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Sunday, March 7, 2021




The two most serious complications of gastric or duodenal peptic ulcers are perforation and hemorrhage. The frequency of acute perforations in patients hospitalized for peptic ulcer varies from 2% to 25%. Perforation occurs with far greater frequency in men than in women. It is also recognized that peptic ulcer tends to perforate more often in individuals between the ages of 25 and 50 years than in younger or older persons. Fortunately, these two complications appear to have decreased over the last several decades with the wide-spread use of flexible upper endoscopy for diagnosis of ulcer disease and the advent of improved medical treatments with proton pump inhibitors and for H. pylori infection.

The previous duration of an ulcer, of either the stomach or the duodenum, seems to have no influence on the speed with which the ulcerative and inflammatory processes penetrate the muscular coat and the serous layer. An acute peptic ulcer may rapidly penetrate or perforate the gastric or intestinal wall, so that, in some instances, the patient may fail to give any history of typical ulcer symptoms. Many chronic ulcers, on the other hand, may exist for years without progressing so far in depth as to implicate the serosa, although no chronic ulcers with severe and persistent symptoms or recurrent or calloused ulcers are ever exempt from the potential danger of a perforation. The rapidity with which the digestive effect of the strongly acid gastric juice destroys the layers of the wall and approaches the serosa cannot be anticipated.

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Once perforation has taken place, the location of the ulcer plays an important role as to the clinical presentation of the patient. Ulcers of the anterior wall of both the stomach and the duodenum have a greater access to the “free” peritoneal cavity than do those on the posterior wall. From the posterior aspects, the ulcer may proceed to penetrate the underlying organs such as the left lobe of the liver, the pancreas, or the gastrohepatic ligament. These may block the ulcer and prevent the entry of gastric or duodenal contents into the peritoneal cavity. This “walled-off” perforation, in which a new floor for the ulcer has been organized outside the visceral wall, has been called chronic perforation or penetration; the term subacute perforation has been reserved for certain tiny ruptures in the serosa, which occur only with a relatively slowly advancing penetration of a chronic gastric ulcer. In such instances, fibrinous adhesions to contiguous parenchymal organs or peritoneal attachments have come into existence, as a result of periinflammatory tissue reactions, long before the ulcer has penetrated to the serosal layer. The adhesions intercept the small amount of gastric content that might escape through what are usually very small apertures, thus enveloping the fluid, which may lead to the development of localized abscesses.

A free perforation occurs most frequently with ulcers of the anterior wall of the duodenal bulb. The hole resulting from an acute perforation is usually round, varying in diameter from 2 to 4 mm. One of the characteristic features of these holes is their sharp edges, which make them appear to have been punched out. The surrounding tissue may fail to show any signs of chronic induration, edema, or inflammation.

The clinical picture of an acute and free perforation, whether it occurs in the stomach or in the duodenum, is often dramatic. At the moment of perforation, the patient is seized by a sudden, excruciating, explosive pain, which is of a severity “almost beyond description.” It is felt all over the abdomen and may radiate to the chest and shoulder. The patient is pale, the haggard face is covered with cold perspiration, and the suffering is expressed in every feature of the countenance. In an effort to reduce the abdominal pain, the patient flexes the thighs toward the abdomen, which is extremely rigid and tender (“doubling up”). During this early phase, which may last from 10 minutes to a few hours, in part depending on the amount and type of gastrointestinal content released into the peritoneal cavity, the body temperature is subnormal; the pulse and blood pressure remain within the normal range (or the rate of the pulse may even be rather slow), though respiration may assume a superficial and panting character. Within a short time, in some instances introduced by a period of apparent subjective improvement, all the typical signs (e.g., nausea, vomiting, dry tongue, rapid pulse, fever, leukocytosis) of a severe, acute, diffuse peritonitis appear. The tenderness, in the early phase confined mostly to the upper part of the abdomen, has spread, as a rule, over the total abdominal area. It may be excessive in the lower right quadrant if, with a perforation of a duodenal ulcer, the intestinal material is dissipated in the right lumbar gutter along the ascending colon.

The differential diagnosis between a perforated gastric or duodenal ulcer and pancreatitis or a mesenteric thrombosis may be rather difficult in some cases, but such difficulties are seldom encountered with a ruptured appendix. Other conditions, such as an ectopic pregnancy, ruptured diverticulum, renal colic, acute episodes of biliary tract diseases, acute intestinal obstruction or volvulus, and, in some instances, coronary thrombosis, must also be considered.

The sign that is most helpful in confirming the suspected diagnosis of ulcer perforation is the presence of free air in the peritoneal cavity, particularly in the sub-phrenic space, demonstrable by upright x-ray examination. If it is possible for the patient to sit or stand, the air will accumulate under the diaphragm. Escaped air is present, in rare cases, under the left diaphragm only; not infrequently air may be detected under both diaphragmatic leaves and, more usually, under the right leaf only.

