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Endoscopy Practice and Safety

Editor: Peter B. Cotton


9. Pathology

David N. Lewin

Fig. 1 Histological sections of well-oriented biopsies from various areas of the gastrointestinal tract. All reveal mucosa to the muscularis mucosa (at the lower portion of the photomicrograph). (A) Esophageal (squamous mucosa). (B) Gastric fundic (or oxyntic) type mucosa with a central parietal (pink cells) zone. (C) Gastric antral type mucosa with the basal mucous gland. (D) Small bowel mucosa with finger-like villi; the gland-to-villus ratio should be at least 3:1. (E) Colon with a parallel 'test-tube' arrangement of the crypts.

Fig. 2 Histological sections of tangentially oriented normal mucosa from various areas of the gastrointestinal tract. (A) Esophageal (squamous mucosa) with relative increased amount of basal cells (center) due to orientation. (B) Gastric fundic (or oxyntic) type mucosa with increased amount of foveolar tissue due to poor orientation. (C) Small bowel mucosa in which it is very difficult to assess the villus-to-crypt ratio. (D) Colonic mucosa with loss of the 'test-tube' arrangement and instead numerous small cross-sections of each crypt.

Fig. 3 Slide view of serial sections of four well-oriented biopsies in parallel.

Fig. 4 Slide view of numerous (greater than 10) biopsies placed in a single container. A few of the biopsies are of reasonable size; however, some are not well represented.

Fig. 5 Section of colonic tissue with central fold (irregular dark line through the center of the biopsy). This artifact, if pronounced, can make areas of the biopsy impossible to evaluate.

Fig. 6 Medium-power view of a tubular adenoma with a subtle shattering of the tissue. This is caused in the histology laboratory by a dull microtome blade and causes linear lines through the tissue. This can cause interpretation problems.

Fig. 7 Slide view of a single well-oriented biopsy with multiple ribbons (sections) of the tissue on a single slide. This allows the pathologist to follow suspicious areas through the depth of the tissue. This can be especially important when trying to identify granulomas for the diagnosis of Crohn's disease.

Fig. 8 Crush artifact: a medium-power view of the edge of a duodenal biopsy with a carcinoid tumor. Crush is present in virtually all biopsies to some degree. Lymphocytes and endocrine cells (as in this biopsy) are often most affected by the crush. The cells lose their usual rounded appearance and become dark, elongated, and uninterpretable.

Fig. 9 Burn/cautery artifact: a medium-power view of a colonic biopsy with moderate cautery artifact. The cells and nuclei elongate and the architecture of the lesion is distorted. Architecturally this polyp appears to be a hyperplastic polyp; however, differentiation from a tubular adenoma or serrated adenoma due to the nuclear enlargement is impossible.

Fig. 10 Burn/cautery artifact: a high-power view of a colonic polyp to illustrate the elongation of the nuclei. The artifact gives the suggestion of dysplastic nuclei; however, it is unclear if this represents an adenoma or not.

Fig. 11 Low-power view of a polypectomy specimen. The adenoma and focal invasive carcinoma are present in the tip at the lower right portion of the specimen. The stalk is covered by normal colonic mucosa and has a loose (pale) fibrovascular core. The margin is present at the other end.

Fig. 12 Low-power view of an endoscopic mucosal resection of a granular cell tumor of the esophagus. The surface (top of picture) is covered with squamous mucosa. There is a pink cellular lesion (granular cell tumor) in the center and the deep portion represents the cauterized submucosal margin.

Fig. 13 High-power view of an EMR of a granular cell tumor. The deep surgical margin (inferior portion of picture) has been inked with black ink. There is an adjacent artery. The tumor is in the top right hand portion of the image.

Fig. 14 Medium-power view of a villous adenoma of the colon. The routine stain used in pathology is the hematoxylin and eosin (H&E) stain. The nuclei stain blue with the hematoxylin and the cytoplasm has a pink (eosinophilic) appearance with the eosin.

Fig. 15 Slide view of a smear using a brush from a pancreatic duct brushing. The brush was smeared onto the slide, depositing cells, the slide fixed in alcohol and stained with a Pap stain.

Fig. 16 Slide view of a smear made from a fine-needle aspiration. A drop of material was placed at the top of the slide and smeared with a second slide to spread the cells. The material was allowed to air dry and stained with Romanovsky stain.

Fig. 17 Slide view of a ThinPrep. The material is placed into a fixative and transported to the lab. The ThinPrep machine creates a monolayer of cells on a slide that are then stained with Pap stain.

Fig. 18 Medium-power view of Pap-stained slide. Image of a cluster of normal glandular epithelial cells. Similar to a H&E-stained histology slide, the nuclei are stained blue (from hematoxylin). There are three cytoplasmic stains: light green (which stains the majority of the cytoplasm in this image), eosin (a pink stain), and orange G.

Fig. 19 High-power image of a Romanovsky (metachromatic stain). These slides are allowed to air dry with subsequent enlargement of the cells' cytoplasm and nuclei.

