搜索结果：Clinical case reports

Cryoglobulinemic vasculitis is an immune-complex-mediated small-vessel vasculitis characterized by complement activation and endothelial injury. Its clinical manifestations are heterogeneous and may range from limited cutaneous involvement to systemic disease. We report the case of a 65-year-old woman who developed a symmetrical violaceous dermatosis involving the upper and lower extremities, accompanied by arthralgias and distal paresthesias. Laboratory investigations revealed marked hypocomplementemia and positive circulating cryoglobulins. Histopathological examination of a skin biopsy demonstrated leukocytoclastic vasculitis, leading to the diagnosis of idiopathic cryoglobulinemic vasculitis after exclusion of hepatitis C virus infection, autoimmune diseases, and associated hematologic malignancies, with no evidence of major systemic organ involvement. Treatment with corticosteroid- and cyclophosphamide-based immunosuppression achieved sustained disease control, resulting in approximately 90% symptomatic improvement. This case highlights the importance of recognizing cardinal manifestations, such as palpable purpura, arthralgias, and hypocomplementemia, when evaluating patients with suspected cryoglobulinemic vasculitis, even in the absence of identifiable secondary causes. Early recognition, histopathological confirmation, and a multidisciplinary approach are essential for establishing an accurate diagnosis and implementing timely therapeutic intervention aimed at preventing disease progression and irreversible organ damage.

To perform signal mining of neuro-ophthalmic immune-related adverse events (irAEs) associated with immune checkpoint inhibitors (ICIs) using the FDA Adverse Event Reporting System (FAERS), and to synthesize their clinical manifestations and temporal patterns, thereby providing evidence-based insights for optimizing clinical drug safety. Reports of neuro-ophthalmic irAEs associated with ICIs were extracted from the FAERS (Q1 2011 to Q4 2025). Signal detection was performed using disproportionality analysis methodologies, specifically the Reporting Odds Ratio (ROR) and Information Component (IC) algorithms, with predefined statistical thresholds for signal significance. A total of 521 reports identified neuro-ophthalmic irAEs with ICIs as primary suspect drugs, predominantly affecting males and elderly patients At the High-Level Group Term (HLGT) level, positive signals were detected for pembrolizumab and avelumab. Preferred Term (PT) analysis revealed six significant signals, with eyelid ptosis being the most frequently reported event. The median time to onset was 28-38 days, with acute presentations (≤24 hours post-infusion) observed for pembrolizumab and nivolumab; both agents exhibited elevated case fatality proportions, with a higher proportion of male patients among fatal cases. This study delineated potential neuro-ophthalmic positive disproportionality signals across seven ICIs, revealing demographic variations in signal reporting frequency with higher susceptibility among males and elderly patients. Pembrolizumab and avelumab were associated with higher reporting frequencies of neuro-ophthalmic adverse events, which were related to poor visual outcomes. Consequently, prompt recognition and management of neuro-ophthalmic irAEs are imperative to enhance ICI safety profiles in clinical practice.

