Cover
Title Page
Notes on contributors
SECTION 1: Approach to specific presentations
1. CHAPTER 1: Approach to dysphagia
  1. Definitions
  2. Differential diagnosis
  3. History and examination
  4. Investigation
  5. Management of dysphagia
  6. Further reading
2. CHAPTER 2: Approach to vomiting
  1. Definition
  2. Etiology
  3. History
  4. Examination
  5. Investigations
  6. Management of acute nausea and vomiting
  7. Further reading
3. CHAPTER 3: Approach to upper gastrointestinal bleeding
  1. Introduction
  2. History
  3. Causes of upper gastrointestinal bleeding
  4. Past medical history
  5. Examination and assessment
  6. Management of UGIB
  7. Summary
  8. References
4. CHAPTER 4: Approach to acute abdominal pain
  1. Introduction
  2. History
  3. Examination
  4. Investigation
  5. Management
  6. References
5. CHAPTER 5: Approach to jaundice
  1. Definition
  2. Differential diagnosis
  3. History and examination
  4. History
  5. Investigations
  6. Management
  7. References
6. CHAPTER 6: Acute severe lower gastrointestinal hemorrhage
  1. Introduction
  2. Definition
  3. Presentation and differential diagnosis
  4. Evaluation
  5. Independent correlates of severe bleeding
  6. Management
  7. Outcomes
  8. Further reading and viewing
7. CHAPTER 7: Approach to diarrhea
  1. Definition
  2. Differential diagnosis
  3. History
  4. Examination
  5. Investigation
  6. Management
  7. Further reading
SECTION 2: Complications of gastrointestinal procedures and therapy
1. CHAPTER 8: Complications of upper gastrointestinal endoscopy
  1. Introduction
  2. Complications of sedation
  3. Cardiopulmonary complications
  4. Management of sedation-related complications
  5. Infectious complications
  6. Perforation
  7. Bleeding
  8. Complications of common endoscopic procedures
  9. Summary
  10. References
2. CHAPTER 9: Complications of percutaneous endoscopic gastrostomy
  1. Introduction
  2. Minor complications
  3. Major complications
  4. References
3. CHAPTER 10: Complications of endoscopic variceal ligation, sclerotherapy, and balloon tamponade
  1. Acknowledgements
  2. References
4. CHAPTER 11: ERCP complications
  1. Introduction
  2. Post-ERCP pancreatitis
  3. Post-sphincterotomy bleeding (PSB)
  4. Infectious complications
  5. Perforation
  6. Cardiopulmonary complications
  7. Contrast media-related reactions
  8. Conclusions
  9. References
5. CHAPTER 12: Complications of laparoscopic surgery
  1. Introduction
  2. Assessment, investigation, and management of laparoscopic complications
  3. Types of complication
  4. Complications of operative injury during laparoscopy
  5. Conversion to open surgery
  6. Complications specific to procedures
  7. References
6. CHAPTER 13: Complications of liver biopsy
  1. Introduction
  2. Complications
  3. Acknowledgments
  4. Further reading
7. CHAPTER 14: Complications of colonoscopy
  1. Introduction
  2. Complications
  3. Rare complications of colonoscopy
  4. References
8. CHAPTER 15: Complications of capsule endoscopy
  1. Introduction
  2. Contraindications
  3. Limitations
  4. References
9. CHAPTER 16: Complications of endoscopic ultrasound
  1. Introduction
  2. Complications
  3. Summary
  4. References
10. CHAPTER 17: Complications of Endoscopic Mucosal Resection (EMR) and Endoscopic Submucosal Dissection (ESD)
  1. Introduction
  2. Stomach
  3. Colon
  4. Esophagus
  5. References
11. CHAPTER 18: Complications of bariatric surgery
  1. Introduction
  2. Roux-en-Y gastric bypass
  3. Gastric banding
  4. Sleeve gastrectomy
  5. Vertical banded gastroplasty
  6. Biliopancreatic-diversion with or without duodenal switch
  7. Conclusion
  8. References
12. CHAPTER 19: Complications of drugs used in gastroenterology
  1. The nature of drug complications
  2. An overview of ADRs for gastroenterology drugs
  3. Principles of prescribing
  4. References
SECTION 3: Specific conditions
1. CHAPTER 20: Foreign body impaction in the esophagus
  1. Introduction
  2. History and examination
  3. Treatment
  4. References
2. CHAPTER 21: Esophageal perforation
  1. Introduction
  2. Etiology
  3. Clinical presentation
  4. Examination
  5. Investigations
  6. Diagnosis
  7. Management
  8. Summary
  9. Future developments
  10. References
3. CHAPTER 22: Acute upper non-variceal gastrointestinal hemorrhage
  1. Introduction
  2. Risk assessment
  3. Diagnosis and etiology
  4. Management
  5. References
4. CHAPTER 23: Acute pancreatitis
  1. Introduction
  2. Clinical presentation (Table 23.1)
  3. Diagnosis: clinical and imaging
  4. Etiology of acute pancreatitis
  5. Assessment of severity and outcome
  6. Treatment of acute pancreatitis
  7. Definition and management of local complications
  8. Management of sterile pancreatic necrosis
  9. References
5. CHAPTER 24: Biliary tract emergencies
  1. Introduction
  2. Gallstone pancreatitis
  3. Cholangitis
  4. Bile leak
  5. Acute cholecystitis
  6. References
6. CHAPTER 25: Variceal hemorrhage
  1. Introduction
  2. Clinical presentation
  3. Prevention of variceal hemorrhage
  4. Secondary prevention of variceal hemorrhage
  5. Initial emergency management of bleeding varices
  6. Acknowledgments
  7. References
7. CHAPTER 26: Acute liver failure
  1. Introduction
  2. Definitions
  3. Epidemiology
  4. Etiology
  5. Clinical manifestations
  6. Treatment
  7. Prognostication and transplantation
  8. Acknowledgment
  9. References
8. CHAPTER 27: Ascites and spontaneous bacterial peritonitis
  1. Introduction
  2. Pathophysiology of ascites in cirrhosis
  3. Clinical presentation of ascites and diagnosis
  4. Treatment of ascites
  5. Treatment and prophylaxis of SBP
  6. References
9. CHAPTER 28: Alcoholic hepatitis
  1. Introduction
  2. Pathogenesis
  3. Clinical features
  4. Biochemical features
  5. Investigations and diagnosis
  6. Prognostic factors
  7. Management
  8. Conclusion
  9. References
10. CHAPTER 29: Perforation of the gastrointestinal tract
  1. Introduction
  2. Clinical presentation
  3. Prognosis
  4. Management
  5. Colonic perforation
  6. References
11. CHAPTER 30: Intestinal obstruction
  1. Introduction
  2. Etiology
  3. Examination
  4. Investigations
  5. Management
  6. Acknowledgment
12. CHAPTER 31: Acute appendicitis
  1. Introduction
  2. Etiology
  3. History
  4. Examination
  5. Unusual presentations
  6. Investigation
  7. Management
  8. Management of complicated appendicitis
  9. Postoperative complications
  10. References
13. CHAPTER 32: Middle gastrointestinal bleeding
  1. Introduction
  2. Evaluation
  3. Management
  4. References
14. CHAPTER 33: Ischemic bowel
  1. Introduction
  2. Acute mesenteric ischemia
  3. Ischemic colitis
  4. Chronic mesenteric ischemia
  5. References
15. CHAPTER 34: Acute severe ulcerative colitis
  1. Introduction
  2. Acute severe crohn’s colitis
  3. Principles of management
  4. Conclusion
  5. References
16. CHAPTER 35: Gastrointestinal infections
  1. Introduction
  2. Gastroenteritis
  3. General management
  4. Specific infections
  5. Other important gastrointestinal conditions
  6. References
  7. Useful links
17. CHAPTER 36: Diverticular disease
  1. Introduction
  2. Acute diverticulitis
  3. Complicated diverticular disease
  4. Diverticular hemorrhage
  5. Further reading
18. CHAPTER 37: Gastrointestinal complications of HIV disease
  1. Overview of HIV/AIDS
  2. HIV testing in the gastrointestinal setting
  3. Upper gastrointestinal diseases associated with HIV
  4. Gastric diseases associated with HIV
  5. Hepatobiliary diseases associated with HIV
  6. Lower gastrointestinal diseases associated with HIV
  7. Investigation of lower gastrointestinal symptoms
  8. Anorectal diseases associated with HIV
  9. Gastrointestinal complications of antiretroviral therapy
  10. Conclusion
  11. References
19. CHAPTER 38: Gastrointestinal complications in the intensive care unit
  1. Introduction
  2. Specific gastrointestinal conditions
  3. References
Index
End User License Agreement

