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00 GI disorders USMLE Step 2 Outline

00 Gi Disorders Usmle Step 2 Outline

by susucapp9, Jul. 2011

Subjects: 00 disorders gi

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Symptoms Dysphagia (often with liquids), regurgitation of undigested food and aspiration while recumbent, minimal pain.	Achalasia Description Motility disorder characterized by a triad of: primary esophageal aperistalsis and atony; megaesophagus; failure of lower esophageal sphincter (LES) relaxation. The LES fails to relax with swallowing. Circular muscle of the LES is thickened. Auerbach’s plexus absent.	Diagnosis Esophagram—Marked dilation above constricted distal esophagus. Abnormal peristalsis. Endoscopy—Excludes an esophageal stricture whether benign or malignant. Esophageal Manometry—Uncoordinated peristalsis, primary peristal- sis absent, gastroesophageal (GE) sphincter has above-normal resting pressure and does not relax with swallowing. Complications of untreated achalasia: megaesophagus, increased risk of squamous cell carcinoma. Treatment Steps 1. Pneumatic dilatation. 2. Botulinum toxin injected in LES. 3. Longitudinal esophageal myotomy (open or laparoscopic) is sur- gical procedure of choice. Usually, antireﬂux procedure (e.g., Nissen or Toupet fundoplication) added to myotomy.
Symptoms Vomiting blood (hematemesis) or melena.	Acute Upper GI Bleeding Description Site of bleeding is esophagogastric (EG) junction (esophageal varices, esophagitis, Mallory–Weiss tears), one-third; stomach (ul- cers, gastritis), one-third; and pyloroduodenal region (ulcers, duo- denitis), one-third. UGIB (gastritis, peptic ulcer disease, Mallory–Weiss tear, cancer, esophageal varices, to mention only a few of the most common ones);	Diagnosis Esophagogastroduodenoscopy (EGD) identiﬁes source in 95%. In ulcers, visible vessel in ulcer base indicates rebleed of 50%, and clean ulcer base, rebleed of 1%. Upper • Nasogastric (NG) positive. • Upper endoscopy. Treatment Steps Mortality unchanged at 10% in past 40 years. leeding ulcer: 1. Intravenous proton pump inhibitor (IV Protonix 80 mg IV (stat), then 8 mg/hr IV), 2. Correct coagulopathy if present. 3. Transfuse as needed. 4. Urgent endoscopy when indicated. 5. Epinephrine injected into visible vessel spurting in an ulcer may stop acute bleeding. 6. Surgery if bleeding is uncontrolled after medical interventions Esophageal varices: 1. Octreotide 50 µg IV bolus, then 50 µg/hr IV constant infusion, or 2. Banding and/or sclerotherapy. 3. Endotracheal intubation may be needed in rapidly bleeding patient. 4. Transjugular intrahepatic portosystemic shunt (TIPS) (can ﬁx varices but very often cause/worsen encephalopathy).
Symptoms Most hiatal hernias are asymptomatic. Symptoms of gastroe- sophageal reﬂux disease (GERD) can occur, including retrosternal burning pain especially lying supine, lifting, or straining; regurgita- tion of bitter ﬂuid; nocturnal cough, recurrent pneumonia from as- piration; dysphagia. Bleeding rare.	Sliding Hiatal Hernia Description Esophagogastric junction and proximal stomach displaced into me- diastinum. Ninety-ﬁve percent of hiatal hernias are sliding. Symp- toms caused by accompanying esophageal reﬂux. There is no true hernia sac	Diagnosis Chest x-ray (CXR): Air–ﬂuid level in mediastinum. GE reﬂux may be evident on esophagram. Esophagoscopy to rule out other lesions and document esophagitis. Distal esophagus pH monitoring most sensitive test. Treatment Steps 1. No treatment if asymptomatic. 2. Treat GERD symmptoms medically (see Chapter 4). 3. Surgical antireﬂux procedures—Nissen fundoplication, Hill repair, Belsey fundoplication
Symptoms Bright red blood per rectum.	Acute Lower GI Bleeding Description Common causes include diverticulosis, angiodysplasia, neoplasm, colitis.	Diagnosis Colonoscopy when bleeding stops. Angiography if bleeding persists. LGIB (atriovenous malformations,malignancies, hemorrhoids, trauma, diverticulitis, colitis[Crohn’s disease,ulcerative, pseudomembranous], and a few others). Lower • NG tube negative, bile no blood. • Colonoscopy if bleeding stops. • Bleeding scan if bleeding continues. • If positive, surgical evaluation—possible angiography with vasopressin at bleeding site. Treatment Steps 1. Replace blood. 2. Correct coagulation factors if needed. 3. Vasopressin infusion at angiographic bleeding site.
Symptoms Fullness after meals, epigastric postprandial pain (69%), bowel sounds in chest, early postprandial vomiting (50%), breathlessness while eating. Chronic blood loss in up to one-third of patients due to recurrent bleeding from the gastric mucosa.	Paraesophageal Hiatal Hernia Description Esophageal junction in normal anatomic position. Stomach herni- ates through hiatus usually to left of esophagus. May strangulate or volvulize leading to rapid death (20–30%).	Diagnosis CXR: air–ﬂuid level in mediastinum. Esophagram establishes the di- agnosis. Esophagoscopy to rule out Barrett’s esophagus. Treatment Steps Because of high rate of complications, all paraesophageal hiatal her- nias should be surgically repaired (abdominal and/or thoracic ap- proach) with or without an accompanying antireﬂux procedure. Good to excellent surgical results in 80–90% of patients.
Symptoms Small, frequent, bloody diarrheal stools often associated with tenesmus. Abdominal pain, fever, and leukocytosis. Fulminant colitis is associated with worsening systemic toxicity and may show colonic dilatation (transverse diameter > 5 cm).	Ulcerative Colitis Diagnosis Rule out antibiotics and other drugs, stool for ova and parasites, culture and sensitivity (O&P, C&S), and Clostridium difﬁcile toxin (Escherichia coli O157:H7-culture negative hemorrhagic colitis, after raw beef or milk causes hemolytic anemia syndrome, 35% mortality in elderly). Histologic exam of mucosa. Colonoscopy and ileoscopy, barium enema if not megacolon, and small bowel series (see Table 4–1). Pathology Crypt abscesses and superﬁcial ulceration compatible with diagnosis.	Treatment Steps Azulﬁdine 4 q/day; folic acid 1 mg daily for 2–3 weeks. Amebiasis should be excluded before beginning steroid therapy. Oral prednisone (30–60 mg daily) responds usually in 2 weeks, taper by 5 mg weekly. Maintenance prophylactic therapy: sulfasalazine 500 mg PO qid and folate 1 mg daily. 6-Mercaptopurine for steroid sparing in steroid-dependent disease, 1–1.5 mg/kg/day.
Symptoms Progressive dysphagia, odynophagia, chest pain, weight loss.	Esophageal Cancer Description Squamous carcinoma most common cell type: distal third (30%), middle third (50%), upper third (20%). Spreads by lymphatics, vas- cular invasion, and direct extension. Adenocarcinoma 5–10% of pri- mary carcinomas of esophagus. Frequency of adenocarcinoma has increased and currently accounts for > 50% all esophageal tumors. Extraesophageal extension present in high percentage of patients at time of diagnosis. Highly aggressive. Five-year survival rate only 3% when lymph nodes are involved.	Diagnosis Esophagram—Irregular mass narrowing lumen of esophagus, mini- mal proximal dilatation. Esophagoscopy—Biopsy for tissue diagnosis, tumor length. Rule out gastric involvement. Bronchoscopy—For upper- and middle-third lesions to rule out tra- cheobronchial involvement. Computed tomographic (CT) scan and endoscopic ultrasonography (EUS) helps with staging. Other imaging studies used for staging are: magnetic resonance imaging (MRI), positron-emission to- mography (PET), and video-assisted thoracoscopic surgery (VATS). Treatment Steps 1. Surgery; only 30% resectable. Esophagectomy (transhiatal blunt esophagectomy or Ivor Lewis procedure), total or partial, de- pending on tumor location and size. Stomach or the left-sided colon are used to reestablish gastrointestinal (GI) tract continu- ity. Resection may also provide palliation in low-risk patients. 2. Radiation therapy preoperative may shrink tumor mass allowing resection. Combined with chemotherapy may be effective adju- vant therapy. However, no deﬁnitive survival advantage to either chemo- or radiation therapy has been demonstrated. 3. Endoscopic laser therapy used to establish esophageal patency in unresectable obstructing tumors.
Symptoms Small intestinal sites cause pain, bloating, diarrhea, weight loss, fever. Obstruction causes crampy abdominal pain followed by vomiting. Pe- rianal disease (ﬁstula, perianal abscess, ﬁssures), ﬁstulae (to the blad- der, vagina, colon, skin, among loops of bowel), or abdominal masses due to abscesses	Crohn’s Disease Description Chronic idiopathic inﬂammation. Pathology Transmural, “fat wrapping” on serosal surface, noncaseating granulomas. There is an increased incidence of gallstones and calcium oxalate kidney stones in Crohn’s disease.	Diagnosis Stomach or small bowel involvement, rectal sparing, ﬁstulization. Deep ﬁssures, ulcer, granulomas, or patchy distribution of colonic inﬂammation. Upper GI/small bowel, barium enema with ﬂexible sigmoidoscopy versus colonoscopy (see Fig. 4–1). Treatment Steps 1. Sulfasalazine: 4 g/day, and if conﬁned to the colon, 1 mg folic acid for 2–4 weeks, if sulfa allergic. Asacol 800 mg tid. 2. Metronidazole: 10 mg/kg/day. If no response in 4 weeks, then 3. Prednisone: 30–60 mg/day should be used instead (start with prednisone if symptoms are severe). If patient responds to treat- ment 1 or 2, continue for 4–6 months; then stop if symptoms gone. Maintenance prophylactic therapy: Asacol (mesalamine) (5ASA) 800 mg PO tid. Twenty percent of cases of IBD are neither speciﬁcally ulcerative colitis nor Crohn’s disease. Sulfasalazine and prednisone appear safe in pregnancy and during lactation. 4. 6-Mercaptopurine in steroid-dependent case (1–1.5 mg/kg/day). 5. Inﬂiximab (Remicade) 5 mg/kg IV over 2 hrs. One infusion for active disease. Three infusions (0, 2, 6 wks) for ﬁstulous disease
Symptoms Dysphagia, pain, fever, neck tenderness and crepitus (with cervical perforations), chest pain, dyspnea, shock, mediastinal air (Hamman’s sign).	Esophageal Perforation 1. Instrumental Perforation Causes The most common cause of esophageal perforation is iatrogenic disrup- tion, which includes endoscopy, dilation, paraesophageal surgery, Seng- staken–Blakemore (SB) tube, intubation, sclerotherapy. Description Susceptible at areas of narrowing: cricopharyngeal area, midportion near aortic arch and mainstem bronchi, diaphragmatic hiatus.	Diagnosis X-rays: soft tissue air, mediastinal air (takes 1 hour to be seen), pleural effusion, pneumothorax, mediastinal widening. Esophagram shows site of perforation (usually into left pleural cavity). Treatment Steps 1. Antibiotics for all patients. 2. Observation for those patients with small localized perforation with minimal symptoms and no sepsis. 3. Surgical repair required in almost all cases. a. Early diagnosis (< 24 hours)—primary repair. b. Late diagnosis—primary reinforced repair, drainage alone (cervical perforation), esophageal exclusion and diversion, or esophagectomy (if underlying signiﬁcant esophageal pathol- ogy, e.g., cancer is present). Criteria for Nonoperative Therapy Contained mediastinal leak, free drainage back into esophagus, min- imal symptoms, no sign of sepsis. Surgical repair possible within 24 hours of perforation. After 24 hours, resection combined with diverting procedures may be necessary (“spit ﬁstula”).
