2504 PART 10 Disorders of the Gastrointestinal System

Presentation and Evaluation Patients commonly present to a

physician for two reasons: bleeding and protrusion. Pain is less common than with fissures and, if present, is described as a dull ache from

engorgement of the hemorrhoidal tissue. Severe pain may indicate

a thrombosed hemorrhoid. Hemorrhoidal bleeding is described as

painless bright red blood seen either in the toilet or upon wiping. Occasional patients can present with significant bleeding, which may be a

cause of anemia; however, the presence of a colonic neoplasm must be

ruled out in anemic patients. Patients who present with a protruding

mass complain about inability to maintain perianal hygiene and are

often concerned about the presence of a malignancy.

The diagnosis of hemorrhoidal disease is made on physical examination. Inspection of the perianal region for evidence of thrombosis

or excoriation is performed, followed by a careful digital examination.

Anoscopy is performed paying particular attention to the known

position of hemorrhoidal disease. The patient is asked to strain. If

this is difficult for the patient, the maneuver can be performed while

sitting on a toilet. The physician is notified when the tissue prolapses.

It is important to differentiate the circumferential appearance of a

full-thickness rectal prolapse from the radial nature of prolapsing hemorrhoids (see “Rectal Prolapse,” above). The stage and location of the

hemorrhoidal complexes are defined.

TREATMENT

Hemorrhoidal Disease

The treatment for bleeding hemorrhoids is based on the stage of

the disease (Table 328-6). In all patients with bleeding, the possibility of other causes must be considered. In young patients without

a family history of colorectal cancer, the hemorrhoidal disease

may be treated first and a colonoscopic examination performed

if the bleeding continues. Older patients who have not had colorectal cancer screening should undergo colonoscopy or flexible

sigmoidoscopy.

With rare exceptions, the acutely thrombosed hemorrhoid can be

excised within the first 72 h by performing an elliptical excision.

Sitz baths, fiber, and stool softeners are prescribed. Additional

therapy for bleeding hemorrhoids includes the office procedures

of rubber band ligation, infrared coagulation, and sclerotherapy.

Sensation begins at the dentate line; therefore, all procedures

can be performed without discomfort either endoscopically or in

the office. Bands are placed around the engorged tissue, causing

ischemia and fibrosis. This aids in fixing the tissue proximally

in the anal canal. Patients may complain of a dull ache for 24 h

following band application. During sclerotherapy, 1–2 mL of a

sclerosant (usually sodium tetradecyl sulfate) is injected using a

25-gauge needle into the submucosa of the hemorrhoidal complex.

Care must be taken not to inject the anal canal circumferentially,

or stenosis may occur.

For surgical management of hemorrhoidal disease, excisional

hemorrhoidectomy with sharp dissection or using a ligator, transhemorrhoidal dearterialization (THD), or stapled hemorrhoidectomy (“the procedure for prolapse or hemorrhoids” [PPH]) is

the procedure of choice. All surgical methods of management

are equally effective in the treatment of symptomatic third- and

fourth-degree hemorrhoids. However, because the sutured hemorrhoidectomy involves the removal of redundant tissue down

to the anal verge, unpleasant anal skin tags are removed as well.

The stapled hemorrhoidectomy is associated with less discomfort;

however, this procedure does not remove anal skin tags, and an

increased number of complications are associated with use of the

stapling device. THD uses ultrasound guidance to ligate the blood

supply to the anal tissue, hence reducing hemorrhoidal engorgement. No procedures on hemorrhoids should be done in patients

who are immunocompromised or who have active proctitis. Furthermore, emergent hemorrhoidectomy for bleeding hemorrhoids

is associated with a higher complication rate.

Acute complications associated with the treatment of hemorrhoids include pain, infection, recurrent bleeding, and urinary

retention. Care should be taken to place bands properly and to avoid

overhydration in patients undergoing operative hemorrhoidectomy.

Late complications include fecal incontinence as a result of injury to

the sphincter during the dissection. Anal stenosis may develop from

overzealous excision, with loss of mucosal skin bridges for reepithelialization. Finally, an ectropion (prolapse of rectal mucosa from the

anal canal) may develop. Patients with an ectropion complain of a

“wet” anus as a result of inability to prevent soiling once the rectal

mucosa is exposed below the dentate line.

■ ANORECTAL ABSCESS

Incidence and Epidemiology The development of a perianal

abscess is more common in men than women by a ratio of 3:1. The

peak incidence is in the third to fifth decade of life. Perianal pain

associated with the presence of an abscess accounts for 15% of office

visits to a colorectal surgeon. The disease is more prevalent in immunocompromised patients such as those with diabetes, hematologic

disorders, or inflammatory bowel disease (IBD) and persons who are

HIV positive. These disorders should be considered in patients with

recurrent perianal infections.

Anatomy and Pathophysiology An anorectal abscess is an

abnormal fluid-containing cavity in the anorectal region. Anorectal

abscess results from an infection involving the glands surrounding the

anal canal. Normally, these glands release mucus into the anal canal,

which aids in defecation. When stool accidentally enters the anal

glands, the glands become infected, and an abscess develops. Anorectal

abscesses are perianal in 40–50% of patients, ischiorectal in 20–25%,

intersphincteric in 2–5%, and supralevator in 2.5% (Fig. 328-7).

Presentation and Evaluation Perianal pain and fever are the

hallmarks of an abscess. Patients may have difficulty voiding and have

blood in the stool. A prostatic abscess may present with similar complaints, including dysuria. Patients with a prostatic abscess will often

have a history of recurrent sexually transmitted diseases. On physical

examination, a large fluctuant area is usually readily visible. Routine

laboratory evaluation shows an elevated white blood cell count. Diagnostic procedures are rarely necessary unless evaluating a recurrent

abscess. A CT scan or MRI has an accuracy of 80% in determining

incomplete drainage. If there is a concern about the presence of IBD,

a rigid or flexible sigmoidoscopic examination may be done at the

time of drainage to evaluate for inflammation within the rectosigmoid

region. A more complete evaluation for Crohn’s disease would include

a full colonoscopy and small-bowel series.

1

1

2

2

3

3

4

4

Fistula

tracts

Abscesses

Intersphincteric

Intersphincteric

Trans-sphincteric

Suprasphincteric

Extrasphincteric

Supralevator

Ischiorectal

Perianal

FIGURE 328-7 Common locations of anorectal abscess (left) and fistula in ano (right).

2505 Diverticular Disease and Common Anorectal Disorders CHAPTER 328

TREATMENT

Anorectal Abscess

As with all abscesses, the “gold standard” is drainage. Office drainage of an uncomplicated anorectal abscess may suffice. A small

incision close to the anal verge is made, and a Mallenkot drain is

advanced into the abscess cavity. For patients who have a complicated abscess or who are diabetic or immunocompromised, drainage should be performed in an operating room under anesthesia.

These patients are at greater risk for developing necrotizing fasciitis.

The role of antibiotics in the management of anorectal abscesses is

limited. Antibiotics are only warranted in patients who are immunocompromised or have prosthetic heart valves, artificial joints,

diabetes, or IBD.

■ FISTULA IN ANO

Incidence and Epidemiology The incidence and prevalence of

fistulating perianal disease parallel the incidence of anorectal abscess,

estimated to be 1 in 10,000 individuals. Some 30–40% of abscesses

will give rise to fistula in ano. Although the majority of the fistulas are

cryptoglandular in origin, 10% are associated with IBD, tuberculosis,

malignancy, and radiation.

Anatomy and Pathophysiology A fistula in ano is defined as a

communication of an abscess cavity with an identifiable internal opening within the anal canal. This identifiable opening is most commonly

located at the dentate line where the anal glands enter the anal canal.

