Babac Vahabzadeh and Dayna S. Early
Dysphagia and Odynophagia
GENERAL PRINCIPLES
· The swallowing mechanism consists of the pharynx, cricopharyngeus (upper esophageal sphincter), body of the esophagus, and lower esophageal sphincter.
· Dysphagia is a sense of difficulty with the passage of food or liquid from the pharynx to the stomach. Dysphagia can be divided into oropharyngeal or esophageal dysphagia. These groups can be further subdivided into mechanical causes or neuromuscular causes. Dysphagia is distinct from globus, which is a subjective feeling of fullness in the throat not related to eating.
· Odynophagia is the presence of pain on swallowing that may or may not accompany dysphagia.
DIAGNOSIS
Clinical Presentation
History
· Progressive difficulty in swallowing solid foods but not liquids indicates mechanical obstruction such as malignancy or benign stricture. Dysphagia is distinct from globus, which is a subjective feeling of fullness in the throat not related to eating. Intermittent dysphagia for solids, usually meat or bread, can result from a lower esophageal ring, known as Schatzki ring.1
· When hoarseness follows the onset of dysphagia, involvement of the recurrent laryngeal nerve by oropharyngeal or esophageal cancer should be considered.
· Symptoms located in the lower part of the sternum are most likely due to abnormality in the distal esophagus. Otherwise, subjective localization of dysphagia is nonspecific.
· Unintended weight loss associated with dysphagia suggests carcinoma. Risk factors for esophageal cancer include heavy tobacco and alcohol use and long-standing gastroesophageal reflux.
· Tracheobronchial aspiration may occur in those with tracheoesophageal fistula, brainstem neuromuscular diseases, achalasia, or severe gastroesophageal reflux.
· A history of chronic heartburn associated with dysphagia is usually present in peptic strictures. These individuals may describe chronic antacid use.
· Chest pain may occur in those with severe reflux, accounting for half of noncardiac chest pain.2
· Odynophagia is frequently related to esophageal infections or pill ulcers.
· Hiccups can be associated with a lesion in the distal esophagus causing diaphragmatic irritation or gastric or esophageal distention from aerophagia.
Physical Examination
· Oral pharyngeal examination should focus on finding evidence of thrush or lesions of pemphigus or epidermolysis bullosa.
· Examination of the neck may reveal structural defects such as thyromegaly, spinal deformity, and neck masses.
· Skin examination is important for features of collagen vascular disease including scleroderma or CREST syndrome (Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias), which is associated with dysphagia and impaired peristalsis.
Differential Diagnosis
· Infections including candidal, herpetic, or other viral esophagitis must be considered in patients who describe odynophagia. Acute odynophagia can be secondary to esophagitis or ulcers from pills such as tetracycline, potassium tablets, bisphosphonates, ferrous sulfate, quinidine, and nonsteroidal anti-inflammatory agents (NSAIDs).
· The differential diagnosis/causes of dysphagia are presented in Table 28-1.3
TABLE 28-1 Causes of Dysphagia
Diagnostic Testing
· When esophageal dysphagia is suspected, endoscopy is the initial test to visualize the mucosa directly with biopsy of suspicious lesions and/or biopsy of the midesophagus for eosinophilic esophagitis.
· Barium swallow can be used to identify structural defects in patients at high risk for sedation and those taking anticoagulants.
· Modified barium swallow is used to evaluate oropharyngeal dysmotility and aspiration.
· Laryngoscopy can identify oropharyngeal lesions.
· Esophageal manometry is the test of choice when esophageal motor disease is suspected.
TREATMENT
· Gastroesophageal reflux disease (GERD) should be treated with proton pump inhibitors.4
· Esophageal strictures or rings can be treated with endoscopy by bougienage (the passage of dilators with or without guidewire assistance) or balloon dilators.
· Achalasia can be treated with the following:
o Pneumatic dilatation via fluoroscopic and endoscopic visualization.
o Heller myotomy (surgical procedure that dissects the smooth muscle of the hypertensive lower esophageal sphincter).
o Botulinum toxin injection can be used for those at high risk for other interventions. The effects of botulinum toxin injection are temporary, usually lasting 3 to 6 months.
· Eosinophilic esophagitis can be treated with aggressive acid suppression, elimination diets, and/or swallowed fluticasone.
· Odynophagia may be treated symptomatically with opioid analgesic agents or topical viscous lidocaine.
o Pill ulcers are generally self-limited.
o Infectious causes of odynophagia should be treated with appropriate antimicrobials.
Nausea and Vomiting
DIAGNOSIS
Clinical Presentation
History
· The initial evaluation should determine the duration and severity of symptoms.
· Association with certain triggers including smells, tastes, emotional or physical stress, headaches, and abdominal pain should be noted.
· If abdominal pain is the main symptom, refer to the Abdominal Pain section of this chapter for the differential diagnosis.
· Nausea and/or vomiting associated with right upper quadrant (RUQ) or epigastric pain could be secondary to biliary colic, pancreatitis, cholecystitis, peptic ulcer disease, or acute viral hepatitis.
· Initial periumbilical pain that relocates to the right lower quadrant accompanied by nausea and vomiting is suggestive of appendicitis.
· Left lower quadrant pain in the presence of vomiting may be secondary to diverticulitis.
· Flank pain along with fever and vomiting may indicate pyelonephritis.
· Occurrence soon after meals can be a result of gastric outlet obstruction.
· Vomiting that is delayed after meals and consists of partially digested food or food consumed several hours earlier may indicate gastroparesis (particularly in diabetics) or intestinal obstruction.
· Vomiting undigested food (regurgitation) is seen with a Zenker diverticulum (pharyngoesophageal diverticulum) and achalasia, which are also associated with severe halitosis.
· Presence of diarrhea may indicate an infectious gastroenteritis.
Physical Examination
· Evaluate for orthostatic hypotension defined by fall of systolic blood pressure of 20 mm Hg or 10 mm Hg diastolic with positional change, which may be present in persistent vomiting due to volume depletion.
· Decreased skin turgor or dry mucous membranes are signs of significant fluid losses.
