Peptic ulcer

Selena Abboud

Outline Anatomy

Definition

Epidemiology

Pathophysiology

Etiology

Classification

Clinical manifestations

Diagnosis

Treatment

Complications

Blood supply: All parts of the stomach are supplied by the branches of the celiac trunk.

• The celiac trunk gives 3 major arteries; left gastric, splenic and common hepatic.

Left gastric artery lesser curvature

The splenic artery left gastroepiploic artery greater curvature

Terminal branches of the splenic artery short gastric arteries fundus of the stomach

Common hepatic artery gives two arteries before becoming the hepatic artery proper

1. right gastric artery (to the lesser curvature)

2. gastroduodenal artery gastroduodenal artery descends posteromedial to the second part of the duodenum and terminates as right gastroepiploic artery greater curvature

and the superior pancreaticoduodenal arteries.

Venous drainage of the stomach:

• Right and left gastric veins →Directly to the portal vein.

• Left gastroepiploic vein → splenic vein.

• Right gastroepiploic vein→ SMV.

Innervation :

• Anterior gastric wall → left vagus nerve.

• Posterior gastric wall→ right vagus nerve.

• Gastroduodenal pain is sensed via sympathetic afferents from T5 to T10

Physiology:

The major secretory cells of the stomach:

1. Parietal cells gastric acid

2. Chief cells pepsinogen

3. Goblet cells mucus cell

4. G-Cells gastrin

5. D cells somatostatin .

Definition

• Peptic ulcers are focal defects in the gastric or duodenal mucosa that extend into the submucosa or deeper.

• Acute or chronic

Epidemiology • Incidence 2%

• Cumulative prevalence 10%

• Peaking around (70 years)

• Incidence is decreasing due to :-

1. Discovery and eradication of H pylori

2. Better medical treatment

3. Improvement in the quality of life

4. More sanitation

5. More precaution in the use of NSAIDs and aspirin

Pathophysiology

• Peptic ulcer disease (PUD) is caused by an imbalance between mucosal defenses and acid/peptic injury.

Common sites for peptic ulcer :-

1- First part of the duodenum

2- Lesser curve of the stomach

3- Stoma after gastric surgery

4- Esophagus

5- Meckels diverticulum

Etiology

1- Helicobacter pylori

2- NSAIDS

3- Acid hypersecretion ( like zollinger Ellison syndrome)

4- Smoking , stress

Helicobacter pylori Infection

• With specialized flagella and a rich supply of urease.

• About 50% of the world’s population is infected with H. pylori (a major cause of chronic gastritis.)

• Has a role in gastric lymphoma

• Urease converts urea into ammonia and bicarbonate, creating an environment that buffers the acid secreted by the stomach.

• The ammonia is damaging to the surface epithelial cells

NSAIDs

• Chronic use of NSAIDs (including aspirin) increases the risk of peptic ulcer disease about 5-fold, upper GI bleeding about 4-fold and increases the complications.

• Duodenal 8%

• Gastric 40%

Smoking, stress and other factors

• Smokers vs non smokers.

• Smoking increases gastric acid secretion and duodenogastric reflux.

• Decreases prostaglandin production and bicarbonate production.

• The use of cocaine has been linked to juxtapyloric peptic ulcers with a propensity to perforate.

Zollinger Ellison syndrome •Gastric acid hyper secretion -> unregulated gastrin release from a non-ß cell endocrine tumor (gastrinoma).

• Incidence 0.1-1%

• Males > females

• Diagnosed between 30-50

• Gastrin stimulates acid secretion through gastrin receptors on parietal cells and by inducing histamine release from ECL cells.

• Pancreatic lipase is inactivated and bile acids are precipitated

• 90% in the pancreatic head or proximal duodenal wall

• Involves: the parathyroid glands (80-90%), pancreas (40-80%) and pituitary gland (30-60%).

• 80% are in gastrinoma triangle.

• Duodenal tumors constitute the most common nonpancreatic lesion, between 50-75% of gastrinomas.

•Less common extrapancreatic sites include stomach, bones, ovaries, heart, liver, and Iymph nodes.

