209 B Mucosal break >5 mm long limited to the space between two mucosal fold tops. C Mucosal break continuous between the tops of two or more mucosal folds but which involves <75% of the esophageal circumference. D Mucosal break involving \211 75% of the esophageal circumference. Treatment \212Lifestyle: Encourage weight loss; raise bed head; small, regular meals. Avoid hot drinks, alcohol, and eating <3 h before be d. Avoid drugs affecting esophageal motility (nitrates, anticholinergics, tricyclic antidep ressants) or that damage the mucosa (NSAIDs, K + salts, alendronate). \212Drugs: Antacids to relieve symptoms. If symptoms persist for >4 wks (or weight \206 \223 ; dysphagia; excessive vomiting; GI bleeding), refer for GI endoscopy . If esophagitis confirmed, try a PPI (the most effective option). Prokinetic drugs: These help gastric emp tying (e.g., metoclopramide; dystonias and tardive dyskinesia can be a serious side effect [see FDA Black Box warning]). \212Surgery: Endoscopic options such as Stretta or EndoCinch (endoscopic plication methods ) have fallen out of use. Laparoscopic fundoplication performed by an experienced surgeon i s a reliable therapeutic option for patients with proven reflux disease to achieve prolonge d symptom relief. Diarrhea The normal daily stool weight is 100 \200\223200 g, and, in the United States, a d aily stool weight >200 g is abnormal. Diarrhea means increased stool water (hence increased stool volume, e.g., >200 mL daily), and thus increased stool frequency and the passage of liquid stool. If it is the stool \200\231s fat content that is increased, the diarrhea is t ermed steatorrhea . Distinguish both from fecal urgency (may be caused by cancers or UC). C onditions that cause diarrhea are broadly classified into osmotic diar- rhea (stool output diminishes with reduced oral intake), secretory diarrhea (stool output persists despite red uction in oral intake), and mucosal injury categories. In reality, high-output diarrhea is usually a combination of these mechanisms. Normal-output diarrhea (stool volume <200 g/d) i s typically related to anorectal dysfunction. Foul-smelling, greasy stools are character- i stic of steatorrhea. See Table 7.1. Clinical features It is important to take a detailed an d accurate history: Is it acute (<3 wks duration) or chronic (>3 wks duration)? Acute : Usu ally infectious or drug-induced. Ask about recent travel, sexual practices, inges- tion of well water or inadequately cooked food and shellfish. Question for exposure to ill contacts Chronic : Usually requires extensive history and further testing. Ask about prior bowel su rgery and a family history. Additional testing should include stool studies for lactoferrin (fecal leukocytes), ova and parasites, cultures, and Clostridium difficile toxin. Check fo r signs of labs of malabsorption, including vitamins, and evaluate stool for steatorrhea (s udan stain). Often, radiographic and endoscopic evaluation with biopsies is required if abo ve testing is normal. \212Is the large or small bowel the source? Large bowel symptoms : W atery stool blood or mucus, pelvic pain relieved by defecation, tenesmus, 210 Table 7.1 Common causes of diarrhea Common causes Gastroenteritis Uncommon Microscopic colitis Rare Autonomic neuropathy Addison \200\231s disease Ischemic colitis Amyloidosis Tropical e nteropathy Viral Bacterial Parasites/protozoa Irritable bowel Celiac disease Chronic pancreatitis Thyrotoxicosis Laxative abuse; food allergy Drugs (below) Colorectal cancer Ulcerative colitis (UC) Crohn disease Lactose intolerance Ileal/gastric resection Bacterial overgrowth Pseudo membranous colitis Gastrinoma, VIPoma Carcinoid syndrome Medullary thyroid ca Pellagra urgency. Small bowel symptoms: Periumbilical (or right iliac fossa [RIF]) right lower quadr ant (RLQ) pain, not relieved by defecation; watery stool or steatorrhea. y g o o r e t n e o r t s a G l \212Is there blood, mucus, or pus? Bloody diarrhea: Campylobacter , Shigella , Salmonella , E. coli , amebiasis, inflammatory bowel disease, malignancy, pseudomembranous colitis, is chemic colitis. Mucus occurs in irritable bowel syndrome (IBS), colonic adenocarcinoma, pol yps. Pus suggests inflammatory bowel disease or diverticulitis. \212Could there be a non-gi cause? Think of drugs (antibiotics, PPIs, cimeti- dine, propra nolol, cytotoxics, NSAIDs, digoxin, alcohol, laxative abuse) and medical conditions (thyrot oxicosis, autonomic neuropathy, Addison \200\231s disease). Examination Look for weight loss, anemia, dehydration, oral ulcers, club- bing, rashes, and abdominal scars. Feel for: Enlarged thyroid or an abdomi- nal mass. Do a rectal examinatio n: Any rectal mass (rectal carcinoma) or impacted feces (overflow diarrhea)? Test stools fo r fecal occult blood. Tests Blood : In addition to above tests, look for evidence of iron d eficiency or celiac sprue. Stool : For pathogens and C. difficile toxin (pseudomembranous c olitis). Fecal fat excretion or 13 C-hiolein breath test if symptoms of chronic pancreatiti s, malabsorption, or steatorrhea are present. Colonoscopy/barium enema: In colitis, and to exclude malignancy. If normal, consider small bowel radiology or capsule endoscopy (Crohn \200\231s) endo- scopic ultrasound or endoscopic retrograde cholangiopancreatography (ER CP) (p. 222, e.g., chronic pancreatitis). Management Treat causes. Oral rehydration is pref erable to IV rehydra- tion. If severely dehydrated, give 0.9% saline + 20 mmol K + /L IVI. Codeine phosphate 30 mg/6 h PO reduces stool frequency. Avoid antibiotics unless the patien t has infective diarrhea and is systemically unwell. See Figure 7.2. 