The clinical significance of appendicitis secondary to acute gastroenteritis is largely unknown. This study is the first to examine the features of pediatric acute gastroenteritis when accompanied by secondary appendicitis in comparison with those with no secondary appendicitis. The findings will contribute to establishing the direction of clinical treatment.
Most primary appendicitis occurs as a result of a series of events resulting from a blockage in the lining of the appendix caused by feces, proliferation of lymphatic tissues, vegetable or fruit seeds, or parasites, which in turn cause closed loop obstructions with continued mucus secretion into the appendiceal lining, thereby distending it and continuously increasing the intraluminal pressure.(8) Continuous elevation of intraluminal pressure causes occlusion of the appendiceal veins and damages the mucosal barrier, thereby inducing bacterial entry and progressing inflammation.(9) By contrast, secondary appendicitis refers to periappendicitis or serositis caused by colonic or periappendiceal lesions spreading inflammation to periappendiceal areas, as opposed to a blockage of the appendiceal lumen, and this results from sympathetic mural edema.(10) Secondary appendicitis is classified as intrinsic or extrinsic, where intrinsic appendicitis is caused by an inflammation of the cecum or large intestine connected to the appendix (e.g., ischemic colitis, infectious colitis, pseudomembranous colitis), and extrinsic appendicitis is caused by inflammation resulting from a spread of lesion in the surrounding organs, such as the gallbladder, liver, bladder, ovaries, kidney, or terminal ileum (e.g., Crohn’s disease, cystitis, cholecystitis, sigmoid diverticulosis).(2, 10) In the present study, many cases of appendicitis secondary to acute gastroenteritis were intrinsic cases caused by acute ileocecitis affecting the ileum and cecum around the appendix. Acute gastroenteritis cases in which the inflammation is confined to the ileum and cecum are called ileocecitis, and most of these cases are caused by infection in these areas by bacteria such as Yersinia enterocolitica, Campylobacter jejuni, and Salmonella enteritidis.(11, 12) Acute gastroenteritis can be diagnosed based on enlarged ileocecal area and normal appendix,(13) and some cases may show appendiceal infection as well.(14)
One shortcoming of diagnostic US is that the diagnosis rate may vary according to the proficiency of the examiner, although it is widely used as the primary test owing to the benefits of US. This includes its noninvasive simple nature. The examiner can talk to the patient while performing the study in real time, observing peristalsis and blood flow distribution of the digestive tract. The test can be safely repeated frequently, and there is no risk of irradiation.(15, 16) In the present study, US was generally the modality chosen, and abdominal CT was performed in the presence of poor acoustic windows, abdominal obesity, and difficulty of ultrasonography. Generally, secondary appendicitis is distinguished from primary appendicitis according to the patterns of cecal wall thickening. Whereas cecal wall thickening is local, asymmetrical, and irregular in primary appendicitis, it is symmetrical, and regular in secondary appendicitis.(3, 17) Appendiceal distention can be observed in both cases; however, appendiceal wall thickening and periappendiceal fat deposition are characteristic findings of primary appendicitis.(12) Color Doppler imaging shows increased blood flow in the thickened appendiceal wall in primary appendicitis, while hyperemia of terminal ileum is characteristic of secondary appendicitis.(18, 19) Similarly, we diagnosed cases featuring absence of blockage in appendiceal lumen with the presence of symmetrical and regular cecal and appendiceal wall thickening along with inflamed large and small intestines as secondary appendicitis.
The mean age of patients with secondary appendicitis was 11.75 years, suggesting that appendicitis was more common in older children. The major symptoms upon hospital visit were abdominal pain and fever among those with secondary appendicitis, while diarrhea was the most common symptom among those without secondary appendicitis. A significantly higher percentage of patients with secondary appendicitis had fever. CRP levels were significantly higher among patients with secondary appendicitis compared to those without. These findings suggest that patients with secondary appendicitis may have more severe inflammation and therefore have fever more frequently with higher levels of acute inflammation indicators.
Of patients with secondary appendicitis, Salmonella spp., Campylobacter spp., and C. perfringens were detected in the stool samples of five patients, with no viruses detected. Rotavirus, norovirus, and enteric adenovirus were detected among patients without secondary appendicitis. These findings suggest that patients with secondary appendicitis may be more likely to have been infected with bacteria, and this should be noted when determining treatment approaches.
The lengths of hospital stay were longer, and the use of antibiotics was more common among patients with secondary appendicitis. The use of antibiotics and additional radiologic testing were greater among these patients after initial diagnosis because of the persistence and high severity of symptoms. Most patients showed rapid improvement of symptoms only with symptomatic treatment for acute gastroenteritis, and antibiotics were used for shorter periods in the earlier stages with severe symptoms and unclear diagnoses. Nevertheless, because it was reported that infectious ileocecitis occurred in one out of 11 cases of acute appendicitis,(1) and secondary ileocecitis can develop along with fat inflammation even in progressed acute appendicitis, we believe abdominal CT should be performed in cases in which US findings are unclear. In the present study, one patient was initially diagnosed with secondary appendicitis with ileocecitis, and CT taken on day 2 of admission indicated by worsening of symptoms revealed intestinal perforation and peritonitis, for which appendectomy and cecectomy were performed. Early diagnosis is often difficult and delayed in children because they usually complain of nonspecific symptoms in the earlier stages and have less ability to express their describe their symptoms than do adults. Because children have more lymphoid tissue in the mucosal layer of the appendiceal wall, proliferation of these lymphoid tissues caused by inflammation can more easily occlude the appendix.(20–22) Children may show quicker progression of inflammation because of their anatomically thin and sparse fiber tissues in the appendiceal wall. They are also at elevated risk for peritonitis because of weak defense systems that might otherwise minimize inflammation in the abdominal cavity; finally, children also have incomplete epiploic development.(23) As shown in the present study, even if appendicitis secondary to acute gastroenteritis had been initially diagnosed, it is possible to have mistaken ileocecitis secondary to progressed primary appendicitis. Even if the diagnosis is correct, it may progress severely and cause peritonitis. Therefore, it is important to continuously and closely monitor symptoms and to perform additional radiologic testing as necessary.
This study has a few limitations. First, the small sample size limits the generalizability of the clinical presentations. Second, bacterial and viral detection rates using stool PCR were low, at 59.4%. Subsequent studies are required to examine larger sample sizes and to strive to enhance bacterial identification and virus detection using various media in order to illuminate the etiology and clinical course of this disease.