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Bloating — Assessment & ManagementIBS Rome IV · ovarian cancer CA125 · coeliac anti-tTG · calprotectin · FODMAP dietitian · ascites · FIT 2WW · gut-directed hypnotherapy NICE NG61
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The full reasoning pathway β€” bloating is usually functional, but in women it is the key prompt to test CA125 and exclude ovarian cancer. Classify the cause, treat, modify diet, and safety-net.StartDecisionInvestigateActionReferStop / Admit
PresentationBloating / distension
Pattern, relation to food/bowels, persistence. In women ask specifically about early satiety, pelvic pain, urinary urgency.
Step 1 Β· Safety β€” ovarian cancer (NG12)Ovarian cancer features?
Woman (especially 50+) with persistent bloating, early satiety, pelvic/abdominal pain, or urinary urgency/frequency β€” particularly >12 times/month.
YES
Stop Β· InvestigateCA125 β†’ USS
Measure CA125; if β‰₯35 IU/mL β†’ urgent pelvic + abdominal ultrasound; calculate RMI.
NO
InvestigateFBC, coeliac, FIT as indicated
Consider coeliac serology; review diet (FODMAP), bowel habit.
Step 3 Β· cause
Functional
Commonest
IBS, dietary (FODMAPs), constipation, swallowed air.
GI
Organic
Coeliac, lactose intolerance, SIBO, constipation.
Sinister
Don't miss
Ovarian / GI malignancy, ascites.
Step 6 Β· ReferEscalation
2WW NICE NG12 CA125 β‰₯35 with suggestive USS or ascites β†’ urgent gynaecology (ovarian cancer). Gastroenterology organic GI cause.
Step 8 Β· diet & self-management
Step 8 Β· Diet & self-managementFirst-line for functional bloating
Treat constipation; regular meals, reduce gas-producing foods, fizzy drinks and chewing gum (swallowed air). Trial a low-FODMAP diet with a dietitian for IBS-type bloating; consider a lactose/gluten trial where suggestive. Encourage activity and stress management (gut–brain axis); probiotics may help some. Review culprit drugs.
Step 9 Β· review & safety-net
Step 9 Β· Review & safety-netRecheck & when to escalate
Review response to dietary/IBS measures at a few weeks; persistent or progressive bloating should not be re-labelled "IBS" without thought. Re-investigate / refer for new persistent bloating in a woman (CA125 + USS β€” ovarian), weight loss, change in bowel habit, rectal bleeding, abdominal/pelvic mass, or iron-deficiency anaemia. Safety-net that new bloating over age 50 warrants assessment, not reassurance.
⚠️ Persistent bloating in a woman is an ovarian-cancer prompt β€” not "just IBS". Measure CA125 and arrange ultrasound rather than reassuring repeatedly.
1
Safety

