Chapter 4 Perforated peptic ulcer

The frequency of peptic ulcer disease is estimated 6% to 15% in the general population. Most individuals do not have clinically significant ulcer. Approximately 10% of young men have H pylori, and the proportion of people with the infection increases steadily with age. The incidence of duodenal ulcer has been decreasing  over the past 3–4 decades.

Lifetime prevalence of perforation in patients with peptic ulcer disease is approximately 5%. With nonsteroidal anti-inflammatory drugs (NSAID)-related ulcers, the incidence of perforation is 0.3%. Emergency operations for peptic ulcer perforation carry a mortality risk of 6–30%. Most deaths result from postoperative complications.

Aetiology

1. Predisposing factor: progressive destruction of stomach or duodenal wall.

Ulcers of the stomach and duodenum are caused chiefly by the effects of hydrochloric acid, produced by the parietal cells of the stomach, and by lack of protection of the mucosa against this acid. Acid production is the most important factor as far as duodenal ulcer is concerned, but cannot be the only factor, since the severity of duodenal ulcers and their responses to therapy do not vary directly with the amount of gastric acid secreted.

Additional factors are important in the production of gastric ulcers. Gastric contents can be retained for a much longer period than duodenal contents and are not neutralized rapidly. The mucous membrane of the stomach must normally be protected continuously from the damaging effect of the hydrochloric acid which it secretes. This protective layer consists of an adherent layer of mucus which is separated from the gastric mucosa by a bicarbonate layer that normally neutralizes any hydrochloric acid diffusing back through the mucous layer. The mucous layer also protects the gastric mucosa against other noxious agents such as bile, alcohol, and aspirin and other irritating drugs.

Secretion of acid by the parietal cells of the stomach is influenced by several mechanisms. Stimulation by the vagus nerves accounts for about 50% of acid secretion. Gastrin that is secreted by the antral mucosa causes 40 to 45% of the secretion and the remaining 5 to 10% is due to gastrin that comes from the intestinal tract from various APUD cells.

Production of gastric mucus should presumably vary according to the blood supply of the organ. Experimental studies have shown that prostaglandins increase the mucosal blood supply and increase the bicarbonate level and thickness of the mucous layer; they may, therefore, play an important role in the protection of the gastric mucosa.

Causes of gastric ulcers vary in importance depending upon the location of these ulcers. In 1965 Johnson observed the different behavior of ulcers in different portions of the stomach and classified them into three groups. In patients with type 1 ulcers, located in the body of the stomach, gastric acid secretion as determined by secretory tests is low. Here inadequate mucosal protection and back-diffusion of hydrochloric acid through the protective bicarbonate and mucous layer into the gastric mucosa seem to be involved in the disease. Silent suggested it is in this location that alternating waves of gastric acid from above and refluxing alkaline secretions from the duodenum destroy the protective layer of mucus.

Johnson’s type 2 gastric ulcers (those combined with a present or past duodenal ulcer) and type 3 (those in the prepyloric region) behave more like duodenal ulcers; here the effects of acid production appear to be more important.

 A peptic ulcer occurs when an alteration occurs in the aggressive and/or protective factors such that the balance is in favor of gastric acid and pepsin. Any process that increases gastric acidity (e.g., individuals with increased maximal and basal acid output), decreases prostaglandin production (e.g., NSAIDs), or interferes with the mucous layer (e.g., Helicobacter pylori infection) can cause such an imbalance and lead to peptic ulcer disease.

H pylori infection that follows an antral predominant pattern leads to an inflammatory state in which high levels of tumor necrosis factor-alpha (TNF-alpha) and other cytokines are produced. These stimulate gastric acid production directly by increasing  gastrin release from G cells and inhibit somatostatin production by antral D cells. This leads to a net increase in gastric acid secretion, which leads to an increased acid load in the duodenum, overwhelming the mucosal defense.

 H pylori can then colonize the duodenal mucosa and adhere to cells. This adherence leads to a variety of second-messenger signals, which invoke an immunologic response against those cells causing mucosal damage by host neutrophils and other inflammatory cells.

H. pylori also affect the gastric and duodenal mucous layer because this organism produces proteases that degrade the protective mucous layer.

Moreover, H pylori infection decreases the production of epidermal growth factor, which normally promotes healing of gastric and duodenal mucosa.

H pylori organisms produce urease. Urease hydrolyzes urea to ammonia end carbon dioxide. Hydroxide ions produced by equilibration of ammonia with water may damage the gastric and duodenal mucosa.

