01OverviewDefinition, clinical context and the essential points that orientate the chapter.
A gallstone can lodge briefly at the ampulla, disrupt pancreatic outflow and trigger enzyme-mediated inflammation before passing. Consequently, ultrasound may show gallbladder stones without a persistent common-duct calculus and bilirubin may fall rapidly. Severe constant epigastric pain radiating to the back, vomiting and raised lipase or amylase support acute pancreatitis, but perforation, ischaemia and myocardial infarction remain dangerous alternatives.
Early work concentrates on physiology rather than predicting severity from appearance alone. Measure oxygenation, perfusion, urine output, renal function and inflammatory trajectory. Excessive fluid can worsen pulmonary oedema and abdominal pressure, while inadequate replacement perpetuates kidney injury. Routine immediate CT is unnecessary when the diagnosis is clear; contrast CT becomes valuable for diagnostic doubt, clinical deterioration or later assessment of necrosis and collections.
Cause-directed prevention matters after recovery. Same-admission cholecystectomy following mild gallstone pancreatitis reduces recurrent biliary events. ERCP is not a universal cleansing test: it is most useful for cholangitis or evidence of persisting obstruction. Severe necrotising disease, large collections or ongoing organ failure requires HPB multidisciplinary timing so gallbladder surgery does not disrupt inflamed tissue or prematurely expose the patient to another physiological insult.
Key points
- Confirm acute pancreatitis from the compatible pain syndrome and raised lipase or amylase, using imaging when the diagnosis remains uncertain.
- Look for gallstones with liver tests and ultrasound while also reviewing alcohol, medicines, calcium, triglycerides and other causes.
- Support perfusion with individualised reassessed crystalloid, effective analgesia, oxygen when required and early enteral nutrition where oral intake is not possible.
- Do not give prophylactic antibiotics for sterile pancreatitis; treat documented or strongly suspected infection and seek source control.
- Use ERCP urgently when acute pancreatitis is accompanied by cholangitis or continuing biliary obstruction, rather than as routine treatment for every biliary attack.
- Offer cholecystectomy during the same admission for mild gallstone pancreatitis when clinically appropriate; severe disease or collections may require delayed, specialist timing.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Ampullary stone migration
A gallstone passing from the common duct can transiently block pancreatic drainage and initiate an acute inflammatory cascade.
Alternative pancreatitis causes
Alcohol, hypertriglyceridaemia, hypercalcaemia, medicines, trauma and structural disease must still be considered when stones are incidental or evidence is weak.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Premature enzyme activation
Acinar injury and obstructed outflow activate digestive enzymes within pancreatic tissue, producing oedema, fat injury and systemic mediator release.
- 2Systemic capillary leak
Inflammation causes intravascular depletion, lung injury and kidney hypoperfusion; severity is defined by organ dysfunction rather than enzyme concentration.
- 3Necrosis and collections
Severe injury can create non-viable pancreatic or peripancreatic tissue and evolving fluid collections that may later become infected or compress organs.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Sudden severe constant epigastric pain often radiates to the back and is accompanied by vomiting, although the pattern is not specific.
Gallbladder stones, transient cholestasis or an early aminotransferase rise support a migrating stone as the trigger.
Hypoxaemia, shock and acute kidney injury define immediate severity and need for a higher level of monitoring.
Fever, jaundice, rigors and obstructive imaging demand urgent biliary drainage in addition to pancreatitis care.
New fever, persistent pain, gastric compression or renewed inflammation after initial improvement suggests necrosis or a pancreatic collection.
05InvestigationsWhat to request, why it matters and how to interpret it.
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
Serum lipase or amylaseFirst step - Why
- Confirm biochemical pancreatic inflammation in a compatible syndrome.
- Interpretation and limitations
- A substantial rise supports acute pancreatitis, but enzyme height does not grade severity and other abdominal or renal conditions can elevate results.
- 02
Liver blood tests - Why
- Identify evidence of recent or continuing biliary obstruction.
- Interpretation and limitations
- Rapidly improving aminotransferases and bilirubin can reflect a passed stone; persistent cholestasis raises the probability of a retained duct stone.
- 03
Abdominal ultrasound - Why
- Detect gallbladder stones and duct dilatation.
- Interpretation and limitations
- Bowel gas can limit the pancreas and distal duct. A stone-bearing gallbladder supports causation but does not prove a common-duct stone remains.
- 04
Contrast-enhanced CT - Why
- Clarify diagnostic uncertainty or assess deterioration and complications.
- Interpretation and limitations
- Early CT may underestimate necrosis. Time the scan to the clinical question and renal risk rather than obtaining it routinely at admission.
- 05
MRCP or EUS - Why
- Assess possible retained common-duct stones in a stable patient.