Symptoms Burning epigastric pain, dull ache, often associated with heart- burn/gastroesophageal reﬂux disease (GERD). Bleeding ulcers may be painless, but cause hematemesis, melena, anemia, or hematochezia. Gastric outlet obstruction may present with repeated vomiting and dehydration.	PEPTIC ULCER (DUODENAL AND GASTRIC ULCER) Description Peptic ulcers are defects in GI mucosa extending to the submucosa, into the muscle layers, and require acid and pepsin. The major com- plications of duodenal ulcers are bleeding, perforation, gastric outlet obstruction, and penetration into the pancreas Risk factors for NSAID ulcers • > 70 years old • History of prior ulcer disease or complications • Co-therapy with corticosteroids or with anticoagulants • Misoprostol (200 mg qid) is the only drug approved by the Food and Drug Administration (FDA) to prevent NSAID-induced ulcer, proton pump inhibitors (PPIs) may be helpful. H. pylori • Urease of CLO-test, H. pylori on gastric biopsy, (+) C14 urea breath test clarithromycin 500 mg bid, omeprazole 20 mg or lansoprazole 30 mg bid, and amoxicillin 1 g bid (with penicillin allergy—metronidazole 500 mg bid) for 2 weeks (other regimens exist). • C14 urea breath test no earlier than 1 month after treatment to check for cure. • Occurs in 90% of patients with duodenal ulcers and 70–80% of patients with gastric ulcer Classically, duodenal ulcer pain is relieved by food, but gastric ulcer pain is worsened by or unrelated to food.	Diagnosis Upper endoscopy, biopsy and brush of gastric ulcers to rule out can- cer). Radiographic exam (upper GI series) somewhat less accurate. Assess for Helicobacter pylori via biopsy, CLO test, or breath test. Treatment Steps If H. pylori infection positive, multiple regimens exist. One example: clarithromycin 500 mg bid, omeprazole 20 mg, or lansoprazole 30 mg bid, and amoxicillin 1 g bid (or with penicillin allergy—metro- nidazole 500 mg bid) for 2 weeks. 1. Stop caustics: alcohol, nonsteroidal anti-inﬂammatory drugs (NSAIDs), caffeine, nicotine. 2. Proton pump inhibitors initially given bid (omeprazole, lansopra- zole, others).
Symptoms Sudden, severe pain in lower chest and upper abdomen; shock; rigid abdomen.	Esophageal Perforation Spontaneous Perforation Description Postemetic transmural perforation usually following an alcoholic binge (Boerhaave syndrome). Patients generally present with medi- astinitis. Posterior, distal esophagus most usual site. Fifty percent with concomitant GERD. Differential Diagnosis Pancreatitis, myocardial infarction, perforated peptic ulcer, dissecting aortic aneurysm.	Diagnosis X-rays: soft tissue air, mediastinal air (takes 1 hour to be seen), pleural effusion, pneumothorax, mediastinal widening. Esophagram shows site of perforation (usually into left pleural cavity). Treatment Steps 1. Antibiotics for all patients. 2. Observation for those patients with small localized perforation with minimal symptoms and no sepsis. 3. Surgical repair required in almost all cases. a. Early diagnosis (< 24 hours)—primary repair. b. Late diagnosis—primary reinforced repair, drainage alone (cervical perforation), esophageal exclusion and diversion, or esophagectomy (if underlying signiﬁcant esophageal pathol- ogy, e.g., cancer is present). Criteria for Nonoperative Therapy Contained mediastinal leak, free drainage back into esophagus, min- imal symptoms, no sign of sepsis. Surgical repair possible within 24 hours of perforation. After 24 hours, resection combined with diverting procedures may be necessary (“spit ﬁstula”).
Oropharyngeal Dysphagia	Description Neuromuscular control of oral and oropharyngeal stage of swallowing is impaired. Skeletal muscle is primarily involved; 50% of nursing home patients in the United States have difﬁculty with eating and drinking. differential diagnosis • Usually caused by CVA,Parkinson’s, or Alzheimer’s. • Evaluate with video swallow. • If aspirates, depending on clinical course and/or family wishes, PEG or G tube	Diagnosis Barium video swallow with liquid to solid foods, neurological evaluation. Occasionally, esophageal manometry (ear, nose, and throat [ENT]) evaluation. Pathology Cerebrovascular accident (CVA) (most common), Alzheimer’s, bulbar and pseudobulbar palsy. Cranial nerve paralysis, myasthenia gravis, skeletal myopathies. Treatment Steps Treat underlying condition where possible. If patient aspirates more than 10% of barium test bolus and develops barium residue in oropharynx with sequential swallows, needs endoscopic (percutaneous endoscopic gastrostomy [PEG]) or surgical gastrostomy for feeds.
Symptoms Epigastric pain, pain relieved by food and/or antacids, nocturnal awakenings, nausea, vomiting, and anorexia. Approximately one- third are asymptomatic.	Duodenal Ulcer Description Associated with acid hypersecretion. Increased number of parietal cells. Peak incidence between the ages of 20 and 60. Typically, peri- ods of remission and exacerbation. Ninety-ﬁve percent occur in duodenal bulb (posterior wall within 2 cm of the pylorus). Risk fac- tors include: Helicobactor pylori (almost 100%), tobacco use, nonsteroidal anti-inﬂammatory drugs (NSAIDs), and Zollinger–Ellison syndrome.	Diagnosis Endoscopy is 95% accurate and is diagnostic procedure of choice. Upper GI series 75–80% accurate, showing an ulcer crater or scar- ring of the duodenal bulb. The saline load test can be used to determine gastric outlet obstruction. Treatment Steps Medical—See Chapter 4. Surgical—Indications for surgery are hemorrhage, perforation (Fig. 18–1), obstruction, and intractability. Surgical procedures: 1. Perforated duodenal ulcer—vagotomy and pyloroplasty, vago- tomy and antrectomy, highly selective vagotomy (laparoscopic or open), omentopexy (Graham patch) with vagotomy. 2. Bleeding duodenal ulcer—oversew the bleeder with pyloro- plasty and truncal vagotomy. 3. Obstructing duodenal ulcer—truncal vagotomy with gastrojejunostomy
ESOPHAGEAL DYSPHAGIA	Structural • Schatzki’s ring—shown on video swallow with tablet; when symptomatic, usually has superﬁcial inﬂammation or erosion; brush cytology, balloon dilatation, and treatment with PPIs • Stricture, benign—brush cytology, balloon dilatation, and treatment with PPI • Carcinoma—biopsy diagnosis; resection if lower, radiation if upper; chemotherapy showing recent promise Nonstructural • Achalasia—aperistalsis, incomplete relaxation of LES with a high resting LES pressure. Botox injection in LES if ≥ 50 years old; pneumatic dilatation; if failed, then surgical myotomy with fundoplication • Scleroderma— aperistalsis, incompetent LES treatment for GERD
Symptoms Similar to duodenal ulcer. Pain localizes to left of midline, mostly postprandial	Gastric Ulcer Description Appear later in life. Peak incidence in ﬁfth decade. More common in men. Usually no acid hypersecretion. Cause factor is mucosal in- jury or defect in “mucosal defense” that renders mucosa susceptible to gastric acid. Majority occur on lesser curve of stomach. Malignant potential (10%). Ninety percent have H. pylori. Types 1. Ulcer located at incisura angularis on the lesser curvature (low acid output, associated with blood group A). 2. Ulcers located in stomach and duodenum (high acid output, as- sociated with blood group O). 3. Ulcer located in pylorus or prepyloric area (high acid output, as- sociated with blood group O). 4. Ulcer located high in stomach (juxtacardia, low acid output). 5. Ulcer located anywhere in stomach (associated with NSAIDs).	Diagnosis Upper GI series can localize (90% sensitive). Endoscopy (97% sensi- tive) important. Must biopsy ulcer 8–12 times to rule out malig- nancy. Treatment Steps 1. Principles of medical treatment are similar to those of treatment of duodenal ulcer. (See Chapter 4.) 2. Because recurrence rate is higher after medical therapy, surgical therapy should be considered earlier. Procedure of choice is antrectomy with Billroth I anastomosis. No vagotomy with type I gastric ulcers. • Type 1: distal gastrectomy (use Billroth I). • Types 2, 3: antrectomy with truncal vagotomy. • Type 4: extended distal gastrectomy or 90% near total gastrec- tomy with Roux-en-Y esophagogastrojejunostomy
Symptoms Dysphagia for liquids, then solids; chest pain, vomiting frequently without sour taste, nocturnal cough, pneumonia, lung abscess.	Achalasia Description Achalasia is characterized by increased basal pressure of the lower esophageal sphincter (LES), incomplete LES relaxation after a swallow, and aperistalsis of the distal two-thirds of the esophageal body. Pathology Abnormalities are found in the dorsomotor nucleus of the vagus nerve and in the postganglionic neurons, which innervate the circu- lar smooth muscle of the esophagus (myenteric plexus).	Diagnosis Air–ﬂuid level near aortic arch with widened mediastinum on chest x-ray. Barium swallow may show dilated distal two-thirds of the esophagus and smooth tapering at EG junction. All patients with achalasia should have upper endoscopy to ex- clude tumors and to enter the stomach to differentiate the tonically contracted LES from a malignant stricture. Esophageal manometry should be done and is the “gold stan- dard” (see Description). Computed tomography may be used to exclude extrinsic circumferential lesions simulating achalasia. Treatment Steps 1. Botoxin injection (80 U) into the lower esophageal sphincter if > 50 years old; if no help, then can be repeated in one month; if no help then #2. 2. Pneumatic dilation—transmural rupture of esophagus is an un- common complication—if no help, then 3. Surgical myotomy (modiﬁed Heller’s) with fundoplication, at- tempting to avoid esophageal stricture (20%) or Barrett’s esopha- gus.
Symptoms • Early—vague, nondescript symptoms. • Late—indigestion, postprandial fullness, eructation, loss of ap- petite, heartburn, vomiting. Pain pattern is similar to peptic ulcer disease.	Gastric Carcinoma Description Adenocarcinoma is the most common (95%); classiﬁed into ulcer- ating (25%), polypoid (25%), superﬁcial spreading (15%, best prognosis), linnitus plastica or “leather bottle” (10%), and ad- vanced (35%). Risk factors include: dietary (nitrosamines, smoked/salted or pickled foodstuffs), tobacco use, alcohol, and en- vironmental factors. Almost all have H. pylori. Adenomatous polyps and atypical gastritis are premalignant lesions. Most have adenocar- cinoma and are located in the antrum. Cancer at the gastroe- sophageal junction is associated with Barrett’s esophagus and GERD. Major factors inﬂuencing survival are level of spread through gastric wall and lymph node involvement. Seventy-ﬁve per- cent have metastasis at the time of diagnosis. Age range: 50–70 years; male-to-female ratio is 2:1.	Diagnosis Barium Meal Upper GI Series (Double Contrast)—polypoid mass, ulcer crater not extending outside boundary of gastric wall, nondisten- sible stomach. Endoscopy—With biopsy, 90% accurate. Endoscopic ultrasound may be of value in determining depth of tumor and presence of enlarged lymph nodes. CT Scan—Evaluation of metastatic spread. Treatment Steps 1. Radical subtotal gastrectomy for cure, distal lesions. 2. Radical total gastrectomy for proximal lesions. Half of those oper- ated on are resectable. 3. Chemotherapy reserved for unresectable or recurrent disease (no impact on survival). 4. Gastrojejunostomy for palliative bypass in unresectable disease. 5. Radiotherapy to control pain and bleeding in unresectable cases.
