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Wound Healing in Immune-compromised Patients

Info: 10149 words (41 pages) Dissertation
Published: 11th Dec 2019

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Tagged: MedicinePharmacology

There are many textbooks and research papers (Dougherty and Lister 2015, Dealey 2012 & Daeschlein 2013) that suggest wound healing in Immune-compromised patients takes longer and is more complex than in patients who are considered immune competent without any other comorbidities that can influence wound healing. Yet despite wound healing in immune-compromised patients being considered a difficult goal to achieve, at present, there appears to be no guidelines to support healthcare professionals when dealing specifically with wounds in immune-compromised patients.

The Nursing and Midwifery Council (NMC) code of conduct (2015) tells us that we should practice in line with the best available evidence. However, there seems to be limited studies with regard to wound healing in immune-compromised patients as it is considered a barrier to healing; it is often in the exclusion criteria for many research studies.

There are many reasons for someone to have a compromised immune system. Some cases are caused directly by a condition like Human Immunodeficiency Virus (HIV) others are induced by medication used to treat a condition like chemotherapy in a person with cancer or immune-suppressant medication used to treat autoimmune conditions including Crohns disease.

Someone who is immune-compromised cannot respond to an infection in the same way someone that is immune-competent would, due to an impaired or weakened immune system (Ochs et al. 2007). This inability to fight infection can be caused by many acute and chronic conditions, malnutrition, and drugs (Schlagenhauf et al. 2011). Some of these conditions come with inherent risks of being more susceptible to chronic wounds and other conditions that can result in surgery.

By surveying the available literature and guidelines, I intend to establish if wounds in immune-compromised patients need to be treated differently to wounds in immune-competent patients, to aid healing and prevent infection. If this is the case, I will also consider, whether we need separate guidelines and policies to set a national standard and establish best practice when treating wounds in immune-compromised patients.

In 2015-16 1.2% of all surgical incisions developed an infection in the UK within 30 days of surgery (Elgohari et al. 2016). There appears to be no reliable statistics at present with regards to the prevalence of infection in chronic wounds. However, Chamanga et al. (2015) found that 60% of chronic wounds have biofilms compared to 6% of surgical wounds. Therefore, it is safe to assume that in chronic wounds healed by secondary intention, the prevalence of infection will be higher than that in acute or surgical wounds healed by primary intention (Downe 2014); due to chronic wounds, already being colonised with bacteria. It is when this bacterial burden increases the infection begins (Dealey 2012).

A study looking at mortality rates among immune-competent patients in comparison to immune-compromised patients undergoing a bowel resection, due to diverticulitis, in the elective and emergency surgery settings; found the death rate of immune-compromised patients requiring emergency surgery, due to bowel perforation, considerably higher (Brandl et al. 2016). They considered this to be due to the immune systems’ inability to fight infection in immune-compromised patients and the overwhelming bacterial burden caused by the bowel perforation, leading to sepsis (Brandl et al. 2016). Although this study and the mortality rate is not directly linked to wound healing; it does demonstrate the need to reduce the risk of infection in immune-compromised patients to prevent further complications.
The immune system

The immune system is comprised of Lymph nodes, bone marrow, tonsils, and the Spleen as well as proteins and cells in the blood, including lymphocytes (B cells and T cells) and phagocytes (neutrophils, monocytes, and macrophages) (Marieb & Hoehn 2010).

Anatomy and physiology of wounds

The skin is the largest organ of the body and makes up approximately 10% of an adults’ body weight (Hess 2005). It functions as an outer barrier for the body and aids in preserving the balance within (Tortora & Derrickson 2011). The integrity of the skin needs to be maintained to enable it to efficiently perform its vital role (Timmons 2006), without it the body would not endure the bacterial invasion, heat and water loss (Marieb & Hoehn 2010).

The skin varies in thickness from 1.5mm to 4mm depending upon which part of the body it is covering (Marieb & Hoehn 2010). The skin is comprised of two main layers; the dermis and the epidermis. These two layers have six primary functions; protection, sensation, thermoregulation, metabolism, excretion and non-verbal communication (Hess 2005, Timmons 2006).

The epidermis is the outermost layer of the skin. It is avascular and thin. It regenerates every four to six weeks and functions as a protective barrier, avoiding environmental damage and microorganism invasion (Hess 2005). The thickness of the epidermis varies, and it is thicker over the palms of the hands and soles of the feet (Marieb & Hoehn 2010). The Stratum corneum, the outermost layer of the epidermis that results from the terminal differentiation of the keratinocytes, forms the primary protection from the external environment (Marieb & Hoehn 2010). This layer of anucleate keratinocytes is comprised of highly cross-linked proteinaceous cellular envelopes with extracellular lipid lamellae comprising of ceramides, free fatty acids, and cholesterol (Okafor 2012). The free fatty acids establish an acidic environment that inhibits colonisation by certain bacteria including Staphylococcus aureus, providing further protection (Okafor 2012). There are many organisms in the skin of the immune-compromised patient that are associated with infection in the skin (Okafor 2012). The infections could be the result of conventional or opportunistic infection. These infections include viral, bacterial, fungal and parasites (Marieb & Hoehn 2010).

The dermis provides support and transports nutrients to the epidermis. It contains blood and lymphatic vessels, sweat and oil glands and hair follicles. The dermis is made up of collagen and fibroblasts, elastins and other extracellular proteins which bind it to keep it healthy (Hess 2005). The dermis’ extracellular matrix contains fibroblasts, macrophages and some mast cells and white blood cells (Marieb & Hoehn 2010). The connective tissue within the dermis is highly elastic and provides strength to maintain the integrity of the skin to combat daily stretching and wear and tear (Tortora & Derrickson 2011).

The subcutaneous layer just below the dermis is the deepest extension and binds the skin to the underlying tissue (Tortora & Derrickson 2011). This layer is also known as the hypodermis or superficial layer and allows movement (Marieb & Hoehn 2010).