Fig. 20 High-power view of an air-drying artifact in a Pap-stained slide. The nuclei breakdown and the nuclear contours become indistinct. There is irregularity to the cytoplasmic borders as well.

Fig. 21 Medium-power view of a cytological crush artifact. The cells can become spindled (as in this example) and may be mistaken as a sarcoma. The nuclei become elongate and, if crushed enough, can be uninterpretable.

Fig. 22 High-power view of Pap-stained slide with cells on top of one another. The three dimensional nature of this preparation makes it very difficult to evaluate the cytological features of each individual cell. The features are obscured by other cells on top of one another.

Fig. 23 Medium-power view of Romanovsky-stained cytology slide with displaced epithelium. Squamous cells (the large purple cells with centrally placed nuclei) are present in this aspirate from a lymph node. The squamous cells are picked up by the fine-needle aspiration through the esophagus lined by squamous epithelium. This is not a significant problem in this case; however, aspirating a lymph node through a malignancy is very problematic, as one may pick up malignant cells going through a tumor and get a false positive lymph node.

Fig. 24 A medium-power view of an unsatisfactory smear (Romanovsky stain). In this case the thickness of the preparation makes it impossible to render a cytological diagnosis.

Fig. 25 A medium-power view (Pap stain) of a benign aspirate of a pancreas. There is a cohesive group of cells present in a 'honeycomb-like' arrangement of cells. The nuclei are relatively homogenous and small. The cells respect each others borders.

Fig. 26 A medium-power view (Pap stain) of a reactive aspirate of the pancreas. Pancreatic ductal epithelial cells are present. The nuclei are enlarged with single prominent nucleoli. These features are typically seen in inflammatory (reactive) conditions.

Fig. 27 A medium-power view (Pap stain) of an atypical smear of pancreatic ductal epithelial cells. The cells are clustered together; however, there is nuclear enlargement and elongation of the nuclei. This is not definitive for malignancy; however, these features are often seen in dysplasia and present in many malignant cases.

Fig. 28 A medium-power view (Pap stain) of a smear suspicious for malignancy. Two cell populations are present in this smear: the inferior aspect of the picture has normal epithelial cells with a nice homogenous appearance. In the superior cluster, the cells are larger. The nuclei are irregular and there is loss of the normal architecture. If this were all that were seen in a smear, the diagnosis of suspicious would be used. The majority of these lesions are malignant; however, there are typically too few diagnostic cells to feel comfortable with the diagnosis.

Fig. 29 A high-power view (Pap stain) of a malignant smear. The cells are enlarged. The nuclei are irregular with focal prominent nucleoli. There are nuclear contour irregularities and loss of the typical architecture. Necrotic individual cells are present as well.

Fig. 30 Summary of diagnostic features of malignancy.

Fig. 31 H&E images of reflux esophagitis. These are (A) low- and (B) medium-power images of the squamous mucosa in reflux esophagitis. There is basal cell hyperplasia (expansion of the basal proliferative zone) and elongation of the rete papilla of the squamous epithelium. In image B, a central eosinophil can be seen in the squamous mucosa.

Fig. 32 H&E image of eosinophilic esophagitis. There is some basal cell hyperplasia and elongation of the rete papilla (as seen in reflux esophagitis); however, in contrast there are numerous eosinophils (typically greater than 20 per high-power field) in the squamous mucosa.

Fig. 33 H&E image of marked elongation of the rete papilla (greater than 90% of the mucosal thickness) and basal cell hyperplasia.

Fig. 34 Low- and high-power H&E images of Barrett's esophagus. There is replacement of the normal squamous epithelial lining of the esophagus by a glandular mucosa (typically gastric type with the presence of goblet cells). (B) is a high-power view of intestinal metaplasia with numerous goblet cells.

Fig. 35 Combination Alcian blue at pH 2.5 and PAS stain on the same biopsy seen in Fig. 34. The goblet cells stain deep blue with the Alcian blue stain, while the gastric-type epithelium with neutral mucins stains pink with the PAS stain. (A) is a low-power view, while (B) is a high-power image.

Fig. 36 High-power images of candida in the esophagus. (A) An H&E stain. (B) A PAS stain. (C) A cytology specimen stained with Pap. All show, with varying degrees of clarity, squamous epithelial cells and candidal spores and hyphae (pink on H&E, purple on PAS, and red on Pap).

Fig. 37 Herpes esophagitis. (A) An H&E high-power view of the base of the epithelium adjacent to an ulcer. There are enlarged multinucleated cells (representing the intranuclear inclusions of the virus). (B) An immunohistochemical stain, with the herpes infected squamous cells staining brown.

Fig. 38 Cytomegalovirus esophagitis. (A) An H&E high-power view of the base of the ulcer. There are enlarged cells with single eosinophilic intranuclear inclusions (representing the intranuclear inclusions of the virus). (B) An immunohistochemical stain, with the CMV-infected endothelial cells staining brown.

Fig. 39 Invasive squamous cell carcinoma. (A) is a medium- and (B) a high-power H&E-stained slide. The lesion consists of infiltrating nests of tumor cells. The cells have intercellular bridges and focal keratinization, characteristic of squamous differentiation.

