Tetanus Infection And Wound Inflammation: Nursing Assessment, Management And Treatment

The anaerobic, rod-shaped, racket like, Gram negative bacterium Clostridium tetani causes tetanus (Marieb & Hoehn, 2016). Since Mary got a cut while working in the garden, the wound was exposed to soil and her chances of getting an infection at the wound site are high. She is 50 years old and may not have received a tetanus booster recently. This means that the antibodies against C. tetani must be quite low, so it is necessary that she be given a tetanus booster.

In Mary’s case a booster dose of the tetanus vaccine would enable her immune system to counter an infection of Clostridium tetani, in case it occurs. At her age, It may have been a gap of several years since Mary was given a tetanus vaccine, the concentration of antibodies against C. tetani would thus be very low, a booster shot would help her to combat an infection if it occurs. Cases of tetanus have been reported even when people have received vaccination in a 10 year period prior to minor injuries. So, clinicians advise booster whenever there is risk of infection (Immunise.health.gov.au, 2017).

As soon as the wound occurs the process of establishing skin homeostasis begins in a number of ways. Preparation also begins for the process of healing of wound.

Wound edges are hot to touch and red. The ruptured skin at the edges of the wound becomes hot to touch and red due to the process of inflammation which is set in motion to protect the exposed tissue from infection due to pathogenic organisms. White blood cells such as neutrophils produce antimicrobial peptides, proteases, reactive oxygen species and cytokines at the wound site (Yin, et al., 2013). Due to the impact of inflammation flow of blood to the skin near the wound increases, this causes the redness and warmth on the edges of the cut. The blood vessels in the vicinity of the wound vasodilate causing the redness of the wound.

Surrounding tissues are swollen because of build up of fluids due to leakage of fluids from the capillaries in the vicinity of the wound. This is called edema and it prevents the action of leukocytes that is necessary for bactericidal action at the wound site and may contribute to the establishment of infection by pathogenic bacteria (Sood, Granick, & Tomaselli, 2014).

Purulent and odorous discharge occurs when the wound is infected by bacteria. It occurs due to formation of pus and is an indication that the wound is infected. Since Mary also has fever, she may require an antibiotic to treat the cause of the infection. A culture test will help determine the antibiotic the causative organism is sensitive to. The pain and warmth at the wound site are also indications that the wound is infected. The fact that the discharge from the wound is odorous is also indicative of the presence of an infection. It means that the healing of the wound will require the systemic administration of an appropriate antibiotic (Demidova-Rice, Hamblin, & Herman, 2012).

Due to inflammation at the wound site, the leukocytes are recruited and are responsible for the release of pyrogens. Endogenous pyrogens include interleukin-1, inetleukin-6 and tumor necrosis factor-α. Release of prostaglandins also causes release of more pyrogens. When the pyrogens travel to the hypothalamus of the brain, the temperature regulation or the body’s thermostat is reset and so fever develops. The cytokines can directly reach the organum vasculosum of the lamina terminalis that is part of the optic recess of the hypothalamus and is located anteroventrally at the end of its third ventricle. It is supplied richly with vasculature and does not have a blood brain barrier (Walter, Hanna-Jumma, Carraretto, & Forni, 2016). This makes it possible for the pyrogens to stimulate it directly. In Mary’s case the inflammation at the wound site must have caused a release of pyrogens and the subsequent fever (Craft, 2015).

When a fever occurs, there is a rise in the body temperature. This rise helps to enhance the immune response and a higher number of lymphocytes and interferons are produced. Besides, bacterial pathogens grow best at a temperature of 37⁰C. Any increase in the body temperature slows down their multiplication. Thus fever works as a defence mechanism and controls the growth of bacterial pathogens. In Mary’s case her wound is infected and the pyrogens produced by the components of the innate immune response could have caused the fever and the elevation of body temperature will help to control the growth of the bacterial pathogen. However, it may not be enough to contain the infection completely, so she may have to take systemic antibiotics.

Since Mary is being treated for an infection by Staphylococcus aureus, it is a part of the normal microbiota that resides on the skin. The rupture of the skin once the wound occurs exposes a warm, nutritious and moist environment for the bacteria to grow in. The bacteria begin to grow and thrive in the environment but their status changes from that of a commensal from the skin surface to that of a pathogen because as an infectious agent the bacteria can cause harm to the host. This is also referred to as the endogenous transmission of pathogen, since the bacteria are normal skin microflora.

On normal skin, several protective mechanisms such as the pH, production of cytokines and chemokines keep the skin protected from an infection. But as soon as the organism finds an environment conducive to its growth, it gets established as an infectious pathogen. Staphylococci also occur as residents of the mucosal membranes of the nasopharynx, the oropharynx and the vaginal mucosa. A transfer of the organism from the nose or mouth of the patient through the hand is also possible and wound also be termed as endogenous transmission of the pathogen (Bowler, Duerden, & Armstrong, 2001).

In Mary’s case, although the wound was exposed to soil there is little chance of S. aureus having infected her wound through this route. Exogenous sources of the infection could be from the hands of the health care staff (Matoušková & Holy, 2014) contaminated gloves, stethescope, handsets, door handles, taps and many other surfaces that the nurse or the first aid provider could have come in contact with (Walia, Manchanda, Narang, Singh, & Kahlon, 2014).

Mary had developed the symptoms of fever and purulent and malodoriferous discharge from the wound meant that it was infected with a pathogenic bacterium. Once a systemic antibiotic is administered to such a patient in appropriate doses for a suitable length of time, the infection by the pathogen can be effectively treated and wound healing can be accelerated. Augmentin is a new generation antibiotic that can treat infections caused by antibiotic resistant organisms. Antibiotic resistance in Staphylococcus aureus is well known and it is important that the infection be treated by an antibiotic that is known for being effective against the causative organism.

Treatment of a Staphylococcus aureus infection with a penicillin analogue, such as amoxycillin became difficult due to development of antibiotic resistance to the beta lactam ring that inhibits cell wall synthesis of bacteria. The resistance developed because the bacteria could produce the enzyme beta lactamase and antibiotics that could earlier impede the development of the peptidoglycan cell wall were rendered ineffective. The methicillin resistant Staphylococcus aureus can also resist action of the antibiotic amoxycillin. Augmentin is  combination of amoxycillin and clavulenic acid. Clavulenic acid is a beta lactamase inhibitor and so it does not allow destruction of the beta lactam ring of amoxycillin by bacteria and it remains active against Staphylococcus aureus. Therefore, augmentin is an appropriate prescription (Bullock & Manias, 2017).