Apart from the physical barriers, the skin also contains other innate immunomodulating substances and cells (Marieb & Hoehn 2010); including cathelicidins, cytokines, neuropeptides, eicosanoids, reactive oxygen species and Langham cells which have phagocytic properties and act as antigen presenting cells (Tortora & Derrickson 2011). The skin is consistently exposed to a host of injuries; because of its size and exposure to the environment (Marieb & Hoehn 2010). These coordinated protective barriers, cells, and substances maintain the integrity of the skin (Okafor 2012).

Wound healing is a cellular and biochemical process which relies principally on an inflammatory process (Hampton & Collins 2004). The processes are dynamic, depend upon each other and overlap (Dealey 2005, Timmons 2006). It is important to support a wound healing environment that encourages progression from one phase to the next without bacterial contamination, as this increases slough and necrosis (Hampton & Collins 2004). These stages are the same for everyone. However, many factors can delay and influence this process.

Stages of healing:


Vasoconstriction occurs within a few seconds of tissue injury, and damaged blood vessels constrict to curtail the flow of blood. When platelets come into contact with exposed collagen from damaged blood vessels, they release chemical messengers that stimulate a clotting cascade (Hampton & Collins 2004, Timmons 2006). Platelets adhere to vessel walls and are stabilised by fibrin networks to form a clot. Bleeding terminates when the blood vessels thrombose, typically within five to ten minutes of injury occurring (Hampton & Collins 2004).

Inflammatory phase (days 1-5)

With the activation of clotting factors comes the release of histamine and vasodilation (Dowdett 2002). The liberation of histamine also increases the penetrability of the capillary walls, and plasma proteins, leukocytes, antibodies, and electrolytes exude into the surrounding tissues. The wound becomes red, swollen and hot. These signs are accompanied by pain and tenderness at the wound site, and last for one to three days and can easily be mistaken for wound infection (Hampton 2013). Polymorphonuclear leukocytes and macrophages migrate to the wound within hours, and these phagocytose debris and bacteria begin the process of repair (Hart 2002). If the number and function of macrophages are reduced which may occur in diseases including diabetes (Springett 2002), healing processes are affected. Nutrients and oxygen are required to produce cellular activity, and therefore malnourished patients and hypoxic wounds are more susceptible to infection (Dealey 2005, Timmons 2006). The breakdown of debris causes an increased osmolality within the area, resulting in further swelling. A chronic wound can become delayed at this phase of wound healing (Dealey 2005, Hampton & Collins 2004). With prolonged healing, there is a tendency for infection and high levels of exudate (Timmons 2006). The stages that follow start the process of repair (Tortora & Derrickson 2011).

Proliferation or reconstructive stage (days 3-24)

Acute wounds will begin to granulate within three days, but inflammatory and proliferative phases can overlap with both granulation and sloughy tissue present (Timmons 2006).

The fibroblasts are activated to divide and produce collagen by processes initiated by macrophages (Timmons 2006). Newly synthesised collagen creates a ‘healing ridge’ below an intact structure line, thus giving an indication of how primary wound healing is progressing. The mechanism is dependent on iron, vitamin C, and oxygen. Vitamin C and lactate are stimulants for fibroblast activity (Hampton & Collins 2004). Fibroblasts are also dependent on a supply of oxygen (Dealey 2005). The wound surface and the oxygen tension within encourage the macrophages to instigate the process of angiogenesis, forming new blood cell vessels. The vessels branch and join other vessels, forming loops. The fragile capillary loops are held within a framework of collagen. This complex is known as granulation tissue (Grey et al., 2010).

Endothelial buds grow, and the fibroblasts continue the process of repair by laying down fibrous tissue (Hampton & Collins 2004). Epithelial cells will burrow under contaminated debris and unwanted material while also secreting an enzyme that separates the scab from the underlying tissue. Through a mechanism called contact inhibition, epithelial cells will cease migrating when they come into contact with other epithelial cells (Tortora & Derrickson 2011).

Epithelisation occurs at an increased rate in a moist wound environment, as do the synthesis of collagen and formation of new capillaries. Wound contraction is a function of myofibroblasts, which are prominent in granulating tissue. The extent of wound contraction is dependent on the number of myofibroblasts present and is maintained by collagen deposition and cross-linking (Giele & Cassell 2008).

Maturation or remodelling phase (21 days onwards)

Twenty-one days following the initial injury the remodelling phase begins. Re-epithelialization occurs at this stage and covers the wound (Benbow 2005). Collagen is reorganised; fibers become enlarged and orientated along the lines of tension in the wound (Silver 1994). This occurs via a process of lysis and resynthesis. Intermolecular cross-linking aids the tensile strength of the wound. During the reorganisation, fibroblasts may constrict the neighbouring collagen fibers surrounding them, causing the contraction of the tissue and reduction of blood vessels within the scar (Cho & Hunt 2001). At the end of the maturation phase, the delicate granulation tissue of the wound will have been replaced with a strong avascular scar (Dealey 2005).

Types of wound closure

Primary wound closure

Primary wound closure describes the process of closing a wound within hours of injury and is possible when the wound edges remain in close proximity, and there is little or no tissue loss or damage. As long as the wound edges can be brought together without tension, the wound can be closed by many methods; including sutures, clips, adhesive strips, or skin adhesives. Wounds closed by primary intention typically have the best aesthetic appearance, and wound healing is faster providing there are no factors to delay wound healing and complications are treated quickly and appropriately.

Secondary closure

If primary closure is impossible, wounds should be left open to spontaneously heal by the process of contraction and re-epithelisation known as secondary closure. Secondary closure is associated with wounds that had substantial damage and tissue loss. These wounds tend to be caused by an underlying, internal etiology and pathology like venous insufficiency, unrelieved pressure or friction. In many of these cases, healing will be delayed due to these local factors.

