Vascular Malformations Research Articles

Spina bifida is a common congenital anomaly caused by the incomplete fusion of the caudal neural tube, classified as spina bifida aperta (open) with a visible lesion and spina bifida occulta (closed) without external lesions. Its causes are diverse, including genetic factors, reduced intake of folate and nutrients, maternal obesity, diabetes and certain teratogens. Most cases may be prevented with maternal folic acid supplementation. Closed spinal dysraphism is harder to diagnose due to the lack of evident lesions, but may be suspected in asymptomatic newborns with midline skin signs. The paper describes the case of a newborn presenting with an atypical lumbosacral dimple linked to a lumbosacral vascular malformation. Radiological imaging (US and MRI) facilitated early detection and treatment of the neural tube defect, preventing progressive neurological and orthopaedic damage linked to tethered cord syndrome.

Vascular anomalies are classified into vascular tumors and vascular malformations. Hemangiolymphangioma (HLA) is a rare vascular malformation that contains both blood and lymphatic components, most commonly diagnosed in infancy or early childhood. Adult cases, especially in atypical locations such as the medial thigh, are exceedingly rare and pose diagnostic challenges. A 27 yo female presented with a slowly enlarging, painless lump on the left medial thigh. Initially misdiagnosed as condyloma acuminata, the lesion was subsequently identified as a vascular malformation through dermoscopic visualization of characteristic vascular lacunae. Histopathological and immunohistochemical analyses confirmed the diagnosis of HLA. Surgical excision was performed with clear margins, and no recurrence was observed after 3 mo. Hemangiolymphangiomas are benign but may exhibit local infiltration and recurrence, especially after incomplete resection. Diagnosis requires a multimodal approach including clinical assessment, dermoscopy, histopathology, and immunohistochemistry. Differential diagnosis includes hemangioma, lymphangioma, and malignancies such as lymphangiosarcoma. Complete surgical excision remains the treatment of choice, with other modalities like electrocautery or cryotherapy considered in selected cases. Long-term follow-up is crucial due to the risk of recurrence. In conclusion, this rare adult case of medial thigh HLA highlights the importance of considering vascular malformations in atypical anatomical sites. Early recognition and comprehensive diagnostic evaluation facilitate appropriate management and improve patient outcomes

Background: Hereditary hemorrhagic telangiectasia (HHT) and hereditary pulmonary arterial hypertension (HPAH) are genetic diseases that affect the pulmonary vasculature. HHT and HPAH are due to a haploinsufficiency in components of the bone morphogenetic protein receptor type 2 (BMPR2) pathway. Despite shared genetics, HHT and HPAH cause different pulmonary vascular lesions. In HHT, pulmonary arteriovenous malformations (pAVMs) can occur. These are abnormal shunts between arteries and veins that can lead to stroke. HPAH is characterized by extensive remodeling of the lung including the formation of plexiform lesions, convolutes of vascular channels that were described as a pathological hallmark of PAH. The pathobiology of pAVMs and plexiform lesions is incompletely understood. Recent studies suggest that a local bi-allelic loss of HHT causing genes in clonally expanding endothelial cells (ECs) might be required for AVMs to form in patients with HHT. In plexiform lesions, clonal EC expansion was also described. Hypothesis: We hypothesized that local somatic mutations in ECs might be involved in the pathogenesis of pulmonary vascular lesions in HHT and HPAH. Aims: We here aimed at detecting somatic mutations in pulmonary vascular lesions of a patient with HHT and end-stage PAH caused by a mutation in ENG . Methods: Targeted deep sequencing of 3 HHT causing genes and 11 vascular malformation associated genes was performed on 4 pAVMs and 14 plexiform lesions of the patient. Results: The disease-causing germline mutation in ENG was detected in every sample. No somatic mutation in the functional allele of ENG was detected in the pulmonary vascular lesions. However, we identified a somatic mutation in the gene encoding for Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Alpha ( PIK3CA) in one of the plexiform lesions. This mutation is a confirmed activating somatic mutation in the Catalogue Of Somatic Mutations In Cancer that was previously functionally confirmed as a moderately potent oncogenic mutation. Conclusion and Outlook: We here describe a rare case of an ENG mutation carrier with HHT and HPAH. We identified a somatic activating mutation in PIK3CA in one of her plexiform lesions. To explore if the mutation contributes to the overgrowth of ECs in a plexiform lesion on a background of a haploinsufficiency in ENG , we are performing functional studies on iPSC-derived ECs from this patient after introduction of the mutation in PIK3CA by Crispr/Cas9.

