Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1499_Библиотеки_им_академика_М_И_Перельмана.pdf
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
REQUIRED MINIMAL STANDARD
Rigid or flexible sigmoidoscopy: usually sufficient to establish diagnosis, full colonic evaluation generally indicated.
Caveat: no biopsy of anterior ulcers/pathology—risk of iatrogenic rectovaginal/rectourinary fistula.
ADDITIONAL TESTS (OPTIONAL)
Contrast studies (barium or Gastrografin enema): only if colonoscopy unfeasible (eg, stricture) or road map needed (eg,
fistula).
Virtual colonoscopy: role not defined, risk of perforation.
MRI, PET, PET-CT: role not defined.
Anophysiology studies: evaluation of anorectal functionality (eg, rectal compliance, etc).
Lab work: nutritional status.
Small bowel follow-through: evidence for short bowel (foreshortening)?
Classification
Radiation proctitis: acute vs chronic, localized vs diffuse.
Radiation enteritis: acute vs chronic, localized vs diffuse.
Secondary radiation-induced complications (stricture, fistula, etc).
Nonoperative Treatment
Acute radiation injury: temporizing measures (stool management, antidiarrheal medication, perianal skin care) and patience;
topical medications (sucralfate, steroid, or 5-ASA enemas), fecal diversion if symptoms severe and poorly tolerated.
Chronic radiation injury: no cure, poor tissue quality
control symptoms:
Antidiarrheals/antispasmodics as needed.
Topical anti-inflammatory medications: suppositories/enemas with steroids, 5-ASA, sucralfate, misoprostol.
Oral antibiotics: metronidazole.
Vitamin supplements: vitamin C and vitamin E.
Possible benefit from home TPN.
Colonic mucosal integrity: short-chain fatty acid enemas (chemically unstable, therefore not practical for use).
Laser ablation: multiple sessions needed.
Formalin instillation: proctoscope/endoscope 50-mL aliquots of 4% formalin 2–3 minutes contact with area of
interest, followed by copious washout with saline. Usually quickly effective, may need repeat treatment if relapse.
Operative Treatment
INDICATIONS
Significant and treatment-refractory symptoms: hemorrhage, tenesmus, discharge, incontinence.
Obstruction: stricture formation.
Fistula formation.
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
Uncertainty about possible tumor recurrence.
OPERATIVE APPROACH
Excision of area with radiation injury, with or without reconstruction (may be very challenging).
Palliation of symptoms without resection of injured tissue: fecal and/or urinary diversion.
Outcome
Acute radiation injury: self-limited, resolution typically within 6–12 weeks.
Chronic radiation injury: frequently responding adequately to nonoperative management, repeated sessions needed. Severe
injuries expected to decrease in the future (more sophisticated radiation techniques).
Anastomosis in radiated area: increased leak rate
temporary fecal diversion recommended.
Diversion alone: some symptoms may persist (mucus discharge, bleeding, pain).
Follow-Up
Frequent clinic visits until symptoms under control, per routine guidelines thereafter.
Cross-Reference
Ulceration (Ch. 1)
IBD–ulcerative colitis (556.9) (Ch. 4)
Rectovaginal fistula (619.1) (Ch. 4)
Complications—leak (997.4) (Ch. 4)
ISCHEMIC COLITIS (557.X)
Overview
Ischemic colitis—caused by inadequate blood flow—is the most common form of intestinal ischemia (~60%). Various degrees
of severity depending on location and extent, acuity of onset, presence of collaterals, and level of occlusion: commonly,
splenic flexure, rectosigmoid junction, and right colon most vulnerable. Numerous different etiologies result in a final common
pathway:
Occlusive disease:
– Major vascular occlusion: infrarenal aortic bypass, SMA thrombosis/embolism, portal vein/SMV thrombosis,
trauma, acute pancreatitis, aortic dissection.
– Microvascular (peripheral vessels): diabetic vasculopathy, thrombosis, embolism, vasculitis, amyloidosis,
rheumatoid arthritis, radiation injury, trauma, interventional radiology embolization (for lower GI bleeding),
hypercoagulable states (protein C and S deficiency, antithrombin III deficiency, sickle cell disease).
