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.

Homocystinuria caused by cystathionine β-synthase (CBS) deficiency is characterized by involvement of the eye (ectopia lentis and/or severe myopia), skeletal system (excessive height, long limbs, scolioisis, and pectus excavatum), vascular system (thromboembolism), and CNS (developmental delay/intellectual disability). All four ‒ or only one ‒ of the systems can be involved; expressivity is variable for all of the clinical signs. It is not unusual for a previously asymptomatic individual to present in adult years with only a thromboembolic event that is often cerebrovascular. Two phenotypic variants are recognized, B6-responsive homocystinuria and B6-non-responsive homocystinuria. B6-responsive homocystinuria is usually milder than the non-responsive variant. Thromboembolism is the major cause of early death and morbidity. IQ in individuals with untreated homocystinuria ranges widely, from 10 to 138. In B6-responsive individuals the mean IQ is 79 versus 57 for those who are B6-non-responsive. Other features that may occur include: seizures, psychiatric problems, extrapyramidal signs (e.g., dystonia), hypopigmentation of the skin and hair, malar flush, livedo reticularis, and pancreatitis.

Vascular complications following hyaluronic acid filler injections are rare but may lead to ischemia and necrosis. Effective management often relies on the early administration of hyaluronidase to restore perfusion and prevent long-term damage. However, delayed presentations pose unique challenges due to prolonged ischemia and increased risk of tissue necrosis. A 35-year-old woman presented 3 days after forehead filler injection with signs of vascular compromise. Initial treatment with 1800 U hyaluronidase failed. On presentation, she exhibited advanced ischemia with erythema, pustules, and livedo reticularis. A high-dose pulsed hyaluronidase protocol totaling 32,000 U for 4 days was initiated. Rapid improvement followed, with complete epithelialization by day 30 and near-complete recovery by day 90 without scarring. Despite delayed presentation, the high-dose pulsed hyaluronidase protocol successfully reversed ischemia and prevented necrosis, supporting its use in late-stage vascular complications.

Congenital dysfibrinogenemia (CD) and antiphospholipid syndrome (APS) are two distinct thrombotic disorders that can have significant clinical implications, especially in pregnancy. CD is a rare inherited condition caused by mutations in fibrinogen genes, leading to abnormal fibrin polymerization and fibrinolysis, and causes bleeding tendencies, thrombosis and pregnancy complications. APS, an acquired autoimmune disorder, increases the risk of recurrent thrombosis and adverse pregnancy outcomes, such as miscarriages and stillbirths. This report describes a 35-year-old woman with genetically confirmed congenital dysfibrinogenemia (CD) (heterozygous FGG c.1001A>C) who subsequently developed antiphospholipid syndrome (APS). Notably, although lupus anticoagulant and β2GP1-IgM positivity were present since 2017, APS remained undiagnosed until 2023, following her third miscarriage. In retrospect, she fulfilled the Sydney criteria with recurrent early pregnancy loss, persistent antibodies, and livedo reticularis. During her successful pregnancy in 2021, management focused exclusively on CD: fibrinogen levels were monitored (0.47-0.98 g/L), and fibrinogen concentrate was administered during cesarean delivery due to fetal growth restriction. This resulted in a live infant birth, despite the later recognition of placental thrombosis as APS pathology. This case highlights how CD may mask the diagnosis of APS. The aunt's uneventful pregnancy, with the same FGG mutation but no APS, confirms CD's limited obstetric impact. The delayed APS recognition underscores the importance of reevaluating antiphospholipid status in CD patients experiencing new thrombotic or obstetric events. However, the management of combined CD and APS remains theoretical.