List of Tables

Chapter 01
1. Table 1.1 Etiology of oropharyngeal dysphagia.
2. Table 1.2 Etiology of esophageal dyphagia.
Chapter 02
1. Table 2.1 Causes of acute vomiting.
2. Table 2.2 Classes of antiemetic drug.
3. Table 2.3 Clinical uses of different antiemetics.
Chapter 03
1. Table 3.1 Causes of upper gastrointestinal bleeding.
2. Table 3.2 Glasgow-Blatchford Score for upper gastrointestinal bleeding.
3. Table 3.3 Rockall Score for upper gastrointestinal bleeding.
4. Table 3.4 Components of the pre-endoscopy AIMS 65 Score.
Chapter 04
1. Table 4.1 Abdominal causes of acute abdomen.
2. Table 4.2 Extra-abdominal causes of acute abdomen.
3. Table 4.3 Causes of abdominal pain based on pathophysiological mechanisms.
4. Table 4.4 Comparison of symptoms of common causes of acute abdominal pain.
5. Table 4.5 Localization of common causes of acute abdominal pain.
6. Table 4.6 Causes of intermittent abdominal pain with periodicity.
Chapter 05
1. Table 5.1 Differential diagnosis of jaundice.
2. Table 5.2 Differentiating obstructive jaundice from hepatic jaundice.
3. Table 5.3 Drugs that can cause dose-independent hepatotoxicity.
4. Table 5.4 Liver enzymes in different types of jaundice.
5. Table 5.5 Management of pruritus.
6. Table 5.6 Monitoring and replacement of fat-soluble vitamin deficiency in prolonged cholestasis.
Chapter 06
1. Table 6.1 Etiology of lower gastrointestinal hemorrhage.
2. Table 6.2 Endoscopic therapies for acute bleeding.
Chapter 07
1. Table 7.1 Physiological mechanisms in acute diarrhea.
2. Table 7.2 Differential diagnosis of acute onset diarrhea.
Chapter 12
1. Table 12.1 Categorization of specific risks of complications in laparoscopic versus open operations.
2. Table 12.2 Complications of laparoscopic cholecystectomy.
3. Table 12.3 Complications of laparoscopic colorectal surgery
Chapter 13
1. Table 13.1 Complications of percutaneous liver biopsy.
Chapter 16
1. Table 16.1 Guidelines for medical and surgical management of esophageal perforation.
Chapter 18
1. Table 18.1 Etiology of marginal ulceration.
2. Table 18.2 Recommended supplement doses after bariatric surgery.
3. Table 18.3 Symptoms of early and late dumping.
Chapter 19
1. Table 19.1 Adverse drug reactions attributed to drugs commonly used in gastroenterology.
Chapter 20
1. Table 20.1 Underlying conditions in esophageal foreign body impaction.
2. Table 20.2 Seven steps in management of esophageal foreign body obstruction.
3. Table 20.3 Appropriate timing for endoscopic retrieval.
4. Table 20.4 Useful endoscopic accessories for esophageal foreign body removal.
Chapter 21
1. Table 21.1 Causes of esophageal perforation [1].
2. Table 21.2 Endoscopic accessories used for esophageal perforations (including manufacturer and product name).
3. Table 21.3 Summary of previous studies on the use of stents in the management of oesophageal perforation.
Chapter 22
1. Table 22.1 The Blatchford Scoring system.
2. Table 22.2 Total Blatchford Score and need for Intervention (i.e. transfusion, endoscopic therapy, surgery).
3. Table 22.3 The Rockall scoring system.
4. Table 22.4 Mortality and rebleeding of patients with peptic ulceration and esophageal varices according to complete Rockall Score.
5. Table 22.5 Causes of hematemesis and melena.
6. Table 22.6 Endoscopic stigmata and the risk of rebleeding.
Chapter 23
1. Table 23.1 Clinical manifestations of acute pancreatitis; the effects of pancreatitis are manifest at three sites.
2. Table 23.2 Diagnostic features of acute pancreatitis.
3. Table 23.3 Etiology of acute pancreatitis.
4. Table 23.4 Ranson’s prognostic scoring criteria.
5. Table 23.5 CT severity index for acute pancreatitis.
Chapter 25
1. Table 25.1 Screening and treatment guidelines.
2. Table 25.2 Technique for endoscopic variceal obliteration using N-butyl-2 cyanoacrylate.
Chapter 26
1. Table 26.1 Causes of acute liver failure.
2. Table 26.2 Course of acute liver failure.
3. Table 26.3 West Haven classification for grading hepatic encephalopathy.
4. Table 26.4 Relative and complete contraindications to liver transplantation.
5. Table 26.5 Criteria of king’s college, london.
Chapter 27
1. Table 27.1 Initial evaluation of patients with cirrhosis and ascites.
2. Table 27.2 Management practice points in patients with ascites and cirrhosis (all patients must be evaluated for liver transplantation).
3. Table 27.3 Definition and diagnostic criteria of refractory ascites in cirrhosis.
4. Table 27.4 Recommendations for the management and prevention of spontaneous bacterial peritonitis.
Chapter 28
1. Table 28.1 The Glasgow alcoholic hepatitis score.
Chapter 29
1. Table 29.1 Etiology of colonic perforation.
2. Table 29.2 Hinchey classification of peritoneal contamination in perforated diverticular disease.
3. Table 29.3 Mannheim peritonitis index.
Chapter 31
1. Table 31.1 Differential diagnosis of acute appendicitis.
Chapter 34
1. Table 34.1 Truelove and Witts classification of ulcerative colitis.
2. Table 34.2 Diseases mimicking severe ulcerative colitis.
3. Table 34.3 Monitoring regimen in acute severe ulcerative colitis.
4. Table 34.4 Principles of salvage therapy in intravenous steroid-refractory patients.
5. Table 34.5 Incidence of adverse events associated with ciclosporin.
Chapter 35
1. Table 35.1 High-risk groups for infectious diarrhea.
2. Table 35.2 Oral rehydration solutions.
3. Table 35.3 Antibiotic treatments for infectious diarrhea.
4. Table 35.4 Approach to recurrent Clostridium difficile infection.
Chapter 36
1. Table 36.1 Definitions of diverticular disease.
Chapter 37
1. Table 37.1 Gastrointestinal manifestations of HIV infection.
2. Table 37.2 Upper gastrointestinal endoscopic findings.
3. Table 37.3 Lower gastrointestinal endoscopic findings.
Chapter 38
1. Table 38.1 GI symptoms associated with mortality.
2. Table 38.2 Risk factors for stress ulcer.
3. Table 38.3 Risk factors for IAH.