Nonocclusive disease:
– Shock, sepsis, and low flow state (eg, atrial fibrillation, myocardial infarction, cardiopulmonary bypass
machine), steal phenomenon, abdominal compartment syndrome.
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
– Colonic obstruction, volvulus, hernia.
– Toxic: cocaine, medications (NSAIDS, vasopressors, digoxin, diuretics, chemotherapy, gold compounds).
Caveat: patients may have other relevant colonic pathology (eg, cancer) in affected or unaffected segments.
Treatment ranging from conservative management (milder to moderate forms) to a segmental or even total abdominal
colectomy (severe and life-threatening form).
Epidemiology
Incidence peak between 6th and 9th decades. Females > males. Results in 1:2000 acute admissions to the hospital. True
incidence unknown: under- or misdiagnosis. Historically: up to 10% ischemic colitis after infrarenal aortic replacement, less
frequent with interventional radiology procedures. Location: 80% on the left side (between splenic flexure and sigmoid), 10–
20% in ascending to transverse colon, < 3% in rectum.
Symptoms
Acute Ischemia
Initial stage: acute ischemia sudden onset of abdominal pain, potentially crampy, hyperperistalsis, potentially
associated with diarrhea or urge to defecate.
Second stage: beginning tissue necrosis (after 12–24 hours) ileus, paradoxical decrease of pain level, bleeding
(hematochezia), subtle peritoneal signs.
Third stage: peritonitis, sepsis—increasing peritoneal signs, signs of toxicity (fever, elevated WBC with left shift,
tachycardia); complete ileus, nausea and vomiting, hemodynamic instability, septic shock.
Complications:
– Colonic dilation and structural weakening
perforation, sepsis, oliguria, multiorgan failure, death.
– Sepsis
bacterial seeding to ischemia-associated implants (eg, valves, aortic graft etc).
Chronic Ischemia
Angina abdominalis: postprandial pain as result of inadequate increase of intestinal blood flow.
Ischemic colonic stricture obstructive signs.
Differential Diagnosis
IBD: ulcerative colitis, Crohn disease.
Infectious colitis: shigella, enterohemorrhagic E coli, salmonella, Campylobacter, etc.
Colorectal cancer.
Diverticulosis, diverticulitis.
Radiation proctocolitis.
Other causes of acute abdominal pain and/or lower GI bleeding.
Pathology
MACROSCOPIC
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
Acute: bowel and mucosal edema geographic areas of ulcerations or necrosis, segmental full-thickness necrosis
segmental gangrene.
Chronic: chronic fibrotic stricture, mucosal surface intact.
MICROSCOPIC
Acute: superficial mucosal necrosis, crypts initially intact hemorrhage and pseudomembranes full-thickness wall
necrosis (loss of nuclei, ghost cells, inflammatory reaction, increasing architectural distortion); potentially visible
thrombus, embolus, cholesterol embolus.
Chronic: largely intact mucosa, but crypt atrophy and focal erosions, thickened/hyalinized lamina propria, crypt
atrophy, diffuse fibrosis.
Evaluation
REQUIRED MINIMAL STANDARD
History:
– Recent cardiovascular surgery, history of embolic disease, "angina abdominalis," history of vasculitis, medications
(including warfarin, ASA).
– Current symptom triad: acute abdominal pain, rectal bleeding, diarrhea.
Clinical examination:
– Vital signs: absolute arrhythmia (atrial fibrillation), hemodynamic stability?
– Abdominal distention, disproportionate abdominal pain, hyperperistalsis vs ileus, peritoneal signs?
– Femoral or distal extremity pulses: maintained? Evidence of diffuse arteriosclerosis?
Blood work: CBC
elevated WBC/anemia/thrombocytopenia?, lactate, acidosis, creatine kinase-BB (CK-BB),
hypophosphatemia, coagulopathy, hypoproteinemia?
Imaging:
– Abdominal x-ray, chest-x-ray: free peritoneal air, thumb printing, loss of haustrations, dilation of loops.
– CT scan with oral/IV contrast if possible (kidney function!): most practical test if pain is the primary symptom
free
peritoneal air, segmental wall thickening, thumb printing, pneumatosis, loss of haustrations, dilation of loops,
pneumatosis coli, double halo sign, portal vein gas? Other causes of abdominal pain? Assessment of main vascular
run-offs: thrombus?
