Central precocious puberty is a rare endocrine disorder characterised by premature activation of the hypothalamic–pituitary–gonadal (HPG) axis, leading to the onset of pubertal development before the defined age criteria. This condition is predominantly seen in girls and is usually sporadic in nature. We report an unusual case of central precocious puberty (CPP) in a 9-month-old female infant who presented with regular
menstrual cycles from 5 months of age. The infant was assessed clinically on an outpatient basis and subsequently investigated with neuroimaging and hormonal studies. She was diagnosed with a hypothalamic hamartoma as the underlying cause of CPP and was successfully initiated on a GnRH analogue (leuprolide depot), with subsequent regression of pubertal signs and cessation of menses.

Normal echocardiographic variants in neonates present a diagnostic challenge because benign intracardiac structures may mimic pathological masses. Accurate differentiation is essential to prevent unnecessary diagnostic investigations and potentially harmful treatments. Diagnostic evaluation should integrate fetal
echocardiography, obstetric and delivery history, neonatal physical examination, and laboratory findings. When transthoracic echocardiography is inconclusive, additional imaging modalities, including transesophageal echocardiography, three-dimensional echocardiography, CT angiography, or cardiac MRI, may be required. Nevertheless, transthoracic echocardiography remains the most accessible, practical, and low-risk imaging technique for distinguishing normal variants from pathological findings in paediatric patients. We report a healthy, one-day-old, preterm female neonate with normal clinical and laboratory findings who exhibited several recognised normal echocardiographic variants, along with a previously undescribed normal right atrial structure resembling the Coumadin ridge typically observed in the left atrium. This case highlights the importance of recognising rare normal neonatal echocardiographic variants to improve diagnostic interpretation and guide decisions regarding further imaging evaluation.

Rifampicin is first-line therapy for drug-susceptible tuberculosis (TB) but rarely causes severe immune-mediated thrombocytopenia, which may be overlooked amid multiple concomitant medications. A 49-year-old man with cavitary pulmonary TB developed severe thrombocytopenia nine days after starting rifampicin-containing therapy; platelets fell abruptly from 311,000/µL to 9,000/µL. He also received prophylactic heparin, vancomycin, and other antimicrobials. The 4Ts score indicated low probability of heparin-induced thrombocytopenia, and peripheral smear excluded microangiopathic processes. Rifampicin-induced immune thrombocytopenia (RIT) was diagnosed based on temporal association, exclusion of major alternatives, and rapid platelet recovery after rifampicin discontinuation. RIT should be considered in acute severe thrombocytopenia during TB treatment, even with other thrombocytopeniaassociated drugs. Early recognition and prompt withdrawal of the offending agent are essential to reduce bleeding risk and permit continuation of effective TB therapy with an alternative regimen.

Left ventricular thrombus is most commonly associated with acute myocardial infarction, significant regional wall motion abnormalities, ventricular aneurysm, or severe left ventricular systolic dysfunction. Its occurrence in a patient with preserved ventricular function and no significant obstructive coronary artery disease is unusual. We report the case of a middle-aged patient who presented with mild acute pancreatitis
and a mature pancreatic pseudocyst measuring 6.8×6.9×6.0 cm. During contrastenhanced abdominal CT performed for evaluation of the pancreatic pathology, an incidental left ventricular apical filling defect was identified. Subsequent transthoracic echocardiography and cardiac magnetic resonance imaging confirmed multiple left ventricular apical thrombi, the largest measuring approximately 1.7 cm, despite a preserved left ventricular ejection fraction of 65% and absence of overt regional wall motion abnormality. Coronary angiography demonstrated non-obstructive coronary artery disease, with a 40% lesion in the left circumflex artery. A thrombophilia evaluation was non-contributory. In view of the known systemic prothrombotic effects of acute pancreatitis, pancreatic inflammation was considered a potential contributor to thrombus formation, although a direct causal relationship could not be established. The patient was treated with apixaban 5 mg twice daily following multidisciplinary cardiology and surgical assessment. Elective intervention for the pancreatic pseudocyst was deferred because of the competing thromboembolic and procedural bleeding
risks. At 6-week follow-up, repeat echocardiography demonstrated partial regression of the thrombus without clinical evidence of systemic embolization. This case highlights an unusual association between acute pancreatitis and left ventricular thrombus formation in the absence of the conventional major cardiac
substrates. It also emphasizes the importance of careful review of cardiac structures visible on abdominal cross-sectional imaging and the need for multidisciplinary decision-making when an intracardiac thrombus is identified in a patient requiring elective surgery.

