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268 Marcello and Metcalf
adaptive response to colectomy over the first few weeks following procto-
colectomy. The gradual reduction of stomal output seen following procto-
colectomy is, however; not typically seen in patients who have undergone
significant ileal resection.
High stool output following proctocolectomy may be due to a multi-
tude of causes including infectious sources, partial obstruction, recurrence
of Crohn’s disease, or further resection of small bowel. Patients who have
undergone proctocolectomy may develop bacterial or viral (more likely)
gastroenteritis at the same frequency as the general population. However,
in comparison to the general population, the consequences of gastroenteritis
are more severe to the patient with an ileostomy. Without an intact colon
and ileocecal valve, stoma patients are much more prone to dehydration
with marked increases in effluent output and must be instructed to maintain
adequate liquid intake. If they develop significant nausea and vomiting with
their illness, dehydration may rapidly ensue. All stoma patients need to be
aware of this phenomenon. Patients are instructed to monitor their urine
output and, before severe dehydration occurs, should present to the emer-
gency room for hydration if the urine volume decreases or becomes more
concentrated.
Partial Obstruction
Small bowel obstruction is common following proctocolectomy. The inci-
dence of such obstruction is highest in the first 3 years following surgery
[2]. Adhesions, volvulus, and internal or parastomal hernias are the most
common sources of bowel obstruction, with the majority being due to adhe-
sion formation. Symptoms of bowel obstruction include a significant change
in ostomy output (either more or less depending on degree of obstruction),
abdominal cramps, bloating, and nausea and vomiting. In cases of partial
small bowel obstruction, stomal output may become quite excessive, with
thin, watery fluid. The mechanism by which partial obstruction leads to
increased effluent is not well understood. With complete obstruction, fluid
and electrolyte absorption is impaired and the bowel proximal to the ob-
struction becomes secretory rather absorptive [3]. With resolution of bowel
obstruction by conservative treatment, there may be a compensatory in-
crease in ostomy output as the obstruction resolves. This is heralded by
thin, watery output through which one could “read a newspaper.” Patients
require commensurate intravenous fluid resuscitation. For output greater than
2 L, patients should be placed on milliliter-for-milliliter replacement with
either 0.45% normal saline or lactated Ringer’s solution, depending on their
electrolyte and metabolic status. The patients’ diet should not be advanced
beyond clear liquids until the stoma output falls and the effluent thickens.
Partial or complete ileostomy obstruction commonly results from di-
etary indiscretion. An ileostomate may eat celery, raw carrots, apples, or
Ileostomy and Pouch Dysfunction 269
other fibrous food. Particularly if eaten quickly and not chewed well, this food
may pass relatively undigested to the ileum just proximal to the stoma. Lodg-
ing immediately proximal to the fascia where the ileal lumen is at its narrow-
est point, this food bolus may cause partial or complete obstruction. In such
instances, patients present with symptoms identical to those of small bowel
obstruction. When questioned, they can often identify the dietary source.
In this circumstance, gentle irrigation of the stoma with water via a
lubricated red rubber catheter (digital evaluation of the ileostomy is unre-
warding, due to its narrow lumen) will commonly dislodge the food parti-
cle. Occasionally dramatic results ensue, as evidenced by large ileostomy
output and relief of obstructive symptoms.
Bacterial Overgrowth
Bacterial overgrowth has been identified in patients with partial bowel ob-
struction and may be a cause for increased stoma output. Small bowel bac-
terial overgrowth is known to cause both deconjugation of bile salts and
vitamin B
12
malabsorption [4]. Unconjugated bile salts impair sugar, water,
sodium, and potassium transport in the small intestine [5]. Anaerobic bacte-
ria are capable of binding to the vitamin B
12
–intrinsic factor complex, mak-
ing it unavailable for absorption. The combination of aerobic and anaerobic
bacterial overgrowth may lead to increased fluid sequestration in the ob-
structed bowel by the above mechanisms.
Recurrent Regional Enteritis
Recurrence rates after colectomy for Crohn’s disease vary. Recurrence fol-
lowing proctocolectomy and ileostomy is less common than segmental co-
lonic or small bowel resection with anastomosis and ranges from 10–20%
[6–7]. High-volume output in these patients may be caused by either muco-
sal disease—with resultant malabsorption of fluid, electrolytes, and nutri-
ents—or partial intestinal obstruction, with its attendant pathophysiology.