Colonoscopy: gold standard: most sensitive test, contraindicated in presence of peritoneal signs: normal rectum (unless
complete aortic occlusion); segmental mucosal changes
hemorrhage, necrosis, ulcers, friability? Stricture?
ADDITIONAL TESTS (OPTIONAL)
Contrast enema: not typically indicated in acute setting (would show: thumbprinting, colonic wall edema, loss of haustration,
ulcers); chronic ischemia colonic road map, stricture?
Visceral angiography (with intervention: eg, thrombolysis): role relatively limited in acute setting unless realistic probability
for successful thrombolysis; evaluation of chronic ischemic symptoms
vascular road map.
CLASSIFICATION
Based on etiology: occlusive vs nonocclusive ischemia.
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
Based on pathology:
Gangrenous ischemic colitis (15–20%):
Nongangrenous ischemic colitis (80–85%):
– Transient, reversible (60–70%).
– Chronic, irreversible chronic segmental colitis (20–25%) stricture (10–15%).
Nonoperative Treatment
Hemodynamic resuscitation: volume rather than vasopressors.
Broad spectrum antibiotics, temporary bowel rest
serial clinical exams.
Heparinization if tolerated.
Possible interventional radiology.
Repeat colonoscopy: as needed to monitor progress, reevaluate colon for other pathology under more optimal conditions.
Operative Treatment
INDICATIONS
Acute ischemia: peritonitis, disproportionate pain (contrast with clinical exam), evidence of gangrene, treatment-
refractory sepsis, pneumoperitoneum; failure to improve, persistent protein-losing colopathy (arbitrary > 14 days'
duration).
Chronic ischemia: recurring sepsis, symptomatic colonic stricture, any stricture for which neoplasia cannot be ruled
out.
OPERATIVE APPROACH
Acute Ischemia
Surgical bowel resection of affected segments intraoperative assessment of colonic viability: bleeding mucosal
edges, venous thrombi, presence of palpable pulse?
– Primary anastomosis vs ostomy (eg, double barrel).
– Questionable viability: planned second look operation vs more extensive primary resection.
Exploratory laparotomy: "open-close"—if extent of ischemia too large to be compatible with life.
Chronic Ischemia
Resection and primary anastomosis of affected segment.
Angina abdominalis: possible vascular intervention and reconstruction.
Outcome
Transient ischemia: relatively good prognosis, largely dependent on prognosis of other organ systems; 50% reversible:
clinical resolution in 48–72 hours, endoscopic resolution in 2 weeks; more severe forms: time healing to healing much longer
(up to 6 months) stricture?
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
Gangrenous ischemia: 50–60% mortality—less favorable patient population (comorbidities) with more severe disease!
Chronic ischemia: morbidity and mortality similar to colon resection for other reasons, but higher cardiovascular risk.
Follow-Up
Full colonic evaluation after 6 weeks (if condition permits).
Emergency surgery:
planning of subsequent surgery, ie, elective restoration of intestinal continuity, after complete
physical/nutritional recovery.
Definition of type and duration of anticoagulation.
Cross-Reference
Magnetic resonance imaging (MRI) (Ch. 2)
Angiography with possible embolization (Ch. 2)
Vascular anatomy (Ch. 3)
PSEUDOMEMBRANOUS/CLOSTRIDIUM DIFFICILE COLITIS (008.45)
Overview
Pseudomembranous or C difficile colitis presents a wide clinical spectrum ranging from mild diarrhea to fulminant and
potentially fatal colitis. Pseudomembranous colitis in the preantibiotic era was caused by various bacteria (eg,
Staphylococcus); nowadays it is most commonly associated with antibiotic use and resulting overgrowth of commensal
anaerobe C difficile.
Pathophysiology: antibiotic-related disruption of normal colonic bacteria (few days to 10 weeks post antibiotic use) allows for
colonization with toxin-producing C difficile by oral-fecal route. Release of toxins A and B causes mucosal damage and
inflammation. Basis for variable disease expression likely related to (1) host immune factors and (2) virulence factors of the
organism.
