Acute pancreatitis

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

Acute pancreatitis is premature pancreatic enzyme activation with local inflammation and a variable systemic response. Mild disease has no organ failure or local complication and usually settles with supportive care. Moderately severe disease includes transient organ failure or local/systemic complications. Severe disease is defined by organ failure persisting beyond forty-eight hours. These categories evolve, so an apparently mild admission needs repeated assessment rather than a one-off score.

Diagnosis should be efficient. Characteristic pain and a diagnostic enzyme rise usually make early CT unnecessary. Lipase is generally more pancreas-specific and remains elevated longer, but renal impairment and other abdominal disorders can cause smaller increases. If the diagnosis is unclear, imaging evaluates alternatives. Ultrasound should assess gallstones even when alcohol use is reported because causes can coexist. Contrast CT is most useful later when complications, non-improvement or diagnostic uncertainty will change management.

Treatment is supportive and cause-directed. Analgesia and antiemetics allow breathing, mobilisation and feeding. Fluid is prescribed to physiological response, not as a ritual volume; pulmonary oedema, abdominal compartment physiology and renal or cardiac disease require particular care. Nutrition protects gut integrity. Antibiotics are withheld unless infection exists. Gallstone disease needs a duct assessment when obstruction is suspected and a cholecystectomy plan; alcohol-associated disease needs non-stigmatising withdrawal-risk assessment, thiamine and ongoing support.

Key points

Diagnose acute pancreatitis when at least two of three features are present: characteristic pain, serum lipase or amylase above three times the upper reference limit, and compatible imaging.
Severe constant epigastric pain commonly radiates to the back and accompanies vomiting, but older, postoperative or critically ill patients can present atypically.
Gallstones and alcohol are common causes; also assess medicines, calcium, triglycerides, trauma, recent ERCP, autoimmune disease, infection, anatomical obstruction and tumour.
Repeatedly measure physiology, urine output, oxygen requirement, renal function and haematocrit or urea trends; an enzyme concentration does not grade severity.
Provide titrated analgesia, antiemesis, oxygen for hypoxaemia and carefully reassessed crystalloid resuscitation; avoid both under-resuscitation and uncritical fixed large volumes.
NICE says not to give prophylactic antimicrobials for acute pancreatitis; treat a demonstrated or strongly suspected infection such as cholangitis, pneumonia or infected necrosis.
Encourage oral feeding in mild disease as tolerated; NICE recommends enteral nutrition within seventy-two hours for moderately severe or severe pancreatitis rather than routine parenteral feeding.
Urgent ERCP is for associated cholangitis or ongoing biliary obstruction, not for every case of gallstone pancreatitis; secure definitive gallbladder management after recovery.

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

Gallstones and alcohol

Transient ampullary obstruction from gallstones and sustained harmful alcohol exposure are common causes; history, liver tests and biliary imaging help distinguish them.

Metabolic and medicine-related

Hypertriglyceridaemia, hypercalcaemia and selected medicines can trigger pancreatitis, requiring interpretation of timing and competing causes rather than an uncritical adverse-effect label.

Procedural, structural and immune

ERCP, abdominal trauma, pancreatic obstruction, anatomical variants and autoimmune pancreatitis are less common but clinically important when initial assessment finds no usual cause.

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

1
Premature enzyme activation
Intra-acinar activation of digestive enzymes initiates pancreatic autodigestion, cellular injury and local inflammatory mediator release within and around the gland.
2
Local inflammatory spread
Oedema, fat necrosis and vascular injury extend into peripancreatic tissues, producing fluid collections, necrosis and sometimes haemorrhage.
3
Systemic inflammatory response
Cytokine release, capillary leak and circulatory disturbance can cause respiratory, cardiovascular and renal failure remote from the pancreas.

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

Typical pancreatic pain

Abrupt severe epigastric pain radiating through to the back with vomiting and upper-abdominal tenderness is characteristic but not unique to pancreatitis.

Evolving organ dysfunctionRed flag

Increasing oxygen need, hypotension, oliguria, rising creatinine, confusion or acidosis signals systemic severity and requires senior and critical-care reassessment.

