Hard-to-heal (chronic) wounds pose significant challenges in healthcare due to their prolonged inflammatory phase and impaired healing processes. These wounds, commonly associated with diabetes, vascular insufficiency or impaired mobility, fail to progress through the orderly phases of haemostasis, inflammation, proliferation and remodelling. Persistent inflammation, driven by M1 macrophages, neutrophils and proteases, disrupts extracellular matrix (ECM) reconstruction and degrades growth factors and cytokines, halting healing. Conventional treatments often fail to address the underlying pathophysiology, prompting interest in advanced autologous therapies. Autologous whole blood clot (AWBC), an innovative autologous therapy, activates the patient's blood to create a biological scaffold rich in growth factors and cytokines. This scaffold promotes wound healing by supporting ECM reconstruction, causing inflammatory M1 macrophages to transition to regenerative M2 macrophages, and enhancing neutrophil clearance. The objective of this review was to summarise the current clinical evidence and elucidate the proposed biological mechanisms by which AWBC promotes healing in hard-to-heal wounds. Clinical studies have demonstrated AWBC's efficacy across multiple wound types, including diabetic foot ulcers, pressure ulcers and surgical wounds. With a robust safety profile, minimal risk of adverse reactions and reported efficacy, AWBC offers a transformative solution for hard-to-heal wound management, addressing unmet clinical needs and improving patient outcomes.
Robert J Snyder (Sat,) studied this question.