Surgery for perforated ulcer. Emergency Ulcer Surgery: A Comprehensive Guide to Perforated Ulcer Treatment

09.02.197617.10.2021 by alexxlab

How has the rate of elective ulcer surgery changed over the past decades. What are the main causes of peptic ulcer disease. How do H. pylori and NSAIDs contribute to ulcer formation. Why is peptic ulcer disease now predominantly seen in older adults. What are the key considerations for emergency surgical management of perforated ulcers.

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The Changing Landscape of Ulcer Surgery

The field of gastric surgery has undergone significant changes over the past few decades, particularly in relation to peptic ulcer disease. Once a common reason for elective surgery, the rate of planned ulcer procedures has seen a dramatic decline. Data from American surgical training programs and Scandinavian national audits reveal a staggering 80-97% decrease in elective ulcer surgeries during the 1980s and 1990s.

Interestingly, while elective procedures have become less frequent, there has been a notable 44% increase in emergency ulcer surgeries during the same period. In 2006, approximately 25,000 operations were performed in the United States for bleeding or perforated peptic ulcers. This shift presents a unique challenge for gastrointestinal surgeons, who are now more likely to encounter urgent cases involving elderly and critically ill patients, often with limited experience in elective peptic ulcer disease surgery.

Understanding the Pathogenesis of Peptic Ulcer Disease

The traditional understanding of peptic ulcer disease viewed it as an imbalance between the corrosive effects of gastric acid and pepsin, and the protective mechanisms of the stomach and duodenal mucosa. This perspective led to the belief that excessive acid secretion, influenced by factors such as smoking, alcohol use, and stress, was the primary culprit.

However, our understanding of peptic ulcer pathogenesis underwent a revolutionary change with the discovery of Helicobacter pylori (H. pylori) in the early 1980s. This bacterium was found to be associated with the majority of gastric and duodenal ulcers, leading to a paradigm shift in ulcer treatment.

The Role of H. pylori in Ulcer Formation

H. pylori infection of the gastric mucosa is now recognized as responsible for many of the observed changes in gastric acid secretion seen in peptic ulcers. The location and extent of the infection within the stomach can lead to different outcomes:

Predominantly antral infection: Impairs negative feedback of acid secretion, resulting in increased gastric acid production and development of duodenal and pre-pyloric ulcers.
Uniform infection throughout the stomach: Often leads to low acid production due to inflammation of the gastric body, impairing the function of acid-secreting mucosa and frequently resulting in gastric ulcers.

The Impact of NSAIDs on Ulcer Development

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs), including aspirin, have long been recognized as significant contributors to peptic ulcer disease. These medications inhibit the production of prostaglandins in the stomach, which play a crucial role in mucosal defense against acid and pepsin-induced injury.

Prostaglandins in the stomach stimulate mucus and bicarbonate production and regulate gastric mucosal blood flow. By inhibiting these protective mechanisms, NSAIDs can cause peptic ulceration independently or synergize with H. pylori infection to exacerbate ulcer formation.

The Evolving Epidemiology of Peptic Ulcer Disease

The demographic landscape of peptic ulcer disease has shifted significantly in recent years. Once prevalent across all age groups, it has now become predominantly a condition affecting the elderly. Patients presenting with complications of peptic ulcer disease are most commonly in their 70s and 80s, with a notable male predominance.

This shift in epidemiology can be attributed to several factors:

Improved hygiene and living conditions, leading to reduced H. pylori infection rates in younger populations
Increased use of NSAIDs and aspirin in older adults for management of chronic conditions
Higher prevalence of comorbidities in elderly patients, which may increase susceptibility to ulcer formation
Potential age-related changes in gastric mucosal defense mechanisms

Emergency Surgical Management of Perforated Ulcers

When faced with a perforated ulcer, emergency surgical intervention is often necessary. The primary goals of surgery for perforated ulcers are to control the source of contamination, prevent further peritoneal soiling, and manage any associated complications.

Preoperative Considerations

Before proceeding with surgery, several key factors must be addressed:

Rapid resuscitation with intravenous fluids and electrolyte correction
Administration of broad-spectrum antibiotics to cover enteric flora
Nasogastric tube placement for gastric decompression
Assessment of comorbidities and optimization of the patient’s condition when possible

Surgical Techniques for Perforated Ulcer Repair

The choice of surgical technique depends on various factors, including the location and size of the perforation, the degree of peritoneal contamination, and the patient’s overall condition. Common approaches include:

Simple closure with omental patch (Graham patch): Often the preferred method for small perforations
Truncal vagotomy and pyloroplasty: May be considered in cases of chronic ulcer disease
Partial gastrectomy: Reserved for large perforations or in cases where malignancy is suspected
Laparoscopic repair: Increasingly utilized in stable patients with minimal contamination

Postoperative Management and Long-term Considerations

Following emergency surgery for perforated ulcers, careful postoperative management is crucial for optimal outcomes. Key aspects of care include:

Continued fluid resuscitation and electrolyte management
Pain control and early mobilization
Nutritional support, potentially including temporary parenteral nutrition
Monitoring for signs of infection or anastomotic leak
Initiation of proton pump inhibitor therapy

Long-term management should focus on addressing the underlying causes of ulcer formation. This typically involves:

Testing for and eradicating H. pylori infection
Reassessing the need for NSAIDs and considering alternative pain management strategies
Lifestyle modifications, such as smoking cessation and alcohol reduction
Regular follow-up to monitor for ulcer recurrence or complications

Complications and Prognosis of Perforated Ulcer Surgery

While emergency surgery for perforated ulcers can be life-saving, it is not without risks. Potential complications include:

Wound infection and dehiscence
Intra-abdominal abscess formation
Anastomotic leak (in cases of resection)
Respiratory complications, particularly in elderly patients
Recurrent ulceration

The prognosis following perforated ulcer surgery is influenced by several factors:

Patient age and overall health status
Duration of perforation before surgical intervention
Extent of peritoneal contamination
Presence of shock or sepsis at presentation
Underlying comorbidities

Early recognition and prompt surgical management, combined with appropriate postoperative care and addressing of underlying risk factors, can significantly improve outcomes for patients with perforated ulcers.

Advances in Ulcer Prevention and Non-Surgical Management

While emergency surgery remains a crucial intervention for perforated ulcers, significant advances have been made in ulcer prevention and non-surgical management. These developments have contributed to the overall decline in elective ulcer surgeries and have implications for long-term patient care following emergency procedures.

Pharmacological Advancements

The introduction of highly effective acid-suppressing medications has revolutionized ulcer treatment and prevention:

Proton Pump Inhibitors (PPIs): These drugs provide potent and long-lasting reduction of gastric acid secretion, promoting ulcer healing and preventing recurrence.
H2 Receptor Antagonists: While less potent than PPIs, these medications offer an alternative for acid suppression in some patients.
Cytoprotective Agents: Drugs like sucralfate and misoprostol can enhance mucosal protection and may be useful in certain clinical scenarios.

H. pylori Eradication Protocols

The development of effective H. pylori eradication regimens has been a game-changer in ulcer management:

Triple Therapy: Combining a PPI with two antibiotics (usually clarithromycin and amoxicillin or metronidazole) for 7-14 days.
Quadruple Therapy: Adding bismuth subsalicylate to the triple therapy regimen or using a different combination of antibiotics for regions with high clarithromycin resistance.
Sequential Therapy: A 10-day regimen involving PPI and amoxicillin for 5 days, followed by PPI, clarithromycin, and metronidazole for another 5 days.

These protocols have shown high success rates in eradicating H. pylori and significantly reducing ulcer recurrence.

NSAID Risk Mitigation Strategies

Given the significant role of NSAIDs in ulcer formation, several strategies have been developed to mitigate this risk:

Co-prescription of PPIs with NSAIDs in high-risk patients
Use of COX-2 selective inhibitors, which may have a lower risk of gastrointestinal complications
Development of novel NSAID formulations with built-in gastroprotective mechanisms
Regular risk assessment and individualized treatment plans for patients requiring long-term NSAID therapy

The Future of Ulcer Management: Emerging Trends and Research Directions

As our understanding of peptic ulcer disease continues to evolve, several exciting areas of research and development are emerging:

Precision Medicine Approaches

Advances in genetic and molecular profiling are paving the way for more personalized approaches to ulcer prevention and treatment:

Identification of genetic markers associated with increased ulcer susceptibility
Development of targeted therapies based on individual patient characteristics and risk factors
Personalized H. pylori eradication protocols based on antibiotic resistance profiles

Novel Therapeutic Targets

Ongoing research is exploring new avenues for ulcer prevention and treatment:

Modulation of the gastric microbiome to promote mucosal health
Development of mucosal protective agents that enhance natural defense mechanisms
Investigation of growth factors and other compounds that promote rapid ulcer healing
Exploration of anti-inflammatory strategies that do not compromise gastric mucosal integrity

Advanced Endoscopic Techniques

Improvements in endoscopic technology and techniques are expanding the role of non-surgical interventions:

Endoscopic closure of small perforations using clips or suturing devices
Development of novel hemostatic agents and techniques for managing bleeding ulcers
Use of artificial intelligence algorithms to enhance early detection and risk stratification of ulcers

Minimally Invasive Surgical Innovations

Advancements in laparoscopic and robotic surgery are refining surgical approaches to ulcer complications:

Refinement of laparoscopic techniques for perforated ulcer repair
Development of robotic-assisted platforms for complex ulcer surgeries
Exploration of natural orifice transluminal endoscopic surgery (NOTES) for select cases

As research in these areas progresses, it is likely that we will see further reductions in the need for emergency ulcer surgery, along with improved outcomes for those patients who do require surgical intervention. The integration of these advances into clinical practice will require ongoing education and adaptation by surgeons and gastroenterologists alike.

Conclusion: The Evolving Role of Surgery in Ulcer Management

The landscape of peptic ulcer disease management has undergone a dramatic transformation over the past few decades. While emergency surgery remains a critical intervention for complications such as perforation, the overall approach to ulcer treatment has shifted towards medical management and prevention.

Key takeaways from this comprehensive review include:

The recognition of H. pylori and NSAIDs as primary causes of peptic ulcers has revolutionized our understanding and treatment approach.
Peptic ulcer disease is increasingly a condition of the elderly, often complicated by comorbidities and medication use.
Emergency surgical management of perforated ulcers requires a tailored approach based on patient factors and ulcer characteristics.
Postoperative care and long-term management should focus on addressing underlying causes and preventing recurrence.
Advances in pharmacology, endoscopic techniques, and minimally invasive surgery are continually refining our approach to ulcer complications.
Future developments in precision medicine and novel therapeutic targets hold promise for further improvements in ulcer prevention and treatment.

As we move forward, the role of the gastrointestinal surgeon in ulcer management will continue to evolve. While the need for emergency interventions may persist, the focus is likely to shift towards more complex cases and the integration of advanced technologies. Surgeons must stay abreast of these developments to provide optimal care for patients with peptic ulcer disease and its complications.

The story of peptic ulcer disease management serves as a powerful example of how advances in medical science can fundamentally change our approach to a common condition. As we look to the future, it is clear that the collaborative efforts of researchers, clinicians, and surgeons will continue to drive progress in this field, ultimately leading to better outcomes for patients suffering from this challenging disease.

Emergency Ulcer Surgery

Introduction

Once one of the most common indications for gastric surgery, the rate of elective surgery for peptic ulcer disease has been declining steadily over the last 3 decades. Data from American surgical training programs and Scandinavian national audits have shown a decrease in the rate of elective ulcer surgery of between 80 and 97% during the 1980’s and 1990’s^{1, 2}. During this same time period the rate of emergency ulcer surgery rose by 44%. In the United States in 2006 roughly 25,000 operations were performed for bleeding or perforated peptic ulcers³. These time trends mean that the gastrointestinal surgeon is likely to be called upon to manage the emergent complications of peptic ulcer disease in an elderly and ill patient without substantial experience in elective peptic ulcer disease surgery⁴. The goal of this review is to familiarize surgeons with our evolving understanding of the pathogenesis, epidemiology, presentation and management of peptic ulcer disease in the emergency setting, with a focus on peptic ulcer disease associated bleeding and perforation.

Pathogenesis of Peptic Ulcer Disease

The classic understanding of the pathogenesis of peptic ulcer disease is that it represents an imbalance between the toxicity of the gastric injurious forces of acid and pepsin and the mucosal defense mechanisms of the stomach and duodenum. Classically, the dictum was “No acid, no ulcer” and most ulcers were thought to be a consequence of excessive acid secretion caused by smoking, alcohol use, stress or other environmental factors⁵. In this model the pathogenesis was multifactorial, and many of the underlying factors were difficult to modify. Treatment of peptic ulcer disease needed to be chronic and was directed at the reduction of acid secretion either by vagotomy and/or surgical elimination of acid secreting gastric mucosa or by chronic use of medications such as h3 antagonists or proton pump Inhibitors (PPI).

Our understanding of peptic ulcer pathogenesis was revolutionized by the discovery of the presence of the bacterium Helicobactor pylori in association with most gastric and duodenal ulcers in the early 1980’s⁶. Over the next ten years multiple trials demonstrated that effective eradication of H. pylori with a short course of antibiotics and PPI’s resulted in relapse free cure of the vast majority of ulcers. This led to an NIH consensus conference in 1994 that recommended treatment of H. pylori as the primary target of ulcer treatment⁷. With our increased understanding of the biology of H. pylori, it is now clear that infection of the gastric mucosa with H. pylori is responsible for most of the observed changes in gastric acid secretion observed in peptic ulcers. Patients with predominantly antral infection have impaired negative feedback of acid secretion, resulting in increased gastric acid production and they develop duodenal and pre-pyloric ulcers. Patients with uniform infection throughout the stomach often have low acid production secondary to inflammation of the gastric body which impair the normal function of the acid secreting mucosal and they frequently develop gastric ulcers. The effects of H. pylori infection on acid secretion are beautifully described in a recent review, and nicely explain the observed clinical finding of differential acid secretion in duodenal and gastric ulcers⁵.

The use of aspirin and Non-Steroidal Anti-Inflammatory Drugs (NSAIDS) has long been recognized as an important case of peptic ulcer disease. These drugs inhibit the production of prostaglandins in the stomach that play a critical role in the mucosal defenses of the stomach against acid and pepsin induced injury⁸. In the stomach prostaglandins stimulate mucus and bicarbonate production, and play an important role in the regulation of gastric mucosal blood flow. By inhibiting mucosal defense mechanisms against acid mediated injury, NSAIDS are able to cause peptic ulceration independently, but also synergize with H. pylori infection to cause peptic ulcers⁹. Our current understanding of peptic ulcer disease suggests that H. pylori and NSAIDS use, either alone or in combination are the causative agents for the vast majority of peptic ulcers. This new understanding of peptic ulcer disease implies that the great majority of peptic ulcer disease is the result of treatable or modifiable causes. Based on this understanding of the pathogenesis of peptic ulcer disease, the classic surgical approach directed at reducing acid production must be carefully reevaluated.

The Epidemiology of Peptic Ulcer Disease

Once relatively common across all age groups, in the 21^st century peptic ulcer disease is predominantly a disease of the elderly. Patients presenting with complications of peptic ulcer disease are most commonly in the 7^th and 8^th decades of life and there is a male predominance with roughly 1.5 times as many cases in men than women^{3, 10}. Overall there has been a marked decline in the incidence of all peptic ulcer disease, with data from multiple countries showing declines in ulcer hospitalization rates of 40–50% over the last three decades^{1, 3, 11}. Duodenal ulcer is more common than gastric ulcer although the largest decreases in ulcer incidence have been seen in duodenal ulcer¹⁰. Despite a declining incidence overall of peptic ulcer disease, the incidence of peptic ulcer disease complicated by either bleeding or perforation has remained constant or in fact even increased. Although the data is inconsistent in different countries, data from Finland and the Netherlands suggest that the rate of ulcer complications and the need for emergent ulcer surgery may have increased slightly over the last 30 years^{1, 11}.