211 Figure 7.2 Management of infective diarrhea Diarrhea Special circumstances: Food poisoning outbreak Travel (p556 & 558) Recent antibiotic use Re ctal intercourse Immunocompromised host Raw sea food ingested Systemic illness Fever> 39 C Bloody diarrhea lasting>2 weeks Dehydration No systemic signs Symptomic treatment Consider noninfectious causes (see text) Admit to hospital Give oral fluids Consider presumptive antimicrobial therapy* Stool culture not needed Routine stool culture and microscopy Prompt, direct fecal smear (then culture) Confer with microbiologist Polymorphs seen No Polymorphs Parasites seen Specific therapy (p616 \216 p620) Likely culture: Shigella** Campylobacter E coli (Yersinia \216 rare) (Samonella \216 rare) (C difficile*) Likely culture: Salmonella** E coli (C difficile*) 212 NB: Alternatively, classify into secretory (e.g., infections, UC/Crohn \200\231s, etc.) or osmotic causes (if water drawn into the gut, as in laxative use). Constipation Constipation is defined as the symptomatic reduction in stool frequency to few er than three bowel movements per week or difficulty in defecation, with straining or disco mfort. Causes of constipation are numerous and relate either to colonic transit impairment or to structure or functional obstruction to fecal evacuation (see Table 7.2). Clinical fea tures Ask about frequency, nature, and consistency of the stool, and in comparison to their past habits. Is there blood or mucus in/on the stools? Is there diarrhea alternating with constipation? Has there been a recent change in bowel habit? Ask about diet and drugs. Rect al examina- tion is essential. Tests Most constipation does not need investigation, especia lly in young, mildly affected patients. Indications for investigation: Age >40 yrs, recent change in bowel habit, associated symptoms (weight loss, rectal bleeding, mucous discharge, or tenesmus). Blood tests: TSH. Colonoscopy and biopsy of abnormal mucosa if testing is ab normal. Special investigations (e.g., tran- sit studies; anorectal physiology) are rarely i ndicated for constipation that responds to basic medical management. Treatment Treat the ca use (see Figure 7.2 ). Advise exercise and adequate fluid intake (a high-fiber diet is ofte n advised, but this may cause bloating without helping the constipation). Consider drugs on ly if these measures fail and try to use them for short periods only. Often, a stimulant su ch as senna a bulking agent is cheaper than agents such as polyethylene glycol solutions . Both methods are effective. Bulking agents increase fecal mass and thus stimulate perista lsis. Contraindications ( CI) : Difficulty in swallowing, intestinal obstruction, colonic a tony, fecal impaction. Stimulant laxatives increase intestinal motility and should be avoid ed in intestinal obstruction. Prolonged use may rarely cause colonic atony and hypokalemia. Pure stimulant laxatives include bisacodyl tablets (5 \200\22310 mg at night) or supposito ries (10 mg in the mornings) and senna (2 \200\2234 tablets at night). Glycerol suppositori es act as a rectal stimulant. Stool softeners : Docusate sodium acts as a stool softener. L iquid paraffin should not be used for a prolonged period. Side effects ( SE) : Anal seepage , lipoid pneumonia, malabsorption of fat-soluble vitamins. Osmotic laxatives retain fluid i n the bowel. Lactulose , a semisynthetic disac- charide, produces an osmotic diarrhea of lo w fecal pH that discourages growth of ammonia-producing organisms. It is useful in hepatic enceph- alopathy and is used frequently for constipation. A major SE is bloating that can o ften worsen the abdominal pain in constipated patients. A better alternative is polyethylen e glycol (MiraLax ), which is an osmotic laxative. Magnesium salts (e.g., magnesium hydrox ide and magnesium sulfate) are use- ful when rapid bowel evacuation is required. Sodium sal ts (e.g., Microlette and Micralax enemas) should be avoided as they may cause sodium an d water retention. Phosphate enemas were useful for rapid bowel evacuation prior to procedu res. Phosphate preparations have largely been removed from U.S. markets over concerns about renal failure and phosphate neph- ropathy when used