West Nile virus neuroinvasive disease (WNND) most commonly presents as meningitis, encephalitis, or acute flaccid paralysis, with variable neuroimaging findings. While MRI abnormalities classically involve deep gray matter and brainstem structures, hemorrhagic manifestations are rarely reported. We report a 77-year-old woman who presented with rapidly progressive altered mental status following a brief febrile prodrome. Cerebrospinal fluid studies demonstrated a lymphocytic pleocytosis consistent with aseptic meningitis. Brain MRI revealed an acute lacunar infarct and diffuse cerebral microhemorrhages initially concerning for cerebral amyloid angiopathy. During hospitalization, she developed livedo reticularis-like peripheral skin changes prompting evaluation for autoimmune or vasculitic etiologies. Extensive infectious and autoimmune testing was ultimately notable for positive serum and CSF West Nile virus serologies, confirming neuroinvasive WNV infection. Despite transient neurologic improvement, her clinical course deteriorated, and she died following transition to comfort-focused care. This case highlights diffuse cerebral microhemorrhages as a potential finding in WNND, although their attribution remains uncertain. These findings may reflect underlying neurovascular inflammatory injury related to WNV or may represent coincident pathology and can mimic other small-vessel or autoimmune pathologies, complicating early diagnostic evaluation. Recognition of this expanded radiographic and clinical spectrum may aid timely diagnosis of WNND in patients with atypical presentations.

Transarterial chemoembolization (TACE) is a commonly used locoregional therapy for hepatocellular carcinoma (HCC), with rare complications related to nontarget embolization. We describe a case of hepatic falciform artery (HFA) embolization following drug-eluting bead TACE (DEB-TACE), resulting in transient ischemic injury of the anterior abdominal wall. A 71-year-old man with Child-Pugh A cirrhosis and multifocal HCC developed a livedo-reticularis-like rash over the epigastrium 2 days after DEB-TACE. Retrospective review of angiographic and cross-sectional imaging identified a hepatic falciform artery arising from the hepatic arterial system, consistent with nontarget embolization. The patient was managed conservatively, with complete resolution over several months. The HFA is an anatomically variable vessel that may be difficult to identify on angiography. Awareness of this entity is important to recognize characteristic imaging findings, guide patient counselling, and minimize procedural complications during TACE.

Vascular occlusion is an uncommon but serious complication of hyaluronic acid filler injections. If not recognized and managed early, it can lead to ischemia and even skin necrosis. Timely diagnosis and intervention are therefore crucial to minimize tissue damage and avoid long-term consequences. With the rising popularity of chin augmentation procedures, awareness of these rare complications is increasingly important for aesthetic practitioners. This report describes the case of a 54-year-old woman who presented with increasing pain, skin discoloration, and livedo reticularis approximately 24 hours after she had received hyaluronic acid filler injections in her chin. Clinical examination revealed delayed capillary refill time and mottled skin changes across the chin and neck. The high-dose pulsed hyaluronidase protocol was initiated 25 hours after injection. A total of 2850 IU of hyaluronidase was administered in a series of doses during a 15-hour period. Alongside enzyme therapy, the patient received oral aspirin, warm compresses, and gentle massage. Her symptoms improved quickly, and by day 21, she had fully recovered with no scarring or volume loss. This case highlights that even minimal filler volumes can trigger vascular occlusion. Preparedness to identify the vascular complications and apply the high-dose pulsed hyaluronidase protocol is essential to ensure full recovery and safeguard patient outcomes.

