Here's how the gallstone pancreatitis case unfolds and what to pick up on the way.

This gallstone pancreatitis case starts with a line you may hear on any take in: "Severe upper tummy pain that came on a few hours ago." It’s easy to miss if you don’t press for the pain boring through to the back or the relief in sitting forward, and easy to misread if you anchor on vomiting after a fatty meal and earlier brief bouts that settled.

This page walks through how the case presents, what to pick up in the history, the tests, and the teaching points: diagnosing acute pancreatitis without defaulting to CT by meeting two of three criteria, why lipase is preferred to amylase, finding the cause with gallstones and alcohol common in the UK, and early repeated severity scoring to decide level of care.

How the case presents

In their own words: "Severe upper tummy pain that came on a few hours ago."

Observations on arrival:

Observation	On arrival
Heart rate	108 beats per minute
Blood pressure	128/80 mmHg
Respiratory rate	20 breaths per minute
Oxygen saturation	96%
Temperature	37.8 °C

What to pick up in the history

These are the findings the case is built around. Each one moves you towards or away from gallstone pancreatitis, and the scorecard checks whether you found it.

Severe constant epigastric pain boring through to the back: constant boring epigastric pain radiating to the back is the classic pancreatitis pattern, not colic.
Pain worse lying flat, eased by sitting forward: relief on leaning forward is highly characteristic of pancreatic inflammation and helps separate it from peritonitis.
Repeated vomiting, unable to keep down even water.
Onset a few hours after a large fatty takeaway meal: A fatty meal trigger points to a biliary cause and away from alcoholic or drug-induced pancreatitis.
Earlier bouts of pain after fatty food that settled.
Drinks only a few beers at weekends, not daily: excluding heavy alcohol intake removes the other major cause and leaves gallstones as the leading aetiology.
No crushing central chest pain, sweating or arm pain: makes inferior myocardial infarction, a classic mimic of epigastric pain, much less likely.
Eyes look a little yellow and urine is dark: jaundice suggests a stone obstructing the common bile duct, raising cholangitis and the need for urgent ERCP.

Red flags you must not miss

The case marks these as must-elicit. They only come out if you ask.

He has not vomited any blood or 'coffee-ground' material and has not passed black tarry stools.
It did not start as a sudden tearing or ripping pain, and it does not go down into his groin.
No crushing central chest pain, sweating or arm pain.

Investigations and what they showed

Lipase: Markedly raised, more than three times the upper limit of normal. Why it helps: the key confirmatory test, a lipase (or amylase) >3× the upper limit of normal, with typical pain, makes the diagnosis of acute pancreatitis; lipase is more specific and stays elevated longer than amylase.
Amylase: Raised (>3× the upper limit of normal). Why it helps: supports the diagnosis, but is less specific than lipase and can be normal late or falsely raised by other causes, the level does not indicate severity.
Liver function tests: Raised ALT, ALP and bilirubin, an obstructive/hepatocellular pattern.
C-reactive protein: Raised and rising.
Urea and electrolytes: Raised urea (dehydration) with a mildly raised creatinine (early acute kidney injury).
Corrected calcium: Low. Why it helps: hypocalcaemia (from fat saponification) is a Glasgow severity criterion and a marker of a more serious attack.
Random glucose: Raised. Why it helps: hyperglycaemia is a Glasgow severity criterion and reflects impaired pancreatic endocrine function during a severe attack.
Arterial blood gas: Mild hypoxia with a metabolic acidosis and a raised lactate. Why it helps: A low PaO2 is a Glasgow severity criterion; the ABG also flags hypoperfusion/organ dysfunction in severe pancreatitis.
Ultrasound hepatobiliary / gallbladder: Multiple gallstones with posterior acoustic shadowing in the gallbladder; the common bile duct is mildly dilated.
CT abdomen and pelvis: Confirms pancreatic inflammation and, done later (72 hours+), grades severity and detects necrosis/collections, it is not needed to make the diagnosis when lipase and the history are typical.
MRCP: A dilated common bile duct with a stone at the lower end (choledocholithiasis).
Inspect the patient's colour: A yellow tinge to the skin and a clearly icteric sclera in a middle-aged man.
Inspect the sclera: Yellow discolouration of the sclera, scleral icterus. Why it helps: he volunteers that his eyes 'may look a little yellow'. The sclera is where jaundice is detected earliest, at a bilirubin far lower than is needed to make the skin look yellow, so it is the first place to look when you suspect a biliary cause.
Inspect the umbilicus: Bluish-brown bruising and discolouration spreading around the umbilicus. Why it helps: cullen's sign is retroperitoneal blood tracking to the umbilicus along the falciform ligament. It is uncommon and appears late (usually days in), but when present it marks haemorrhagic/necrotising pancreatitis and demands severity scoring and HDU-level care rather than a ward bed.
Inspect the tongue: A dry, furred tongue with tacky mucous membranes. Why it helps: he has vomited repeatedly, cannot keep water down, feels thirsty and has passed little urine.
Inspect the urine: A small volume of dark, concentrated, tea-coloured urine. Why it helps: two things at once: conjugated bilirubin from biliary obstruction darkens the urine, and the small volume reflects hypovolaemia.
Inspect the back: Bluish-purple bruising and discolouration over both flanks, between the lower ribs and the iliac crests. Why it helps: grey Turner's sign, retroperitoneal haemorrhage tracking to the flanks. Like Cullen's sign it is late and uncommon, but it is a marker of severe necrotising pancreatitis and should trigger immediate severity scoring and escalation of care.
Inspect the patient's posture and position: He will not lie flat. He sits hunched forward over his knees, and every attempt to lay him back for examination makes him grimace and pull himself upright again. Why it helps: pain relieved by sitting forward and worsened by lying flat is the classic positional signature of retroperitoneal pancreatic pain, and it is one of the three diagnostic criteria (typical pain + lipase >3x ULN + imaging).
Inspect the abdomen: The abdomen is distended and quiet, moving poorly with respiration, and he guards the epigastrium, flinching before your hand reaches him. Why it helps: he has not opened his bowels or passed wind since the pain began: this is the paralytic ileus that accompanies severe pancreatitis. The distension also explains the vomiting and supports early NG decompression and early enteral rather than parenteral feeding.
Inspect the work of breathing: He is breathing shallowly at 20/min, splinting the upper abdomen, each deeper breath is cut short by the pain. Why it helps: shallow splinted breathing in pancreatitis is both a pain sign and an early warning: pleural effusions, atelectasis and ARDS are recognised complications, and a rising respiratory rate is one of the earliest severity markers to act on.

