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• W2318744941 abstract "Nontraumatic colonic perforation is an uncommon cause of acute abdomen in children (1). It may be caused by diverticulitis, malignancy, severe appendicitis, ischemic colitis, tuberculosis, Ehlers-Danlos syndrome, or infection (2,3); however, other much rarer etiologies, such as nonsteroidal anti-inflammatory drugs (NSAIDs), may also cause colonic perforation (2,4). In this report, we present a boy who developed nontraumatic colonic perforation after taking diclofenac sodium for 3 weeks. He showed no evidence of the common causes of nontraumatic colon perforation; therefore, diclofenac was considered the cause of colonic perforation. The boy, who was 2 years and 7 months old, had fever and sore throat 3 weeks before admission. Cephalexin, acetaminophen, and diclofenac sodium (25 mg/day; 1.6 mg · kg−1 · day−1) had been prescribed at a pediatric clinic. Two days before admission, he was transferred to another hospital because of recurrent fever. Plain roentgenogram showed minimal free air at the left subphrenic area, which was not noted at that time. Intravenous ceftriaxone was administered, and diclofenac was continued to treat the fever. No gastric protectors such as omeprazole or ranitidine had been used associated with diclofenac during these 3 weeks. Seven hours before admission, he developed abdominal pain and distension, and a second plain roentgenogram revealed ileus and pneumoperitoneum (Fig. 1). He was then transferred to our hospital. On admission, his abdomen was diffusely distended with muscle guarding. Generalized abdominal tenderness with rebound pain was noted. His white blood cell count was 8.71 × 103/μL, with myelocyte 1.0%, band form 2.0%, segment form 50.0%, and lymphocyte 39.0%. The serum biochemistry was normal. He then underwent surgery after a diagnosis of hollow organ perforation and peritonitis. Laparoscopic exploration of the abdomen revealed a large amount of brownish yellow fluid and stool in the peritoneal cavity (Fig. 2A). Severe adhesion of the intestines was observed, especially at the right upper abdomen. A 5-mm perforation with fibrin coating (Fig. 2B) was noted at the antimesenteric border of the ascending colon, near the hepatic flexure. No granuloma, diverticulosis, or malignancy was noted. Primary repair of the perforation and loop ileostomy were performed. After surgery, antibiotic treatment was continued. The peritoneal fluid culture grew Escherichia coli, Klebsiella pneumoniae, β-Streptococcus Group D, and Enterococcus species, but did not grow Clostridium difficile or Salmonella. Serum virology studies were negative. Therefore, antibiotics were changed according to the drug sensitivity tests. His clinical condition improved gradually; however, a fever up to 39.6°C developed 21 days after the operation. Abdominal sonogram and computed tomography (CT) revealed an abscess measuring 5 × 2 × 1 cm3 at the right subphrenic space. CT-guided drainage of the abscess was performed and his condition improved. He was discharged in good condition 26 days after operation. The ileostomy was closed 2 months after operation; during operation, only mild adhesion of the colon near the previous perforation site was noted. Neither tumor nor diverticulum was found. After 1 year of follow-up, his condition was found to be satisfactory and he showed smooth oral intake and regular stool passage.FIGURE 1: Plain roentgenogram on the day of surgery showed significant free air and diffuse paralytic ileus.FIGURE 2: Laparoscopic pictures of the Morrison pouch. A, Whitish fibrin coating on the peritoneum (P) and green exudate on the area of colonic perforation. B, Colonic perforation (arrow) near the hepatic flexure was noted after removing exudates on the colon (C) and fibrins on the peritoneum (P).DISCUSSION Our patient was a boy and had no history of trauma, which indicated that he had childhood nontraumatic colonic perforation. He had no history of Ehlers-Danlos syndrome, and no granulomatous lesion, appendicitis, diverticulosis, malignancy, or other anatomical abnormality in the colon was noted during the 2 surgeries. In addition, he had no history of diarrhea or rectal bleeding, and the culture of peritoneal fluid did not grow specific pathogens such as Salmonella or C difficile. Furthermore, serum virology studies were negative. Therefore, the patient presented no evidence of the common causes of nontraumatic colon perforation in pediatric patients (1–3); however, he had taken diclofenac sodium, an NSAID, for 3 weeks before colonic perforation, and this drug is the NSAID that most commonly causes colonic perforation (3). Because no other common causes of colon perforation were observed in our patient, NSAID-induced colonic perforation was considered the cause of his colonic perforation. In the literature, only 13 patients have been reported as having NSAID-related colonic perforations (Table 1) (1–8). Three were boys and 10 were girls. Their ages ranged from 15 to 79 years (mean 46.1 years). The NSAIDs used in these patients included slow-release indomethacin trihydrate in 2 patients; indomethacin in 1; piroxicam in 1; nimesulide in 1; diclofenac in 7; and a combination of naproxen, diclofenac, and piroxicam in 1. Diclofenac was the most common NSAID used in these patients. Five patients had 2 or more perforations and 8 had a single perforation. Among the 8 patients with a single perforation, the locations of the perforation included cecum in 2, ileocecal area in 1, transverse colon in 3, and sigmoid colon in 2. For the 5 patients who exhibited multiple perforations, 1 had 2 perforations at terminal ileum and ascending colon, 1 had 2 perforations at transverse colon, 1 had 2 perforations at transverse colon and sigmoid colon, 1 had 3 perforations at cecum, ascending colon, and transverse colon, and 1 had 4 perforations, including 1 at transverse colon, 1 at sigmoid colon, and 2 at jejunum. The locations of the perforations were distributed along the entire colon, and the transverse colon was the most commonly affected area. The duration of drug intake ranged from 1.5 to 21 days in 11 patients (mean 10.4 days), 3 years in 1, and 5 years in 1. Four patients received resection for the diseased intestine, 1 received resection surgery followed by resection of the distal ileum and ileostomy at a second operation, 1 received primary repair and colostomy followed by resection surgery at a second operation, 3 received colostomy only for the diseased portion, 2 received primary repair, 1 received surgery with an unknown procedure, and 1 did not undergo surgery. Eleven patients showed favorable recovery and 2 died. Our patient exhibited a single perforation at the ascending colon, and, according to a review of the literature, is the youngest patient exhibiting NSAID-related colonic perforation.TABLE 1: Summary of the clinical features of patients with colonic perforation related to NSAIDsFor patients exhibiting nontraumatic colonic perforation, NSAID should be considered a possible cause if other possibilities are excluded. The colonic perforation may have been caused as a result of diclofenac adverse reaction but also by its long-term use. In addition, diclofenac may have interactions with the antibiotics (cephalexin and ceftriaxone) used before colonic perforation; however, there is no report mentioning such interactions may cause colonic perforation. The treatment for the NSAID-related colonic perforation, in addition to surgery and antibiotics, should include discontinuation of NSAID therapy. Furthermore, we would like to point out that the use of diclofenac in children is off-label." @default.
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• W2318744941 title "Colonic Perforation After Nonsteroidal Anti-Inflammatory Drug Use in a 2.7-Year-Old Boy" @default.
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