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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1784_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •Contributors
- •History of Stomas*
- •Stoma Physiology
- •Preoperative Considerations
- •Stoma Therapy
- •Quality of Life with a Stoma
- •Diverting Stomas
- •Cecostomy
- •End Ileostomy
- •Continent Stomas
- •Ostomy Take-Down
- •Methods of Urinary Diversion
- •Minimally Invasive Stomas
- •Ilestomy and Pouch Dysfunction
- •Parastomal Hernias
- •Stomal Prolapse
- •Management of Intestinal Fistulas
- •Pediatric Intestinal Stomas
- •Appendix A

38 Cataldo
56. Rankin FW. Total colectomy: its indication and technic. Trans Am Surg
Assoc 1931; 49:263–290.
57. Dragstedt LR, Dack GM, Kisner JB. Chronic ulcerative colitis: a summary
of evidence implicating Bacterium neocrophorum as an etiologic agent. Ann
Surg 1941; 114:654.
58. Turnbull RB Jr. Management of the ileostomy. Am J Surg 1953; 86:617–624.
59. Kock NG. Continent ileostomy. Progr Surg 1973; 12:180–201.
60. Dozois RR, Kelly KA, Beart RW Jr, Beahrs OH. Improved results with conti-
nent ileostomy. Ann Surg 1980; 192:319–324.
61. Turnbull RW, Turnbull GB. The history and current status of paramedical
support for the ostomy patient. Semin Colon Rectal Surg 1991; 2:131–140.
62. Brooke BN. Historical Perspectives: Alternatives to Ileostomy. Chicago: Year
Book, 1985:21.
63. Smith D. Status of colostomy. JAMA 1932; 99:1129–1130.

2
Stoma Physiology
William E. Taylor
Mayo Graduate School of Medicine, Mayo Foundation,
Rochester, Minnesota, U.S.A.
John H. Pemberton
Mayo Medical School and Mayo Clinic, Rochester, Minnesota, U.S.A.
INTRODUCTION
Over a million people in the United States have an intestinal stoma which
has been fashioned for a variety of reasons. Patients with properly function-
ing stomas retain normal physiology except for some well-compensated
changes in fluid and electrolyte homeostasis. Furthermore, with modern
techniques of stomal construction and proper postoperative care, the meta-
bolic complications from the creation of a stoma have fortunately been min-
imized. Through a better understanding of normal physiology and the sys-
temic response to fecal diversion, physicians are able to help maintain and
improve the lifestyles of their patients with stomas.
CONVENTIONAL ILEOSTOMY
Ileostomy Output
There appear to be three distinct phases of adaptation during the initial
postoperative period following stoma construction. Ileostomy effluent dur-
ing the first 1–3 days is bilious and liquid in nature, and each day the
output increases. During the second phase, beginning between days 3 and
5, the output stabilizes or decreases slightly. The third phase is character-
ized by steadily declining outputs until a steady state is reached 6–8 weeks
postoperatively [1]. Subsequently, a relatively constant stool volume rang-
ing from 200–700 mL/day is expected when the ileostomy is well estab-
lished. This process of small intestinal adaptation allows conservation of
the majority of the 1500–2000 mL/day that normally enters the colon from
the small intestine. Dietary changes have minimal influence on the ultimate
stomal output, and once the ileostomy has “matured,” there is little daily
39

