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16 Gastrointestinal Diseases

Cho điểm
Gastrointestinal Diseases
Chandra Prakash
Gastrointestinal Bleeding
General Principles
Gastrointestinal (GI) bleeding may manifest as passage of bright or altered blood with emesis or bowel movements. Acute GI bleeding typically presents with overt blood loss that can be readily recognized by the patient or treating physician.
Overt GI bleeding is the passage of fresh or altered blood in emesis or in the stool.

Occult bleeding refers to a positive fecal occult blood test (stool guaiac) or iron-deficiency anemia without visible blood in the stool.

Obscure bleeding consists of GI blood loss of unknown origin that persists or recurs after negative initial endoscopic evaluation; obscure bleeding can be either overt or occult.

The following segments refer primarily to overt bleeding.
Clinical Presentation
Hematemesis, coffee-ground emesis, and aspiration of blood or coffee grounds from a nasogastric (NG) tube suggest an upper GI source of blood loss.

Melena, black sticky stool with a characteristic odor, indicates an upper GI source of blood loss, although small-bowel and sometimes right colonic bleeds can result in melena.

Various shades of red blood are seen in the stool with distal small-bowel or colonic bleeding, depending on the rate of blood loss and colonic transit.
Bleeding from the anorectal area typically results in bright blood coating the exterior of formed stool, sometimes associated with distal colonic symptoms (e.g., rectal urgency, straining or pain with defecation).

Although patients with upper GI bleeding can also present with red blood in their stool, this is almost invariably associated with hemodynamic compromise and circulatory shock.
Other symptoms may include fatigue, weakness, abdominal pain, pallor, or dyspnea.

Estimation of amount of blood lost can be attempted, but is often inaccurate. If the baseline hematocrit is known, the drop in hematocrit provides a rough estimate of blood loss. In general, patients with lower GI bleeding have less hemodynamic compromise compared to those with upper GI bleeding.
Emesis preceding upper GI bleeding may suggest a Mallory-Weiss tear.

Hypotension and hypovolemic shock preceding the bleeding episode may suggest ischemic colitis.

Radiation therapy to the prostate or pelvis suggests radiation proctopathy, and prior aortic graft surgery raises suspicion of an aortoenteric or aortocolonic fistula.

Chronic constipation may suggest bleeding from stercoral (stool-induced) ulceration of the rectum.

Recent polypectomy may indicate postpolypectomy bleeding.
Chronic renal disease may be associated with GI angiodysplasia, while patients with hereditary hemorrhagic telangiectasia can have GI telangiectasia as a source for blood loss.
Coagulation abnormalities can propagate bleeding from a pre-existing lesion in the GI tract. Disorders of coagulation, such as liver disease, von Willebrand disease, vitamin K deficiency, and disseminated intravascular coagulation can influence the course of GI bleeding (see Chapter 18, Disorders of Hemostasis).

Medications known to affect the coagulation process include warfarin, heparin, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), clopidogrel (Plavix), and thrombolytic agents. Newer antithrombotic agents can also propagate bleeding and include glycoprotein IIb/IIIa receptor antagonists (abciximab [ReoPro], eptifibatide [Integrilin], tirofiban [Aggrastat]) (see Chapter 5, Ischemic Heart Disease) and direct thrombin inhibitors (argatroban, bivalirudin). NSAIDs and aspirin can result in mucosal damage anywhere in the GI tract.

Physical Examination
Color of stool. Direct examination of spontaneously passed stool or stool obtained during a digital rectal examination can provide important clues as to the level of bleeding. In addition to assessing the color of stool, a digital rectal examination may identify a potential source of bleeding in the anorectum. Anal fissures, typically seen in the posterior midline, can result in extreme pain during a rectal examination.

NG aspiration. An NG aspirate is useful in the diagnosis of upper GI bleeding. Hemoccult testing of a normal-appearing NG aspirate is of no clinical utility; the aspirate should be considered positive only if blood or dark particulate matter (“coffee grounds) is seen. Gastric lavage with water or saline may be useful in assessing the activity and severity of upper GI bleeding and in clearing the stomach of blood and clots before endoscopic examination. After a diagnosis of upper GI bleeding is made, the NG tube is not required further in a stable patient, especially if endoscopy is to follow. In a small fraction of patients, a bleeding source in the duodenum can result in a negative NG aspirate.

Intravascular volume and hemodynamic status. Constant monitoring or frequent assessment of vital signs is necessary early in the evaluation, as a sudden increase in pulse rate or decrease in blood pressure (BP) may be an early indicator of recurrent or ongoing blood loss.

If the baseline BP and pulse are within normal limits, sitting the patient up or having the patient stand may result in orthostatic hemodynamic changes (drop in systolic BP of >10 mm Hg, rise in pulse rate of >15 bpm). Orthostatic changes in pulse and BP are seen with loss of 10%÷20% of the circulatory volume; supine hypotension suggests a >20% loss. Hypotension with a systolic blood pressure of <100 mm Hg or baseline tachycardia suggests significant hemodynamic compromise that requires urgent volume resuscitation.
Laboratory Studies
Complete blood count
Coagulation parameters (prothrombin time, partial thromboplastin time, platelet count)

Blood group, cross matching of 2÷4 units of blood

Comprehensive chemical profile (including liver function tests, serum creatinine)
Restoration of intravascular volume. Two large-bore IV lines with 14- to 18-gauge catheters or a central venous line should be urgently placed. Isotonic saline, lactated Ringer solution, or 5% hetastarch can be initiated; patients in shock may require volume administration using pressure infusion devices or hand infused using large syringes

and stopcocks. Packed red blood cell (RBC) transfusion should be used for volume replacement whenever possible; O-negative blood or simultaneous multiple-unit transfusions may be indicated if bleeding is massive. Transfusion should be continued until hemodynamic stability is achieved and the hematocrit reaches ≥25%; patients with cardiac or pulmonary disease may require transfusion to a hematocrit of ≥30%. The rate of volume infusion should be guided by the patient's condition and the rate and degree of volume loss. Vasopressors are generally not indicated, although transient IV pressor therapy is sometimes beneficial until enough volume is infused.
Correction of coagulopathy. Discontinuation of anticoagulant, if possible, followed by infusion of fresh frozen plasma (FFP) can be used to correct prolonged coagulation parameters from warfarin. An initial infusion of 2÷4 units of FFP can be supplemented with further infusion based on reassessment of the coagulation parameters. Parenteral vitamin K (10 mg SC or IM) may be indicated for prolonged prothrombin time from warfarin therapy or hepatobiliary disease but takes several hours to days for adequate reversal; it should be repeated daily for a total of three doses in hepatobiliary disease. Protamine infusion (1 mg antagonizes ~100 units of heparin) can be used for immediate reversal of anticoagulation from heparin infusion. Platelet infusion may be indicated when the platelet count is <50,000/mm3.

Airway protection. Endotracheal intubation to prevent aspiration should be considered when altered mental status (shock, hepatic encephalopathy), massive hematemesis, or active variceal hemorrhage is present.

Specific Tests for Localizing and Treating the Bleeding Source
Esophagogastroduodenoscopy (EGD) is the preferred method of investigation and therapy of upper GI bleeding and is associated with high diagnostic accuracy, therapeutic capability, and low morbidity. Volume resuscitation or blood transfusion should precede endoscopy in hemodynamically unstable patients. Patients with ongoing bleeding benefit most from urgent EGD, while stable patients with minimal bleeding (e.g. “coffee ground emesis with stable hematocrit) can have the procedure performed electively during the hospitalization.

Early colonoscopy can be performed after a rapid bowel purge in patients whose condition has clinically stabilized and who can tolerate an adequate bowel purge. The yield of finding a potential bleeding source in the colon is greatest if colonoscopy is performed within the initial 24 hours of presentation.
Patients unable to drink adequate amounts of the balanced electrolyte solution can have an NG tube placed for infusion of the bowel purge. All patients with acute lower GI bleeding from an unknown source should eventually undergo endoscopic evaluation of the colon during the initial hospitalization, regardless of the initial mode of investigation. Although early diagnostic endoscopy does not reduce mortality, therapeutic endoscopy reduces transfusion requirements, need for surgery, and length of hospital stay.
Anoscopy may be useful in the detection of internal hemorrhoids and anal fissures. In an outpatient or emergency room setting, anoscopy and sigmoidoscopy may be useful in rapid diagnosis of the level of bleeding before patient triage, but is usually followed by colonoscopy after bowel preparation.

Push enteroscopy allows evaluation of the proximal small bowel if a bleeding source is not seen within reach of a standard upper endoscope, especially if the colon has been excluded as a bleeding source by careful colonoscopy.

Tagged red blood cell (TRBC) scanning. RBCs labeled with technetium-99m remain in circulation for as long as 48 hours and extravasate into the bowel lumen with active bleeding. This extravasation can be detected as pooling of the radioactive tracer on gamma camera scanning. The pattern of peristaltic movement of the pooled tracer can help identify the potential site of bleeding.

A positive TRBC scan identifies patients likely to require invasive intervention and with high in-hospital morbidity, while a negative test may imply a better short-term prognosis. However, the scan is only positive 45% of the time. When positive, it
is accurate in identification of the location of the bleeding source in 80% of cases. The false localization rate of approximately 20% precludes use of this test alone in directing surgical resection of the bleeding bowel segment. Therefore, the clinical utility of this test is for assessing location and intensity of bleeding before more invasive tests are performed, especially in patients who demonstrate evidence of ongoing active bleeding.
Arteriography allows rapid localization and potential therapy of GI bleeding by demonstrating extravasation of the dye into the intestine when bleeding rates exceed 0.5 mL/min.

Arteriography may also identify the bleeding lesion, especially bleeding diverticula or angiodysplasia. A tumor blush or a late draining vein of angiodysplasia may be seen even in the absence of active bleeding.
When an actively bleeding lesion is found during angiography, intra-arterial infusion of vasopressin can cause vasoconstriction and stop bleeding. Superselective cannulation and embolization of the bleeding artery is sometimes performed.
In upper GI bleeding, arteriography is reserved for situations where brisk bleeding makes endoscopy difficult.
In small-bowel or lower GI bleeding, arteriography is utilized for both diagnosis and therapy of the bleeding lesion, typically after initial localization with TRBC scanning. Immediate or early extravasation on TRBC scanning carries the greatest likelihood of a positive arteriogram.
In stable patients with recurrent, difficult-to-localize GI bleeding, infusion of anticoagulants (e.g., heparin), thrombolytic agents (e.g., streptokinase), or intra-arterial vasodilators in a controlled fashion may increase the diagnostic yield of angiography. These provocative measures can be associated with excessive bleeding and should only be used in specialized centers in stable patients without comorbid illnesses.
Capsule endoscopy. A tiny camera, a light source, and a transmitter sealed in a biocompatible capsule resistant to digestive juices collect 50,000 images over 8 hours, mostly from the small bowel. This technique is most useful after the upper gut and the colon have been thoroughly examined, and the bleeding source is expected in the small bowel. Disadvantages are that the images cannot be viewed in real time, exact localization within the small bowel cannot be pinpointed, and therapy cannot be administered.

Intraoperative enteroscopy. When an actively bleeding source is identified within the small bowel, endoscopic therapy or surgical intervention can be facilitated by performing intraoperative enteroscopy. The surgeon, through an abdominal incision, advances the endoscope (inserted either through the mouth, the anus, or an enterotomy) by pleating bowel over the instrument.