Even a pathologically confirmed diagnosis of ulcerative colitis does
not preclude the possibility of regional enteritis (Crohn’s disease) as a cause
of ileostomy diarrhea. In a small percentage (<5%) of patients thought to
have ulcerative colitis, an ultimate diagnosis of Crohn’s disease will be
identified postoperatively when regional enteritis develops in the small in-
testine. This is especially true following ileoanal pouch surgery. In a study
from the Lahey Clinic, 3% of patients with a pathological diagnosis of
ulcerative colitis were eventually found to have Crohn’s disease in the re-
sidual small intestine [8]. In more than half of these patients, high stool
frequency related to the Crohn’s disease was identified, thus highlighting
the need to consider recurrent regional enteritis in all patients with an ileos-
tomy regardless of the original colonic pathology.
270 Marcello and Metcalf
Ileal Resection
Resection of even small lengths of terminal ileum can have significant
long-term effects on the volume of effluent from a conventional stoma. In
addition to a chronically elevated effluent volume, patients have higher-
than-normal output of sodium and potassium. They may also have higher-
than-normal fecal concentrations of nitrogen and fat [9]. This phenomenon
may be a result of more rapid transit of intestinal contents, loss of the portion
of small bowel that is most responsive to mineralocorticoids, or steatorrhea.
Steatorrhea after resection is probably secondary to impairment of bile salt
absorption from loss of the terminal ileum, with secondary depletion of the
bile salt pool. Whatever the precise mechanism, patients who require ileal
resection will have persistently high effluent volumes.
Gastric Hypersecretion
Gastric hypersecretion is rarely seen after proctocolectomy alone. It occurs
more commonly when proctocolectomy is combined with excessive small
bowel resection. The period of hypersecretion may last up to several months.
H
2
blockers or proton pump inhibitors may curtail some of the effects. If
untreated, acid hypersecretion results in low jejunal pH, impaired micellar
solubilization of fat, steatorrhea, and diarrhea [10].
CONTINENT ILEOSTOMY OR ILEOANAL POUCH
Pouchitis
Patients with a continent ileostomy or ileoanal pouch are prone to develop a
type of ileostomy dysfunction that is not seen in patients with conventional
ileostomies. This syndrome, termed pouchitis, may occur in up to 50% of
patients following either of these procedures. Patients will complain of in-
creased stool frequency, abdominal or pelvic cramps, and tenesmus (if they
have a pelvic pouch). They may sometimes complain of fever, arthralgias,
anorexia, or weight loss. Arthralgias are often seen in patients who had
arthralgias associated with their inflammatory bowel disease. Patients with
a continent ileostomy may have difficulty intubating their pouch. More than
any single symptom, a patient with an ileoanal reservoir who develops pou-
chitis will complain that his or her “colitis” has returned. The precise mech-
anism of pouchitis remains unknown, but most theories center around bac-
terial overgrowth of the ileal reservoir. This alone, however, is insufficient.
Patients with continent ileostomies and ileoanal reservoirs who develop
pouchitis almost universally have inflammatory bowel disease; pouchitis
rarely occurs in patients with familial adenomatous polyposis who undergo
similar procedures [11]. This suggests that pouchitis is multifactorial, in-
volving genetic, immune, and microbial mediators. Ileal reservoirs are colo-
nized with high concentrations of bacteria, which—combined with incom-
Ileostomy and Pouch Dysfunction 271
plete evacuation and stasis—may be a major factor in the pathogenesis of
pouchitis. The role of bacterial overgrowth is further supported by the use
of antibiotics and probiotics in the treatment of pouchitis. Metronidazole
and ciprofloxacin are the most commonly prescribed antibiotics in the treat-
ment of pouchitis. A recent randomized control trial compared these two
antibiotics; both were found to be highly effective, and they significantly
lowered pouchitis activity indices [12]. Further studies have demonstrated
the efficacy of probiotics for the treatment and remission of pouchitis. Pro-
biotics, by restoring the microbial imbalance in the pouch, are a new alterna-
tive for the treatment of chronic pouch inflammation. In a placebo-controlled
trial by Gionchetti and colleagues, a highly concentrated mixture of probiotic
bacteria was highly effective as a maintenance treatment for pouchitis [13].
Future studies will evaluate the role of probiotics in the prevention of pou-
chitis. Until then, oral antibiotics will likely remain the mainstays of therapy.
Patients with an ileoanal pouch may also be at risk for long-term met-
abolic consequences, which are most prominent in patient with chronic
pouchitis. In a recent evaluation of 104 patients with an ileoanal J pouch
for more than 5 years, the incidence of pouchitis was 42% and was strongly
associated with villous atrophy [14]. In patients with severe villous atrophy,
serum levels of albumin, calcium, cholesterol, triglycerides, and vitamin E
were significantly reduced. Rates of vitamin B
12
absorption were lowest in
patients whose inflammation extended into the afferent limb. Vitamin D
deficiency was seen in 10%, and deficiencies of vitamins A and B
12
were
noted in 5%. In patients with chronic pouch inflammation, therefore, an
assessment of these metabolic disturbances should be considered.
