Myriad gastrointestinal (GI) maladies may affect patients in the intensive care unit (ICU), from GI bleeding to complications from liver cirrhosis. In this chapter, we review several of the most common GI-related clinical scenarios encountered in the ICU.

Upper Gastrointestinal Bleeding

Upper GI bleeding (UGIB) is a common indication for ICU admission. With advances in critical care and endoscopy, the in-hospital mortality of patients admitted for UGIB has modestly decreased over the past several decades, but remains around 2.1%.¹ Etiologies of UGIB can be divided into variceal and nonvariceal hemorrhage; in this section, we will primarily discuss nonvariceal hemorrhage.

Peptic ulcer disease (PUD) is the most common etiology of nonvariceal UGIB, accounting for up to 40% of cases, followed by gastritis or esophagitis, Mallory-Weiss tears, cancer, angiodysplasias, and Dieulafoy lesions.² The most common risk factors for PUD are infection with Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs (NSAIDs).³ Ulcer disease may present with epigastric pain but is frequently asymptomatic until a patient presents with signs and symptoms of GI bleeding. If a patient does have pain related to a duodenal ulcer, it typically improves with food and recurs 1 to 3 hours after a meal. In contrast, gastric ulcers are often made worse with eating. Patients with UGIB related to PUD or any etiology typically present either with melena or with hematemesis. If UGI bleeding is very brisk, patients may present with hematochezia. Labs suggestive of an acute UGIB include a decrease of hemoglobin/hematocrit from baseline values, a mildly elevated white blood cell (WBC) count, and an elevated blood urea nitrogen (BUN) out of proportion to creatinine.

The risk of mortality can be estimated using the pre-endoscopic Rockall score (Table 24-1), and the Glasgow-Blatchford score can be utilized to estimate the need for inpatient endoscopic intervention.^4,5 Patients with a Blatchford score of 0 (BUN < 18.2 mg/dL, hemoglobin [Hgb] ≥ 13 g/dL, systolic blood pressure [SBP] ≥ 100 mmHg, heart rate [HR] < 100 beats/min, no melena, no syncope, no heart disease, no liver failure) have a low likelihood of requiring endoscopic intervention and may be discharged from the emergency department (ED).⁶

Initial therapy for UGIB, as for hemorrhage of any etiology, is timely resuscitation. Patients should have adequate intravenous (IV) access placed with 2 large-bore IVs, infusion of IV fluids to correct volume deficits, and transfusion of packed red blood cells to a goal hemoglobin of 7 g/dL. This transfusion goal has been validated in a large clinical trial comparing a hemoglobin goal of 7 g/dL to a goal of 9 g/dL.⁷ Coagulopathy also should be corrected via transfusion of fresh frozen plasma (FFP) and/or platelets, as appropriate. In addition to resuscitation, initial medical therapy should include an IV proton pump inhibitor (PPI). Typically, a PPI is initially given as a high-dose bolus, followed by a continuous infusion.⁸ While pre-endoscopic PPI therapy has not been shown to improve mortality or the risk of re-bleeding, it does appear to reduce the incidence of finding ulcers with high-risk stigmata of hemorrhage and, therefore, to reduce the need for endoscopic therapy.⁹ Erythromycin may also be given prior to endoscopy to accelerate gastric emptying, so that intragastric blood does not obscure the endoscopist’s view. While nasogastric (NG) lavage is frequently attempted to document an upper GI source of bleeding, a negative NG aspirate does not necessarily rule out an upper GI source; therefore, its utility is limited.

Endoscopy should be performed within 24 hours of admission in a patient presenting with an upper GI bleed and should perhaps be performed within 12 hours in high-risk patients (ie, those with hematemesis and hemodynamic instability).⁸ Very early endoscopy (within 2 hours of presentation) may actually be deleterious, as there may not be enough time for adequate resuscitation.¹⁰

Appropriate management of PUD depends in large part upon endoscopic findings. Stigmata of recent hemorrhage (SRH) are utilized to describe the appearance of an ulcer at endoscopy, and to prognosticate the risk of rebleeding and therefore dictate postendoscopic management. The Forrest classification is also used to describe the appearance of an ulcer and corresponds to specific stigmata of recent hemorrhage (Table 24-2). Endoscopic therapy is indicated in the presence of active bleeding, a nonbleeding visible vessel, or an ulcer with overlying clot (if the clot cannot be washed away to reveal lower-risk stigmata underlying it). Endoscopic therapy can be accomplished via cautery or with mechanical clipping of the vessel or bleeding site. Injection of epinephrine may be used as an adjunct to cautery or clipping, but is insufficient to be used alone.⁸

