Intestinal Perforation

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History of the Procedure

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 rate 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:

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.

Problem

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.

Epidemiology

Frequency

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 rate is relatively high (~20-40%), largely because of complications, such as septic shock and multiorgan failure.

In elderly patients, acute appendicitis has a mortality rate of 35% and a morbidity rate 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.[3]

Etiology

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.

Presentation

History

A careful medical history often suggests the source of the problem, which is subsequently confirmed by clinical examination and radiologic study findings. Possible etiologies include the following:

Physical

Differential diagnosis

Relevant 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 WBCs/µL; in other words, the fluid becomes an exudate.

Contraindications

Laboratory Studies

Imaging Studies

Other Tests

Diagnostic Procedures

Medical Therapy

The mainstay of treatment for intestinal perforation is surgery.[16] Emergency medical care includes the following steps:

However, if symptoms and signs of generalized peritonitis are absent, a nonoperative policy may be used with antibiotic therapy directed against gram-negative and anaerobic bacteria.[17, 18]

Antibiotics

Antibiotics have proven effective in decreasing the rate of postoperative wound infection and in improving outcome in patients with intraperitoneal infection and septicemia.

Metronidazole (Flagyl) is typically used in combination with an aminoglycoside to provide broad gram-negative and anaerobic coverage. It is reduced to a product that interacts with deoxyribonucleic acid (DNA) to cause a loss of helical DNA structure and strand breakage, resulting in inhibition of protein synthesis and cell death in susceptible organisms. Adult dosing is 7.5 mg/kg IV before surgery. Pediatric dosing is 15-30 mg/kg/d IV divided bid/tid for 7 d. It is a pregnancy category B drug.

Gentamicin (Garamycin, Genoptic, Gentacidin) is an aminoglycoside antibiotic with gram-negative coverage. It is used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Although it is not the DOC, consider gentamicin if penicillins or other less-toxic drugs are contraindicated, when clinically indicated, and in mixed infections caused by susceptible staphylococci and gram-negative organisms. Dosing regimens are numerous; adjust dose based on CrCl and changes in volume of distribution. It may be given IV/IM. In adults, the loading dose before surgery is 2 mg/kg IV; thereafter, dosing is 3-5 mg/kg/d divided tid/qid. In infants, dosing is 7.5 mg/kg/d IV divided tid. In children, dosing is 6-7.5 mg/kg/d IV divided tid. It is a pregnancy category C drug.

Cefotetan (Cefotan) is a second-generation cephalosporin that inhibits bacterial cell wall synthesis by binding to 1 or more of the penicillin-binding proteins. It inhibits the final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Adult dosing is 2 g IV once before surgery. In children < 3 months, dosing is not established. In those >3 months, dosing is 30-40 mg/kg IV once before surgery. It is a pregnancy category B drug.

Cefoxitin (Mefoxin) is also a second-generation cephalosporin that inhibits bacterial cell wall synthesis by binding to 1 or more of the penicillin-binding proteins. It inhibits the final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Adult dosing is 2 g IV once before surgery, followed by 4 doses of 2 g IV q4-6h. In children < 3 months, dosing is not established. In those >3 months, dosing is 30-40 mg/kg IV before surgery, followed by 3 doses of 2 g IV q4-6h for 24 h. It is a pregnancy category B drug.

Cefoperazone sodium (Cefobid) is a third-generation cephalosporin that inhibits bacterial cell wall synthesis by binding to 1 or more of the penicillin-binding proteins. It inhibits the final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Adult dosing is 2-4 g/d IV divided q12h. Pediatric dosing is 100-150 mg/kg/d IV divided q8-12h, not to exceed 12 g/d. It is a pregnancy category B drug.

Surgical Therapy

The goals of surgical therapy are as follows:

Preoperative Details

Intraoperative Details

Operative management depends on the cause of perforation. Perform urgent surgery either on patients not responding to resuscitation or following stabilization and maintenance of adequate urine output. All necrotic material and contaminated fluid should be removed and accompanied by lavage with antibiotics (tetracycline 1 mg/mL). Decompress distended bowel via a nasogastric tube.

Laparoscopic or laparoscopic-assisted (minilaparotomy) surgery is also being increasingly used with outcomes comparable with conventional laparotomy. Experience and the advancement in accessories have enabled endoscopic repair of a significant number of intestinal perforations, such as iatrogenic perforation. Management of such cases needs to be individualized to the patient.

