Surgical management of ulcerative colitis

Introduction

Ulcerative colitis (UC) is the most common inflammatory bowel disease, with a rising prevalence¹. Classical presentation is with bloody diarrhoea, mucus, and abdominal pain, with the first presentation as an emergency in 10 per cent of patients. Predominant aetiological theories relate to environmental factors, the gut microbiota, and autoimmune dysregulation as triggering factors for those with a genetic predisposition¹. UC only affects the colon and rectum, with contiguous inflammation meaning surgical excision is ‘curative’ for the intestinal disease. UC usually follows a relapsing/remitting course managed with de/escalating medical therapy and a lifetime colectomy risk of approximately 20 to 30 per cent^1,2.

Diagnosis

Raised serum C-reactive protein (CRP), white blood cell count, and faecal calprotectin are observed³. Plain abdominal radiograph may demonstrate the featureless ‘lead pipe’ or ‘cobblestone’ appearance of the colon secondary to colonic mural oedema, while CT demonstrates hyperenhancement of the mucosa, with thickening and oedema of the bowel wall. In severe disease, mural abscesses and thinning of the bowel wall or colonic distension to a diameter of 6 cm indicates impending perforation⁴.

Endoscopy allows severity grading using the modified Mayo score or the Ulcerative Colitis Endoscopic Index of Severity (UCEIS)⁵, as well as definitive histological diagnosis. Neutrophil-mediated epithelial injury, resulting in cryptitis and crypt abscesses, are classical findings on histology. Chronicity of inflammation manifests as crypt architectural distortion, basal lymphoplasmacytosis, or Paneth cell metaplasia.

Classification

The Montreal classification of UC, derived from the original Truelove and Witts criteria⁶, is the most widely used classification system categorizing by disease severity and extent (Table 1). The Mayo severity score categorizes endoscopic appearance, stool frequency, and bleeding, as well as incorporating the physician’s global assessment.

Table 1

Montreal classification of ulcerative colitis (UC)

Extent		Anatomy
E1	Ulcerative proctitis	Involvement limited to the rectum (i.e. proximal extent of inflammation is distal to the rectosigmoid junction)
E2	Left-sided UC (distal UC)	Involvement limited to a proportion of the colorectum distal to the splenic flexure
E3	Extensive UC (pancolitis)	Involvement extends proximal to the splenic flexure
Severity		Definition
S0	Clinical remission	Asymptomatic
S1	Mild UC	Passage of ≤4 stools/day (with or without blood), absence of physiological compromise, and normal inflammatory markers (ESR/CRP)
S2	Moderate UC	Passage of >4 stools per day but with minimal signs of physiological compromise
S3	Severe UC	Passage of ≤6 bloody stools daily, pulse rate ≤90 beats/minute, temperature ≤37.5˚C, haemoglobin <10.5 g/100 ml, and ESR ≤30 mm/h (commonly now substituted for CRP rather than ESR)

ESR, erythrocyte sedimentation rate; CRP, C-reactive protein⁷.

Summary of medical management

Traditional escalation of medical therapy has been replaced in recent years by the concept of ‘top-down’ therapy, using biological therapy as a first- or second-line treatment to aggressively pursue disease control. Therapies are guided by disease extent, severity, response to treatment, and pattern of remission. There are several categories of medical treatment which can be de/escalated as required (Table 2). UK guidelines suggest discontinuing anti-tumour necrosis factor-α agents 14 to 30 days before elective surgery, and steroids should be weaned preoperatively, if possible².

Table 2

Summary of the medical agents available for the treatment of ulcerative colitis

Category	Mechanism of action	Significant adverse effects	Method of delivery	Indication
5-ASA (mesalazine)	Unknown. Proposed suppression of several proinflammatory pathways. Direct effect on mucosal inflammation	Caution in renal impairment. Hypersensitivity reactions	Topical rectal preparations or oral	Mild and moderate proctitis and pancolitis
Corticosteroids (prednisolone, hydrocortisone)	Intracellular binding to glucocorticoid receptors with inhibition of protein transcription for PLA2, COX2, proinflammatory cytokines, including TNF-α	Adrenal suppression and insufficiency, increased susceptibility to infection, osteoporosis, psychiatric effects, oedema	Oral or i.v.	Moderate disease of any distribution. Severe disease in high dose, commonly i.v.
Immunomodulators (thiopurines, methotrexate, JAK inhibitors, ciclosporin)	Inhibition of interleukins and T-lymphocyte activity	Bone marrow suppression, lymphoma, pancreatitis.	Oral preferable	Moderate disease refractory to steroids or in combination therapy with a biological agent. Ciclosporin as rescue therapy in acute severe disease
Biological agents (monoclonal antibodies: infliximab, adalimumab, vedolizumab, ustekinumab)	Infliximab and adalimumab—high affinity for TNF-α, interrupting the inflammatory cascade Vedolizumab—binds to α4β7 integrin receptor on memory T lymphocytes. Ustekinumab—binds to the p40 subunit of IL-12 and IL-23	Hypersensitivity reactions, increased susceptibility to infections, psychological side effects, lymphoma, melanoma	i.v. infusion, subcutaneous	Moderate-to-severe disease. Infliximab as rescue therapy to steroid refractory severe disease

5-ASA, 5-aminosalicylic acids; PLA2, phospholipase A2; COX-2, cyclooxygenase-2; TNF, tumour necrosis factor; i.v., intravenous; JAK, Janus kinase; IL, interleukin.

