucosal ulceration, bleeding, and tenesmus months to years after completion of therapy. Late
radiation enteritis produces a gray, matted small intestine
with extensive fibrosis and thickening as well as mucosal
ulcerations. As the endarteritis progresses, the ischemic
bowel tends to depend on blood supply from adhesions
that form. The irradiated bowel therefore tolerates surgical mobilization poorly and is subject to failure of anastomoses and development of fistulas. When an operation
must be performed for obstruction caused by radiation
enteritis, the overall mortality rate is 25% with a 50%
chance that more surgery will be required.
2
P athophysiology ................................................................................................................................. 257
When pelvic irradiation is necessary, several methods
are used to reduce damage to the small intestine. These
include positioning the patient on the radiotherapy table
so that the intestine is displaced out of the pelvis. When a
laparotomy precedes radiation, the small bowel may be
kept out of the pelvis by the use of omentum or absorbable
mesh slings. Following low anterior resection, all attempts
are made to approximate the peritoneum over the pelvic
floor to prevent the small intestine from being fixed in the
pelvic floor.
SHORT BOWEL SYNDROME
The small intestine is about 6 meters in length. Massive
small bowel resection implies resection of more than 50%
of the bowel, which invariably results in the development
of serious malabsorption problems. The reasons for
massive small bowel resection in the pediatric population
are congenital atresia and necrotizing enterocolitis. In
adults, massive resection is most commonly performed for
acute mesenteric ischemia, trauma, radiation enteritis,
strangulated small bowel obstruction, and radiation
enteropathy.
The seriousness of the consequences of massive small
bowel resection depend on several factors:
1. Extent of resection. When 2 meters or less of bowel
remains following surgery, critical malnutrition will
develop.
2. Segment resected. In general, ileal resection is less
well tolerated because of ileal function in absorption of fat,
bile acids, and vitamin B
12
. After jejunal resection, the
ileum accommodates to take over its function. The reverse
is not as true.
3. Preservation of the ileocecal valve. The presence of
the ileocecal valve, up to a point, allows for preservation
of adequate absorptive function with less remaining
intestine.
4. Function. The functional health and adaptability of
the remaining intestine determines the extent of recovery
of its absorptive function.
Consequences of Massive Small
Bowel Resection
Early Physiological Consequences
In the days or weeks following massive small bowel resection, a number of physiological changes occur.
L
OSS OF ABSORPTIVE SURFACE Loss of small intestine
deprives the bowel of absorptive surface, resulting in loss
of water and electrolytes. The results are diarrhea and malabsorption of nutrients, the severity of which depends on
the first three factors listed above.When proximal intestine
is resected, malabsorption of iron, folate, and calcium
occurs. In distal resection, absorption of vitamin B
12
and
bile salts is impaired.
B
ASAL AND POSTPRANDIAL HYPERGASTRINEMIA While
the cause of resection-related hypergastrinemia is
unknown, it is thought to arise from two factors: (1)
removal of intestinal inhibitors of gastrin release, and (2)
loss of intestinal microcirculation, which has an important
role in gastrin degradation.
H
YPERSECRETION OF GASTRIC ACID Acid hyper-
secretion, while due partly to hypergastrinemia, is further
explained by the loss of enterogastrones, inhibitors of
intestinal origin. Acid hypersecretion is time-limited, and
normal gastric acid secretion resumes within a few weeks.
E
NTEROGLUCAGONEMIA Elevated levels of enteroglu-
cagon are due to increased colonic release of the peptide
and serve to stimulate adaptive hypertrophy of the remaining small intestine.
Late Changes
ADAPTIVE CHANGES Hyperplasia of the remaining
enterocytes leads to increased cell renewal, lengthening of
the villi, and deepening of crypts. This process, which
increases the absorptive surface of the small intestine, takes
several weeks to months to reach equilibrium. Growth
factors that may be involved include enteroglucagon, neurotensin and insulin-like growth factor-1 (IGF-1).
D
ISRUPTION OF ENTEROHEPATIC CIRCULATION Resec-
tion of the ileum disrupts the enterohepatic circulation.
The consequences are several:
1. Excessive amounts of bile acids are lost into
the colon, where they injure the colonic mucosa.
This inhibits water and electrolyte absorption and stimulates excessive water and electrolyte secretion, resulting in
diarrhea.
2. Increased hepatic synthesis of bile salts, which leads
to even greater losses of bile salts in the stool.
3. Enteric hyperoxaluria occurs when unabsorbed
fatty acids bind calcium, making the cation unavailable to
form insoluble calcium oxalate. As a result, oxalate
remains soluble and available for absorption. Hyperoxaluria develops, leading to formation of oxalate kidney
stones.
BACTERIAL OVERGROWTH
SYNDROMES
Under normal physiological conditions, several mechanisms prevent bacterial overgrowth in the intestine. One
such mechanism is the migrating motor complex (MMC),
which, during the fasting state, moves from the duodenum
258 ................................................................................................................ Small and L arge Intestine
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