Exposure to arsenic comes from contamination of drinking water (India), burning of arsenic coal (China), or medicinal administration (Fowler \200\231s solution, used worldwide for ch ronic myeloid leukemia 1931 \200\2231953). The polymerization of vinyl chloride in the poly vinyl chlo- ride (PVC) industry since the mid 1930s lead to high levels of exposure among w orkers in the industry. The first case of angiosarcoma because of this occupational exposur e was identified in 1974. Since then tight controls on the work environment have been imple mented and cases caused by this exposure now occur rarely, if at all. Further reading Kim HR, Rha SY, Cheon SH et al. (2009). Clinical features and treatment outcomes of advanced stage primary hepatic angiosarcoma. Ann Oncol; 20: 780 \200\2237. Maluf D, Cottere ll A, Clark B et al. (2005). Hepatic angiosarcoma and liver transplantation: Case report and literature review. Transplant Proc; 37: 2195 \200\2239. Mu ller AF, Toghill PJ (1995). Hyposplenism in gastrointestinal disease. Gut 1995; 36: 165 \200\2237. Van Kampen RJW, Erdkamp FLG, Peters FPJ (2007). Thorium dioxide-related haemangiosarcoma of the liver. Neth J Med; 65: 279 \200\22382. OXFORD CASE HISTORIES 328 Case 49 A 49-year-old female carer developed severe abdominal pain over the course of a fortnight, with diarrhea, weight loss, and vomiting. She was admitted via the emergency department, wh ere a CT scan showed intestinal obstruction, a stenosing tumor in the transverse colon, and liver metastases. She was taken to theater, where an extended right hemicolectomy was perf ormed, with resection of a gangrenous loop of small bowel. This was complicated by an anast omotic leak requiring further laparotomy and ileostomy, following which there was wound deh iscence and discharge through two enterocutaneous fistulas. Seventeen days after the initia l admission, on a Friday, parenteral nutrition was requested urgently. On examination, the patient weighed 61kg, had lost 15kg in the previous 4 weeks, and had an output through the wound manager of 1650mL in the past 24 hours. Investigations showed: 9/L, platelets 100 x 109/L Hb 10.3g/L, WCC 9.4 x 10 mol/L, ALT 39 IU, ALP 157 IU Bilirubin 45 Albumin 20g/dL, phosphate 0.61mmol/L, magnesium 0.82mmol/L CRP >160mg/L. Questions 49a) Interpret the blood results. 49b) What are the dangers of starting parenteral nutrition immediately? 49c) What is the best advice? 49d) What is the optimal management strategy? This page intentionally left blank OXFORD CASE HISTORIES 330 Answers 49a) Interpret the blood results. This patient is dehydrated, evidenced by a disproportionate increase in urea compared with creatinine, in the context of a high stoma output (>1200ml/d) and high potassium (see Case 33). She is almost certainly septic given the low albumin (20g/dL). Sepsis is also consiste nt with the high CRP (>160mg/L). The anemia and hyperbilirubinaemia are most probably due t o haematoma formation and resorption after two major operations. The thrombocytopenia is li kely to be caused by bone marrow suppression from sepsis, which will also be contributing t o the anemia. Sepsis and hypovolaemia are therefore the key messages in this complex situat ion: both are surprisingly easy to overlook, because the patient is apyrexial and the stoma output is frequently not measured except on a specialist ward. 49b) What are the dangers of starting parenteral nutrition immediately? This patient is at risk of refeeding syndrome, which is defined as severe fluid and electro lyte shifts with related metabolic mayhem in malnour- ished patients undergoing refeeding ( see Case 37). The principal bio- chemical features of refeeding syndrome are hypophosphatae mia, hypomagnesaemia, hypokalaemia, glucose intolerance, fluid overload, and thiamine defic iency. Clinical consequences can include congestive heart failure, cardiac arrhythmias, ske letal muscle weakness, respiratory failure, metabolic acidosis, ataxia, seizures, encephalo pathy, and death. Patients at risk include those who have had: complete starvation for >7 days >20% loss of body weight in <3months catabolic state caused by sepsis. Because this patient has been referred on a Friday afternoon (as so often happens, when the urgency of the situation is recognized before the weekend!), there is greater risk of the clinical consequences of refeeding syndrome if feeding is started immediately, simply becau se monitoring over the weekend is often suboptimal. Designated central venous access for pa renteral nutrition is also a problem, unless insertion has already been organized, or if (i mprobably) the patient has an untouched central line port. Parenteral nutrition is never an emergency: the risk of death from refeeding exceeds the risk of delaying nutrition pending appropri- ate preparation. CASE 49 331 49c) What is the