List of Illustrations

Chapter 01
1. Fig. 1.1 Diagnostic algorithm for the symptomatic assessment of the patient with dysphagia.
2. Fig. 1.2 Approach to management of total dysphagia.
Chapter 05
1. Fig. 5.1 Bilirubin metabolism.
2. Fig. 5.2 Diagnostic algorithm for assessment of the patient with jaundice. ERCP endoscopic retrograde cholangiopancreatography, EUS endoscopic ultrasound, MRCP magnetic resonance cholangiopancreatography, PTC percutaneous transhepatic cholangiogram.
Chapter 06
1. Fig. 6.1 Approach to the patient with acute lower gastrointestinal hemorrhage.
2. Fig. 6.2 Diverticular bleed with stigmata of an adherent clot.
3. Fig. 6.3 Radiation proctopathy (a) treated with argon plasma coagulation (b).
Chapter 09
1. Fig. 9.1 Endoscopic appearance of a buried bumper at endoscopy.
Chapter 11
1. Fig. 11.1 Temporary pancreatic duct stent with single external pigtail, inserted for post-ERCP pancreatitis prophylaxis in a high-risk patient.
2. Fig. 11.2 Delayed post-sphincterotomy bleeding in a patient who had to start full anticoagulation therapy soon after ERCP with sphincterotomy.
3. Fig. 11.3 Cholangitis with immediate release of intraductal stones and pus from the bile duct after biliary sphincterotomy.
4. Fig. 11.4 Perforation of the afferent enteral limb with a duodenoscope in a patient with Billroth II anatomy. After obtaining an emergent surgical consultation in the endoscopy unit, the defect was immediately managed endoscopically with a cap-fitted, forward-viewing gastroscope with complete clip-closure of the perforation. The ERCP was then able to be completed in the same session with the cap-fitted, forward-viewing instrument [53].
5. Fig. 11.5 Retroperitoneal air (white arrows) on computerized tomography (CT) of the abdomen and pelvis in a patient with retroperitoneal perforation during ERCP. Despite the CT findings and subcutaneous air leading to clinical crepitus and periorbital edema, the patient was successfully managed conservatively after obtaining an emergent surgical consultation in the endoscopy unit.
Chapter 12
1. Fig. 12.1 CT scan: port site hernia following laparoscopic Incisional hernia repair.
Chapter 15
1. Fig. 15.1 Small bowel tumor causing capsule retention.
2. Fig. 15.2 Agile patency capsule causing small bowel obstruction before disintegration. The capsule dissolved on the specified time and symptoms were relieved.
Chapter 16
1. Fig. 16.1 Intracystic hemorrhage after fine needle aspiration using a 22 gauge needle of a pancreatic cyst.
2. Fig. 16.2 Injection of fibrin glue into the cyst cavity after an arterial bleeding occurred and did not stop spontaneously 20 minutes after EUS FNA of a pancreatic cyst. The bleeding stopped instantaneously after injection of fibrin glue.
3. Fig. 16.3 Esophageal tear after passage of the echoendoscope.
4. Fig. 16.4 Esophageal stent placed over the site of perforation.
Chapter 17
1. Fig. 17.1 (a) Perforation occurred during gastric ESD. (b) Perforation closed successfully with “omental-patch method” using endoclips.
2. Fig. 17.2 (a) Arterial bleeding during gastric ESD. (b) Arterial bleeding managed by electrocautery using hemostatic forceps.
Chapter 18
1. Fig. 18.1 Bariatric surgeries including: Roux-en-Y gastric bypass (a), gastric banding (b), sleeve gastrectomy (c), vertical banded gastroplasty (d), biliopancreatic-diversion (e), and biliopancreatic diversion with duodenal switch (f).
2. Fig. 18.2 Endoscopic examples of complications and/or treatments including marginal ulceration (a), gastrogastric fistula (b), dilated gastrojejunal anastamosis (c), and an endoscopic suturing procedure to decrease stoma size (d) following Roux-en-Y gastric bypass, and gastric outlet obstruction at the incisura angularis (e) with subsequent endoscopic balloon dilation (f) following sleeve gastrectomy.
Chapter 19
1. Fig. 19.1 The metabolism of azathioprine (AZA) and 6-mercaptopurine (6-MP). 6-mMP = 6-methylmercaptopurine, 6-MMP(R) = 6-methylmercaptopurine ribonucleotides, 6-TGNs = 6-thioguanine nucleotides, 6-TIMP = 6-thioinosine monophosphate, HGPRT = hypoxanthine guanine phosphoribosyltransferase, TPMT = thiopurine S-methyl-transferase, XO =xanthine oxidase.
Chapter 20
1. Fig. 20.1 Chicken meat bolus impacted above a distal esophageal mucosal (Schatzki’s) ring (not shown). The bolus was grasped using the polypectomy snare and lifted off the distal esophageal stenosis before being removed by mouth using the Roth net.
