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Fibrous obliteration of the appendiceal lumen (neural hyperplasia)
Clinical features
There are no specific features as this is typically an incidental finding in about one third of appendices excised for a variety of reasons.
Definition
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A spindle cell proliferation that fills and “obliterates” the appendix lumen, usually at the tip
Incidence and location
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Found in about one third of excised appendices
Morbidity and mortality
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None
Gender, race, and age distribution
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All ages, without race or gender predisposition
Clinical features
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Incidental finding in appendices excised for all reasons
Pathologic features
Gross findings
The tip of the appendix is usually affected and appears whitish on cut surface. The appendix is not enlarged and the serosa is normal.
Microscopic findings
Obliteration of the appendiceal lumen is by spindle cells in a collagenous and myxoid backdrop. The process may be confined to the mucosa (“intramucosal variant”) or may replace the entire lumen and underlying crypts. These phenomena are believed to be overall proliferative, with attendant phases of growth, involution, and finally fibrosis.
Gross findings
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Normal appendix diameter with firm white process involving lumen
Microscopic findings
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Bland spindle cell population effacing appendix lumen with no residual mucosa
Immunohistochemistry
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S-100-positive and NSE-positive cells with scattered endocrine cells
Differential diagnosis
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With benign mesenchymal tumors, the luminal location is the key
Ancillary studies
Immunohistochemistry
Immunohistochemical staining discloses S-100 protein and neuron-specific enolase-reactive spindle cells (intermingled Schwann cells and axons, respectively), and scattered endocrine cells (if neuroendocrine stains are performed).
Differential diagnosis
The differential diagnosis is with the host of spindle cell tumors of the gastrointestinal tract that are discussed in Chapter 7 . However, it is the pattern that is specific here—namely, a process with its epicenter in the lumen of the appendix.
Prognosis and therapy
Fibrous obliteration is a benign and incidental lesion.
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Anatomic anomalies of the appendix
Clinical features
The appendix can have a host of anatomic abnormalities including atypical location, duplication, and congenital absence. There can be complete or incomplete septa, which are seen principally in children and young adults and associated with acute appendicitis. An abnormally long appendix (normal is 7 to 10 cm) has been linked to primary acute torsion, although torsion has also been reported in appendices of normal length. Diverticula of the appendix can be congenital, in which case the muscularis propria is part of the diverticular wall, or acquired, in which case the diverticulum results from increased intraluminal pressure and mucosal herniation through a defect of the muscularis propria, often at the site of a penetrating artery. Acquired diverticula are more common than congenital diverticula and are seen in 1% to 2% of the population. However, acquired diverticula are greatly increased in patients with cystic fibrosis, in whom they are found in up to 22% of appendectomy specimens ( Fig. 8-1 ).
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Acute and chronic appendicitis
Clinical features
Acute appendicitis is a disease of the young, most typically presenting in children and adolescents (5-15 years), but even the elderly can be affected. Perforation is most likely in the very young and in older adults. An approximate incidence of acute appendicitis is 7% to 10%. The pathogenesis of appendicitis is believed by some clinicians to reflect an initial insult to the mucosa resulting from luminal obstruction by a fecalith, fragment of undigested food, or lymphoid hyperplasia, followed by bacterial infection that progressively spreads from the mucosa into the wall. Approximately 70% of patients suspected to have appendicitis on clinical and imaging grounds have it on resection. Some observers believe that all appendices should be removed during surgery for suspected acute appendicitis, even when grossly normal, because nearly 20% of normal-appearing appendices may have acute inflammation on microscopic examination. A possible exception is those patients who might require urologic surgery in the future, because their appendices may later serve as urinary conduits. Patients with appendicitis in the setting of human immunodeficiency virus (HIV) infection have similar clinical presentations, although sometimes with a less striking elevation in the peripheral white blood cell count. In one surgical series of appendicitis and HIV infection, delays before operation increased the likelihood of perforation.
Definition
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An acute inflammatory process attributed to local obstruction and autoinfection involving the appendix
Incidence and location
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Involves the appendix
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Incidences reported up to 7%
Morbidity and mortality
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Complications include wound infection, urinary retention, bowel obstruction, intra-abdominal abscesses, urinary tract infections, and pneumonia, all more likely if the appendix has perforated
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Overall mortality for appendectomy is about 0.3%; in individuals older than 65 years, this percentage is closer to 5%
Gender, race, and age distribution
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Peak presentation is from 5 to 15 years but occurs at any age
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Male predominance in all races, but acute appendicitis is more common in whites than in African-Americans and Asian-Americans.