best advice? After explaining the dangers of starting intravenous nutrition immedi- ately and over the w eekend to the surgeons looking after her, the ward nurses, the patient, and her family, pre paration includes rehydration, electrolyte and vitamin replacement, with daily monitoring a ccording to refeeding guidelines below. This is enough to keep the team looking after the p atient occupied over the weekend, knowing that they are doing the best thing for the patien t. Electrolyte replacement: electrolytes need immediate replacement if the potassium is <2.5mm ol/L, magnesium <0.5mmol/L, or phosphate <0.3mmol/L. \200 .5mmol): intravenous potassium is always more Low potassium (<2 appropriate than oral potas sium pending parenteral nutrition. A care- fully monitored infusion pump should be used to administer 120mmol/L through a central line over 12 hours. Oral potassium usu- ally tastes disgusting. Remember that for the commonly prescribed Sando K, one tablet contains 12mmol, so 5 tablets/day (=60mmol) only meet (and do not exceed) ordinary daily requirements. .3mmol/L): intravenous Addiphos \204 20ml vial) Low phosphate (<0 in 500ml normal saline s hould be administered over 6 hours. Shake the bag well. One vial of Addiphos \204 contains phosphate 40mmol, potassium 30mmol, and sodium 30mmol. Oral phosphate causes diarrhea and should therefore be avoided. Low magnesium (<0 .5mmol/L): 50% magnesium sulfate 6g (=24mmol, or 12ml) in 500ml normal sa line should be given over 6 \200\22312 hours. The maximum infusion rate is 4mmol/hour of Mg . Oral magnesium causes diarrhea. : in practice, calcium is not too much of a problem. Low calcium If it is low, it is likely to be secondary to magnesium or phosphate deficiency; when these are replaced, the calcium usually returns to normal. If necessary, intravenous calcium gluconate can be given. In practice, any electrolyte concentration below the normal range (K <3.5mmol/L, P <0.6mmol /L, Mg <0.7mmol/L) merits proactive replacement during the weekend, or 48 hours before pare nteral nutrition is started. This is because the refeeding syndrome is characterized by fur ther electrolyte depletion, owing to intracellular shifts of electrolytes. Intravenous vitamins: thiamine is required. Pabrinex \204 1 pair of ampoules (= 250mg thia mine) should be given in 50 \200\223100ml normal saline over 30 minutes, daily for 3 days. OXFORD CASE HISTORIES 332 Insertion of a designated central venous line ONLY to be used for intravenous feeding: this can be done after the weekend, ideally as a peripherally inserted central catheter (PICC). Commence intravenous feeding after the weekend, after all the above has been done: if all b iochemistry is normal, start feeding. Ensure that the intravenous vitamins are given at lea st 30 minutes before feeding starts. Start feeding at 20kcal/kg for the first 24 hours, the n increase gradually within the first week to full feeding, with daily monitoring of electr olytes, magnesium, and phosphate (too frequently forgotten), and further electrolyte replac ement for the first 2 weeks. 49d) What is the optimal management strategy? The optimal management strategy is to ask for help from a team experi- enced in the managem ent of intestinal failure. Be guided by the SNAP acronym: S: Sepsis (drain abscess, treat infection) N: Nutrition (est ablish appropriate route and type of nutritional support) A: Anatomy (use contrast radiolog y and cross-sectional imaging to define anatomy when the first two steps have been addresse d) P: Procedure (timely surgery, often many months down the line). When managing patients with intestinal failure, it is important to manage expectations. Pat ients want a rapid resolution of appalling com- plications, but precipitate re-operation to restore continuity and repair of enterocutaneous fistulae simply leads to further wound br eak down, fistulation, and loss of bowel. That way lays dependency on intravenous nutrition and the law courts for inappropriate management. Consequently, these complex patients are best managed in a specialist unit with access to multidisciplinary care. Patients need to understand that short cuts (such as surgery within weeks) carries high ris ks, and that patience, months of nutritional sup- port, and timely re-operation are the qui ckest way to recovery. It is a sad fact that many surgeons and physicians are simply unawar e of the avail- ability of specialist centers dealing with intestinal failure, or feel that their patients are not sick enough to merit transfer. The least that can be done is to dis cuss management with appropriate specialists. CASE 49 333 Further reading Lal S, Teubner A, Shaffer JL. Review article: intestinal failure. Aliment Pharmacol Ther 2006; 24: 19 \200\22331. Mehanna HM, Moledina J, Travis J (2008). Refeeding syndrome: what it is, and how to prevent