2. Fig. 20.2 Endoscopic appearance of a distal esophageal mucosal (Schatzki’s) ring severed by the passage of the food bolus into the stomach under direct endoscopic visualization, water and air instillation, and gentle pressure by the endoscope tip. Mucosal rings account for many episodes of acute esophageal impaction, typically with a meat bolus (Steak house syndrome).
3. Fig. 20.3 Characteristic appearance of eosinophilic esophagitis, a clinical condition that underlies many foreign body impactions today. This endoscopic photograph, depicting multiple rings along the esophageal body, was taken upon introduction of the endoscope in the proximal esophagus and hence provided with an endoscopic clue to the etiology of impaction, which occurred more distally in this patient (not shown).
4. Fig. 20.4 Anatomical areas associated with esophageal bolus impaction.
5. Fig. 20.5 Food impaction in a patient with severe scleroderma esophagus and secondary esophageal candidiasis. Note the dilated esophagus and the esophageal mucosal changes consistent with Candida infection. Careful water instillation allowed the endoscope to break up the food residue that initially appeared as a cast of the esophageal body. The repeated use of the Roth retrieval net eventually relieved the patient’s impaction and associated acute dysphagia.
6. Fig. 20.6 Food impaction in a patient with esophageal achalasia. Note the distorted appearance of the distal esophageal mucosa consistent with stasis esophagitis. Because of the associated atony and dilation of the esophageal body, water instillation allowed the endoscope to bypass the impaction and break up the food residue in small particles. Using the endoscope, the food particles were then pushed into the stomach and relieved the patient’s dysphagia.
7. Fig. 20.7 Management of esophageal foreign body impaction.
Chapter 21
1. Fig. 21.1 Gastrografin swallow showing leakage of contrast outside the esophagus.
2. Fig. 21.2 Patient presenting with a perforation due to Boerhaave’s syndrome (a). A fully covered Wallflex stent was placed (b), which was extending just below the gastroesophageal junction (c).
Chapter 22
1. Fig. 22.1 Algorithm for acute gastrointestinal bleeding. SRH, stigmata of recent haemorrhage; PPI, proton pump inhibitors.
Chapter 23
1. Fig. 23.1 ERCP of pancreatic ductal system in pancreas divisum. The upper duct (dorsal pancreas) was obtained by injecting contrast into the duct of Santorini. The lower duct (ventral pancreas) was obtained by injecting the duct of Wirsung.
2. Fig. 23.2 Proposed algorithm for evaluation of patients with idiopathic pancreatitis.
3. Fig. 23.3 Computed tomography scan of a patient with a large pancreatic pseudocyst.
4. Fig. 23.4 Contrast-enhanced CT scans demonstrating interstitial pancreatitis (a) and necrotizing pancreatitis (b).
5. Fig. 23.5 Algorithm for management of acute pancreatitis.
Chapter 25
1. Fig. 25.1 Placement of Sengstaken–Blakemore balloon tube for esophageal variceal bleeding (left), Linton–Nachlas balloon tube for variceal bleeding from the cardia and fundus (right).
Chapter 26
1. Fig. 26.1 Definitions of acute liver failure.
Chapter 27
1. Fig. 27.1 Treatment modalities for patients with ascites and cirrhosis.
Chapter 29
1. Fig. 29.1 Algorithm for management of a colonic perforation.
Chapter 31
1. Fig. 31.1 Algorithm for the management of RIF pain and suspected appendicitis. RIF = right iliac fossa, CT = computerized tomography scan, USS = ultrasound scan.
Chapter 32
1. Fig. 32.1 Deep enteroscopy images. (a) Duodenal ulcer with a visible vessel. (b) Duodenal ulcer with visible vessel after endoscopic clipping. (c) Same under NBI. (d) Jejunal tumor.
2. Fig. 32.2 Capsule endoscopy images. (a) Intestinal AVM. (b) Meckel’s diverticulum opening. (c) Duodenal ulcer with bleeding visible vessel. (d) NSAID enteropathy with a visible clot. (e) Bleeding ileal tumor. (f) Active gastric bleeding in a patient with portal hypertensive gastropathy.
3. Fig. 32.3 Overt obscure gastrointestinal bleeding algorithm.
4. Fig. 32.4 Occult obscure gastrointestinal bleeding with significant anemia algorithm.
Chapter 34
1. Fig. 34.1 Scandinavian randomized controlled trial of infliximab in acute severe ulcerative colitis.
2. Fig. 34.2 90 day colectomy rate in infliximab arm compared to placebo arm in IV steroid refractory ulcerative colitis.
3. Fig. 34.3 Ciclosporin versus infliximab study (CYSIF) – primary efficacy endpoint of treatment failure at day 98.
4. Fig. 34.4 Endoscopic appearance of severe colitis despite treatment with infliximab for 7 days. The patient underwent colectomy.
5. Fig. 34.5 A management algorithm for short-term management of acute severe colitis.
Chapter 36
1. Fig. 36.1 Diverticulosis of the colon.
2. Fig. 36.2 Active diverticular bleed.