At the full-term birth of a healthy girl, a swelling was observed in her mouth. Clinical examination revealed a firm, elastic swelling, pedunculated to the superior alveolar process. The swelling, larger than 2 centimeters, hindered mouth closure and prevented normal feeding. It did not interfere with breathing. An MRI scan ruled out vascular malformations, after which the pedicle was surgically removed under general anaesthesia. Histopathological examination showed a subepithelial mass consisting of cells with abundant granular cytoplasm, consistent with the diagnosis of congenital epulis. Congenital epulis is a rare benign tumour, occurring on the upper jaw of newborns. The condition has an incidence of 6 in 1,000,000 and predominantly occurs in girls. Its aetiology is unknown. If there are no feeding or breathing issues, one can await spontaneous regression.

ABSTRACTBronchial artery‐pulmonary artery fistula (BPAF) is an uncommon vascular malformation with a left‐to‐right shunt. We report a case of a 72‐year‐old woman diagnosed with BPAF with two arterial feeders who had no underlying lung diseases and presented with intermittent haemoptysis. Her digital subtraction angiography confirmed BPAF supplied by the right bronchial artery (BA) from the intercostobronchial trunk and another ectopic accessory right BA originating from the right subclavian artery. Considering the future risk of catastrophic rupture due to high systemic pressure exerted on the fistula, prophylactic embolisation procedures via a percutaneous approach were performed. The pulmonary artery was first embolised for outflow control, followed by coil and microvascular plug embolisation on the right BA. The ectopic accessory right BA was later embolised with coil and microvascular plug as a staged procedure. A 14‐month post‐procedure computed tomography scan confirmed complete thrombosis of both BAs. Our case highlights the efficacy and safety of endovascular embolisation in BPAF.

Sclerotherapy with Polidocanol for Head and Neck Vascular Anomalies: A Single-Center Experience.

Introduction: Cognard-type V arteriovenous fistulas are rare forms of dural arteriovenous malformations. This specific subtype is characterised by spinal venous drainage into peri-medullary veins, which presents as progressive or ascending myelopathy in 50% of cases. Case Presentation: A 59-year-old man with three weeks of worsening quadriparesis, along with abnormal sensory findings, gait deterioration, and bowel and bladder dysfunction, was admitted to the hospital. MRI revealed extensive T2 hyperintense signal changes in the brainstem and myelopathy in the cervical spinal cord extending down to C7. The differential diagnosis for extensive myelopathy and brainstem lesions seen on MRI included a tumour, autoimmune inflammation, and suspicion of vascular malformation. The administration of corticosteroids resulted in a worsening of the patient’s neurological symptoms. Conventional angiography confirmed the presence of a dural AVF (a small arteriovenous short shunt receiving arterial supply from the middle meningeal and occipital artery) in the territory of the left external carotid artery. A minimally invasive endovascular treatment was successfully performed. Conclusion: We present this case considering that only 100 patients with Cognard type V fistula have been reported to date. Additionally, we aim to highlight the importance of caution when administering corticosteroids in cases of diagnostic uncertainty.

Background:Aberrant anterior tibial artery (AATA) is an uncommon variation of the anterior tibial artery. It is an important vascular variation that increases the risk of vascular complications in some knee surgeries (high tibial osteotomy, posterior cruciate ligament reconstruction, etc).Hypothesis:The anatomic and morphometric features of AATA remain unclear. The authors hypothesize that the posterior femoral morphology and popliteus muscle-related features may be associated with the presence of AATA.Study Design:Cross-sectional study; Level of evidence, 3.Methods:Between December 2022 and December 2024, knee magnetic resonance imaging (MRIs) were analyzed to detect AATA. Images in which image analysis was not optimal due to artifacts, images of patients with previous surgery around the knee, and patients with vascular malformations in the lower extremity were excluded. A control group was formed through computer-assisted randomization, comprising an equal number of men and women with AATA as patients. The condylar twist angle, posterior condylar angle (PCA), posterior tibiofemoral angle, popliteus sulcus depth (PSD), and PSD/lateral condylar width (LCW) parameters were measured on the MRIs of all patients and recorded for each patient. Patients with AATA variation were scanned for the presence of MRI of the opposite knee outside the time interval determined for the study, and it was analyzed whether patients with opposite knee MRIs had bilateral AATA.Results:After applying the inclusion and exclusion criteria, 4075 knee MRIs were analyzed. A total of 78 AATA variations were detected, with a prevalence of 1.91%. The prevalence of AATA was 2.04% in women and 1.78% in men. The PCA was statistically higher in patients with AATA compared with the control group (P < .005). PSD and PSD/LCW were found to be lower in patients with AATA compared with the control group (P = .012, P = .05). The prevalence of bilateral AATA in patients with AATA variation was 48.5%.Conclusion:The prevalence of AATA was found to be 1.91%. High PCA, low PSD, and PSD/LCW are radiologic parameters associated with AATA variation. Both the popliteus musculature and posterior femoral morphometry are related to the occurrence of AATA variation.