Red Flags β€” Malignancy, Obstruction & Serious Pathology

Bloating + unintentional weight loss + change in bowel habit + age >50 or rectal bleeding Colorectal cancer. β†’ 2WW colorectal. NICE NG12: quantitative FIT (faecal immunochemical test) for lower GI symptoms + age β‰₯40. FIT >10 mcg Hb/g β†’ 2WW.
Bloating + progressive abdominal distension + shifting dullness + fluid thrill Ascites. Causes: cirrhosis (most common), peritoneal malignancy (ovarian, colorectal, gastric), cardiac failure, TB peritonitis. USS abdomen urgently. LFTs + albumin + AFP.
Abdominal bloating + new-onset ascites in a woman + elevated CA125 Ovarian cancer. β†’ 2WW gynaecology. NICE NG12: CA125 >35 IU/ml in a woman with bloating + early satiety + increased urinary frequency β†’ urgent USS.
Severe abdominal distension + absolute constipation + vomiting + bowel sounds absent/tinkling Acute large bowel obstruction. β†’ 999. CT abdomen. Causes: colorectal cancer, volvulus, adhesions.
Bloating + persistent diarrhoea + fatigue + iron deficiency anaemia + weight loss Coeliac disease or inflammatory bowel disease. Anti-tTG IgA + total IgA. Calprotectin. Colonoscopy (IBD).
Bloating in a post-menopausal woman that is new, persistent, and daily Ovarian cancer until proved otherwise. CA125 + USS pelvis. Do NOT attribute to IBS in a post-menopausal woman without excluding gynaecological malignancy.
The ovarian cancer bloating connection is one of the most important cancer safety-net rules in primary care β€” the classic symptoms of ovarian cancer are frustratingly non-specific and frequently attributed to IBS or functional bowel disorders, causing diagnostic delays averaging 3–6 months. The NICE NG12 2023 guidance specifies: in women presenting with any of β€” abdominal or pelvic pain, increased abdominal size/bloating, early satiety/appetite loss, urinary urgency or frequency β€” that are persistent, unexplained, or new, CA125 should be measured. A CA125 β‰₯35 IU/ml (the validated threshold) should prompt USS pelvis within 2 weeks. The concept of 'persistent' bloating is the key qualifier β€” functional bloating varies day to day and relates to meals and bowel activity. The bloating of ovarian cancer is progressive, persistent (daily, not intermittent), and does not respond to the usual dietary or laxative measures. GPs who see post-menopausal women with new persistent bloating or early satiety must have ovarian cancer as the primary working diagnosis until USS excludes it. The IBS label should never be applied to a post-menopausal woman with new GI symptoms without a prior negative gynaecological screen.
2
Diagnose

Classification β€” Causes of Bloating

Functional (most common β€” approximately 80%)
Irritable bowel syndrome (IBS): most common cause in primary care. Bloating + abdominal pain + altered bowel habit (diarrhoea, constipation, or alternating). Rome IV criteria: recurrent abdominal pain >1 day/week in past 3 months + β‰₯2 of: related to defaecation; onset associated with change in stool frequency; associated with change in stool form. Bloating in IBS: visceral hypersensitivity + impaired gas handling rather than excess gas production. Functional bloating/distension: visible abdominal distension Β± discomfort, no pain, other Rome criteria not met.
Dietary / fermentation
FODMAP foods (Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols): lactose (dairy), fructose (apples, honey, HFCS), fructans (wheat, garlic, onions), galacto-oligosaccharides (legumes), polyols (sorbitol, xylitol in "sugar-free" products). These are osmotically active + rapidly fermented by gut bacteria β†’ gas production. Lactase deficiency (lactose intolerance): especially East/Southeast Asian populations (80% prevalence). Swallowed air (aerophagia): rapid eating, carbonated drinks, chewing gum.
Organic GI causes
Coeliac disease (NICE NG20 β€” anti-tTG IgA + total IgA). SIBO (small intestinal bacterial overgrowth β€” hydrogen/methane breath test). Gastroparesis (delayed gastric emptying β€” diabetes, post-vagotomy). Intestinal dysmotility (constipation β€” hard stools ferment β†’ gas). Post-infectious IBS (post-gastroenteritis gut dysbiosis). IBD. Diverticular disease.
Extraintestinal causes
Ascites (malignancy, cirrhosis β€” progressive distension not influenced by meals). Ovarian mass. Uterine fibroids (large). Hepatomegaly/splenomegaly. Abdominal mass (lymphadenopathy).
The FODMAP mechanism explains the majority of dietary-related bloating β€” FODMAPs are short-chain fermentable carbohydrates that are osmotically active (drawing water into the intestinal lumen) and rapidly fermented by colonic bacteria (producing hydrogen and methane gas). The key clinical insight: the symptoms are reproducible and food-dependent (bloating develops 1–4 hours after consuming high-FODMAP foods), distinguishing dietary bloating from functional bloating (which is less predictably related to specific foods). The low-FODMAP diet (developed at Monash University, Australia) reduces GI symptoms in approximately 70% of IBS patients β€” it is the most evidence-based dietary intervention for IBS with predominant bloating and pain. However, it requires dietitian supervision (it is a complex elimination diet with a reintroduction phase), and long-term strict adherence may reduce prebiotic fibre intake and gut microbiome diversity. GPs should arrange dietitian referral (not just give a FODMAP leaflet) for patients with bloating who are suitable for this intervention. Small intestinal bacterial overgrowth (SIBO) is a frequently over-diagnosed condition β€” breath testing is poorly standardised and has high false-positive rates. The clinical picture of SIBO: bloating + diarrhoea predominantly after fermentable foods + risk factors (prior GI surgery, gastroparesis, small bowel dysmotility, PPI use, immunodeficiency). Treatment: rifaximin 550 mg TDS Γ— 14 days (gold standard β€” non-absorbable antibiotic targeting gut luminal bacteria).
3
Diagnose