40 Taylor and Pemberton
variation in output volume in a given individual. Hill [2] classified individ-
uals with ileostomies into two groups; patients with a low stomal effluent
(less than 700 mL/day) and those with outputs exceeding 1000 mL/day. Pa-
tients with Crohn’s disease characteristically have a higher stomal output.
Since the development of eversion and primary maturation as de-
scribed by Brooke in 1952 [3], high ileostomy outputs have become less
common. Prior to this, high stomal outputs were caused by serositis of the
exposed ileostomy, with subsequent localized inflammation and partial
small bowel obstruction at the level of the abdominal wall. The inflamma-
tory obstruction led to proximal partial small intestinal dilation and watery
diarrhea [4]. Today bowel obstruction is caused by local edema, food im-
paction, ileus, or early adhesive complications. Partial obstruction can be
recognized by either scant output or high-volume, thin, bile-stained efflu-
ent: this most often resolves with the use of conservative measures, includ-
ing nasogastric decompression and bowel rest with intravenous hydration.
By 4–6 months postoperatively, the volume of ileostomy effluent var-
ies little from day to day; the consistency is porridge-like, with a yellow-
brown color, and food particles are present. Formed feces are extremely
unusual and generally associated with marked dehydration, since normal
ileostomy effluent is 90% water (Fig. 1). Variations in consistency and
volume are governed by the amount of water in the stool. Hill [5] observed
that body mass had a direct correlation with stomal output, such that a 40-
kg individual might expect outputs of 300–400 mL/day, while an 80-kg
individual could expect outputs of 800 mL/day.
High stomal output in the perioperative period is initially managed
with aggressive rehydration and replacement of depleted electrolytes.
Should the initial recovery phase to a steady state be prolonged, the output
can be decreased by the use of antimotility agents such as loperamide, di-
phenoxylate-atropine, or tincture of opium. Caution must be employed to
ensure these agents are not used if a partial small bowel obstruction is the
underlying cause of high stomal output.
High outputs in a patient with a mature ileostomy are dealt with first
by modifying the diet. Avoiding foods that frequently quicken transit time
(fruit juices, heavily spiced foods, chocolate, and alcoholic beverages) and
the use of stool-thickening foods (breads, pastas, cheeses, bananas, and creamy
peanut butter) will often decrease the output to an acceptable level. Should
dietary measures prove ineffective, the use of antimotility agents can be
initiated and monitored.
Effects of Oral Intake
The influence of diet and fluid intake on the consistency and volume of
ileal effluent has been well studied and characterized. Water intake plays
virtually no role in determining ileostomy output except that dehydration is

Stoma Physiology 41
Figure 1 Intestinal consistency and erosiveness. The stool becomes more solid as
it progresses through the gastrointestinal tract. A stoma from the colon rather than
the small bowel emits stool that is far less injurious to the skin. (From Keighley
MRB. Ostomy Management. In: Pemberton JH, ed. Shackelford’s Surgery of the
Alimentary Tract, 5th ed. Vol. IV. Philadelphia: W. B. Sau nde rs Co., 2002:3 05–333.)
associated with decreased outputs and thicker consistency. Fasting dramati-
cally decreases ileostomy output to between 50 and 100 mL/day. Studies
of individual dietary components show that ileostomies respond to the insti-
tution of an elemental diet with decreased output and concentration of di-
gestive enzymes and bile acids [6]. Diets with high fat content have been
associated with increases of stomal output to 20% above baseline [6,7].
Increases in fiber content in excess of 16 g/day likewise are reported to
increase output by 20–25%, [8] and also cause increased stool frequency
and flatus. The quantity of sodium in the diet correlates directly with the
volume of stomal output without affecting the dry weight of stool. Grape
or fruit juices, however, do increase the wet weight of the stool. The vast
majority of patients report maintaining or gaining weight after ileostomy
construction, with tolerance of most food types.

42 Taylor and Pemberton
Nutritional Effects
Normal nutrition is the goal and generally also the rule in patients with
established ileostomies. As long as terminal ileal resections are limited (less
than 100 cm), there are few nutritional consequences. Normally, nutrients
are readily absorbed from the small intestine. When malabsorption does
occur though, osmotic diarrhea may result and is suggested by malodorous
floating stools. Fat malabsorption, from impaired bile salt absorption or a
reduced bile salt pool, is a common cause of osmotic diarrhea. Bile salts
may increase outputs either by absorptive inhibition or perhaps by a direct
secretory stimulation on the intestinal mucosa [6,9]. Other disorders of nu-
trient malabsorption occur with carbohydrates (lactase deficiency) and pro-
tein (enterokinase deficiency). Body composition is preserved if patients
increase their dietary consumption of fluid, nutritious foodstuffs, and min-
erals. However, fat losses cannot be compensated for by dietary measures
if the terminal ileum has been resected.
Malabsorption of vitamin B
12
is unusual in patients who have under-
gone resection of less than the distal third of the ileum [10]. Transient
malabsorption of vitamin B
12
may be related to a temporary alteration in
the ileal microflora, and vitamin B
12
supplementation is unnecessary in such
patients. However, resection of more than 100 cm of ileum (especially in-
volving the distal ileum and ileocecal valve) and stagnation from distal
obstruction or bacterial overgrowth predispose the patient to the need for
vitamin B
12
supplementation.
Metabolic Effects
In individuals with well-adapted ileostomies, electrolyte, mineral, and vita-
min deficiencies are uncommon. Intestinal water absorption is controlled
by solute transport across the epithelium, with sodium transport being the
major determinant of small bowel water absorption. Kramer [11] observed
that variations in dietary Na
+
do not markedly influence the Na
+
content of
the stomal effluent. However, chronic systemic water and sodium depletion
associated with ileostomy are accompanied by profound changes in urine
volume, osmolality, and Na
+
content. These observations are consistent
with more recent studies indicating that, after ileostomy, the kidneys pro-
mote systemic conservation of salt and water through the release of mineral
corticoids and their precursors. Thus, after ileostomy, urine volume and
sodium ion concentrations—[Na
+
]—fall, accompanied by increases in [H
+
]
and [K
+
] [12–14]. Early on, there may be disturbances in total body water
and [K
+
] homeostasis [15]. Subsequently, when the ileostomy is estab-
lished and the patient has achieved a steady state, the chronic stimulation
of endogenous mineral corticoid secretion is sufficient to restore body water
and ion composition [12,13,15].

