Open access peer-reviewed chapter

Peptic Ulcer Disease

Written By

Carlos A. Casalnuovo, Pedro A. Brégoli, Cesar J. Valdivieso Duarte and Carlos A. Vera Cedeño

Submitted: 09 December 2021 Reviewed: 09 February 2022 Published: 25 August 2022

DOI: 10.5772/intechopen.103150

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Peptic Ulcer Disease - What's New?

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Peptic ulcer disease, including duodenal and gastric ulcers, is associated with potentially life-threatening complications, including bleeding, perforation, and gastric outlet obstruction. Stomach lesions are located preferentially along the small curvature in the transition zone between the body and the antrum; in the duodenum those lesions are located in the duodenal bulb, where posterior lesions are usually associated with hemorrhage and the anterior ones with perforation. Peptic ulcer disease affects approximately 5–10% of the population worldwide and represents an important cost for public health. Peptic ulcers pathogenesis is complex and involves multifactorial processes, which basically occurs by an imbalance between aggressive and defensive factors of the gastric mucosa. Gastric mucosa is continuously exposed to harmful substances and factors, whether endogenous (acid secretion, peptic activity, and biliary secretion) or exogenous (Helicobacter pylori infection, alcohol abuse, smoking habit, and nonsteroidal anti-inflammatory drugs (NSAIDs)) and stressful life habits.


  • peptic ulcer disease
  • bleeding
  • perforation
  • gastric outlet obstruction
  • gastric ulcer complications

1. Introduction

Peptic ulcer disease (PUD) is common with a lifetime prevalence in the general population of 5–10% and an incidence of 0.1–0.3% per year. Peptic ulceration occurs due to acid peptic damage to the gastroduodenal mucosa, resulting in mucosal erosion that exposes the underlying tissues to the digestive action of gastroduodenal secretions. This pathology was traditionally related to a hypersecretory acid environment, dietary factors, and stress. However, the increasing incidence of the Helicobacter pylori infection, the extensive use of NSAIDs, and the increase in alcohol and smoking abuse have changed the epidemiology of this disease. Despite a sharp reduction in incidence and rates of hospital admission and mortality over the past 30 years, complications are still encountered in 10–20% of these patients. Complications of peptic ulcer disease include perforation and bleeding, and improvement in medical management has made obstruction from chronic fibrotic disease a rare event [1].


2. Bleeding

Bleeding is a common complication and the leading cause of death from peptic ulcer. Requiring endoscopic therapy in the onset of bleeding, rebleeding and multiple comorbidities are predictive of mortality. Treatment often requires the participation of a multidisciplinary team.

2.1 Definition

Upper gastrointestinal bleedings (UGBs) are those originating proximal to Treitz angle, including diseases of the esophagus, stomach, duodenum, and those generating haemobilia, such as tumors or trauma of the liver, bile duct, and pancreas. Approximately 20% of peptic ulcers have an episode of bleeding, and 25–30% of them repeat it.

2.2 Pathophysiology

The wall of the stomach has a complex irrigation. By eroding the wall, peptic ulcers may injure a large vessel causing bleeding; once it starts, gastric acid becomes more harmful because a pH of 6 or below diminishes platelet aggregation and clots get unstable. In the duodenum, irrigation comes from the gastroduodenal and pancreaticoduodenal arteries, which are larger in the posterior wall, and that’s why the majority of hemorrhage complications are related to posterior wall duodenal ulcers. Loss of intravascular volume leads to shock, the severity of which is determined primarily by the amount, speed, and body’s ability to compensate blood lost. Hypovolemia causes a reduction in tissue perfusion. The first compensation phenomena are the release of catecholamines that generate vasoconstriction.

2.3 Clinical presentation

The initial management is essential. Based on the grade of hypovolemia, the patient may be hemodynamically compensated or need an urgent transfusion. Treatment depends on patient’s general condition after bleeding onset. Clinical presentation may be oligosymptomatic, with or without history of PUD symptoms, and without rebleeding it would whether go unnoticed or be diagnosed in a follow-up check, usually by anemia; it would also be presented as a complication in the evolution of a previously diagnosticated peptic ulcer. Almost 30% of ulcers begin their clinical manifestations with bleeding.

Bleeding can also be classified based on the percentage of blood lost, into:

MILD, if the loss is less than 10% of the total blood volume.

MODERATE, when it is 10 to 20%.

SEVERE, with a loss of more than 20% of the total blood volume.

