Gastrointestinal perforation overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]

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Overview

Perforation is full-thickness injury of the bowel wall. The gastrointestinal tract includes the esophagus, stomach, small intestine, and large intestine. Gastrointestinal perforation may also be divided based on age of the patient into adult type and neonatal type perforation. Instrumentation of the gastrointestinal tract includes upper endoscopy, sigmoidoscopy, colonoscopy, stent placement, endoscopic sclerotherapy, nasogastric intubation, esophageal dilation, and surgery is the commonest cause of gastrointestinal perforation. Perforation of the gastrointestinal tract can be due to many causes but main causes are instrumentation during surgery or bowel obstruction. Spontaneous perforation can be caused by inflammation, connective tissue disorders, and medications. Terminal ileum is the commonest site for spontaneous perforation and may be the jejunum and colon. In neonatal perforation, the terminal ileum and colon are the commonest sites for perforation. The pathogenesis of NEC remains unknown but there are many factors for infection such as: Ninety percent of NEC cases occur in preterm infants due to immaturity of the gastrointestinal tract. The incidence of iatrogenic esophageal perforation from instrumentation has decreased, but the number of esophageal perforations from external trauma and spontaneous rupture has increased to 1 per 8,000 admissions. Incidence rates of gastric perforation varied from 1.5 to 7.8/100000 per year and from 5.2 to 40.2 regarding peptic ulcer bleeding. A perforation rate of 110 per 100,000 for rigid endoscopy and 30 per 100,000 regarding flexible endoscopy. Sclerotherapy perforation rate is 1,000 to 5,000 per 100,000. Gastrointestinal perforation should be differentiated from other causes of chest pain and abdominal pain according to the site of perforation. Acute onset of chest or epigastric pain may also be seen with disorders such as Mallory-Weiss syndrome, acute pancreatitis, myocardial infarction, and peptic ulcer disease. History of recent instrumentation, surgery, or ingested foreign bodies is usually related to gastrointestinal tract (GIT) perforation. Main symptoms are pains in chest or abdomen, abdominal mass, dysphagia, fistula formation, or sepsis. Diverticulitis is the most common etiology leading to intra-abdominal abscess formation. Chest computed tomography (CT) is done when fluoroscopy is equivocal, and there is persisting suspicion of perforation. Signs of perforation on abdominal CT scanning include extraluminal oral contrast, free fluid or food collections, discontinuity of the intestinal wall, localized peritoneal fat stranding, and Bowel wall thickening. Initial management of the patient with gastrointestinal perforation includes intravenous fluid therapy and broad-spectrum antibiotics. Patients with intestinal perforation can have severe volume depletion. The administration of intravenous proton pump inhibitors. Electrolyte abnormalities correction especially metabolic alkalosis if fistula developed. The severity of any electrolyte abnormalities depends upon the nature and volume of material leaking from the gastrointestinal tract. Intravenous vasopressors are useful in patients who remain hypotensive despite adequate fluid resuscitation or who develop cardiogenic pulmonary edema. Norepinephrine is the first-line single agent in septic shock. The addition of a second or third agent to norepinephrine may be required. Surgery is the mainstay therapy for gastrointestinal tract (GIT) perforation. The main indications are abdominal sepsis, worsening abdominal pain, signs of diffuse peritonitis, complete bowel obstruction, bowel ischemia. In esophageal perforation, surgical options include primary repair, repair over a drain. Primary repair is the best procedure for thoracic esophageal rupture. It is performed when the closure can heal. Endoscopically-placed-stents can be used to manage some patients with esophageal perforation. In perforated stomach, if the patient is unstable or deteriorating, urgent operation and closure with a piece of omentum is the standard of care. If the patient is stable or improving, nonoperative management with close monitoring is a reasonable option. If patients did not show clinical improvement after 24 hours, surgery was performed. In colonic resection, A one-stage colon resection for diverticulitis can be performed open or laparoscopically.