Mucopolysaccharidosis type I (MPS-I) is an inherited lysosomal storage disorder characterized by alpha-L-iduronidase deficiency, leading to progressive multi-organ damage and fatal complications. Early treatment is crucial to improve outcomes, particularly in patients with severe phenotypes. We present the first case of successful allogeneic bone marrow transplantation (BMT) for MPS-I in Vietnam. A 10-month-old girl experienced coarse facial features, congenital dermal melanocytosis spots, kyphoscoliosis developmental delay. Laboratory analyses revealed reduced alpha-L-iduronidase activity and elevated urinary glycosaminoglycans, genetic mutations identified two heterozygous mutations in the IDUA gene, confirmed the diagnosis of MPS-I. At 3 years old, she underwent allogeneic BMT from an HLA-matched sibling donor following conditioning regimen with busulfan, cyclophosphamide, antithymocyte globulin. Neutrophil engraftment was achieved on day +24, and platelet engrafted on day +32. The post-transplant course was complicated by respiratory deterioration requiring 5 days of mechanical ventilation, which was promptly managed and resolved. No graft-versus-host disease occurred. Post-transplant chimerism showed 95.77% donor-derived cells on day +30 and remained stable at 100% from 2 months. The patient demonstrated improvement in clinical symptoms, accompanied by alpha-L-iduronidase activity returned to normal range, urinary glycosaminoglycan levels decreased and remained stable during follow-up. At 12 months, she demonstrated complete immune reconstitution. This case suggests that allogeneic BMT may be a therapeutic approach for patients with MPS-I in resource-limited settings. First case of MPS-I treated with bone marrow transplantation in Vietnam This article reports a case of a 3-year-old girl who was diagnosed with mucopolysaccharidosis type I also known as Hurler syndrome, a rare lysosomal storage disease where the body lacks the enzyme alpha-L-iduronidase, causing fats and glycosaminoglycans to build up in cells and organs. This disorder affects skeletal abnormalities, cognitive impairment, distinct facial features, an enlarged liver and spleen, and heart and respiratory issues. Without appropriate treatments, including enzyme replacement therapy and/or allogeneic hematopoietic stem cell transplantation, outcome of MPS-I patients was very poor. We reported the first bone marrow transplantation was done for MPS-I girl in Vietnam. This transplant relieved her symptoms, and the patient did not require any further treatment. 1 year follow-up after transplantation, patient has normal enzyme level without any complications, and improved quality of life.

Diffuse hepatic hemangiomatosis (DHH) in adults is a rare benign vascular tumor of the liver that histologically resembles a hepatic hemangioma but is characterized by an infiltrative growth pattern despite the absence of cytologic atypia typical of hepatic angiosarcoma. Although generally indolent, its clinical course is variable, and rapidly progressive or fatal cases have been reported. Due to its rarity and overlapping radiological and histopathological features with those of other vascular lesions, its diagnosis can be challenging. We present the case of a 51-year-old female with multiple hepatic lesions, initially suspected to be hepatic hemangiomas. Six months later, the lesions had progressed rapidly. A percutaneous liver biopsy revealed dilated sinusoids lined with endothelial cells without marked atypia, thus suggesting a benign vascular lesion. However, the rapid clinical course raised concerns regarding hepatic angiosarcoma, and the patient received weekly paclitaxel followed by durvalumab. No therapeutic response was observed, and the patient died of tumor rupture. Autopsy revealed diffuse replacement of the hepatic parenchyma with multiloculated cystic vascular spaces lined with pleomorphic endothelial cells. No histological heterogeneity or extrahepatic lesions are observed. These findings supported the diagnosis of DHH. This case report contributes to the current knowledge of the clinical and pathological features of this rare entity. In addition, pleomorphic endothelial cells observed during autopsy may be attributable to treatment-related artifacts.

Coronectomy is a nerve-sparing technique used to reduce the risk of inferior alveolar nerve (IAN) injury during removal of mandibular third molar (M3) in close proximity to the mandibular canal. This case describes a 45-year-old female with a history of an uneventful coronectomy of the right M3 performed 2 years earlier, currently presenting with a late-onset inferior alveolar nerve (IAN) paresthesia and discomfort at the same site. Intraoral examination showed partial exposure of the retained roots to the oral cavity and the clinical neurosensory examination confirmed Level A paresthesia of the right lower lip and chin, characterised by loss of light touch and directional discrimination. Follow-up imaging revealed approximately 2.4 mm of migration of the retained roots towards the oral cavity. In the absence of clinical or radiographic signs of infection, the radiographic findings strongly supported a mechanical etiology. A secondary surgical procedure was performed to section and remove the roots individually, preserving the nerve, resulting in complete sensory recovery within one month. This case highlights that late-onset sensory disturbance may still occur after an initially uneventful coronectomy, in cases having intimate root-canal relationships. Timely surgical management, when indicated, may result in complete neurological recovery, as observed in this patient.

