Ministry of Health of the Republic of Moldova Public Institution [301533]

Ministry of Health of the Republic of Moldova Public Institution

“Nicolae Testemițanu” State University of Medicine and Pharmacy of the

Republic of Moldova

FACULTY OF MEDICINE

Department Of Surgical Diseases No 2

DIPLOMA THESIS

Peptic ulcer disease

Name and surname of scientific advisor: Toader Timiș.

Name and surname of student: [anonimizat]: VI

Group: M1043

Position and scientific degree: Conferențiar Universitar.

Introduction

2.Peptic ulcer disease

2.1 Introduction

2.2 Anatomy

2.3 Pathophysiology and etiology

2.4 Epidemiology and prognosis

2.5 History

2.6 Approach and diagnosis

2.7 Differential diagnosis

2.8 Classification of peptic ulcers

3.role of surgery in the management of peptic ulcer disease

3.1 The fundamental goals of surgical therapy

3.2 Indications for emergent surgery

3.3 Indications for elective surgery

4. Perforated Peptic Ulcer

4.1Surgical management
4.2 Types of surgical procedures

4.3 Laparoscopic repair of perforated peptic ulcer:

5.Complication pf PUD

5.1 Bleeding Peptic Ulcer

5.2 Gastric Outlet Obstruction

6. non healing or recurrent ulcers

7.Case history

8. References

1. Introduction

Peptic ulceration: [anonimizat], [anonimizat]. Healing was an uncertain process; recurrence and relapse were common; scarring often resulted in gastric outlet obstruction; [anonimizat]. [anonimizat]-[anonimizat]. However, [anonimizat]-enterostomy stoma. [anonimizat], duodenum, or lower oesophagus remained obscure. [anonimizat]-[anonimizat] “mucosal resistance”. On the basis of these two postulated mechanisms a [anonimizat]. The management of these diseases has more recently been revolutionized with the discovery that much gastritis and peptic ulceration is causally associated with chronic bacterial infection. Antimicrobial therapy has become the mainstay of treatment; suppression of gastric acid production has become of secondary importance; and, [anonimizat]-term therapy now holds the prospect of prolonged remission for the vast majority of patients — and at a cost that is minuscule compared to that of the prolonged maintenance therapy which was required in the past.

2.Peptic ulcer disease:

2.1 indtroduction

Peptic ulcers are focal defects in the gastric or duodenal mucosa that extend into the submucosa or deeper. [anonimizat],are caused by an imbalance between mucosal defenses and acid/peptic injury.Peptic ulcer remains a [anonimizat], hospital admissions, and elective operations for PUD has decreased steadily and dramatically over the past three decades.

Interestingly, the start of these trends all predated the use of H2 receptor blockers, fiber-optic endoscopy, and HSV. However, the incidence of emergency surgery and the death rate associated with peptic ulcers has not decreased nearly so dramatically. These epidemiologic changes probably represent the net effect of several factors, including (beneficially) decreased prevalence of H. pylori infection, better medical therapy, and increased outpatient management; and (detrimentally) the use of NSAIDs and aspirin (with and without ulcer prophylaxis) in an aging population with multiple risk factors.

Balance of aggressive and defensive factors in the gastric mucosa.

PUD is one of the most common GI disorders in the United States with a prevalence of about 2%, and a lifetime cumulative prevalence of about 10%, peaking around age 70 years.50 The costs of PUD, including lost work time and productivity, are estimated to be above $8 billion per year in the United States. In 1998, approximately 1.5% of all Medicare hospital costs were spent treating PUD, and the crude mortality rate for peptic ulcer was 1.7 per 100,000 individuals. Gastric ulcer has a higher mortality than duodenal ulcer because of its increased prevalence in the elderly. Recent studies have shown an increase in the rates of hospitalization and mortality in elderly patients for the peptic ulcer complications of bleeding and perforation. Presumably, this is due to the increasingly common use of NSAIDs and aspirin in this elderly cohort, many of whom also have H. pylori infection.

2.2 anatomy:

The Stomach Nerve Supply There are two types of nerve supply of the stomach; sympathetic and parasympathetic. The sympathetic constricts the sphincters, however the parasympathetic is a secreto-motor and stimulate smooth muscles for peristaltic movement and induce evacuation. Therefore, to empty the pyloris, the sympathetic stimulation must be inhibited and the parasympathetic excited. Distribution of the vagus innervation to the stomach; the right vagus nerve innervates the posterior portion of the stomach while the left vagus supplies the anterior part of the stomach(posterior gastric and posterior gastric, respectively).

*Parasymathetic innervation of the stomach:

I-The anterior gastric nerve(left vagus):

1. mainly supplies the anterior portion of the body

2. it also innervates the liver(hepatic branch)

3. and the laterjet nerve to the pyloris(which is specific to the pyloris to increase control on the emptying of the stomach).

II-The posterior gastric nerve(right vagus):

1. innervates a small portion of the anterior body

2. a main fiber innervates the posterior body

3. and another celiac branch which innervates all the small intestines, up until the lateral third of the transverse colon(innervates the medial two thirds), along with the pancreas, (Note: the lateral third and the descending colon are innervated by parasympathetic fibers from S2,S3 and S4)

4. and a laterjet nerve to the posterior and anterior walls of the pyloris. (Note: although the parasympathetic fibers pass the celiac and superior mesenteric ganglia, they do not synapse with other fibers till they reach the myenteric plexus)

*Sympathetic innervation of the stomach:

Those fibers are mainly derived from T5-T9 spinal cords, and supply their targets by the splanchnic chain, which is a branch from the thorax ganglia that penetrates the diaphragm to the abdomen.

