Intestinal Perforation

Updated: Dec 22, 2016
  • Author: Samy A Azer, MD, PhD, MPH; Chief Editor: John Geibel, MD, DSc, MSc, AGAF  more...
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Overview

Background

Upper-bowel perforation can be described as either free or contained. Free perforation occurs when bowel contents spill freely into the abdominal cavity, causing diffuse peritonitis (eg, duodenal or gastric perforation). Contained perforation occurs when a full-thickness hole is created by an ulcer, but free spillage is prevented because contiguous organs wall off the area (as occurs, for example, when a duodenal ulcer penetrates into the pancreas).

Lower-bowel perforation (eg, in patients with acute diverticulitis or acute appendicitis) results in free intraperitoneal contamination.

Lau and Leow have indicated that perforated peptic ulcer was clinically recognized by 1799, but the first successful surgical management of gastric ulcer was by Ludwig Heusner in Germany in 1892. In 1894, Henry Percy Dean from London was the first surgeon to report successful repair of a perforated duodenal ulcer. [1]

Partial gastrectomy, although performed for perforated gastric ulcer as early as 1892, did not become a popular treatment until the 1940s. This was carried out as a result of the perceived high recurrence rate of ulcer symptoms after simple repair. The physiologic effects of truncal vagotomy on acid secretion had been known since the early 19th century, and this approach was introduced to the treatment of chronic duodenal ulcer in the 1940s.

The next development in the management of peptic ulcer disease was the introduction of high selective vagotomy in the late 1960s. However, neither of these approaches proved to be useful, and several postoperative complications, including high rates of ulcer recurrence, have limited their use. Currently, in patients with gastric perforation, simple closure of perforated ulcers is more commonly performed than is gastric resection. [2]

During World War I, the mortality following isolated injuries of the small intestine and colon was approximately 66% and 59%, respectively. The possible reasons for the high mortality and morbidity rates at that time may have been related to the following factors:

  • Knowledge in the area of bowel injuries and the pathophysiologic changes triggered by such injuries was inadequate
  • Clinical skills and diagnostic techniques that allow early detection of such injuries were lacking
  • Intravenous saline solutions or blood transfusions were not used in the management of hypovolemia and hemodynamic changes of these patients
  • No antibiotics were available
  • Laparotomy was not recommended in abdominal injuries
  • The technical maneuvers to assess bowel injuries and to mobilize ascending and descending colon were generally not recommended

During the early years of World War II, Ogilvie, a leading surgeon in the British Army, recommended colostomy for management of all colonic injuries. This notion was supported by a publication from the office of the Surgeon General of the United States. However, the data presented in Ogilvie's series were not convincing. He reported a mortality rate of 53% for colonic injuries treated with colostomy, a rate similar to that observed during World War I.

According to Ogilvie, colostomy apparently failed to improve the mortality rate in World War II because primary repairs were used to treat less-severe injuries during World War I. Many patients in World War I were treated expectantly and were not included in the mortality data. On the other hand, Ogilvie's data included all patients with bowel injuries. These apparent differences in the methodology used convinced surgeons to continue using colostomies in such injuries after World War II.

Several reports clearly indicated that surgeons used colostomy during the Korean and Vietnam wars, particularly in the management of left colonic injuries. However, in civilian injuries, it has been reported that primary repair can be successfully used. By the end of 1980s, primary repair was considered to the management strategy of choice, and it has replaced the use of colostomies in the treatment of civilian patients in most hospitals in the United States, the United Kingdom, Europe, and Australia. At present, primary repairs are widely used for such bowel injuries.

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Anatomy

The peritoneal cavity is lined with a single layer of mesothelial cells, connective tissue (including collagen), elastic tissues, macrophages, and fat cells. The parietal peritoneum covers the abdominal cavity (ie, abdominal wall, diaphragm, pelvis); the visceral peritoneum covers all of the intra-abdominal viscera, forming a cavity that is completely enclosed except at the open ends of the fallopian tubes.

The peritoneal cavity is divided by the transverse mesocolon. The greater omentum extends from the transverse mesocolon and from the lower pole of the stomach to line the lower peritoneal cavity. Abdominal organs, such as the pancreas, duodenum, and ascending and descending colon, are located in the anterior retroperitoneal space; the kidneys, ureters, and adrenal glands are found in the posterior retroperitoneal space. Other abdominal organs, the liver, stomach, gallbladder, spleen, jejunum, ileum, transverse colon, sigmoid colon, cecum, and appendix are found within the peritoneal cavity.

A small amount of fluid sufficient to allow movement of organs is usually present in the peritoneal space. This fluid is normally serous (protein content of <30 g/L, <300 WBCs/µL). In the presence of infection, the amount of this fluid increases, its protein content climbs to more than 30 g/L, and the white blood cell (WBC) count increases to more than 500/µL; in other words, the fluid becomes an exudate.

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Pathophysiology

Normally, the stomach is relatively free of bacteria and other microorganisms because of its high intraluminal acidity. Most persons who experience abdominal trauma have normal gastric functions and are not at risk of bacterial contamination following gastric perforation. However, those who have a preexisting gastric problem are at risk of peritoneal contamination with gastric perforation.

Leakage of acidic gastric juice into the peritoneal cavity often results in profound chemical peritonitis. If the leakage is not closed and food particles reach the peritoneal cavity, chemical peritonitis is succeeded by gradual development of bacterial peritonitis. Patients may be free of symptoms for several hours between the initial chemical peritonitis and the later occurrence of bacterial peritonitis.