Double balloon enteroscopy. This is a new technique that allows visualization of most of the small bowel, using a special endoscope with an overtube. Balloons at the endoscope tip and the overtube can be consecutively inflated and deflated while inserting and pulling out the endoscope to allow bowel to pleat over the overtube, thus allowing deep endoscope insertion into the small bowel, either through the mouth or the anus. This procedure is only available in advanced centers.

Nonvariceal upper GI bleeding
Intravenous proton pump inhibitors (PPIs) or high-dose PPIs administered orally (e.g., omeprazole, 40 mg PO bid) reduce the rate of recurrent bleeding and the need for surgery in patients with upper GI bleeding awaiting endoscopic treatment or if endoscopy is contraindicated or postponed; mortality is reduced in peptic ulcer bleeding, but not other causes of upper GI bleeding. Conventional oral doses of PPIs may suffice after endoscopic therapy has been administered. PPI therapy, oral or IV, is better than IV histamine-2 receptor antagonist (H2RA) therapy in bleeding peptic ulcers.
Variceal bleeding
When variceal bleeding is suspected, octreotide infusion should be initiated immediately (50- to 100-mcg bolus, followed by infusion at 25÷50 mcg/hr). Octreotide infusion acutely reduces portal pressures and controls variceal bleeding with very few
side effects, improving the diagnostic yield and therapeutic success of subsequent endoscopy.
Vasopressin (0.3 units/min IV, titrated by increments of 0.1 units/min q30min until hemostasis is achieved, side effects develop, or the maximum dose of 0.9 units/min is reached) is an alternative agent, rarely used because of significant cardiovascular complications including cardiac arrest and myocardial infarction. Concomitant infusion of nitroglycerin may reduce undesirable cardiovascular side effects and provide more effective control of bleeding. Nitroglycerin is administered only if the systolic BP is >100 mm Hg, at a dose of 10 mcg/min IV, increased by 10 mcg/min q10÷15min until the systolic BP falls to 100 mm Hg or a maximum dose of 400 mcg/min is reached.

Endoscopic Therapy
Therapeutic endoscopy offers the advantage of immediate treatment and should be implemented in all patients early in the hospital course (within 24 hours). Fluid resuscitation and hemodynamic stability are essential before endoscopy. Administration of promotility agents such as metoclopramide (10 mg IV) or erythromycin (150÷250 mg IV) may accelerate gastric emptying, and thereby help clear the stomach of blood or clots prior to endoscopy in patients with significant or ongoing bleeding.

Variceal ligation or banding is the endoscopic therapy of choice for esophageal varices. Intensive care unit (ICU) admission and endotracheal intubation for airway protection should be considered when active bleeding from varices is suspected. It is effective in controlling active hemorrhage and achieves variceal eradication rapidly, with lower rates of rebleeding and fewer complications compared to sclerotherapy. Complications of banding include superficial ulceration, dysphagia, transient chest discomfort, and, rarely, esophageal strictures.

Sclerotherapy is also effective but is used less frequently because of complications (ulcerations, strictures, perforation, pleural effusions, adult respiratory distress syndrome, sepsis). Recurrent bleeding may be seen in up to 50% of patients but usually responds to repeat sclerotherapy. Fever may be seen in 40% of patients within the first 2 days of therapy; fever that lasts longer than 2 days should prompt investigation for bacteremia.

Other Therapy
Transjugular intrahepatic portosystemic shunt (TIPS) is a radiologic procedure wherein an expandable metal stent is deployed between the hepatic veins and the portal vein to decompress the portal system and reduce portal venous pressure. Indications include refractory variceal bleeding unresponsive to variceal ligation or sclerotherapy, and bleeding from gastric varices in the setting of portal hypertension. Encephalopathy may occur in up to 25% of patients but is usually controlled with medical therapy (see Complications of Hepatic Insufficiency, Chapter 17, Liver Diseases). Shunt stenosis is another significant complication that may respond to balloon dilation. Screening for shunt stenosis with duplex Doppler ultrasound is recommended if the patient redevelops variceal bleeding or has recurrence of esophageal or gastric varices on endoscopy.

Emergent total colectomy may rarely be required as a lifesaving maneuver for massive, unlocalized, colonic bleeding; this should be preceded by emergent EGD to rule out a rapidly bleeding upper source whenever possible. Certain lesions (e.g., neoplasia, Meckel's diverticulum) require surgical resection for a cure.

Splenectomy is curative in bleeding gastric varices from splenic vein thrombosis. Ongoing bleeding with transfusion requirements exceeding 4÷6 units over 24 hours or 10 units overall, or more than two to three recurrent bleeding episodes from the same source have been considered indications for surgery.

Shunt surgery (portacaval or distal splenorenal shunt) should be considered in patients with good hepatic reserve if the patient (a) fails endoscopic or pharmacologic therapy, (b) is unable to return for follow-up visits, (c) is at high risk of death from recurrent

bleeding because of cardiac disease or difficulty in obtaining blood products, or (d) lives far from medical care. Although bleeding may be controlled in 95% of cases, hospital death rates are high, and there is a significant incidence of postoperative encephalopathy, especially among patients with higher grades of Child's classification (see Chapter 17, Table 17-5).
Esophageal Disorders
Gastroesophageal Reflux Disease
General Principles
Gastroesophageal reflux disease (GERD) is defined as symptoms or tissue damage resulting from reflux of gastric acid into the esophagus and more proximal structures.
Clinical Presentation
The predominant symptoms of GERD are heartburn and regurgitation.
Atypical symptoms include cough, asthma, hoarseness, chest pain, hiccups, and dental erosions.

Symptom response to a therapeutic trial of PPIs can be diagnostic.
Endoscopic evaluation is recommended for patients with warning symptoms of dysphagia, odynophagia, early satiety, weight loss, or bleeding, and atypical symptoms (cough, asthma, hoarseness, chest pain, aphthous ulcers, hiccups, dental erosions).
Patients with symptoms refractory to empiric acid suppression or requiring continuous medication for prolonged periods should also undergo endoscopy.
Ambulatory pH monitoring is used to establish elevated esophageal acid exposure and symptom-reflux correlation in patients with ongoing symptoms despite acid suppression (especially if endoscopy is negative) or those with atypical symptoms. It is also used to determine adequacy of acid suppression in patients with established GERD and ongoing symptoms.
Lifestyle Modification
The basics of lifestyle modification include eating small meals; refraining from eating for 2÷3 hours before lying down; elevating the head of the bed 4÷6 in.; decreasing intake of fatty foods, chocolate, coffee, cola, and alcohol; and smoking cessation.
Lifestyle modification also includes avoiding medications such as calcium channel blockers, theophylline, sedatives/tranquilizers, and anticholinergics, as they may potentiate reflux.
Lifestyle modifications alone are unlikely to resolve symptoms in the majority of GERD patients, but should be recommended in conjunction with medications.
In patients with mild or intermittent symptoms, over-the-counter antacids and H2RAs can be used intermittently or prophylactically if necessary.
PPIs have been demonstrated to be more effective than placebo or standard-dose H2RA in symptomatic relief as well as endoscopic healing of GERD. Higher doses (omeprazole, 20÷40 mg PO bid or equivalent) may be required in severe esophagitis or persistent symptoms. Continuous long-term PPI therapy is safe and effective in maintaining remission of GERD symptoms, and is recommended for patients with erosive esophagitis, Barrett's esophagus, and severe symptoms.

Standard doses of H2RAs (Table 16-1) can result in symptomatic benefit in up to 60% of patients and endoscopic healing in 50%. Higher doses of H2RAs (equivalent to ranitidine, 600 mg daily) improve the healing rate to 75% at a higher cost. Dosage adjustments are required in renal insufficiency.
Indications for fundoplication include the need for continuous or increasing doses of medication in patients who are good surgical candidates. Patients who require aggressive long-term medical therapy should be offered the surgical option. Other indications include patient preference for surgery and noncompliance with medical therapy.
The success rate of laparoscopic fundoplication in controlling GERD symptoms exceeds 90%, with fewer complications compared to the open technique. Elevated esophageal acid exposure and correlation of symptoms to reflux events on ambulatory pH monitoring predict a higher likelihood of a successful outcome.
Patients with medical treatment failures need careful evaluation to determine whether symptoms are indeed related to acid reflux before surgical options are considered; these patients often have other diagnoses including visceral hypersensitivity and functional heartburn.
Esophageal ulceration and stricture formation can occur in patients with GERD. Iron-deficiency anemia is less common.
GERD can contribute to laryngitis, laryngeal ulcers, asthma, and dental caries.
Barrett's esophagus is a change in the esophageal mucosa from normal squamous epithelium to specialized intestinal metaplastic epithelium due to longstanding acid related injury. It carries a small risk of progression to esophageal adenocarcinoma. Endoscopic surveillance for Barrett's esophagus should be considered in patients with a symptom history that exceeds 5 years.
Differential Diagnosis
Other disorders that can result in esophagitis include:

TABLE 16-1 Dosage of Acid-Suppressive Agents
Eosinophilic Esophagitis
Eosinophilic esophagitis is an idiopathic disorder characterized by eosinophilic infiltration of the esophageal mucosa, resulting in mucosal changes (furrows, corrugations, whitish plaques) as well as luminal narrowing (narrow-caliber esophagus, strictures, solid food dysphagia). Food antigens are thought to play a role in the pathogenesis. The diagnosis should be suspected in young men with solid food dysphagia, episodes of food impaction, or reflux symptoms not responsive to maximal antisecretory therapy. Mucosal biopsies during endoscopy will demonstrate marked eosinophilic infiltration. Management includes topical and systemic corticosteroids, leukotriene receptor antagonists, elimination diets, and cautious dilation of tight strictures.
Infectious Esophagitis
Infectious esophagitis is seen most often in immunocompromised states (AIDS, organ transplant recipients), esophageal stasis (abnormal motility [e.g., achalasia, scleroderma]; mechanical obstruction [e.g., strictures]), malignancy, diabetes mellitus, and antibiotic use. However, herpes simplex virus (HSV) and varicella esophagitis can occur in the normal healthy host. The presence of typical oral lesions (thrush, herpetic vesicles) may suggest an etiologic agent. The usual presenting symptoms are dysphagia and odynophagia.
Candida esophagitis results from fungal overgrowth of the esophagus, impaired cell-mediated immunity, or both. Fungal overgrowth typically occurs in the setting of esophageal stasis, impaired cell-mediated immunity from immunosuppressive therapy (e.g., with steroids or cytotoxic agents), malignancies, or AIDS. Chronic mucocutaneous candidiasis is a congenital immunodeficiency state that is also associated with Candida esophagitis.

Symptomatic relief can be achieved with 2% viscous lidocaine swish and swallow (15 mL PO q3÷4h PRN) or sucralfate slurry (1 g PO qid). Concomitant acid suppression should also be administered.
Fluconazole 100÷200 mg/d or itraconazole 200 mg/d for 14÷21 days is recommended as initial therapy for Candida esophagitis. For infections refractory to azoles, a short course of parenteral amphotericin B (0.3÷0.5 mg/kg/d) should be considered.

