to the brain along the lateral spinothalamic tract and esting Staining the nociceptive dorsal column pathovay and ae then perceived. Other afferent fibers synapse in the pre vertebral ganglia and reflely modulate intestinal mo- ay, LWTESTINAL FLUID ABSORPTION AND SECRETION On an av erage day, 91, of fui enters the gastrointestinal act, | Pusorctale approximately IL of residual fod reaches the colon: the stool excretion of fsid consis about 0.2L | xr! an The colon has a large capacitance and functional re- serve and may recover upto four times its usual vt Pax ein coceyx econ ume of 0 84, provided the rat of flow permits reah- somption to occur, ‘Thus, the colon can partially compensate for intestinal absorpave or secretory ds onder In the colon, soium absorption i predominanily electrogenic, and uptake takes place atthe apical membrane it is com- pensaled for bythe export functione of the basolateral sodium pump, ‘A vanity of neural and non-newral mediators regulate colonic Avid tnd electrolyte balance, including cholinergic, adrenergic, and sero- tonergic mediators. Angiotensin and aldosterone also influence colonic absorption, reflecting the common embryologic development of sistal colonic epithelium and the renal tubules SMALL INTESTINAL MOTILITY During fasting, the motility of the small sntestine is characterized by acychcal even called the migrating motor complex (MMC), which serves to clesrnondigestible resid ftom the smal intestine. This organized propagated series of contractions lasts ‘on average 4 min, oceuts every 60 t0 90 min, nd usually involves the cntze small intestine. After food ingestion, the small intestine pro- «duces regular, mixing contactions of relatively low amplitude, ex- cept in the distal ileum where more powerful contractions eccur it~ fermittenty and empty the ileum by bolus transfers. 'NEOCOLONIC STORAGE AND SALVAGE ‘The distal eum ate a reservoir emplying intermstently by bolas movements, This ation allows time for salvage of fluids, electrolytes, and nuvients. Segmentation by haus- ‘va comparimestalizes the colon and facihlace mixing, retention of residue, and formation of slid stools, In health, the ascending and tranaverte regions of colon function as reservoir (average tant, 15 hy, andthe descending colon acts as a conduit (average transi, 3 8). The colons efficent at conserving sodium and water, a function ‘hat is particularly important in sodiumdepleted patent in whom the ‘smal intestine alone is unable to maintain sodium balance. Diarrhea for constipation may result from alteration inthe reservoir function of the proximal colon ofthe propulsive Tunetion of the let olen, Con- sipution may also result from disturbance of the rectal or sigmoid reservoir, typically as a result of dysfunction ofthe pelvi floor or the ‘coordination of defecation. COLONIE MOTLITY AKD TONE The small ineatinal MMC only rately con- tinues into the colon, However, hort duration o phasic contractions mix colonic contents, and high-ampltude propagated contractions (HAPCs) ate sometimes associated with mass movements through the colon and occur approximately five times per day, usally on awak- ning in the morning and postprandlly. Ineeased frequency of APCs may result in dianhea. The predominant phasic contractions sae irregular and nonpropagated and serve as a “mixing” Iunclion, Colonic tone refers to the background contractility upon which phasic contractile activity (ypically contractions lasting <15 3) is su perimposed, isan important cofactor inthe colon capacitance (vol- ume accommodation) and sensation, FHGunE 35-1, COLONIC MOTIUTY AFTER MEAL INGESTION After meal ingestion, colonic phasic and tonic contactity increase for a period of approximately 2h The iil phase (about 10 min) is mediated by the vagus nerve in response to mechanical distention ofthe stomach, The subsequent response of the colon requires caloric stimulation and is atleast in par mediated by hormones, e.g, eatin and serotonin. ech sah in cetnene a func. Crane eegutes:anYacion of pbsecat, martersce a arc 2a eetuaton Notte pata of eve fora reo ot sone Deen ees od elaine. ‘ston, ae reanaton of berets, DEFECTION Tonic contraction ofthe puboretalis muscle, which forme 4 