Symptoms Heartburn (can manifest as chest/epigastric pain), occasionally chronic cough, nocturnal cough, choking, wheezing, laryngospasm, hoarseness, earache.	Gastroesophageal Reﬂux Disease (GERD) Description Reﬂux of gastric acid into lower esophagus causing irritative symp- toms	Diagnosis Upper GI endoscopy to rule out ulcers, Barrett’s esophagus. How- ever, can diagnose GERD clinically and start empiric therapy. Treatment Steps 1. Lifestyle changes include not lying down after eating (and not eating close to bedtime) and reduction in foods that trigger GERD (often fatty foods, alcohol, spicy foods). 2. Empiric treatment with PPI (although H2 blockers are less expensive, the PPIs are more effective, therefore cost effective, in the end. 3. If symptoms refractory despite compliance with above, may use esophageal pH monitoring to look at physiologic response. 4. Refractory cases of GERD may respond to surgery (Nissen fundoplication).
Symptoms Crampy abdominal pain, vomiting, obstipation, distention, failure to pass ﬂatus.	SMALL INTESTINE A. Obstruction Description Can be classiﬁed into: • Simple—no vascular compromise. • Strangulating—vascular obstruction. • Paralytic ileus—impairment of muscle function, closed-loop block- age at two points. Can be caused by adhesions (70%), hernia (8%), tumor (9%), inﬂammatory disease (4%), volvulus, or intussusception. SMALL BOWEL OBSTRUCTION • Adhesions • Malignancy • External hernia • Volvulus • Crohn’s disease • Intra-abdominal abscess • Intussusception • Radiation stricture • Foreign body • Gallstone ileus	Diagnosis High-pitched bowel sounds on physical examination. Peritoneal signs signify peritonitis secondary to strangulation and/or perfora- tion. X-ray: distended small-bowel loops in stepladder pattern, air–ﬂuid levels. Small bowel follow-through and CT scan may delineate the point of obstruction. Treatment Steps 1. Nonsurgical management for partial small bowel obstruction (SBO), which includes replacing electrolyte losses, intravenous ﬂuids, nothing by mouth (NPO), and often nasogastric tube de- compression. 2. Consider trial of long-tube decompression. Uncommonly used secondary to risk of perforation or intussusception. 3. Complete SBO––surgery as needed. 4. Operative therapy: exploratory laparotomy with lysis of adhesions and small bowel resection if indicated. 5. Septraﬁlms (hyaluronic acid) can be used to reduce adhesions (by 50%). Results Morbidity—30% (60% with strangulated bowel, 20% with neoplasia, 20% with adhesion and hernia).
Symptoms Heartburn, dysphagia for liquids, then solids.	Scleroderma Esophagus Description A patulous esophagus leads to reﬂux disease and dysphagia associ- ated with Raynaud’s phenomenon in 90% of cases	Diagnosis Air-ﬁlled esophagus on chest ﬁlm. Prone view of esophagogram fails to empty. Esophageal manometry in advanced state includes de- creased LES pressure, low amplitude or absent contractions in the smooth muscle esophagus, normal peristalsis in the striated muscle esophagus, and a normal upper esophageal sphincter (UES). Treatment Steps See treatment for GERD. Surgery is unnecessary and probably con- traindicated here because of the limited ability to empty the esophagus
Symptoms Bleeding and obstruction. Weight loss in nearly all malignant tu- mors. Carcinoid syndrome (ﬂushing, pain, diarrhea, bronchocon- striction, valvular disease) from release of vasoactive substances from metastatic carcinoid tumors.	SMALL INTESTINE Neoplasms Description Jejunum and ileum, 5% of all tumors of GI tract. Benign are more common. Most are asymptomatic; 10% become symptomatic. Benign Tumors—Leiomyomas (18–20%), lipomas (15%), neuroﬁ- bromas (10%), adenomas (15%), polyps (15%), hemangiomas (13%), ﬁbromas (10%). Malignant Tumors—Adenocarcinomas (30–50%), lymphomas (15%), leiomyosarcomas (20%), carcinoids (30–50%). Less than 5% metastatic tumors (melanoma, gastric carcinoma).	Diagnosis Often made at time of laparotomy. Bowel obstruction with no previ- ous surgery is suspicious for neoplasm. Small-bowel series (entero- clysis is most sensitive). Endoscopy (procedure of choice with duo- denal neoplasms). Arteriography (useful with vascular neoplasms: hemangiomas). CT/MRI may complement staging. Biochemical analysis of urine samples (5-hydroxyindoleacetic acid in carcinoid tumors). Treatment Steps 1. Wide resection. 2. Bypass for palliation.
Symptoms Nausea, vomiting, bloating, upper abdominal discomfort.	Gastroparesis Description Delayed gastric emptying without mechanical cause. Pathology and Associated Conditions Acute with intact vagi (blood sugar > 300 mg/dL, acute pancreatitis, trauma, abdominal surgery, porphyria, severe hypokalemia, or drugs [opiates, digitalis, ganglionic blockers, anticholinergic]). Chronic (most frequently caused by neuropathy [postvagotomy or diabetic] or myopathy [scleroderma]).	Diagnosis Retained barium in stomach on upper GI series (UGI). Delayed nu- clear medicine gastric emptying scan. Upper endoscopic exam within normal limits. Treatment Steps Metoclopramide (a dopaminergic antagonist, 30% neurologic, and psychiatric side effects). Erythromycin (oral).
Symptoms Obstruction due to stricture, bleeding from ulcerated mucosa, necrosis with perforation, ﬁstula formation, abscess formation	SMALL INTESTINE Radiation Injury Description Pathogenesis involves progressive obliterative vasculitis. May be diag- nosed many years remote from time of radiation therapy.	Treatment Steps 1. Avoid surgery if possible. (Total parenteral nutrition [TPN] used with severe symptomatic disease, poor nutritional status.) Mini- mal dissection. 2. Resection or bypass with wide margins. May need to exteriorize if bowel viability is in question.
Description Symptomatic decrease in frequency of bowel movements and may also mean (to some patients) passage of dry stools, excessive straining, lower abdominal fullness, and a sense of incomplete evacuation.	Constipation	Diagnosis Rule out organic disease (endocrine pharmacologic, neurologic, and structural). Treatment Steps Insoluble dietary bulk 15 g of crude ﬁber (e.g., wheat bran [methyl- cellulose] or commercial psyllium products with 32 oz of water per day). Lactulose can be tolerated well for long periods. Occasionally, mineral oil enemas can help relieve distal fecal impaction
Symptoms May mimic appendicitis if Meckel’s diverticulitis is present. Bleeding (more common in children). Intestinal obstruction from intussusception (more common in adults).	Meckel’s Diverticulum Description Congenital anomaly, persistent omphalomesenteric duct. A true di- verticulum found on the antimesenteric border. Found in 2% of the population. Two feet from ileocecal valve; 2 inches long. May con- tain heterotopic tissue (pancreas, gastric mucosa, other types). Four percent symptomatic, usually in childhood MECKEL’S DIVERTICULUM “RULE OF TWOS” • 2% of population • 2 feet from ileocecal valve • 2 inches long • 2 types of heterotopic tissue (pancreas, gastric mucosa) • Shaped like a 2 • 2x more common in males • 2% symptomatic	Diagnosis X-ray and small-bowel series unreliable. Technetium scan will local- ize heterotopic gastric mucosa, if present (accuracy, 90%). Treatment Steps 1. Surgical resection (with GI bleeding, excise diverticulum with suf- ﬁcient margin of ileum to encompass ulceration). The contralat- eral ileal wall is usually the source of the bleeding and therefore, a wedge resection is not appropriate. 2. Incidental ﬁnding at laparotomy: leave alone.
Description Twenty-four-hour excretion weight or volume greater than 200 g/24 hours and greater than 10 g/kg in infants, and change in consistency—more liquid. Not incontinence (the involuntary release of rectal contents).	Diarrhea Always think of the common ones ﬁrst: gastroenteritis, food intoxication/poisoning, infections (bacterial— Salmonella, Shigella, Vibrio, Clostridium), parasitic (Giardia, Entamoeba), as well as human immunodeﬁciency virus (HIV)-related; absorption syndromes (sprue, tropical sprue, lactose intolerance).	Diagnosis Osmotic diarrhea stool: 290 − 2 (Na + K) => 50 (Osm gap). Diarrhea should disappear when patient fasts.
Symptoms Crampy abdominal pain, diarrhea, nausea and vomiting, fear of eating, weight loss. Diagnosis Physical Examination—Abdominal mass right lower quadrant. Check for other sites of disease (e.g., perianal area for ﬁstula). Endoscopy—Reddened mucosa, skip lesions. Biopsy. Small Bowel Series—String sign, ﬁstulas. Thickened bowel wall.	Crohn’s Disease Description Chronic inﬂammatory disease of the GI tract. There are three types: inﬂammatory, ﬁbrostenotic, and ﬁstulizing. Unknown cause. Peak age of onset is between second and fourth decades. Transmural in- volvement of bowel wall, noncaseating granulomas, aphthous ulcers, malignant potential, extraintestinal manifestations are common. Ob- struction and perforation with abscess and ﬁstula formation. Skip le- sions. Seventy percent progress to operation for complications of the disease. Anal manifestations of the disease are common.	Treatment Steps Medical Therapy—Antibiotics, steroids, sulfasalazine, 5-aminosali- cyclic acid (ASA), immunosuppressive agents (6-mercapto- purine, azathioprine), bowel rest, central hyperalimentation. Surgical Therapy—(Use eventually required in 75%). Indications: failure of medical therapy or complications of the disease. Surgery: excision, bypass, stricturoplasty. Contraindications to stricturoplasty are ﬁstula, open perforation, abscess, associated inﬂammatory mass. Recurrence—(40% within 5 years, 60% within 10 years, 75% within 15 years). The major problem in surgical treatment.
Noninﬂammatory Diarrhea	Noninﬂammatory Enterotoxigenic E. coli (ETEC) Clostridium perfringens Staphylococcus aureus Bacillus cereus Vibrio cholera Rotavirus Norwalk virus Giardia lamblia Cryptosporidium
Symptoms 1) Dull abdominal pain, occult bleeding. 2)Change in bowel habits, visible blood, change in stool caliber. 3)Tenesmus, incomplete evacuation, blood-streaked stool.	Carcinoma of the Colon and Rectum 1)Right-Sided Lesions 2)Left-Sided Lesions 3)Rectal Lesions Description Second most common malignancy. Pathogenesis unclear. Likely environmental inﬂuence. Diets high in fat, low in ﬁber: higher incidence. Other risk factors (25%): ﬁrst-degree relatives, inherited genetic syndrome, prior colorectal cancer or adenomatous polyp,inﬂammatory bowel disease, hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome, familial polyposis coli. 75% no speciﬁc risk factors. The sigmoid colon in the most common primary site and the liver, the most common site of metastasis. Screening: digital examination, stool for occult blood, sigmoidoscopy, colonoscopy.	Diagnosis Digital examination, barium enema, colonoscopy, CT scan, endorectal ultrasound, liver function tests, CXR. Carcinoembryonic antigen level (provides a baseline level for future comparison). Screen 50 years or older annually for fecal occult blood and every 5 years with ﬂexible sigmoidoscopy, or colonoscopy every 10 years. Treatment Steps Operative excision with adequate margins. Rectal carcinoma: level of resection depends on location of tumor. Lesions < 8 cm from anal verge may need abdominoperineal resection; > 8 cm, low anterior resection. Adjuvant therapy in colorectal cancer: (1) for stage 2 and 3 rectal cancer, 5-ﬂuorouracil (5-FU) and postoperative radiation therapy; (2) no role for radiation therapy in colon cancer. Additional chemotherapy is appropriate for stage 3 and 4 colon cancer.
