Extensive surgical resections due to conditions such as mesenteric ischemia and Crohn's disease or congenital disorders like gastroschisis or intestinal malformations can cause short bowel syndrome (SBS) [1,2]. In adults, SBS is generally defined by the presence of less than 200 cm of functional small intestine [1]. The small intestine is the primary site for the digestion and absorption of nutrients and fluids, playing a vital role in maintaining overall health and physiological homeostasis. However, in SBS, these essential functions are significantly impaired.

The SBS classification is based on the anatomical configuration of the remaining bowel and includes three main anatomy types: end-jejunostomy (type 1), jejuno-colic anastomosis (type 2) and jejuno-ileal anastomosis (type 3) (Fig. 1) [3,4]. Patients with either a type 2 or type 3 anatomy have the presence of (at least part of) the colon-in-continuity (CiC) in common. The anatomical SBS classification is of importance as it provides insights in the degree of malabsorption and the potential for intestinal adaptation, a spontaneous compensatory process where the remaining intestine undergoes changes, both structural and functional, to enhance nutrient and fluid absorption [5]. Furthermore, the degree of malabsorption distinguishes between intestinal insufficiency (II) and intestinal failure (IF). IF is defined by the ESPEN consensus as the loss of absorptive gut function to such an extent that intravenous supplementation of nutrients and/or fluids and electrolytes, also called parenteral support (PS), is required for survival [1,2]. In contrast, patients with II retain partial enteral autonomy and therefore do not require PS. IF can be further classified into three types based on duration and complexity [1]. Type 1 IF is acute and short-term; typically occurring in the postoperative period. Type 2 IF is less common and represents a prolonged acute condition which often takes place in metabolically unstable patients that require complex care. Type 3 IF is a chronic condition (CIF) where patients require PS for longer periods.

Patients with SBS often present with symptoms such as chronic diarrhea, abdominal pain, flatulence, nausea, dehydration and fatigue. Furthermore, PS, while life-sustaining, is associated with risks including catheter-related infections, intestinal-failure associated liver disease (IFALD) and impaired sleep. Treatment options remain limited and are primarily focused on symptom relief and prevention of complications [6]. The pharmacological management of SBS includes anti-secretory and anti-motility/antidiarrheal agents to reduce gastrointestinal secretions and slow transit time, thereby improving time for absorption, reducing the nutrient and fluid losses and increasing quality of life. Recently, analogs of the glucagon-like peptide-2 (GLP-2) have emerged as disease-modifying treatments for patients with SBS-IF [[7], [8], [9], [10]].

Nutrition plays a central role in the management of patients with SBS. While PS remains the cornerstone of treatment in patients with SBS-IF, dietary modifications are recommended for all patients with SBS; regardless of whether they have IF. The nutritional management of SBS is a dynamic process that integrates oral, enteral and parenteral strategies tailored to the patient's clinical status. Although oral intake may seem ineffective due to reduced intestinal length and limited absorption capacity, it remains a vital component of the nutritional management of SBS and also improves general well-being and quality of life. Oral nutrient intake supports residual nutrient uptake, stimulates intestinal adaptation, and can help to reduce the dependence on PS [11]. The overarching goals of nutritional therapy in SBS are to maintain hydration, ensure adequate macro- and micronutrient intake, and promote intestinal adaptation. In this review, we will elaborate on the key aspects of the oral nutritional management in SBS, highlighting evidence-based strategies, potential risks and practical guidelines.