• 60% are considered malignant

Clinical manifestations:-

•Peptic ulcers in unusual sites such as the post-bulbar duodenum, jejunum or oesophagus

•Poor response to standard ulcer therapy

•Bleeding and perforation are common

•Diarrhoea

•Steatorrhoea

•Abdominal pain

•Nausea and vomiting

•Weight loss and decreased appetite

Diagnosis

Biochemical test

1. Fasting gastrin levels <150 pg/mL.

2. pH <3

3. BAO > 15 meq/h in the presence of hypergastrinemia

4. BAO/MAO ratio >0.6

5. An increase in gastrin of <120 pg within 15 min of secretin injection

´ Imaging

An abdominal CT scan or MRI to exclude metastatic disease

Endoscopic ultrasound (EUS)

Gastric ulcer • Resource poor countries

• Older age

• Men = women

• Larger than duodenal ulcers

• Type I (near angularis incisura on the lesser curvature, close to the border between antral and corpus mucosa) / Normal or decreased acid secretion.

• Type II (associated with active or quiescent duodenal ulcer disease) / normal or increased gastric acid secretion

• Type III (Prepyloric) /normal or increased gastric acid secretion.

• Type IV ( near the GE junction) /acid secretion is normal or below normal.

• Type V (anywhere in the stomach) (medication induced) .

Duodenal ulcer

• Resource rich countries

• More common

• Men:Women (2:1)

• First part of the duodenum, most commonly anterior wall

• A chronic ulcer penetrates the mucosa into the muscle coat leading to fibrosis which can cause pyloric stenosis.

• Kissing ulcer : posterior and anterior duodenal ulcer present at the same time.

• Anterior : perforate

• Posterior : bleed

• Malignancy is uncommon

Clinical Manifestations • Sometimes asymptomatic

• Abdominal pain 90% , epigastric, no radiation, burning and gnawing in nature, intermittent.

• Relieved by food or antacid ingestion for duodenal ulcers.

• Exacerbated by food intake for gastric ulcers.

• Duodenal ulcer : (2/3 wake up from sleep due to pain).

• Gastric ulcer is less likely to awaken the patient at night.

• A history of PUD, use of NSAIDs, over-the-counter antacids or antisecretory drugs.

• Nausea

• Vomiting

• Bloating

• Weight loss

• Stool positive for occult blood, upper GI bleeding

• Anemia

Diagnosis

• Young patient with dyspepsia and/or

epigastric pain initiate empirical PPI therapy

for PUD without confirmatory testing.

1- Flexible upper endoscopy

• To confirm the diagnosis.

• All patients >= 45 years old with the above symptoms.

• If any alarm symptoms are present / rule out malignancy

1. Anemia

2. Loss of weight

3. Anorexia

4. Recent onset of progressive symptoms

5. Melena, Hematemesis

6. Swallowing difficulty

• After confirmation of an ulcer endoscopically or radiologically, investigate the cause

2- H. Pylori infection tests

➢ Non-invasive: Serological antibody tests, Urea breath test and Fecal antigen test.

➢ Invasive: Biopsy (gold standard) → to rule out malignancy, Culture and Urease test.

3- Fasting serum gastrin levels

• To rule out gastrinoma, zollinger Ellison syndrome.

• If there is no history of NSAIDs, with -ve H. pylori test.

• If a patient is experiencing recurrent ulcers despite medical treatment.

• If a patient has multiple ulcers or ulcers in unusual sites.

4- Biopsy for all gastric ulcers and any sites of gastritis to rule out H. pylori and for histologic evaluation.

5- Double-contrast upper GI X-ray

Oral contrast and barium

Medical treatment

• Helicobacter pylori eradication

• Stop NSAIDs then initiate anti-secretory Treatment.

• Smoking cessation

• Avoid alcohol

•Hospitalized patients : continuous IV infusion PPI

and Life long PPI when discharged

• Follow up with endoscopy to see if the ulcer recovered

• Acid suppression can be stopped after 3 months

if the ulcerogenic stimulus has been removed.

• Sucralfate acts locally on mucosal defects,

is well tolerated and useful as a supplement

to acid suppression.