Delayed primary closure

Delayed primary closure sometimes referred to as tertiary closure occurs when wound closure is delayed by three to six days due to adverse local conditions such as poor vascularity, uncontrolled bleeding or risk of infection (Gottrup 1999). Once conditions improve wounds are closed with sutures or other primary closure techniques. Delayed wound closure is a balancing act between primary closure and waiting for optimal conditions to close the wound.

Wound healing influences

Some wounds progress toward wound healing with no complications. However, not all wounds follow the expected stages of wound healing; some become stuck in the inflammation phase due to wound infection as well as many other local and systemic factors such as immune-compromised individuals (Chamanga et al. 2015). There are many factors that can influence and delay wound healing; these can be broken down into local and systemic factors (Guo & DiPietro 2008).

Local factors


The supply of oxygen to wound tissue is necessary to promote wound healing and to encourage resistance to infection (Gottrup 2004). Wound hypoxia is described as oxygen levels lower than 30mmHg and is related to poor wound healing, inhibition of fibroblast replication and impaired collagen reproduction (Burns et al. 2003). Oxygen plays a dual role in angiogenesis, the formation of new blood vessels. Initially, Hypoxia stimulates the initial growth of new vessels. However, the later stages of angiogenesis are stimulated by Hyperoxia and wounds will not progress to heal without higher oxygen levels (Chambers & Leaper 2011). Therefore, oxygen is required to optimise wound healing and create a well-vascularised wound bed. Even though, immune-compromise does not directly influence oxygenation of the wound bed. There are conditions such as chronic obstructive pulmonary disease (COPD) that is treated with immunosuppressing medications, steroids, which link immunosuppression and wound bed oxygenation.

Bacterial burden

The wound environment is the ideal environment for bacterial growth. Devitalised tissue and slough caused by chronic wound hypoxia provide a food supply for the bacteria. This can lead to a prolonged inflammatory response and can be detrimental to normal wound healing. The bacteria burden or biofilm needs to be removed to allow the wound to move out of the inflammatory stage, allowing normal wound healing to continue. The bacterial burden of wounds, or biofilm, in immune-compromised patients leaves an opening for opportunistic infections. Therefore, it is imperative to reduce the bacterial burden of the wound bed to minimise the risk of opportunistic infections.

Wound pH (Potential of hydrogen)

A pH value of 7 represents neutral; above seven is alkaline and below 7 is an acid environment. A non-healing wound is usually an alkaline environment. A healing wound typically progresses into an acidic environment. The pH of the wound bed is an important factor in promoting an optimal wound healing environment. Protease, an enzyme that breaks down proteins and peptides, is pH dependent. If protease levels are elevated, this can cause delayed wound healing. pH also plays a substantial role in infection control and wound oxygenation. In addition to the effects on protease activity and oxygen release, the acidic environment also enhances the destruction of abnormal collagen in the wound bed, increased macrophages and fibroblast activity and controls activities of various enzymes participating in the wound healing process. There is no available evidence to suggest that wound bed pH is influenced by immunosuppression.

Foreign bodies

It is essential to remove any foreign objects from the wound where possible to reduce the risk of infection and delayed healing. Suturing a wound is also considered a foreign object in a wound and can occasionally lead to pain and inflammation around the sutures. Although sutures are sterile on insertion they do create the opportunity for bacteria to enter the wound, leaving the wound open to opportunistic infection in immune-compromised patients.

Wound temperature

All cellular activity within the body occurs at an optimal rate when the body is at normal core body temperature. Tissue repair occurs when the body surface temperature is between 33 and 42 degrees Celsius. Therefore, dressing changes and wound cleansing can reduce the temperature of the wound bed, delaying wound healing until the wound bed once again reaches optimal temperature.

Systemic factors

Age and gender

Increased age, over 60, has a significant impact on wound healing. This impact on wound healing is due to an altered inflammatory response. However, this does not have a bearing on the quality of wound healing. Every stage of healing undergoes characteristic age-related changes, including enhanced platelet aggregation, increased secretion of inflammatory mediators, delayed infiltration of macrophages and lymphocytes, impaired macrophage function, decreased secretion of growth factors, delayed re-epithelialisation, delayed angiogenesis and collagen deposition, reduced collagen turnover and remodelling, and decreased wound strength

Sex hormones

Sex hormones play a role in age-related wound healing deficits. Compares with elderly females, elderly males have shown to have delayed healing of acute wounds. A potential explanation for this is that female oestrogen, and male androgens and their steroid precursors appear to have significant effects on the wound healing process. Oestrogen effect wound healing by regulation of genes primarily associated with inflammation.


Stress has always been renowned for its effects on health and social behaviour. Many diseases are associated with stress and can be aggravated by it. The pathophysiology of stress results in a dysregulation of the immune system. This dysregulation of the immune systems makes the patient more susceptible to infections that in turn impair and delay the wound healing process.


The prevalence of obesity continues to increase across all generations in Weston society. Obesity is well known to increase the susceptibility to many health conditions including heart disease, stroke, and diabetes. However, it also has an impact on wound healing. Obese individuals frequently face complications with wound healing including wound infection, wound dehiscence, haematoma and scab formation.


Many medications such as those that interfere with normal clotting and platelet formation or inflammatory response and cell proliferation have the capacity to affect wound healing.

The following types of medications are used to treat immune system disorders and to prevent the rejection of transplanted organs; Monoclonal antibodies, Anti-lymphocyte, Anti-metabolites, Calcineurin inhibitors, Purie synthesis inhibitors, T-cell activation inhibitors, Thalidomide and Interleukin inhibitors. They work by suppressing the immune system, therefore preventing it from attacking the healthy tissue of organs;

Glucocorticoid steroids are frequently used as anti-inflammatory’s and are well known to inhibit wound repair. Due to anti-inflammatory effects; and suppression of cellular activity, this includes fibroblast proliferation and collagen synthesis. Steroids cause wounds to heal with incomplete granulation tissue and reduced wound contraction. As well as the effects on the wound healing systemic steroids also increase the risk of infection due to their immune-suppressing effects. While systemic steroids have adverse effects on wound healing, low-dose topical steroids have the opposite effect; there is evidence to suggest that topical steroids used on chronic wounds have been found to accelerate wound healing, reduce pain and exudate and suppress hyper granulation.