· Severe halitosis may be associated with intestinal obstruction, gastroparesis, gastrocolic fistula, bacterial overgrowth, achalasia, and Zenker diverticulum.
· Oral examination may reveal poor dentition and enamel erosion in those with eating disorders such as bulimia.
· High-pitched bowel sounds may suggest small bowel obstruction, while succussion splash (the movement of gastric fluid within the stomach heard on auscultation) may be seen in gastric outlet obstruction or gastroparesis.
· Palpation to find areas of tenderness, abdominal masses, or Murphy sign.
Differential Diagnosis
The differential diagnosis of nausea and vomiting is presented in Table 28-2.
TABLE 28-2 Causes of Nausea and Vomiting
Data from Quigley EM, Hasler WL, Parkman HP. AGA technical review on nausea and vomiting. Gastroenterology 2001;120:263–286.
Diagnostic Testing
Laboratories
· Serum chemistries evaluating electrolytes, bilirubin, amylase, lipase, alkaline phosphatase, and transaminases. Hyponatremia and azotemia may cause nausea and vomiting. Hyponatremia and hyperkalemia can be seen in adrenal insufficiency. Check AM cortisol if adrenal insufficiency is suspected.
· Complete blood cell count (CBC) evaluating for leukocytosis indicating acute inflammation or infection as well as anemia indicating possible blood loss within the gastrointestinal (GI) tract.
· Pregnancy test should be obtained in women of childbearing age.
Imaging
· If nausea and vomiting are associated with pain, an obstructive series is important to identify intestinal obstruction, air-fluid levels, bowel gas pattern, and free air.
· Upper GI endoscopy can detect mechanical sources of nausea and vomiting. If negative, a small bowel exam should be considered, such as small bowel follow-through, capsule endoscopy, or CT enterography.
· Radionuclide gastric-emptying scan and manometry can evaluate for motility disorders of the stomach.
· CT may be obtained to evaluate for intra-abdominal processes, such as pancreatitis or appendicitis.
· CT scan or MRI of the brain may be pertinent if an intracranial process is suspected.
TREATMENT
· Identify and treat underlying process, using antiemetic agents to temporarily alleviate symptoms.
o Prochlorperazine starting at 5 to 10 mg PO tid/qid or 25-mg suppositories every 12 hours.
o Promethazine starting at 12.5 to 25 mg PO every 4 to 6 hours or 25-mg suppositories every 4 to 6 hours.
o Also, refer to Chapter 36 for a more detailed discussion of antiemetic therapy.
· Prokinetic medication such as metoclopramide may be used for delayed gastric emptying; the starting dose is 10 mg PO/IM/IV 1 hour before meals and at bedtime.
o Mechanical obstruction must be excluded before using prokinetics.
o Metoclopramide should not be used for prolonged periods and/or in high doses, particularly in the elderly, because of the risk of drug-induced tardive dyskinesia.
· A number of serotonin receptor inhibitors, such as ondansetron, or antagonists of substance P/neurokinin-1 receptors, such as aprepitant, are frequently used in nausea and emesis related to chemotherapy.
· Indications for hospitalization:
o Clinical evidence of severe volume depletion
o Electrolyte derangements that require correction under monitored conditions
o Patients at extremes of age and those with diabetes and/or accompanying debilitating illnesses
Dyspepsia
GENERAL PRINCIPLES
· Persistent or recurrent discomfort or pain located in the upper abdomen. Pain can be accompanied by bloating, heartburn, nausea, and food intolerance.
· Divided into two categories: peptic ulcer disease and nonulcer dyspepsia.
DIAGNOSIS
Clinical Presentation
History
· Pain in the preprandial state or nocturnal pain that results in awakening several hours after ingestion of food is suspicious for peptic ulcer disease. Similar pain that is relieved by food is suggestive of a duodenal ulcer.
· Pain from nonulcer dyspepsia is difficult to distinguish from ulcer-related dyspepsia.
· Pain radiating to the back and somewhat improved on leaning forward suggests pancreatitis, perforated peptic ulcer, or leaking abdominal aneurysm.
· Pain referred to the right scapula may originate in the gallbladder or from any process causing diaphragmatic irritation.
· Constipation, diarrhea, tenesmus, or nonspecific lower abdominal discomfort in association with upper abdominal complaints may be due to irritable bowel syndrome.
· Early satiety can result from ulcers at the gastric outlet or infiltrating tumors creating reduced gastric wall compliance.
· Fear of eating because of subsequent abdominal pain is suggestive of mesenteric ischemia or intestinal angina.
· History of peptic ulcer disease, gastric surgery, cigarette smoking, or alcohol use are risk factors for the development of dyspepsia.
· Early satiety, recurrent vomiting, or bloating that is not accompanied by visible distention or pain may indicate dysmotility.
· Aerophagia is excess swallowing of air that results in fullness, belching, or reflux-like symptoms relieved by repetitive belching. Aerophagia is usually psychiatric in origin.
· Red flags: weight loss, GI bleeding, recurrent vomiting, dysphagia, and NSAID use.
Physical Examination
· Abdominal tenderness to palpation is nonspecific and may be seen in most disorders that cause dyspepsia. RUQ tenderness increased by palpation with inspiration (Murphy sign) indicates cholecystitis.
· Evaluate for peritoneal signs such as guarding and rebound tenderness (i.e., discomfort induced by movement of an irritated peritoneum during the release of pressure from palpation).
· Jaundice suggests a hepatic or biliary process.
· Evaluate for blood in stool.
Diagnostic Testing
Laboratories
CBC looking for anemia, if GI bleeding is suspected, and leukocytosis indicating possible intra-abdominal infection.
Diagnostic Procedures
· Endoscopy of the upper GI tract is indicated for those with alarm symptoms, for new-onset dyspepsia in a patient over 50, and for whom trials of acid-suppressing medications are inadequate.5
· Helicobacter pylori testing is appropriate if mucosal abnormalities, such as peptic ulcers, erosive gastropathy, or duodenitis, are detected, or in the case of documented prior peptic ulcer disease and mucosa-associated lymphoid tissue (MALT) lymphoma.
· Upper GI barium radiographs are reserved for patients who cannot undergo endoscopy.
