Level 2 of 6Must-remember

Acute pancreatitis

Assess, manage and stay safe — enough on its own

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The card — assess, manage, caution

Assessment— look, ask, measure

Make the diagnosis on two of three criteria: typical abdominal pain — epigastric, often radiating to the back; serum lipase and/or amylase greater than three times the upper limit of normal; or characteristic findings on cross-sectional abdominal imaging. Because two of three suffice, imaging is unnecessary when the history is classical and the enzymes diagnostic, and a normal enzyme does not exclude the diagnosis when pain is typical and imaging confirmatory.
Carry the rule that any severe acute pain in the abdomen or back should raise the possibility of acute pancreatitis.
The typical pain is severe and constant, building over 15–60 minutes and radiating to the back — steady and boring rather than colicky, centred on the epigastrium, and it may also be felt in chest, flanks and lower abdomen; the patient is distressed, cannot lie still, and often gains partial relief by sitting forward.
Ask for the cause: gallstones and alcohol account for 80–90% of identified cases — gallstones 30–60%, alcohol 15–30% — so ask about biliary colic and previous stones, alcohol intake and the time of the last drink, recent ERCP (which is followed by pancreatitis in 5–10%), drugs, trauma, and known hypertriglyceridaemia or hypercalcaemia.
On examination expect marked epigastric tenderness with absent guarding and rebound early on — unlike a perforated peptic ulcer — because the inflammation is retroperitoneal; the signs may be unimpressive against the intensity of the pain, and bowel sounds become quiet or absent as ileus develops.
Measure and record the vital signs that define severity: systolic blood pressure (below 90 mmHg or hypotension unresponsive to fluid is a red flag), heart rate, respiratory rate, oxygen saturation, temperature (low-grade fever is common), conscious level, and hourly urine output through a catheter (persistently below 0.5 mL/kg/hour is a red flag).
Take a blood gas: an increasing oxygen requirement or PaO₂ of 8 kPa (60 mmHg) or less is present in 5–10% and heralds ARDS; the gas also supplies lactate and the pH used for scoring.Not available at your setup — Arterial blood gas.
Look for the specific but insensitive signs: Grey Turner sign (blue-red-purple or green-brown discoloration of the flanks) and Cullen sign (faint blue discoloration around the umbilicus from haemoperitoneum) — both rare and late, so absence means nothing but presence marks the worst category.
Jaundice is infrequent and suggests compression by peripancreatic oedema or a head mass, or obstruction by a duct stone or sludge; with fever, rigors and right upper quadrant pain it indicates cholangitis.
Look for pulmonary findings, present in 10–20% — basilar crackles, atelectasis and pleural effusion, most often left-sided; the effusion is a formal severity criterion, not an incidental finding.
Severity is defined by organ failure, not by the height of the enzymes — there is no correlation between the degree of amylase or lipase elevation, or its serial trend, and the severity of the attack.
Grade organ failure with the modified Marshall score, all three systems derivable at the bedside from a blood gas, a creatinine and a blood pressure; a score of 2 or more in any single system means organ failure, and persistent organ failure >48 hours is severe pancreatitis.Not available at your setup — Arterial blood gas, Renal function (creatinine/urea).
Take the other red flags seriously: haematocrit above 44% with a rising urea; new confusion; a change in the character of the pain or new peritonism (perforation, infarction or haemorrhage); a tense distended abdomen with rising ventilatory pressures (abdominal compartment syndrome); and fever or a rising CRP after the first week, suggesting infected necrosis.Not available at your setup — Renal function (creatinine/urea).
Older patients present atypically — confusion, hypotension, falls or simply being off legs, with less pain than the pathology warrants and fever may be absent — so the threshold for measuring lipase should be very low, and a first unexplained attack after the age of 50 warrants investigation for malignancy after recovery.
In children the aetiology differs — trauma including inflicted injury, infection, drugs, congenital anomalies, hereditary pancreatitis, cystic fibrosis, hypercalcaemia and hypertriglyceridaemia, not gallstones and alcohol — and a parent will describe a child who refuses to lie flat, draws the knees up and vomits repeatedly; hypotension in a child is a pre-terminal sign, so use capillary refill, pulse pressure, respiratory rate, urine output and conscious level, and check the glucose because small glycogen stores mean hypoglycaemia develops far faster than in adults.
Exclude the mimics before you commit: perforated peptic ulcer (board-like rigidity, free gas on an erect chest radiograph — which also raises the amylase), acute cholangitis (Charcot's triad), intestinal obstruction, mesenteric occlusion, inferior myocardial infarction, aortic dissection, diabetic ketoacidosis (amylase raised non-specifically in 16–25%, but lipase is often not raised), renal colic, basal pneumonia, vasculitis, and ruptured ectopic pregnancy — a pregnancy test is required in every woman of childbearing age.