Inﬂammatory diarrhea	white blood cells in the stool. Blood may also be present. Inﬂammatory Campylobacter jejuni Shigella species Enterohemorrhagic E. coli (EHEC) Clostridium difﬁcile Vibrio parahaemolyticus Entamoeba histolytica Salmonella species
Symptoms Blood per rectum, minimal pain.	Diverticulosis Description Colonic outpouching from bowel wall. Males and females equal inci- dence. Sixty-ﬁve percent of population by age 85. Bleeding occurs in 15%. Hemorrhage arises in right colon in 70–90%. Seventy percent stop bleeding spontaneously; 30% have recurrent bleeding.	Diagnosis Endoscopy, bleeding scan, arteriography. Treatment Steps (Lower GI Bleed or Diverticulosis) 1. Selective infusion of vasopressin or rarely angioembolization. 2. Segmental colonic resection if bleeding site is localized. 3. Subtotal colectomy if bleeding not localized.
Description Prior antibiotic use alters the normal GI ﬂora and C. difﬁcile causes diarrhea. Can occur with any antibiotic (even one dose as long as 2 months before).	Pseudomembranous Colitis (Clostridium difﬁcile Diarrhea)	Diagnosis Identifying C. difﬁcile toxin in the stool. On colonoscopy: yellow ad- herent plaques on the colonic mucosa. Treatment Steps 1. Remove the offending antibiotic whenever possible. 2. Oral metronidazole is the treatment of choice, although patients can have recurrence. 3. If multiple recurrences, use oral vancomycin. 4. Alternatives include cholestyramine and Saccharomyces boulardii 500 mg PO bid.
Symptoms Left lower quadrant (LLQ) pain, anorexia, nausea and vomiting, fever, abdominal mass.	Diverticulitis Description Inﬂammation of diverticulae. Limited to sigmoid colon in 90%. Inﬂammation is usually contained by pericolic fat and mesentery.	Diagnosis Clinical presentation, CT scan. Barium enema and colonoscopy only after acute inﬂammation lessened (usually > 1 week following acute episode). Treatment Steps 1. Bowel rest, antibiotics, intravenous ﬂuids, analgesia. 2. If there is an abscess, CT-guided drainage. 3. Elective surgical resection in young, diabetic, immunocompro- mised, or one prior episode of diverticulitis. Surgical resection when inﬂammation has subsided (approximately 8 weeks follow- ing recent attack). 4. Operations for diverticular disease: One-Stage Procedure—Resection and primary anastomosis. Two-Stage Procedure—Hartman operation (sigmoid resection, and decending colostomy, mucous ﬁstula or leaving a rectal stump as a “Hartman’s pouch”). Operating room sigmoid resection, pri- mary anastomosis, and proximal diverting colostomy. Three-Stage Procedure—Colostomy and drainage. Subsequent resec- tion as a second procedure. Subsequent takedown of colostomy and primary ananstomosis. This series of procedures is uncom- monly done secondary to prolonged hospital stay, increased morbidity and mortality.
Symptoms Rectal bleeding, change in bowel habits. Sometimes asymptomatic, but found on routine screening colonoscopy	COLORECTAL CANCER Description Cancer of colon is the most frequent neoplasm of the GI tract and is the second most common cause of cancer mortality in the United States. Early detection may lead to a substantial improvement in out- come (see Fig. 4–2). Pathology Ninety-ﬁve percent of malignancies of the colon and rectum are ade- nocarcinoma.	Diagnosis American Cancer Society recommends fecal occult blood testing (FOBT) of passed stool yearly after age 50 and ﬂexible sigmoidoscopy every 4 years. Start earlier age with colonoscopy if genetic predisposi- tion or prior disease. More recent studies have suggested screening all normal-risk individuals with colonoscopy starting at age 50, regardless of results of FOBT. The presence of heme in an asymptomatic person at risk is an indication for colonoscopy.Colonoscopy is more sensitive, a biopsy can be made (and polyps can be removed); especially in high-risk patients whose ﬁrst-degree relatives have colorectal cancer or who themselves have IBD, previ- ous breast or genital cancer, prior colonic adenomas, or familial polyposis. Finding even one adenoma on ﬂex sig should lead to total colonoscopy and polypectomy. Repeat colonoscopy in 3 years; if nor- mal, can be followed by exams every 5 years depending on the com- pleteness of the exam and type of polyp. Treatment Steps The only curative therapy is surgical resection of the primary tumor and of the isolated hepatic metastases. Rule out synchronous lesions by doing full colonoscopy preop. Colonoscopy in 1 year to exclude recurrence and at 3–5 years to prevent the 8–10% incidence of sec- ond cancers, which occur within 10 years of the initial surgery. Chemotherapy for metastatic disease.
Symptoms Bloody diarrhea, fever, crampy abdominal pain, tenesmus, urgency, incontinence.	Ulcerative Colitis Description Mucosal inﬂammation, crypt abscesses, mucosa sloughs, colon becomes shortened. Two peaks in incidence: second and sixth decades Can involve rectum alone or entire colon. Malignant potential in- creases with time (2–5% at 10 years, then 1% 1 year thereafter). Ex- traintestinal manifestations (arthralgias, ankylosing spondylitis, sclerosing cholangitis, and liver dysfunction, uveitis, nephrolithiasis).	Diagnosis Endoscopy—Friable, erythematous mucosa. Barium Enema—Loss of haustral markings, stricture, stovepipe colon. Treatment Steps Medical—Intravenous ﬂuids, NPO, steroid enemas, correct elec- trolyte abnormalities, sulfasalazine. Surgery—Reserved for treatment of complications (hemorrhage, perforation, toxic megacolon, carcinoma, intractability). Total proctocolectomy with ileostomy. Proctocolectomy with ileoanal anastomosis (ileal J pouch).
Symptoms • Fatigue • Increasing abdominal girth (due to ascites) • Jaundice • Spider angiomas • Bleeding (GI bleeding due to hemorrhoids or esophageal varices) Signs • Palmar erythema • Hepatosplenomegaly • Gynecomastia • Testicular atrophy Labs • Elevated AST and ALT • Elevated PT and INR • Thrombocytopenia, anemia (often macrocytic), or pancytopenia • Hyponatremia • Hypoalbuminemia	Chronic Liver Disease Description A variety of conditions can cause chronic liver disease (see Cram Facts). With recent increases in hepatitis C and obesity (and there- fore fatty liver disease) the incidence of liver disease is increasing. If chronic liver disease progresses to end-stage liver disease, the patient can have a multitude of problems, including hepatic encephalopa- thy, coagulopathy (elevated prothrombin time [PT] and interna- tional normalized ratio [INR] due to impaired synthesis of coagula- tion factors), thrombocytopenia (due to portal hypertension causing hepatosplenomegaly and consumption of platelets), esophageal varices (due to portal hypertension), and hepatorenal syndrome (re- nal failure due to liver disease) CAUSES OF CHRONIC LIVER DISEASE • Autoimmune hepatitis • Hereditary hemochromatosis • Chronic alcohol use • Fatty liver disease (non- alcoholic steatohepatitis) • Wilson’s disease • Viral (hepatitis B, C)	Treatment Steps Varies according to the underlying condition. With any etiology, if cirrhosis/end-stage liver disease is present, patients may be consid- ered for liver transplantation if they are abstaining from alcohol
Symptoms Bleeding, pruritus ani, pain (secondary to thrombosis).	Hemorrhoids Description Internal hemorrhoids above dentate line. External below dentate line. Location of internal hemorrhoids: right anterior, right posterior, left lateral. Causes: Hereditary, straining, portal hypertension,and pregnancy.	Diagnosis Physical examination, anoscopy. Treatment Steps 1. Medical symptomatic relief (high-ﬁber diet, stool softeners, bulk agents [psyllium]). 2. Rubber band ligation. Contraindication to banding—presence of foreign material (e.g., breast or penile implant, or pacemaker). 3. Surgical excision. Indication for surgical hemorrhoidectomy— SURGICAL PRINCIPLES Colon, Rectum, Anus 502 ULCERATIVE COLITIS VS. CROHN’S DISEASE OF THE COLON Ulcerative Colitis Crohn’s Disease Rectum Involved Spared in 25% Colon Begins in rectum with proximal Neocolonic pattern frequent spread Ileum Rarely involved Commonly involved as “skip lesions” Mucosal involvement Circumferential Patchy, segmental cram facts Ustage 4 hemorrhoids that fail conservative therapy. Contraindica- tion to surgical hemorrhoidectomy—inﬂammatory bowel disease, suspicion of neoplasm. 4. Anal dilatation. Uncommonly done secondary to incontinence issue
Symptoms CAAH is suspected when physical examination reveals signs of chronic liver disease (e.g., spider angiomata, ascites, and elevated serum glutamic oxaloacetic transaminase [SGOT] or serum gluta- mate pyruvate transaminase [SGPT]). Often, the patient may have only increased fatigue and persistent elevated enzymes for 6 months or more.	Autoimmune Hepatitis Description Chronic active autoimmune hepatitis (CAAH) can present with striking increases in enzymes resembling viral hepatitis, but stigmata of chronic liver disease or marked elevations in gamma globulins may help identify it as chronic without evidence of other causes. A positive antinuclear antibody (ANA) strongly suggests the diagnosis. Pathology Piecemeal necrosis and bridging necrosis (ﬁbrosis can lead to cir- rhosis). This disease is associated with three important patterns of au- toantibodies in serum: 1.The ﬁrst pattern characteristically has positive ANA, anti- smooth muscle antibody (ASMA) liver membrane autoantibod- ies. 2.The second pattern is associated with antibodies to a soluble liver antigen (antisoluble liver antigen [anti-SLA]). 3.The third is associated with anti-liver-kidney microsomal-1 anti-body (mainly in Europe). Drugs producing a hepatitis that mimics CAAH are α-methyl- dopa and nitrofurantoin (especially women).	Treatment Steps Steroid therapy achieves symptomatic, clinical, and histologic remis- sion, but relapse occurs in 90% over 2 years, requiring long-term maintenance therapy leading to increases in life expectancy, but does not appear to stop progression to cirrhosis. 6-Mercaptopurine may be used with steroids.