Postendoscopic medical therapy is driven by endoscopic findings and the need for endoscopic therapy. If endoscopic therapy has been applied, then IV PPI should be continued for at least 72 hours. American College of Gastroenterology (ACG) guidelines recommend a continuous infusion of PPI after endoscopic therapy.⁸ However, a recent meta-analysis suggests that intermittent dosing of a PPI (eg, pantoprazole every 12 hours) post–endoscopic therapy may be equivalent to continuous dosing, with the advantage of decreased resource utilization.¹¹ Further data is necessary, and for now, guidelines recommend continuous PPI infusion postendoscopy. If a patient has low-risk stigmata (ie, a flat pigmented spot or clean-based ulcer), he or she may be transitioned to a standard-dose oral PPI and discharged after assuring that he or she is hemodynamically stable and has stable hemoglobin. Routine second-look endoscopy is not recommended in the absence of evidence of ongoing bleeding.⁸

In the setting of ongoing upper GI bleeding not amenable to endoscopic therapy, assistance from interventional radiology may be helpful. Angiography may be performed to identify the vessel from which bleeding is occurring (eg, the gastroduodenal artery in the case of a posterior wall duodenal bulb ulcer), and said vessel may be embolized by interventional radiology with excellent technical success.¹² In the modern era, surgery is less commonly performed for peptic ulcer disease, although it may be necessary in cases where bleeding does not resolve after endoscopic or angiographic therapy. Surgical options include oversewing of the ulcer to ligate the bleeding vessel, coupled with truncal vagotomy in the acute setting. In the nonemergent setting, antrectomy, vagotomy, and gastrojejunal anastomosis (Billroth II) can be performed for the treatment of PUD; however, given the effectiveness of medical therapy with PPIs, the need for this type of surgery is increasingly uncommon.¹³

Lower Gastrointestinal Bleeding

Overt lower GI bleeding (LGIB) accounts for approximately 20% of all cases of GIB.¹⁴ Patients may present with hematochezia or maroon-colored stools. Melena may be seen if there is slow bleeding from the proximal colon. Hemodynamic instability should prompt suspicion for a brisk UGIB, which may occur in up to 15% of patients presenting with hematochezia.¹⁵ Diverticular bleeding accounts for up to 50% of LGIB cases. Other common etiologies include angiodysplasias, colonic ischemia, infectious or inflammatory colitis, radiation proctopathy, and anorectal disorders such as hemorrhoids.¹⁶

Initial management should focus on appropriate resuscitation, including blood transfusion, if necessary. For patients on systemic anticoagulation, ACG guidelines suggest that endoscopic therapy is safe in patients with an international normalized ratio (INR) of 1.5 to 2.5, so for hemodynamically stable patients, reversal of anticoagulation may not be necessary.¹⁴ Platelets should be transfused in the setting of thrombocytopenia (platelet count < 50 × 10³/μL). For patients requiring massive transfusion (> 3 units packed red blood cells [PRBC] in 1 hour), 1 unit each of platelets and FFP should be transfused per unit of PRBC to prevent transfusion-related coagulopathy.¹⁷ In the great majority of patients (~80%), LGIB will stop spontaneously. However, in patients with ongoing hemorrhage, therapeutic intervention is required to halt bleeding.

In hemodynamically stable patients, colonoscopy should be the first diagnostic and therapeutic procedure attempted. Colonoscopy allows visualization of the colonic mucosa to identify a bleeding site as well as a means for therapeutic intervention. Colonoscopy can identify a definitive or potential bleeding source in 45% to 90% of patients.¹⁸ Early colonoscopy within 8 to 12 hours of presentation (compared with delayed colonoscopy at 36 to 90 hours after presentation) was shown in 1 randomized controlled trial to lead to an increased yield in identification of a bleeding source but did not improve length of stay or rates of rebleeding or surgery.^19,20 Early colonoscopy should be attempted only if the patient is able to tolerate rapid bowel preparation. Nasogastric tube (NGT) placement may facilitate this, as long as the patient is at low risk for aspiration.¹⁶ Endoscopic therapy depends on the bleeding source, and may involve a combination of epinephrine injection, clipping, and/or argon plasma coagulation.¹⁴