These epidemiologic changes make sense with our new understanding of the pathophysiology of peptic ulcers. The rate of H. pylori infection has been decreasing over time, both as a consequence of improved sanitation, treatment of infection and a cohort effect. This likely explains the decrease overall in ulcer disease and aging of the ulcer patient. At the same time with an aging population and increased use of NSAIDS, the reasons for increase in ulcer complications particularly in elderly seems clear. For the surgeon dealing with patients with ulcer emergencies, this means increasingly being called on to offer surgical therapy to elderly frail patients.

Bleeding Peptic Ulcer

PRESENTATION AND INITIAL MANAGEMENT

Patients with bleeding from peptic ulcer will usually present with hematemesis, melana or both. In the cases of massive bleeding they can occasionally present with hematochezia. Many patients will present with hemodynamic findings of significant volume loss or even shock. Patients may also report a history of syncope prior to presentation that should suggest significant blood loss. The initial management of all non-variceal upper GI bleeding is directed at obtaining IV access, ensuring the availability of blood for possible transfusion, and initiating resuscitation of the patient with either crystalloid solutions or blood if evidence of significant blood loss exists. The primary therapeutic goal in a patient with acute upper GI bleeding is control of bleeding, and the goal of a surgeon in managing a bleeding peptic ulcer is to provide definitive hemostasis. The challenge in managing bleeding peptic ulcers, is that many patients will stop bleeding spontaneously, and only 5–10% of patients with bleeding ulcers will require surgery. To help identify patients likely to require intervention for bleeding control, and those at high risk for re-bleeding and death from bleeding ulcers, several scoring systems based on clinical and endoscopic variables have been developed. The use of the prognostic systems for risk stratification is one of the major recommendations of a recently published international consensus statement on UGIB, and surgeons managing peptic ulcers should be familiar with their use¹². The Blatchford score uses clinical and laboratory data such as hemodynamic parameters, hemoglobin, and BUN level, and co-morbid conditions to assess patients and can accurately identify patients at low risk of requiring intervention. The full scoring system is outlined in . Based on Blatchford’s initial data, patients with a score of 3 or less have a less than 6% chance of requiring intervention for hemostasis while those with a score of 6 or higher have a greater than 50% chance of requiring intervention for control of bleeding¹³.

Table 1

Blood Urea Nitrogen (BUN mg/dl)
18.2–22.4	2
22.4–28	3
28–70	4
> 70	6
Hemoglobin for Men (g/dl)
12–13	1
10–12	3
<10	6
Hemoglobin for Womens (g/dl)
10–12	1
< 10	6
Systolic Blood Pressure mmHg
100–109	1
90–99	2
<90	3
Heart Rate >100 Bpm	1
Presentation with Melena	1
Presentation with Syncope	2
Hepatic Disease	2
History of Heart Failure	2

ENDOSCOPIC INTERVENTION

The most important step in the management of a patient with a bleeding peptic ulcer is to arrange for urgent upper GI endoscopy. Upper GI endoscopy is critical in establishing the etiology of the bleeding, of which up to 60% is related to peptic ulcer disease¹⁴. More importantly in most cases of active GI bleeding, endoscopic hemostatic techniques will be successful in controlling the source of bleeding. Meta-analysis of data in the early 1990’s demonstrated that endoscopic therapy is effective at controlling peptic ulcer bleeding and reducing the risk of mortality and the need for surgical intervention^{15, 16}. More recent data has shown that the use of epinephrine injection combined with an additional technique such as thermal contact, sclerosant or clipping improves success in controlling initial bleeding¹⁷. In the hands of a skilled endoscopist, bleeding can initially be controlled in almost all cases. Essentially all patients with bleeding peptic ulcers should undergo upper endoscopy prior to the consideration of surgical therapy. It is important, however for the surgeon to be present at the time of endoscopy, as important anatomic information will be gained during the endoscopic procedure. Failure of initial endoscopic hemostasis attempts is one of the indications for surgery in bleeding peptic ulcers.

Despite the high success rates of initial endoscopic hemostasis, roughly 15–20% of patients will experience re-bleeding from their ulcer. Rockall and colleagues identified in 1996 that re-bleeding in patients with peptic ulcer disease is an important contributor to mortality risk¹⁸. Based on a large cohort of patients they devised a clinical scoring system based on patient characteristics and endoscopic findings that could be used to predict mortality and risk of re-bleeding in patients with peptic ulcer disease. Patients with a Rockall score of 3 or less have a risk of re-bleeding of 11% and a mortality rate of less than 5%, while those with a score of 5 or higher have a re-bleeding rate of 25% and a greater than 10% risk of death. The components of the Rockall score are summarized in . Further study of the Rockall score has suggested that it is better at predicting mortality than re-bleeding, and has lead to multiple attempts to better define the risk factors for re-bleeding. In a recent systematic review, six factors were identified as independent predictors of rebleeding: hemodynamic instability, comorbid illnesses, active bleeding at endoscopy, >2 cm ulcer size, and ulcer location in either the posterior duodenum or lesser curvature of the stomach¹⁹.

Table 2

Variable	0	1	2	3
Age	<60	60–79	≥80
Shock	No Shock	Tachycardia	Hypotension
Comorbidity	None		Cardiac Disease	Liver or Kidney Failure
Diagnosis	Mallory-Weiss or no diagnosis	All other Diagnoses	Upper GI Malignancy
Stigmata of recent Hemmorhage	None or Dark Spot		Blood in GI tract, bleeding or visible vessel, adherent clot

The role of the surgeon in patients at risk for re-bleeding after endoscopic hemostasis remains an area of controversy. Data from the 1980’s before wide spread availability of modern endoscopic techniques for hemostasis could not prove that early operation for ulcers without active bleeding improved mortality, but it did show that it resulted in an increase in the number of patients undergoing operation^{20, 21}. One small trial using modern endoscopic hemostasis techniques that compared early elective operation with endoscopic retreatment per protocol after initial endoscopic control of ulcer bleeding. This trial showed that patients who underwent early elective surgery were less likely to re-bleed, but showed no difference in overall mortality or need for emergency surgery²². It is worth noting that more than 75% of the patients receiving endoscopic therapy achieved definitive hemostasis without surgery. This data agrees with the results of an elegant randomized controlled trial performed by Lau and colleagues that demonstrated that endoscopic retreatment of peptic ulcers that re-bled after initial endoscopic treatment was successful in nearly 75% of patients and associated with similar mortality and significantly fewer complications than immediate surgery for re-bleeding²³. In this study two factors predicted failure of endoscopic retreatment for recurrent bleeding, an ulcer larger than 2 cm and patients who developed hypotension with the recurrent bleeding. Taken altogether these studies suggest that early elective surgery for bleeding peptic ulcer does not reduce the mortality risk, but it does reduce the risk of re-bleeding. It seems reasonable to consider early elective operative intervention in those patients who are at high risk of recurrent bleeding such as those with ulcers > 2cm, hypotension on presentation, with posterior duodenal or lesser curvature gastric ulcers. This recommendation must be balanced against significant risk of complications and death in this elderly frail patient population, and requires the exercise of careful surgical judgment.

OPERATIVE APPROACH

The primary goal of any operation for a bleeding peptic ulcer is hemorrhage control. Classically, the secondary goal of surgery was treatment of the underlying ulcer diathesis. With our current understanding of the underlying causes of peptic ulcers and the advent of potent acid suppressive medications, the need for surgical reduction of acid secretion is less clear. The preferred operative approach to a peptic ulcer will depend on the location of the ulcer, and for this reason it is important for the surgeon caring for the patient to be present during upper GI endoscopy to obtain precise information on the location of the ulcer.

Bleeding gastric ulcers are generally best treated by excision of the ulcer and repair of the resulting gastric defect. Excision or biopsy of the ulcer is important, as 4–5% of benign appearing ulcers are actually malignant ulcers²⁴. For ulcers along the greater curvature of the stomach, antrum or body of the stomach wedge excision of the ulcer and closure of the resulting defect can easily be achieved in most cases without causing significant deformation of the stomach. Gastric ulcers along the lesser curvature of the stomach are more problematic. Because of the rich arcade of vessels from the left gastric artery, wedge excision of these ulcers is more difficult than in other locations, and the subsequent closure of the gastric defect is much more likely to result in deformation of the stomach and ether luminal obstruction or gastric volvulus of the resulting J-shaped stomach. For distal gastric ulcers along the lesser curvature in the area of the incisura angularis, a distal gastrectomy with either a Bilroth I or Bilroth II reconstruction is often the easiest method of excising the ulcer and restoring GI continuity. A special case is the proximal gastric ulcer near the gastroesophageal (GE) junction. Wedge excision of these ulcers will often result in compromise of the GE junction and leak. In most patients the easiest approach is an anterior gastrotomy with biopsy and oversewing of the ulcer from inside the gastric lumen. With this approach it is relatively easy to avoid compromising the GE junction. In the event that ulcer excision is necessary, a Csendes procedure, a distal gastrectomy with tongue shapped extension of the lesser curve resection margin to include the ulcer and subsequent Roux-Y esophagogastrojenjunostomy is an excellent option²⁵.

The standard approach to a bleeding duodenal ulcer is to perform an anterior longitudinal duodenotomy extending across the pylorus to the distal stomach. The bleeding vessel, often the gastroduodenal artery is ligated in the ulcer crater by placing a figure of eight suture at the top and the bottom of the ulcer crater to control the artery proximally and distally. A third suture is placed as a U-stitch underneath the ulcer to control the transverse pancreatic branches that enter the GDA posteriorly. The transverse duodenal incision is then closed vertically to construct a Heineke-Mikulicz pyloroplasty. Classically a truncal vagotomy is then performed to reduce the risk of recurrent ulceration. The role of the vagotomy in 2011 is unclear. Our modern understanding of the pathogenesis of peptic ulcer suggests that treatment of H. pylori and elimination of NSAID use should result in cure of the underlying risk of ulcer. Further, with the advent of PPI’s it is now possible to medically eliminate gastric acid production without the side effects of vagotomy. Although level one data exists for perforated duodenal ulcer demonstrating that H. pylori treatment eliminates the need for definitive ulcer surgery, there is to date no trial that confirms this finding in the case of bleeding duodenal ulcer²⁶. Despite the lack of level one evidence, surveys of surgeons in the United Kingdom²⁷, and national data from the United States³ suggest that most surgeons no longer perform a vagotomy as a component of operation for bleeding duodenal ulcer.

Although duodenotomy with direct control of the bleeding site with or without vagotomy is the most commonly used approach for a bleeding duodenal ulcer, there is some data to suggest that a more extensive operation may be associated with a lower re-bleeding rate. In 1993 Millat and colleagues published a randomized controlled trial comparing vagotomy and pyloropasty with gastric resection combined with ulcer excision. The found that the re-bleeding rate was higher (17% vs 3%) with vagotomy and pyloroplasty, but the overall mortality was not different²⁸. The major complication rate, mostly duodenal leaks, was significantly higher after gastric resection. An important caveat to this data is that this study was performed prior to widespread use of PPI’s and H pylori treatment, and it is unclear that there is still a place for aggressive surgical treatment of the underlying ulcer disease now that medical therapy has replaced surgical therapy as the mainstay of ulcer treatment. In patients without significant comorbidities, who are not in shock at the time of operation, a more aggressive surgical approach may be warranted in patients with large posterior duodenal ulcers. Given the challenges of dealing with the difficult duodenal stump in a large posterior duodenal ulcer, this approach should only be undertaken by surgeons with significant experience in ulcer surgery.

Despite the best surgical efforts, re-bleeding after vagotomy and pyloroplasty occurs in between 6–17% of cases^{28, 29}. Endoscopic therapy is generally not an option after a recent duodenotomy, leaving two options either reoperation or transcatherter arterial embolization (TAE). Classically reoperation was the procedure of choice for rebleeding after duodenotomy. In the case of reoperation for recurrent bleeding most surgeons have advocated a more extensive operation, usually distal gastrectomy with or without vagotomy and ulcer excision or exclusion. This approach is unfortunately fraught with complications and associated with high operative mortality^{28, 29}. More recently several authors have advocated TAE as a viable alternative to operative treatment for ulcer bleeding refractory to endoscopy. Without a head to head trial, it is unclear whether TAE should replace surgery as a primary approach to bleeding control, but data from two large series suggest that TAE can achieve long-term hemostasis in roughly 75% of patients with recurrent bleeding after duodentomy and ulcer oversewing^{30, 31}. Given the significant risk of complication or mortality in reoperation for recurrent bleeding, TAE, when available should be the first line therapy for recurrent bleeding after duodenotomy and ulcer oversewing.

PERFORATED ULCER

The therapeutic goal in a perforated peptic ulcer is to repair the hole in the GI tract and treat peritoneal contamination. Unlike in the case of bleeding duodenal ulcers, surgery is the mainstay of treatment for perforated peptic ulcers. The majority of perforated ulcers occur in the duodenum and pyloric channel; in an analysis of 40 trials of perforated peptic ulcer disease, perforation was most common at the duodenal bulb (62%), followed by the pyloric region (20%), and the gastric body (18%)³². Although the majority of patients who present with ulcer perforation have no prior history of ulcer disease, risk factors for perforation include the prior history of ulcer disease or use of NSAIDs ³³. In patients on NSAID therapy, there is a greater risk of ulcer perforation with a history of prior ulcer, age greater than 60 years, concomitant use of alendronate, selective serotonin reuptake inhibitors, steroids, or anticoagulants ^34–37.

PRESENTATION

Classically, the presentation of a perforated peptic ulcer is described as a three-stage process ³⁸. Initial symptoms, occurring within 2 hours of perforation, include the abrupt onset of abdominal pain. The pain may initially be focused at the epigastrum, but it can quickly become generalized. Between 2 and 12 hours of perforation, the abdominal pain worsens and there may be significant pain with palpation of the hypogastrum and right lower quadrant secondary to drainage of succus from the perforation. 12 hours after perforation, in addition to increasing pain, the patient may have fever, signs of hypovolemia, and abdominal distention.

EVALUATION

It is important to quickly diagnose a perforated peptic ulcer. The prognosis is improved if treatment is provided within 6 hours of perforation, whereas a delay in treatment beyond 12 hours following perforation is associated with an increase in both morbidity and mortality ^{38, 39}. A prospective study of patients with duodenal ulcer perforations, Boey and colleagues identified that perforations >48 hours, pre-operative shock, and concurrent medical illness were associated with an increase in mortality ⁴⁰. In a patient with an appropriate history, if free air is present on an upright chest or abdominal x-ray or computed tomography (CT) scan, no additional testing is required before proceeding with treatment. However, direct findings of perforation are not identified in 10–20% of patients with a perforated duodenal ulcer ⁴¹. An upper GI study or abdominal CT scan with oral contrast may be performed to confirm the diagnosis.

The patient should be evaluated for Helicobacter pylori infection as knowledge of a patients H. pylori status can play an important role in treatment decisions. H. pylori infection is present in 70–90% of duodenal ulcers and 30–60% of gastric ulcers and antibiotic therapy is very effective at eradication⁴². Non-invasive testing options include urea breath testing, stool antigen testing, and serology. Stool antigen testing is a modern and rapid method of gaining information on a patients H. pylori status in the preoperative period. A monoclonal stool antigen test has a 94% sensitivity, 97% specificity, and is processed in an hour ⁴³. A rapid stool antigen test may be processed within 5 minutes; however the sensitivity is 76% and specificity 98% ⁴⁴.

TREATMENT

Medical management of a perforated peptic ulcer consists of fluid resuscitation, nasogastric decompression, acid suppression, and empiric antibiotic therapy. Antibiotic therapy should cover enteric gram-negative rods, anaerobes, oral flora and fungus ^{45, 46}. A non-surgical treatment plan consisting of only the aforementioned medical management has been proposed for patients with contained perforation at high risk for operative complications ⁴⁷. Despite the appeal of non-operative therapy in high risk patients, the application of this strategy is likely limited, as was demonstrated in a randomized, controlled trial of non-operative treatment for perforated peptic ulcers in which patients over 70 years of age were less likely to improve with conservative management ⁴⁸.