· Gastroparesis can be demonstrated by gastric-emptying scintigraphy but must be interpreted in conjunction with the clinical setting.
· Transabdominal ultrasound can be used to evaluate for liver and biliary tract abnormalities.
TREATMENT
· Peptic ulcer disease should be managed with acid suppression. Documentation of healing is recommended for gastric ulcer.6 Helicobacter pylori should be tested for and eradicated if found.
· Nonulcer dyspepsia may not respond to specific treatment but may improve with acid suppression or neuromodulators such as tricyclic antidepressants. In those with alarm symptoms or new-onset dyspepsia after age 50, upper endoscopy is warranted.7
· Reflux should be treated symptomatically with regularly scheduled proton pump inhibitors as well as weight reduction, dietary changes, and elevation of the head of bed.4
· Dysmotility-like dyspepsia may benefit from prokinetic agents such as metoclopramide. Metoclopramide should not be used for prolonged periods and/or in high doses, particularly in the elderly, because of the risk of drug-induced tardive dyskinesia.
Abdominal Pain
GENERAL PRINCIPLES
One of the most valuable diagnostic tools in evaluating the patient with abdominal pain is the history. The location and features of pain are useful in narrowing the differential diagnosis to an organ (e.g., hepatobiliary, gastric, and intestinal) as well as to a cause (e.g., inflammation, infection, obstruction, ischemia, and neurogenic).
DIAGNOSIS
Clinical Presentation
History
· The initial evaluation should focus on the chronology of events and determine the duration of symptoms (e.g., acute [Table 28-3] or chronic [Table 28-4]).
· The first consideration for a patient with acute abdominal pain is whether they can be evaluated in an outpatient setting or whether an emergency room is more appropriate.
· Some causes of abdominal pain can be well localized, particularly if they result from inflammation in the parietal peritoneum (Table 28-3).
· Substernal chest pressure or pain can be indicative of esophageal disorders. This can result in pain that radiates to the neck, jaw, arms, and back and may mimic cardiac angina.
· Epigastric discomfort may be secondary to a process affecting the stomach, duodenum, and pancreas, while stretching of the liver capsule or gallbladder distention or inflammation can result in RUQ pain. Small bowel obstruction and appendicitis may localize to the periumbilical area. Colonic pain may be localized to the lower abdomen but can be generalized. Abdominal disease causing inflammation under the diaphragm can produce referred pain in the shoulder.
· Non-GI abdominal pain can result from the following:
o Urinary tract disease (e.g., cystitis, pyelonephritis, obstructive uropathy, and nephrolithiasis) is often associated with dysuria or hematuria and can cause pain in the flanks or suprapubic area as well as abdominal discomfort.
o Pleural, pulmonary, or pericardial etiologies may cause upper abdominal pain.
o Gynecologic etiologies must be considered in women with lower abdominal symptoms (Tables 28-3 and 28-4).
· Description of pain that is sharp, tearing, and cutting may indicate an acute process, whereas descriptors such as gnawing, burning, dull, or boring point toward a chronic process.
· Colic describes pain with a waxing and waning intensity.
· Certain movements can generate abdominal pain due to musculoskeletal disorders or nerve root compression.
· Pain that is worse while supine may indicate pancreatic disease.
· Postprandial pain may indicate a process such as cholecystitis, pancreatitis, bowel obstruction, or gastric ulcer. In contrast, pain from duodenal ulcers generally improves with food ingestion. Intestinal angina may be associated with a fear of eating due to pain and result in weight loss.
· Nausea and emesis are nonspecific symptoms and can occur in association with abdominal pain due to a number of causes. Diarrhea associated with nausea and emesis suggests an infectious source.Hiccups can result from distention of the esophagus or stomach or irritation of the diaphragm.
· Patients should be questioned about changes in bowel movements, stool caliber, and stool volume. Constipation can result in diffuse abdominal discomfort, while diarrhea can be accompanied by cramping. Patients with alternating complaints of diarrhea and constipation may have irritable bowel syndrome.
· GI bleeding raises concern for ulcers, infections, inflammation, or ischemia. Melena (dark, tarry stool) usually signals an upper GI source, although it can occur during right-sided colonic bleeding or small bowel bleeding. Hematochezia (bright red blood from the rectum) usually reflects a colonic source but sometimes presents during massive upper bleeding.
· Menstrual cycles, irregularity, or abnormalities in bleeding may cause abdominal pain or worsening of underlying GI disorders. Symptoms of inflammatory bowel disease or irritable bowel syndrome can clearly worsen during and around the time of menses. Pain that follows a close pattern of menstrual cycles may be due to underlying endometriosis.
· Psychiatric causes should be considered in patients with underlying depression and anxiety, after organic causes are eliminated.
· Red flags: pain that awakens the patient from sleep, fever, prolonged severe pain of more than several hours duration, persistent vomiting, changes in patterns or location, significant alterations in appetite or mental status, unintentional weight loss, and GI bleeding.
TABLE 28-3 Common Causes of Acute Abdominal Pain by Location
Data from Yamada T, Alpers DH, Laine L, et al. Textbook of Gastroenterology, 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.
Physical Examination
· Inspection and assessment for signs of systemic illness such as cachexia, pallor, severity of distress, presence of ascites, masses, prior surgical procedures, or other abnormalities, and presence of cutaneous findings of underlying cirrhosis.
· Auscultation for presence or absence of bowel sounds. High-pitched sounds may indicate bowel obstruction, whereas absence of sounds may be a feature of ileus or peritonitis.
· Tympanic percussion can indicate gas-filled or dilated loops of bowel. Dullness may indicate a mass or ascites, particularly if percussed in the flanks. Dullness below the left costal margin may indicate splenomegaly, and dullness below the right costal margin may indicate hepatomegaly.
· Palpation for the detection of hepatomegaly or splenomegaly. Palpation for masses, localized tenderness, or ascites. Murphy sign is tenderness to palpation in the RUQ, which induces a midinspiratory pause in breathing, and is suggestive of cholecystitis.
· Mesenteric ischemia classically presents with pain that is out of proportion to findings on physical examination.
