nueva etapa, supone la inauguración del modelo de la protección integral que
III. Derecho a una jurisdicción especializada
eating and relieved with fasting or a clear liquid diet suggests car- bohydrate malabsorption, whereas persistent or nocturnal diar- rhea suggests a secretory process. The presence of persistent, severe or aching abdominal pain suggests an invasive process asso- ciated with inflammation or destruction of the mucosa. Skin find- ings, when present, may provide significant diagnostic clues. For example, flushing may indicate carcinoid syndrome; dermatitis herpetiformis may occur in patients with celiac sprue; and erythe- ma nodosum or pyoderma gangrenosum may suggest underlying inflammatory bowel disease. Bloody diarrhea typically indicates an invasive process with loss of intestinal mucosal integrity. An oily residue or evidence of undigested food in the toilet bowl is more suggestive of malabsorption.
Consider irritable bowel syndrome in patients with a long- standing history of abdominal pain and abnormal bowel habits (constipation, diarrhea, or variable bowel movements) in the absence of other defined illnesses. The presence of weight loss, blood, or nocturnal diarrhea almost always indicates that the patient does not have irritable bowel syndrome.
The number and variety of diagnostic tests available for patients with chronic diarrhea is extensive, and further testing should be guided by information obtained from history and physical. A com- plete blood count and chemistry panel can reveal anemia, leuko- cytosis, electrolyte and nutritional status. Bacterial infections rarely cause chronic diarrhea in immunocompetent patients, but com- mon infectious causes of acute diarrhea such as Campylobacter or
Salmonella can cause persistent diarrhea in immunocompromised
patients. Infection should always be ruled out in patients with
chronic diarrhea before proceeding with more extensive testing (Table 2).
A fecal fat study is usually indicated for evaluating a patient with noninvasive diarrhea. However, test results are valid only if the patient ingests an adequate amount of dietary fat (>100 g/d). Any cause of diarrhea may mildly elevate fecal fat values (6-10 g/24 hr), but values in excess of 14 g/24 hr almost always indi- cate primary fat malabsorption.
The presence of fecal leukocytes or lactoferrin suggests an inflammatory process but rarely provides more specific clues about the cause of diarrhea. If infection is excluded in a patient with chronic inflammatory diarrhea, colonoscopy or flexible sigmoi- doscopy with biopsies are usually required for diagnosis.
Measurement of stool electrolytes is valuable for only a subset of patients who remain a diagnostic challenge despite the exclu- sion of infectious, iatrogenic, and inflammatory causes of diarrhea. Stool electrolytes help differentiate osmotic from secretory diar- rhea. If factitious diarrhea is suspected, a fresh liquid stool sample should be obtained for determination of total osmolarity, stool sodium and potassium concentrations, and the osmotic gap should be calculated.
Celiac sprue (gluten-sensitive enteropathy) occurs in approx- imately 1:120 to 1:300 persons in the United States and other northern European countries. Classic symptoms include steator- rhea and weight loss, but many have only mild or nonspecific symptoms that often result in erroneous diagnosis of irritable bowel syndrome. Laboratory tests that aid the diagnosis include anti-tissue transglutaminase and antiendomysial antibodies; con- firmation is by endoscopic small-bowel biopsy.
62 • Gastroenterology and Hepatology
Table 1. Causes and Evaluation of Chronic Noninfectious Diarrhea
Condition Notes
Ulcerative colitis Bloody diarrhea, tenesmus. Obtain colonoscopy and biopsies.
Crohn's disease Weight loss, anemia, and hypoalbuminemia. Obtain small bowel imaging and/or ileocolonoscopy with biopsy. Microscopic colitis (collagenous Diarrhea unrelated to food intake (e.g., nocturnal diarrhea). Colonoscopy or sigmoidoscopy with biopsy. colitis, lymphocytic colitis)
Irritable bowel syndrome Bloating, abdominal discomfort relieved by a bowel movement; no weight loss or alarm features.
Celiac sprue Dermatitis herpetiformis, iron deficiency anemia. Obtain anti-tissue transglutaminase antibody and (if positive) small bowel biopsy.
Whipple’s disease Arthralgias, neurologic or ophthalmologic symptoms. Polymerase chain reaction for T. whippleii; small bowel biopsy. Carbohydrate intolerance Excess lactose—use of artificial sweeteners (sorbitol, mannitol), or fructose. Attempt dietary exclusion or breath
hydrogen test.
Pancreatic insufficiency Chronic pancreatitis, hyperglycemia, history of pancreatic resection. Obtain tests for excess fecal fat, x-ray for pancreatic calcifications, and pancreatic function tests (e.g., secretin stimulation test).
Small bowel bacterial overgrowth Intestinal dysmotility (e.g., diabetes mellitus, systemic sclerosis), jejunal diverticula. Response to empiric antibiotics, duodenal aspirate.