Fig. 40 Adenocarcinoma of the esophagus. Medium-power H&E section with overlying squamous mucosa and infiltration of the lamina propria and muscularis mucosa by a gland-forming tumor. The nests of tumor cells have enlarged hyperchromatic nuclei and irregular contours.

Fig. 41 Poorly differentiated tumor of the esophagus. Medium-power H&E section of a poorly differentiated malignancy of the esophagus. Immunohistochemical stains would be required to exclude sarcomas, lymphomas from carcinoma. No distinguishing elements (gland or mucin formation for an adenocarcinoma or keratinization for a squamous cell carcinoma) are present.

Fig. 42 Reactive gastropathy. Medium-power H&E section of gastric antral type mucosa. There is elongation of the foveolar (surface epithelium) with focal erosion and an inflammatory exudate. The inflammatory cells present are predominately neutrophils, with a relative paucity of lymphocytes (chronic inflammatory infiltrates).

Fig. 43 H. pylori-associated chronic active gastritis. (A) Medium-power H&E section with a superficial infiltrate of lymphocytes and plasma cells in the lamina propria (what was once called a superficial gastritis). (B) High-power H&E of the superficial foveolar epithelium to illustrate some Helicobacter organisms. (C) High-power Giemsa stain of Helicobacter organisms (staining blue). (D) High-power silver stain (Steiner stain) where the Helicobacter organisms are black. (E) High-power H&E revealing the infiltration of the gastric epithelium by neutrophils (acute or active gastritis). (F) Medium-power H&E revealing a lymphoid aggregate at the base of the epithelium, typical of Helicobacter infection.

Fig. 44 Medium-power PAS-stained section of an infiltrative signet ring carcinoma of the stomach. There is loss of the normal glandular architecture. Residual normal surface epithelium (staining pink at the top) is present and there is an infiltration of single malignant cells in the lamina propria. These cells are filled with mucin that stains pink with the PAS stain.

Fig. 45 Mucosal associate lymphoid tissue (MALT) lymphoma. H&E medium-power view with intense infiltration of the lamina propria by a lymphoid infiltrate (blue) with associated parietal gland (pink) loss on the right hand portion of the image.

Fig. 46 Stomach with granuloma: H&E medium-power view with two large epithelioid granulomas at the base of the mucosa, surrounded by a lymphoid aggregate in a Crohn's patient.

Fig. 47 Hyperplasic polyp: H&E low-power image of antral mucosa with surface erosion (top of image), foveolar hyperplasia, and glandular dilatation lined by mucinous cells.

Fig. 48 Fundic gland polyp. H&E low-power image of fundic-type mucosa with glandular dilatation lined by a mixture of parietal, chief, and mucinous cells.

Fig. 49 Gastric adenocarcinoma. H&E medium-power image of an adenocarcinoma of the stomach. There is an increased number of glands with enlarge nuclei and relatively little cytoplasm. The normal gastric glands are not present.

Fig. 50 Endocrine (carcinoid) tumor. H&E medium-power image with tumor comprised of nests and lobules of cells. Gland formation is not identified.

Fig. 51 Lymphoma. H&E medium-power image of a high-grade lymphoma. The cells are enlarged with prominent vesicular nuclei and prominent nucleoli. Numerous mitotic figures are present.

Fig. 52 Gastrointestinal stromal tumor. H&E medium-power image of a spindle cell neoplasm with numerous admixed lymphocytes. There is relatively little mitotic activity. Immunohistochemical stains are needed to subclassify this mesenchymal neoplasm. The primary prognostic factors are tumor size and mitotic activity.

Fig. 53 Normal small bowel mucosal biopsies. H&E medium-power image. (A) has the normal gland-to-villus ratio of 3:1, while (B) is a biopsy from the duodenal bulb with Brunner's glands and relative villous blunting, but no increased inflammatory infiltrate.

Fig. 54 Celiac sprue. This is a severe mucosal lesion with almost total villous atrophy ((A) medium-power H&E), an increased lymphoplasmacytic infiltrate in the lamina propria, and increased numbers of intraepithelial lymphocytes ((B) high-power H&E).

Fig. 55 Whipple's disease. There is a lamina propria infiltration by histiocytes. Focal fat (clear spaces) are present as well. (A) is a medium-power H&E, (B) a high-power H&E, and (C) a high-power PAS-stained section. The histiocytes are positive (pink) with the PAS stain.

Fig. 56 Mycobacterium avium–intracellulare (MAI). Similar to Whipple's disease, there is a significant infiltration of histiocytes in the lamina propria. These are filled with the organisms and can be identified on a modified acid fast stain (Fite). (A) medium-power H&E, (B) high-power H&E, and (C) high-power fite stain.

Fig. 57 Giardia. High-power H&E of small bowel mucosa. The organisms can be seen in the lumen adjacent to the surface epithelium. They are purple concave or pear shaped.

