Oxford Handbook of Clinical Surgery (4 edn)
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Ulcerative colitis 392
Crohn's disease 394
Other forms of colitis 396
Colorectal polyps 398
Colorectal cancer 400
Restorative pelvic surgery 402
Minimally-invasive colorectal surgery 403
Diverticular disease of the colon 404
Rectal prolapse 406
Pilonidal sinus disease 408
Fistula-in-ano 410
Haemorrhoids 412
Acute anorectal pain 414
Acute rectal bleeding 416
Acute severe colitis 418
Post-operative anastomotic leakage 420
Ulcerative colitis
Key facts
An acute and chronic inflammatory disease originating in the colonic columnar mucosa.
Precise aetiology is unknown, but an environmental trigger combined with a genetic predisposition (family history) are factors.
Often precipitated by an apparent acute GI infection; peak age of diagnosis is the late teens and twenties, but may present in late adulthood.
Commonest in white Anglo-Saxon Caucasians.
Pathological features
Granular, hypervascular, and mildly oedematous mucosa with loss of vascular pattern seen at endoscopy.
Acute neutrophil infiltration of the colonic mucosa and submucosa; mucosal crypt abscesses with goblet cell mucin depletion.
With more severe inflammation, there are multiple aphthous ulcers, which may become confluent with only islands of inflamed mucosa and granulation tissue remaining (‘pseudopolyposis’).
Transmural inflammation may occur in severe disease secondary to the widespread loss of mucosa and subsequent severe inflammation.
Chronic ‘burnt-out’ disease leads to a pale, featureless, ahaustral pattern to the colon.
Disease tends to be present in the distal colon and rectum and spread proximally with increasing extent of disease.
Clinical features
Proctitis. Commonest presentation. Rectum ‘always’ involved unless already on topical treatment. Symptoms of urgency and frequency of defecation due to rectal irritability; bloody mucus mixed with loose stools (frank bloody diarrhoea rare).
Left-sided colitis. Disease up to the splenic flexure. Symptoms of rectal irritation plus extensive bloody mucus in stools, often leading to bloody diarrhoea; mild associated systemic features.
Pancolitis. Disease involving the entire colon. May be associated with mild secondary inflammation of the terminal ileum (‘backwash ileitis’). Diarrhoea predominant feature; systemic features common (fever, malaise, anorexia, tachycardia). May be associated with anaemia (due to blood loss), hypoalbuminaemia, and hypokalaemia (due to mucus loss).
Diagnosis and investigations
Basic tests
↑ WCC and CRP; ↓ Hb and albumin, especially during episodes of inflammation. AXR may show oedematous colonic mucosa (‘thumbprinting’), but is unreliable for diagnosis or extent of disease. Proctosigmoidoscopy usually shows erythematous, granular, or frankly ulcerated rectal mucosa with mucus and blood. Biopsies should be taken before starting treatment. Always send stool M,C,&S and test for parasites and cysts in any acute presentation to exclude infectious causes.
Advanced tests
Extent of disease is best assessed with colonoscopy and biopsies; will also usually exclude colonic Crohn's disease.
Treatment
See 
p. 418 for management of acute severe colitis.
Medical treatment
Principles are to reduce inflammation and prevent complications. Acute derangements in blood results should be corrected (e.g. blood transfusion for severe anaemia, potassium supplementation, nutritional support for hypoalbuminaemia).
Proctitis
Topical steroids—Predsol® suppositories.
Topical 5-aminosalicyclic acid (5-ASA) suppositories.
Left-sided colitis
Topical steroids—Predsol® foam enemas (penetrate up as far as the splenic flexure).
Topical 5-ASA foam enemas.
May require systemic steroid treatment (prednisolone).
Pancolitis
Topical steroids or 5-ASA treatments for local symptoms.
Usually need systemic treatment, e.g. oral steroids (prednisolone), 5-ASA treatment.
Oral immunosuppressives, e.g. azathioprine, 6-mercaptopurine.
Systemic affectors of lymphocyte function, e.g. cyclosporin A, anti-TNFα (infliximab)
Surgical treatment
Surgery is indicated for acute colitis that fails to respond to treatment (see p. 418) and for chronic colitis when:
Chronically symptomatic despite maximal medical therapy.
Medical therapy controlling symptoms, but associated with unacceptable side effects, e.g. osteoporosis, immunosuppression.
Recurrent exacerbations affecting growth or development in adolescents.
Confirmed diagnosis of either high grade dysplasia or dysplasia-associated lesion or mass (DALM), or carcinoma of colon.
Surgical treatment may be:
Proctocolectomy (removal of colon and rectum) with ileoanal pouch formation (see p. 402).
Panproctocolectomy (removal of colon, rectum, and anus) with end ileostomy formation (permanent).
Total abdominal colectomy (removal of colon) with ileostomy (used when the patient is too unwell for major pelvic surgery, e.g. for acute severe colitis).
Crohn's disease
Key facts
A chronic inflammatory non-caseating, granulomatous disease affecting any part of the GI tract.
Associated with several extraintestinal disorders (see Box 11.1).
Precise aetiology is unknown, but products from the bacterial flora combined with a genetic predisposition (family history) are factors.
Peak age of onset of symptoms is the teens and early twenties, but diagnosis is often several years later.
Commonest in white Anglo-Saxon Caucasians.
Associated with disease activity • Pyoderma gangrenosum • Erythema nodosum • Primary biliary cirrhosis | Independent of disease activity • Ankylosing spondylitis • Polyarthritis • Chronic active hepatitis |
Associated with disease activity • Pyoderma gangrenosum • Erythema nodosum • Primary biliary cirrhosis | Independent of disease activity • Ankylosing spondylitis • Polyarthritis • Chronic active hepatitis |
Pathological features
Commonly focused in the terminal ileum and caecum, but may affect the anus, colon, or entire small bowel.
Anal Crohn's disease is not common, but may be severe and associated with active small bowel disease.
Colonic Crohn's disease is a long-term risk factor for colorectal cancer formation.
Affected bowel looks blue-grey, thickened, with spiral surface vessels and encroachment of the mesenteric fat around the bowel (‘fat wrapping’).
Transmural inflammation in the form of lymphoid aggregates, particularly in the subserosal tissues (‘Crohn's rosary’), mucosal crypt ulceration, and fissuring ulceration.
Mucosal thickening and serpiginous longitudinal ulceration combine to give the appearance of ‘cobblestoning’.
Perforation, fistulation, and abscess formation are occasional ‘fistulizing’ sequelae of transmural inflammation.
Extensive fibrosis and smooth muscle hyperplasia may occur, giving rise to stenosis.