without sufficient hydration technique s. Chloride-channel(CIC-2) activators, such as lubiprostone (Amitiza ), have been demonstr ated to be effective in treating chronic constipation. Selective -opioid receptor antago nist , such as methylnaltrexone (Relistor ), when used as a subcutaneous injectable produc t has been shown to relieve constipation in opioid-induced constipation. y g o o r e t n e o r t s a G l 213 Agonist of guanylate cyclase C, such as linaclotide (Linzess )is now FDA approved for cont rol of constipation and IBS with constipation predomi- nant symptoms. What if laxatives don \200\231t help? A multidisciplinary approach with behav- ior therapy, psychological suppor t, habit training sphincter-action bio- feedback may help. Clinical trials are under way to evaluate prucalopride (selective 5HT-4 agonist) on safety and efficacy. This agent is u nder FDA review. Table 7.2 Causes of constipation Poor diet Inadequate fluid intake or dehydration Immobility (or lack of exercise) Irritable bowel syndrome Elderly Postoperative pain Anorectal disease Anal fissure Anal stricture Rectal prolapse Intestinal obstruction Colorectal carcinoma Strictures (e.g., Crohn \200\231s disease) Pelvic mass (e.g., fibroids ) Diverticular disease (stricture formation) Congenital abnormalities Pseudo-obstruction Metabolic/endocrine Hypothyroidism Hypercalcemia Hypokalemia Porphyria Lead poisoning 214 Drugs Opiate analgesics (e.g., morphine, codeine) Anticholinergics (tricyclics, phenothiazines) I ron Neuromuscular (slow transit with reduced propulsive activity) Spinal or pelvic nerve injury Aganglionosis (Chagas \200\231 disease, Hirschsprung \200\231 s disease) Systemic sclerosis Diabetic neuropathy Other causes Chronic laxative abuse (rare; diarrhea is more common) Idiopathic slow transit Idiopathic m egarectum/colon Psychological (e.g., associated with depression or abuse as a child) Jaundice Jaundice (icterus) refers to a yellow pigmentation of skin, sclera, and mucosa due to an elevated plasma bilirubin level (visible at >3 mg/dL). Jaundice may be classified by the type of circulating bilirubin (conjugated or unconjugated) or by the site of the probl em (prehepatic, hepatocel- lular, or cholestatic/obstructive). Bilirubin metabolism: Biliru bin is formed from the breakdown of hemoglobin. It is conjugated with glucuronic acid by he patocytes, making it water soluble. Conjugated bilirubin is secreted into bile and passes i nto the duodenum. In the small intestine, bile is con- verted to urobilinogen by the gut fl ora. Most (>90%) of the urobilinogen is actively reabsorbed in the ileum and transported vi a the portal circulation to the liver. Some of the portal urobilinogen is retaken by the he patocytes and resecreted into the bile ( enterohepatic circulation ). A portion of the bile bypasses the liver and is excreted by the kidneys into the urine. The remainder of urobili nogen that is not reabsorbed in the ileum is converted to stercobilin in the distal small i ntestine or proximal colon, giving feces its characteristic brown color. Prehepatic jaundic e If there is excess bilirubin production (hemolysis, inadequate liver uptake, or deficient hepatic conjugation), unconjugated bili- rubin enters the blood. Because unconjugated bili rubin is water insoluble, it is not excreted in urine, resulting in an unconjugated (indire ct) hyperbilirubine- mia . Causes: Physiological (neonatal), hemolysis, ineffective erythro poiesis, glucuronyl transferase deficiency (e.g., Gilbert \200\231s syndrome, Crigler \200 \223Najjar \200\231s syndrome). Hepatocellular jaundice occurs with hepatocyte damage ch olesta- sis. Causes: Viruses: Hepatitis (p. 564, e.g., A, B, C, etc.), cytomegalovirus (CMV ), EBV (p. 559); drugs (see Table 7.3); alcoholic hepatitis; cirrhosis; liver metastases/ab scess; hemochromatosis; autoimmune hepatitis (AIH); sepsis; leptospirosis; 1 -antitrypsi n deficiency; Budd \200\223Chiari syndrome; Wilson \200\231s disease (p. 233); failure to e xcrete conjugated bilirubin (Dubin \200\223Johnson and Rotor \200\231s syndromes); right-he art failure, causing sinusoidal congestion; tox- ins, e.g., carbon tetrachloride; fungi ( A manita phalloides ). Cholestatic (obstructive) jaundice Blockage or obstruction of the comm on bile duct results in conjugated hyperbilirubinemia. Conjugated bilirubin is water solubl e and thus easily excreted into the urine. Jaundiced patients complain of dark, tea-colored urine. The lack of conjugated biliru- bin reaching the gut (due to bile duct obstruction) prevents adequate uro- bilinogen formation. This causes the feces to become clay-colored. C auses: Choledocholithiasis, pancreatic cancer, lymph nodes at the porta hepatis, drugs (see Table 7.3), cholangiocarcinoma, sclerosing cholangitis, primary biliary cirrhosis (PBC) (s ee Table 7.4), choledochal cyst, biliary atresia. Clinical features Ask about clues to a po ssible viral hepatitis