If a patient presents with hemodynamic instability and hematochezia, esophagogastroduodenoscopy (EGD) should be performed first to rule out UGIB. Patients who remain hemodynamically unstable in whom a UGI source of bleeding has been ruled out are unlikely to tolerate bowel preparation for colonoscopy and typically require radiographic intervention to localize and treat the source of bleeding. Radiographic methods for identifying the source of GI bleeding include RBC scintigraphy, computed tomography angiography (CTA), and conventional angiography. Red blood cell scintigraphy can identify bleeding at rates as low as 0.05 to 0.1 mL/min, but it has limited accuracy in identifying a bleeding site (66%).²¹ CTA is more accurate, with a sensitivity and specificity of 85% and 92%, respectively. It requires a patient to be bleeding at a rate of 0.3 to 0.5 mL/min. It can also be performed more rapidly than RBC scintigraphy. Its drawbacks include exposure to ionizing radiation and IV contrast media, with attendant risks of contrast allergy as well as contrast-induced nephropathy. If a bleeding site is identified on either RBC scintigraphy or CTA, the patient can be referred for conventional angiography and embolization.²² Conventional angiography requires a patient to be bleeding at a rate of 0.5 to 1 mL/min to visualize extravasation of contrast media. Superselective angiographic embolization can control bleeding in 40% to 100% of cases; rebleeding occurs in 0% to 50% of patients. Aside from exposure to radiation and contrast, 1 potential risk of embolization includes bowel ischemia, which may occur in 1% to 4% of patients.¹⁴ Finally, surgical management may be necessary if endoscopic and radiologic intervention fails; if the bleeding source cannot be accurately localized, subtotal colectomy is the procedure of choice.

Mesenteric Ischemia

Patients with mesenteric ischemia typically present with the acute onset of continuous abdominal pain, the location of which may vary, but it typically begins in the periumbilical region. As symptoms progress, the pain may become more diffuse. While initially patients will present with the classic “pain out of proportion” to physical exam findings, as ischemia progresses, peritonitis develops and patients may have findings consistent with an acute abdomen, including rebound and involuntary guarding. It is important to suspect the diagnosis of mesenteric ischemia in patients presenting with these symptoms and who have a history of ischemic heart disease, atrial fibrillation, hypertension, diabetes, and other cardiovascular risk factors.²³ Mesenteric ischemia most often develops due to embolism of clot into the superior mesenteric artery or as a result of mesenteric artery thrombosis. Patients with mesenteric thrombosis may have a history of chronic mesenteric ischemia, characterized by “mesenteric angina” whenever the patient eats, leading to sitophobia (fear of eating) and weight loss. This pattern of disease may be found in patients with diffuse atherosclerotic disease.²⁴

In addition to clinical findings, laboratory studies may show an elevated white blood cell count, amylase, and lactate, although these are nonspecific findings. CTA is especially useful, with a high sensitivity and specificity (93% and 95%, respectively). CTA should be performed without oral contrast, as oral contrast may obscure the mesenteric vessels and reduce sensitivity.²⁵

Management of acute mesenteric ischemia involves general supportive measures, including NGT placement, nothing-by-mouth (NPO) status, IV fluids, and initiation of broad-spectrum antibiotics given the risk of bacterial translocation and sepsis. Anticoagulation with unfractionated heparin should be initiated to prevent propagation of clots. Vasopressors should be avoided if possible, as they may exacerbate splanchnic vasoconstriction and worsen ischemia.²⁶ For patients with clinical or radiographic evidence of peritonitis or for those who are hemodynamically unstable, emergent laparotomy is indicated. For all others, revascularization may be attempted with either open surgical thrombectomy or endovascular therapy with thrombolysis or balloon angioplasty and stenting.²⁷

Ischemic Colitis

Of patients hospitalized for LGIB, ischemic colitis (IC) may be the etiology in up to 24% of cases.²⁸ The most common area of the colon affected is the splenic flexure, where the vascular distributions of the superior and inferior mesenteric arteries form a “watershed” area, leading to increased susceptibility to ischemia during episodes of low blood flow. Although the left colon is most commonly affected, the right colon can be involved in an isolated manner in up to 25% of cases.²⁹ Risk factors for IC include advanced age, comorbid cardiovascular disease, hypertension, diabetes, hypercoagulable states, and the presence of comorbid GI disease, including irritable bowel syndrome and constipation. Ischemic colitis also can complicate shock, in which hypotension leads to decreased blood flow to watershed areas of the colon. Ischemic colitis may be seen after repair of an abdominal aortic aneurysm if there is occlusion or injury of the inferior mesenteric artery. Numerous medications have been implicated in the etiology of IC, including opiates (vis-à-vis induction of constipation), immunomodulatory drugs, and illicit drugs that induce vasospasm such as cocaine and amphetamines.²⁸