The microbiology of the small bowel changes from its proximal to its distal part. Few bacteria populate the proximal part of the small bowel, whereas the distal part of the small bowel (the jejunum and ileum) contains aerobic organisms (eg, Escherichia coli) and a higher percentage of anaerobic organisms (eg, Bacteroides fragilis). Thus, the likelihood of intra-abdominal or wound infection is increased with perforation of the distal bowel.

The presence of bacteria in the peritoneal cavity stimulates an influx of acute inflammatory cells. The omentum and viscera tend to localize the site of inflammation, producing a phlegmon. (This usually occurs in perforation of the large bowel.) The resulting hypoxia in the area facilitates growth of anaerobes and produces impairment of bactericidal activity of granulocytes, which leads to increased phagocytic activity of granulocytes, degradation of cells, hypertonicity of fluid forming the abscess, osmotic effects, shift of more fluids into the abscess area, and enlargement of the abdominal abscess. If untreated, bacteremia, generalized sepsis, multiorgan failure, and shock may occur.

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Etiology

Causes of intestinal perforation include the following:

  • Penetrating injury to the lower chest or abdomen (eg, knife injuries) - In cases of penetrating trauma, the small bowel is the most commonly injured intra-abdominal viscus, because it is coiled in the abdomen and occupies most of the area of the peritoneal cavity. In addition, the small bowel is attached to a mesentery and is highly mobile.
  • Blunt abdominal trauma to the stomach - Such injuries are more common in children than they are in adults and include vehicle-related trauma, bicycle handlebar injuries, and seatbelt syndrome.
  • Ingestion of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), [3] and steroids - Intestinal perforation from such causes is particularly observed in elderly patients. Prescribing NSAIDs to patients with diverticular disease carries an increased risk of colonic perforation.
  • Presence of a predisposing condition - Predisposing conditions include peptic ulcer disease, acute appendicitis, acute diverticulitis, and inflamed Meckel diverticulum. Indeed, acute appendicitis is still one of the common causes of bowel perforation in elderly patients and is associated with relatively poor outcomes. [4]
  • Bowel injuries associated with endoscopy - Injuries can occur with ERCP and colonoscopy. [5, 6, 7, 8]
  • Endoscopic biliary stent - Dislocation and migration of biliary stents to the intestine may cause bowel perforation. [9]
  • Intestinal puncture as a complication of laparoscopy - Factors that may predispose patients to this complication are obesity, pregnancy, acute and chronic bowel inflammation, and bowel obstruction.
  • Bacterial infections - Bacterial infections (eg, typhoid fever) may be complicated by intestinal perforation in about 5% of patients. Perforation in these patients may unexpectedly occur after their condition has started to improve.
  • Inflammatory bowel disease - Bowel perforation may occur in patients with acute ulcerative colitis, and perforation of the terminal ileum may occur in patients with Crohn disease (CD); the CD-associated gene SLCO3A1 has been shown to mediate inflammatory processes in intestinal epithelial cells and thereby result in a higher incidence of bowel perforation in CD patients [10]
  • Perforation secondary to intestinal ischemia (eg, ischemic colitis)
  • Bowel perforation by intra-abdominal malignancy, lymphoma, or metastatic renal carcinoma - Even benign tumours, such as desmoid tumours (eg, those originating from the fibrous tissues of the mesentery), may cause bowel perforation. [11]
  • Radiotherapy of cervical carcinoma and other intra-abdominal malignancies - This may be associated with late complications, including bowel obstruction and bowel perforation. [12]
  • Necrotizing vasculitis - Wegener’s granulomatosis affecting the viscera, although uncommon, may cause bowel ulcerations and perforations. [13]
  • Kidney transplantation - Following kidney transplantation, gastrointestinal perforations may occur as a complication. In these cases, the perforation is usually related to the use of high doses of immunosuppressive medications, a treatment employed in the early postoperative period and in the management of acute rejection episodes. [14]
  • Ingestion of caustic substances - Accidental or intentional ingestion of caustic substances may result in acute intestinal perforation and peritonitis. Delayed perforation may occur up to 4 days after acid exposure.
  • Foreign bodies (eg, toothpicks) - These may cause perforation of the esophagus, stomach, or small intestine, with intra-abdominal infection, peritonitis, and sepsis.
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Epidemiology

In children, small-bowel injuries following blunt abdominal trauma are infrequent, with an incidence of 1-7%. Evidence shows, however, that the incidence of these injuries is increasing.

In adults, perforations of peptic ulcer disease were a common cause of morbidity and mortality with acute abdomen until the latter half of the 20th century. The rate has fallen in parallel with the general decline in the prevalence of peptic ulcer disease. Duodenal ulcer perforations are 2-3 times more common than are gastric ulcer perforations. About a third of gastric perforations are due to gastric carcinoma.

Approximately 10-15% of patients with acute diverticulitis develop free perforation. Although most episodes of perforated diverticulum are confined to the peridiverticular region or pelvis, patients occasionally present with signs of generalized peritonitis. The overall mortality is relatively high (~20-40%), largely because of complications, such as septic shock and multiorgan failure.

In elderly patients, acute appendicitis has a mortality of 35% and a morbidity of 50%. A major contributing factor to morbidity and mortality in these patients is the presence of 1 or more severe medical conditions coexisting with, but predating, the appendicitis.

Endoscopy-associated bowel injuries are not a common cause of perforation. For example, perforations related to endoscopic retrograde cholangiopancreatography (ERCP) occur in about 1% of patients. [5]

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Prognosis

Outcome is improved with early diagnosis and treatment. The following factors increase the risk of death:

  • Advanced age
  • Presence of preexisting underlying disease
  • Malnutrition
  • The nature of the primary cause of bowel perforation
  • Appearance of complications
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