Patients experiencing continuous drainage following the treatment of a

perianal abscess likely have a fistula in ano. These fistulas are classified

by their relationship to the anal sphincter muscles, with 70% being

intersphincteric, 23% transsphincteric, 5% suprasphincteric, and 2%

extrasphincteric (Fig. 328-7).

Presentation and Evaluation A patient with a fistula in ano will

complain of constant drainage from the perianal region associated

with a firm mass. The drainage may increase with defecation. Perianal

hygiene is difficult to maintain. Examination under anesthesia is the

best way to evaluate a fistula. At the time of the examination, anoscopy

is performed to look for an internal opening. Diluted hydrogen peroxide will aid in identifying such an opening. In lieu of anesthesia, MRI

with an endoanal coil will also identify tracts in 80% of the cases. After

drainage of an abscess with insertion of a Mallenkot catheter, a fistulagram through the catheter can be obtained in search of an occult fistula

tract. Goodsall’s rule states that a posterior external fistula will enter the

anal canal in the posterior midline, whereas an anterior fistula will enter

at the nearest crypt. A fistula exiting >3 cm from the anal verge may

have a complicated upward extension and may not obey Goodsall’s rule.

TREATMENT

Fistula in Ano

A newly diagnosed draining fistula is best managed with placement

of a seton, a vessel loop or silk tie placed through the fistula tract,

which maintains the tract open and quiets down the surrounding

inflammation that occurs from repeated blockage of the tract. Once

the inflammation is less, the exact relationship of the fistula tract

to the anal sphincters can be ascertained. A simple fistulotomy can

be performed for intersphincteric and low (less than one-third of

the muscle) transsphincteric fistulas without compromising continence. For a higher transsphincteric fistula, an anorectal advancement flap in combination with a drainage catheter or fibrin glue

may be used. Very long (>2 cm) and narrow tracts respond better to

fibrin glue than shorter tracts. Simple ligation of the internal fistula

tract (LIFT procedure) has also been used in the management of

simple fistula with good success.

Patients should be maintained on stool-bulking agents, nonnarcotic pain medication, and sitz baths following surgery for a fistula.

Early complications from these procedures include urinary retention and bleeding. Later complications are rare (<10%) and include

temporary and permanent incontinence. Recurrence is 0–18% following fistulotomy and 20–30% following anorectal advancement

flap and the LIFT procedure.

Fistulizing disease of the anus is common in Crohn’s disease, and

recent evidence has suggested that the use of mesenchymal stem

cell therapy may improve healing rates of fistula associated with

Crohn’s disease. The ADMIRE study examined the use of allogeneic

expanded adipose-derived mesenchymal stem cells in the treatment

of complex fistula in ano in Crohn’s disease. The study included 212

patients randomized to stem cell therapy or placebo. Fistula remission rates at 52 weeks were significantly higher with the use of stem

cell therapy over placebo (59 vs 42%, respectively). Currently, there

is an international multicenter trial underway.

■ ANAL FISSURE

Incidence and Epidemiology Anal fissures occur at all ages but

are more common in the third through the fifth decades. A fissure is

the most common cause of rectal bleeding in infancy. The prevalence is

equal in males and females. It is associated with constipation, diarrhea,

infectious etiologies, perianal trauma, and Crohn’s disease.

Anatomy and Pathophysiology Trauma to the anal canal occurs

following defecation. This injury occurs in the anterior or, more commonly, posterior anal canal. Irritation caused by the trauma to the anal

canal results in an increased resting pressure of the internal sphincter.

The blood supply to the sphincter and anal mucosa enters laterally.

Therefore, increased anal sphincter tone results in a relative ischemia

in the region of the fissure and leads to poor healing of the anal injury.

A fissure that is not in the posterior or anterior position should raise

suspicion for other causes, including tuberculosis, syphilis, Crohn’s

disease, and malignancy.

Presentation and Evaluation A fissure can be easily diagnosed

on history alone. The classic complaint is pain, which is strongly

associated with defecation and is relentless. The bright red bleeding

that can be associated with a fissure is less extensive than that associated with hemorrhoids. On examination, most fissures are located in

either the posterior or anterior position. A lateral fissure is worrisome

because it may have a less benign nature, and systemic disorders should

be ruled out. A chronic fissure is indicated by the presence of a hypertrophied anal papilla at the proximal end of the fissure and a sentinel

pile or skin tag at the distal end. Often the circular fibers of the hypertrophied internal sphincter are visible within the base of the fissure. If

anal manometry is performed, elevation in anal resting pressure and

a sawtooth deformity with paradoxical contractions of the sphincter

muscles are pathognomonic.

TREATMENT

Anal Fissure

The management of the acute fissure is conservative. Stool softeners

for those with constipation, increased dietary fiber, topical anesthetics, glucocorticoids, and sitz baths are prescribed and will heal

60–90% of fissures. Chronic fissures are those present for >6 weeks.

These can be treated with modalities aimed at decreasing the anal

canal resting pressure including nifedipine ointment applied three

times a day and botulinum toxin type A, up to 20 units, injected into

the internal sphincter on each side of the fissure. Both treatments

are associated with a fissure healing rate of >80%. Surgical management includes anal dilatation and lateral internal sphincterotomy.

Usually, one-third of the internal sphincter muscle is divided; it is

easily identified because it is hypertrophied. Recurrence rates from

medical therapy are higher, but this is offset by a risk of incontinence following sphincterotomy. Lateral internal sphincterotomy

may lead to incontinence more commonly in women.

2506 PART 10 Disorders of the Gastrointestinal System

Acknowledgment

The author thanks Cory Sandore for providing some illustrations for this

chapter. Gregory Bulkley, MD, contributed to this chapter in an earlier

edition, and some of that material has been retained here.

■ FURTHER READING

Bharucha AE et al: Surgical interventions and the use of device-aided

therapy for the treatment of fecal incontinence and defecatory disorders. Clin Gastroenterol Hepatol 15:1844, 2017.

Daniels L et al: Randomized clinical trial of observation versus antibiotic treatment for a first episode of CT-proven uncomplicated acute

diverticulitis (DIABOLO trial). BJS 104:52, 2017.

Guttenplan M: The evaluation and office management of hemorrhoids for the gastroenterologist. Curr Gastroenterol Rep 19:30, 2017.

Panes J et al: Long-term efficacy and safety of stem cell therapy

(Cx601) for complex perianal fistulas in patients with Crohn’s disease.

Gastroenterology 154:1334, 2018.

Prichard D, Bharucha AE: Management of pelvic floor disorders:

Biofeedback and more. Curr Treat Options Gastroenterol 12:456,

2014.

Salfity HV et al: Minimally invasive incision and drainage technique

in the treatment of simple subcutaneous abscess in adults. Am Surg

83:699, 2017.

Sugrue J et al: Sphincter-sparing anal fistula repair: Are we getting

better? Dis Colon Rectum 60:1071, 2017.

Tursi A: Dietary pattern and colonic diverticulosis. Curr Opin Clin

Nutr Metab Care 20:409, 2017.

329 Mesenteric Vascular

Insufficiency

Maryam Ali Khan, Jaideep Das Gupta,

Mahmoud Malas

Left phrenic a.

Right phrenic a.

Marginal a.

Arc of

Riolan

Aorta

IIA

Pancreaticoduodenal a.

Griffiths’

point

Sudeck’s

point

SMA

IMA

Hemorrhoidal aa.

Superior

Middle

Inferior

Celiac trunk

Splenic a.