There is also another classification according to the volume lost and the consequent management (Table 1).

mlBlood volume (%)Treatment
III1500–200030–40Fluids + blood
IV>2000>40Fluids + blood

Table 1.

Hypovolemic classification.

Taking the history of the patient should identify those patients with systemic diseases that may predispose or promote bleeding such as gastric or duodenal pathology, liver disease that predisposes to coagulopathies, portal hypertension, stress situations, and use of NSAIDs or anticoagulants.

2.3.1 Signs and symptoms

Hematemesis is usually absent in mild bleeding, while melena (tarry stools) is evident with 50–100 ml of blood. The presence or absence of hematochezia depends on the bleeding rate and the speed of bowel transit. The paleness of the skin and mucous membranes depends on the degree of anemia, while orthostatism is one of the first symptoms of hypovolemia.

2.4 Diagnosis

In cases with doubts, a nasogastric tube may show traces of blood or active bleeding, with a 10% of false-negatives.

2.4.1 Physical examination

As bleeding progresses, tachycardia, arterial hypotension, tachypnea, oliguria, poor peripheral perfusion, Glasgow deterioration, and shock appear. Digital rectal exam can evaluate rectal content and differentiate between melena and red blood.

2.4.2 Laboratory

Hematocrit: In acute bleeding and the first hours, it is practically not modified then it is more useful for the replacement of the blood volume lost and control for eventually rebleeding scenario. Anemia without signs of hypovolemia suggests slow bleeding (chronic anemia). In UGB, the elevation of urea in the blood is very common, without being part of diagnostic criteria.

2.4.3 Endoscopy

It is the main diagnostic procedure with an efficiency of 80 to 90%. It has three goals: to make a diagnosis, to stop bleeding, and to assess the risk of rebleeding.

Endoscopy should not be deferred. It evaluates:

  1. Topographic diagnosis. Location of the bleeding lesion (esophagus, stomach, or duodenum) and other possible lesions. Endoscopy is essential due to the possibility of treatment, since bleeding endoscopic treatment may avoid gastrotomies or duodenotomies.

  2. Etiological diagnosis. Both tactics and opportunity change depending on the cause and pace of bleeding.

  3. Evaluation of the “Type of Bleeding”. Forrest et al. [2] (Table 2) described the characteristics of bleeding lesions, to unify diagnostic and prognostic criteria.

  4. Application of a therapeutic procedure (Figures 14).

Forrest classificationRebleeding (%)
I. Active bleedingIa. Spurting hemorrhage (Figure 1)90–100
Ib. Oozing hemorrhage (Figure 2)80–85
II. Signs of recent bleedingIIa. Non-bleeding visible vessel (Figure 3)40–45
IIb. Adherent clot on lesion (Figure 4)20–30
IIc. Hematin-covered lesion5
III. Lesion without bleeding<3

Table 2.

Forrest classification.

Figure 1.

Spurting hemorrhage.

Figure 2.

Oozing hemorrhage.

Figure 3.

Non-bleeding visible vessel.

Figure 4.

Adherent clot on lesion.

Other options of exceptional need, given the persistence of bleeding without endoscopic findings, are:

2.4.4 Selective arteriography

Sensitivity depends on the bleeding extent and the operator. Lesions such as tumors or vascular malformations can be detected even if they are not bleeding at the time of the study. Arteriography could also be therapeutic by the possibility of eventual embolization, making this technique analog to endoscopy (diagnostic and therapeutic). Topographically locates the bleeding area if there is a loss greater than 0.5 cc/minute.

2.4.5 99mTc-labeled red cell scintigraphy

A technetium Tc 99m-labeled red cell scan is another diagnostic resource with specific indications and may be helpful in localizing the source of bleeding, although with brisk bleeding the time required for the scan is problematic and urgent surgical intervention may be more expeditious. Topographically locates the bleeding area if there is a loss greater than 0.2 cc/minute.

2.5 Natural evolution

It is estimated that more than 70% of UGB by peptic ulcer respond to medical treatment. Adding endoscopic to medical treatments, the bleeding control reach 90%. Rebleeding is a proven prognostic factor. With an effective endoscopic procedure, it is only seen in 10% of those under 60 years old and in 15–20% of those over 60 years. The worst scenario of rebleeding is when the endoscopic treatments are already exhausted and the patient remains with hypovolemia, and increasingly in worse conditions which usually contraindicates getting the patient to the operation room. Between 5 and 10%, they are discharged without etiological diagnosis.