Clinical features
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Classically, right lower quadrant pain accompanied by fever and elevated white blood cell count, but many variants occur
Prognosis and therapy
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Treatment is appendectomy
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Preoperative antibiotics followed by appendectomy (“interval appendectomy”) have been advocated in patients with perforated appendices
- ■
Overall prognosis is good
Radiologic features
Both ultrasound and computed tomography (CT) are useful in diagnosing acute appendicitis.
Overall sensitivity of 85% and specificity of 92% have been reported for sonography. The normal appendix is usually not visualized at graded-compression sonography. The inflamed appendix appears as a fluid-filled, noncompressible blind-ending structure measuring greater than 6 mm in maximal diameter. In early nonperforated appendicitis, an inner echogenic lining representing submucosa can be identified. If fluid is present within the appendiceal lumen, a target appearance, characterized by a fluid-filled center, surrounded by echogenic mucosa and submucosa and hypoechoic muscularis, may be seen when imaging in the axial plane. Other findings of appendicitis include an appendicolith, which appears as echogenic foci with acoustic shadowing, pericecal or periappendiceal fluid, and increased periappendiceal echogenicity representing fat infiltration. The only sonographic sign that is specific for appendicitis is an enlarged, noncompressible appendix measuring greater than 6 mm in maximal diameter. The appendix may not be visible following perforation. The characteristic sonographic findings associated with perforated appendicitis are nonspecific, but, in the proper clinical situation, still suggest the diagnosis. The findings include focal periappendiceal or pelvic fluid collections, or a complex mass representing intraperitoneal abscess.
The reported sensitivity of CT using rectal contrast medium has ranged from 97% to 100%, and the specificity has ranged from 94% to 98%. The normal appendix can be identified with CT as a tubular structure arising from the posteromedial aspect of the cecum, approximately 1 to 4 cm below the ileocecal junction. The normal appendix is identified on CT in approximately one half of children. The appendix is usually curved and may be tortuous. The free end of the appendix is mobile and can be directed medially, caudally, laterally, or retrocecally. A segment of the appendix is commonly noted at a level higher than the ileocecal valve. The maximal normal appendiceal diameter is typically 7 mm or less. The lumen of the normal appendix may fill with contrast material and may contain intraluminal air or fluid.
CT signs of acute appendicitis include a distended appendix greater than 7 mm in maximal diameter, appendiceal wall thickening and enhancement, an appendicolith, circumferential or focal cecal apical thickening, pericecal fat stranding, adjacent bowel-wall thickening, focal or free peritoneal fluid, mesenteric lymphadenopathy, and intraperitoneal phlegmon or abscess. The identification of cecal apical thickening is particularly useful in allowing a confident diagnosis of acute appendicitis if there is difficulty in identifying an enlarged appendix. Cecal apical thickening can result in a triangular-shaped space that becomes filled with contrast medium. This has been labeled the arrowhead sign and is a useful indicator of disease.
Pathologic features
Gross findings
The appendix may appear grossly normal when inflammation is limited to the mucosa and submucosa. However, when inflammation extends into the muscularis propria, the appendix frequently becomes swollen and erythematous. When the serosa is affected, the peritoneum is initially dull and gray, followed by a purulent exudate. Perforation secondary to mural necrosis (gangrenous appendicitis) can follow, which may lead to abscess formation. At times, an appendix resected in the clinical setting of acute appendicitis is grossly and histologically normal, even after submission of the complete specimen for histologic examination. In these cases, an etiology is rarely found.
Microscopic findings
On microscopic examination, early lesions display mucosal erosions and scattered crypt abscesses ( Figs. 8-2 and 8-3 ). Later, the inflammation extends into the lamina propria, and collections of neutrophils are also seen in the lumen. When the inflammation damages the muscularis propria extensively, mural necrosis can lead to perforation.