Colectomy for ulcerative colitis

There are three indications for colectomy: acute severe UC (ASUC), chronic symptoms intractable to medical therapy, and dysplastic or malignant change². Approximately 10 per cent of patients undergoing an episode of acute severe colitis will require colectomy during the same admission, some during their first presentation.

Acute severe ulcerative colitis and emergency colectomy

ASUC is defined by six or more bloody stools/day and one of CRP above 30 mg/l, fever above 37.8°C, heart rate above 90 beats/minute, or haemoglobin below 10.5 g/dl^6,8. Such patients can become quickly dehydrated, hyponatraemic, and hypokalaemic; early intensive management is required to avoid significant deterioration. The mortality rate for ASUC is approximately 2 per cent in a recent series⁹.

The principles of management for ASUC are detailed in Fig. 1. Baseline CT is required with serial plain abdominal radiographs to monitor progress. Urgent unprepped flexible sigmoidoscopy within 24 hours of admission facilitates severity grading and histological diagnosis. Following fluid resuscitation, first-line therapy is intravenous corticosteroids (e.g. hydrocortisone 100 mg q6h) with early surgical referral^2,3. CRP, albumin, and endoscopic severity are useful predictors of response to steroids. After 3 days of steroid therapy, the Oxford index and Edinburgh Colitis Risk Scores can be used to predict the need for colectomy during the same admission. Using the Oxford index, more than eight stools per day or a CRP higher than 45 mg/l, and stool frequency of 3 to 8 per day predicts an 85 per cent risk of colectomy during that admission. The Edinburgh Score incorporates stool frequency, toxic dilatation, and hypoalbuminaemia, with a score of 4 or more suggesting a colectomy risk of 85 per cent^10,11.

Fig. 1

Principles for effective management of acute severe ulcerative colitis

Lack of response to steroids is an indication for second-line ‘rescue’ therapy, commonly ciclosporin or infliximab, which has a less severe side effect profile in the short term. If there is no or partial response at day five of rescue therapy, a total colectomy should be considered, with worse outcomes associated with a longer delay to colectomy. Steroids should be weaned in expectation of surgery to reduce complications. Perioperative nutrition should be optimized, fluid balance corrected, and stoma nurse specialist counselling provided^2,3. A laparoscopic approach is preferable to maintain abdominal wall integrity, reduce surgical stress response, decrease postoperative pain, and minimize adhesions—especially relevant in those likely to undergo subsequent restorative surgery⁴. In the absence of dysplasia or adenocarcinoma, high ligation of vascular pedicles is not indicated.

Elective colectomy for disease refractory to medical management

The choice of elective total colectomy versus pan-proctocolectomy requires shared decision-making regarding fitness, long-term cancer risk, preference for ‘restorative’ surgery, and engagement with surveillance. Interaction with relevant support groups should be encouraged, for example through the Ileostomy and Internal Pouch Association.

Endoscopic surveillance is required for a rectal remnant given the incidence of adenocarcinoma of 2 per cent at 10 years from diagnosis, and 18 per cent at 30 years¹. Patients may suffer mucus discharge, bleeding, tenesmus, and pain due to active UC or diversion proctitis in the rectal stump. Suppositories or enemas of 5-aminosalicylic acids or steroids may alleviate these symptoms¹. Completion proctectomy may be required for dysplasia, carcinoma, or refractory symptoms.

For patients wishing to avoid permanent end ileostomy, restorative options include an ileoanal pouch. The terminal ileum is folded with longitudinal enterotomies and anastomosed together to increase capacity, then anastomosed to an anorectal cuff roughly 2 cm above the dentate line. Other options are an ileorectal anastomosis or a continent ileostomy. The rate of ileoanal pouch failure is approximately 10 per cent at 10 years postoperatively, and ileorectal anastomosis approximately 20 to 30 per cent at equivalent follow-up.

Conclusions

UC is associated with significant morbidity. Management requires close collaboration between gastroenterology and surgical teams, with widely accepted and validated classification and predictive scoring systems aiding shared decision-making around medical treatment and need for colectomy.

Acknowledgements

G.W. (writing—original draft), P.V.-S. (conceptualization, writing—review and editing), and K.S. (conceptualization, writing—review and editing).

Funding

The authors have no funding to declare.

Disclosure

The authors declare no conflict of interest.