Operative intervention is almost always indicated in the treatment of perforated peptic ulcers. Unfortunately, emergency surgery for a perforated peptic ulcer has a 6–30% risk of mortality ³⁹. In the setting of emergency surgery for perforated peptic ulcer, several variables have been independently associated with an increase risk of mortality, including age, American Society of Anesthesiologists (ASA) class, shock on admission, hypoalbuminemia on admission, an elevated serum creatinine, and pre-operative metabolic acidosis ⁴⁹. Unfortunately most of these adverse prognostic factors are not modifiable, and despite substantial advances in medical care, there has been little change in the mortality of perforated ulcer over the last 15 years³.

The choice of operation will depend on the site of perforation found at exploration. Duodenal and pyloric channel perforations are the most common site of ulcer perforation and are functionally grouped as duodenal perforations. The most common technique for the management of a perforated duodenal ulcer is a patch repair with an omental pedicle commonly referred to as a Graham patch or omentopexy⁵⁰. In this technique the ulcer is not closed, but instead a pedicle of vascularized omentum is sutured over the perforation site with multiple interrupted sutures. These repairs may be performed by a laparoscopic or open approach, but ulcers over 10 mm in size appear to increase the risk of conversion to open surgery. In a randomized controlled trial of 121 patients with perforated peptic ulcer disease Siu and colleagues demonstrated significantly lower analgesic requirements, post-operative hospital length of stay, and time away from work in patients receiving a laparoscopic repair. Importantly, there were no significant differences between the groups receiving an open or laparoscopic repair in terms of mortality, incidence of reoperation, or in the identification of post-operative intra-abdominal fluid collections ⁵¹. Classically repair of a perforated duodenal ulcer was accompanied by a definitive ulcer operation either a vagotomy and pyloroplasty or a patch repair and a parietal cell vagotomy. However with our improved understanding of the pathogensis of peptic ulcers, it appears that definitive ulcer surgery is no longer necessary in most cases. Patch repair of the perforation with concomitant medical therapy is often sufficient for patients with ulcer disease secondary to H. pylori infection or NSAIDs. A randomized study of 99 patients with perforated duodenal ulcers infected with H. pylori treated with a patch repair demonstrated that successful treatment of H. pylori significantly decreased ulcer recurrence from 38% to 5%, leading the authors to conclude that a definitive ulcer procedure is not necessary in this setting ⁵². In light of this data knowledge of a patients H. pylori status prior to surgery cannot be understated.

In the rare patient with a history of H. pylori negative peptic ulcer disease or those who are unable to stop NSAID therapy, a definitive ulcer procedure may be performed if the patient is hemodynamically stable and has minimal intra-abdominal contamination. In this setting, a truncal vagotomy and pyloroplasty, omental patch and parietal cell vagotomy, or an antrectomy with truncal vagotomy have all been advocated as suitable repairs. Vagotomy and pyloroplasty is the easiest operation to perform, but has an 10–15% ulcer recurrence rate and exposes the patient to all of the complications of dumping and post vagotomy syndromes. Omental patch with parietal cell vagotomy avoids most of the complications of dumping and post vagotomy syndrome, but is a more challenging operation and high ulcer recurrence rates have been reported in inexperienced hands⁵³. The benefits of a vagotomy with antrectomy are that the procedure may be applied to a variety of situations, and that the ulcer recurrence rate is very low. The disadvantages are that the operative mortality is higher than either of the other procedures, and the surgeon is forced to deal with an often chronically scared duodenal stump and the complications of duodenal stump leak or anastomotic failure. The choice of definitive operation should depend on the experience of the surgeon, but in the absence of significant experience with ulcer surgery, vagotomy and pyloroplasty or not performing definitive surgery in the emergent setting seems prudent.

In the case of a perforated gastric ulcer, either ulcer excision and repair of the defect or biopsy and omental patch are the most expeditious approach in the emergency setting. Because malignancy has been reported in 4–14% of gastric perforations, biopsy or excision of the ulcer when feasible is important⁵⁴. For a gastric ulcer located along the greater curvature, antrum or body of the stomach, simple wedge excision of the ulcer is easy to perform, often with a single fire of a linear stapler, simultaneously obtaining tissue for biopsy and closing the perforation. Although no trials have been conducted comparing the techniques, this could be performed either with an open or laparoscopic approach. As with bleeding ulcers, ulcers along the lesser curvature of the stomach are more challenging because of the left gastric artery arcade, and the GE junction in high lesser curve ulcers. For distal lesser curve ulcers distal gastrectomy can be performed with similar mortality to that seen with patch or simple excision⁵⁵. The operative approach to perforation of an ulcer located next to the esophagogastric junction may include a subtotal gastrectomy to include the ulcer with a Roux-en-Y esophagogastrojejunostomy as described above for bleeding ulcers.

A particularly challenging clinical scenario is the perforated giant duodenal ulcer. With a duodenal ulcer perforation greater than 2 cm, there is an increased risk of repair failure with omental patch repair, with leak rates of up to 12% reported ⁵⁶. In the setting of a giant perforated duodenal ulcer there is no standard management. Recommendations for repair include: omental patch, controlled tube duodenostomy, jejunal pedicled graft, jejunal serosal patch, pedicled omental plug, partial gastrectomy, and gastric disconnection ^56–58. The pedicled omental plug is an intriguing and easy option for this problem. In this procedure an NG tube is passed out through the perforation and a tongue of omentum sutured to the NG tube. This is withdrawn back into the stomach and the omental plug is then sewn to the edges of the ulcer. In a single randomized trial comparing omental plug with standard omental patch, plug repair was associated with a lower recurrent leak and duodenal stenosis rate⁵⁶. The choice of repair should be influenced by the patient’s clinical status, the size of the perforation, the degree of intraperitoneal contamination, and the surgeon’s experience.

Emergency Ulcer Surgery

Introduction

Pathogenesis of Peptic Ulcer Disease

The Epidemiology of Peptic Ulcer Disease

Bleeding Peptic Ulcer

PRESENTATION AND INITIAL MANAGEMENT

Table 1

Blood Urea Nitrogen (BUN mg/dl)
18.2–22.4	2
22.4–28	3
28–70	4
> 70	6
Hemoglobin for Men (g/dl)
12–13	1
10–12	3
<10	6
Hemoglobin for Womens (g/dl)
10–12	1
< 10	6
Systolic Blood Pressure mmHg
100–109	1
90–99	2
<90	3
Heart Rate >100 Bpm	1
Presentation with Melena	1
Presentation with Syncope	2
Hepatic Disease	2
History of Heart Failure	2

ENDOSCOPIC INTERVENTION

Table 2

Variable	0	1	2	3
Age	<60	60–79	≥80
Shock	No Shock	Tachycardia	Hypotension
Comorbidity	None		Cardiac Disease	Liver or Kidney Failure
Diagnosis	Mallory-Weiss or no diagnosis	All other Diagnoses	Upper GI Malignancy
Stigmata of recent Hemmorhage	None or Dark Spot		Blood in GI tract, bleeding or visible vessel, adherent clot

OPERATIVE APPROACH

PERFORATED ULCER

PRESENTATION

EVALUATION

TREATMENT

Background, Indications for Surgery vs Conservative Management, General Surgical Considerations

The patient is placed in a supine position. A midline incision is the incision of choice, and it can be extended to the symphysis pubis if necessary. After entry into the abdomen, a thorough inspection of the abdominal cavity is performed. The stomach and duodenum are carefully examined to determine the exact site of perforation. If the anterior surfaces of the stomach and duodenum show no abnormalities, the posterior surface of the stomach should be examined.

Truncal vagotomy and drainage

The esophagus is retracted to patient’s left, and the left hemiliver is retracted to the patient’s right side. A transverse incision is made in the peritoneum overlying the esophagus at the hiatus in the diaphragm. This opening is widened. A right-angle clamp can be used to pass a Penrose drain around the esophagus. The anterior vagal trunk is then sought and separated from the esophagus. The posterior vagus is usually felt as a cord lying posterior to the esophagus.

After the vagal trunks have been transected, the distal 5-6 cm of the esophagus should be cleared by meticulous dissection and division of nerve fibers and blood vessels. The criminal nerve of Grassi, which is a branch of the posterior vagus nerve, must be sought and divided. Careful attention to operative technique is essential to ensure complete vagotomy. The drainage procedure depends on the condition of the duodenum. Pyloroplasty (see below) is preferred by most surgeons; if the duodenum is inflamed, a gastrojejunostomy (see below) is the safest alternative.

Pyloroplasty

A Kocher maneuver is performed to mobilize the second part of the duodenum. Two silk stay sutures are made at the superior and inferior aspects of the pylorus. A 6- to 10-cm longitudinal incision is made, starting from the antrum and extending across the pylorus and into the first part of the duodenum. This incision is closed transversely with an inner layer of interrupted 3-0 absorbable sutures encompassing all layers; this is followed by a seromuscular layer of 3-0 silk Lembert sutures.

Gastrojejunostomy

A loop of jejunum approximately 12-15 cm from the ligament of Treitz is lifted and brought next to the greater curvature of the stomach through an opening in the transverse mesocolon, usually to the left of the middle colic vessels. A gastrotomy is made in the prepyloric region or at the most dependent portion of the stomach.

Before the bowel is opened, noncrushing clamps are placed on both sides of the proposed anastomosis sides. The area of the anastomosis is isolated with moist laparotomy pads to avoid spillage and contamination. The stomach and the adjacent jejunum are then opened. A full-thickness inner layer is started posteriorly with 3-0 absorbable sutures and completed anteriorly with inverting Connell sutures. Alternatively, a stapled anastomosis can be performed by putting one limb of stapler in the gastrotomy and the other in the jejunotomy.

Billroth I and II gastrectomy

The greater omentum is identified at the greater curvature of the stomach. It is separated from the proximal half of the transverse colon. Next, branches from the gastroepiploic arcade to the greater curvature are divided. The posterior wall of the first part of the duodenum is separated from the pancreas and divided with a gastrointestinal anastomosis (GIA)-60 linear stapler. The right gastric artery above the pylorus is identified and divided. The gastrohepatic ligament is divided proximally with an electrocautery along the lesser curvature. The left gastric vessels lying along the lesser curvature are ligated. The stomach is divided with a GIA-90 linear stapler.

Billroth I

A Billroth I gastroduodenal anastomosis can be constructed if an adequate length normal duodenum is available. A two-layer anastomosis is performed, with an outer layer of interrupted Lembert sutures and an inner layer of full-thickness continuous absorbable sutures.

Billroth II

If a Billroth II gastrojejunostomy is chosen, a loop of proximal jejunum is selected and brought in an antecolic or retrocolic fashion toward the transected stomach. For a handsewn anastomosis, a posterior layer of interrupted Lembert sutures is placed. A longitudinal enterotomy is made in the loop of jejunum, and the appropriate length of adjacent gastric staple line is excised. The inner layer of continuous 3-0 absorbable sutures is placed. Then, anterior interrupted Lembert 3-0 silk sutures are placed.

For a stapled Billroth II anastomosis, stay sutures are placed so that the loop of jejunum is held adjacent to the gastric remnant. A small stab incision is made in the jejunum and at the adjacent posterior wall along the greater curvature of the stomach. The limbs of the GIA stapler are inserted and fired.

Highly selective vagotomy

Patient positioning and incision are the same as for truncal vagotomy and pyloroplasty. The key step is identification of the anterior nerve of Latarjet, which leaves the esophagogastric junction and runs in the lesser omentum parallel to the lesser curvature. In order to enter the lesser sac, the gastrocolic ligament is divided. Neurovascular branches are carefully ligated with the help of a fine clamp. Next, the stomach is turned upward, and posterior denervation is conducted in a similar fashion.

Ulcer Surgery and its Complications. Peptic ulcer surgery

Historical and global perspective

This article will summarise the elective surgical procedures that were historically used for peptic ulcer disease and the consequences of such surgery. These procedures are now almost obsolete but there may some elderly patients who will have had such surgery.

It will also describe the indications for emergency surgery for peptic ulcers and the resulting morbidity and mortality.

Data analysis from the UK^[1]and the USA^[2]shows that elective surgery for peptic ulcer disease has now ‘virtually disappeared’. This is attributed to antacid medications, the treatment of Helicobacter pylori, and an awareness of the gastric erosive effect of non-steroidal anti-inflammatory drugs (NSAIDs). However, the need for elective surgery was declining even before these treatments came about, which suggests a change in the natural history of peptic ulcer.

Nevertheless, there are some elderly patients still alive who have had elective surgery, so it is useful to know the effects of the procedures.

Furthermore, the rate of emergency surgery for peptic ulcer disease, although infrequent, has remained almost constant since the 1980s. The main indications for emergency surgery are haemorrhage and perforation. Stenosis with gastric outflow obstruction and potential malignant change are less common indications.

Smoking, heavy alcohol use, cocaine use and HIV are risk factors for perforation of a peptic ulcer^[3].

In some parts of the developed world it is estimated that 90% of children are infected with H. pylori by the age of 5 years. It is hypothesised that this leads to high rates of peptic ulcer disease, although data are hard to come by^[4].

Indications for surgery

The options for malignant ulcers are discussed in the separate Gastric Cancer article.

Elective surgical procedures

Various elective procedures for peptic ulceration have been assessed^[5]. The operations that have been used traditionally are:

Billroth I gastrectomy.
Billroth II or Pólya gastrectomy.
Truncal vagotomy and pyloroplasty.
Highly selective vagotomy.

Gastric ulcers were in the past best removed together with the gastrin-secreting zone of the antrum (achieved by the Billroth I gastrectomy).

Duodenal ulcers were treated either by removing the body and lesser curve of the stomach (where acid secretion mainly occurs) or by dividing the vagi. As this could interfere with gastric emptying, it was performed with either gastrojejunostomy or pyloroplasty. Gastrojejunostomy alone was used occasionally in elderly patients but this was often complicated by stomal ulcers. In theory this achieved ulcer healing by introducing alkali secretions from the jejunum. Partial gastrectomy with a gastrojejunal anastamosis is called a Pólya gastrectomy.

The partial gastrectomies are largely superseded by the vagotomy operations but many patients may be found who had such operations many years ago. Nowadays even operations to repair perforated ulcers are often performed laparoscopically and there may be a lower risk of immediate complications in low-risk patients^{[6, 7]}. Gastric resection can also be achieved laparoscopically^[8].

Complications after elective surgery

Complications can occur soon after surgery. Early complications usually occur whilst the patient is still in hospital and include wound infections, anastomotic leaks, or recurrence of bleeding.

Late complications vary according to the surgical procedure but they are generally more marked after partial gastrectomy than after vagotomy. Simple truncal vagotomy would lead to failure of gastric emptying and so a drainage procedure such as pyloroplasty is performed but this leads to poor control of gastric outflow. Highly selective vagotomy is supposed to overcome the problem in that it does not require a drainage procedure. It requires great skill to get enough denervation to heal the ulcer but not too much to cause delayed gastric emptying. Highly selective vagotomy has a much lower incidence of complications but a significantly higher incidence of recurrence.

Late complications after peptic ulcer surgery include:

Recurrent ulceration.
Diarrhoea.
Dumping syndrome.
Iron deficiency, vitamin B12 deficiency, folate deficiency.

Post-gastrectomy syndromes

The stomach transforms the intermittent intake of food into a more gradual release into the duodenum and small intestine as well as initiating the process of digestion. The control of gastric emptying is both neural and hormonal. The post-gastrectomy syndromes include:

Small capacity or ‘small stomach’ syndrome – this is associated with fullness after only moderate-sized meals and may be associated with weight loss and reduced appetite.
Dumping syndrome – can be early or late, as set out in more detail under the heading ‘Dumping syndrome’, below.
Bile gastritis and bilious vomiting – can occur particularly after emptying of the afferent loop of a Pólya gastrectomy into the stomach remnant.
Blind loop syndrome (sometimes called stasis syndrome or stagnant loop syndrome) – this affects digestion and absorption, causing:
- Bloating, loss of appetite, abdominal pain and nausea.
- Fatty stools (steatorrhoea).
- Diarrhoea with weight loss.
- Food unable to move through the bypassed section of bowel, producing a bacterial overgrowth syndrome. The bacteria may produce toxins as well as interfere with the absorption of nutrients.
Anaemia usually results from iron deficiency from failure of iron absorption. It can also occur with loss of intrinsic factor and less B12 absorption (typically about two years after total gastrectomy).
Steatorrhoea occurs particularly with a long afferent loop when fatty food is less well absorbed.
Stomal ulceration may occur following gastrectomy for duodenal ulcer.
Metabolic bone disease.

