Minimising wound‐related pain at dressing change: evidence‐informed practice

Abstract

Pain is a common concern in patients with chronic wounds. The purpose of this article is to inform clinicians of empirical evidence for practice based on a recent published consensus document on wound related pain. A team approach is needed to address the experience of living with wound related pain within a holistic framework. The importance of regular pain assessment and strategies to minimize traumatic during wound care are highlighted.

Introduction

Pain is a common in patients with chronic wounds 1, 2, 3. Although mounting evidence 4, 5 suggests that pain is often exacerbated by local treatments (dressing changes and other procedures), a substantial proportion of patients also experience wound‐related pain at rest (5). As a subjective experience, pain is more than merely a sensory perception (6). In response to a similar noxious stimulation, the ultimate pain experience can be modulated by variable individual perceptual factors (7). These personal and situational factors include negative thoughts about pain, emotional distress, expected painful experience, heightened awareness (vigilance) and anxiety (8). The impact of chronic unrelenting pain is often enormous, permeating activities of daily living and quality of life including physical and mental functioning, sense of well‐being, mood and social/family relationships 9, 10, 11, 12. It is within this patient‐centred context that the patient’s pain can be assessed and successfully managed to break the cycle of pain, inadequate coping and further intensified pain. The consequences of pain include activation of the stress response and the potential impeding of normal wound healing (13). Despite many efforts to raise awareness about wound‐related pain, the majority of patients continue to suffer from painful wound‐related symptoms. Many clinicians still feel uncomfortable assessing pain and are often unsure what strategies to institute to provide effective treatment (14).

Over the past decade, a number of clinical guidelines and consensus statements have been published, drawing attention to the extent of wound‐related pain and its treatment 6, 15, 16. A recent wound‐related pain consensus document has been published reflecting the burgeoning international concern (http://www.molnlycke.com/item.asp?id=12187). Where empirical research is lacking, clinical experience and patient preference are considered as equally important to inform the consensus process. This longer version of the pain consensus document is intended to provide a scientific rationale for the consensus statements. The companion short paper is designed for clinicians to translate the recommendations for improved patient care. The short paper is available through the Woundpedia website of the World Union of Wound Healing Societies (WUWHS) [http://www.cnomy.com/?dn=woundpedia.com&pid=1PO00Y3D5&prvtof=8b2VkUqfXDCNzAFPpQpuNUZ6X8jlUg%3D%3D (website under construction)] and the Mölnlycke website (http://www.molnlycke.com/item.asp?id=12187).

Goal and objectives

The goal of this article was to raise awareness of pain in patients living with chronic wounds. By fulfilling the following objectives, the readers will

• • Identify appropriate routine practice assessment/documentation tools and procedures for wound‐related pain;
• • Appraise scientific evidence relating to wound‐related pain;
• • Evaluate strategies to reduce pain during dressing change;
• • Optimise wound healing by minimising pain and adequately preparing the wound bed.

Method for wound‐related pain consensus

A panel of international wound experts were identified and assembled to generate clinical recommendations for practice. Wound pain‐related literature was searched through Medline by combining the MeSH terms ‘pain’ with ‘varicose ulcers’, ‘foot ulcers’, ‘pressure ulcers’ and ‘skin ulcers’. An extensive bibliography of references was provided to the panel. Draft statements were developed based on the identified literature. The panel appraised the draft statements and developed their conclusions based on the scientific evidence and their expert opinion (knowledge) from the treatment of wound‐related pain.

Prior to the consensus meeting, each individual panel member was asked to rate the scientific merit and expert opinion of a series of statements on a four‐point Likert scale: strongly agree, somewhat agree, somewhat disagree and strongly disagree with the content. Using a modified Delphi method, the members were given their own personal ratings along with the cumulative totals of the ratings for all the panel members. After a facilitated discussion of each item, panel members were asked to reaffirm their previous rating or change their rating based on the group consensus and discussion. All individual initial and final votes were confidential. If any of the items did not receive an 80% agreement rating, the statements were adjusted based on the participants’ comments, and the voting procedure was repeated on an iterative basis until a consensus was reached.

Consensus statements

Identify and treat the cause of the chronic wound and address concerns expressed by the patient including pain assessment at every visit

Chronic wounds are often recalcitrant to healing because of the underlying aetiology and comorbidities that delay healing. Depending on the wound type, delayed healing may be associated with persistent (chronic) pain or acute (temporary) pain that may be cyclical.