Fig. 58 Gastric metaplasia. (A) Medium-power H&E of duodenal mucosa with the typical goblet cells. In the center of the picture the surface epithelium has the foveolar epithelium typically seen in gastric mucosa (gastric surface metaplasia). (B) Low-power H&E of duodenal mucosa with gastric surface metaplasia and gastric fundic-type glands.

Fig. 59 Brunner's gland nodule. Low-power H&E image of surface duodenal mucosa and prominent submucosal Brunner's glands (endoscopically a nodular appearance).

Fig. 60 Adenoma. (A) Low-power H&E image of an adenomatous polyp. The lesion is blue from low power due to the enlargement and hyperchromasia of the epithelium (dysplasia). (B) Higher-power H&E of the dysplastic epithelium with enlargement and stratification of the nuclei typical of adenoma (dysplasia, low grade in this instance).

Fig. 61 Abnormal endoscopy and biopsy findings in 205 patients with diarrhea.

Fig. 62 Normal colonic mucosa, H&E stains. (A) Low-power image of the right side of the colon and left side of colon. (B) The architecture is similar with the crypts lined up as 'test tubes' in a rack. There is a difference in the inflammatory infiltrate, with more lymphocytes, plasma cells, and eosinophils typically present on the right side of the colon. (C) There is some mild architectural distortion adjacent to this normal lymphoid aggregate in the center of this biopsy.

Fig. 63 Collagenous colitis. (A) Low-power H&E view of a colonic biopsy in collagenous colitis. The architecture is similar to the normal mucosa (Fig. 62A) with crypts arranged parallel to one another and extending to the base of the biopsy. There is a mild increase in the lymphocytes in the lamina propria. A prominent acellular band is present below the surface epithelium. This 'collagenous' expansion of the basement membrane is the characteristic finding in collagenous colitis. (B) High-power H&E view of the thickened basement membrane. This basement membrane should be thicker than 15 µm (a normal lymphocyte is 7 µm, so at least the thickness of two lymphocyte nuclei). There are often entrapped lymphocytes and blood vessels in the collagen band. Additionally there are increased numbers of lymphocytes, eosinophils, and plasma cells in the lamina propria. There is focal epithelial detachment from the basement membrane and some epithelial apoptosis. (C) Medium-power trichrome stain of normal colonic epithelium. The blue strip below the epithelium is the normal basement membrane thickness. This is to be contrasted with (D), a trichrome stain in collagenous colitis that highlights the marked basement membrane thickening (blue) below the surface epithelium.

Fig. 64 Lymphocytic colitis. (A) Medium-power H&E view of lymphocytic colitis. Similar to normal and collagenous colitis, the architecture of the mucosa is intact, with parallel crypts that extend to the muscularis mucosa. There is an increased lymphocytic infiltrate in the lamina propria, no thickening of the basement membrane, and a characteristic increase in the number of intraepithelial lymphocytes (lymphocytes above the basement membrane and between the colonic epithelial cells). This increase in the number of intraepithelial lymphocytes is best identified in (B), a high-power H&E view of the mucosa. There should be greater than one lymphocyte per five epithelial cells.

Fig. 65 Crypt architectural changes in idiopathic inflammatory bowel disease. Medium-power H&E view of a biopsy from a patient with ulcerative colitis. The normal crypt architecture is disrupted. There is crypt branching. Some of the crypts are markedly expanded with the presence of neutrophils in the lumen (crypt abscess). A number of the crypts are foreshortened with the base of the crypt not extending all the way to the muscularis mucosa at the base of the biopsy. The surface of the biopsy has an undulating, almost villiform appearance, not the typical flat surface.

Fig. 66 Acute self-limited colitis (infectious colitis). A medium-power H&E view of colonic mucosa with an increase in the number of lamina propria inflammatory cells. The majority of inflammatory cells are in the upper half of the lamina propria (as opposed to the predominance of deep inflammatory cells in typical inflammatory bowel disease. There is no crypt architectural distortion.

Fig. 67 Crohn's disease. Medium-power H&E view of mucosa and superficial submucosa with an epithelioid granuloma, typical of that seen in Crohn's disease. The granuloma is seen in the middle of the image, at the base of the crypts. There is an increase in the number of inflammatory cells in the lamina propria and some crypt architectural distortion.

Fig. 68 Granuloma associated with a ruptured crypt. High-power H&E image of a ruptured crypt in the center of the image with an associated granuloma composed of epithelioid histiocytes. These lesions can be seen in both ulcerative colitis and Crohn's disease and are not the characteristic granuloma (Fig. 67) virtually diagnostic of Crohn's disease.

Fig. 69 Crohn's disease. Medium-power H&E view of colonic mucosa illustrating patchy microscopic inflammation typical of Crohn's disease. In addition to the gross patchiness present on endoscopic examination, microscopic patchiness is also present. There is a focus of inflammation on the left side of the image, while the right side of the image has a normal inflammatory component.