Abstract Spinal cavernous malformations are rare vascular malformations with an unclear natural history, especially in de novo cases without prior radiation exposure or genetic predisposition. Although surgery is often recommended for symptomatic hemorrhagic lesions, spontaneous regression is extremely rare. A 74-year-old man presented with isolated neck pain after a minor head trauma. Computed tomography revealed a hyperdense lesion in the C2 spinal canal, and magnetic resonance imaging (MRI) showed a 16 × 9 × 20 mm intradural, intramedullary mass with protruding extramedullary hemorrhagic features, consistent with a cavernous malformation. A previous MRI 1 year earlier showed no abnormalities, confirming its de novo nature. Surgery was initially planned due to the risk of rebleeding. However, the patient's symptoms resolved spontaneously. A follow-up MRI 9 days later revealed significant regression, with continued involution observed over 5 years. This is the first reported case of spontaneous regression of a de novo spinal cavernous malformation, suggesting that in selected patients, conservative management with serial imaging may be safe in asymptomatic or minimally symptomatic patients showing early regression. Possible mechanisms include hematoma resorption, vascular thrombosis, or cerebrospinal fluid mediated clearance. Further studies are needed to identify predictive factors for regression and refine treatment strategies.

Tumor Metabolic Behavior modulates the immunosuppressive microenvironment through multiple pathways, thereby compromising anti-tumor immune responses. To date, there have been limited studies assessing the role of metabolic plasticity or immunometabolism in the tumor microenvironment (TME) during metastasis. Notably, emerging evidence suggests the presence of an immunosuppressive niche in brain metastases. This research aims to delineate distinct metabolic signatures in brain metastatic, investigate the impact of tumor-associated glycolysis on the development of brain metastases in lung adenocarcinoma, and characterize the lactylation regulation in this immunosuppressive microenvironment. The GSE131907 and GSE198291 datasets were retrieved for bioinformatic analysis. Combined with the results of proteomic and transcriptomic sequencing conducted on the lung adenocarcinoma brain metastasis model, differentially expressed signaling pathways were systematically identified through KEGG and GO functional annotations. A multimodal approach encompassing immunohistochemical (IHC) staining, immunofluorescence (IF) imaging, enzyme-linked immunosorbent assay (ELISA) quantification, and co-immunoprecipitation (Co-IP) assays was employed to experimentally validate the characteristics of the immunosuppressive microenvironment and the levels of tumor lactate/lactylation. Rescue experiments were performed by adding a lactylation-specific inhibitor (LDHi) or an H3K18la site-specific inhibitor. Finally, immunohistochemical staining was used to verify the expression level of H3K18la in clinical samples. A total of 86,215 cells were extracted from the GSE131907 dataset, and the metabolic profiles of different cell types were analyzed. The results showed that glycolysis plays a dominant role in tumor cell metabolism. Further analysis revealed that early-stage primary lesions exhibit an inflammatory response signature, while advanced-stage primary lesions and brain metastatic lesions display an immunosuppressive signature. Elevated glycolytic flux showed a significant positive correlation with both the progression of brain metastasis and the immune evasion capacity of brain metastatic lesions. Pathological evaluation of tumor tissues from the LLC-BM (Lewis Lung Cancer Brain Metastasis) model confirmed its immunosuppressive characteristics. Additionally, obvious hypoxia was observed in the tumor tissues, accompanied by intratumoral vascular malformation and dysfunction. Significant lactate accumulation was present in the tumor microenvironment of LLC-BM tumors, and prominent lactylation modifications were detected in the tumor regions. In this model, Rac2 was identified as a potential core mediator of lactylation modification in macrophages, promoting the M2 polarization of macrophages. Meanwhile, CD40, TNFSF13 and CCL22 were identified as key immunoregulatory factors regulated by lactylation signaling. Notably, H3K18la was significantly highly expressed in lung cancer brain metastatic lesion samples. The glycolytic pathway plays a critical role in the metabolic reprogramming of tumor cells during lung adenocarcinoma brain metastasis. Tumor glycolysis is closely associated with lung cancer progression, brain metastasis, and immune evasion. The Rac2 could be affected by lactylation, and then facilitate the formation of an immunosuppressive tumor microenvironment by induce the M2 polarization of macrophages.