The classical presentation of IC is the sudden onset of left lower quadrant (LLQ) cramping abdominal pain, followed within 24 hours by bloody diarrhea or maroon-colored stools Patients may have LLQ tenderness. In cases of right-sided IC, pain is the predominant presenting symptom, and hematochezia is less common. The degree of rectal bleeding in patients with colonic ischemia is usually mild, and transfusion is rarely required. While the diagnosis of IC may be made on clinical findings alone, colonoscopic evaluation and/or imaging studies may be helpful to confirm the diagnosis. A CT scan may show segmental wall thickening, thumb printing (subepithelial hemorrhage/edema), and pericolonic fat stranding. CTA is usually unnecessary, unless a patient presents with severe disease (eg, sepsis, peritoneal signs, isolated right IC), in which it is essential to rule out vascular occlusion.²⁸ Colonoscopy should be performed within 48 hours to confirm the diagnosis. Typical findings on colonoscopy include erythema, edema, friability, and superficial ulcerations. Deep ulcerations, luminal narrowing, and dusky mucosa are present in more severe disease.³⁰

The management of IC varies depending upon its severity. In most cases, symptoms will resolve within 2 to 3 days with supportive care, including bowel rest and intravenous hydration, and up to 80% of patients will require no surgical intervention.³¹ In addition to supportive care, ACG practice guidelines recommend the use of broad-spectrum antibiotics for colonic flora in patients with moderate or severe disease.²⁸ Patients with moderate or severe disease should have a surgical consultation and should be considered for transfer to the ICU. Aside from frank peritonitis, other indications for surgical intervention include the presence of massive hemorrhage, fulminant colitis, or a failure to respond to medical therapy after 2 to 3 weeks. The type of surgery performed depends upon the involved segment of colon, but most commonly requires total or subtotal colectomy. Postoperative mortality can be as high as 48%.³²

Diverticular Disease

Colonic diverticuli are sac-like outpouchings of the colon wall that occur at points of weakness where the vasa recta enter the muscle layer of the colon.³³ They develop over time due to increased pressure within the colon lumen and are more common among patients with constipation and abnormalities of colonic motility. Up to 40% of patients undergoing screening colonoscopies may be found to have diverticulosis; 20% of these patients will become symptomatic. The manifestations of diverticular disease include diverticular bleeding, diverticulitis, segmental colitis associated with diverticulosis (SCAD; inflammation of the mucosa surrounding diverticuli, without involvement of the diverticuli themselves), and symptomatic uncomplicated diverticular disease (SUDD).³⁴ Typically, only management of diverticular bleeding (see “Lower Gastrointestinal Bleeding,” discussed previously) and diverticulitis may require ICU-level care; SCAD and SUDD are managed as chronic outpatient conditions.

Similar to appendicitis, diverticulitis occurs when a diverticulum becomes obstructed by a fecalith or other material, leading to bacterial stasis, inflammation, and ultimately microperforation.³⁵ Patients present with a constellation of symptoms, including LLQ pain, fever, and leukocytosis. In patients with a redundant sigmoid colon, the pain may be on the right side. Nausea and vomiting due to an ileus may be present. Rarely, patients with severe inflammatory changes may present with obstruction. Typical findings on CT, including colonic wall thickening and pericolonic fat stranding in close proximity to colonic diverticuli, are used to support the diagnosis.³⁶ Ultrasound may be used in patients who have a contraindication to CT, with sensitivity and specificity of 84% and 98%, respectively.³⁷

Uncomplicated diverticulitis often can be managed in the outpatient setting with oral antibiotics. Recommended regimens include ciprofloxacin plus metronidazole, trimethoprim-sulfamethoxazole plus metronidazole, amoxicillin-clavulanate, or moxifloxacin, all given for 7 to 10 days.³⁸ Outpatient treatment is successful in up to 97% of cases.³⁹ In patients who either fail outpatient therapy or are unable to tolerate oral (PO) therapy, hospitalization and use of IV antibiotics is indicated. Intravenous antibiotic regimens for acute uncomplicated diverticulitis include ciprofloxacin or a third-generation cephalosporin plus metronidazole, or in a patient with risk factors for antimicrobial resistance, piperacillin-tazobactam or a carbapenem.⁴⁰ Antibiotics are given for a 7- to 10-day course, although they may be transitioned to oral to complete the course if the patient’s condition improves.⁴¹ American Gastroenterological Association guidelines recommend that a colonoscopy should be performed after recovery from an episode of diverticulitis if the patient has not recently undergone a colonoscopy for colorectal cancer screening in order to rule out a concomitant colorectal carcinoma or advanced adenoma.⁴²