Common variable immunodeficiency Pulmonary diseases, recurrent Giardia infection. Obtain tests for hypogammaglobulinemia (multiple subclasses). Medications History. Review a drug database.
Enteral feedings History. Classic osmotic diarrhea.
Bile acid malabsorption History of resection of <100 cm of distal small bowel. Diagnosis of exclusion, empiric response to cholestyramine. Bile acid deficiency Cholestasis, history of resection of >100 cm of small bowel. Diagnosis of exclusion, test for excess fecal fat. Dumping syndrome Postprandial flushing, tachycardia, diaphoresis. History of previous gastrectomy or gastric bypass surgery. Self-induced diarrhea Somatization or other psychiatric syndromes. History of laxative use. Obtain tests for stool pH, sodium, potassium,
Excessive bacterial colonization of the small bowel lumen may result in diarrhea and malabsorption. A clue to the presence of bacterial overgrowth is finding a low-serum vitamin B12level and a high-serum folate level (from bacteria production). Common conditions that predispose patients to bacterial overgrowth include diabetes, systemic sclerosis, and surgically created blind loops (i.e., gastrojejunostomy). Although the gold standard is aspiration of duodenal luminal contents for quantitative culture at the time of upper endoscopy, many clinicians first attempt an empiric trial of antibiotics (e.g., amoxicillin–clavulanate or norfloxacin) to see if the patient’s symptoms improve.
Therapy
Treatment of chronic diarrhea should be based on the underlying cause. Symptomatic therapy may be considered if a diagnosis is pending, if a diagnosis cannot be confirmed, or if the condition diagnosed does not have a specific treatment. Symptoms may be controlled with stool-modifying agents such as fiber, opiate-based
medications, bile-acid binding agents, and bismuth-containing medications.
Book Enhancement
Go to www.acponline.org/essentials/gastroenterology-section .html to view a DFA stool test for Giardia, and to review the skin lesions and gastrointestinal histopathology associated with celiac disease. In MKSAP for Students 4, assess yourself with items 18- 20 in the Gastroenterology and Hepatology section.
Bibliography
American College of Physicians.Medical Knowledge Self-Assessment Program 14. Philadelphia: American College of Physicians; 2006.
Fine KD, Schiller LR.AGA technical review on the evaluation and man- agement of chronic diarrhea. Gastroenterology. 1999;116:1464-86. [PMID: 10348832]
Guerrant RL, Van Gilder T, Steiner TS, et al.Practice guidelines for the management of infectious diarrhea. Clin Infect Dis. 2001;32:331-51. [PMID: 11170940]
Approach to Diarrhea • 63
Table 2. Common Tests for Chronic Noninfectious Diarrhea
Condition Notes
Qualitative fecal fat Detects >90% of significant steatorrhea; low dietary fat leads to false-negative results. (Sudan stain of stool)
Quantitative fecal fat Gold standard. Must be on high-fat diet (>100 g/d); Values >10–24 g/24 hr indicate fat malabsorption. (48- or 72-hour)
Fecal leukocytes or lactoferrin For inflammatory bowel diseases. Limited usefulness (poor sensitivity and specificity). Stool osmolarity Normal is 280–300 mosm/kg; <250 mosm/kg suggests factitious diarrhea.
Stool electrolytes Osmotic gap [290 mosm/kg – 2 (Na + K)] >125 mosm/kg suggests osmotic diarrhea; <50 mosm/kg suggests (sodium, potassium) secretory diarrhea.
Stool magnesium Spot sample >90 meq/L is abnormal; use of antacids is a common source. Stool pH pH <6.0 suggests carbohydrate malabsorption.
Anti–tissue transglutaminase Most reliable screening test for celiac sprue; diagnosis is confirmed by small bowel biopsies. (anti-tTG) antibody assay
Breath hydrogen test For carbohydrate malabsorption. Increased hydrogen excretion after carbohydrate challenge.
Small bowel biopsy For malabsorption. Loss of villi (e.g., celiac sprue)- inflammatory infiltrates (Whipple's disease, mastocytosis). Duodenal aspirates For small bowel overgrowth. Quantitative bacterial culture >105is positive.
Neuropeptide assays (gastrin, For secretory diarrhea. Useful if persistent diarrhea >1 L/24 hr despite fasting and other indications of possible tumor vasoactive intestinal peptide, (hypokalemia, mass, skin findings, etc.) are present.
glucagon, somatostatin, pancreatic peptide, neurotensin, substance P, calcitonin, motilin, urine 5-hydroxyindoleacetic acid)
Radiographic small bowel For inflammatory diarrhea or bacterial overgrowth. Strictures, ulcers, fistulas suggests Crohn's disease; diverticulosis follow-through predisposes to bacterial overgrowth.