Notes on contributors

Seiichiro Abe
National Cancer Center Hospital, Tokyo, Japan

Aijaz Ahmed MD
Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA, USA

Patrick B. Allen MB, FRCP, BSc
Consultant Gastroenterologist, Ulster Hospital, Belfast, Northern Ireland, UK

Constantinos P. Anastassiades MBBS (Lond), FACP
Consultant, Division of Gastroenterology & Hepatology, Khoo Teck Puat Hospital, Singapore
Adj. Assistant Professor of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA

Stephen Attwood MCh, FRCS, FRCSI
Consultant Upper GI and Laparoscopic Surgeon, Honorary Professor, Durham University, Durham, UK

Andrés Cárdenas MD, MMSc, PhD, AGAF
Faculty Member/Senior Specialist, GI Unit, Institute of Digestive Diseases, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain

David L. Carr-Locke MB, Bchir, FRCP, FASGE
Chief, Division of Digestive Diseases, Associate Chair of Medicine, Mount Sinai Beth Israel Medical Center, New York, USA
Professor, Icahn School of Medicine, New York, USA

W. Johnny Cash MD, FRCP
Consultant Hepatologist, Royal Victoria Hospital, Belfast, Northern Ireland, UK

John S. A. Collins MD
Associate Postgraduate Dean, Northern Ireland Medical and Dental Training Agency
Formerly Consultant Gastroenterologist, Royal Victoria Hospital, Belfast, Northern Ireland, UK

Wallace Dinsmore MD, FRCP, FRCPI, FRCPEd
Professor of Medicine, Department of GU Medicine, Royal Victoria Hospital, Belfast, UK

Shai Friedland MD
Assistant Professor, Stanford University School of Medicine and VA Palo Alto, Stanford, CA, USA

Subrata Ghosh MD, FRCP, FRCPE, FRCPC, FCAHS
Professor of Medicine, Microbiology & Immunology, University of Calgary, Alberta, Canada

Pere Ginès MD, PhD
Chief of Hepatology, Liver Unit, Institute of Digestive Diseases Hospital Clinic, IDIBAPS, Professor of Medicine, University of Barcelona, Spain

Isabel Graupera
Institut de Malalties Digestives i Metabolisme, Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain

Philip S. J. Hall MRCP, MB, BCh
Specialty registrar in Gastroenterology, Gastroenterology training program, Altnagelvin Hospital, Londonderry, Northern Ireland, UK

Paul Kevin Hamilton BSc (Hons), MD, FRCPE
Specialty Registrar, Department of Clinical Biochemistry; Formerly Consultant Physician and Clinical Pharmacologist; Belfast Health and Social Care Trust, Belfast, Northern Ireland, UK