Clinical features
Inflammatory features. Fever, malaise, abdominal pain (often RIF), change in bowel habit (usually diarrhoea without blood), and weight loss. Children and adolescents may have failure to thrive or have retarded growth. Rectal bleeding is rare except in Crohn's colitis.
Fistulizing features. Para-enteric abscess formation often with a tender abdominal mass, fistula formation (ileocolic, ileoileal, ileocutaneous); rarely free perforation with features of peritonitis.
Stenosing features. Colicky abdominal pain, weight loss due to poor food intake (‘food fear’), palpable or visible distended small bowel loops.
Anal disease. Atypical severe anal fissures, fistula in ano, anal mucosal thickening, and discoloration.
Diagnosis and investigations
Basic tests
↑ WCC and CRP; ↓ Hb and albumin, especially during episodes of inflammation.
Advanced tests
In acute presentations, an abdominal CT may show an inflammatory mass, abscess formation, localized or free perforation.
In subacute or chronic presentations, small bowel disease may be shown by a small bowel contrast study (shows mucosal irregularity and narrowing) or a white cell scan showing ileal ‘hot spots’.
Crohn's colitis is diagnosed by endoscopy and biopsy.
Anal disease may require, EUA, anal ultrasound, or MRI scanning for assessment.
OGD and biopsies may show features of Crohn's in gastric mucosa.
Treatment
Medical treatment
Principles are to reduce inflammation and control complications. Acute derangements in blood results should be corrected.
Systemic (5-ASA) drugs are first-line acute and long-term treatment.
Systemic steroids (hydrocortisone, prednisolone) control acute exacerbations of inflammation and steroids with very high first pass metabolism (budesonide) can be used chronically.
Immunosuppressives (azathioprine, 6-mercaptopurine) are used as maintenance therapy and anti-TNFA antibodies (infliximab) may be effective in fistulizing complications.
Dietary manipulation (elemental diet) may reduce inflammatory factors.
Surgical treatment
Principles are to deal with septic complications, relieve significant bowel obstruction, and remove as little bowel as possible. Indications for surgery include the following.
Acute. Free perforation, severe haemorrhage, acute severe colitis, complete intestinal obstruction.
Subacute. Inflammatory mass, subacute obstruction, abscess formation, symptomatic fistulation.
Chronic. Steroid dependency or complications, growth retardation, cancer treatment or prevention.
Other forms of colitis
Key facts and pathological features
Various insults of widely differing origin may give rise to colitis other then idiopathic inflammatory bowel disease.
Acute infective colitis
Typically caused by pathological variants of normal enteric organisms, e.g. enteropathogenic E. coli; only rarely progresses to acute severe colitis.
Typhoid colitis (Salmonella typhi) (rare in the UK). Typified by acute bloody diarrhoea, but few if any colonic mucosal neutrophils on biopsy due to bone marrow suppression.
Clostridium (C.) difficile-related colitis
Caused by C. difficile infestation. Associated with antibiotic use, particularly third generation cephalosporins (even a single dose), prolonged inpatient stay. Toxin A produced by the organism causes acute severe inflammation in the mucosa.
Clinical picture may be varied.
C. difficile diarrhoea. Foul green liquid without bloody stools.
Acute C. difficile colitis. Caused by progressive rapid mucosal loss, acute neutrophil infiltration, and inflammation
Pseudomembranous colitis. Exudate and slough forms grey-white ‘plaques’ of material on the denuded colonic surface called pseudomembranes. May rapidly progress to acute severe ‘invasive’ colitis, especially in the immunocompromised or acutely unwell. Typified by secondary infections associated with mucosal loss.
Neutropenic colitis
Occurs in the severely immunocompromised with neutropenia and/or neutrophil dysfunction. Caused by multiple, normally non-pathogenic, enteric organisms colonizing the colonic mucosa.
Radiation colitis
Acute, transient colitis caused by mucosal injury secondary to external beam radiotherapy. May progress to chronic mucosal damage, haemorrhagic telangectasia, and possible stricturing after months or years.
Ischaemic colitis
Commonest in the upper left colon where the collateral blood supply between the middle and inferior colic arteries is poorest. Usually precipitated by an acute occlusion of part or all of the inferior mesenteric artery. May progress to infarction, but often presents with acute onset bloody diarrhoea and abdominal pain; may settle spontaneously although occasionally forms an ischaemic stricture.
Clinical features
Broadly similar, independently of the underlying cause. Typical features are vague abdominal pain, mild fever (absent in neutropenic colitis), diarrhoea (may be bloody, especially in ischaemic, radiation, severe pseudomembranous, and typhoid colitis). Cessation of diarrhoea, except with treatment, suggests acute severe colitis is developing and should be investigated urgently.
Diagnosis and investigations
Depending on the suspected cause:
Stool sent for C. difficile toxin (CDT), three samples.
Stool for M,C,&S (if atypical infective causes possible, also send for cysts, parasites, and ova (C,P,&O)).
Plain abdominal radiograph may show thickened colonic haustrae.
CT abdomen often shows typical mucosal thickening in colitis and may be diagnostic for pseudomembranous colitis.
Flexible endoscopy (usually flexible sigmoidoscopy) with biopsy.
Treatment
Medical treatment
Acute infective colitis. Antibiotics only if severely symptomatic.
C. difficile diarrhoea/colitis. Oral vancomycin up to 200mg PO daily or metronidazole 400mg PO tds; treatment may be as for pseudomembranous colitis if severe.
Pseudomembranous colitis. Oral vancomycin up to 200mg PO daily or metronidazole 400mg PO tds; adjuvant systemic treatment may be added in severe cases, e.g. IV vancomycin or tigicycline.
Neutropenic colitis. Broad-spectrum antibiotics, bone marrow support.
Radiation colitis. Symptomatic treatment only; anti-diarrhoeals.
Ischaemic colitis. Supportive treatment; anticoagulation may be appropriate if the underlying cause is thromboembolic.
Surgical treatment
Rarely indicated. Any form of colitis may progress to acute severe colitis and require emergency colectomy (see 
p. 418). Indications are:
Failure to respond to maximal medical therapy with life-threatening colitis (usually requires perioperative ITU support).
Complications of colitis. Uncontrollable bleeding, perforation (especially in ischaemic or neutropenic colitis).
Anastomosis of the colon/rectum may be in several ways.
Hand sewn. Either end to end or end to side, usually single layer of sutures (dissolvable), either interrupted or continuous.
Stapled colonic. By mechanical stapler (‘linear stapler’), usually side to side.
Stapled colorectal. By mechanical stapler (‘endoluminal stapler’), end to end.
Defunctioning (loop) ileostomy typically for rectal anastomosis when:
Below the peritoneal reflection.
Comorbidities (diabetes, age, previous DXT, acute illness).