2.6 Treatment

2.6.1 Medical treatment

After initial evaluation of the patient, fluid resuscitation may be achieved by canalizing two peripheric veins with 14 Fr catheters. Due to persistence of hypovolemia (hypotension) without response to fluid resuscitation, blood transfusion is mandatory. Hypovolemic shock would require the placement of a central venous catheter that measures venous pressure, or Swan-Ganz catheter placement to measure the pressure in the pulmonary artery when the shock is severe. Simultaneously and according to severity, a mechanical ventilation is evaluated in order to achieve integral life support management.

Catheterization of the bladder is to control urine output. A nasogastric tube is useful if there is Glasgow deterioration, to prevent regurgitation of gastric contents to the airway. It can also evaluate bleeding; aspiration favors an eventual endoscopy.

A gastric pH > 6 is ideal to decrease the risk of rebleeding. In 95% of cases, it is achieved with proton pump inhibitors (PPIs) in intravenous doses of 40–80 mg/day.

2.6.2 Endoscopic treatment

Until the mid-80s, endoscopy was only diagnostic. Nowadays, it is very common to attempt for endoscopic hemostasia before indicating surgical treatment.

The most accepted technique is the adrenaline or epinephrine 1:10,000 injection, and better results would be obtained if sclerosing agents such as ethanolamine oleate, human thrombin, or cauterization are added. Other methods such as bipolar electrocautery (Figure 5), laser (Figures 6 and 7), elastic bands, or hemo-clips are effective but require more training and specific equipment. Currently, endoscopic treatments are effective in more than 90% of cases.

Figure 5.


Figure 6.

Figure 7.

Endoscopic electrocoagulation of an active bleeding.

Hemostasis in lesions with pulsatile bleeding have more than a 50% chance of rebleeding, but it also facilitates hemodynamic stabilization until surgical intervention. In those with a visible vessel without active bleeding, the incidence of rebleeding is 40–50%, while lesions with a clot adhered rebleeding rate is estimated around 20–30%, so a second endoscopic treatment is suggested at 48 h.

2.7 Rebleeding

It is defined as a new episode of hematemesis and/or melena, associated with signs of hypovolemia or anemia. This must be confirmed by endoscopy. The risk of rebleeding depends on several factors, such as, massive UGB, persistence of hemodynamic instability, delay endoscopic treatment, larger size of the ulcer, those having a visible vessel or a clot attached, even without active bleeding and posterior duodenal ulcers.

After endoscopic treatment, administration of proton pump inhibitors decreases rebleeding risk.

2.8 Surgical treatment

Modern medical and endoscopic treatments have decreased the frequency of operations for upper gastrointestinal bleeding.

Surgical indication:

The criteria or guides that stand out are:

  1. Magnitude of bleeding

    Hypovolemic shock has a “period of reversibility,” so if hemodynamic stability is not achieved, an operation should be chosen.

    According to this criterion, surgery is indicated when bleeding requires more than five blood units in the first 24 h.

  2. Persistence of bleeding

    Between 5 and 10% of patients with UGB keep bleeding once the initial hypovolemia is controlled and even after medical and endoscopic treatments.

    With these criteria, the operation is indicated when there is a daily requirement of two blood units, for 4 days or more.

  3. Rebleeding

    It occurs between 10 and 30% of the hemorrhages already treated. It is recommended that patients at high risk of rebleeding should have a new evaluation in the following 2 or 3 days. In the face of new bleeding, the surgical indication is urgent, because treatment alternatives are exhausted, the failure of a new endoscopic procedure is very high, and the patient deteriorates rapidly.

Surgical tactics:

The main objectives of the operation are:

  1. Control of bleeding

  2. The cure of ulcerative disease, if feasible, but is not the main objective. Maintaining postoperative PPI therapy is mandatory.

In the plan matters patient general condition, the history of the PUD, its location, the operative risk, and the experience of the surgical team.

2.8.1 Gastric ulcer (GU)

Surgeons have two options:

  1. Hemostatic suture

    It is the first option because of its simplicity and results and is indicated also in patients who had not received right medical treatment. The hemostatic suture consists of making deep suture throughout the extension of the ulcer, with nonabsorbable material or very slow absorption and using semicircular and strong needles, due to sclerosis of the peri-ulcerous tissue.

  2. Gastrectomy

    It is feasible in compensated patients. As the most frequent gastric ulcers are in the middle and distal thirds, the most used operations are antrectomies and hemigastrectomies, trying to avoid subtotal resections. The need for a total gastrectomy for PUD is exceptional. When the procedure does not include resection of the ulcer, biopsies should be taken before hemostasia, for the chance of having a bleeding carcinoma.