HSV esophagitis can be treated with acyclovir 400÷800 mg PO five times a day for 14÷21 days or 5 mg/kg IV q8h for 7÷14 days. Famciclovir and valacyclovir are alternate agents.
IV therapy with ganciclovir, foscarnet, or cidofovir are all effective for a variety of GI cytomegalovirus (CMV) infections in immunocompromised hosts (see Chapter 15, Solid Organ Transplant Medicine). Ganciclovir 5 mg/kg IV q12h or foscarnet 90 mg/kg IV q12h for 3÷6 weeks can be used as initial therapy. Oral valganciclovir may also be effective.
Chemical Esophagitis
Ingestion of caustic agents (alkalis, acids) or medications such as oral potassium, doxycycline, quinidine, iron, NSAIDs, aspirin, and bisphosphonates can result in mucosal irritation and damage.
Cautious early endoscopy is recommended to evaluate the extent and degree of mucosal damage. With caustic ingestions, the optimal time to perform endoscopy is 24÷72 hours from ingestion.
The offending medication should be discontinued if possible. Mucosal coating agents (sucralfate) and acid suppressive agents may help. A second caustic agent to neutralize the first is contraindicated.
Nonspecific Ulceration
Nonspecific ulceration can be seen with medications, malignancy, or AIDS (idiopathic ulcer).
Multiple biopsies, brushings, and culture specimens should be obtained at endoscopy.
Idiopathic ulcer of AIDS may respond to oral steroid or thalidomide therapy.
Concomitant acid suppression should always be administered.
General Principles
Achalasia is the most easily recognized motor disorder of the esophagus, characterized by failure of the lower esophageal sphincter (LES) to relax completely with swallowing and aperistalsis of the esophageal body.

Clinical Presentation
Presenting symptoms can include dysphagia, regurgitation, chest pain, weight loss, and aspiration pneumonia.
Objective Testing
Esophageal manometry is the gold standard for diagnosis. The characteristic findings include a nonrelaxing LES and aperistalsis of the esophageal body.

Barium radiographs may demonstrate a typical appearance of a dilated intrathoracic esophagus with impaired emptying, an air÷fluid level, absence of gastric air bubble, and tapering of the distal esophagus with the appearance of a bird's beak.

Endoscopy may help exclude a stricture or neoplasia of the distal esophagus; the esophageal body may be dilated and contain food debris, whereas the LES, although pinpoint, typically allows passage of the endoscope into the stomach with minimal resistance.

Smooth muscle relaxants such as nitrates or calcium channel blockers administered immediately before meals may afford short-lived symptom relief. Overall, medications are not very effective and are only indicated as temporizing measures.

Botulinum toxin injection into the LES at endoscopy can result in relief of achalasia symptoms that can last several weeks to months. This approach may be useful in elderly and frail patients who are poor surgical risks or as a bridge to more definitive therapy. Botulinum toxin injection may induce fibrosis in the region of the LES, making subsequent surgery more cumbersome.

Disruption of the circular muscle of the LES using pneumatic dilation can result in lasting reduction of LES pressure and symptomatic relief. Gastroesophageal reflux can result, treated with lifelong acid suppression. Esophageal perforation occurs in 3%÷5%, requiring prompt surgical repair.
A surgical (Heller) myotomy offers good efficacy and lasting symptom relief. It can be performed laparoscopically with minimal complications. Laparoscopic myotomy is typically combined with an antireflux procedure to prevent symptoms from acid reflux.
Complications include aspiration pneumonia and weight loss.
Achalasia is associated with a 0.15% risk of squamous cell cancer of the distal esophagus, a 33-fold higher risk relative to the nonachalasic population.
Diffuse Esophageal Spasm
General Principles
Diffuse esophageal spasm is a spastic disorder characterized by simultaneous, nonperistaltic contractions in the esophageal body.
Concomitant incomplete LES relaxation may be present. The major symptoms are dysphagia and chest pain.
Esophageal manometry is essential for diagnosis.

Barium studies may show a beaded or “corkscrew esophagus, sometimes with epiphrenic diverticula.

Smooth muscle relaxants such as nitrates and calcium channel blockers are commonly used.

Low-dose tricyclic antidepressants (TCAs) can be effective for symptom relief not only in diffuse esophageal spasm, but also in other nonspecific spastic motor disorders of the esophagus.
Botulinum toxin injection may be required for resistant cases.

Resistant cases may require empiric esophageal dilation.
Surgical myotomy is rarely indicated for patients with severe symptoms.

Esophageal Hypomotility Disorders
General Principles
Esophageal hypomotility disorders are characterized by feeble or absent esophageal peristalsis, with LES hypomotility, leading to severe GERD.
While typically idiopathic, hypomotility disorders can be associated with connective tissue diseases, Barrett's esophagus, and diabetes mellitus.
Scleroderma can cause fibrosis that results in aperistalsis and atony of the distal esophagus and LES; the esophagus is involved in 75%÷85% of cases.
Dysphagia and heartburn are the predominant symptoms.

Esophageal manometry may demonstrate weak or absent peristaltic sequences and LES hypomotility.

Barium swallow may reveal a dilated esophageal body, an open LES, and free reflux of gastric contents into the esophagus.

Endoscopy may show a dilated esophagus with gaping gastroesophageal junction and evidence of GERD.

No specific therapy exists for esophageal hypomotility from connective tissue diseases.
Acid suppression with a proton pump inhibitor is recommended for acid reflux. Fundoplication is relatively contraindicated.
Periodic dilation may be necessary for strictures.
Peptic Ulcer Disease
General Principles
Peptic ulcer disease (PUD) is characterized by breaks in the lining of the stomach and duodenum when corrosive effects of acid and pepsin overwhelm mucosal defense mechanisms. Peptic ulcers can also occur in the esophagus, in the small bowel adjacent to gastroenteric anastomoses, and within a Meckel's diverticulum.
Helicobacter pylori, a spiral, Gram-negative urease-producing bacillus, is thought to be responsible for 80% of ulcers that are not due to NSAIDs.

NSAIDs and aspirin can result in mucosal damage anywhere in the GI tract and are responsible for most peptic ulcers not due to H. pylori. Past history of PUD, age >60 years, concomitant corticosteroid or anticoagulant therapy, high-dose or multiple NSAID therapy, and presence of serious comorbid medical illnesses all increase risk for PUD.
A gastrin-secreting tumor or gastrinoma can result in uncontrolled acid secretion, and accounts for <1% of all peptic ulcers.
When none of the above etiologies is evident, the ulcer is designated idiopathic.
Cigarette smoking doubles the risk for peptic ulcers.
Clinical Presentation
Epigastric pain or dyspepsia may be presenting symptoms; however, symptoms are not always predictive of the presence of ulcers.
Epigastric tenderness may be elicited on abdominal palpation.
Ten percent may present with a complication. The important complications are gastrointestinal bleeding, perforation, penetration, and gastric outlet obstruction.
In the presence of alarm symptoms (weight loss, early satiety, bleeding, anemia, and lack of appropriate response to acid suppression), endoscopy is indicated to evaluate for a complication or an alternate diagnosis.
Endoscopy is the gold standard for diagnosis of peptic ulcers.

Barium studies also have good sensitivity for diagnosis of ulcers, but smaller ulcers and erosions may be missed; further, biopsies cannot be taken.

Serum H. pylori antibody testing is the cheapest noninvasive test for diagnosing H. pylori infection; the antibody remains detectable as long as 18 months after successful eradication, and therefore this test cannot be used to document successful eradication of the organism.

Stool H. pylori antigen testing also has high sensitivity and specificity for the diagnosis of H. pylori infection. This test can be used to confirm eradication of H. pylori after triple therapy.

Rapid urease assay (Campylobacter-like organism [CLO] test) and histopathologic examination of endoscopic biopsy specimens are commonly used for diagnosis in patients undergoing endoscopy; these tests may be falsely negative in patients on PPI therapy.

Carbon-labeled urea breath testing is the most accurate noninvasive test for diagnosis. This test is often used to document successful eradication after therapy in patients with ongoing dyspeptic symptoms or complicated ulcer disease.

Regardless of etiology, acid suppression forms the mainstay of therapy of PUD. Gastric ulcers are typically treated for 12 weeks, and duodenal ulcers for 8 weeks.
Oral PPI or H2RA therapy will suffice in most instances; parenteral administration of PPIs may be necessary, especially in the presence of GI bleeding or when oral administration is not tolerated or not possible (see Table 16-1). Dosage intervals should be prolonged for H2RAs in the presence of renal insufficiency. Side effects are uncommon, but headache and mental status abnormalities (lethargy, confusion, depression, hallucinations) can result from H2RA therapy; abdominal pain and diarrhea are common side effects of PPI therapy. Rare hepatotoxicity, thrombocytopenia, and leukopenia have been observed with H2RA use. Cimetidine can impair metabolism of many drugs, including warfarin anticoagulants, theophylline, and phenytoin (see Appendix C).
Sucralfate acts by coating the mucosal surface without blocking acid secretion and can be as effective as H2RAs or high-dose antacids in healing duodenal ulcers. Side effects include constipation and reduction of bioavailability of certain drugs (e.g., cimetidine, digoxin, fluoroquinolones, phenytoin, and tetracycline) when administered concomitantly.

Antacids are rarely used as primary therapy for PUD but can be useful as supplemental therapy for pain relief. The choice of antacid is determined by buffering capacity, formulation, and side effects. A typical dose is 30 mL of a high-potency liquid antacid, administered four to six times a day. Magnesium-containing antacids should be avoided in renal failure.

Antimicrobial therapy in addition to antisecretory medication for eradication of H. pylori promotes healing and markedly reduces recurrence of gastric and duodenal ulcers. Several antimicrobial and antisecretory agent regimens are available (Table 16-2), and eradication is recommended in all H. pylori÷infected patients with PUD. Metronidazole resistance (predominantly in females and patients of Asian descent) and poor compliance with therapy may affect eradication rates.

Nonpharmacologic measures. Dietary modification should only include the avoidance of foods that are reproducibly associated with dyspeptic symptoms. Cigarette smoking doubles the risk of peptic ulcer development, delays healing, and promotes recurrence; therefore, cessation of cigarette smoking should be encouraged in all instances. Alcohol in high concentrations can damage the gastric mucosal barrier, but no evidence exists to link alcohol with ulcer recurrence.

NSAIDs and aspirin should be avoided if possible.
Surgery is still occasionally required for intractable symptoms, GI bleeding, Zollinger-Ellison syndrome, and other complications of PUD. Surgical options vary depending on the location of the ulcer and the presence of associated complications.
Significant morbidity can occur after surgical therapy of PUD, and adequate therapy requires a thorough understanding of the postsurgical complications.
EGD or upper GI series should be performed 8÷12 weeks after initial diagnosis of all gastric ulcers to document healing; repeat endoscopic biopsy should be considered for nonhealing ulcers to exclude the possibility of a malignant ulcer.
Duodenal ulcers are almost never malignant, and therefore documentation of healing is unnecessary in the absence of symptoms.
GI bleeding (see Gastrointestinal Bleeding)

TABLE 16-2 Examples of Regimens Used for Eradication of Helicobacter pylori
Gastric outlet obstruction is more likely to occur with ulcers that are close to the pyloric channel. Nausea and vomiting, sometimes several hours after meals, may occur. Plain abdominal radiographs often show a dilated stomach with an air÷fluid level. NG suction should be maintained for 2÷3 days to decompress the stomach while repleting fluids and electrolytes intravenously.

Although medical management may be temporarily effective, recurrence is common, and endoscopic balloon dilation or surgery is often necessary for definitive correction.
Perforation occurs in a small number of PUD patients and usually necessitates emergency surgery. Perforation may occur in the absence of previous symptoms of PUD, and may be asymptomatic in patients who are receiving glucocorticoids. A plain upright radiograph of the abdomen may demonstrate free air under the diaphragm.