Post-vagotomy syndromes

Highly selective vagotomy aims to maintain the nerves of Latarjet (branches of the vagus nerve which supply the pyloric sphincter) and obviate the need for an accompanying drainage procedure (usually pyloroplasty). Complications afterwards include:

Steatorrhoea and diarrhoea, which are common after vagotomy (although this is less of a problem after highly selective vagotomy). Often such symptoms are transient or episodic. However, in about 2% of cases symptoms are severe or persistent.
Stomal ulceration, which can occur particularly if the vagotomy is incomplete.

Dumping syndrome

^[9]

This is the most troublesome of the syndromes after surgery to eradicate peptic ulcer. Dumping syndrome is a frequent complication of oesophageal, gastric or bariatric surgery.

There is rapid gastric emptying, with the delivery to the small intestine of a significant proportion of solid food as large particles that are difficult to digest. This causes excessive intravascular fluid to move to the intestinal lumen, which results in cardiovascular symptoms, release of several gastrointestinal and pancreatic hormones and late postprandial hypoglycemia.

Early dumping
Early dumping causes symptoms 30-60 minutes after a meal. Early dumping symptoms include both gastrointestinal and vasomotor symptoms. Symptoms include:

Desire to lie down (with fatigue, faintness and possibly syncope).
Palpitations.
Headache.
Flushing.
Epigastric fullness.
Nausea, vomiting and diarrhoea.
Abdominal cramps and borborygmi (abdominal gurgling or rumbling sounds).

Late dumping
Late dumping occurs between one and three hours after a meal. Late dumping symptoms are the result of reactive hypoglycaemia. Symptoms include:

Sweating and tremor.
Hunger.
Difficulty concentrating and even reduced level of consciousness.

Malabsorption

Causes
Failure to absorb essential nutrients may be caused by a combination of factors:

Poor dietary intake (as a result, for example, of bloating and decreased appetite).
Intestinal hurry (with, for example, changes in the gut flora in blind loop syndromes).
Reduced intrinsic factor (for example. after gastrectomy).
Reduced acid secretion (after gastrectomy).

Presenting features
These may be vague and the onset is usually slow:

Iron-deficiency anaemia may be accompanied by fatigue. FBC will show a microcytic, hypochromic anaemia and ferritin will be low.
Folate deficiency will cause macrocytosis and macrocytic anaemia. Poor intake and blind loop syndromes are probably to blame for this common problem.
Pernicious anaemia occurs after partial gastrectomy. Production of intrinsic factor is reduced (and hence absorption of B12). This produces a macrocytic anaemia.
A mixed picture results from a combination of deficiencies in iron, B12 and folate.
Chronic intake of an inadequate number of calories will cause weight loss and even muscle wasting.

Patients who have had such surgery need long-term follow-up with periodic weighing, FBC, ferritin, folate and B12 levels.

Management

Small, frequent meals may enable an adequate intake of nutrients and reduce dumping syndrome. Avoid simple sugars and reduce fluid intake with meals.
Iron and folic acid supplements may be required.
Hydroxocobalamin injections to prevent vitamin B12 deficiency.
Acarabose can reduce the absorption of glucose and help prevent late dumping but it may also aggravate bloating and diarrhoea.
Octreotide is a somatostatin antagonist that can inhibit the release of insulin and various gut peptide hormones. Trials have shown benefit in severe dumping syndrome but it is not licensed for this purpose.
A number of surgical reconstructions are possible of which the best known is the Roux-en-Y gastrojejunostomy. Symptoms may improve with time and so remedial surgery should not be undertaken without giving time.

Emergency surgical procedures

Endoscopic haemostasis can be attempted in upper gastrointestinal haemorrhage where the patient is not compromised.
If surgery is needed, an omental patch is usually stitched over the perforation (a Graham’s omentopexy). This can be done laparoscopically or at laparotomy. Medical therapy for H. pylori eradication usually follows^{[3, 10]}. If the perforation is too large to be patched, a Roux-en-Y gastrojejunostomy or a subtotal gastrectomy may be needed.
For small perforations that are difficult to localise, methylthioninium chloride (methylene blue) dye can be introduced via a nasogastric tube^[11].
Simple suturing of the perforation was generally shown to be ineffective, with a high chance of needing re-operation, from data in the 1970s^[12]and 1980s^[13].

The 30-day mortality after surgery for perforated peptic ulcer, derived from data in the western world, varies between 10%^[3], 16%^[14]and 29%^[15].

The advent of the novel oral anticoagulant drugs, which at present do not have an antidote^[16], may present difficulties in the future management of haemorrhage or perforation of peptic ulcers.

Laparoscopic Repair of Perforated Duodenal Ulcers: Outcome and Efficacy in 30 Consecutive Patients | Gastroenterology | JAMA Surgery

Hypothesis
Laparoscopic management of perforated duodenal ulcers is safe and effective.

Design
Prospective nonrandomized controlled trial.

Setting
Tertiary care academic center.

Patients and Methods
Between October 1993 and October 1997, 30 patients underwent laparoscopic Graham patch repair of perforated duodenal ulcers and 16 had an open repair.

Main Outcome Measures
Morbidity, operating time, analgesic requirements, length of hospital stay, and time to return to work.

Results
There was no difference in morbidity between the 2 groups. Operating time was longer in the laparoscopy group (106 vs 63 minutes; P=.001). Patients with shock on admission or symptoms for more than 24 hours had a higher conversion rate (P<.05). The laparoscopy group required fewer analgesics, had a shorter stay, and a quicker recovery.

Conclusions
Laparoscopic repair for perforated ulcers is safe and maintains benefits of the minimally invasive approach. Laparoscopy is not beneficial in patients with shock.

SINCE THE INITIAL reports of successful laparoscopic management of perforated duodenal ulcers using various operative methods,¹^-4 several larger comparative series have been published confirming the technical feasibility and demonstrating some of the established advantages of the laparoscopic approach.⁵^-11 From these reports, it appears that the main benefits of the laparoscopic repair are decreased postoperative analgesic requirements and diminished trauma to the abdominal wall with its inherent potential complications of wound infection and incisional hernia formation. Other proven advantages of the minimally invasive approach were less evident in these studies because of the presence of sepsis, the systemic effects of which often offset the advantages of the laparoscopic approach.

Despite the appeal of the minimally invasive approach to perforated peptic ulcer, no definitive criteria have been established to select patients who may benefit the most from this approach and those in whom its use may be detrimental. This is particularly true today with the current effective antiulcer medications including Helicobacter pylori eradication regimens, which may obviate the need to perform an additional definitive antiulcer procedure. Furthermore, in analyzing published results, no strict parameters to evaluate outcome measures have been established, thus potentially underestimating the true benefits of laparoscopy in this setting.

The aims of this study were to compare outcome and efficacy of laparoscopic and open surgery for perforated duodenal ulcers, and to define the group of patients who might benefit from the laparoscopic approach.

Between October 1993 and October 1997, 30 patients who underwent laparoscopic omental patch repair for perforated duodenal ulcers at the Los Angeles County–University of Southern California Medical Center were evaluated prospectively. During the same period, 16 patients had an open procedure. All patients were operated on by residents and assisted by senior attending physicians. The decision to perform laparoscopy or an open repair was left to the discretion of the supervising surgeon, and was dependent on his level of laparoscopic expertise. Patients with shock on admission, defined as a systolic blood pressure less than 80 mm Hg, were not excluded from the laparoscopic approach. All patients received appropriate management of their septic condition, including resuscitative measures for the patients with shock. Postoperative pain assessment included careful monitoring of doses of intramuscular or intravenous analgesics (meperidine hydrochloride, 75 mg). Postoperatively, all patients received triple therapy for eradication of H pylori. Liquid diet was started when bowel sounds were present, and patients were discharged home when they tolerated an oral diet, were afebrile, and had a normal white blood cell count.

A comparison was done between the 2 groups by assessing morbidity and mortality, operative time, amount of analgesics required after surgery, time to return to normal diet, length of hospital stay, and time to return to work. Follow-up endoscopy was done at 6 months and ulcer recurrence was assessed.

A pneumoperitoneum was created using a Veress needle or a Hassan open technique in the presence of abdominal distension. Insufflation pressure was maintained below 11 mm Hg to minimize the risk of transperitoneal translocation of bacteria and endotoxemia. Four ports were inserted: the upper trocar was placed in the subxiphoid area and used for irrigation and suction and/or retraction of the liver. An umbilical port was used for the camera and the 2 remaining working ports were placed on each side of the camera port in a triangulated fashion. The surgeon stands between the legs of the patient, with an assistant on each side. The gallbladder, which usually covers the perforation, was retracted upward and held by the assistant. Inflammatory adhesions were divided using harmonic shears (LCS; Ethicon Endosurgery Inc, Cincinnati, Ohio). This device allows a faster dissection while limiting lateral thermal damage. The exposed area was examined and the perforation identified. For the purpose of the study, the tip of the suction-irrigation tube (5 mm) was used to measure the size of the perforation. The next step was careful and thorough irrigation and suction of all intra-abdominal fluid, requiring about 10 L of isotonic sodium chloride solution mixed with local antibiotics. Each quadrant was cleaned methodically, starting at the right upper quadrant and moving in a clockwise fashion. Special attention was given to the vesicorectal pouch retracting the sigmoid colon and accessing all loculated pelvic spillage. Fibrinous membranes on the small bowel were removed as much as possible without damaging the serosal surfaces.

The perforation was closed using the classic Graham patch technique with the omental patch inserted between 2 or 3 stitches with nonabsorbable sutures (Prolene; Ethicon Inc, Sommerville NJ) before tying the knots intracorporeally. This method was preferred to the technique of suturing the perforation closed and buttressing the repair with an omental patch.

Decision to convert to an open approach was dictated by the patient’s intolerance to carbon dioxide insufflation and consequent hemodynamic instability, and the inability to obtain appropriate laparoscopic closure due to the size of the perforation or the friability of the ulcer edges. No drains were placed at the end of the procedure, and the fascia was closed in all ports. The open repair was conducted through a midline incision and followed the same technical guidelines.

All data are expressed as median and interquartile range unless otherwise stated. Comparison between the 2 groups was made using nonparametric methods (Mann-Whitney test). Comparisons between categorical data were made using a χ² test.

The 2 groups were categorized based on an intention-to-treat basis. Thus, patients in the laparoscopy group who were converted to an open procedure remained in the laparoscopy group for the statistical comparisons. P<.05 was considered statistically significant.

Patient demographics are summarized in Table 1. There was no difference in age, weight, duration of symptoms, and time to surgery between the groups. Of the 30 patients treated laparoscopically, 6 (20%) were in shock on admission, compared with 4 (25%) in the open surgery group. Sixteen (53%) of the 30 patients in the laparoscopy group had a history suggestive of chronic peptic ulcer disease. Alcohol and cocaine use were similar between the 2 groups.

The median operating time of the laparoscopic patch repair was significantly longer than the open procedure (106 minutes [range, 76-122] vs 63 minutes [range, 51-86]; P=.001). Five (17%) patients in the laparoscopy group underwent conversion to an open procedure. The reasons for conversion were large perforations (diameter >6 mm) precluding safe laparoscopic closure in 3 patients and cardiovascular instability in the remaining 2 patients.

Of the 6 patients in the laparoscopy group who presented with shock on admission, 3 underwent conversion, as opposed to only 2 conversions of the 24 patients without evidence of shock on admission (P=.04). No patients with symptoms for less than 24 hours underwent conversion (n=15), as opposed to 15 patients who had symptoms for more than 24 hours, 5 of whom underwent conversion (33%; P=.01).

The postoperative complications are summarized in Table 2. There was no difference in morbidity between the laparoscopy and open surgery groups (6 of 30 patients vs 5 of 16 patients; P=.09). One death occurred in each group.

The opiate analgesic requirements were significantly less in the laparoscopy group compared with the open surgery group (3 doses [range, 2-7] vs 9 doses [range, 7-11]; P=.002). Time to return to a normal diet was also significantly shorter in the laparoscopy group (3 days [range, 1-4] vs 5 days [range, 4-7]; P<.001). This was also reflected in the median length of hospital stay that was significantly shorter in the laparoscopy group (3 days [range, 3-7]) compared with the open surgery group (8 days [range, 6-10]) (P=.003). The time to return to work in the patients in the laparoscopy group (21 days [range, 18-27]) was also significantly shorter than that in the open surgery group (30 days [range, 27-38]) (P=.001).

Outcome of patients with shock on admission treated laparoscopically was considerably worse than those without shock (Table 3). Not only was the conversion rate higher, but the rate of complications, length of hospital stay, and time to return to work were all significantly higher. The rate of complications in patients with shock on admission in the open surgery group was also significantly higher than in patients without shock (Table 4). Both deaths occurred in patients who presented with shock.

A follow-up endoscopy at 6 months was performed in 13 patients from the laparoscopy group and in 7 patients from the open surgery group. A recurrent ulcer was documented in only 1 patient in the open surgery group.

The widespread use of histamine₂ (H₂)–receptor blockers, proton pump inhibitors, and, more recently, effective treatment protocols for eradication of H pylori, have reduced the surgeon’s role in the elective treatment of peptic ulcer disease. The frequency of complicated ulcer disease requiring surgery has not changed, and the incidence of perforated ulcers is still about 5% of all duodenal ulcers and may be rising with the increased use of nonsteroidal anti-inflammatory drugs in elderly women.¹² With the advancement of laparoscopic techniques, the feasibility and safety of laparoscopic closure of perforated ulcers has been shown in several large series.⁶^,10^,11

There are several potential advantages to the minimally invasive approach. Simple patch closure of the perforation can be accomplished relatively easily laparoscopically and is probably a sufficient treatment. Following simple closure and postoperative treatment with H₂-receptor blockers, less than 20% of the patients will require subsequent definitive ulcer surgery. Furthermore, Sebastian et al¹³ and Tokunaga et al¹⁴ demonstrated that in more than 83% to 90% of patients with perforated ulcers, H pylori infection is present. The addition of anti–H pylori treatment postoperatively may even further reduce the number of patients who might require an acid-reducing procedure. The routine addition of an antiulcer procedure such as parietal cell vagotomy as recommended by Jordan and Thornby¹⁵ is therefore probably not necessary and might lead to a prolonged operation in gravely ill patients.

Simple laparoscopic patch closure is also an adequate treatment in perforations not associated with acid hypersecretion, as is the case in patients with crack cocaine–induced perforated ulcers and ulcers secondary to use of nonsteroidal anti-inflammatory drugs.¹⁶

The laparoscopic approach offers advantages demonstrated in other well-established procedures. In contrast to published data where the main benefit of the laparoscopic repair was decreased postoperative analgesic requirements,⁵^,10 we have demonstrated additional significant advantages: quicker resumption of oral intake, shorter hospital stay, and quicker return to work. This difference may reside in the younger age of our patient population compared with the older age group in other series. In addition, we have used strict criteria in defining the stages of postoperative recuperation, whereas in other series the postoperative course was less defined, and in many cases prolonged because of social and nursing problems leading to a mean hospital stay of up to 17 days in one series.⁶

Moreover, the minimally invasive approach has the considerable advantages of diminished trauma to the abdominal wall and improved cosmesis. Large abdominal incisions in the face of peritonitis carry a significant risk of wound infection and postoperative incisional hernias in up to 15% of cases.¹⁷

An added benefit of laparoscopy is its diagnostic value. Proponents of selective nonoperative management of perforated ulcers by demonstrating the absence of gastrointestinal leakage on a gastrografin swallow test and showing improvement on serial physical examinations do still not address the problem of possible erroneous diagnosis.¹²^,18^,19 Performing a routine laparoscopy as the initial step in managing patients with a suspected perforated ulcer has the advantage of identifying an occasional different abnormality. In addition, laparoscopy enables one to perform a thorough cleansing of the abdominal cavity thus decreasing the risk of developing intra-abdominal abscesses, which, as reported by Crofts et al,¹⁸ occurred in 15% of patients treated conservatively.