sling around the rectoanal junction, i importa to maintain conti- rence: during defecation, sacral parasympathetic nerves relax this muscle, facilitating the seaightening of the rectoanal angle Fig 35-1) Distention ofthe rectum reels im transient relaxation of the internal anal sphincter via ntinsic and elexsympatheti innervation, [As sigmoid and rectal contractions increase the presse within the ‘ect, the rectosigmoid angle opens by 15°. Voluntary relaxation fof the extemal anal sphincter (ited muscle innervated by the pur dence nerve) permits the evacuation of feces; his evacuation process can be augmented by an increase in itrabdominal pressure created by the Valsalva maneuver. DIARRHEA DEFINION Diarhea is loosely dened as passage of abnormally igi ‘or unformed stools at an increased frequency, For adults on a typical ‘Westem det, stool weight >200 g/d can generally e considered di- amheal, Because of the fundamental importance of duration to diag- nostic considerations, diatrhea may he further defined as acute if “£2 wooks, persistent if 2 to 4 weeks, and chronic s >4 weeks in duration ‘Two commen conditions, usually associated with the passage of stool Iotaling 200 id, must be distinguished from dirthea, a8 die Agnostic and therapeutic algorithms differ. Pseudediarrhe, ofthe ee quent passage of small volumes of stool is often associated with rectal ‘urgency and accompanies the snstable bowel syndrome or anorectal disorders such az proctitis. Fecal incontinence i the svokutary dit~ charge of rectal contents and is most oflen caused by neuromuscular disorders or structural anorectal problems. Dirthea and urgency, e= pecially i severe, may aggravate er cause incontinence. Pseudodi- tsthea and fecal incontinence occur at prevalence tates comparable to forhigher than that of chronic diarthes and should always be considered in patents complaining of “dirthea.” A careful history and physical ‘examination generally allow these conditions to he discriminated from true diame, ACUTE DIARRHEA More than 90% of caes of acute dare ae caused by infectious agents; these cases are often accompanied by vomiting, fever, and abdominal pain. The remaining 10% or so are caused bY medications, toxic ingestons schema, and other conditions Infectious Agents Mos infectious diarheas are acquited by feal-oal transmission via direct personal contact or, more commonly, via in- estion of food or water contaminated with pathogens from human or ‘animal feces. In the immunelogieally competent person, the resident fecal microllora, containing >500 taxonomically distinct species, are rarely the source of diartea and may actualy play a role in suppress ing the growth of ingested pathogens. Acute infection or injury occurs when the ingested agent overwhelms the host's mucosal immune and nonimmune (gatic acid, digestive enzymes, mucus secretion, peri- stasis, and suppressive resident flora) defenses. Established clinical ‘ssociations with specific enteropathogens may offer diagnostic chesTHBLE 35-2 sssecation betes Patty of Cavave Apts en nal ears oo ‘Toxin producers Preformed toxin Bail cereus Stphyfococeus Copia perngent Enctotonin Vivi cholerae, ‘nerotorigeie Beterths col, Klebrla reaming, Aeromonas species Yonitig _Abemin aln_—_ fer enh 24 Lat neoudherent TEnleropatogenic and ‘nroadheret (ob, end cgi, ppiesporidioss, simi ‘Cyotoin produces {Clas dite ott Hemonage colt ony Invasive erganions ‘Minima nfammsion Rotaine and ‘Norwal ag! Voit falbestion “Salmonella ‘Campyobacte. snd Aeromonat speves Vibro orchaeroitns, Foraia Severe indammsion ‘Shigella species, ‘nerosnvanve E (a, Examecbe stole ise pend rahe a fete te Soure Adige tam DW Powel = T Yama (Teh of Garvcnioy and pot Wis Wiki 06 nd DR Syma, SL Cates nec ihe. Lami inkl 96 In the United States, hgh tsk groups ae recognized! 1. Travelers. Neary 40% of tourists to endemic regions of Latin America, Aca, and Asia develop so-called traveler’ diahea, most ‘commonly due to enterotoxigenic Eschevichia cll as well as to Cam= vlobacter Shigella, and Salmonella, Visitors to Resta especialy St Petersburg) may have increase rik of Giardi-associated dante; visitors to Nepal may aegire Cyclospora. Campers, backpackers, and Swimmers in wikdemess areas may Become infected with Giardia 2. Consumers of certain foods. Diathea closely following food ‘consumption at a picnic, Banquet, o restaurant may suggest infection with Salmonctla, Campylobacter, ot Shgelta from chicken; entero- hhemorthapic E coli (O157:H1) tom underconked hamburger: Bai!