Non-steroidal anti-inflammatory drugs (NSAIDs) including Aspirin and Ibuprofen are widely used for the treatment of inflammation and rheumatoid arthritis and pain management. There is some evidence to suggest that short-term use of NSAIDs has a negative effect on wound healing. However, since Aspirin is used long term as a therapeutic, preventative treatment for cardiovascular disease further research is required with regards to its long-term effects on wound healing. Conversely, Aspirin is also a medication that interferes with clot formation: it therefore delays the first stage of wound healing, haemostasis.

Chemotherapy drugs are designed to inhibit cellular metabolism, rapid cell division, and angiogenesis. Therefore, inhibit many of the processes critical for wound repair. Chemotherapy medications inhibit protein synthesis resulting in decreased production of fibroblasts and neovascularisation of wounds. Chemotherapy drugs also delay cell migration into the wound, reducing early wound matrix formation, lower collagen production, impair proliferation of fibroblasts and inhibit contraction of wounds. Also, these medications suppress the immune system increasing the risk of wound infection for the patient.

Chemotherapy can induce; neutropenia, anaemia and thrombocytopenia. Therefore, leaving wounds vulnerable to infection, causing less oxygen delivery to the wound and making the patient susceptible to excessive bleeding at the wound site.

Alcohol and cigarette consumption

Alcohol consumption and smoking have been linked to increased risk of wound infection. Alcohol consumption decreases the patients’ resistance to infection and leaves them vulnerable. Alcohol also suppresses the inflammatory response which in turn increases the risk of infection. Smoking interferes with oxygen saturation which can have an adverse effect on healing due to wound hypoxia.


Malnutrition or deficiency in specific nutrients can have a profound impact on the wound healing process. Carbohydrates, proteins, amino acids, and fats that are the primary sources of energy for the wound healing process.


Immune-suppression and immune-compromised refers to a state where the body’s immune system is intentionally stopped from working or is made less efficient for the body to accept an organ that has been transplanted or to put an autoimmune condition into remission. Immunodeficiency is defined as a condition arising, in which the body is unable to produce enough antibodies to fight bacteria and viruses, often resulting in infection or disease.

Causes of immune-compromise

As previously discussed, there are many medications that can compromise the immune system. There are also many conditions can cause immune compromise, either on their own or due to the treatment that was given; Cancer, Crohns disease, HIV, uncontrolled diabetes, neutropenia, pancytopenia, malnutrition, Ataxia-telangiectasia, Complement deficiencies, DiGeorge syndrome, Hypogammaglobinaemia, Job syndrome, Leukocyte adhesion defects, Bruton disease and Wiscott-Aldrich syndrome.

To analyse the papers found I will use the appropriate Critical Appraisal Skills Program (CASP) tools for the type of literature I am looking at. CASP was initially developed by Sir Muir Gray in 1993, in response to the need for developing skills in health care staff to meet the challenge of moving towards evidence-based practice. CASP was designed for the use of healthcare professionals, to enable learning to evaluate and critically appraise texts to inform their practice. I have decided to use the CASP tool to assess the sources as it is designed specifically for evaluating literature within the context of health and social care.

My research is limited by the fact there is no single piece of research looking at all areas of wound care in immune-compromised individuals, and many are published in condition-specific fields. Therefore, I am limited by time and my ingenuity to be able to successfully search for all of the available research on this subject to perform a comprehensive and systematic literature review.

Primarily, I will be looking to use quantitative research from randomised control trials for my literature review. However, I will also be looking at some mixed-method studies and be considering information from evidence-based textbooks from background research.

The literature and anecdotal evidence suggests many of the practices used by healthcare professionals when treating patients with a compromised immune system lack an evidence base, but are used because they appear prudent and reasonable (Schlagenhauf et al. 2011). To give an example; low microbial foods, personal protective equipment and skin antiseptic regimes are all used to reduce the risk of an immune-compromised patient developing an opportunistic infection (Schlagenhauf et al. 2011).

Aseptic technique is assumed to prevent infection and promote healing (Stotts et al. 1997), but how true is this assumption? Gruber et al. (1981) and Tenorio et al. (1976) both suggested that aseptic technique is not required to prevent infection in immune competent wound healing and that a clean technique is acceptable. Gruber et al. (1981) and Levenson et al. (1983) take this further by suggesting that a small amount of bacterial burden can stimulate healing.

The two primary sources of infection are the patient’s skin flora and the environment. Cross-contamination from these two sources is the leading cause of wound infection in surgical patients. Hand washing and clean gloves are interventions that can reduce the risks of cross-contamination wound infection in surgical patients (Stotts et al. 1997).

It is notable that the study by Stotts et al. (1997) looked at clean technique and aseptic technique as an intervention in wound healing and found the incidents of infection were the same in each group. One participant in each group developed a wound infection. However, the participant from the aseptic technique group developed such a severe infection it was no longer safe for that person to participate in the trial. There were three immune compromised participants in this trial; however, their outcomes are not documented.

I also looked at studies from Wound ostomy and continence nurse society (2012), Gillespie & Fenwick (2009), Creamer et al. (2012), Barber (2002) and Rodgers et al. (2006) all of which concluded there is no increased risk of infection when a clean dressing technique is used over aseptic technique. Ultimately, as clean technique is more cost-effective than and just as safe as aseptic technique there is no reason not to use clean technique as standard practice when providing wound care. However, these trials did not document the use or exclusion of immune-compromised patients. Therefore, it cannot be generalised to be safe practice within this group of patients without further research.

