Truelove and Witts criteria (1955) remain the gold standard for identifying acute severe UC requiring inpatient IV corticosteroids. Toxic megacolon (colonic dilatation >6 cm) occurs in ~5% of acute severe UC and carries 30% mortality without surgical intervention. Patients on biological therapy (infliximab, vedolizumab) or immunomodulators are immunocompromised — fever requires urgent assessment for opportunistic infections including CMV colitis.

C.difficile superinfection in UC patients increases mortality 4-fold compared to UC alone. Steroids worsen C.diff infection — this is a critical safety issue. Faecal calprotectin distinguishes inflammatory from functional symptoms with 80–90% sensitivity, reducing unnecessary colonoscopy. NSAIDs cause UC flares in 20–30% of cases through prostaglandin inhibition — stopping them can resolve a flare without immunosuppression.

Truelove and Witts criteria have been validated for over 60 years and remain the primary triage tool for UC flare severity. Correct severity classification prevents both under-treatment (missing severe colitis needing IV therapy) and over-treatment (admitting mild flares). Steroid dependency (defined as inability to wean below 10 mg prednisolone) is the trigger for escalation to steroid-sparing immunomodulators — this conversation should happen with the gastroenterologist, not be deferred indefinitely in primary care.

Abdominal examination is critical — toxic megacolon can develop silently and presents with distension disproportionate to reported symptoms. Extra-intestinal manifestations (EIMs) occur in 25–40% of UC patients — arthritis often flares in parallel with gut disease, uveitis requires ophthalmology review and can cause blindness if missed. Pyoderma gangrenosum is a clinical diagnosis requiring gastroenterology and dermatology collaboration — it should not be debrided surgically.

Albumin <30 g/L in a UC flare is a marker of severe systemic disease and poor nutritional status — these patients often need hospital admission regardless of stool frequency. CRP >45 mg/L on day 3 of IV steroids predicts need for colectomy (Oxford criteria) — this monitoring happens in hospital. Faecal calprotectin tracks mucosal healing and is increasingly used to guide step-down of therapy, though this decision is made with the gastroenterologist.

Many UC patients have access to an IBD nurse specialist who can advise on whether a flare can be managed with an existing rescue therapy protocol (e.g., patient-held steroid prescription). This prevents unnecessary GP and hospital contacts. Direct phone referral to gastroenterology on-call for severe flares is faster than A&E for most patients. Steroid-dependent UC has a significantly worse prognosis and quality of life — early escalation to biologic therapy is associated with higher remission rates and fewer hospitalisations.

Topical mesalazine achieves mucosal drug concentrations 100× higher than oral formulations for distal disease and is the most effective treatment for proctitis (NNT ~3 for remission induction). Long-term oral mesalazine reduces colorectal cancer risk by 75% — UC patients have a 2–3× higher risk of colorectal cancer after 10 years. TPMT enzyme testing before azathioprine prevents potentially fatal myelosuppression in 0.3% of the population who are TPMT-deficient. Prednisolone should never be used as long-term maintenance — it has no mucosal healing effect and causes significant morbidity.

The NSAID-UC relationship is clinically important — many patients take OTC ibuprofen without realising it precipitates flares. Psychological co-morbidity (anxiety, depression) affects 30–40% of IBD patients and worsens disease course — psychological support is part of disease management, not an optional extra. Vaccination is critical: patients on biologics have significantly higher infection rates, and live vaccines (MMR, yellow fever, oral typhoid) are contraindicated in significant immunosuppression. Cancer surveillance colonoscopy is the GP's responsibility to ensure is arranged via gastroenterology.

Early review at 48–72 hours catches patients not responding to steroids before they deteriorate severely — this is the most important safety intervention in moderate UC. Mucosal healing (confirmed endoscopically) is now the treatment target in UC — symptom resolution alone does not predict remission. Patients who do not achieve mucosal healing have higher relapse rates, colectomy rates, and cancer risk. Abrupt steroid cessation after >3 weeks causes adrenal crisis — always taper.