Laparoscopic versus open surgical treatment of perforated peptic duodenal ulcer

Abstract

The stomach is the most dilated part of the digestive tube. It is situated between the end of the esophagus and the duodenum.

The length of the duodenum is approximately 20-30 cm. The duodenum is divided into four parts: the first (or superior) portion, the second (or vertical or descending portion); the third (or horizontal or transverse) portion; and the fourth (or oblique or ascending) portion.

DUs occur most often in the first portion of duodenum (>95%), with ~90% located within 3 cm of the pylorus. They are usually 1 cm in diameter but can occasionally reach 3-6 cm (giant ulcer).

Hellicobacter Pylori (H. pylori) and NSAID-induced injury account for the majority of DUs. Many acid secretory abnormalities have been described in DU patients. H. pylori infection is virtually always associated with a chronic active gastritis.

NSAIDs interruption of prostaglandin synthesis can impair mucosal defense and repair, thus facilitating mucosal injury. Topical NSAIDs can also alter the surface mucous layer, permitting back diffusion of H+ and pepsin, leading to further epithelial cell damage.

Abdominal pain is common to many (GI) gastrointestinal disorders, including DU and GU, but has a poor predictive value for the presence of either DU or GU. Epigastric tenderness is the most frequent finding in patients with GU or DU.

Several additional disease processes that may present with “ulcer-like” symptoms include proximal gastrointestinal tumors, gastroesophageal reflux (GERD), vascular disease, pancreaticobiliary disease and gastroduodenal Crohn’s disease.

Documentation of an ulcer requires either a radiographic or an endoscopic procedure.

Complications of peptic ulcer disease include bleeding, perforation, penetration, and gastric outlet obstruction and vary in frequency geographically.

GI bleeding is the most common complication observed in PUD. It occurs in ~15% of patients and more often in individuals >60 years old.

The second most common ulcer-related complication is perforation, being reported in as many as 6-7% of PUD patients. Duodenal perforation tends to occur in the anterior wall while gastric ulcers may perforate anteriorly or posteriorly. Concomitant hemorrhage should suggest the presence of a „kissing‟ ulcer (ulcers involving anterior and posterior duodenal walls simultaneously)

Gastric outlet obstruction is the least common ulcer-related complication, occurring in 1-2% of patients. Patients with gastric outlet obstruction are frequently malnourished, hypovolemic and have metabolic alkalosis.

Bleeding, potentially is the most serious and common complication of peptic ulcers. Bleeding can be both overt or occult blood loss, presenting with iron-deficient anemia. Associations have been shown between drugs with ulcerogenic and/or bleeding promoting side-effects; aspirin, other NSAIDs, warfarin and SSRIs, and bleedings from both the upper and lower GI tract.

Penetration of duodenal ulcer is rare in nowadays because of efficacy of therapy; however it remains a serious complication associated with operative difficulties and postoperative morbidity.

Before the discovery of H. pylori, the therapy of PUD was centered on the old dictum by Schwartz of “no acid, no ulcer”. Although acid secretion is still important in the pathogenesis of PUD, eradication of H. pylori and therapy/prevention of NSAID-induced disease is the mainstay of treatment.

Antacids are now rarely used as a primary therapy and used for symptomatic relief of dyspepsia.

H2-blockers, although each has different potency, all will significantly inhibit basal and stimulated acid secretion to comparable levels when used at therapeutic doses.

Proton pump (H+, K+-ATPase) inhibitors are the most potent acid inhibitory agents available.

Cytoprotective agents as sucralfate, Bismuth drevatives and prostaglandin analogues also help in peptic ulcer disease therapy.

Ideally, the injurious agent should be stopped as the first step in the therapy of an active NSAID-induced ulcer.

Surgical intervention in PUD can be viewed as being either elective, for treatment of medically refractory disease, or as urgent/emergent, for the treatment of an ulcer-related complication.

Bleeding patients unresponsive or refractory to endoscopic intervention will require surgery.

Surgical treatment for PUD is designed to decrease gastric acid secretion. Operations most commonly performed include  vagotomy and drainage,  highly selective vagotomy and  vagotomy with antrectomy.

The procedure that provides the lowest rates of ulcer recurrence but has the highest complication rate is vagotomy (truncal or selective) in combination with antrectomy.

Complications seen after surgery for PUD are related primarily to the extent of the anatomical modification performed.

Management of gastrointestinal bleeding commences with full resuscitation, followed by investigation to determine the site of bleeding and then treatment to arrest hemorrhage and prevent rebleeding and promote ulcer healing.

Interventional radiologists in many institutions have developed increasing experience in vascular embolization to arrest hemorrhage over the past decade.

Surgery is indicated when the patient is actively bleeding and the source cannot be seen or controlled endoscopically. Timing for surgery depends on surgeon experience.

For select, nonseptic patients, nonoperative management of a perforated benign gastric ulcer can occasionally be successful in a stable patient without peritonitis. For all other patients with a symptomatic presentation, the treatment is surgical after a short period of aggressive resuscitation.

The options for surgical treatment of perforated duodenal ulcer are simple patch closure, patch closure and highly selective vagotomy (HSV), or patch closure and vagotomy and drainage (V+D).

simple patch closure, currently the most commonly performed operation for perforated peptic ulcer, should be done in patients with hemodynamic instability and/or exudative peritonitis signifying a perforation >24 hours old.

In the stable patients without longstanding perforation, the addition of HSV may be considered.

Perforation of GDUs is considered particularly hazardous because of the extensive duodenal tissue loss and surrounding tissue inflammation, which are said to preclude simple closure with omental patch, often resulting in postoperative leak or gastric outlet obstruction.