Colorectal polyps
‘Polyp’ is a purely descriptive term and any growth from the lining of the large bowel can be described as a polyp. Polyps may be predominantly raised with a stalk attachment (pedunculated), flat and spreading over the surface of the bowel wall (sessile), or occasionally a combination of the two.
Key facts and pathological features
Polyps may arise for many different reasons.
Juvenile polyps
Mucin-filled cystic swellings of the lower rectal mucosa. Rarely part of a hereditary syndrome (juvenile polyposis) with multiple juvenile polyps throughout the colon; small increased risk of colorectal cancer.
Hamartomatous polyps
Polyps containing excessive amounts of the normal architectural components of the bowel wall, usually isolated. May be part of a hereditary syndrome (Peutz–Jeghers syndrome, with polyps characterized by extensive branched growth of the muscularis mucosa); small increased risk of colorectal and other GI cancers.
Hyperplastic polyps
Small sessile polyps formed from normal elongated mucosal crypts. Only associated with risk of colorectal cancer if numerous (‘hyperplastic polyposis’).
Adenomatous polyps
True neoplastic polyps formed by excessive growth of the colorectal epithelium; divided by the morphology of the glandular tissue into tubular, tubulovillous, and villous types.
May be sessile, pedunculated, or mixed.
Thought to be the precursor of most colorectal cancers; the risk of cancerous change within an adenomatous polyp increases with size (particularly >1cm), villous morphology, and sessile form.
Majority are sporadic (either isolated or in small numbers), although occasionally part of a hereditary syndrome.
Familial adenomatous polyposis (FAP)
Caused by an autosomal dominant defect in the APC gene on chromosome 5. Characterized by between dozens and thousands of adenomatous polyps in the colorectum and an increased risk of polyp formation in the stomach and duodenum. The risk of cancerous transformation in any given polyp is similar to that in normal polyps, but the overall risk is very high due to the vastly increased number present.
Associated with:
Desmoid formation, particularly in the abdominal tissues.
Multiple osteomata, fibromata, and thyroid inflammation (called Gardner's syndrome).
Hereditary non-polyposis colorectal cancer (HNPCC)
A range of abnormalities of the mismatch repair (MMR) genes that predispose adenomas to acquire multiple genetic defects and so progress more rapidly than normal to cancer, although the overall rate of adenoma formation is similar to that in normals.
Clinical features
Most polyps are asymptomatic, although symptoms may occur with increasing size and with proximity to the anus. Typical symptoms are:
Bleeding. Usually low volume, dark red, often flecks or mixed with stool.
Mucus discharge. White, clear, or watery; commonest with large villous adenomas and may cause hypokalaemia and hypoproteinaemia if the villous adenoma is large with copious mucus discharge.
Prolapse. If pedunculated and low in the rectum polyps, may prolapse out of the anus.
Diagnosis and investigations
Most polyps are diagnosed by colonoscopy.
Most patients with polyps require further follow-up investigations to keep them under surveillance for future polyp formation; the frequency and length of follow-up depends on the number, size, and histology of the polyp.1
Hereditary polyposis syndromes may be investigated by genetic mutation analysis.
Treatment
Medical treatment
Surgical treatment
Surgical excision is required for polyps that are too large or unsuitable for colonoscopic removal and in which there is a risk of current or future malignant change; for colonic polyps this means either resection or open excision.
Rectal polyps may be removed by transanal microsurgery (see p. 403).
FAP is usually treated by proctocolectomy (usually with ileoanal pouch formation) or colectomy and ileorectal anastomosis before early adulthood; other polyposis syndromes may also be treated by prophylactic colectomy.
Reference
Colorectal cancer
Key facts
Colorectal cancer (CRCa) is the second commonest tumour and commonest GI malignancy. One in 18 of the population will suffer CRCa; ♂:♀ ≈ 3:1. Peak age of incidence 55–75y, but is increasing in younger ages.
Pathological features
The predominant type is adenocarcinoma (mucinous, signet ring cell, and anaplastic subtypes). Classified as well, moderately, or poorly differentiated. Predisposing factors include:
Polyposis syndromes (including FAP, HNPCC, juvenile polyposis).
Strong family history of colorectal carcinoma.
Previous history of polyps or CRCa.
Chronic ulcerative colitis or colonic Crohn's disease.
Diet poor in fruit and vegetables.
Morphology
CRCa may occur as a polypoid, ulcerating, stenosing, or infiltrative tumour mass. The majority (75%) lie on the left side of the colon and rectum (rectum, 45%; descending-sigmoid, 30%; transverse, 5%; right-sided, 20%). Three to five per cent have a synchronous carcinoma at time of diagnosis.
Clinical features
Rectal location
PR bleeding. Deep red on the surface of stools.
Change in bowel habit. Difficulty with defecation, sensation of incomplete evacuation, and painful defecation (tenesmus).
Descending-sigmoid location
PR bleeding. Typically dark red, mixed with stool, sometimes clotted.
Change in bowel habit. Typically increased frequency, variable consistency, mucus PR, bloating, and flatulence.
Right-sided location
Iron deficiency anaemia may be the only elective presentation.
Emergency presentations
Up to 40% of colorectal carcinomas will present as emergencies.
Large bowel obstruction (colicky pain, bloating, bowels not open).
Perforation with peritonitis.
Acute PR bleeding.
Diagnosis and investigations
Elective diagnosis
By PR examination or rigid sigmoidoscopy for rectal carcinoma. Colonoscopy is the preferred diagnostic investigation (alternatives are barium enema and CT colonography).
Emergency presentations
Commonly diagnosed by abdominal CT scan. Single contrast enema may be used when the diagnosis of large bowel obstruction is possible and CT scanning is unavailable. Acute PR bleeding is sometimes investigated by urgent colonoscopy.
Staging investigations
Assessment of the presence of metastases (liver, lung, or para-aortic). Thoracoabdominopelvic CT scanning is gold standard; CT PET scan may be used to evaluate equivocal lesions.
Assessment of local extent. For colonic carcinoma, CT scanning is adequate; for rectal cancer, pelvic MRI and TRUS are commonly used.
Assessment of synchronous tumours. If not diagnosed by colonoscopy or barium enema, one of these two tests is usually performed to identify synchronous tumours.
Tumour marker (CEA) is of no use for diagnosis or staging, but can be used to monitor disease relapse if raised at diagnosis and falls to normal after resection.