Symptoms Exquisite pain, painful defecation, blood on toilet paper. Diagnosis Sentinel pile, painful digital examination, endoscopy when acute episode resolved.	Anal Fissure Description Superﬁcial linear ulceration in the posterior midline. Sentinel pile (skin tag), seen in chronic ﬁssures. Ulceration occurs in the squa- mous epithelium; therefore, very painful. Straining at stool. Consti- pation. Condition is cyclic. Secondary anal ﬁssures occur secondary to inﬂammatory bowel disease, malignancy, acquired immune deﬁciency syndrome (AIDS), syphilis, tuberculosis	Treatment Steps 1. Acute ﬁssure is treated nonsurgically. Chronic ﬁssure is treated operatively with consideration for biopsy. 2. Local cleansing agents. 3. Sitz baths. 4. Topical ointments. 5. Stool softeners. 6. Anal dilatation. 7. Lateral internal sphincterotomy (open or closed).
Description A genetic condition (usually autosomal recessive with variable pene- trance) that causes iron overload. Iron can be deposited in many or- gans. The classic tetrad includes cirrhosis, diabetes, skin hyperpigmentation, and cardiac failure. Sometimes called “bronze diabetes.”	Hereditary Hemochromatosis	Treatment Steps Removal of excess iron through phlebotomy. Chelation therapy (with deferoxamine) is usually indicated only when phlebotomy is inappropriate.
Symptoms Pain, anorexia, vomiting, diarrhea, cutaneous hyperesthesia, guarding and rebound at McBurney’s point, Rovsing’s sign, psoas sign, obturator sign, Blumberg’s sign.	APPENDIX––APPENDICITIS Description Appendix: variable location in relation to the cecum. Teniae converge on appendix. Closed-loop obstruction of lumen, vascular congestion, serosal inﬂammation, perforation.	Diagnosis Physical examination. Fecalith in right lower quadrant (RLQ) is diagnostic, altered right psoas shadow. Leukocytosis (may be absent).Ultrasound and CT scan useful in equivocal cases. However, use clinical judgment. If appendicitis is still clinically suspected despite negative lab or radiologic workup, seek surgical opinion. Treatment Steps 1. Intravenous ﬂuids and antibiotic therapy. 2. Appendectomy (open or laparoscopic). Normal appendix is removed as an incidental ﬁnding of malrotation or if an explo- ration is done for possible appendicitis (to avoid future confusion over the diagnosis).
Description Liver disease due to alcohol consumption. Can range from asympto- matic liver function test (LFT) abnormalities to alcoholic hepatitis to cirrhosis/end-stage liver disease. Women are at higher risk from liver damage due to alcohol than are men because ethanol is metab- olized differently. Any chronic liver condition will be worsened by al- cohol use.	Chronic Alcohol Use	Treatment Steps Cessation of drinking alcohol, which can be very difﬁcult. Support groups (Alcoholics Anonymous) have been effective. A patient must demonstrate cessation of alcohol before he/she can be considered for a liver transplant
Symptoms Right upper quadrant (RUQ) or epigastric pain. Pain radiates to tip of scapula. Nausea and vomiting.	Acute Cholecystitis Description Bacterial or chemical inﬂammation of the gallbladder. Cystic duct obstruction and altered bile chemistry are two conditions necessary to cause acute cholecystitis. Occurs in the 4th to 8th decade. Inci- dence higher in females. Obstruction of the cystic duct. Bacteria in 50–75% (Escherichia coli, Klebsiella, Enterobacter).	Diagnosis Physical examination: Murphy’s sign. Mild jaundice. Ultrasound is the most sensitive and speciﬁc diagnostic test to detect stones and surrounding inﬂammation, and can provide other anatomic infor- mation in the hepatobiliary system. Hepatoiminodiacetic acid (HIDA) scan 90% accurate (normal HIDA, gallbladder ﬁlls in 30 minutes). Treatment Steps Antibiotics. Cholecystectomy, delayed or immediate. Percutaneous cholecystostomy in poor-risk patients. Not to be performed in the presence of gallbladder gangrene or perforation (Fig. 18–2). Variant forms: empyema of gallbladder, gangrene, acalculous cholecystitis
elevated LFTs in people who do not ingest alcohol. There is often a common clinical picture: Patients have obesity, diabetes, hyperlipidemia, and/or high-fat diet.	Fatty Liver Disease (Nonalcoholic Steatohepatitis [NASH]) Unfortunately, this condition is becoming exceedingly common in the United States, as the number of people with diabetes and obesity is higher now than ever before. It is now felt that many people who have presented with cryptogenic cirrhosis may have actually had NASH that was undiagnosed. Description A condition in which lipids accumulate in the hepatocytes. Fatty change in the liver is known as steatosis, and steatosis with inﬂammation is called steatohepatitis. Because steatohepatitis is common in patients who drink alcohol, this particular subset (NASH) occurs in people who do not ingest alcohol. There is often a common clinical picture: Patients have obesity, diabetes, hyperlipidemia, and/or high-fat diet.	Diagnosis Technically, NASH is a pathologic diagnosis seen on liver biopsy.However, patients are suspected of having NASH, or “fatty liver disease” in the correct clinical setting (overweight/obese, diabetes, hyperlipidemia), and elevated LFTs. Ultrasound of the liver can show changes consistent with fatty liver. All other causes of chronic liver disease should be ruled out Treatment Steps 1.Varying opinions exist as to whether all patients should have a liver biopsy. The argument is that pathology (inﬂammation, ﬁbrosis/cirrhosis) can be followed serially. 2.Evidence exists that a low-fat diet, weight loss, and control of diabetes and hyperlipidemia will help fatty liver. However, if cirrhosis develops, supportive care and consideration of liver transplant are needed.
Signs and Symptoms Pain in RUQ and epigastric pain. May radiate to tip of scapula. Nausea and vomiting. Attacks often follow large meals.	Chronic Cholecystitis Description Repeated attacks of acute cholecystitis. Stones almost always present.	Diagnosis Physical examination. Ultrasound to identify stones. Oral cholecys- tography if symptoms are typical but ultrasound negative. Endo- scopic retrograde cholangiopancreatography (ERCP) to identify cholesterol crystals if other tests negative and symptoms persist Treatment Steps Laparoscopic cholecystectomy for routine management. An open cholecystectomy is indicated in cases of cirrhosis, bleeding disorders, pregnancy, gallbladder cancer, and severe cardiopulmonary disor- ders.
Diagnosis Patients may present with acute hepatitis. Psychiatric manifestations may include confusion, aggression. Labs that are basically diagnostic for Wilson’s include serum ceruloplasmin (< 20 mg/dL), low total serum copper, and increased urinary copper excretion. One clue to the diagnosis is the presence of hemolytic anemia. Computed tomo- graphic (CT) scan of the brain can reveal hypodense regions in the basal ganglia. Liver biopsy can conﬁrm the diagnosis: a hepatic copper content > 250 µg dry weight of the liver in the correct clinical setting. Two clues to the diagnosis: • Hemolytic anemia. • Kayser–Fleischer rings–– asymptomatic color changes that occur in the Descemet membrane of the eye. They are always found if there is neurologic involvement. The rings can disappear with appropriate treatment.	Wilson’s Disease Description Wilson’s disease (hepatolenticular degeneration) is an inherited (autosomal recessive) genetic disorder. While it is rare, it is impor- tant to recognize as it can be fatal if unrecognized/untreated. (See also Chapter 11, section IX.C.)	Treatment Steps Copper chelating medications include penicillamine. The disease is uniformly fatal if untreated.
Symptoms Fever and chills, jaundice, biliary colic (Charcot’s triad). Severe: additional hypotension and mental confusion (Reynolds’ pentad).	Cholangitis Description Infection in the biliary tree. Bacteria (commonly E. coli, Klebsiella, Enterococcus), obstruction, increased pressure. Most commonly associated with choledocholithiasis.	Diagnosis Clinical presentation. RUQ tenderness. Elevated white blood cell count, bilirubin, and alkaline phosphatase. Ultrasound of RUQ to document gallstones. CT scan to rule out periampullary malignancies or liver abscesses. Treatment Steps Antibiotics. Triple antibiotics if severe (60% of cases with multiple organisms). Endoscopic sphincterotomy with stone extraction. Ex- ploratory laparotomy, cholecystectomy with common bile duct exploration and T-tube drainage.
Description Almost any virus can cause an acute and often self-limited hepatitis. Classically, hepatitis viruses B and C are capable of causing chronic liver disease. Hepatitis A virus is never a cause of chronic liver dis- ease. However, acute hepatitis A infection can worsen a patient’s condition in the setting of chronic liver disease.	Viral Hepatitis	Immunization against hepatitis A and B is indicated in patients with chronic liver disease if they are not already immune.
Symptoms Pain in RUQ. Distention. Nausea. Vomiting. Colicky abdominal pain.	Gallstone Ileus Description Antecedent cholecystointestinal or choledochointestinal ﬁstula. Gallstone obstructs at intestinal narrowing (usually in distal ileum). Occurs more likely in the elderly (70s) and is four times more com- mon in women. Less commonly Bouveret’s syndrome (stone enters and obstructs the duodenum). Gallbladder carcinoma occurs in 15% of those with gallstone ileus.	Diagnosis Air in biliary tree (pneumobilia) occurs in 40%. Dilated small-bowel loops. Opaque stone in the intestinal tract (15–20%). Nonopaque stone in intestinal tract identiﬁed by ultrasound. Treatment Steps 1. Fluid resuscitation, correction of electrolyte abnomalities, naso- gastric decompression, antibiotic prophylaxis. 2. Exploratory laparotomy, enterotomy proximal to the impacted stone with removal of the stone. Repair of biliary–enteric ﬁstula. 3. Cholecystectomy if medically stable.
HYPERBILIRUBINEMIA differential diagnosis	Conjugated 1.Bilary obstruction: choledocholithiasis, biliary atresia, malignancy, pancreatitis, sclerosing cholangitis, others. 2.Hereditary: Gilbert syndrome, Crigler–Najjar syndrome, Dubin–Johnson syndrome. 3.Hepatocellular dysfunction: hepatitis, hepatic cirrhosis, biliary cirrhosis, sepsis, postop, drugs, infections, mononucleosis, cholangitis, sarcoidosis, toxins, lymphomas. Unconjugated 1.Hemolytic anemias. 2.Posthepatitis. 3.Gilbert syndrome.
BILIARY OBSTRUCTION differential diagnosis	• Gallstones • Benign strictures • Malignant strictures • Pancreatitis • Extrinsic compression • Obstructed biliary stents
Complications of Cirrhosis	Portal hypertension causes hepatosplenomegaly, hemorrhoids, ab- dominal and esophageal varices. Pancytopenia can occur, due to hypersplenism––the spleen con- sumes cells from all three cell lines. (Alcohol can also suppress bone marrow.) • Coagulopathy––elevated PT and INR due to the lack of production of the vitamin K–dependent clotting factors in the liver (factors II, VII, IX, X). Ascites, spontaneous bacterial peritonitis, hepatic encephalopathy (see next three sections).	In a patient with chronic liver disease, endoscopy should be per- formed, and if esophageal varices are present, β-blockers should be started to decrease portal pressures and decrease risk of bleeding. Bleeding esophageal varices can be a signiﬁcant cause of morbidity and mortality
Symptoms Nonspeciﬁc. Pain. Weight loss. Jaundice. Anorexia. RUQ mass.	Gallbladder Carcinoma Description Most common malignancy of biliary tract. Association with gallstones (95%, particularly larger ones), porcelain gallbladder (calciﬁed wall, should have cholecystectomy even if asymptomatic), biliary adenoma, biliary infection with Salmonella. Adenocarcinoma in 82%. More common in females. 1-2% undergo cholecystectomy. Tends to be diagnosed in advanced stage. Seventy percent have liver metastases at the time of diagnosis.	Diagnosis Advanced disease: CT scan. Curable, localized disease found at time of cholecystectomy. Treatment Steps If tumor localized to mucosa and submucosa, cholecystectomy. Serosal or lymph node involvement: cholecystectomy with node resection and hepatic wedge resection. If N2 nodes (peripancreatic,duodenal, portal, celiac, or superior mesenteric artery [SMA]) are present, do not proceed with resection. Results: overall 5-year survival rate, 2–5%.