Assessment β€” Diagnostic Approach & Investigations

History (ALARM symptoms first)
Red flags (age >50, weight loss, rectal bleeding, anaemia, nocturnal symptoms, family history CRC/ovarian) β†’ exclude malignancy before IBS diagnosis. Bloating character: timing (post-prandial vs constant), relation to specific foods (dairy, wheat, onions, garlic, beans), variation during day (worse evening = fermentation; constant = structural), visible distension vs sensation only, associated symptoms (diarrhoea, constipation, urgency, tenesmus, early satiety).
Examination
Abdominal distension (visually assess β€” ask patient to stand). Percussion: generalised tympany (gas) vs dullness (fluid/mass/faeces). Shifting dullness + fluid thrill (ascites). Palpation: organomegaly, masses. Bowel sounds. Rectal examination (constipation with faecal loading, rectal mass).
Investigations β€” red flags present
FIT (faecal immunochemical test β€” NICE NG12: quantitative FIT for all lower GI symptoms in age β‰₯40) · CA125 (women with persistent bloating/pelvic pain) · USS pelvis/abdomen (ascites, ovarian mass, organomegaly) · FBC + ferritin (anaemia, iron deficiency) · Colonoscopy (CRC/IBD β€” 2WW or urgent)
Investigations β€” no red flags
Anti-tTG IgA + total IgA (coeliac) · FBC + CRP + ESR · TFTs (hypothyroidism β†’ constipation/bloating) · Faecal calprotectin (>100 mcg/g = IBD likely β†’ colonoscopy; <50 = IBS likely) · Hydrogen/methane breath test (lactose intolerance, SIBO β€” selected cases) · HbA1c (diabetic gastroparesis)
The faecal calprotectin test is the most important investigation distinguishing IBS from IBD in primary care β€” calprotectin is a protein released by neutrophils into the gut lumen during intestinal inflammation. A faecal calprotectin above 100 mcg/g has approximately 90% sensitivity for IBD (particularly Crohn's disease and ulcerative colitis), while a result below 50 mcg/g makes IBD very unlikely (sensitivity 80–90%) in patients with functional bowel symptoms. NICE recommends faecal calprotectin as the first-line investigation for distinguishing IBD from IBS in adults with lower GI symptoms before proceeding to colonoscopy β€” avoiding unnecessary colonoscopy in the majority of patients who have IBS. Important caveats: calprotectin can be elevated by: NSAIDs (causes gut mucosal inflammation), PPI use (modest elevation), bowel preparation, recent GI infection, and colorectal cancer (sometimes). Ensure the patient has not taken NSAIDs for 2 weeks before the test for accurate interpretation. A calprotectin between 50–100 mcg/g is borderline β€” clinical judgement required (consider repeat test in 4–6 weeks or discuss with gastroenterology).
4
Diagnose