- Interpretation and limitations
- These tests can prevent unnecessary ERCP when obstruction probability is uncertain; neither provides drainage if cholangitis is present.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Perforated peptic ulcer
Sudden epigastric pain and peritonism may resemble pancreatitis, but free gas and direct imaging findings require urgent surgical management.
Mesenteric ischaemia
Severe pain with limited early tenderness, vascular risk and lactate change requires urgent vascular imaging and must not be dismissed after a modest enzyme rise.
Acute coronary syndrome
Inferior myocardial ischaemia can produce epigastric pain and vomiting, so ECG and troponin remain appropriate when risk supports them.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Worked case: mild biliary pancreatitisPrevent the second eventFirst stepA patient has typical pain, lipase eight times the upper limit, gallbladder stones and falling liver tests; organ function is normal and symptoms improve over forty-eight hours.+
- 1Confirm acute pancreatitis and a likely gallstone cause while documenting that no cholangitis or persistent organ failure is present.
- 2Provide analgesia, reassessed fluids and oral feeding as tolerated; avoid prophylactic antibiotics and routine urgent ERCP.
- 3Offer same-admission laparoscopic cholecystectomy once clinically ready, with duct imaging only if retained-stone probability remains significant.
- 4Verify stable physiology, improving renal and liver tests, nutritional tolerance and a completed operative plan before discharge.
02Pancreatitis with cholangitisDrain the infected ductA jaundiced patient with pancreatitis develops rigors and hypotension.+
- 1Begin sepsis resuscitation and cultures followed by prompt local intravenous biliary antibiotics.
- 2Call therapeutic endoscopy urgently for biliary decompression alongside critical-care support.
- 3Do not wait for pancreatic inflammation to resolve before treating infected obstruction.
- 4Confirm post-drainage perfusion and cholestatic improvement and monitor for ERCP complications.
03Severe necrotising courseDelay anatomy-sensitive surgeryPersistent organ failure and necrotic collections develop.+
- 1EscalationEscalate to critical care and an HPB multidisciplinary team.
- 2Use enteral nutrition when feasible and treat infection only when suspected or confirmed.
- 3DefinitiveDefer gallbladder surgery until inflammation and collections permit a safer definitive plan unless another urgent indication arises.
- 4Reimage and intervene on collections according to symptoms, infection and maturation rather than size alone.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Paracetamol 500 mg tablets as a non-opioid analgesic component
For an adult aged 16 years or over using this 500 mg tablet formulation, give 500–1,000 mg orally every 4–6 hours when required, leaving at least four hours between doses; give no more than four doses and do not exceed 4,000 mg, eight tablets, in 24 hours. Stop as acute pain resolves and reassess promptly if pain remains uncontrolled rather than exceeding the ceiling.Check every prescription and over-the-counter product for duplicate paracetamol. Use a lower patient-specific maximum with low body weight, malnutrition, chronic alcohol excess or hepatic impairment, and use an intravenous or alternative supervised plan if vomiting prevents absorption. Suspected overdose requires urgent toxicology assessment even if the person feels well.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Persistent organ failure
Respiratory, cardiovascular or renal failure persisting for more than 48 hours defines severe acute pancreatitis. Organ dysfunction requires immediate escalation and support while its duration is still evolving.
Infected necrosis
Colonisation of necrotic tissue can cause late sepsis and often requires a staged drainage and debridement strategy.
Recurrent biliary events
Before definitive gallbladder treatment, further stone migration can cause recurrent colic, cholecystitis, common-duct obstruction, cholangitis or another pancreatitis attack.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Measure oxygen requirement, perfusion, urine output and renal function repeatedly during the first days.
- Track oral intake and start dietetic or enteral support when normal eating is insufficient.
- Review liver tests and duct imaging for retained obstruction, especially when jaundice does not resolve.
- Watch for late fever, recurrent pain, early satiety or inflammatory relapse that may indicate necrosis or collections.
- Before discharge confirm the cholecystectomy plan, alcohol and medicine review, and exact return symptoms.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Enzyme height is not severity
A very high lipase confirms inflammation but does not predict organ failure or necrosis.
A passed stone leaves clues
Transient liver-test disturbance can be the only evidence that ampullary obstruction initiated the attack.
Feeding supports recovery
When oral intake is not possible, enteral nutrition is generally preferred to avoid unnecessary parenteral feeding.
Timing follows phenotype
Mild resolving disease favours same-admission cholecystectomy, while severe necrotising disease requires anatomy-aware specialist delay.
11Common pitfallsFrequent interpretation and management errors.
- 01
Giving antibiotics simply because CRP is high in otherwise sterile pancreatitis.
- 02
Using routine urgent ERCP in every gallstone pancreatitis presentation.
- 03
Equating a falling enzyme concentration with resolution of organ failure.
- 04
Discharging after mild biliary pancreatitis without a definitive gallbladder plan.