Stoma Physiology 43
If dietary sodium is decreased, a diuresis with reduced renal sodium
excretion and increased ileal potassium losses occurs, which maintains a
normal plasma sodium concentration. Importantly, this renal response may
lead to hypovolemia in ileostomates who are already at risk for dehydration
because of fixed salt and water losses. The mechanism for this response is
unknown but may be related to changes in the secretion of arginine vaso-
pressin. However, previous studies have failed to show significant changes
arginine vasopressin levels in plasma [16,17]. Sutters et al. [18] have
shown that diuresis from sodium restriction in ileostomy patients is blunted
with synthetic vasopressin administration without affecting renal sodium
losses or the composition of ileal effluents.
The normal amount of sodium lost in the ileostomy effluent is approx-
imately 60 mEq daily, as compared to 2 to 10 mEq lost in the stool daily
in a normal individual. Stomal sodium losses average 1 mEq/hr in the fast-
ing state but increase to 3–4 mEq/hr postprandially. However, symptomatic
salt depletion in well-established ileostomates is rare. Instead, urine output
and sodium excretion are decreased because of enhanced renal conservation
of salt and water [19]. Hill [2] showed that, despite adaptation, a decreased
amount of total body water and exchangeable sodium exists in ileostomy
patients compared to healthy persons. This obligatory ileal sodium loss is
normally overcome with a standard diet. Importantly, however, the onset
of volume depletion is rapid in patients who develop high ileostomy outputs
for any reason.
The terminal ileum is an important region for water and sodium re-
sorption, and the extent of small bowel resection directly effects the ileos-
tomy adaptation process. Ileostomy output is susceptible to the loss of as
little as 9 cm of terminal ileum, and salt and water absorption are progres-
sively impaired as the extent of resection increases [20]. In patients who
have undergone ileal resection, ileostomy outputs and electrolyte losses are
higher early postoperatively as compared with those in patients with preser-
vation of small bowel; furthermore, the volume and electrolyte composition
are unchanged by 6 months [21]. In addition, losses of fat and nitrogen
are higher following more extensive small bowel resection and can further
influence water and electrolyte losses [22].
A proximally located loop ileostomy has an effect comparable to that
of extended ileal resection. In performing the ileal pouch–anal anastomosis
(IPAA), 50–100 cm of terminal ileum is often excluded from absorption
by creating the diverting loop ileostomy. Patients have higher fecal outputs,
which are more liquid in nature. Poor weight gain and episodes of dehydra-
tion cease once the loop ileostomy is closed.
Total body potassium depletion is rare in a patient with an uncompli-
cated ileostomy. Normal individuals and ileostomy patients lose about 9
mEq K
+
each day, regardless of the magnitude of the output of feces or

