Physiological Basis Of Wound Observations: Contamination And Antibiotic Choices For Wound Healing

Physiological basis of the wound observations

Research shows that there are four stages of wound healing: Hemostasis, Inflammation, Proliferation and Remodelling. (Orsted et al, 2018). Immediately Mary’s injury occurred, the body reacted and the healing process began. Hemostasis is the immediate phase and occurs within minutes of the injury. The platelets are the cells involved, their job being sealing off the damaged blood vessels, which constrict in response to injury by forming a stable clot. Adenosine Diphosphate (ADP) influences the working of platelets by leaking from injured cells and they stick to the uncovered type 1 Collagen. They then secrete sticky glycoprotein which causes more platelet aggregation. Thrombin is released which initiates the conversion of fibrinogen to fibrin. Fibrin forms a mesh which strengthens the aggregate, forming a clot. Platelets also secrete growth factors which recruit cells like neutrophilis and monocytes and initiate the recruiting of fibroblasts  by the epithelial cells bring about the the next stage, inflammation (Altmeyer, Hoffmann, Gammal, & Hutchinson, 2012).

Inflammation is the second phase. (Orsted et al, 2018). It is characterized by erythema (redness of the skin), warmth and swelling, often linked to pain This is the stage Mary’s wound currently is and lasts upto four days after injury. The constriction of vessels in the hemostasis stage is follwed by dilation in the inflammation phase. Here, cleaning of the debris occurs done by neurophilis cells or polymorphonuclear neutrophilic leukocytes (PMNs).The blood vessels in response release plasma and PMN’s. So as to provide defence against infection, the neutrophilis phagotize debris. They also take part in oxidative bacteria killing, increasing the effectiveness of antibiotics, but as they digest bacteria and debris, they die. Monocytes then come in and digest the tissue further. Cytokines and growth factors help cells communicate. They bind to receptors on target cells and stimulate them to move and they synthesize releasing substances needed to form the extracellular matrix which plays a role in healing. Macrophages and extracellular matrix come into contact and are able to phagotize bacteria providing a second streak of defence. They help in resolving inflammation by degrading enzymes from the matrix metalloproteinasis (MMPs). Uncontrolled activities in MMPs may cause degradation in the new formed tissue thus a delay in would healing (Altmeyer et al., 2012). 

One example is Enterobactericeae (Samuelsson, 2013). Enterobacteria pathogens cause urinary tract contagions and septicaemia cases. The most common mode of bacterial transmission is contact transmission and it is divided into two; direct and indirect transmission. Sometimes body surfaces of the clinical providers come into touching base with patients, for example while taking blood pressure or pulse, touching the patients groin twice for a few seconds then cleaning with soap and afterwards to manipulate a sterile foley catheter can lead to Enterobactericeae being transmitted (Long, Prober & Fischer, 2017). In Mary’s case, the microorganism that caused her condition was the bacteria Staphylococcus aureus which is often a commensal organism on the skin and upper respiratory tract. 

Possible sources of contamination and modes of transmission

The most common source of human infection is other humans. Some agents are more transmissible than others, for example, measles. Outbreaks occur and human beings transmits pathogens to others. An example of an exogenous mode of transmission is sexual transmission of agents, for example, Neisseria gonorrheae. Others are HIV and Treponoma pallidum, Chlamydia trachomatis. These agents may be transmitted sexually and they survive in hosts as a result of killing of the white blood cells and weakening immunity, hence they thrive in the body of the host. (Wright, 2013). Staphylococcus aureus can be carried on hands by people like healthcare personnel and end up spreading to the patients. (Bush & Schmidt, 2018). In Mary’s case, the bacteria was possibly present on the glass that cut her, hence was spread to her through the glass. 