Management— do this, in order

Fluid replacement is the intervention that most influences outcome and should begin before confirmatory results return. Correct hypovolaemia with Ringer's lactate or Hartmann's solution; balanced crystalloid is preferred to 0.9% sodium chloride, which in volume causes hyperchloraemic acidosis.
In a shocked adult give 500 mL over about 15 minutes and reassess immediately, repeating as required, then continue an infusion titrated to physiological endpoints; in a volume-depleted but non-shocked patient, a continuous infusion with hourly reassessment is appropriate.
Titrate to endpoints, not to a formula: urine output at least 0.5 mL/kg/hour (which requires a catheter), a falling haematocrit, a falling urea, a falling lactate, and normalising heart rate and blood pressure, with haematocrit and urea measured every 8–12 hours — both under- and over-resuscitation cause harm.Not available at your setup — Renal function (creatinine/urea), Arterial blood gas.
In children give 10–20 mL/kg of isotonic crystalloid as a bolus, reassessed after each bolus, then weight-appropriate isotonic maintenance; hypotonic maintenance fluid (plain 5% dextrose or 0.45% sodium chloride) must not be used in a sick child — it causes hyponatraemia and cerebral oedema.
Give opiate analgesia promptly and without rationing: tramadol 50–100 mg IV/IM 6-hourly, or fentanyl 25–50 micrograms IV titrated, or morphine 2.5–5 mg IV slowly repeated every 5–10 minutes to effect; in children morphine 0.1 mg/kg IV titrated in increments or fentanyl 1 microgram/kg IV. Where pain does not settle promptly, patient-controlled analgesia provides continuous relief.Doctor / Nurse
Add regular intravenous paracetamol as background analgesia: 1 g IV or orally 6-hourly (maximum 4 g/24 h); children 15 mg/kg IV or orally 6-hourly (maximum 60 mg/kg/24 h).Doctor / Nurse
Give an antiemetic — ondansetron 4–8 mg IV 8-hourly or metoclopramide 10 mg IV 8-hourly (children ondansetron 0.1–0.15 mg/kg IV, maximum 4 mg/dose) — since nausea and vomiting are near-universal.Doctor / Nurse
Give oxygen to hypoxic patients, titrated to saturations of 94–98%, and take baseline arterial gases, which are both a resuscitation measurement and a severity criterion; patients who develop SIRS may need ventilatory support.Not available at your setup — Arterial blood gas. If ventilatory support is unavailable, escalate urgently to a facility with ICU/ventilator capacity.
Prescribe thromboprophylaxis on admission for every patient: enoxaparin 40 mg subcutaneously daily (reduce in renal impairment) or unfractionated heparin 5000 units subcutaneously 12-hourly — these patients are immobile, dehydrated, inflamed and often obese, and splenic and portal vein thrombosis are recognised complications; in children thromboprophylaxis is usually mechanical, pharmacological only on specialist advice.Doctor / Nurse
Correct hyperglycaemia with a variable-rate intravenous insulin infusion in severe disease (soluble insulin 50 units in 50 mL of 0.9% sodium chloride) titrated to hourly capillary glucose, rather than subcutaneous sliding scales in a poorly perfused patient; children 0.05–0.1 units/kg/hour with hourly glucose.Doctor / NurseNot available at your setup — Infusion pump.
Correct symptomatic or severe hypocalcaemia (tetany, Chvostek or Trousseau signs, seizures, prolonged QT) with 10% calcium gluconate 10 mL IV over 10 minutes into a large vein with cardiac monitoring (children 0.5 mL/kg IV over 10 minutes, maximum 20 mL), and measure magnesium at the same time — hypomagnesaemia renders hypocalcaemia refractory to calcium; give magnesium sulfate 2 g (8 mmol) IV over 20 minutes (children 25–50 mg/kg IV over 20 minutes, maximum 2 g) if hypomagnesaemic.Doctor / NurseNot available at your setup — Serum electrolytes.
In alcohol-related disease give parenteral high-dose thiamine or B-complex intravenously before any glucose-containing fluid, document the time of the last drink (withdrawal begins at 6–24 hours) and prescribe a withdrawal regimen pre-emptively; give phytomenadione 10 mg IV for the coagulopathy of obstructive jaundice (children 300 micrograms/kg IV, maximum 10 mg).Doctor / Nurse
Insert a nasogastric tube only if paralytic ileus is present — it prevents distension, vomiting and aspiration but is not therapeutic, and routine insertion is unjustified.Doctor / Nurse
Feed the patient. In mild disease enteral feeding should begin as soon as abdominal pain has settled; in severe disease it should be considered only after about 48 hours nil by mouth and full resuscitation. Nasogastric feeding is as effective as nasojejunal; total parenteral nutrition carries a high infection risk and has largely been replaced by enteral nutrition.
Do not give prophylactic antibiotics. Reserve them for cholangitis, strongly suspected infected necrosis, or proven extrapancreatic infection, guided by blood cultures: meropenem 1 g IV 8-hourly, or ciprofloxacin 400 mg IV 12-hourly plus metronidazole 500 mg IV 8-hourly, or piperacillin-tazobactam 4.5 g IV 8-hourly; children meropenem 20 mg/kg/dose IV 8-hourly (maximum 1 g) and metronidazole 7.5 mg/kg/dose IV 8-hourly (maximum 500 mg).Doctor / NurseNot available at your setup — Blood culture.
Treat the cause: patients with cholangitis in association with severe acute pancreatitis should undergo urgent ERCP, with sphincterotomy and stone extraction where there is duct obstruction; cholecystectomy should follow as soon as feasible after resolution — within about two weeks, and preferably during the same admission in mild disease — because a further, potentially fatal attack is otherwise likely.
In hypertriglyceridaemic pancreatitis, and in contrast to standard nutritional management, the patient should fast for the initial 24–36 hours to promote resolution of the triglyceride elevation, with a variable-rate insulin infusion and concurrent glucose targeting a triglyceride below 10 mmol/L (880 mg/dL), and removal of precipitants such as alcohol and oestrogens.Doctor / Nurse
Get the CT timing right: do not scan in the first 72 hours merely to confirm the diagnosis; do scan immediately if a surgical catastrophe cannot be excluded; do scan at 48–72 hours or later in any patient with persisting organ failure, sepsis or deterioration.Not available at your setup — CT scan.