Fig. 70 Pseudomembranous colitis. Medium-power H&E view of colonic mucosa with pseudomembrane formation. There is a predominantly neutrophilic (acute) inflammatory infiltrate present in the biopsy. The pseudomembrane is present on the right upper portion of the image. There is a loss of the surface epithelium and the pseudomembrane is comprised of inflammatory cells and pink fibrin.

Fig. 71 Ischemic colitis. Medium-power H&E view of colonic mucosa in ischemia. There is surface erosion and a pseudomembrane present in the top right portion of the image. In contrast to Fig. 70, there is atrophy (loss) of the crypt glandular epithelium and the lamina propria has a pink hyalinized quality.

Fig. 72 Tubular adenoma. High-power H&E image of tubular adenoma. The top of the image has the adenomatous (dysplastic) epithelium and is to be compared with the normal colonic mucosa in the lower portion of the image. The dysplasia is characterized by a dark blue appearance to the tissue. This is secondary to the increased size of the nuclei, stratification of the nuclei, and a loss of pale mucin.

Fig. 73 Tubular adenoma. Low-power H&E image of tubular adenoma. The extreme left portion of the image contains normal colonic mucosa and the remainder of the darker glandular tissue is the (dysplastic) tubular adenoma. This image should be compared to Fig. 74, of a villous adenoma. The tubular adenoma is comprised of tubular forms of the dysplastic glands.

Fig. 74 Villous adenoma. Low-power H&E image of a dysplastic (adenomatous) epithelium with tall finger-like projections. The architecture is similar to the villi present in small bowel mucosa (Fig. 53), however, there are increased nuclear atypia and enlargement.

Fig. 75 Flat adenoma. Low-power H&E view of colonic mucosa with dysplastic epithelium. On the far right of the image there are a couple of normal crypts present. Unlike usual adenomatous polyps, there appears to be no protrusion of the dysplastic epithelium above the normal mucosa (the lesion appears flat, or even depressed).

Fig. 76 Hyperplastic polyp. Medium-power H&E view of a typical hyperplastic polyp. There is an increased number of epithelial cells, giving a serrated (saw-like) appearance to the surface epithelium and into the crypts. There is no increase in the nuclear size (no dysplasia).

Fig. 77 Serrated adenoma. Medium-power H&E view of a lesion that has the architecture of the hyperplastic polyp (Fig. 76), but nuclear atypia and hyperplasia (dysplasia) typically seen in a tubular adenoma (Fig. 72).

Fig. 78 Sessile serrated adenoma. Medium-power H&E view of a lesion with architecture of the hyperplastic polyp (Fig. 76), but more architectural distortion (dilatation of the basal glands and arrangement of the glands parallel to the muscularis propria). There should not be significant dysplasia (nuclear atypia) in contrast to a serrated adenoma (Fig. 77).

Fig. 79 Adenocarcinoma of the colon. Medium-power H&E view of a moderately differentiated invasive adenocarcinoma. The lesion is forming glands (best seen in the top of the image). At the base of the image, the glandular cells are infiltrating into the lamina propria. There is a characteristic desmoplastic response to the tumor, comprised of a fibroblastic response around the tumor cells.