Pancreatitis can result from penetration into the pancreas, most commonly seen with ulcers in the posterior wall of the duodenal bulb. The pain becomes severe and continuous, radiates to the back, and is no longer relieved by antisecretory therapy. Serum amylase may be elevated. Computed tomography (CT) scanning may be diagnostic. These patients frequently require surgery.

Postsurgical Complications
Abdominal symptoms. Postoperative abdominal discomfort or vomiting after meals can be secondary to recurrent ulcer, afferent loop obstruction, bile reflux gastritis, gastric outlet obstruction, or stump carcinoma (a late complication). Dumping syndrome is caused by rapid gastric emptying of a large osmotic load into the small intestine and occurs after gastroenteric anastomosis with or without subtotal gastrectomy, vagotomy, and pyloroplasty.

Early dumping syndrome occurs 15÷30 minutes after eating and is due to osmotic fluid shifts into the gut lumen. Symptoms can be abdominal (nausea, vomiting, abdominal pain) or vasomotor (palpitations, sweating, dizziness).

Late dumping syndrome consists of similar symptoms 2÷4 hours after meals, due to excessive serum insulin response to rapid delivery and absorption of sugars from the small intestine.

Dietary modification to multiple small meals high in protein and low in refined carbohydrates can be beneficial; liquids with meals should be avoided. Anticholinergics, fiber supplements, and ephedrine may relieve the vasomotor symptoms. In refractory situations, SC administration of octreotide may be necessary.
Malabsorption. Mild steatorrhea can occur as a result of decreased intestinal transit time and inadequate mixing of food with bile and pancreatic secretions. Bacterial overgrowth due to afferent loop stasis can also lead to steatorrhea (see Other Gastrointestinal Disorders).

Anemia. Deficiencies of folate, vitamin B12, and iron can lead to anemia. Postoperative iron-deficiency anemia is usually a result of dietary iron malabsorption, but blood loss from gastritis or recurrent ulcers may contribute.

Special Considerations
Zollinger-Ellison syndrome is caused by a gastrin-secreting, non-β islet cell tumor of the pancreas or duodenum. Multiple endocrine neoplasia type I can be associated with this syndrome in 25% of patients. The resultant hypersecretion of gastric acid can cause multiple peptic ulcers in unusual locations, ulcers that fail to respond to standard medical therapy, or recurrent ulceration after surgical therapy. Diarrhea and gastroesophageal reflux symptoms are common.

Gastric acid output is typically >15 mEq/L, and gastric pH <1.0. A fasting serum gastrin level while off acid suppression for at least 5 days serves as a screening test; a value >1,000 pg/mL is seen in 90% of patients. When serum gastrin is elevated but <1,000 pg/mL, a secretin stimulation test may demonstrate a paradoxical 200-pg increment in serum gastrin level after IV secretin in patients with gastrinomas. PPIs are generally required in higher doses than those used for PUD. Specialized nuclear medicine scans (octreotide scans) can be useful in localizing the neoplastic lesion for curative resection.
Inflammatory Bowel Disease
General Principles
Ulcerative colitis (UC) is an idiopathic chronic inflammatory disease of the colon and rectum, characterized by mucosal inflammation and typically presenting with bloody diarrhea. Rectal involvement is almost universal.

Crohn's disease is characterized by transmural inflammation of the gut wall and can affect any part of the tubular GI tract.

Clinical Presentation
Both disorders can present with diarrhea, weight loss, and abdominal pain. Ulcerative colitis typically presents with bloody diarrhea. Crohn's disease can also present with fistula formation, strictures, abscesses, or bowel obstruction.
Endoscopy and imaging studies are useful diagnostic modalities.
5-Aminosalicylic acid (ASA) compounds
Sulfasalazine reaches the colon intact, where it is metabolized to 5-ASA and a sulfapyridine moiety. It is therefore used for colonic disease (UC and Crohn's disease limited to the colon), either as initial therapy (0.5 g PO bid, increased as tolerated to 0.5÷1.5 g PO qid) or to maintain remission (1 g PO bid÷qid).

Adverse effects are mainly caused by the sulfapyridine moiety and include headache, nausea, vomiting, and abdominal pain; a reduction in dose may be beneficial.
Hypersensitivity reactions are less common and include skin rash, fever, agranulocytosis, hepatotoxicity, and aplastic anemia. Reversible reduction in sperm counts can be seen in males. Paradoxic exacerbation of colitis is a rare adverse effect.
Folic acid supplementation is recommended, as sulfasalazine impairs folate absorption.
Newer 5-ASA preparations lack the sulfa moiety of sulfasalazine and are associated with fewer side effects.

Mesalamine (5-ASA) is available in several formulations. An oral preparation released at pH >7 (Asacol, 800÷1,600 mg PO tid) is useful in UC as well as ileocecal/colonic Crohn's disease. A second preparation, balsalazide (Colazal, 2.25 g PO tid for active disease, 1.5 g PO bid for maintenance), is cleaved by colonic bacteria to mesalamine and an inert carrier molecule and is useful for colonic inflammation. A third preparation with time- and pH-dependent release of the active ingredient throughout the GI tract (Pentasa, 0.5÷1.0 g PO qid) is useful in diffuse Crohn's disease that also affects the small bowel; it can be used in UC as well. Rare hypersensitivity reactions occur and include pneumonitis, pancreatitis, hepatitis, and nephritis. Mesalamine preparations can be used for initiation and maintenance therapy.

Olsalazine is a 5-ASA dimer that is cleaved by bacteria in the colon and can be used in UC and Crohn's colitis. Diarrhea is a major side effect and can limit its use.

Glucocorticoids are beneficial in inducing remission of active UC and Crohn's disease. They are not recommended for mild disease; they can be used concurrently with other anti-inflammatory agents in moderate to severe disease, especially with flare-ups of disease activity. Extracolonic manifestations of inflammatory bowel disease (ocular lesions, skin disease, and peripheral arthritis) also respond to glucocorticoids.

A typical starting oral dose of prednisone is 40÷60 mg given once a day in the morning. Depending on response, the dose can be reduced by 10 mg every 5÷10 days and tapered off in 3÷6 weeks. In severe disease or in patients who cannot tolerate oral medication, IV administration (methylprednisolone, 20÷40 mg daily to bid, up to 1 mg/kg/d) may be necessary for brief periods; higher doses are used in refractory disease. Glucocorticoids are not recommended for maintenance therapy, and alternatives should be sought for the patient who appears dependent on these medications.
Oral or parenteral glucocorticoids should not be prescribed before ruling out an infectious process and should not be initiated for the first time over the telephone.
Budesonide (Entocort, 9 mg/d) may have less systemic side effects compared to glucocorticoids when used for mild to moderate ileocolonic Crohn's disease.

Immunosuppressive agents
6-Mercaptopurine, a purine analog, and azathioprine, its S-imidazole precursor, cause preferential suppression of T-cell activation and antigen recognition. They are used orally in doses of 1.0÷1.5 mg/kg body weight daily. Both agents have more favorable side effect profiles than do glucocorticoids and are used as steroid-sparing agents in severe or refractory inflammatory bowel disease (IBD). Response may be delayed for up to 1÷2 months. Side effects include reversible bone marrow suppression, pancreatitis, and allergic reactions.

Methotrexate (15÷25 mg IM or PO weekly) has also been used as a steroid-sparing agent in Crohn's disease. Side effects include hepatic fibrosis, bone marrow suppression, alopecia, pneumonitis, allergic reactions, and teratogenicity.

IV cyclosporine has been used in refractory cases of UC; however, the benefit is temporary. Side effects include nephrotoxicity, hepatotoxicity, hypertrichosis, seizures, and lymphoproliferative disorders.
Metronidazole (250÷500 mg PO tid) can be used as an alternate first-line agent or adjunctive therapy in mild to moderate Crohn's disease. Peripheral neuropathy is a concern with long-term use.

Ciprofloxacin (500 mg PO bid) has also been used in Crohn's disease. The two agents can be used concurrently in perianal Crohn's disease for prolonged periods with good results.

An alternative agent that is sometimes used is sulfamethoxazole-trimethoprim.
Infliximab (Remicade) is a monoclonal antibody against tumor necrosis factor-α that induces inflammatory cell lysis by binding to tumor necrosis factor receptors on the cell surface. Infliximab (IV infusions of 5 mg/kg) is used for therapy of fistulous Crohn's disease, refractory inflammatory-type Crohn's disease unresponsive to conventional therapy, and more recently, severe ulcerative colitis.

Induction regimens typically consist of doses at 0, 2, and 6 weeks, with maintenance doses every 8 weeks. Congestive heart failure may worsen after therapy.
Sepsis and reactivation of latent tuberculosis or histoplasmosis may occur; a tuberculin test may be indicated to evaluate for latent tuberculosis.
Serious infusion reactions may occur, and constant monitoring is essential during infusion.
Sargramostim (granulocyte macrophage colony stimulation factor [GM-CSF], 6 mcg/kg/day SC for continuous periods of up to 2 months) may benefit patients with refractory Crohn's disease by stimulating the innate immune system in the gastrointestinal tract. Side effects can include injection site reactions and bone pain.

Local therapy. UC that is limited to the rectum or distal left colon can be treated effectively with 5-ASA and/or glucocorticoid enemas or suppositories administered once to twice a day; concurrent systemic therapy may be required in severe cases. Symptomatic benefit may be achieved in perianal Crohn's disease with sitz baths, analgesic, and hydrocortisone creams and local heat, in addition to systemic anti-inflammatory agents and antibiotics.

Antidiarrheal agents may be useful as an adjunctive therapy in selected patients with mild exacerbations or postresection diarrhea. They are contraindicated in severe exacerbations and toxic megacolon.

Other measures. A low-roughage diet often provides symptomatic relief in patients with mild to moderate disease or in patients with strictures. Elemental diets have been used in acute phases of the diseases, especially Crohn's disease, but are unpalatable and disliked by patients.

Total parenteral nutrition and bowel rest may be required in severe disease, for nutritional maintenance and symptom relief while waiting for the effects of medical treatment, or as a bridge to surgery.

Patients with Crohn's ileitis or ileocolonic resection may need vitamin B12 supplementation. Specific oral replacement of calcium, magnesium, folate, iron, vitamins A and D, and other micronutrients may be necessary in patients with small-bowel Crohn's disease.
Surgery is generally reserved for patients with fistulas, obstruction, abscess, perforation, or bleeding, and rarely for medically refractory disease and neoplastic transformation.
Recurrence close to the resected margins is common after bowel resection. Efforts should be made to avoid multiple resections in Crohn's disease because of the risk of short-bowel syndrome. Immunosuppressive agents should be discontinued before surgery and reinstituted if necessary during the postoperative period.
Special Considerations
Colon cancer surveillance. In patients with colitis lasting longer than 8÷10 years (both UC and Crohn's colitis), annual colonoscopic surveillance for neoplasia with four-quadrant mucosal biopsies every 5÷10 cm is recommended. Histopathologic evidence of any grade of dysplasia is an indication for total colectomy.