2.8.2 Duodenal ulcer (DU)

There are several options.

  1. Hemostatic suture (Figure 8): currently, it is the most used technique in non-compensated and compensated patients. Because PPIs and H. pylori eradication cure more than 90% of DU, hemostatic suture and medical treatment from the immediate postoperative period have goods results and lowers risks. The technique of hemostasia is like in GU, adding an important difference in posterior wall ulcers due to their proximity to the bile duct. Another complementary option is the external ligation of the vessel that irrigates the anatomic portion where the ulcer is located.

  2. Hemostasia and vagotomy with gastric drainage: in compensated patients and with chronic ulcer disease, adding a vagotomy with drainage to the hemostatic suture is a physio-pathologically correct criterion, but less used today. The reduction in acid secretion achieved with vagotomy is lower or the same in some cases as with proton pump inhibitors.

Figure 8.

Longitudinally pyloro-duodenotomy and posterior defect transversal closure (pyloroplasty).

2.9 Mortality

Mortality in patients admitted to hospital with UGB ranges between 5 and 10%, while in intensive care units, when there is bleeding as a complication of another serious disease, it can exceed 25%.


3. Perforated peptic ulcers

Perforations begin penetrating the layers of the viscera until they open freely in the peritoneum or are blocked by neighboring tissues or organs. They occur between 2 and 10% of patients with PU.

Perforation is a frequent cause of acute abdomen. The perforation causes the leak of chlorohydric acid in to the peritoneum, constituting over time in to septic shock.

3.1 Diagnosis

3.1.1 History

In 70% of those perforated, there is a history of ulcerative disease or a known diagnosis of GU or DU. The remaining 30% is divided between those who are perforated without previous symptoms and those who present symptoms of PU a few weeks before perforation. The pain of the perforation is very intense, with an abrupt beginning and mid-abdominal predominance. Then it becomes continuous and spreads to the rest of the abdomen with propagation to the chest and shoulders. The intensity of the pain causes sweating, paleness, and superficial breathing. Peritoneal irritation causes an antalgic position to be adopted with the thighs flexed over the abdomen.

With time, fever, arterial hypotension, ileus, and oliguria are added, and eventually if not treated achieving systemic failure.

3.1.2 Physical examination

Paleness of the skin and mucous membranes, tachycardia, and hypotension are common findings. When peritonitis is already installed, the patient is still and does not try to move. In the palpation of the abdomen, there is muscle contracture, (rigid abdomen) defense, and pain to decompression (Blumberg sign). The disappearance of hepatic dullness to percussion is a classical semiological maneuver (Jobert’s sign), which must be followed by radiological studies. It means the interposition of air between the liver and the abdominal wall (Popper’s sign).

Perforated ulcers are a constant surgical pathology at pace with advances in the medical treatment of peptic ulcer disease.

In 1987, Boey and Wong [3] scientifically analyzed several risk factors to conclude that mortality significantly increased

  1. when there was preoperative shock;

  2. when there were serious associated diseases; and

  3. when treatment was started more than 24 h after perforation (most studies had used a 12-h parameter). Diffuse peritoneal contamination aged over 60 years and less than 3 months of ulcerative history had no value as isolated factors, but when they were associated with others.

The analysis of 613 perforations in Hong Kong recorded only 22.2% with one or more of the three main risk factors, which influenced the low overall mortality of 4.7%.

In 1989, we applied several risk factors to a retrospective series of 105 perforated at the “Hospital de Clinicas” [4]. Ninety-two percent had one or more of the following factors: (a) onset time of more than 12 h; (b) concomitance of associated serious diseases; (c) over 60 years of age, which led to a mortality of 26.7%. The first factor is related to the delay in treatment (58.1% had more than 12 h of perforation). Sometimes, the blame lays with the patient and their family members, but other times it is due to failures of primary medical care.

In our series, 33.3% were over the age of 60 years and 28.6% received corticosteroids or NSAID, figures similar to those of Watkins et al. [5].

When we evaluated patients without risk factors, mortality decreased significantly similar to Boey’s [3].

The preoperative shock is associated with a misdiagnosis, late diagnosis, or medical mismanagement; therefore, its reduction depends on medical education.

In terms of diagnosis, experience plays a leading role, and the health organization of many countries means that care services are composed of doctors in training.

3.1.3 Imaging

A simple chest X-ray with visualization of the diaphragmatic domes shows pneumoperitoneum in 65–70% of perforated patients (Popper’s sign) (Figure 9).