Wound cleansing

The purpose of wound cleansing is to create an optimal environment for healing. If the wound is clean with little exudate and granulated tissue present, repeated cleaning can damage the new tissue and decrease the temperature of the wound (Downe & Khatun 2016). A temperature drop of 12 degrees centigrade is possible during the wound cleansing process, and it can take up to three hours for the temperature to return to normal (Flanagan 2013). During this time, there is a reduction in cellular activity, therefore, slowing the healing process. Downe & Khatun et al. (2016) suggests that cleansing can be just as effective at managing bacterial burden as some of the softer debridement techniques.

Studies by Goldberg (1981), Riederer (1997) and Neues (2000); all looked at tap water versus no cleansing and considered prevalence of infection in immune competent surgical wounds. All these trials demonstrated no increase in wound infections, and none of the wounds showed signs of delayed wound healing. The trial by Neues (2000) also considered soapy tap water and demonstrated no increased risk of infection or delay in wound healing.

Studies by Angeras (1992), Grithiths (2001), Grodinez (2002) and Moscati (2007) looked at tap water versus normal saline in sutured acute wounds and found no statistical significance to suggest use of one cleansing solution over another. However, Angeras (1992) did note an increased infection rate in the normal saline group which may have been due to the water being stored at room temperature. However, the study by Grithiths (2001) showed increased patient satisfaction if they were allowed to cleanse the wound themselves in the shower before dressing the wound.

A study by Museru (1989) designed a three-armed trial looking at the infection prevalence between wounds cleansed with distilled water, cooled boiled water and normal saline. When considering distilled water versus cooled boiled water, 17% of the wounds cleansed with distilled water developed infection compared to 29% of wound cleansed with cooled boiled water developed an infection. Whereas, 35% of wounds cleansed with normal saline developed an infection. Unfortunately, this trial had small sample sizes in each group. Therefore, it was not a big enough trial to have any clinical significance but does suggest the need for further studies to establish an evidence base.

Sodium chloride 0.9%, also known as normal saline, is favoured as a wound cleansing solution as it is readily available in many settings and does not interfere with the wound healing process. This is due to sodium chloride having a similar osmotic pressure to the wound bed. Therefore, it is compatible with human tissue. Although sodium chloride has no antiseptic properties, it dilutes the bacteria and is non-toxic to tissue. However, in the community setting tap water is favoured due to easy access and cost-effectiveness. There is no evidence to suggest this increases the risk of infection or influences the healing process.

Looking at numbers alone, these would suggest that cleansing wounds with normal saline is putting the patient at a marginally higher risk of infection. However, there appears to be not enough in-depth trials with large enough sample sizes to establish an alternative as best practice. At present, none of the data suggests a single cleansing solution be optimal. Therefore, more trials are needed. None of the trials found considered co-morbidities or dressings. There is also minimal data looking at chronic wounds and no research available looking at cleansing solutions used in immune-compromised patients.

A comprehensive literature review by Fernandez & Griffiths (2012) considered 11 trials were looking at different cleansing solutions for wound care and also found there was no increased risk associated with any of the cleaning solutions considered; they also found there was no increased risk associated with not cleaning the wound. This would suggest that wound cleansing does not need to be a standard practice unless it is required to help the healthcare professional visualise the wound bed to accurately assess the wound.


Debridement refers to deep removal of adherent, dead or contaminated tissue from the wound and is a separate act of wound cleansing. It is the act of removing necrotic material, eschar, devitalised tissue, scabs, infected tissue, hyperkeratosis, slough, pus, haematomas, foreign bodies, debris, bone fragments or any other types of bio burden from the wound with the objective of promoting wound healing. There are many types of debridement; autolytic, enzymatic, mechanical, surgical or sharp and biologic. Debridement of the wound enables the nurse to visualise and assess the wound bed.

Autolytic debridement is a process by which the body attempts to get rid of devitalised tissue by using moisture. When tissue is kept moist, it will naturally degrade and be de-sloughed from the underlying healthy structures ( ). This process is helped by the presence of enzymes called matrix metalloproteinases, which are produced by damaged tissue and which disrupt the proteins that bind the dead tissue to the body ( ). This process can be enhanced by the application of wound management products which promote a moist environment ( ). These products can be divided into two categories: those that donate moisture to the dead tissue and those that absorb excess moisture produced by the body. Both are designed to facilitate the autolytic debridement process ( ).

There are various enzyme preparations which are effective at digesting dead tissue, e.g., collagenase and papain, but these are not currently available in the UK (Bellingeri and Hofman, 2006).

Surgical debridement involves the removal of dead tissue from the wound bed. It is carried out under surgical conditions and results in a bleeding wound bed following the complete removal of necrotic material. This is carried out by surgeons, podiatrists and specialist nurses who have been trained in the procedure, using scalpel and forceps.

Sharp debridement is the removal of dead tissue with scissors or scalpel. This should only be carried out by a healthcare professional trained in the procedure.

Larvae or maggots have been used in the UK to debride wounds for many years and are a fast, effective and safe method of debridement (Thomas, 1998). Maggots are now available both as ‘free- range’ (and placed directly into the wound) or contained in bags. The powerful enzymes in their saliva dissolve necrotic tissue, which the maggots then ingest. They do not have to be in direct contact with the wound bed. However, free-range maggots have the advantage of being in a position to penetrate crevices and sinuses more effectively. The disadvantage is they can escape and cause distress to both patient and practitioner.