- lus aureus from fried see; Stophslococeus aureus ot Salmonella trom ‘mayonnaise or creams; Salmonella fom eggs; and Vibrio species, Sal- ‘monella, or acute hepatitis A or B trom sealood, especially i ra 3. Immunodeficient persons. Individual at tsk for diathea in- clude those with either primary immunodeficiency (eg. IgA def- sieney, common variable hypogammaglobulinemia, chronic gran Tomatcus disease) or the much more commen secondary Jmmunodeficency states (eg. AIDS, senescence, pharmacologic sup- pression). Common enteropathogens often cause a mote severe and protracted danteal ines, and, patc= ‘larly in persons with AIDS, opportu istic infections, such as by Mycobacte- rium species, certain vituses (to rmegalovirus, adenovirus, and herpes simplex), and protozoa (Cryprospori jum, Icapora belli, Mierospoidia, and Blastocystis hominis) may also play a tole (Chap, 173) In patients with AIDS, agents ransmitted veneeally prrectuma (eg, Neisseria gonorrhoeae, Trepo nema pallidm, Chlamydia) may con- Inbute to proctocobis “4, Daycare participants and their family members, Infections with Shi «ella, Giardia, Cryptosporidium, rota ‘irus, and other agents are very common, ani should be considered 5. Instiuionalized persons, Yeo tious diarrhea ie one ofthe most requeat categories of nosocomial infetions in many hospitals and long-term cate fs calles; the causes area variety of mi ‘roorganisms but most commonly Clas: vidi dificil. ‘The pathophysiology underlying acute diathea By infectious agents pro: duces specific clinical features that may also be helpful in diagnosis Table 35 2), Profuse watery diathea secondary small bowel hypersecretion occurs with ingestion of preformed bacterial toxins, «enterotoxin-producing bacteria, and en teroadherent pathogens, Diathea 2:80 ‘ated with masked vomiting and mini imal of no fever may occur abruptly ‘within afew hours afer ingestion of the former two types: vomiting 3s usually Tess, and abdominal cramping or bloat ing iz grealer fever is higher withthe later, Cytotoxin-producing and inva sive microorganisms all cause high fe ver and abdominal pain. Invasive be feria and Entamoeba histolytica often cause bloody diamhea (refered to as dysentery), Yersinia nade the tem ‘al ileal and proximal colon mucosa and ray cause especially severe abdominal pan with tendemness mimick: Ing acute appendicitis Finally, snfectious dianhea may be associated with systemic man- itestations, Reiter's syndrome (arthritis, urethritis, and conjunctivitis) ray accompany oF follow infections by Salmonella, Campylobacter, Shigella, aul Yerrni, Yersniosis may also lead to an autoimmune. type thyroiditis, pericarditis, and glomerulonephntis. Both entero hemorthagi E.coli (0157:H7) and Shigella can lead the hemotyte: uremic syndrome with an attendant high morality rae. Acute diarrhea ‘an alzo be a major symptom: of several eystemic infections including ral hepatitis, lateriosis,legionellois, and tose shock syndrome. rte ae, watey sa watery 1225, watery 123, sally watery, eccaomaly Hoody 225 tally watery, ‘uk Bloody 123+, watery >. watery o bloody 122+, Bloody Other Causes Side elfecte from medications are probably the most ‘common noninfectious cause of acute diarthes, and etiology may be suggested by a temporal association between use and symptom ons ‘Although innumerable medications may produce diarthea, some ofthe more Hrequenty incriminated include antbioucs, cardiac anidys wthmice, anhypertensives, nonsteroidal anisinilammatory drugs SAID), certain antidepressants, chemotherapeutic agents, bros ‘hodilators antacids, and laxatives. Occlusive of nonosclsiveitche ‘mic cole typically oceuts in petsons 250 year, offen presents asacute lower abdominal pain preceding watery, then bloody dianhea, tnd generally results im acute snflarumatory changes inthe sigmoid or Jef colon wile sparing the rectum. Acvle arches may accompany colonic divericulitir and