Copyright © Blackwell Publishing, 2005

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  A (very) brief history of endoscopy
  Professionalism and quality
Synopsis
Introduction
Unit design
  Space planning
   Daily room volumes
   Procedure room size
   Preparation and recovery ratios
   Separate entrances
   Common space problems
  Physical infrastructure
  Intake and recovery areas
   Intake areas
   Managing clothes and valuables
   Recovery facilities
  Procedure room reprocessing and storage
   Standard procedure rooms
   Scope reprocessing and storage
   Patient flow issues
   Complex procedure rooms
   Storage of supplies and medications
   Travel carts for emergencies
Unit management
  Major areas of responsibility
  Staffing design
   Staffing emergencies
  Procedure schedules
   Relative time requirements
   Barriers to efficiency
  Purchasing
   Endoscopes
   How many endoscopes?
   Endoscope repair costs
   Databases
   Devices
  Endoscope reprocessing
  Coding and billing
  Accreditation
Outstanding issues and future trends
  Capsule endoscopy
  Colon screening technologies
  Endoscopy by non-specialists
  Growth of advanced endoscopy
Summary
References
Synopsis
Introduction
  Moderate sedation
  Deep sedation/analgesia
Advances in monitoring during sedation
  Standard pulse oximetry
  CO2 monitoring
   Transcutaneous CO2 monitoring
   Capnography
  BIS monitoring
Topical anesthetics: are they worth the effort?
Titration vs. bolus administration of sedation and analgesia
Propofol
  Problems with propofol
  Specific training for use of propofol
  Contraindications of propofol
  Clinical trials of propofol
   Propofol or midazolam?
   Upper endoscopy
   ERCP
   Upper endoscopy and colonoscopy
   Propofol with or without midazolam
   Patient-controlled administration of propofol
   Nurse-administered propofol
   Gastroenterologist-administered propofol
Droperidol
  Complications
Outstanding issues and future trends
References
Synopsis
Gastrointestinal endoscopes
  Endoscope design
   Control section
   Insertion tube
   Connector section
  Imaging
   Light source/processors
  Endoscope equipment compatibility
  Endoscope categories
   Esophagogastroduodenoscope (gastroscope)
   Enteroscope
   Duodenoscope
   Choledochoscope
   Echoendoscopes
   Colonoscope
   Sigmoidoscope
   Wireless capsule endoscopy
Gastrointestinal endoscopic accessories
  Tissue sampling
   Biopsy forceps
   Single-bite cold-biopsy forceps
   Biopsy cup jaws
   Multi-bite forceps
   Other specialty forceps
   Monopolar hot biopsy forceps
   Reusable vs. disposable biopsy
   Cytology brushes
   Needle aspiration
  Polypectomy snares
  Retrieval devices
  Injection devices
   Injection needles
   Spray catheters
   ERCP catheters
  Hemostatic and ablation devices
   Contact and non-contact thermal devices
   Heater probe
   Laser fibers
   Argon plasma beam coagulator
   Mechanical hemostatic devices
   Band ligation
   Metallic clip application via flexible endoscopes
   Marking with clips
   Detachable loops
  Transparent cap
  Dilation devices
   Push-type fixed-diameter dilators
   Hurst and Maloney dilators
   Savary-type dilators
   American Dilation System dilators
   TTS fixed diameter dilators
   Threaded-tip stent retrievers
   Radial expanding balloon dilators
   TTS dilators
  Achalasia balloon dilators
Conclusion
Outstanding issues and future trends
References
Synopsis
  Fiberoptic imaging
   Teaching attachments and photography
  Videoscopes
   Image capture
   Standardized image terminology
   Structured reporting
   The opportunities and challenges of the digital revolution
Digital imaging
  Imaging the gastrointestinal tract using a videoendoscope requires several steps
  Color models
   RGB
   CMYK
   HSB
Digitization of color
Color depth
Pixel density
File size
  What detail is needed?
  File compression
  Compression techniques
   Lossless compression
   Lossy compression
  Image file formats
  Color and black and white compression
  JPEG 2000 and beyond
DICOM standard
  Information Objects
   Patient name attributes
  DICOM conformance
  DICOM in endoscopy
  Expanding the scope of DICOM
How much compression is clinically acceptable?
  Studies of compression acceptability
   Vakil and Bourgeois
   Kim (personal communication)
  Developments in compression
Still pictures or live video?
  Video storage developments
What images should be recorded in practice?
  Lesion documentation
  Recording negative examinations
  Structured image documentation
  Costs of image documentation
Image enhancement
  Color manipulation
  Narrow band imaging and spectroscopy
Terminology standardization
  OMED standardized terminology
  Minimal standard terminology—MST
   Problems with MST
Outstanding issues and future trends
Acknowledgments
References
Editor's note
Introduction
Relevant thermal effects in biological tissues
  Thermal devitalization
  Thermal coagulation
  Thermal desiccation
  Thermal carbonization
  Thermal vaporization
Generation of temperature in thermal tissue
  Heater probe
  High-frequency surgery
   General principles of high-frequency electric devices
   Electric arcs
Principles of high-frequency surgical coagulation
  Monopolar coagulation instruments
  Electro-hydro-thermo probes
  Bipolar coagulation instruments
Principles of high-frequency surgical cutting with particular regard to polypectomy
Technical aspects of polypectomy
  Polypectomy snares
  The polypectomy snare handle
  Polypectomy snare catheters
Safety aspects of high-frequency surgery
Argon plasma coagulation
  The principle of argon plasma coagulation
  Equipment for argon plasma coagulation
  Safety aspects of argon plasma coagulation
Laser
  Principle of Nd:YAG laser
  Specific characteristics of Nd:YAG lasers in flexible endoscopy
Safety aspects of Nd:YAG laser in flexible endoscopy
Summary
References
Synopsis