Biliary infection overlapRed flag

Jaundice, fever and rigors with pancreatitis may represent ascending cholangitis; urgent antibiotics and biliary decompression take priority over routine pancreatitis observation.

Unusual underlying cause

First idiopathic episodes in older adults, recurrent attacks, duct dilatation, weight loss or new diabetes should prompt review for tumour, microlithiasis, autoimmune or structural disease.

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
Serum lipase or amylaseFirst step
Why
Provide one diagnostic criterion in a patient with compatible acute upper-abdominal pain.
Interpretation and limitations
More than three times the laboratory upper limit supports pancreatitis; the absolute height does not measure necrosis or predict outcome.
02
FBC, urea, creatinine, electrolytes and glucose
Why
Establish haemoconcentration, renal injury, metabolic disturbance and a baseline for repeated severity assessment.
Interpretation and limitations
Rising urea or creatinine, worsening thrombocytopenia or persistent hyperglycaemia can indicate complicated illness but must be integrated with physiology.
03
Liver profile and abdominal ultrasound
Why
Identify gallstones, cholestasis and duct dilatation as clues to a biliary aetiology needing definitive treatment.
Interpretation and limitations
A transient aminotransferase rise can reflect a passed stone; absent visualised calculi do not exclude microlithiasis or prior migration.
04
Calcium, triglycerides and medicine review
Why
Search for treatable metabolic or iatrogenic causes when gallstone and alcohol explanations are incomplete.
Interpretation and limitations
Measure triglycerides early because fasting lowers them; correct calcium for albumin and avoid declaring a medicine causal without temporal evidence.
05
Contrast-enhanced CT abdomen
Why
Clarify uncertain diagnosis, failure to improve, necrosis, collection, haemorrhage or another abdominal emergency when results will change care.
Interpretation and limitations
Very early CT can underestimate necrosis and is unnecessary in straightforward mild disease; timing and protocol should be agreed with radiology and specialists.
06
Blood gas, lactate and chest imaging
Why
Assess hypoxaemia, acidosis, perfusion and pulmonary complications in patients with systemic illness.
Interpretation and limitations
Respiratory deterioration can result from atelectasis, effusion, inflammatory lung injury, aspiration or fluid overload, each needing different management.

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

Peptic ulcer or perforation

Epigastric pain may overlap, but free gas, peritonism, endoscopic ulceration or absence of diagnostic pancreatitis criteria redirects assessment.

Biliary sepsis

Fever, jaundice, cholestatic tests and duct obstruction suggest ascending cholangitis, which requires urgent drainage planning rather than supportive pancreatitis care alone.

Vascular or cardiac disease

Mesenteric ischaemia, aortic catastrophe and myocardial ischaemia can mimic upper abdominal pain; vascular risk, shock, ECG findings and targeted imaging discriminate them.

Additional chapter-specific clues

Haemorrhage or perforation mimicRed flag

Peritonism, gastrointestinal bleeding, abrupt collapse, pulsatile mass or pain out of proportion requires emergency imaging and surgical or vascular pathways rather than diagnostic anchoring.

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

01InitialFirst-day supportive careFirst stepTwo diagnostic criteria establish pancreatitis or the clinical probability is high while confirmation proceeds.

1Use ABCDE, prescribe appropriate monitored analgesia and antiemesis, correct hypoxaemia and establish venous access plus urine-output observation.
2Give crystalloid for demonstrable hypovolaemia in reassessed increments, considering age, heart or kidney disease and signs of pulmonary congestion.
3Send diagnostic and cause-focused blood tests, perform gallbladder ultrasound and take a non-judgemental alcohol and medicine history.
4Allow oral food as symptoms permit in mild illness; engage dietetics early when intake will be inadequate or disease is more severe.

02EscalateDeteriorating pancreatitisEscalationOrgan function worsens, systemic inflammation persists or pain and feeding do not improve as expected.

1Repeat structured physiology and blood tests, involve critical care early, and support respiratory, cardiovascular and renal failure in the appropriate environment.
2Review fluid balance for both continuing depletion and harmful overload; use haemodynamic information rather than automatic repeated boluses.
3Obtain specialist-timed contrast CT for necrosis or another complication, avoiding routine daily scanning without a management question.
4Start enteral nutrition within the NICE window for moderately severe or severe disease and investigate infection before prescribing antimicrobials.