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Surgical intervention is nearly always required in the form of exploratory laparotomy and closure of perforation with peritoneal wash. Conservative treatment, including intravenous fluids, antibiotics, nasogastric aspiration, and bowel rest, is occasionally used with consultation with surgery, if the patient is nontoxic and clinically stable. With the finding of air, operation is usually indicated without delay. The prognosis of a perforated gastric or duodenal ulcer is better the earlier an operation is performed. The mortality rate increases when the operation is performed more than 6 hours after perforation. The operation of choice is often a subtotal gastric resection in younger individuals who are in good general condition. This is true if the surgeon is permitted to work within the first 6 hours after the ulcer has perforated, under optimal hospital conditions, with carefully supervised anesthesia, with the support necessary to combat successfully the vascular collapse and infection. When the patient is in poor general condition, efforts to treat conservatively with suction through an indwelling catheter in the stomach, massive antibiotics, and supportive therapy entail a greater risk and are less successful than is surgical treatment, although in some isolated instances the life of the patient so treated has been saved. The simple closure of the perforation, postponing the more definitive surgery, if necessary, until such time as the patient may be in a more favorable condition, should be reserved for cases that come to the surgeon’s attention later than 6 hours after the onset of the acute illness, or for elderly patients (over 60 years of age), when the shock tends to be massive, or when the cardiopulmonary situation requires an operation of the shortest possible duration. In approximately 60% of cases in which the perforation is closed by simple suture, the more radical operation becomes inevitable at a later time.

The symptoms of a spontaneously closing ulcer perforation (so-called subacute perforation) lack the dramatic accents of an “acute” or free perforation. The majority of these patients may not feel more than some intensification of their usual ulcer pains. It happens, not infrequently, that a perforation is not detected preoperatively in the assessment of a bleeding or intractable ulcer but becomes evident only at surgery or with examination of the pathologic specimen. In other instances the patient, as well as the physician, may have been well aware of the acute event, but the signs pointing to a perforation (e.g., sharp epigastric pain, abdominal rigidity, elevated temperature and pulse rate) disappeared within such a short period of time that operation was deferred as not critical. Sooner or later, however, most of these patients must be operated upon because of a localized peritonitis, an abscess that may form in the subphrenic or subhepatic regions, or, later, a partial gastric or duodenal obstruction caused by the massive scar formation.

The erosion of the serosal layer by a chronic peptic ulcer on the posterior walls of the stomach and duodenum and its penetration into a contiguous organ is such a slow process that the actual perforation is rarely detected by the patient. The typical ulcer pains and their relation to and relief as a result of food intake gradually give way to continuous, gnawing, boring pain, which no longer responds to the ingestion of food. The pain may radiate to the back, shoulder, clavicular areas, or umbilicus, or downward to the lumbar vertebrae and the pubic or inguinal regions. Considering the peripheral distribution of pain pathways and their origin in a spinal segment, the site where the patient allocates the radiating pain or the detection of a hyperesthesia in a certain region of the skin may give a clue to determining the organ involved. A classic example of a chronic perforation is the ulcer of the posterior wall of the duodenal bulb, penetrating into and walled off by the pancreas. In operating for this condition and attempting to remove the entire ulcer with its floor in the pancreatic tissue, one runs the risk of producing a pancreatic lesion that may open accessory pancreatic ducts. It is, therefore, advisable in these cases to leave the ulcer floor untouched after careful dissection of the ulcer from the duodenal wall.

Ulcers located in the upper parts of the posterior duodenal wall have a great tendency to penetrate the hepato-duodenal ligament. This process is usually accompanied by the development of extensive, fibrous, and thickened adhesions, to which the greater omentum may contribute. The supraduodenal and retroduodenal portions of the common bile duct, taking its course within the leaves of the ligament, may become compromised in these adhesions. As a result of a constriction or distortion of the common duct, a mild obstructive icterus may confuse the clinical picture. Fortunately, perforation into the duct, with a subsequent cholangitis, is a rare event. In the surgical approach to an ulcer of that kind, the anatomic relations of the common bile duct must be kept acutely in mind, whether or not signs of duct involvement are present. Disastrous lesions can be avoided by a preliminary exposure of the duct and by the introduction of a T tube, which serves as a good guide in disentangling the adhesions and exposing the duodenal wall and the ulcer. Very seldom does an acute perforated ulcer of the posterior gastric wall release chyme into the bursa omentalis, producing only signs of localized peritonitis without free air in the abdominal cavity.


