Abstract
Background: Colorectal cancer (CRC) predominately affects adults over the age of 50, however it occasionally occurs in young patients. Case: This case observes the presentation and management of a 14-year-old African American male (AAM) who presented to the emergency department with a two-week history of insidious onset RLQ abdominal pain. Evaluation of suspected small bowel obstruction with computed tomography raised alarm for a mass lesion causing the obstruction. Subsequent barium enema, colonoscopy, and histological analysis diagnosed colorectal cancer. The patient then underwent surgery, chemotherapy, and radiation for stage IIIc CRC. Conclusion: We use this case to argue for the development of a genetic panel that can screen for high-risk mutations so detected patients can pursue early and frequent screening protocols such as colonoscopy. We demonstrate the importance of early intervention by discussing the prognosis of patients that are discovered after a change in bowel habits.
Highlights
Colorectal cancer (CRC) is the second leading cause of cancer related death in the US overall
Pathway, where sequential mutations in The patient received a colonoscopy with biopsy oncogenes [e.g., APC, KRAS, TP53, DCC], on the 4th day of admission, which was cause development of an adenomatous polyp consistent with lymphoid nodular hyperplasia and progression of a polyp to cancer.[1] and a large colonic mass proximal to the hepatic
Case Presentation: Mr WS is a 14-year-old male with a past medical history of ADHD, ODD, and eczema who presented to the Henry Ford Fairlane emergency department with a two-week history of moderate and intermittent RLQ abdominal pain associated with four episodes of nonbilious vomiting, weight loss, and anorexia
Summary
CRC is the second leading cause of cancer related death in the US overall. The prevalence of CRC reaches .4%, the peak incidence occurs within the age range of 65 to 74. Pathway, where sequential mutations in The patient received a colonoscopy with biopsy oncogenes [e.g., APC, KRAS, TP53, DCC], on the 4th day of admission, which was cause development of an adenomatous polyp consistent with lymphoid nodular hyperplasia and progression of a polyp to cancer.[1] and a large colonic mass proximal to the hepatic
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