IntroductionThe urachus is a vestigial embryologic structure resulting from the obliteration of the allantois, which connects the fetal bladder to the umbilicus [1]. Failure of this canal to completely involute after birth leads to a spectrum of urachal anomalies, including patent urachus, sinus, diverticulum, and cyst, with the cystic form being the most common variant [2]. Urachal cysts are typically located in the extraperitoneal space between the bladder dome and the umbilicus and often remain clinically silent throughout childhood [1, 3].The most frequent complication that renders these anomalies symptomatic is secondary infection [4], which can mimic other common causes of acute abdomen, such as appendicitis, Meckel’s diverticulitis, or mesenteric cysts [5]. This non-specific presentation, characterized by suprapubic pain, fever, and a palpable infra-umbilical mass, can lead to significant diagnostic delays [6]. While chronic inflammation may result in adhesion to adjacent structures, progression to a severe inflammatory phlegmon causing bowel ischemia and necessitating intestinal resection is an exceptionally rare and poorly documented complication in the pediatric population.Herein, we report the case of a 14-year-old male with a long-standing infected urachal cyst that precipitated segmental small bowel ischemia requiring en-bloc resection and primary anastomosis. This report aims to highlight this severe and unusual complication, underscoring the potential for significant morbidity and the critical importance of timely diagnosis and definitive surgical management for symptomatic urachal anomalies.

IntroductionApocrine hidrocystomas are benign cystic neoplasms arising from the secretory components of apocrine sweat glands. While commonly encountered as translucent nodules on the eyelid margin, where they originate from the glands of Moll, their presence within the subconjunctival space is exceedingly rare due to the absence of native apocrine glands in this tissue. The pathogenesis in such atypical locations is hypothesized to involve ectopic glandular tissue, post-traumatic implantation, or metaplasia [1-3].Clinically, a subconjunctival apocrine hidrocystoma can mimic a variety of more common entities, including conjunctival inclusion cysts, mucoceles, and, importantly, parasitic cysts, creating a significant diagnostic pitfall for clinicians. Definitive diagnosis relies on characteristic histopathological features—namely a bilayered epithelial lining with apical ”decapitation” secretion—which can be confirmed with a specific immunohistochemical profile [1, 4].Here, we report the case of a large, long-standing subconjunctival apocrine hidrocystoma in a young man, emphasizing the diagnostic journey from a clinical suspicion of a parasitic cyst to definitive immunohistochemical confirmation and successful management via complete surgical excision.

Proactive Management of Gestational Hypertension in a Patient with Uterine Fibroids: A Case Report of a Successful Outcome

Diagnostic Discordance in a Compromised Host: Acinetobacter Meningitis with Atypical Cerebrospinal Fluid in Pediatric Sturge-Weber Syndrome

IntroductionHydrocephalus is a neurological condition marked by abnormal cerebrospinal fluid (CSF) accumulation, causing ventricular enlargement and potential brain damage [1,2]. It results from CSF overproduction, flow obstruction, or impaired absorption, presenting with headaches, nausea, visual disturbances, and cognitive decline, which is diagnosed via CT or MRI [3]. Ventriculoperitoneal (VP) shunts, which divert CSF to the peritoneum, treat various forms of hydrocephalus, including congenital, tumor-related, and normal pressure hydrocephalus [4]. However, VP shunts carry 2-20% complication risks like infection, hemorrhage, and obstruction [4]. A rare but serious complication of VP shunt is trapped fourth ventricle (TFV), where CSF accumulates due to aqueductal and foraminal blockages [5,6], which may be discovered incidentally during imaging studies [7]. This typically occurs post-multiple shunt surgeries, potentially causing brainstem compression and neurological deficits [8,9]. Symptomatic TFV requires surgical intervention [10]. The choice of surgical approach remains subject to institutional resources and expertise, with endoscopic techniques emerging as the preferred modality in well-equipped centers [11]. Early recognition of TFV and intervention are critical to prevent irreversible neurological deficits. We present a case of TFV in a pediatric patient with a history of post-traumatic hydrocephalus, initially misdiagnosed as a space-occupying lesion.

Sanjad-Sakati Syndrome: Severe Intracranial Calcification in a Child with Misleading Normocalcemia

Sanjad-Sakati Syndrome: Severe Intracranial Calcification in a Child with Misleading Normocalcemia

Anomalous Single Coronary Ostium from the Right Sinus of Valsalva Complicated by Severe Triple-Vessel Atherosclerosis

IntroductionJuvenile systemic lupus erythematosus (jSLE), defined by disease onset before the age of 18 [1], accounts for 15-20% of all SLE cases and is characterized by a more aggressive disease course, higher rates of major organ damage, and a twofold higher mortality rate compared to adult-onset SLE [2-4]. While renal, hematologic, and cutaneous manifestations are common, jSLE can also present with atypical and life-threatening complications that create significant diagnostic and therapeutic challenges.Acute pancreatitis is a recognized but uncommon complication of jSLE, occurring in approximately 4.2% of patients and associated with high fatality rates, often linked to underlying vasculitis or immune dysregulation [5]. Similarly, significant peripheral nervous system involvement is rare, with pure axonal motor polyneuropathy being an infrequently detailed pattern compared to sensory or central nervous system manifestations [6]. Furthermore, the coexistence of jSLE with other autoimmune disorders, such as type 1 diabetes mellitus (T1D), remains a rare clinical scenario, though one that is mechanistically plausible due to shared genetic susceptibility factors, including HLA-DR3 and HLA-DR4 haplotypes [7].The simultaneous or rapidly sequential development of this specific triad—acute pancreatitis, axonal motor polyneuropathy, and T1D—in a single patient represents an exceptionally rare clinical convergence that has not been previously described in the literature. This constellation of severe complications underscores an extreme disease phenotype and poses a formidable challenge in distinguishing primary disease activity from treatment-related toxicities. In this report, we detail the case of a 14-year-old female who presented with this life-threatening triad during a severe jSLE flare to highlight the complex management required and to emphasize the importance of maintaining a high index of suspicion for multiple, concurrent systemic attacks in this vulnerable population.

Delayed Ileal Perforation with Psoas Abscess and Fistulization into the Inferior Vena Cava Post-Dilation and Curettage - A case report

Sporadic Neurofibroma

Successful Perinatal Outcome in a Giant Placental Chorioangioma Without Fetal Intervention: A Case Report