Caution— what harms

Never use the height of the amylase or lipase to judge severity — there is no correlation between the degree of elevation, or its serial trend, and the severity of the attack. Severity is defined by organ failure.
Do not repeat the amylase daily — it has no prognostic value; the one exception is that a persistently elevated amylase suggests pseudocyst formation. Use CRP as the serial marker, measured daily.
Do not exclude pancreatitis because the enzyme is normal: only about 85% of patients show a threefold elevation — roughly one in seven does not. Amylase is spuriously low in hypertriglyceridaemia and spuriously high in acidaemia (arterial pH ≤7.32), which explains the diabetic ketoacidosis mimicry — and lipase is often not raised in DKA.
Do not scan in the first 72 hours merely to confirm the diagnosis: perfusion defects take 48–72 hours to develop, so an early scan under-estimates necrosis and needlessly exposes a hypovolaemic patient to contrast nephropathy. Contraindications to intravenous contrast are creatinine above 2 mg/dL (about 177 µmol/L) and severe previous reaction to iodinated contrast — restore volume before scanning.Not available at your setup — CT scan, Renal function (creatinine/urea).
Do not withhold opiates for fear of the sphincter of Oddi. The concern that morphine and diamorphine aggravate pancreatic ductal hypertension is theoretical; there are no clinical data supporting this risk, untreated severe pain is a real harm, and if morphine is the available opiate, give it.
NSAIDs should generally be avoided in a patient who is hypovolaemic, at risk of acute kidney injury and liable to gastric erosion — the exception is rectal diclofenac 100 mg given at the time of an ERCP, which is prophylaxis against post-ERCP pancreatitis rather than treatment.
Do not give prophylactic broad-spectrum antibiotics to prevent infection of pancreatic necrosis — controlled trials have not uniformly shown benefit, particularly in mortality; the only positive signal concerns imipenem, which may reduce the incidence of infected necrosis.
Hospital-acquired infections occur in up to 20% of patients, so pneumonia, urinary and line infection should be sought before a new fever is blamed on the pancreas.
Do not over-resuscitate: high fixed-rate regimens cause fluid overload, pulmonary oedema, worsening hypoxaemia and abdominal compartment syndrome without reducing progression to severe disease. Reassess after every bolus and titrate to endpoints.
Never give hypotonic maintenance fluid (plain 5% dextrose or 0.45% sodium chloride) to a sick child — it causes hyponatraemia and cerebral oedema.
Do not treat pain that suddenly becomes generalised with rigidity as a failure of analgesia — it signals a new event: perforation, infarction or haemorrhage.
Do not rely on scoring systems in the first hours: Glasgow and Ranson achieve about 80% sensitivity only after 48 hours — they mature *after* the window in which resuscitation determines outcome — and all scoring systems have proved to have only modest utility in practice. Resuscitate on clinical impression first and score second.
Manage moderately severe pancreatitis as severe until sustained improvement is seen, because it can convert without warning; and absence of Grey Turner and Cullen signs means nothing since both are rare and late.
Do not attribute hypoalbuminaemia to a need for albumin infusion — it reflects capillary leak and is a severity marker, not a target; and do not read leucocytosis of 15,000–20,000/µL as proof of infection, since it occurs frequently without it. Always correct calcium for albumin.

Refer / escalate

Refer urgently for critical care and specialist surgical or gastroenterological input in any patient with organ failure (modified Marshall score 2 or more in any system), persisting shock or hypoxaemia despite adequate fluid, systolic blood pressure below 90 mmHg, PaO₂ of 8 kPa (60 mmHg) or less, urine output persistently below 0.5 mL/kg/hour or a rising creatinine, a tense distended abdomen, or cholangitis needing urgent ERCP; and prompt contrast-enhanced CT with percutaneous aspiration for culture if deterioration or sepsis occurs after 72 hours.

The card — assess, manage, caution

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