Inflammatory and infective
Appendicitis, cholecystitis, pancreatitis, diverticulitis and intra-abdominal infection commonly generate acute pain through local inflammation, oedema and peritoneal irritation.
Recognise physiological danger and time-critical surgical causes of acute abdominal pain, resuscitate in parallel with diagnosis, and choose examination and imaging that lead to a definitive disposition.
Acute abdominal pain is an anatomical and physiological problem before it is a named diagnosis. Establish onset, speed to peak, migration, site, character, radiation and relation to movement, meals, vomiting, stool, urine and menstruation. Visceral pain is often diffuse and poorly localised; parietal irritation becomes sharper and movement-sensitive; referred pain appears away from the affected organ. These patterns guide but do not prove a cause. Appendicitis need not start centrally, myocardial infarction can present epigastrically, lower-lobe pneumonia can mimic an acute abdomen, and diabetic ketoacidosis can produce pain without primary intra-abdominal disease.
Examination begins at the bedside rather than with palpation. Note distress, stillness versus writhing, colour, hydration, respiratory pattern, scars, distension, visible hernia and monitoring trends. Auscultation has limited discriminatory value and should not postpone more important assessment. Palpate gently away from pain, seeking focal tenderness, involuntary guarding, masses and organ enlargement; percussion or cough can reveal peritoneal irritation without repeated rebound testing. Examine groins and external genitalia when obstruction, torsion or hernia is possible. Rectal or pelvic examination should answer a specific question, be consented and use a chaperone rather than being performed ceremonially.
Appendicitis, cholecystitis, pancreatitis, diverticulitis and intra-abdominal infection commonly generate acute pain through local inflammation, oedema and peritoneal irritation.
Bowel obstruction, volvulus, strangulated hernia and perforated viscus cause distension, traction, ischaemia or contamination and may deteriorate rapidly.
Mesenteric ischaemia, aneurysmal rupture, myocardial ischaemia, basal pneumonia, urinary disease and gynaecological emergencies can present primarily as abdominal pain.
Distension, ischaemia or inflammation activates poorly localised visceral afferents, often producing midline pain with autonomic nausea, sweating or pallor.
Extension to the parietal peritoneum produces sharper, localised pain, guarding and pain on movement or percussion.
Ongoing bleeding, contamination, necrosis or inflammation drives hypovolaemia, sepsis and organ hypoperfusion, so physiology may worsen before diagnostic certainty is achieved.
Sudden abdominal, flank or back pain with syncope, shock or a known aneurysm should trigger immediate vascular consideration. The classic pulsatile mass may be absent, and transient response to fluid does not remove rupture risk.
Severe pain disproportionate to early abdominal findings, atrial fibrillation, atherosclerosis, low-flow state or postprandial chronic symptoms raises bowel ischaemia. Peritonism indicates advanced injury; normal early lactate cannot safely exclude it.
Abrupt severe pain, generalised guarding or rigidity, sepsis and free intraperitoneal gas support perforation. Absence of visible free gas on plain radiography does not exclude a contained or early perforation.
Colicky pain, vomiting, distension and obstipation suggest obstruction; constant worsening pain, focal tenderness, fever, tachycardia, acidosis or a closed-loop configuration raises compromised blood supply and demands urgent surgery.
Persistent upper abdominal pain radiating to the back with compatible lipase or imaging supports pancreatitis. Organ failure, systemic inflammation, hypoxaemia, kidney injury or hypotension determines severity more than enzyme height.
Right iliac fossa migration supports appendicitis, left lower-quadrant pain with fever supports diverticulitis, and right upper-quadrant pain with Murphy-type tenderness supports gallbladder inflammation; atypical anatomy and age alter presentation.
Abrupt severe pain, vascular risk, pain out of proportion, pulse deficit or shock favours ischaemia or rupture and requires urgent vascular imaging.
Migration or localisation of pain, fever, focal tenderness and rising inflammatory markers support appendicitis, cholecystitis, diverticulitis or another local inflammatory process.
Chest symptoms, hypoxia, electrocardiographic change, urinary findings, pregnancy possibility or pelvic symptoms redirect assessment towards cardiopulmonary, renal or gynaecological causes.
Perforation, infection, haemorrhage or bowel necrosis can cause circulatory collapse, acute kidney injury and multiorgan failure without timely resuscitation and source control.
Unrelieved obstruction or vascular compromise progresses from venous congestion to infarction, contamination and peritonitis, substantially increasing operative risk.
False reassurance from early normal tests, analgesic response or atypical examination can postpone definitive imaging or surgery until physiological reserve is lost.
Appropriate analgesia does not erase involuntary guarding or physiological deterioration. Withholding it harms patients and can make examination less reliable through fear and voluntary muscle tension.
Mesenteric ischaemia can precede systemic lactate elevation, particularly before extensive infarction. Strong clinical probability should lead to urgent arterial imaging and surgical discussion despite an early normal value.
Intermittent colic can become constant when bowel perfusion is compromised. That transition, especially with focal tenderness or systemic change, is more concerning than absolute pain score alone.
Frailty, immunosuppression, neuropathy and corticosteroids can blunt fever, guarding and leucocytosis. New functional decline, delirium or unexplained acidosis may be the dominant presentation of abdominal catastrophe.
Inferior myocardial infarction, pneumonia, ketoacidosis, porphyria and testicular torsion can present as abdominal pain. A focused chest, cardiac, metabolic and genital assessment prevents an anatomically narrow error.
Waiting for a complete classic triad before considering ruptured abdominal aortic aneurysm.
Using a normal early lactate to exclude mesenteric ischaemia despite disproportionate pain and vascular risk.
Withholding analgesia in the belief that pain relief makes surgical examination impossible.
Relying on absent bowel sounds or a plain abdominal radiograph to exclude obstruction or perforation.
Omitting pregnancy testing or groin examination from an apparently gastrointestinal presentation.
Choosing routine portal-venous CT when an arterial vascular question requires CT angiography.
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A 74-year-old with atrial fibrillation develops sudden severe central abdominal pain. The abdomen is soft with mild tenderness, lactate is initially normal and haemodynamics are stable. What is the best next action?
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.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. ·
Investigations test the leading mechanisms and dangerous alternatives. Blood results describe inflammation, anaemia, organ injury, pancreatitis and physiological compromise but rarely replace imaging. A pregnancy test changes radiation, ectopic and medication decisions. Bedside ultrasound rapidly answers selected questions yet does not survey bowel or retroperitoneum comprehensively. CT abdomen and pelvis with intravenous contrast is central for many stable adults with peritonism, obstruction, diverticulitis or uncertain severe pain; CT angiography is required for suspected mesenteric ischaemia and often for stable suspected aortic catastrophe. Reassess after analgesia and resuscitation, communicate directly with the relevant surgeon and name the trigger for escalation if observation is chosen.
Monitor sedation, respiration and blood pressure; avoid NSAIDs when bleeding, kidney injury or perforation is plausible, and do not let symptom improvement cancel reassessment.
Antibiotics cannot replace drainage or surgery. Record indication and review against cultures, imaging and source control; local resistance and stewardship policy determine selection and duration.