Large Bowel Disorders

Key Clinical Questions

When should ischemic colitis be suspected?
What are the key diagnostic tests for ischemic colitis, diverticulitis, acute appendicitis, colonic obstruction, and colonic pseudoobstruction?
How is diverticulitis medically managed? What are the indications for surgery in patients with diverticulitis?
What are the therapeutic options for colonic obstruction? for colonic pseudoobstruction?

Introduction

Large bowel disorders (LBD) impose a substantial burden on Americans, accounting for more than 1% of all inpatient admissions, contributing as comorbidities to other hospitalizations, and resulting in expenditures of more than $20 billion annually, which is likely to increase as the population ages. This chapter describes disorders of ischemic colitis, diverticulitis, acute appendicitis, colonic obstruction, and colonic pseudoobstruction. Other disorders, including lower gastrointestinal bleeding, inflammatory bowel diseases, tumors and cancer of the colon, and diarrhea are described in chapters dedicated to those disorders. Table 162-1 describes key diagnostic tests and therapeutic options for important large bowel disorders, while Table 162-2 describes the colonoscopic findings.

Table 162-1 Key Diagnostic Tests and Therapies for Important Large Bowel Diseases in Hospitalized Patients

Disease or Disorder	Key Diagnostic Tests	Major Therapeutic Options
Lower gastrointestinal bleeding	Colonoscopy – localizes site and determines etiology. Nuclear scintigraphy using radio-labelled erythrocytes – locates approximate site. Mesenteric angiography – can determine site and cause if lesion is actively bleeding. CT enterography or capsule endoscopy – second line tests if other tests are unrevealing.	Colonoscopy – injection, ablation, or mechanical therapy to stop the bleeding. Angiography – intra-arterial vasopressin infusion or gelfoam or coil embolization. Surgery – for ongoing bleeding refractory to colonoscopic or angiographic therapy.
Ischemic colitis	Colonoscopy – highly sensitive and specific. Mesenteric angiography – can be diagnostic and therapeutic, test mandatory for involvement of major branches of superior mesenteric artery. Abdominal computed tomography – important to exclude other conditions and often helps suggest the diagnosis.	Medical therapy – usually supportive, including bowel rest, intravenous fluids, antibiotic therapy, and reversal of precipitating factors. Surgery – required for frankly infarcted bowel, impending peritonitis, and sepsis refractory to antibiotic therapy.
Inflammatory bowel disease (IBD)	Blood tests – complete blood count, ESR or C reactive protein. Stool tests – for bacterial culture, fecal leukocytes, ova and parasites, C difficile toxin. Abdominal computed tomography – helpful to suggest IBD and to diagnose alternative conditions. Colonoscopy – highly diagnostic in combination with colonic biopsies; examination of terminal ileum recommended for Crohn disease.	General therapy – bowel rest, intravenous hydration, correct electrolyte disorders. Medications – typically first corticosteroids, consider biologic anti-TNF alpha therapy, antibiotics for abscesses or fistulas. Surgery – for large or refractory abscesses, refractory toxic megacolon, severe disease refractory to medical therapy.
Diverticulitis	Abdominal computed tomography – radiologic test of choice for diagnosis and evaluating complications. Colonoscopy – avoided in the setting of acute diverticulitis.	Medical therapy – bowel rest, intravenous antibiotics, intravenous hydration. Percutaneous drainage – for large, walled-off abscess. Surgery – multiple recurrent attacks, advanced Hinchey stage III or IV disease, severe abscesses, refractoriness to medical therapy, colonic perforation.
Acute appendicitis	Abdominal computed tomography – inflamed, distended appendix that fails to fill with contrast or air, appendicolith, mural thickening, pericecal fluid collection, periappendiceal fat stranding. Abdominal ultrasound – valuable only in certain circumstances such as pediatric patients, pregnant women, and thin adults.	Preoperative resuscitation – intravenous hydration, antibiotics, replete electrolytes. Surgery – either open or laparoscopic appendectomy.
Acute diarrhea	Stool studies – for bacterial culture and sensitivity, for ova and parasites, for C difficile toxin, stool for fecal leukocytes, stool for fecal occult blood. Abdominal CT – helpful to exclude other diseases and can help define extent of colitis. Colonoscopy – generally only indicated if stool studies do not reveal a cause and if patient is still having diarrhea despite medical therapy.	Supportive therapy – bowel rest, intravenous fluids, replete missing electrolytes. Antibiotic therapy – indicated for certain specific infections or for systemic toxicity.
C difficile colitis	Stool assay for C difficile toxin or PCR of stool specimen for C difficile gene encoding for toxin B. Colonoscopy – sometimes required to detect characteristic pseudomembranes.	Established therapy – discontinue offending antibiotic, treat with flagyl or vancomycin. Novel or experimental therapies – immunglobulin, rifaxmin, cholestramine, nitazoxanide or fecal transplant.
Colonic obstruction	Radiologic tests – obstructive series, abdominal computerized tomography, occasionally barium enema or CT colonography. Small bowel series or small bowel enterography – for suspected small bowel obstruction.	Supportive therapy – complete bowel rest, antibiotics, intravenous hydration, replete lost electrolytes. Treatment – depends upon etiology. Malignant obstruction or any complete obstruction refractory to medical therapy requires surgery. Sigmoid volvulus often initially responds to sigmoidoscopy or colonoscopy.
Colonic pseudoobstruction	Daily abdominal flat plates – to monitor cecal and transverse colon diameters. Colonoscopy – mostly for therapeutic decompression, but helpful diagnostically to exclude other disorders such as mechanical obstruction (eg, volvulus), and detect severity of colonic involvement (especially secondary colonic ischemia).	General measures – bowel rest, correct underlying reversible etiologic factors, discontinue narcotics, nasogastric tube suction, rectal tube, antibiotics in selected circumstances. Neostigmine – must be administered in an ICU. Colonoscopic decompression – usually done on an unprepared colon, emphasis on aspirating air. Surgery – for pseudoobstruction refractory to general measures, neostigmine therapy, and colonoscopic decompression.