graj-vertu-hort dveave. Acute dhathes, of ten associated with systemic compromise, can follow ingestion of tox~ ins including organophosphate intecticides, smanita and other mush- ooms, arsenic, and preformed environmental toxins in seafoods, such as ciguatera and scombroid. The conditions causing chronic diarrhea fan also be confused with acute diarthea early in their course, This ‘confusion may occur with inflammatory bowel ditease and some of the other invlammatery chronic ciatheas that may have an abrupt rather than insidious onest and exhibit features tht mimic infection, ene "The decision to evaluate acue danthea depends on it severity and uration and on various host tactors (Fig. 35-2). Most episodes of acute diathea ae mild and self-limited and do not justify the cost and potential morbidity of diagnostic or pharmacologic interven ‘ons Indications for evaluation include profuse dames with de hydration, grossly bloody stools, fever =38.5°C, duration >48 h ‘without improvement, new community outbreaks, aszocited se vere abdominal ain inpatients 50 yeats, ad elderly (=70 yeats) for immunocompromised patients, In some cases of moderately se vere febrile diaztheaaseociated with fecal leukocytes (or increased. fecal levels of the leukocyte proteins) or with gross blood, adi agnestic evaluation might be avoided in favor ofan empiical an ‘ibiowe til (see below) “Tae comerstone of diagnosis in those suspected of severe acute infectious diathea is microbiologic analysis ofthe stool. Workup includes cultures for bacterial and vial pathogens, diectnepecton {for ova nd parasites, and immuncassays fr certain bacteial toxins (C dite), vizal antigens (otavius), and protoroal antigens Hit ana brveleal exam 1 Tikty infectious T ‘acivtes atered) and leat replacerart I Fave: 200. bledy scale, eel WA, ‘runoconramtes or ley host Evalaie and Trea accordingly ia Turwesbiees) 1 Severe Tinespactate) Teste ta Es on Teeigesoaney Pesaro ol! Paneae a toy Get "Peer | [Stance = ak AGINE 35-2 grt ee gee se ae. Cer np ix ate van wih (*) metal are (wt gamle Prt a Giardia, #. histolytica). The aforementioned clinical and epi- Aensologic associations may assist in focusing the evaluation, Ira particular pathogen or set of possible pathogens is so implicated, then ether the whole panel of routine studies may not be necessary for, in some instances, special cultures may be appropriate as for enterohemorthagic and other types of E coli Vibrio species, and Yersinia. Molecular diagnosis of pathogens in sto0] cane made by identification of unique DNA sequences: and evolving microar- ray technologies could lad to amore rapid, sensitive speci, and ‘ostetfective diagnortic approach inthe fare Persistent diamhea is commonly due to Giardia, but aditional eausative organisms that should be considered include C.difiile (especialy if antibiotics had been administered), F. histolytica, Cryptosporidium, Campylobacter, and others. If stool studies are unrevealing, then flexible sigmoidoscopy with biopsies and upper endoscopy with duodenal aspirates an biopsies may be indicated ‘Structural examination by sigmoidoscopy, colonoscopy, of ab- dominal computed tomographic scanning (or other imaging ap- roaches) may be appropriate in patients wth uncharacterized per- fistent dines to exclude inflammatory bowel dseate, of a= an ‘ntl approach in patients wath suspected noninfectious acute di hea such as might be caused by ischemic colitis, diveticul or patal bowel obstruction, [&] TREATMENT Fluid and electeolyte replacement ae of central impontance to all forms of acute diarthea. Fluid replacement alone may sufice for mild cases, Oral saguelecrolyte solutions (sport drinks or designed formula. tions) shoul be instituted promptly with severe diarhea to init de- hydration. which isthe major cause of death Profoundly dehydrated patients, especially infants and the elderly, requite intzavenous tehy- dration. In moderately severe nonfebrile and noabloody diahea,antimo- Ulty anusecretory agents such as loperamide can be useful adjuncts to contol symptoms. Such agents should be avoided with febrile dys- entry, which may be exacerbated or prolonged by them. Bismth subsaicylate may reduce symptoms of vomiting and