such as blood transfusions before 1990, IV drug use, body piercing, tattoos, sex- ual activity, travel abroad, jaundiced contacts, etc. Also, query family his- tory, alcohol consumption, and all medications (e.g., old drug charts and records). Examin e for signs of chronic liver disease, hepatic encephalopathy, lymphadenopathy, hepatomegaly , splenomegaly, palpable gallbladder, and ascites. Pale stools and dark urine suggest obstr uctive jaundice. Tests Urine: Bilirubin is absent in prehepatic causes; urobilinogen is abs ent in obstructive jaundice. Hematology : Signs of hemolysis (anemia, elevated lactate dehy drogenase (LDH), low haptoglobin, elevated reticulocyte count, positive Coombs \200\231 tes t). Biochemistry: Liver function tests (LFT; bilirubin \200\224 direct and indirect, aspart ate aminotransferase/alanine aminotransferase (AST/ALT), alk phos, total protein, albumin). Virology: EBV, CMV, hepa- titis virus A, B, C (HVA, HVB, HVC) serologies. Other specific t ests , e.g., for hemochromatosis (elevated ferritin and iron-to-total iron binding y g o o r e t n e o r t s a G l 215 capacity (TIBC) ratio, causing a high serum % iron saturation (>55 \200\22360%); 1 -anti trypsin deficiency (serum for genetic analysis), Wilson \200\231s disease (e.g., low serum and high urine copper levels, low serum ceruloplasmin [p. 233]); PBC (high antimitochondria l antibody titers, AMA), and AIH (high antinuclear and anti-smooth muscle antibodies). Ultr asound: Are the bile ducts dilated (obstruction)? Are there gallstones, hepatic metastases, or pancreatic masses? Request magnetic resonance cholangiopancreatography (MRCP) (p. 223), endoscopic ultrasound (EUS ), or ERCP if bile ducts are dilated. Consider performing a liv er biopsy (p. 222) if the bile ducts are normal. Consider abdominal computed tomography (CT ) or magnetic reso- nance imaging (MRI) scan . Table 7.3 Drug-induced jaundice Phenytoin, carbamazepine, valproic acid Anti-tuberculosis (TB) meds (isoniazid, rifampin, Hepatitis pyrazinamide), nitrofurantoin, antifungals (ketocon- azole, fluconazole, itraconazole), ant ivirals (DDI, AZT) Statins Angiotensin-converting enzyme (ACE)-inhibitors, methyldopa, calcium channel blockers Monoamine oxidase inhibitors (MAOIs), amitriptyline, imipramine Halothane (general anesthetic); NSAIDs (ibuprofen, sulindac, diclofenac, indomethacin) Cholestasis Antibiotics (erythromycin, nitrofurantoin, rifampin) Anabolic steroids Oral contraceptives Chlorpromazine Prochlorperazine, Sulfonylureas, chlorpropamide Gold salts, cyclosporin 216 Table 7.4 Causes of jaundice in a previously stable patient with cirrhosis \212 \212 \212 \212 \212 Sepsis Alcohol Drugs Malignancy (e.g., hepatocellular carcinoma) GI bleeding Upper GI bleeding 1 Hematemesis is vomiting of blood. It may be bright or resemble coffee g rounds. Melena is black, tarry stool (signifies altered blood) with a charac- teristic odor . Both can indicate upper GI bleeding. y g o o r e t n e o r t s a G l Causes Common Peptic ulcers Gastritis/gastric erosions Mallory \200\223Weiss tear Duodeniti s Rare Bleeding disorders Portal hypertensive gastropathy Aortoenteric fistula; angiodysplasi a Hemobilia (bleeding from biliary tree) Esophageal varicesEsophagitis Dieulafoy lesion (rupture of a submucosal arteriole) Malignancy Drugs (NSAIDs, steroids thrombolytics, anticoagulants) Meckel \200\231s diverticulum Peutz \200\223Jeghers \200\231 syndrome Osler \200\223Weber \200\223Rendu syndrome Assessment Brief history and examination to assess severity. History: Elicit a focused hist ory evaluating for risk factors or conditions that are associated with severe GI bleeding. Assess for prior history of GI bleed- ing, history of PUD, known bleeding diathesis, underl ying cirrhosis and portal hypertension, dysphagia, vomiting, weight loss, NSAID use, alcoho l consumption. Examination: Look for stigmata of chronic liver disease and perform a digita l rectal examination to check for melena. Assess for signs of vascular shock: \212 \212 Peripheral vasoconstriction (cool and clammy) Tachycardic (pulse >100 bpm, and jugular veno us pressure (JVP) not elevated) Hypotensive (systolic BP <100 mm Hg) Postural drop in BP (o rthostatic) Poor urine output, e.g., <30 mL/h 217 \212 \212 \212 Calculating the Rockall risk score (see Table 7.5) may help to risk-strat ify the patient. Acute management (p. 769) Critical to management is early resuscitation of a bleeding patient (Table 7.6). In summary: \212 Protect airway and give high-flow oxygen . Insert two large-bore (14 \200\22316 G) IV cannula and draw blood for hemoglo- \212 bin levels, clotting assessment, and type and cross for 4 \200\2236 U packed red blood cells (P RBCs) (1 U/g/dL <14 g/dL). Give IV colloid while waiting for blood to be cross-matched. In an emer- gency, give group O Rh \200\223ve blood. Transfuse until hemodynamically stable. C orrect clotting abnormalities (vitamin K, frozen