Table 162-2 Colonoscopic Findings with Large Bowel Disorders in Hospitalized Patients

Disease or Disorder	Colonoscopic Findings
Colonic diverticular bleeding	Stigmata of recent hemorrhage: active bleeding, feeding vessel, adherent clot. Blood pooling in area around diverticulum. No other significant lesion seen at colonoscopy.
Internal hemorrhoids	Purplish lesions just proximal to dentate line bulging into the lumen detected by anoscopy or by rectal retroflexion during colonoscopy.
Angiodysplasia	Macular, intensely erythematous, reticular lesions with an internal structure (eg, starburst pattern or fern tree). Must distinguish lesion from colonoscopic trauma.
Colon cancer	Irregular, exophytic mass with induration and superficial Ulceration, or irregular or asymmetric stricture.
Dieulafoy lesion	Raised, pigmented (visible) vessel without surrounding ulceration. Most common in proximal stomach but can occur in colon or rectum.
Radiation colitis	Acute – sloughed off mucosa, mucosal exudate, edema. Chronic – irregular telangiectasias, mucosal friability, active bleeding, mucosal pallor, fibrotic strictures.
Ischemic colitis	Mottled, grey, or dusky bowel, mucosal friability, mucosal edema, mucosal erythema, superficial ulcers, abrupt transition from normal colon to colitis, rectal sparing, hemorrhagic nodules, de novo colitis, colonoscopic changes rapidly disappear.
Ulcerative colitis	Mucosal granularity, erythema, blunting of normal vascular pattern, mucosal friability or bleeding, mucopus, superficial ulcers, pseudopolyps, rectum involved, continuous involvement without skip lesions.
Crohn disease	Deep linear ulcers, cobblestoning, fistulas, fibrotic strictures, rectal sparing, terminal ileal involvement, skip lesions.
Diverticulitis	Colonoscopy not recommended in the setting of acute diverticulitis due to increased risk of colonic perforation because of colonic spasm and tortuosity. Colonoscopy generally recommended about six weeks after acute diverticulitis to exclude colon cancer in the elderly.
Pseudomembranous colitis	Characteristic raised, yellow-to-green, densely adherent, plaques that are 2–8 mm wide and are randomly scattered over colonic mucosa with relatively normal intervening mucosa.
Colonic pseudoobstruction	Highly dilated, air-filled, compliant colon with poor or no muscular activity and no mechanical obstruction or stricture. At colonoscopy evaluate colon for mucosal ischemia. Abort colonoscopy if dusky or frankly necrotic bowel encountered during the procedure.