Gastrointestinal perforation historical perspective

Boerhaave syndrome was first described by the physician Herman Boerhaave, Professor of Medicine at Leiden University, in a publication entitled “History of a Grievous Disease Not Previously Described”. Hundred years ago, polish clinical researcher professor W.Jaworski was the first to describe the spiral-shaped microorganism at Cracow Jagiellonian University In 1586, Marcellus Donatus of Mantua described gastric ulcers by performing autopsies. In 1688, Johannes von Murault gave detailed description of duodenal ulcers. The appropriate therapy for intestinal perforation in typhoid fever has been controversial since the late 1880s.

Gastrointestinal perforation classification

Gastrointestinal perforation may be classified based upon the etiology into instrumental perforation, perforation due to systemic diseases, perforation due to inflammatory causes, medications and neoplasms. Gastrointestinal perforation may also be divided based on age of the patient into adult type and neonatal type perforation.

Gastrointestinal perforation causes

Instrumentation of the gastrointestinal tract includes upper endoscopy, sigmoidoscopy, colonoscopy, stent placement, endoscopic sclerotherapy, nasogastric intubation, esophageal dilation, and surgery is the commonest cause of gastrointestinal perforation. Other causes include medications, foreign bodies, violent retching, peptic ulcer disease. Perforation of the small intestine can be related to bowel obstruction, acute mesenteric ischemia, inflammatory bowel disease. Colonic diverticulosis is common cause of perforation in large intestine. Causes of spontaneous intestinal perforation in adults include Crohn’s disease, Celiac disease, graft-vs-host disease, and infection. Causes of intestinal perforation in neonates include necrotising enterocolitis, iatrogenic, umbilical catheterization, umbilical cord clamping, nasogastric tube, obstruction, and ileal atresia.

Gastrointestinal perforation pathophysiology

Perforation is full-thickness injury of the bowel wall. Perforation of the gastrointestinal tract can be due to many causes but main causes are instrumentation during surgery or bowel obstruction. Spontaneous perforation can be caused by inflammation, connective tissue disorders, and medications. Terminal ileum is the commonest site for spontaneous perforation and may be the jejunum and colon. In neonatal perforation, the terminal ileum and colon are the commonest sites for perforation. The pathogenesis of NEC remains unknown but there are many factors for infection such as: Ninety percent of NEC cases occur in preterm infants due to immaturity of the gastrointestinal tract. Preterm infants have lower concentrations or more immature function of contributing mucosal defense factors than do term infants and adults. Regarding anatomy of GIT, the esophagus travels 3 regions of the body: the neck, thorax, and abdomen. Accordingly, it is divided into 3 parts: cervical, thoracic, and abdominal. The gastrointestinal tract has a form of general histology with some differences that reflect the specialization in functional anatomy. The GI tract can be divided into four concentric layers in the following order: Mucosa, Submucosa, muscular layer, and Adventitia or serosa. Perforation of the gastrointestinal tract can be due to many causes but main causes are instrumentation during surgery or bowel obstruction. Spontaneous perforation can be caused by inflammation, connective tissue disorders, and medications. With bowel obstruction, perforation occurs proximal to the obstruction as pressure builds up within the bowel, exceeding intestinal perfusion pressure, and leading to ischemia and subsequently necrosis. Acute colonic pseudo-obstruction is an acute dilatation of the colon without mechanical obstruction of the flow of intestinal contents. The mechanism of perforation in patients with acute colonic pseudo-obstruction is unknown. Spinal anesthesia and pharmacologic agents are suggested to be the causes due to impairment of autonomic system.

Gastrointestinal perforation epidemiology and demographics

The incidence of iatrogenic esophageal perforation from instrumentation has decreased, but the number of esophageal perforations from external trauma and spontaneous rupture has increased to 1 per 8,000 admissions. Incidence rates of gastric perforation varied from 1.5 to 7.8/100000 per year and from 5.2 to 40.2 regarding peptic ulcer bleeding. A perforation rate of 110 per 100,000 for rigid endoscopy and 30 per 100,000 regarding flexible endoscopy. Sclerotherapy perforation rate is 1,000 to 5,000 per 100,000. The incidence of colonic perforation could be as low as 16 per 100,000 of all diagnostic colonoscopy procedures and may be seen in up to 5% of therapeutic colonoscopies. The incidence of CP following flexible sigmoidoscopy varies from 27 to 88 per 100,0000. Screening colonoscopy perforation rates are 1000 to 10,000 per 100,000. Anastomotic stricture dilation perforation rates are 0 to 6000 per 100,000.