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Another complication of the chronic relapsing duodenal, pyloric, or prepyloric ulcer is stenosis of the pylorus, which develops gradually as the result of the little-by-little thickening of the duodenal wall and the progressive fibrotic narrowing of the lumen. The incidence of complete pyloric stenosis as a sequel to an ulcer has decreased in recent decades, apparently because of improved medical management of this type of ulcer and prompt recognition of its initial phases. Medical management involves the use of proton pump inhibitor therapy; treatment of H. pylori infection, if present; and, if needed, endoscopic pyloric dilation. When the pyloric lumen begins to narrow, the stomach tries to overcome the impediment by increased peristalsis, and its muscular wall becomes hypertrophic. This is the stage that has been called compensated pyloric stenosis because, with these adaptation phenomena, the stomach succeeds in expelling its contents with only mild degrees of gastric retention. Later, when the lumen is appreciably narrowed, the expulsive efforts of the stomach fail, and the clinical picture will be dominated by incessant vomiting and by distress, owing to a progressive dilatation of the stomach, which, at times, may become massive. This condition of decompensated pyloric stenosis, which results in the retention of ingested material and the products of gastric secretion, is, as a rule, irreversible and is an unequivocal indication for surgical intervention. The operation of choice is a subtotal gastrectomy, but, in view of the characteristically poor general condition of the patient, the surgeon may sometimes have to resort to less radical procedures, such as a gastrojejunostomy. In the presence of a still-active ulcer, those operations which reroute the gastric content around the duodenum in the simplest fashion should be supplemented by a bilateral vagotomy.


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Minor bleeding occurs in the majority of patients with acute or chronic peptic ulcer. “Occult” blood can be found with fair regularity in the stools or gastric juice of most ulcer patients. This is the result of the oozing characteristic of ulcerative lesions. Massive hemorrhage, which, together with perforation, typifies the most dangerous of all ulcer complications, is fortunately far less frequent. Reliable figures of its incidence are not available, but it has been estimated that, of all massive hemorrhages of the gastrointestinal tract, 60% to 75% stem from a peptic ulcer. Obliterative endarteritis or thrombosis of the mucosal and submucosal vessels in the ulcerated tissue may be a natural protection against bleeding from the more superficial ulcers. As a rule, the hemorrhage is caused by erosion into a large vessel, though excessive bleeding occasionally also derives from smaller arteries or veins whose drainage is impaired. A decisive factor for the degree of bleeding is the location of the ulcer. Gastric ulcers have often caused excessive blood loss, but the most frequent origin of a massive hemorrhage is the ulcer of the posterior portion of the duodenal bulb, because here the ulcer can penetrate into the walls of the gastroduodenal and retroduodenal (posterior and superior pancreaticoduodenal) arteries, which course just behind the first portion of the duodenum.

The essential clinical signs of a duodenal ulcer perforated into an artery are massive melena and acute vascular collapse. The shock may appear suddenly and very shortly after the opening of an artery, or it may be delayed for several hours. In striking contrast to the hemorrhages due to gastric ulcer and esophageal ulcers or varices, hematemesis is rare with bleeding from a duodenal ulcer, because the blood, originating from beyond the spastic pylorus, is propelled into the small intestine and does not regurgitate to the stomach. In some cases sudden bleeding comes as a complete sur- prise to patients who have had no previous complaints or signs pointing to the presence of an ulcer, and this may be the first event to indicate the existence of a “silent” ulcer. The differential diagnosis of the origin of the bleeding and its localization may, at times, be extremely difficult. Emergent upper endoscopy in patients with upper gastrointestinal bleeding is usually indicated. X-ray examination is often of little help, because such a bleeding ulcer may fail to show the usually typical perifocal changes, and because the niche may be filled with blood coagulum. Endoscopic therapy with electrocautery, clipping, or injections is attempted to stop the bleeding, along with giving intravenous fluids and/or blood and with proton pump inhibitor therapy.

Massive and continuous bleeding from an ulcer which cannot be stopped endoscopically should be treated surgically. Repeated hemorrhages are adequate indication for surgical intervention. A rapid major blood loss, the advanced age of a patient, and the presence of shock not immediately responsive to appropriate measures make operation imperative.

Even during operation, it may often be difficult to establish the origin of hemorrhage if it has not been determined before surgery by upper endoscopy.

However, endoscopic localization can also be difficult if the bleeding is massive. A bluish discoloration of the upper jejunal loops permits no more than a suspicion that the bleeding has originated in the gastroduodenal or esophageal area. The ulcer itself cannot always be palpated, and only after duodenotomy may the ulcer crater be found. The bleeding can then be provisionally secured by ligation of the bleeding vessel. The final arrest of the hemorrhage, however, may require subtotal resection.

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