Brian J. Hogan
Specialty Registrar, Sheila Sherlock Liver Centre, Royal Free London NHS Foundation Trust, Royal Free Hospital, London, UK

Marietta Iacucci MD, PhD
Clinical Associate Professor of Medicine Division of Gastroenterology, University of Calgary, Alberta, Canada

Tonya Kaltenbach MD, MS
Veterans Affairs Palo Alto Health Care System, Clinical Assistant Professor of Medicine (Affiliated), Stanford University, Palo Alto, CA, USA

Joseph K. N. Kim
Icahn School of Medicine, New York, USA

Jennifer M. Kolb MD
Icahn School of Medicine at Mount Sinai, Internal Medicine, New York, NY, USA

Bee Chan Lee MB, MRCP
Consultant Gastroenterologist, Warwick Hospital, Warwicks, England, UK

David R. Lichtenstein MD
Director of Endsocopy & Associate Professor of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, MA, USA

Ian McAllister MD
Consultant Surgeon, Ulster Hospital, Dundonald, Belfast, Northern Ireland, UK

Daniel F. McAuley
Professor and Consultant in Intensive Care Medicine, Royal Victoria Hospital and Queen’s University of Belfast, Belfast, Northern Ireland, UK

Kevin McCallion
Consultant Surgeon, Ulster Hospital, Dundonald, Belfast, Northern Ireland, UK

Emma McCarty
Consultant in Genitourinary Medicine, Royal Victoria Hospital, Belfast, Northern Ireland, UK

James J. McNamee FCARCSI, FRCA, FCICM, FFICM
Consultant in Intensive Care Medicine, Royal Victoria Hospital, Belfast, Northern Ireland, UK

Graham Morrison MB, MRCP
Consultant Gastroenterologist, Altnagelvin Hospital, Londonderry, Northern Ireland, UK

Ichiro Oda MDNational Cancer Center Hospital, Tokyo, Japan

Khalid Osman FRCS
North Tyneside General Hospital, Tyne & Wear, UK

Kelvin Palmer FRCP(Edin)
Formerly Consultant Gastroenterologist, Western General Hospital, Edinburgh, UK

Ioannis S. Papanikolaou
Department of Internal Medicine and Research Unit, “Attikon” University General Hospital, University of Athens, Greece

David W.M. Patch MBBS, FRCP
Consultant Hepatologist, Department of Hepatology, Royal Free Hospital, London, UK

Ryan B. Perumpail MD
Stanford Hospital and Clinics, Stanford, CA, USA

Aarti K. Rao MD
Resident Physician, Department of Internal Medicine, Stanford University; Department of Gastroenterology, Veterans Affairs Palo Alto Health Care System, CA, USA

Michele B. Ryan
Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

Andres Sanchez-Yague MD, PhD
Chief, Gastroenterology Unit, Vithas Xanit International Hospital, Benalmadena, Spain
Consultant, Gastroenterology Unit, Hospital Costa del Sol, Marbella, Spain

Allison R. Schulman
Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

Reza Shaker MD, FACP
Professor and Chief, Division of Gastroenterology and Hepatology; Director, Digestive Disease Center, Medical College of Wisconsin, Milwaukee, WI, USA

Peter D. Siersema MD, PhD
Professor of Gastroenterology and Chief, Department of Gastroenterology and Hepatology, University Medical Center, Utrecht, The Netherlands

Maria Cecilia M. Sison-Oh
Medical Center Manila, Manila, Philippines

Roy Soetikno MD, MS (Health Service Research)
Chief, GI Section, Veterans Affairs Palo Alto Health Care System, Palo Alto
Associate Professor, Stanford University, Stanford, CA, USA

Daniel J. Stein MD
Assistant Professor of Medicine, Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, WI, USA

Matthias Steverlynck
Centre Hospitalier de Mouscron, Belgium

Haruhisa Suzuki
National Cancer Center Hospital, Tokyo, Japan

Tony C. K. Tham MD, FRCP, FRCPI
Consultant Gastroenterologist, Dundonald, Ulster Hospital, Belfast, Northern Ireland, UK

Christopher C. Thompson
Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

Philip Toner MRCP
Specialty Registrar, Department of General Medicine, Belfast Health and Social Care Trust, Belfast City Hospital, Belfast, UK

George Triadafilopoulos MD, DSc
Clinical Professor of Medicine, Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA, USA

Jo Vandervoort MD
Department of Gastroenterology, Onze-Lieve-Vrouw Ziekenhuis, Aalst, Belgium

Barbara Willandt
KU Leuven, Netherlands

Richard C. K. Wong BSc, MBBS(Lond), FASGE, FACG, AGAF, FACP
Professor of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH, USA
Medical Director, DHI Endoscopy Unit, University Hospitals Case Medical Center, Cleveland, OH, USA

Robert J. Wong MD, MS
Stanford University School of Medicine, Stanford, CA, USA

CHAPTER 1
Approach to dysphagia

John S. A. Collins

Northern Ireland Medical and Dental Training Agency, Royal Victoria Hospital, Belfast, UK

Definitions

Dysphagia refers to a subjective sensation of the obstruction of swallowed solids or liquids from mouth to stomach. Patients most frequently complain that food “sticks” in the retrosternal area or simply will “not go down.” Patients may complain of a feeling of choking and chest discomfort. In some cases food material is rapidly regurgitated to relieve symptoms.

Dysphagia can be divided into two types:

oropharyngeal dysphagia, where there is an inability to initiate the swallowing process and may involve disorders of striated muscle. There may be a sensation of solids or liquids left in the pharynx.
esophageal dysphagia, which involves disorders of the smooth muscle of the esophagus and results in symptoms within seconds of the Initiation of swallowing.