and treat it. BMJ; 336: 1495 \200\2238. Stanga Z, Brunner A, Leuenberger M et al. (2008). Nutrition in clinical practice: the refeeding syndrome: illustrative cases and guidelines for management and treatment. Eur J C lin Nutr; 62: 687 \200\22394. OXFORD CASE HISTORIES 334 Case 50 A 60-year-old Dutch woman with a history of colitis for 20 years presented to the emergency department with central abdominal pain and vomiting. Symptoms had started an hour after ta king bowel preparation for colonoscopy. In the preceding month, she had lost 9kg in weight, with loss of appetite and borborygmi. Her bowels opened once or twice a day, with no diarr hea. She had previously had a deep vein thrombosis but no other medical history. She did no t smoke, and drank alcohol infrequently. On examination, her pulse rate was 112bpm and blood pressure 130/80mmHg. She was not pale, or jaundiced. The abdomen was soft and non-tender, without palpable masses or organs. Investigations showed: 9/L, platelets 545 x 109/L, MCV 96fL Hb 13.5g/dL, WCC 13.7 x 10 CRP 19mg/L U&E, LFT, and amylase normal Abdominal radiograph: prominent small bowel loops scattered through- out the abdomen; no co lonic dilatation Small bowel enema (performed subsequently): delayed small bowel transit CT of the abdomen: segmental colitis with inflammation of terminal ileum; biliary dilatatio n in the right lobe of the liver MRCP: shown in Fig. 50.1. Questions 50a) What do the patient \200\231s symptoms suggest? 50b) The MRCP is diagnostic: what does it show? 50c) Discuss the relationship between this condition and inflammatory bowel disease. 50d) How is this condition managed? 50e) What complications can occur with this condition? 50f) The patient did not respond to medical therapy. A repeat CT scan was carried out (Figs 50.2a and 50.2b). Describe the findings. CASE 50 335 Fig. 50.1 OXFORD CASE HISTORIES 336 Answers 50a) What do the patient \200\231s symptoms suggest? The clinical picture indicates partial small bowel obstruction. The abdominal radiograph sh owed prominent small bowel loops, with no evidence of colonic dilatation. The most likely c auses are stricturing small bowel disease or a carcinoma obstructing the ileocaecal valve. Adhesions are a common cause, but the patient had not previously had abdominal surgery. The initial CT scan suggested terminal ileal Crohn \200\231s disease, although the small bowel radiology did not show diagnostic images. 50b) The MRCP is diagnostic: what does it show? The MRCP shows marked irregularity of the intrahepatic biliary tree, typical of primary scl erosing cholangitis (PSC). This is a chronic chole- static liver disease of the intrahepati c and/or extrahepatic biliary tree, with inflammation and fibrosis, leading to progressive cholestasis and eventually to biliary cirrhosis with endstage liver disease. Most cases are associated with inflammatory bowel disease. PSC is typically a male-predominant disease, with a 2:1 male to female ratio. Liver functio n tests are abnormal in 90% of patients at diagnosis, and are the usual reason for investig ation (initially by ultrasound, then MRCP) that leads to diagnosis. Endoscopic retrograde c holangiopancre- atography (ERCP) used to be used, but MRCP is now the diagnostic test of ch oice, because it avoids the complications of ERCP. ERCP is reserved for biliary sampling fo r cytology, or biliary drainage. Liver biopsy is required only if the MRCP looks normal. Li ver function tests may occasionally be normal (in about 10%). The diagnosis in this patient was coincidental to presentation with small bowel obstruction. Both intrahepatic and extrahepatic bile ducts are involved in 69% with PSC, and 25% have is olated intrahepatic PSC, as in our patient. Just 4% have exclusive extrahepatic involvement , and the remaining 2% have typical biochemical and histological features of PSC, but norma l cholan- giograms. This is termed \200\230small duct PSC \200\231 and is thought to have a con- siderably better prognosis than typical PSC. Progression to cirrhosis and endstage l iver disease is slower, and cholangiocarcinoma, the most important complication of PSC, doe s not occur. Nevertheless, a propor- tion of patients with small duct PSC (20% in one study ) progress to typical PSC. CASE 50 337 The median time to death or liver transplantation in PSC is 9 \200\22318 years after diagno sis. Jaundice usually precedes other features of cirrhosis, such as ascites. 