diarhea but should not be used to eeatimmunocompremised patents because of the is of biemth encephalopathy. Jdicious use of antibiotics is appropriate in selected instances of acute diartea and may reduce ts seventy and duration (Fig. 35-2) “Many physicians teat moderately to severely ill patients with febrile Aysentery empirically without diagnostic evaluation using a quinolone such a5 ciprofloxacin (500 mg bid for 3 to 5 d). Empirical teatment an also be considered for supected giardiasis with metronidazole (250 mg gid for 74), Section of antibiotics and dosage regimens are these dictated by speciic pathogens and conditions found (Chaps 13, 134, 137-143), Antibiotic coverage i indicated whether ot not 1 causative organism is discovered in patients who are immunocom- mised, have mechanical hear valves or recent vascular gras, of te elderly. Anibioue prophylaxis ie indeated fr certain patients rave ling to high-risk countries im whom the ikelihood or seriousness of Acquired diathea would be especially high, including those with m= ‘munecempromise, inflammatory bowel disease, or gasic achloshy dia. Use of timethoprinysulfamethoxazole or ciprofloxacin may re- duce bacterial diarhes in such travelers by 90% CHRONIC DIARRHEA. Dischea lasting >4 weeks warrants evaluation to exclude serious underlying pathology. In contrast to acute diarthea, ‘most of the many causes of chronic diarthea are noninfectious. The Classification of chron diasthea by pathophysiologic mechanism fa- cites a rational approach to management (Table 35-3) Seeretory Causes Secretory dhartbess are de to derangements in Hid ani elecitolye transport across the enterocolie mucosa They ate charSm ad Pret TABLE 35-3 War Coss of Casi ares Arg ta Predoninnt Patios Mecbans Secretory eases ‘Exogenous rimlant axaives (Chri easel geeten Other drugs and toxins Taflammatory cases eto nlsmmatry bowel ucase (Cros evens eerie cobs) Endogenons laxatives (Shyéroxy Microscope and olagenous Tale acid) cals ice secetoy dartea Te elled mtcoealdose Crt bce fection (Cor 2 immsodetceaces, Bowel resection, dete or ‘stl (absorption) Parl bowel bron o eel ‘iapction omoneproducingtamaes (acciotd, VIPoma, medullary ‘canter of thyroid, masoeyons, [psinoma. colorectal vise food allergy eosinophilic gastoeneis,grafevbost fiscae) Infect vate haters "ruses, ad puraies) Radiation jy Garton malignancies Dysmotile anes Seneca) "isc! newernyepatier ‘Addison ease Hperthyrotie, Congenital lecoiyteabeorpion Drug prokinetc ages) ‘tects acta eaees Ome enueer Munemasses ‘Onmovielanatives (Mg! PO,", Bulimia 302") Lactate and other dxcchaide “efeiencee [Nonabvorbabe carbobydatee "Gerace, polyetiiene eyecl) Stestombeal eases Tham! malgseon IGaocretic etocton ‘auletecy, bacterial overgowi liver disease) ‘Moco malabsarion (eine spre, Whipple's dns, tection, sbvubpoprotenenia,tchemia) Postmueosel abstuction (or lymphatic ebotection} acterized clinically by watery, large-volume Lecal outpats that are 1yp- ically painless and persist with tasting. Because there is no malab- sorbed solute, stool osmolality is arcounted for by normal endogenous leeteolytes with no fecal ormotie gap. [MeICATONS Side effects from regular ingestion of drugs and toxins axe the most common seretory eauses of chron dizthen, Hundreds ‘of prescription and over-the-counter medications (see "Other Causes fof Acute Diarhea.” above) may produce unwanted dianhea. Surep- tions or hastual use of stimulant laxatives [eg senna, caseat, bit acodyl,ricinoleic acd (cate oil) must also be considered. Chronic ‘ethanol consumption may cause a seeretory-type diarthea due to en- tesoeyte injury with impaired sodium and water absorption as wel as to rapid trait and other alterations. Inadvertent ingestion of certain ‘environmental toxins (eg, arsenic) may Tea to chtonic rather tha acute forms of diathea. Certain bacterial infections may oceascnally persist and he associated wath a seeretory.type diarhea, OWE RESTON, Most OSES, OR EATEROCOC FTA These conditions say resul in a secretory-type dirshea because of inadequate surface for resospsion of secreted ids and electralytes Unlike other secretory artheas, this subset of conditiens tends to worsen with eating. With sisease (¢.g, Crohn's