Gastrointesinal perforation risk factors

Risk factors for gastrointestinal perforation varies between instrumentation during upper endoscopy, sigmoidoscopy, colonoscopy, stent placement, endoscopic sclerotherapy, nasogastric intubation, esophageal dilatation, and surgery. Other risks include medications especially Aspirin, potassium supplements, disease-modifying antirheumatic drugs (DMARDs), and nonsteroidal anti-inflammatory drug. Peptic ulcer disease is the most common cause of stomach and duodenal perforation. Colonic diverticulosis is common risk for colonic perforation in the developed world. Mesenteric ischemia increases the risk for perforation. Embolism, mesenteric occlusive disease, and heart failure lead to gastrointestinal ischemia. In neonatal perforation, prematurity is the commonest risk factor. Antenatal administration of glucocorticoids, nonsteroidal antiinflammatory drugs, indomethacin, and magnesium sulfate had been initially reported to increase the risk of perforation.

Gastrointestinal perforation differential diagnosis

Gastrointestinal perforation should be differentiated from other causes of chest pain and abdominal pain according to the site of perforation. Acute onset of chest or epigastric pain may also be seen with disorders such as Mallory-Weiss syndrome, acute pancreatitis, myocardial infarction, and peptic ulcer disease.

Gastrointestinal perforation natural history, complications, and prognosis

If left untreated, all of patients with gastrointestinal perforation (GIT) may progress to develop shock, abdominal abscess, and sepsis. Complications of GIT perforation include systemic complications such as pneumonia, renal dysfunction and thromboembolism, Surgical site infection, sepsis, intraabdominal abscess, and Shock. Prognosis of GIT perforation depends on site of perforation, age of patient, and time of intervention. A delay in diagnosis more than 24 hours in patients found to have isolated blunt small bowel injury was associated with a higher mortality compared with diagnosis at <24 hours. Patients with small bowel injury has worse prognosis than patients without small bowel injury. Mortality rates for patients sustaining a ruptured stomach have been reported between 28 and 66 percent. Colon-injury-related mortality rate of 1.3 percent. Sepsis has a high mortality rate. Sepsis is responsible for 6 percent of all deaths. Long-term survival of infants with spontaneous intestinal perforation has improved over the past 30 years with reported survival rates of 64 to 90 percent. Patients with spontaneous intestinal perforation appear to have a lower mortality rate compared with patients with surgically treated necrotizing enterocolitis.

Gastrointesinal perforation screening

There is no specific screening for gastrointestinal perforation.

Gastrointestinal perforation history and symptoms

History of recent instrumentation, surgery, or ingested foreign bodies is usually related to gastrointestinal tract (GIT) perforation. Main symptoms are pains in chest or abdomen, abdominal mass, dysphagia, fistula formation, or sepsis. Diverticulitis is the most common etiology leading to intra-abdominal abscess formation. Patients who develop an external fistula will complain of the sudden appearance of drainage from a postoperative wound, or from the abdominal wall or perineum in the case of spontaneous fistulas. 

Gastrointestinal perforation physical examination

Patients may appear tired, weak, diaphoretic and anxious especially if sepsis developed. Tachycardia and rapid weak pulse may develop if sepsis developed. In esophageal perforation, asymmetric chest expansion/ decreased chest expansion may develop. Abdominal distention, tenderness, guarding or mass may develop in intestinal perforation. Infants with spontaneous intestinal perforation present with an acute onset of abdominal distension and hypotension. Abdominal distention usually occurs without the abdominal wall erythema, crepitus, and induration commonly seen in patients with necrotitzing enterocolitis.

Gastrointestinal perforation laboratory findings

Laboratory studies for gastrointestinal perforation include Complete blood count, electrolytes, liver function tests, and renal function tests.