A disadvantage of the laparoscopic approach is a longer operating time, but this had no effect on the overall results. Some authors were able to shorten the operating time by using sutureless techniques to close the perforation with the use of a gelatin plug and application of fibrin sealant (Tisseel; Baxter Immuno, Deerfield, Ill).⁴^,5 We think that this method is elegant and can be added to the surgical armamentarium.

A major concern is the effect of high-pressure insufflation in the face of peritonitis and possible endotoxemia and bacterial translocation through peritoneal surfaces into the bloodstream. Experimental work done in pigs with gastric perforation and peritonitis has shown no difference in mortality between laparoscopic and open repair if surgery was performed less than 12 hours from perforation. After 12 hours, the incidence of bacteremia and endotoxemia was significantly higher in the laparoscopy group.²⁰ Lau et al,²¹ examining acute-phase response markers and endotoxemia in patients with perforated ulcers receiving laparoscopic repair, found no difference in these parameters compared with patients who had open repair. It appears that if the laparoscopic repair is performed relatively early following perforation and insufflation pressures are kept at low levels, the risk from bacterial translocation and endotoxemia is not significant.

In analyzing our results, we found 2 clinical parameters that may preclude safe laparoscopic repair of perforated ulcers—shock and symptom duration more than 24 hours. Patients who presented with evidence of shock and were treated laparoscopically had a high conversion rate and a significantly worse postoperative course than patients without shock on admission. In this clinical situation, a laparoscopic approach that has a high likelihood of failure should not be attempted, and the patient should have an expeditious open repair. Patients with symptoms for more than 24 hours represent another group where laparoscopy may be attempted with a high risk of conversion to an open procedure. These risk factors are consistent with the operative risk factors in perforated duodenal ulcers defined by Boey et al.²²

In conclusion, despite the limitation of a nonrandomized trial, our study shows that laparoscopic repair of perforated duodenal ulcers is safe and carries many of the established advantages of minimally invasive techniques. Nevertheless, it should be used selectively, reserving the traditional open approach for patients presenting with shock on admission. Patients with symptoms for more than 24 hours have a higher chance of conversion to an open technique.

Presented at the 70th Annual Session of the Pacific Coast Surgical Association, San Jose del Cabo, Baja California Sur, February 14, 1999.

Corresponding author: Namir Katkhouda, MD, USC Department of Surgery, Healthcare Consultation Center, 1510 San Pablo St, Los Angeles, CA 90033.

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Edward H. Phillips, MD, Los Angeles, Calif: Virtually every major treatment for perforated ulcer has been studied at LA County–USC Medical Center, from definitive therapy to nonoperation for patients in whom the ulcer has sealed. Now, with recognition of the role of H pylori in its pathophysiology and the application of laparoscopy, a new therapy is under investigation at the very center that has already taught us so much. The authors have compared laparoscopic with open omental patch closure of perforated duodenal ulcers and found that patients who were treated laparoscopically resumed oral diets and left the hospital sooner than patients with open procedures. A subset of patients who were in shock on admission had longer hospitalizations, more complications, and more conversions to open operations following attempted laparoscopic repair. Their data show that laparoscopic omental patch repair of perforated ulcers is feasible in skilled hands and has a superior outcome.

I have several questions for the authors. First, treatment protocols for perforated ulcer have always been stratified based upon the presence or absence of shock. Your patients in shock were operated on significantly earlier than those not in shock, with worse outcome. Might they have done better after a longer period of resuscitation, particularly in the laparoscopic group, where abdominal insufflation exacerbates hemodynamic abnormalities? What are your resuscitation protocols? Were the outcomes of laparoscopic, converted, and open techniques in just shock patients compared?

I was impressed that laparoscopic patients were fed on average 3 days after operation. I’ve never been accused of being timid when it comes to laparoscopy, and these experiences have taught me that we can feed patients sooner than we thought. What’s your protocol for oral alimentation? Were nasogastric tubes used? Also, what diagnostic studies were performed preoperatively to see if the ulcer was sealed already, such as a Hypaque upper GI [gastrointestinal study]? Finally, there is considerable opinion today that simple patch closure is not optimal therapy for chronic ulcer disease, as was the case in 53% of your laparoscopic group. While the emergency general surgeon inside of us may wish to just close the perforation and get back to bed, the foregut surgeon in us says that stable patients should be treated with ulcer closure and parietal cell vagotomy (PGV). Does this mean that the laparoscopic procedure should be reserved only for stable patients without a prior history of ulcer? Or should we be performing a laparoscopic PGV? Perhaps we’ll be hearing from you about this next year in San Francisco. What are your current thoughts on this subject?

Some of the best years of my life were spent as a student and resident at LA County–USC Medical Center, and I expect that the current residents will agree when I say that their faculty are world experts when it comes to giving ulcers. As we have heard today, they are also masters when it comes to fixing them.

Lawrence Way, MD, San Francisco, Calif: I have a couple of questions. First, can you describe the technique used for closing the perforations? The photograph shown during the presentation looked as if it could have represented a simple approximation instead of a genuine Graham patch. Incidentally, while I have the chance I want to condemn the use of hernia staples for closing perforated ulcers, a method likely to result in a leak. I know that you did not do this, but I have heard of this shortcut being tried in practice.

Second, was there a relationship between the outcome of the operation and the results of cultures of abdominal fluid taken during the laparoscopy?

John Payne, MD, Honolulu, Hawaii: This is a good approach. In your comments on the learning curve and the duration that it takes to do this operation did you notice a difference as you stratified your patients between your first 10, your second 10, and your most recent patients, if there was a difference in the time of the operation?

Carlos A. Pellegrini, MD, Seattle, Wash: You looked at length of stay and you looked at consumption of analgesics. Are these populations matched enough to compare them? For example, the patients who were excluded from the laparoscopic technique, in particular, cirrhosis, advanced cardiac disease, and so forth, were those part of the 16 patients who were operated on? And, second, it has become clear to many of us that the way we approach the patients preoperatively bears significantly in length of stay and return to work. Those 2 parameters are influenced by us telling the patient you have to stay off work for 6 weeks vs you have had a limited approach, you should go back to work in 8 days. In fact, can you comment as to how you handle these aspects?

James J. Peck, MD, Portland, Ore: Do these patients have nasogastric tubes, or do they not? If at the time of surgery you find a callus or evidence of chronic peptic ulcer disease, is that an indication to open or to do the laparoscopic parietal cell procedure?

Karen E. Deveney, MD, Portland: Was the length of stay equivalency possibly due to duration of use of intravenous antibiotics, or what was responsible for that fairly long length of stay in the group repaired laparoscopically?

Bruce E. Stabile, MD, Torrance, Calif: Dr Katkhouda, I am not clear whether there was a bias in the selection of patients. Could you tell us whether it was surgeons’ preference whether the patient had an open operation, or were some surgeons doing only laparoscopic and others doing only open operation?

Dr Berne: To get right to the questions, Dr Phillips pointed out the fact that the patients in shock got to the operating room earlier than the stable patients. He wondered if a longer period of resuscitation wouldn’t have been better for them. The patients in this series were all basically resuscitated to the same end points, that is, slowing of the pulse, good blood pressure, and good urine output. They went to the operating room when we thought that they were resuscitated, and this was done rather quickly. The difference in the time to the operating room is that the sicker patients in our operating room triage system tend to get to the operating room earlier than stable patients.

The next question was about the protocol regarding feeding and the use of nasogastric tubes. I have to say that does seem worrisome, but in the laparoscopic era we have gotten used to giving people food earlier on than we used to. It just doesn’t seem to cause much trouble. Somebody else asked about the leak rate: we did not experience leaks in either group.

Dr Phillips also asked about the use of water-soluble upper GI studies. When he was a resident we felt strongly about the use of water-soluble upper GIs to select patients with perforated ulcer disease for nonoperative management. Today there is clear evidence that Helicobacter infection is the major cause. As many as 95% of patients with perforated ulcers can be demonstrated as harboring Helicobacter. Now we only use water-soluble GIs in situations where there is a patient who we don’t want to operate on; one of those that Dr Katkhouda mentioned with a bad heart, bad cirrhosis, or some other reason why we want to stay out of their abdomen, we believe you can do a water-soluble upper GI. About half of the patients will be sealed and you don’t need to do anything more. But that is the rare patient, and those patients were not included in this study.

In regard to the technique, it is a reversion back to the simple Graham patch where the omental tab is pulled up and then sutures are placed over it and tied down, trying not to necrose the patch. We do not use hernia staplers as there is no direct attempt to close the hole itself.

Dr Way asked about the outcome vs cultures. We did not look at that. Dr John Payne asked about whether the technique was difficult to learn. Our guess would be that this procedure is one of the next things to teach residents after they have mastered cholecystectomy. It is a relatively simple procedure to do. It is a little tedious, particularly the washing out of the peritoneal cavity, but it is not technically challenging.

Dr Pellegrini, you are right. This study was not randomized, controlled, or prospective. Dr Stabile asked a question about the bias for selection for each group in this study. It depended on whether the attending on that day felt that he or she was comfortable with laparoscopic surgery. Our policy with emergency abdominal, nontrauma surgery is that if the attending is comfortable starting with laparoscopic surgery we do that, but with the caveat that if it seems to be not going well or possibly dangerous, that the case is converted to open. If the attending surgeon is starting the case with laparoscopy, then they don’t do that. Therefore, it was by attending staff choice.

Also, the patients were not told when to go back to work. The patients generally decided on their own. We don’t think they were led into returning to work earlier in one group than the other by the instructions from the doctors.

Dr Deveney, we do not think that the length of stay was due to differences in the antibiotics. That didn’t seem to be the limiting factor in the patient’s recovery.

Perforated Peptic Ulcer Disease: A Review of History and Treatment – FullText – Digestive Surgery 2010, Vol. 27, No. 3

Abstract

Background: In the last one hundred years much has been written on peptic ulcer disease and the treatment options for one of its most common complications: perforation. The reason for reviewing the literature was evaluating most common ideas on how to treat perforated peptic ulcers (PPU) in general, opinions on conservative treatment and surgical treatment and summarizing ideas about necessary pre-, per- and postoperative proceedings. Method: All relevant articles found by Medline, Ovid and PubMed search were used. Results: A hundred articles written between 1929 and 2009 were reviewed. Of these, 9 were about the history of treatment, 7 about conservative treatment, and 26 were about the surgical procedure of which 8 were addressing laparoscopic correction. Overall there is no consensus, but some advice is given. For conservative treatment there are only a few indications. Use of an omental patch is recommended, irrigation and drainage are not. Laparoscopic correction of PPU as well as for definitive ulcer surgery has many advantages. Conclusions: Surgery for PPU is still a subject of debate despite more than an era of published expertise, indicating the need for establishing guidelines.

History

For thousands of years healthy people have had acute abdominal pain, nausea, vomiting and diarrhea followed by death in a few hours or days. Often these symptoms were attributed to poisoning and people have been sent to prison for this [1]. King Charles I’s daughter, Henriette-Anne, died suddenly in 1670 (at 26 years of age) after a day of abdominal pain and tenderness. Since poisoning was suspected autopsy was performed 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 [1,2]. Necropsies were first allowed since 1500 and became more routine between 1600 and 1800 [2,3]. As a consequence, perforation of the stomach was more often observed. Johan Mikulicz-Radecki (1850–1905), often referred to as the first surgeon who closed a 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 inflammation by careful cleansing of the abdominal cavity’ [4]. Surprisingly enough, treatment has not changed much since, still consisting of primary closure of the perforation by a single stitch suture and a convenient tag of adjacent omentum on top of this [5,6,7,8]. Although this therapy sounds very simple PPU still remains a dangerous surgical condition, associated with high morbidity and mortality, not to be underestimated [9].

Clinical Presentation and Investigation

In 1843, Edward Crisp was the first to report 50 cases of PPU and accurately summarized the clinical aspects of perforation, concluding: ‘The symptoms are so typical, I hardly believe it possible that anyone can fail to make the correct diagnosis’ [10]. Patients with PPU have a typical history of sudden onset of acute, sharp pain usually located in the epigastric area and sometimes with shoulder pain, indicating free air under the diaphragm [11]. Bases on collected data from 52 papers on PPU clinical characteristics have been summarized in table 1. The typical patient with PPU is male with an average age of 48 years. He may have a history of peptic ulcer disease (PUD) (29%), or nonsteroidal anti-inflammatory drugs (NSAIDs) usage (20%). Vomiting and nausea are present in 50% of the cases. At physical examination, pulse might be quickened, but seldom goes beyond 90 bpm. About 5–10% of patients experience shock with a mean arterial pressure of less than 80 mm Hg [12]. Hypotension is a late finding as is high fever. Obliteration or complete absence of liver dullness was only noted in 37%, so as a diagnostic tool, this has its limitations [7]. In blood analysis a moderate leukocytosis will be found. The main reason for taking a blood sample is excluding other diagnoses like pancreatitis [4]. An X-ray of the abdomen/thorax in the standing position will reveal free air under the diaphragm in about 80–85% [7,13]. Some centers perform abdominal ultrasonography, or computerized tomography (CT) scans with oral contrast [14]. With current radiological techniques, 80–90% of cases are correctly diagnosed [12]. As soon as diagnosis is made resuscitation is started with large volume crystalloids, nasogastric suction to empty the stomach, and administration of broad-spectrum antibiotics [13,15]. When PPU has been diagnosed, there are a few different therapeutic options to be taken into consideration [12]. Firstly, it must be evaluated if the patient is suitable for surgery or if conservative treatment should be considered instead. If surgery is indicated, is a simple closure with or without omentoplasty sufficient or is there a need for definitive ulcer surgery and if so which specific operation is indicated? Finally, can the operation be performed laparoscopically or are there risk factors that would make laparotomy a safer option [12,16]?

Table 1

Demographics of patients with perforated peptic ulcer disease [12, 13, 16, 31, 41–43, 45, 49, 51, 52, 58–100]

Pathogenesis

The pathogenesis of PUD may best be considered as representing a complex scenario involving an imbalance between defensive (mucus-bicarbonate layer, prostaglandins, cellular renovation, and blood flow) and aggressive factors (hydrochloric acid, pepsin, ethanol, bile salts, some medications, etc.) [15]. In recent years, Helicobacter pylori infection and NSAIDs have been identified as the two main causes of peptic ulcer [17]. The use of crack cocaine has also led to an increase in PPU, but with a different underlying mechanism, since PPU secondary to the use of crack cocaine is caused by ischemia of the gastric mucosa, and treatment of these perforations does not require acid reducing definitive surgery [12]. Three clinical phases in the process of PPU can be distinguished [4]:

Phase 1: Chemical peritonitis/contamination. The perforation causes a chemical peritonitis. Acid sterilizes the gastroduodenal content; it is only when gastric acid is reduced by treatment or disease (gastric cancer) that bacteria and fungi are present in the stomach and duodenum.

Phase 2: Intermediate stage. After 6–12 h many patients obtain some relief of pain. This is probably due to the dilution of the irritating gastroduodenal contents by ensuing peritoneal exudates.

Phase 3: Intra-abdominal infection. After 12–24 h intra-abdominal infection supervenes.