ileitis) or resection of 100 cm of terminal ileum, dihydroxy bile acids may escape absorption and stimulate co- lonie secretion (cholortheie darchea). This mechanism may contribute to so-aled idiopathic secretory diarrhea, in which bil aids ae fune= tionally malabserbed frem a normal-appearing terminal ileum. Partial Dowel obstruction, ostomy stricture, of fecal smapaction may paradon= ically lead to increased fecal output due to hypersecretion onNoWES Altyough uncommon the classic examples of secretory di ahea ae those mediated by hormenes. Metastatic gastrointestinal carcinoid tumors or rarely, primary bronchial carcinoids may pr ‘duce watery darts alone o as past af the carcinoid syndrome that ‘comprises episodic flushing, wheering, dyspnea, and right-sided val- vulat heart disease, Diarthea itd to the release ino the citealation of potent intestinal secretagogues including serotonin, histamine, pros taglandins, and various kinins. Pellagra-like skin lesions may rarely ‘occur a the result of serotonin overproduction wth niacin depletion Gastrinoma, one of the mest common neuroendocrine tumors, most ‘ypiealy presents with refractory peptic ueers, but anes oscars tp to one-third of eases and may be the only clinical manifestation in 10%. While various secretagogues released with gastrin may play a role, the dinthea most often resus from fat maldigestion owing to pancreatic enzyme inactivation by low intaduodenal pH. The watery Aiarthes hypokalemia achlorhydria syndrome, also ealled pancreatic cholera, is due to 2 non-B cell pancreatic adenoma, refered 10 as a ViPoma, that secretes vasoactive intestinal peptide (VIP) and a hor of other peptide hormones including pancreatic polypeptie, secretin, gsinn, gastinsinhibitory polypeptide, neurotensin, calcitonin, and prostaglandins. The seeetory dante soften massive with stool vol lames >3 Li daily volumes as high as 20 L have been reported. Lite threatening dehydration: neuromuscular dysfunction {rom associated hypokalemia, hypomagnesemia, of hypercalcemia; Bushing; and by: peselycemia may accompany a ViPoma. Medullary carcinoma ofthe thyroid may present with watery diarthea caused by caleonin, other secreory peptides or prostaglandins. This tumor occurs sporadically for in 25 to 30% of eases, a8 Tealre of multiple endocrine neoplasia {ype Ils with pheochremocytomas and hypesparathyoidism, Prom sent diatheaisolten associated wath melastai dtease aad poor prog: nosis. Systemic mastocytais, which may be associated with the skin lesion urticaria pigmentosa, may cause diazthea that is either secretory and mediated by histamine or inflammatory and due to intestinal Gl tention by mast cells. Large colorectal villous adenomas may rately be asvoctated witha secretory diaries that may case hypokalemia, can be sahibited by NSATDs, and is apparently mediated by pros slandins CONGENITAL DEFECTS 10 ABSORPTION. Rarely, these defects cause watery siathea rom bith snd include detective CI-/HICO,” exehange (con genital chloridorriea) with alkalosis and detective Na'/H exchange ‘with acidosis, Some hormone deicieneies may be associated with wa tery darts, such ae occurs with adrenocomical insufficiency (Addi son's disease) that may be accompanied by hyperpigmentaion. Osmati Causes Osmoic dirthea occurs when ingested, poorly a. sotbuble, osmotically active solutes draw enough id lumenward to exceed the resorpive capacity of the colon. Fecal water output i treats in proportion to such a solute load, Oxmove darthea charac~ tevstically ceases with fasting of with discontinued oral intake ofthe olfending agent. SWOT LATS Ingestion of magnesium-containing antacids, health supplements, of laxatives may induce osmosie ditshea typified by 4 stool osmotic gap: 2[Na] + [K]) <290 mosmvkg. Anionic laxatives containing slfates or phosphates produce osmotic diashea without an ‘osmotic gap, a8 sodium accompanies the anionic sluts; direct meas ‘urement of stool sulfates and phosphates may be necessary 1 con, the cause of diarrhea ‘AgoonroRATe waAasonrTON Carbohydrate malabsorption dve to a quired or congenital defects in brush-border disaccharidases and other ‘enzymes lead to osmotic darzhea with alow pl. One of the most common causes