Closed-loop small bowel obstruction is a surgical emergency associated with a high risk of strangulation and bowel ischemia. Clinical presentation may be deceptively mild, and imaging findings can be subtle, leading to delayed diagnosis. We report a case of closed-loop mid-ileal obstruction with progressive free intraperitoneal fluid and preserved bowel wall enhancement on contrast-enhanced computed tomography. Despite minimal clinical symptoms and transient pain relief, surgical exploration revealed gangrenous bowel requiring resection. This case highlights the importance of recognizing free intraperitoneal fluid as a critical indirect imaging marker of bowel ischemia and emphasizes the need for early surgical intervention based on radiological suspicion rather than clinical severity alone.

Trauma is a leading cause of mortality in individuals between 1 and 44 years of age. Among thoracic traumas, blunt cardiac injury (BCI) represents a relatively uncommon but potentially fatal entity. Approximately 20% of blunt chest traumas involve some form of cardiac injury, with this number increasing to 76% in cases of polytrauma. BCIs span a clinical spectrum from benign myocardial contusions to fatal multi-chamber
ruptures. Blunt cardiac rupture, although rare, carries a high pre-hospital mortality rate and accounts for only 0.16–2% of hospital trauma admissions. We report a case of a 24-year-old male involved in a high-speed car-to-car collision, who arrived at the emergency department in cardiac arrest. He underwent immediate resuscitative thoracotomy, revealing a full-thickness rupture of the left ventricle. Although spontaneous circulation was restored after pericardial decompression and bleeding was temporarily controlled using a Foley catheter, the patient later developed cardiac edema and refractory arrhythmia and did not survive.
This case emphasizes the rarity and lethality of blunt cardiac rupture, the need for rapid surgical intervention, and the critical role of multidisciplinary trauma care, including emergency medicine, surgery, and anesthesiology, in optimizing outcomes.

Fibroepithelial polyps are rare benign lesions of mesodermal origin that may arise within the urinary tract. Urinary bladder involvement is uncommon, particularly in children. Because these lesions may appear as vascularized polypoid bladder masses, they may mimic other bladder tumors. Histopathological examination is therefore essential for definitive diagnosis. A 10-year-old girl presented on 24/07/2026 with a 9–10-day history of gross hematuria and a sensation of incomplete bladder emptying. She was clinically well, with mild
suprapubic tenderness. Laboratory evaluation demonstrated hematuria, and urine culture grew Escherichia coli (>10⁵ CFU/mL). Antibiotic treatment was initiated; however, hematuria persisted. Abdominal and pelvic ultrasonography subsequently demonstrated a well-defined, approximately 1 × 1 cm vascularized hyperechoic lesion arising from the right posterior wall of the urinary bladder. The patient underwent cystoscopic excision of the lesion. Histopathological examination demonstrated a fibroepithelial polyp composed of fibrovascular stroma lined by urothelium, with reactive urothelial changes, acute inflammatory cell infiltration, and focal stromal infarction with hemorrhage and degenerative changes. No significant cytologic atypia, carcinoma in situ, or invasive malignancy was identified. The final diagnosis was fibroepithelial polyp with focal infarction and inflamed/reactive urothelium, negative for malignancy. The patient had a favorable postoperative course through 04/08/2026. Fibroepithelial polyp should be considered in the differential diagnosis of a bladder
mass in children presenting with gross hematuria. Although imaging can identify the lesion, histopathological examination is essential for definitive diagnosis and exclusion of malignancy. Cystoscopic excision provides tissue for definitive diagnosis and treatment of an appropriate localized lesion. 

Von Hippel–Lindau (VHL) disease is an autosomal dominant hereditary tumor predisposition syndrome caused by pathogenic variants in the VHL gene located on chromosome 3p25.3. It is characterized by the development of multiple benign and malignant neoplasms and cystic lesions involving various organs, with most
manifestations presenting in early to middle adulthood. We report the case of a young female who initially presented with back pain andwas found to have a spinal hemangioblastoma. A concomitant adrenal mass identified incidentally on lumbosacral MRI raised suspicion of an underlying hereditary syndrome.
Subsequent brain MRI demonstrated a fourth ventricular hemangioblastoma. The constellation of multisystem lesions prompted germline genetic testing, which confirmed a pathogenic VHL gene variant, establishing the diagnosis of VHL disease. The coexistence of CNS, spinal, adrenal, renal, or other characteristic tumors should
raise suspicion for VHL syndrome. Diagnosis is established through a combination of clinical evaluation, multimodal imaging, and genetic testing, despite considerable phenotypic heterogeneity.  

