Describe Complications of Peptic Ulcer Disease in detail.

The Concept

Peptic ulcers matter chiefly because of their complications, which may be the first presentation of a previously silent ulcer. There are four to know, and a simple way to remember them is that an ulcer can bleed, perforate, obstruct, or (if gastric) turn malignant. Each has a characteristic mechanism that explains its clinical picture.

Haemorrhage

Bleeding is the commonest complication. It is classically caused by a posterior duodenal ulcer eroding the gastroduodenal artery that lies behind it, producing brisk bleeding. The patient presents with haematemesis and/or melaena and may be shocked. Management is to resuscitate first (ABC, IV access, fluids/blood), then perform urgent endoscopy — which is both diagnostic and therapeutic (injection, clips or thermal coagulation) — with a PPI; surgery or angiographic embolisation is reserved for uncontrolled bleeding.

Perforation

Perforation is a dramatic surgical emergency, classically from an anterior duodenal ulcer that erodes through the wall, releasing gastroduodenal contents into the peritoneum. There is sudden, severe epigastric pain that rapidly becomes generalised (peritonitis), with a rigid, 'board-like' abdomen, absent bowel sounds and shock. An erect chest X-ray shows free gas under the diaphragm (pneumoperitoneum) in most cases. Treatment is resuscitation followed by surgery — closure with an omental (Graham) patch and peritoneal lavage — plus later H. Pylori eradication.

Gastric Outlet Obstruction

Chronic ulceration near the pylorus heals by fibrosis and scarring, which narrows the gastric outlet (cicatrising 'pyloric stenosis'). The stomach cannot empty, so there is projectile vomiting of large volumes of undigested, non-bile-stained food, a visible gastric peristalsis and a succussion splash, weight loss and dehydration. Persistent vomiting of gastric acid produces the classic hypochloraemic, hypokalaemic metabolic alkalosis. Treatment is to correct the fluid and electrolyte derangement, decompress the stomach with a nasogastric tube, and then relieve the obstruction (endoscopic balloon dilatation or surgery).

Malignant Change

A chronic gastric ulcer may harbour or develop into malignancy, which is why gastric ulcers are always biopsied and followed to healing. Duodenal ulcers do not become malignant.

Assessing the Bleeding Patient

Because upper GI haemorrhage is common and potentially fatal, its assessment is standardised. Resuscitation comes first (two large-bore cannulae, fluids and blood, correcting coagulopathy). Risk is scored — the Glasgow-Blatchford score before endoscopy (identifying who can be managed as an outpatient) and the Rockall score after, to predict rebleeding and mortality. Endoscopy within 24 hours is both diagnostic and therapeutic, and the appearance of the ulcer (the Forrest classification — active spurting, oozing, a visible vessel or a clean base) predicts rebleeding and guides whether endoscopic therapy is needed.

Principles Common to the Complications

Across all four complications the same principles apply: resuscitate before you investigate or operate, correct fluid and electrolyte derangement, and treat the underlying ulcer disease after the emergency is controlled (PPI, H. Pylori eradication, stopping NSAIDs). Modern management has become far less operative — most bleeding is controlled endoscopically and most obstruction is dilated or stented — but the surgeon must still recognise the patient who needs the operating theatre without delay, particularly in perforation and uncontrolled haemorrhage.

Recognising WHO Needs Theatre

The judgement that defines good surgical care here is recognising the patient who cannot be managed conservatively: a perforation with peritonitis, haemorrhage not controlled at endoscopy (or that rebleeds), and obstruction refractory to dilatation all require operation. Delay in these situations — persisting with medical measures while the patient deteriorates — is the classic error, so a low threshold for senior surgical review and intervention is essential in the complicated ulcer.

• Perforation: erect CXR shows free sub-diaphragmatic gas (~70%); treat by resuscitation + omental (Graham) patch.
• Bleeding: resuscitate → endoscopic haemostasis + PPI; posterior DU erodes the gastroduodenal artery.
• Gastric outlet obstruction → hypochloraemic hypokalaemic metabolic alkalosis; correct fluids/electrolytes first.

Posterior ulcers bleed; anterior ulcers perforate.

• Four complications: haemorrhage, perforation, gastric outlet obstruction, and (gastric) malignant change.
• Haemorrhage (commonest): posterior DU erodes gastroduodenal artery → haematemesis/melaena; resuscitate → endoscopic haemostasis + PPI.
• Perforation: anterior DU → sudden pain, board-like rigidity, gas under diaphragm → resuscitation + omental (Graham) patch.
• Gastric outlet obstruction: pyloric scarring → projectile non-bilious vomiting, succussion splash, hypochloraemic hypokalaemic metabolic alkalosis → correct electrolytes then relieve.
• Gastric ulcers may be malignant (biopsy); duodenal ulcers are not.