In a study involving 934 patients with sigmoid diverticulitis, Ritz et al found that the risk of free perforation in acute sigmoid diverticulitis decreases with the increases in the number of previous episodes of sigmoid diverticulitis. They concluded that the first episode has the highest risk for a free perforation. Therefore, the indication for colectomy should not be made based on the potential risk of free perforation.[19]

Postoperative Details

Intravenous replacement therapy

The aim of intravenous replacement therapy is to maintain intravascular volume and hydrate the patient. Monitor by CVP measurement and urinary output.

Nasogastric drainage

Perform nasogastric drainage continuously until drainage becomes minimal. At that stage, the nasogastric tube may be removed.

Antibiotics

Continue administration of the antibiotics commenced preoperatively unless the results of cultures taken at the time of the operation reveal that the causative organisms are resistant to them.

The goal of antibiotic therapy is to achieve levels of antibiotics at the site of infection that exceed the minimum inhibitory concentrations for the pathogens present.

In the presence of intra-abdominal infections, gastrointestinal function is often impaired; therefore, oral antibiotics are not efficacious, and intravenous antibiotics are recommended.

If no obvious improvement in the patient's condition occurs within 2-3 days, consider the following possibilities:

Analgesics

Analgesics, such as intravenous morphine, should be given continuously or in small doses at frequent intervals.

Follow-up

For patients treated with a nonsurgical approach, follow-up care consists of the following:

Complications

Outcome and Prognosis

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

Future and Controversies

Medicolegal pitfalls include the following:

Author

Samy A Azer, MD, PhD, MPH, Professor of Medical Education and Head of Curriculum Development Unit, King Saud University, Riyadh, Saudi Arabia; Visiting Professor of Medical Education, Faculty of Medicine, University of Toyama, Japan; former Professor of Medical Education, Chair of Medical Education Research and Development Unit, Faculty of Medicine, Universiti Teknologi MARA, Malaysia; former Consultant to the Victorian Postgraduate Medical Foundation, Melbourne, Australia; former Senior Lecturer in Medical Education, Faculty Education Unit, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne and University of Sydney, Australia

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Michael A Grosso, MD, Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Disclosure: Nothing to disclose.

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy

Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA, Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital

Disclosure: AMGEN Royalty Consulting; Ardelyx Ownership interest Board membership