Duke's (approx. % 5y survival) • A, confined to bowel wall only (75–90) • B, through bowel wall (55–70) • C, any with +ve lymph nodes (30–60) • D, any with metastases (5–10) | TNM • T1–4,stages of invasion of bowel wall • N0/1/2, no/up to 4/more than 4 lymph nodes involved • M0/1, metastases not present/present |
Duke's (approx. % 5y survival) • A, confined to bowel wall only (75–90) • B, through bowel wall (55–70) • C, any with +ve lymph nodes (30–60) • D, any with metastases (5–10) | TNM • T1–4,stages of invasion of bowel wall • N0/1/2, no/up to 4/more than 4 lymph nodes involved • M0/1, metastases not present/present |
Treatment
Potentially curative treatment
Suitable for technically resectable tumours with no evidence of metastases (or metastases potentially curable by liver or lung resection).
Surgical resection (with lymphadenectomy) is the only curative treatment. Typical operations:
Right/transverse. Right/extended right hemicolectomy.
Left. Left hemicolectomy.
Sigmoid/upper rectum. High anterior resection.
Lower rectum. Low anterior resection/abdominoperineal resection (APER).
Anorectal. APER.
Preoperative (neoadjuvant) chemoradiotherapy may be used in rectal cancer to increase the chance of curative resection.
Adjuvant chemotherapy (5-FU based) is offered for tumours with positive lymph nodes or evidence of vascular invasion.
Hepatic or lung resection may be offered to patients with suitable metastases and a clear resected/resectable primary tumour.
Palliative treatment
For unresectable metastases or unresectable tumours.
Chemotherapy may effectively extend life expectancy with a good quality of life.
Obstructing tumours may be endoluminally stented with self-expanding metal stents or transanally ablated if rectal.
Surgery reserved for untreatable obstruction, bleeding, or severe symptoms.
Restorative pelvic surgery
Low/ultralow anterior resection
Anterior resection = removal of part or all of the rectum and anastomosis of the left colon to the remaining stump of tissue.
Low anterior resection refers to a join that takes place below the level of the peritoneal reflection. i.e. to a short stump of rectum.
Ultralow anterior resection refers to a join that takes place on to the top of the anal canal, i.e. no native rectum remains. The anastomosis may be stapled or sewn by hand.
The lower the level of the anastomosis, the higher the risk of complications of anastomosis, particularly anastomotic leakage (see p. 420). Most low and almost every ultralow anastomosis will have a temporary loop ileostomy formed to reduce the risk of major septic complications and consequences of leakage, but cannot prevent them.
Indications
Rectal carcinoma.
Rectal adenoma untreatable by other means (very rare with transanal endoscopic microsurgery (TEMS).
Severe or complex anorectal sepsis (including rectovaginal fistula).
Ileoanal pouch formation
For operations that remove all the colon and rectum, but do not require removal of the anus, a permanent stoma can be avoided by the formation of an ileal pouch. Formed from a side-to-side double fold of ileum (‘J’ pouch) or three folds sewn together (‘W’ pouch), joined either by hand or by staples to the upper anal canal (ileoanal anastomosis). A temporary loop ileostomy is often formed for the same reasons as for a low anterior resection (above).
Indications
Ulcerative colitis not responding to medical management.
FAP or multiple colorectal polyposis.
Crohn's disease of the colon (controversial).
Multiple colonic tumours including the rectum.
Complications of pelvic anastomosis (anterior resection and ileoanal pouch)
Leakage. Occurs in up to 15% of cases; highest in the lowest anastomosis. Typically presents as fever, abdominal pain, and tachycardia (see p. 420).
Bleeding. Uncommon; usually settles with supportive treatment.
Ischaemia. The proximal bowel involved in the anastomosis may become ischaemic. This may present as a leak, bleeding PR, or fever and tachycardia. Diagnosis is by careful flexible sigmoidoscopy. May resolve spontaneously; progressive ischaemia results in perforation and death if not corrected by surgery.
Stenosis. Narrowing of the anastomosis or bowel used to form it is an occasional late complication. Presents with difficulty in defecation and small volume frequent stools. Treatment is dilatation under anaesthetic; very rarely requires re-operation.
Minimally-invasive colorectal surgery
Transanal endoscopic microsurgery (TEMS)
Large calibre operating protoscope with operating microscope allows microsurgery within the rectum.
Indications
Excision of large adenomas of the rectum (up to the rectosigmoid junction) in a single specimen either by mucosectomy (or occasionally full thickness).
Excision of early rectal carcinoma (only if <3cm size, early tumour (T1), no adverse features or in elderly/comorbid patients) by single specimen full thickness excision.
Repair of a rectovaginal fistula.
Advantages
Include entirely endoscopic technique, very low risk of pararectal/pelvic sepsis, single complete specimen for histological assessment, may avoid more radical surgery.
Complications
Include bleeding (rarely requires active treatment), infection in the pelvic tissues (rare, presents with deep pelvic pain, fever, tachycardia, and disturbance of bowel habit; treat with IV antibiotics).
Laparoscopic surgery
Several variants now exist. All use the same principles: minimal incisions, avoidance of exposure of viscera, light anaesthetic techniques with minimal opiates, and often enhanced recovery post-operatively.
Typical Indications
Any colorectal resection can be performed by laparoscopic surgery.
Rectopexy for prolapse.
Combined treatment of large/extensive colonic polyps.
Formation of some stomas.
Two newer variants have been used:
SILS. Single incision laparoscopic surgery; one larger port for camera and instruments used at the umbilicus.
LESS. Combined laparoscopic and endoscopic single site surgery; combines laparoscopic mobilization and handling with endoluminal endoscopic techniques to remove very large lesions.
Advanced polypectomy
Several advanced endoscopic techniques are used to remove large and often sessile colonic polyps.
EMR. Endoscopic mucosal resection; excision (usually piecemeal) of (presumed) adenoma with use of submucosal fluid injection to facilitate snaring of the polyp.
ESD. Endoscopic submucosal dissection; attempted complete excision of (presumed) adenoma using submucosal injection and endoscopic diathermy ‘knife’.
Diverticular disease of the colon
Key facts
Colonic diverticula are acquired outpouchings of colonic mucosa and overlying connective tissue through the colonic wall.
Tend to occur along the lines where the penetrating colonic arteries traverse the colonic wall between the taenia coli.
Associated with hypertrophy of the surrounding colonic muscle with thickening of the colonic mucosa. This is probably due to the underlying pathological process, which is high pressure contractions of the colon, causing chronic pressure on the colonic wall.
Peak age of presentation is 50–70y, but diverticular disease is increasing in frequency and occurring at a progressively younger age.
Clinical and pathological features
Asymptomatic
The majority of diverticular disease is found incidentally on barium enema examination.
Painful diverticular disease
Intermittent LIF pain may be due to diverticular disease, but irritable bowel syndrome commonly coexists and may be the cause of symptoms.
