Bowel Necrosis

Etiology

The most common causes of bowel necrosis are acute arterial obstruction from a thromboembolism with underlying atrial fibrillation, through a patent foramen ovale, or from frank perforation and bacterial invasion. Less common causes are venous thrombosis, chronic ischemia, autoimmune disease, mechanical obstruction, and nonobstructive mesenteric ischemia. These conditions are typically seen in patients with severe vascular pathology and other comorbidities and are theorized to be a combination of infectious agents, inflammatory mediators, and reperfusion injury leading to ischemia, perforation, and bowel necrosis.[2][3]

Epidemiology

Bowel necrosis is the end stage of several different disease processes making an accurate determination of prevalence difficult. One of the most common causes of bowel necrosis, acute ischemic bowel, is a rare disease accounting for only .09% to .2% of surgical admissions.[4] About 50% of cases are due to embolic events, 30% due to plaque rupture, 10% to 20% from venous obstruction, and less than 5% due to dissection, vasospasm, and inflammation.[2]

Pathophysiology

Bowel necrosis is the widespread cellular death of any part of the gastrointestinal tract below the stomach. The necrosis is due to the body’s inability to meet the tissue's metabolic demands. The cells, starved of oxygen, switch to anaerobic metabolism, which does not produce enough energy to maintain the electrochemical gradient and hydrostatic equilibrium, resulting in cell swelling and rupture. Physiologically, this results in bowel edema and breakdown of the immunological barrier, permitting bacteria to invade the dying tissue. Once inside the bowel tissue, they begin to produce proinflammatory mediators resulting in further damage and edema. Initially, cells farthest from the blood supply die, and as time passes, the entire thickness of the bowel wall becomes necrotic. Bacteria, toxins, and breakdown products return to systemic circulation, resulting in systemic inflammation and sepsis.[1] This cascade is usually precipitated by a low-flow state such as an acute embolic, thrombotic, inflammatory, or obstructive event.[2]

History and Physical

For patients in the early stages of the disease process, history is crucial for determining the underlying etiology since vital signs and physical exams may not reveal the diagnosis. Up to one-half of patients will have a history of embolic diseases such as deep vein thrombosis and pulmonary embolism, or a history of atrial fibrillation. They will also frequently have a preceding history of postprandial pain, loss of appetite, nausea and vomiting, and unintentional weight loss.[5][6][7]

Patients with bowel necrosis secondary to perforation and bacterial invasion will likely have a history of risk factors predisposing to perforation such as peptic ulcer disease, alcoholism, heavy nonsteroidal anti-inflammatory drug use, inflammatory bowel disease, or corticosteroid use with acute onset of abdominal pain. Their exam will be concerning for evidence of an acute abdomen, fevers, nausea, and vomiting with progression to sepsis and septic shock without intervention.

Lastly, there are a variety of less common precipitators of bowel necrosis, though most of them cause either an acute or chronic low-flow state. These patients typically have vascular risk factors such as diabetes, peripheral vascular disease, or smoking. They will present with acute-on-chronic pain, diffuse abdominal pain, and signs of sepsis or septic shock.

The description of the type and severity of abdominal pain depends on several factors, including the cause of ischemia, the affected vasculature, and comorbidities. Acute arterial obstruction of the superior mesenteric artery will present with severe, periumbilical pain with nausea and vomiting. Chronic mesenteric ischemia will present with progressively worsening postprandial abdominal pain with appetite and weight loss. Venous thrombosis is subtle with waxing and waning non-specific pain. Lastly, nonocclusive mesenteric ischemia has a variable presentation and generally co-exists with other serious disease processes such as peripheral vascular disease, congestive heart failure, or dialysis-dependent renal failure. On physical examination, patients will appear distressed and diaphoretic. Their abdominal exam can vary from severe pain out of proportion to physical examination findings to an acute rigid abdomen with peritonitis.[2]

Evaluation

Evaluation of a patient with bowel necrosis must proceed quickly, with a high index of suspicion. As with any critically ill patient, rapid evaluation of the airway, breathing, and circulation, along with establishment of intravenous access and hemodynamic monitoring, is essential upon presentation. Definitive airway treatment may be indicated, but blood pressure should be optimized before intubation. Often, the underlying etiology of the patient’s shock is unclear, and a bedside Rapid Ultrasound for Shock and Hypotension ultrasonography examination, electrocardiography, portable chest radiography, basic metabolic panel, and arterial blood gas analysis can be used to quickly evaluate for cardiogenic, hypovolemic, obstructive, or distributive shock and help narrow the differential diagnosis. Further laboratory evaluation should include a complete blood count, a complete metabolic panel, the international normalized ratio, blood cultures, partial thromboplastin time, and a lactate level.[2][3]