2. Causative factor: increasing of pressure in stomach lumen (more food intake, physical training).

Classifications

Forms of perforation (Savelyev V. S.,1976)

perforation of duodenal or gastric ulcer into the free abdominal cavity.

covered perforation.

atypical perforation (into the lesser sac, retroperitoneal fatty tissue).

Clinical stages (Neimark N. I., 1972) 

stage of shock.

stage of illusion.

stage of peritonitis.

Clinical manifestations

Clinically the perforations are divided into three stages: of shock, illusion and peritonitis (Mondor, 1939).

Stage of shock (lasts for about 6 hours)

Intensive upper abdominal pain at the time of perforation (Delafua compares it with “pain due to stabbing with a dagger”).

Elicer’s sign – irradiation of pain to the right shoulder or scapula.

Tenderness of abdominal wall. In elderly patients tension of muscles of abdominal wall is absent or insignificant through old-age relaxation of muscles.

Percussion of liver will reveal attenuated dullness due to free gas.

Auscultation will reveal a silent abdomen.

Blumberg’s sign.

Temperature is normal.

Blood pressure may be lost.

Pulse is rapid.

Stage of illusion (lasts for about 6–12 hours)

As more exudate accumulates, chemical irritation of peritoneum becomes less, the patient feels better with less pain.

The same signs may be found by rigidity becomes less.

Abdominal distention will start.

Temperature becomes elevated.

Stage of peritonitis

The patient is extremely toxic with tachycardia and high temperature.

The abdomen is rigid, distended and silent.

Blumberg’s sign.

Blood pressure is often lost.

Covered perforation (A. M. Shnicler, 1912). In this pathology the perforation is closed by fibrin, by omentum or sometimes _ by food particle. After that some amount of stomach content and air left into the abdominal cavity. This protective mechanism leads to relief from stomachache, but moderate tenderness of abdominal wall in right epigastria region persists (Ratner’s sign). On percussion hepatic dullness is doubtful. During X-ray examination it is not always possible to mark gas in right hypochondrium

Consequences of the covered perforation are: repeated perforation with development of classic clinical signs; subdiaphragmatic or subhepatic abscess; complete closing of defect by surrounding tissue with gradual convalescence of patient.

The atypical perforation is the perforation, at which gastric or intes­tinal content does not enter the abdominal cavity, but enters the retro­peritoneal space (ulcers of posterior wall of duodenum), large or small omentum (ulcers of lesser curvature of stomach), hepatoduodenal liga­ment.

In such patients during the perforation pain is not acutely expressed. During palpation insignificant rigidity of muscles of anterior abdominal wall is observed. On occasion, especially in the late stages of disease, can be hypodermic emphysema and crepitation.

The differential diagnosis includes acute cholecystitis, acute pancreatitis, strangulating intestinal obstruction, acute appendicitis, perforation of some other portion of the intestinal tract, and mesenteric thrombosis. A past history of ulcer disease is predictive, but in 30% of patients perforation is the first manifestation of peptic ulcer disease.

Diagnosis programmer

X-ray examination of abdominal cavity organs for presence of free gas (pneumoperitoneum, fig. 17).

Fibergastroduodenoscopy (FGDS) + X-ray examination.

Ultrasonic of abdominal cavity (pneumoperitoneum, fig. 18) + laparocentesis (peritoneal exudate).

Laparoscopy.

Laparotomy.

CT with oral contrast may also demonstrate extravasation of contrast in the presence of a perforated ulcer. If history and physical examination raise the possibility of perforation, upright chest radiography and an upper digestive tract contrast study with water-soluble contrast are the diagnostic studies of choice. Do not perform CT scanning in this situation.

Laboratory Studies

CBC count (leucocytosis with left shift is found in most cases).

Serum gastrin level. Gastrin levels greater than 1000 pg/mL are suggestive of gastrinoma.

Serum H pylori antibody detection. Antibodies (immunoglobulin G [IgG]) to H pylori can be measured in serum, plasma, or whole blood. However, results from whole blood tests using finger sticks are less reliable.

Urea breath tests. Urea breath tests are used to detect active H pylori infection by testing for the enzymatic activity of bacterial urease. In the presence of urease produced by H pylori, labeled carbon dioxide (heavy isotope, carbon-13, or radioactive isotope carbon-14) is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled.

Faecal antigen tests. Faecal antigen testing is used to identify active H pylori infection by revealing the presence of H pylori antigens in stools.

This test is more accurate than antibody testing and less expensive than urea breath tests.

Treatment of perforated peptic ulcer

Treatment policy in patients with perforated peptic ulcer is surgical.