fresh plasma [FFP], platelets). Monitor pu lse, BP, and central venous pressure (CVP) at least hourly until stable. Consider insertion of a urinary catheter and monitor hourly urine output. Consider a CVP line to monitor CVP and guide fluid replacement. Remember that standard CVP catheters infuse more slowly than p eriph- eral large-bore IV. \212 \212 \212 \212 \212 \212 \212 Obtain a chest x-ray (CXR), electrocardiogram (ECG), and arterial blood gas (ABG) in high-r isk patients. Consult gastroenterologist and arrange for an urgent endoscopy (p. 221). Begi n PPI therapy. May wish to notify surgery team of all severe bleeds on admission. If liver disease present, consider octreotide infusion. \212 \212 \212 Further management \212 \212 Reexamine after 4 h and give FFP if >4 U transfused. Monitor pulse, BP, CVP, and urine outp ut hourly; decrease frequency to 4 h if hemodynamically stable. Check CBC, CMP, LFT, and cl otting daily. Transfuse to goal Hb based on comorbidities; always keep 2 units of blood in reserve. Keep \200\234NPO \200\235 for 24 h. Allow clear fluids after 24 h and light diet after 48 h if no evidence of rebleeding. Discuss with consulting gastroenterologist, if nee ded. Start IV or oral PPI pending clinical status. \212 \212 \212 \212 Table 7.5 Rockall risk-scoring system for gi bleeds Score Age Shock: Systolic bp pulse rate 0 <60 yrs BP >100 mm Hg<100/ min 1 60 \200\22379 yrs BP >100 mm HgPulse >100/min 2 80 yrs BP <100 mm 3 Hg 218 Co-morbidity No major Cardiac Renal failure Liver failure Metastases failureIs- chemic heart disease All other- diag- noses Diagnosis Mallory \200\223 Weiss tear; no lesion; no sign of recent bleeding None, or dark-red spot Upper GI malignancy Bl ood in upper GI tract; adherent clot;visible vessel Signs of recent hemorrhage on endoscopy Rockall scores help predict risk of rebleeding and death after upper GI bleeding. A score > 6 is said to be an indication for surgery, but decisions relating to surgery are rarely tak en on the basis of Rockall scores alone. y g o o r e t n e o r t s a G Table 7.6 gi bleeding management plan: Resuscitate (p. 769) l Any suspicion of variceal bleeding? See p. 206 No Yes Endoscopy (at <24 h if shock) Emergency endoscopy (at <4 h if shock) Are there bleeding varices? Peptic ulcer Other diagnosis Yes No Sclerotherapy/banding; No risk fac- tors: Conservative treatment One risk factor: Surgery v s. endo- scopic therapy; surgery is most relevant in the context of ongo- ing bleeding desp ite endoscopic therapy, and in rebleeding if \211 6 U already transfused Are risk factors present? \212 \211 6 units transfused \212 \212 \212 Hematemesis Rebleeding Bleeding vessel seen on endoscopy, or clot in an ulcer and melena 219 Upper GI bleeding 2 and bleeding varices Endoscopy should be arranged after resuscitation, within 4 h if variceal hemorrhage is suspected or bleeding is ongoing, and otherwise within 12 \200\22324 h of admission. It can identify the site of bleeding, be used to estimate th e risk of rebleeding, and to administer endoscopic treatment. Stigmata of high-risk rebleed ing lesions for PUD include actively bleeding vessel (60%), adherent clot (40%), visible ve ssel (20%), flat spot (10%), and clean base (5%). Rebleeding Since rebleeders have increase d mortality, identify these patients and monitor them closely for signs of rebleeding. Guid elines for considering surgery \212 Severe bleeding or bleeding despite transfusing 6 U if >60 yrs (8 U if <60 yrs) Rebleeding Active bleeding at endoscopy that cannot be controlled Rockall score >6 (p. 218) \212 \212 \212 Varices Portal hypertension causes dilated collateral veins (varices) at sites of porto-systemic anastomosis. Varices are most prevalently in the distal esophagus, but may also be found in the stomach (gastric varices), around the umbilicus (caput medusa \200\224 rare) and in the rectum (rectal varices) and duodenum (duodenal varices). Varices develop in patients with cirrhosis once portal pressure (measured by hepatic venous pressure gradient) is >10 mm Hg; if >12 mm Hg, variceal bleeding may develop; associated with a mortality of 30 \200\22350% per episo de. Causes of portal hypertension can be divided into: Prehepatic: Portal vein thrombosis; splenic vein thrombosis, arterioportal fistula, splenom- egaly. Intrahepatic: Cirrhosis; fu lminant hepatitis, veno-occlusive disease, Budd-Chiari syndrome, schistosomiasis (common wo rldwide); sarcoidosis; myeloproliferative diseases; congenital hepatic fibrosis, metastatic malig- nancy. Posthepatic: Budd \200\223Chiari syndrome, right-heart failure, constrictive pericarditis, inferior vena cava web. Risk factors for variceal hemorrhage : Increased por tal pressure; variceal size, endoscopic features of the variceal wall, e.g., fresh clot, re d wale sign, etc.; and Child \200\223Pugh score \211 8 (see Table 7.12 ). Suspect varices as a cause of gi bleeding if there is alcohol abuse or cirrhosis. Look for signs of chroni c liver disease, encephalopathy, splenomegaly ascites. Prophylaxis (primary): Variceal h emorrhage occurs annually in 5 \200\22315% of patients with varices and cirrhosis. 