Complications of diverticulitis include the development of a pericolic abscess, fistulization, obstruction, or free perforation. Although free perforation is a clear indication for emergent surgery, due to a recurrence rate greater than 40%, surgical resection of the involved segment is recommended after any complicated episode of diverticulitis.⁴³ Abscesses occur in about 15% of patients who develop diverticulitis, and management varies depending upon the size of the abscess. Small (< 3 cm) abscesses may be managed with antibiotics alone if the patient is clinically stable.⁴⁴ Larger abscesses require either percutaneous drainage by interventional radiology or, less commonly, by surgical management. Percutaneous drainage also may act as a bridge to surgery, allowing a 1-stage procedure (with primary colocolonic anastomosis) rather than an ostomy with subsequent reanastomosis.⁴⁵ Abscesses that are unable to be successfully drained percutaneously require surgical management.^40-42 Fistulae and obstruction also require resection of the involved segment of the colon; if fistulae are complicated (eg, colovesical), multidisciplinary surgical involvement may be required.⁴³

Diverticular bleeding is discussed in “Lower Gastrointestinal Bleeding.”

Ulcerative Colitis

Ulcerative colitis (UC) is 1 of the 2 forms of idiopathic inflammatory bowel disease (IBD). As opposed to Crohn disease (and as the name implies), only the colon is affected, typically with contiguous inflammation that begins in the rectum at the anal verge. The disease may be isolated to the rectosigmoid in 45% of patients, or it may extend to involve the left colon in 35% of patients. A minority of patients have pancolitis.³⁵ Patients present with a variety of symptoms, including diarrhea, rectal bleeding, tenesmus, and abdominal pain. Whereas patients usually present with longstanding symptoms, a minority of patients may present acutely with severe or fulminant disease requiring hospitalization. Laboratory findings may include anemia and hypoalbuminemia; serologic evidence of inflammation may be present, including elevations in C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and platelets.⁴⁶ Diagnosis is supported by typical endoscopic findings, which include the presence of inflammation contiguous from the anal verge, ulcerations (superficial or deep), erythema, and friability. Patients with longstanding disease may have pseudopolyps, which are regenerative growths of mucosa that form in response to chronic inflammation. Biopsy findings include cryptitis, crypt abscesses, and a mixed inflammatory infiltrate in the lamina propria. Inflammation is confined to the mucosa, as opposed to Crohn disease where inflammation may be transmural.³⁵

As with Crohn disease, the management of UC mainly takes place in the outpatient setting. Treatment includes the use of steroids; topical mesalamine agents; immunomodulators like 6-mercaptopurine, azathioprine, and methotrexate; and biologic agents including anti–tumor necrosis factor (TNF) therapies (infliximab, adalimumab, and golimumab) and integrin inhibitors (vedolizumab). Inpatient management is necessary for patients who fail outpatient therapy or for those with severe or fulminant disease. Severe disease is defined by the Montréal classification as 6 or more bowel movements per day with blood, as well as evidence of systemic toxicity including one of the following: HR greater than 90 beats/min, temperature greater than 37.5°C, hemoglobin less than 10.5 g/dL, or ESR greater than 30 mm/h.⁴⁷

Initial steps in management include general resuscitative measures, including IV hydration and correction of electrolyte abnormalities. Testing for Clostridium difficile infection should be performed. If significant abdominal distension or tenderness is present, plain abdominal radiography or CT may be indicated to rule out complications including toxic megacolon or perforation. Flexible sigmoidoscopy should be performed to assess endoscopic grade of disease and to perform biopsies to assess for concomitant cytomegalovirus infection, which requires appropriate antiviral therapy. Despite the presence of mild bleeding, all patients admitted to the hospital with a flare of inflammatory bowel disease should be started on some form of pharmacological venous thromboembolism (VTE) prophylaxis, as the inflammatory state places patients at increased risk for VTE.⁴⁸ Initial therapy should include intravenous steroids at a dose of 100 mg IV hydrocortisone every 6 hours or 20 mg IV methylprednisolone every 8 hours. Oral and rectal mesalamine may be continued. The patient should be allowed to eat (or if they are unable to maintain adequate PO intake, supplemental enteral nutrition via nasogastric or nasojejunal tube should be provided), as nourishment of the colonic mucosa may improve outcomes. Bowel rest and parenteral nutrition do not provide any additional benefit and actually may worsen outcomes.⁴⁹ Electrolyte abnormalities should be corrected, as hypokalemia or hypomagnesemia may promote the development of toxic megacolon.⁵⁰ Antibiotics are not indicated for the treatment of acute UC per se, although they may be appropriate in patients with signs of systemic infection.⁵¹