50c) Discuss the relationship between this condition and inflammatory bowel disease. Inflammatory bowel disease, most often pancolitis, is present in 63 \200\22390% of patients with PSC in Northern Europe and North America. PSC devel- ops in 2.4 \200\2237.5% of patie nts with ulcerative colitis and in 1.4 \200\2233.4% with Crohn \200\231s disease, although in a recent study the prevalence of MRCP fea- tures of PSC in patients with ulcerative coli tis affecting the whole colon was as high as 17%. The diagnosis of inflammatory bowel disea se usually precedes that of PSC by several years, reflecting the insidious nature of PSC an d the debilitating symptoms of inflammatory bowel disease. PSC may present years after cole ctomy. However, the diagnosis of PSC can precede that of inflammatory bowel disease: colono scopy is appropriate if a patient is found to have PSC, even in the apparent absence of bow el symptoms. Ulcerative colitis in such patients exhibits relative rectal spar- ing. Crohn \200\231s disease in patients with PSC always involves the colon, with or without small bow el involvement. 50d) How is this condition managed? PSC is relentlessly progressive and no current medical therapy improves survival. Liver tra nsplantation is the only life-extending therapy. Although PSC is thought to be immunologica lly mediated, it does not have the characteristics of a typical autoimmune disease: witness the male predominance, no absence of a specific autoantibody, and poor response to immunos uppression. Ursodeoxycholic acid is recommended for treatment. Ursodeoxycholic acid is a hy drophilic bile acid that may displace toxic bile acids, be cytoprotective, and promote bile flow. Studies have shown improvement of biochemical, cholangiographic, and histo- logical characteristics. Ursodeoxycholic acid also appears to reduce the risk of colon cancer in pa tients with PSC and inflammatory bowel disease. The risk of colon cancer in patients with i nflammatory bowel disease and PSC is higher than in inflammatory bowel disease alone. Tumor s are more often proximal and subject to late diagnosis. Patients with inflammatory bowel d isease and PSC should be enrolled in a sur- veillance program at diagnosis, with complete c olonoscopy on an annual basis. OXFORD CASE HISTORIES 338 50e) What complications can occur with this condition? In addition to the typical features of PSC on the MRCP (Fig. 50.1), there was marked dilata tion of the right intrahepatic biliary system. No expla- nation was found, but this asymmet ry should raise a concern about cho- langiocarcinoma. The lifetime risk of cholangiocarcino ma in patients with PSC is about 23%, but only in those with underlying ulcerative colitis, and very rarely (if at all) in Crohn \200\231s colitis. A third of patients who develop ch olangiocarcinoma do so within a year of diagnosis of PSC. The annual risk is then about 1.5 %. Risk factors for cholangiocarcinoma in patients with PSC include older age, longer durat ion of ulcerative colitis, and smoking. Therapy for cholangiocarcinoma is usually palliative, since it is consid- ered a contraindi cation to liver transplantation. When cholangiocarci- noma complicates PSC it has a dismal prognosis, with a median survival from diagnosis of 5 \200\22311 months. The diagnosis rema ins challenging. Once jaundice and weight loss occur, the disease is advanced. The tumor ma rker CA19-9 is insufficiently sensitive and specific, and may be elevated in cholestasis of any cause. CT scan and MRCP cannot reliably distinguish benign from malignant stenosis. Po sitron emission tomogra- phy (PET) has shown inconsistent results. The mainstay of diagnosis of cholangiocarcinoma remains ERCP with endoscopic brush cytology . The specificity is 89 \200\223100% but the sensitivity is only 69 \200\22375%. Biliary fl uorescence in situ hybridization (F.I.S.H) and digital image analysis are more sensitive. T ranspapillary cholangiography Fig. 50.1 Irregular intrahepatic bile ducts (small arrows). The gallbladder (large arrow) a nd common bile duct (long arrow) looked normal on this and other images. CASE 50 339 with intraductal ultrasonography may help differentiate benign from malignant biliary stric tures in the future. 50f) The patient did not respond to medical therapy. A repeat CT scan was carried out (Figs 50.2a and 50.2b). Describe the findings Fig. 50.2a shows wall thickening in the distal transverse colon (arrow) and colonic dilatat ion, highly suggestive of a carcinoma. Fig. 50.2b shows a mass in the caecum (arrow) highly suggestive of a caecal carcinoma. An emergency subtotal colectomy was carried out for colonic obstruc- tion. Pathological exa mination showed synchronous adenocarcinomas of the colon, one in the distal transverse colo n and one in the caecum. The colon showed chronically active ulcerative colitis. The findin g of colon cancer is not surprising, in view of the longstanding colitis, asso- ciation wit h PSC (note the proximal cancer), and presentation with bowel obstruction. This case illust rates some of the difficulty in classify- ing colitis, the indolent nature of PSC, and the complications of longstanding colitis associated with PSC. Fig. 50.2a Repeat CT scan. OXFORD CASE HISTORIES 340 Fig. 50.2b Repeat