Acute diverticulitis
Rapid onset of LIF pain, nausea, fever, frequently with loose stools. Usually febrile with moderate tachycardia and LIF tenderness. Colonic wall shows acute neutrophil infiltration around the inflamed diverticulum and in the subserosal tissues.
Bleeding diverticular disease
Usually spontaneous in onset with no prodromal symptoms. Presenting with large volume dark red, clotted rectal blood. Due to rupture of a peridiverticular submucosal blood vessel. Not typically associated with inflammation.
Complications
Pericolic/paracolic mass/abscess
Acute diverticulitis may progress to persistent pericolic infection with thickening of surrounding tissues and the formation of a mass. If this suppurates, a pericolic abscess forms. Enlargement and extension of this into the paracolic area leads to a paracolic abscess. The features are those of acute diverticulitis with a swinging fever, fluctuating tachycardia, unresolving abdominal pain, and a tender LIF mass.
Peritonitis
Perforation of a pericolic or paracolic abscess usually leads to purulent peritonitis. Direct perforation of the acute diverticular segment leads to faeculent peritonitis. The features are of acute diverticulitis with high fever, severe abdominal pain, and generalized guarding and rigidity.
Diverticular fistula
Acute infection with paracolic sepsis may drain by perforation into adjacent structures. This is typically the posterior vaginal vault in women or the bladder in either sex. Colovesical fistula leads to recurrent UTI caused by enteric organisms with bubbles and debris in the urine. Colovaginal fistula leads to faeculent per vagina (PV) discharge.
Stricture formation
Chronic or repetitive inflammatory episodes may lead to fibrosis and narrowing of the colon. A history of recurrent diverticulitis with recurrent colicky abdominal pain, distension, and bloating suggests stricture formation.
Diagnosis and investigations
Elective diagnosis is usually by double contrast barium enema. Colonoscopy is a relatively poor investigation to assess number and extent of diverticula.
Hb, WCC, CRP during acute episodes of inflammation.
CT scanning is the test of choice to identify complications, including abscess formation and perforation.
Double contrast barium enema is used to assess for possible stricture formation.
Colonoscopy is indicated if there is any suggestion of coexistent malignancy.
Treatment
Medical treatment
High fibre diet, high fluid intake, and stool softeners to reduce intracolonic pressure.
IV antibiotics (amoxycillin 500mg IV tds, metronidazole 500mg IV tds, gentamicin IV od) during acute infective exacerbations.
Recurrent infective episodes may be prevented by a 6-week course of oral antibiotics (e.g. ciprofloxacin 500mg PO od).
Significant paracolic abscesses may be drained by radiological guidance.
Surgical treatment
Resection is indicated for:
Acute inflammation failing to respond to medical management.
Undrainable paracolic sepsis.
Free perforation.
The affected region should be resected (segmental colectomy). The ends may be re-anastomosed if they are healthy and the patient's general condition is suitable. If not, a proximal end colostomy and oversewing of the distal end is usual (Hartmann's type resection).
Stricture may be treated by elective resection or balloon dilatation.
Diverticular fistula may be treated by elective resection to prevent recurrent infections.
Rectal prolapse
Key facts
Rectal prolapse may be partial thickness (usually just mucosa) or full thickness involving all the layers of the rectal wall. Full thickness may be contained within the rectum (internal prolapse also called intussusception). Commonest in post-menopausal women, multiple vaginal deliveries, associated with chronic straining and chronic disorders of defecation (which cause weakness of the pelvic floor and sphincter complex), and slow transit constipation. Occasionally occurs in children suffering constipation (usually self-limiting).
Pathological features
Mucosa involved in prolapse undergoes chronic changes.
Typically glandular branching and occasional gland misplacement.
Thickening of the muscularis mucosae and excess submucosal collagen deposition.
Mucosal inflammation and focal ulceration may also occur. Extensive mucosal ulceration associated with mucosal prolapse may result in an appearance called ‘solitary rectal ulcer’.
Clinical features
Mucosal prolapse. Discharge of mucus and small volume faecal staining, pruritus ani, and occasionally small volume bright red rectal bleeding.
Internal full thickness prolapse. Sensation of rectal fullness/mass, incomplete defecation, dissatisfaction after defecation and repeated defecation.
External full thickness prolapse. External prolapsing mass after defecation (usually requiring manual reduction), mucus and faecal soiling, occasional bright red rectal bleeding (may be large volume if prolapse becomes ulcerated).
Diagnosis and investigations
Rigid sigmoidoscopy may show features of mucosal inflammation, particularly the anterior rectal mucosa.
Prolapse may be demonstrable on straining in clinic.
Defecating proctogram may be performed to confirm the diagnosis if it is unclear and surgery is contemplated. Proctogram required to confirm the diagnosis of internal prolapse if suspected. May also demonstrate associated problems of pelvic floor and rectocele.
Colonic transit studies may be used if there is suspected slow transit constipation and resection is possible.
Treatment
Medical treatment
Avoidance of straining and adaptation of defecatory habit (biofeedback).
Avoidance of constipation (stool softeners and bulking agents, rather than stimulants).
Surgical treatment
Mucosal prolapse
Recurrent banding or dilute phenol injection of excess mucosa.
Mucosal excision.
Stapled anopexy (also called procedure for prolapse and haemorrhoids (PPH)) sometimes used.
Full thickness prolapse (internal or external)
Surgery indicated for failure of control of symptoms. Choice of operation depends on age and extent of prolapse.
Delorme's perineal rectopexy (mucosal excision with sutured plication of the excessively long rectal muscle tube in an effort to shorten it to prevent prolapse). Ideal for very frail and elderly, but least successful with highest recurrence rate of all surgical procedures.
Altmeier's perineal rectal resection (mucosal and rectal muscle tube excision with sutured perineal anastomosis). Avoids abdominal operation, but has increased morbidity due to perineal anastomosis.
Transabdominal rectopexy (mobilization of the rectum and suturing to the presacral fascia). May be done via a laparotomy or laparoscopically. May be just to ventral surface of the rectum with suspensory mesh (ventral mesh rectopexy). Highest success rate for prevention of recurrence of prolapse. May be combined with a sigmoid resection if there is marked associated constipation on transit studies.
The internal anal sphincter is smooth muscle and under involuntary control of the pelvic autonomic system. Relaxants include nitric oxide donors (e.g. GTN) and calcium antagonists (e.g. diltiazem).
The external anal sphincter is skeletal muscle and under voluntary control of the pudendal nerve (S2, 3, 4). Relaxation (by temporary partial paralysis) may be achieved by botulinum toxin injection.
Defecation is a complex sensorimotor process that requires intact pelvic autonomics, sacral spinal nerves, and pelvic floor muscle function.