Outlet Obstruction
Patients with an ileoanal reservoir may develop frequent stools and inconti-
nence secondary to poor emptying of the pelvic pouch as a result of me-
chanical outlet obstruction. For patients with a J-type pouch, this likely
relates to stricture at the pouch’s anal anastomosis. This typically responds
to in-office or operative dilatation. For patients with an S-shaped pouch,
outlet obstruction occurs secondary to elongation of the efferent limb, which
results in a kink at the junction of the efferent limb and pouch. This typi-
cally requires abdominal revision of the pouch by shortening the efferent
limb and reseating the pouch. An alternative is a transanal approach that
divides the obstructing septum between the pouch and the efferent limb.
This approach has been highly effective in a small series of patients [15].
Afferent Limb Obstruction
Afferent limb obstruction should be suspected in patients with recurrent
obstruction following the construction of an ileoanal reservoir [16]. Patients
often present with chronic symptoms of intermittent obstruction. The bowel
272 Marcello and Metcalf
proximal to the ileoanal pouch becomes adherent to the ileoanal pouch;
thus, when the pouch distends, external compression worsens the obstruc-
tion. Symptoms are relieved when the patient evacuates the ileal reservoir.
The diagnosis is difficult to establish, although radiographic demonstration
of dilated bowel to the level of the pouch is suggestive. Because the obstruc-
tion is distal in the small bowel and often not complete, antegrade contrast
studies may not be definitive. Retrograde contrast enema using fluoroscopy
is probably the most effective study to demonstrate the site of obstruction.
The obstruction is treated by resection or preferably by bypassing the ob-
structed afferent limb. Resection of the afferent limb may result in inadver-
tent injury to the pouch or its blood supply. Afferent limb obstruction
should be considered in a pouch patient who has chronic intermittent ob-
struction without evidence of proximal adhesive obstruction.
MANAGEMENT OF ILEOSTOMY DIARRHEA
Since many patients with a well-functioning ileostomy are prone to mild
dehydration, it is no surprise that severe dehydration can develop quite rap-
idly when diarrhea occurs. With a reduction in both total body water and
exchangeable sodium, serum sodium levels may be normal. A secondary
potassium deficiency can develop, as the kidney will excrete potassium in
an attempt to conserve sodium. Occasionally magnesium and calcium
depletion may be identified in patients with long-standing high ileostomy
output. Vitamin B
12
deficiency is a well-known sequela of ileal resection,
and patients with chronic ileostomy diarrhea are prone to develop uric acid
or calcium oxalate kidney stones and cholelithiasis.
CLINICAL EVALUATION
History
Knowledge of the details of the original diagnosis, the type of procedure
performed, and the postoperative complications helps in narrowing the dif-
ferential diagnosis. Symptoms beginning early after surgery suggest ileal
resection, chronic obstruction, or a preexisting condition (such as lactose
intolerance) as a cause of high stomal outputs. The volume of stool effluent
can be estimated by the frequency of ostomy device emptying. The charac-
ter of the stool and the presence of blood can also provide clues. The patient’s
volume status can be estimated by the frequency and volume of urination
and recent weight loss. Associated intestinal symptoms such as cramping,
bloating, and difficult evacuation or intubation should be ascertained, as should
extraintestinal symptoms of stomatitis, arthritis, or uveitis. Such symptoms
are suggestive of partial intestinal obstruction, bacterial overgrowth, pou-
chitis, or recurrent Crohn’s disease. Current medications or recent changes
Ileostomy and Pouch Dysfunction 273
of medication should be reviewed, as should similar diarrheal symptoms in
other family members and any preceding travel history that might suggest
an infectious source.
Physical Examination
Physical examination should focus on hydration status, abdominal evalua-
tion, stomal appearance, and the perineum. In patients with an ileoanal res-
ervoir, the perianal skin should be examined for manifestations of Crohn’s
disease and digital examination should be performed to exclude anasto-
motic stricture. Flexible or rigid endoscopy through the stoma or anus will
allow assessment of the small bowel mucosa.
Laboratory Studies
The history and physical examination will dictate which studies should be
obtained. Blood chemistries—including complete blood count, serum electro-
lytes, creatinine, and blood urea nitrogen—are appropriate in most patients.