2007 Ame rican Association for the study of Liver Disease (AASLD) guidelines 3 recommend primary pro phylaxis for patients with large varices or small varices at risk for bleeding with: (1) No nselective -blockers (propranolol or nadolol) titrated to maximum tolerated dose. (2) En doscopic ligation (banding) is indicated for large and at risk varices. Banding reduces ris k of first bleeding when compared with -blockers. Endoscopic sclerotherapy is no longer recommended as com- plications outweigh benefits. Secondary: After an initial variceal blee d, risk of further bleeding is high. Options are (1) and (2) as above, + transjugular intra hepatic portosystemic shunting (TIPS) or surgical shunts. TIPS is also used in uncontrolled variceal hemorrhage. Consider surgical shunts if TIPS is impossible for technical reasons. Acute variceal bleeding : Get expert help at the bedside. \212 220 Resuscitate until hemodynamically stable or Hg goal of 8 g/dL. Beyond this, increased reble eding and mortality rise. Avoid excess saline infusion. Correct clotting abnormalities with vitamin K and FFP. Start IVI of octreotide (for 5 d). Endoscopic therapy: Band ligation is recommended when possible. Banding may be impossible when visualization is poor due to rap id bleeding. If bleeding uncontrolled, a Minnesota tube or Sengstaken \200\223Blakemore tub e should be placed by someone with experience \200\224or TIPS as above (see Table 7.7). \212 \212 \212 In cirrhotic patients with active GI bleed, initiate antibiotic treatment to reduce mortali ty; recommended agents include ceftriaxone and norfloxacin. 3 Garcia-Tsao G, et al. AASLD Practice Guidelines: Prevention and management of gastroesoph ageal varices and variceal hemorrhage in cirrhosis. Hepatology . 2007;46(3):922 \200\223938 . y g o o r e t n e o r t s a G Table 7.7 Balloon tamponade with a Sengstaken \200\223 Blakemore tube l In life-threatening variceal bleeding, this can buy time to arrange transfer to a specialty liver center. It uses balloons to compress gastric and esophageal varices. Before insertio n, inflate balloons with a measured volume (120 \200\223300 mL) of air giving pressures of 60 mm Hg (check with a sphygmomanometer). \212 \212 Deflate, and clamp exits. Pass the lubricated tube and inflate the gastric balloon with the pre- determined volume of air in stomach. Tug gently back into position against the upper stomach. Inflation of the gastric balloon within the esophagus will lead to perforation. If there is any question as to loca- tion, confirm with x-ray. Inflate the esophageal balloon . Check pressures (should be 20 \200\22330 mm Hg higher on the trial run). This phase of th e procedure is dangerous: Do not overinflate the balloon (risk of esophageal necrosis or ru pture). Often, hemodynamic stability can be achieved with inflation of the gas- tric balloo n alone. Again, may confirm position with imaging. Many balloons come with a helmet to prop erly attach and apply ten- sion to the balloon to maintain tamponade. Tie or tape to patien t \200\231s helmet or forehead to ensure the gastric balloon impacts gently on the gastroes ophageal junction. Place the esophageal aspiration channel on continuous low suction and ar range for the gastric channel to drain freely. \212 \212 \212 Leave in situ for just enough time to stabilize, transfer, or determine definitive treatmen t course. These tubes should be removed within 24 h; long duration risks necrosis and perfo ration. Various other techniques of insertion may be used, and tubes vary in structure. Do not try to pass one yourself if you have no or little experience: Ask an expert; if unavail able locally, call a specialist liver center and transfer urgently. 221 Endoscopy and biopsy Upper GI endoscopy Diagnostic indications \212 Dyspepsia, especially if >50 yrs old Gastric biopsy (suspected malignancy) Duodenal biopsy (e.g., celiac disease) \212 Hematemesis \212 \212 Persistent vomiting \212 \212 Iron-deficiency anemia. Therapeutic: Primarily injection/coagulating of bleeding lesions. Also: \212 \212 \212 Banding of esophageal varices Dilatation of strictures (esophageal, pyloric) Palliation of esophageal cancer (stent insertion, laser therapy, mucosal resection therapy) Palliation of malignant obstruction (stent insertion) Removal of foreign bodies Radiofrequency ablation of Barrett esophagus Placement of feeding tubes \212 \212 \212 \212 Preprocedure: NPO after midnight except for medications. Obtain inf ormed written consent. Advise the patient not to drive for 24 h if sedation is being given. Arrange follow-up. Procedure: Conscious sedation may be given (e.g., midazolam 2 mg IV; moni- tor O 2 saturati on with a pulse oximeter). Anesthesia-directed