Colonic Anatomy

The colon is a tubular structure approximately 30 to 40 cm in length at birth, but grows to nearly 150 cm in adulthood. It has a much larger diameter than that of the small bowel. The colon extends from the small bowel at the ileocecal valve to terminate at the anal verge. The longitudinal muscle fibers coalesce around the colonic circumference to form three discrete bands called teniae. The colon is divided into cecum, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon, and rectum. The first portion of the ascending colon, called the cecum, is a sacculated structure 6 to 8 cm in length and breadth that generally lies in the right iliac fossa and projects downward as a blind pouch below the entrance of the ileum. The large diameter of the cecum makes it particularly vulnerable to rupture from distal colonic obstruction. Its large diameter also provides ample space for cecal tumors to grow before producing obstruction. The mobility of the cecum is normally restricted by a small mesocecum, but 10% to 20% of people lack this mesocecum and are thereby predisposed to cecal volvulus. The vermiform appendix is a blind, digitiform outpouching of the cecum that begins inferior to the ileocecal valve. The ascending colon extends about 20 cm along the right side of the peritoneal cavity from the cecum to the hepatic flexure. The colon turns medially and anteriorly at the hepatic flexure to emerge as the transverse colon, which drapes itself across the anterior abdomen for 40 to 50 cm between the hepatic and splenic flexures. This is the most mobile colonic segment. This segment may dip down into the pelvis in the upright posture. The temporary festooned arrangement of transverse colon can become entrenched by adhesions, such as adhesions after hysterectomy. Such adhesions can result in a technically difficult colonoscopy. The descending colon, about 30 cm in length, continues as the S-shaped sigmoid colon in the retroperitoneum. The colonic diameter is narrowest (2.5 cm) in the sigmoid colon. The sigmoid colon does not provide ample space to accommodate local tumors or strictures and therefore sigmoid colon tumors or strictures result in early obstruction. The shape, tortuosity, mobility, and spasticity of the sigmoid colon create challenges for the colonoscopist, as well as render it susceptible to volvulus.

Despite individual anatomic variations, the colon generally has a specific vascular arrangement. The superior mesenteric artery (SMA) in addition to supplying nearly the entire small intestine, supplies the entire right colon, including the cecum, ascending colon, hepatic flexure, and most of the transverse colon. The inferior mesenteric artery (IMA) supplies most of the left colon including the descending colon, sigmoid colon, and part of the rectum. The rectum is also supplied by the inferior and middle rectal (hemorrhoidal) arteries derived from the internal pudendal and internal iliac arteries. Ischemia of the rectum is rare because it is supplied by both the IMA and the systemic circulation via the internal pudendal and internal iliac arteries. Contrariwise, the splenic flexure is vulnerable to ischemia because it lies at a watershed area that is supplied by end arteries of the SMA and the IMA, which have a low perfusion pressure. The splenic flexure can become ischemic when the systemic blood pressure declines in shock.

Extensive anastomotic and collateral circulations exist individually within the SMA and within the IMA and between these two arteries. A series of arcades interconnect neighboring branches of the SMA, while a similar series of arcades interconnect neighboring branches of the IMA. These collateral pathways protect against intestinal ischemia because they open up immediately when one branch of a major vessel is occluded.

The venous system generally parallels the arterial system. The superior mesenteric vein (SMV) drains the cecum, ascending colon, hepatic flexure, and transverse colon, whereas the inferior mesenteric vein (IMV) drains the descending colon, sigmoid colon, and proximal rectum. The IMV drains into the splenic vein, which then joins the SMV to form the portal vein.

Ischemic Colitis

Ischemic colitis (IC) is defined as inflammation of the colon secondary to diminished blood perfusion that leads to bowel wall ischemia. The colon is the most common site of gastrointestinal ischemic injury. Ischemic colitis encompasses numerous clinical entities that produce insufficient blood perfusion to a segment or the entire colon, and result in variably severe ischemic necrosis ranging from superficial mucosal involvement to full-thickness transmural necrosis. The term ischemic colitis describes the phenomenon of colonic ischemic injury, especially as observed on colonoscopy, but lacks specificity because it fails to specify the obstructed vessel, mechanism, and etiology. The physician should not accept ischemic colitis as a final diagnosis but should assiduously analyze the cause to determine the site of occlusion, including colonic branches of the SMA, SMV, IMA, and IMV; the mechanism of occlusion, including embolus, thrombus, or vasospasm; and the cause of occlusion, including atherosclerosis, vasculitis, low flow states, and hypercoagulable states.