Conservative treatment is temporary measure when surgery is impossible. Conservative treatment includes the following (Taylor’s method):

nasogastric decompression;

replacement of fluid and electrolytes;

proton pump inhibitor;

broad-spectrum antibiotics;

hypothermia of abdominal wall.

Conservative treatment is associated with high risk of septic complications (formation of abscess, peritonitis).

Surgical treatment

Preoperative details. Fluid resuscitation should be initiated as soon as the diagnosis is made. Essential steps include insertion of a nasogastric tube to decompress the stomach and a Foley catheter to monitor urine output. Intravenous infusion of fluids is begun, and broad-spectrum antibiotics are administered. In select cases, insertion of a central venous line may be necessary for accurate fluid resuscitation and monitoring. As soon as the patient has been adequately resuscitated, emergent surgery should be performed.

Simple closure of perforation. Simple closure of perforation may be performed by laparotomy or laparoscopy.

The 1st step of the operation is the exploration of the abdominal cavity, which allows confirming the diagnosis of generalized peritonitis. In addition, it allows differentiating between the septic and the clinical peritonitis, and especially it permits to determine the possibility of the laparoscopic repair.

A very important step of the operation is the aspiration of peritoneal fluid, which should be as complete as possible. This is followed by extensive irrigation of the abdominal cavity.

The next step is the exact localization of the perforation, which sometimes may be covered by the liver, gallbladder or omentum. In this case, the perforation is identified on the anterior aspect of the duodenum.

Ideal repair of the perforation is direct closure by absorbable or non-absorbable sutures. Treatment of perforation may include also an epiploplasty in addition to the closure. An omental flap is chosen and is placed over the suture and fixed with 1 or 2 absorbable stitches. When a reliable direct suture of the opening cannot be achieved, closure can be completed by application of biological glue. The operation is completed by final extensive abdominal irrigation.

Ulcer excision, pyloroduodenoplasty

Ulcer excision and pyloroduodenoplasty is the simplest open surgical treatment for duodenal ulcer and in selected instances it can be used in the treatment of bleeding, obstruction, perforation. The operation carries low morbidity and mortality rates.

The operation usually consists of a Judd procedure. A longitudinal excision is made around the ulcer defect beginning from distal stomach to the proximal duodenum and closed transversely, so that the action of the pyloric valve is obliterated.

In other cases, when the proximal duodenum is badly deformed by scar, a Finney procedure (essentially a side-to-side gastroduodenostomy) or a Jaboulay procedure (gastric resection plus side-to-side gastroduodenostomy) is used after ulcer excision.

Various types of vagotomy

Three types of vagotomy require consideration. Bilateral truncal vagotomy denervates the entire stomach and the gastrointestinal tract to the left colon. When combined with other operations it is extremely effective in reducing the number of recurrent ulcers.

However it does carry some deleterious side effects, reducing the ability of the stomach to empty and being followed by other late motility disturbances, occasional vagus diarrhoea, and reflux alkaline gastritis.

Selective vagotomy denervates the entire stomach but leaves nerves to the gallbladder, pylorus, and bowel intact. From a practical point of view this operation is more difficult and time-consuming than truncal vagotomy, appears to have nearly equivalent results, and has attracted few supporters. Proximal gastric vagotomy can be used without pyloroplasty.

 

 

Partial gastrectomy

The usual procedure involves resection of the distal two-thirds of the stomach followed by either a Billroth I or a Billroth II anastomosis. In our opinion the operation is neater and more accurate when sutures are inserted by hand, although stapling instruments can be used. Partial gastrectomies are usually performed for type 1 gastric ulcer and for combination of duodenal ulcer perforation with decompensate stenosis.

Postoperative treatment

Administer intravenous antibiotics postoperatively. The length of administration is based on the operative findings and the recovery of the patient.

Antiemetics and analgesics are administered to patients experiencing nausea and wound pain.

A liquid diet may be started when bowel function returns.

To prevent gastric and duodenal ulcer recurrence and their complications proton pump inhibitor or H2 – receptors antagonist is administered.

Follow-up care

After hospital discharge, patients must have a light diet and limit their physical activity for a period of 4 weeks – 3 months based on the surgical approach (i.e., laparoscopic or open procedure).

The patient should be evaluated by the surgeon in the clinic to determine improvement and to detect any possible complications.

Continuous supportive therapy (for a month or even years) with half the dose of proton pump inhibitors or            H2 receptors antagonists is administered.

Prognosis

For uncomplicated surgery, the prognosis is excellent, with a very low mortality rate.