Open pyeloplasty in children is often associated with significant postoperative pain, and providing effective analgesia while limiting opioid exposure remains challenging. We describe our experience with the ultrasound-guided Quadro-Iliac Plane Block (QIPB), a recently described fascial plane block, in five children aged 2-7 years undergoing open pyeloplasty. Following induction of general anesthesia, a unilateral QIPB was performed using 0.2% ropivacaine (0.5 mL/kg). Postoperative pain was assessed using the FLACC scale over 24 hours, and the need for rescue analgesia was documented. All children had low pain scores in the early postoperative period, with median FLACC scores remaining ≤3. Three patients required a single dose of rescue fentanyl between 13 and 16 hours postoperatively, likely corresponding to block wear-off. No adverse effects, motor weakness, nausea, or vomiting were observed. Our experience suggests that QIPB may offer effective, opioid-sparing, and motor-preserving analgesia for pediatric open pyeloplasty, although larger controlled studies are needed.

A 7-year-old male neutered Miniature Schnauzer was assessed due to an acute and progressive history of pelvic limb weakness and incoordination. At the examination, the dog was non-ambulatory paraparetic, the postural reaction were abscent in both pelvic limbs, with intact withdrawal and patellar reflexes and increased pelvic limb muscle tone, which lead into paraplegia with intact nociception in the follow 24 h. A T3-L3 myelopathy was suspected, and an MRI of the thoracolumbar vertebral column was performed under general anaesthesia. An ill-defined, solitary, T2W hyperintense and strongly contrast enhancing intramedullary lesion was found, extending from the caudal endplate of T12 to the midbody of T13 and associated with severe spinal cord oedema and meningeal enhancement. A lumbar CSF analysis revealed a severe mononuclear pleocytosis (309 cells/μL) and markedly increased protein level; serology against Neospora caninum and Toxoplasma gondii was negative, and treatment with steroids for a suspected focal meningomyelitis of unknown origin was started. The patient deteriorated over the following days, becoming paraplegic with reduced nociception in the right pelvic limb. An exploratory surgery was carried out via T12-T13 right-sided hemilaminectomy, durotomy and myelotomy, and a well-defined, firm intramedullary mass was removed and sent for histopathology. The mass was consistent with an inflammatory pyogranuloma with intralesional fungal hyphae. Panfungal PCR was negative. Treatment with fluconazole was started, and a follow-up MRI was performed 6 months after surgery. At this time the dog was ambulatory paraparetic and MRI revealed complete resolution of the previous mass. Repeat CSF analysis revealed a mild mononuclear pleocytosis (6 cells/μL) and a mild increase in protein. Fluconazole treatment was continued for another 12 months; during all this time, the patient remained ambulatory with a mild paraparesis. The patient died for unrelated reasons 18 months after surgery when under general anaesthesia for routine removal of a subcutaneous lipoma.

Near-infrared spectroscopy-based cerebral oximetry is commonly used to detect cerebral hypoxia during anesthesia. However, the clinical significance of extremely low regional cerebral oxygen saturation (rSO2) in noncardiac surgery in severe sepsis remains unclear. We report two patients with severe sepsis who underwent emergency noncardiac surgery under general anesthesia. In both cases, systemic parameters, including arterial blood pressure, arterial oxygen saturation, and bispectral index, were within clinically acceptable ranges. Nevertheless, intraoperative rSO2 decreased to 15% (the lowest measurable value) bilaterally and persisted throughout the surgery. Both patients developed refractory shock and severe metabolic derangements and died shortly thereafter. We report these cases to highlight an unusual monitoring pattern in which extreme rSO2 depression occurred in the context of severe sepsis and to raise the question of its physiological significance and clinical implications.