Pilonidal sinus disease
Key facts
Single or multiple sinuses (‘pits’) that exist in the midline of the buttock clefts. Usually contain hair, inspissated secretions, and debris. Commonest in men, dark-haired, hirsute people, especially eastern Mediterranean races. Probably caused by local trauma, causing retention of hairs within initially normal midline pits. May be precipitated by long periods seated, e.g. lorry drivers, computer operators.
Pathological features
Typified by chronic inflammation. Once inflammation has started, sinuses often extend and may become interlinked. Lateral tracks may run out into the neighbouring buttock tissue.
Clinical features
Irritative features. Intermittent discharge and inflammation with pain and swelling.
Acute sepsis. Acute abscess formation is common with swelling, pain, and erythema; may discharge spontaneously or may cause fistulation with sinuses appearing in the lateral buttock tissue.
Chronic sepsis. Usually follows unresolved acute sepsis either after spontaneous discharge or surgical drainage.
Diagnosis and investigations
Ensure the patient is tested for occult diabetes mellitus.
Very extensive sinus formation and fistulation may be assessed by MRI scanning of the natal cleft and buttocks.
Treatment
Medical/non-surgical
Shaving of local hairs and washing of accessible cavities (usually by a partner or family member) may control local symptoms.
Intermittent courses of antibiotics may be required for septic episodes.
Formed pilonidal abscess or collection requires surgical drainage (under local or general anaesthetic).
Recurrent acute sepsis or persistently symptomatic chronic sepsis usually requires surgical treatment.
Surgical
Principles of surgical treatments are:
Excision of all sinus openings.
Obliteration of all infected or chronically inflamed tissue.
Obliteration of the natal cleft by flattening (thought to be most important in the prevention of recurrence by reducing the risk of further hair implantation).
Surgical options are:
Primary excision with laying open of wound and closure by secondary intention is very rarely used, except in extensive recurrent disease; it requires daily dressings for many weeks or months.
Tension-free apposition of the skin edges (may be by lateral flaps, e.g. Karyadakis or Bascom procedures, or by plastic surgical flaps, e.g. rhomboid, rotational, or Z plasty flaps).
Main features of large intestine structure:
Complete layer of circular smooth muscle throughout, but incomplete bands of longitudinal muscle (taeniae coli) in colon (complete in rectum).
Fatty appendages along taeniae (appendices epiploicae).
Folded internal mucosal appearances (haustrations).
‘Segmented’ external appearances (sacculations).
Four main arterial (and lymph node) territories (used for resections):
Ileocolic and right colic arteries (from SMA): last terminal ileal loop, caecum, and ascending colon.
Middle colic artery (from SMA): transverse colon up to the splenic flexure.
Left colic (from IMA): splenic flexure and descending colon.
Superior rectal artery (from IMA): rectum and upper anal canal.
Autonomic nerve supply:
Sympathetic, mainly from greater splanchnic nerves via SMA and IMA plexuses.
Parasympathetic, from vagus via SMA and IMA plexus from caecum to splenic flexure and from pelvic parasympathetics (S2, 3, 4) via hypogastric plexuses and retroperitoneal nerves from splenic flexure to upper anal canal.
Fistula-in-ano
Key facts
A fistula is an abnormal connection of two epithelial surfaces and the two surfaces joined in fistula in ano are the anorectal lining and the perineal or vaginal skin. Very common, especially in otherwise fit young adults. May occur in the presence of Crohn's disease; minor association with obesity and diabetes mellitus, very rarely due to trauma or ulceration of anorectal tumours.
Pathological features
Commonest cause is sepsis arising in an anal gland that forces its way out through the anal tissues to appear in the perianal or in women, vaginal skin (cryptoglandular theory of fistula in ano). Often presents initially as an acute perianal abscess. The tissues through which the track pushes determines the classification of fistulas (see Fig. 11.1).
Classification of fistula-in-ano.
Clinical features
Acute perianal abscess. Rapid onset of severe perianal or perineal pain. Swelling and erythema of the perianal skin with fever and tachycardia.
Recurrent perianal sepsis. Recurrent intermittent sepsis typified by gradual build-up of ‘pressure’ sensation and swelling in the perianal skin and eventual discharge of bloodstained purulent fluid.
Chronic perianal discharge. Persistent low grade sepsis of the track with chronic discharge of seropurulent fluid via a punctum that is usually clearly identified by the patient.
Diagnosis and investigations
Diagnosis and investigation should aim to confirm the presence of a fistula and identify the course of the track to determine the type of fistula:
Examination of the perineum and rectal examination may reveal a palpable fibrous track.
EUA with probing of any external opening to aid identification of the course of the track.
Endoanal ultrasound (sometimes with hydrogen peroxide injected into the track) identifies the course of the track.
MRI scanning is probably the most sensitive method of determining the course of the track and identifying any occult perianal or pelvic sepsis.
Flexible sigmoidoscopy if associated colorectal disease, e.g. Crohn's disease, is suspected.
Treatment
Medical treatment
Antibiotics may reduce symptoms from recurrent sepsis, but cannot treat the underlying fistula.
Medical treatment of inflammatory bowel disease may dramatically reduce symptoms from associated fistulas.
Surgical treatment
Principles of surgical treatment are as follows:
Drainage of any acute sepsis if present.
Prevention of recurrent sepsis. Usually by insertion of a loose seton suture, e.g. silastic sling.
Low fistula in ano. Lay open track, remove all chronic granulation tissue, and allow to heal spontaneously (fistulotomy); little risk of impairment of continence due to minimal division of sphincter tissues.
High fistula in ano:
Remove fistula track and close the internal opening (core fistulectomy and endorectal flap advancement).
Slowly divide the sphincter tissue between the fistula and the perianal skin (cutting seton); low risk of incontinence.
Fill the fistula with fibrin glue.
Haemorrhoids
Key facts
Broad term, often incorrectly used to refer any perianal excess tissue. True haemorrhoids are excessive amounts of the normal endoanal cushions that comprise anorectal mucosa, submucosal tissue, and submucosal blood vessels (small arterioles and veins). Commonest age of onset is in young adulthood. Associated with constipation, chronic straining, obesity, and previous childbirth. May become ulcerated and inflamed if recurrently prolapsing.
If confined to the tissue of the upper anal canal, they are referred to as ‘internal’.
If extend to the tissues of the lower anal canal, they are referred to as ‘external’.
Typically occur in the same location as the main anal blood vessel pedicles (described as 3, 7, and 11 o'clock positions as seen in the supine position).
Clinical features
Features of irritation. Pruritus ani, mucus discharge, and perianal discomfort.
Features of damage to mucosal lining. Recurrent post-defecatory bleeding—bright red, not mixed with stools, on paper or splashing in the toilet pan.
Features of prolapse. Intermittent lump appearing at anal margin, usually after defecation, may spontaneously reduce or require manual reduction.