Moisture donating methods of debridement use dressings such as Hydrocolloids and hydrogels (amorphous gel in a tube or hydrogel sheets), to donate moisture to the dead tissue to facilitate autolytic debridement. These dressings are particularly useful in wounds that are not heavily exuding. The use of second-generation hydrogel sheets such as Actiform Cool will absorb a certain amount of moisture while also donating it so, in many cases; will provide a good moisture balance at the wound surface. If desired the dressing can be cut to fit the wound. The white backing should be peeled off, and the dressing laid gel side down onto the wound surface. Dressings should be changed when there is strike-through but may possibly be left on for up to seven days if there is no leakage. A second-generation hydrogel sheet dressing may continue to be used after debridement has occurred through to healing as it promotes granulation tissue and maintains a clean wound bed

Alginates, cellulose dressings and foams are designed to absorb exudate. By absorbing excess wound fluid, these products avoid damage to the surrounding skin from maceration. The structure of some foam dressings alters under compression so that the moisture remains in contact with the skin. Care should be taken to select appropriate foam. Dressings which reduce bacteria in a wound such as honey, silver, or iodine may help reduce slough and promote healthy granulation.

The process of debridement will increase exudate and this, in turn, may damage surrounding skin. The frequency of dressing change may have to be increased and surrounding skin treated to reduce the risk of the healthy tissue breaking down.

Dressings which donate moisture (such as hydrogels) should not be used on a wet wound as the increase in moisture will macerate the skin. Honey dressings, although increasing exudate in the initial phase, will, by reducing bacterial load, also eventually reduce exudate.

The choice of method of debridement depends on wound severity and patient preference. Many patients like the idea of a natural product such as honey. The only reason to avoid this dressing would be pain as patients often find the drawing sensation intolerable. Maggot treatment is more rapid than autolytic debridement if the wound is offensive and there is significant sloughy/necrotic tissue larval therapy should be considered.

If the wound is painful, it is unlikely that maggot treatment will be tolerated, and some patients are repelled by the idea of larval therapy. In a painful wound, using a second-generation hydrogel sheet should be considered.

Primary dressings

Modern wound management offers a varied selection of materials and dressings that provides various benefits in the wound healing process. Some of these dressings have already been introduced due to their debridement properties and fit into some of the following categories; non-adherent dressings, semi-permeable films, hydrogels, hydrocolloids, alginates, foams and anti-microbial and growth-factor dressings. So, which dressings should we be using and does it make a difference if the patient has a compromised immune system? I have considered the following types of dressings, looking at their use and their advantages and disadvantages:

Activated charcoal is a non-adherent dressing that contains a layer of charcoal which traps and reduces odour causing molecules. It can be used as a primary or secondary dressing. It is easy to apply and can be used with another absorbent dressing. However, for it to be effective it needs to have a good seal around the dressing to prevent any odour from leaking out. Some brands of the dressing have been found to lose their effectiveness as they get wet.

Alginates are a textile fibre dressing made from seaweed; the soft woven fibres gel as they absorb exudate and promote autolytic debridement. It is available as sheet, ribbon or packing and is suitable for use in wounds with moderate to heavy exudate. It requires a secondary dressing. It can be used on infected wounds and is useful for sinus cavities and fistula drainage. It also has a haemostatic property and can be irrigated out of a wound with warm saline. However, it cannot be used on dry wounds or wounds with hard necrotic tissue. Research has found; reports of mild burning or drawing sensation on application.

Antimicrobials dressings are topical solutions or dressings that can be used as primary or secondary dressing. They are available in primary layer or impregnated in other dressings or creams and are suitable for use in chronic wounds with heavy exudate that needs protection from bacterial contamination. They provide this protection by a broad range of antimicrobial activity. They can be used to reduce or prevent infection. Research suggests there can be some sensitivity with silver dressings; and the silver dressing has a limited time period when it is effective, this is considered to be approximately 2 weeks. Occasional, an undesirable side effect of these dressing is skin staining. Instructions can vary with different products and the dressings are more expensive than other types of dressings.

Capillary wound dressing are comprised of a 100% polyester filament outer layers and 65% polyester, 35% cotton woven inner layer. The outer layer draws exudate, interstitial fluid and necrotic tissue into the inner layer via a capillary action. It is suitable for light to heavy exudate. It has the ability to debride necrotic tissue and insulate the wound. whilst Maintaining a moist environment and prevent maceration. Capillary wound dressings also encourage the development of granulation tissue. It can be cut to any shape and are available in large rolls it can also be used as a wick  to drain sinus and cavity wounds. It can be hard to cut and is quite stiff to fit in to wounds. It cannot be used in wounds where there is a risk of bleeding due to the drawing action. It is expensive and should be used on a named patient basis as an infection control precaution.

Collagen dressings are protein based dressings. They are fibrous and insoluble. Collagen encourages fibres into granulation tissue. It is available in sheets and gels, and conforms well to the wound surface. Collagen dressings have the ability to Maintain a moist wound environment and are suitable for most wounds to support healing. However, collagen dressings are not recommended for necrotic wounds and it requires a secondary dressing to absorb exudate.

Foam dressing products can be produced in a variety of forms, most are constructed of polyurethane foam and may have one or more layers. Foam cavity dressings are also available and are suitable for use with open exuding wounds. They are highly absorbent, non-adherent and maintains a moist wound bed. They are available for low to high exudate wounds and can be obtained with or without an adhesive border. However, these dressing can be difficult to use in wounds with deep tracks and Occasionally needs a combined approach with an alginate dressing.

Honey is available in tubes of cream and ointment or impregnated dressing. It is suitable for use in acute, chronic, infected, necrotic or sloughy wounds. It helps provide a moist wound environment. It is non-adherent and anti-bacterial, and can assist with wound debridement. Honey also effectively eliminates wound malodour and has an anti-inflammatory effect. However, it can be messy to use and cause leakage if excess exudate if present. It requires a secondary dressing to absorb exudate and research suggests it may have a burning or drawing effect when first applied.

Hydrocolloid dressings usually consist of a base material containing gelatine, pectin and carboxymethylcellulose combined with adhesive polymers. The base material may be bonded to a semi permeable film or a film plus polyurethane foam; some hydrocolloid dressings are available with an adhesive border. Hydrocolloid dressings are suitable for acute and chronic wounds with low to no exudate. They provide a moist wound environment that promotes wound debridement as well as provide thermal insulation and protective waterproof barrier that is also a barrier to micro-organisms. The dressing is easy to apply and use. However, some hydrocolloid dressing brands cannot be used on infected wounds and may release degradation products into the wound which can lead to strong odour production as dressing interacts with exudate.