Pediatric acute myocarditis often presents with dominant respiratory symptoms, creating a significant diagnostic overlap with common lower respiratory tract infections. This clinical mimicry frequently results in misdiagnosis, such as pneumonia, and potentially fatal delays in specialized cardiac care. We report three consecutive male patients (aged 6 months to 3.5 years) initially referred to a Pediatric Pulmonology
Service for presumed consolidative pneumonia. The diagnosis was shifted to acute myocarditis only after identifying cardiac “red flags,” including tachycardia disproportionate to fever, cardiomegaly on imaging, and elevated cardiac biomarkers or pericardial effusions. Clinical management included intravenous immunoglobulin, pulse steroids, and supportive therapy. One patient required electrical cardioversion
for refractory ventricular tachycardia. All three patients achieved clinical recovery or significant improvement, with normalization of cardiac function or resolution of effusions. Emergency medicine specialists and pediatricians must maintain a high index of suspicion for acute myocarditis in children presenting with respiratory distress. Recognizing clinical findings that are disproportionate to the degree of parenchymal
lung involvement is essential to prevent diagnostic delays and ensure the timely initiation of life-saving interventions.

Acute mesenteric venous thrombosis is an uncommon but potentially fatal cause of mesenteric ischemia, whose nonspecific presentation can delay diagnosis. We report a 46-year-old man with no prior thromboembolic, hepatic, or malignant disease who presented with five days of periumbilical pain, vomiting, and melena. Upper endoscopy revealed hematin without an identifiable bleeding source. Computed tomography angiography revealed extensive portal, splenic, and superior mesenteric venous thrombosis with jejunal ischemia. Intravenous heparin was started, and the patient was monitored closely because his abdomen remained soft and non-tender. After approximately 48 hours, he developed sudden hemodynamic
collapse; emergency laparotomy revealed 100 cm of necrotic jejunum, which was resected without primary anastomosis. Despite intensive postoperative support, he died of cardiovascular collapse approximately 24 hours later. This case shows that extensive portomesenteric thrombosis can cause severe and fatal intestinal ischemia despite reassuring abdominal findings, underscoring the need for prompt imaging, anticoagulation, and vigilant reassessment.

Onychogryphosis is a disorder of nail plate growth characterized by an opaque, yellow-brown discoloration,
marked thickening, elongation, and increased curvature of the nail plate associated with hyperkeratosis. It is
often characterized as “ram’s horn” or “oyster-like” in appearance [1]. It may be congenital, inherited in an autosomal dominant pattern, involving all twenty nails, or acquired, usually associated with neglect, trauma, or impaired self-care. This deformity occurs because of two proposed mechanisms: insufficient nail matrix beneath the posterior fold to exert a flattening effect on the nail plate, or excessive keratin production by the nail bed. Although the great toenail is most often affected, the fingernail may be involved in rare cases [2].
The authors report a case of an elderly female who presented with progressive thickening, elongation,
yellow-brown discoloration, and marked curvature of all fingernails and toenails over several years. She was malnourished, socially isolated, and had poor self-care. Examination revealed significant hypertrophy of all twenty nails with exaggerated transverse and longitudinal curvature, producing characteristic ram’s horn-like deformities (Figure 1a, b). Several nails showed distal tapering with claw-like projections and subungual hyperkeratosis. Onychoscopy revealed nail plate hyperkeratosis, brownish-yellow discoloration, longitudinal or
transverse ridges and grooves with loss of normal nail plate architecture, and dense subungual keratotic
debris (Figure 2a, b). The patient reported difficulty performing household activities and discomfort while wearing footwear. There was no history of psoriasis, peripheral vascular disease, trauma, or systemic illness. Mucocutaneous examination was unremarkable. A clinical diagnosis of generalized onychogryphosis was made. Treatment options include conservative management, nail avulsion with or without matricectomy, V-Y
advancement flap, or the Syme technique [3]. In this case, simultaneous extensive involvement of all
fingernails and toenails is uncommon and presents a striking clinical appearance, emphasizing the need for
prompt evaluation and management.