They synapse in the celiac ganglia, or the superior mesenteric ganglia, which incapsulates the blood vessels(the post ganglionic fibers pass the myenteric plexus without synapsing with it).

(Note: sympathetic stimulation has no direct effect on motility. i.e when parasympathetic system is activated, the sympathetic system is inhibited, therefore motility decreases. Sympathetic stimulation also causes vasoconstriction).

Anatomy-7 21/4/2013 REFER TO THE SLIDES FOR FIGURES AND EXTRA INFORMATION NOT MENTIONED IN THE LECTURE 1 Sensation in the stomach is supplied by both sympathetic and parasympathetic fibers. The vagus nerve contains 80% sensory fiberb (afferent fibers) and 20% secretomotor fibers(efferent fibers). Stomach ache is sensed by afferent fibers in the vagus nerve.

2.3 Pathophysiology and Etiology:

H. pylori infection plays a crucial role in the pathogenesis of peptic ulcer disease. More than 95 % of patients suffering from the duodenal ulcers and about 70 % – 80 % of patients with gastric ulcers are H. pylori positive. H. pylori is a gram-negative, motile, microaerophilic, curved bacillus that is found in the mucus layer overlying the gastric epithelium. In 1981, Marshall and Warren conducted a prospective study of 100 consecutive patients undergoing endoscopy to correlate gastric mucosal biopsy findings with clinical and endoscopy data. In this investigation, they isolated microaerophilic, catalase-positive bacterium. H. pylori infection has been recognized as the primary cause of chronic gastritis and peptic ulcer disease. In 1994, United States (U.S.) National Institutes of Health Consensus Development Panel concluded that infection appears to play an important contributory role in the pathogenesis of peptic ulcers. The role of H. pylori infection is well explained in peptic ulcer disease by O’connor.

Currently, 70 % of all gastric ulcers occurring in the U.S. can be attributed to H. Pylori infection. In addition to an increase in acid secretion, bacterial infection also predisposes patients to ulcer disease by disrupting mucosal integrity. In developed countries, however, infection with H. pylori is uncommon before age 10 and increases to 10 % in 18 – 30 years old, compared with 50 % in those older than 60. In developing nations, 60 % – 70 % of children are infected with the bacteria by age 10, probably because of overcrowding and poor sanitation. Chronic gastritis associated with H. pylori infection is often observed in children with primary duodenal ulcer. Colonization of the gastric mucosa by H. pylori is currently uncommon among children who live in industrialized countries, compared to those who live in developing countries, with prevalence upto the tenth year of life of 5 % – 10 % and up to 80 %, respectively.

There are several strains of H. pylori along with two phenotypes of the bacterium. Both make a vacuolating cytotoxin Vac A. Type I also has a cytotoxin-associated gene (cag A) that may be necessary for transcription, function, or excretion of Vac A cytotoxin. This type I phenotype is associated with ulcer formation. Type II organisms lack cag A and do not produce as much of an inflammatory response. This bacterium also makes mucolytic enzymes, platelet activating factor, and lipopolysaccharide. Each of these can cause cellular injury. Covacci et al have suggested that only bacteria expressing the cag A antigen are associated with ulcer disease. These findings explain the link between H. pylori cytotoxin expression and ulcer disease.

A variety of factors may contribute to the development of PUD. Although it is now recognized that the large majority of duodenal and gastric ulcers are caused by H. pylori infection and/or NSAID use, the final common pathway to ulcer formation is acid-peptic injury of the gastroduodenal

mucosal barrier. Thus, the adage "no acid, no ulcer" remains true even today. Acid suppression remains a mainstay in healing both duodenal and gastric ulcers and in preventing recurrence. It generally is thought that H. pylori predisposes to ulceration, both by acid hypersecretion, and by compromise of

mucosal defense mechanisms including damage to SECs. NSAID use is thought to lead to PUD predominantly by compromise of mucosal defenses.

Duodenal ulcer has typically been viewed as a disease of increased acid-peptic action on the duodenal mucosa, whereas gastric ulcer has been thought of as a disease of weakened mucosal defenses in the face of relatively normal or even decreased acid-peptic activity. However, an increased understanding of peptic ulcer pathophysiology has blurred this overly simplistic distinction. Clearly, weakened mucosal defenses play a role in many duodenal and most gastric ulcers (e.g., duodenal ulcer in an H. pylori–negative patient on NSAIDs or a patient with a typical type I gastric ulcer with acid hyposecretion), whereas increased aggressive activity of peptic acid may result in a duodenal or gastric ulcer in the setting of normal mucosal defenses.

SMOKING, STRESS, AND OTHER FACTORS

Epidemiologic studies suggest that smokers are about twice as likely to develop PUD as nonsmokers. Smoking increases gastric acid secretion and duodenogastric reflux. Smoking decreases both gastroduodenal prostaglandin production and pancreaticoduodenal bicarbonate production. These

observations may be related, and any or all could explain the observed association between smoking and PUD.

Although difficult to measure, both physiologic and psychologic stress undoubtedly play a role in the development of peptic ulcer in some patients. In 1842, Curling described duodenal ulcer and/or duodenitis in burn patients. Decades later, Cushing described the appearance of acute peptic ulceration in patients with head trauma (Cushing's ulcer). Even the ancients recognized the undeniable links between PUD and stress. Patients still present with ulcer complications (bleeding, perforation, and obstruction) that are seemingly exacerbated by stressful life events. The use of crack cocaine has been linked to juxtapyloric peptic ulcers with a propensity to perforate. Alcohol is commonly mentioned as a risk factor for PUD, but confirmatory data are lacking.