If the patient remains hemodynamically unstable despite adequate resuscitation, the patient should be transferred emergently to the operating room for exploratory laparotomy. Otherwise, urgent CT of the abdomen and pelvis with intravenous contrast should be ordered to evaluate for the cause and extent of ischemia or necrosis. Radiologic evaluation should not be delayed while awaiting laboratory results, and the benefits of contrast outweigh the risk of contrast-associated nephropathy in patients with critical illness. Often, the bowel wall contains air, known as pneumatosis intestinalis, which suggests a breakdown of protective mechanisms and bacterial invasion. Another sign is gas in the portal vasculature. Results from one meta-analysis found the sensitivity and specificity of contrast-enhanced CT for acute mesenteric ischemia to be 93.3% and 96%, respectively. If the diagnosis remains unclear, angiography is recommended and may reveal filling defects or arterial stenoses.[2][3]

Treatment / Management

Bowel necrosis is a surgical emergency. Initial treatment requires early recognition with aggressive fluid resuscitation, vasopressor support, broad-spectrum antibiotics such as vancomycin and piperacillin-tazobactam, and pain control. If the patient is profoundly septic and has altered mental status, the patient may not be able to protect the airway and will need intubation. Treatment algorithms recommend emergency exploratory laparotomy in all patients who remain hemodynamically unstable despite aggressive resuscitation. In patients who stabilize, advanced imaging with CT angiography is recommended to tailor the surgical intervention.[8]

If imaging reveals acute arterial embolism, without evidence of peritonitis, perforation, or necrosis, angiography with embolectomy or systemic or catheter-directed thrombolysis may be indicated. Mesenteric arterial thrombosis may be amenable to surgical revascularization, angioplasty, or stenting depending on severity, time course, and comorbidities. If CT imaging or angiography reveals venous thrombosis, anticoagulation may be the only intervention required. In any patient who remains hemodynamically unstable, septic, or with radiographic evidence of perforation, free air, or necrosis, exploratory laparotomy with excision of nonviable tissue is recommended.

If nonocclusive mesenteric ischemia is suspected, initial resuscitation is still recommended but with a focus on underlying factors such as heart failure, arrhythmias, vasoconstrictive medications, or dialysis. If the patient improves, admission for optimization is indicated. If they continue to complain of abdominal pain without peritonitis, contrasted CT imaging is recommended for perforation, free air, or signs of necrosis. In cases of stenotic or spasming arteries, catheter-directed vasodilators are indicated. If the patient continues to exhibit peritoneal signs or remains hemodynamically unstable, exploratory laparotomy without imaging is recommended. Many patients with nonocclusive mesenteric ischemia will require a second look either via laparotomy or angiography despite initial approach therapy.

Differential Diagnosis

Patients with bowel necrosis can present with a variety of symptoms secondary to the underlying etiology of their disease, varying from severe abdominal pain to altered mental status and septic shock. The differential should include sources of infection such as pyelonephritis, cholangitis, and diverticulitis; causes of shock, including septic, cardiogenic, hemorrhagic, and distributive shock; as well as causes of bowel necrosis, such as acute versus chronic ischemia, perforation, thrombotic emboli, and obstruction.

Prognosis

In patients with this disease process who receive adequate and appropriate treatment, including timely operative intervention, mortality remains exceedingly high. Bowel necrosis without appropriate intervention and surgical management carries mortality approaching 100%. The pooled operative mortality rate for acute mesenteric ischemia has been reported at 47%, and patients who survive the initial event have a high probability of postoperative complications.

Complications

Bowel necrosis can have many complications. Sepsis associated with bacterial overgrowth can cause hypotension and end-organ damage, particularly renal and hepatic failure. Patients requiring emergency surgery may develop postoperative infections and obstructions. For those who survive the initial intervention, mortality remains elevated secondary to underlying comorbidities and frequently results in long-term disability.[3][4]