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    Pathogenesis: Pseudomonas Species (

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    Sharon Angélica Vargas Quisca
    The document summarizes the pathogenesis of appendicitis. It begins with appendiceal obstruction leading to increased luminal pressure, thrombosis, and ischemia. This causes inflammation and eventually perforation of the appendix or peritonitis. The mechanism of obstruction varies by age but can include fecaliths, tumors, parasites, or lymphoid hyperplasia. Bacterial overgrowth occurs and further propagates the inflammatory response. Within 24 hours, 90% develop inflammation but not perforation. Perforation risk increases with time and is associated with fecaliths or true calculi.

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    Pathogenesis: Pseudomonas Species (

    Uploaded by

    Sharon Angélica Vargas Quisca
    20 views2 pages
    The document summarizes the pathogenesis of appendicitis. It begins with appendiceal obstruction leading to increased luminal pressure, thrombosis, and ischemia. This causes inflammation and eventually perforation of the appendix or peritonitis. The mechanism of obstruction varies by age but can include fecaliths, tumors, parasites, or lymphoid hyperplasia. Bacterial overgrowth occurs and further propagates the inflammatory response. Within 24 hours, 90% develop inflammation but not perforation. Perforation risk increases with time and is associated with fecaliths or true calculi.

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    patogénesis

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    PATHOGENESIS-Uptodate

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    The document summarizes the pathogenesis of appendicitis. It begins with appendiceal obstruction leading to increased luminal pressure, thrombosis, and ischemia. This causes inflammation and eventually perforation of the appendix or peritonitis. The mechanism of obstruction varies by age but can include fecaliths, tumors, parasites, or lymphoid hyperplasia. Bacterial overgrowth occurs and further propagates the inflammatory response. Within 24 hours, 90% develop inflammation but not perforation. Perforation risk increases with time and is associated with fecaliths or true calculi.

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    20 views2 pages

    Pathogenesis: Pseudomonas Species (

    Uploaded by

    Sharon Angélica Vargas Quisca
    The document summarizes the pathogenesis of appendicitis. It begins with appendiceal obstruction leading to increased luminal pressure, thrombosis, and ischemia. This causes inflammation and eventually perforation of the appendix or peritonitis. The mechanism of obstruction varies by age but can include fecaliths, tumors, parasites, or lymphoid hyperplasia. Bacterial overgrowth occurs and further propagates the inflammatory response. Within 24 hours, 90% develop inflammation but not perforation. Perforation risk increases with time and is associated with fecaliths or true calculi.

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    © All Rights Reserved
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    PATHOGENESIS — The natural history of appendicitis is similar to that of other

    inflammatory processes involving hollow visceral organs. Initial inflammation of the


    appendiceal wall is followed by localized ischemia, perforation, and the development of
    a contained abscess or generalized peritonitis.

    Appendiceal obstruction has been proposed as the primary cause of appendicitis [3,8-
    11]. Obstruction is frequently implicated but not always identified. A study of patients
    with appendicitis showed that there was elevated intraluminal pressure in only one-third
    of the patients with nonperforated appendicitis [12].

    Appendiceal obstruction may be caused by fecaliths (hard fecal masses), calculi,


    lymphoid hyperplasia, infectious processes, and benign or malignant tumors. However,
    some patients with a fecalith have a histologically normal appendix, and the majority of
    patients with appendicitis do not have a fecalith [13,14].

    When obstruction of the appendix is the cause of appendicitis, the obstruction leads to
    an increase in luminal and intramural pressure, resulting in thrombosis and occlusion of
    the small vessels in the appendiceal wall, and stasis of lymphatic flow. As the appendix
    becomes engorged, the visceral afferent nerve fibers entering the spinal cord at T8-T10
    are stimulated, leading to vague central or periumbilical abdominal pain [8]. Well-
    localized pain occurs later in the course when inflammation involves the adjacent
    parietal peritoneum.

    The mechanism of luminal obstruction varies depending upon the patient's age. In the
    young, lymphoid follicular hyperplasia due to infection is thought to be the main cause.
    In older patients, luminal obstruction is more likely to be caused by fibrosis, fecaliths, or
    neoplasia (carcinoid, adenocarcinoma, or mucocele). In endemic areas, parasites can
    cause obstruction in any age group. (See "Cancer of the appendix and pseudomyxoma
    peritonei".)

    Once obstructed, the lumen becomes filled with mucus and distends, increasing
    luminal and intramural pressure. This results in thrombosis and occlusion of the small
    vessels, and stasis of lymphatic flow. As lymphatic and vascular compromise
    progresses, the wall of the appendix becomes ischemic and then necrotic.

    Bacterial overgrowth occurs within the diseased appendix. Aerobic organisms


    predominate early in the course, while mixed infection is more common in late
    appendicitis [15]. Common organisms involved in gangrenous and perforated
    appendicitis include Escherichia coli, Peptostreptococcus, Bacteroides fragilis, and
    Pseudomonas species [16]. Intraluminal bacteria subsequently invade the appendiceal
    wall and further propagate a neutrophilic exudate. The influx of neutrophils causes a
    fibropurulent reaction on the serosal surface, irritating the surrounding parietal
    peritoneum [6]. This results in stimulation of somatic nerves, causing pain at the site of
    peritoneal irritation [5].

    During the first 24 hours after symptoms develop, approximately 90 percent of patients
    develop inflammation and perhaps necrosis of the appendix, but not perforation. The
    type of luminal obstruction may be a predictor of perforation of an acutely inflamed
    appendix. Fecaliths were six times more common than true calculi in the appendix, but
    calculi were more often associated with perforated appendicitis or periappendiceal
    abscess (45 percent) than were fecaliths (19 percent). This is presumably due to the
    rigidity of true calculi as compared with the softer, more crushable fecaliths [13].

    Once significant inflammation and necrosis occur, the appendix is at risk of perforation,
    which leads to localized abscess formation or diffuse peritonitis. The time course to
    perforation is variable. One study showed that 20 percent of patients developed
    perforation less than 24 hours after the onset of symptoms [17]. Sixty-five percent of
    patients in whom the appendix perforated had symptoms for longer than 48 hours.

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