Introduction
Abdominal bloating is a common condition affecting up to 3.5% of people globally (4.6% in women and 2.4% in men),1 with 13.9% of the US population reporting bloating in the past 7 days.2 The prevalence of bloating and distention exceeds 50% when linked to disorders of gut-brain interaction (DGBIs) such as irritable bowel syndrome (IBS), constipation, gastroparesis, and functional dyspepsia (FD).3,4 According to the Rome IV criteria, functional bloating and distention (FABD) patients are characterized by recurrent symptoms of abdominal fullness or pressure (bloating), or a visible increase in abdominal girth (distention) occurring at least 1 day per week for 3 consecutive months with an onset of 6 months and without predominant pain or altered bowel habits.5
Prolonged abdominal bloating and distention (ABD) can significantly impact quality of life and work productivity and can lead to increased medical consultations.2 Multiple pathophysiological mechanisms are involved in ABD that complicate the clinical management.4 There is an unmet need to understand the underlying mechanisms that lead to the development of ABD such as, food intolerance, abnormal viscerosomatic reflex, visceral hypersensitivity, and gut microbial dysbiosis. Recent advancements and acceptance of a multidisciplinary management of ABD have shifted the paradigm from merely treating symptoms to subtyping the condition and identifying overlaps with other DGBIs in order to individualize treatment that addresses the underlying pathophysiological mechanism. The recent American Gastroenterological Association (AGA) clinical update provided insights into the best practice advice for evaluating and managing ABD based on a review of current literature and on expert opinion of coauthors.6 This article aims to deliberate a practical approach to diagnostic strategies and treatment options based on etiology to refine clinical care of patients with ABD.
University of Nevada, Reno
Dr. Rajan Singh
Pathophysiological Mechanisms
ABD can result from various pathophysiological mechanisms. This section highlights the major causes (illustrated in Figure 1).
Food intolerances
Understanding food intolerances is crucial for diagnosing and managing patients with ABD. Disaccharidase deficiency is common (e.g., lactase deficiency is found in 35%-40% of adults).7 It can be undiagnosed in patients presenting with IBS symptoms, given the overlap in presentation with a prevalence of 9% of pan-disaccharidase deficiency. Sucrase-deficient patients must often adjust sugar and carbohydrate/starch intake to relieve symptoms.7 Deficiencies in lactase and sucrase activity, along with the consumption of some artificial sweeteners (e.g., sugar alcohols and sorbitol) and fructans can lead to bloating and distention. These substances increase osmotic load, fluid retention, microbial fermentation, and visceral hypersensitivity, leading to gas production and abdominal distention. One prospective study of symptomatic patients with various DGBIs (n = 1372) reported a prevalence of lactose intolerance and malabsorption at 51% and 32%, respectively.8 Furthermore, fructose intolerance and malabsorption prevalence were 60% and 45%, respectively.8 Notably, lactase deficiency does not always cause ABD, as not all individuals with lactase deficiency experience these symptoms after consuming lactose. Patients with celiac disease (CD), non-celiac gluten sensitivity (NCGS), and gluten intolerance can also experience bloating and distention, with or without changes in bowel habits.9 In some patients with self-reported NCGS, symptoms may be due to fructans in gluten-rich foods rather than gluten itself, thus recommending the elimination of fructans may help improve symptoms.9
