Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Classify persistent or episodic abdominal pain by pattern, identify inflammatory, malignant, metabolic and gynaecological warning features, and make a positive, reviewable diagnosis without indiscriminate testing.
Chronic abdominal pain is best organised by phenotype. Pain related to defecation with altered stool frequency or form supports irritable bowel syndrome; postprandial upper pain or fullness points towards dyspepsia or gastroduodenal disease; biliary-type episodes build to a steady right upper-quadrant or epigastric intensity; pancreatic pain may radiate to the back and accompany malabsorption; exertional or food-avoidant pain with vascular risk raises chronic mesenteric ischaemia. Cyclical pelvic pain, dyspareunia or infertility requires a gynaecological lens, and focal pain worsened by movement may arise from the abdominal wall. These are probability shifts, not definitive diagnoses.
The first consultation should establish impact as well as anatomy. Ask about nutrition, weight trajectory, sleep, work, mood, trauma, health anxiety and previous investigations without implying symptoms are imagined. Review opioids, NSAIDs, metformin, iron, laxatives, GLP-1 receptor agonists and other medicines that can cause or amplify gastrointestinal symptoms. Family history should cover colorectal, ovarian and gastric cancer, inflammatory bowel disease and coeliac disease. Examination includes nutritional state, pallor, nodes, oral or skin manifestations, focal masses, organomegaly, hernias and appropriate rectal or pelvic assessment when it will change the question.
Irritable bowel syndrome, functional dyspepsia and centrally mediated pain cause genuine recurrent symptoms through altered sensation, motility and pain processing.
IBD, ulcer, coeliac disease, cancer, chronic pancreatitis, adhesions and mesenteric ischaemia cause persistent pain through inflammation, obstruction or tissue injury.
Urinary, gynaecological, abdominal-wall, spinal, endocrine and metabolic disease may mimic visceral pain and require history beyond bowel symptoms.
Normal distension or motility may generate amplified discomfort when enteric sensory signalling and central processing become sensitised.
Inflammation, ischaemia, distension or partial obstruction repeatedly activates nociceptors, often linking pain to meals, stool or movement.
Sleep disturbance, fear, mood, prior trauma and repeated medicalisation can reinforce neural pain pathways without implying that symptoms are imagined.
Recurrent abdominal pain related to defecation with altered stool frequency or form, bloating and symptom fluctuation supports IBS after limited exclusion testing. Nocturnal progressive symptoms, bleeding, anaemia or objective inflammation argue against simple closure.
Chronic diarrhoea, urgency, blood, nocturnal stool, weight loss, fever, perianal disease, extra-intestinal inflammation or raised calprotectin supports intestinal inflammation and specialist assessment rather than symptom-only treatment.
Unexplained weight loss, iron-deficiency anaemia, rectal bleeding, persistent change in bowel habit, abdominal or rectal mass and relevant age or family history require the current suspected-cancer pathway even when pain is longstanding.
Postprandial pain leading to food avoidance and weight loss in a person with smoking, peripheral vascular disease or other atherosclerotic risk raises intestinal angina. Sudden escalation may indicate acute-on-chronic ischaemia.
A small localised tender point reproducible by movement and persisting or worsening when abdominal muscles tense supports somatic wall or nerve-entrapment pain. Hernia and intra-abdominal red flags still require exclusion.
Pain linked to menstruation, intercourse, fertility symptoms, urinary symptoms or a pelvic mass suggests endometriosis, ovarian or bladder pathology. A normal gastrointestinal work-up is not a substitute for appropriate pelvic assessment.
Pain linked to defaecation and altered stool pattern, with limited negative tests and no alarm features, supports a positive IBS diagnosis.
Weight loss, anaemia, bleeding, nocturnal symptoms, fever, mass or objective inflammation requires targeted endoscopy or imaging rather than a functional label.
Back radiation, postprandial attacks, jaundice, food fear or vascular risk directs ultrasound, pancreatic assessment or arterial imaging towards a non-luminal cause.
Meal-associated pain, nausea or restrictive self-management can cause weight loss, micronutrient deficiency and avoidant eating even without malabsorptive disease.
Escalating opioids, NSAIDs or unstructured polypharmacy can cause dependence, constipation, ulceration, dysmotility and worsening pain sensitivity.
Failure to review evolving alarm features can miss organic disease, while repeated unfocused testing can entrench uncertainty, work loss and functional impairment.
Disorders of gut-brain interaction involve altered motility, sensation and central processing. A positive explanation can coexist with vigilance for later organic change and avoids the false choice between real and psychological symptoms.
Its value is greatest when deciding whether compatible lower gastrointestinal symptoms reflect inflammation. Infection, NSAID use and increasing age reduce specificity, so the threshold must sit inside a clinical pathway.
Postprandial pain often drives progressive restriction before a diagnosis is made. Measuring weight trajectory and involving dietetics can prevent malnutrition while biliary, vascular, inflammatory and gut-brain mechanisms are investigated.
Pain unchanged or worse during abdominal-muscle contraction suggests a wall source because tensing shields the viscera but activates somatic structures. It is supportive rather than an exclusion test for internal disease.
Long-term opioid exposure may worsen constipation, nausea and visceral pain sensitivity. Escalating doses in chronic unexplained abdominal pain can create a self-reinforcing syndrome requiring coordinated pain and prescribing review.
Diagnosing IBS solely because one scan was normal without confirming a compatible symptom phenotype.
Starting a gluten-free diet before coeliac serology and specialist confirmation have been completed.
Using faecal calprotectin as a colorectal cancer exclusion test or ignoring confounding infection and NSAID exposure.
Repeating CT scans for unchanged symptoms without identifying a new question or accounting for radiation burden.
Treating cyclical pelvic pain as gastrointestinal after normal endoscopy without appropriate gynaecological assessment.
Escalating opioids for chronic unexplained pain while overlooking opioid-induced constipation and hyperalgesia.
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A patient with recurrent bloating, loose stool and abdominal pain plans to start a gluten-free diet tomorrow. Coeliac disease has not yet been investigated. What is the most appropriate advice?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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Investigation should be proportionate. A baseline blood count, inflammatory markers, renal and liver profiles and coeliac serology often address common organic alternatives. Stool calprotectin helps in the inflammatory-versus-non-inflammatory bowel question; quantitative FIT belongs to the current suspected colorectal cancer pathway and should not be used as a generic inflammation test. Endoscopy, ultrasound, CT, MR enterography or pelvic imaging follow a defined hypothesis. When criteria support a disorder of gut-brain interaction and warning features are absent, explain the diagnosis positively, agree treatments and plan review. Diagnostic safety comes from continuity and explicit reassessment triggers, not from either endless testing or premature closure.
Anticholinergic effects can worsen constipation, urinary retention, glaucoma or cognitive impairment. Stop ineffective treatment and do not use symptomatic improvement to dismiss newly emerging warning features.
Check overdose risk, cardiac history, sedation, anticholinergic burden and constipation. Explain the analgesic purpose, avoid abrupt escalation and use specialist advice when uncertainty or comorbidity is substantial.