Remimazolam is an ultra-short-acting benzodiazepine that is increasingly used for the induction and maintenance of general anesthesia owing to its favorable hemodynamic profile. However, severe perioperative hypersensitivity reactions associated with its use have been reported. We report three cases of elderly patients who experienced severe cardiovascular collapse immediately after anesthetic induction with remimazolam. Additionally, an institutional review conducted over an 18-month study period identified six suspected perioperative hypersensitivity reactions. All six patients were elderly and developed sudden cardiovascular or respiratory instability shortly after induction of anesthesia with remimazolam and rocuronium. Of these, three patients experienced severe cardiovascular collapse requiring epinephrine administration or cardiopulmonary resuscitation, and two progressed to cardiac arrest. Cutaneous manifestations were absent or minimal in several cases, whereas a marked reduction in end-tidal CO₂ and refractory hypotension were the predominant clinical features. In selected cases, elevated histamine or tryptase levels provided evidence of mast-cell activation. Although rocuronium remains an important alternative causative agent, the temporal relationship with remimazolam administration, the recurrence pattern within the institution, and the uneventful subsequent anesthesia with alternative regimens in some patients suggest that remimazolam or its formulation components should be considered among the potential triggers. These cases highlight the need for early recognition of perioperative hypersensitivity when abrupt cardiovascular collapse and a sudden decrease in end-tidal CO₂ occur during induction, even in the absence of skin findings.

Giant chronic splenic infarction is an extremely rare condition with insidious onset and atypical imaging features, carrying a high risk of misdiagnosis as splenic neoplasm. This case highlights the atypical clinical features and important diagnostic considerations of this uncommon disorder. A 73-year-old female presented with recurrent epigastric pain for 2 years, with a medical history of rheumatic heart disease and hypertension. Contrast-enhanced abdominal computed tomography showed a huge splenic mass measuring approximately 18.0 × 14.2 × 19.1 cm with heterogeneous enhancement and calcification, which was highly suggestive of splenic neoplasm. The patient received splenectomy, and pathological examination confirmed extensive splenic infarction with focal fibrosis and calcification. The patient had an uneventful postoperative recovery, with no evidence of thrombosis or infectious complications during the 3-month follow-up period. Rheumatic heart disease with mitral stenosis may have contributed to splenic infarction as a possible cardioembolic source in this patient. Giant chronic splenic infarction may be misdiagnosed because of atypical clinical manifestations, tumor-mimicking imaging features, and insufficient integration of clinical, laboratory, and imaging findings. A comprehensive assessment of clinical history, laboratory results, imaging findings, and cardiac status may help reduce misdiagnosis and guide appropriate management.

Rhabdomyolysis is characterized by skeletal muscle breakdown resulting in the release of intracellular contents into the circulation. Although trauma, medications, and metabolic disorders are common causes, viral infections are increasingly recognized as potential triggers. A 26-year-old previously healthy male presented with a 2-day history of abdominal pain, diarrhea, vomiting, bilateral thigh pain, and dark urine. Laboratory evaluation demonstrated severe rhabdomyolysis with a peak creatine phosphokinase (CK) level of 25,036 U/L, elevated aminotransferases, and preserved renal function. A stool gastrointestinal multiplex polymerase chain reaction (PCR) panel was positive for adenovirus and did not identify other enteric pathogens. Alternative etiologies, including significant recent exertion, medication-related muscle injury, toxin exposure, autoimmune myopathy, and inherited metabolic disorders, were considered but were not supported by the clinical history or disease course. The patient was treated with early intravenous isotonic fluid 1L every 6 hours and experienced progressive biochemical and clinical improvement without developing acute kidney injury. Adenovirus-associated rhabdomyolysis is an uncommon but increasingly recognized clinical entity in adults. The pathogenesis may involve direct viral muscle injury, immune-mediated inflammation, and contributory factors such as dehydration associated with gastrointestinal illness. Although adenovirus was considered the most likely precipitating factor in this case, a definitive causal relationship cannot be established. This case highlights probable adenovirus-associated rhabdomyolysis in an immunocompetent young adult presenting predominantly with gastrointestinal symptoms and preserved renal function despite marked creatine kinase elevation. Early recognition, careful evaluation of alternative etiologies, and prompt supportive management are important for preventing complications and achieving favorable outcomes.