2.4 epidemiology and prognosis:

Perforation occurs in 2-10% of patients with PUD and accounts for more than 70% of deaths associated with PUD. Often perforation is the first clinical presentation of PUD. The incidence of duodenal perforation is 7-10 cases/ 100.000 adults per year. The perforation site usually involves the anterior wall of the duodenum (60%), although it might occur antral (20%) and lesser-curvature gastric ulcers (20%). Duodenal ulcer is the predominant lesion of the western population, whereas gastric ulcers are more frequent in oriental countries, particularly in Japan. Gastric ulcers

have a higher associated mortality and a greater morbidity resulting from haemorrhage, perforation and obstruction. PPU used to be a disorder mainly of younger patients (predominantly males), but recently the age of PPU patients is increasing (predominantly females). Current peak age is 40-60 years. The need for surgery for PPU has remained stable or even increased and the mortality of peptic ulcer surgery have not decreased since the introduction of H2 receptor antagonists and peptic ulcers are still responsible for about 20.000-30.000 deaths per year in Europe. This may be due

to an increase in use of aspirin and/ or NSAID’s .

2.5 history:

For thousands of years healthy people have had acute abdominal pain, nausea, vomiting and diarrhoea followed by death in a few hours or days. Often these symptoms were contributed to poisoning and people have been sent to prison for this. King Charles I’s daughter, Henriette-Anne, died suddenly in 1670 (at age 26) after a day of abdominal pain and tenderness. Since poisoning was suspected autopsy was performed and revealing peritonitis and a small hole in the anterior wall of the stomach. However, the doctors had never heard of a perforated peptic ulcer (PPU) and attributed the hole in the stomach to the knife of the dissector. Necropsies were !rst allowed since 1500 and became more routine between 1600 and 1800. As a consequence more often perforation of the stomach was observed. Johan Mikulicz- Radecki (1850-1905), often referred to as the !rst surgeon who closed a perforated peptic ulcer (PPU) by simple closure said: “ Every doctor, faced with a perforated duodenal ulcer of the stomach or intestine, must consider opening the abdomen, sewing up the hole, and averting a possible in"ammation by careful cleansing of the abdominal cavity” . Surprising enough treatment since has not changed much, still consisting of primary closure of the perforation by single stitch suture and a convenient tag of adjacent omentum on top of this . Although this therapy sounds very simple still PPU remains a dangerous surgical condition, associated with high morbidity and mortality, not to be underestimated.

2.6 Approach and diagnosis:

DIAGNOSTIC TESTS

Until early 20th century, the diagnosis of peptic ulcer was made on clinical grounds. In 1950’s various flexible endoscopies revolutionized the direct visualization of ulcer disease. Various diagnostic tests which are frequently employed by gastroenterologists depending upon patient’s symptoms are summarized in the following text.

Esophagogastroduodenoscopy

This is a special test performed by gastroenterologists in which a thin tube with a camera on the end is inserted through mouth into the GI tract to see stomach and small intestine. During this examination, the doctor may take a biopsy from the wall of stomach for detection of H. pylori.

x-ray

In this, patient is made to swallow a white chalky substance called barium that is visible on X-ray and then patient is made to lie down on a tilted examining table. The tilting distributes the barium evenly around upper digestive tract and X-ray can capture images at different angles. This allows the doctor to locate the ulcer and determine its type and severity.

Computed tomography

It is a rapid way to confirm an uncertain diagnosis of perforation and penetration associated with peptic ulcer disease. This study is carried out retrospectively to review the abdominal computed tomography findings in patients with peptic ulcer disease and correlated them with the clinical history, endoscopic and upper GIT series findings, and surgery when it is performed.

DIAGNOSIS OF H. PYLORI

Diagnosis of H. pylori in peptic ulcer needs to be established before treatment is initiated. This can be done via noninvasive and/or invasive testing. The noninvasive tests include urea breath test, stool antigen test, and serology testing.

Urea breath test involves radioisotopes 13C or 14C, which help in identifying the production of urease by H. pylori. Patients ingest 13C or 14C labeled urea and then exhales labeled carbon dioxide. If H. pylori are present, since the bacterium produces urease this splits urea thereby, detecting the presence of the organism. False negative tests can occur if H. pylori is suppressed but not completely eliminated after treatment.

Several commercial stool antigen tests are also available. This test checks whether substances that trigger the immune system to fight an H. pylori infection are present in the feces of the patients infected with the bacterium. Serology testing includes presence of human IgG antibodies against H. pylori.

Antibody levels decline after treatment for infection and hence the positive antibody levels may indicate current or past infection. Antibodies for H. pylori can be measured in serum, plasma or whole blood.

Invasive testing includes endoscopy with subsequent histology, urease production testing and cultures allowing the clinician to identify the organism. Hematoxylin-eosin, Giemsa, or Warthin-Starry stains can be used in the detection and easier visualization of bacterium. Thus, many gastroenterologists utilizes urease test first, followed by histology, if the urease test is negative or if confirmation of the urease is desired. Culture is difficult to perform but it is helpful in evaluating treatment failure since antibiotic sensitivity can be evaluated. The diagnostic tests for H. pylori are represented in table 1 along with their advantages.