As appendices heal, two basic patterns may be seen. In the first, more typical pattern, there are mixed inflammatory infiltrates ranging from patchy and mild to diffuse and transmural ( Figs. 8-4 and 8-5 ). In some appendices, there may be intramural or serosal foreign body–type giant cells surrounded by granulation tissue suggestive of prior rupture. Serositis and fibrous adhesions can be present, as well as prominent submucosal fibrosis. Mucin extravasation is often seen. A second pattern, which has been termed xanthogranulomatous appendicitis , features a xanthogranulomatous infiltrate composed of foam cells, scattered multinucleated histiocytes, abundant hemosiderin, and luminal obliteration with spared lymphoid follicles. These latter cases share features with Crohn’s disease but differ by lacking epithelioid granulomas, having fewer lymphoid aggregates, and having less profound subserosal fibrosis. However, occasional patients having features similar to those described previously are found to have Crohn’s disease on follow-up, so careful clinical correlation is always important in such cases.
More recently, patients who present with a ruptured acute appendicitis are treated with antibiotic therapy and drainage followed by a delayed or “interval appendectomy.” In this setting, about two thirds of cases contain granulomas compared with less than 10% of acute appendicitis controls. About one third of interval appendectomy cases have xanthogranulomatous inflammation (cases with acute appendicitis do not display this pattern). A Crohn’s-like appearance is found about half the time in interval appendices. Without the appropriate clinical history, these changes may be misinterpreted as Crohn’s disease.
Gross findings
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Thickened diameter, depending on severity of process. There may be perforation. Serosa may be dulled (from periappendicitis).
Microscopic findings
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Early lesions display mucosal erosions and scattered crypt abscesses; later, the inflammation extends into the lamina propria and collections of neutrophils are also seen in the lumen
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When the inflammation extensively damages the muscularis propria, mural necrosis can lead to perforation
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In appendectomies performed in patients with prior appendicitis, there are mixed inflammatory infiltrates ranging from patchy and mild to diffuse and transmural
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In some appendices, there may be intramural or serosal foreign body–type giant cells surrounded by granulation tissue suggestive of prior rupture
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Serositis and fibrous adhesions, as well as prominent submucosal fibrosis, may be present
- ■
Mucin extravasation is often seen
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A second pattern, xanthogranulomatous appendicitis , features a xanthogranulomatous infiltrate composed of foam cells, scattered multinucleated histiocytes, abundant hemosiderin, and luminal obliteration with spared lymphoid follicles
Differential diagnosis
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Interval appendices share features with Crohn’s disease but differ by lacking epithelioid granulomas, having fewer lymphoid aggregates and having less profound subserosal fibrosis.
Differential diagnosis
The differential diagnosis is with inflammatory bowel disease, which is described in subsequent text, and with infections. The diagnosis is often one of exclusion.
Prognosis and therapy
Treatment is appendectomy. Complications include wound infection, urinary retention, bowel obstruction, intra-abdominal abscesses, urinary tract infections, and pneumonia, all more likely if the appendix has perforated. Rarer complications include fistula formation, pylephlebitis, and liver abscesses. The overall mortality for appendectomy is about 0.3%. In individuals older than 65 years, this figure is closer to 5%.
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Periappendicitis
Clinical features
Preoperative mechanical manipulation of the appendix alone may result in mild diffuse granulocytic infiltration of the serosa, but when inflammation is accompanied by fibrin deposition and/or adhesions in the absence of luminal active inflammation, this is a potentially clinically significant finding. Periappendicitis alone is found in 1% to 5% of appendices resected for clinically acute appendicitis, the majority of which are attributable to salpingitis. In two large series, periappendicitis was attributable to a variety of processes: gonococcal and chlamydial salpingitis; yersiniosis, Meckel’s diverticulitis, and associated intraperitoneal abscess; urologic disorders; colon neoplasms; infectious colitis; abdominal aortic aneurysm; bacterial peritonitis; and gastrointestinal perforation.
Definition
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Inflammatory process confined to the appendix serosa without luminal involvement (and thus with an extra-appendiceal source)
Incidence and location
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Periappendicitis alone is found in 1% to 5% of appendices resected for clinically acute appendicitis, the majority of which are attributable to salpingitis
Morbidity and mortality
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Depends on the source of the periappendicitis
Clinical features
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Attributable to a variety of processes: gonococcal and chlamydial salpingitis; yersiniosis, Meckel’s diverticulitis, and associated intraperitoneal abscess; urologic disorders; colon neoplasms; infectious colitis; abdominal aortic aneurysm; bacterial peritonitis; and gastrointestinal perforation
Prognosis and therapy
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Depends on the source of the periappendicitis
Radiologic features
These vary with the etiology of the periappendicitis.
Pathologic features
Gross findings
The appendix is not enlarged, and the serosa is dulled or whitish depending on the severity of the periappendicitis. The lumen and mucosa appear normal.