IBS Diagnosis & Subtypes

Rome IV IBS criteria
Recurrent abdominal pain at least 1 day/week in the last 3 months, AND associated with β‰₯2 of: (1) related to defaecation; (2) onset associated with change in stool frequency; (3) onset associated with change in stool form/appearance. Plus: criteria fulfilled for the last 3 months with symptom onset β‰₯6 months before diagnosis.
IBS subtypes
IBS-C (constipation-predominant): >25% hard stools (Bristol type 1–2), <25% loose stools. IBS-D (diarrhoea-predominant): >25% loose stools (Bristol type 6–7), <25% hard. IBS-M (mixed): >25% both hard and loose on different occasions. IBS-U (unclassified): criteria met but stool pattern does not fit above categories.
Positive diagnosis of IBS β€” do not just exclude everything
IBS is a positive clinical diagnosis based on characteristic symptom pattern β€” NICE NG61 recommends making a positive IBS diagnosis in patients with typical symptoms rather than exhaustive investigations. Investigations are used to exclude red-flag conditions, not to confirm IBS (IBS has no diagnostic test). Over-investigating IBS increases patient anxiety and healthcare utilisation without improving outcomes.
When NOT to diagnose IBS
Age >50 with new symptoms. Post-menopausal woman with bloating/pelvic symptoms. Weight loss. Rectal bleeding. Anaemia. Nocturnal symptoms (diarrhoea or pain waking from sleep β€” IBS does not typically cause nocturnal symptoms). Abnormal investigations (elevated CRP, FIT positive, anaemia).
The positive IBS diagnosis principle (NICE NG61) is one of the most important quality improvements in primary care gastroenterology β€” NICE specifically recommends that IBS should be diagnosed positively based on characteristic symptoms, rather than as a diagnosis of exclusion after exhaustive investigation. The clinical rationale: over-investigating patients with typical IBS symptoms (particularly with invasive investigations like colonoscopy) increases anxiety, medicalises a functional condition, and has not been shown to improve outcomes or patient satisfaction compared to positive clinical diagnosis with appropriate safety-netting. The key is that the positive diagnosis must be accompanied by: appropriate red-flag exclusion (age, alarm symptoms, investigations if indicated), clear explanation of the diagnosis (not 'nothing is wrong with you' β€” which is unhelpful and inaccurate), and management planning. The IBS explanation that improves patient outcomes: 'Your bowel is structurally normal, but it is more sensitive to certain stimuli β€” food, stress, infection. This is a real condition that affects approximately 20% of people, and there are effective treatments. It will not progress to cancer or IBD.'
5
Refer

Referral Pathways

999
Suspected acute large bowel obstruction Β· Peritonitis
2WW colorectal / gynaecology
FIT >10 mcg/g + any lower GI symptom in age β‰₯40 Β· CA125 β‰₯35 + USS ovarian mass Β· Suspected ovarian cancer (new persistent bloating + pelvic symptoms + post-menopausal)
Gastroenterology (urgent)
Calprotectin >100 mcg/g (suspected IBD) Β· Persistent unexplained weight loss + GI symptoms Β· Coeliac not improving on GFD Β· Suspected SIBO (refractory bloating + risk factors)
Dietitian
Low-FODMAP dietary advice for IBS with predominant bloating Β· Coeliac disease education (gluten-free diet) Β· Lactose intolerance management
GP management
IBS (typical Rome IV, red flags excluded, negative investigations): positive diagnosis + dietary advice + FODMAP referral + antispasmodics. Functional bloating: reassurance + dietary fibre regulation + probiotics. Constipation-related: laxatives + fibre + hydration.
The dietitian referral for low-FODMAP is a NICE NG61 recommendation β€” NICE specifies that the low-FODMAP diet for IBS should be supervised by a dietitian, not self-implemented from a handout. The reason is important: the low-FODMAP diet has three phases (elimination, reintroduction, and personalisation), and incorrect implementation commonly leads to: (1) permanent restriction of many nutritious foods that do not actually trigger symptoms in that individual (the reintroduction phase is designed to identify which specific FODMAPs are problematic for each patient β€” most patients can tolerate at least some categories); (2) significant reduction in prebiotic fibre intake, potentially adversely affecting the gut microbiome; and (3) patient frustration and abandonment after initial elimination phase without personalisation. A properly trained dietitian conducts the elimination phase (typically 6 weeks), supervises systematic reintroduction of individual FODMAP categories, and helps the patient develop a personalised diet that excludes only their specific triggers. This approach achieves equivalent symptom reduction to full FODMAP restriction while maintaining better nutritional quality and gut microbiome diversity.
6
Treat