CT scan (separate level). Further reading Bjornsson E, Lindqvist-Ottosson J, Asztely M, Olsson R (2004). Dominant strictures in patients with primary sclerosing cholangitis. Am J Gastroenterol; 99: 502 \200\2238. Bj rnsson E, Olsson R, Berqquist A et al. (2008). The natural history of small-duct primar y sclerosing cholangitis. Gastroenterology; 134: 975 \200\22380. Tischendorf JJW, Geier A, Trautwein C (2008). Current diagnosis and management of primary sclerosing cholangitis. Liver Transpl; 14: 735 \200\22346. Tischendorf JJW, Meier PN, Schneider A et al. (2007). Transpapillary intraductal ultrasound in the evaluation of dominant bile duct stenoses in patients with primary sclero sing cholangitis. Scand J Gastroenterol; 42: 1011 \200\22317. Loftus EV, Harewood GC, Loftus CG et al. (2005). PSC-IBD: a unique form of inflammatory bowel disease associated with primary sclerosing cholangitis. Gut; 54: 91 \200 \2236. LIST OF CASES BY DIAGNOSIS 341 List of cases by diagnosis Case 1: Acute liver failure due to isoniazid Case 2: Autoimmune hepatitis Case 3: Intrahepatic cholestasis of pregnancy Case 4: Primary biliary cirrhosis Case 5: Variceal bleeding Case 6: Haemochromatosis Case 7: HIV-associated diarrhea Case 8: Ascites Case 9: Ampullary carcinoma Case 10: Small bowel bacterial overgrowth Case 11: Hepatorenal syndrome Case 12: Pancreatic insufficiency Case 13: Autoimmune pancreatitis Case 14: Hepatocellular carcinoma Case 15: Functional outlet obstruction Case 16: Hepatitis A Case 17: Hereditary non-polyposis colon cancer Case 18: Crohn \200\231s disease Case 19: Perianal Crohns \200\231s disease Case 20: Dyspepsia Case 21: Portal vein thrombosis Case 22: Clostridium difficile-associated diarrhea Case 23: Pregnancy in inflammatory bowel disease Case 24: Abdominal lymphoma Case 25: Hepatic encephalopathy Case 26: Intestinal tuberculosis Case 27: Eosinophilc oesophagitis Case 28: Peptic ulcer disease Case 29: Intrapapillary mucinous neoplasm Case 30: Pernicious anemia Case 31: Cytomegalovirus colitis OXFORD CASE HISTORIES 342 Case 32: Irritable bowel syndrome Case 33: High-output stoma Case 34: Colorectal cancer Case 35: Azathioprine toxicity Case 36: Lymphocytic colitis Case 37: Anorexia nervosa Case 38: Coeliac disease Case 39: Pancreatic pseudocyst Case 40: Hepatic adenomas Case 41: Severe ulcerative colitis Case 42: Granulomatous hepatitis Case 43: Hepatitis C Case 44: Hepatitis B Case 45: Non-alcoholic steatohepatitis Case 46: Leptospirosis Case 47: Wilson \200\231s disease Case 48: Angiosarcoma Case 49: Total parenteral nutrition and refeeding syndrome Case 50: Primary sclerosing cholangitis LIST OF CASES BY PRINCIPAL CLINICAL FEATURES AT DIAGNOSIS 343 List of cases by principal clinical features at diagnosis Abdominal pain 2, 13, 19, 21, 26, 28, 39, 50 Abnormal LFTs: 1, 3, 4, 5, 6, 25, 40, 42, 43, 44, 45, 47, 48 Anemia: 10, 18, 30, 39, 47 Ascites: 8, 11, 24, 25, 45 Vomiting 16, 50 Constipation 15 Diarrhea 7, 10, 12, 18, 22, 31, 32, 33, 35, 36, 41 Dysphagia: 27 Encephalopathy 1, 11, 25, 47 Family history: 17, 21, 27 Gastrointestinal bleeding 5, 34 Jaundice: 1, 2, 3, 9, 11, 13, 46 47 Pruritus: 3, 4 Weight loss 9, 10, 12, 13, 18, 29, 30, 37, 39, 49, 50 Other: 14, 33 This page intentionally left blank LIST OF CASES BY AETIOLOGICAL MECHANISMS 345 List of cases by aetiological mechanisms Autoimmune conditions: 3, 4, 13, 30 Drug induced: 1, 35 Infectious disease: 2, 7, 11, 16, 22, 26, 28, 31, 32, 42, 43, 44, 46 Inflammatory: 18, 19, 23, 27, 36, 39, 41, 50 Inherited conditions: 6, 8, 17, 21, 47 Malignancy: 9, 14, 17, 24, 29, 34, 40, 48 Physiological: 15, 33, 49 Psychological: 32, 37 Toxic: 5, 25 Other: 10, 12, 45 This page intentionally left blank Index Bold indicates the diagnosis of the case discussed within the page range. abdominal lymphoma 152 \200\22360 abdominal pain 7, 77, 80, 110, 133, 134, 138, 167, 171, 1 84, 187, 188, 189, 220, 232, 245, 265, 296, 300 \200\2231, 328, 334 antibiotic prophylaxis acute liver failure 4 endoscopic retrograde cholangiopancreatography 57 abdominal tuberculosis 170, 171 abnormal liver function tests 1, 15, 20, 27, 34, 161, 271, 282, 290, 296, 302, 314, 322 spontaneous bacterial peritonitis 52 variceal bleeding 28 antibiotic therapy acaeruloplasminaemia 38 acalculous cholecystitis 186 achalasia 180 \200\2231 acupuncture 22 5 acute angioedema 188 \200\2239 acute cholangitis 186 acute decompensation of chronic live r Clostridium difficile-associated diarrhea 143 \200\2234, 145 Helicobacter pylori 131 infective colitis 278 leptospirosis 311 perianal Crohn \200\231s di sease 122, 124 \200\2235 small bowel bacterial overgrowth 65 spontaneous bacterial peritoni tis 51 disease 2 \200\2233 acute fatty liver of pregnancy 16 \200\22317 acute hepatitis 10, 100 acute liver failure 1 \200\2236, 100 \200\2231 acute liver injury 10 acute pancreatitis 186, 200, 201 