Figure 9.

Frontal chest X-ray. The air bubble below the right hemidiaphragm (on the left of the image) is a pneumoperitoneum.

When radiology does not show air in the cavity, it does not invalidate the clinical diagnosis.

If the patient has been perforating for a while and the hemodynamic conditions of the patient make it impossible for him to stand up, a chest X-ray can be performed with the lateral position and the patient in the left lateral decubitus position in order to visualize air between the liver and the chest wall.

When is not found, it may be due to the immediate blockage of perforation by the omentum. It is more frequent in the elderly.

Because pneumoperitoneum is not objectifiable in 30–35% of those perforated, an alternative is pneumogastrophagy, which consists of injecting air into the stomach through the nasogastric tube. In this way, a pneumoperitoneum could become visible and have a more accurate diagnosis, reducing to one-third the time between perforation and surgery and therefore also decreasing mortality to one-third (K. Maull [6]).

3.2 Treatment

The initial management in the perforated PU is the usual performed on every visceral perforation.

Urgent hospitalization in a center with possibilities of laboratory, images, intensive care unit, and eventual surgery. Replacement of fluids with crystalloids and administration of analgesics. Nasogastric tube to reduce the effusion of gastroduodenal contents to the peritoneum and to evacuate the stomach before a possible emergency surgery. Antibiotics since the diagnosis is made. In case of shock, the placement of a central line, bladder catheter and hospitalization in an intensive care unit, antibiotics, continuous gastric aspiration, and PPIs are added, since the diagnosis of perforation is confirmed.

3.2.1 Surgical treatment

As a fact, every perforation is a surgical treatment emergency with three objectives: closure of the perforation, washing the cavity, and culture of the peritoneal fluid. The classic procedure for closing the perforation is by laparoscopy or laparotomy, making trans-parietal points with resorbable material and omentoplasty if feasible (Graham technique). In the GU, biopsy of the edges is done due to the eventuality of a perforation related to malignancy, but it is also done in the DU to identify HP infection. Laparoscopic treatment is the gold standard [7], and laparotomy is reserved for those patients with general contraindications for laparoscopy as it happens with patients on established shock.

The conversion from laparoscopy to laparotomy rate varies between 0% and 29%, being higher in patients who underwent surgery in shock. Postoperative

The nasogastric tube should remain until intestinal peristalsis is reestablish. The administration of proton pump inhibitors, first intravenous, and then oral should continue until the healing of the ulcer. The presence or absence of H. Pylori is controlled by endoscopy.

At present time with the progress of medical treatment, practically only simple closure of the ulcer is performed [8]. The simple closure is a short and simple operation, and it is available to every surgeon; you can spend more time washing the peritoneal cavity, since peritonitis is the main cause of mortality. It forces a postoperative medical treatment for the possibility of another ulcer of acute lesions, perforation, or bleeding from the sutured ulcer. Complications

Once the acute condition has been treated even with adequate antibiotic coverage, subphrenic abscesses, pelvic abscesses, or between the intestinal loops may be develop.

3.3 Morbidity and mortality

The prognosis of a patient with perforated PU depends on multiple factors:

Age is a non-modifiable factor, and comorbidities can be modified. The doctor is responsible for a quick diagnosis, and the surgeon is responsible of having good training and about choosing an appropriate tactic to each particular case.

Hermon Taylor in 1956 [9] described the nonsurgical treatment of perforated peptic ulcer, in which he considers that aspiration of the nasogastric tube and blocks the perforation with the omentum.

It is not convenient to replace surgery with this method, because more than 25% of patients had to be operated. This method has more complications, longer hospitalization time, and more failure in the elderly. Gastric aspiration is useful in the preoperative or in the period when patients need preoperative stabilization of any previous conditions.

While the patient already diagnosed waits for the surgery and thus by some medical indication (anesthesiologist or other specialist), it is decided to delay it briefly in order to improve some associated disease.

The simplest effective treatment in a perforated peptic ulcer, as soon as possible, is simple closure and lavage of the abdominal cavity.

In summary, mortality in PU perforations for both laparoscopic and laparoscopic surgery remains high and varies between 4.8% and 10.2%.

In order to improve the prognosis in perforated ulcers, we must follow certain statements:

  • Culture of the population in order to alert them of symptoms and awareness to hospitals.

  • Effective primary care, that is, the first doctor who attends the patient makes an accurate and rapid diagnosis.