IBS Treatment Ladder

First line Dietary + lifestyleDietary modifications: reduce gas-producing foods (carbonated drinks, beans, onions, garlic, brassicas). Regular meals (3 small meals, avoid skipping). Adequate water (not fizzy). Physical activity (improves gut motility). Mindfulness/relaxation (gut-brain axis). Soluble fibre (ispaghula husk/Fybogel β€” not insoluble bran which worsens IBS-D and bloating). Probiotic trials (Lactobacillus acidophilus or Bifidobacterium longum β€” modest but consistent benefit in RCTs β€” NNT ~7). Continue Γ— 4 weeks, stop if no benefit.
Second line PharmacologicalAntispasmodics: hyoscine butylbromide (Buscopan) 10–20 mg QDS as needed OR mebeverine 135 mg TDS 20 min before meals (smooth muscle relaxant). IBS-C: linaclotide 290 mcg OD (guanylate cyclase agonist β€” reduces pain + improves stool frequency β€” NICE TA318) or lubiprostone. Macrogol (osmotic laxative) for constipation. IBS-D: loperamide 2 mg (as needed, not regular). Colestyramine (bile acid malabsorption β€” post-cholecystectomy IBS-D or suspected BAM β€” SeHCAT test).
Third line PsychologicalGut-directed hypnotherapy (NICE NG61 β€” recommend for IBS if first/second line fail): 6–12 sessions, significant evidence base (NNT ~4 for meaningful symptom improvement). CBT (IAPT β€” individual or group-based CBT for IBS β€” evidence-based, NICE NG61). Mindfulness-based cognitive therapy. Antidepressants: low-dose TCAs (amitriptyline 10–30 mg nocte) for IBS pain with or without IBS-D effect (reduces gut transit); SSRIs (fluoxetine 20 mg OD) for IBS-C (increases gut motility) and anxiety component.
Gut-directed hypnotherapy (GDH) is one of the most evidence-based yet underutilised treatments for IBS β€” NICE NG61 specifically recommends it for IBS patients who have not improved after 12 months of dietary and pharmacological management. The Gut-Focused Hypnotherapy protocol (Manchester protocol, developed by Whorwell) involves 7–12 sessions focusing specifically on gut symptoms and visceral perception rather than general relaxation. Meta-analyses show response rates of approximately 80% and remission in approximately 50% of treated patients β€” significantly superior to standard medical therapy. The mechanism is thought to involve: modification of visceral hypersensitivity (changing central pain processing), reduction in rectal urgency and colonic motility, and improvement in psychological distress that drives the gut-brain axis dysregulation. Access in the NHS: some clinical psychology services offer GDH; some gastroenterology departments have clinical psychologists who provide it; private practitioners are also available. The Gutsy app and other digital health tools are emerging as accessible GDH delivery platforms with early positive evidence.
7
Treat

Specific Scenarios β€” Coeliac, SIBO & Ascites

Coeliac disease bloating
Strict gluten-free diet: wheat, barley, rye (and contaminated oats) excluded. Dietitian referral mandatory. Annual anti-tTG IgA monitoring (dietary compliance). Nutritional supplements: calcium, vitamin D, B12, folate (often deficient at diagnosis). Symptoms improve dramatically within 4–8 weeks of strict GFD. Refractory symptoms: consider: FODMAP (wheat contains both gluten and fructans β€” some "GFD" patients improve further with low-FODMAP), SIBO (common in coeliac), or refractory coeliac disease (gastroenterology).
SIBO management
Rifaximin 550 mg TDS Γ— 14 days (non-absorbable antibiotic β€” targets gut luminal bacteria, minimal systemic absorption, low resistance risk). Alternatively: metronidazole 400 mg TDS Γ— 14 days or co-amoxiclav 625 mg TDS Γ— 14 days (less specific). Address underlying cause: PPI reduction if possible, treat gastroparesis, treat underlying motility disorder. Probiotic supplementation after treatment (restores microbiome). Elemental diet (exclusive liquid nutrition Γ— 2 weeks) β€” alternative for antibiotic-intolerant patients.
New-onset ascites β€” investigation
USS abdomen (confirm ascites + identify cause). Diagnostic paracentesis (ascitic tap): cell count (>250 neutrophils/ml = SBP β€” empirical antibiotics immediately: cefotaxime 2g IV), protein (exudate >25g/L = malignancy/TB; transudate <25g/L = cirrhosis/CCF), SAAG (serum-ascites albumin gradient >11g/L = portal hypertension), cytology (malignant cells), glucose + LDH (infection/malignancy), culture + sensitivity (SBP). Hepatology referral urgently.
Spontaneous bacterial peritonitis (SBP) is a life-threatening complication of cirrhotic ascites that GPs must recognise β€” it occurs in approximately 10–30% of hospitalised patients with cirrhotic ascites and has a mortality of approximately 20% even with treatment (higher without). SBP is caused by translocation of gut bacteria (predominantly E. coli, Klebsiella, Streptococcus) through the bowel wall into the peritoneal fluid, where the immune response is impaired by low complement and protein levels in the ascites. Clinical presentation: fever, abdominal pain, confusion (hepatic encephalopathy triggered by infection), and deterioration in hepatic function. Importantly, SBP can present without classical peritonitis features β€” up to 30% are essentially asymptomatic, presenting only with hepatic encephalopathy or unexplained deterioration. Any patient with cirrhotic ascites presenting with unexplained deterioration, new confusion, or fever should be referred to hospital for diagnostic paracentesis. GPs managing cirrhotic patients should advise: any new confusion, fever, or abdominal pain in a cirrhotic patient = hospital assessment same day.
8
Lifestyle