Epidemiology

Perforation occurs in 2–10% of patients with PUD and accounts for more than 70% of deaths associated with PUD. Perforation is often the first clinical presentation of PUD [18]. The incidence of duodenal perforation is 7–10 cases/100,000 adults per year [9,15,16,19,20,21,22]. The perforation site usually involves the anterior wall of the duodenum (60%), although it might occur in antral (20%) and lesser-curvature gastric ulcers (20%) [19]. 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 hemorrhage, perforation and obstruction [17]. PPU used to be a disorder mainly of younger patients (predominantly males), but recently the age of PPU patients is increasing (predominantly females) [16,20]. The current peak age is 40–60 years [16]. The need for surgery for PPU has remained stable or even increased and the mortality of peptic ulcer surgery has 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 [19,23]. This may be due to an increase in use of aspirin and/or NSAIDs [12].

Role of

Helicobacter pylori

Until the discovery of the role of H. pylori in gastric and peptic ulcers by Barry J. Marshall and Robin Warren in 1982, stress and life style factors were believed to be the most important factors contributing to PUD and PPU [24]. H. pylori infection can be held responsible in more than 90% of duodenal ulcers and in up to 80% of gastric ulcers [17,24]. H. pylori infection and the accompanying inflammation disrupts the inhibitory control of gastrin release by decreasing antral somatostatin, and this is more marked if the infecting organism is a cagA-positive strain [19]. The resulting increase in gastrin release and gastric acid secretion is a key mechanism by which the H. pylori infection induces PUD [19]. In most instances, infection with H. pylori seems to be acquired in early childhood. In contrast to many other infections, the immune system does not contribute to the healing [3,17]. Another problem with eradicating H. pylori is that it is not only located on the surface of the gastric mucosa but also in the layer of mucus protecting it. In 1994, the National Institutes of Health Consensus Development Panel on Helicobacter pylori in Peptic Ulcer Disease recommended that ulcer patients positive for H. pylori should be treated with antimicrobial agents [25]. The type, number of drugs given and treatment duration differ enormously [25]. Although the problem of antibiotic resistance of H. pylori is increasing, combination therapies such as metronidazole with clindamycin or metronidazole with tetracycline can achieve eradication rates of 80% or more [19,26]. According to the Maastricht III consensus report, first line treatment for H. pylori infection should be triple therapy which should compromise a proton pump inhibitor (PPI) plus clarithromycin plus amoxicillin or metronidazole [17,27]. Monotherapy by just giving antibiotics has proven not to be successful (<30% eradication rate) [17]. Traditionally, peptic ulcer is diagnosed endoscopically, but this is an expensive tool and not well tolerated by patients [22]. The carbon-13-urea breath test is expensive, but represents a reliable indicator of H. pylori infection. The preferred method to diagnose H. pylori is by taking peroperative biopsies [22]. Even in patients with PPU and NSAID usage, it is advisable to look for the presence of H. pylori, since it can be eradicated easily. To avoid missing gastric cancer, gastroendoscopy should be performed in patients >45 years of age with alarming features like weight loss, anemia, or dysphagia [17].

Current Management Perforated Peptic Ulcer

Nonoperative Management

Conservative treatment is known as the Taylor method and consists of nasogastric aspiration, antibiotics, intravenous fluids and nowadays H. pylori triple therapy [23,26]. In 1946, Taylor presented the first series of successful outcome of conservatively treated patients with PPU, based on the theory that effective gastric decompression and continuous drainage will enhance self-healing [9,26]. The fundamental idea for conservative treatment came from Crisp who in 1843 noted that perforations of the stomach were filled up by adhesions to the surrounding viscera which prevented leakage from the stomach into the peritoneum [26]. Since then, many reports have been published on this topic, with different success rates [9]. But still there is an ongoing debate whether PPU generally needs to be operated on or not. It has been estimated that about 40–80% of the perforations will seal spontaneously and overall morbidity and mortality are comparable [19,23,26,28]. However, delaying the time point of operation beyond 12 h after the onset of clinical symptoms will worsen the outcome in PPU [9,19]. Also in patients >70 years of age conservative treatment is unsuccessful with a failure rate as high as 67% [9,28]. Shock at admission and conservative treatment were associated with a high mortality rate (64%) [9,23]. Patients likely to respond well to conservative treatment can be selected by performing a gastroduodenogram as described by Donovan et al. [26]. Nonsurgical treatment in these patients, who had proven sealing of their perforation site, was safe, only resulting in 3% intra-abdominal abscess formation and <2% repeat leak [26]. The advantages of conservative treatment are avoidance of operation with associated morbidity caused by surgery and anesthesia, reduction in formation of intra-abdominal adhesion induced by surgery which makes elective surgery for PUD or for other indications in a later phase less complicated and hospital stay perhaps shorter [29]. However, there are also studies that showed a prolonged hospital stay after conservative treatment [13,19]. Disadvantages are a higher mortality rate in case conservative treatment fails. Another disadvantage is the lack of the benefit of laparoscopy or laparotomy as a diagnostic tool in case the patient was misdiagnosed [28,29]. Finally, one always has to bear in mind that PPU can be a symptom of gastric cancer, so if conservative treatment has been chosen after a few weeks endoscopy should be performed [9,28]. In conclusion, one can say that nonoperative treatment is limited to patients <70 years of age who are not eligible for surgical repair due to associated morbidity, with documented contrast studies showing that the perforation has sealed completely. When the patient is in shock or when the time point between perforation and ‘start of treatment’ is >12 h, simple closure should be the first treatment of choice.

Simple Suture

Open Repair Technique. All surgical procedures start by giving prophylactic antibiotics at induction of anesthesia. In conventional surgery, an upper midline incision is performed. Identification of the site of perforation is not always easy: sometimes a perforation has occurred at the dorsal site of the stomach, only to be detected after opening of the lesser sac through the gastrocolic ligament. Also, double perforations can occur. In case of a gastric ulcer, a biopsy is taken to exclude gastric cancer. Simple closure of the perforation can be done in different ways (fig. 1): simple closure of the perforation by interrupted sutures without omentoplasty or (free) omental patch, simple closure of the perforation with a pedicled omentum sutured on top of the repair, representing omentoplasty, a pedicled omental plug drawn into the perforation after which the sutures are tied over it, and finally the free omental patch after Graham. The repair can be tested by either filling the abdomen with warm saline and inflating some air into the nasogastric tube. If no bubbles appear, the perforation has been sealed appropriately. Also, dye can be injected through the nasogastric tube [30]. Thorough peritoneal toilet is then performed. A drain is not left routinely [31]. The abdominal wound can be infiltrated with bupivacaine 0.25% at the end of the procedure.

Fig. 1

Different suture techniques for closure of the perforation.

Omentoplasty or Omental Patch: Necessary or Not? Cellan-Jones [32] published an article in 1929 entitled ‘a rapid method of treatment in perforated duodenal ulcers’. Treatment of choice at that time was, after excision of friable edges if indicated, the application of purse string sutures and on top an omental graft. An encountered problem was narrowing of the duodenum. To avoid this, he suggested omentoplasty without primary closure of the defect. His technique consisted of placing 4–6 sutures, selecting a long omental strand passing a fine suture through it, the tip of the strand is then anchored in the region of the perforation and finally the sutures are tied off [32]. It was not until 1937 that Graham published his results with a free omental graft [33]. He placed three sutures with a piece of free omentum laid over these sutures, which are then tied. No attempt is made to actually close the perforation [33]. The omental graft provides the stimulus for fibrin formation. His approach has been the golden standard since [34]. Very often surgeons mention they used a Graham patch, but they actually mean they used the pedicled omental patch described by Cellan-Jones [32]. Schein [4] could not have outlined it any clearer: ‘Do not stitch the perforation but plug it with viable omentum and patch a perforated ulcer if you can, if you cannot, then you must resect’.

Irrigation of the Peritoneal Cavity. Although some surgeons doubt the usefulness of irrigation, nothing has been found in the literature supporting this theory. Generally, it is reflected on to be one of the most important parts of the surgery and irrigation with 6–10 liters and even up to 30 liters of warm saline are recommended [16]. However, the rational for the routine use of intraoperative peritoneal lavage seems to be more a historically based custom lacking any evidence-based support [35].

Drainage or Not. There seems to be no unanimity of opinion on this topic [16,30]. In a questionnaire 80% of the responders answered that they would not leave a drain [30]. A drain will not reduce the incidence of intra-abdominal fluid collections or abscesses [30]. On the other hand, the drain site can become infected (10%) and can cause intestinal obstruction [30,36]. Often, a drain is left as a sentinel. However, in case of suspected leakage, a CT scan will provide all the information needed, probably better than a nonproductive drain.

Definitive Surgery

Indications for elective surgery are still not defined [19]. The number of elective procedures performed for PUD has declined by more than 70% since the 1980s [19,22]. The results of a questionnaire with 607 responders showed that only 0.3% of the surgeons routinely perform a vagotomy for duodenal ulcer complications and 54.5% mentioned they never include it [37]. Reasons for decline in definitive ulcer surgery are: lower recurrence rate of PUD and PPU because of good results of H. pylori eradication and elimination of NSAID use. Also patients nowadays operated for PPU are older with higher surgical risk which make them less suitable candidates for definitive ulcer surgery. Finally, many surgeons practicing today have limited experience with definitive ulcer operations [22]. Patients in whom definitive ulcer surgery should be considered are those with PPU who are found to be H. pylori-negative, or those with recurrent ulcers despite triple therapy [12,19,26,38,39]. In these patients, a parietal cell vagotomy is recommended if necessary combined with anterior linear gastrectomy [40]. This procedure can be safely and relatively easily performed laparoscopically [19,22].

Laparoscopy

Since the 1990s laparoscopic closure of a PPU has been described. Laparoscopic surgery offers several advantages. First of all, a laparoscopic procedure serves as a minimally invasive diagnostic tool [41]. Other benefits from laparoscopic repair are postoperative pain reduction and less consumption of analgesics and a reduction in hospital stay [42]. Also, a reduction in wound infections, burst abdomen and incisional hernia due to shorter scars has been noted [16,42]. Avoiding upper laparotomy might lower the incidence of postoperative ileus and chest infections [16,42]. Drawbacks are a prolonged operating time, higher incidence of re-operations due to leakage at the repair site and a higher incidence of intra-abdominal collection secondary to inadequate lavage [16,42,43]. If the presence of these fluid collections has any clinical relevance is unclear. The higher incidence of leakage might be caused by the difficulty of the laparoscopic suturing procedure. First of all, this emphasizes the need for a dedicated laparoscopically trained surgeon to perform this procedure [13]. Alternative techniques to simplify the suturing process have been thought of [13,42]. Some laparoscopic surgeons use omentopexy alone [12,41]. Sutureless techniques have been tried, in which fibrin glue alone or a gelatin sponge has been glued into the ulcer [12]. The downside of this technique is that it can only be used to close small perforations. To overcome this problem, a biodegradable patch that can be cut into any desirable size has been tested in rats with good results [44]. Finally, combined laparoscopic-endoscopic repair has been described as well [45].

Postoperative Management

In reviewing the literature, all patients receive nasogastric probes for at least 48 h [16]. This, however, seems to be a more ‘common practice’ than evidence-based medicine [46]. A recently published Cochrane review concludes that routine nasogastric decompression does not accomplish any of its intended goals and should only be applied in selected cases, which has been supported by other trials as well [46,47,48]. This also means that oral feeding can be started early, as in colorectal surgery, and that waiting for 3 days, as is often done according to protocol, is unnecessary [48,49]. As can be seen in table 2, wound infections represent the second most common complication after surgery for PPU. Also, the incidence of sepsis is 2.5%. Preoperative intravenous administration of antibiotics has proven to lower the overall infection rate [50]. Though for most surgical procedures a single dose seems to be sufficient, in the case of H. pylori infection triple therapy is recommended consisting of a PPI combined with clarithromycin and amoxicillin for 14 days [16,27,49,50]. Upper gastrointestinal endoscopy is suggested to be performed after 6 weeks to assess healing of the ulcers and to evaluate H. pylori status [49].

Table 2

Overview of complications after surgery for PPU [13, 16, 19, 20, 42, 43, 51–55]

Postoperative Complications

The most commonly observed postoperative complication was pneumonia followed by wound infection. An overview of all the complications and their incidences based on literature reviews is listed in table 2 [13,16,19,20,42,43,51,52,53,54,55].

Risk Factors Influencing Outcome

Mortality after surgery for PPU is between 6 and 10% [20]. There are four main factors which can increase this mortality rate even up to 100%. These are age >60 years, delayed treatment (>24 h), shock at admission (systolic BP <100 mm Hg) and concomitant diseases [19,21]. Also, gastric ulcers are associated with a two- to threefold increased mortality risk [19,22]. Boey’s score, which is a score based on scoring factors as shock on admission, confounding medical illness, and prolonged perforation, has been found to be a useful tool in predicting outcome (table 3) [16,23,39,51].

Table 3

Boey’s score related to morbidity and mortality

Perforated Peptic Ulcer in the Elderly

Mortality rate after surgery for PPU is three to five times higher in the elderly (up to 50%) [56]. This can be explained by the occurrence of concomitant medical diseases but also by difficulties in making the right diagnosis resulting in a delay of >24 h [56]. In case of a perforated gastric ulcer or recurrent PUD (hemi)gastrectomy with vagotomy might be indicated, but overall simple closure is a safe procedure and there seems to be no need for definitive surgery in this group of patients since ulcer recurrence is only 14% [12,56,57].

Conclusion

Surgery for PPU still is a subject of debate despite more than an era of published expertise. Reviewing different policies regarding for instance the indication for conservative treatment, sense or no sense of drains, the need for omentoplasty or not, performing the procedure laparoscopically and the need for definitive ulcer surgery, might contribute to establishing consensus. Reviewing results of laparoscopic correction of PPU and correction by upper laparotomy one may conclude that the complications seen after laparoscopic procedure (longer operation time and higher incidence of re-leakage), which can be reduced by allowing only surgeons trained in laparoscopy to perform this surgery, do not outweigh the benefits of performing this procedure laparoscopically (lower pain, morbidity and mortality), even in the elderly. Therefore, a laparoscopic procedure should be the first choice.

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Author Contacts

Mariëtta J.O.E. Bertleff

Department of Plastic and Reconstructive Surgery

P. Debeyelaan 25

NL–6229 HX Maastricht (The Netherlands)

Tel. +31 43 517 7481, Fax +31 43 387 5612, E-Mail [email protected]

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Is Laparoscopy a New Paradigm?

Introduction. Laparoscopic repair of perforated peptic ulcer (PPU) remains controversial mainly due to its safety and applicability in critically ill patients. The aim of this study is to compare the outcomes of laparoscopy versus laparotomy in the treatment of PPU. Methods. Single-institutional, retrospective study of all patients submitted to surgical repair of PPU between 2012 and 2019. Results. During the study period, 169 patients underwent emergent surgery for PPU. A laparoscopic approach was tried in 60 patients and completely performed in 49 of them (conversion rate 18.3%). The open group was composed of 120 patients (included 11 conversions). Comparing the laparoscopic with the open group, there were significant differences in gender (male/female ratio 7.2/1 versus 2.2/1, respectively; ) and in the presence of sepsis criteria (12.2% versus 38.3%, respectively; ), while the Boey score showed no differences between the two groups. The operative time was longer in the laparoscopic group (median 100’ versus 80’, ). Laparoscopy was associated with few early postoperative complications (18.4% versus 41.7%, ), mortality (2.0% versus 14.2%; ), shorter hospital stay (median 6 versus 7 days, ), and earlier oral intake (median 3 versus 4 days, ). Conclusion. Laparoscopic repair of PPU may be considered the procedure of choice in patients without sepsis criteria if expertise and resources are available. This kind of approach is associated with a shorter length of hospital stay and earlier oral intake. In patients with sepsis criteria, more data are required to access the safety of laparoscopy in the treatment of PPU.

1. Introduction

Peptic Ulcer Disease (PUD) is a clinical condition that results from an imbalance between ulcerogenic factors and mucosal defence barriers of the stomach and duodenum.

Recent data show a heterogeneous incidence and prevalence of PUD worldwide [1]. However, almost all of the authors agree that both of them are decreasing especially due to the eradication of Helicobacter pylori and the use of Proton Pump Inhibitors (PPI) [2]. Over the past 3 decades, the median age of diagnosis increased from the 40 s to the 60 s; a previously male-predominant disease affects now both sexes equally and the ulcer location is now more frequent in the stomach than in the duodenum [3, 4].