Despite aggressive therapy with intravenous steroids, some patients go on to develop complications of disease, including toxic megacolon, refractory hemorrhage, or frank perforation. It is essential for providers to realize when medical therapy with steroids has failed and when an escalation of therapy is appropriate. Multiple scoring systems have been developed to assist providers in decision making regarding the appropriate timing of colectomy. One of the simplest is the Oxford index, in which a stool frequency of more than 8 bowel movements per day on day 3 of intravenous steroids, along with a CRP greater than 45 mg/L, are predictive of requiring a colectomy during admission in 85% of cases.⁵²

For patients who do not have toxic megacolon or refractory bleeding but who have not had a good clinical response to 3 to 5 days of IV steroid therapy (defined as a Lichtiger index < 10 for 2 consecutive days; Table 24-3), rescue therapy with IV infliximab or cyclosporine can be considered. The decision of which agent to use depends in large part upon local practice patterns. Two large, open-label trials found no difference in rates of colectomy, mortality, or serious infectious complications between the 2 therapies. Infliximab is given as a single weight-based infusion, followed by further induction infusions at weeks 2 and 6; maintenance therapy is given every 8 weeks. Cyclosporine is given as a continuous, weight-based infusion and is typically administered for 8 days. Monitoring of serum levels of cyclosporine, as well as monitoring of kidney function, blood pressure, and serum electrolytes are required when administering cyclosporine induction therapy. Serum triglycerides should also be monitored, as hypotriglyceridemia is associated with adverse neurologic side effects (including seizures) in patients on IV cyclosporine. Patients who respond to IV cyclosporine must be transitioned to oral cyclosporine and a thiopurine (such as 6-mercaptopurine or azathioprine), as cyclosporine cannot be continued long term as a maintenance therapy.⁵⁰ For that reason, patients who have previously failed maintenance therapy with a thiopurine may not be good candidates for salvage therapy with cyclosporine and may benefit more from use of infliximab. If salvage therapy with either infliximab or cyclosporine fails, it is not recommended to again attempt medical salvage therapy with the other agent, as following infliximab with cyclosporine, or vice versa, has been found to significantly increase the risk of infectious complications and mortality.⁵³

Crohn Disease

Crohn disease (CD) is a chronic, idiopathic inflammatory bowel disease characterized by transmural inflammation that can affect the entire GI tract. Most commonly, it affects the distal small bowel, with or without involvement of the colon, although occasionally only the colon is affected.⁵⁴ Although patients will rarely be admitted to the ICU for management of their Crohn disease per se, management of the complications of CD or its treatment (including sepsis in patients on immunosuppressive therapy) may necessitate ICU-level care. Those on total parenteral nutrition may also be at risk for fungal infections.⁴⁶ Patients requiring surgery may be at risk for postoperative complications, including anastomotic leaks and anastomotic bleeding, which may occur in 8% and 5% of patients, respectively.^55,56 Finally, patients with high-output enterocutaneous fistulae that have developed because of refractory CD or postsurgical complications may present with profound hypovolemia, volume depletion, and electrolyte imbalances that may necessitate admission to the ICU. Multidisciplinary care involving gastroenterology, nutrition, and surgery is essential in the management of these complex patients.^57,58

Sigmoid Volvulus

Sigmoid volvulus is one of the most common etiologies of large bowel obstruction. It develops when a redundant loop of sigmoid colon twists upon its vascular pedicle to cause a closed-loop obstruction, ultimately leading to bowel ischemia. Risk factors include older age, a history of chronic constipation, and a history of colonic dysmotility.^59,60 Patients often present with abdominal pain, obstipation, nausea and vomiting, and abdominal distension. Diagnosis is confirmed radiographically, with abdominal x-ray demonstrating a classic “coffee-bean” sign. Computed tomography may demonstrate a “whirl” pattern around the site of obstruction, with dilated bowel proximal to it.⁶¹

Treatment for sigmoid volvulus includes IV fluids, nasogastric decompression, and correction of electrolyte abnormalities. Excluding patients with peritoneal signs who should proceed directly to exploratory laparotomy, flexible sigmoidoscopy should be performed emergently to reduce the volvulus. The sigmoidoscope is inserted past the spiral-shaped area of torsion, and air and stool are suctioned from it. A rectal tube may be placed to allow for continued decompression. Because the recurrence risk is up to 60%, surgical resection of the redundant sigmoid colon is indicated after sigmoidoscopic decompression.⁶²