Diagnosis and investigations
Diagnosis is usually by rigid sigmoidoscopy and proctoscopy.
Flexible sigmoidoscopy or colonoscopy may be appropriate if there is concern about the cause of symptoms; remember—haemorrhoids rarely start over the age of 55y and it is often best to assume another cause until proven otherwise in these cases.
Treatment
Medical treatment
Avoidance of constipation and straining; bulking or softener laxatives.
Surgical treatment
Banding or excessive tissue. Best for prolapse symptoms (not possible for external components due to excellent nerve supply of lower anal canal).
Dilute phenol injections (5% in almond oil). Best for bleeding symptoms.
Haemorrhoidal devascularization procedures (e.g. arterial ligation ‘HALO’ either Doppler ultrasound-guided or blind). For failed topical treatments and surgery not indicated/desired.
Stapled anopexy (also called PPH). Sometimes used for circumferential prolapsing haemorrhoids.
Haemorrhoidectomy for large external haemorrhoids or haemorrhoids failing to respond to conservative treatment. Associated with a small risk of impaired continence and anal stenosis.
Lower third of the anal canal is somatic tissue in origin—stratified squamous epithelium; very sensitive (pudendal and distal sacral nerves); relatively poor blood supply and healing.
Upper third of the canal is visceral tissue in origin—columnar epithelium; insensitive; excellent blood supply and healing.
Acute anorectal pain
Causes and features
Fissure-in-ano
Acute severe, localized, ‘knife-like’ pain in the anus during defecation. Often associated with deep throbbing pain for minutes or hours afterwards due to pelvic floor spasm. Blood on the paper when wiping (small volume, red-pink streaks or spots).
Haemorrhoids
Usually acutely prolapsed and inflamed with associated perianal lump, soreness, and irritation. May bleed, often profuse, bright red.
Perianal abscess
Gradual onset, constant localized perianal pain. Associated swelling with tenderness and possible discharge. May have associated systemic features of fever, malaise, anorexia.
Perianal haematoma
Usually sudden onset; acutely painful with associated perianal swelling (dark red coloured).
Rectal prolapse
Acute full thickness rectal prolapse, occasionally causes pain. Obvious large perineal lump, dark red blue with surface mucus and occasionally some surface ulceration.
Emergency management
Establish a diagnosis
Good inspection and careful digital rectal examination is usually all that is required.
Rigid sigmoidoscopy may be painful and is often unnecessary.
Flexible sigmoidoscopy is rarely indicated.
Early treatment
Give adequate analgesia; opiates may be necessary.
Topical treatment is highly effective; cool pads, topical local anaesthetic gels.
Definitive management
Fissure-in-ano
Mainstay of acute treatment is analgesia and anal sphincter muscle relaxants, e.g. topical GTN 0.2% ointment, diltiazem 2% ointment. Local anaesthetics are helpful early in treatment.
Haemorrhoids
May require bed rest with continued topical treatment until swelling resolves and spontaneous reduction begins. Acute haemorrhoidectomy is almost always best avoided due to the risk of over-excision of anal tissue. Minimal anal dilatation under GA is rarely necessary.
Perianal abscess
Incision and drainage is a surgical emergency, particularly if the patient is diabetic or immunosuppressed.
Perianal haematoma
Incision to allow decompression of acute haematoma may be necessary, often done under topical LA.
Rectal prolapse
Swelling may be reduced by cool packs, elevation, and sometimes icing sugar applied to the swollen mucosa as a dessicant! Very rarely requires emergency surgery.
Acute rectal bleeding
Causes and features
Acute rectal bleeding is broadly divided into regions of the colon from which it comes and the blood is typically different according to the origin.
Anorectal
Bright red blood, on the surface of the stool and paper, after defecation.
Haemorrhoids.
Acute anal fissure.
Distal proctitis.
Rectal prolapse.
Rectosigmoid
Darker red blood, with clots, in surface of stool and mixed.
Rectal tumours (benign or malignant).
Proctocolitis.
Diverticular disease.
Proximal colonic
Dark red blood mixed into stool or altered blood.
Colonic tumours (benign or malignant).
Colitis.
Angiodysplasia.
NSAID-induced ulceration.
Upper GI bleeding occasionally produces dark red rectal bleeding, but it is usually associated with significant haemodynamic instability when sufficiently large.
Features (signs)
Tachycardia and hypotension suggests substantial loss.
LIF tenderness suggests diverticular inflammation with bleeding.
Emergency management
Resuscitation
Establish large calibre IV access; give crystalloid fluid up to 1000mL if tachycardic or hypotensive.
Catheterize and place on a fluid balance chart if hypotensive.
Send blood for FBC (Hb, WCC), U&E (Na, K), LFTs (albumin), group and save, clotting.
Establish a diagnosis
Rigid proctosigmoidoscopy should be performed in all cases to exclude a simple anorectal cause.
Urgent flexible sigmoidoscopy and colonoscopy may be undertaken. It is higher risk than elective endoscopy, but may confirm an origin and may allow therapeutic intervention (adrenaline injection, heater probe coagulation, argon plasma coagulation (APC)).
Urgent selective mesenteric arteriography for obscure or persistent bleeding; needs active bleeding of 0.5mL/min.
Urgent gastroscopy should be used to exclude massive upper GI bleeding if suspected.
Early treatment
Consider blood transfusion if major bleed (persisting haemodynamic instability despite resuscitation, Hb <8g/dL).
Definitive management
Anorectal causes
Most can be controlled by local measures, such as injection, coagulation, or packing.
Acute colitis
IV or PO metronidazole if thought to be infective until organism identified.
IV hydrocortisone 100mg qds if thought to be ulcerative or Crohn's colitis.
Surgery may be necessary whatever the aetiology if bleeding persists (subtotal colectomy and ileostomy formation).
Diverticular disease
IV antibiotics (cefuroxime 750mg tds + metronidazole 500mg tds).
Angiographic embolization if bleeding fails to stop and patient not critically unstable for time in radiology.
Surgery is high risk, but may be unavoidable. If the location is known, a directed hemicolectomy may be performed (on-table colonoscopy may be used). If not, a subtotal colectomy is safest.
Angiodysplasia
Colonoscopic therapy (injection, heater probe, APC) is ideal.
Angiographic embolization may be possible.
Right hemicolectomy is occasionally unavoidable.
Undiagnosed source
Rarely, the patient remains unstable with active bleeding and no cause can be reliably confirmed. Surgical options to deal with this include:
On-table colonoscopy with washout via colostomy to locate bleeding source.
Formation of mid-transverse loop colostomy and subsequent targeted hemicolectomy.