Lane-Hamilton syndrome is a rare association between idiopathic pulmonary hemosiderosis (IPH) and celiac disease that can present with isolated hemoptysis. We describe a case of a previously healthy 15-year-old female who presented with 1 month of intermittent hemoptysis, chest pain, and severe iron deficiency anemia. Physical examination was remarkable for mild conjunctival pallor and livedo reticularis. Extensive laboratory studies were obtained to rule out infectious, rheumatological, and oncological explanations of anemia. A chest radiograph showed an increased density in the left mid-lung and bilateral opacities, and computed tomography showed scattered multifocal ground glass opacities. Bronchoalveolar lavage revealed hemosiderin-laden macrophages consistent with the diagnosis of IPH. Additional workup for IPH revealed elevated celiac titers. Upper endoscopy confirmed the diagnosis of celiac disease, which led to a final diagnosis of Lane-Hamilton syndrome, a rare co-occurrence of IPH and celiac disease. The treatment plan included a course of systemic steroids and a gluten-free diet. Given this known association, workup for IPH should include testing for celiac disease since a gluten-free diet may prevent future occurrences of alveolar hemorrhage.

Abdominal aortic aneurysm is defined as the abnormal dilation of the abdominal aorta to a diameter of three centimeters or greater. The risk of rupture increases significantly when the aneurysm is greater than 6 centimeters in diameter. Ruptured abdominal aortic aneurysms carry a mortality rate of up to 83%, with up to a third of these deaths occurring before the patient reaches the hospital. Symptoms of dissection or rupture of the abdominal aorta include a tearing sensation in the back, lower extremity weakness, sudden and severe abdominal pain, and hypotension. Symptoms are often vague, and some patients have few symptoms until they develop hypotension and shock. In this case presentation, a 65-year-old male presented to the emergency department with sudden onset of leg weakness, and was noted to have a well demarcated livedo reticularis rash. A computed tomography scan showed a large abdominal aortic aneurysm with evidence of active hemorrhage within the aneurysm. He underwent surgical repair and was discharged in good condition.

STING‑associated vasculopathy with onset in infancy (SAVI) is a rare autoinflammatory disorder that causes systemic inflammation, vasculopathy, and progressive interstitial lung disease (ILD). The pulmonary manifestations of SAVI typically resemble a nonspecific interstitial pneumonia (NSIP) pattern both radiologically and histologically. We present a case of a 20‑year‑old male with genetically confirmed SAVI who developed acute hypoxic respiratory failure triggered by respiratory syncytial virus infection, despite appropriate treatment. Imaging revealed extensive subpleural fibrosis, traction bronchiectasis, and honeycombing. These findings were observed in the setting of a CT appearance strongly consistent with a definite usual interstitial pneumonia (UIP) pattern. Ultimately, the patient underwent a lung transplant, and histopathology of the explanted lungs revealed fibrotic changes, including diffuse interstitial thickening, lymphoid aggregates, and honeycombing, without definitive fibroblastic foci, indicating a mixed UIP and NSIP pattern of fibrosis. This case illustrates a rare UIP‑pattern imaging phenotype in SAVI‑associated ILD, despite a mixed UIP‑NSIP histologic pattern of pulmonary fibrosis, and highlights the potential for acute viral infection to precipitate decompensation in patients with interferon‑driven pulmonary fibrosis. Written informed consent was obtained from the patient for publication of this report and accompanying images.

We report a rare case of cholesterol embolization syndrome (CES) presenting with multifocal cerebral infarctions following thoracic endovascular aortic repair (TEVAR). A 75-year-old male with a 6.1 cm thoracic aortic aneurysm and extensive atherosclerotic disease ("shaggy aorta") underwent zone 2 TEVAR with left subclavian artery embolization after left carotid-subclavian bypass surgery. Postoperatively, the patient developed altered mental status with multifocal cerebral infarctions involving the left middle cerebral artery territory, bilateral cerebellar hemispheres, and pons. The characteristic findings included livedo reticularis, blue toe syndrome, leukocytosis (21,190/μL), elevated C-reactive protein (11.4 mg/dL), and acute kidney injury (creatinine 3.81 mg/dL). Despite supportive care, including continuous renal replacement therapy, the patient died of sudden cardiac arrest on hospital day 123. This case demonstrates the devastating potential of CES following TEVAR in patients with a shaggy aorta, emphasizing the importance of preoperative risk stratification and early recognition of the characteristic clinical triad of neurological symptoms, cutaneous lesions, and renal dysfunction.