of chronic diarthea in adults i lactase deficiency, ‘which atfects three-fourths of non-Caucastans worldwide and 50 0% fof petsons in the United States; most leat to avoid milk products ‘without an intervention. Some sugars, suchas sorbitol, ae universally malabsorbed, and diamea ensues with ingestion of ample medica tons, rum, or candies sweetened with these nonabsorbable sugat,Lactulose, used to ai stools in patients with hepatie failure, also causes diarea on this basis Steatonheal Causes Fat malabsorption may led to greasy, foul-smell~ ing, diticutto-tush diambea oltenazcocited with weightloss and nutsitional deiiencies due to concomitant malabsorption of amino fscide and vitamins. Increased fecal output is caused by the osmotic fleets of fatty acid, especially after bacterial hydzoxylaton, and, (0 ‘lesser exten, bythe burden of neusal fat. Quansitatively, steatorrea 4s dened as stool fat exceeding the normal 7 gf: daily fecal fat av rages 15 t0 25 g with small intestinal diseases and is often >40 ‘with pancretic exocrine inuticiency. intraluminal maldigestion, m= cosal malabsorption, or lymphatic obstruction may produce steator- thes, nTRAOUINA, MADIGESTON Ths Condition mest commonly results fom. pancreatic exocrine insufficiency, which occurs when >90% of pan- reatie secretory function i lost, Chronic pancreas, usualy a 8 ucla of ethanol abuse, most frequently. causes pancreatic insu ciency. Other causes include cyst fibrosis, pancreatic. duct ‘obtrucion, and rately, somatastatinoma, Bacterial qvergeowth in the small intestine may deconjugat ile acids and alter micelle formation ‘hat impairs ft digestion; st occurs with stasis from a blind-loop small bowel diverticulum or dysmotiliy and is especially Iikely in the cl- erly. Finally. cithoss o biliary obstruction may lead to mild stez- torthea due to defieient intraluminal bile acid concentation, Macosse maeasonrion Mucosal malabsorption occurs from a variety of enteropathies but most prottypiclly and perhaps most commonly from celiac sprue. Tis gluten-sensitive enteropathy characterized by villous atophy and crypt hyperplasia in the proximal small bowel often presents with fatty diarhea associated with molipe nusitenal Aehciencies of varying severity and affects all ages. Tropical sprue ‘may produce a similar histologic and clinical syndrome but cecurs in residents of or travelers to topical climates: its often abrupt onset and response o antibiotics suggest an infectious etiology. Whipple's dis ase, doe to the actinomycete Treponema whipped! and histiocytic ‘inflation ofthe small howel mucosa, is a ess common cause of steatorhea that most ypically occurs in young or middle-aged men: sts frequently associated with arthralgias, fever. lymphadenopathy, and extteme fatigue and may alfect the central nervous system and endocardium, A simular clinical and histologic picture resale Kom, Mycobacterium aviun-iniracelludare ifection in patients with AIDS, “Abetalipoproteinemia ie rare defect of chylomicron formation and fat malabsorpion in children asiociaed with acanthocytc erythro= cytes, alaxia, and retinitis pigmentosa. Several other conditions may ‘use mucosal malabsorption including infections, especially withro- tozoa such at Giardia, numerous mediestons (e..,calehicine, cho- Jestyramine, neomycin), and chronic ischemia, PasTMcosit LYMPWAT OASTRUCON “The pathophysiology of this condi tion, which is due tothe rare congenital intestinal Iymphongiecasia oF 0 acquired iymphatic obstruction secondary to trauma, tumor, of infection, leads tothe unigue constellation of fat malabsorption with enteric losses of protein (often causing edema) and Tymphocytes (With resultant Iymphocytopenia) that enter the portal circulation directly Carbohydrate and amino aid absorption ate preserve. Inflammatory Cases Inflammatory diarheas are generally accompa- nied by pain, fever, bleeding, of other manifestations of iaftansmation. ‘The mechanism af diarthea may not only be exudation but, depending on lesion site, may include fat malabsorption, disrupted Muidelecto~ Ite absorption, and hypersecretion or hypermotiity from release of cytokines and other inflammatory mediators. The unifying feature on soo! analysis isthe