acute renal colic 187 acute severe ulcerative colitis 276 \200\22380 adalimumab 114, 115, 117, 125, 15 0 Addiphos \204 331 adenocarcinoma colon 339 gastric 207, 208 mucinous 202 small bowel 155 \200\2236 antidepressants 225 antihistamines 18 antimitochondrial antibodies 22 antiphospholipid synd rome 15 antiretroviral therapy 42 \200\2233, 287 \200\2238 antispasmodics 225 anti-TNF ther apy 114, 115 \200\22316, 117, 149 \200\22350 antituberculous treatment 5, 174 appetite loss 156, 205, 208, 334 arsenic exposure 327 arth ropathy 36 \200\2237, 113, 320 ascites 45 \200\22352, 67, 70, 152, 161, 302 astrocytes 162 autoimmune hepatitis 7 \200\22314, 17 autoimmune markers 3 autoimmune pancreatitis 77 \200 \22384 autonomic neuropathy 63 azathioprine therapy AIDS cholangiopathy 285 albumin infusion 51, 70 alcoholic hepatitis 3, 10 allopregnanolone 163 alosetron 225 -fetoprotein 88 aminoglycoside antibiotics 51 amitriptyline 132, 225 am monia 162 \200\2233 amoxicillin 131, 192, 194 ampicillin 311 ampullary carcinoma 53 \200 \22360 Amsterdam II Criteria 107, 108 amyloidosis 188, 208, 324, 325 anemia 61, 110, 265 pe rnicious 205 \200\22311 for autoimmune hepatitis 12 breast-feeding 117, 150 \200\2231 Crohn \200\231s disease 114, 115, 116 hepatitis risk 17 perianal fistula 125 pregnancy 17, 117, 148 \200\2239 toxicity 2 41 \200\2234 back pain 152, 154, 184, 245, 290 bacterial diarrhea 42, 214 bacterial overgrowth 61 \200 \2236, 74, 217, 228 balloon tamponade 31 Barcelona-Clinic Liver Cancer stage 89 barium enem a 235 beta-blockers 33 biliary colic 186 angioedema 188 \200\2239 angiosarcoma 322 \200\2237 ankylosing spondylitis 113 anorexia ner vosa 251 \200\2236 anthraquinones 97 INDEX 348 bisacodyl 98 bismuth 131 blind loop syndrome 63 bone fractures 20, 23 breath tests 64 \200 \2235, 130 bronze diabetes 37 brucellosis 310 Budd Chiari syndrome 2 budesonide 114, 149, 2 49 bulk-forming laxatives 97 colonic ischaemia 215 colonoscopy 236 colorectal cancer 232 \200\22340 hereditary non-polyposis 104 \200\2239 computerized tomography, see CT headings confusion 1, 31, 161 constipation 93, 94, 95, 224 laxatives 96 \200\2238 contrast-enhanced CT abdomen 134 copper measurements 317 \200\22318 corkscrew esophagus 181 corticosteroid therapy C282Y 36, 37 \200\2238 caeruloplasmin 317 caffeine 224, 249 calcium 331 capacity to consent 255 capecitabine 238 carcinoid tumors 157 cellulitis 68 cephalosporin 4, 51 certolizumab p egol 114, 115 Charcot \200\231s triad 186 chelating agents 318 \200\22319 chemotherapy regi mens 210 \200\22311, 237 \200\2238 Child \200\223Pugh score 48 cholangiocarcinoma 338 chola ngitis, acute 186 cholecystitis, acalculous 186 cholestasis 101 cholestyramine 18 chronic a trophic gastritis Type A 206 ciclosporin 279 ciprofloxacin 52, 65, 278 cirrhosis 304 autoimmune hepatitis 12 autoimmune pancreatitis 83 Clostridium difficile-associated diarrhea 144 Crohn \200\231s disease 114, 149 eosinophilic oesophagitis 182 pregnancy 117, 149 side effects 114 ulcerative colitis 278 cracked linseed 93, 97 Creon \204 76 Crohn \200\231s disease 110 \200\22318 differentiation from TB 175 \200\2236, 242 perianal 119 \200\22326 pregnancy 116 \200\22317 , 147 \200\22351 cryptosporidiosis 44 CT, dual-phase 81 \200\2232 CT abdomen, contrast-enhanced 134 CT colon 236 CT colonography 94, 236 CT enteroclysis 158 CT pneumocolon 94, 236 culture-negative ne urocytic ascites 50 cyst fluid 202 \200\2233 cytomegalovirus Child \200\223Pugh score 48 hepatic encephalopathy 162 hepatitis B 300 hepatitis C 292 hepa tocellular carcinoma risk 88 primary biliary 20 \200\2236 colitis 42, 43 \200\2234, 212 \200\22318 liver infection in HIV 285 clarithromycin 131, 192, 194 Clostridium difficile-associated diarrhea 138 \200\22346, 216 De-Noltab 194 decompensated chronic liver disease 2 \200\2233, 48 descending perineum syn drome 94 diabetes 37, 80 diarrhea 72, 110, 167, 171, 212, 216 \200\22317, 220, codanthrusate 98 codeine 225, 231 coeliac disease 62, 258 \200\22364 colesevalam 25, 225, 2 49 colestyramine 24, 25, 225, 249 colitis 224, 227, 241, 245, 246, 276, 328 Clostridium difficile 138 \200\22346, 216 HIV 41 \200\223 4 nocturnal 61, 62 collagenous 247 cytomegalovirus 42, 43 \200\2234, 212 \200\22318 lymphocytic 245 \200\22350 microscopic 247 \200\2239 pseudomembranous 142, 143, 145, 214 severe ulcerative 276 \200 \22380 viral 42 diverticulosis 62, 63, 66, 72, 138 docusate sodium 98 domperidone 132 donor feces 144 Doppl er ultrasonography 134 double duct sign 57, 58, 81 drug resistant TB 175 dual-phase scan 81 \200\2232 Dukes \200\231 classification 237 collagenous colitis 247 colon adenocarcinoma 339 INDEX 349 Dulcolax 98 duodenal ulceration 190, 191 \200\2233 dyspepsia 127 \200\22332 dysphagia 178, 180, 181 dystrophia myotonica 181 gastric adenocarcinoma 207, 208 gastric cancers 108, 208 \200\22311 gastric outlet obstruct ion 