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The evidence of postoperative laceration contamination has a tri-factorial basis; the local host impairment associated with both the injury and the operation, the overall systemic trauma and the other impacts of premorbidity along with the bacterial infection of the laceration (Bertesteanu et al., 2014). The amount of the factor of host damage as a result of operation and injury could be directly influenced by a surgeon who should make sure that his surgical mechanisms are non-aggressive and in line with the present knowledge management. However, the factor of overall systemic trauma and the other impacts of premorbidity are moderately open to intervention (Bertesteanu et al., 2014).
The two aspects are in direct connection to the hypothesis that every injury is capable of tolerating some local host impairment and some bacterial inoculum with no indication of contamination. Furthermore, it is also directly related to the hypothesis that the bacterial laceration flora is the outcome of the bacterial infringement force together with the local laceration state (Bertesteanu et al., 2014).
The factor of intraoperative bacterial inoculum could be improved through hygiene observation (Bertesteanu et al., 2014). The bacterial laceration flora along with the local situation of the injury is interrelated, and if either of the factors transcends the endurable threshold, the infection becomes manifest. This means that there will exist an unmanageable multiplication of microorganisms and the degree of the breaking point will reckon particular systemic host factors like immunodeficiency, age or even diabetes. Consequently, the contamination hindrance should concentrate concurrently on reducing the local bacterial inoculum and enhancing local injury condition (Bertesteanu et al., 2014).
The primary endogenous root of infection is the victim's carriers (Glassing, Dowd, Galandiuk, Davis & Chiodini, 2016). An estimation of fifty percent of the population is colonized with microorganism like Staphylococci aureus in the anterior nasal passages. Over time, this rate has reduced as a result of changes in socioeconomic class, smaller families along with excellent personal hygiene (Glassing, Dowd, Galandiuk, Davis & Chiodini, 2016). The mode of transmission is direct contact. Pathogens gain access to the underlying bloodstream and blood tissue and are transferred to the injury resulting in infection (Manaia, 2017).
Name one exogenous source of contamination and discuss the mode of transmission from the source to the new host.
The exogenous root of contamination is the surrounding (Glassing, Dowd, Galandiuk, Davis & Chiodini, 2016). The contact with the environment whereby the pathogens are in the air, sharp objects or those introduced by traumatic accident. The mode of infection transmission is via an indirect connection which happens in case contaminated objects with bacteria transfer the microorganisms to the host by coming into contact (Manaia, 2017).
Rationalefor choices of antibiotics
The stat dose of ceftriaxone was delivered directly to hinder the growth of microorganisms (Zaheer & Latif, 2017). This drug stops the pathogens from developing so that they may not lead to infection after surgery is conducted. Its choice is selected because the preceding step will be a medical procedure for the laceration so that after the operation there is a low peril of infection. Ceftriaxone only stops the microbes from reproducing but does not eliminate the organisms' cell wall hence discontinued, and cephalexin is introduced (Zaheer & Latif, 2017).
The purpose of the administration of oral cephalexin was to interfere with the creation of the microbe’s cell wall and also to rupture and kill the microorganisms (Rao et al., 2014). Its selection was based on the fact that the initial antibiotic was incapable of destroying the bacteria and it is discontinued because of its inefficacy against diseases caused by microorganisms such as Staphylococcus aureus.
The change of antibiotics to dicloxacillin is because this antibiotic operates versus microbes which are resistant to other penicillins such as Staphylococcus aureus. Also, dicloxacillin assists in clearing up the contamination of the microorganisms via inhibiting their growth (Chu et al., 2016). Its selection was based on its lower peril of antibiotic-induced liver injury and also because it does not have cautions on the hazard of severe cholestasis hepatitis. Consequently, dicloxacillin react through impeding the synthesis of bacterial cell walls. It impedes cross-linkage amidst the linear peptidoglycan polymer supply chains that constitute a significant element of the Gram-positive bacterial cell wall (Chu et al., 2016).
The adverse reactions of dicloxacillin more so when administered orally will result in signs of gastrointestinal irritation such as vomiting and diarrhea (Macy & Chen, 2017).
Hemostasis stage is the initial stage which begins once the wound starts to bleed and its work is to close the laceration through clotting. Once blood is limited to flow platelets join to block the break in the blood vessel wall, then clotting occurs and support the platelet plug with fibrin threads which operate as a molecular binding agent (Olczyk, Mencner & Komosinska-Vassev, 2014). In the second stage called inflammatory phase, the injured victim starts to feel the physical repercussions of the injury like redness, warmth, and tenderness. This stage is essential since it controls bleeding and averts contamination (Olczyk, Mencner & Komosinska-Vassev, 2014).
Proliferation stage is the preliminary phase where the laceration starts to be restored with new and healthy tissues and is achieved through an adequate supply of oxygen together with nutrients. The newly created membrane is made of collagen along with extracellular matrix which permits the growth of new blood vessel connection to restore the weary ones (Olczyk, Mencner & Komosinska-Vassev, 2014). Finally, in the maturation stage, the collagen is remodeled and the laceration closes completely. The cells utilized to rebuild the injury and not required anymore are replaced by programmed cell death or apoptosis (Olczyk, Mencner & Komosinska-Vassev, 2014).
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