Antibiotics associated with C difficile colitis: any antibiotic (with few exceptions: eg, vancomycin), frequency largely reflecting
overall use of the respective agents: penicillins, cephalosporins, quinolones, clindamycin, even metronidazole (despite being
used in treatment of C difficile colitis).
Treatment ranges from conservative management (milder to moderate forms) to total abdominal colectomy (severe and life-
threatening form), which is potentially lifesaving if performed before point of no return.
Epidemiology
C difficile is the most common nosocomial infection of the GI tract. Epidemically rising incidence from 6–7 per 1000
admissions in 1990 to 23 per 1000 admissions in 2004; > 3 million cases per year in the US, > 60 per 100,000 short-stay
discharges with C difficile as primary diagnosis.
Clusters of particularly virulent strains (6% of isolates) with increasing severity of C difficile–associated disease: toxinotype
III, CD binary toxin, ribotype 027.
Asymptomatic colonization with C difficile:
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
> 50% of healthy neonates.
1–3% of healthy adults.
25% of adults recently treated with antibiotics important hidden reservoir of C difficile.
20–25% of inpatients become colonized with C difficile during hospital stay.
Symptoms
Variations in severity and dynamics of the disease: asymptomatic, self-limited/intestinal only, progressive/systemic, chronic
smoldering/systemic, fulminant/multiorgan failure:
Asymptomatic carrier status.
Simple antibiotic-associated diarrhea: diarrhea mild, no macroscopic colitis, systemic symptoms absent: C difficile
accounts for only 20% of this category.
C difficile–associated diarrhea/colitis (without pseudomembrane formation): more serious illness, watery diarrhea,
some malaise, some abdominal pain, nausea, anorexia, low-grade fever, peripheral leukocytosis. Endoscopy:
nonspecific diffuse or patchy erythematous colitis without pseudomembranes.
Pseudomembranous C difficile colitis: more profound symptoms, more systemic impact. Endoscopy: classic
pseudomembranes present, but in 10–20% of patients not in reach of flexible sigmoidoscopy.
Chronic smoldering C difficile colitis: persistent diarrhea, persistent colonic inflammation with colonic thickening (CT),
varying but rather mild systemic impact, leukocytosis (leukemoid reaction: massive WBC increase up to 50,000).
Fulminant, life-threatening colitis: 3% of patients with C difficile infection, acutely ill, lethargy, mental status change,
fever, tachycardia, abdominal pain, oliguria. Symptom sequence: diarrhea
paralytic ileus and colonic dilation
paradoxical decrease in diarrhea, but increasing abdominal distention and marked tenderness; loss of colonic muscular
tone
toxic dilation/megacolon. Rebound tenderness: suspicious for colonic perforation and peritonitis?
Complications: colonic dilation (initial presentation as Ogilvie syndrome)
toxic megacolon, perforation, sepsis, oliguria,
multiorgan failure, death.
Rare presentations:
C difficile enteritis or pouchitis after proctocolectomy with ileostomy or ileoanal pouch.
Superinfection/exacerbation of active ulcerative colitis.
Differential Diagnosis
Antibiotic-associated diarrhea not caused by C difficile (80%): unspecific diarrhea, other pathogens (Staphylococcus,
Clostridium perfringens, Candida albicans, etc).
Diarrhea not associated with antibiotics: eg, secretory, dietary, medications (eg, NSAIDS, prokinetics), neuroendocrine
tumors, etc.
Post–C difficile colonic dysfunction: may last for weeks to months after clearing of C difficile.
IBD: exacerbation of ulcerative colitis with C difficile superinfection.
Infectious colitis: Shigella, enterohemorrhagic E coli, Salmonella,Campylobacter, etc.
Ischemic colitis.
Diverticulitis.
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
Pathology
MICROBIOLOGY
C difficile: ubiquitous anaerobic gram-positive bacillus, forming heat-resistant spores able to persist in environment
for months or years
differentiation between nonpathogenic strains (do not produce toxins) vs pathogenic strains
(produce toxins that cause diarrhea and colitis).
Infection from oral ingestion of spores, which can survive the acidic stomach environment conversion to vegetative
forms in colon.
