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Surgery - Peptic Ulcer Disease
Introduction
GI tract ulceration brought on by exposure to pepsin and stomach acid. mostly duodenum and stomach (may also develop in the oesophagus and Meckel's diverticulum).
Etiology
The cause is an imbalance between the mucosal defense systems and the harmful effects of pepsin and acid. Although there is a clear association with Helicobacter pylori infection, the exact mechanism by which the bacteria induces ulcer formation remains unknown.
NSAID use and H. pylori, which is linked to 95% of duodenal and 70–80% of stomach ulcers, are common.
Zollinger-Ellison syndrome (ZE) is uncommon.
Epidemiology
Typical. The incidence is roughly 1-4/1000 per year. more typical among men. The average age of gastric ulcers is in the fifties, but the average age of duodenal ulcers is in the thirties. The majority of cases of H. pylori are acquired during childhood, and the prevalence is approximately correlated with age.
History
Antacids: Provide relief from epigastric belly pain.
The link between symptoms and food varies: if they worsen shortly after eating, they are more likely to be gastric ulcers; if they worsen several hours later, they are more likely to be duodenal.
Complications (e.g., haematemesis, melaena) may manifest.
Examination
There might not be any tangible results.
soreness in the stomach area.
indications of problems (such as anemia or a succession splash in pyloric stenosis).
Investigational studies
Blood tests: clotting screen (if GI bleeding), amylase (to rule out pancreatitis), FBC (for anemia), LFT, cross-match if bleeding is occurring. If ZE is suspected, consider the secretin test: intravenous secretin elevates serum gastrin in ZE patients but not in controls.
Endoscopy: Duodenal ulcers do not require a biopsy; four quadrant stomach ulcer biopsies are necessary to rule out cancer.
According to Rockall scoring (see Gastrointestinal Haemorrhage, Upper), a GI bleeding's severity score indicates the prognosis: <3 indicates a positive prognosis; >8 indicates a high chance of death.
Test for H.pylori
The 13C-Urea breath test is used to test for H. pylori. Radiolabelled urea is administered orally, and 13C is found in the exhaled air.
Serology: H. pylori-specific IgG antibody; indicates exposure but not eradication.
stool antigen examination. Test for organisms similar to Campylobacter.
A pH indicator and urea substrate are used for the gastric biopsy. If H. pylori is present, the urea produces ammonia and the sample's color changes from yellow to red.
Biopsia histology: H. pylori is difficult to see, hence its usefulness is restricted.
Imaging: To look for signs of a perforation, set up a CT or CXR.
Management
Acute: Providing endoscopic or surgical treatment and resuscitation if bleeding or punctured.
Endoscopy: Electrocoagulation, laser, or injectable sclerotherapy hemostasis.
Surgical: If an ulcer is ruptured, it can be covered with an omental patch or oversewn. Suturing the damaged vessels (usually the gastroduodenal artery) stops the bleeding.
Trans-arterial embolization, vagotomy, and/or partial gastrectomy may be used in chronic situations where ulcer-related bleeding is uncontrollable.
Medical: "Triple therapy" to eradicate H. pylori for 1-2 weeks: It is advised to use one PPI/ranitidine bismuth sulphate and two antibiotics in different combinations (e.g. metronidazole ÷ tetracycline; clarithromycin ÷ amoxicillin).
PPIs or H2-antagonists can be used to treat if H. pylori is not involved. If you must use an NSAID, stop using them, especially diclofenac. Instead, try misoprostol, an analogue of prostaglandin E1.
Complications
Major complications, such as haematemesis, melaena, iron deficiency anemia, perforation, obstruction/pyloric stenosis (caused by scarring), and pancreatitis, occur at a rate of 1% annually.
Prognosis
Lifetime risk overall: 10%. Generally excellent since H. pylori-related peptic ulcers can be healed with removal.
Introduction
GI tract ulceration brought on by exposure to pepsin and stomach acid. mostly duodenum and stomach (may also develop in the oesophagus and Meckel's diverticulum).
Etiology
The cause is an imbalance between the mucosal defense systems and the harmful effects of pepsin and acid. Although there is a clear association with Helicobacter pylori infection, the exact mechanism by which the bacteria induces ulcer formation remains unknown.
NSAID use and H. pylori, which is linked to 95% of duodenal and 70–80% of stomach ulcers, are common.
Zollinger-Ellison syndrome (ZE) is uncommon.
Epidemiology
Typical. The incidence is roughly 1-4/1000 per year. more typical among men. The average age of gastric ulcers is in the fifties, but the average age of duodenal ulcers is in the thirties. The majority of cases of H. pylori are acquired during childhood, and the prevalence is approximately correlated with age.
History
Antacids: Provide relief from epigastric belly pain.
The link between symptoms and food varies: if they worsen shortly after eating, they are more likely to be gastric ulcers; if they worsen several hours later, they are more likely to be duodenal.
Complications (e.g., haematemesis, melaena) may manifest.
Examination
There might not be any tangible results.
soreness in the stomach area.
indications of problems (such as anemia or a succession splash in pyloric stenosis).
Investigational studies
Blood tests: clotting screen (if GI bleeding), amylase (to rule out pancreatitis), FBC (for anemia), LFT, cross-match if bleeding is occurring. If ZE is suspected, consider the secretin test: intravenous secretin elevates serum gastrin in ZE patients but not in controls.
Endoscopy: Duodenal ulcers do not require a biopsy; four quadrant stomach ulcer biopsies are necessary to rule out cancer.
According to Rockall scoring (see Gastrointestinal Haemorrhage, Upper), a GI bleeding's severity score indicates the prognosis: <3 indicates a positive prognosis; >8 indicates a high chance of death.
Test for H.pylori
The 13C-Urea breath test is used to test for H. pylori. Radiolabelled urea is administered orally, and 13C is found in the exhaled air.
Serology: H. pylori-specific IgG antibody; indicates exposure but not eradication.
stool antigen examination. Test for organisms similar to Campylobacter.
A pH indicator and urea substrate are used for the gastric biopsy. If H. pylori is present, the urea produces ammonia and the sample's color changes from yellow to red.
Biopsia histology: H. pylori is difficult to see, hence its usefulness is restricted.
Imaging: To look for signs of a perforation, set up a CT or CXR.
Management
Acute: Providing endoscopic or surgical treatment and resuscitation if bleeding or punctured.
Endoscopy: Electrocoagulation, laser, or injectable sclerotherapy hemostasis.
Surgical: If an ulcer is ruptured, it can be covered with an omental patch or oversewn. Suturing the damaged vessels (usually the gastroduodenal artery) stops the bleeding.
Trans-arterial embolization, vagotomy, and/or partial gastrectomy may be used in chronic situations where ulcer-related bleeding is uncontrollable.
Medical: "Triple therapy" to eradicate H. pylori for 1-2 weeks: It is advised to use one PPI/ranitidine bismuth sulphate and two antibiotics in different combinations (e.g. metronidazole ÷ tetracycline; clarithromycin ÷ amoxicillin).
PPIs or H2-antagonists can be used to treat if H. pylori is not involved. If you must use an NSAID, stop using them, especially diclofenac. Instead, try misoprostol, an analogue of prostaglandin E1.
Complications
Major complications, such as haematemesis, melaena, iron deficiency anemia, perforation, obstruction/pyloric stenosis (caused by scarring), and pancreatitis, occur at a rate of 1% annually.
Prognosis
Lifetime risk overall: 10%. Generally excellent since H. pylori-related peptic ulcers can be healed with removal.
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