Intestinal obstruction. Stricture formation can result in intestinal obstruction in Crohn's disease. Presentation may resemble a flare, and a careful history, physical examination, and imaging studies are essential for diagnosis. NG tube decompression, parenteral hydration, and bowel rest may resolve minor episodes, but surgery may be necessary. Stricturoplasty is an accepted procedure for focal tight strictures; biopsies should be obtained to rule out cancer at stricture sites. Patients with intermittent obstructive symptoms should avoid highly indigestible foods such as nuts, pits, hulls, skins, seeds, and pulps that may precipitate obstruction.

Fulminant colitis and toxic megacolon. Acute fulminant colitis presents as severe diarrhea with abdominal pain, bleeding, fever, sepsis, electrolyte disturbances, and dehydration. Toxic megacolon occurs in 1%÷2% of patients with UC; the colon becomes atonic and modestly dilates, but systemic toxicity is the dominant feature.

Patients should be kept NPO, with NG suction if there is evidence of small-bowel ileus.
Dehydration and electrolyte disturbances should be treated vigorously.
Anticholinergic and opioid medication should be discontinued.
Intensive medical therapy with IV corticosteroids (hydrocortisone, 100 mg IV q6h or equivalent) and broad-spectrum antimicrobials should be initiated.
Clinical deterioration/lack of improvement despite 7÷10 days of intensive medical management, evidence of bowel perforation, or peritoneal signs are indications for urgent total colectomy.
Functional Gastrointestinal Disorders
General Principles
Functional GI disorders are characterized by the presence of abdominal symptoms in the absence of a demonstrable organic disease process. Symptoms can arise from any part of the luminal gut.
Irritable bowel syndrome (IBS), primarily characterized by abdominal pain linked to altered bowel habits, is the best-recognized functional bowel disease and the most commonly diagnosed GI illness.

Clinical evaluation and investigation should be directed toward prudently excluding organic processes in the involved area of the gut while initiating therapeutic trials when functional symptoms are suspected.
Older patients with new-onset bowel symptoms, patients with longstanding symptoms or symptoms not responsive to empiric therapy, and patients with alarm symptoms (gastrointestinal bleeding, anemia, weight loss, early satiety) need further workup with endoscopy and imaging studies.
In young individuals with short-lived symptoms and no other explanation for dyspepsia, noninvasive testing for H. pylori (serology or urea breath test) can be considered.
Nonspecific Measures
Patient education, reassurance, and help with diet and lifestyle modification are key to an effective physician÷patient relationship. The psychosocial contribution to symptom exacerbation should be determined, and its management may be sufficient for many patients.
Low-dose TCAs (e.g., amitriptyline, nortriptyline, imipramine, doxepin: 25÷100 mg at bedtime) have neuromodulatory and analgesic properties that are independent of their psychotropic effects and can be beneficial, especially in pain-predominant functional GI disorders.
Selective serotonin reuptake inhibitors (e.g., fluoxetine, 20 mg; paroxetine, 20 mg; sertraline, 50 mg, duloxetine 20÷60 mg) are less effective but have better side effect profiles.

Symptomatic management
Antiemetic agents are useful in functional nausea and vomiting syndromes, in addition to neuromodulators.

When pain and bloating are the predominant symptoms, antispasmodic or anticholinergic medications (hyoscyamine, 0.125÷0.25 mg PO/sublingual up to qid; dicyclomine, 10÷20 mg PO qid) may be beneficial.
Constipation-predominant IBS may benefit from increased dietary fiber (25 g/d) supplemented with laxatives PRN.
Loperamide (2÷4 mg, up to qid/PRN) can reduce stool frequency, urgency, and fecal incontinence.

Newer 5-HT4 receptor agonists such as tegaserod (Zelnorm, 6 mg bid) may be useful in women with constipation-predominant IBS, but studies in men are inconclusive.
Alosetron (Lotronex, 1 mg daily to bid), a 5-HT3 antagonist, is useful in women with diarrhea-predominant IBS; its use is restricted to women with symptoms refractory to other measures because of the potential for ischemic colitis in a small proportion of patients.

Patients with cyclic vomiting syndrome (stereotypic episodes of vigorous vomiting with asymptomatic intervals between episodes) benefit from treatment with low-dose TCAs or antiepileptic medications (Zonegran, Keppra) as maintenance options. Anecdotal evidence suggests that these patients may also benefit from sumatriptan (25÷50 mg PO, 5÷10 mg transnasally, or 6 mg SC at the beginning of an episode), especially if it is administered during a prodrome or early in the episode.
Acute Intestinal Pseudo-Obstruction (Ileus)
General Principles
Acute intestinal pseudo-obstruction or ileus consists of obstructive symptoms (nausea, vomiting, abdominal distension, lack of bowel movements) and intestinal dilation on imaging studies without a mechanical explanation.

Ogilvie syndrome or acute colonic pseudo-obstruction describes colonic dilation without a mechanical obstruction in the presence of a competent ileocecal valve, which may be complicated by cecal rupture when dilation is rapid or massive.

Predisposing causes include virtually any medical insult, particularly life-threatening systemic diseases, infection, vascular insufficiency, surgery, and electrolyte abnormalities.
A careful history and physical exam are essential in the initial evaluation of these patients.
Conventional laboratory studies (blood count, complete metabolic profile, amylase, lipase) help in assessing for a primary intra-abdominal inflammatory process.
Obstructive series (supine and upright abdominal radiograph with a chest radiograph) determines the distribution of intestinal gas and assesses for the presence of free intraperitoneal air.

Additional imaging studies may be required to assess for mechanical obstruction and inflammatory processes and include CT scanning, contrast enema, and small-bowel series.

Nonspecific Measures
Basic supportive measures consist of nothing by mouth (NPO), fluid replacement, and correction of electrolyte imbalances. Prompt antimicrobial therapy is indicated if an infectious process is suspected. Medications that slow GI motility (adrenergic agonists, TCAs, sedatives, narcotic analgesics) should be withdrawn or doses reduced. The ambulatory patient is encouraged to remain active and to undertake short walks.
Intermittent NG suction prevents swallowed air from passing distally. In protracted cases, gastric decompression, either using an NG tube or a percutaneous endoscopic gastrotomy tube, eliminates upper GI secretions and decreases vomiting and gastric distension.

Rectal tubes help decompress the distal colon; more proximal colonic distension may necessitate colonoscopic decompression, especially when the cecal diameter approaches 9÷10 cm. A flexible decompression tube can be left in the proximal colon during colonoscopy. Turning the patient from side to side may potentiate the benefit of colonoscopic decompression.

Temporary total parenteral nutrition may be required in protracted cases.
Neostigmine (2 mg IV administered slowly over 3÷5 minutes) is beneficial in selected patients with acute colonic distension. The drug can induce rapid re-establishment of colonic tone and is contraindicated if mechanical obstruction remains in the differential diagnosis. Side effects include abdominal pain, excessive salivation, symptomatic bradycardia, and syncope. A trial of neostigmine may be warranted before colonoscopic decompression in patients without contraindications.

Erythromycin (200 mg IV) acts as a motilin agonist and stimulates upper gut motility; it has been used with some success in refractory postoperative ileus.

Guanethidine, bethanechol, and metoclopramide have all been used with mixed results.

Surgical consultation is required when the clinical picture is suggestive of mechanical obstruction or if peritoneal signs are present.

Cecostomy is rarely required when colonoscopic decompression fails in acute colonic distension.

Surgical exploration is reserved for acute cases with peritoneal signs, ischemic bowel changes, or other evidence for perforation.
Pancreaticobiliary Disorders
Acute Pancreatitis
General Principles
Acute pancreatitis is inflammation of the pancreas and peripancreatic tissue from activation of potent pancreatic enzymes within the pancreas, particularly trypsin.
The most common causes are alcohol and gallstone disease. Less common causes include abdominal trauma, hypercalcemia, hypertriglyceridemia, and a variety of drugs. Postendoscopic retrograde cholangiopancreatography (ERCP) pancreatitis occurs in 5%÷10% of patients undergoing ERCP.
Dual-phase (pancreatic protocol) CT scanning is useful in the initial evaluation of severe acute pancreatitis. The Ranson criteria (Table 16-3) may provide prognostic information.

General Measures
Aggressive volume repletion with IV fluids must be undertaken, with careful monitoring of fluid balance and awareness of the potential for significant fluid sequestration within the abdomen. Serum electrolytes, calcium, and glucose levels should be monitored and supplemented as necessary. Patients with severe pancreatitis and hemodynamic instability often require admission to the ICU.

TABLE 16-3 Ranson Criteria for Severity Assessment in Acute Pancreatitisa
Urine output, hemodynamics, and laboratory parameters help assess adequacy of volume repletion.
Patients should receive nothing by mouth until they are free of pain and nausea. NG suction is reserved for patients with ileus or protracted emesis. Total parenteral nutrition (TPN) may be necessary when inflammation is slow to resolve. Enteral nutrition through a tube placed distal to the ligament of Treitz is usually tolerated, and may be safer than TPN.
Acid suppression may be necessary in severely ill patients with risk factors for stress ulcer bleeding (see Gastrointestinal Bleeding).

Narcotic analgesics are usually necessary for pain relief.

Meperidine is the most commonly used agent. Though morphine is frequently avoided, there is no conclusive evidence that morphine has deleterious effects on sphincter of Oddi pressure. Patient-controlled analgesia is frequently necessary for adequate relief of pain.

Endoscopic Therapy
Urgent ERCP and biliary sphincterotomy within 72 hours of presentation can improve the outcome of severe gallstone pancreatitis in the presence of elevated liver numbers and/or a dilated common bile duct. This is thought to result from reduced biliary sepsis rather than true improvement of pancreatic inflammation.
Necrotizing pancreatitis represents a severe form of acute pancreatitis, usually identified on dynamic dual-phase CT scanning with IV contrast. The presence of radiologically identified pancreatic necrosis increases the morbidity and mortality of acute pancreatitis. Increasing abdominal pain, fever, marked leukocytosis, and bacteremia suggest infected pancreatic necrosis that requires broad-spectrum antibiotics and often surgical debridement. CT-guided percutaneous aspiration for Gram stain and culture can confirm the diagnosis of infected necrosis.

The presence of pseudocysts is suggested by persistent pain or hyperamylasemia. Complications include infection, hemorrhage, rupture (pancreatic ascites), and obstruction of adjacent structures. Generally, asymptomatic nonenlarging pseudocysts can be followed clinically with serial imaging studies. Decompression of symptomatic, rapidly enlarging, or complicated pseudocysts can be performed by percutaneous, endoscopic, or surgical techniques.
Infection. Potential sources of fever include pancreatic necrosis, abscess, infected pseudocyst, cholangitis, and aspiration pneumonia. Cultures should be obtained, and broad-spectrum antimicrobials that are appropriate for bowel flora should be administered. In the absence of fever or other clinical evidence for infection, prophylactic antimicrobial therapy has no clear role in acute pancreatitis.

Pulmonary complications. Atelectasis, pleural effusion, pneumonia, and acute respiratory distress syndrome can develop in severely ill patients (see Chapter 9, Pulmonary Disease).

Renal failure. Severe intravascular volume depletion or acute tubular necrosis can cause renal failure.

Other complications. Metabolic complications include hypocalcemia, hypomagnesemia, and hyperglycemia. Gastrointestinal bleeding can result from stress gastritis, pseudoaneurysm rupture, or gastric varices from splenic vein thrombosis.

Gallstone Disease
General Principles
Asymptomatic cholelithiasis is a common incidental finding for which no specific therapy is generally necessary.

Symptomatic cholelithiasis, when upper abdominal symptoms are thought to be related to the presence of gallstones, is typically treated surgically with cholecystectomy.