FIGURE 329-1 Blood supply to the intestines includes the celiac artery, superior

mesenteric artery (SMA), inferior mesenteric artery (IMA), and branches of the

internal iliac artery (IIA). Griffiths’ and Sudeck’s points, indicated by shaded areas,

are watershed areas within the colonic blood supply and common locations for

ischemia.

INTESTINAL ISCHEMIA

■ INCIDENCE AND EPIDEMIOLOGY

Intestinal ischemia occurs when splanchnic perfusion fails to meet the

metabolic demands of the intestines, resulting in ischemic tissue injury.

Mesenteric ischemia affects 2–3 people per 100,000, with an increasing

incidence in the aging population. Mortality with acute presentation

remains high, between 50 and 80%, and early diagnosis with prompt

intervention is crucial in improving clinical outcomes. Intestinal

ischemia is further classified as chronic mesenteric ischemia (CMI) or

acute mesenteric ischemic (AMI). CMI is secondary to multiple major

visceral arterio-occlusive disease, with involvement of the superior

mesenteric artery (SMA) most worrisome. AMI is most commonly

associated with (1) arterio-occlusive mesenteric ischemia, (2) nonocclusive mesenteric ischemia, and (3) mesenteric venous thrombosis.

CMI is the failure to achieve normal postprandial hyperemic intestinal blood flow. This occurs due to an imbalance between the supply

and demand of oxygen metabolites to the intestinal tract similar to

cardiac angina. CMI occurs due to significant atherosclerotic disease

leading to the narrowing of the SMA and/or celiac artery origins.

AMI is the occurrence of an abrupt cessation of mesenteric blood

flow, usually embolic or thrombotic in nature. Approximately 50% of

AMI is due to embolus to the mid to distal SMA. Embolus etiology

includes atrial fibrillation, recent myocardial infarction, soft atherosclerotic plaque, infective endocarditis, valvular heart disease, and

recent cardiac or vascular catheterization. Approximately 25–30% of

cases are characterized by an acute-on-chronic thrombosis in patients

with preexisting mesenteric atherosclerosis. Thrombotic occlusion

most commonly occurs in areas of severe atherosclerotic narrowing at

the SMA and celiac artery.

Nonocclusive mesenteric ischemia represents 20% of the cases and

is secondary to intestinal ischemia when subjected to acute hemodynamic instability. Hypovolemia, shock, and the use of vasoconstrictive

agents (digoxin, α-adrenergic agonists, cocaine) can precipitate ischemia in these patients. It is the most prevalent gastrointestinal disease

complicating cardiovascular surgery. The incidence of ischemic colitis

following elective aortic repair is 5–9%, and the incidence triples in

patients following emergent repair.

Mesenteric venous thrombosis accounts for <10% of cases and is

generally precipitated by a hypercoagulable state due to an underlying

inherited disorder such as factor V Leiden, prothrombin mutation,

protein S deficiency, protein C deficiency, antithrombin deficiency, and

antiphospholipid syndrome. It may also occur as a result of acquired

thrombophilia in malignancies, hematologic disorders, or use of oral

contraceptives.

■ ANATOMY AND PATHOPHYSIOLOGY

The blood supply to the intestines is supplied by the celiac artery, SMA,

and inferior mesenteric artery (IMA) (Fig. 329-1). Extensive collateralization occurs between major mesenteric trunks and branches of

the mesenteric arcades. Collateral vessels within the small bowel are

numerous and meet within the duodenum and the bed of the pancreas.

Collateral vessels within the colon meet at the splenic flexure and

descending/sigmoid colon. These areas, which are inherently at risk for

decreased blood flow, are known as Griffiths’ point and Sudeck’s point,

respectively, and are the most common locations for colonic ischemia

(Fig. 329-1, shaded areas). The splanchnic circulation can receive up

to 30% of the cardiac output. Protective responses to prevent intestinal

ischemia include abundant collateralization, autoregulation of blood

flow, and the ability to increase oxygen extraction from the blood.

2507 Mesenteric Vascular Insufficiency CHAPTER 329

Occlusive ischemia is a result of disruption of blood flow by an

embolus or progressive thrombosis in a major artery supplying the

intestine. In >75% of cases, emboli originate from the heart and preferentially lodge in the SMA just distal to the origin of the middle colic

artery. Progressive thrombosis of typically two of the major vessels

supplying the intestine is required for the development of chronic

intestinal angina. The involvement of the SMA is most worrisome.

Nonocclusive ischemia is disproportionate mesenteric vasoconstriction (arteriolar vasospasm) in response to severe physiologic stress

such as shock. If left untreated, early mucosal stress ulceration will

progress to full-thickness injury.

■ PRESENTATION, EVALUATION,

AND MANAGEMENT

Patients with CMI typically present with insidious onset of symptoms

and classically with recurrent episodes of acute, dull, crampy, postprandial epigastric pain, which has also been referred to as “intestinal

angina.” Weight loss and chronic diarrhea may also be noted. Duration of symptoms is typically 6–12 months. Physical examination

often reveals a malnourished patient with other manifestations of

atherosclerosis.

Duplex ultrasound has gained popularity as a screening tool for

the evaluation of the mesenteric vessels due to high sensitivity and

specificity. Mesenteric duplex scan demonstrating a high peak velocity of flow in the SMA is associated with an ~80% positive predictive

value of mesenteric ischemia. More significantly, a negative duplex

scan virtually precludes the diagnosis of mesenteric ischemia. It is

important to perform the test while the patient is fasting because the

presence of increased bowel gas prevents adequate visualization of flow

disturbances within the vessels or the lack of a vasodilation response to

feeding during the test.

The management of CMI includes medical management of the atherosclerotic disease by exercise, cessation of smoking, and antiplatelet

and lipid-lowering medications. A full cardiac and vascular evaluation

should be performed before intervention on CMI. Before intervention,

a CT angiogram is recommended to assess the degree of atherosclerotic

disease of the aortic and visceral vessels.

Treatment involves either endovascular or open surgical revascularization and should be individualized based on the patient’s comorbidities and anatomy. Endovascular revascularization involves targeted

vessel treatment with visceral stents, with the SMA anatomy being the

key determinant. Open revascularization involves antegrade bypass

from the supraceliac aortic or retrograde bypass, typically the common

iliac arteries, with a synthetic graft to the targeted vessels, usually the

SMA and/or celiac artery. In patients requiring revascularization, the

endovascular approach is recommended as first-line therapy. It is especially favorable for short segment stenosis with minimal to moderate

calcification or thrombus. Angioplasty with endovascular stenting in

the treatment of CMI is associated with an 80% long-term success

rate. Open revascularization should be considered in patients with

lesions not amenable to endovascular treatment such as severe calcification, longer lesions, small vessel diameter, or failed endovascular

interventions.

Acute intestinal ischemia remains one of the most challenging

diagnoses. The mortality rate of AMI is >50%. The most significant

indicator of survival is the timeliness of diagnosis and treatment. An

overview of diagnosis and management of each form of intestinal

ischemia is given in Table 329-1.

AMI resulting from an arterial embolus or thrombosis presentation

is nonspecific and requires a high index of suspicion for diagnosis.

Severe, acute, unremitting abdominal pain strikingly out of proportion to the physical findings is the most common complaint (95%).

This may be associated with nausea (44%), vomiting (35%), diarrhea

(35%), and blood per rectum (16%). Later findings will demonstrate

peritonitis and cardiovascular collapse. Specific clinical features can

help differentiate the underlying etiology, whether embolic or thrombotic. Patients with embolic ischemia are typically older adults with an

underlying condition that predisposes to embolism such as atrial fibrillation, prior embolic event, or recent infective endocarditis. Thrombotic ischemia typically presents as an acute occlusion in patients with

the underlying atherosclerotic disease who may have been previously

diagnosed with CMI.