Odynophagia is the sensation of pain on swallowing which is usually felt in the chest or throat. Globus is the sensation of a lump, fullness or tightness in the throat.

Differential diagnosis

The causes of the above types of dysphagia are shown in Tables 1.1 and 1.2.

Table 1.1 Etiology of oropharyngeal dysphagia.

Neurological disorders
Cerebrovascular disease
Amyotrophic lateral sclerosis
Parkinson’s disease
Multiple sclerosis
Bulbar poliomyelitis
Wilson’s disease
Cranial nerve injury
Brainstem tumors

Striated muscle disorders
Polymyositis
Dermatomyositis
Muscular dystrophies
Myasthenia gravis

Structural lesions
Inflammatory – pharyngitis, tonsillar abscess
Head and neck tumors
Congenital webs
Plummer–Vinson syndrome
Cervical osteophytes

Surgical procedures to the oropharynx
Pharyngeal pouch (Zenker diverticulum)
Cricopharyngeal bar

Metabolic disorders
Hypothyroidism
Hyperthyroidism
Steroid myopathy

Table 1.2 Etiology of esophageal dyphagia.

Neuromuscular/dysmotility disorders
Achalasia
CRST syndrome
Diffuse esophageal spasm
Nutcracker esophagus
Hypertensive lower esophageal shincter
Nonspecific esophageal dysmotility
Chaga disease
Mixed connective tissue disease

Mechanical strictures – intrinsic
Peptic related to GERD
Carcinoma
Esophageal webs
Esophageal diverticula
Lower esophageal ring (Schatzki)
Benign tumors
Foreign bodies
Acute esophageal mucosal infections
Pemphigus/pemphigoid
Crohn’s disease

Mechanical lesions – extrinsic
Bronchial carcinoma
Mediastinal nodes
Vascular compression
Mediastinal tumors
Cervical osteoarthritis/spondylosis

History and examination

Acute dysphagia is a relatively uncommon, but dramatic, presenting symptom and constitutes a gastrointestinal emergency. The patient will complain of difficulty initiating swallowing or state that food is readily swallowed but results in the rapid onset of chest discomfort or pain, which is only relieved by passage or regurgitation of the swallowed food bolus. The latter sensation can result after swallowing a mouthful of liquid. In the acute case it is important to ask the patient about the presence of other neurological symptoms.

If oropharyngeal dysphagia is suspected, the following points are important:

The patient may complain of nasal regurgitation of liquid, coughing or choking during swallowing or a change in voice character which may indicate nasal speech due to palatal weakness.
Patients may describe repeated attempts at the initiation of swallowing.
Symptoms are noticed within a second of swallowing.
Patients with cerebrovascular disease may give a history of symptoms of transient ischemic attacks (TIA) – these would include visual disturbance, dysphasia, or transient facial or limb weakness.
There may be progressive muscular weakness and dysphagia is only part of the symptom complex, in contrast to esophageal dysphagia where swallowing disorder is the most prominent symptom.
Patients should have a careful neurological examination and evaluation of the pharynx and larynx including direct laryngoscopy.
In cases of esophageal dysphagia, the following points are important:
Is the sensation of dysphagia worse with liquids or solids? If a progressive obstructive lesion is the cause of symptoms, the patient will notice difficulty swallowing solids initially and liquids later. Difficulty with both solids and liquids suggests dysmotility.
Is the dysphagia intermittent or progressive? Intermittent dysphagia may indicate a motility disorder such as diffuse esophageal spasm whereas a progressive course is more characteristic of an esophageal tumor.
How long have symptoms been present? A long history usually greater than 12 months suggests a benign cause, whereas a short history less than 4 weeks suggests a malignant etiology.
Has the patient a history of heartburn suggesting gastroesophageal reflux disease (GERD)? While a history of heartburn does not rule out gastroesophageal cancer as a cause of dysphagia, a long history in the presence of slow onset, non-progressive symptoms may point to a benign peptic stricture as the cause.

A diagnostic algorithm for the symptomatic assessment of the patient with dysphagia is shown in Fig. 1.1.

Diagnostic algorithm for the symptomatic assessment of a patient with dysphagia that may lead to lower esophageal ring, peptic stricture, carcinoma, diffuse esophageal spasm, scleroderma, and achalasia. — **Fig. 1.1** Diagnostic algorithm for the symptomatic assessment of the patient with dysphagia.
Source: Yamada 1995. Reproduced with permission of Wiley.

The etiology of esophageal dysphagia is summarized in Table 1.2.

While acute dysphagia may be painful, especially in relation to foreign body or food bolus impaction above an existing stricture, a history of odynophagia usually suggests an inflammatory condition or disruption of the esophageal mucosa leading to the irritation of pain receptors. The causes of odynophagia are:

Candida
herpes simplex
cytomegalovirus
pill-induced ulceration
reflux disease/stricture
radiation esophagitis
caustic injury
motility disorders stimulated by swallowing
cancer
graft-versus-host disease
foreign body.

Clinical signs in patients who present with dysphagia are uncommon. On examination, the following signs should be noted:

loss of weight
signs of anemia
cervical lymphadenopathy
hoarseness
concomitant neurological especially bulbar signs
respiratory signs if history of cough/choking
hepatomegaly
oral ulcers or signs of Candida
goiter.

