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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1499_Библиотеки_им_академика_М_И_Перельмана.pdf
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Epidemiology
Ulcerative colitis: 40–50% of patients develop at least one episode of pouchitis, 60% of patients with one pouchitis episode
will experience recurrent episodes; 5–10% of patients per decade develop treatment-refractory ileoanal dysfunction risk of
pouch loss. FAP: risk of pouchitis is lower (10–15%).
Symptoms
Primary symptoms: diarrhea, increased/unacceptable frequency/urgency above expected normal range of 4–8 bowel
movements per day, fecal incontinence or soilage, gas formation, passage of mucous and blood.
Secondary symptoms: perianal dermatitis with/without excoriations
perianal/perirectal pain, itching/burning.
Systemic symptoms: fever, flulike symptoms may occur, particularly in acute-onset pouchitis; flare-up of extraintestinal
manifestations.
Differential Diagnosis
Pouchitis: most common long-term adverse event after technically successful IPAA, nonspecific pouch inflammation of
unknown etiology. Defined by (1) clinical criteria: increased frequency, diarrhea, gas formation, flulike symptoms; (2)
morphologic criteria: mucosal inflammation, ulcerations.
Irritable pouch syndrome (IPS): same symptoms as pouchitis but complete absence of inflammatory changes.
Anal transitional zone (ATZ) cuffitis: morphologically normal-appearing pouch (pouchogram, pouchoscopy) but significant
acute and chronic ATZ cuff inflammation with/without ulcerations
topical mesalamine or steroid suppositories,
mucosectomy with pouch-anal advancement if treatment-refractory cuffitis.
Specific pouch infection: C difficile, candidiasis, CMV
specific treatment.
Insufficient pouch volume: technical problem (too-short limbs, incomplete division) or result of extrinsic or intrinsic process
(abscess, desmoids, pouch tumor, etc)
pouch augmentation or revision, completion of septum division (transanal
endoscopic linear stapler division or pouch revision), pelvic "clean-out" depending on etiology.
Pouch prolapse (IPAA, continent ileostomy)
pouchopexy, local trimming of redundancy, complete pouch revision.
Stricture: result of chronic leak, ischemic segment, postradiation, desmoid formation
treatment with serial dilations,
stricturoplasty, salvage pouch.
Fistula: result of anastomotic leak, underlying Crohn disease, cryptoglandular origin
rediversion, drainage procedure,
pouch revision with axial rotation and reinsertion, collagen plug, advancement flap, muscle interposition.
Sinus: resulting from confined anastomotic leak
marsupialization/incorporation into pouch vs pouch revision.
Pouch polyp
pouch cancer. Prophylaxis: adequate pouch surveillance; once cancer present oncologic resection and
management.
Pouch outlet obstruction: low-pressure reservoir anastomosed to high-pressure segment, ie, S-pouch with long efferent
limb, J-pouch to high rectum:
functional outlet obstruction (as opposed to morphologic stricture) surgical revision vs
supportive measures (tube insertion, stool management).
Crohn disease: incidence 2–7%. Diagnosis difficult: mucosal inflammation/ulcerations in afferent small bowel mucosa
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proximal to the pouch, pouch fistula or other perianal complication more than 3 months after closure of temporary ileostomy.
Pathology
MACROSCOPIC
Diffuse or focal erythema and granularity, loss of vascular pattern, friability of the mucosa with bleeding tendency, exudates,
focal ulcerations, aphthoid lesions; while changes are generally diffuse, the posterior pouch portions are more exposed to the
stool stasis and may show more extensive inflammation; afferent limb to pouch unaffected, otherwise suspicious for
secondary Crohn disease.
MICROSCOPIC
Depending on the course and acuity of pouchitis: varying degrees of inflammatory infiltrates (chronic: lympho-/plasmocytes;
acute/subacute: neutrophils and eosinophils), focal epithelial ulceration with fibrinoid exudates, superficial acute
(neutrophils) and chronic (lymphocytes).
Evaluation
REQUIRED MINIMAL STANDARD
Clinical assessment: inspection: perianal skin irritation with/without excoriations. Digital rectal exam: stricture, evidence for
fistula, etc.
Pouchoscopy (rigid or flexible): assessment of mucosa in ATZ cuff and the pouch (suspicion of Crohn disease only if
ulcerations in afferent small bowel).
