Healing II: Complications

Contractures develop when scar tissue tightens and shrinks over time, restricting movement. Excessive collagen cross-linking and myofibroblast activity cause this deformity, which is especially common after severe burns affecting large dermal areas. Contractures limit joint mobility in highly mobile areas like fingers and elbows, significantly impairing function and quality of life.

Scar tissue lacks adnexal structures such as hair follicles, sebaceous glands, and sweat glands present in normal skin. This absence reduces tactile sensitivity, impairs thermoregulation, and limits epidermal lubrication. Healed areas consequently exhibit dryness, decreased sensation, and reduced heat dissipation, compromising the skin's protective and regulatory functions.

Hypertrophic scars are raised and thick, caused by excess collagen confined to the original wound boundaries. Keloids, by contrast, grow beyond the initial injury and extend into surrounding skin, forming bulky scars that project above the surface. Both reflect dysregulated fibroblast activity and impaired extracellular matrix remodeling during healing.

Adhesions are internal bands of scar tissue that connect adjacent body structures. After abdominal surgery, fibrous adhesions may form between intestinal loops, potentially tethering them and increasing the risk of bowel obstruction. These complications can cause significant morbidity and may require surgical intervention to restore normal organ function.

Scar tissue has reduced vascularity compared with normal tissue, compromising regional blood flow and limiting oxygen and nutrient delivery. When fibrosis mechanically disrupts local circulation, tissue breakdown occurs, predisposing the area to chronic ulcers. This risk increases in regions subjected to mechanical stress or where perfusion is already compromised, such as the lower extremities.

Abnormal scar formation results from altered collagen deposition, dysregulated fibroblast activity, and impaired extracellular matrix remodeling. Local and systemic factors disrupt normal tissue repair, leading to excessive or insufficient collagen cross-linking. These changes compromise the biomechanical properties of healing tissue and reduce vascular supply, preventing restoration of normal structure and function.

Scar tissue lacks sweat glands and other adnexal structures necessary for thermoregulation. Without functional sweat glands, the healed area cannot effectively dissipate heat through perspiration. This loss of thermoregulatory capacity reduces the body's ability to maintain optimal temperature in scarred regions, particularly problematic after extensive burns affecting large skin areas.