Acute cholecystitis is caused most often by obstruction of the cystic duct by gallstones, but acalculous cholecystitis can occur in severely ill or hospitalized patients.

Clinical Presentation
Cholelithiasis may present as biliary colic, a constant pain lasting for hours, located in the right upper quadrant, radiating to the back or right shoulder, and sometimes associated with nausea or vomiting.
Other presentations of gallstone disease include acute cholecystitis, acute pancreatitis, and cholangitis. Gallstone disease may rarely be associated with gallbladder cancer.
Patients with acute ascending cholangitis present with right upper quadrant pain, fever with chills, and jaundice (Charcot's triad), usually in the setting of biliary obstruction (choledocholithiasis, neoplasia, sclerosing cholangitis, biliary stent occlusion). Elderly patients may lack abdominal symptoms.
Ultrasound scans have a high degree of accuracy in diagnosis.

Hydroxyiminodiacetic acid (HIDA) scan can demonstrate nonfilling of the gallbladder in patients with acute cholecystitis.
Cholecystectomy is the therapy of choice for symptomatic gallstone disease and acute cholecystitis. Laparoscopic cholecystectomy compares favorably with the open procedure, with lower morbidity, shorter hospital stay, and better cosmetic results.

Supportive measures include IV fluid resuscitation and broad-spectrum antimicrobial agents, especially in the event of complications such as acute cholecystitis with sepsis, perforation, peritonitis, abscess, or empyema formation.

Percutaneous cholecystotomy and decompression of the gallbladder can be performed under fluoroscopy in severely ill patients with acute cholecystitis who are not surgical candidates.
Ursodeoxycholic acid (8÷10 mg/kg/d PO in two to three divided doses for prolonged periods) might be prudent in a small select group of patients with small cholesterol stones in normally functioning gallbladders who are at high risk for complications from surgical therapy. Side effects include diarrhea and reversible elevation in serum transaminase levels.

Another option is percutaneous instillation of contact solvents such as methyl-tertiary-butyl ether into the gallbladder and extracorporeal shock-wave lithotripsy combined with oral bile acid dissolution therapy. Experience with these therapies is limited, and neither is definitive as the gallbladder remains in place.
Acute pancreatitis. See section on acute pancreatitis above.

Choledocholithiasis. In patients who have undergone cholecystectomy, retained common bile duct stones can complicate the postoperative course. Common bile duct obstruction, jaundice, biliary colic, cholangitis, or pancreatitis can result. The diagnosis can be made on ultrasonography, CT scanning, or magnetic resonance cholangiography. ERCP with sphincterotomy and stone extraction is curative.

Acute ascending cholangitis can present with right upper quadrant pain, fever with chills, and jaundice (Charcot's triad), usually in the setting of biliary obstruction (choledocholithiasis, neoplasia, sclerosing cholangitis, biliary stent occlusion). Cholangitis represents a medical emergency with high morbidity and mortality if biliary decompression

is not performed urgently. The condition should be stabilized with IV fluids and broad-spectrum antibiotics. Drainage of the biliary tree can be performed through the endoscopic (ERCP with sphincterotomy) or percutaneous approach under fluoroscopic guidance.
Chronic Pancreatitis
General Principles
Chronic pancreatitis represents changes resulting from recurrent acute or chronic inflammation of the pancreas. This is commonly seen with chronic alcohol abuse.
Endocrine insufficiency may result from destruction of islet cells.

Clinical Presentation
Pain, exocrine insufficiency (manifesting as weight loss and steatorrhea), and endocrine insufficiency (manifesting as brittle diabetes) are the main clinical manifestations.

Laboratory Studies
In the presence of steatorrhea, a serum trypsinogen level of <10 ng/mL is diagnostic of chronic pancreatitis.
Narcotic analgesics are frequently required for control of pain, and narcotic dependence is common. In patients with mild to moderate exocrine insufficiency, the addition of oral pancreatic enzyme supplements may be beneficial for pain control.

Pancreatic enzyme supplements are the mainstay of management of pancreatic exocrine insufficiency, in conjunction with a low-fat diet (<50 g fat/d). Enteric-coated preparations (Pancrease or Creon, one to two capsules with meals) are stable at acid pH and should not be given with concomitant acid suppression.

Fat-soluble vitamin supplementation may be necessary.
Insulin therapy is generally required for endocrine insufficiency, as the resultant diabetes mellitus is characteristically brittle.

Patients with pancreatic duct obstruction from stones, strictures, or papillary stenosis may benefit from ERCP and sphincterotomy.
Intractable pain may necessitate celiac ganglion block or even surgery.
Dysphagia and Odynophagia
General Principles
Oropharyngeal dysphagia: Difficulty in transferring food from the mouth to the esophagus, often associated with symptoms of nasopharyngeal regurgitation and pulmonary aspiration.

Esophageal dysphagia: The sensation of difficulty in passage of food down the esophagus.

Odynophagia: Pain on swallowing food and fluids; may indicate the presence of esophagitis, particularly infectious esophagitis and pill esophagitis.

Oropharyngeal dysphagia is typically caused by neuromuscular or structural disorders involving the oropharynx and proximal esophagus.

Esophageal dysphagia can occur from an obstructive process in the esophagus. Progressive dysphagia may be seen with neoplasia, while intermittent symptoms can result from webs or rings. Acute onset of dysphagia in temporal relationship to a meal may suggest food impaction. In the absence of a structural obstructive process, esophageal manometry may be necessary to exclude a motility disorder (achalasia, diffuse esophageal spasm).

Oropharyngeal Dysphagia
Assessment is initiated with a detailed neurologic exam.
Barium videofluoroscopy (modified barium swallow) evaluates the oropharyngeal swallow mechanism, and may identify laryngeal penetration.
Ear, nose, and throat exam including flexible nasal endoscopy may identify structural etiologies.
Imaging studies (CT scans) may demonstrate a structural process.
Laboratory tests for polymyositis, myasthenia gravis, and other neuromuscular disorders can be considered.
Esophageal Dysphagia
Endoscopy is typically used for initial investigation of esophageal dysphagia. Endoscopy provides information on mucosal abnormalities, allows tissue sampling, and offers the option of dilation if a narrowing is seen.
Barium swallow is also a suitable initial test for esophageal dysphagia, although biopsies and esophageal dilation require endoscopy. Subtle rings and webs may not be visualized unless a barium swallow is performed using a solid bolus or a barium pill.
Esophageal manometry can characterize esophageal motor disorders when other studies are normal or suggest a motility disorder.
Acute esophageal obstruction is best investigated with endoscopy.
General Measures
Modification of diet and swallowing maneuvers may benefit patients with dysphagia, especially oropharyngeal dysphagia.
Enteral feeding through a gastrostomy tube may be indicated in patients with frank tracheal aspiration on attempted swallowing.
Endoscopic retrieval of an obstructing food bolus can result in dramatic resolution of acute dysphagia from food impaction.
Nutrition needs to be addressed in patients with prolonged dysphagia causing weight loss; patients with dysphagia are typically advised to chew their food well and eat foods of soft consistencies.
Mucosal inflammation from reflux disease can be treated with acid suppression, typically with a PPI.
Odynophagia generally responds to specific therapy of the condition causing esophagitis (e.g., PPIs for reflux disease, antimicrobial agents for infectious esophagitis). Viscous lidocaine swish-and-swallow solutions may afford symptomatic relief.
Patients with oropharyngeal dysphagia and drooling of saliva can be treated with anticholinergic medication (e.g., transdermal scopolamine).
Glucagon (2- to 4-mg IV bolus) can be attempted in patients with acute dysphagia from food impaction, but is frequently unsuccessful. Sublingual nitroglycerin can also be given, but meat tenderizer should not be administered.

Endoscopic Therapy
Esophageal dilation is performed for anatomic narrowings visualized during endoscopy. Empiric dilation is sometimes performed even when a defined narrowing is not identified, and may result in symptomatic benefit.
Aggressive pneumatic dilation of the LES is sometimes performed for achalasia, but laparoscopic myotomy is gaining popularity over pneumatic dilation. Botulinum toxin injections to the LES may result in temporary symptom relief in achalasia.
Esophageal stent placement can alleviate dysphagia in inoperable neoplasia.
Nausea and Vomiting
General Principles
Nausea and vomiting may result from side effects of medications, systemic illnesses, central nervous system (CNS) disorders, and primary GI disorders.
Vomiting that occurs during or immediately after a meal can result from a pyloric channel ulcer or from functional disorders.
Vomiting within 30÷60 minutes after a meal may suggest gastric or duodenal pathology.
Delayed vomiting after a meal with undigested food from a previous meal can suggest gastric outlet obstruction or gastroparesis.
Bowel obstruction and pregnancy should be ruled out.
The patient's medication list should be scrutinized.
General Measures
Correction of fluid and electrolyte imbalances is an important supportive measure.
Oral intake should be withheld or limited to clear liquids. Many patients with self-limited illnesses require no further therapy.
NG decompression may be required for patients with bowel obstruction or protracted nausea and vomiting of any etiology.
Patients with protracted nausea and vomiting may sometimes require enteral feeding through jejunal tubes, or rarely even total parenteral nutrition.
Empiric pharmacotherapy is often initiated while investigation is in progress, or when the etiology is thought to be self-limited.
Phenothiazines and related agents. Prochlorperazine (Compazine), 5÷10 mg PO tid÷qid, 10 mg IM or IV q6h, or 25 mg PR bid; promethazine (Phenergan), 12.5÷25.0 mg PO, IM, or PR q4÷6h; and trimethobenzamide (Tigan), 250 mg PO tid÷qid, 200 mg IM tid÷qid, or 200 mg PR tid÷qid are effective. Drowsiness is a common side effect, and acute dystonic reactions or other extrapyramidal effects may occur.

Dopamine antagonists include metoclopramide (10 mg PO 30 minutes before meals and at bedtime), a prokinetic agent that also has central antiemetic effects. IV metoclopramide

can be used in nausea and vomiting associated with chemotherapy (see Chapter 20, Medical Management of Malignant Disease). Metoclopramide can also be tried in chronic cases where dysmotility of the upper GI tract is thought to play a significant role in symptoms. Drowsiness and extrapyramidal reactions may occur; tachyphylaxis may limit long term efficacy. Domperidone is an alternate agent that does not cross the blood-brain barrier and therefore has no CNS side effects; however, it is not uniformly available.
Antihistaminic agents are most useful for nausea and vomiting related to motion sickness, but may also be useful for other causes. Agents used include diphenhydramine (Benadryl, 25÷50 mg PO q6÷8h, or 10÷50 mg IV q2÷4h), dimenhydrinate (Dramamine, 50÷100 mg PO or IV q4÷6h), and meclizine (Antivert, 12.5÷25 mg 1 hour before travel).

Serotonin 5-HT3 receptor antagonists. Ondansetron (Zofran, 0.15 mg/kg IV q4h for three doses or 32 mg IV infused over 15 minutes beginning 30 minutes before chemotherapy) is effective in chemotherapy-associated emesis. It can also be used in emesis that is refractory to other medications (4÷8 mg PO or IV up to q8h). Constipation may occur (see Chapter 20, Medical Management of Malignant Disease). Granisetron(Kytril, 10 mcg/kg IV for one to three doses 10 minutes apart, or 1 mg PO bid) is also effective.