Microscopic findings
Depending on the stage of the lesion, there is a serosa-confined (or possibly with extension into muscularis propria) lesion ( Fig. 8-6 ) consisting of neutrophils and fibrin if the process is acute or with adhesions (scarring) and chronic inflammation if the process is chronic. The lumen is unaffected.
Gross findings
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Serosal thickening or exudates with normal muscularis and lumen
Microscopic findings
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Serosal fibroinflammatory process and normal lumen
Differential diagnosis
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With appendicitis
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Diagnosing periappendicitis as appendicitis is misleading to the clinician, who needs to find the true source of the inflammatory process; appendicitis has luminal involvement
Ancillary studies
The pathologist’s finding of periappendicitis on an appendectomy specimen in the absence of luminal disease should alert the surgeon to take measures to identify the source of the serosal injury. If the patient is a woman, the female genital tract is a likely source, but as noted previously, any abdominal process may result in periappendicitis.
Prognosis and therapy
The treatment and prognosis depend on the inciting extra-appendiceal lesion.
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Infectious causes of acute appendicitis
Clinical features
Infections of the appendix can be caused by bacteria, viruses, fungi, or parasites. In most cases of acute appendicitis, no organisms are identified by histology. Although specific infectious causes of acute appendicitis are only rarely identified, certain agents can occasionally be implicated. A few specific infections are noted in the following sections.
Bacterial infections
Cultures reveal mixed aerobic and anaerobic isolates in almost all cases. In one study of 41 children with acute appendicitis, an average of 14.1 isolates per specimen was detected. Bacterial isolates are almost always limited to normal flora and believed to play a secondary role following mucosal injury. Bacteria belonging to the Bacteroides fragilis group are the most frequently isolated anaerobes, whereas Escherichia coli is the most frequently isolated aerobe. Bacteria belonging to the Streptococcus milleri group are also common aerobes, but may be of greater significance because they have been linked to a markedly increased (seven-fold) risk of abscess formation.
Actinomyces
Actinomyces israelii is a rare cause of appendicitis. A. israelii can rarely lead to infections of the small intestine, appendix, or colon. Histologically, the long filamentous organisms stain dark blue on routine hematoxylin and eosin preparations and are particularly easy to recognize when associated with characteristic sulfur granules. Active inflammation in the mucosal wall is typically present, and fistula formation, rupture of the appendix, and abscess formation may complicate the clinical course. Actinomyces turicensis has also been implicated in appendicitis and is frequently accompanied by aerobic bacterial isolates of the Streptococcus anginosus group.
Campylobacter
Campylobacter jejuni is an uncommon cause of bacterial appendicitis (approximately 2%). The patients are generally young children with grossly normal appendices. Histologically, the active inflammatory changes are limited to the mucosa, consisting of cryptitis and surface erosions with focal accumulations of histiocytes that occasionally result in a granulomatous appearance.
Clostridium difficile and shigella
Clostridium difficile infections and shigellosis involving the appendix are almost always associated with more general colonic disease, although appendicitis can be a rare clinical presentation. Overall, the histologic findings are identical to those seen in the colon (see Chapter 9 ).
Malakoplakia
Malakoplakia is most commonly seen in the urinary tract but can occasionally be found in the appendix ( Figs. 8-7 and 8-8 ). In general malakoplakia results from an abnormal immune response in which bacteria are incompletely digested and accumulate in histiocytes. The histologic findings typically consist of a diffuse or nodular thickening of the mucosal wall resulting from the accumulation of numerous macrophages, including many that are eosinophilic, with scattered lymphocytes and plasma cells. Most characteristic are the admixed Michaelis-Gutmann bodies, which are round, laminated structures with a targetoid appearance that can be highlighted with iron or calcium stains.
Spirochetosis
Spirochetosis is caused by Brachyspira aalborgi and can occasionally be seen in the appendix. In one study, spirochetosis was detected in 1.9% of incidentally removed appendices, 0.7% of appendices in patients with clinical acute appendicitis plus histologic acute appendicitis, and 12.3% of patients with clinical acute appendicitis but no histologic changes. Therefore, spirochetosis may contribute to clinical symptoms in patients with otherwise normal appendices. Spirochetosis of the small intestine and colon is more commonly found in HIV-infected patients than in non-HIV-infected patients, but little information is available on whether this is also true for the appendix. Overall, adults appear to be more commonly infected than children. From a histologic standpoint, spirochetosis is characterized by a hazy hematoxylin-positive band of about 3 μm in thickness that lies along the epithelial brush border ( Fig. 8-9 ). Silver stains highlight the organisms ( Fig. 8-10 ). Typically, there is no inflammatory response, even though organisms can be seen by electron microscopy within epithelial cells and macrophages.