AMI is a surgical emergency, and emergent admission to a monitored bed or intensive care unit is recommended for resuscitation with

fluids and administration of broad-spectrum antibiotics in addition

to further evaluation. If the diagnosis of intestinal ischemia is being

considered, consultation with a surgical service is necessary. Often

the decision to operate is made on a high index of suspicion from

the history and physical exam despite normal laboratory findings. In

patients with suspected AMI, CT angiography with a 1-mm or thinner

cut should be used to detect mesenteric arterial occlusive disease most

likely due to embolic or thrombotic etiology and is the gold standard.

TABLE 329-1 Overview of the Management of Acute Intestinal Ischemia

CONDITION KEY TO EARLY DIAGNOSIS

TREATMENT OF UNDERLYING

CAUSE TREATMENT OF SPECIFIC LESION

TREATMENT OF SYSTEMIC

CONSEQUENCE

Arterio-occlusive

mesenteric ischemia

1. Arterial embolus

Computed tomography (CT)

angiography

Early laparotomy

Anticoagulation

Cardioversion

Thrombectomy

Broad-spectrum antibiotics

Laparotomy

Embolectomy

Assess viability and resect

nonviable bowel

Anticoagulation

Resuscitation

Broad-spectrum antibiotics

Emergent surgical intervention

Assessment of bowel

2. Arterial thrombosis Duplex ultrasound

CT angiography

Anticoagulation

Broad-spectrum antibiotics

Resuscitation

Endovascular approach:

thrombolysis, angioplasty, and

stenting

Endarterectomy/thrombectomy or

vascular bypass

Assess viability and resect

nonviable bowel

Anticoagulation

Resuscitation

Broad-spectrum antibiotics

Emergent surgical intervention

Assessment of bowel

Mesenteric venous

thrombosis

Venous thrombosis

CT with venous phase Anticoagulation

Resuscitation

Anticoagulation

Hypercoagulable workup

Anticoagulation

Resuscitation

Broad-spectrum antibiotics

Support cardiac output

Avoid vasoconstrictors

Nonocclusive mesenteric

ischemia

Vasospasm: CT

Hypoperfusion: CT

Resuscitation

Support cardiac output

Avoid vasoconstrictors

Broad-spectrum antibiotics

Vasospasm: intraarterial

vasodilators

Hypoperfusion: assess viability

and resect dead bowel

Resuscitation

Broad-spectrum antibiotics

Support cardiac output

Avoid vasoconstrictors

Source: Modified from GB Bulkley, in JL Cameron (ed): Current Surgical Therapy, 2nd ed. Toronto, BC Decker, 1986.

2508 PART 10 Disorders of the Gastrointestinal System

Additional diagnostic modalities that can be useful in diagnosis but

that should not delay surgical therapy include an electrocardiogram

(ECG), echocardiogram, and abdominal radiographs. Patients with

AMI should be given a heparin bolus and started on a therapeutic heparin drip. Correction of electrolyte abnormalities and empiric broadspectrum antibiotic therapy should also be initiated immediately.

If the CTA verifies the acute embolic occlusion of SMA, surgical

exploration should not be delayed. The goal of operative exploration is

to resect the compromised bowel and restore blood supply. The entire

length of the small and large bowel beginning at the ligament of Treitz

should be evaluated. The SMA artery should be localized, typically at

the mesocolon of the transverse colon. A transverse arteriotomy of the

SMA should be made with the removal of the embolus with a Fogarty

catheter passed in a retrograde and antegrade manner to restore blood

flow. In the case of SMA occlusion where the embolus usually lies just

proximal to the origin of the middle colic artery, the proximal jejunum

is often spared, while the remainder of the small bowel up to the transverse colon may become ischemic. Nonviable bowel should be resected.

Questionable bowel should undergo a second-look laparotomy in a 24-

to 48-h period. After revascularization, peristalsis and return of pink

color of the bowel wall should be observed. Palpation of major arterial

mesenteric vessels can be performed, as well as applying a Doppler

flowmeter to the antimesenteric border of the bowel wall, but neither

is a definitive indicator of viability.

In the assessment of acute-on-chronic mesenteric ischemia, typically

involvement of the orifice of the SMA is seen. Therefore, the entire

small bowel is compromised. Revascularization using an endovascular, open, and/or hybrid approach should be individualized based on

the patient’s critical status, comorbidities, and anatomy. Endovascular

stenting, suction thrombectomy, and/or thrombolysis catheter should

be considered for intervention. The bowel should be evaluated for viability, typically via an exploratory laparotomy.

Nonocclusive or vasospastic mesenteric ischemia presents with

generalized abdominal pain, anorexia, bloody stools, and abdominal

distention. Often these patients are obtunded, and physical findings

may not assist in the diagnosis or may be obscured by the underlying

etiology. The presence of leukocytosis, metabolic acidosis, and/or

lactic acidosis is useful in support of the diagnosis of advanced intestinal ischemia; however, these markers may not be indicative of either

reversible ischemia or frank necrosis.

Emergent admission to a monitored bed or intensive care unit is recommended for resuscitation, broad-spectrum antibiotics, and further

evaluation. Anticoagulation is not recommended as the goal of resuscitation is to maintain hemodynamics. For select patients, intramesenteric infusion of vasodilators such as papaverine, prostaglandins,

and nitroglycerin for reversal of mesenteric ischemia can be used, but

resuscitation and the treatment of the underlying pathology should be

the priority.

If ischemic colitis is a concern, colonoscopy should be considered

to assess the integrity of the colon mucosa. Ischemia of the colonic

mucosa is graded as mild with minimal mucosal erythema or as

moderate with pale mucosal ulcerations and evidence of extension to

the muscular layer of the bowel wall. Severe ischemic colitis presents

with severe ulcerations resulting in black or green discoloration of the

mucosa, consistent with full-thickness bowel-wall necrosis. Laparoscopy can also be employed for assessment. Ischemic colitis is optimally

treated with resection of the ischemic bowel and the formation of a

proximal stoma.

Onset of mesenteric venous thrombosis can be acute or subacute

based on the location of thrombosis in the splanchnic circulation.

Patients often present with vague abdominal pain associated with nausea and vomiting. Physical examination findings include abdominal

distention with mild to moderate tenderness and signs of dehydration.

Findings on CT venous phase include diffuse bowel-wall thickening

and thrombus within the splanchnic system. IV therapeutic anticoagulation, broad-spectrum antibiotics, and correction of electrolyte abnormalities should be performed. Surgical intervention is not performed

unless there is evidence of peritonitis and/or bowel perforation. If there

is evidence of bowel compromise, an exploratory laparotomy should be

performed with resection of compromised bowel. Second-look laparotomy after 24–48 h should be attempted as anticoagulation can help

prevent resection of viable bowel. Hypercoagulability testing should

be performed, and if underlying inherited disorders are diagnosed,

lifelong anticoagulation is recommended.

Acknowledgments

We thank Cory Sandore for providing the illustration for this chapter.

Susan Gearhart contributed to this chapter in the 18th edition, Rizwan

Ahmed contributed to the 19th edition and Satinderjit Locham to the

20th edition.

■ FURTHER READING

Deng QW et al: Risk factors for postoperative acute mesenteric ischemia among adult patients undergoing cardiac surgery: A systematic

review and meta-analysis. J Crit Care 42:294, 2017.

Salsano G et al: What is the best revascularization strategy for

acute occlusive arterial mesenteric ischemia: Systematic review and

meta-analysis. Cardiovasc Intervent Radiol 41:27, 2018.