presence of leukocytes or leukocyte-derived pro- teins such as calprotecun. With severe inflammation exudative protein loss can Tead to anasarca (generalized edema). Any middle-aged of ‘older person with chronic iflammatory-type dara, especially with blood, shouldbe carefully evaluated to exclude a colorectal or large Prt ro EE loiparic MpiaMNATORY BOWEL DISEASE ‘The illnesses in this category, Which include Crofn's disease and chronic adcerative colt, ate among the most common organic causes of chronic diathea in adults and range in seventy from mild to fulminant and hfe-heatening. They ‘may be associated with uveitis, polyarthralgias, cholestatic liver dis- ‘ease (primary sclerosing cholangitis), and various skin lesions (ry ‘hema nodosum, pyoderma gangrenosum). Microscopic colitis. ine cluding collagenous colt, i an inreasingly recognized cause of ‘chronic watery diathea; biopsy of a normal appearing coloectum is ‘required for histologic diagnosis. ‘RUA On SECONDARY FORMS OF MMUNGDEFCENCY ImOdefciency may lead to prolonged infectious diasthea. With common, variable hypo: gammaglobulinemia, darhea is particularly prevalent and often the esl of giardiasis osinopmccasmoenenns Eosinophil infiltration ofthe mucosa, mus vlan, or serosa at any level ofthe gastrointestinal tract may cause diane, pain, vomiting, of ascites Affected patients often have an atopic history, Charcot Leyden crystals due to extruded eosinophil contents may be seen on microscopic inspection of stool, and pesih- ‘era eosinophilia is present in 50 to 75% of patients. While hypersen Svity t certain foods occurs in adults, tue food allergy causing ‘conic dara stare UTIR USES Chronic inflammatory diahea may be caused by radi- lation enterocolii, chronic graftversuthost diseate, Behe ¢ drome, and Cronkite-Canada syndrome, among others. Dysmotle Causes Rapid transit may accompany many diarbeas as a secondary or contributing phenomenon, bat primary dysmotliy is an ‘unusual eGology of tue dara, Stool features often suggest secre tory diathea, but mild steatorhea of up to 14 of fat per day can be produced by maldigestion from rapid transit alone. Hyperthyroidism, ‘carcinoid syndrome, and certain drugs (prostaglandins, rokinetic agents) may produce hypermotiity with resultant diashea, Primary visceral neuromyepathies or idiopathic acquired intestinal pseudo- dbstrction may lead to stasis with secondary bacterial overgrowth ‘using diatiea. Diabetic diarrhea, olten accompanied by peripheral tux generalized autonomic newopathies, may occur in part hecause of intestinal dysmouiy. ‘The exceedingly common iritable Bowel syndrome (10% point prevalence, 1 to 2% per year incidence) is characterized by disturhed intestinal and colonic motor and sensory responses to various stu Symptoms of stool frequency typically cease at might, altemate with periods of constipation, are accompanied by abdominal pain relieved with defecation, and rarely result in weight loss or true diarhea Facial Gusts Facuital diartiea accounts for up (o 15% of unex: plained dianteas referred to tertiary care centers. Ether as form of Muchausen syndrome (deception or set-injury for secondary gain) ‘or bulimia, some patents covertly sel-admnister laxatives alone or in combination with other medications (eg. durtics) or sutepti lously add water or urine to stool sent for analysis. Suck patents are ‘ypically women, often with histories of psychiatic illness, and dis- proportionately fom careers in health care. Hypotension and hypo- kealemia are common co-presenting features, Such patients often deny ‘this possibilty when confronted, but they do benefit tom psychiatric counseling when they acknowledge their behavior. ‘The laboratory tools available to evaluate the very common prob- Jem of chronic iantea are extensive, and many are cosly and snvasive. As such, the diagnostic evaluation must be rationally di- rected by « careful history and physical examination, and simple Ueage tests ae often warranted before complex investigations are launched (Fig. 35-2). The history, physical examination, and rou- tine blood studies should attempt to characterize the mechanism of| diathea identify diagnostically Relpful associations, and assess the