03CausePrevent recurrenceThe acute diagnosis is secure and immediate physiological threats are controlled.

1For gallstone disease, assess persistent obstruction or cholangitis for ERCP and ensure cholecystectomy timing is explicitly owned by surgery.
2For alcohol-related illness, assess withdrawal risk, provide thiamine where indicated and arrange compassionate alcohol-care follow-up rather than advice alone.
3Treat hypercalcaemia or severe hypertriglyceridaemia with relevant specialists and discontinue a culprit medicine only after benefit-risk review.
4Refer unexplained, recurrent or atypical disease for EUS, MRCP, autoimmune, genetic or malignancy evaluation according to age and phenotype.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Relieves severe pancreatic pain so the patient can ventilate, mobilise and participate in feeding and assessment.

Opioid analgesia

Titrate a short-acting intravenous, subcutaneous or oral regimen under the acute-pain protocol with frequent effect and sedation review.

Reduce exposure in frailty or renal and hepatic impairment; monitor respiration, ileus, nausea, delirium and cumulative doses, and reassess escalating pain anatomically.

Corrects extracellular depletion caused by vomiting, reduced intake and inflammatory third spacing.

Crystalloid fluid replacement

Give reassessed adult boluses or maintenance matched to perfusion, urine output, losses, comorbidity and local intravenous-fluid guidance.

Over-resuscitation can worsen pulmonary oedema, effusions and abdominal pressure; seek critical-care support when shock persists despite an appropriate trial.

Prevents or treats thiamine deficiency during admission in people with harmful alcohol use or prolonged poor intake.

Thiamine for alcohol risk

Use the current local oral or parenteral prophylaxis or treatment regimen according to nutrition, withdrawal and Wernicke risk.

Give before carbohydrate when Wernicke encephalopathy is suspected and do not wait for laboratory confirmation of a neurological emergency.

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

Persistent organ failure

Inflammatory capillary leak and vasodilatation can cause hypoxaemia, shock and acute kidney injury, defining the most dangerous disease trajectory.

Necrosis and infection

Pancreatic or peripancreatic tissue may become necrotic and later infected, creating sepsis and a need for specialist step-up drainage or necrosectomy.

Collections and structural effects

Acute collections may mature into pseudocyst or walled-off necrosis, causing pain, gastric or biliary obstruction, bleeding or fistulation.

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

Repeat heart rate, blood pressure, respiratory rate, oxygen requirement, temperature, cognition, urine output and fluid balance according to instability.
Trend renal function, urea, haematocrit, electrolytes, glucose, calcium and liver tests; enzyme levels need not be serially chased for severity.
Review pain control, sedation, bowel function, nausea and the ability to eat at least daily.
Watch for new fever, late deterioration, falling haemoglobin, abdominal distension or recurrent organ failure that may signal necrosis, infection or bleeding.
Before discharge, confirm cause review, alcohol or metabolic intervention, gallstone surgery ownership and written recurrence safety-netting.

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

Two criteria suffice

When characteristic pain and a diagnostic enzyme rise coexist, routine early CT adds radiation and may not improve care.

Lipase is not severity

A spectacular enzyme value can accompany mild disease, while necrotic pancreatitis may later have a modest concentration.

Causes can overlap

Alcohol exposure should not stop an ultrasound finding gallstones, and visible stones do not eliminate a medication or metabolic contribution.

Feeding is treatment

Early oral or enteral nutrition supports gut barrier function; prolonged nil-by-mouth practice is not benign.

ERCP needs an indication

Gallstone aetiology alone does not justify emergency cannulation when cholangitis and persistent duct obstruction are absent.

11Common pitfallsFrequent interpretation and management errors.

01
Using the lipase height to label disease severe or mild.
02
Ordering immediate CT for every straightforward enzyme-positive presentation.
03
Giving prophylactic antibiotics because inflammatory markers are high.
04
Keeping mild pancreatitis nil by mouth after nausea has settled.
05
Delivering repeated fixed fluid boluses without checking lungs and urine output.
06
Discharging gallstone pancreatitis without a named definitive surgical plan.