Sise MJ: Acute mesenteric ischemia. Surg Clin North Am 94:165, 2014.

■ EPIDEMIOLOGY

Morbidity and mortality from acute intestinal obstruction have been

decreasing over the past several decades. Nevertheless, the diagnosis

can still be challenging, and the type of complications that patients suffer has not changed significantly. The extent of mechanical obstruction

is typically described as partial, high grade, or complete—generally

correlating with the risk of complications and the urgency with which

the underlying disease process must be addressed. Obstruction is also

commonly described as being either “simple” or, alternatively, “strangulated” if vascular insufficiency and intestinal ischemia are evident.

Acute intestinal obstruction occurs either mechanically from blockage or from intestinal dysmotility when there is no blockage. In the

latter instance, the abnormality is described as being functional.

Mechanical bowel obstruction may be caused by extrinsic processes,

intrinsic abnormalities of the bowel wall, or intraluminal abnormalities

(Table 330-1). Within each of these broad categories are many diseases

that can impede intestinal propulsion. Intrinsic diseases that can cause

intestinal obstruction are usually congenital, inflammatory, neoplastic,

or traumatic in origin, although intussusception and radiation injury

can also be etiologic.

Acute intestinal obstruction accounts for ~1–3% of all hospitalizations and a quarter of all urgent or emergent general surgery admissions. Approximately 80% of cases involve the small bowel, and about

one-third of these patients show evidence of significant ischemia. The

mortality rate for patients with strangulation who are operated on

within 24–30 h of the onset of symptoms is ~8% but triples shortly

thereafter.

Extrinsic diseases most commonly cause mechanical obstruction of

the small intestine. In the United States and Europe, almost all cases

are caused by postoperative adhesions, carcinomatosis, or herniation

of the anterior abdominal wall. Carcinomatosis most often originates

from the ovary, pancreas, stomach, or colon, although rarely, metastasis

from distant organs like the breast and skin can occur. Adhesions are

responsible for the majority of cases of early postoperative obstruction

that require intervention. It is important to note many patients who

are successfully treated for adhesive small-bowel instruction will experience recurrence. Approximately 20% of patients who were treated

330 Acute Intestinal

Obstruction

Danny O. Jacobs

2509Acute Intestinal Obstruction CHAPTER 330

is often the most common reason why hospital discharge is delayed.

Pseudo-obstruction of the colon, also known as Ogilvie’s syndrome, is

a relatively rare disease. Some patients with Ogilvie’s syndrome have

colonic dysmotility due to abnormalities of their autonomic nervous

system that may be inherited.

■ PATHOPHYSIOLOGY

The manifestations of acute intestinal obstruction depend on the

nature of the underlying disease process, its location, and changes in

blood flow (Fig. 330-1). Increased intestinal contractility, which occurs

proximally and distal to the obstruction, is a characteristic response.

Subsequently, intestinal peristalsis slows as the intestine or stomach

proximal to the point of obstruction dilates and fills with gastrointestinal secretions and swallowed air. Although swallowed air is the

primary contributor to intestinal distension, intraluminal air may also

accumulate from fermentation, local carbon dioxide production, and

altered gaseous diffusion.

Intraluminal dilation also increases intraluminal pressure. When

luminal pressure exceeds venous pressure, venous and lymphatic

drainage is impeded. Edema ensues, and the bowel wall proximal to

the site of blockage may become hypoxemic. Epithelial necrosis can be

identified within 12 h of obstruction. Ultimately, arterial blood supply

may become so compromised that full-thickness ischemia, necrosis,

and perforation result. Stasis increases the bacteria counts within the

jejunum and ileum. Bacteria, such as Escherichia coli, Streptococcus

faecalis, and Klebsiella, and other pathogens may be recovered from

intestinal cultures, mesenteric lymph nodes, the bloodstream, and

other sites.

Other manifestations depend on the degree of hypovolemia, the

patient’s metabolic response, and the presence or absence of associated

intestinal ischemia. Inflammatory edema eventually increases the

production of reactive oxygen species and activates neutrophils and

macrophages, which accumulate within the bowel wall. Their accumulation, along with changes in innate immunity, disrupts secretory and

neuromotor processes. Dehydration is caused by loss of the normal

intestinal absorptive capacity as well as fluid accumulation in the gastric or intestinal wall and intraperitoneally.

Anorexia and emesis tend to exacerbate intravascular volume

depletion. In the worst-case scenario that is most commonly identified after high-grade distal obstruction, emesis leads to losses of gastric potassium, hydrogen, and chloride, while dehydration stimulates

proximal renal tubule bicarbonate reabsorption. Intraperitoneal fluid

accumulation, especially in patients with severe distal bowel obstruction, may increase intraabdominal pressure enough to elevate the diaphragm, inhibit respiration, and impede systemic venous return and

promote vascular instability. Severe hemodynamic compromise may

elicit a systemic inflammatory response and generalized microvascular leakage.

TABLE 330-1 Most Common Causes of Acute Intestinal Obstruction

Extrinsic Disease

Adhesions (especially due to previous abdominal surgery), internal or external

hernias, neoplasms (including carcinomatosis and extraintestinal malignancies,

mostly commonly ovarian), endometriosis or intraperitoneal abscesses, and

idiopathic sclerosis

Intrinsic Disease

Congenital (e.g., malrotation, atresia, stenosis, intestinal duplication, cyst

formation, and congenital bands—the latter rarely in adults)

Inflammation (e.g., inflammatory bowel disease, especially Crohn’s disease,

but also diverticulitis, radiation, tuberculosis, lymphogranuloma venereum, and

schistosomiasis)

Neoplasia (note: primary small-bowel cancer is rare; obstructive colon cancer

may mimic small-bowel obstruction if the ileocecal valve is incompetent)

Traumatic (e.g., hematoma formation, anastomotic strictures)

Other, including intussusception (where the lead point is typically a polyp or

tumor in adults), volvulus, obstruction of duodenum by superior mesenteric

artery, radiation or ischemic injury, and aganglionosis, which is Hirschsprung’s

disease

Intraluminal Abnormalities

Bezoars, feces, foreign bodies including inspissated barium, gallstones (entering

the lumen via a cholecystoenteric fistula), enteroliths

TABLE 330-2 Acute Small-Intestinal and Colonic

Obstruction Incidences

CAUSE INCIDENCE

Postoperative adhesions >50%

Neoplasms ~20%

Hernias (especially ventral or internal types, where the

risk of strangulation is increased)

~10%

Inflammatory bowel disease, other inflammation

(obstruction may resolve if acute inflammation and

edema subside)

~5%

Intussusception, volvulus, other miscellaneous

diseases

<15%

conservatively and between 5 and 30% of patients who were managed

operatively will require readmission within 10 years.

Open operations of the lower abdomen, including appendectomy

and colorectal and gynecologic procedures, are especially likely to create adhesions that can cause bowel obstruction (Table 330-2). The risk

of internal herniation is increased by abdominal procedures such as

laparoscopic or open Roux-en-Y gastric bypass. Although laparoscopic

procedures may generate fewer postoperative adhesions compared

with open surgery, the risk of obstructive adhesion formation is not

eliminated.

Volvulus, which occurs when bowel twists on its mesenteric axis,

can cause partial or complete obstruction and vascular insufficiency.

The sigmoid colon is most commonly affected, accounting for approximately two-thirds of all cases of volvulus and 4% of all cases of largebowel obstruction. The cecum and terminal ileum can also volvulize,

or the cecum alone may be involved as a cecal bascule. Risk factors

include institutionalization, the presence of neuropsychiatric conditions requiring psychotropic medication, chronic constipation, and

aging; patients typically present in their seventies or eighties.

