Steroid is injurious to wound when given
Wound healing is delayed in patients who are malnourished, or have vitamin A and C deficiency. Steroids also inhibit the adequate healing of wounds as they inhibit protein synthesis and fibroblast proliferation. Poorly-controlled diabetes delays wound healing and increases the risk of infection at the surgical site. Wound Healing This is variously described as taking place in three or four phases, the most commonly agreed being: the inflammatory phase; the proliferative phase; the remodelling phase (maturing phase). Occasionally, a haemostatic phase is referred to as occurring before the inflammatory phase, or a destructive phase following inflammation consisting of the cellular cleansing of the wound by macrophages The inflammatory phase begins immediately after wounding and lasts 2-3 days. Bleeding is followed by vasoconstriction and thrombus formation to limit blood loss. Platelets stick to the damaged endothelial lining of vessels, releasing adenosine diphosphate (ADP), which causes thrombocytic aggregates to fill the wound. When bleeding stops, the platelets then release several cytokines from their alpha granules. These are platelet-derived growth factor (PDGF), platelet factor IV and transforming growth factor beta (TGFb). These attract inflammatory cells such as polymorphonuclear leukocytes (PMN) and macrophages. Platelets and the local injured tissue release vasoactive amines, such as histamine, serotonin and prostaglandins, which increase vascular permeability, thereby aiding infiltration of these inflammatory cells. Macrophages remove devitalised tissue and microorganisms while regulating fibroblast activity in the proliferative phase of healing. The initial framework for structural suppo of cells is provided by fibrin produced by fibrinogen. A more historical (Latin) description of this phase is described in four words: rubor (redness), tumor (swelling), calor (heat) and dolor (pain). The proliferative phase lasts from the third day to the third week, consisting mainly of fibroblast activity with the production of collagen and ground substance (glycosaminoglycans and proteoglycans), the growth of new blood vessels as capillary loops (angioneogenesis) and the re-epithelialisation of the wound surface. Fibroblasts require vitamin C to produce collagen. The wound tissue formed in the early pa of this phase is called granulation tissue. In the latter pa of this phase, there is an increase in the tensile strength of the wound due to increased collagen, which is at first deposited in a random fashion and consists of type III collagen. This proliferative phase with its increase of collagen deposition is associated with wound contraction, which can considerably reduce the surface area of a wound over the first 3 weeks of healing. The remodelling phase is characterised by maturation of collagen (type I replacing type III until a ratio of 4:1 is achieved). There is a realignment of collagen fibres along the lines of tension, decreased wound vascularity, and wound contraction due to fibroblast and myofibroblast activity. This maturation of collagen leads to increased tensile strength in the wound which is maximal at the 12th week post injury and represents approximately 80% of the uninjured skin strength. Ref: Bailey and love 27th edition Pgno : 24, 299
On 1st day
< 2 weeks
2-4 weeks
>4 weeks
Urology