Introduction

Inflammatory bowel disease (IBD) is increasing in prevalence around the world.1 It can be divided into Crohn’s disease (CD), an inflammatory condition of the entire gastrointestinal tract, or ulcerative colitis, which predominantly affects the large bowel. Advances in therapy, such as anti-integrins, anti IL12/23 and particularly anti-tumour necrosis alpha biologics, have contributed to a decrease in surgical intervention.2 Unfortunately, there is a cohort of patients with a severe phenotype, who are refractory to available therapy and ultimately develop intestinal failure (IF). Risk factors which have been identified for this phenotype include a younger age at diagnosis or at first surgery, ileocolonic and perianal disease, family history, smoking and initial need for corticosteroids.3 4 In fact, a recent study has shown surgical complications (abdominal sepsis) as being the most common cause of IF in patients with CD.4 This may explain why, in combination with the development of targeted biological therapies, a study from a national IF unit found a decrease in the number of patients with IF due to CD directly and an increase in those whose aetiology was from surgical complications.5 A 40-year study from a Danish IF unit showed the number of home parenteral nutrition (HPN) patients due to IBD increased by around 30 patients a decade but reduced as percentage of total cases.6 The accepted definition of IF is “the reduction of gut function below the minimum necessary for the absorption of macronutrients and/or water and electrolytes, such that intravenous supplementation is required to maintain health and/or growth”.7 IF still remains rare, with a prevalence of patients on parenteral nutrition (PN) of between 5 and 20 patients per million7 and around one-third of these patients have CD.3