Contrast studies (pouchogram)
road map, leak, sinus, fistula, stricture, pouch configuration, volume and size, distance to
the sacral curvature.
ADDITIONAL TESTS (OPTIONAL)
Defecation proctogram/pouchogram: configuration, prolapse.
CT/MRI with possible 3D reconstruction: extrinsic problem (compression, abscess, etc).
Pouch cultures (in treatment-refractory or recurrent episodes): C difficile toxin, Candida, CMV, stool cultures (Salmonella,
Shigella, E coli, Campylobacter, etc).
Classification
Idiopathic pouchitis: acute, recurrent, chronic.
Specific pouchitis: identifiable/treatable pathogen.
Morphologic ileoanal dysfunction.
Nonoperative Treatment
General Measures
Improvement of perianal skin care: barrier creams; avoidance of moisture; petroleum jelly–based creams (eg,
Vaseline) are generally counterproductive. Severe skin excoriations/ulcerations
application of topical Maalox mixed
with nystatin powder until area improved.
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Adjustment or change of antidiarrheal medication, addition of fibers.
Adjustment of diet and meal schedule.
Specific Measures
1. Pouchitis:
a. Empirical initial treatment of suspected pouchitis:
(1) Antibiotic treatment (eg, metronidazole, ciprofloxacin, rifaximin): 10–14 days.
(2) Optimization of diet, antidiarrheal medication (diphenoxylate/atropine, loperamide, glycopyrrolate),
protection of perianal skin.
b. Treatment options for recurrent pouchitis episodes:
(1) Same as above, but tapering of medication, prolonged low-dose antibiotic maintenance therapy
(caveat: metronidazole-induced polyneuropathy), alternating antibiotic schedules.
(2) Specific pouchitis
adjustment of antibiotic regimen according to culture result.
(3) Oral bismuth medication.
(4) Antibiotic course, followed by probiotics prophylaxis.
(5) Mesalamine enemas.
2. Stricture: dilation
digital, or with dilator (eg, Hegar), Foley catheter balloon (office), or self-dilation by patient
using dilators (expensive) or candle (cheap).
3. Cuffitis: mesalamine suppositories.
4. Functional outlet obstruction: insertion of tube for evacuation, possible combination with enemas.
Operative Treatment
INDICATIONS
Failure of nonoperative management with unacceptable quality of life.
Morphologic ileoanal dysfunction.
OPERATIVE APPROACH
Transanal Approach
Examination under anesthesia.
Dilation of stricture.
ATZ mucosectomy.
Local fistula repair.
Septum division with stapler.
Marsupialization of sinus.
Abdominal Approach
Pouch revision, redo pouch.
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Pouchopexy.
Pouch excision end-ileostomy or continent ileostomy.
Outcome
Depending on underlying cause of ileoanal dysfunction: 5–10% pouch loss per decade. Risk of peripheral neuropathy with
long-term metronidazole use.
Follow-Up
Careful patient guidance and reassurance.
Pouch surveillance (bi-)annually.
Cross-Reference
Diarrhea (Ch. 1)
IBD—ulcerative colitis (556.9) (Ch. 4)
IBD—Crohn disease (555.X) (Ch. 4)
"Pouchology"—the science of pouches (Ch. 4)
"Stomatology"—the science of ostomies (Ch. 4)
Proctocolectomy, ileal J-pouch anal anastomosis (open) (Ch. 5)
Medical management of Crohn disease (Ch. 6)
Medical management of ulcerative colitis (Ch. 6)
Medications against tumor or inflammation (App. 1)
KOCK POUCH DYSFUNCTION
Overview
Continent ileostomy remains one of the options (rarely used since IPAA) for patients who are either not candidates for an
IPAA, have failed an IPAA, or for other reasons ended up with a permanent ileostomy. A continent ileostomy consists of an
internal reservoir equipped with a valve that prevents stool leaking through a skin-level ostomy. The pouch is emptied
several times per day by inserting a tube through the stoma.
Invented in 1969 by Dr Nils Kock, subsequently several different modifications/alternatives:
1969 Kock pouch.
1984 Barnett pouch (BCIR [Barnett continent intestinal reservoir]).
2002 T-pouch (Kaiser).
The valve mechanism in the first 2 techniques relies on an intussuscepted bowel segment. Paradox: naturally occurring
intussusception usually is not considered a good thing, but it is intentionally created for these pouches. This construction
triggers the problem that natural force tends to dis-intussuscept the valve over time (Figure 4–15A): common either early
(within the 1 year) or long term (after 15–20 years):
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Axial transfascial desintussusception: leakage and stoma prolapse.