Colonic volvulus is more common in Eastern Europe, Russia, and

Africa than it is in the United States. It is rare for adhesions or hernias

to obstruct the colon. Cancer of the descending colon and rectum

is responsible for approximately two-thirds of all cases, followed by

diverticulitis and volvulus.

Functional obstruction, also known as ileus and pseudo-obstruction,

is present when dysmotility prevents intestinal contents from being

propelled distally and no mechanical blockage exists. Ileus that occurs

after intraabdominal surgery is the most commonly identified form

of functional bowel obstruction, but there are many other causes

(Table 330-3). Although postoperative ileus is most often transient, it

TABLE 330-3 Most Common Causes of Ileus (Functional or

Pseudo-Obstruction of the Intestine)

Intraabdominal procedures, lumbar spinal injuries, or surgical procedures on the

lumbar spine and pelvis

Metabolic or electrolyte abnormalities, especially hypokalemia and

hypomagnesemia, but also hyponatremia, uremia, and severe hyperglycemia

Drugs such as opiates, antihistamines, and some psychotropic (e.g., haloperidol,

tricyclic antidepressants) and anticholinergic agents

Intestinal ischemia

Intraabdominal or retroperitoneal inflammation or hemorrhage

Lower lobe pneumonias

Intraoperative radiation (likely due to muscle damage)

Systemic sepsis

Hyperparathyroidism

Pseudo-obstruction (Ogilvie’s syndrome)

Ileus secondary to hereditary or acquired visceral myopathies and neuropathies

that disrupt myocellular neural coordination

Some collagen vascular diseases such as lupus erythematosus or scleroderma

2510 PART 10 Disorders of the Gastrointestinal System

Closed-loop obstruction results when the proximal and distal

openings of a given bowel segment are both occluded, for example,

due to volvulus or a hernia. It is the most common precursor for strangulation, but not every closed loop strangulates. The risk of vascular

insufficiency, systemic inflammation, hemodynamic compromise,

and irreversible intestinal ischemia is much greater in patients with

closed-loop obstruction. Pathologic changes may occur more rapidly,

and emergency intervention is indicated. Irreversible bowel ischemia

may progress to transmural necrosis even if obstruction is relieved.

It is also important to remember that patients with high-grade distal

colonic obstruction who have competent ileocecal valves may present

with closed-loop obstruction. In the latter instance, the cecum may

progressively dilate such that ischemic necrosis results in perforation

especially when the cecal diameter exceeds 10–12 cm, as informed by

Laplace’s law. Patients with distal colonic obstruction whose ileocecal

valves are incompetent tend to present later in the course of disease and

mimic patients with distal small-bowel obstruction.

■ HISTORY AND PHYSICAL FINDINGS

Even though the presenting signs and symptoms can be misleading,

many patients with acute obstruction can be accurately diagnosed after

a thorough history and physical examination is performed. However,

small-bowel obstruction with strangulation can be especially difficult

to diagnosis promptly. Early recognition allows earlier treatment that

decreases the risk of progression or other excess morbidity.

The cardinal signs are colicky abdominal pain, abdominal distention, emesis, and obstipation. More intraluminal fluid accumulates in

patients with distal obstruction, which typically leads to greater distention, more discomfort, and delayed emesis. This emesis is feculent

when there is bacterial overgrowth. Patients with more proximal

obstruction commonly present with less abdominal distention but

more pronounced vomiting. Elements of the history that might be

helpful include any prior history of surgery, including herniorrhaphy,

as well as any history of cancer or inflammatory bowel disease.

Most patients, even those with simple obstruction, appear to be critically ill. Many may be oliguric, hypotensive, and tachycardic because

of severe intravascular volume depletion. Fever is worrisome for strangulation or systemic inflammation. Bowel sounds and bowel functional

activity are notoriously difficult to interpret. Classically, many patients

with early small-bowel obstruction will have high-pitched, “musical”

tinkling bowel sounds and peristaltic “rushes” known as borborygmi.

Later in the course of disease, the bowel sounds may be absent or

hypoactive as peristaltic activity decreases. This is in contrast to the

common findings in patients with ileus or pseudo-obstruction where

bowel sounds are typically absent or hypoactive from the beginning.

Lastly, patients with partial blockage may continue to pass flatus and

stool, and those with complete blockage may evacuate bowel contents

present downstream beyond their obstruction.

All surgical incisions should be examined, and the presence of a

tender abdominal or groin mass strongly suggests that an incarcerated

hernia may be the cause of obstruction. The presence of tenderness

should increase the concern about the presence of complications such

as ischemia, necrosis, or peritonitis. Severe pain with localization or

signs of peritoneal irritation is suspicious for strangulated or closedloop obstruction. It is important to remember that the discomfort may

be out of proportion to physical findings mimicking the complaints of

patients with acute mesenteric ischemia. Patients with colonic volvulus

present with the classic manifestations of closed-loop obstruction:

Inflammatory

wall edema

Point of obstruction

from extrinsic, intrinsic,

or intraluminal disease

Patients with distal

obstruction may still

discharge intraluminal

contents

Note: intraluminal obstruction is displayed

Collapsed

bowel distal

to obstruction

Air

Fluid

Inflammatory

mediators

released

Abnormal

bacteria

colonization

Fluid and air

accumulate; bacteria

overgrowth may occur

Epithelial

necrosis

Proximal

bowel

dilatation

FIGURE 330-1 Pathophysiologic changes of small-bowel obstruction.

2511Acute Intestinal Obstruction CHAPTER 330

severe abdominal pain, vomiting, and obstipation. Asymmetrical

abdominal distension and a tympanic mass may be evident.

Patients with ileus or pseudo-obstruction may have signs and

symptoms similar to those of bowel obstruction. Although abdominal

distention is present, colicky abdominal pain is typically absent, and

patients may not have nausea or emesis. Ongoing, regular discharge of

stool or flatus can sometimes help distinguish patients with ileus from

those with complete mechanical bowel obstruction.

■ LABORATORY AND IMAGING STUDIES

Laboratory testing should include a complete blood count and serum

electrolyte and creatinine measurements. Serial assessments are often

useful. Mild hemoconcentration and slight elevation of the white blood

cell count commonly occur after simple bowel obstruction. Emesis and

dehydration may cause hypokalemia, hypochloremia, elevated blood

urea nitrogen–to–creatinine ratios, and metabolic alkalosis. Patients

may be hyponatremic on admission because many have attempted

to rehydrate themselves with hypotonic fluids. The presence of

guaiac-positive stools and iron-deficiency anemia are strongly suggestive of malignancy.

Higher white blood cell counts with the presence of immature forms

or the presence of metabolic acidosis are worrisome for severe volume

depletion or ischemic necrosis and sepsis. Presently, there are no laboratory tests that are especially useful for identifying the presence of

simple or strangulated obstruction, although increases in serum d-lactate, creatine kinase BB isoenzymes, or intestinal fatty acid binding

protein levels may be suggestive of the latter.

