Your skin is the organ from the body that bears the responsibility of protecting it from environmental pathogens. It is important to understand, however, that the skin surface is not germ-free. In fact, healthy skin could be colonized with multiple types of virulent organisms. Therefore, the mere presence of bacteria in a wound doesn't in itself define infection. Rather, it is the amount and kind of bacteria that determines whether a wound is really infected.
There's a continuum spanning in the sterile wound to the grossly infected wound, and determining where a wound falls about this continuum is really a challenge for the bedside clinician. It is necessary for that plastic surgeon to become proficient in this skill, since it will help predict the likelihood and rate of wound closure versus the opportunity of the wound to become a systemic threat. Understanding the severity of bacterial involvement will even help to steer therapy.
Your skin is covered with microorganisms. It may be either resident organisms, those that can typically be found on the subject's skin, or transients that in many cases are seen on the skin surface but they are quickly shed during normal body hygiene or by skin sloughing. While these organisms are often bacteria, the yeast Pityrosporum and skin mite Demodex are also commonly found. These colonizing microbes take residence in the crypts and crevices that favor bacterial growth, and stop pathologic species from accessing these areas.
Human beings are protected from bacterial overgrowth and invasion in the surface with a quantity of disease fighting capability. A layer of dead, keratinous epithelial cells known as the stratum corneum is the outermost layer of skin. Since the keratin sloughs, it removes attached organisms with it. Skin oil glands secrete an oily, lipid-rich, acidic substance, (pH range of 4.2 to 5.6) that acts to retard bacterial growth. Bacteria become more active on the skin since the pH rises above 6.5, as is seen with the use of many cleansing and moisturizing agents.
Should foreign organisms get past these defenses, the antigen-presenting Langerhans cells found in the epidermis and also the phagocytosing macrophages and immune-stimulating mast cells present in the dermis rapidly mobilize the body's cellular and humoral immune responses.
Cutaneous wounds, by definition, have forfeit their protective barrier and therefore are subject to invasion by not only foreign bacteria introduced through the environment, but additionally the local bacterial flora that is present on intact skin. These wounds occur in the setting of numerous pathologies and are usually chronic in nature before being delivered to the attention of the plastic surgeon. Unlike most surgical incisions, these wounds heal by secondary intention and therefore are always colonized by bacteria.
They require extensive granulation tissue formation and keratinocyte migration for closure, involving endothelial cells and fibroblasts for that purpose of neovascularization and matrix production, respectively. For this to happen, macrophages and a varying milieu of growth factors must be present. Along with neutrophils, macrophages also act to disinfect the wound, killing foreign organisms by the generation of peroxide and superoxide radicals. The clinical spectrum of bacterial invasion exists on a continuum from least to many severe: contamination, colonization, local infection or critical contamination, invasive infection and sepsis.
Contaminated wounds have nonreplicating organisms within their borders. These wounds will go onto heal normally.
Colonized wounds have replicating bacteria, however these bacteria are nondestructive and contained inside the wound. A hallmark of colonization is that it doesn't delay the wound recovery process.
Local infection or critical contamination is an intermediate level of bacterial invasion seen as a granulation tissue that comes with an unhealthy appearance, and wound healing that may be delayed. In this type of wound, however, tissue invasion is not present. This stage is notable for that lack of other signs and symptoms of infection for example cellulitis or pus formation.
Invasive infection occurs once bacteria have invaded through the wound bed, tissue destruction has begun, as well as an aggressive immune fact is present. Signs and symptoms of invasive infection include pain, edema, erythema and fever. The finding of a chronic, nonhealing wound, often with pus formation and tissue necrosis is usually evident.
Sepsis occurs when the infection spread systemically, and cardiovascular instability and organ-system dysfunction develop.
Low levels of bacteria in wounds actually help to advertise wound healing by stimulating brisk monocyte and macrophage activity. However, his or her number or virulence increases, the tissue response to their presence disrupts and prolongs the inflammatory phase of wound healing, depletes the constituents from the complement cascade, interferes with normal clotting mechanisms, and alters leukocyte function.
The amount of pro-inflammatory cytokines, including interleukin-1 and tumor necrosis factor-alpha, rises and stays elevated. Elevated levels of matrix metalloproteinases and a insufficient their inhibitors lead to tissue breakdown and growth factor inhibition. Bacteria also compete with local cells for oxygen, reducing its availability to those cells and stimulating an angiogenic response, leading to friable granulation tissue that is vulnerable to bleeding.
Our website is not responsible for the information contained by this article. Webworldarticles.com is a free articles resource thus practically any visitor can submit an article. However if you notice any copyrighted material, please contact us and we will remove the article(s) in discussion right away.
This article was sent to us by:
Ralph C. Bennett at
02092011
1. How is latissimus dorsi flap reconstruction performed
All articles in this directory are property of their respective authors. Additionally, read our Privacy Policy
© 2010 WebWorldarticles.com - All Rights Reserved. Partners: Gunblade Saga