Relevance. Telangiectasia is a vascular malformation characterized by a network of thin, interconnected blood vessels with multiple anastomoses. It occurs most commonly on the skin and less frequently on mucosal surfaces. One of the etiological factors in its development is exposure of tissues to ionizing radiation. Case presentation. This article presents a clinical case of oral mucosal telangiectasia in a female patient as a late complication of radiation therapy for a malignant tumor of the tongue. Conclusion. Recognizing the manifestations of primary and secondary radiation-induced complications allows dental practitioners to make an accurate diagnosis and choose an appropriate treatment strategy.

Advances in genetic sequencing technology have enabled identification of the somatic and germline variants that underlie many vascular anomalies. These pathogenic variants often affect one of two signalling pathways: (1) the PI3K (phosphoinositide 3-kinase)/AKT (protein kinase B)/mTOR (mammalian target of rapamycin) pathway and (2) the RAS (rat sarcoma)/RAF (rapidly accelerated fibrosarcoma)/MEK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) pathway. This narrative review aims to synthesize the existing knowledge on the genetic origin of vascular anomalies and the targeted therapeutic approaches. A literature search was conducted using PubMed, Google Scholar and EMBASE, with a key focus on genetic pathways and emerging therapies. mTOR inhibitors have shown efficacy in a range of venous, lymphatic, capillary and syndromic vascular malformations. PIK3CA inhibitors are already commonly used in the treatment of PIK3CA-related overgrowth spectrum (PROS), with current research into new mutant-specific inhibitors aiming to improve selectivity and reduce toxicity. AKT inhibitors are being trialled in Proteus syndrome and PROS. MEK inhibitors have shown efficacy in the treatment of capillary malformations with arteriovenous malformations (CM-AVM) and both MEK and BRAF inhibitors are being investigated for use in extracranial AVMs. Vascular anomalies were previously orphan diseases with minimal effective therapeutic approaches. The discovery of the precise molecular pathways underlying these anomalies has allowed existing drugs to be repurposed for genotype-guided management, enabling a 'personalized' approach to patient care.

Pelvic Puzzles: Imaging Non-Traumatic Emergencies of the Female Pelvis: A Comprehensive Review.

Vascular anomalies (VAs) require specialized multidisciplinary management. Bleomycin electrosclerotherapy (B)EST combines electroporation with intralesional bleomycin to enhance drug uptake while preserving surrounding tissue. Its role in treating VAs remains largely unexplored. This systematic review evaluates the efficacy, safety, and procedural protocols of BEST in VA treatment. Following PRISMA guidelines, a systematic search was conducted in PubMed, Web of Science, and Scopus. Inclusion criteria included peer-reviewed studies on (B)EST for VAs, excluding reviews, editorials, and animal studies. Among 1237 records, 15 studies met the inclusion criteria, published between 2012 and 2025, primarily from Europe (13/15). A total of 566 patients were treated, including 445 with vascular malformations and 121 with vascular tumors (Kaposi sarcoma, angiosarcoma). (B)EST was mainly applied to slow-flow malformations. Across VA types, lesion-volume or symptom reduction rate was high, with five studies each reporting a 100% rate. Complete response in vascular tumors ranged from 65 to 100%. Most studies followed current guidelines, with bleomycin doses between 200 and 10,000 IU per session. Adverse effects were primarily local and self-limiting (Cardiovascular and Interventional Radiological Society of Europe classification CIRSE 1a-2); ulcerations occurred mainly in vascular tumors (CIRSE 3a); and skin hyperpigmentation (CIRSE 1a) was observed frequently, often partially resolving over time. BEST shows promise for VA treatment, particularly venous and lymphatic malformations. While results suggest efficacy and safety, treatment heterogeneity and long-term outcomes require further investigation. Optimizing tailored protocols for each VA subtype and presentation is essential for defining (B)EST's role in VA management. Question What is the role and efficacy of (bleomycin) electrosclerotherapy (B)EST in managing vascular anomalies resistant to conventional treatments, including tumors and malformations? Findings (B)EST demonstrated significant efficacy, achieving 65-100% complete responses in vascular tumors and 54.9-100% lesion or symptom reduction in vascular malformations. Clinical relevance (B)EST offers an option for patients with treatment-resistant or recurrent vascular anomalies, improving symptom-related outcomes. This is tempered by the absence of controlled trials, the need for cumulative dose pulmonary monitoring and the potential cosmetic burden of hyperpigmentation.