Recommendations for diagnostic imaging continue to evolve. In

all cases, the key is not to delay operative intervention unnecessarily

when the patient’s signs or symptoms strongly suggest that high-grade

or complete obstruction or bowel compromise is present. Abdominal

radiography, which must include upright or cross-table lateral views,

can be completed quickly and may indicate the need for emergency

surgical intervention in patients who are not in the immediate postoperative period. A “staircasing” pattern of dilated air and fluid-filled

small-bowel loops >2.5 cm in diameter with little or no air seen in the

colon are classical findings in patients with small-bowel obstruction,

although findings may be equivocal in some patients with documented

disease. Little bowel gas appears in patients with proximal bowel

obstruction or in patients whose intestinal lumens are filled with

fluid. Upright plain films of the abdomen of patients with large-bowel

obstruction typically show colon dilatation. Small-bowel air-fluid levels may not be obvious if the ileocecal valve is incompetent. Although

it can be difficult to distinguish from ileus, small-bowel obstruction is

more likely when air-fluid levels are seen without significant colonic

distension. Free air suggests that perforation has occurred in patients

who have not recently undergone surgical procedures. A gas-filled,

“coffee bean”–shaped dilated shadow may be seen in patients with

volvulus.

More sophisticated imaging, which may be unnecessarily time consuming and expensive, can nevertheless be beneficial when the diagnosis is unclear. Computed tomography (CT) is the most commonly used

imaging modality. Its sensitivity for detecting bowel obstruction is ~95%

(78–100%) in patients with high-grade obstruction, with a specificity of

96% and an accuracy of ≥95%. Its accuracy in diagnosing closed-loop

obstruction is much lower (60%). CT may also provide useful information regarding location or to identify particular circumstances where

surgical intervention is needed urgently. Patients who have evidence

of contrast appearing within the cecum within 4–24 h of oral administration of water-soluble contrast can be expected to improve with high

sensitivity and specificity (~95% each). For example, contrast studies

may demonstrate a “bird’s beak,” a “c-loop,” or “whorl” deformity on CT

imaging at the site where twisting obstructs the lumen when a colonic

volvulus is present. Although abdominal radiography is usually the initial examination, unlike CT imaging, it may not accurately distinguish

obstruction from other causes of colonic dysmotility. Examples of some

CT images are reproduced in Fig. 330-2.

Ultrasonographic evaluations are especially difficult to interpret but

may be sensitive and appropriate studies to evaluate patients who are

pregnant or for whom x-ray exposure is otherwise contraindicated or

inappropriate.

CT imaging with enteral and IV contrast can also identify ischemia.

Altered bowel wall enhancement is the most specific early finding, but

its sensitivity is low. Mesenteric venous gas, pneumoperitoneum, and

pneumatosis intestinalis are late findings indicating the presence of

bowel necrosis. CT scanning after a water-soluble contrast enema may

help distinguish ileus or pseudo-obstruction from distal large-bowel

obstruction in patients who present with evidence of small-bowel

and colonic distention. CT enteroclysis, though rarely performed, can

FIGURE 330-2 Computed tomography with oral and intravenous contrast

demonstrating (A) evidence of small-bowel dilatation with air-fluid levels consistent

with a small-bowel obstruction; (B) a partial small-bowel obstruction from an

incarcerated ventral hernia (arrow); and (C) decompressed bowel seen distal to

the hernia (arrow). (Reproduced with permission from D Longo et al: Harrison’s

Principles of Internal Medicine, 18th ed. New York: McGraw-Hill; 2012.)

2512 PART 10 Disorders of the Gastrointestinal System

accurately identify neoplasia as a cause of bowel obstruction. Contrast

enemas or colonoscopies are almost always needed to identify causes

of acute colonic obstruction.

Barium studies are generally contraindicated in patients with firm

evidence of complete or high-grade bowel obstruction, especially when

they present acutely. Barium should never be given orally to a patient

with possible obstruction until that diagnosis has been excluded. In

every other case, such investigations should only be performed in

exceptional circumstances and with great caution because patients with

significant obstruction may develop barium concretions as an additional

source of blockage and some who would have otherwise recovered will

require operative intervention. Barium opacification also renders crosssectional imaging studies or angiography uninterpretable.

TREATMENT

Acute Intestinal Obstruction

An improved understanding of the pathophysiology of bowel

obstruction and the importance of fluid resuscitation, electrolyte

repletion, intestinal decompression, and the selected use of antibiotics has likely contributed to a reduction in mortality from acute

bowel obstruction. Every patient should be stabilized as quickly

as possible. Nasogastric tube suction decompresses the stomach,

minimizes further distention from swallowed air, improves patient

comfort, and reduces the risk of aspiration. Urine output should

be assessed using a Foley catheter. In some cases, for example, in

patients with cardiac disease, central venous pressures should be

monitored. The use of antibiotics is controversial, although prophylactic administration may be warranted if operation is anticipated.

Complete bowel obstruction is an indication for intervention. Stenting may be possible and warranted for some patients with highgrade obstruction due to unresectable stage IV malignancy. Stenting

may also allow elective mechanical bowel preparation before surgery is undertaken. Because treatment options are so variable, it

is helpful to make as precise a diagnosis as possible preoperatively.

ILEUS

Patients with ileus are treated supportively with intravenous fluids

and nasogastric decompression while any underlying pathology is

treated. Pharmacologic therapy is not yet proven to be efficacious

or cost-effective. However, peripherally active μ-opioid receptor

antagonists (e.g., alvimopan and methylnaltrexone) may accelerate

gastrointestinal recovery in some patients who have undergone

abdominal surgery.

COLONIC PSEUDO-OBSTRUCTION (OGILVIE’S DISEASE)

Neostigmine is an acetylcholinesterase inhibitor that increases cholinergic (parasympathetic) activity, which can stimulate colonic

motility. Some studies have shown it to be moderately effective

in alleviating acute colonic pseudo-obstruction. It is the most

common therapeutic approach and can be used once it is certain

that there is no mechanical obstruction. Cardiac monitoring is

required, and atropine should be immediately available. Intravenous administration induces defecation and flatus within 10 min in

the majority of patients who will respond. Sympathetic blockade by

epidural anesthesia can successfully ameliorate pseudo-obstruction

in some patients.

VOLVULUS

Patients with sigmoid volvulus can often be decompressed using a

flexible tube inserted through a rigid proctoscope or using a flexible

sigmoidoscope. Successful decompression results in sudden release

of gas and fluid with evidence of decreased abdominal distension

and allows definitive correction to be scheduled electively. Cecal

volvulus most often requires laparotomy or laparoscopic correction.

INTRAOPERATIVE STRATEGIES

Approximately 60–80% of selected patients with mechanical bowel

obstruction can be successfully treated conservatively. Indeed, most

cases of radiation-induced obstruction should also be managed

nonoperatively if possible. In most circumstances, early consultation with a surgeon is prudent when there is concern about

strangulation obstruction or other abnormality that needs to be

addressed urgently. Deterioration signifies a need for intervention.

At this time, the decision as to whether the patient can continue to

be treated nonoperatively can only be based on clinical judgment,

although, as described earlier, imaging studies can sometimes be

helpful. The frequency of major complications after operation

ranges from 12 to 47%, with greater risk being attributed to resection therapies and the patient’s overall health. Risk is increased for

patients with American Society of Anesthesiologists (ASA) physical

status of class III or higher.

At operation, dilation proximal to the site of blockage with distal

collapse is a defining feature of bowel obstruction. Intraoperative

strategies depend on the underlying problem and range from lysis

of adhesions to resection with or without diverting ostomy to

primary resection with anastomosis. Resection is warranted when

there is concern about the bowel’s viability after the obstructive process is relieved. Laparoscopic approaches can be useful for patients

with early obstruction when extensive adhesions are not expected

to be present. Some patients with high-grade obstruction secondary

to malignant disease that is not amendable to resection will benefit

from bypass procedures.

ADULT INTUSSUSCEPTION AND GALLSTONE ILEUS

Primary resection is prudent. Careful manual reduction of any

involved bowel may limit the amount of intestine that needs to be

removed. A proximal ostomy may be required if unprepped colon

is involved. The most common site of intestinal obstruction in

patients with gallstone “ileus” is the ileum (60% of patients). The

gallstone enters the intestinal tract most often via a cholecystoduodenal fistula. It can usually be removed by operative enterolithotomy. Addressing the gallbladder disease during urgent or

emergent surgery is not recommended.

