Advancements in medical technology and an aging population are leading to a rapid expansion in the use of medical devices, a market that is predicted to double over the next ten years. Coupled with the reality that half of all Americans suffer from one or more chronic diseases (e.g., diabetes, cancer, or heart disease), has resulted in the creation of a rapidly expanding market for implanted medical devices that can perform longer-term with reduced complications. Mechanical improvements to these devices have been dramatic, yet improvements in controlling the interface of the body and the device have been minimal. As a result, nearly half of all medical devices implanted in the body are plagued with one or more severe complications – such as infection, thrombosis, improper healing, and cell overgrowth:
Healthcare Associated Infections (HAIs) result in 100,000 preventable deaths annually, more than AIDS, auto accidents, and breast cancer deaths combined. The majority of the 2 million HAIs contracted each year by Americans originate with the colonization of implantable medical devices – which provide a source of contamination and a surface for bacterial growth1.
Once these infections take hold on the device surface, they form complex “biofilms,” which are catalysts for infection and are often untreatable by conventional antibiotics. As biofilms grow, they serve as a recurrent source of bloodstream infections, due to shedding bacteria. The virulence of biofilms is especially problematic on medical devices used in patients who are immuno-compromised (e.g., dialysis or oncology patients.)
When an infection reaches the bloodstream, it lengthens average hospital stays by approximately two weeks, costs up to $50,000 to treat, and increases mortality by up to 25 percent, resulting in nearly $30 billion per year in direct medical expenses every year2,3.
The continuous growth of antibiotic resistance to certain bacteria and the lagging development of novel antibiotics render the treatment of HAIs increasingly difficult.
Device thrombosis, or blood clotting, can clog catheters in up to 25% of cases4. Once a “foreign body” such as a catheter is implanted into the blood stream, an immediate biological response begins. Within seconds, blood proteins and host cells (such as platelets) begin to deposit on the device surface, leading to the formation of a large, complex thrombus, or blood clot, on the surface.
“Openness” to blood flow is a critical concern for catheters, vascular grafts, and stents. Thrombus formation on the surface of these devices can constrict or block flow entirely, often requiring costly device replacement and increasing the risk of severe complications and death.
Improper healing can necessitate device removal. The interaction of device surfaces with the surrounding tissues is critical for implants:
- Despite recent advances in orthopedic joint implants, these implants have a high failure rate when implanted into osteoporotic bone that does not fully integrate into the implant surface.
- Inflammation surrounding intravenous catheters (known as phlebitis) is a common cause of discomfort and device replacement.
- Contracture of breast implants is caused by the excessive formation of a “fibrous capsule” as the body attempts to isolate the foreign body. Excessive encapsulation can cause cosmetic changes, pain, and eventually necessitate device replacement.
Engineering the device surface to closely mimic the properties of the surrounding tissue may help prevent these complications by reducing the foreign body response.
Hyperplasia, or cell overgrowth, often leads to device failure. The use of pharmaceuticals known as “restenosis inhibitors” in the drug-eluting stent market has made marked advances to reduce hyperplasia. However, a range of other devices, such as vascular grafts, are still in need of improved protection from cell overgrowth in long-term use. The development of a single technology which could simultaneously prevent restenosis and thrombosis would address the multi-functional demands of many vascular devices.
1. Klevens et al. (CDC),2002.
2. Maki et al., 2006.
3. Scott (CDC), 2009.
4. Stephens et al., 1995.