Environmental C difficile particularly common in hospitals/long-term care facilities:
– Hospital floors, toilets, bedpans, bedding, mops, scales, furniture.
– Increased risk after recent treatment of patients with diarrhea from C difficile infection.
– Health care personnel acting as carriers: hands, ties, rings, stethoscopes.
Pathogens:
– Toxin A (308-kD enterotoxin): fluid secretion, mucosal damage, and intestinal inflammation.
– Toxin B (250-to-270-kD cytotoxin): in tissue culture 1000 times more cytotoxic than toxin A but not
enterotoxic in animals. Causes disintegration of filamentous actin
collapse of the microfilament cytoskeleton
cell rounding and cell death.
MACROSCOPIC/MICROSCOPIC (FIGURE 4–12A)
Figure 4–12A.
Clostridium difficile colitis specimen.
Characteristic yellow-white pseudomembranous plaques that bleed when scraped:
Type I (earliest lesion): patchy epithelial necrosis, exudation of fibrin and neutrophils into colonic lumen discrete
yellow-white plaques of < 10 mm separated by normal or mildly hyperemic and friable mucosa.
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
Type II lesion: "volcano" or "summit" lesions with focal intercrypt necrosis and ballooned crypts rise of
pseudomembrane (fibrin, neutrophils, mucin); intact or mildly hyperemic/friable surrounding mucosa.
Type III lesion: diffuse epithelial necrosis and ulceration, overlaid by pseudomembrane consisting of mucin, fibrin,
leukocytes, and cellular debris.
After resolution of C difficile infection: normalization of mucosa, residual glandular irregularity, often persistent dysfunction
for months.
Evaluation
REQUIRED MINIMAL STANDARD
Diarrhea Only
Stool analysis for C difficile toxins A and B (cultures for C difficile are not indicated!):
– Stool cytotoxin test: 95% sensitivity, 99% specificity, result in 2–3 days.
– ELISA for toxin: 70–90% sensitivity, 99% specificity, result in 4–6 hours.
– PCR of toxin B gene: sensitivity 96%, specificity 100%, result within hours.
Diarrhea and Abdominal/Systemic or Uncertain Symptoms
Rigid or flexible sigmoidoscopy: sufficient to establish diagnosis in 75–80% of patients: characteristic adherent yellow
plaques, diameter 2–10 mm.
Plain abdominal x-ray: mucosal edema (thumbprinting) and abnormal haustral pattern, ileus pattern (28% of patients)
toxic megacolon or perforation?
CT scan: distention and diffuse segmental or pan-colonic thickening of colon wall, pericolonic inflammation (Figure 4–12B).
In that situation, CT alone is often diagnostic when pain, fever, leukocytosis is present, but diarrhea is absent.
Figure 4–12B.
AccessSurgery | Print: Chapter 4. Diseases and Problems
file:///C|/...RIANA/McGrawHillManual%20ColorectalSurgery%201stEdition/Chapter%204_%20Diseases%20and%20Problems.htm[9/5/2009 19:15:58]
CT diagnosis of C difficile colitis.
Colonoscopy (potentially with decompression): diagnostic in 90% of the patients, including the 20% of the cases with disease
only proximal to splenic flexure. Perforation hazard in patients with colonic dilation.
Blood work: CBC (leukocytosis with WBC varying from 10,000–50,000/mL), creatinine, albumin.
ADDITIONAL TESTS (OPTIONAL)
Fecal leukocytes: positive test with > 3–5 leukocytes/HPF excludes benign diarrhea; but negative result does not exclude
colitis.
Classification
Antibiotic-associated diarrhea (ABAD).
C difficile–associated diarrhea (CDAD).
Pseudomembranous C difficile colitis (PMC).
Chronic smoldering C difficile colitis.
Fulminant/toxic C difficile colitis with/without megacolon.
Nonoperative Treatment
Outpatient or Inpatient with Mild Symptoms
Discontinuation of offending antibiotic.
Correction of underlying process.
Perianal skin care: barrier ointments.
Single antibiotic treatment for at least 10 days with one of the following:
– Metronidazole 3
x 250–500 mg PO (cheap).