CIRRHOSIS—COMPLICATIONS	Fourth most common (25–45%) cause of death in U.S. urban areas. •Ascites: Na, ﬂuid restriction and diuretics; Aldactone 50–400 mg/24 hr; if no help, furosemide; if no help, large-volume paracentesis can be done 1-3 times a month for life, if no help TIPS may help. •Spontaneous bacterial peritonitis: > 250 polys; 10–100 mL blood culture bottles at bedside; treat with cefotaxime 2 g IV q8 to 12h for 5–10 days. If polys not decreased 50% by 48 hr, change med and reevaluate problem. •Encephalopathy: protein restriction, lactulose 30 cc qh until diarrhea, then q6h; if PO not available, then 300 mL lactulose plus 700 mL tap water enema one to three times daily if deemed safe to give enemas. Treat underlying condition.
Symptoms Pain, distention, weight loss, fatigue, anorexia, fever, jaundice, ascites. Diagnosis The tumor marker, α-fetoprotein (AFP) is elevated (although ﬁbro- lamellar type seen in younger patients, it is not associated with AFP elevation). CT scan with or without percutaneous biopsy. Arteriogra- phy. Intraoperative ultrasound.	Hepatocellular Carcinoma Description More common in Africa and Asia. Risk factors include: cirrhosis, hepatitis B, hemochromatosis, schistosomiasis, aﬂatoxin, and α1- antitrypsin deﬁciency. Eighty percent of primary liver tumors. Very often presents in advanced stage.	Treatment Steps 1. Only 25% are resectable (5-year survival rate: 18–36%). Can re- move up to 80% of liver. 2. Transplantation. 3. Palliation: intra-arterial chemotherapy, hepatic artery ligation. 4. Cryoablation developing as alternative to resection.
Diagnosis Ultrasound (US) or CT more sensitive than physical exam. Paracentesis 10 mL into blood culture bottles, acid-fast bacteria (AFB), fungal cultures, cytology, amylase, total protein, white blood count (WBC) and differential.	Ascites Description Fluid in peritoneal cavity Pathology All the factors in ascites mechanism and formation are not known	Treatment Steps 1.Sodium and ﬂuid restriction and diuretics. 2.Initially with spironolactone 50–400 mg/24 hr. 3.If no help in 3–4 days, start furosemide 40 mg daily. 4.If no response, double daily up to 240–320 mg daily. 5.Failure: other drugs, bumetanide, ethacrynic acid, or metola- zone, watch for large diuresis. 6.If no help, large-volume paracentesis if > 5 L needed to give albu- min 6–8 g/L of ﬂuid removed. Can be done one to three times per month for life. 7.Patient with intractable ascites who has bled from varices may beneﬁt from intrahepatic shunting by a stent radiologically placed through hepatic vein to the portal vein (TIPS
Symptoms Fever, malaise, chills, anorexia, weight loss, abdominal pain, RUQ tenderness, jaundice, hepatomegaly Diagnosis Leukocytosis (very high); CXR: atelectasis, pneumonia, effusion (all right-sided), CT scan, ultrasound, arteriography.	Pyogenic Liver Abscess Description Follows an acute abdominal infection. Routes: portal system, ascen- sion from the biliary tree, hepatic artery, direct extension, trauma. Untreated, 100% mortality rate; treated, 20% mortality rate. Right lobe more common. Solitary or multiple. Bacteria: E. coli, Klebsiella, enterococcus, bacteroides. May rupture into adjacent peritoneal, pericardial, or thoracic cavities.	Treatment Steps 1. Eliminate abscess and underlying cause. 2. Percutaneous drainage if single. 3. Operative drainage if multiple or multilocated abscess. 4. Long-term antibiotics, especially for multiple small hepatic ab- scesses.
Symptoms Fever, abdominal pain, encephalopathy in cirrhotic patient with ascites, but many patients may be asymptomatic. Diagnosis Greater than 250/mL polys is reliable even if ﬂuid is sterile, if symp- toms are suggestive. Best ascites culture yields (> 80%) obtained by inoculation of 10 mL of ascites into each of three 100-mL blood culture bottles (aero- bic, anaerobic, and microaerophilic) at the bedside, protein usually less than 1 g/mL. WBC greater than 10,000/mL, protein greater than 2.5 with free air suggests ruptured viscus	Spontaneous Bacterial Peritonitis Description Bacteria most likely reaches ascites through hematogenous spread; E. coli is most common pathogen. Mortality and recurrence is high even with antibiotics	Treatment Steps 1.Cefotaxime 2 g IV every 8–12 hours for 5–10 days. 2.Repeat paracentesis in 48 hours after initiation of antibiotics; if ascitic ﬂuid poly count not decreased by at least 50%, antibiotics should be changed and the problem reevaluated.
Symptoms Recent diarrheal syndrome in minority. Similar to pyogenic abscess.	Amebic Liver Abscess Description Prevalence higher in tropical zones, travelers to tropical countries. More common in males, peak incidence fourth decade. Spread by fecal–oral route of E. histolytica. Typically reaches the liver by way of the portal vein from intestinal amebiasis. Only 5% of people in- fected with amebiasis develop liver abscess. Ninety percent in right lobe. May grow to large size. History to separate from hydatid cyst. Amebic abscess ﬂuid looks like anchovy paste.	Diagnosis Serum antibody for E. histolytica (indirect hemagglutinin test). Only one-third have positive amebic stool cultures. Treatment Steps 1. Metronidazole 750 mg by mouth, three times a day for 10 days. 2. Operative treatment reserved for rupture. 3. Percutanous drainage may be considered. In cases of abscess re- fractory to Flagyl, large left liver lobe abscess, bacterial contami- nation (10–15%). There is danger of anaphylaxis from spillage with open drainage of cyst.
Symptoms Starting with lethargy and progressing to stupor or coma, with dropping things and making mistakes as early signs.	Hepatic Encephalopathy Description Abnormal mental state and neuromuscular dysfunction due to hepatic failure. Often associated with elevated ammonia level.	Diagnosis Can be spontaneous. Seek precipitating cause (e.g., diuretics, hypokalemic alkalosis, hypovolemia, hyponatremia, azotemia, tranquilizer, sedative, analgesic drugs, infection, severe constipation, hypoxia, excessive dietary protein, and progressive liver damage). Treatment Steps Lactulose 30 cc PO hourly until diarrhea, then every 6 hours. If PO not available, then 300 cc lactulose plus 700 cc tap water enema 1-3 times daily if deemed safe to give enemas. Treat underlying condition. If refractory to lactulose, consider oral neomycin
Symptoms Ascites. Hepatic encephalopathy, hypersplenism, hemorrhoids, caput medusa, esophageal variceal bleed. Stigmata of cirrhosis: spider angiomata, palmar erythema, testicular atrophy, gynecomastia, hepatomegaly. Jaundice.	PORTAL HYPERTENSION/ESOPHAGEAL VARICEAL BLEEDING Description Present when portal venous pressure exceeds 15 mm Hg. Collaterals between portal and systemic venous circulations lead to splenic varices, hemorrhoids, and esophageal varices. Commonly associated with cirrhosis (United States) and schistosomiasis (worldwide).	Diagnosis Liver function tests, liver biopsy, hepatitis proﬁle, endoscopy if bleeding. Treatment Steps Acute variceal bleed (50% mortality): 1. Injection sclerotherapy by way of esophagogastroduodeno- scopy (EGD); 90% initial success. 2. Vasopressin infusion or octreotide (somatostatin) infusion. 3. Balloon tamponade (Sengstaken–Blakemore tube). 4. Transjugular intrahepatic portosystemic shunt (TIPS). 5. Emergency portosystemic shunt. Shunt procedures: 1. End-to-side and side-to-side shunts are nonselective and are associated with encephalopathy. 2. Selective shunts (e.g., distal splenorenal Warren shunt) is associated with cirrhosis. Prophylactic treatment: β-blocker (propranolol) long-term prophylactic medication in portal hypertension (HTN) to prevent esophageal varices from bleeding.
Liver Transplantation Description For end-stage liver disease, usually in postnecrotic cirrhosis, primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC). Five- year survival from 55 to 85%. Absolute contraindication: active sepsis outside biliary tree, metastatic hepatobiliary malignancy, advanced cardiopulmonary disease, and acquired immune deﬁciency syn- drome (AIDS).	Relative contraindications: active alcohol (EtOH)-induced liver disease (only 13–16% resume EtOH after), portal vein thrombosis, or previous portacaval shunt surgery. Clinically apparent hepatocel- lular carcinoma or cholangiocarcinoma, Hepatitis B surface antigen (HBsAg)-positive liver disease, and advanced chronic renal disease. In fulminant hepatic failure, decide before stage IV coma (e.g., drug-induced, hepatitis C viral hepatic failure, and fulminant Wil- son’s disease).
Symptoms Epigastric and back pain, fever, tachycardia, hypotension, nausea,vomiting, epigastric tenderness, ﬂank ecchymosis (Grey–Turner’s sign), periumbilical ecchymosis (Cullen’s sign).	Acute Pancreatitis Description Inﬂammation from escape of active pancreatic enzymes. 80%due to alcohol and biliary disease (predominantly gallstones). Trauma, hyperlipidemia, hypercalcemia, pancreas divisum. Also caused by scorpion, Ascaris, or Clonorchis sinensis. Drugs causing pancreatitis: azithioprine, furosemide, Tylenol/ﬂagyl/Zantac, erythromycin/tetracycline. Ninety percent mild cases; 10% life-threatening. RANSON’S CRITERIA (PREDICTING THE SEVERITY OF ACUTE PANCREATITIS) On Admission (GA LAW) G Glucose > 200 mg/dL A Age > 55 yr L LDH > 350 IU/L A AST > 250 IU/dL W WBC > 16,000/mm3 At 48 Hours (HUB PEC) P PaO2 < 60 mm Hg E Estimated ﬂuid gain > 6 L C Calcium < 8 mg/dL H Hct fall > 10% U Urea rise > 5 mg/dL B Base deﬁcit > 4 mEq/L	Diagnosis Serum amylase and lipase, hypocalcemia,hyperbilirubinemia, leukocytosis, CT scan (dynamic angio-CT also measures amount of pancreatic necrosis). CT-guided ﬁne-needle aspiration (FNA) differentiates infected compared to sterile pancreatic necrosis. Upper gastrointestinal (UGI) series, sentinal loop on plain ﬁlm abdomen, ultrasound of biliary tree. Treatment Steps 1. Bowel rest, NPO, intravenous ﬂuids, analgesia, nasogastric tube,antibiotics. Antibiotics especially if pancreatic necrosis is present. 2. TPN for prolonged cases. 3. ERCP and endoscopic sphincterotomy to treat gallstone pancreatitis. 4. Surgery: correct biliary disease (e.g., cholecystectomy for gallstone pancreatitis); reserved for complications of pancreatitis (abscess, ascites, hemorrhagic, pseudocyst). Pancreatic debridement and open packing/closed lavage for pancreatic necrosis; 50% develop infection and mostly with gram-negative rod bacteria.