POSTOPERATIVE BOWEL OBSTRUCTION

Early postoperative mechanical bowel obstruction is that which

occurs within the first 6 weeks of operation. Most are partial and

can be expected to resolve spontaneously. It tends to respond

and behave differently from classic mechanical bowel obstruction

and may be very difficult to distinguish from postoperative ileus.

A higher index of suspicion for a definitive site of obstruction is

warranted for patients who undergo laparoscopic surgical procedures. Patients who first had ileus and then subsequently develop

obstructive symptoms after an initial return of normal bowel function are more likely to have true postoperative small-bowel obstruction. The longer it takes for a patient’s obstructive symptoms to

resolve after hospitalization, the more likely the patient is to require

surgical intervention.

Acknowledgment

The wisdom and expertise of Dr. William Silen are gratefully

acknowledged.

■ FURTHER READING

Catena F et al: Adhesive small bowel adhesions obstruction: Evolutions in diagnosis, management and prevention. World J Gastrointest

Surg 27:222, 2016.

Ferrada P et al: Surgery or stenting for colonic obstruction: A practice

management guideline from the Eastern Association for the Surgery

of Trauma. J Trauma Acute Care Surg 80:659, 2016.

Jaffe T, Thompson WM: Large-bowel obstruction in the adults:

Classic radiographic and CT findings, etiology and mimics. Radiology 275:651, 2015.

Paulson EK, Thompson WM: Review of small-bowel obstruction:

The diagnosis and when to worry. Radiology 275:332, 2015.

Perry H et al: Relative accuracy of emergency CT in adults with nontraumatic abdominal pain. Brit Inst Rad 89:20150416, 2016.

Taylor MR, Lalani N: Adult small bowel obstruction. Acad Emerg

Med 20:528, 2013.

2513Acute Appendicitis and Peritonitis CHAPTER 331

ACUTE APPENDICITIS

■ INCIDENCE AND EPIDEMIOLOGY

Appendicitis occurs more frequently in westernized societies, but

its incidence is decreasing for uncertain reasons. Nevertheless, acute

appendicitis remains the most common emergency general surgical disease affecting the abdomen, with a rate of ~100 per 100,000

person-years in Europe and the Americas or ~11 cases per 10,000

people annually. Approximately 9% of men and 7% of women will

experience an episode during their lifetime. Appendicitis occurs most

commonly in 10- to 19-year-olds; however, the average age at diagnosis appears to be gradually increasing. Overall, 70% of patients are

<30 years old, and most are men.

One of the more common complications and most important

causes of excess morbidity and mortality is perforation, whether it is

contained and localized or unconstrained within the peritoneal cavity. The incidence of perforated appendicitis (~20 cases per 100,000

person-years) may be increasing. The explanation for this trend is

unknown. Approximately 20% of all patients will present with evidence

of perforation, but the percentage risk is much higher in patients <5 or

>65 years of age.

■ PATHOGENESIS OF APPENDICITIS AND

APPENDICEAL PERFORATION

Appendicitis was first described in 1886 by Reginald Fitz. Its etiology is

still not completely understood. Fecaliths, incompletely digested food

residue, lymphoid hyperplasia, intraluminal scarring, tumors, bacteria,

viruses, and inflammatory bowel disease have all been associated with

inflammation of the appendix and appendicitis with potentially different outcomes depending on pathogenesis.

Although not proven, obstruction of the appendiceal lumen is

believed to be an important step in the development of appendicitis—

at least in some cases. Here, obstruction leads to bacterial overgrowth

and luminal distension, with an increase in intraluminal pressure that

can inhibit the flow of lymph and blood. Then, vascular thrombosis

and ischemic necrosis with perforation of the distal appendix may

occur. Therefore, perforation that occurs near the base of the appendix

should raise concerns about another disease process. Most patients

who will perforate do so before they are evaluated by surgeons.

Appendiceal fecaliths (or appendicoliths) are found in ~50% of

patients with gangrenous appendicitis who perforate but are rarely

identified in those who have simple disease. As mentioned earlier,

the incidence of perforated, but not simple, appendicitis appears to

be increasing. The rate of perforated and nonperforated appendicitis

is correlated in men but not in women. Together these observations

suggest that the underlying pathophysiologic processes are different

and that simple appendicitis does not always progress to perforation.

It appears that at least some cases of simple acute appendicitis may

resolve spontaneously or with antibiotic therapy with limited risk of

recurrent disease. The use of antibiotics to treat uncomplicated appendicitis continues to be studied intensively. Some data indicate that

some patients who present with uncomplicated appendicitis based on

computed tomography (CT) and who are treated with antibiotics alone

will not experience a recurrence within a year. These findings highlight

the importance of clinical decision-making and risk assessment when

deciding and discussing treatment options with patients who presumably have simple disease, for example, deciding who is an appropriate

candidate for nonoperative management and who is not. The latter

is especially pertinent given the difficulty in assessing which patients

might progress to perforation and which will not.

331

Increasingly it appears that there are two broad categories of patients

with appendicitis—those with complicated disease like gangrene or

perforation and those without. When perforation occurs, the resultant

leak may be contained by the omentum or other surrounding tissues

to form an abscess. Free perforation normally causes severe peritonitis.

These patients may also develop infective suppurative thrombosis

of the portal vein and its tributaries along with intrahepatic abscesses.

The prognosis of the very unfortunate patients who develop this rare

but dreaded complication is very poor.

■ CLINICAL MANIFESTATIONS

Improved diagnosis, supportive care, and surgical interventions are

likely responsible for the remarkable decrease in the risk of mortality

from simple appendicitis to currently <1%. Nevertheless, it is still

important to identify patients who might have appendicitis as early

as possible. Patients who have persistent symptoms that have not

improved over 48 h may be more likely to perforate or develop other

complications.

Appendicitis should be included in the differential diagnosis of

abdominal pain for every patient in any age group unless it is certain

that the organ has been previously removed (Table 331-1).

The appendix’s anatomic location, which varies, may directly influence how the patient presents. Where the appendix can be “found”

ranges from local differences in how the appendiceal body and tip

lie relative to its attachment to the cecum (Figs. 331-1 and 331-2), to

where the appendix is actually situated in the peritoneal cavity—for

example, from its typical location in the right lower quadrant, to the

pelvis, right flank, right upper quadrant (as may be observed during

pregnancy), or even the left side of the abdomen for patients with malrotation or who have severely redundant colons.

Because the differential diagnosis of appendicitis is so extensive,

deciding if a patient has appendicitis can be difficult (Table 331-2).

Many patients may not present with the classically described history or

Acute Appendicitis

and Peritonitis

Danny O. Jacobs

TABLE 331-1 Some Conditions That Mimic Appendicitis

Crohn’s disease

Cholecystitis or other gallbladder

disease

Diverticulitis

Ectopic pregnancy

Endometriosis

Gastroenteritis or colitis

Gastric or duodenal ulceration

Hepatitis

Kidney disease, including

nephrolithiasis

Liver abscess

Meckel’s diverticulitis

Mittelschmerz

Mesenteric adenitis

Omental torsion

Pancreatitis

Lower lobe pneumonia

Pelvic inflammatory disease

Ruptured ovarian cyst or other cystic

disease of the ovaries

Small-bowel obstruction

Urinary tract infection

64%

0.5%

1%

32%

2%

FIGURE 331-1 Regional anatomic variations of the appendix.