Breast edema is a clinically significant but underrecognized complication following breast-conserving surgery (BCS) and radiotherapy. It involves parenchymal and cutaneous changes that can cause pain, functional impairment, and reduced quality of life. Despite overlapping risk factors and shared lymphatic pathophysiology with breast cancer-related lymphedema (BCRL), breast edema remains poorly defined, with no standardized diagnostic criteria and wide variability in reported incidence. In contrast to the extensive literature on arm lymphedema, breast edema, particularly in patients who develop BCRL, has not been systematically synthesized. A clearer understanding of this relationship is needed to improve recognition, diagnosis, and clinical management. This systematic review aims to analyze the association between breast edema and BCRL, focusing on the development of breast edema and its quantitative diagnostic criteria following BCS. Three databases (Ovid MEDLINE, EMBASE, and Web of Science) were searched for studies pertaining to breast edema and arm lymphedema following BCS. Studies underwent a multistep screening process to ensure they met the inclusion criteria before inclusion in this systematic review. To be included in this review, studies must have been peer-reviewed, published between 2015 and 2025, written in the English language, and relevant to the topic of breast cancer-related lymphedema following BCS. A total of 23 studies met our inclusion criteria, representing 10,402 women across 14 countries who underwent BCS. The prevalence of breast edema varied widely, ranging from 2.7% to 24.8% in clinically assessed cohorts and up to 72% in ultrasound (US)-based studies. Breast edema was more frequently observed following axillary lymph node dissection, larger breast volume, higher body mass index (BMI), postoperative cellulitis, and in patients with BCRL. Women with breast edema reported worse quality of life, greater breast pain, and poorer body image. Quantitative assessment methods, including US and tissue dielectric constant (TDC) measurements, identified both clinical and subclinical breast tissue changes, though diagnostic thresholds and assessment approaches varied substantially across studies. Overall, this review illustrates multiple factors that contribute to breast edema and arm lymphedema, yet also points to the need to improve assessment measures to both identify and prevent edema following BCS.

ObjectivePhlebolymphedema is a progressive condition caused by combined venous and lymphatic dysfunction. Although complete decongestive therapy (CDT) is widely used in clinical practice, objective evidence regarding its effectiveness across different disease stages is limited. This study aimed to evaluate the short-term effectiveness of CDT in patients with lower extremity phlebolymphedema and to examine the influence of disease stage and body mass index (BMI) on treatment response.MethodsThis retrospective study included patients with phlebolymphedema treated at a tertiary lymphedema clinic between 2020 and 2024. Chronic venous insufficiency was diagnosed by lower-extremity venous duplex Doppler ultrasonography, and lymphatic dysfunction was confirmed by lymphoscintigraphy. All patients completed a standardized intensive CDT program consisting of manual lymphatic drainage, multilayer compression bandaging, and therapeutic exercises for 10 sessions over 2 weeks. Extremity volume was measured using circumferential measurements and calculated with the truncated cone formula. Pre- and post-treatment volumes were compared, and associations with disease stage and BMI were analyzed.Results62 patients (72.2% female), corresponding to 108 affected lower extremities, were analyzed. The mean BMI was 36.5 ± 6.3 kg/m2. CDT resulted in a statistically significant reduction in extremity volume (median reduction: 0.55 L; p < .001). Treatment response differed across disease stages, with greater absolute volume reduction observed in Stage 3 disease (p = .007). A positive correlation was identified between BMI and volume reduction (ρ = 0.322, p = .0007). Age, sex, and history of venous surgery were not associated with treatment response.ConclusionCDT is an effective treatment modality for achieving a significant short-term reduction in extremity volume in patients with phlebolymphedema. Clinically meaningful volume reduction can be achieved across all disease stages, including patients with advanced-stage disease and elevated BMI. These findings support the role of CDT as a primary conservative treatment option in routine phlebolymphedema management.