sedation may be given (e.g., propofol) for s elected cases. The pharynx may be sprayed with local anesthetic, and a flexible endoscope i s swallowed. Continuous suction must be available to prevent aspiration. Complications: Tra nsient sore throat, amnesia following sedation, perforation (<0.1%), cardiorespira- tory ar rest (<0.1%). Duodenal biopsy is the gold standard for diagnosing celiac disease. Endoscopy with biopsy is also useful in investigating unusual causes of mal- absorption (e.g., giard iasis, lymphoma, Whipple \200\231s disease, amyloid, eosino- philic gastroenteritis, or mic roscopic colitis). Colonoscopy Diagnostic indications: Lower GI bleeding, iron deficiency, persistent diarrhea, biopsy of a known lesion or polyp, to assess for Crohn \200\231s or UC , colorectal cancer surveillance, Strep. bovis endocarditis. Therapeutic indications: Polyp ectomy, lower GI bleeding treatment, treat- ing IBD strictures with dilation, treating mali gnant obstruction (stenting), pseudo-obstruction or volvulus (decompression). Preparation: Various prep solutions exist. Most commonly used is polyeth- ylene glycol solution (1 gallo n). Procedure: Sedation and analgesia are given before a flexible colonoscope is passed per rectum around the colon. Complications: Abdominal discomfort, incomplete examination, perf oration (0.2%), hemorrhage after biopsy or polypectomy. Transjugular or ultrasound-guided p ercutaneous liver biopsy Indications: Abnormal LFT, chronic viral hepatitis, alcoholic hepa titis, AIH, suspected cirrhosis, suspected carcinoma, biopsy of hepatic lesions, inves- tig ation of FUO. Preprocedure: NPO after midnight. Check clotting (International Normalized Ra tio [INR] <1.3) and platelet count (>100 \227 10 9 /L). Obtain written con- sent. Prescrib e analgesia. Procedure: Sedation (e.g., diazepam 5 mg IV) may be given, but usually not req uired. If percutaneous, ultrasound guidance is recommended, the liver borders are percussed and local anesthetic (2% lidocaine) is injected to the region of maximal dullness in the m idaxillary line during expiration that correlates with target area on ultrasound. Breathing is rehearsed, and a needle biopsy is taken with the breath held in expiration. Afterward t he patient lies on the right side for 2 h, then in bed for 6 h while regular pulse and BP o bservations are taken. Transjugular biopsies are recommended for patients with ascites, low platelets, morbid obesity, etc., in whom the percutaneous approach may be difficult to per form safely. Some academic centers perform transluminal endoscopic peritoneoscopy and liver biopsy; added advantages include direct visualization and immediate treatment of any bleed ing lesion. Still in early research trials. Complications: Local pain, pneumothorax/hemotho rax, bleeding (<0.5%), death (<0.1%), biopsy of adjacent organ (e.g., gallbladder, kidney). 222 Radiological and other GI procedures Abdominal ultrasound is used for the investigation of abdominal pain, abnormal LFT, jaundice, hepatomegaly, or abdominal masses. Patients should be NPO by mouth for 4 h before the scan to allow visualization of the gallbladder. Pelvic u ltrasound requires the bladder to be full. Ultrasound may also be used to guide diagnostic biopsy or therapeutic aspiration. Endoscopic retrograde cholangiopancreatography Diagnostic indica- tions: With the advent of MRCP (below), diagnostic ERCP is uncommonly performed. Indications to perform ERCP prior to MRCP are for therapeutic intervention or wh en clinical suspicion is high for therapeutic interven- tion. Indications for ERCP include cholangitis, jaundice with dilated intrahe- patic ducts, recurrent pancreatitis, symptomati c choledocholithiasis, biliary obstruction, biliary strictures. Preprocedure: Check clottin g and platelet count. NPO after midnight. Obtain informed consent. Sedation is accom- plish ed similarly to other endoscopic procedures. Procedure: A catheter is advanced from a side- viewing duodenoscope via the ampulla into the common bile duct and/or pancreatic duct. Cont rast medium is injected and x-rays taken to show lesions in the biliary tree and pancreatic ducts. Complications: Pancreatitis, bleeding, cholangitis, perforation. Mortality: <0.2% o verall; 0.4% if stone removal. Small bowel follow-through After bowel preparation, barium i s ingested and serial x-ray films are taken every 30 min until barium reaches the cecum. En hanced films are taken of areas of interest (e.g., terminal ileum). Small bowel enema After bowel preparation, barium is introduced via duodenal intubation. Although technically more demanding than a barium follow-through, this method results in better mucosal definition. Barium enema Always do a rectal exam first rigid sigmoidoscopy and biopsy. Preparation i s per colonoscopy (p. 222). For double-contrast bar- ium enema, barium and air are introduc ed per rectum. Special views may be needed to visualize the