Subfascial desintussusception: unfolding and kinking of valve segment leakage and difficulty intubating the pouch.
Figure 4–15A.
Kock pouch dysfunction from valve desintussusception.
Epidemiology
Rare.
Symptoms
Chronic: leakage of gas or feces, increasing difficulty to intubate the pouch, stoma prolapse. Secondary symptoms:
peristomal skin irritation.
Acute: sudden inability to intubate a pouch that is still continent
closed loop, SBO risk of pouch rupture.
Differential Diagnosis
Pouchitis in the continent reservoir.
Pouch-valve fistula.
Pathology
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As described above: shortened effective valve segment.
Evaluation
REQUIRED MINIMAL STANDARD
History: suggestive circumstances and symptoms.
Clinical examination: pouchoscopy: difficult course of the valve? Pouchitis? Traumatized valve segment? Visible fistula
opening?
X-rays: pouchogram or CT-pouchogram (3D reconstruction).
ADDITIONAL TESTS (OPTIONAL)
Stool analysis: C difficile toxin, cultures (including fungi).
Small bowel follow-through: assessment of residual small bowel length.
Classification
Transient vs progressive Kock pouch dysfunction.
Valve dysfunction vs reservoir dysfunction.
Functional pouch dysfunction: clogged system from lack of dietary compliance, inadequate intubation, kinking of
intubation tube.
Morphologic pouch dysfunction: secondary Crohn disease, leak, fistula, chronic pouchitis.
Nonoperative Treatment
Optimization of drainage schedule.
Antibiotic trial
suppress element/variable of pouchitis.
Operative Treatment
INDICATION
Chronic Kock pouch dysfunction.
Acute inability to intubate.
Need for minor service operations.
OPERATIVE APPROACH
Inability to Intubate
Emergency pouch decompression: insert narrow rigid sigmoidoscope and advance to reservoir to decompress the
pouch
slide in an adequate guidance tube that fits through the scope, followed by a larger tube with cut-off tip that
is slipped over guidance tube.
Common mistake: placement of NGT only because of assumption that lack of output results from "garden-variety"
SBO rather than from the valve
insertion of tube is mandatory!
Options for Chronic Kock Pouch Dysfunction
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Minor revision.
Detachment of existing valve pouch rotation and creation of new intussuscepted valve.
Conversion of Kock pouch into T-pouch (Figure 4–15B).
Shortening of competent but kinked valve segment.
Pouch removal with creation of end-ileostomy.
Figure 4–15B.
T-pouch valve intraoperatively and on a pouchogram.
Minor Service Operations
Stenosis of skin-level stoma stricturoplasty.
Mucosal redundancy of stoma infrared coagulation, formalin ablation, surgical trimming of redundancy.
Dilatation of valve segment stricture.
Outcome
Continent ileostomy business time-consuming but rewarding: most patients are convinced of the continence concept they
would rather undergo several operations than abandon bag-free life. Increased perioperative morbidities (eg, 10–15% leak,
abscess or enterocutaneous fistula formation) need to carefully select patients and document information to minimize risk
of litigation.
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Follow-Up
Functional reassessment in regular intervals. FAP pouch surveillance.
Cross-Reference
Small bowel obstruction (SBO) (Ch. 1)
Familial adenomatous polyposis (FAP; 211.3, 235.2, V84.09) (Ch. 4)
IBD—ulcerative colitis (556.9) (Ch. 4)
"Pouchology"—the science of pouches (Ch. 4)
Pouchitis—ileoanal dysfunction (569.60) (Ch. 4)
"Stomatology"—the science of ostomies (V44.2) (Ch. 4)
Proctocolectomy, ileal J-pouch anal anastomosis (open) (Ch. 5)
Medical management of ulcerative colitis (Ch. 6)
Medications against tumor or inflammation (App. 1)
TOXIC MEGACOLON (556.9)
Overview
Toxic megacolon is the common final pathway of numerous unrelated pathologies of the colon and carries a high risk of fatal
outcome. Definition: combination of segmental or total colonic distention (superimposed on acute colitis) and signs of
systemic toxicity (Jalan criteria: fever, tachycardia, elevated WBCs). Proactive aggressive treatment is the only chance for
survival. Very high probability that patient will require colectomy—emergency, urgent, or in future.