Tuberculosis
Tuberculosis of the appendix is almost always accompanied by gastrointestinal or pulmonary tuberculosis, although isolated infections have been reported. The histologic findings are identical to those seen elsewhere in the body.
Yersinia
When Yersinia enterocolitica is specifically sought, infections are found in approximately 4% of cases of acute appendicitis. In general, Yersinia tends to cause acute enteritis in young children and terminal ileitis and mesenteric adenitis in older children and young adults. Y. enterocolitica and Y. pseudotuberculosis infection can cause granulomatous inflammation with large epithelioid noncaseating granulomas surrounded by prominent lymphoid cuffs. In these cases of granulomatous inflammation, prominent acute inflammation is common and lymphoid hyperplasia is essentially always present ( Figs. 8-11 and 8-12 ).
Fungal infections
Fungal infections such as aspergillosis and mucormycosis can involve the appendix, typically as a component of systemic infection. Patients are typically immunosuppressed owing to organ transplantation or chemotherapy.
Parasite infections
Enterobius vermicularis is one of the most common parasites seen in the appendix. However, at our hospital, only 4 of 1584 appendices removed over a 17-year period from patients 15 years of age or younger had Enterobius infections. Individuals in late childhood and early adolescence have the highest frequency of infection (ages 5 to 15 years), which can reach as high as 24% in some studies. The organism is most commonly found in the lumen with no mucosal inflammatory response ( Figs. 8-13 and 8-14 ). In one study in which close to 22,000 appendices were evaluated, granulomatous inflammation and increased eosinophils in the lamina propria were quite rare and were both noted in less than 2% of infections. It is of interest to note that an inverse relationship between active mucosal inflammation and pinworm infection has been noted in several studies. Mucosal inflammation, when present, has been more strongly linked to the presence of parasite ova.
Viral infections
Viral gastroenteritis does not typically result in appendectomy, although some examples of appendicitis are, no doubt, caused by viral agents. Viral enteritis classically results in surgical excision of the appendix when it leads to ileocecal intussusception and ileocolectomy. Intussusception is most often attributable to lymphoid hyperplasia in the terminal ileum, which can form a “leading edge,” classically in infants and young children. The viral agents most commonly implicated in this setting are rotavirus, echovirus, and adenovirus. The latter is detected most frequently and is so named based on its isolation from adenoids. In appendices infected with adenovirus, lymphoid hyperplasia is prominent. Erosions may be identified, but viral inclusions are found in intact mucosal epithelial cells. Zones in which inclusions may be found are selected by scanning at low magnification for areas with frayed-appearing epithelium showing loss of nuclear polarity and an eosinophilic appearance imparted by loss of goblet cell mucin. Such zones are frequently in close association with lymphoid follicles. Intranuclear adenovirus inclusions are typically of the Cowdry B type, consisting of nuclear smudging, although Cowdry A inclusions, featuring sharply demarcated globules surrounded by a clear zone, are found in a minority of cases ( Figs. 8-15 and 8-16 ).
Cytomegalovirus may also be found in the appendices of immunocompromised hosts, where it displays the features found in other sites with endothelial cells, rather than epithelial cells, tending to be infected. It is occasionally responsible for clinical acute appendicitis.
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Actinomyces
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Campylobacter
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Clostridium difficile
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Shigella sp .
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Malakoplakia
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Spirochetosis
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Tuberculosis
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Yersiniosis
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Fungal infections
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Parasitic infections (usually Enterobius vermicularis )
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Viral agents (adenovirus)
Ulcerative colitis involving the appendix
Clinical features
The appendix may play an interesting role in inflammatory bowel disease because an appendectomy has been touted as a protective factor in ulcerative colitis in more than one study, although some evidence suggests that it is the appendicitis rather than the appendectomy that is protective. The prevalence of prior appendectomy is far lower in patients with ulcerative colitis than in control groups, although this observation does not necessarily indicate causation. Similar findings have also been observed in a murine model.