References

  1. Lau WY, Leow CK. History of perforated duodenal and gastric ulcers. World J Surg. Oct 1997;21(8):890-6. [View Abstract]
  2. Sarath Chandra S, Siva Kumar S. Definitive or conservative surgery for perforated gastric ulcer? - An unresolved problem. Int J Surg. Dec 25 2008;[View Abstract]
  3. Stapfer M, Selby RR, Stain SC, et al. Management of duodenal perforation after endoscopic retrograde cholangiopancreatography and sphincterotomy. Ann Surg. Aug 2000;232(2):191-8. [View Abstract]
  4. Goh H, Bourne R. Non-steroidal anti-inflammatory drugs and perforated diverticular disease: a case-control study. Ann R Coll Surg Engl. Mar 2002;84(2):93-6. [View Abstract]
  5. Lee JF, Leow CK, Lau WY. Appendicitis in the elderly. Aust N Z J Surg. Aug 2000;70(8):593-6. [View Abstract]
  6. Anderson ML, Pasha TM, Leighton JA. Endoscopic perforation of the colon: lessons from a 10-year study. Am J Gastroenterol. Dec 2000;95(12):3418-22. [View Abstract]
  7. Iqbal CW, Cullinane DC, Schiller HJ, et al. Surgical management and outcomes of 165 colonoscopic perforations from a single institution. Arch Surg. Jul 2008;143(7):701-6; discussion 706-7. [View Abstract]
  8. Teoh AY, Poon CM, Lee JF, et al. Outcomes and predictors of mortality and stoma formation in surgical management of colonoscopic perforations: a multicenter review. Arch Surg. Jan 2009;144(1):9-13. [View Abstract]
  9. Namdar T, Raffel AM, Topp SA, et al. Complications and treatment of migrated biliary endoprostheses: a review of the literature. World J Gastroenterol. Oct 28 2007;13(40):5397-9. [View Abstract]
  10. Kim JB, Kim SH, Cho YK, Ahn SB, Jo YJ, Park YS, et al. A case of colon perforation due to enteropathy-associated T-cell lymphoma. World J Gastroenterol. Mar 21 2013;19(11):1841-4. [View Abstract]
  11. Cheung CP, Chiu HS, Chung CH. Small bowel perforation after radiotherapy for cervical carcinoma. Hong Kong Med J. Dec 2003;9(6):461-3. [View Abstract]
  12. Deniz K, Ozseker HS, Balas S, et al. Intestinal involvement in Wegener's granulomatosis. J Gastrointestin Liver Dis. Sep 2007;16(3):329-31. [View Abstract]
  13. Catena F, Ansaloni L, Gazzotti F, et al. Gastrointestinal perforations following kidney transplantation. Transplant Proc. Jul-Aug 2008;40(6):1895-6. [View Abstract]
  14. Kim JH, Ahn HD, Kwon KA, Kim YJ, Chung JW, Park DK, et al. Spontaneous healing of gastric perforation after endoscopic ligation for gastric varices. J Korean Med Sci. Apr 2013;28(4):624-7. [View Abstract]
  15. Butler J, Martin B. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. Detection of pneumoperitoneum on erect chest radiograph. Emerg Med J. Jan 2002;19(1):46-7. [View Abstract]
  16. Langell JT, Mulvihill SJ. Gastrointestinal perforation and the acute abdomen. Med Clin North Am. May 2008;92(3):599-625, viii-ix. [View Abstract]
  17. Crofts TJ, Park KG, Steele RJ. A randomized trial of nonoperative treatment for perforated peptic ulcer. N Engl J Med. Apr 13 1989;320(15):970-3. [View Abstract]
  18. Donovan AJ, Berne TV, Donovan JA. Perforated duodenal ulcer: an alternative therapeutic plan. Arch Surg. Nov 1998;133(11):1166-71. [View Abstract]
  19. Ritz JP, Lehmann KS, Frericks B, Stroux A, Buhr HJ, Holmer C. Outcome of patients with acute sigmoid diverticulitis: Multivariate analysis of risk factors for free perforation. Surgery. May 2011;149(5):606-13. [View Abstract]
  20. Cappendijk VC, Hazebroek FW. The impact of diagnostic delay on the course of acute appendicitis. Arch Dis Child. Jul 2000;83(1):64-6. [View Abstract]
  21. De Blaky M. Acute perforated gastroduodenal ulceration; statistical analysis and review of the literature. Surgery. 1940;8:850.
  22. Herrington JL Jr. Historical aspects of gastric surgery. In: Scott HW Jr, Sawyers JL, eds. Surgery of the Stomach, Duodenum and Small Intestine. Boston, Mass: Blackwell Scientific; 1992.
  23. Holland AJ, Cass DT, Glasson MJ, et al. Small bowel injuries in children. J Paediatr Child Health. Jun 2000;36(3):265-9. [View Abstract]
  24. Isaacman DJ, Scarfone RJ, Kost SI, et al. Utility of routine laboratory testing for detecting intra-abdominal injury in the pediatric trauma patient. Pediatrics. Nov 1993;92(5):691-4. [View Abstract]
  25. Lim JH. Ultrasound examination of gastrointestinal tract diseases. J Korean Med Sci. Aug 2000;15(4):371-9. [View Abstract]
  26. Putcha RV, Burdick JS. Management of iatrogenic perforation. Gastroenterol Clin North Am. Dec 2003;32(4):1289-309. [View Abstract]
  27. Saxe JM, Cropsey R. Is operative management effective in treatment of perforated typhoid?. Am J Surg. Mar 2005;189(3):342-4. [View Abstract]
  28. Saxena V, Basu S, Sharma CL. Perforation of the gall bladder following typhoid fever-induced ileal perforation. Hong Kong Med J. Dec 2007;13(6):475-7. [View Abstract]
  29. Schnoll-Sussman F, Kurtz RC. Gastrointestinal emergencies in the critically ill cancer patient. Semin Oncol. Jun 2000;27(3):270-83. [View Abstract]
  30. Shah M, Azam B. Case report of an intra-abdominal desmoid tumour presenting with bowel perforation. Mcgill J Med. Jul 2007;10(2):90-2. [View Abstract]
  31. Velitchkov NG, Losanoff JE, Kjossev KT, et al. Delayed small bowel injury as a result of penetrating extraperitoneal high-velocity ballistic trauma to the abdomen. J Trauma. Jan 2000;48(1):169-70. [View Abstract]