Colonoscopy with biopsies For inflammatory or secretory diarrhea. Diagnostic for ulcerative colitis, microscopic colitis, strictures, radiation enteropathy.
64
G
allstones are the most common cause of biliary disease in the United States. The incidence of gallstones increases with increasing age and is higher in women than in men. Ninety percent of gallstones in the United States are cholesterol stones. Gallstones form when there is excess cholesterol relative to bile salts and lecithin in bile, resulting in cholesterol crystal pre- cipitation. Risk factors for the formation of cholesterol stones include age, estrogen (female gender, pregnancy, estrogen ther- apy), obesity, physical inactivity, Native American or Mexican- American ancestry, impaired gallbladder emptying (total par- enteral nutrition, biliary strictures), rapid weight loss, and medications (thiazide diuretics, ceftriaxone). Risk factors for pig- ment stones include hemolytic disease (including sickle cell dis- ease), biliary stasis, and biliary infection.The majority of patients with gallstones remain asymptomatic. When gallstones obstruct the cystic duct, symptoms of biliary colic develop. Prolonged obstruction can cause inflammation of the gallbladder (cholecystitis). Gallstones may migrate to the common bile duct (choledocholithiasis) where obstruction can lead to the more serious complications of cholangitis (infection of the biliary tree) and pancreatitis.
Prevention
As obesity and a sedentary lifestyle are major modifiable risk fac- tors for gallstones, primary prevention includes counseling patients about the importance of eating a diet high in fiber and plant- based foods, increasing physical activity, and maintaining a nor- mal body weight. In most patients with asymptomatic gall- stones, the risks of developing symptoms or complications are less than the risk of surgery, so prophylactic cholecystectomy is not indicated. Some patient populations have an increased risk of developing complicated gallbladder disease or gallbladder can- cer: Pima Indian women, patients with calcified (porcelain) gall- bladders, gallstones >3 cm, patients with sickle cell anemia, and organ transplant candidates. These patients may be candidates for prophylactic cholecystectomy.
Diagnosis
No single sign or symptom is sensitive or specific enough to estab- lish or rule out the diagnosis of biliary disease. An appropriate his- tory and physical examination, with selected laboratory and imag- ing studies, is required. History should focus on eliciting characteristic symptoms as well as evaluating risk factors. Classic biliary colic is constant epigastric abdominal pain that develops
over 1 hour or less, radiates to the right scapula or shoulder, and subsides in several hours. Associated symptoms may include bloat- ing, flatulence, and dyspepsia. In acute cholecystitis, the pain fre- quently starts in the epigastric area then localizes in the right upper quadrant. Pain lasting >6 hours, especially if accompanied by fever, chills, and diaphoresis, suggests cholecystitis. A history of jaun- dice, pruritis, acholic stools, and dark urine indicates biliary obstruction due to choledocholithiasis. The physical exam in bil- iary colic may be benign, although there may be right upper quad- rant tenderness and a positive Murphy’s sign (inspiratory arrest when the gallbladder fossa is palpated during deep inspiration). Patients with cholecystitis infrequently have a tender right upper quadrant mass. Jaundice supports the diagnosis of choledo- cholithiasis and, in the presence of fever, cholangitis. Peritoneal signs point to a perforated or inflamed viscus.
Suspect cholecystitis or cholangitis in patients with leukocyto- sis. Mild increases in transaminase and bilirubin concentrations may be seen. Bilirubin >4 mg/dL is not a feature of cholecystitis and should prompt an evaluation for cholangitis (Table 1).
Ultrasound is the initial imaging modality of choice in sus- pected biliary disease. It is the most sensitive and specific test for detecting gallstones, has no risk, is widely available, and is rela- tively inexpensive (Table 2). Ultrasound will demonstrate dilata- tion of the cystic or biliary duct if there is an obstructing stone. In cholecystitis, ultrasound will show pericholecystic fluid and a thick- ened gallbladder wall. A sonographic Murphy’s sign further sup- ports the diagnosis. If ultrasound is nondiagnostic, cholescintig- raphy (e.g., HIDA scan) should be obtained; nonvisualization of the gallbladder suggests cholecystitis. Abdominal CT scan should be used when other studies are equivocal or when complications of cholecystitis, such as perforation, cholangitis or gangrenous cholecystitis, are suspected. If bile duct stones are suspected, mag- netic resonance cholangiography is more sensitive than ultra- sonography and is the preferred noninvasive imaging modality. Untreated acute cholecystitis can progress to perforation, gan- grenous cholecystitis (especially in diabetic patients), and acute cholangitis. In cholangitis, bacterial infection proximal to a bile duct obstruction may result in bacteremia and rapid septic shock. Acalculous cholecystitis may present with fever and abnormal transaminases without characteristic abdominal pain, particularly in critically ill and elderly patients. Biliary dyskinesia may have symptoms indistinguishable from biliary colic.