Sterilization and disinfection
  Sterilization
  High-level disinfection
  What level of disinfection is required?
   Critical items
   Semi-critical items
  The practical problem
  Biocides
  The organisms
  The critical points in reprocessing
Risks of infections associated with endoscopic procedures
  Mechanisms of infection
  Clinical infections
   Infecting organisms
   Bacteria
   Vegetative bacteria
   Clostridium difficile
   Mycobacterium tuberculosis
   Atypical mycobacteria
   Serratia marcescens
   Helicobacter pylori
   Pseudomonas
   Viruses
   Human immunodeficiency virus (HIV)
   Hepatitis B
   Hepatitis C (HCV)
   Prions
   CJD
   What to do in practice about CJD?
   New variant CJD (vCJD)
   Other infections
  The endoscopic procedures
   Upper gastrointestinal endoscopy
   Lower gastrointestinal endoscopy
   Endoscopic retrograde cholangiopancreatography
   Percutaneous endoscopic gastrostomy
   Endoscopic ultrasound
   Mucosectomy
  Host factors
   Immune competence
   The degree of tissue damage
   Intrinsic sources of infection
   Damaged valves and implants
Antibiotic prophylaxis for endoscopic procedures
  Principles of prevention of bacterial endocarditis
  High risk cardiovascular conditions [43]
  Moderate risk cardiovascular conditions [43]
  Recommendations for antibiotic prophylaxis
   Who should receive antibiotics?
   Clinical problems where opinions diverge
   What antibiotic regimen?
Antibiotic prophylaxis for ERCP
  Prophylactic antibiotic regimens for ERCP
Principles of effective decontamination protocols
  Cleaning is essential
  Effectiveness of recommended protocols
  Endoscope structure
   Common features
   External features
   Common internal features
   Special internal features
   Cleaning equipment
   Cleaning fluids
   Rinsing
   Disinfectants
   Soaking time
   General maintenance
   Lubrication
  Recommendations
   Work areas
Reprocessing regimens
  Disinfect before and after procedures
  Manual cleaning
  Manual disinfection
  At the end of the list
  Endoscopic accessory equipment
   Cleaning accessories
   Disinfection
   Special accessory items
   Sclerotherapy needles
   Water bottles and connectors
   Dilators
Problem areas in endoscope reprocessing
  Rinsing water
   Poor quality water
   Infections from rinsing water
   Bacteria free water
   Water testing
   Recommendations for rinsing water
Variation in cleaning and disinfection regimens depending upon the supposed infective status of the patient
Compliance with cleaning and disinfection protocols
The investigation of possible endoscopy infection transmission incidents
  Common causes
  Golden rules for investigating potential infection incidents
  The investigation process
  Transmission of viral disease
Automatic flexible endoscope reprocessors (AFERs)
  Machine design and principles
   Contamination
   Water supply
   Alarm function
   Self-sterilization
   Fume containment
   Disinfectant supply
   Reprocessing time
   AFERs cannot guarantee to sterilize endoscopes
   Cost
   Plumbing pathway
   Rinse and dry cycle
   Regular bacteriological surveillance
Quality control in endoscope reprocessing
  Quality control measures
Microbiological surveillance in endoscopy
  Duodenoscopes
  Bronchoscopes
  Recommendations
  Testing procedures
  Interpretation of cultures
  Microbiological surveillance of AFERs
Outstanding issues and future trends
References
Synopsis
Introduction
The contract with the patient; informed consent
  Responsibility
  Educational materials
  Humanity
What are 'risks' and 'complications'?
  Definitions
  Threshold for 'a complication'
  Severity
  Attribution
  Timing of unplanned events
  Direct and indirect events
  Data set for unplanned events
General issues of causation and management
  Technical and cognitive performance
  Fitness for procedures
   ASA score
   Other risk indices
  Prompt recognition and management
   Communication
   Distress
   Document
   Act promptly
  Specific unplanned events
   Failure to diagnose
   Perforation
   Risk factors
   Recognition
   Treatment
   Bleeding
   Risk factors
   Recognition
   Treatment
   Cardiopulmonary and sedation complications
   Infection
   Endocarditis
   Infections
   Instrumentation
   Allergic reactions
   IV site issues
   Miscellaneous and rare events
Preventing unplanned events
Outstanding issues and future trends
References
Synopsis
Introduction
Gastroenterologist–pathologist communication
  Endoscopist communication responsibility
  Pathologist communication responsibility
  Question-orientated approach
  Common terminology
Endoscopic biopsy specimens
  Specimen handling and interpretation issues
   Orientation
   Fixation
   Number of biopsies per container
   Tissue processing
   Prep-induced artifact
   Endoscopy-induced artifacts
   Biopsy-induced artifacts
   Crush artifact
   Burn/cautery artifact
   Polypectomy
   Endoscopic mucosal resection
   Core biopsy
  Regular stains
Exfoliative and fine-needle cytology
  Specimen handling; staining and fixation
   Artifacts
   Cytological diagnosis
  Fine-needle aspiration
Organ system overview
  Esophagus
   Where and when to biopsy
   Gastroesophageal reflux disease
   Barrett's esophagus
   Infective esophagitis
   Candida
   Herpes simplex virus
   Cytomegalovirus
   Adenocarcinoma and squamous cell carcinoma
  Stomach
   Where and when to biopsy
   Inflammatory conditions; gastritis
   NSAIDS
   H.pylori gastritis
   Hypertrophic folds
   Polyps
   Mass lesions
  Small bowel
   Celiac sprue
   Infective enteropathies
   Whipple's disease
   Mycobacterium avium–intracellulare
   Giardia lamblia
   Polyps
   Mass lesions
  Colon
   Defining 'normal'
   Inflammatory colitides
   Normal colonoscopy
   Abnormal colonoscopy
   Inflammatory bowel disease
   Pseudomembranous colitis
   Ischemic colitis
   Polyps
   Adenomatous
   Hyperplastic
   Mass lesions
 