Hydrofiber dressings have the same consistency as hydrocolloid dressings except they are formed into a soft woven sheet. Hydrofiber dressings are also available impregnated with silver. When in contact with the wound the dressing forms a soft hydrophilic gas-permeable gel that manages exudate whilst preventing maceration of the wound edge. The dressing is easy to remove therefore preventing trauma to the wound bed. However, this dressing does not have the haemostatic properties of alginates.

Hydrogel dressing contain 17.5% – 90% water depending of brand, as well as various other components to form a gel or solid sheet. Hydrogel dressings are suitable for wounds with exudate as the dressing in only able to absorb small amounts of exudate. It is a moisture donating dressing that donates fluid to dry necrotic tissue to facilitate autolytic debridement. Due to the cooling effect of the dressing there is evidence to suggest it reduces pain and there is a low risk of trauma to the wound bed on dressing change. This type of dressing can also be used as mode of medication administration to the wound bed. However, the cooling effect of the dressing has the potential to delay wound healing as it cools the wound surface. This type of dressing should be used with caution in infected wounds. It also has the potential to cause skin maceration due to leakage if too much gel is applied or the wound has moderate to heavy exudate. Care should be taken with dressing sheets to ensure they do not dry out.

Semi-permeable films consist of a polyurethane film with a hypoallergenic acrylic adhesive. It has a variety of application methods, often consisting of a plastic or cardboard carrier to aid application. This type of dressing is only suitable for shallow superficial wounds or for prophylactic use against friction damage. It can also be useful as a retention dressing. This type of dressing allows water vapour to pass through it and for the monitoring of the wound. However, there is the possibility of adhesive trauma if removed incorrectly. This type of dressing does not have the ability to contain exudate, and can cause maceration of the skin surrounding the wound. There is also an issue with the dressing slipping and leaking in the presence of exudate.

Skin barrier films are non-cytotoxic alcohol free lipid polymers that form a protective film on the skin. It does not sting on application to excoriated areas of skin. It has a high wash off resistance and can protect the skin from bodily fluids, friction and shear and the effects of adhesive products for up to 72 hours after application. However, skin barrier films require good manual dexterity to apply, and may cause skin warming on application.


A review by Robson et al. (2008) developed recommendations for guidelines to aid healing in patients with compromised wound healing. As immune-compromise is considered a factor that delays wound healing they considered this in their guidelines. They diligently reviewed the causes of immune-compromise separately.

In patients with HIV and AIDS Robson et al. (2008) recommend maximising pharmaceutical treatment before any elective surgery. They suggest Antiretroviral therapy be initiated, viral load minimised and absolute lymphocyte count maximised. Controversially, Robson et al. (2008) also recommend an effective prophylaxis against wound infection should be used. Although this research was published several years before the NICE recommendations pertaining to antimicrobial stewardship (2015); the presence of antibiotic-resistant ‘superbugs’ was already well documented and discussed with the healthcare industry. Notably, Graeb & Jauch et al. (2008) recognised the significant impact of infection on wound healing in immune-compromised patients. However, they rebutted the idea of prophylactic antibiotics to prevent postoperative infection stating it would put the patient at greater risk of fungal and viral infections, which often prove harder to treat than the original bacterial infection.

For medication induced immune-suppression, Robson et al. (2008) recommend reducing the medication as much as safely possible before any procedure and until the wound has completely healed. In particular, Robson et al. (2008) suggest, that steroids be reduced or where possible, and safe to do so, discontinued before surgery and only restarted if needed, once the wound has completely healed. Alternatively, in the case of emergency surgery, Robson et al. (2008) suggest weaning the patient off the steroids postoperatively. Conversely, Graeb & Jauch (2008) suggest the complete removal of immune-suppressing medication where possible, and if not switching to azathioprine. Although, this was contradicted by Colombel et al. (2004) when looking at post-operative complications in Crohns patients on immune-suppressing medication as they found no increased risk for patients receiving steroids, infliximab or azathioprine before surgery. This is supported by an earlier study by Odabasi at al (2000) that looked at immune-compromised patients in receipt of a Cochlear implant. Of the 13 patients that participated in the study, only one patient who was immune-suppressed; as well as having multiple comorbidities, developed a wound infection. There were no adjustments made to the medications for these patients and the treatment and care remained the same for the immune-compromised patient as it was for immune-competent patients. This led to a conclusion by the author that although it is prudent to practice in a way that reduces the risk of infection, it is not necessary to change practice and treatment for immune-compromised patients.

A study by Howard et al., looked at the incidents of infection and wound healing following surgical fixation of open fractures in HIV positive and negative patients. Unfortunately, the study was limited by poor compliance with follow-up, but of the 51 patients that completed the follow-up only one patient developed a wound infection and this patient was in the HIV negative group. It is also noted no patients developed a chronic non-healing wound following the surgery. The authors conclude there should be no concerns of delayed wound healing or increased infection risk in infected patients surgically treated for open fractures. As this study was performed on patients receiving emergency surgery, there was no medication adjustments performed prior to surgery; once again suggesting that medication optimisation, to prevent wound infections is unnecessary in immune-compromised patients.

For patients with Leukopenia Robson et al. (2008) recommends correcting it where possible before any elective surgery. They consider Granulocyte-monocyte colony-stimulating growth factors or blood transfusions a potential treatment to correct the Leukopenia as white blood cells are also sources for tissue growth factors, macrophages are required for normal wound healing, therefore rationalising the need to correct Leukopenia to enable normal wound healing. Unfortunately, I found no other research to support or reject this theory.