2.7 differential diagnosis:

Acute Cholangitis

Acute Coronary Syndrome

Acute Gastritis

Cholecystitis

Cholecystitis and Biliary Colic in Emergency Medicine

Chronic Gastritis

Diverticulitis

Emergent Treatment of Gastroenteritis

Esophageal Rupture and Tears in Emergency Medicine

2.8 Classification of peptic ulcers

Ulcers are classified either by their state, acute or chronic, or by their site (Table 1). Acute ulcers are those that have not had time to produce any fibrotic reaction around them and they may be very superficial. When they are multiple and widespread they are often referred to as ‘erosions’. A useful classification of gastric ulcers is based on that of Johnson (Table 2). Nearly all chronic duodenal ulcers occur in the bulb (or ‘cap’), and those occupying a more distal site raise the suspicion of Zollinger–Ellison syndrome (or an ulcerating carcinoma of the pancreas). Acute ulcers tend to perforate easily because there is no fibrotic reaction, and they may bleed from superficial mucosal vessels rather than from the major vessels, such as the splenic or pancreaticoduodenal arteries, that are eroded by chronic ulcers.

The classification is important because ulcers differ in their pathogenesis and their management. The management of a patient with multiple, recurrent, aggressive chronic ulcers from Zollinger–Ellison syndrome is very different from that of a patient with acute gastric erosions from non-steroidal anti-inflammatory drugs.

The most common, Johnson type I gastric ulcer, is typically located near the angularis incisura on the lesser curvature, close to the border between the antrum and the body of the stomach. Patients with type I gastric ulcer usually have normal or decreased acid secretion. Type II gastric ulcer is associated with active or quiescent duodenal ulcer disease, and type III gastric ulcer is prepyloric ulcer disease. Both type II and type III gastric ulcers are associated with normal or increased gastric acid secretion. Type IV gastric ulcers occur near the GE junction, and acid secretion is normal or below normal. Type V gastric ulcers are medication induced and may occur anywhere in the stomach.

Modified Johnson classification for gastric ulcer:

I. Lesser curve, incisura. II. Body of stomach, incisura + duodenal ulcer (active or healed).

III. Prepyloric. IV. High on lesser curve, near gastroesophageal junction. V. Medication-induced (NSAID/acetylsalicylic acid), anywhere in stomach.

role of surgery in the management of peptic ulcer disease

The management of peptic ulcer disease has changed dramatically over the last several decades. With the advent of potent antisecretory agents (H2 blockers and proton pump inhibitors) and the recognition of the pathogenetic role of helicobacter pylori infection, medical therapy has replaced surgery as the cornerstone of the elective treatment of this disorder. Nevertheless, surgery remains the mainstay for the emergency treatment of lifethreatining complications of aggressive and advanced disease.

3.1 the fundamental goals of surgical therapy are to:

1.permit ulcer healing

2.Prevent of treat ulcer complications

3.Address the underlying ulcer diathesis

4.Minimize postoperative digestive relapse

No single procedure satisfies all of the stated goals, nor is any specific operation applicable to all clinical scenarios. To optimize therapy, the surgeon must consider characteristics of the ulcer (location,chronicity,presence of complications), the patient (age,nutrition,comorbid illness,condition on presentation), and the operation (moratality rate, side effects). In some respects, all ulcer operations represent a compromise: the morbidity of ulcer disease is replaced by the morbidity of the operation.

The efficacy of indications for the different surgical techniques used in the treatment of duodenal and gastric ulcers will be reviewed here. The management of patients with complications of ulcer disease (perforation, gastric outlet obstruction,and bleeding) is discussed separately.

3.2 Indications for emergent surgery

Elective surgery is uncommonly needed for peptic ulcer disease in current medical practice. Currently accepted indications, elective and emergent, for surgery in the management of peptic ulcer disease include bleeding, perforation, obstruction, intractable disease, and suspected malignancy.

Today, most patients undergoing operation for PUD have simple oversewing of a bleeding ulcer, or simple patch of a perforated ulcer, or distal gastrectomy. Simultaneous performance of vagotomy either truncal or highly selective is increasingly uncommon, probably due to surgeon unfamiliarity with the procedure and reliance on postoperative PPIs to decrease acid secretion.

Unfortunately, the data from many excellent randomized clinical trials evaluating elective operation for peptic ulcer over the last several decades may be irrelevant to most patients presenting for ulcer surgery today. The large majority of these excellent studies were done in the pre-PPI, pre-Helicobacter, pre-NSAID era, and focused on elective operation for intractable disease, an unusual indication in the modern era. Thus, today's surgeon should take great care in applying this literature to inform surgical decision making.

Classically, in the previous era, the vast majority of peptic ulcers were adequately treated by a variant of one of the three basic operations: HSV, vagotomy and drainage (V+D), and vagotomy and distal gastrectomy. Recurrence rates were lowest but morbidity highest with the latter procedure.

3.3 Indications for elective surgery

With the introduction of H2-receptor antagonists in 1976, the frequency of elective hospital admissions for peptic ulcer started to decline, but overall the frequency of emergency surgery stayed the same, and, as mentioned above, actually increased in elderly men and women over the following 7 years . Elective surgery was the alternative to lifelong drug treatment or for the 10 per cent or so of patients whose ulcers failed to heal. With very few treatment failures with proton-pump inhibitors, and the ability to eliminate H. pylori in most cases, the need for elective surgery is even less. The present indications can be summarized as follows: z The occasional patient whose ulcer fails to heal with medical treatment or who relapses frequently and is H. pylori negative. z Prevention of recurrent complications when the patient is at high risk. z Possibly as a protection in patients who cannot be without non-steroidal antiinflammatory drugs. z For financial reasons, either from the patient's or supplier's viewpoint: in some countries the patient has to pay for drugs but the operation is free, and, in many countries, surgery is considerably cheaper than long-term drug therapy.