Special stains
  Histochemical stains
  Immunohistochemical stains
  In situ hybridization
  Flow cytometry
  Electron microscopy
  Cytogenetics
  Molecular pathology
Outstanding issues and future trends
References
Synopsis
Introduction
The endoscopy facility and personnel
  Endoscopy facility
  Equipment
   Endoscopes
   Endoscopy instruments
   Ancillary equipment
  Personnel
   The endoscopist
   Nursing and ancillary personnel
The pediatric patient and procedural preparation
  Patient preparation
   Psychological preparation
   Medical preparation
   Recommendations for fasting
   Bowel preparation
   Antibiotic prophylaxis
  Informed consent
Endoscopic procedures currently performed in pediatric patients
  Indications and limitations
  Patient sedation
  Endoscopic technique
   Esophagogastroduodenoscopy
   Colonoscopy
   Sigmoidoscopy
   Therapeutic endoscopy
   Other endoscopic modalities
   Small bowel enteroscopy
   Wireless capsule endoscopy
   Endoscopic ultrasonography
   Endoscopic retrograde cholangiopancreatography (ERCP)
Selected gastrointestinal pathologies in pediatric patients
  Eosinophilic esophagitis
  Food allergic enteropathy and colitis
  Foreign body ingestion
  Helicobacter pylori gastritis
  Polyps in the pediatric patient
  Lymphonodular hyperplasia
Outstanding issues and future directions
References
Synopsis
General principles of endoscopy training
  Traditional standard means of instruction
   Teachers
   Environment
   Is self-teaching still acceptable?
  What to teach and how to teach it
  Defining competency and how to access it
   Linking diagnosis and therapy
   How competent?
   Varying rates of learning
   Outcomes
   Learning beyond the training period
Training and competency in specific endoscopic procedures
  Esophagogastroduodenoscopy (EGD)
   Published guidelines for training in EGD
   Defining competence for EGD
   Data on acquisition of competency in diagnostic EGD
   Competency and EGD outcome
  Therapeutic EGD techniques
   Standard upper GI endoscopy techniques
   Hemostasis techniques
   Simulation
   Bleeding team
   Retaining competence
   Other specialized therapeutic upper GI endoscopy techniques
  Flexible sigmoidoscopy
   Published guidelines for training in flexible sigmoidoscopy
  Colonoscopy
   Published guidelines for training in colonoscopy
   Defining competence for colonoscopy
   Technical components
   Cognitive objectives
   Minimum training requirements to achieve competency for colonoscopy
   The Cass study
   Conclusion
   Competency and colonoscopy outcome
   Acceptable outcomes
   Non-gastroenterologists
   Rate of skills acquisition for colonoscopy
   Cases per week
   Too many cases?
  Therapeutic colonoscopy (biopsy, polypectomy, hemostasis techniques, stricture dilation, stent deployment)
   Standard therapeutic techniques (integral to performance of diagnostic colonoscopy)
   Advanced therapeutic colonoscopy techniques
  Diagnostic and therapeutic ERCP
   Published guidelines for training in ERCP
   Non-technical training
   Defining competence for ERCP
   Technical success
   Varying case difficulty
   Judgement
   Minimum training requirements to achieve competency for ERCP
   Case numbers
   What is a case?
   Competency and ERCP outcome
   Improving after training
   Annual volume
   Competence affects complication rates
   Rate of acquisition of ERCP skills
   Therapeutic ERCP
   Rate of acquisition of therapeutic skills
  Diagnostic and therapeutic EUS
   Defining competency in EUS
   Learning curve for EUS
   Therapeutic EUS
   EUS training opportunities
Complementary methods for instructions in GI endoscopy
  Advances in didactic methods
   Self-instruction
   Group instruction
   Laboratory demonstrations
  Endoscopy simulators
   Static models
   Courses with static models
   Ex vivo artificial tissue models: the 'phantom' Tübingen models
   Ex vivo animal tissue simulators: EASIE and Erlangen models
   Live animals
   Computer simulation
   AccuTouch®
   GI Mentor™
   Current status of simulators
   Costs of simulators
   EUS models and simulators
  Use of training resources: summary
Endoscopy training 2010—a glimpse into the future
Credentialing and granting of privileges
  Credentialing
  Privileging
  Proctoring
   ASGE guidelines
Renewal of privileges and privileging in new procedures
  New procedures
Privileging for non-gastroenterologists and non-physician providers
The future of credentialing and privileging
  The use of new technology for credentialing
The role of endoscopic societies in training and credentialing
  Guidelines
  Society courses
  Materials
  Hands-on courses
  Research in training
  Influencing credentialing
Outstanding issues and future trends
References
Synopsis
Introduction
Achieving competence—the goal of training
What experience is necessary in training? The fallacy of numbers
Beyond numbers: tools to measure competence
What level of competence is good enough? How is it recognized?
Endoscopic performance beyond training
Issues in measuring endoscopic performance
The report card agenda
Benchmarking
The quality of endoscopy units
Conclusion
Outstanding issues and future trends
References
Synopsis
Most endoscopists are not interested
Is the problem declining?
Newly recognized infections
Compliance with guidelines
What can be done to remedy this sorry state of affairs?
  Infection control staff
  Microbiological surveillance
   British practice
The role of industry
Manual cleaning is key
References

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