Etiology

IC is caused by diminished colonic perfusion due to a decrease in systemic perfusion or an anatomic occlusion that is so severe that colonic metabolic demands are not met. Anatomic factors predisposing to colonic ischemia include the narrow caliber of the IMA and occasional vascular variations that lack significant collaterals between the SMA and IMA. Predisposing physiologic factors include the low perfusion pressure at the splenic flexure, a watershed area, a decrease in perfusion associated with colonic motility, and sustained mesenteric vasospasm associated with systemic hypotension or other severe physiologic stress produced by sympathetic activity. Table 162-3 lists various conditions associated with ischemic colitis.

Table 162-3 Etiologies of Ischemic Colitis

Primary circulatory abnormalities
- Atherosclerosis with thrombosis of the IMA or SMA
- Systemic hypotension with a low-flow state (nonocclusive mesenteric ischemia, NOMI)
  - Shock
  - Hypovolemia or dehydration
  - Long distance running
- Emboli of SMA or IMA
Aortic injury
- Aortic surgery (intraoperative injury to IMA)
- Aortic dissection
Extrinsic disease compressing the vasculature
- Cancer infiltrating the mesentery
- Retroperitoneal fibrosis
Vasculitis
- Behcet disease
- Buerger disease (thromboangiitis obliterans)
- Polyarteritis nodosa
- Rheumatoid arthritis with vasculitis
- Systemic lupus erythematosus with vasculitis
- Takayasu disease
- Wegener granulomatosis
Hypercoagulopathy/blood dyscrasia
- Anticardiolipin antibodies
- Antithrombin III deficiency
- Factor V Leiden mutation
- Protein C deficiency
- Protein S deficiency
- Sickle cell disease
Extrinsic compression of bowel vasculature associated with intestinal obstruction
- Incarcerated hernia
- Sigmoid volvulus
- Cecal volvulus
- Intussusception
- Bowel adhesions
Colonic obstruction with colonic distention
- Colon cancer with stricture
- Benign colonic stricture
- Colonic diverticular stricture
- Toxic megacolon
- Colonic pseudoobstruction
Drug induced injury (see Table 162-4)
Other
- Amyloidosis

Ischemic colitis most often occurs in the elderly; the average age is 70 years. Age-related tortuosity of colonic arteries as well as cumulative atherosclerotic disease increases vascular resistance and contributes to colonic ischemia in elderly patients. Mesenteric arterial emboli, thrombosis, or trauma may lead to occlusive vascular disease and impaired colonic perfusion. Colonic hypoperfusion due to congestive heart failure, transient perioperative hypotension, strenuous physical activity, or shock due to various causes, such as hypovolemia or sepsis, can result in IC. About 10% to 15% of patients with ischemic colitis have colonic obstruction from colon cancer, benign colonic stricture, or colonic diverticulitis.

A hypercoagulable state is often a significant factor in the pathogenesis of IC in young patients. Vasculitidies can cause thrombosis and occlusion of small vessels perfusing the colon, resulting in IC (Table 162-3). Various medications predispose to colonic ischemia (Table 162-4). Rare causes of ischemic colitis include aortic dissection, intra-abdominal inflammatory disease, and colonic infections such as schistosomiasis or cytomegalovirus. Severe constipation is a risk factor for ischemic colitis. Constipation, however, is an exceedingly common complaint so that patients with mild to moderate constipation without other risk factors rarely develop ischemic colitis.

Table 162-4 Drugs Associated with Colonic Ischemia

Well-established associations – proposed mechanisms
- Cocaine – vasoconstriction due to noradrenergic stimulation
- Ergotamine – vasospasm
- Estrogen (with progesterone) contraceptives – thrombosis due to hypercoagulability
- Pseudoephedrine – alpha-adrenergic vasoconstrictor
- Sodium polystyrene (kayexalate) – electrolyte shifts due to medication
- Vasopressin – vasospasm
Probable associations – proposed mechanisms
- Amphetamines – sympathetic vasoconstriction
- Digitalis – mesenteric vasoconstrictor at toxic levels
- Dopamine – potent vasoconstrictor
- Epinephrine or norepinephrine – potent vasoconstrictors
- Methysergide – mesenteric vascular compression from retroperitoneal fibrosis
- Nonsteroidal anti-inflammatory drugs – decreased synthesis of local prostaglandins that promote intestinal vasodilation
Possible associations – proposed mechanisms
- Alosetron – unknown mechanism related to 5-HT(3) antagonism, induced constipation may play a role
- Alpha-interferon – unknown mechanism
- Danazol – ischemia from constipation and bowel dilatation
- Diuretics – cause volume depletion and decreased colonic perfusion
- Tegaserod – serotonin 5HT(4) antagonist that may cause severe diarrhea and ischemic colitis.
- Tricyclic antidepressants – may decrease colonic perfusion

Infectious colitis and ischemic colitis may present similarly with acute abdominal pain. Various clinical characteristics can help differentiate ischemic colitis from infectious colitis (Table 162-5).