areas of interest. Gastrografin may be used instead of barium in suspected colonic obstruction. It may show diverticular d is- ease or cancers (e.g., an irregular \200\234apple-core \200\235 narrowing of the lumen ). In Crohn \200\231s disease, look for \200\234cobblestoning, \200\235 \200\234rose thor n \200\235 ulcers, colonic strictures with rectal sparing. Disadvantages: Significant radia tion dose; no biopsy possible. Computed tomography is indicated if ultrasound is technicall y difficult or nondiagnostic. It allows better visualization of retroperitoneal structures but requires skilled interpretation. Oral or IV contrast may be given to enhance definition . The main disadvantage is the high radiation dose. Magnetic resonance imaging provides sup erior soft tissue imaging and enables the distinction of benign and malignant lesions. The other advantage over CT is the lack of radiation. Disadvantages are that patients with pace - makers and certain metal implants cannot be scanned and that the scanner itself can induc e claustrophobia. Magnetic resonance cholangiopancreatography MRCP enables in vivo anatomic exploration of the main pancreatic duct. Horizontal sections provide helpful radioanatomic information. The tech- nique nevertheless remains limited by poor spatial resolution. MRCP had a sensitivity of 83% and a specificity of 99% for diagnosing common bile duct stones, and according to some authorities, is the investigation of choice \200\224 partly, no doubt , due to lack of side effects. Endoscopic ultrasound An ultrasound transducer is placed at the tip of an endoscope, allowing for unprecedented visualization of the GI tract and its a djacent structures. The layers of the GI tract can be discerned (allows for unprecedented e valuation of submucosal lesions) and adjacent organs (pancreas, mediastinal structures). A fine-needle aspiration (FNA) or core biopsy can be accomplished through the endoscope, allo wing for tissue acquisition. EUS has revolutionized cancer diagnosis and staging of esopha- geal, pancreaticobiliary, gastric, and colorectal cancers. Imaging via a wireless enterosc opy capsule This capsule is swallowed and sends images to a recorder worn by the patient. I t allows for visualiza- tion of the small bowel mucosa and is indicated for obscure GI blee ding, detection of inflammatory bowel disease (IBD), etc. Recently, it is approved y g o o r e t n e o r t s a G l 223 for evaluation of the esophagus as well. Robotic biopsy and therapeutic procedures are not yet possible. Deep bowel enteroscopy with double balloon, single balloon, or spiral enteros copy . An enteroscope (a long endoscope) and an added balloon-like device can be used in ta ndem to allow the scope to be inserted deep into the small bowel. The entire length of smal l bowel can be reached in most cases. The sequential advancement of balloon and scope allow s for plication and folding of the bowel to shorten the length and advance the scope furthe r. This technique is useful to reach the small bowel and provide diagnosis of small bowel d iseases such as lymphoma or Crohn \200\231s with ERCP in patients with Roux-en-Y gastric by pass or therapy for bleeding. It can also be used in retrograde fashion to advance a scope through the colon and into the distal ileum. Liver failure Definitions Acute liver failure may occur suddenly in the previously healthy liver, precipitating elevated INR ( \211 1.5), rapid deterioration of liver function, ons et of encephalopathy, or change in mental status] Acute hepatic failure is liver failure of <26 wks duration). Liver failure more commonly may occur as a result of decompensation of chronic liver disease; i.e., acute-on-chronic hepatic failure . Many terms are used, includ ing fulminant hepatic failure, which refers to severe acute liver injury with synthetic dys function and encephalopathy occurring within 8 wks of the onset of symptoms. Subfulminant h epatic failure refers to impaired synthetic function and encephalopathy occurring within 9 \200\22326 wks (<6 months). Immediately upon development of acute liver failure (<26 wks du ration): Elevated INR ( \211 1.5) and encephalopathy in a patient: Must initiate contact with a transplant center as early transfer essential. Causes Infections: Viral hepatitis, y ellow fever, leptospirosis. Drugs: Acetaminophen overdose, halothane, isoniazid. Toxins: Am anita phalloides mushrooms, carbon tetrachloride. Vascular: Budd \200\223Chiari syndrome, v eno-occlusive disease. Others: Primary biliary cirrhosis, hemochromatosis, autoimmune hepat itis, 1 -antitrypsin deficiency, Wilson \200\231s disease, fatty liver of pregnancy, mal ig- nancy, drug-induced liver disease. Clinical features Hepatic encephalopathy is graded a s follows: 224 Grade I Altered mood or behavioral changes, day-night reversal, hyperreflexia Increased drowsiness or hypersomnia, confusion, Grade II slurred speech, asterixis Grade III