195 gastric ulceration 191 \200\2233 gastric varices 29 gastritis Type A/B 206, 209 gas trointestinal bleeding 27, 232 gastrointestinal stromal tumors (GIST) 157 gastro-oesophagea l reflux disease 180 genetic disease 36, 37 \200\2239, 106, 107, 108 \200\2239, 113 glucose , intravenous 188 glucose hydrogen breath test 64 \200\2235 glutamine synthetase 163 gluten -free diet 263 glycerin suppositories 98 golden linseed 97, 224 granulomatous hepatitis 282 \200\2239 ECF regimen 210 ectopic pregnancy 187 elastase, fecal 74 \200\2235 electrolyte replacement 331 elimination diets 182 ELLISPOT 172, 242 endometrial cancer 107, 108 endoscopic retrog rade cholangiopancreatography 56 \200\2238 endoscopic therapy, variceal bleeding 29 enterochroma fin cells 223 eosinophilic oesophagitis 178 \200\22383 EOX regimen 211 epithelioid cell gra nulomas 172 erythema nodosum 113 esomeprazole 193 ethambutol 174 ethanol, percutaneous 90 e xocrine pancreatic insufficiency 62, 72 \200\2236 extensively drug resistant TB 175 eye, Cr ohn \200\231s disease 114 HAART 42 \200\2233, 287 \200\2238 haematin 188 haemochromatosis, hereditary 34 \200\22340 h emorrhage 194 \200\2235 HBeAg-negative chronic hepatitis B 299 HBeAg-positive chronic hepat itis B 296 \200\223301 heavy metal poisoning 189 Helicobacter pylori 127, 129 \200\22331, 1 90, 191, 192, 193 \200\2234, 209 HELLP syndrome 16 hepatic adenomas 271 \200\2235 hepatic artery chemoemb olization 90 hepatic encephalopathy 30, 31 \200\2232, 161 \200\2236 hepatic haemangiomas 27 2 hepatic resection 90 hepatic venous pressure gradient 30 \200\2231 hepatitis, acute 10, 1 00 hepatitis, alcoholic 3, 10 hepatitis, autoimmune 7 \200\22314, 17 hepatitis, granulomato us 282 \200\2239 hepatitis, ischaemic 100 hepatitis A 10, 99 \200\223103 hepatitis A virus vaccine 101 \200\2232 hepatitis B 292, 296 \200\223301 hepatitis B virus fecal donation 144 fecal elastase 74 \200\2235 fecal softeners 98 familial Mediterranean fe ver 188 fatigue 15, 20, 23, 25 \200\2236, 290, 300 \200\2231 fatty liver acute fatty liver of pregnancy 16 \200\22317 non-alcoholic fatty liver disease 304 \200\223 7 ferritin 36 ferroportin disease type A/B 38 -fetoprotein 39, 88, 273 fever 133, 134, 138, 167, 171 finger clubbing 167, 174 fistulae 123, 124 Fleet enema 98 flexible sigmoidoscopy 235 fluoroquinolones 51, 131 5-fluorouracil 237 \200\2238 fluticasone 182 focal nodular hyp erplasia 272 fractures 20, 23 frusemide 51, 161, 212 functional dyspepsia 128, 129, 131 \200\2232 functional outlet obstruction 93 \200\2238 fungal infections 42, 285 Fybogel 97 coinfection in HIV 287 \200\2238 hepatocellular carcinoma 89 hepatitis C 290 \200\2234 hepatitis C virus coinfection in HIV 288 hepatocellular carcinoma 88 \200\2239 hepatocellular carcinoma 39, 8 5 \200\22392 hepatorenal syndrome 51, 67 \200\22371 hepcidin 39 hereditary acaeruloplasmina emia 38 hereditary haemochromatosis 34 \200\22340 hereditary hypotransferrinaemia 38 \200 \2239 hereditary non-polyposis colon GABA 163 gall bladder wall thickening 11 gastric acid hypersecretion 229 cancer 104 \200\2239 HFE haemochromatosis 37 \200\2238 INDEX 350 high-output stoma 227 \200\22331 highly active antiretroviral therapy (HAART) jaundice 1, 7, 15, 16, 23, 53, 67, 77, 80, 99, 100, 290, 292, 308, 314 42 \200\2233, 287 \200\2238 jejunal diverticulosis 62, 246 juvenile haemochromatosis 38 HIV diarrhea 41 \200\2234 enteropathy 44 HBV/HCV coinfection 287 \200\2238 liver malignancies 2 84 opportunistic infections 284 \200\2235 tuberculosis 173 \200\2234, 284 \200\2235, 287 Kaposi \200\231s sarcoma 284 Kayser \200\223Fleischer rings 318 lactic acidosis syndrome 288 lactose intolerance 62, 217 lactulose 30, 97, 164 lactulose hy drogen breath test 64 \200\2235 lansoprazole 131, 192, 193, 194 laxatives 96 \200\2238 Laxo beral 97 left flank mass 152, 154 leptospirosis 308 \200\22312 levofloxacin 131 lipase 76 liver biopsy HLA typing 260, 262 Howell \200\223Jolly bodies 324 \200\2235 hydrocortisone 278 hyoscine b utylbromide 225 hyperammonaemia 162 \200\2233 hyperthyroidism 181 hypnotherapy 225 hyponatr aemia 51 \200\2232 hypothyroidism 181 hypotransferrinaemia 38 \200\2239 hypovolaemia 28, 68 , 330 autoimmune hepatitis 11 haemochromatosis 36 hepatocellular carcinoma 88 non-alcoholic fatty liver disease 305, 306 \200\2237 primary biliary cirrhosis 22 transjugular 305 IFL regimen 211 IgA deficiency 261 \200\2232 IgG4 82 ileostomy dysfunction 227 \200\22331 i matinib mesylate 157 immunoproliferative small intestinal liver failure, acute 1 \200\2236, 100 \200\2231 liver injury, acute 10 liver lesion charact erization 88 liver screen 3 liver transplantation disease 156 immunosuppression therapy 12 inactive carrier state 298 infective colitis 278 inflammatory bowel disease in pregnancy 147 \200\22351 primary sclerosing cholangitis and 337 acute liver failure 4 \200\2235 hepatocellular