Variety of underlying diseases: IBD (ulcerative colitis, Crohn colitis), infectious colitis (C difficile, Salmonella, Shigella,
Campylobacter, Yersinia, Entamoeba, CMV, etc), ischemic colitis, etc.
Pathogenesis: inflammation with complex mediator interaction with cytokine and nitric oxide release
colonic dysmotility
impaired smooth muscle contractility reduction of luminal pressure via dilation. Toxic decompensation may be triggered in
an acute episode of colitis by instrumentation or contrast enemas.
Complications: perforation, sepsis, coagulopathy, abdominal compartment syndrome, multiorgan failure, death.
Epidemiology
Incidence: depends on cause; eg, up to 5–10% risk in admissions for ulcerative colitis, up to 3% of C difficile colitis.
Symptoms
Signs of severe/fulminant exacerbation of colitis: diarrhea, bleeding, passage of mucus per rectum, abdominal pain.
Later development of systemic effects: fever, anemia, anorexia, malnutrition/weight loss, dehydration, transition of diarrhea
to ileus with increasing abdominal distention.
Differential Diagnosis
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Other causes of colonic distention (without signs of toxicity, without inflammatory trigger):
LBO.
Colonic pseudoobstruction (Ogilvie syndrome).
Hirschsprung disease, Chagas disease.
Severe/fulminant colitis without toxic dilation.
Pathology
MACROSCOPIC
Massive colonic distention, colonic wall either paper-thin or thickened/edematous (edema extension to retroperitoneum),
focal areas of hemorrhagic and ischemic necrosis, covered or free perforation, mucosal pathology according to underlying
disease.
MICROSCOPIC
Combination of mostly acute and some chronic inflammation involving all layers of colonic wall, with muscle necrosis,
vascular congestion, hemorrhage.
Evaluation
REQUIRED MINIMAL STANDARD
History: Known underlying colitis vs toxic megacolon as primary presentation, abdominal pain, diarrhea or constipation,
nausea, vomiting, fever? Triggering events: instrumentation, contrast studies, opiates, antidiarrheals? Previous medications:
steroids ( masking of clinical signs), other immunosuppressives?
Clinical examination: vital signs: high fever, tachycardia, hemodynamic instability, mental status change, signs of systemic
toxicity? Abdominal tenderness and distention, decreased bowel sounds, peritoneal signs (may often be absent)?
Blood work: CBC (WBC?, anemia?, thrombocytopenia?), electrolyte imbalances, renal failure, coagulopathy, increased
lactate?
Imaging:
Plain abdominal x-rays: colonic dilation > 6 cm (1
1
/
2
vertebrae) in transverse colon or > 12 cm for cecum, abnormal
haustration, rule out perforation (Figure 4–16). Caveat: extent of colonic diameter does not accurately predict risk of
perforation!
CT abdomen/pelvis: colonic dilation, wall thickening, mucosal edema/hyperemia, pericolonic stranding, ascites, free
extraluminal air, pneumatosis intestinalis, portal vein gas?
Figure 4–16.
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Toxic megacolon and rigid pipe in ulcerative colitis.
ADDITIONAL TESTS (OPTIONAL)
Colonoscopy (for diagnosis and decompression) in selected patients.
Contrast studies (barium or Gastrografin) contraindicated in acute colitis: may precipitate toxic deterioration.
Classification
Toxic megacolon without associated organ dysfunction.
Toxic megacolon with associated organ dysfunction (kidney, liver, cardiopulmonary, etc), perforation, or peritonitis.
Nonoperative Treatment
Initial conservative management acceptable only if no evidence of perforation, compartment syndrome, or multiorgan
dysfunction serial examinations: no deterioration but marked improvement should be noted in all parameters within
maximal 3–5 days, otherwise surgical management.
Supportive care with ICU monitoring, hemodynamic resuscitation.
Antibiotics appropriate adjustment (and possible addition of antiviral medication) if specific infectious cause or C
difficile colitis found.
Immunosuppressives (for IBD-related toxic megacolon only): steroids (and/or steroid stress dose if on steroids < 6
months), cyclosporine A, etc.