Surgical treatment

Indications For surgery:

1. Non-healing ulcers/ intractable.

2. Perforated Ulcers.

3. Bleeding Ulcers.

4. Gastric outlet obstruction.

5. Malignant Ulcers

Principles of Surgical treatment:

1. Reduce gastric acid secretion by cutting the parasympathetic stimulation (vagus nerve) through surgical vagotomy.

2. In Vagotomy, the higher level you cut the vagus nerve, the more you paralyze the stomach (especially the antrum) and delay gastric emptying.

So in Truncal Vagotomy, it’s mandatory to perform a drainage procedure; pyloroplasty, antrectomy, or gastrojejunostomy.

1- Highly selective vagotomy (HSV) / parietal cell / proximal

• Lowest postoperative morbidity (3% to 8%) and mortality rates.

• Most satisfactory operation, but demanding.

• Transection of the vagal fibers to the body of the stomach without interruption of fibers to the pylorus.

• Advantages: we don’t remove any part of the stomach, we don’t interfere with the process of emptying (no need for drainage procedure).

• Side effects: loss of receptive relaxation of the stomach leading to epigastric fullness and sometimes mild dumping.

• Higher recurrence rates (5% to 15%)

2- Selective Vagotomy ( total gastric ): We cut the nerve supply to the whole stomach, except the hepatobiliary and celiac branches.

3- Truncal vagotomy: The vagus in nerve is cut (perform a drainage procedure).

a) Truncal vagotomy with pyloroplasty

• Reduces the maximal acid output by 50%.

• Because the vagal nerves are motor to the stomach, denervation of the antropyloroduodenal segment results in gastric stasis.

• The most popular drainage procedure is the Heineke–Mikulicz pyloroplasty (simple, involves the longitudinal section of the pyloric ring).

• The incision is closed transversely.

b) Truncal Vagotomy with antrectomy and anastomosis

• Transection of the vagus nerve trunk, then the distal 40% of the stomach is removed and anastomosed with the duodenum Billroth I (gastroduodenostomy) or jejunum Billroth II (gastrojejunostomy).

• Recurrence rate (1% to 2%)

• Postoperative morbidity rate (15% to 30%)

• Mortality rate (1% to 2%)

Gastric ulcers:

1. Wedge excision

2. Antrectomy with inclusion of the ulcer

Concurrent acid-reducing operation is reserved for acid hypersecreting patients (type II and III) or refractory ulcer despite maximal medical management.

Complications of surgery

1- Recurrent ulceration

• Easiest problem

• Heal with potent antisecretory agents

• Gastrojejunal colic fistula: the anastomotic ulcer penetrates into the transverse colon causing severe diarrhea after every meal, foul breath, vomit formed faeces, severe weight loss and dehydration

Mistaken for malignancy.

Nutritional disturbance from contamination of the jejunum with colonic bacteria.

CT with oral contrast or barium enema.

Endoscopy isn’t useful in half of such cases

Treatment : rehydration and nutrition and then performing revisional surgery.

2- Bile vomiting

• Abdominal pain and reflux symptoms after eating.

• Bile chelating agents are usually ineffective.

• In intractable cases, revisional surgery may be indicated.

• Following gastrectomy, roux-en-y diversion is the best treatment.

• In patients with a gastroenterostomy this can be taken down and a small pyloroplasty can be performed.

• In patients with a pyloroplasty, reconstruction of the pylorus has been attempted (poor results)

• Antrectomy and Roux-en-Y reconstruction is the best option.

3- Early and late dumping ( early rapid gastric emptying).

4- Post-vagotomy diarrhea

5- Malignant transformation

•The lag phase between operation and the development of malignancy is at least 10 years.

• Highly selective vagotomy is not associated with an increased incidence of gastric cancer in the long term.

6- Nutritional consequences

Small meals are often more useful.

Anaemia due to iron or vitamin b12 deficiency.

7- Gallstones

8- Small stomach syndrome

Early satiety (there is loss of receptive relaxation), gets better.

Complications of peptic ulcer disease

1- Bleeding (mortality rate 5-10%)

• Presentation: melena and/or hematemesis.

• Abdominal pain is uncommon.