Soft tissue synovial sarcoma is a rare mesenchymal tumor that mainly affects deep soft tissues of the extremities in young adults, but it is also recognized as a primary pulmonary neoplasm. Primary pulmonary synovial sarcoma (PPSS) accounts for less than 0.5% of all primary lung malignancies. Unlike other primary lung malignancies, PPSS has no known association with tobacco exposure and environmental carcinogens. It is characterized by an aggressive clinical course and a defining chromosomal translocation, t(X,18)(p11;q11), resulting in the fusion of the SYT gene on chromosome 18 with SSX1 or SSX2 on chromosome X. A 60-year-old woman with a 50-pack-per-year smoking history presented with gross hematuria and was incidentally found to have a right lower lobe lung mass on chest radiography. Positron emission tomography (PET) and computed tomography (CT) demonstrated a 7.1 x 6.6 cm supradiaphragmatic pulmonary mass without lymphadenopathy or distant metastases. Biopsy confirmed synovial sarcoma. Due to borderline pulmonary function, she was initially deemed a poor surgical candidate and referred to a sarcoma specialty center, where neoadjuvant chemotherapy with Adriamycin, Ifosfamide, and Mesna was initiated locally. After four cycles, follow-up imaging showed tumor reduction greater than 30% and no evidence of metastatic disease. Her lung function improved following smoking cessation, and she subsequently underwent a right lower lobectomy, with pathology revealing a largely necrotic synovial sarcoma with peripheral residual tumor, negative margins, and negative lymph nodes. Then, 4 months postoperatively, surveillance imaging revealed widespread metastatic sarcoma with innumerable pulmonary metastases, a large omental mass, and invasion of the right supraspinatus and scapula. Palliative management was initiated, but subsequent imaging demonstrated metastatic disease progression, showing more than 50 metabolically active pulmonary nodules, omental carcinomatosis, peritoneal metastases, and abdominopelvic ascites. This case highlights the aggressive clinical course of PPSS despite optimal multimodal therapy including neoadjuvant chemotherapy and complete surgical resection. Recurrence and metastasis remain common even following apparent initial response to therapy, underscoring the need for improved targeted systemic therapies and broader access to clinical trials for this rare malignancy.

Von Hippel-Lindau (VHL) disease is a rare familial autosomal dominant disorder with an incidence rate of approximately 1 in 36,000. It primarily results from mutations or inactivation of the VHL tumor suppressor gene located on chromosome 3p25-p26. The hallmark of this disease is hereditary hemangioblastoma, which can affect multiple organs and systems, including the brain (commonly infratentorial), spinal cord, retina, and internal organs such as the kidneys, adrenal glands, and pancreas. Less commonly, lesions may include papillary cystadenomas and endolymphatic sac tumors (ELST), which can form in the epididymis or broad ligament. The leading causes of death in these patients are hemangioblastomas and renal cell carcinoma of the central nervous system. Due to the multidisciplinary nature of the disease, diagnosis and management require a multidisciplinary team (MDT) consultation and collaboration among various specialties. Clinical diagnosis, genetic implications, and prognosis must be assessed comprehensively, with genetic testing confirming the diagnosis. Cases of VHL are exceptionally rare in clinical practice, and there remains a significant unmet need for effective treatments, particularly in rare tumors. Misdiagnosis and mistreatment are common, and repeated surgical interventions can exacerbate kidney damage. Early and accurate diagnosis, followed by proactive treatment, can significantly improve prognosis. Recently, our department admitted two patients with VHL-deficient renal cell carcinoma. Through surgery, radiofrequency ablation, and subsequent targeted therapy, the therapeutic outcomes were highly favorable. This report introduces the treatment of these two cases and provides a literature review on the current progress in the diagnosis, treatment, and prognosis of VHL-deficient renal cell carcinoma. Additionally, it discusses data on the screening of VHL patients and their close relatives, while emphasizing the optimization of individualized management for renal cell carcinoma to enhance the understanding, diagnosis, and treatment of the disease.