· Signs worrisome for surgical abdomen include guarding and peritoneal signs (rebound tenderness or a rigid abdomen), fever, Murphy sign, iliopsoas sign (hyperextension of right hip causing abdominal pain associated with appendicitis or terminal ileal disease, absent or high-pitched bowel sounds.)
Diagnostic Testing
Laboratories
· CBC, looking for the following: leukocytosis suggesting acute inflammatory response; anemia, which can indicate GI bleeding; and thrombocytopenia suggesting liver disease.
· Serum chemistries evaluating electrolytes, bilirubin, amylase, lipase, alkaline phosphatase, and transaminases
· Urinalysis to assess hydration, proteinuria, infection, and renal disease
Imaging
· Plain films (obstructive series) are easy, inexpensive, and low risk. They can detect obstruction or perforation (free air under the diaphragm). However, when there is no real concern for obstruction or perforation, plain films are rarely diagnostic.
· Ultrasound to evaluate for organomegaly, masses, ascites, or biliary tract disease.
· CT scan may be more sensitive in detecting intra-abdominal processes.
TABLE 28-4 Causes of Chronic Abdominal Pain
Diarrhea
GENERAL PRINCIPLES
· A subjective increase in the frequency of stools as well as liquid consistency may be described as diarrhea by patients.
· Diarrhea is defined as stool quantity that exceeds 200 g/24-hour period.
· Diarrhea that has been present for <2 to 4 weeks is classified as acute, while chronic diarrhea describes symptoms of >4 weeks.
DIAGNOSIS
Clinical Presentation
History
· Relation to eating can be important in determining if the diarrhea is due to an osmotic or secretory cause, as the latter does not improve with fasting (Table 28-5).
· Nighttime diarrhea could indicate organic causes including infectious, secretory, inflammatory, or diabetic diarrhea. Functional diarrhea such as irritable bowel syndrome tends not to disturb the patient during sleep.
TABLE 28-5 Causes of Chronic Diarrhea
· Ascertain if the patient has had recent travel or contact with others at work, home, or otherwise who have similar symptoms.
· Blood, mucus, or pus in the stool and/or fever may indicate an invasive bacterial pathogen.
· Localized abdominal pain to the lower quadrants or rectum in the presence of bleeding, tenesmus, and weight loss are features of inflammatory bowel disease. Tenesmus is the sense of incomplete rectal evacuation accompanied by pain, cramping, and involuntary straining and strongly suggests proctitis. Pain is more commonly associated with Crohn disease than ulcerative colitis. Nonspecific diffuse pain or discomfort may be reported with irritable bowel syndrome.
· Patients with steatorrhea (fat malabsorption) often describe light-colored loose stools that are difficult to flush and stick to the toilet bowl. Fatty food intolerance may be observed in disorders of pancreatic exocrine insufficiency.
· Nighttime visual impairment and bone pain may be associated with fat-soluble vitamin malabsorption of vitamins A and D, respectively.
· Frequent small volumes of stool output with urgency suggest distal colorectal pathology, whereas larger volumes with less frequency suggest small bowel or proximal colonic disorders.
Physical Examination
· Dehydration should be assessed: orthostatic hypotension and pulse changes, poor skin turgor, and dry mucous membranes.
Differential Diagnosis
· Sugar substitutes and sugar-free candy or chewing gum containing sorbitol, mannitol, or olestra are a common cause of diarrhea.
· Antibiotic use within the preceding 8 weeks is a predisposing factor for Clostridium difficile–associated pseudomembranous colitis,8 although infection can occur in the absence of predisposing factors.
· Acute diarrhea is usually infectious (also see Chapter 26).
o Viruses such as Norovirus in adults and older children and rotavirus in young children.
o Enterotoxigenic bacteria such as Escherichia coli (traveler’s diarrhea), Bacillus cereus, Clostridium perfringens, and Staphylococcus aureus.
o Enteropathic agents, which can be invasive, include Campylobacter, Salmonella, Shigella, and certain species of Yersinia.
o Protozoa including Giardia species, which can be acquired from spring or well water consumption, as well as amebiasis being common in travelers and homosexual men.
· Bloody diarrhea may be secondary to the following:
o Invasive infections particularly Campylobacter and Shigella.
o Acute onset of watery diarrhea that becomes bloody within 24 to 48 hours and is accompanied by fever suggests hemorrhagic colitis caused by E. coli O157:H7.
o Inflammatory bowel disease.
o Drug-induced colitis.
o Mesenteric ischemia.
o Ischemic colitis.
· Diverticular diarrhea can have features of left lower quadrant discomfort, rectal urgency, pain with defecation, tenesmus, and fever.
· Fecal impaction may paradoxically cause diarrhea in the elderly or in those who consume opioid pain medications with small liquid stool leakage around an impacted hard stool.
· Several categories of chronic diarrhea exist including osmotic, secretory, malabsorptive, and inflammatory (Table 28-5).
· Dumping syndrome is voluminous diarrhea occurring shortly after eating, commonly seen in postgastrectomy states. Within a few hours, some may experience the latent phase characterized by weakness, light-headedness, flushing, and hypoglycemia due to reactive insulin release.
· Irritable bowel syndrome can be characterized by alternating features of diarrhea and constipation with abdominal pain and frequently coexists with depression or anxiety.
· Diabetic diarrhea occurs in those with poorly controlled and/or long-standing diabetes and usually coexists with other signs of peripheral neuropathy.
o Factitious diarrhea is the surreptitious use of laxatives resulting in severe watery diarrhea, nausea, vomiting, and weight loss. The majority of these individuals are women <30 years of age who have eating disorders or middle-aged women with extensive medical histories who derive secondary gain from being chronically ill.9
· Significant intestinal resection, particularly segments of the ileum that exceed 100 cm, can result in malabsorption and a bile acid–induced diarrhea.10
· Microscopic colitis manifests as chronic diarrhea with few associated symptoms and is divided into lymphocytic colitis or collagenous colitis.
TABLE 28-6 Causes of Abnormal Liver Tests
NSAIDs, nonsteroidal anti-inflammatory agents.
Diagnostic Testing
Laboratories
· Electrolytes, blood urea nitrogen (BUN), and creatinine can assist in identifying severity of dehydration or metabolic acidosis.