A study by the Centre of Health Protection (2017) shows that Methicillin-resistant Staphylococcus aureus (MRSA) is mainly transmitted through contact with wounds, soiled and discharge areas. Unhygienic, crowded conditions and places, close contact with people or objects infected with the bacteria, breaks in the skin due to wounds or indwelling catheters. 
Outbreaks of MRSA have also been seen in communities and households. In a variety of community based reservoirs including Sports clubs day care facilities, jails, schools and work places. Within households, the risk of infections from one household member to another is high. This is because of contact between people and contact with objects. ( Knox, Uhlemann & Lowy, 2015)

A study by ISMP Canada (2016) shows that ceftriaxone is an antibiotic and for Mary’s wound, it was used for completion. It fights staphylococcus aureus, which was the primary microorganism affecting Mary’s wound. Ceftriaxone can be used on skin and skin structures, based on susceptible organisms (West Suffolk NHS Foundation Trust, 2018). 

Research by Auro Pharma Inc (2017), shows that cephalexin is bactericidal. In Mary’s case,

cephalexin can be used to treat her wound, because it is used for treatment of bacterial infections for her wound, on the skin and soft tissues. This drug is administered orally, preferably on an empty stomach and following the doctors dosage instructions and precautions 

In this case, Mary’s wound was most likely infected by community-related methicillin-resistant Staphylococcus aureus (CA-MRSA). The use of cephalexin was discontinued because this type of bacteria (Staphylococcus aureus) was methicillin-resistant and empiric therapy with penicillins or cephalosporin might have been inadequate. Dicloxacillin was therefore taken up to be used because it is a penicillinase-resistant penicillin (Baorto, 2017).

Rationale for choices of antibiotics

Hematologic adverse reactions which include agranulocytosis, eosinophili and neutropenia, as studies from antimicrobe.org show (Walsh & Cuppett, 2017). 

Renal adverse reactions which include interstitial nephritis-rash, fever, eosinophilia, hepatitis, protenuria, renal insufficiency. ((DailyMed, 2018). 

Mary should be subjected to the correct zinc therapy as it has been confirmed to improve the healing of wounds (Galbraith, Hunt, Richards, Bullock, & Manias, 2015). Chlorinated lime can be useful in wound dressing (Bullock & Manias, 2017).  The healing process follows as follows.

Mary’s injury will begin to heal during acute inflammation. Healing is a process and involves fill in, seal and shrinking. The three processes take different durations and vary in importance. Mary’s wound would heal through collagen synthesis as is not a very serious one (Craft et al., 2014). The process of wound healing is a multifaceted process involving a selection of cells, cytokines and repair substances (Marieb & Hoehn, 2016; Lee & Bishop, 2012).

As seen, there are four phases of wound healing. After the Hemostasis and inflammation phases described above, the proliferation stage begins around 4 days until 21st day, depending on the wound. (Osterd et al, 2018). Angiogenesis, collagen deposition, granulation tissue formation, wound contraction and epithelialization are the processes involved in this phase. Fibroblasts secrete collagen on which more dermal regeneration occurs. Angiogenesis is the manner of progress of new vessels that takes place through pericytes. They generate the superficial layers of capillaries and endothilial cells which secrete the lining. Keratinocytes cause epithelialization and they further differentiate forming stratum cormeum, which is the outer layer. Growth factors in a healing wound cause cell reproduction and migration (by cytokines). 

The remodelling phase is the final stage and it involves realignment of collagen. (Osterd et al, 2018). The collagen I replaces collagen III. The fibres then align and join along tension links increasing ductile strength of the wound. Myofibroblasts, which are a subcategory of fibroblasts too assist the shrinking of the wound. Reedy layers of scar tissue form and coagulate with time. Colour of the blemish tissue is initially profound pink, but later turns into bright pink. Fibroblasts play an active role in remodelling but this process can take upto two years after injury depending on the type and extent of the wound (Flanagan, 2013). 

References:

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Auro Pharma Inc. (2017). Product Monograph Auro Cephalexin. Retrieved 23rd Sep. 2018 from https://auropharma.ca/products/
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