A chronic or complex wound deviates from the body’s normal, orderly healing process, often resulting in a prolonged inflammatory state that leads to tissue destruction instead of regeneration. When a wound develops a narrow channel or tract extending deep into the underlying structures, it is known as tunneling. This complication indicates a significant, unresolved problem beneath the surface of the skin and requires specialized attention for resolution.
Defining Tunneling and Undermining
Tunneling is characterized by a narrow passageway, often called a sinus tract, that extends from the visible wound opening into the deeper subcutaneous tissue, muscle, or fascia. This tract usually follows a single, linear direction and can extend several centimeters deep.
Tunneling is distinct from undermining, although both involve tissue destruction beneath the skin surface. Undermining is the separation of the wound edges from the underlying tissue around the perimeter, creating a wider, often circumferential pocket. While both complications create a “dead space” that impedes healing, tunneling is a narrow, deep tract, whereas undermining is a wider, shallower separation of tissue layers.
Underlying Pathophysiology of Tunnel Formation
The biological mechanism driving tunnel formation involves a destructive cycle of inflammation and tissue breakdown in the deeper layers. Tunneling begins with localized deep tissue necrosis, often due to intense pressure or trauma. The body responds by initiating a sustained, localized inflammatory response to wall off and clear the damaged area.
This prolonged inflammation recruits high numbers of immune cells, such as neutrophils and macrophages, to the deep tissue site. These cells release large quantities of proteolytic enzymes, including Matrix Metalloproteinases (MMPs). While these enzymes are necessary to remove damaged tissue, their overproduction leads to the excessive breakdown of the extracellular matrix, the structural scaffolding made of collagen and connective tissue.
This enzymatic destruction of collagen and fascia creates a path of least resistance for inflammatory exudate to travel toward the skin surface, forming the narrow tract or channel.
Primary Causes and Contributing Factors
Specific external and systemic conditions initiate the deep tissue damage necessary for tunneling to occur. Deep-seated infection is a major cause, where an abscess in the deeper tissues seeks a natural path to the surface to drain. As bacteria colonize, they release toxins and proteases that actively erode the surrounding tissue and create the tunnel.
Persistent mechanical force, particularly localized pressure and shear, is a common factor in pressure injuries. Prolonged pressure compresses blood vessels, causing tissue ischemia and subsequent necrosis in deep tissue planes near the bone. This deep damage results in a wound that presents on the surface but tunnels inward to the initial injury site.
Underlying disease states significantly compromise tissue viability and healing capacity. For example, diabetes impairs blood flow and weakens the immune response, hindering the ability to clear infection and repair tissue. Vascular insufficiency or the presence of a foreign body, such as a retained suture, can also perpetuate the inflammation and deep tissue destruction necessary for tract formation.
Clinical Implications and Management Strategies
The presence of tunneling is a serious clinical finding because it significantly increases the risk of complications like deep-space infections, abscess formation, and osteomyelitis (bone infection). The narrow channel traps bacteria and exudate, preventing the wound from healing from the base upward and creating an ideal environment for microbial proliferation.
Effective management begins with accurate assessment to determine the full extent of the tissue damage. A healthcare professional must gently probe the wound with a sterile instrument to determine the depth, direction, and number of tracts, often using the face of a clock for documentation. Probing is essential because the full depth of the tunnel is often not visible on the surface.
Treatment strategies focus on cleaning the deep tract and promoting tissue growth from the bottom upward. This requires thorough cleansing and debridement to remove necrotic tissue and reduce the bacterial load within the channel. The tract must then be lightly packed with specialized materials, such as sterile gauze strips or hydrogel fillers, to ensure the tunnel walls do not prematurely close and form a new abscess. This method promotes healing by secondary intention, eliminating the deep space through the gradual formation of healthy granulation tissue.