· CBC to assess for anemia or leukocytosis.
· Thyroid-stimulating hormone (TSH) level in those with chronic diarrhea.
· Presence of elevated IgA anti–tissue transglutaminase antibody is highly sensitive and specific for celiac sprue.11,12 About 10% of celiac sprue patients have selective IgA deficiency, so total IgA levels should be checked as well.
· Stool should be examined for the following: ova, parasites, and culture; C. difficile toxin; fecal leukocytes, which are nonspecific but indicate inflammatory cause; stool electrolytes and osmolality to calculate osmotic gap; and Sudan staining of stool for fat (if abnormal, obtain 24-hour stool specimen for fat and volume).
Diagnostic Procedures
· Sigmoidoscopy with biopsies for infectious and inflammatory colitis can be a useful tool for those who have had diarrhea for >1 week. If initially negative or if colitis is present, a full colonoscopy may be necessary to determine the extent of involvement.
· Colonoscopy with terminal ileum exam is frequently performed to evaluate chronic diarrhea. It is highly sensitive for inflammatory bowel disease, microscopic colitis, and diverticular disease.
· Upper endoscopy with small bowel biopsies can be performed in chronic diarrhea to identify celiac sprue histologically. Alternatively, serologic testing can be performed, and upper endoscopy is performed only if serology is abnormal.
TREATMENT
· Oral rehydration with noncaffeinated and nonalcoholic products is preferred, but intravenous fluid administration may be necessary.
· Antidiarrheal medications
o Kaolin and pectin-containing agents may add bulk to stool.
o Bismuth subsalicylate has antisecretory, antimicrobial, and anti-inflammatory properties.
o Loperamide is initially given as 4 mg dose followed by 2-mg capsules with a maximum of 8 mg/day.
o Diphenoxylate plus atropine can be given as 5 mg initially and then 2.5 mg after each loose stool to a maximum of 20 mg/day.
o Systemically absorbed opiates are sometimes given including tincture of opium (0.6 mL every 4 hours), belladonna/opium (1 suppository every 12 hours), and codeine (30 - 60 mg PO every 4 hours).
o All of these agents impair intestinal motility and should be avoided in bacterial infectious states, as they may delay clearance of the organism.
· Anticholinergic agents such as atropine and hyoscyamine products are useful to some, particularly with cramping that accompanies diarrhea.
· Bulk-forming substances such as psyllium and methylcellulose may ameliorate functional diarrhea but are otherwise rarely effective in controlling symptoms.
· Cholestyramine can improve refractory diarrhea of malabsorption or bile acid–induced diarrhea, which can occur as a result of distal small bowel resections.
· Antibiotics are not required for most acute infectious diarrhea, as it is usually self-limited. Severe traveler’s diarrhea that presents as dysentery with bloody stools with/without fever may require antibiotics (discussed in Chapter 26).
Constipation
GENERAL PRINCIPLES
· Constipation is the subjective feeling of infrequent stools or difficulty in passing stools. Absolute inability to pass stools can be referred to as obstipation.
· By ROME III criteria for functional constipation ≥2 of the following must be present: straining during ≥25% of defecations, lumpy or hard stools in ≥25% of defecations, sensation of incomplete evacuation for ≥25% of defectations, sensation of anorectal obstruction/blockage for ≥25% of defecations, manual maneuvers to facilitate ≥25% of defecations (e.g., digital evacuation, support of the pelvic floor), and <3 defecations per week.13
· The frequency of bowel movements may decrease with age.
DIAGNOSIS
Clinical Presentation
History
· Significant alterations in bowel habits without previous problems should alert the clinician to search for organic causes. Intermittent constipation may be due to medications, dietary habits, or functional bowel disease. Unrelenting symptoms should be investigated for serious illness such as obstruction from a mass.
· Patients with a rectal mass may sometimes describe a gradual reduction of stool caliber and often have accompanying hematochezia.
· Constipation in association with pain could indicate either inflammatory or obstructive causes such as: diverticulitis (left lower quadrant pain), anal fissures (anorectal pain), inflammatory colitis (diffuse pain), thrombosed external hemorrhoids (anal pain), and cancer. Cramping abdominal pain associated with bloating relieved by defecation may indicate irritable bowel syndrome if organic pathology has been excluded.
· Digital manipulation through either the vagina or the rectum may be described by the patient as a routine practice to induce bowel movements.
Physical Examination
· Abdominal examination evaluating for distention, tenderness, and masses. Tympanic distention may indicate ileus or obstruction. Perineal and rectal examination to identify external deformities, such as rectal prolapse and hemorrhoids. Digital examination of the rectum assessing for fissures, distal fixed stenosis, masses, or fecal impaction as well as to test perineal sensation, rectal sphincter tone, and reflexes.
Differential Diagnosis
· Medications including narcotic analgesics, calcium channel blockers, anticholinergic agents, iron supplements, and many others.
· Constipation that accompanies urinary incontinence, particularly in postmenopausal women, could indicate the following: abnormal pelvic floor relaxation, rectocele, and cystoceles.
· Inadequate intake of fiber or fluid (6 to 8 glasses daily).
· Colonic inertia.
· Constipation—predominant irritable bowel syndrome.
· Colorectal neoplasia.
· Stricture (postoperative, diverticular, and radiation).
· Hypothyroidism.
· Neurologic/autonomic dysfunction (e.g., diabetes, Parkinson disease, Hirschsprung disease).
Diagnostic Testing
Laboratories
· Serum electrolytes, particularly low potassium and magnesium, and abnormally low or high calcium levels, may become clinically significant. Thyroid studies to evaluate for hypothyroidism. Hyperglycemia may identify diabetics who have delayed transit time.
Diagnostic Procedures
· In the setting of new-onset or progressive constipation (especially in those >50 years of age), colonoscopy is essential to evaluate for colon cancer or strictures. Melanosis coli, a dark pigmentation that is most often seen in the distal colon, may be seen during colonoscopy in patients who use excess laxatives.
· Barium enema may be helpful when combined with flexible sigmoidoscopy to exclude obstructive colonic process in patients who are unable to undergo colonoscopy.
