Chronic and recurrent abdominal pain

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

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.

Key points

Describe duration, episodic versus continuous course, exact relation to defecation, meals, posture, movement, menstruation and medicines before attaching a diagnostic label.
Weight loss, iron-deficiency anaemia, rectal bleeding, nocturnal symptoms, fever, mass, family cancer history, persistent vomiting and older-age new onset shift the pathway towards prompt investigation.
A positive diagnosis of irritable bowel syndrome rests on a compatible symptom pattern, limited exclusion tests and absence of warning features; it is not a synonym for all unexplained pain.
Inflammatory markers and faecal calprotectin help discriminate inflammatory bowel disease in suitable adults, but infection, NSAIDs, cancer and age can alter calprotectin and local thresholds vary.
Test for coeliac disease while the patient continues eating gluten; starting a gluten-free diet before serology and biopsy planning can make diagnosis unnecessarily difficult.
Consider abdominal-wall pain when a small reproducible tender point worsens as the abdominal muscles tense, but do not use that sign to dismiss deeper pathology without context.
Endometriosis, ovarian disease, bladder pain, chronic pancreatitis, mesenteric ischaemia, adhesions and neuropathic pain may not be revealed by routine luminal tests.
Management should match the dominant mechanism and patient goals: dietetic support, bowel-pattern treatment, activity, sleep, psychological therapy and selected neuromodulation often work as a combined plan.
Repeated normal tests are evidence only for the questions they answered. Revisit the diagnosis when the pattern changes instead of repeating the same investigation automatically.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Disorders of gut-brain interaction

Irritable bowel syndrome, functional dyspepsia and centrally mediated pain cause genuine recurrent symptoms through altered sensation, motility and pain processing.

Inflammatory or structural disease

IBD, ulcer, coeliac disease, cancer, chronic pancreatitis, adhesions and mesenteric ischaemia cause persistent pain through inflammation, obstruction or tissue injury.

Extra-gastrointestinal causes

Urinary, gynaecological, abdominal-wall, spinal, endocrine and metabolic disease may mimic visceral pain and require history beyond bowel symptoms.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Visceral hypersensitivity
Normal distension or motility may generate amplified discomfort when enteric sensory signalling and central processing become sensitised.
2
Ongoing tissue stimulus
Inflammation, ischaemia, distension or partial obstruction repeatedly activates nociceptors, often linking pain to meals, stool or movement.
3
Pain amplification and disability
Sleep disturbance, fear, mood, prior trauma and repeated medicalisation can reinforce neural pain pathways without implying that symptoms are imagined.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Irritable bowel syndrome phenotype

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.

Inflammatory bowel disease signal

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.

Cancer warning patternRed flag

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.

Chronic mesenteric ischaemiaRed flag

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.

Abdominal-wall pain

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.

Pelvic or cyclical mechanism

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Full blood count and ferritinFirst step
Why
Detect anaemia, iron deficiency, thrombocytosis or other evidence that changes inflammatory and cancer probability.
Interpretation and limitations
Iron deficiency requires a cause, not simple replacement alone. Normal haemoglobin does not exclude early disease, while macrocytosis may point to nutrition, alcohol, medicines or marrow pathology.
02
CRP and ESR
Why
Look for systemic inflammation when inflammatory bowel, infection or other inflammatory disease is plausible.
Interpretation and limitations
Raised values support further evaluation but are non-specific; normal markers cannot fully exclude isolated intestinal inflammation or endometriosis, particularly when warning symptoms persist.
03
Coeliac serology with total IgA
Why
Screen for coeliac disease as a treatable cause of pain, bloating, altered stool and nutritional deficiency.
Interpretation and limitations
Testing is valid while gluten is being consumed. IgA deficiency requires an appropriate IgG-based strategy, and positive serology usually leads to specialist diagnostic confirmation under current guidance.
04
Faecal calprotectin
Why
Differentiate inflammatory bowel disease from a non-inflammatory bowel disorder in an appropriate symptomatic population.
Interpretation and limitations
Interpret against local age and repeat thresholds, infection, NSAID exposure and cancer risk. A low result supports but does not guarantee a non-inflammatory diagnosis; a persistently raised value has a defined referral consequence.
05
Quantitative faecal immunochemical test
Why
Guide suspected colorectal cancer referral when the patient's symptoms meet the current NICE pathway.
Interpretation and limitations
Use the locally commissioned assay and threshold. A result below threshold does not override a rectal or abdominal mass, persistent unexplained symptoms, anaemia or strong clinical concern.
06
Targeted imaging or endoscopy
Why
Investigate a defined structural, mucosal, pancreatic, biliary, vascular or pelvic hypothesis after clinical stratification.
Interpretation and limitations
Ultrasound, endoscopy, CT, MR enterography and CT angiography answer different questions. Choose deliberately and track incidental findings; a normal luminal test does not exclude abdominal-wall, pelvic or vascular disease.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Irritable bowel syndrome

Pain linked to defaecation and altered stool pattern, with limited negative tests and no alarm features, supports a positive IBS diagnosis.

Inflammatory or malignant bowel disease

Weight loss, anaemia, bleeding, nocturnal symptoms, fever, mass or objective inflammation requires targeted endoscopy or imaging rather than a functional label.