4.Perforated Peptic Ulcer

Abstract

Background Perforated peptic ulcer (PPU), despite anti-ulcer medication and Helicobacter eradication, is still the most common indication for emergency gastric surgery associated with high morbidity and mortality. Outcome might be improved by performing this procedure laparoscopically, but there is no consensus on whether the bene!ts of laparoscopic closure of perforated peptic ulcer outweigh the

disadvantages such as prolonged surgery time and greater expenses. Methods An electronic literature search was done by using PubMed and EMBASE databases. Relevant papers written between January 1989 and May 2009 were selected and scored according to E#ective Public Health Practice Project guidelines.

Results Data were extracted from 56 papers, as summarized in tables 1-7. The overall conversion rate for laparoscopic correction of perforated peptic ulcer was 12.4%, with main reason for conversion being the diameter of perforation. Patients presenting with PPU were predominantly men (79%) with an average age of 48 years. One-third had a history of peptic ulcer disease, and one-!fth took nonsteroidal anti-in"ammatory drugs (NSAIDs). Only 7% presented with shock at admission. There seems to be no consensus on the perfect setup for surgery and/ or operating technique. In the laparoscopic groups, operating time was signi!cant longer and incidence of recurrent leakage at the repair site was higher. Nonetheless there was signi!cant less postoperative pain, lower morbidity, less mortality, and a shorter hospital stay. Conclusion There are good arguments that laparoscopic correction of PPU should be first treatment of choice. A Boey score of 3, age over 70 years, and symptoms persisting longer than 24 h are associated with higher morbidity and mortality and should be considered contraindications for laparoscopic intervention.

Staging of perforation according to:

Boey's score

Mannheim peritonitis index

Hacetteppe score

4.1. Surgical management

4.2 Types of surgical procedures

Classically, in the previous era, the vast majority of peptic ulcers were adequately treated by a variant of one of the three basic operations: HSV, vagotomy and drainage (V+D), and vagotomy and distal gastrectomy. Recurrence rates were lowest but morbidity highest with the latter procedure.

HSV, also called parietal cell vagotomy or proximal gastric vagotomy, is safe (mortality risk <0.5%) and causes minimal side effects. The operation severs the vagal nerve supply to the proximal two thirds of the stomach, where essentially all the parietal cells are located, and preserves the vagal innervation to the antrum and pylorus, and the remaining abdominal viscera (Fig. 26-33). Thus, the operation decreases total gastric acid secretion by about 75%, and GI side effects are rare. Elective HSV has largely been supplanted by long-term PPI treatment, but the operation, which has a learning curve, may still be useful in the patient (elective or emergent) who is noncompliant with, intolerant of, or cannot afford medical treatment. Historically, HSV has not performed particularly well for type II (gastric and duodenal) and III (prepyloric) gastric ulcer, perhaps because of hypergastrinemia caused by gastric outlet obstruction and persistent antral stasis. The Taylor procedure consists of a posterior truncal vagotomy and anterior seromyotomy (but anterior HSV is probably equivalent), and is an attractive and simple alternative to HSV with similar results.

Fig. 26-33. ”highly selective vagotomy”

Truncal vagotomy and pyloroplasty, and truncal vagotomy and gastrojejunostomy

are the paradigmatic vagotomy and drainage procedures. HSV may be substituted for truncal vagotomy. The advantage of V+D is that it can be performed safely and quickly by the experienced surgeon. The main disadvantages are the side effect profile (10% of patients have significant dumping and/or diarrhea). During truncal vagotomy (Fig. 26-34), care must be taken not to perforate the esophagus, a potentially lethal complication. Intraoperative frozen section confirmation of at least two vagal trunks is prudent; additional vagal trunks are common. Unlike HSV, V+D is widely accepted as a successful operation for complicated PUD. It has been described as a useful part of the operative treatment for bleeding duodenal and gastric ulcer, perforated duodenal and gastric ulcer, and obstructing duodenal and gastric (type II and III) ulcer. When applied to gastric ulcer, the ulcer should be excised or biopsied.

Fig. 26-34. “Truncal vagotomy.”

Truncal vagotomy

denervates the antropyloric mechanism, and therefore, some sort of procedure is necessary to ablate or bypass the pylorus. Gastrojejunostomy is a good choice in patients with gastric outlet obstruction or a severely diseased proximal duodenum. The anastomosis is done between

the proximal jejunum and the most dependent portion of the greater gastric curvature, in either an antecolic or retrocolic fashion (Fig. 26-35). Marginal ulceration is a potential complication. Pyloroplasty is useful in patients who require a pyloroduodenotomy to deal with the ulcer complication (e.g., posterior bleeding duodenal ulcer), in those with limited or focal scarring in the pyloric region, or when gastrojejunostomy is technically difficult. The most commonly performed pyloroplasty is the Heineke-Mikulicz type (Fig 26-36). Other occasionally useful techniques include the Finney (Fig. 26-37) and the Jaboulay pyloroplasties (Fig. 26-38).

Fig. 26-35.” Retrocolic gastrojejunostomy. Note mesocolon sutured to stomach (b, c, d).”

