Your next patient has sudden, severe tummy pain that started 3 hours ago. Here's how the perforated peptic ulcer case unfolds and what to pick up on the way.

A perforated peptic ulcer case can be easy to get wrong in the history: months of grumbling epigastric indigestion sound mundane, until sudden severe epigastric pain has the patient lying still because any movement makes it worse. With no chest pain, no tearing pain to the back and no relief sitting forward, it is easy to be misled.

This page walks through how the case presents, what to pick up in the history, and the tests and teaching points. Expect pain that becomes generalised with a rigid board-like abdomen, rising heart rate and falling blood pressure as sepsis and shock evolve. We cover the erect chest X-ray for free air under the diaphragm, and CT for sensitive localisation, while noting that absence of these findings does not fully exclude it. It also flags the catastrophic mimics to exclude: ruptured abdominal aortic aneurysm, mesenteric ischaemia and inferior myocardial infarction.

How the case presents

Your next patient has sudden, severe tummy pain that started 3 hours ago. In their own words: "Severe tummy pain that came on suddenly a few hours ago."

Observations on arrival:

Observation	On arrival
Heart rate	116 beats per minute
Blood pressure	104/68 mmHg
Respiratory rate	24 breaths per minute
Oxygen saturation	97%
Temperature	37.9 °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 perforated peptic ulcer, and the scorecard checks whether you found it.

Sudden severe epigastric pain, now generalised: instantaneous onset with rapid spread across the abdomen is characteristic of a perforated viscus rather than colic.
Lies completely still; any movement worsens the pain: classic peritonism, contrasting with the restless patient of renal or mesenteric colic.
Months of grumbling epigastric indigestion beforehand: establishes pre-existing peptic ulcer disease as the source of the perforation.
Rising heart rate and falling blood pressure.
No back radiation and no relief sitting forward: argues against acute pancreatitis, which a modestly raised amylase might otherwise suggest.
No chest pain and no tearing pain to the back: weighs against inferior myocardial infarction and aortic catastrophe, the mimics that must be excluded.

Red flags you must not miss

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

Rising heart rate and falling blood pressure.
He has eaten and drunk nothing since the pain began and feels faint on sitting up.

Investigations and what they showed

Full blood count: Raised white cell count (neutrophilia); haemoglobin may fall if bleeding.
C-reactive protein: Raised. Why it helps: reflects the inflammatory/septic response to perforation and peritonitis.
Amylase: May be mildly raised, but not to the >3× upper-limit levels of acute pancreatitis. Why it helps: amylase can rise modestly in a perforation, so a mildly raised level must not be mistaken for pancreatitis; a very high level points to pancreatitis instead.
Urea and electrolytes: May show acute kidney injury/dehydration from third-space losses and sepsis.
Venous blood gas: A raised lactate with metabolic acidosis suggests hypoperfusion/sepsis.
X-ray erect chest for free air: Free AIR (a crescent of gas) beneath the diaphragm, pneumoperitoneum, indicating a perforated viscus.
CT abdomen and pelvis: G. duodenal/gastric wall defect) and surrounding inflammation.
Inspect the patient's posture and position: He lies absolutely still and flat on his back with his knees slightly drawn up and his hands off the abdomen. He will not roll over, will not sit forward, and asks you not to shake the bed. Why it helps: this is the single most discriminating bedside observation in the acute abdomen. Peritonitis makes any movement agony, so the patient freezes, the exact opposite of the writhing, cannot-get-comfortable patient with renal or biliary colic. Stillness plus a rigid abdomen is peritonitis until proven otherwise.
Inspect the abdomen: The abdomen is flat and held rigid, and it does not move at all with breathing. The abdominal wall is visibly tensed, 'board-like', and he tenses further as your hand approaches. Why it helps: an abdomen that does not move with respiration means generalised peritonitis. With a sudden-onset severe epigastric pain that spread across the whole abdomen, this is a perforated viscus and needs an erect chest X-ray and a surgeon now, not a period of observation.
Inspect the work of breathing: Rapid, shallow, entirely upper-chest breathing at about 24 a minute. He splints the diaphragm deliberately and refuses to take a deep breath or cough. Why it helps: shallow splinted breathing is a compensatory response to peritonitis, not primary lung disease, but it also contributes to the tachypnoea of metabolic acidosis from evolving sepsis, and it predicts postoperative atelectasis.
Inspect the patient's colour: He looks grey and peripherally shut down, with a cold clammy sweat beading on the forehead and upper lip and pale, mottled hands. Why it helps: with a heart rate of 116 and a blood pressure drifting down to 104/68, this is early shock from chemical peritonitis and evolving sepsis.
Inspect the patient's level of alertness and demeanour: Fully alert but frightened, guarded and speaking in short sentences, reluctant to be examined and visibly bracing before you touch him. Why it helps: A patient who looks this unwell and this apprehensive is a clinical alarm in itself; preserved alertness alongside shock is also reassuring against the profound obtundation of advanced septic shock, and it lets you consent him for theatre now.