Quantification of gastric acid secretion and serum gastrin levels may be indi-
cated. Fecal studies for Campylobacter, Yersinia, Shigella, Salmonella, Clos-
tridium difficile toxin, other pathogens, and ova and parasites may be required.
Quantification of 24-hr fecal volumes, electrolytes, and fat is appropriate
in most chronic cases. Contrast examinations of the small intestine and
endoscopy are useful to exclude obstruction or recurrent Crohn’s disease.
MEDICAL MANAGEMENT
For patients in whom a surgically correctable source of the diarrhea has
been identified, resection is appropriate. In patients with recurrent Crohn’s
disease, appropriate medical therapy may avoid the need for surgery.
For patients with a continent ileostomy or ileoanal pouch with symp-
toms consistent with pouchitis, antibiotic therapy should be instituted. A 2-
week course of metronidazole or ciprofloxacin should be tried and then the
antibiotics discontinued. Other broad-spectrum antibiotics may also be
used. If symptoms recur, patients may be retreated. There is increasing evi-
dence that probiotics may be used as a primary or supplemental treatment
for recurrent pouchitis. For patients with persistent symptoms, endoscopic
examination of the pouch is useful in documenting the degree and location
of the inflammation and is best done when patients are symptomatic. In
some cases inflammation may occur in the distal pouch or retained rectal
mucosa if a stapled anastomosis was performed. These patients will re-
spond well to steroid suppositories or steroid foam injections. For patients
with chronic recurrent pouchitis, resumption of 5-aminosolicyclic acid (5-
ASA) class medications, 6-mercaptopurine, or systemic steroids may be
required. Also in this group, repeated endoscopic examination of the affer-
274 Marcello and Metcalf
ent limb proximal to the pouch along with a small bowel series should be
performed to exclude Crohn’s disease.
In patients who have high ileostomy output after ileal resection in whom
other treatable conditions have been excluded, it is important to quantitate
the amount of steatorrhea on a diet with a known amount (70–100 g) of
daily fat intake. Patients with a stomal output of greater than 15 g of fat a
day generally have fat malabsorption should be treated with a 50 to 70-g
fat diet. In more severe cases, further reduction to a 40-g fat diet may be
tried with medium-chain triglyceride supplementation. Patients should also
be on maintenance antidiarrheal agents, such as loperamide or codeine.
Supplemental fiber may be used to thicken the effluent. If response is mini-
mal, opium may be added. For patients with steatorrhea, there has been
some success from treatment with an H
2
blocker.
A host of other therapies have been utilized to maintain fluid and
electrolyte balance, with varying results. Active absorption of an orally ad-
ministered glucose polymer solution (Polycose; Ross Laboratories, Colum-
bus, OH) in the proximal jejunum is believed to result in passive absorption
of salt and water [17]. There are also scattered case reports of good re-
sponse to long-acting somatostatin analogues. Somatostatin leads to de-
crease water secretion and prolonged small bowel transit time. Gastric
emptying and glucose and nitrogen excretion were not altered in the pa-
tients studied, although fat excretion was increased [18].
In patients with truly uncorrectable ileostomy diarrhea and problems
maintaining fluid and electrolyte balance, fluid therapy through a perma-
nent indwelling intravenous catheter may be necessary. If a patient with
long-term high ileostomy output develops urolithiasis, alkalinization of the
urine should be considered. For patients who develop symptomatic choleli-
thiasis, cholecystectomy is required. Elective cholecystectomy should be
considered in a patient with an ileostomy who requires further small bowel
resection resulting in the development of short bowel syndrome.
SUMMARY
Most patients with ileostomy and or pouch dysfunction have an underlying
cause that is relatively easy to diagnose and treat. In most instances the
cause relates to the underlying disease or the type of surgical procedure
performed. Successful management, often without surgery, is possible in
the majority of cases.
REFERENCES
1. Kramer P, Levitan R. Effect of 9-fluorohydrocortisone on the ileal excreta of
ileostomized subjects. Gastroenterology 1972; 62:235–241.
Ileostomy and Pouch Dysfunction 275
2. Watts J, deDombal FT, Goligher JC. Long-term complications and prognosis
following major surgery for ulcerative colitis. Br J Surg 1966; 53:1014–1023.
3. Sheilds R. The effect of experimental obstruction on the intestinal absorption
of water, sodium, and potassium. In: Smith AN, ed. Surgical Physiology of
the Gastrointestinal Tract. Edinburgh: Royal College of Surgeons of Edin-
burgh, 1963:166.
