This is a case presentation of Perforated Duodenal Ulceration seen in a 43 yr old man followed by some background, discussion and suggestions for further reading.

Case Report
Mr CC - Perforated Peptic Ulcer

Presenting Complaint

A 43 year old male presents to Accident and Emergency at midnight with severe upper abdominal pain.

History of Presenting Complaint

• At 5.30 pm Mr CC developed a sudden onset of severe upper abdominal pain that was constant with no radiation. He described no nausea or vomiting.
• For the previous two days he had experienced vague symptoms of heartburn and upper abdominal discomfort.
• There was no change in bowel habit and no malaena. He had not felt feverish.

Past Medical History

Mr CC’s GP had diagnosed a peptic ulcer 3 years previously. This had been confirmed with a barium study. He had never had an OGD.

Social History

Mr CC returned from a holiday in the Caribbean one week previously where he confessed to some binge drinking. He is a smoker with a twenty pack year history.

On Examination

Pulse 92, BP 117/63, Temp 37.0 94% on air
In obvious distress.
Pale, clammy.

Abdomen: distended, rigid upper abdomen, with absent bowel sounds.

Bloods

Aterial Blood Gas

Note: There is no sub-diaphragmatic air on the admission CXR.

Immediate Management

MR CC was resuscitated and admitted to hospital.
A clinical diagnosis of perforated duodenal ulcer was made.
His case was discussed with the consultant General Surgeon on call.
A urinary catheter was inserted, IV fluid was commenced and regular analgesia was administered. He was placed under hourly observations.

Further Management

The following morning the patient was reviewed and had not improved.
An urgent CT scan was performed.

This was reported as follows:
Within the abdomen there is a large amount of fluid around the right liver lobe. There is free gas within the abdomen as well as free fluids. There is also a small amount of air within the lesser sac suggesting a perforated ulcer.
There is a bilateral pleural effusion and atelectasis of the basal part of both lungs.

Operative Management

The patient was urgently transferred to theatre.

An upper midline incision was made. There was seropurulent fluid in the peritoneal cavity. A perforated Duodenal Ulcer was identified on the D1 anterior surface.
An omental flap was mobilised and the perforation was over sewn with an omental patch.
The patient was washed out in all four quadrants.

PDS loop was used for mass closure.

Post operatively

The patient was transferred to HDU. He received 5 days of Cefuroxime and Metronidazole IV.
Three days post operatively he developed a right sided pneumonia, from which he made an uneventful recovery with the aid of physiotherapy.
Oral intake was commenced three days post operatively and increased as tolerated.
The patient was discharged home nine days post operatively.

Discussion

Peptic ulceration:
Definition
A peptic ulcer is a break in the epithelial surface of the oesophagus, stomach or duodenum caused by the action of gastric secretions and in the case of duodenal ulcers, H. pylori.

Epidemiology:
0.8% of the population per year develop a duodenal ulcer
0.2% of the population per year develop a gastric ulcer.
Worldwide the incidence is increasing but decreasing in developed countries.
The peak age for duodenal ulceration is increasing (35-45 years)
Gastric ulceration occurs in older age groups.

Aetiology:
Peptic ulcers are caused by the action of gastric acid and pepsin on the mucosa of the gastrointestinal tract.

Predisposing factors:

H. pylori infection:
A gram negative spiral microaerophilic bacillus specific for human gastric mucosa. It produces urease creating an alkaline microenvironment. It is probably causative in duodenal ulcer and may be associated with gastric ulceration.

Chemicals:
NSAIDs, Alcohol, Cigarettes

Associated diseases:
Alcoholic cirrhosis, chronic renal failure COPD and hyperparathyroidism all act to increase serum calcium which promotes gastrin secretion.

Familial:
There is a familial predisposition. Duodenal ulcers are also more common in HLA B5 and blood group O patients.

Gastrin Hypersecretion:
Zollinger Ellison Syndrome

Pathology:

80% solitary
80% in duodenum
90% in the first part of the duodenum on the anterior surface within a few centimetres of the pyloric ring
19% in Stomach usually in the lesser curvature of the body.

Clinical Features:

Duodenal ulcers and type II gastric ulcers (prepyloric and antral)
• Male: Female 4:1
• Epigstric pain during fasting relieved by food and antacids
• Boring back pain if ulcer is penetrating posteriorly.
• Haematemesis from ulcer penetrating gastro duodenal artery posteriorly
• Peritonitis if perforation
• Vomiting if gastric outlet obstruction occurs.

Type I gastric ulcer (i.e. body of stomach)
• Male :Female 3:1 peak incidence 50+ years
• Epigastric pain induced by eating
• Weight loss
• Nausea and vomiting
• Anaemia from chronic blood loss

Investigations

Endoscopy:
The gold standard. This is essential to exclude malignancy in:
• Patients > 45 at first presentation
• Concomitant anaemia
• Short history of anaemia

At least six biopsies should be taken from any ulcer seen. Clo (campylobacter like organism) test can be performed to test for H pylori.

Barium Meal
Can be used for patients unable to tolerate OGD

Tests for H pylori
• Blood can be tested for antibodies
• Urea breath test
• Biopsy of mucosa