  • Prompt diagnosis reduces the time until surgical intervention, reducing morbidity and mortality.

  • Antibiotic-onset prophylaxis to counteract the progression of infection.

  • Emergency surgery and proper operation (limited to simple closure and peritoneal lavage in most cases).


4. Pyloroduodenal obstruction

For many years, pyloroduodenal obstruction (PDO) by peptic ulcer (PU) was one of the classic indications of gastric surgery.

As mentioned in this chapter, the big change occurred by the appearance of H2 blockers and then proton pump inhibitors (PPIs) and eradication of H. Pylori. Before these treatments, the PUs had as a characteristic an extended chronicity.

PDO is always preceded by week or months of dyspepsia. In general, they are progressive and rarely become total because consultations are earlier, except in areas of insufficient medical coverage.

There are two mechanisms of obstruction:

  1. By edema and pylorus spams, in active ulcers. They were formerly called “soft pyloric syndromes” because of their good response to medical treatment

  2. By the healing of old ulcers, causing fibrosis. They were known as “hard pyloric syndromes” because they did not respond to antiulcer treatment and were surgically indicated.

4.1 Symptomatology

A minority of patients with PU begin their disease with PDO. The first symptoms are usually postprandial fullness for weeks or months. In more advanced stages, there are belching, nausea, and vomiting. The latter usually have traces of food from previous days and generally do not have bile. When provoked, they relieve symptoms immediately.

In cases of gastric retention by an active PU, the classic pain of ulcerative crises is added. In chronic PDO, anorexia leads to malnutrition and persistent vomiting causes dehydration, thirst, and hypokalemic and hypochloremic alkalosis due to the loss of hydrochloric acid and potassium.

4.2 Diagnosis

The symptomatology is so evident, that with the interrogation a diagnosis of gastric retention is made, although the etiology cannot be assured. The physical examination predominates weight loss, dryness of skin, and mucous membranes and oliguria. The abdomen presents with an asymmetrical distension to the left and can reach the pelvis, often with the shape of the distended stomach. Direct radiology of the abdomen shows large gastric dilatation and air liquid interphase characteristic of retention. X-rays contrasted with barium, which used to be routine, are contraindicated before an endoscopy and rarely help to establish the etiological diagnosis. Endoscopy is essential to detect pathology of the esophageal mucosa by reflux, ulcerative lesions of the gastric body, associated with PDO, and discard a carcinoma or other non-ulcerative gastric pathology. In cases of retention due to active ulcers, if the endoscope passes to the duodenum, the need for further dilations decreases.

4.3 Treatment

Medical treatment: The replacement of fluids and electrolytes is a priority due to the abundant loss/lack of intake, meaning the correction of dehydration and the underlying acid-base disorder and in this way permitting the reversion of duodenal edema and transit reestablish. The nasogastric tube should remain as a permanent drain for several days. PPIs are the main medication to maintain a gastric pH > 4.

Endoscopic treatment: The pneumatic dilation of a stenosis due to PU is one of the main advances of the last decade, both for active ulcers and for scars stenosis. In most patients, several dilations are needed. The main risk is perforation, but its incidence is low. Pneumatic dilation is a first line of instrumental therapy, which relieves symptoms and can prevent or defer the need for surgical treatment.

Surgical treatment: Operations, along with the eradication of HP, are the most commonly used treatment. The percentage of patients who are operated is variable and is related to the time of evolution of the PUD. In PDO due to an ulcer in activity it can reach 64%, while in chronic ones with fibrous stenosis it exceeds 98%.

PDO operations are not an emergency and are indicated in clinically compensated patients, which are achieved in the first week before intervention.

The surgery has two objectives. It decreases acid secretion, which is obtained with vagotomy (can be replace by PPI treatment), and improves gastric emptying, with gastrojejunostomy or antral resection.

Postoperative complications are the same as the ones for uncomplicated PU surgery. The most frequent is the delay in evacuation due to gastric hypotonia secondary to prolonged obstruction and usually improves in days or a few weeks.



Mario A. Suarez García, Centro de Cirugía de la Obesidad—CCO, Buenos Aires, Argentina,

Claudia A. Refi, Centro de Cirugía de la Obesidad—CCO, Buenos Aires, Argentina,


Conflict of interest

The authors declare no conflict of interest.


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Written By

Carlos A. Casalnuovo, Pedro A. Brégoli, Cesar J. Valdivieso Duarte and Carlos A. Vera Cedeño

Submitted: 09 December 2021 Reviewed: 09 February 2022 Published: 25 August 2022