Robson et al. (2008) also consider the effects of chemotherapy on wound healing and recommend an appropriate gap before any surgical intervention takes place dependent on the type of chemotherapy and its lasting effect. It is certainly prudent to allow the patient time to recover from chemotherapy before any surgery, as this is a lot of trauma to inflict on the human body. Depending on the type of chemotherapy and its effects on the bone marrow, platelet and white cell count, it would be appropriate to give the patient a period of recovery between chemotherapy and surgery to ensure the patients safety whilst undergoing the surgery.

Inopportunely, the recommendations by Robson et al. (2008), while related to wound healing in immune-compromised patients do not consider the treatment of the wound itself. They only consider reducing the risk of a problems during the wound healing process by making changes before elective surgery. However, there is always a potential for the need of emergency surgery or the wound being sustained outside of the heath care environment.

An observational study using medical honey as a topical treatment for wounds in paediatric haematology-oncology patients with wound infections; shows dramatic results in treating the infection and preventing further infection in continued use, allowing the wounds to heal on the expected trajectory (Santos et al. 2006). Honey is also documented to be an effective treatment when treating Vancomycin-Resistant Enterococci (VRE) and Methicillin-Resistant Staphylococcus Aureus (MRSA) (White 2005). All of the patients in this study (Santos et al. 2006) were treated using aseptic technique and monitored daily for signs of infection. Many of the patients in this study were severely immune-compromised due to chemotherapy treatment (Santos et al. 2006). However, the study was limited to the one type of antimicrobial dressing and did not compare the honey dressing to the effectiveness of alternative treatments.

A study by Pucca (2017) looking at wound infections in immune-compromised diabetic patients; found that uncontrolled non-insulin dependent Type 2 Diabetic patients were more likely to develop a wound infection compared to insulin dependent Type 2 Diabetics and Type 1 Diabetics. Imaginably, this finding is due to the similarity between risk factors for Type 2 diabetes and the local and systemic factors that can delay wound healing. However, Pucca (2017) postulated that the cause was the uncontrolled blood glucose levels of these patients and advocated tighter blood glucose level control for these patients and commencing them on insulin.

Nutrition has long been considered an important factor in the wound healing process; with malnutrition being a cause of delayed wound healing. Casey (2003) also suggests that chronic or infected wounds can also cause malnutrition due to the increased metabolic and nutritional demands placed on the body. Ward (2002) takes the idea of nutrition and wound healing further and suggests the need for a balanced diet to maintain the immune system and prevent wound infections. Ward (2002), suggests that Protein, Vitamin A, Vitamin C, Vitamin D, Vitamin E, Iron, Zinc and Copper are all required to maintain an effective immune system to reduce a person’s susceptibility to infection. These are the same nutrients that Casey (2003) suggest aid wound healing. Both authors suggest that nutritional support for patients with wounds may improve healing rates particularly in those with poor nutrition; either before the wound or due to the wound.

Conclusion and Recommendations

Upon commencement of this research project I intended to establish whether there was a need to treat wounds in immune-compromise patients different to those in immune-competent patients, and if this was the case was there a need to establish separate wound care guidelines for this group of patients. Having considered all of the research and evidence with regards to the care of wounds in immune-compromised patients I have formed recommendations for the treatment of these wounds. These recommendations have the potential to evolve with advances in research and practice. However, there is a need for the creation of guidelines to support and inform the decision-making processes of healthcare professionals caring for this group of patients. At present the evidence base for the creation of such guidelines is inadequate. Further control trials are needed in this area; although, ethics approval is likely to be difficult to gain for studies within this category of patients’ due to their susceptibility to severe infections.

Although, I have found many statements with regards to delayed wound healing and increased susceptibility to infection in patients with a compromised immune system the studies found did not demonstrate higher rates of infection in immune-compromised patients. Considering an individual’s vulnerability to infection is an important aspect of patient assessment. Patients who are immune-compromised have an increased susceptibility to infection. However, this does not necessary mean they will develop a wound infection as detailed throughout this review.

When caring for a wound in patients that have a compromised immune system, it is imperative to pay meticulous attention to infection control policies and procedures to prevent the contamination or cross-contamination of the wound wherever possible. The surface of any wound suspected to be infected needs to be cleaned or debrided to ensure that organic matter such as slough, extracellular products, biofilm, and exudate are removed as they are the ideal growth media for microorganisms. The most effective wound cleanser still needs to be determined by further research and clinical trials. Therefore, the choice is down to local policy and practitioner discretion. Selection of debridement technique once again is down to the healthcare professionals’ assessment and discretion and should be considered in conjunction with local policy and guidelines.

If wound infection is suspected, a holistic review of the patient, the wound and the care plan is required. In the case of localised infection, the first line treatment should be to consider antimicrobial or honey dressings, bearing in mind the evidence base to suggest that silver only has a short window of effectiveness, rotation of antimicrobial dressings may be required where clinical appropriate. Furthermore, keeping in mind the need for antimicrobial stewardship, antibiotic therapy should only be considered if there is evidence of spreading or systemic infection that has been confirmed by wound swabs, blood cultures or clinical assessment. Antibiotics should not be used indiscriminately and should be used for limited periods of time, and their effectiveness should be reviewed at regular intervals. There is no evidence at present to suggest the need for stringent control of antimicrobial dressings and therefore can be used more freely than antibiotics and can be used prophylactically where clinically necessary.

Management of any patient with an infected wound, immune-compromised or immune-competent, requires the practitioner to have a sound understanding of the significance of microorganisms in wounds, a good knowledge of the criteria to identify localised and systemic infections and the ability to select the appropriate treatment options. Adoption of effective infection control and management practices will decrease the risk of wound infection.

The care of a problematic wound in an immune-compromised patient requires a multidisciplinary team approach, including; doctors or prescribers, nurses, dieticians, microbiologists and tissues viability specialists. It is important to involve the patient in the decision-making process, and health promotion strategies may need to be implemented to encourage any required lifestyle strategies to decrease the risk of infection and influence another factor that have a negative impact on the wound healing process.

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