A lymphocele is a collection of lymphatic fluid without epithelial lining, commonly occurring as a postsurgical complication. Most lymphoceles do not require treatment, but symptomatic lymphoceles can be successfully treated with surgery, percutaneous drainage and sclerotherapy, or lymphangiography with lymphatic embolization. Although drainage and sclerotherapy are effective in treating lymphoceles, their efficacy decreases in the setting of larger volume, ruptured, or multiseptated lymphoceles. Lymphangiography allows direct visualization of lymphatic vessels and identifies lymphatic leaks and guiding targeted interventions. Moreover, lymphangiography itself has therapeutic potential to directly treat lymphatic leakages. This case report describes a ruptured postkidney-transplant lymphocele, which dehisced the incision resulting in recalcitrant lymphorrhea. After drainage failed to resolve the lymphocele and sclerotherapy was deemed potentially risky to the kidney transplant, repeated lymphangiography sessions successfully treated the lymphocele and facilitated incisional healing.
BACKGROUND: Hypertension is a major driver of neurovascular dysfunction and cognitive decline, yet the molecular mechanisms linking elevated arterial pressure to impaired cerebral blood flow remain poorly defined. Piezo1, a mechanosensitive cation channel enriched in the brain endothelium, is a candidate mediator of cerebral blood flow deficits during hypertension. METHODS: Using 2 distinct mouse models of hypertension—BPH/2J mice (genetically hypertensive strain) and angiotensin II–infused C57BL/6J mice—we assessed brain endothelial Piezo1 activity using patch-clamp electrophysiology. Endothelial-specific Piezo1 deletion models were used to evaluate the role of the channel in hypertension-associated cerebrovascular impairment. Cerebral blood flow responses were measured in vivo by laser speckle contrast imaging, and super-resolution nanoscopy was used to quantify Piezo1 nanoscale organization. Behavioral testing was used to assess cognition. RESULTS: Genetic manipulation of endothelial Piezo1 had minimal impact on baseline blood pressure. However, cerebral endothelial Piezo1 activity was markedly elevated in different hypertension models. Deletion of endothelial Piezo1 protected against hypertension-induced cerebrovascular deficits, including impaired vasomotion, reduced functional hyperemia, and blunted CO 2 -evoked hyperemia. Super-resolution imaging revealed that hypertension increased Piezo1 clustering, consistent with electrophysiological findings of enhanced channel coupling and open probability. Mechanistically, Piezo1 hyperactivity was PKC (protein kinase C)–dependent, and the PKC-Piezo1 spatial association was enhanced during hypertension. Importantly, PKC inhibition normalized brain endothelial Piezo1 activity, restored cerebral blood flow responses, and rescued cognitive performance. CONCLUSIONS: Hypertension increased the gain of Piezo1 function in brain endothelial cells, promoting dysfunctional neurovascular signaling and cognitive impairment. Targeting Piezo1 or PKC signaling selectively restored cerebrovascular regulation. This work identifies a mechanosensitive pathway that could be leveraged to protect the hypertensive brain.
Background/Objectives: Radiofrequency (RF) wire energy can be used for tissue ablation across many conditions. Adjusting RF generator parameters allows RF energy to puncture tissue with minimal adjacent damage. When RF energy is applied to tissue, however, microbubbles are produced, obstructing intravascular ultrasound (IVUS). Mitigation of RF-generated microbubbles has been studied for ablation but not for puncture. Methods: This paper describes an in vitro bench study using ex vivo bovine live tissue. A model was created with bovine liver tissue and an IVUS catheter submerged in a saline bath. Tissue was punctured with an RF guidewire to recreate microbubbles. Following the puncture, various methods were applied: altering the mechanical index of the IVUS, applying a VF10-5 Linear probe (Siemens), and applying a L12-3 Linear probe (Philips). Regions of interest (ROIs) were selected to track pixel brightness as a proxy for microbubbles. Results: The control increased ROI brightness by 1.5%. Altering the mechanical index of IVUS reduced ROI brightness by 1.2%. VF10-5 probe application increased ROI brightness by 1.2%. L12-3 probe application reduced ROI brightness by 33.0% (p = 0.046, n = 3, one-sample t-test). Brightness reduction was most pronounced at the site of initial RF wire puncture, where microbubbles accumulated. Tip visualization improved, allowing for more precise wire trajectory adjustments. Conclusions: External US with an L12-3 probe was able to dissipate microbubbles effectively to improve IVUS guidance following RF wire puncture in an in vitro exploratory bench model.
External jugular venous pseudoaneurysms are rare and have been previously reported as spontaneous or congenital occurrences. This case describes a 72-year-old female who initially underwent ultrasound-guided needle aspiration of a complex, left supraclavicular cystic mass which subsequently resolved after 2 months. Approximately 4 years later, she returned with complaints of non-tender, left neck swelling in the location of her prior aspiration. Duplex ultrasonography revealed an active, iatrogenic external jugular vein pseudoaneurysm which was confirmed by CT angiography. While complications from venous pseudoaneurysm can arise, most asymptomatic patients do not require treatment and can be followed clinically and with imaging. This case report demonstrates the unusual presentation of an iatrogenic external jugular vein pseudoaneurysm following fine needle aspiration of a neck cyst.
Sclerosing peritonitis is uncommon and often arises as sequala of inflammation and may be asymptomatic or present with variable gastrointestinal symptoms. This case describes a 41-year-old female with decompensated alcoholic cirrhosis and refractory ascites who developed recurrent spontaneous bacterial peritonitis. Months later, she presented with failure to drain ascites on repeated paracentesis. Loculations and echogenic debris were visualized on abdominal ultrasound and percutaneous removal was performed revealing a 40 cm long pale white cord. Histopathologic analysis indicated features of sclerosing peritonitis without evidence of malignancy. This case demonstrates the unusual presentation, diagnosis, and treatment of sclerosing peritonitis, which only came to clinical attention when it impeded paracentesis in a patient with contraindications to other management options. Removal of this sclerotic tissue restored the ability to perform successful large-volume paracentesis for her refractory ascites.