Although the incidence of PUD is decreasing, the total number of PUD complications, such as bleeding and perforation, remains stable [3]. Peptic ulcer perforation is the second most frequent complication after bleeding but it represents the main indication for emergent surgery for PUD, with short-term mortality and morbidity as high as 30 and 50%, respectively [2, 5].

Some perforations may resolve spontaneously and these patients can be managed nonoperatively. The presence of sepsis, generalized peritonitis, or failed nonoperative management is an indication for emergent surgery [6, 7]. Suture of the perforation, with or without an omental patch, has been accepted as the ideal procedure for the majority of cases. Usually, this procedure is performed by laparotomy, but with the widespread of laparoscopic procedures and concomitant surgeon expertise, a minimally invasive approach is increasingly being preferred. Recent studies stated that laparoscopic repair of PPU is performed in 1/3 of the patients [8, 9].

The aim of this study is to assess the feasibility and safety of laparoscopic repair of PPU, even in patients with sepsis criteria, compared to the classic open approach.

2. Materials and Methods

All patients submitted to surgery for gastric or duodenal PPU between January 2012 and December 2019 in our tertiary hospital were identified from the internal electronic database (Sclinico®). Demographic and clinical data were retrieved. Patients treated nonoperatively and those with gastric or duodenal malignancies were excluded.

A per-protocol analysis was performed to compare patients submitted to laparoscopic repair of PPU (n = 49) with patients submitted to open repair of PPU (n = 120, including 11 patients with the conversion of laparoscopic procedures to open surgery). Several parameters were evaluated: demographic and clinical-pathological characteristics (sex, age, comorbidities, presence of sepsis/septic shock, Boey score, ulcer localization, and symptoms-to-surgery time interval), surgical procedure (suture versus resection; ulcer biopsy), and outcomes (operative time, suture dehiscence, reintervention, morbidity, mortality, Clavien-Dindo classification, resumption of oral intake, and length of hospital stay).

Analysis of the subgroup of patients who presented with sepsis/septic shock criteria at the moment of diagnosis (n = 52, 30.8%) was also performed.

2.1. Severity Scores

To assess the presence of sepsis or septic shock at the moment of diagnosis, the 3rd International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) [10] were used. In patients with PPU, sepsis was assumed if ≥ 2 points were present on the Sequential Organ Failure Assessment (SOFA) score; the septic shock was assumed if vasopressors were needed to maintain mean arterial pressure ≥65 mmHg and serum lactate level was ≥2 mmol/L in the absence of hypovolemia.

Boey score was evaluated based on three criteria: the presence of major comorbidities, preoperative systolic arterial pressure <90 mmHg, and duration of symptoms >24h [11].

2.2. Statistical Analysis

Chi-square test was used to compare categorical variables and the nonparametric Mann–Whitney U test for the continuous data analysis. Odds ratios were assumed by logistic regression and adjusted for sex and age. A value < 0.05 was considered statistically significant. SPSS 24.0 for Mac (SPSS Inc., Chicago, IL) was used to perform all statistical analysis.

3. Results

Between January of 2012 and December of 2019, 169 patients were submitted to surgical repair of PPU. Of these patients, 125 (74%) were males and 44 (26%) females. The median age was 52 years (range 21–97). Previous medical comorbidities were present in 97 patients (57.4%). Clinical-pathological characteristics, surgical procedures, and outcomes are presented in Table 1.


Variable	Laparoscopy n = 49 (29%)	Laparotomy n = 120 (71%)	Total n = 169 (100%)	value

Sex				0.009
Male	43 (87.8%)	82 (68.3%)	125 (74%)
Female	6 (12.2%)	38 (31.7%)	44 (26%)
Age (years, median, and range)	48 (21–81)	53 (21–97)	52 (21–97)	0.002
Comorbidities	25 (51%)	72 (60%)	97 (57.4%)	0.284
Sepsis criteria	6 (12.2%)	46 (38.3%)	52 (30.8%)	0.001

Sepsis group				0.003
Nonsepsis	43 (87.8%)	74 (61.7%)	117 (69.2%)
Sepsis	5 (10.2%)	28 (23.3%)	33 (19.5%)
Septic shock	1 (2%)	18 (15.0%)	19 (11.2%)

Boey score				0.317
0	22 (44.9%)	43 (35.8%)	65 (38.5%)
1	17 (34.7%)	35 (29.2%)	52 (30.8%)
2	7 (14.3%)	28 (23.3%)	35 (20.7%)
3	3 (6.1%)	14 (11.7%)	17 (10.1%)

Categorical Boey score				0.062
Boey score <2	39 (79.6%)	78 (65%)	117 (69.2%)
Boey score ≥2	10 (20.4%)	42 (35%)	52 (30.8%)

Symptoms-surgery delay (hours)				0.700
<12	19 (38.8%)	41 (34.2%)	60 (35.5%)
12 < 24	13 (26.5%)	29 (24.2%)	42 (24.9%)
>24	17 (34.7%)	50 (41.7%)	67 (39.6%)

Ulcer localization				0.305
Gastric	22 (44.9%)	58 (48.3%)	80 (47.3%)
Pyloric	16 (32.7%)	47 (39.2%)	63 (37.3%)
Duodenal	11 (22.4%)	14 (11.7%)	25 (14.8%)
Gastrojejunal anastomosis	0 (0%)	1 (0.8%)	1 (0.6%)

Procedure				0.323
Suture (nonresection procedure)	49 (100%)	115 (95.8%)	164 (97%)
Resection procedure	0 (0%)	5 (4.2%)	5 (3%)

Biopsy (only gastric location)				<0.001
Yes	8 (36.4%)	48 (82.8%)	56 (70%)
No	14 (63.6%)	6 (10.3%)	20 (25%)
Not applied	0 (0%)	4 (6.9%)	4 (5%)
Operative time (minutes, median, and range)	100 (40–188)	80 (40–260)	90 (40–260)	0.01
Early complications (<30 days)	9 (18.4%)	50 (41.7%)	59 (34.9%)	0.004

Complications (Clavien-Dindo)				0.032
Grade I	0 (0%)	1 (2%)	1 (1.7%)
Grade II	3 (33.3%)	12 (24%)	15 (25.4%)
Grade III	5 (55.6%)	7 (14%)	12 (20.3%)
Grade IV	0 (0%)	13 (26%)	13 (22%)
Grade V	1 (11.1%)	17 (34%)	18 (30.5%)
Mortality	1 (2.0%)	17 (14.2%)	18 (10.7%)	0.02
Suture dehiscence	2 (4.1%)	5 (4.2%)	7 (4.1%)	0.980
Reoperation	3 (6.1%)	13 (10.8%)	16 (9.5%)	0.343
Late complications (>30 days)	5 (10.4%)	15 (16%)	20 (14.1%)	0.369
Hospital stay (days, median, and range)	6 (4–79)	7 (1–152)	7 (1–152)	0.001
Oral intake (days, median, and range)	3 (1–7)	4 (2–42)	3.50 (1–52)	0.021

Laparoscopic repair of PPU was attempted in 60 (35.5%) patients and 81.7% of these patients (49/60) completed surgical treatment by this kind of approach. There was a conversion rate of 18.3% (11/60). Causes of conversions were technical difficulties in 7 patients, perforation on the posterior gastric wall in 2 patients, perforation of the abdominal aorta with the Veress needle in one patient, and ventilatory intolerance to pneumoperitoneum in another patient.

Patients were divided into two groups: laparoscopy group (49 patients) and laparotomy group (120 patients). Those patients who required conversion were included in the open surgery group.

When both groups were compared, significant differences were observed in gender distribution (male : female ratio was 7.2 : 1 in the laparoscopy group and 2.2 : 1 in the laparotomy group, ) and in age (median age in the laparoscopy group was 48 years and in the laparotomy group was 53 years, ).

At diagnosis, 33 (19.5%) patients presented with sepsis and 19 (11.2%) patients with septic shock. Those 52 patients were operated preferentially by laparotomy (38.3% versus 12.2%, ). Similarly, patients with a Boey score ≥2 were operated preferentially by laparotomy (35% versus 20.4%, ).

The majority of the patients (n = 102; 60.4%) were operated in less than 24 hours after the onset of the symptoms. No differences were found between the two groups regarding the symptoms-to-surgery time interval ().

Gastric PPU was observed in 80 (47.3%) patients, pyloric PPU in 63 (37.3%) patients, and duodenal PPU in 25 (14.8%) patients. One patient (0.6%) had PPU on a previous gastrojejunal anastomosis.

A nonresection procedure (suture ± omental or round ligament patch) was performed in 164 (97%) patients. There were 5 patients submitted to gastric resection; all of them performed by open surgery: 4 atypical gastrectomies and 1 distal gastrectomy with gastrojejunal anastomosis (Billroth 2).

Regarding only gastric location, biopsy of the ulcer wall was performed intraoperatively in 56 (70%) patients: 8 (36.4%) patients in the laparoscopy group and 48 (82.8%) patients in the laparotomy group, . All patients presented no signs of malignancy.

The median operative time in the laparotomy group and in the laparoscopy group was 80 and 100 minutes, respectively ().

Early complications (<30 days) were found in 59 (34.9%) patients: 9 (18.4%) in the laparoscopy group and 50 (41.7%) in the laparotomy group, . Regarding the Clavien-Dindo classification, grade I/II complications (mainly respiratory or wound infections treated with antibiotic therapy) were observed in 16 (27.1%) patients, grade III complications were recorded in 12 (20.7%) patients, and grade IV complications were present in 13 (22.0%) patients. Overall mortality was 10.7% (18 patients): 1 (2%) patients in the laparoscopic group and 17 (14.2%) in the laparotomy group, . Sepsis with multiorganic failure was the most frequent cause of death.

Reoperation was needed in 16 patients: 3 (6.1%) in the laparoscopy group and 13 (10.8%) in the laparotomy group (). There were 7 cases of ulcer suture dehiscence: 2 (4.1%) in the laparoscopic group and 5 (4.2%) in the open surgery group (). Suture dehiscence led to surgical reintervention in 6 patients and one patient was treated nonoperatively with antibiotics and percutaneous drainage. All reoperations were performed by midline laparotomy. Other causes of reoperation were tertiary peritonitis (5 patients), evisceration (3 patients), iatrogenic lesion of the spleen (one patient), and ulcer relapse (one patient).

Laparoscopy was associated with a median length of hospital stay of 6 days (4–79) compared to 7 days (1–152) in the laparotomy group, . The median time for resumption of oral intake after surgery was 3 days in the laparoscopy group compared to 4 days in the laparotomy group, .

Late complications (>30 days) were present in 5 (10.4%) patients submitted to laparoscopy repair of PPU and in 15 (16%) patients who underwent open surgery (). The majority (14/20) of these complications were incisional hernias.

Despite any selection bias, laparoscopy reduced the probability of postoperative complications and mortality in 68.5% (crude OR 0.315; CI 95% 0.140–0.707, ) and 87.4% (crude OR 0.126; CI 95% 0.016–0.967, ), respectively.

Female gender (crude OR 2.378; CI 95% 1.175–4.812, ) and age (crude OR 1.057; CI 95% 1.034–1.081, ) were risk factors for postoperative early complications and mortality (crude OR 4.301; CI 95% 1.574–11.752, , and crude OR 1.047; CI 95% 1.016–1.079, , resp.). Therefore, when laparoscopy was adjusted for gender and age, no significance was reached regarding postoperatory complications () or mortality ().

3.1. Sepsis Subgroup Analysis

In the group of patients with sepsis (n = 52), 46 (88.5%) patients were submitted to open repair of PPU. In these subgroups of patients, significant differences were observed in postoperative complications (33.3% in the laparoscopy group and 76.1% in the laparotomy group, ). Laparoscopy was associated with a decrease of 84.3% in postoperative complications (crude OR 0.157; CI 95% 0.025–0.977, ). Gender and age were not associated with postoperative complications in this subgroup. However, when the laparoscopy group was adjusted for these 2 variables, no significance was reached regarding postoperative complications (). No other differences between the laparoscopy and the laparotomy group were found: results are summarized in Table 2.


Variable	Laparoscopy n = 6 (11.5%)	Laparotomy n = 46 (88.5%)	Total n = 52 (100%)	value

Sex				0.243
Male	5 (83.3%)	27 (58.7%)	32 (61.5%)
Female	1 (16.7%)	19 (41.3%)	20 (38.5%)
Age (years, median, and range)	48 (41–78)	68 (39–94)	62.5 (39–94)	0.078
Comorbidities	5 (83.3%)	39 (84.8%)	44 (84.6%)	0.926

Boey score				0.132
0	1 (16.9%)	1 (2.2%)	2 (3.8%)
1	0 (0%)	16 (34.8%)	16 (30.8%)
2	2 (33.3%)	15 (32.6%)	17 (32.7%)
3	3 (50%)	14 (30.4%)	17 (32.7%)

Categorical Boey score				0.651
Boey score <2	1 (16.7%)	17 (37%)	18 (34.6%)
Boey score ≥ 2	5 (83.3%)	29 (63%)	34 (65.4%)

Symptoms-surgery delay (hours)				0.382
<12	2 (33.3%)	7 (15.2%)	9 (17.3%)
12 < 24	0 (0%)	7 (15.2%)	7 (13.5%)
>24	4 (66.7%)	32 (69.6%)	36 (69.2%)

Procedure				0.519
Suture (nonresection procedure)	6 (100%)	43 (93.5%)	49 (94.2%)
Resection procedure	0 (0%)	3 (6.5%)	3 (5.8%)

Biopsy (only gastric location)				0.848
Yes	1 (100%)	21 (75%)	22 (75.9%)
No	0 (0%)	5 (17.9%)	5 (17.2%)
Not applied	0 (0%)	2 (7.1%)	2 (6.9%)
Operative time (minutes, median, and range)	122.5 (60–165)	100 (42–245)	100 (42–245)	0.483
Early complications (<30 days)	2 (33.3%)	35 (76.1%)	37 (71.2%)	0.047

Complications (Clavien-Dindo)				0.262
Grade I	0 (0%)	0 (0%)	0 (0%)
Grade II	0 (0%)	6 (17.1%)	6 (16.2%)
Grade III	1 (50%)	3 (8.6%)	4 (10.8%)
Grade IV	0 (0%)	11 (31.4%)	11 (29.7%)
Grade V	1 (50%)	15 (42.9%)	16 (43.2%)
Mortality	1 (16.7%)	15 (32.6%)	16 (30.8%)	0.653
Late complications (>30 days)	1 (20%)	9 (32.1%)	10 (30.3%)	0.586
Hospital stay (days, median, and range)	7.5 (5–79)	13.5 (1–152)	13 (1–152)	0.354
Oral intake (days, median, and range)	3 (1–5)	4 (2–42)	4 (1–42)	0.029

4. Discussion

In this series of patients, PPU occurred more frequently in male patients and within a median age of 52 years, in line with historical cohorts. The trend observed in recent occidental reports [3, 9] of equal gender distribution and older age was not confirmed in this specific population. However, like these and other recent papers reported, PPU is now more frequent in the stomach than in the duodenum [3, 4, 6, 9].

Since PPU is a serious complication of PUD, the symptoms-to-surgery interval is an important prognostic factor and is related to increased morbidity and mortality [11–13]. Every hour of delay may reduce the probability of survival by 2–4% [12]. The majority of patients in this series were operated in the first 24 hours.

Risk stratification was performed using the Boey score, one of the most specific validated scores used for PPU [11, 14]. Furthermore, this study used the new Sepsis-3 criteria to assess the severity and to predict outcomes of patients with PPU: to our knowledge, these criteria have never been used before in patients with PPU.

According to Sepsis-3 criteria, in this series, patients with sepsis were operated preferentially by laparotomy and had higher rates of postoperative complications and mortality. Although a Boey score ≥2 is referred to be a marker of poor prognosis, in this series, only 34 of the 52 patients with Boey score ≥2 presented sepsis at the same time. Patients with Boey score ≥2 were not significantly associated with laparotomy repair of PPU or higher rates of complications. Consequently, in our series, Boey score was less accurate than the Sepsis-3 criteria to predict patients’ outcomes.