Diet, Gut Microbiome & Patient Self-Management

Regular meal pattern Three regular meals per day without prolonged fasting. Eating quickly or while stressed increases aerophagia (swallowed air). Sit down to eat. Chew food thoroughly. Avoid eating late in the evening (reduced gut motility during sleep amplifies bloating overnight). Avoid skipping meals (irregular eating patterns disrupt gut motor patterns).
Physical activity Regular moderate exercise (150 min/week) improves gut motility and significantly reduces IBS symptoms (NNT ~4 for any meaningful improvement β€” Johannesson 2011 RCT). Walking, cycling, swimming. Yoga has specific evidence for IBS bloating (abdominal yoga poses reduce gas pooling + parasympathetic activation). Prescribe exercise as a treatment, not just an adjunct.
Stress and the gut-brain axis IBS is fundamentally a disorder of gut-brain axis communication β€” psychological distress worsens gut symptoms, and gut symptoms worsen psychological distress. Explain this bidirectional mechanism clearly. Mindfulness-based stress reduction (MBSR) Γ— 8 weeks significantly improves IBS symptoms (Zernicke 2013). CBT via IAPT addresses catastrophising about symptoms (common driver of healthcare utilisation in IBS). Apps: Nerva (gut-directed hypnotherapy app β€” accessible, evidence-based).
Probiotic guidance Some probiotic strains have modest evidence for IBS bloating: Bifidobacterium longum NCC3001 (Alflorex β€” available OTC), Lactobacillus plantarum 299v (Symprove), multi-strain products (VSL#3 for IBD-related bloating). Take consistently for 4 weeks β€” if no benefit, stop. Probiotics are not regulated as medicines β€” quality varies. Advise: choose products with published RCT evidence rather than generic "probiotic" capsules.
Food diary A 2-week food and symptom diary helps identify specific triggers in individual patients. Low-tech: notebook or smartphone notes app. High-tech: Monash University FODMAP app (identifies high-FODMAP foods). Diary review with dietitian directs personalised dietary modification. Most effective when kept prospectively (not retrospectively).
Reducing aerophagia Avoid carbonated drinks, chewing gum, and eating while anxious. Avoid drinking through straws. Eat more slowly (fork-down technique between bites). Simethicone (Infacol, Wind-eze β€” gas-dispersing agent) β€” modest benefit for trapped gas causing acute discomfort. Activated charcoal capsules β€” weak evidence but safe for occasional use.
Bowel habit regularity Straining at stool (IBS-C, constipation) creates backdraft that moves gas from colon to small bowel β€” worsening bloating. Adequate fluid intake (1.5–2 L/day), soluble fibre (ispaghula), regular toilet time (use the gastrocolic reflex β€” sit on toilet 20 minutes after breakfast). Squatting position (foot stool under feet when on toilet) improves anorectal angle and reduces straining.
Alcohol and bloating Alcohol directly irritates the gastric and intestinal mucosa, alters gut microbiome composition (dysbiosis), and increases intestinal permeability β€” all of which worsen IBS symptoms. Alcohol intolerance is significantly more common in IBS patients than the general population. Advise reduction (NHS guidelines <14 units/week). Red wine (tannins + high FODMAP content) and beer (high FODMAP) are particularly common IBS triggers.
The gut-brain axis explanation is the single most therapeutic communication in managing IBS β€” patients who understand the mechanism (bidirectional communication between the enteric nervous system and the central nervous system, mediated by the vagus nerve, the hypothalamic-pituitary axis, and the gut microbiome) are better equipped to understand why stress worsens their symptoms, why psychological treatments are effective, and why there is nothing 'in their head' about their symptoms. The most useful analogy: 'Just as your heart races when you're nervous, your gut responds to stress too β€” it's connected to your brain through a major nerve called the vagus nerve. The gut is sometimes called the second brain because it has 100 million nerve cells of its own. When you're anxious or stressed, your gut receives the same stress signals and becomes more sensitive and reactive.' This explanation reduces the stigma of functional diagnosis and increases engagement with psychological interventions that have the strongest evidence base.
9
Safety

