Hepatic Abscess Following NSAID Use in an Adolescentq

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Hepatic Abscess Following NSAID Use in an Adolescentq J Ped Surg Case Reports 2 (2014) 33e36 Contents lists available at ScienceDirect Journal of Pediatric Surgery CASE REPORTS journal homepage: www.jpscasereports.com Hepatic abscess following NSAID use in an adolescentq Margaret E. Clark a,*, Andrew W. Osten b, Mazen I. Abbas b, Mary J. Edwards a a Department of General Surgery, Tripler Army Medical Center, 1 Jarrett White Rd., Honolulu, HI 96859, USA b Department of Pediatrics, Tripler Army Medical Center, 1 Jarrett White Rd., Honolulu, HI 96859, USA article info abstract Article history: Non-steroidal anti-inflammatory drugs (NSAIDs) are a known cause of peptic ulcer disease, resulting in Received 3 December 2013 gastrointestinal bleeding or perforation. We present a case of a sixteen year old male athlete who pre- Received in revised form sented with abdominal pain and was found to have a pyogenic liver abscess secondary to a gastrohepatic 7 December 2013 fistula due to a deeply penetrating ulcer from NSAID use. This patient was successfully managed with Accepted 11 December 2013 antibiotics, a proton pump inhibitor (PPI), percutaneous drainage, and bowel rest. Perforating peptic ulcer disease (PPU) is rare in children, and this is a novel report of a resulting gastrohepatic fistula and subcapsular hepatic abscess. In otherwise healthy adolescents with abdominal complaints, a careful Key words: NSAID history of NSAID use should be obtained. Peptic ulcer Published by Elsevier Inc. Adolescent Gastrohepatic fistula Ulcer perforation Peptic ulcer disease (PUD) is a significant source of morbidity (CT) of the abdomen. He was hospitalized for pain control and and mortality in adults, but is rare in the pediatric population. The further evaluation. An upper gastrointestinal series (UGI) demon- etiology is classified as either primary or secondary, with secondary strated non-specific small bowel wall thickening. He underwent an peptic ulcers being associated with physiological stress, systemic extensive laboratory evaluation which was unremarkable, including illnesses or drugs such as NSAIDs [1]. In a healthy adolescent, negative stool Helicobacter pylori (H. pylori) antigen, and normal NSAIDs are often first or second line medications taken for sports- inflammatory bowel disease (IBD) serology. The patient improved related injuries. In an otherwise healthy active adolescent with after a several day hospitalization and was discharged home with a abdominal pain, complications of ulcer disease are not often high diagnosis of irritable bowel syndrome-constipation predominant on the differential diagnoses, but warrant consideration. This case and treated with laxatives. One year later, he presented as an highlights the potential for an insidious presentation of NSAID outpatient with similar complaints and was initially diagnosed as induced ulcer disease, and the success of non-operative treatment having an abdominal wall muscle strain. Subsequently he began self in patients who are clinically stable. medicating with 1000 mg ibuprofen three to four times a day, frequently on an empty stomach. At follow up he complained of fatigue, anorexia and an involuntary eight percent weight loss (5 kg) 1. Case report over the past few weeks. On physical exam he had a palpable, tender epigastric mass. An A previously healthy fifteen year old male athlete initially pre- abdominal ultrasound was performed and demonstrated two sented with a several week history of severe abdominal pain. hypovascular lesions in the left lobe of the liver concerning for he- Physical exam was unremarkable, as was computed tomography patic abscesses (Fig. 1). A CT scan demonstrated a 7.3 Â 6.4 Â 11.1 cm multiloculated mass in the left hepatic lobe, with the most inferior q This is an open-access article distributed under the terms of the Creative portion appearing contiguous with the antrum of the stomach Commons Attribution-NonCommercial-ShareAlike License, which permits non- (Fig. 2). Laboratory analysis was notable for an elevated erythrocyte commercial use, distribution, and reproduction in any medium, provided the sedimentation rate (ESR) to 110 mm/h, C-reactive protein (CRP) to original author and source are credited. 34.8 mg/dL, and a leukocytosis of 21.9 Â 109/L with a granulocytosis * Corresponding author. Tel.: þ1 808 433 3479, þ1 262 442 5405; fax: þ1 808 433 of 77.4% and no eosinophilia. His aspartate aminotransferase (AST) 6539. E-mail addresses: [email protected], [email protected] was elevated at 239 Units/L, but the remainder of his hepatic (M.E. Clark). function panel was unremarkable. 