According to the recent guidelines from the World Society of Emergency Surgery (WSES), a laparoscopic approach in PPU is recommended in “stable” patients, while an open approach should be performed in the absence of laparoscopic skills and equipment as well in “unstable” patients [15]. In our series, laparoscopic repair of PPU was performed essentially in patients with a better prognosis (patients with no sepsis). Interestingly, we observed that sepsis at admission was more frequent in women than in men. So, when comparing the laparoscopic group with the open one, the male : female ratio was higher in the laparoscopic group.

This study has some limitations. The patients were not randomized to laparotomy or laparoscopic treatment of PPU. The surgical approach was decided case by case and taking into account the surgeons’ expertise in laparoscopy. We observed that laparoscopic repair of PPU was accomplished in 29% of patients which is in line with recently published data reporting that laparoscopic repair is used in 3–33% of patients with PPU [6, 8, 9].

The conversion rate of this series (18,3%) is lower than other reports (25–44%) [8, 9, 16, 17]. Mean operative time was longer in the laparoscopic group, as observed in these recent papers.

Biopsy of the ulcer wall was done less frequently when the treatment was performed by laparoscopy. We assume that intraoperative adverse conditions were the main reason for this difference. Although controversial, we may consider that surgical repair of PPU is a life-saving surgery often performed in a “damage-control” setting and definitive diagnosis may be postponed for postoperative endoscopic biopsies of nonhealing ulcers. This strategy may delay diagnosis. However, it is an acceptable strategy in selected cases with no effects on prognosis, especially if we take into account the fact that the optimal oncologic treatment of a perforated gastric cancer in the acute setting is difficult to achieve. As malignancy was considered as an exclusion criterion, we could not analyse such differences and few data are available regarding this topic.

PPU is a serious complication of PUD with mortality and mobility that can reach 30% and 50%, respectively [2, 5]. Postoperative early complications occurred in 59 (34.9%) of our patients with an overall mortality of 10.7%. When analysed by groups, the laparoscopic group had a significantly lower rate of complications and mortality compared to the laparotomy group. However, there was a selection bias of patients with better prognosis (younger, males, and without sepsis criteria). When the analysis was adjusted for sex and age, statistically significant differences were not found regarding complications or mortality. Accordingly, other studies reported no significant differences between laparoscopy and laparotomy regarding postoperative complications or mortality [8, 17, 18]. However, a shorter hospital stay is observed for patients submitted to laparoscopic repair of PPU, as already reported [6, 17].

When sepsis was present, there were few patients treated by laparoscopy. Nonetheless, we observed that outcomes after laparoscopic repair are noninferior to the outcomes of open repair of PPU, even in the presence of severity criteria. We expect that, as surgical expertise and perioperative care continuously improve, we may observe in the near future the full spectrum of advantages attributed to the minimally invasive techniques, as described for other procedures.

5. Conclusion

Recent guidelines started to suggest which kind of patients could benefit from a laparoscopic approach instead of a classic open one for the treatment of PPU. However, the selection criteria for a correct assignment are not very clear yet. Specific criteria to identify a “stable” or “unstable” patient like WSES are required. Sepsis-3 criteria proved to be an accurate score in predicting outcomes for PPU and maybe they could be used for this purpose. In our opinion, patients without sepsis criteria benefit from minimally invasive approaches. The presence of sepsis or septic shock may not be considered an absolute contraindication for laparoscopic repair of PPU but additional studies are required to assess feasibility and safety outcomes in this subset of patients.

Data Availability

The demographic and clinical-pathological characteristics and data related to the surgical procedures and outcomes used to support the findings of this study are included within the article. All data were retrieved from the internal electronic database (“SClinic”).

Conflicts of Interest

The authors declare no conflicts of interest related to this paper.

Recovery after gastric ulcer surgery

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Operations on the stomach belong to the category of complex surgical interventions and involve not only careful care in the postoperative period, but also long-term rehabilitation, including spa treatment. As practice shows, the best place for rehabilitation are health resorts that have their own medical base and the possibility of balneotherapy with natural mineral waters. “Gorny” is rightfully considered one of the best sanatoriums for recovering from stomach surgery in the Krasnodar Territory.

Benefits of rehabilitation in the sanatorium “Gorny”

The rehabilitation program is drawn up taking into account the patient’s age, his mood, the severity and volume of the surgical intervention performed, the state of the digestive system and the time that has passed since the operation.

1. Rest under the supervision of doctors

The psychological atmosphere surrounding the patient is extremely important for recovery from stomach surgery, stomach ulcers and other severe diseases of the digestive system. Comfortable living conditions, high level of service are conducive to rest, contribute to the normalization of the nervous system and the adaptation of the body to new conditions.Careful medical supervision ensures early detection of abnormalities in the state of health and timely correction of the treatment program.

2. Physiotherapy exercises, taking into account the individual characteristics of the organism

A sharp decrease in motor activity in the postoperative period requires further gradual restoration of physical form. Walking in the fresh air, Scandinavian walking, a special set of exercises can normalize the work of the cardiovascular and respiratory systems, improve the peristalsis of the digestive tract.

3. Diet therapy

Diet therapy is the most important component of the treatment of patients who have undergone surgery. Sparing fractional reusable meals are the main thing that is necessary for the restoration of the stomach, and in the sanatorium “Gorny” all conditions have been created for a full-fledged therapeutic nutrition. Always fresh products, the choice of dishes and the creation of an individual menu will satisfy even the most demanding guests.

4. Balneotherapy

Drinking courses of treatment with mineral waters take a special place in the rehabilitation of gastroenterological patients.After the operation, the stomach becomes smaller in volume, its secretion decreases. Lack of digestive juices leads to indigestion, heaviness and pain in the abdomen, flatulence, diarrhea and constipation. The mineral water of the Psekupskoye deposit used in “Gorny” has unique healing properties, helps to restore gastric secretion and normal digestion of food. The drinking regime is determined individually and, according to the doctor’s prescription, is supplemented with general and local balneological procedures with the use of Matsesta mineral waters.

Treatment in a sanatorium at the stage of recovery after surgery for stomach ulcers allows you to avoid the development of complications and return to a full life.

“Choosing the right sanatorium is a significant step towards maintaining and improving health. Gorny is a resort complex that combines the experience and knowledge of Russian and Soviet balneology. The presence of modern medical equipment and innovative installations, the professionalism of the staff and love for their work will serve as a guarantee for the extension of longevity ”- chief physician of the sanatorium Karaulov Alexander Olegovich.

Drug or surgical treatment for peptic ulcer of the stomach and upper small intestine, resistant to drug treatment

Review Question

Which is better, medical or surgical treatment is best for people with stomach or upper small intestine ulcers (peptic ulcers) that do not heal with eight to 12 weeks of treatment (refractory peptic ulcers) or that come back after healing (recurrent peptic ulcers) ?

Relevance

About 1 in 100 to 1 in 800 people have peptic ulcers.The main causes of peptic ulcer disease are infection with the bacterium Helicobacter pylori , the use of non-steroidal anti-inflammatory drugs (NSAIDs), and smoking. People with peptic ulcers experience pain in the upper abdomen, which is sometimes accompanied by indigestion (that is, feeling full, bloating, loss of appetite after eating small amounts of food, or nausea). The most serious complications of peptic ulcer disease are bleeding from the ulcer and perforation of the peptic ulcer, which results in leakage (contents) into the abdominal cavity (abdomen) from the stomach or upper small intestine.About 1 in 10 people with bleeding ulcers and 1 in 4 with ulcer perforation die. Peptic ulcers cause an estimated 3,000 to 4,500 deaths per year in the United States.

Currently, the basic treatment for uncomplicated peptic ulcers is usually the use of a group of agents called proton pump inhibitors (eg omeprazole and lansoprazole). Recently, there have been concerns about the risk of fractures with long-term use of proton pump inhibitors. An alternative to drug treatment for refractory and recurrent peptic ulcer disease is surgery to reduce gastric acid secretion in order to heal peptic ulcers.It is not known if medical or surgical treatment is the best option for people with refractory or recurrent peptic ulcers. We have attempted to address this issue by searching the medical literature for studies comparing medical versus surgical treatment in people with refractory or recurrent peptic ulcers.

Characteristics of research

We found no randomized controlled trials and found only one non-randomized study published 30 years ago on this topic.The study included 77 participants who had stomach ulcers and in whom drug therapy had no effect after treatment for an average of 29 months. Medications included histamine h3 receptor blockers (drugs that block the action of a chemical called histamine, which leads to decreased production of stomach acid, such as ranitidine), antacids, and diet. It should be emphasized that this form of treatment is not considered to be as effective as treatment with proton pump inhibitors.The authors do not report whether these were recurrent or refractory ulcers. Of the 77 participants included, 37 continued to receive drug therapy, while 40 participants received surgical treatment. Whether to use therapeutic (drug) or surgical treatment was determined by the preference of the participant or the treating physician. This evidence is current to September 2015.

Key Outcomes

The study authors reported that two participants in the drug treatment group (5%) had stomach cancer, which was diagnosed after repeated examinations with a camera that allows you to look inside the body (endoscope), in this case, the stomach and small intestine.The authors did not report the percentage of participants who had stomach cancer in the surgical treatment group. They also did not report the consequences of delayed diagnosis of stomach cancer in the drug treatment group. They did not report any other outcomes (outcomes) of interest (measures by which one treatment can be considered better than another) for this review (i.e. health-related quality of life, treatment-related complications, complications of peptic ulcer , abdominal pain, and long-term mortality).Accordingly, there is no study that provides information on the relative benefits and harms of medicinal and surgical treatment for recurrent or refractory peptic ulcers. Research on this topic is urgently needed.

Quality of evidence

Because the only study comparing medical versus surgical treatment in people with refractory or recurrent ulcers did not report any outcome in sufficient detail, we were unable to assess the quality of the evidence in a formal way.

Fast food shock: teenagers in Moscow bring themselves to a perforated ulcer

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Moscow doctors rescued a teenager with a rare form of the disease, aggravated by fast food

Metropolitan gastroenterologists sound the alarm. Since the beginning of the year, the Morozov Children’s Hospital has recorded the fourth case of an ulcer caused by the children eating fast food, two of them were complicated by the formation of through injuries to the stomach walls.What was considered very rare for children 3-4 years ago – this complication was more common in 40-60-year-olds – has now, alas, become a trend in pediatric clinical practice. We talked about its reasons with the chief pediatric gastroenterologist in Moscow, head of the gastroenterology department of the Morozov Children’s Clinical Hospital Tamara SKVORTSOVA.

Recently, a 17-year-old teenager with suspected acute appendicitis was admitted to the emergency and abdominal surgery department of the Morozov Children’s Hospital of the Moscow Healthcare Department.The guy was tormented by incessant, gradually increasing pain in the abdomen. The clinical picture corresponded to the inflammatory process in the abdominal cavity – peritonitis, which is fatal in 15–20 percent.

During diagnostic laparoscopy, doctors discovered a 5-mm hole in the stomach in a teenager – a perforated ulcer, which was the cause of the inflammatory process. Fortunately, the urgently performed surgical operation to suture the ulcer, which lasted an hour and a half, ended successfully, and on the seventh day the patient was discharged home in satisfactory condition.

All this could be considered a common case from the life of the Morozov hospital, if not for one thing … Perforated ulcer in childhood and adolescence, according to Tamara Skvortsova, is an extremely rare diagnosis, – earlier it accounted all abdominal (affecting the abdominal organs) surgical pathology. In 2019, only in the Morozov hospital, this is already the second case, there were two more cases of acute ulcers, not complicated by perforation.

It is noteworthy that all the patients – adolescents – told the doctor that they love fast food.Doctors, referring to the words of their patients, name two, perhaps, the most popular fast food restaurants among Muscovites.

– Almost everyone said that they were lovers of fast food, they visited the restaurant two or three times a week, says Tamara Andreevna. – As a rule, patients come to us who have abused large quantities of spicy, fried, fatty foods from the fast food menu.

– They must have had weak stomachs since childhood?

– Among those who came to us this year with an exacerbation, there was not one of those whom we observe from early childhood.

– How can you explain the increase in acute pathological cases? There used to be fast food too.

– Fast food restaurants became available to the general public, affordable prices and varied menus. The frequency of visits, including family visits, has increased. Add to this hot seasonings, all kinds of spices, food additives, sweet soda.

– Maybe the addiction to fast food is due to the fact that mothers have stopped preparing the right meals at home?

– Chances are, once-expensive fast food restaurants have become more affordable.You can always sit in them with a company, no restrictions. After such overeating, adolescents are most often brought to us.

– Probably after surgery for a perforated ulcer, the patient promised never to approach a fast food outlet?

– After such operations, and even after an exacerbation of peptic ulcer or gastritis, our patients are forced to follow a strict diet for a long time. The slightest error, especially at first, can lead to severe pain, nausea.After a perforated ulcer, many have to follow a diet for a long time.

To avoid stomach problems, the nutrition of children and adolescents should be balanced and thermally properly processed, reminds the gastroenterologist. – We recommend not eating spicy, smoked, fried and fatty foods in large quantities. Nuts, fruits, kefir, yoghurts, and dark chocolate are best for snacks.

Published in the newspaper “Moskovsky Komsomolets” No. 28026 dated July 19, 2019

Newspaper headline:
Young victims of fast food

Abdominal surgery

Cytological laparoscopy

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Suturing of perforated gastric ulcer, duodenal ulcer laparoscopic 2 category of complexity

31,000 90 120

Suturing of a perforated ulcer of the stomach, duodenum laparoscopic 2 category of complexity

31,000 90 120

Suturing of the perforated ulcer

Suturing of perforated gastric ulcer, duodenal ulcer, laparoscopic 4th category of complexity

41,000

Video-assisted gastric resection, 2nd category of complexity

51,000

Video-assisted gastric resection, 3rd category of complexity

71,000

Surgery for pancreatic cysts, laparoscopic, 1st category of complexity

31,000

Surgery for pancreatic cysts, laparoscopic, 2nd category of complexity

36,000

36,000
0

41,000

Surgery for pancreatic cysts laparoscopic 4th category of complexity

46,000

Video-assisted resection of the small intestine, 1st category of complexity

31,000

Video-assisted resection of the small intestine, 2nd category of complexity

36,000

Video-assisted resection

46,000 90 120

Alloplasty of giant ventral hernias 1 category of complexity 90 120 90 121 31,000 90 120 90 124

Alloplasty of giant ventral hernias 2 category of complexity 90 120

41,000

Alloplasty of giant ventral hernias, complexity level 4

46,000

Liver resection, laparoscopic without stapling devices 1st category of complexity

25,000

Liver resection laparoscopic without stapling devices 2nd category of complexity

30,000 90 120

Liver resection laparoscopic without stapling devices

Liver resection laparoscopic without stapling devices 4th category of complexity

40,000

Biliodigestive anastomoses laparoscopic 1st category of complexity

31,000

Biliodigestive

laparoscopic

Biliodigestive

anastomoses

laparoscopic

Biliodigestive

anastomoses

anastomosis 3rd category of complexity

41,000

Biliodigestive anastomoses laparoscopic 4th category of complexity

46,000 9012 0

Adrenalectomy 1st category of complexity

31,000 90 120

Adrenalectomy 2nd category of complexity

36,000 90 120

Adrenalectomy 3rd category of complexity

Video-assisted resection of the pancreas 1st category of complexity

31,000

Video-assisted resection of the pancreas 2nd category of complexity

36,000

Video-assisted resection

Video-assisted resection 9012 9011 pancreatic resection

glands 4 category of complexity 90 120 90 121 46,000 90 122 90 120 90 124 90 118 90 119 Video-assisted colon resection 1 category of complexity 90 120 90 121 31,000 90 122 90 120

Video-assisted colon resection, complexity level 2 90 120

36,000

Video-assisted colon resection, complexity level 3 90 120

41,000 90 120