Follow-Up & Safety-Netting

IBS β€” review schedule
6–8 weeks after initiating treatment: symptomatic response? Dietary adherence? Any new alarm symptoms emerging? If no improvement at 6 weeks: step up treatment (antispasmodics β†’ low-dose TCA β†’ referral). Annual review: stable IBS, routine. Document Rome IV criteria met and red flags excluded at diagnosis.
Post-coeliac diagnosis follow-up
Anti-tTG IgA at 6 months and 12 months (falling titre = dietary compliance). Annual thereafter. FBC + ferritin + calcium + B12 + folate annually. DEXA at 18 years or at diagnosis if adult (coeliac + osteoporosis).
New ascites β€” after diagnostic paracentesis
Treat SBP (if neutrophils >250) immediately with cefotaxime. Long-term SBP prophylaxis after first episode: norfloxacin 400 mg OD or co-trimoxazole 960 mg OD. Hepatology follow-up. Address variceal surveillance.
999 / Same-day
Bowel obstruction (absolute constipation + distension + vomiting) Β· Peritonitis Β· Acute variceal bleed (haematemesis in cirrhosis) Β· Suspected SBP (confusion + fever in ascitic patient)
Within 2 weeks
Persistent bloating not responding to treatment + new weight loss at any follow-up visit β†’ FIT + CA125 + referral Β· Calprotectin rising on serial tests despite IBS diagnosis β†’ gastroenterology Β· Post-menopausal woman with new or worsening bloating at any point β†’ CA125 + USS
The CA125 monitoring principle for post-menopausal women with bloating is a NICE recommendation that is frequently not implemented β€” NICE CG122 (Ovarian Cancer Recognition) and the subsequent NICE NG12 both specify that CA125 should be measured in women with persistent bloating. The word 'persistent' means occurring more than 12 times per month β€” daily or near-daily bloating is the threshold, not occasional bloating. The most common error: attributing persistent bloating in a post-menopausal woman to IBS, GORD, or 'just ageing' without measuring CA125 or USS pelvis. The Ovarian Cancer Action charity estimates that in the UK, approximately 4,000 women per year receive a diagnosis of ovarian cancer only after the cancer has reached stage III or IV β€” when 5-year survival is approximately 30%, compared to approximately 90% at stage I. Most of these delayed diagnoses involve GI symptoms (bloating, early satiety, change in bowel habit) that were attributed to functional disorders. CA125 + USS pelvis at the first presentation of persistent unexplained bloating in a post-menopausal woman is a non-negotiable safety standard.
Educational use only. Based on NICE NG61 IBS 2017, NICE NG12 Suspected Cancer 2023, NICE NG20 Coeliac Disease 2015, NICE TA318 Linaclotide, BSG Ascites guidelines 2006 (updated), Johannesson exercise RCT 2011.