Strongyloides stercoralis is an intestinal nematode with a unique autoinfective life cycle that enables decades-long persistence in the human host. Its gastrointestinal manifestations may resemble inflammatory bowel disease (IBD), creating a clinically important diagnostic pitfall. Misdiagnosis is particularly hazardous because corticosteroids or other immunosuppressive therapies may precipitate Strongyloides hyperinfection syndrome or disseminated disease. We report a 52-year-old immunocompetent woman from northern Iran who presented with a 20-day history of persistent watery inflammatory diarrhea, severe hypokalemia (2.4 mEq/L), leukocytosis, and thrombocytosis. Serial stool examinations for ova and parasites were repeatedly negative for larvae; however, fecal leukocytes and erythrocytes, together with erosive duodenopathy, initially raised concern for IBD. Duodenal biopsy established the diagnosis by demonstrating marked eosinophilic infiltration of the lamina propria, reaching 45-50 eosinophils per high-power field, and rhabditiform larvae within the mucosal crypts. The larvae showed morphologic features supporting Strongyloides stercoralis, including a short buccal cavity/canal and a characteristic rhabditiform esophagus. Molecular testing, serology, and independent expert parasitologist confirmation were not performed, which represents a diagnostic limitation. The patient was treated with oral ivermectin plus adjunctive albendazole. The addition of albendazole was an individualized, non-standard clinical decision rather than a routine evidence-based recommendation. Her symptoms improved rapidly, and she remained asymptomatic at one-month follow-up. This case emphasizes the clinical and histopathological overlap between duodenal strongyloidiasis and IBD, particularly when stool parasitology is unrevealing. The novelty of this report lies primarily in its didactic value for clinicians in endemic regions: Strongyloides should remain in the differential diagnosis of IBD-like presentations with unexplained eosinophilic mucosal inflammation before immunosuppressive therapy is considered.

Cushing's syndrome in early childhood is rare and may be particularly challenging to diagnose when adrenal imaging is unrevealing. We report the case of a 23-month-old girl who presented with rapid weight gain, cushingoid appearance, hypertrichosis, severe hypertension, irritability, and developmental regression. Biochemical assessment confirmed adrenocorticotropic hormone (ACTH)-independent hypercortisolism, with suppressed ACTH, loss of circadian cortisol rhythm, lack of cortisol suppression following dexamethasone administration, and increased 24-hour urinary free cortisol excretion. Adrenal magnetic resonance imaging showed morphologically normal adrenal glands. Adrenal computed tomography was not performed, to avoid additional ionising radiation after a non-diagnostic adrenal MRI in a 23-month-old child. Adrenal scintigraphy with ¹³¹I-NP-59 after metyrapone-induced suppression demonstrated bilateral adrenal uptake, slightly more prominent on the right. The patient underwent right adrenalectomy. Histopathological examination showed micronodular adrenocortical hyperplasia without pigmentation, atypia, or malignant features, consistent with isolated micronodular adrenal disease. Following surgery, blood pressure, metabolic abnormalities, cutaneous manifestations, and motor function improved markedly. Steroid supplementation was required for only 3 days post-operatively, with no evidence of persistent adrenal insufficiency. At 3 years of follow-up, there were no clinical features of recurrent hypercortisolism, blood pressure remained normal without antihypertensive therapy, body mass index had markedly improved, and available biochemical parameters were reassuring. This case highlights that isolated micronodular adrenal disease should be considered in very young children with ACTH-independent Cushing's syndrome even when adrenal magnetic resonance imaging is normal. Functional adrenal imaging may be useful in selected cases, and unilateral adrenalectomy may achieve durable remission while delaying permanent adrenal insufficiency.

Leadless pacemakers offer an important alternative for patients with recurrent cardiac implantable electronic device infections. However, clinical data on long-term management and sequential implantation strategies after battery depletion remain limited. We aimed to evaluate the feasibility and safety of a sequential leadless-only pacing strategy in a patient with a multi-decade history of pacing-related complications. We report the long-term clinical course of a patient with a 26-year history of cardiac pacing (2000-2026). Following multiple transvenous system failures and recurrent infections, the patient transitioned to a leadless platform in 2017. We describe the clinical rationale and procedural outcome of upgrading from a depleted first-generation leadless pacemaker (Micra VR, implanted 2017, left in situ at the right ventricular septum) to an AV-synchronous leadless pacemaker (Micra AV, implanted 2025 because of battery depletion of the prior device, not infection) using a leave-in-situ approach. Sequential implantation was successfully performed in 2025, with the new device implanted at the right ventricular mid-septum while the previously implanted device was left in situ. Acute electrical parameters were satisfactory (pacing threshold 0.63 V, R-wave amplitude 9.8 mV, impedance 720 Ω), with no evidence of inappropriate sensing. At follow-up, electrical parameters remained stable (pacing threshold 0.50 V, impedance 670-650 Ω), with atrioventricular synchrony of 80% at 1 month and 84-85% at 3-6 months. No clinical or device-telemetry evidence of mechanical interaction or electrical interference between the devices was observed during follow-up. No device-related complications occurred during follow-up. A sequential leadless-only pacing strategy, including a leave-in-situ approach, may represent a feasible and safe long-term option in selected high-risk patients with device-related infections and a history of transvenous system extraction.

