Rapid hemostasis is an urgent need in management of trauma and surgical wounds. While hemostasis is in a simple sense just one step in the process of wound healing, it represents an opportunity in medtech due to both the high clinical value of stopping bleeds and the number and type of ways hemostasis can be produced.
The wounding event—whether caused by trauma or by a surgical procedure—leads to damage of blood vessels, initiating a clotting cascade involving complement factors in the blood and resulting in the formation of fibrin clots. This clotting cascade also helps to block pathogens from accessing the blood or tissues at the injury site. Vasoconstriction occurs to aid the biochemical cascade and cause hypoxia, which attracts white blood cells into the tissue and causes a humoral and cellular inflammatory response. This occurs extremely quickly and leads to the release of vasoactive factors such as histamine and bradykinin; these maintain the flow of blood factors to deal with the damaged tissue and any pathogens at the wound site. Wound exudates are allowed to seep through to the damaged area carrying inflammatory immune factors for repair. Plasma factors, including lysozyme, white blood cells (WBC) and macrophages, then begin the process of removing dead cells and debris from the tissue. Macrophages and WBC play an important role in regulating the healing process through cytokines and growth factors.
Hemostasis is a general term given to the process which is initiated to stop the bleeding and thus prevent significant loss of blood, and to close the wound and block the entry of pathogens as quickly as possible. Central to hemostasis is the clotting process; denatured polymers such as collagen and other foreign bodies in the injured site activate substances known as complement factors in the blood; these act on a soluble, blood-borne thrombin precursor (prothrombin) to cause it to change to thrombin. Thrombin brings about the cleavage of the protein fibrinogen to form an insoluble fibrin clot; fibrin is then further cross-linked by an enzyme in blood called Factor XIII. The cascade of events also results in the release of vasoactive factors to accelerate blood clotting.
The extent of the clotting process, the biochemical makeup of the hemostasis cascade, and the density of the fibrin clot are dictated by a combination of genetic and environmental factors. It is thought that the clotting process has evolved, over many millennia of evolutionary development, to be very efficient at stopping bleeding rapidly, preventing infection, and stimulating repair, albeit at some cost in terms of the resultant cosmetic appearance of the healed skin.
The evolved ability of the human body to stop bleeding has limits when the size and/or nature of the wound overwhelms the clotting process. Additionally, patients with compromised abilities in their clotting process can be at extreme risk from relatively minor wounds. As a result, hemostasis products have seen, and will continue to see, strong growth in the overall wound closure and management market.
Given the opportunity and the relatively low barrier to market entry, there are many active companies in the hemostasis market. Such opportunity is responsible for the U.S. market (often near 50% share of the worldwide market for medtech) representing a scant 32% of the global market.
Source: MedMarket Diligence, LLC; "Worldwide Surgical Sealants, Glues, Wound Closure and Anti-Adhesion Markets, 2010-2017." Report #S190.
Growth in the global hemostasis market is near 10% with some of the highest growth seen in the U.S. and Asia/Pacific markets, although driven by different dynamics.