• Shock

• Nasogastric aspiration confirms upper GI bleeding.

• Spontaneous cessation 70% ( if given acid suppression and nothing by mouth.)

• 25% will continue to bleed or rebleed after an initial quiescent period (mortalities and operations occur in this group).

• admit the patient

•Aggressive resuscitation… abcde

•Iv flud

•PPI infusion

• NPO

• Nasogastric tube

• Correction of any coagulopathy

• EGD

Endoscopic therapy using thermal coagulation/ electrocautery +- epinephrine for hemodynamic instability, need for continuous transfusion, hematemesis or red stool, older than 60 years, and with comorbidities because these patients have a higher risk of recurrent bleeding.

• Exposed vessel: mechanical hemostasis using a clip.

• Indications for surgery : age > 60 years, shock, those requiring more than four units of blood in 24 hours or eight units of blood in 48 hours, rebleeding, more than one unsuccessful endoscopic intervention and those with ulcers >2 cm in diameter.

• Bleeding duodenal ulcers (posterior duodenal wall within 2 cm of the pylorus) erode into the gastroduodenal artery and (lesser curvature) erode left gastric artery.

• Bleeding is controlled by duodenotomy and three-point ligation of the bleeding vessels.

• Postoperative H. pylori eradication is important to reduce the risk of recurrence.

• Bleeding gastric ulcers : biopsy followed by oversewing or wedge excision of the ulcer is generally preferred.

2- perforation

• Severe sudden abdominal pain.

• Chemical peritonitis develops from the gastric and/or duodenal secretions but within hours a bacterial peritonitis supervenes.

• Generalized peritonitis (localized when the perforation is walled off by adjacent viscera and structures).

• Examination: fever, tachycardia, guarding and board like rigidity, decreased bowel sounds.

• Laboratory evaluation: leukocytosis and maybe high amylase.

• Chest X-ray / upright: free sub diaphragmatic air (80% to 85%)

• Amit the patient

•Aggressive fluid resuscitation (isotonic)

• Analgesia

• Broad-spectrum antibiotics

• NPO and Nasogastric tube

•Foley catheter

• Operation

• Sometimes the perforation has sealed spontaneously by the time of presentation and surgery can be avoided if the patient is doing well.

• Non-operative treatment : poor operative candidates (perforation present for more than 24 hours, localized pain, no evidence of ongoing extravasation on upper GI water-soluble contrast studies, leak has sealed and in the absence of clinical peritonitis.

• Perforated duodenal ulcers : simple omental patching and peritoneal debridement followed by H. pylori eradication.

• Perforated gastric ulcers: simple wedge resection to eliminate the perforation and exclude malignancy.

If cannot be performed due to its juxtapyloric location, multiple biopsies are taken and omental patching is performed

3- Gastric outlet obstruction 5%

• Due to duodenal or prepyloric ulcer disease.

• Acute or chronic.

• Present with nonbilious recurrent vomiting of poorly digested food, profound hypokalemic hypochloremic metabolic alkalosis. ( like pyloric stenosis)

• Pain or discomfort is common.

• Weight loss depending on the duration of symptoms.

• Succussion splash may be audible with stethoscope placed in the epigastrium.

• The diagnosis is confirmed by endoscopy.

• Admission

• Correction of volume and electrolyte abnormalities

• Nasogastric suction (NG tube)

• Intravenous antisecretory agents

• EGD for evaluating the nature of the obstruction and for ruling out malignancy (pancreatic, gastric, or duodenal)

• Endoscopic hydrostatic balloon dilation

This is feasible in up to 85% of patients but fewer than 40% have sustained improvement at 3 months

• The standard operation for obstructing PUD is vagotomy and antrectomy.

4- Intractable or Nonhealing Peptic Ulcer

• Noncompliant patient (not taking prescribed PPI, still taking NSAIDs, still smoking).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4714294/

• Current interest in probiotic effectiveness against H. pylori and its activity in reducing bacterial colonization and decreasing gastric inflammation have been stimulated because it provides a large-scale and low-cost alternate solution to prevent or decrease H. pylori colonization.

• Photodynamic therapy and vaccine are still in the experimental phase

Thank you