ACETAMINOPHEN TOXICITY	• Acute liver injury occurs after a toxic ingestion of acetaminophen. • In the acute setting, it is often taken by a patient as a suicide attempt in a large dose, with or without alcohol. • It is the drug most commonly ingested in overdoses.	• Acetaminophen-induced liver failure is the second most common cause of liver transplantation. • Immediate treatment with N-acetylcysteine needed.
Symptoms Epigastric and back pain, anorexia and weight loss, pancreatic insuf- ﬁciency with malabsorption, steatorrhea, possibly diabetes.	Chronic Pancreatitis Description Recurrent abdominal pain of pancreatic origin. Irreversible damage. Exocrine and endocrine insufﬁciency. Most often alcohol related (70%). Ten-year survival rate only 43%.	Diagnosis Clinical ﬁndings: Plain Films—Pancreatic calciﬁcations. CT Scan—Calciﬁcations, size of pancreas. ERCP—Identify ductal abnormalities (“chain of lakes”). SMA and Celiac Arteriogram—Pseudo-aneurysm with or without splenic/portal vein thrombosis. Treatment Steps 1. Analgesia, correct exocrine and endocrine function. 2. Surgery: indications: intractable abdominal pain, local complica- tions, main duct stenosis, pancreas divisum, rule out malignancy. Ampullary procedures; transduodenal sphincteroplasty. 3. Ductal drainage procedures: side-to-side pancreaticojejunostomy (Puestow procedure).
Symptoms Easy fatigability, jaundice, anorexia, fever, but often not diagnosed because of mild anicteric disease.	Hepatitis A (HAV) Description The RNA virus: almost exclusive fecal–oral routes, usually early childhood. Rarely fulminant and fatal. Chronic A not described.	Diagnosis Immunoglobulin M (IgM) anti-HAV (+) indicates acute infection; immunoglobulin G (IgG) indicates previous infection with A. SGPT greater than SGOT, usually > 1,000. Treatment Steps 1.Prevent with vaccination. Vaccines of killed and attenuated types produced. 2.Immune serum globulin within 2 weeks of close contact. 3.Supportive care for acute infection.
Symptoms Jaundice, weight loss, abdominal pain, pain in epigastrium and back, palpable gallbladder (Courvoisier’s sign). Diagnosis Liver function tests (LFTs) reﬂect ductal obstruction. Elevated carci- noembryonic antigen (CEA), CA 19–9, occult blood in stool. CT scan to evaluate size of tumor and relation to surrounding structures (Fig. 18–3), ERCP or percutaneous transhepatic cholangiography, arteriog- raphy (deﬁne anatomy/resectability), percutaneous biopsy. Prognos- tic factors in pancreatic carcinoma include lymph node status, margin involvement, vascular invasion, and need for blood transfusion.	Pancreatic Carcinoma Description Ninety percent duct cell adenocarcinoma (remainder are cystade- noma and acinar cell carcinoma); 65% arise in pancreatic head. Pre- sent in advanced stage. Fifth leading cancer-related death. Other risk factors include advanced age, smoking, diabetes, alcohol abuse, exposure to benzidine, naphthylamine, and partial gastrectomy.	Treatment Steps Resection for cure, if possible: pancreaticoduodenectomy. Five-year survival rate, 15–35%. Bypass for palliation: choledochojejunostomy, gastrojejunostomy. Adjuvant chemo- and radiation therapy improve survival. CONTRAINDICATIONS FOR PANCREATIC RESECTION • Liver or peritoneum involvement • Periaortic lymph node metastasis • Celiac lymph node metastasis • SMA and superior mesenteric vein (SMV) tumor involvement
Symptoms Flulike illness, jaundice in one-third. Incubation a few weeks to 6months. Ten percent to 20% (high) incidence of serum sickness—fever, arthralgia or arthritis, or skin rash, most frequently maculopapular or urticarial.	Hepatitis B (HBV) Description DNA virus: Transmitted perinatally, parenterally, and sexually, but not fecal–oral. HBsAg is earliest marker, can be negative in fulminant hepatitis B. IgM anti-hepatitis B core (HBc) will become rapidly positive and diagnostic. HBsAg > 6 months = chronic B. Hepatitis Be antigen (HBeAg): whole virus replication (likely HBV DNA is detectable in serum and is highly infective). IgM anti-HBc AB titer can become low and persist in chronic hepatitis. IgG anti-HBc with normal enzymes and no anti-HBs may have had viral B in the past, but failed to develop anti-HBs or lost it. IgG anti-HBc found alone in a case may be associated with HBV detectable by polymerase chain reaction (PCR) technique Pathology Cytotoxic T cells recognize hepatitis B core antigen receptors on liver cells. T cells attach to receptors, leading to cellular necrosis.	Hepatitis B vaccine is now recommended for all infants. Diagnosis Clinical picture and serologies Treatment Steps Prevent with active (vaccine) and passive hepatitis B immunoglobulin (HBIG) immunization. Interferon-α stops replications in chronic hepatitis. HBV DNA and HBeAg disappear from serum. Patient is less infective in 35% of cases. In 10%, cure, HBsAg gone, and anti-HBs appeared; or lamivudine 100 mg PO qd for 12 months (and possible adefovir 10 mg/day); limitation resistance and mutation • A patient with immunity from hepatitis B due to vaccination has a + hepatitis B surface antibody, but a – hepatitis B core antibody. • If the core antibody is positive, it means the patient has been exposed to the virus. Treatment Steps Prevent with active (vaccine) and passive hepatitis B immunoglobulin (HBIG) immunization. Interferon-α stops replications in chronic hepatitis. HBV DNA and HBeAg disappear from serum. Patient is less infective in 35% of cases. In 10%, cure, HBsAg gone, and anti-HBs appeared; or lamivudine 100 mg PO qd for 12 months (and possible adefovir 10 mg/day); limitation resistance and mutation.
Whipple’s triad. Fasting hypoglycemia (insulin:glucose ratio > 0.3). Elevated C- peptide and proinsulin.	Insulinoma Most common. β-cell origin. Equal distribution throughout the pan- creas. Eighty percent solitary benign; 10% malignant. Whipple’s triad. Fasting hypoglycemia (insulin:glucose ratio > 0.3). Elevated C- peptide and proinsulin.	Preoperative localization: CT scan localizes tu- mors > 1 cm. Arteriography. Intraoperative ultrasound used in local- ization. Resection is curative for large lesions, and enucleation also adequate for small lesions. Debulk for palliation. Medical therapy: diazoxide.
Symptoms Similar to B, but the acute attack is usually unrecognized. No fea- tures predicting chronicity, except for concomitant alcohol use.	Hepatitis C (HCV) Description Ribonucleic acid (RNA) viral infection. Pathology Direct viral cytopathic injury postulated. Fatty change in 75% of cases. Mild chronic hepatitis is characteristic	Diagnosis Anti-HCV antibody and positive HCV RNA by PCR. Treatment Steps 1.Goals of treatment: Sustained virologic response (absence of HCV RNA in serum) and prevention of cirrhosis. 2.PEG interferon-α-2b (1.5 µg/kg/wk) plus ribavirin (800 mg/ day). 3.If normal serum alanine aminotransferase (ALT) and negative HCV RNA by PCR does not occur by 3 months, treatment is stopped. 4.Continue regimen for 12 months in responders
Hypergastrinemia and PUD (especially in unusual locations). Zollinger–Ellison syndrome. Elevated fasting gas- trin and secretin stimulation test.	Gastrinoma Second most common. Hypergastrinemia and PUD (especially in unusual locations). Zollinger–Ellison syndrome. Elevated fasting gas- trin and secretin stimulation test. Fifty percent malignant.	Resection for cure. Preoperative localization. Explore if localization attempts fail. Eighty percent of lesions found in the gastrinoma triangle (boundaries are: cystic–common bile duct, second to third part of duodenum, and neck–body junction of the pancreas). Somatostatin and high-dose omeprazole for treatment
Description Unique RNA, requiring outer envelope of HBsAg for replication, coinfection, or superinfection (which is more likely to produce ful- minant hepatic failure). Prevalent among parenteral drug addicts, hemophiliacs, and homosexual men	Hepatitis D	Treatment Steps Interferon-α treats D but relapses after therapy. Immunity to B pre- vents D.
Elevated plasmin glucagon is diagnostic. Hyperglycemia. Necrolytic migratory erythema.	Glucagonoma From α cells. Mainly in the body and the tail of the pancreas. Ele- vated plasmin glucagon is diagnostic. Hyperglycemia. Majority are malignant. Necrolytic migratory erythema.	Present in advanced stage. Resect for cure. Debulk for relief of symptoms.
Symptoms The disease is self-limited and does not evolve into chronic hepatitis, but has often been observed to be cholestatic; unique fulminant dis- ease in pregnant women	Hepatitis E Description Transmitted by fecal–oral route—waterborne epidemics, especially in India, Nepal, Pakistan, and Southeast Asia.	Treatment Steps Standard gamma globulin is ineffective and there are no active vaccines available.
Watery Diarrhea, Hypokalemia, Achlorhydria, or Verner–Morrison	VIPoma (Vasoactive Intestinal Polypeptide Tumors) or WDHA Syndrome (Watery Diarrhea, Hypokalemia, Achlorhydria, or Verner–Morrison Syndrome)	Fifty percent have metastasis at presentation, and treatment is subto- tal pancreatectomy if no tumor found in the presence of the syndrome.
Drug-Induced Liver Disease	Description Acute hepatitis (isoniazid [INH]), chronic active hepatitis (nitrofu- rantoin, α-methyldopa), cirrhosis (methotrexate), cholestasis (sul- fonamides), fatty liver (corticosteroids), granuloma (allopurinol), benign and malignant neoplasms (estrogens), vascular lesions (vita- min A) and sclerosing cholangitis (5-ﬂuorodeoxyuridine [5-FUDR]). Acetaminophen is suicide—> 15 g causes massive necrosis; gen- erates toxic metabolites through P450 cytochrome. Cimetidine com- petes for oxidation by cytochrome P450. Alcohol increases P450 activity and toxic metabolites. Doses aver- aging 6 to 7 g/day (acetaminophen) taken by alcoholic have been as- sociated with severe hepatotoxicity characterized by increased aspar- tate aminotransferase (AST) > 3,000 to 10,000. The mortality in one series was 20%. Antiarrhythmic amiodarone like alcoholic hepatitis (e.g., steato- sis, hepatocellular necrosis, and Mallory bodies). Verapamil and captopril mixed hepatocellular cholestatic pat- terns; ketoconazole variable hepatocellular and in 40% cholestatic. Methotrexate cirrhosis > 1.5 g total dose; low dose 7.5 mg/week for 2 years; not associated with bridging ﬁbrosis or cirrhosis. Most NSAIDs are found to be associated with some form of hepa- totoxicity. Total parenteral nutrition (TPN) associated with fragment cholestatic jaundice, much mixed origin but not characterized.