Breast lymphedema is characterized by skin thickening/swelling of the breast and is common following partial mastectomy and radiation. Oncoplastic reduction performed during partial mastectomy removes additional breast tissue compared to partial mastectomy alone to optimize breast contour. Recent literature has suggested oncoplastic reduction in patients with macromastia undergoing breast-conservation surgery is protective of breast lymphedema, decreasing rates from 11% to 3%. The purpose of this study is to assess the rates of breast lymphedema after partial mastectomy and oncoplastic reduction and identify risk factors. A single-center retrospective study was performed of breast cancer patients following partial mastectomy and oncoplastic reduction (2018-2023). Patients underwent contralateral breast reduction for symmetry. Breast lymphedema was assessed. Demographics data and risk factors were evaluated. This study included 158 patients who underwent partial mastectomy and oncoplastic reduction. Breast lymphedema incidence was 3.2% (5/158). Including contralateral non-cancerous breast symmetry reduction, lymphedema occurred in 3.6% (5/140) of irradiated breasts and 0% (0/176) of non-irradiated breasts (p = 0.0164). Among irradiated breasts, skin necrosis occurred in 11.4% (16/140) compared to 4.5% (8/176) of non-irradiated breasts (p = 0.031). Breast lymphedema developed 207.4 ± 37.6 days postoperatively and 101.6 ± 15.9 days following adjuvant radiation. Mean follow-up was 639 days. Breast lymphedema incidence following partial mastectomy and oncoplastic reduction was 3.6% in this series and occurs 3-4 months after radiation. Radiation was the only significant risk factor for developing breast lymphedema. This largest series on breast lymphedema after oncoplastic reduction corroborates that oncoplastic reduction may be protective.

Breast cancer incidence rates are rising due to early detection, improved screening methods and advances in treatment options. As mortality rates reduce, there is a growing population living longer with treatment side-effects who require assistance. Prevalent issues arising after breast cancer treatment include pain, fatigue, lymphoedema and arm and shoulder mobility issues. Evidence demonstrates that upper limb exercises help reduce these common side effects and improve day-to-day functioning and quality of life. However, access to physiotherapy and rehabilitation services remains limited due to resource and access constraints. Despite a growing interest in digital health resources, little is known about the effectiveness of using digital exercise interventions to help resolve this problem.

Intestinal lymphatic vessels are essential for dietary lipid absorption and immune cell trafficking. Villus lymphatic capillaries, lacteals, undergo continuous VEGF-C-dependent renewal to function in a hyperosmolar, inflammatory environment exposed to dietary and microbial by-products. To define mechanisms underlying this adaptation, we integrated new and published single-cell RNA-sequencing datasets of murine small intestinal lymphatic endothelial cells (LECs). Lacteal LECs resembled Ptx3+ immune-interacting LECs and were characterized by high expression of water channel AQP1. LEC-specific Aqp1 deletion reduced lacteal length, impaired lipid uptake, and limited weight gain on a high-fat diet, while mosaic deletion revealed a cell-autonomous requirement for AQP1 in LEC positioning at hyperosmolar tip regions. AQP1 promoted LEC migration under hyperosmotic stress by preserving cytoskeletal and junctional remodeling and alleviating osmotic stress-induced transcriptional programs. AQP1 was upregulated during inflammatory remodeling in lymphedema and lymphatic malformations, but not during embryonic lymphangiogenesis. These findings link lacteal regeneration to inflammatory lymphatic remodeling and highlight tissue osmolarity as a biophysical determinant of postnatal lymphangiogenesis.

Streptococcus canis (S. canis) is an underrecognized zoonotic pathogen capable of causing invasive human infection. We report a case of sepsis with acute hypoxic respiratory failure due to S. canis bacteremia in a 73-year-old woman with multiple comorbidities, including breast cancer complicated by chronic lymphedema and cardiovascular disease. She presented with fever, progressive dyspnea, hypoxemia, leukocytosis, acute kidney injury, and rising cardiac troponin levels. Imaging demonstrated bilateral interstitial opacities consistent with pulmonary edema, and her clinical course required intensive care management. Two sets of blood cultures grew S. canis, a group G β-hemolytic streptococcus most commonly associated with dogs and cats. Species-level identification was achieved using polymerase chain reaction-based blood culture testing followed by automated biochemical confirmation. The patient was initially treated with broad-spectrum antibiotics and subsequently transitioned to intravenous penicillin G after susceptibility testing demonstrated β-lactam sensitivity. Further history revealed frequent exposure to a household dog without history of bites or scratches, supporting probable non-traumatic zoonotic transmission. The patient improved with targeted therapy and completed a 13-day course of intravenous antibiotics. This case demonstrates that S. canis can cause severe cardiopulmonary compromise in elderly patients and highlights the epidemiologic value of species-level identification in recognizing zoonotic transmission and prompting targeted assessment of animal exposure in patients with group G streptococcal sepsis.