Disclosure: K. Taquechel: None. P. Sinha: None.Background: Paragangliomas are rare neuroendocrine tumors that arise from autonomic paraganglioma and can potentially secrete excess catecholamines. Radiographic diagnosis of paragangliomas can present challenges as they often share features of other lesions including vascular malformations. Clinical Case: We present a case of a paraganglioma initially diagnosed as a renal artery aneurysm. A 55-year-old woman with a history of hypertension, multinodular goiter, and resected endometrial adenocarcinoma underwent a CT scan of the abdomen and pelvis for postmenopausal bleeding. She was incidentally found to have what appeared to be a right renal artery aneurysm and underwent endovascular stenting of the lesion. Five years later, she had a follow-up CT scan to evaluate the renal artery stent. The lesion originally thought to be an aneurysm had increased in size with new areas of heterogeneity. An MRI of the abdomen was thus performed, and imaging characteristics appeared consistent with a paraganglioma. She was referred to endocrinology. Blood testing was notable for an elevated plasma normetanephrine level (777 pg/mL) and chromogranin A (279 ng/mL). Urine testing showed an elevated normetanephrine level (1615 mcg/24h) and norepinephrine level (261 mcg/24h). She was pre-treated with doxazosin and metoprolol before undergoing successful resection of the paraganglioma and radical nephrectomy. Subsequently, her blood pressure improved and she required only one, rather than three antihypertensive agents. She also noted an improvement in mood and energy after surgery. Genetic testing was negative for any known mutations associated with paragangliomas. Conclusion: Paragangliomas can present a diagnostic challenge as they can resemble other lesions including, rarely, vascular malformations. To our knowledge, this case is the first to describe a paraganglioma mimicking a renal artery aneurysm. When such lesions demonstrate atypical characteristics (such as growth over time) rarer pathologies such as paragangliomas may need to be considered as they require a multidisciplinary approach for appropriate treatment. Reference: 1) Neumann, H. P. H., Young, W. F., & Eng, C. (2019). Pheochromocytoma and Paraganglioma. The New England Journal of Medicine, 381(6), 552-565. 2) Chow S, Chu R, Ho S, Chan A, Burd A. Paraganglioma Presenting as a Vascular Malformation: Case Report. Journal of Plastic, Reconstructive & Aesthetic Surgery : JPRAS. 2006;59(1):90-3. 3) Rajoo AR, Kannairan S, Habeebullah Khan HA, Md Idris MA, Tan GC, Chandra Sakaran KR, Safri LS. Case report: Paraganglioma masquerading as angiosarcoma: diagnostic-dilemma in vascular tumors. Front Oncol. 2024 Dec 5;14:1462956.Presentation: Sunday, July 13, 2025