carcinoma 90 hepatorenal syndrome 70 King \200\231s College Hospital criteria 4 \200\2235 primary biliary cirrhosis 23, 25 variceal b leeding 31 Wilson \200\231s disease 318 inflammatory pseudocysts 200 infliximab 114, 115, 117, 125, 149 \200\22350, 279 interferon- -release assays 172, 242 interferon therapy 293 \200\2234, 299 international normalized r atio (INR) 56 intestinal infarction 135 intestinal lymphoma 43 intestinal tuberculosis 42, 167 \200\22376 intraductal papillary mucinous LOLA 65 long preparation CT colonography 236 loperamide 225, 230, 231 lupus hepatitis 17 ly mph node clearance 210 lymph node enlargement 81 lymphocytic colitis 245 \200\22350 lymphom a neoplasm 197 \200\223204 intrahepatic cholestasis of pregnancy 15 \200\22319 abdominal 152 \200\22360 azathioprine/mercaptopurine-related 243 \200\2234 intestinal 43 no n-Hodgkin \200\231s 284 Lynch syndrome 104 \200\2239 intraluminal maldigestion 74 intravenous immunoglobulin 144 iron balance regulation 39 iron deficiency 130 iron overload 36, 37 \200\2238 irritable bowel syndrome 220 \200\2236 ischa emic hepatitis 100 isoniazid 174 isoniazid-associated acute liver failure 1 \200\2236 isoto nic fluids 230 isphagula husk 97 magnesium sulfate 331 magnetic resonance cholangiography 56 magnetic resonance cholangiopancreatography (MRCP) 336 meal-related/unrelated functional dyspepsia 131 \200\2232 INDEX 351 mebeverine 225 mechanical balloon tamponade 31 megaloblastic anemia 206 megaloblastic madne ss 206 mercaptopurine 115, 125, 243 oral rehydration solution 230 organic dyspepsia 128 osmotic laxatives 97 osteoporosis 23 \200\2234 ovarian cancer 108 ovarian torsion 187 oxaliplatin 237, 238 breast-feeding 150 \200\2231 pregnancy 148 \200\2239 mesalazine 115, 249 mesenteric ischaem ia 186 methotrexate 115, 243 metoclopramide 132 metronidazole 65, 122, 131, 143 \200\2234, 192, 194, Pabrinex \204 331 pancreas, sausage-shaped 81 pancreatic atrophy 74, 75 \200\2236 pancreat ic biopsy 82 pancreatic calcification 81 pancreatic cancer 80, 83 pancreatic cysts 200 \200 \2233 pancreatic enzyme replacement 76 pancreatic insufficiency 62, 72 \200\2236 pancreatic pseudocyst 200, 265 \200\22370 pancreatitis 230, 278 Micralax 98 microsatellite instability (MSI) 106, 107 microscopic colitis 247 \200\2239 Milan criteria 90 minimal CT colonography 236 mismatch repair genes 106, 107 miso prostil 192 \200\2233 Model for Endstage Liver Disease (MELD) acute 186, 200, 201 autoimmune 77 \200\22384 endoscopic retrograde 48 \200\2239 monoclonal antibodies 211 Montr al classification 112 Movicol 97 mucinous adenocarcinoma 202 multi-drug resistant TB 175 Murphy \200\231s sign 186 muscular dystrophy 181 myastheni a gravis 181 Mycobacterium avium complex 285 myelopathy 206 cholangiopancreatography risk 57 recurrent 200, 201 pancreatoduodenectomy 59, 83 pantoprazole 193 paracentesis 51, 70 paracetamol overdose 3 pa rtial small bowel obstruction 336 pegylated interferon 293 \200\2234, 299 penicillamine 319 penicillin G 311 peptic ulcer disease 184 \200\22396 peptic ulcer perforation 186 \200\223 7, 195 perianal abscess 122 perianal Crohn \200\231s disease 119 \200\22326 perianal fistul a 123 \200\2235 perianal pain 119, 122 perianal sepsis 122 peripheral neuropathy 206 periph eral plasmacytosis 102 \200\2233 peritonitis 186 \200\2237 naltrexone 25 neomycin 165 neuropsychiatric symptoms 206, 319 \200\22320 neurosteroids 163 night sweats 171 non-alcoholic fatty liver disease 304 \200\2237 non-alcoholic steatohepati tis 302 \200\2237 non-Hodgkin \200\231s lymphoma 284 non-steroidal anti-inflammatory drugs (NSAIDs) 190, 191, 193 spontaneous bacterial 50, 51, 52 non-ulcer dyspepsia 128 norofloxacin 52 pernicious anemia 205 \200\22311 phlebotomy 39 phosphate 331 phosphate enemas 30 pituitary failure 36 plasmacytosis 102 \200\2233 polyethylene glycol 97 polyglandular autoimmune synd rome occupational carcinogen exposure 326 octreotide 29, 231 ocular involvement, Crohn \200\231s disease 114 oculopharyngeal dystrophy 181 oesophageal dilatation 182 oesophageal spasm 181 oesophageal varices 24, 29 omeprazole 131, 192, 193, 194, 195, 230, 231 opioid antagonists 25 opportunistic infections, HIV 284 \200\2235 oral contraceptives, hepatic adenoma type II 207 polymerase chain reaction 171 polyvinyl chloride 326, 327 porphyria 187 \200\2238 portal hy pertension 24, 30, 135 \200\2236 portal vein thrombosis 133 \200\2237 post-cholecystectomy syndrome 301 link 273 INDEX 352 post-infective irritable bowel syndrome 220 \200\2236 post-transplant lymphoproliferative serum-ascites albumin gradient 50 \200\2231 seton drain 122 severe CDAD 142 shellfish 10 sh ort bowel 229 skin pigmentation 34, 37 small bowel adenocarcinoma 155 \200\2236 small bowel bacterial overgrowth 61 \200\2236, 74, disorder 217 potassium 331 prednisolone 12, 83, 114, 149, 182 pre-eclampsia 16 pregnancy