Laparoscopic repair of perforated peptic ulcer

Flore Varcus1, Ion Paun2, Ciprian Duta1

  • 1Victor Babes University of Medicine and Pharmacy, Timisoara, Romania.

Minerva Chirurgica
|January 26, 2018
PubMed

Insights

Laparoscopic perforation repair (LPR) for perforated peptic ulcers (PPUs) offers shorter hospital stays and lower morbidity/mortality compared to open repair (OR). However, LPR has a higher leakage rate, necessitating improved surgeon training.

Area of Science:

  • Gastroenterology
  • Surgical Innovation
  • Minimally Invasive Surgery

Background:

  • Perforated peptic ulcers (PPUs) are a common surgical emergency, leading to significant morbidity and mortality.
  • Laparoscopic perforation repair (LPR) offers a minimally invasive approach compared to open repair (OR).

Purpose of the Study:

  • To evaluate the latest reported outcomes of laparoscopic perforation repair (LPR) for perforated peptic ulcers (PPUs).
  • To compare LPR with traditional open repair (OR) for PPUs.

Main Methods:

  • Extensive literature search of PubMed and EMBASE databases (1989-2017) for studies on LPR for PPU.
  • Inclusion of 32 studies (3488 LPR patients, 5208 OR patients) comparing outcomes, excluding animal studies, pediatric trials, and studies with <30 LPR cases.

Main Results:

  • LPR patients experienced shorter hospital stays (2 days less) and lower morbidity (11.12% vs. 14.71%) and mortality (1.95% vs. 8.35%) compared to OR.
  • OR patients presented with higher rates of shock and higher ASA risk class.
  • LPR had a higher leakage rate (2.18% vs. 0.79%) and conversion rate (4.18%) due to perforation size, localization issues, or technical difficulties.

Conclusions:

  • LPR demonstrates comparable or superior outcomes to OR regarding morbidity, mortality, operation time, and hospital stay.
  • Caution is advised due to the higher leakage rate in LPR, highlighting the need for enhanced surgeon training and safety measures.
Abstract

Related Concept Videos

Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
2.2K
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
900
Peptic Ulcer Disease IV: Management01:26

Peptic Ulcer Disease IV: Management

Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
545
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
1.3K
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
1.3K
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids01:31

Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids

In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
722