Fig. 26-36.” A through D. Heineke-Mikulicz pyloroplasty.”

Fig. 26-37.” A through D. Finney pyloroplasty. ant. = anterior; Duod. = duodenum; Stom. = stomach.”

Fig. 26-38.” A through D. Jaboulay pyloroplasty. ant. = anterior; Duod. = duodenum; Stom. = stomach.”

The advantages of vagotomy and antrectomy (V+A)

are the extremely low ulcer recurrence rate and the applicability of the operation to many patients with complicated PUD (e.g., bleeding duodenal and gastric ulcer, obstructing peptic ulcer, nonhealing gastric ulcer, and recurrent ulcer). When applied to gastric ulcer disease, the resection is usually extended far enough proximally to include the ulcer. The disadvantage of V+A is the higher operative mortality risk (when compared with HSV or V+D), and its irreversibility. Following antrectomy, GI continuity may be re-established with a Billroth I gastroduodenostomy (Fig. 26-39) or a Billroth II loop gastrojejunostomy (Fig. 26-40). Since antrectomy routinely leaves a 60 to 70% gastric remnant, reconstruction as a Roux-en-Y gastrojejunostomy should be avoided (Fig. 26-41). Although the Roux-en-Y operation is an excellent procedure for keeping duodenal contents out of the stomach and esophagus, in the presence of a large gastric remnant, this reconstruction will predispose to marginal ulceration and/or gastric stasis.

Fig. 26-39.” A though C. Billroth I gastroduodenostomy.”

Fig. 26-40.” A through D. Billroth II antecolic gastrojejunostomy.”

Fig. 26-41.” Roux-en-Y gastrojejunostomy.”

V+A should be avoided in hemodynamically unstable patients, and in patients with extensive inflammation and/or scarring of the proximal duodenum, because secure anastomosis (Billroth I) or duodenal closure (Billroth II) may be difficult.

Distal gastrectomy without vagotomy

(usually about a 50% gastrectomy to include the ulcer) has traditionally been the procedure of choice for type I gastric ulcer. The addition of vagotomy should be considered for type II and III gastric ulcers (because the pathophysiology is more analogous to duodenal

ulcer), or if the patient is believed to be at increased risk for recurrent ulcer, or perhaps even if Billroth II reconstruction is contemplated (to decrease the chance of marginal ulcer). Subtotal gastrectomy (75% distal gastrectomy) without vagotomy is rarely used to treat PUD today, although it was the most popular ulcer operation at the middle of the last century.

4.3 Laparoscopic repair of perforated peptic ulcer:

SURGICAL TECHIQUE

Patient position At the beginning of the procedure the patient is placed in supine position with legs straight and spread out. The patient position is changed several times during procedure: in steep anti-Trendelenburg position during suture and in lateral decubitus and Trendelenburg position during peritoneal lavage.

Team position The surgical team is placed as for laparoscopic cholecystectomy. The surgeon stands between patient’s legs and the assistant to the patient’s left . This position is changed during peritoneal lavage with the surgeon to the left of the patient and assistant between patient’s legs. Equipement position The laparoscopic unit is placed on the patient’s left side toward the shoulder. The instrument table is placed at patient’s legs. Trocar position The position and size of the trocars used vary from one center to the other. The standard technique utilizes four trocars. An optical trocar of 10 to 12 mm is introduced in the periumbilical region. One operating trocar of 5 mm is placed in the inferior aspect of the right upper quadrant on the anterior axillary line for the atraumatic grasper. A 5 or 10/11mm trocar is placed in the left flank. generally at umbilicus level on the midclavicular line for the needle holder which should be perpendicular to the pyloroduodenal axis. A fourth trocar of 5 mm is placed in the epigastric region and accomodates one or several means of liver and viscera retraction. Some surgeons place the trocars in the same position as for laparoscopic cholecystectomy (French position). In obese patients the position of the trocars needs to be adapted to the morphology of the patients that is to move the trocars closer to the operative region.

A three trocar technique can be used, the liver being retracted with the help of a percutaneous suture that suspends the round ligament toward the upper left side of the abdomen. The instruments are similar to those used in most laparoscopic procedures. A 0° laparoscope is commonly used, but a 30° laparoscope may be useful to see better a perforated ulcer placed on the superior surface of the duodenum. The other instruments necessary for this operation are: 2 atraumatic graspers, needle holder, suction-irrigation device, scissors. A liver retractor may be preferred my some surgeons instead of a grasper. Endotracheal anaesthesia is generally used. Close anesthetic monitoring must be done for such a patient and intravenous antibiotic therapy should be done before insufflation. A H2 receptor antagonist or a proton pump inhibitor injection is also advisable.