Symptoms Nonspeciﬁc abdominal pain. Left upper quadrant (LUQ) pain. Pain referred to left shoulder (Kehr’s sign).	SPLEEN A. Trauma Description Most commonly injured organ in blunt trauma. Associated with left chest rib fractures.	Diagnosis Clinical suspicion (e.g., multiple left-sided rib fractures). Gross blood on diagnostic peritoneal lavage. Focused abdominal sonogra- phy for trauma (FAST) is frequently the ﬁrst study done on a trauma patient with a suspected splenic injury. CT scan ﬁndings in stable pa- tients. Treatment Steps Splenectomy. Splenic salvage in appropriate cases. Nonoperative therapy in children. Vaccinate the splenectomy patient against Haemophilus inﬂuenzae B, pneumococcus, and meningococcus (en- capsulated organism).
Symptoms Most common symptoms are insidious onset of pruritus and fatigue, early hepatomegaly, and elevation of serum alkaline phosphatase be- fore symptoms. Description Autoimmune disease characterized by antimitochondrial antibodies in the serum. Anti-M2 are the major marker-speciﬁc mitochondrial antibodies against the inner mitochrondrial membrane (see Fig. 4–3).	Primary Biliary Cirrhosis Pathology Destruction of intrahepatic bile ducts in the ﬁrst stage with progres- sion to macronodular cirrhosis in the ﬁnal stage, with mononuclear inﬁltrate in the portal tracts and paucity of bile ducts.	Treatment Steps No speciﬁc effective treatment; ursodeoxycholic acid; transplanta- tion in advanced stages. Benadryl for pruritus.
Symptoms Spontaneous bleeding. Spleen normal size or small.	Immune Thrombocytopenic Purpura Description Persistently low platelet count. Antiplatelet factor (circulating im- munoglobulin G [IgG]) directed against a platelet antigen. Majority are young women. Childhood cases typically occur after a viral ill- ness under age 6. Also associated with human immunodeﬁeciency virus (HIV).	Diagnosis Thrombocytopenia, bone marrow aspirate megakaryocytes. Treatment Steps 1. Steroids, response in 3–7 days. Complete remission with steroids is rare. 2. IV gamma globulin (1–2 g/kg), plasmapheresis. 3. Elective splenectomy, when refractory to medical management (75% of cases), i.e., persistent thrombocytopenia (platelets < 80,000) or recurrence after tapering or discontinuation of steroids. 4. Emergent splenectomy with central nervous system (CNS) bleeding. 5. Laparoscopic splenectomy is an option.
Symptoms Epigastric pain, which can be colicky, advances to prolonged constant pain, lasting more than 30 minutes, and usually moderately severe. May radiate to the midscapular area or to the top of the right scapula, the right shoulder, or neck. May be mistaken for angina.	GALLSTONES Description Twenty percent with asymptomatic gallstones develop biliary colic,cholecystitis, or pancreatitis.No indication for prophylactic cholecystectomy or nonsurgical treatment in asymptomatic patient. Cholecystectomy standard or laparoscopic cholecystectomy best therapy for symptomatic disease. For symptomatic gallstones, if no major contraindications to surgery, operative mortality overall 1%. Lower for elective in 50-year-old, and as high as 10% in emergency situation in elderly	Diagnosis •US is often diagnostic. •Hepatobiliary scan (Disida) is used when ultrasound is nondiagnostic. Treatment Steps Laparoscopic cholecystectomy in qualiﬁed hands and appropriate cases is treatment of choice; second, open cholecystectomy (less frequently used). 1.Magnetic resonance cholangiopancreatography (MRCP) if suspected common bile duct stone and/or pancreatitis. 2.Endoscopic retrograde cholangiopancreatography (ERCP), sphincterotomy (where safe and feasible), and stone removal to remove common bile duct stones; subsequent cholecystec- tomy in selected cases. 3.Transhepatic techniques with radiologic guidance may be used as well.
Symptoms Asymptomatic lymphadenopathy, night sweats, weight loss, pruritus, malaise.	Hodgkin’s Disease Description Malignant lymphoma; Reed–Sternberg cells; asymptomatic lym- phadenopathy: cervical (70%), axillary, inguinal. Four pathologic subtypes: lymphocyte predominance (best prognosis), nodular scle- rosis (most common), mixed cellularity, lymphocyte depletion (worst prognosis). Metastasize in predictable patterns (spread via lymphatics).	Diagnosis Hematologic tests, bone marrow aspirate, LFTs, CT scan abdomen and chest, CXR, lymph node biopsy, lymphangiogram. Staging lap- arotomy: splenectomy, liver biopsy (bilateral), lymph node sampling, oophoropexy. Bilateral bone marrow biopsy from the iliac crest. In women of childbearing years, ﬁx ovary to the pelvic wall or behind uterus to protect it from radiation. Treatment Steps 1. Radiation (all stages). 2. Chemotherapy (stage III A or above). 3. Staging laparotomy: when result may change therapy. It is contro- versial and mainly for stages I and II. Improved imaging and liberal use of chemotherapy has made staging laparotomy less common.
Description/Symptoms Strangulation obstruction of the small bowel—most common form of mesenteric ischemia. Splanchnic vasospasm: nonocclusive mesen- teric ischemia. Classic presentation is severe abdominal pain with a paucity of clinical ﬁndings	MESENTERIC ISCHEMIA	Diagnosis Angiography is the standard. Leukocytosis, acidosis, abdominal pain and tenderness. Treatment Steps Prompt laparotomy: reestablish arterial ﬂow; assess bowel viability; resect frankly ischemic segments. Embolectomy or revascularization with second-look laparotomy 24–48 hours later to reveal intestine left in situ; 50–90% mortality from acute intestinal arterial occlusion.
Two-thirds have asymptomatic lymphadenopathy. Onset may be in extranodal site (e.g., gastric non-Hodgkin’s lym- phoma). May appear as asymptomatic splenomegaly. Constitutional symptoms commonly present.	Non-Hodgkin’s Lymphoma (NHL) Clinical course and natural history more diverse than Hodgkin’s. Usu- ally older patients are more common than with Hodgkin’s disease. Pattern of spread is variable; two grades: high-grade (diffuse) or low- grade (nodular).	Chemotherapy and radiation therapy. It is spread via the bloodstream and can present as a superior vena cava (SVC) syndrome, acute spinal cord compression syndrome, central obstruction or meningeal involvement. Indications for splenectomy in NHL are hypersplenism, pancytopenia, symptomatic splenomegaly, and recurrent splenic infarcts.
Symptoms Epigastric pain radiating to midback, better sitting up. Jaundice and fever are possible.	ACUTE PANCREATITIS See also Chapter 18. Description Inﬂammation from escape of active pancreatic enzymes, causing necrosis of pancreatic tissue, and peripancreatic fat. Mortality is about 5–10%, major causes are alcohol and gallstones.	Diagnosis Elevated serum amylase; swollen, inﬂamed pancreas on CT scan (Fig. 4–4). Elevated amylase also seen in perforated ulcer, mesenteric infarc- tion, intestinal obstruction, pancreas, pseudocyst, and chronic pancre- atitis; also in mumps parotitis, renal failure (if creatinine > 3, serum amylase can be three times normal on that basis), ovarian and oat cell tumor of lung, ruptured ectopic pregnancy, and macroamylasemia. Lipase is slower to rise and fall and may also become elevated due to renal failure. Treatment Steps 1.Supportive care with NPO. 2.Analgesia. 3.Nasogastric tube if nausea and vomiting or ileus with abdominal distention. 4.Watch for poor prognostic signs: hypotension, serum calcium < 8, Cr > 2 , WBC > 20,000, PO2 < 60, decreased Hgb. 5.If hyperalimentation used, use H2 blocker and avoid IV lipids. 6.With severe gallstone pancreatitis, a gallstone impacted at duode- nal ampulla may beneﬁt from early ERCP with sphincterotomy and stone extraction, or if unsuccessful. (MCRP may be helpful preliminarily.) 7.Surgical intervention, especially in the nonalcoholic with pancreatitis.
Symptoms Preceded by upper respiratory infection (URI). Followed by nausea, vomiting, headache, confusion, shock, coma, death within 24 hours.	Postsplenectomy Sepsis Description Risk highest for splenectomy for thalassemia and reticuloendothelial (RE) diseases like Hodgkin’s, lowest for trauma and idiopathic thrombocytopenic purpura (ITP). Risk may be as high as 1% per year. Risk greatest for children younger than 4 years, and within 2 years of splenectomy. Fifty percent mortality rate	Diagnosis Clinical suspicion. Blood cultures positive for Streptococcus pneumo- niae in 50%. Encapsulated organisms predominate (pneumococci, H. inﬂuenzae). Treatment Steps 1. Broad-spectrum antibiotics. 2. Supportive care. 3. Prophylaxis: Pneumovax, prophylactic antibiotics.
Description and Symptoms Worsening of pain, nausea, and vomiting after initial improvement, with fever, increased WBC, and positive blood culture	COMPLICATIONS OF ACUTE PANCREATITIS— PSEUDOCYST VERSUS ABSCESS Diagnosis CT of pancreas with Chiba aspiration, culture, and Gram stain. If cyst without signiﬁcant pancreatitis, rule out cystic neoplasm.	Treatment Steps 1.Antibiotics for proven abscess and possibly for phlegmon. 2.Surgical drainage of abscess reduces mortality from > 50% to 10–20%, if aspiration used for early diagnosis. 3.Present thinking is that pseudocysts that are asymptomatic should be managed medically. Report pain, chills, or fever immediately. 4. Late surgery for sterile necrosis if asymptomatic—4–6 weeks of TPN. 5.If extrapancreatic pseudocyst is associated with signiﬁcant pancre- atic necrosis, it may need surgical evacuation.
Symptoms Vague midabdominal pain, anorexia, and weight loss. Jaundice can occur in the absence of pain. Nausea and vomiting.	PANCREATIC CANCER Description Fifth leading cause of cancer deaths in United States. Five-year sur- vival of 1–5%. Pathology Adenocarcinoma arising from ductular epithelium account for three- fourths of pancreatic cancer; 60–80% arise in the head; 10–20%, body; 5–7%, tail. At surgery, 85% have disseminated disease.	Diagnosis US or CT biopsy of mass. If negative, ERCP, because 90–95% of pan- creatic cancers arise from the pancreatic duct system. Rare to do lap- arotomy for tissue diagnosis. CA 19-9 in nonjaundiced patient has some validity and can be used as tumor marker after apparently curative surgery. Treatment Steps Ten to 20% are candidates for attempted curative resection with small tumor in head of pancreas and no evident spread. Modiﬁed Whipple (pancreaticoduodenectomy) 5–10% mortality in the best centers. Endoscopic and percutaneous stent for biliary obstruction. Palliative gastric bypass and pain control.
Diagnosis Steatorrhea (excess fat in stool): 100 g fat/diet/day × 3, after which stool is collected for another 3 days; greater than 7 g/24 hr is abnor- mal. D-xylose, if abnormal, suggests small bowel disease. Normal value suggests focus on pancreatic disease: CT scan of the abdomen, serum amylase, γ-glutamyl transferase. If overgrowth considered, note response of malabsorption to antibiotic therapy. Celiac sprue panel: antiendomysial antibody, tissue transglutaminase, total serum IgA; antigliadin antibody IgA and IgG; at least three biopsy speci- mens from distal duodenum—gold standard.	MALABSORPTION Description Any condition in which nutrients are not properly absorbed by the GI tract. Abnormal labs; anemia; low serum iron, folate, vitamin C, vitamin B12, calcium, phosphorus, magnesium, zinc, and other trace metals; elevated alkaline phosphatase (bone disease or cholestasis), or folate (blind-loop syndrome), and a prolonged protime	Treatment Steps Treat underlying condition.

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