2213-5766/$ e see front matter Published by Elsevier Inc. http://dx.doi.org/10.1016/j.epsc.2013.12.006 34 M.E. Clark et al. / J Ped Surg Case Reports 2 (2014) 33e36 Fig. 1. Initial ultrasound demonstrated 2 large heterogenous, hypovascular lesions in the left lobe of the liver. The larger lesion, pictured above, measured 7.2 Â 5.0 Â 5.1 cm. Fig. 3. EGD revealed a deeply penetrating ulcer near the pylorus and antrum. Biopsy fi The patient was again hospitalized and treated with intrave- was signi cant for chronic focally active gastritis without any evidence of Helicobacter pylori or malignancy. nous piperacillin/tazobactam and metronidazole. EGD was per- formed which revealed multiple prepyloric ulcers, one of which appeared deeply penetrating (Fig. 3). The hepatic abscess was revealed intermittent, significant use of ibuprofen around the time percutaneously drained and instillation of contrast into the cavity of his prior hospitalization. He admitted to abuse of ibuprofen, confirmed a connection between the hepatic abscess and the often exceeding the maximum recommended adult dose of 3.2 g/ gastric antrum (Fig. 4). Gram stain of the abscess fluid was sig- day, treating various musculoskeletal strains and discomfort nificant for gram positive cocci, but cultures were without growth. intermittently for the past several years. As this was not a regularly Another extensive evaluation was performed to determine an in- prescribed medication, he had not disclosed this on prior history. fectious or autoimmune etiology for his ulcer and abscess. This After 3 weeks of antibiotics and one month of a proton pump included serology for Entamoeba histolytica and Echinococcus as inhibitor (PPI) therapy, bowel rest, and parenteral nutrition, he was well as another IBD panel, all of which were unremarkable. Stool clinically well and the abscess was resolving radiographically. The ova and parasites as well as H. pylori antigens were negative and drain was removed and he continued to do well. At 3 months fecal calprotectin levels were normal. Colonoscopy and magnetic follow-up a repeat EGD showed complete resolution of the gastric resonance enterography were normal as well. Fasting serum ulcer (Fig. 5). He was advised to remain on a PPI and to avoid NSAIDs gastrin level was also within normal limits. Careful history indefinitely. At six month follow up, he has regained his lost weight, is back in competitive sports, and is symptom free. Fig. 2. CT scan demonstrated a multiloculated mass in the left hepatic lobe, measuring 7.3 Â 6.4 Â 11.1 cm. The inferior most portion appeared contiguous with the antrum of the stomach. The asterisk labels a portion of the hepatic mass with an arrow pointing Fig. 4. Fluoroscopic imaging demonstrating the fistula between the stomach and he- to the antrum of stomach. patic abscess cavity (catheter in abscess cavity). M.E. Clark et al. / J Ped Surg Case Reports 2 (2014) 33e36 35 laparoscopy with 24% requiring a conversion to an open operation [10]. 51 of the 52 patients in Hua et al.’s study underwent lapa- rotomy, and the other was managed with laparoscopic repair [8]. Though children with PPU have a lower complication rate and more favorable outcomes than adults [8], these complications may still lead to significant morbidity and even mortality. Another study of 29 children requiring surgery for peptic ulcer disease revealed a 30% complication rate, a 10% reoperation rate and 14% mortality. In this series 13 of the patients had ulcers due to NSAID use [11]. An ulcer on the posterior duodenal wall is in contact with sur- rounding structures, so it tends to penetrate into adjacent organs, such as the pancreas or biliary system, rather than freely into the abdomen [12]. Although the standard treatment for this is surgical antrectomy, percutaneous treatment has been described in adults [12,13], and was successful in this case. If a subcapsular liver abscess is in close proximity to the stomach or duodenum a penetrating ulcer should be considered as an etiology. Misdiagnosis may occur after a CT scan, given that the extravasation of contrast can be misinterpreted as a loop of bowel [12,13]. In this case, a careful history of NSAID use, both prescribed and over the counter, was essential in establishing the diagnosis. As this patient was only taking this medication intermittently for sports related injuries, he did not consider it a “regular” medication. As such he did not disclose it when asked at presentation for both hospitalizations. Fig. 5. Repeat EGD 3 months after patient started antibiotics and treatment. Normal appearance of esophagus, stomach, and duodenum, with biopsies significant only for chronic gastritis. 3. Conclusion Perforation of a gastric ulcer causing a gastrohepatic fistula and 2. Discussion hepatic abscess has not previously been reported in the pediatric population, but is an example of the risk that ulcerogenic medi- fi NSAIDs are thought to cause gastrointestinal ulcers due to their cations pose. NSAIDs cause a signi cant risk for PUD in an other- inhibition of protective mucosal prostaglandins as well as neutro- wise well patient, and a complication of NSAID use should be phil mediated vascular endothelial damage [2]. In adults, endo- considered an etiology for otherwise unexplained abdominal pain. scopic studies have shown a prevalence of peptic ulcers in 20e30% Chronic NSAID use, and potential abuse, in teenage athletes should of regular NSAID users [3].
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