· Obstructive series and abdominal CT may evaluate for obstruction and megacolon (grossly dilated colon with significant abdominal distention).
· Proctoscopy may be useful to identify rectal pathology such as hemorrhoids, fissures, and masses.
· Anorectal manometry is used to identify anorectal dyssynergia and pelvic floor dysfunction.
· Defecography is a radiologic procedure that is helpful in identifying rectocele and pelvic floor dysfunction.
TREATMENT
· Treatment of constipation symptoms presumes that serious etiologies have been excluded.
· For mild symptoms
o Increased fiber and fluid intake increases stool bulk and intestinal motility, which is generally only effective for mild constipation or constipation alternating with diarrhea. Most individuals with mild constipation are able to achieve a positive response with 20 to 30 g of daily fiber supplementation.14
o Bulk-forming fiber supplements can be used.
§ Psyllium (e.g., Metamucil, 1 tsp in liquid or packet with liquid PO bid-qid)
§ Methylcellulose (e.g., Citrucel, 1 tbsp in 8 oz water qd-tid)
§ Polysaccharide derivatives (e.g., FiberCon, 1 g qid prn; 500-, 625-, and 1,000-mg tablets accompanied by 4 to 6 glasses of water)
o Stool softeners including docusate (100 mg PO bid) can be used along with bulk-forming therapy for maintenance.15
· For moderate symptoms
o Hyperosmolar agents
§ Polyethylene glycol (17 g PO qid) is well tolerated and available over the counter.
§ Lactulose (15 to 30 g PO every 2 to 3 hours prn) can cause bloating, which may be limiting.
o Emollient laxatives may be used; however, mineral oil (15 to 45 mL PO every 6 to 8 hours) should be used with caution because of the risk of aspiration and lipid pneumonia.
o Saline laxatives
§ Magnesium citrate (200 mL PO qid); should not be used with impaired renal function.
§ Fleet phospho soda if no contraindications; should not be used with impaired renal function.
· For severe symptoms
o Stimulant laxatives
§ Castor oil (15 to 60 mL qid)
§ Cascara (1 tsp [5 mL] PO bid)
§ Senna (2 tsp [10 mL] PO bid)
§ Bisacodyl (10 to 15 mg PO qid-bid)
§ Lubiprostone (24 mcg PO bid)
§ Colchicine (0.6 mg PO bid). It is important to remember, however, that the margin between therapeutic and toxic is rather narrow with this drug and it should not be used in patients with impaired renal function.16–18
§ Enemas
§ Saline enemas (120 to 240 mL)
§ Tap water enemas (500 to 1,000 mL)
§ Oil-retention enemas such as cottonseed with docusate
· Routine long-term use of stimulant laxatives should be avoided.
· Surgical treatment for rectal deformities, intestinal obstruction and masses, resuspension of rectal intussusception or prolapsed, and pelvic floor disorders.
Anorectal Disorders
DIAGNOSIS
Clinical Presentation
· Evaluation for anal pruritus, pain with defecation, bleeding, and fever
· Association with underlying constipation, inflammatory bowel disease, or other medical illness
· Evaluation of bowel habits, incontinence, and rectal pain changing with position
· Simple visual inspection after spreading the buttocks can often identify a tear, lesion, or fluctuant mass with purulence.
· Digital examination of the rectum for impacted stool, anal sphincter tone, blood, fissure, or mass.
· A lateral or anterior fissure found on examination may suggest Crohn disease, proctitis, leukemia, syphilis, tuberculosis, or carcinoma, but can be benign as well. Posterior fissures are often benign and self-limited.
Differential Diagnosis
· External hemorrhoids (below dentate line) manifesting as anal pruritus and sometimes pain. Severe pain may occur with thrombosis of an external hemorrhoid. Internal hemorrhoids (above dentate line) may produce mild discomfort, but significant pain is seen primarily in prolapse and strangulation. Bleeding from internal hemorrhoids is usually minimal but may be alarming to patients. It tends to be bright red in color and is found on the outside of stool, on toilet paper, or in the toilet bowl.
· Anal fissure is a linear tear of the anal canal tissue and is often associated with pain and rectal bleeding.
o Perirectal fistula characterized as a chronic purulent, foul-smelling discharge from the rectum, or a small opening in the perineum is found with Crohn disease. Perirectal abscess should raise suspicion for Crohn disease or immunosuppression.
· Rectal prolapse manifests as extrusion of the rectum during defecation and may need manual reduction by the patient. This is often seen in women and may be associated with urinary symptoms.
· Rectosigmoid intussusception presents with hematochezia and pain.
· Proctalgia fugax is characterized by sudden brief episodes of severe rectal pain occurring along the midline. Symptoms are typically mild and are a result of levator ani musculature spasm.
· Fecal incontinence with episodes of rectal urgency and fecal soiling of garments.
· Pruritus ani is the itching sensation of the anus or perianal skin. It is a manifestation of residual fecal material, hemorrhoids, rectal fistula, anal fissures, malignancy, psoriasis, or ingestion of certain foods. It can also be caused by infection with pinworms, scabies, pubic lice, and certain sexually transmitted diseases.
Diagnostic Testing
· Anoscopy is used to evaluate for anal fissures with 90% of lesions found at the posterior midline.
· Direct visualization via sigmoidoscopy or colonoscopy may be necessary to evaluate for hemorrhoids, perirectal fistula, intussusception, malignancy, or inflammatory bowel disease.
· Perineal sensory disturbances, identifiable by nerve conduction studies, can be a sign of low back injury or degenerative disk disease with nerve damage.
· Endoscopic ultrasound can assess the sphincter for mechanical disruption.
TREATMENT
· Increased dietary fiber, resulting in softer bulky stools and less straining, as well as stool softeners, analgesic suppositories, and warm sitz baths given two to three times a day can alleviate most anorectal pain.19
· Topical nitroglycerin or injection with botulinum toxin has achieved temporary relaxation of sphincter tone to permit healing of anal fissures.20
· Antibiotics such as ciprofloxacin and metronidazole may aid in healing of perirectal fistulas, but additional medical therapy may be needed when due to Crohn disease.