Neurokinin-1 (NK-1) receptor antagonist. Aprepitant (Emend, 125 mg PO day 1, 80 mg PO days 2 and 3) is an alternative agent currently indicated only for chemotherapy-induced nausea and vomiting.

General Principles
Acute diarrhea consists of increased frequency and/or fluidity of bowel movements of abrupt onset. Infectious agents, toxins, and drugs are the major causes of acute diarrhea. In hospitalized patients, pseudomembranous colitis, antibiotic- or drug-associated diarrhea, and fecal impaction should be considered.

Chronic diarrhea consists of passage of loose stools with or without increased stool frequency for more than 3÷4 weeks.

Clinical Presentation and Etiology
Acute Diarrhea
Bacterial and viral infections. Viral enteritis and bacterial infections with Escherichia coli, Shigella, Salmonella, Campylobacter, and Yersinia species constitute the most common causes of acute diarrhea.

Pseudomembranous colitis is usually seen in the setting of antimicrobial therapy and is caused by toxins produced by Clostridium difficile.

Parasitic infections
Amebiasis may cause acute diarrhea, especially in travelers to areas with poor sanitation and in homosexual men. Demonstration of trophozoites or cysts of Entamoeba histolytica in the stool, or a serum antibody test, confirms the diagnosis.

Giardiasis is confirmed by identification of Giardia lamblia trophozoites in the stool, in duodenal aspirate, or in small-bowel biopsy specimens. A stool immunofluorescence assay is also available for rapid diagnosis.

Diarrhea related to medication use. Common offending agents include laxatives, antacids, cardiac medications (e.g., digitalis, quinidine), colchicine, and antimicrobial agents. Symptoms usually respond to discontinuation of the offending agent.

Graft versus host disease needs to be considered in patients who develop diarrhea after organ transplantation, especially bone marrow transplantation.

Chronic Diarrhea
After a careful history, thorough physical examination, and routine laboratory tests, chronic diarrhea can typically be classified into one of the following categories: watery diarrhea (secretory or osmotic), inflammatory diarrhea, or fatty diarrhea (steatorrhea).
Stool cultures, C. difficile toxin assay, ova and parasite examinations, and flexible sigmoidoscopy may be warranted in patients with severe, prolonged, or atypical symptoms.
The fecal osmotic gap can be calculated in patients with chronic diarrhea and voluminous watery stools as follows: 290 ÷ 2(stool [Na+] + stool [K+]).
Secretory diarrhea: Stool osmotic gap is <50 mOsm/kg.

Osmotic diarrhea: Stool osmotic gap is >125 mOsm/kg.

A positive fecal occult blood test or fecal leukocyte test suggests inflammatory diarrhea.
Steatorrhea is traditionally diagnosed by demonstration of fat excretion in stool of >7 g/d in a 72-hour stool collection while the patient is on a 100-g/d fat diet. Sudan staining of a stool specimen is an alternate test; >100 fat globules per high-power field is suggestive of steatorrhea.
Laxative screening should be considered in any patient with chronic diarrhea that remains undiagnosed.
General Measures
Adequate hydration is an essential part of the therapy of diarrheal disease. IV hydration is required in severe cases.
Long-term IV fluids or parenteral nutrition is sometimes necessary in refractory diarrhea.
Symptomatic therapy is recommended in simple self-limiting GI infections where diarrhea is frequent or troublesome, while diagnostic workup is in progress, when specific management fails to improve symptoms, or when a specific etiology is not identified.
Loperamide, 2÷4 mg up to four times a day, opiates (tincture of opium; belladonna; and opium capsules), and anticholinergic agents (diphenoxylate and atropine [Lomotil], 15÷20 mg/d of diphenoxylate in divided doses) are the most effective nonspecific antidiarrheal agents.

Pectin and kaolin preparations (bind toxins) and bismuth subsalicylate (antibacterial properties) are also useful in symptomatic therapy of acute diarrhea.

Bile acid÷binding resins (e.g., cholestyramine, 1 g up to qid) are beneficial in bile acid÷induced diarrhea.

Octreotide (100÷200 µg bid÷qid PRN) is useful in hormone-mediated secretory diarrhea, but can be of benefit in refractory diarrhea.

Empiric antibiotic therapy is only recommended in patients with moderate to severe disease and associated systemic symptoms, while awaiting stool cultures.

Fluoroquinolones (ciprofloxacin, 500 mg PO bid for 3 days, or norfloxacin, 400 mg PO bid for 3 days)

Trimethoprim-sulfamethoxazole (160 mg/800 mg PO bid for 5 days)

Oral metronidazole is the treatment of choice for pseudomembranous colitis. Oral vancomycin is reserved for resistant cases or intolerance to metronidazole (see Chapter 13, Treatment of Infectious Diseases, for further details).
Treatment of symptomatic amebiasis is with metronidazole, 750 mg PO tid or 500 mg IV q8h for 5÷10 days. This should be followed by paromomycin, 500 mg PO tid for 7 days, or iodoquinol, 650 mg PO tid for 20 days, to eliminate cysts.
Therapy for giardiasis consists of metronidazole, 250 mg PO tid for 5÷7 days, or tinidazole, 2-g single dose. Quinacrine, 100 mg PO tid for 7 days, is an alternative agent. More prolonged therapy may be necessary in the immunocompromised patient.
Special Considerations
Diarrhea in HIV disease
Opportunistic agents, including Cryptosporidium, Microsporidium, CMV, Mycobacterium avium complex, and Mycobacterium tuberculosis, may cause diarrhea in patients with advanced HIV and should be looked for specifically.
Venereal infections (syphilis, gonorrhea, chlamydiosis, HSV infection) as well as other nonvenereal infections (amebiasis, giardiasis, salmonellosis, shigellosis) may also cause diarrhea.
Other causes of diarrhea in this population include intestinal lymphoma and Kaposi's sarcoma. Stool studies (ova and parasites, culture), endoscopic biopsies, and serologic testing may assist diagnosis.
The most likely cause of undiagnosed diarrhea is missed pathogens; however, drugs, antibiotics, HIV acting as a pathogen, autonomic disturbance, and abnormal intestinal motility may also contribute to diarrhea. Management consists of specific therapy if pathogens are identified; symptomatic measures may be of benefit in idiopathic cases.
General Principles
Constipation consists of infrequent (and frequently incomplete) bowel movements.
A recent change in bowel habits may indicate an organic cause, whereas constipation of several years' duration is more likely due to a functional disorder.
Medication (e.g., calcium blockers, opiates, anticholinergics, iron supplements, barium sulfate) and systemic disease (e.g., diabetes mellitus, hypothyroidism, systemic sclerosis, myotonic dystrophy) may contribute.
Other predisposing factors include lack of exercise, disorders that cause pain on defecation (e.g., anal fissures, thrombosed external hemorrhoids), and prolonged immobilization.
Colonoscopy and barium studies help rule out structural disease and may be particularly important in older individuals.
Colonic transit studies, anorectal manometry, and defecography are reserved for resistant cases without an organic explanation.
Regular exercise and adequate fluid intake are nonspecific measures that may be of benefit.
Fiber supplementation. An increase in dietary fiber intake to 20÷30 g/d may be beneficial in many adults with constipation. Fecal impactions should be resolved before fiber supplementation is initiated. A fiber supplement such as wheat bran or psyllium with

water two to four times a day can be initiated; fluid intake should be increased with these preparations. Transient bloating often occurs.
Emollient laxatives consist of docusate salts and mineral oil. Docusate sodium, 50÷200 mg PO daily, and docusate calcium, 240 mg PO daily, allow water and fat to penetrate the fecal mass. Mineral oil (15÷45 mL PO q6÷8h) can be given orally or by enema. Tracheobronchial aspiration of mineral oil can result in lipoid pneumonia.

Stimulant cathartics such as castor oil, 15 mL PO, stimulate intestinal secretion and increase intestinal motility. Anthraquinones (cascara, 5 mL PO daily; senna, one tablet PO daily to qid) stimulate the colon by increasing fluid and water accumulation in the proximal colon. Chronic use can result in benign staining of the colonic mucosa (melanosis coli) and colonic atony from smooth muscle atrophy and damage to the myenteric plexus. Bisacodyl (10÷15 mg PO at bedtime, 10-mg rectal suppositories) is structurally similar to phenolphthalein and stimulates colonic peristalsis. Lubiprostone (24 mcg PO bid) is a selective intestinal chloride channel activator, causing movement of fluid into the bowel lumen and stimulating peristalsis.

Osmotic cathartics include nonabsorbable salts or carbohydrates that cause water retention in the lumen of the colon. Magnesium salts include milk of magnesia (15÷30 mL q8÷12h) and magnesium citrate (200 mL PO); they should be avoided in renal failure. Lactulose (15÷30 mL PO bid÷qid) can cause bloating as a side effect.

Enemas. Sodium biphosphate (Fleet) enemas (one to two rectally PRN) can be used for mild to moderate constipation and for bowel cleansing before sigmoidoscopy. However, these should be avoided in patients with renal failure because of the risk of developing hyperphosphatemia and subsequent hypocalcemia. Tap water enemas (1 L) are also useful for bowel cleansing. Oil-based enemas (cottonseed Colace, Hypaque) are reserved for refractory constipation.

Other agents. Polyethylene glycol in powder form (MiraLax, 17 g PO daily to bid) can be used regularly or intermittently for the treatment of constipation. Serotonin 5-HT4 receptor agonists (tegaserod, 6 mg bid) may be of benefit for some women with constipation-predominant irritable bowel syndrome. Lubiprostone (Amitiza, 24 mcg bid) is a newly available bicyclic fatty acid that increases frequency of bowel movements.

Bowel-cleansing agents. Patients should be placed on a clear liquid diet the previous day and kept NPO for 6÷8 hours or overnight prior to the bowel examination (colonoscopy or barium enema).

An iso-osmotic polyethylene glycol solution (GoLYTELY or NuLYTELY, 1 gallon, administered at a rate of 8 oz every 10 minutes) is commonly used as a bowel-cleansing agent before colonoscopy. This agent has a mildly salty taste, and can be more palatable if chilled; it can also be administered through an NG tube if necessary. Flavored preparations are also available.
Nonabsorbable phosphate (Fleet phosphosoda, 20÷45 mL with 10÷24 oz liquid, taken the day before and morning of the procedure) produces bowel movements in 0.5÷6 hours. The dose can be taken with 4 oz of liquid and followed with at least 8 oz more of liquid, or 15 mL each can be mixed with three 8-oz glasses of liquid and taken within 30 minutes. Phosphosoda can result in severe dehydration, hyperphosphatemia, hypocalcemia, hypokalemia, hypernatremia, and acidosis. It should be avoided in the elderly and patients with electrolyte imbalances, congestive heart failure, and ascites; it is contraindicated in renal failure and hepatic dysfunction.

Two-day bowel preparation is sometimes indicated in elderly or debilitated individuals when the above agents are contraindicated. This consists of magnesium citrate (120÷300 mL PO) administered on 2 consecutive days while the patient remains on a clear liquid diet; bisacodyl (30 mg PO or 10-mg suppository) can also be administered on both days. Oral bowel-cleansing agents should be avoided in patients with suspected bowel obstruction, ileus, bowel perforation, toxic colitis, or toxic megacolon. Tap water enemas (1-L volume, repeated one to two times) can cleanse the distal colon when colonoscopy is indicated in patients with proximal bowel obstruction.