Table 162-5 Distinguishing Ischemic Colitis from Infectious Colitis

Clinical Characteristic	Ischemic Colitis	Infectious Colitis
Symptoms
Acuity of symptoms	Often sudden	Often gradual
Abdominal pain	Predominant symptom, may be severe	Secondary symptom
Diarrhea	May occur early as minor symptom	Predominant symptom
Gastrointestinal bleeding	Frequent, mild blood per rectum	Sometimes bloody diarrhea
Risk factors
Risk factors for atherosclerosis	Frequent	Sometimes
Prior manifestations of vascular disease	Frequent	Occasionally
Risk factors for ischemic colitis (Table 162-3)	Frequent	Occasionally
Physical examination
Physical findings of dehydration (eg, dry mucous membranes)	Occasional	Frequent with severe diarrhea
Bowel sounds	Early hyperactive, then hypoactive	Hyperactive bowel sounds
Lab tests
Serum bicarbonate level	Often low	Often normal
Serum lactate	Often elevated	Usually normal
Fecal leukocytes	Often present	Often present
Stool culture	Nondiagnostic	May be diagnostic
Plain abdominal roentgenogram
Thumbprinting	Characteristic later finding	Uncommon
Thickened colonic wall	Common	Common
Colonoscopy
Grey or dusky bowel	Characteristic of colonic infarction	Rare
Rectal involvement	Rectum spared due to dual blood supply	Rectum often involved
Splenic flexure involvement	Frequent due to “watershed effect”	Sometimes involved
Segmental involvement	Characteristic	Frequently widespread colitis
Skip lesions	Uncharacteristic	Occasionally occurs
Abrupt transition from normal to abnormal colon	Characteristic	Uncommon
Hemorrhagic nodules	Fairly characteristic finding	Rare

Clinical Presentation

The clinical presentation varies with the underlying cause, extent of vascular obstruction, rapidity of ischemic insult, degree of collateral circulation, presence of comorbidities, and time of presentation. Patients typically present with a sudden onset of crampy abdominal pain, diarrhea, and an urge to defecate. The pain is commonly localized to the left lower quadrant because the left colon is most commonly affected, but localized ischemia to other areas of the colon will often lead to pain localized within the corresponding area of the abdomen. Gastrointestinal bleeding, manifesting as bright red or maroon blood mixed with stool, frequently occurs. The bleeding is generally mild and does not cause hemodynamic instability or require blood transfusion. Other symptoms include anorexia and nausea and vomiting from an associated ileus.

Signs include mild to moderate tenderness over the involved intestinal segment, abdominal distention, low-grade pyrexia, tachycardia, and fecal occult blood. In 10% to 20% of cases, marked tenderness with peritoneal signs may be present on physical examination accompanied by metabolic acidosis and septic shock due to severe ischemia, especially with transmural infarction.

Diagnosis

Because mild to moderate IC is nonspecific and variable, the diagnosis largely depends on a high index of clinical suspicion, often based on predisposing conditions, as those presented in Table 162-3.

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Practice Point

In ischemic colitis, the degree of laboratory abnormalities parallels the severity of ischemia. Severe ischemia manifests with leukocytosis, neutrophilia, and a shift to immature leukocyte forms on the leukocyte differential. Necrosis can cause metabolic acidosis, as well as elevations of the serum lactate. Patients with a clinical suspicion of IC should have stool cultures for Salmonella, Shigella, Campylobacter, and Escherichia coli O157:H7. Infection with parasites or viruses such as cytomegalovirus should also be excluded.

Plain abdominal roentgenogram shows nonspecific findings in about 20% of cases such as dilated and air-filled (exhausted) bowel loops, colonic aperistalsis, and mural thickening, but it is often valuable to exclude other abdominal disorders. Barium enema may suggest colonic ischemia, with thumbprinting, from submucosal hemorrhage and edema. Computed tomography (CT), often the initial diagnostic test to assess patients with nonspecific abdominal pain, can reveal mural thickening, thumbprinting, and pericolonic stranding, with or without peritoneal fluid. Mural thickening with IC is typically concentric, symmetric, and smooth.

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