Disclosure: H.C. Davuluri: None. A. Thomas: None.Introduction: Adrenal insufficiency can present in a dramatic manner with a myriad of initiating events. Case: A 20-year-old woman with history of Arnold-Chiari type I malformation presented to her physician’s office with complaints of shortness of breath, palpitations, lightheadedness, and fatigue. She had abnormal T-wave changes on EKG, prompting a referral to the ED. Workup revealed: Sodium 134 mEq/L [range: 135-145], potassium 5.4 mEq/L [3.5-5], D-dimer 0.37 (negative), Troponin normal x 2, FT4 0.977 ng/dl [0.8-1.9], TSH 6.260 mIU/L [0.4-5]. After ondansetron and IV fluid administration, she was markedly improved and discharged with a plan for close follow-up. A week later, repeat labs showed: sodium 131 mEq/dl, K 3.7 mEq/dl, TSH 5.500 mIU/L, fT4 1.09 ng/dl, fT3 5 ng/dl. TPO antibody was negative. She started on levothyroxine 25 mcg daily. Four days later, she presented again to the ED with confusion, generalized weakness, altered mental status, and symptoms concerning for stroke. On exam, she was hypotensive, lethargic, not oriented to time, place or person, with incoherent speech and generalized skin hyperpigmentation. Labs were remarkable for sodium 119 mEq/dl, Cr 0.77 [<1.2], glucose 117, urine tox negative. Initial head CT showed diffuse brain swelling with loss of dilation and descent of the cerebellar tonsils, which was attributed to Arnold-Chiari type I malformation. CTA was negative for large vessel occlusion, aneurysm, or vascular malformation. She was given hypertonic saline followed by normal saline to correct her sodium at a rate of 8 to 10 mEq per 24 hours, treated as acute severe hyponatremia. Endocrinology and nephrology teams were consulted. Her random cortisol was 0.9 ng/dl [2-25], and ACTH of 1620 pg/ml [7.2-63.3], which raised concern for primary adrenal insufficiency. An ACTH stimulation test was done which showed no cortisol response. CT abdomen showed small adrenal glands with no evidence of hemorrhage. After the administration of hydrocortisone, her sodium began to normalize. To prevent overcorrection of her sodium, she received one dose of DDAVP to help maintain sodium stability and address polyuria. 21-hydroxylase antibody was negative. FSH, LH, and prolactin levels were normal. Her presentation was attributed to the initiation of levothyroxine in the context of previously undiagnosed adrenal insufficiency. The patient was started on hydrocortisone and fludrocortisone, which she continued as outpatient therapy with stability in her labs and clinical status. Conclusion: The initiation of levothyroxine in this patient, who had an underlying undiagnosed adrenal insufficiency, likely triggered her severe adrenal crisis. Although rare, this serious and life-threatening presentation underscores the importance of a comprehensive approach to the evaluation and treatment of adrenal crisis.Presentation: Monday, July 14, 2025

A clinical nomogram for predicting recurrence after percutaneous radiofrequency ablation in the management of primary hemifacial spasm.

Intravascular papillary endothelial hyperplasia (IPEH), also known as Masson tumor, is a rare vascular benign tumor of blood vessels. It may occur in any part of the body, especially the deep dermis and subcutaneous tissue of the head, neck, fingers and trunk. The imaging and histopathology of IPEH are similar to hemangiosarcoma, especially in the case of active vascular endothelial hyperplasia. IPEH is a reactive proliferative lesion of vascular intima. The etiology is still unclear. After some studies showed that IPEH was a benign lesion, few reports on the etiology of it were reported. IPEH is usually limited to the thrombotic vessels or lumens of vascular malformations, usually accompanied by a clear history of trauma. IPEH usually does not cause any symptoms. It looks like a slow-growing lump. Some cases have been reported with pain and swelling. Although IPEH is relatively rare, its accurate diagnosis is crucial because it may be similar to malignant angiogenic lesions in clinical practice. There were few reports of cases related to intravascular papillary endothelial hyperplasia located in the sternocleidomastoid muscle after reviewing the domestic and foreign literature in recent 10 years. This case reports that a young male, who was admitted to the hospital one month after finding a subcutaneous tumor in the left neck. After admittance, relevant preoperative examinations were completed. After multi-disciplinary discussion and elimination of surgical contraindications, a specific surgical plan was formulated. The tumor was removed under local anesthesia on the second day after admission. During the operation, it was found that the tumor was located between the sternocleidomastoid muscle bundles, and it was sent for pathologic examination. Paraffin section pathology was reported after operation. Histological examination showed that the morphology was consistent with vascular endothelial papillary hyperplasia. There were no related surgical complications and recurrence in the 3-month follow-up. The purpose of this paper is to provide clinicians with a certain understanding of this rare disease through the report of this case of IPEH, and to identify it in later clinical work, and at the same time, to avoid confusion with malignant diseases, such as hemangiosarcoma, leading to unnecessary treatment and increase the cost of treatment.

Exophytic Jejunal GIST Masquerading as a Vascular Malformation: A Important Diagnostic Pitfall.

Extracranial arteriovenous malformations (AVMs) are high-flow vascular malformations that are challenging entities to treat and are primarily managed with embolization alone. Single-stage embolization and resection is a technique occasionally used for treating intracranial arteriovenous malformations. This manuscript describes combined embolization and surgical resection for localized superficial extracranial AVMs by presenting three cases from our experience. A retrospective review of the medical records of patients in this series including clinical notes, procedural imaging, and follow-up documentation was performed. A total of three AVMs near the antecubital fossa, deltoid, and forehead were embolized and resected. There was no evidence of recurrence on follow-up imaging, and no complications were observed, specifically, overlying skin injury. Embolization and resection of localized superficial extracranial AVMs with overlying skin changes offer an alternative treatment option to existing paradigms.