Which phase of acute wound healing is prolonged during progression to a chronic wound?
B. Inflammation. An acute wound is defined by its ability to normally progress, in a predictable and timely manner, through all of the phases of wound healing; coagulation, inflammation, fibroplasia, angiogenesis, and remodeling. A protracted inflammatory phase is the usual mechanism for the formation of a chronic wound. All clinical efforts should be made to reduce chronic wound inflammation in an effort to support healing.
Which cell is most important for signaling wound healing?
C. Macrop14. The macrophage is the most important source of growth factor signals for wound healing. Experimental studies show that wound healing is most impaired in the absence of macrophages. Although fibroblasts are the main source of collagen synthesis and endothelial cells are required for revascularization, they are dependent on macrophage signaling to stimulate and direct tissue repair. A platelet is not a cell.
Which is the most predictive direct measure of impaired or delayed wound healing?
E. TcO2 less than 30 mm Hg
E. TcO2 less than 30 mm Hg. Wounds will not heal when the tissue concentration of oxygen falls below 30 mm Hg. It is the most powerful predictive measure of delayed or impaired wound healing. Vitamin C deficiency may result in impaired collagen cross linking (scurvy) and weak scars. Low serum albumin predicts increased wound complications, like wound infection. The microangiopathy of radiated tissue indirectly reduces perfusion and therefore, TcO2 levels. Finally, smoking impairs wound healing through the vasoconstrictive effects of chronic nicotine and relative hypoxia as well.
Which of the following is not a clinical impediment to wound healing?
C. A moist wound environment
C. A moist wound environment. A moist or even wet wound environment is critical to normal wound healing. The cellular and molecular biological activity within a wound requires hydration to proceed. Clinical use of dry dressings to support wound debridement, for example, should be limited. Similarly, poor dressing resulting in repeated trauma and mechanical instability to the wound is often overlooked as a source for wound healing failure. Wound infection is the most clinically important, and expensive, impediment to surgical wound healing. Foreign bodies in the wound, such as synthetic surgical meshes, also delay normal wound healing. Finally, experimental and clinical data support that obesity contributes to abnormal wound healing, primarily through a metabolic pathway, and secondarily by increasing the risk of wound infection.
The fundamental mechanism for incisional hernia formation is
A. Long-term fascial scar failure
C. Suture pulling through the fascia
D. Early fascial dehiscence and wound failure
D. Early fascial dehiscence and wound failure. Pollock and Evans showed in a classic clinical study that 94% of incisional hernias were the result of 1.2 cm fascial dehiscence before POD 30. The majority of the time, these were clinically occult wound closure failures, progressing to incisional hernias over the subsequent 3 years. It is no longer believed that many incisional hernias are the result of abnormal scar formation or suture breaking, stretching or even pulling through the fascia. Poor technique certainly will contribute to incisional hernia formation, but the fundamental mechanism is early fascial dehiscence.