44 Taylor and Pemberton
ileostomy effluent [23,24]. A chronic state of salt depletion causes ileal
potassium secretion to increase in exchange for maximizing ileal sodium
absorption. Excess potassium and total-body nitrogen losses reflect exten-
sive small bowel resection. The mature ileostomy excretes approximately
1.5 g of nitrogen daily. Cooper et al. [25] found patients to have a normal
body weight, with normal fat and water content, if the ileal resection was
limited to 4 cm. This was associated with reduced total body nitrogen and
potassium, implying a decreased fat-free body mass. In patients with more
than 50 cm of ileum resected, total body weight was reduced due to de-
creased total fat content.
Losses of calcium and magnesium are unaffected unless extensive il-
eal resection has been performed. In this instance, malabsorption of dietary
calcium is compounded by abnormal bile salt and vitamin D metabolism
from terminal ileal resection.
Intestinal Transit
Patients with an ileostomy adapt to the loss of their colon by slowing their
small bowel transit time. Soper et al. [26] studied the orostomal transit time
in ileostomy patients (Table 1). Using a dual radioisotope technique, they
demonstrated that the gastric emptying of liquids in patients with ileosto-
mies was not altered. However, orostomal transit time was significantly
longer in ileostomy patients compared to controls (348 min vs. 243 min,
respectively, P < 0.01). These observations confirmed the conclusion of a
previous study, which found that proctocolectomy and ileostomy slowed
small bowel transit [27]. A recent study by Bruewer et al. [28], employing
a lactulose breath test, likewise showed that oropouch transit is prolonged
following proctocolectomy with IPAA. The authors found that the adapta-
Table 1 Gastrointestinal Transit After Proctocolectomy
Group (mean ± SD)
Control Ileostomy
Parameter (min) (n = 8) (n = 5) p value
Gastric emptying
a
120 ± 22 109 ± 10 NS
Small bowel transit
b
243 ± 32 348 ± 12 < 0.01
a
T
3/4
of gastric emptying of a liquid marker.
b
Interval to reaching cecum in controls and ileostomy bag in
ileostomy subjects.
Source: From Soper NJ et al. Gastrointestinal transit after proc-
tocolectomy with ileal pouch-anal anastomosis or ileostomy. J
Surg Res 46:300, 1989. Modified with permission of the author .

Stoma Physiology 45
tion process takes longer than a year and that the initial oropouch transit
times in the early postoperative period were significantly accelerated.
The mechanisms behind this adaptive response of the small bowel
following colectomy remain unclear but may be related to epithelial hyper-
trophy, resulting in an increased absorptive surface [29,30]. Furthermore,
an inverse relationship between electrolyte and nutrient absorption and in-
testinal transit has been demonstrated [31].
Bacteriological Environment
The bacterial flora of the ileum after ileostomy is intermediate in nature
between small intestinal and colonic. Gorbach et al. [32] found an 80-fold
increase in organisms in the terminal ileum; furthermore, coliforms were
2500 times more common than in normal ileal fluid. Overall, the ileostomy
effluent bacterial count was still considerably less than that of normal feces.
Staphylococci, streptococci, and fungi were increased in number, while
Bacteroides fragilis was rarely found in the ileostomy effluent.
Systemic Effects
Urinary stone formation is a widely recognized complication of inflamma-
tory bowel diseases, particularly in association with ileal resection. The re-
ported incidence is 3–13% and is related to dehydration and excess sodium
losses experienced by patients with ileostomies. The incidence of stone for-
mation in the general population is approximately 4% [33]. Uric acid stones
usually make up less than 10% of all stones but 60% of all stones found in
patients with ileostomies [34]. Christie et al. [35] found ileostomy and
IPAA patients to have a significantly lowered urinary volume and pH, with
increased concentrations of calcium and oxalate. Patients with ileostomies
were at increased risk for forming uric acid and calcium stones, while those
with IPAA showed only a propensity to form uric acid stones. High-output
ileostomies and extensive ileal resection predispose patients to stone forma-
tion. The etiology is likely related to the reduced urinary volume and pH
facilitating stone precipitation. Prophylaxis is directed toward increasing
daily fluid intake and urine output.
The association between ileostomy construction and increased gall-
stone formation is controversial. Well-adapted patients excrete bile acids in
amounts similar to those excreted by a person with an intact colon [36,37].
However, with extensive terminal ileal resection or inflammation, the enter-
ohepatic circulation is disrupted. Subsequently, bile acid malabsorption or
depletion alters the saturation of bile, promoting precipitation and stone
formation. Ritchie [38] found no difference in the number of ileostomy
patients who required cholecystectomy compared to those without ileosto-
mies. However, Kurchin et al. [39] urged consideration of prophylactic cho-