Ulcerative appendicitis, the appendiceal counterpart of ulcerative colitis, is typically present in patients with pancolitis but is also common as a “skip lesion” in patients who have left-sided or rectal disease, occurring in 20% to more than 80% of cases. In some cases, the active inflammatory disease in the appendix may be prominent, whereas that in the nearby cecum is mild.
Definition
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Appendiceal inflammatory disease (usually active chronic) in patient with ulcerative colitis
Incidence and location
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Common in patients with ulcerative colitis and more predominantly involving the orifice than the tip
Morbidity and mortality
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Same as for ulcerative colitis
Gender, race, and age distribution
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Same as that for ulcerative colitis
Pathologic features
Gross findings
In patients with pancolitis, the appendix may appear swollen in contiguity with the cecum and displays a smooth serosa. Like a “skip lesion” in ulcerative colitis, the appendiceal opening will display a red edematous surface in contrast to the unaffected cecal mucosa.
Microscopic findings
Ulcerative appendicitis shows the same histologic features as ulcerative colitis. There is mucosal-based active inflammation with crypt abscesses, panmucosal plasmacytosis, suppurative luminal exudate, and crypt distortion. Ulcerative appendicitis is distinguished from early acute appendicitis partly on clinical grounds, although early acute appendicitis features less crypt distortion and minimal plasmacytosis.
Gross findings
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Found either in continuity with pancolitis in ulcerative colitis or as a “skip” lesion in left-sided disease
Microscopic findings
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Like those of ulcerative colitis elsewhere, featuring cryptitis, crypt distortion, basal plasmacytosis
Differential diagnosis
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With acute appendicitis. Differs by having more crypt distortion
Ancillary studies
Immunohistochemistry
In ulcerative colitis, but not in acute appendicitis, immunostains can show prominent S-100 protein-reactive dendritic cells, MAC387-positive dendritic cells, as well as upregulated HLA class II antigens.
Differential diagnosis
The differential diagnosis is with acute appendicitis, which often has serosal involvement. Crypt distortion is more typical of ulcerative colitis, but the separation of these entities is made by clinicopathologic correlation.
Prognosis and therapy
Prognosis and therapy is related to the patient’s underlying ulcerative colitis.
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Crohn’s disease involving the appendix
Clinical features
The appendix is often examined in terminal ileal resections from patients with Crohn’s disease, and involvement is found affected in anywhere from 0% to 60% of cases. Such operations are usually performed in adults. The majority of appendices resected from patients with typical Crohn’s disease elsewhere in the gastrointestinal tract are normal, and most patients who present with isolated granulomatous appendiceal disease do not later manifest typical Crohn’s disease elsewhere in the gastrointestinal tract, so many observers believe that there are two diseases: true Crohn’s disease of the appendix and idiopathic granulomatous appendicitis. In contrast to the case with ulcerative colitis, prior appendectomy is thought to be a risk factor for the subsequent development of Crohn’s disease.
Radiologic features
Both CT and ultrasound display mural thickening when Crohn’s disease involves the appendix. However, in contrast to the typical pattern of acute appendicitis, this thickening usually extends into the ileum and or cecum.
Pathologic features
Gross findings
The appendiceal wall is thick and fibrotic in Crohn’s disease and involvement may be patchy.
Microscopic findings
In cases with clinical Crohn’s disease, the appendices have the typical histologic features of Crohn’s seen elsewhere in the gastrointestinal tract, with fissures, ulcers, active inflammation, and occasional granulomas ( Figs. 8-17 and 8-18 ). The numbers of granulomas per cross-section of the appendix were studied by Dudley and Dean in appendices resected from patients with typical Crohn’s disease and compared with cases of isolated “idiopathic granulomatous appendicitis.” They found that cases with clinical Crohn’s disease had 0.3 granulomas per tissue section in contrast to about 20 granulomas per tissue section in patients with “idiopathic granulomatous appendicitis.” Furthermore, none of the “idiopathic granulomatous appendicitis” had recurrent disease in a mean follow-up period of 4.5 years. In another series, none of nine patients (identified among 1133 consecutive appendectomy specimens) with idiopathic granulomatous appendicitis developed Crohn’s disease in a mean follow-up period of just longer than 7 years. In contrast, one patient reported in a series by Huang and Appelman with 21 granulomas per cross-section later developed Crohn’s disease elsewhere in the gut, so the number of granulomas per cross-section is not entirely reliable in separating these entities ( Table 8-1 ).
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