Enterocolitis-Associated Pseudo-Obstruction in a Sickle Cell Patient: A Rare Abdominal Catastrophe
Acute colonic pseudo-obstruction, also known as Ogilvie's syndrome, is a rare but critical cause of abdominal pain and distension, potentially mimicking mechanical obstruction or toxic megacolon. Patients with sickle cell disease (SCD) have additional risk factors such as vaso-occlusive crises, chronic hemolysis, and susceptibility to infections, which further complicate diagnosis. We report the case of a 14-year-old male patient with SCD who presented with severe generalized abdominal pain, vomiting, and progressive distension with no fever. Imaging revealed significant colonic dilation and pneumatosis, suggesting pseudo-obstruction or ischemic bowel. Infectious evaluations ultimately identified enteropathogenic Escherichia coli. Despite initial concern for toxic megacolon, a multidisciplinary evaluation by hematology, gastroenterology, infectious disease, and surgery confirmed acute colonic pseudo-obstruction associated with enterocolitis. The patient's condition was managed nonoperatively with nasogastric decompression, intravenous antibiotics, total parenteral nutrition, and prokinetic agents. Serial imaging demonstrated gradual improvement in colonic distension, facilitating a safe return to oral feeding and subsequent discharge. This case underscores the importance of early recognition of enterocolitis-associated colonic pseudo-obstruction in patients with SCD, highlighting the value of comprehensive infection screening and a careful, multidisciplinary management approach to avoid unnecessary surgery and improve outcomes.
Authors
- Munir Ahmad (ORCID: https://orcid.org/0000-0002-5240-0984)
- Masih Abdul Kader
- Mohammed Alblooshi
- Abdalla Aboelkheir
Institutions
- Al Jalila Foundation (AE)
- Tawam Hospital (AE)
Publication Details
- Journal
- Cureus
- Published
- 2025-04-08
- DOI
- https://doi.org/10.7759/cureus.81886
- Primary Topic
- Hemoglobinopathies and Related Disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00