Lower legs
Richard Ashton, Barbara Leppard in Differential Diagnosis in Dermatology, 2021
The cause of venous ulceration is loss of the valves in the deep or perforating veins. The venous blood returns from the lower legs back to the heart by the calf muscle pump. Compression of the calf muscles (by walking or running) squeezes blood up the legs. Blood is drawn from the superficial veins and pushed upwards by valves which prevent back flow. Loss or incompetence of these valves results in enormous pressure (venous hypertension) in the superficial veins which is transmitted back to the capillaries resulting in venous disease and ulceration. Venous ulcers occur on the lower third of the leg either over the medial or lateral malleolus. They are typically large, superficial and painless; if painful then there may be an element of arterial insufficiency or infection present.
Wound and Soft Tissue Complications: Complications of Wound Repair
Stephen M. Cohn, Matthew O. Dolich in Complications in Surgery and Trauma, 2014
Genetic variants have also been implicated as risk factors for the development of abnormal scar patterns and poor healing. Unlike the aforementioned syndromes, these DNA mutations, which are relatively common in the general population, have not been shown to be causative. Rather, they have been shown to be present in greater percentages among those patients with specific scarring or healing phenotypes. Examples include single nucleotide polymorphisms (SNPs) that have been associated with the development of keloids [34,35] as well as several SNPs that have been associated with increased risk of chronic venous leg ulcers [36]. Conversely, one study identified a variant associated with shorter healing time in venous ulcers following superficial venous surgery [37].
Conservative treatment
Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland in Manual of Venous and Lymphatic Diseases, 2017
After cleansing an ulcer to remove devitalized tissue and exudate, apply a suitable dressing to protect the region and promote moist wound healing.7 Measure wound healing by planimetry of the surface area or by time to complete healing. In addition, assess progress by changes in the wound bed for the phases of healing, the haemostatic phase then the inflammatory phase, granulation phase and epithelialization. Simple venous ulcers should heal in 8–12 weeks with best care, and if not, then a review for an alternative diagnosis is required.
Enhanced healing efficacy of an optimized gabapentin-melittin nanoconjugate gel-loaded formulation in excised wounds of diabetic rats
Published in Drug Delivery, 2022
Hani Z. Asfour, Nabil A. Alhakamy, Osama A. A. Ahmed, Usama A. Fahmy, Shadab Md, Mohamed A. El-Moselhy, Waleed Y. Rizg, Adel F. Alghaith, Basma G. Eid, Ashraf B. Abdel-Naim
Among various types of wounds, the management and treatment of diabetic wounds have remained an area of concern for health care professionals (Deng et al., 2021). Based on numerous clinical and preclinical evidence, connecting link between hyperglycemia and impaired wound healing has been well established (Patel et al., 2019). It is well established that normal wound healing is a controlled anticipated process, and any alteration in the steps of the healing process may result in “venous ulcer,” ‘intractable ulcers or chronic wounds that sometimes become lethal. Hyperglycemic condition hinders the delivery of nutrients and other immunological factors that automatically reflect impaired wound healing (Jiang et al., 2022). In diabetic patients, delayed wound healing is related to impaired growth factor production, inflammatory cell function, angiogenesis and fibroblast production and migration (Rose & Kam, 2002). Therefore, novel and targeted pharmacological approaches are urgently needed to expedite the healing of diabetic wounds.
An appraisal of vascular endothelial growth factor (VEGF): the dynamic molecule of wound healing and its current clinical applications
Published in Growth Factors, 2022
Aakansha Giri Goswami, Somprakas Basu, Farhanul Huda, Jayanti Pant, Amrita Ghosh Kar, Tuhina Banerjee, Vijay Kumar Shukla
Widely accepted to arise in the background of chronic venous insufficiency and its antecedent microcirculatory dysfunction (Jünger et al. 2000), the venous ulcers are a significant cause of morbidity. The tissue hypoxia emanating from microcirculatory failure is a strong stimulant for VEGF expression and angiogenesis. It is believed that leukocyte activation as the result of ambulatory venous hypertension activates ECs to stimulate VEGF expression from keratinocytes, macrophages, and vascular stromal cells as part of the repair process. Kolano et al. (2020) observed a significant correlation between micro-vessel density and VEGF expression in patients with venous ulceration. The serum levels of VEGF can be directly correlated with the dermatological manifestation of venous ulcers (Shoab, Scurr, and Coleridge-Smith 1998) and increased VEGF expression pattern has been consistently observed in the advanced stages of chronic venous disease (Peschen et al. 1998). The resultant neo-vascularization and the long-term microvascular permeability cause fibrin cuff deposition and tissue edema, which interferes with tissue nutrition, and are credited for clinical skin damage.
A review of upper extremity deep vein thrombosis
Published in Postgraduate Medicine, 2021
Oneib Khan, Ashley Marmaro, David A Cohen
PTS is characterized as signs and symptoms of venous insufficiency following deep vein thrombosis [17]. Typical symptoms could be extremity pain, extremity heaviness, vein dilation, edema, skin pigmentation, and venous ulcers. It is thought to occur due to venous hypertension, leading to valve damage [18]. One meta-analysis found a 19% risk of PTS in UEDVT. This risk was more profound in primary UEDVT than secondary UEDVT (20% vs. 14%) [19]. This seems lower relative to the risk of PTS in LEDVT which has been noted in 20%-50% of patients [20]. Although not thoroughly validated, a modified Villalta score has been used previously to diagnose and evaluate PTS of the upper extremity [21]. One problem with this score is that it does not capture the effects of PTS affecting the dominant arm. This can drastically alter a patient’s quality of life and functionality; improvement on this score is necessary.
Related Knowledge Centers
- Chronic Venous Insufficiency
- Chronic Wound
- Lipodermatosclerosis
- Varicose Veins
- Vein
- Venous Stasis
- Heart Failure
- Wound
- Arterial Insufficiency Ulcer
- Ankle Flare