· Pelvic floor muscle strengthening with biofeedback can be used in appropriate patients.
· Patients with proctalgia fugax benefit from reassurance and symptomatic relief with local heat and massage.
· Pruritus ani benefits from the following treatment:
o Antimicrobial therapy for the specific organism, if indicated
o Oral antihistamines for nocturnal symptoms
o Short-term topical treatment with hydrocortisone cream 1% (not to exceed 2 weeks’ duration) or zinc oxide ointment
· Surgical intervention
o Persistent, symptomatic hemorrhoids may require endoscopic band ligation or hemorrhoidectomy.
o Chronic anal fissures require anal sphincterotomy.
o Excision and drainage of perirectal fistulas.
o Incision and drainage of perirectal abscesses.
o Reduction of rectal prolapse or frequent partial prolapse.
o Refractory fecal incontinence.
Approach to Abnormal Liver Chemistries
GENERAL PRINCIPLES
· Laboratory evaluation should be interpreted in conjunction with the clinical history and physical examination. A full discussion of liver diseases is presented in Chapter 30.
· Liver test abnormalities can be grouped into the following categories:
o Hepatocellular disease: aspartate aminotransferase (AST) and alanine aminotransferase (ALT) elevated more than bilirubin and alkaline phosphatase
o Cholestatic disease: bilirubin and alkaline phosphatase elevated more than AST and ALT
DIAGNOSIS
Clinical Presentation
History
· Screen for exposure to hepatitis A, B, or C, and obtain history of blood transfusions, intravenous drug use, and sexual contacts.
· The constellation of RUQ pain, fever, and jaundice is known as Charcot triad and suggests acute cholecystitis. The addition of altered mental status and hypotension to this triad is known as Reynolds pentad and can indicate ascending cholangitis.
· Pain in the midabdomen that radiates to the back suggests acute pancreatitis, which is most commonly caused by choledocholithiasis and may be accompanied by abnormal liver tests.
· Rapid intense RUQ pain may also imply choledocholithiasis, particularly in those with prior cholelithiasis or cholecystectomy.
· Evaluate for nonspecific symptoms including nausea, vomiting, chills, fevers, anorexia, and weight loss. Fatigue alone is frequently reported as the primary presenting symptom in patients with liver disease.
· Dark urine is often noted earlier than jaundice and is an indication of increased urobilinogen due to biliary obstruction or hepatocellular dysfunction.
· Pruritus is usually generalized and present in almost all cases of jaundice that exceed 3 to 4 weeks’ duration.
· Painless jaundice should raise suspicion for pancreaticobiliary disorders, as neoplasms of the pancreatic head may result in extrahepatic biliary obstruction.
· Acute onset of abnormal liver tests may indicate hemolysis or biliary tract obstruction.
· Abdominal pain may reflect stretching of the liver capsule from a space-occupying lesion.
· Congestive heart failure and passive hepatic congestion can account for up to 10% of all jaundice in those >60 years of age.21
Physical Examination
· Evaluate for stigmata of chronic liver disease such as parotid gland enlargement, spider angiomas (most commonly found on the trunk), palmar erythema, Dupuytren contractures (fibrous contractures of the palmar fascia), gynecomastia, hepatomegaly or small liver size, splenomegaly, caput medusa, testicular atrophy, and ascites.
· Fever can be found in acute and chronic illness and may be suggestive of infection.
· Hepatomegaly >15 cm in span can be found in passive congestion, malignant or fatty infiltration, or other infiltrative disorders.
· Splenomegaly is found in patients with portal hypertension and cirrhosis and may also be found in those with hemolysis and a vast array of hematologic disorders and malignancies.
· Murphy sign (RUQ tenderness palpated during inspiration) may indicate cholecystitis. Palpable distended gallbladder without tenderness (Courvoisier sign) is commonly found in pancreaticobiliary malignancy with obstruction.
· Ascites may be present in cirrhosis of various causes and intra-abdominal malignancy as well as congestive heart failure and pancreatitis.
· Cutaneous findings include xanthomas, which may be seen in chronic cholestasis of primary biliary cirrhosis. Gray-bronze discoloration of the skin may suggest hemochromatosis with hepatic involvement. Urticaria may be a sign of acute hepatitis B infection.
Differential Diagnosis
The differential diagnosis for abnormal liver tests is presented in Table 28-6.22
Diagnostic Testing
Laboratories
Evaluate for hemolysis with a CBC, peripheral blood smear, reticulocyte count, lactate dehydrogenase, haptoglobin, and indirect bilirubin.
· Bilirubin:
o Impaired excretion of bilirubin results in an increase in the conjugated form, and clinical icterus presents if the total bilirubin level exceeds 2.5 mg/dL.
o Bilirubin elevation can be prolonged despite convalescence of the acute illness.
o An isolated indirect hyperbilirubinemia that does not exceed 5 mg/dL with normal transaminases and no indication of hemolysis may be the result of a benign familial disorder known as Gilbert syndrome, in which hyperbilirubinemia occurs in response to fasting and physiologic stress.
· Prothrombin Time:
o Impaired liver synthesis of vitamin K–dependent coagulation factors in the extrinsic pathway results in an abnormal PT.
o Cirrhosis, hepatitis, and cholestatic syndromes may produce prolonged PT, which, as a result, can serve as a useful prognostic indicator in patients with cirrhosis.
· Albumin:
o Another measure of the liver’s synthetic function.
o Half-life of 20 days, which makes it better indicator of chronic liver disease.
o Low levels may be present in some patients with poor nutrition, but the finding is nonspecific and should not be used independently to assess a patient’s nutritional status or liver function.
o Loss of this protein can occur through the GI tract or kidneys.
o Dilutional effect should also be considered in volume overload states, in normal pregnancy, and in acute or chronic inflammatory states.
· Aminotransferases:
o AST can be released into the blood from numerous tissues, including liver, cardiac and skeletal muscle, kidney, and brain.
o ALT is more specific to the liver, and serum levels rise with hepatocyte death.
o Elevations in the thousands can be seen in viral hepatitis and toxin- or ischemia-induced hepatic injury.
o Elevation of AST and ALT in a ≥2:1 ratio, high serum γ-glutamyl transpeptidase (GGT), and an elevated mean corpuscular volume of red cells are highly suspicious for alcoholic liver disease.
o Injury from alcohol almost never results in elevations that exceed 10 times the normal values.