Pancreatic, biliary or vascular pain

Back radiation, postprandial attacks, jaundice, food fear or vascular risk directs ultrasound, pancreatic assessment or arterial imaging towards a non-luminal cause.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First assessmentPhenotype before testingFirst stepAbdominal pain has persisted or recurred over weeks to months.

1Build a symptom timeline linked to stool, meals, movement, menstruation and medicines, and document weight, nutrition and functional impact.
2Actively seek bleeding, anaemia symptoms, nocturnal disturbance, fever, vomiting, mass, family history and a recent qualitative change from baseline.
3Examine for pallor, nutrition, nodes, masses, organomegaly, hernias and focal wall tenderness, adding rectal or pelvic assessment only for a defined indication.
4Agree a leading phenotype and dangerous alternatives, then select limited tests that will alter referral or treatment rather than ordering an indiscriminate panel.

02Likely IBSMake a positive reviewed diagnosisSymptoms fit IBS and no warning feature or objective inflammatory signal is present.

1Explain the disorder of gut-brain interaction model in neutral language, validate symptom severity and identify the bowel pattern and most troublesome feature.
2Complete recommended limited exclusion testing, including coeliac serology and inflammatory assessment appropriate to age and presentation.
3First lineOffer regular meals, activity and first-line dietary advice, using a trained dietitian for restrictive strategies; match soluble fibre, antispasmodic, laxative or antidiarrhoeal treatment to phenotype.
4EscalationSet a review point and escalation triggers, considering psychological therapy or low-dose neuromodulation when persistent pain remains functionally important.

03Warning featuresEscalate the correct pathwayEscalationPain coexists with weight loss, bleeding, anaemia, inflammation, mass or progressive nocturnal symptoms.

1Assess current stability and admit if obstruction, sepsis, severe bleeding or acute deterioration is present.
2Use quantitative FIT, calprotectin, endoscopy or cross-sectional imaging according to the suspected colorectal, inflammatory, upper gastrointestinal, pancreatic or vascular process.
3Refer on the current urgent pathway and identify who will review results; do not let a single negative screening test cancel persistent high-risk clinical findings.

04Persistent unexplained painReassess mechanism and iatrogenesisInitial targeted assessment is unrevealing but symptoms continue to impair life.

1Review original reports and pathology rather than relying on 'all normal', and check whether the relevant anatomical question was actually examined.
2Revisit medicines, opioid-related hyperalgesia, abdominal wall, pelvic, neuropathic, metabolic and vascular mechanisms, and assess nutrition and psychosocial contributors collaboratively.
3Avoid repeating low-yield investigations without a new hypothesis; agree a multidisciplinary plan focused on function, safety-netting and a named reassessment interval.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

May reduce episodic bowel spasm and pain as one component of an IBS management plan.

Antispasmodic for IBS-type pain

Use a time-limited trial at the current BNF dose chosen for the individual preparation, then continue only if a meaningful benefit is demonstrated.

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.

Can reduce persistent IBS pain through central and peripheral neuromodulatory effects when simpler measures have not worked.

Low-dose tricyclic neuromodulator

Start below antidepressant dosing at night and titrate slowly under the current NICE and BNF approach, reviewing benefit and adverse effects regularly.

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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Reduced intake and malnutrition

Meal-associated pain, nausea or restrictive self-management can cause weight loss, micronutrient deficiency and avoidant eating even without malabsorptive disease.

Medicine-related harm

Escalating opioids, NSAIDs or unstructured polypharmacy can cause dependence, constipation, ulceration, dysmotility and worsening pain sensitivity.

Delayed diagnosis and disability

Failure to review evolving alarm features can miss organic disease, while repeated unfocused testing can entrench uncertainty, work loss and functional impairment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track weight, appetite, stool pattern, nocturnal symptoms, bleeding and functional impairment rather than relying only on a numerical pain score.
Review pending FIT, calprotectin, coeliac and imaging results through a named clinician, with a clear action for borderline or discordant findings.
For dietary restriction, monitor nutritional adequacy and unintended weight loss and involve a dietitian before prolonged low-FODMAP or exclusion diets.
Assess response and adverse effects after each medicine trial, deprescribing agents without meaningful benefit and watching cumulative anticholinergic or opioid burden.
Re-open the diagnosis promptly when pain changes in site or tempo or new anaemia, bleeding, fever, vomiting, weight loss or nocturnal disturbance appears.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Functional is not imaginary

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.

Calprotectin needs a population

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.

Food fear causes harm

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.

Carnett localises probability

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.

Opioids can amplify pain

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.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing IBS solely because one scan was normal without confirming a compatible symptom phenotype.
02
Starting a gluten-free diet before coeliac serology and specialist confirmation have been completed.
03
Using faecal calprotectin as a colorectal cancer exclusion test or ignoring confounding infection and NSAID exposure.
04
Repeating CT scans for unchanged symptoms without identifying a new question or accounting for radiation burden.
05
Treating cyclical pelvic pain as gastrointestinal after normal endoscopy without appropriate gynaecological assessment.
06
Escalating opioids for chronic unexplained pain while overlooking opioid-induced constipation and hyperalgesia.