Imaging findings

X-ray erect chest for free air: No free air under the diaphragm; no basal effusion. Normal.
X-ray abdomen: A non-specific dilated 'sentinel' loop of small bowel; no obstruction. Normal/non-specific.
Endoscopic ultrasound: Would detect small stones/microlithiasis or sludge if the transabdominal ultrasound were negative.
12-lead ECG: Sinus tachycardia, no acute ischaemic changes. Normal.

Why the diagnosis is gallstone pancreatitis

The decisive diagnosis is acute pancreatitis due to gallstones (biliary/gallstone pancreatitis), severe constant epigastric pain boring to the back, relieved by sitting forward, with vomiting, a lipase >3× the upper limit of normal, and gallstones on ultrasound with obstructive LFTs pointing to the cause. Severity must also be scored (Glasgow/apache, CRP). Naming only 'biliary colic' or 'gastritis' misses the pancreatitis, and the can't-miss mimics, perforated peptic ulcer, myocardial infarction, ruptured AAA and mesenteric ischaemia, must be excluded.

Gallstone pancreatitis at a glance

What it is

Acute pancreatitis is sudden inflammation of the pancreas, causing severe, boring epigastric pain that often radiates to the back.

Pathogenesis

When a gallstone lodges at or near the ampulla of Vater, it obstructs the outflow of pancreatic digestive enzymes. These enzymes back up and activate prematurely within the pancreas itself, rather than in the intestine where they are meant to work, causing the gland to digest its own tissue. This triggers intense local inflammation, and in severe cases, enzymes and blood can track along tissue planes to the flanks or around the umbilicus, producing the bruising of Grey Turner's or Cullen's sign.

Who it affects

Gallstone pancreatitis is more common in older adults and in women, which reflects the higher prevalence of gallstones in these groups, though anyone with gallstones can be affected.

How serious it is

Most cases are mild and self-limiting, but a significant minority progress to severe pancreatitis with organ failure, necrosis or infected necrosis, which carries substantial mortality. Severity must be assessed and reassessed early, since it determines the level of care needed.

Causes and risk factors

Gallstones and alcohol together cause the great majority of cases (remembered as "I GET smashed" for the fuller differential). A raised ALT alongside gallstones on ultrasound points strongly to a biliary cause. Obesity, a family history of gallstones, and rapid weight loss all raise the risk of gallstone formation itself.

Investigations and lab tests

Diagnosis needs two of three: typical pain, a lipase (more specific and longer-lasting than amylase) over three times the upper limit of normal, or characteristic imaging, a CT is not required to make the diagnosis. Severity should be scored early and repeated (Glasgow/apache II, CRP at 48 hours). Ultrasound looks for gallstones and biliary dilation to confirm the cause.

At a glance: Diagnosis: two of three (pain, lipase >3× ULN, imaging). Confirms the cause: ultrasound (gallstones), raised ALT. Scores severity: Glasgow/apache II, CRP at 48 hours.

Teaching points

Diagnose acute pancreatitis on two of three: typical pain (severe epigastric → back, eased sitting forward), a lipase/amylase >3× the upper limit of normal, and characteristic imaging, you do not need a CT to make the diagnosis.
Lipase is more specific and stays raised longer than amylase; the enzyme level does not reflect severity.
Always find the cause, 'I GET smashed', but in the UK the big two are Gallstones and Alcohol; a raised ALT and gallstones on ultrasound point to a biliary cause.
Score severity early and repeat it (Glasgow/apache II, CRP >150 at 48h), it decides the level of care (ward vs HDU/ICU).
Feed early, early enteral/oral nutrition is preferred over prolonged 'nil by mouth'; use NG feeding if oral is not tolerated and avoid TPN if the gut works.
Exclude the can't-miss mimics of severe epigastric pain: perforated peptic ulcer (erect CXR for free air), inferior MI (ECG/troponin), ruptured AAA and mesenteric ischaemia.
Watch for complications: organ failure/ARDS, necrosis and infected necrosis, pseudocyst, hypocalcaemia, hyperglycaemia and AKI.

Practise a similar case

Reading a tidy write up is different from steering a live history when you have to decide which thread to pull first. You need to pick up that the pain worsens when lying flat and eases when sitting forward, and tie it to a fatty takeaway a few hours earlier, while the clock is ticking. Try another simulated surgical patient next.

Here's one from the same specialty, with the diagnosis left for you to find. Your next patient is a 72-year-old man with a suddenly cold, painful right leg for 4 hours. Take this patient's history in Diagnosica. It's free to start, no card needed.

Gallstone pancreatitis case presentation: history, findings and tests