· Alkaline phosphatase:
o Elevated serum levels can arise from processes that affect the liver, skeletal system, intestines, placenta, kidneys, and leukocytes.
o GGT levels can differentiate between biliary and other sources of alkaline phosphatase.
o The largest increases are seen in cholestatic syndromes and intrahepatic and extrahepatic biliary ductal obstruction.
o Markedly increased levels without associated liver disease are sometimes seen in congestive heart failure, bone diseases, and Hodgkin lymphoma.
· Elevated antimitochondrial antibody (AMA) indicates primary biliary cirrhosis.
· Elevated anti–smooth muscle antibody (ASMA) and antinuclear antibody and immunoglobulins indicate autoimmune hepatitis.
· Elevated iron studies suggest hemochromatosis.
· Viral hepatitis panel can diagnose viral etiologies.
· α-Fetoprotein (AFP) is used as a screening test for hepatocellular malignancy in patients with cirrhosis.23
Diagnostic Procedures
· Ultrasound should be used initially for rapid evaluation of the biliary system. Sensitivity is 95% for detection of cholelithiasis and acute cholecystitis and identifying ductal dilation.
· CT scan should be obtained for liver parenchyma examination as well as for distinction between stones, tumors, and stricture.
· Endoscopic retrograde cholangiopancreatography (ERCP) is most useful in diagnosing and treating obstructive jaundice in the setting of choledocholithiasis, cholangitis, intra- and extrahepatic strictures, and pancreatic ductal disease. Magnetic resonance cholangiopancreatography (MRCP) is also useful diagnostically but has no therapeutic use.
· Liver biopsy is helpful in diagnosing the etiology of liver disease in those with abnormal enzymes for >6 months, assuming obstruction is excluded.
· If ascites is present, consider paracentesis to check the following:
o Cell count to rule out infection.
o Serum ascites-albumin gradient (SAAG, the difference between serum and ascites albumin measurements); values of >1.1 indicate portal hypertension.
o Cytology to evaluate for malignancy.
TREATMENT
Treatment depends on the underlying illness. See Chapter 30 for specific management.
REFERENCES
1.Jalil S, Castell DO. Schatzki’s ring: a benign cause of dysphagia in adults. J Clin Gastroenterol 2002;35:295–298.
2.Hewson EG, Sinclair JW, Dalton CB, et al. Twenty-four-hour esophageal pH monitoring: the most useful test for evaluating noncardiac chest pain. Am J Med 1991;90:576–583.
3.Domenech E, Kelly J. Swallowing disorders. Med Clin North Am 1999;83:97–113.
4.DeVault KR, Castell DO. Updated guidelines for diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol 2005;100:190–200.
5.Talley NJ, Vakil NB, Moayyedi P. American Gastroenterological Association technical review on the evaluation of dyspepsia. Gastroenterology 2005;129:1756–1780.
6.Cohen J, Safdi MA, Deal SE, et al.; ASGE/ACG Taskforce on Quality in Endoscopy. Quality indicators for esophagogastroduodenoscopy. Am J Gastroenterol 2006;101:886–891.
7.Fisher RS, Parkman HP. Management of nonulcer dyspepsia. N Engl J Med 1998;339:1376–1381.
8.Hurley BW, Nguyen CC. The spectrum of pseudomembranous enterocolitis and antibiotic-associated diarrhea. Arch Intern Med 2002;162:2177–2184.
9.Ewe K, Karbach U. Factitious diarrhoea. Clin Gastroenterol 1986;15:723–740.
10.Potter GD. Bile acid diarrhea. Dig Dis 1998;16:118–124.
11.Carroccio A, Vitale G, Di Prima L, et al. Comparison of anti-transglutaminase ELISAs and an anti-endomysial antibody assay in the diagnosis of celiac disease: a prospective study. Clin Chem2002;48:1546–1550.
12.Rostom A, Dubé C, Cranney A, et al. The diagnostic accuracy of serologic tests for celiac disease: a systematic review. Gastroenterology 2005;128:S38–S46.
13.Longstreth GF, Thompson WG, Chey WD, et al. Functional bowel disorders. Gastroenterology 2006;130:1480–91.
14.Soffer EE. Constipation: an approach to diagnosis, treatment, referral. Cleve Clin J Med 1999;66(1):41–46.
15.Schiller LR. Clinical pharmacology and use of laxatives and lavage solutions. J Clin Gastroenterol 1999;28(1):11–18.
16.Frame PS, Dolan P, Kohli R, Eberly SW. Use of colchicine to treat severe constipation in developmentally disabled patients. J Am Board Fam Pract 1998;11:341–6.
17.Verne GN, Davis RH, Robinson ME, et al. Treatment of chronic constipation with colchicine: dandomized, double-blind, placebo-controlled, crossover trial. Am J Gastroenterol 2003;98:1112–6.
18.Raghavi SA, Shabani S, Mehramiri A, et al. Colchicine is effective for short-term treatment of slow transit constipation: a double-blind placebo-controlled clinical trial. Int J Colorectal Dis 2010;25:389–94.
19.Herzig DO, Lu KC. Anal fissure. Surg Clin North Am 2010;90:33–44.
20.Dhawan S, Chopra S. Nonsurgical approaches for the treatment of anal fissures. Am J Gastroenterol 2007;102:1312–1321.
21.Qureshi WA. Intrahepatic cholestatic syndromes: pathogenesis, clinical features and management. Dig Dis 1999;17:49–59.
22.Zimmerman HJ. Update of hepatotoxicity due to classes of drugs in common clinical use: non-steroidal drugs, anti-inflammatory drugs, antibiotics, antihypertensives, and cardiac and psychotropic agents. Semin Liver Dis1990;10(4):322–338.
23.Frank BB. Clinical evaluation of jaundice. A guideline of the Patient Care Committee of the American Gastroenterological Association. JAMA 1989;262:3031–3034.