Imaging findings

X-ray abdomen erect and supine: G. Rigler's sign) but is less sensitive than an erect CXR or CT.
ECG (bedside 12-lead): Normal 12 lead ECG sinus rhythm.

Why the diagnosis is perforated peptic ulcer

The decisive diagnosis is a perforated peptic ulcer, sudden, severe epigastric pain that becomes generalised, with a rigid 'board-like' abdomen (generalised peritonitis) and evolving sepsis/shock, on a background of dyspepsia and NSAID use (± smoking, H. pylori). 'Peptic ulcer disease' is the correct umbrella but misses the surgical emergency, free perforation with peritonitis. Confirm with an erect chest X-ray showing free air under the diaphragm (pneumoperitoneum) or, more sensitively, CT; a modestly raised amylase must not be mistaken for pancreatitis. pylori eradication and stopping the NSAID. The main mimics to exclude are acute pancreatitis, a ruptured abdominal aortic aneurysm, mesenteric ischaemia and an inferior myocardial infarction.

Perforated peptic ulcer at a glance

What it is

A perforated peptic ulcer is a full-thickness breach of the stomach or duodenal wall, usually at the site of an existing ulcer, that lets gastric or duodenal contents spill into the peritoneal cavity. It presents with sudden, severe epigastric pain that becomes generalised as peritonitis develops.

Pathogenesis

Acid, pepsin, NSAID use, or H. pylori infection erode progressively deeper into the stomach or duodenal wall until the ulcer breaches it completely. Gastric contents and air escape into the peritoneal cavity, causing chemical then bacterial peritonitis, generalised peritoneal irritation (a rigid, "board-like" abdomen), and rapidly evolving sepsis and shock if untreated. The patient classically lies very still, since any movement worsens the peritoneal pain.

Who it affects

Perforation complicates a minority of peptic ulcers, more often in older patients, NSAID users and smokers. It affects men more than women and is more common where H. pylori infection and NSAID use are prevalent.

Causes and risk factors

Background dyspepsia, NSAID use, smoking and H. pylori infection are the main risk factors, with the same factors that cause the underlying ulcer also predisposing to its perforation. Patients often lie very still, as movement worsens the peritoneal pain.

Investigations and lab tests

An erect chest x-ray showing free air under the diaphragm confirms pneumoperitoneum, though its absence does not exclude a perforation. CT abdomen is more sensitive and localises the perforation. Amylase can rise modestly with perforation, but a level over 3× the upper limit points to pancreatitis instead.

At a glance: First: erect CXR for free air. More sensitive: CT abdomen. Watch: lactate/acidosis for shock.

Teaching points

A perforated peptic ulcer causes sudden, severe epigastric pain that becomes generalised, with a rigid 'board-like' abdomen (generalised peritonitis) and evolving sepsis/shock.
Look for the background: dyspepsia, NSAID use, smoking and H. pylori, and the classic finding that the patient lies very still because movement worsens the pain.
Confirm with an erect chest X-ray showing free air under the diaphragm (pneumoperitoneum); CT is more sensitive and localises the perforation, but their absence does not fully exclude it.
Always exclude the catastrophic mimics: ruptured abdominal aortic aneurysm, mesenteric ischaemia and inferior myocardial infarction.
After recovery, eradicate Helicobacter pylori and stop the NSAID to prevent recurrence.
Perforation and bleeding are the two major ulcer complications, recognise which one you are dealing with (peritonitis vs haematemesis/melaena).

Practise a similar case

Reading a tidy write-up is one thing. Sitting with a patient, under a little time pressure, and teasing out that the pain was epigastric then suddenly became generalised while they lay completely still because movement made it worse, is another. Try a fresh surgical history next, without hints.

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.

Perforated peptic ulcer case presentation: history, findings and tests