Malignant Large Bowel Obstruction

Colonic adenocarcinoma is the most common etiology of large bowel obstruction, accounting for more than 50% of cases.⁶³ Non-GI malignancies, such as ovarian and other gynecological cancers, may cause large bowel obstruction via extrinsic compression. In the setting of an obstructing colon cancer, timely relief of the obstruction is indicated to avoid perforation. Options for decompression include emergency surgery with colostomy placement proximal to the point of obstruction (followed by resection of the primary lesion), or endoscopic placement of an uncovered self-expanding metal stent.⁶⁴

Colonic Pseudo-obstruction/Ogilvie Syndrome

Acute colonic pseudo-obstruction (ACPO), also known as Ogilvie syndrome, is characterized by sudden colonic dilatation in absence of a mechanical obstruction. It typically affects older patients, especially those who are immobile or bedbound due to hospitalization or recent surgery. Significant dilatation of the ascending and transverse colon may be seen on abdominal imaging. Bowel ischemia and perforation can occur in 3% to 15% of cases and is associated with a mortality as high as 50%.⁶⁵ The risk of perforation is increased with a cecal diameter of more than 10 to 12 cm and when the dilatation has been present for more than 6 days.⁶⁶ Conservative management should be initiated with NPO status, IV fluids, NGT decompression, and correction of electrolyte abnormalities. Medications that can contribute to decreased bowel motility (eg, opioids and anticholinergics) should be discontinued. The patient should change positions frequently to encourage bowel motility; prone positioning with hips elevated frequently leads to evacuation of flatus.⁶⁶

If conservative management is unsuccessful after 24 to 48 hours, pharmacologic therapy with neostigmine, an anticholinesterase parasympathomimetic agent, can be attempted. Its side effects include bradycardia, asystole, hypotension, and bronchoconstriction; patients therefore must be on a cardiac monitor while receiving the drug, and atropine must be at the bedside in the case of development of bradyarrhythmias. Administration of neostigmine is successful in approximately 80% of patients, with a rate of recurrence of 10%.⁶⁷ If successful, a low-dose polyethylene glycol–based laxative may be started to encourage colonic motility and reduce the risk of recurrence.⁶⁸ Colonoscopic decompression is an option if conservative and pharmacologic therapy has failed; success rates range from 61% to 95%.⁶⁹ Surgical management with either subtotal colectomy or placement of a tube cecostomy carries a high rate of morbidity and mortality and is reserved for patients who have failed other therapies.^65,66

Up to 20% of patients with gallstones seen on ultrasound may develop symptoms.⁷⁰ Classic biliary pain (“biliary colic”) results from transient obstruction of the cystic duct with a gallstone and presents as transient right upper quadrant (RUQ) pain that often radiates to the right shoulder. The pain typically lasts for at least 30 minutes to 1 hour, although it may continue for as long as 6 hours and may be associated with nausea and vomiting. Exam findings are often normal, although patients may exhibit mild tenderness in the RUQ. Laboratory results are usually normal, with no elevations in liver enzymes.⁷¹ Diagnosis of cholelithiasis is usually obtained via RUQ ultrasound, which has a sensitivity and specificity of 84% and 99%, respectively.⁷² Cholecystectomy is recommended for patients with symptomatic gallstone disease, as the rate of complications, including cholecystitis, cholangitis, and gallstone pancreatitis, increases 1% to 2% per year.⁷³

Cholecystitis

Acute calculous cholecystitis is the most common manifestation of gallstone disease. It occurs when a stone becomes lodged in the neck of the gallbladder, leading to sustained obstruction of the cystic duct. Patients present with RUQ pain typically of a greater intensity and longer duration than that which is seen with biliary colic. Fever, RUQ tenderness, and Murphy sign (inspiratory arrest on palpation of the inflamed gallbladder) may be present. Labs may reveal a leukocytosis, with mild elevations in transaminases and bilirubin (although bilirubin will typically be < 2–4 mg/dL; higher values suggest possible bile duct stones with biliary obstruction). Ultrasound may reveal a dilated gallbladder with a thickened gallbladder wall (> 3 mm) and pericholecystic fluid; the presence of a sonographic Murphy sign together with gallstones has a 90% positive predictive value for cholecystitis. If the diagnosis is unclear, cholescintigraphy with a hepatobiliary iminodiacetic acid (HIDA) scan may help to confirm the diagnosis, with nonvisualization of the gallbladder demonstrating sensitivity and specificity greater than 90%.^74,75