Other Gastrointestinal Disorders
General Principles
Gastroparesis consists of abnormally delayed emptying of stomach contents into the small bowel, usually as a result of damage to the nerves or smooth muscle involved in gastric emptying.
Gastroparesis can result from chronic disorders (diabetes mellitus, scleroderma, intestinal pseudo-obstruction, previous gastric surgery) or, less frequently, from acute metabolic derangements (hypokalemia, hypercalcemia, hypocalcemia, hyperglycemia) or medications (narcotic analgesics, anticholinergic agents, chemotherapy agents).
Mechanical obstruction should always be excluded.
Clinical Presentation
Symptoms include nausea, bloating, and vomiting, usually hours after a meal.
A gastric-emptying study consisting of gamma camera scanning after a radiolabeled meal can help with the diagnosis.
Endoscopic evidence of retained food debris in the stomach after an overnight fast may be an indirect indicator of delayed gastric emptying.
Underlying metabolic derangements should be corrected.
Patients should avoid high-fat, high-fiber meals.
High-calorie liquid iso-osmotic meals may be beneficial in refractory situations.
Prokinetic agents have been used with varying degrees of success.

Metoclopramide (10 mg PO qid half an hour before meals) has variable efficacy, and side effects (drowsiness, tardive dyskinesia, parkinsonism) may be limiting.

Erythromycin (250 mg PO tid or 200 mg IV) also stimulates gastric motility.

Tegaserod, a 5-HT4 agonist with prokinetic properties, is being studied for use in gastroparesis.

Celiac Sprue
General Principles
Celiac sprue is a sensitivity to gluten, the protein found in wheat, barley, and rye. The resulting inflammation in the small-bowel mucosa causes malabsorption of dietary nutrients.
Noninvasive tests include antiendomysial and antitissue transglutaminase antibodies.
Endoscopic biopsy revealing severe blunting or complete absence of villi is highly suggestive.
A gluten-free diet results in prompt improvement in symptoms.
If symptoms persist despite strict gluten-free diet, radiologic and endoscopic evaluation of the small bowel should be performed to rule out complications including collagenous colitis and small-bowel lymphoma.
Patients may require iron, folate, calcium, and vitamin supplements.
Corticosteroids (prednisone, 10÷20 mg/d) may be required in refractory cases, although the most common cause of refractory disease is dietary indiscretion.

Lactose Intolerance
General Principles
Selective deficiency of lactase in the intestinal brush border results in prompt symptoms upon ingestion of dairy products.
Temporary lactase deficiency may result from bacterial or viral enteritis.
Clinical Presentation
Undigested lactose in the intestinal lumen causes osmotic diarrhea, abdominal cramps, and flatulence.
Symptom resolution on avoidance of dairy products is usually sufficient for diagnosis.
Lactose tolerance and hydrogen breath tests can be used for diagnosis in difficult cases.
Patients are advised to avoid dairy products.
Lactase supplements (two to four tablets or capsules with each lactose meal)
Small Intestinal Bacterial Overgrowth
General Principles
Bacterial overgrowth of the small intestine can result from any condition that causes intestinal stasis (small-bowel diverticulitis, afferent loop obstruction, scleroderma, intestinal pseudo-obstruction, strictures, adhesions). Hypochlorhydria and immunodeficiency are other predisposing conditions.
Deconjugation of bile salts by the bacteria causes fat malabsorption. The bacteria also may compete for dietary vitamin B12, causing anemia.
The diagnosis is suspected from patient presentation.
Imaging of the abdomen may demonstrate intestinal stasis.
Lactulose-hydrogen breath testing may confirm the diagnosis.
Culture of small-bowel aspirate obtained at endoscopy is rarely required.
Broad-spectrum antimicrobials (tetracycline, 250 mg PO qid; amoxicillin/clavulanate, 250÷500 mg PO tid; ciprofloxacin, 250 mg PO bid) can be used in 2-week courses intermittently.

Vitamin supplementation may be necessary.
Surgical correction of the predisposing disorder may be indicated.
General Principles
Diverticula consist of outpouchings in the bowel, most commonly in the colon, but also rarely seen elsewhere in the gut.

Diverticular bleeding can rarely occur from an artery at the mouth of the diverticulum.

Diverticulitis results from microperforation of a diverticulum and resultant extracolonic or intramural inflammation.

Clinical Presentation
Diverticulosis is most frequently asymptomatic. Though diverticulosis may be found in patients being investigated for symptoms of abdominal pain and altered bowel habits, a causal link is difficult to establish.
Diverticular bleeding can be profuse, and presentation can consist of bright red blood per rectum associated with hemodynamic compromise.
Typical symptoms of diverticulitis include left lower quadrant abdominal pain, fevers and chills, and alteration of bowel habits.
Diverticula are frequently seen on screening colonoscopy.
Presentation with GI bleeding may require investigation as outlined at the beginning of this chapter.
Diverticulitis may be associated with an elevated white blood cell (WBC) count with a left shift.
Imaging studies, most commonly CT scans, are useful in the diagnosis of diverticulitis. A sodium diatrizoate (Hypaque) enema may demonstrate extracolonic leakage of contrast in difficult cases.
Colonoscopy is contraindicated for 4÷6 weeks after acute diverticulitis.
General Measures
Increased dietary fiber is generally recommended in patients with diverticulosis, although no hard data exist to support its benefit.
Management of diverticular bleeding may require invasive measures, including angiography, intra-arterial vasopressin infusion, or surgery for control (see Gastrointestinal Bleeding).
A low-residue diet is recommended for mild diverticulitis.
Oral antibiotics (e.g., ciprofloxacin, 500 mg PO bid, and metronidazole, 500 mg PO tid for 10÷14 days) may suffice for mild diverticulitis.
Hospital admission, bowel rest, IV fluids, and broad-spectrum IV antimicrobial agents are typically required in moderate to severe cases.
Surgical resection of the bleeding segment may be necessary if diverticular bleeding cannot be controlled conservatively.
Surgical consultation should be obtained early in moderate to severe diverticulitis, as operative intervention may be necessary should complications arise.
Ischemic Intestinal Injury
General Principles
Acute mesenteric ischemia results from arterial (or rarely venous) compromise to the superior mesenteric circulation.
Emboli and thrombus formation are the most common causes of acute mesenteric ischemia, although nonocclusive mesenteric ischemia from vasoconstriction can also give rise to the disorder.
Ischemic colitis results from mucosal ischemia in the inferior mesenteric circulation during a low-flow state (hypotension, arrhythmias, sepsis, aortic vascular surgery) in patients with atherosclerotic disease.
Vasculitis, sickle cell disease, vasospasm, and marathon running can also predispose to ischemic colitis.
Clinical Presentation
Patients with acute mesenteric ischemia may present with abdominal pain, but physical examination and imaging studies can be unremarkable until infarction has occurred. As a result, diagnosis is late and mortality is high.
Ischemic colitis may manifest as transient bleeding or diarrhea; severe insults can lead to stricture formation, gangrene, and perforation.
Urgent angiography is indicated if the suspicion for acute mesenteric ischemia is high.
In patients with ischemic colitis, characteristic “thumbprinting of the involved colon may be seen on plain radiographs of the abdomen.
Colonoscopy may reveal mucosal erythema, edema, and ulceration, sometimes in a linear configuration; evidence of gangrene or necrosis is an indication for surgical intervention.
Treatment of acute mesenteric ischemia is essentially surgical.
In patients with ischemic colitis, in the absence of peritoneal signs or evidence of gangrene or perforation, expectant management with fluid and electrolyte repletion, broad-spectrum antimicrobials, and maintenance of an adequate BP usually suffices.
Evidence of gangrene or necrosis in the setting of ischemic colitis is an indication for surgery.
Anorectal Disorders
Thrombosed external hemorrhoids present as acutely painful, tense, bluish lumps covered with skin in the anal area. The thrombosed hemorrhoid can be surgically excised under local anesthesia for relief of severe pain. In less severe cases, oral analgesics, sitz baths (sitting in a tub of warm water), stool softeners, and topical ointments may provide symptomatic relief.Internal hemorrhoids commonly present with either bleeding or a prolapsing mass with straining. Bulk-forming agents such as fiber supplements are useful in preventing straining at defecation. Sitz baths and Tucks pads (cotton soaked in witch hazel) may provide symptomatic relief. Ointments and suppositories that contain topical analgesics, emollients, astringents, and hydrocortisone (e.g., Anusol-HC Suppositories, one per rectum bid for 7÷10 days) can also be used to decrease edema. Hemorrhoidectomy or band ligation can be curative, and is indicated in patients with recurrent or constant bleeding.Anal fissures present with acute onset of pain during defecation and are often caused by passage of hard stool. Anoscopy reveals an elliptical tear in the skin of the anus, usually in the posterior midline. Acute fissures generally heal in 2÷3 weeks with the use of stool softeners, oral or topical analgesics, and sitz baths. Topical nitroglycerin ointment, 0.2%, applied three times a day may be beneficial. Chronic fissures often require surgical therapy.Perirectal abscess commonly presents as a painful induration in the perianal area. Patients with IBD and immunocompromised states are particularly susceptible. Prompt drainage is essential to avoid the serious morbidity associated with delayed treatment. Antimicrobials directed against bowel flora (metronidazole, 500 mg PO tid, and ciprofloxacin, 500 mg PO bid) should be administered in patients with significant inflammation, systemic toxicity, or immunocompromised states.Suggested ReadingsGibril F, Reynolds JC, Doppman JL, et al. Somatostatin receptor scintigraphy: its sensitivity compared with that of other imaging methods in detecting primary and metastatic gastrinomas. A prospective study. Ann Intern Med 1997;126(9):741÷742.Khuroo MS, Farahat KL, Kagevi IE. Treatment with proton pump inhibitors in acute non-variceal upper gastrointestinal bleeding: a meta-analysis. J Gastroenterol Hepatol 2005;20:11÷25.Barkun A, Mardou M, Marshall JK. Consensus recommendations for managing patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med 2003;139:843÷857.Leontiadis GI, McIntyre L, Sharma VK, et al. Proton pump inhibitor treatment for acute peptic ulcer bleeding. Cochrane Database Syst Rev 2004;(3):CD002094.Saad R, Chey WD. A clinician's guide to managing Helicobacter pylori infection. Cleve Clin J Med 2005;72:109÷118.Hoedema RE, Luchtefeld MA. The management of lower gastrointestinal hemorrhage. Dis Colon Rectum 2005;48:2010÷2024.Green BT, Rockey DC, Portwood G, et al. Urgent colonoscopy for evaluation and management of acute lower gastrointestinal hemorrhage: a randomized controlled trial. Am J Gastroenterol 2005;100:2395÷2402.DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol 2005;100:190÷200.Clouse RE. Spastic disorders of the esophagus. Gastroenterologist 1997;5:112÷127.Korzenik JR, Dieckgraefe BK, Valentine JF, et al. Sargramostim for active Crohn's disease. N Engl J Med 2005;352:2193÷2201.Schiller LR. Chronic diarrhea. Gastroenterology 2004;127:287÷293.Brandt LJ, Prather CM, Quigley EM, et al. Systematic review on the management of chronic constipation in North America. Am J Gastroenterol 2005;100(Suppl 1):S5÷21.Brandt LJ, Bjorkman D, Fennerty MB, et al. Systematic review on the management of irritable bowel syndrome in North America. Am J Gastroenterol 2002;97(Suppl 11):S7÷26.Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudoobstruction. N Engl J Med 1999;341:137.

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