Porth's Essentials of Pathophysiology, 4e

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Cell Proliferation and Tissue Regeneration and Repair

C h a p t e r 4

Wound contraction

Wound Contraction and Remodeling Phase. This phase begins approximately 3 weeks after injury with the development of the fibrous scar, and can continue for 6 months or longer, depending on the extent of the wound. During this phase, there is a decrease in vascu- larity and continued remodeling of scar tissue by simultaneous synthesis of collagen by fibroblasts and lysis by collagenase enzymes. As a result of these two processes, the architec- ture of the scar becomes reoriented to increase its tensile strength, and the scar shrinks so it is less visible. 3

Fibrous scar

Blood vessel

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The role of minerals in wound healing is less clearly defined. The major minerals, including sodium, potas- sium, calcium, and phosphorus, as well as trace min- erals such as copper and zinc, must be present for normal cell function. Zinc is a cofactor in a variety of enzyme systems responsible for cell prolifera- tion. In animal studies, zinc has been found to aid in reepithelialization. Blood Flow and Oxygen Delivery Impaired healing due to poor blood flow and hypoxia may occur as a result of wound conditions (e.g., swell- ing) or preexisting health problems. 24,25 Arterial disease and venous pathology are well-documented causes of impaired wound healing. In situations of trauma, a decrease in blood volume may cause a reduction in blood flow to injured tissues. For healing to occur, wounds must have adequate blood flow to supply the necessary nutrients and to remove the resulting waste, local toxins, bacteria, and other debris. Molecular oxygen is required for collagen synthesis and killing of bacteria by phago- cytic white blood cells. It has been shown that even a temporary lack of oxygen can result in the forma- tion of less-stable collagen. 24 Wounds in ischemic tis- sue become infected more frequently than wounds in well-vascularized tissue. Neutrophils and macro- phages require oxygen for destruction of microorgan- isms that have invaded the area. Although these cells

can accomplish phagocytosis in a relatively anoxic environment, they cannot digest bacteria. Oxygen also contributes to signaling systems that support wound healing. Recent research suggests that almost all cells in the wound environment are fitted with specialized enzymes to convert oxygen to reactive oxygen species (ROS). 24 These ROS function as cellular messengers that support wound healing, stimulating cytokine action, angiogenesis, cell motility, and extracellular matrix formation. The availability of respired oxygen to wound tis- sues depends on vascular supply, vasomotor tone, the partial pressure of oxygen (PO 2 ) in arterial blood, and the diffusion distance for oxygen (see Chapter 21). The central area of a wound has the lower oxygen level, with dermal wounds ranging from a PO 2 of 0 to 10 mm Hg centrally to 60 mm Hg in the periphery, while the PO 2 of arterial blood is approximately 100 mm Hg. 24 Transcutaneous oxygen sensors are available for use in measuring wound oxygenation. From a therapeu- tic standpoint oxygen can be given systemically or administered locally using a topical device. Although topical oxygen therapy is not likely to diffuse into the deeper tissues, it does have the advantage of oxygen- ating superficial areas of the wound not supported by intact vasculature. Hyperbaric oxygen therapy delivers 100% oxygen at two to three times the normal atmo- spheric pressure at sea level. 26 The goal of hyperbaric oxygen therapy is to increase oxygen delivery to tissues by increasing the partial pressure of oxygen dissolved in