technique

The Veress needle or an open technique can be used. The abdomen is entered through a small incision just above the umbilicus. A CO2 intraabdominal pressure between 8 and 12mmHg is usually sufficient to realize enough room to work properly. The optic is inserted through the 10-12 mm trocar placed in the supraombilical position. Once the diagnosis is confirmed the other three ports are placed as mentioned above. Bacteriological samples are done and sends immediately to the laboratory. The abdomen is explored to identify the perforation and to assess the magnitude of peritonitis. The gallbladder, which usually adheres to the perforation, is retracted by the surgeon’s left instrument and moved upwards. The gallbladder is passed to the assistant using the instrument placed in the subxyphoid port. Once the liver is retracted the exposed area is carefully checked and the perforation is usually clearly identified as a small hole on the anterior aspect of the first portion of the duodenum. Next step is cleaning the abdomen. The whole abdomen must be irrigated and aspirated with warm saline solution. Each quadrant is cleaned methodically, starting at the right upper quadrant, going to the left, moving down to the left lower quadrant, and then finally over to the right. The tilt of the operating table should be adapted as necessary. Special attention should be given to the rectovesical (-uterine) pouch and to the intestinal loops. Fibrous membranes are removed as much as possible, since they might contain bacteria. Once the abdominal cavity is clean the attention is returned to the perforation. Two techniques are generally employed to treat the perforation. 1. The most common technique is suturing the perforation using standard stitches. Biopsy of a duodenal ulcer is not necessary. However, for a gastric ulcer, samples of the gastric wall at the level of the perforation should be taken and sent for histological examination. Suturing is realized with 2/0 or 3/0 slowly absorbable or non absorbable sutures. Interrupted sutures are used and usually two or three stitches are placed in a transversal manner over the perforation focused on the pyloroduodenal axis in case of duodenal ulcer. Once the perforation is sealed, a small fragment of the greater omentum can be fixed over the suture line using the upper thread which was left loose after making the knot. Some surgeons prefer to use instead of omental patch fibrin glue which is spread over the suture. When is difficult to approximate the edges of the ulcer, as is the case with chronic callous ulcers, woven sutures of bigger caliber (0 or 1) must be used in order to avoid cutting the gastroduodenal wall. 2. Closure of the perforation with an omental patch (Graham patch). A floppy piece of greater omentum flap is mobilized. The assistant holds the patch of the omentum just over the perforation and the surgeon sutures it to the edges of the perforation with several interrupted sutures. 3. Alternative options to seal the perforation may include the use of biological glue and sponge plug as a plasty with the round ligament. The peritoneal lavage is continued after the suture. Warm saline solution is used until the returned liquid is clear. About 4 to 6 liters of saline are generally used, but sometimes as much as 10 liters are necessary to clean the abdomen . Routine drainage of the peritoneal cavity is performed using silicone drains (from 12 to 18 French). Depending on the severity of peritonitis, 1 to 3 drains are placed: one drain in the subhepatic region coming out via the trocar site situated on the right flank, another drain at the level of the rectovesical pouch coming out via the trocar site situated on the left flank and a left subphrenic drain coming out via the epigastric trocar site . Before ending the operation the abdomen must be examined for any possible bowel injury or haemorrhage. Trocars are removed one after the other and hemostasis of the trocar sites is checked. The telescope is removed leaving the gas valve of umbilical port open to let out all the gas.

The musculo-aponeurotic plane is closed only at the level of the 10/11mm trocar sites. The skin is closed using staples or sutures. Postoperative management. The patient may have slight pain initially but usually resolves with mild pain killers. Intravenous H2 receptor antagonists or proton pump inhibitors are given intravenously and then orally once infusions are stopped. Intravenous antibiotic therapy is maintained depending on the severity of the peritonitis and at least until a culture of the peritoneal fluid taken during the procedure is obtained. If the culture is negative intravenous antibiotic therapy is discontinued after 72 hours. However, if the culture is positive, intravenous antibiotic therapy is continued for 10 days first and then orally after return of bowel function and food intake. The aims of antibiotic therapy are to combat peritonitis and Helicobacter pylorus. The nasogastric tube is removed once peristalsis resumes and a clamping test is successful. Food intake is then restored. Drains are removed once the effluent is less than 100mL per day. When suturing is difficult or bowel function is resumed late, the gastric tube can be left in place longer. Water-soluble gastroesophageal contrast (GastrografinTM) examination is then performed to check the integrity of the closure and ensure the absence of pyloroduodenal stenosis. Control gastroscopy is performed usually 4 to 6 weeks after the operation. Patient may be discharged 3 days after operation if every things goes well.

5.Complication pf PUD

5.1 Bleeding Peptic Ulcer

Bleeding is the most common cause of ulcer-related death, but most patients admitted to hospital with bleeding gastric or duodenal ulcer today will not require an operation. The success of endoscopic treatment and medical therapy in treating and preventing bleeding PUD has resulted in the selection of a subgroup of high-risk patients for today's surgeon. It is likely that patients currently coming to operation for bleeding PUD are at higher risk for a poor outcome than ever before. The surgical options for treating bleeding PUD include suture ligation of the bleeder; suture ligation and definitive nonresective

ulcer operation (HSV or V+D); and gastric resection (usually including vagotomy and ulcer excision). Gastric ulcer requires biopsy if not resected.

All patients admitted to hospital with bleeding peptic ulcer should be adequately resuscitated and started on continuous IV PPI.72 Seventy-five percent of patients will stop bleeding with these measures alone, but 25% will continue to bleed or will rebleed in hospital. It is important to identify this high-risk group early with clinical and endoscopic parameters because, essentially, all the deaths from bleeding ulcer occur in this group. Surgical consultation is mandatory, and endoscopic hemostatic therapy (cautery,

epinephrine injection, clipping) is indicated and usually successful in these high-risk patients. Indications for operation include massive hemorrhage unresponsive to endoscopic control, and transfusion requirement of more than four to six units of blood, despite attempts at endoscopic control. Lack of availability of a therapeutic endoscopist, recurrent hemorrhage after one or more attempts at endoscopic control, lack of availability of blood for transfusion, repeat hospitalization for bleeding ulcer, and concurrent indications for surgery such as perforation or obstruction, are also indications for surgery. Patients with massive bleeding from high-risk lesions (e.g., posterior duodenal ulcer with erosion of gastroduodenal artery, or lesser curvature gastric ulcer with erosion of left gastric artery or branch) should be considered for early operation. Early operation should also be considered in patients more than 60 years of age, those presenting in shock, those requiring more than four units of blood in 24 hours or eight units of blood in 48 hours, those with rebleeding, and those with ulcers >2 cm in diameter.