Investigation

Dysphagia is considered to be an “alarm symptom” and should be investigated as a matter of urgency in all cases. Upper gastrointestinal endoscopy is a safe investigation in experienced hands provided the intubation is carried out under direct visualization of the oropharynx and upper esophageal sphincter. The endoscopist should be alert to the possibility of a high obstruction and the likelihood of retained food debris or saliva if dysphagia has been present for some time. If there is a history of choking, the patient should have a liquid-only diet for 24 hours followed by a 12-hour fast prior to the procedure. In some cases, the careful passage of a nasoesophageal tube to aspirate retained luminal contents may be necessary. At endoscopy, obstructing lesions can be biopsied and peptic strictures can be dilated with a balloon or bougie.

The presence of a dilated food and saliva-filled esophagus in the absence of a stricture raises the possibility of achalasia.

Barium studies are not a prerequisite for endoscopy but should be considered complementary in dysphagia. Barium swallow may give additional information in the following situations:

in cases of suspected oropharyngeal dysphagia, especially if videofluoroscopy is employed;
where a high esophageal obstruction is suspected prior to endoscopy;
where a motility disorder is suspected as a method to assess lower esophageal relaxation.

In some cases, a barium swallow may be a useful investigation in certain circumstances:

Where there is suspected proximal obstruction, e.g. laryngeal cancer, Zenker's diverticulum;
Following a negative endoscopy or obstructive symptoms as lower esophageal rings may be more easily detected at fluoroscopy.

Esophageal manometry is indicated if both endoscopy and barium studies are inconclusive in the presence of persistent symptoms. Manometry requires intubation of the esophagus with a multilumen recording catheter attached to a polygraph. Pressure changes are recorded during water bolus swallows along the esophageal body and at the upper and lower esophageal sphincters.

Management of dysphagia

The management of dysphagia depends on the underlying cause. In a patient presenting with total dysphagia who is unable to swallow even small amounts of liquid or saliva, urgent treatment is indicated (Fig. 1.2).

Total dysphagia management algorithm: Admit the patient to a hospital for IV fluids and nil by mouth and urgent barium meal-lurgent EGD to determine if esophageal stricture (dilatation) or foreign body impaction. — **Fig. 1.2** Approach to management of total dysphagia.

The management of oropharyngeal dysphagia can be treated by control of the underlying neurological or metabolic disorder. Dietary modification under the supervision of a speech and language therapist may maintain oral swallowing and avoid gastrostomy tube placement in patients with stroke and pseudobulbar or bulbar palsy. Gastrostomy tube placement may be the only management option in patients with inoperable mouth or throat tumors, or in cases where recurrent pulmonary aspiration is life threatening.

Peptic stricture

When the endoscopic appearances are characteristic of a benign peptic stricture, dilatation can usually be carried out at the time of the procedure using either wire-guided bougies or a balloon. If the stricture is complex, very tight or associated with esophageal scarring, it may be safer to carry out wire-guided dilatation using graded bougies. The majority of patients will gain symptomatic relief and the risk of complications is low (see Chapter 21, Esophageal Perforation).

It is essential that all patients are treated with an adequate dose of a proton pump inhibitor to prevent recurrence. Repeat dilatations are necessary in some cases and repeat inspection and biopsy is advised if there is any concern about mucosal dysplasia or malignancy.

Esophageal carcinoma

Suspected carcinoma, which is detected at endoscopy, requires biopsy confirmation and subsequent staging so that a management plan can be formulated. The most accurate modality for staging is endoscopic ultrasound which can assess depth of local invasion and regional lymph node status. Chest and abdominal computerized tomography (CT) is a less accurate technique but CT/positron emission tomography (PET) scanning enhances staging accuracy, especially in adenocarcinomas.

Surgery offers the only chance of cure but only 30% of tumors are resectable and 5-year survival is 10% in European studies. Contraindications to surgery include invasion of vascular structures, metastatic disease and patients with comorbidity and high operative risk.

Palliative management will be indicated in 70% of patients following staging. Esophageal dilatation, followed by the endoscopic placement of a metal stent, gives adequate swallowing relief in the majority of cases. In situations where there is complete obstruction of the esophageal lumen by tumor, endoscopic laser therapy can provide adequate palliation of dysphagia. The prognosis is poor with a mean survival of 10 months after diagnosis with a 5-year survival of 5%. Where surgical resection is completed after staging and selection, 5-year survival can be up to 25%.

Radiation injury

Following radiotherapy to the thorax or head and neck, some patients develop esophagitis, which may progress to stricturing and fibrosis. The diagnosis is confirmed by endoscopy and biopsy. Treatment consists of balloon or bougie dilatation and may have to be repeated in severe cases.

Esophageal webs and rings

Both of these esophageal lesions can result in dysphagia or lead to food bolus impaction. Webs are typically composed of thin mucosal tissue covered with squamous epithelium. They tend to occur proximally in the upper cervical esophagus and may be missed or ruptured at endoscopy, which is both diagnostic and therapeutic in these cases. They have been associated with chronic iron deficiency anemia. Rings are mucosal circular structures associated with dysmotility and seen at the esophagogastric junction. A Schatzki ring is a solitary thin rim of mucosa usually seen in the distended lower oesophagus. They are usually treated by dilatation and may be recurrent.

Food bolus impaction

See Chapter 20, Foreign Body Impaction in the Esophagus.

Eosinophilic esophagitis

This is an increasingly recognized cause of dysphagia and is diagnosed by characteristic endoscopic appearances and the finding of a dense eosinophilic infiltrate in esophageal mucosal biopsies (>15 per high power field). Dilatation is rarely required and the condition responds to low-dose swallowed topical steroids, administered by a metered inhaler.

Gastrointestinal Emergencies

THIRD EDITION