Initial management of uncomplicated cholecystitis includes initiation of pain control, IV fluids, and antibiotics. Recommended antibiotics include a third-generation cephalosporin for patients with mild-to-moderate disease with no known risk factors for resistant organisms. For patients at risk of antimicrobial resistance, or for those with severe disease (suspected empyema of the gallbladder, perforation, or sepsis) broad-spectrum coverage with piperacillin-tazobactam or a carbapenem is recommended.⁷⁶ In otherwise healthy patients, early cholecystectomy within 72 hours of symptom onset has been shown to lead to improved outcomes, including shorter length of stay.⁷⁷ For patients with multiple comorbidities with a high operative risk, conservative management with antibiotics alone may be more appropriate, with percutaneous cholecystostomy performed in patients who do not improve with nonoperative management alone.⁷⁸

Nonoperative management is also typically necessary for patients with acalculous cholecystitis. The pathophysiology is thought to involve inflammation related to prolonged exposure of the biliary epithelium to bile (owing to a lack of gallbladder contraction in prolonged fasting states, especially in the setting of total parenteral nutrition administration) as well as relative gallbladder ischemia. The diagnosis should be suspected in a critically ill patient with new-onset RUQ pain, leukocytosis, and concerning imaging findings. Ultrasound has a sensitivity and specificity for the diagnosis of acalculous cholecystitis of 67% to 92% and greater than 90%, respectively.⁷⁹ The use of HIDA scintigraphy may be less reliable in critically ill patients because of its higher false-positive rate, especially among those with liver enzyme abnormalities. In addition to antibiotics, drainage of the gallbladder with percutaneous cholecystostomy is necessary for successful treatment. Initial technical and clinical success with this technique may be as high as 93%.⁸⁰ Elective cholecystectomy is indicated once the patient recovers from the acute critical illness. Of note, percutaneous cholecystostomy should not be performed in patients with ascites, as tubes have a high chance of dislodgement from the gallbladder into the peritoneum, leaving a free perforation in the gallbladder wall.

Choledocholithiasis

Choledocholithiasis is defined as the presence of stones within the common bile duct (CBD).⁸¹ Patients with choledocholithiasis may present with biliary colic and/or jaundice owing to extrahepatic biliary obstruction. Pain may be constant if there is persistent blockage at the level of the ampulla, or it may be transient due to a “ball-valve” effect of the stone causing intermittent obstruction. Liver enzymes may be elevated; aminotransferases will elevate first, followed by alkaline phosphatase, γ-glutamyl transferase, and direct and total bilirubin.⁸²

Right upper quadrant ultrasound has poor sensitivity for identifying CBD stones (~50%), although it can be helpful in assessing the presence of CBD dilation (> 6 mm).⁸³ Magnetic resonance cholangiopancreatography (MRCP) has a sensitivity and specificity of 93% and 94%, respectively.⁸⁴ Endoscopic ultrasound (EUS), although invasive, provides an excellent view of the CBD, with positive and negative predictive values of 99% and 98%, respectively. When the clinical and noninvasive radiographic picture is equivocal, EUS is often helpful in avoiding unnecessary endoscopic retrograde cholangiopancreatography (ERCP), which is considered the gold standard for diagnosis and treatment of choledocholithiasis; success rates for stone removal with ERCP range from 87% to 100%.⁸⁵ In the absence of cholangitis, ERCP may be performed on a nonurgent basis. Complications of ERCP include post-sphincterotomy bleeding, perforation, and pancreatitis. Post-ERCP pancreatitis may occur in up to 10% of patients; the risk is higher in younger patients, in women, and in patients with prior post-ERCP pancreatitis. Procedure-related risk factors include excessive cannulation time, injection of the pancreatic duct with contrast, and balloon dilation of an intact sphincter.⁸⁶ In patients with an intact gallbladder, cholecystectomy should be planned soon after ERCP and stone extraction, as a longer interval between ERCP and cholecystectomy has been associated with an increased risk of biliary complications.⁸⁷ Finally, choledocholithiasis can be confirmed on an intraoperative cholangiogram (IOC) performed at the time of cholecystectomy, which should prompt a referral for postoperative ERCP and stone extraction.

The American Society for Gastrointestinal Endoscopy (ASGE) has published criteria⁸¹ to assign risk of choledocholithiasis based on clinical, lab, and imaging parameters (Table 24-4).