5.2 Gastric Outlet Obstruction

Currently, gastric outlet obstruction is the least common indication for operation in PUD. Acute ulcers associated with obstruction due to edema and/or motor dysfunction may respond to intensive antisecretory therapy and nasogastric suction. But most patients with significant obstruction from chronic ulceration will require some sort of more substantial intervention. Endoscopic balloon dilation can often transiently improve obstructive symptoms, but many of these patients ultimately fail and come to operation.

The most common operations for obstructing PUD are V+A and V+D. HSV and gastrojejunostomy is comparable to V+A in this setting77 and is an appealing operation for obstruction, both because it can readily be done using laparoscopic techniques, and because it does not complicate future resection, should this be needed. However, potentially curable gastric or duodenal cancers can be missed with this approach.

6. Non healing or recurrent ulcers.

The definition of a non-healing ulcer is failure to heal, after appropriate treatment, in two months for DU or three months for GU. It must be said that these are rare, especially in the developing world. A diagnostic dilemma in these cases has been observed. H. pylori persistence or reinfection needs to be ruled out, as does Zollinger Ellison syndrome (a gastrinoma secreting abnormally high levels of gastrin). Other aggravating factors – NSAIDS, smoking, alcohol – need to be eliminated if possible. If the ulcer recurs, one option is long term PPI therapy. If there is failure to heal on these, surgery becomes indicated. In GUs, particularly Type I, the standard procedure has been the Bilroth I gastrectomy with excision of the ulcer. Pre/peri-operative biopsies should be performed to make sure the ulcer is not malignant and a larger resection not required. For DUs, the modern options have been some form of vagotomy, truncal vagotomy with drainage or highly selective vagotomy (parietal cell vagotomy) versus vagotomy and antrectomy. The latter procedure has an improved cure rate with increased side effects. Recurrence of ulcer after surgery has long been a problem, often requiring more aggressive surgery.

7.Case history
A 54-year-old Caucasian Greek man presented to the Accident and Emergency department of our hospital with a 20-day history of abdominal pain, vomiting and loss of appetite. He mentioned an eight kg weight loss over the last 20 days, as he had been drinking almost exclusively water due to his symptoms. He had not presented to any hospital facility earlier because he lived in a remote area in the mountains. On admission, he had the septic image of paleness, tachypnea, tachycardia (110 beats/minute) and a fever of 38.5°C, as well as a rigid abdomen. Abdominal and plain chest X-rays demonstrated free gas under both the hemidiaphragms. After initial resuscitation (placement of intravenous lines and nasogastric tube followed by adequate administration of fluids), our patient underwent an emergency exploratory laparotomy. Our patient's worsening clinical image and his deteriorating clinical signs (tachypnea and tachycardia), along with the presence of his acute abdomen led us to conclude that an emergency laparotomy constituted the treatment of choice. In the face of the emergency situation a computed tomography (CT) scan was not performed. Laparotomy revealed peritonitis due to a perforated ulcer on the anterior wall of the duodenum, which was sutured, while the suture line was reinforced with an omental patch (Figure 1). After a thorough lavage of the peritoneal cavity, further exploration of the intra-abdominal organs revealed a second posterior pre-pyloric ulcer on the lesser curvature of the stomach, perforated into the lesser sac (Figure 2). A wedge resection with staplers was carried out (Figure 3), while no further acid reduction procedures were undertaken due to sepsis. A Nissen fundoplication was performed as an anti-reflux measure. Our patient recovered uneventfully and was discharged home on the 13th post-operative day; at this time we administered an appropriate eradication therapy. More specifically, we followed the protocol of triple therapy: a proton pump inhibitor, amoxicillin and clarithromycin were administered. After discharge our patient was referred to gastrointestinal specialists. Our colleagues planned a surveillance endoscopy according to their protocol.

Figure1 Omental patch-reinforced suture on the anterior wall of the duodenum.

Figure 2 The second, posterior pre-pyloric ulcer on the lesser curvature of the stomach.

Figure 3 Wedge resection with staplers.

Discussion

Perforation of a peptic ulcer is a surgical emergency that still carries a risk of mortality. We successfully managed a rare and difficult case of simultaneous perforation of duodenal and gastric ulcers that could have been easily misdiagnosed and undertreated. Retrospectively studying our case, we can state that there is a growing experience with laparoscopic techniques for management of peptic ulcers. A Graham patch, with or without a laparoscopic vagotomy for perforated peptic ulcers is probably the most appropriate minimally invasive approach when in experienced hands [8, 9]. Nevertheless, this case raises doubts as to the extent laparoscopy would have been a safe procedure in our case in terms of revealing both lesions.

Finally, every surgeon should strictly follow one of the basic principles of abdominal surgery and perform a thorough examination of the peritoneal cavity in every case of diffuse peritonitis, even if the underlying pathology appears to be obvious.

Conclusions

In summary, emergency physicians and surgeons should maintain a high level of clinical suspicion as a second perforative peptic lesion, though a rare possibility, could exist and could potentially be lethal.

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