Meningioma-associated acute subdural hematoma (ASDH) is an exceedingly rare clinical entity, and its hemorrhagic mechanisms remain poorly understood. A 65-year-old man presented with progressive headache without a history of trauma. Neurological examination revealed no focal deficits. Computed tomography demonstrated a left convexity acute subdural hematoma, while magnetic resonance imaging revealed a small adjacent extra-axial lesion with mild contrast enhancement. Digital subtraction angiography showed only minimal tumor staining and no evidence of vascular malformation. The patient underwent gross total resection of the tumor and evacuation of the hematoma. Histopathological examination confirmed a meningothelial meningioma with focal disruption of intratumoral venous structures, intratumoral hemorrhage, necrosis, and focal areas of increased proliferative activity. The postoperative course was uneventful, and the patient recovered without neurological deficits. Previously reported cases are discussed to provide clinical context and highlight the diverse presentations and management strategies of this rare condition. Although rare, meningioma should be considered a potential source of non-traumatic ASDH. Because reliable preoperative predictors of hemorrhage have not been established, management should be individualized according to tumor-hematoma continuity, neurological status, surgical feasibility, and patient preferences.

Perioperative dexamethasone is commonly used in enhanced recovery protocols, yet its safety in adrenalectomy remains underevaluated. We report a 33-year-old woman who developed postoperative adrenal crisis-like deterioration 54 hours after right adrenalectomy for a radiologically and biochemically non-functioning adrenal tumor on basal preoperative testing. A single 5 mg intravenous dose of dexamethasone was administered intraoperatively for antiemetic prophylaxis. During clinical deterioration, the patient exhibited marked suppression of ACTH and cortisol, consistent with pharmacological glucocorticoid effects in the perioperative period. However, the clinical presentation was non-specific and alternative postoperative complications, including infection, thromboembolic disease, and metabolic disturbances, could not be fully excluded. The patient improved following combined supportive therapy and stress-dose hydrocortisone. Preoperative endocrine evaluation did not include a 1 mg overnight dexamethasone suppression test, and mild autonomous cortisol secretion could not be excluded. Dynamic assessment of adrenal reserve was not performed preoperatively. This case highlights that perioperative dexamethasone may be temporally associated with postoperative endocrine perturbations that mimic adrenal crisis in susceptible patients. However, causality cannot be established, and careful differential diagnosis is essential in the postoperative setting following adrenal surgery.

Congenital neck anomalies in neonates often present diagnostic dilemmas, particularly when they communicate with the aerodigestive tract. This report describes a rare case of a large, compressive neck cyst in a 28-day-old neonate. Initially presenting as a progressively enlarging cervical mass, the lesion's potential for airway communication was identified by the presence of intralesional air-fluid levels on computed tomography and magnetic resonance imaging. Advanced diagnostic techniques, including virtual bronchoscopy and intraoperative laryngoscopy, were utilized to successfully localize a direct communication between the cyst and the left false vocal cord. This finding confirmed the diagnosis of a rare branchial apparatus anomaly rather than a simple cervical abscess or cystic hygroma. The patient underwent definitive management through complete surgical excision and ligation of the communicating tract, resulting in a full recovery without recurrence. This case highlights the importance of recognizing specific radiological markers, such as air-fluid levels, as indicators of airway communication. It further emphasizes that while these lesions may mimic infectious processes, successful outcomes rely on a high index of clinical suspicion, precise anatomical localization through multimodal imaging, and definitive surgical intervention over simple drainage procedures.