‘Blind’ hemicolectomy (left if significant diverticular disease present; right if no other cause obvious and angiodysplasia is likely).
Acute severe colitis
Causes and features
Any cause of colitis may progress to acute severity. Common causes include:
Severe ulcerative colitis (UC; usually pancolitis); occasionally, acute severe colitis is the presentation of UC with no prior history;
Acute infective colitis (e.g. Salmonella, C. difficile, amoebae, parasites);
Neutropenic colitis;
Pseudomembranous colitis (C. difficile-related);
Progressive Crohn's colitis (usually with a clear prior history).
Symptoms
Diarrhoea (usually bloody with urgency and frequency). ‘Constipation’ may be an ominous feature, suggesting acute colonic dilatation.
Abdominal pain (generalized).
Malaise, anorexia, and fever (systemic inflammatory features).
Signs
Fever, tachycardia, possible hypotension.
Abdominal tenderness; peritonism suggests perforation.
Complications
Any acute severe colitis may develop any of these complications.
Haemorrhage.
Hypokalaemia.
Hypoalbuminaemia;.
Perforation (localized or generalized).
‘Toxic dilatation’ is a term used to describe the situation of acute severe colitis with colonic dilatation usually associated with reduced bowel frequency and impending perforation.
Fulminant severe colitis is defined as: tachycardia >120bpm or stool frequency >10 times/24h or albumin <25g/dL.
Emergency management
Resuscitation
Establish large calibre IV access; give crystalloid fluid up to 1000mL if tachycardic or hypotensive.
Catheterize and place on a fluid balance chart if hypotensive.
Send blood for FBC (Hb, WCC), U&E (Na, K), LFTs (albumin), group and save, clotting.
Establish a diagnosis
Send ‘hot’ stools for M,C,&S as well as microscopy for C,P,&O. Even known colitics may catch acute infective colitis.
Plain AXR (looking for colonic dilatation) and erect CXR (looking for free gas).
Rigid sigmoidoscopy and biopsy only if not unstable.
Flexible endoscopy may be indicated, but carries a risk of perforation.
Early treatment
Give IV hydrocortisone if the diagnosis of UC is likely; if infective colitis is suspected, consider withholding steroids until the M,C,&S results are back.
Blood transfusion if anaemic.
Surgery if peritonitis or free gas on CXR (the operation for any acute colitis is usually total abdominal colectomy and end ileostomy formation).
Definitive management
Acute ulcerative colitis
IV hydrocortisone 100mg qds, converted to oral prednisolone if responding to treatment.
IV cyclosporin if fulminant/not responding to IV steroids.
Surgery for failure to respond to medical treatment or acute complications of haemorrhage or perforation.
Regular blood investigations and plain abdominal radiography to monitor treatment.
Infective colitis
IV or PO metronidazole until organism identified.
Salmonella, C. difficile—metronidazole.
Surgery for failure to respond to medical treatment or acute complications of haemorrhage or perforation.
Neutropenic colitis
IV antibiotics.
Bone marrow support.
Surgery for failure to respond to medical treatment or acute complications of haemorrhage or perforation.
Post-operative anastomotic leakage
Causes and features
Any intra-abdominal anastomosis may leak. Highest risk of leak occurs with oesophageal and rectal anastomosis and lowest with small bowel anastomosis (see Table 11.1).
| Patient factors | Disease factors | Operative factors |
|---|---|---|
Chronic malnutrition Immunosuppression | Unprepared bowel, e.g. obstruction | Poor blood supply or bowel ends |
High dose steroid use Diabetes mellitus | Local or generalized sepsis Metastatic malignancy | Tension on bowel ends |
| Patient factors | Disease factors | Operative factors |
|---|---|---|
Chronic malnutrition Immunosuppression | Unprepared bowel, e.g. obstruction | Poor blood supply or bowel ends |
High dose steroid use Diabetes mellitus | Local or generalized sepsis Metastatic malignancy | Tension on bowel ends |
Anastomotic leakage may present as one of several clinical pictures.
Peritonitis
Acute severe generalized abdominal pain with generalized guarding and rigidity. Fever, tachycardia, and tachypnoea are common. Diagnosis is usually clinical, but may require CT scanning if unsure.
Intra-abdominal abscess
(see p. 308)
Swinging fever and tachycardia, commonly around 5–7 days post-operatively. Localized tenderness related to the anastomosis may be present. Diagnosis should be sought by CT scanning.
Enteric fistula
A fistula between the anastomosis and the wound or another organ may occur. Usually occurs as a result of a subclinical leak and abscess formation that discharges through a pathway of low resistance. Often presents late as an apparent wound infection that discharges with enteric content. Diagnosis made by CT scanning or occasionally, fistulography if presents very late.
Cardiovascular complications
Sepsis originating from an initially subclinical leak may present with apparent cardiovascular complications, e.g. AF, SVT, chest pain, and sinus tachycardia. A wise precautionary rule is, ‘Any acute post-operative disturbance of physiology in a patient with an intra-abdominal anastomosis is due to leak until proven otherwise.’
Emergency management
Resuscitation
Establish large calibre IV access; give crystalloid fluid up to 1000mL if tachycardic or hypotensive.
Catheterize and place on a fluid balance chart if hypotensive.
Send blood for FBC (Hb, WCC), U&E (Na, K), LFTs (albumin), group and save, clotting.
Give appropriate analgesia if not on an epidural or PCA.
Establish a diagnosis
Acute peritonitis needs no diagnostic investigation. Emergency re-look laparotomy should be organized immediately.
CT scanning with IV and PO contrast is the investigation of choice for all other suspected leaks.
For rectal anastomoses, a water-soluble contrast study may delineate a leak.
Early treatment
Give IV antibiotics (e.g. IV cefuroxime 750mg tds + metronidazole 500mg tds).
Monitor fluid balance hourly.
Definitive management
Peritonitis
Always requires surgical intervention unless the patient is deemed unfit.
Prepare for theatre. Ensure blood results from resuscitation are available. Stoma care review is not always necessary and often not practical or useful.
Once the leak has been identified, options for management include:
Dividing the anastomosis, closing the distal end, and forming the proximal end into a stoma;
Emptying the bowel (lavage) and forming a proximal defunctioning stoma;
Re-forming or repairing the anastomosis (only suitable for fit patients with minimal contamination and an otherwise healthy anastomosis);
Placing a large drain(s) next to the anastomosis.
Intra-abdominal abscess
Radiologically guided drainage and antibiotics, provided patient does not become peritonitic or show signs of secondary complications.
Open surgical drainage if inaccessible or unresponsive to radiological drainage.
Enteric fistula
Usually managed by antibiotics. May close spontaneously; if fails to close, surgical repair may be required.
Treat as for abscess or peritonitis if either develops.