Gastrointestinal perforation x-ray

X-ray may be useful to diagnose gut perforation. Findings of chest x-ray in esophageal perforation include Pneumomediastinum, ring-around-the-artery sign in cases of pneumomediastinum, and widening of the mediastinum. Findings of abdominal x-ray in esophageal perforation include free gas under the diaphragm is a classic sign of pneumoperitoneum on erect chest, cupola sign is an arcuate lucency over the lower thoracic spine, and rigler sign is seen as gas outlines the inner and outer surfaces of the intestine. Signs of perforation on plain neck imaging include subcutaneous emphysema tracking into the neck, anterior displacement of the trachea, and air in the prevertebral fascial planes on lateral view.

Gastrointestinal perforation CT

Chest computed tomography (CT) is done when fluoroscopy is equivocal, and there is persisting suspicion of perforation. Signs of perforation on abdominal CT scanning include extraluminal oral contrast, free fluid or food collections, discontinuity of the intestinal wall, localized peritoneal fat stranding, and Bowel wall thickening.

Gastrointestinal perforation MRI

Abdominal and chest MRI may be useful to diagnose gastrointestinal perforation. It shows the same imaging signs of CT.

Gastrointestinal perforation echocardiography or ultrasound

There are no echocardiography or ultrasound findings associated with gastrointestinal perforation.

Gastrointestinal perforation other imaging findings

Esophageal fluoroscopy is most sensitive within the first 24 hours. Small bowel follow through is inferior to CT of the abdomen and pelvis with oral contrast for detection and localization of small bowel perforation.

Gastrointestinal perforation other diagnostic studies

Endoscopy can be used to evaluate patients with suspected esophageal perforation. CT is obtained first because it is non-invasive and sensitive.

Medical therapy

Initial management of the patient with gastrointestinal perforation includes intravenous fluid therapy and broad-spectrum antibiotics. Patients with intestinal perforation can have severe volume depletion. The administration of intravenous proton pump inhibitors. Electrolyte abnormalities correction especially metabolic alkalosis if fistula developed. The severity of any electrolyte abnormalities depends upon the nature and volume of material leaking from the gastrointestinal tract. Intravenous vasopressors are useful in patients who remain hypotensive despite adequate fluid resuscitation or who develop cardiogenic pulmonary edema. Norepinephrine is the first-line single agent in septic shock. The addition of a second or third agent to norepinephrine may be required.

Surgery

Surgery is the mainstay therapy for gastrointestinal tract (GIT) perforation. The main indications are abdominal sepsis, worsening abdominal pain, signs of diffuse peritonitis, complete bowel obstruction, bowel ischemia. In esophageal perforation, surgical options include primary repair, repair over a drain. Primary repair is the best procedure for thoracic esophageal rupture. It is performed when the closure can heal. Endoscopically-placed-stents can be used to manage some patients with esophageal perforation. In perforated stomach, if the patient is unstable or deteriorating, urgent operation and closure with a piece of omentum is the standard of care. If the patient is stable or improving, nonoperative management with close monitoring is a reasonable option. If patients did not show clinical improvement after 24 hours, surgery was performed. In colonic resection, A one-stage colon resection for diverticulitis can be performed open or laparoscopically. The laparoscopic approach is preferred when feasible. A two-stage procedure is primarily used for patients with Hinchey III or IV diverticulitis, and for those with Hinchey I or II diverticulitis who have excessive contamination or inflammation of the surrounding tissues or other risk factors for anastomotic leakage. In perforated appendix, stable patients with perforated appendicitis who have symptoms localized to the right lower quadrant can be treated with immediate appendectomy or initial nonoperative management. Patients with an appendiceal abscess should be treated with intravenous antibiotics and percutaneous image-guided drainage. For patients who are septic or unstable, and for those who have a free perforation of the appendix or generalized peritonitis, emergency appendectomy is required. 

Gastrointestinal perforation primary prevention

There is no specific primary prevention associated with gastrointestinal perforation.

Gastrointestinal perforation secondary prevention

There is no specific secondary prevention associated with gastrointestinal perforation.