4. Tabaqchali S, Hatz J, Booth CC. Bile salt deconjugation and steatorrhea in
patients with stagnant loop syndrome. Lancet 1968; 2:12–16.
5. Gracey M, Burke V, Oshin A. Reversible inhibition of intestinal sugar trans-
port by deconjugated bile salt in vitro. Biochim Biophys Acta 1971; 225:
308–314.
6. Marcello PW. Large bowel Crohn’s disease. Clin Colon Rectal Surg 2001;
14:159–165.
7. Ritchie JK, Lockart-Mummery HE. Nonrestorative surgery in the treatment
of Crohn’s disease of the large bowel. Gut 1973; 14:263–270.
8. Marcello PW, Schoetz DJ, Roberts PL, et al. Evolutionary changes in the
pathologic diagnosis following the ileoanal pouch procedure. Dis Colon Rec-
tum 1997; 40:263–269.
9. Neal OE, Williams NS, Barker MCJ, et al. The effect of resection of distal
ileum on gastric emptying, small bowel transit and absorption after proctoco-
lectomy. Br J Surg 1984; 71:666–670.
10. Cortot A, Fleming RC, Malagelada JR. Improved nutrient absorption after
cimetidine in short bowel syndrome with gastric hypersecretion. N Engl J
Med 1979; 300:79–80.
11. Marcello PW, Roberts PL, Schoetz DJ, et al. Long-term results of the ileoanal
pouch procedure. Arch Surg 1993; 128:500–504.
12. Shen B, Achkar JP, Lashner BA, et al. A randomized clinical trial of cip-
rofloxacin and metronidazole to treat acute pouchitis. Inflamm Bowel Dis
2001; 7:301–305.
13. Gionchetti P, Rizzello F, Venturi A, et al. Oral bacteriotherapy as mainte-
nance treatment in patients with chronic pouchitis: a double-blind, placebo
controlled trial. Gastroenterology 2000; 119:305–309.
14. Kuisma J, Nuutinen H, Luukkonen P, Jarvinen H, Kahri A, Farkkila M. Long-
term metabolic consequences of ileal pouch–anal anastomosis for ulcerative
colitis. Am J Gastroenterol 2001; 96:3110–3116.
15. Bruce CJ, Coller JA, Murray JJ, Marcello PW. Transanal repair in patients
with S-pouch efferent limb obstruction. Dis Colon Rectum 1996; 39:A36.
16. Read TE, Schoetz DJ, Marcello PW, et al. Afferent limb obstruction compli-
cating ileal pouch-anal anastomosis. Dis Colon Rectum 1996; 40:566–569.
17. Saunders DR, Daunders MD, Sillery JK. Beneficial effects of glucose poly-
mer and H2 receptor blocker in a patient with proximal ileostomy. Am J
Gastroenterol 1989; 84:192–194.
18. Cooper JC, Willliams NS, King RF, et al. Effect of a long-acting somatostatin
analogue in patients with severe ileostomy diarrhea. Br J Surg 1986; 73:
128–131.
15
Parastomal Hernias
Marc S. Rubin
Harvard Medical School and The North Shore Medical Center,
Salem, Massachusetts, U.S.A.
INTRODUCTION
Parastomal hernia, an incisional hernia at the site of an intestinal stoma,
has been a recognized complication of stoma surgery for a long time. Ac-
cording to Goligher [1], “Some degree of herniation around a colostomy is
so common that this complication may be regarded as inevitable.” Although
hernias associated with ileostomy and urostomy are less frequent, they are
still common. The potential complications of parastomal hernia can be mild
and easily managed or serious and potentially life-threatening. The patient
may present with a cosmetic problem, with difficulty managing the stoma,
or with any of the usual complications of a hernia. Repair is complex,
although infrequently necessary. The poor results with standard local repair
have caused surgeons to favor relocation of the stoma or techniques using
prosthetic material. Even with these methods, results are often less than
ideal. As is often the case, the best solution to the problem is prevention.
Good preoperative planning and careful attention to technical detail can
minimize parastomal herniation.
INCIDENCE AND PREDISPOSING FACTORS
Identifying the incidence of parastomal hernia is difficult. Various authors
have reported frequencies ranging from 0–100%. Table 1 lists the incidence
in the published series to date. Clearly the rate varies with the type and age
of the stoma and with the technique and circumstances of the operation.
Patient characteristics and postoperative events also affect the likelihood of
hernia development.
Table 2 lists identified or suggested predisposing factors for parasto-
mal hernia formation. Despite the long list of factors that might predispose
an individual with an ostomy to hernia development, only a handful of
277