46 Taylor and Pemberton
lecystectomy in female patients undergoing proctocolectomy or small in-
testinal resection for inflammatory bowel disease because of a threefold
increase in asymptomatic gallstones in women receiving ileostomies. At
Mayo, prophylactic cholecystectomy is rarely performed. If, during laparot-
omy, gallstones are discovered and the remainder of the operation has gone
smoothly, cholecystectomy is usually performed.
KOCK POUCH
Continent Ileostomy Output
The majority of Kock patients appear to have no major long-term physio-
logic sequelae. The physiological consequences of creating a continent
ileostomy have been well described. The initial postoperative fecal output
is approximately 1500 mL/day. By 6 months, the volume is between 400
and 600 mL/day. Well-established continent reservoirs and conventional
ileostomies have similar stool volumes [40]. However, unlike the conven-
tional ileostomy, the continent reservoir accommodates to increasing intra-
luminal volume passively, like the rectum. At the time of operation, the
reservoir typically can accommodate a volume of 70–100 mL. At a month’s
time, the volume is approximately 200 mL, and it increases steadily to a
maximum of around 600 mL at 6 months. The fecal volume may increase
to over 1000 mL/day if undue small bowel is sacrificed at the time of
operation and in the presence of recurrent Crohn ’s disease or pouchitis [41].
Bacteriological Environment
The ileal reservoir luminal flora changes to resemble colonic bacteria in
both quantity and the ratio of anaerobic to aerobic bacteria [40,42]. The
contents of the Kock pouch are more fecal than those of the conventional
ileostomy. These changes are noted soon after creation of the pouch and
presumably occur because of the pouch. Subsequently, increased bacterial
flora then competes with the host for nutrients, bile acids, and vitamin B
12
for substrate. However, bacterial overgrowth tends not to be a significant
clinical problem. Increased anaerobic bacteria in the pouch have been im-
plicated as an etiology of pouchitis because of its common response to
metronidazole therapy. Data from this institution have not confirmed a cor-
relation between stomal microbial effluent and pouch dysfunction, although
it certainly remains a likely component of a multifactorial etiology [42,43].
The bacterial counts in the proximal small bowel also increase in pa-
tients with a continent ileostomy. Qualitatively, the flora is similar to that
of the normal jejunum. Kelly et al. [42] postulated that decreased jejunal
motility and impaired clearance of swallowed bacteria are plausible expla-
nations for this finding.

Stoma Physiology 47
Histological Alterations
Histologically, the small intestinal villi in the pouch become blunted and
undergo a metaplastic response to resemble colonic epithelium [40,44]. The
number of crypt cells and mucosal volume increase while the neuroendo-
crine cell population is unaltered. These changes occur within the first year
of reservoir construction but stabilize by 6–10 years postoperatively [45].
The metaplastic changes are not necessarily permanent and may normalize
back to small intestinal villi with time. The etiology of the altered mucosa
is unknown but may be related to prolonged exposure to bacterial metabo-
lites and toxins from fecal stasis in the pouch. However, oxidative enzy-
matic and secretory activities appear unaltered by the morphological
changes [45]. Furthermore, structural changes in the ileal mucosa are not
correlated with pouch dysfunction [42,43]. The long-term effects of these
changes are uncertain, but in isolated cases, progression of pouch dysplasia
to invasive carcinoma have been reported in both a Kock pouch and an
IPAA [46,47].
Metabolic Effects
The metabolic consequences of constructing a continent ileostomy are mi-
nor despite the altered histology and bacterial environment in the pouch.
The absorptive pattern of the continent ileostomy is similar to that of the
conventional ileostomy. Absorption of fat, water, xylose, and phenylalanine
as well as bicarbonate secretion are not different from what is seen with
standard ileostomies [48]. Mucosal transport of sodium, chloride, and water
within the reservoir is also unaltered despite large concentration gradients
[49]. Total body water and urinary excretion of sodium and potassium are
also similar. Furthermore, Ojerskog et al. [50] found no evidence of potas-
sium or water depletion in conventional ileostomy patients who underwent
conversion to a continent pouch. The pH of the reservoir contents is less
than that of the conventional ileostomy, presumably due to increased bacte-
rial fermentation of polysaccharides and production of short-chain fatty
acids within the reservoir [51].
Bile acid excretion is not different from that associated with conven-
tional ileostomies (Table 2) [48,52]. Normal daily fecal bile acid loss is
approximately 200 mg or 5% of the bile acid pool. Bile acid depletion of
up to 20% is balanced by enhanced hepatic synthesis. Hence, disruption of
the enterohepatic circulation is uncommon unless bacterial overgrowth or
extended ileal resection is present. Hylander et al. [53] reported that bile
acid deconjugation may occur in the reservoir; however, this is disputed by
others [49,51]. Furthermore, the incidence of cholelithiasis is similar with
a continent or conventional stoma [54]. With preservation of the bile acid
pool, the ability to absorb fat is retained in most patients with continent
ileostomies (Table 3).
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