Table 1 links the types of wound‐related pain to the mechanisms and approaches to treatment. Direct excitation of free nerve endings and skin/underlying structure nociceptors activates the sensory aspects of pain (17). Pain is often elicited in response to trauma and tissue damage incurred by mechanical forces (pressure, friction and shear), chemical irritation, vascular damage (venous hypertension and arterial insufficiency), infectious agents and inflammation as outlined in Table 1. For example, patients with early stages of venous disease often describe a dull aching or heaviness in their legs because of leakage of fluid or pitting oedema. As the disease progresses, non pitting oedema develops with the leakage and deposition of fibrin, resulting in dermal sclerosis and hyperpigmentation (leakage of red blood cells with haemosiderin and melanin deposits). This condition is known as lipodermatosclerosis, and it may be painful. Superficial or deep phlebitis must also be considered when patients describe new or increasing lower limb pain (2).

Table 1.

Types of injury and potential pain mechanisms

Type of injury	Pain mechanism	Treatment options
Inflammation	Increase proteases such as matrix metalloproteinases	Topical and systemic anti‐inflammatory
	Immune complex deposition
	Bradykinin, histamine and related substances activate nociceptors
Trauma (including friction and shear)	Activated inflammatory mediators and tissue injury associated with nerve damage	Protect exposed nerve fibres (gels and soft silicones)
	Potential deep tissue injury
	Reperfusion injury
	Underlying pathologies
Pressure	Ischaemic injury with tissue damage and nerve fibre irritation	Pressure redistribution
	Reperfusion injury
Oedema (venous, lymphatic, CHF and ↓albumin)	↑ local interstitial pressure leading to tissue injury (impaired nutrient exchange: accumulation of waste products)	Venous and lymphatic: compression and mechanical pump
		CHF and ↓ albumin: treat the cause

CHF, congestive heart failure

In contrast, intermittent claudication is a common yet extremely painful condition in patients with advanced lower extremity peripheral arterial disease (18). The formation of pressure ulcers is directly related to unrelieved pressure, causing ischaemic tissue damage and precipitating pain. Local irritation can aggravate pain in the presence of excess moisture from incontinence of stools and urine in addition to mechanical friction and shear forces (1).

Despite the diagnosis of neuropathy and loss of protective sensation, patients with diabetes (PWD) may experience neuropathic pain. In fact, up to 75% of PWD with foot ulcers experience painful symptoms compromising their abilities to perform activities of daily living and overall quality of life (19). The differential diagnosis of pain may entail deep and surrounding wound infection 20, 21 or underlying inflammation associated with a Charcot joint involving deep plantar structures. It is not until the wound cause is determined that an appropriate treatment regimen can be instituted to remove factors that are perpetuating the wound and associated pain (22).

Although complete healing may seem to be the logical goal for most patients, some wounds do not have the ability to heal because of inadequate vasculature, a cause that is not treatable, or coexisting medical conditions/medications. If wound healing is not plausible, provision of care should focus on symptom management including minimising pain to optimise patients’ quality of life (3).

Evaluate and document pain intensity/characteristics on a regular basis (before, during and after dressing change)

The process of a dressing change involves multiple steps including removal of the dressing, cleansing of the wound and reapplication of the dressing. While dressing change is often identified as the most painful aspect of wound care, emerging evidence substantiates the fact that the majority of patients with wounds experience pain even when they are at rest. Szor and Bourguignon (5) reported that as many as 84% of their subjects experienced pressure ulcer‐associated pain at rest in contrast to 88% who acknowledged pain at dressing change. Consistent with previous findings, Meaume et al. (4) reported that 79·97% of a large sample of chronic wound patients (n = 2936) experienced moderate‐to‐severe pain during dressing change. Seventy‐seven percent of these patients experienced spontaneous pain in between procedures. Assessment of pain should initially determine the background pain and differentiate that from procedural pain (e.g. dressing change). The ongoing evaluation and documentation of pain serve multiple purposes. Assessment using a standardised pain evaluation tool enables the clinician to

• • establish a baseline to benchmark treatment effectiveness,
• • document temporal pain patterns to schedule appropriate treatment,
• • identify potential aggravating and alleviating factors,
• • detect potential barriers to effective pain management and
• • develop a common treatment goal in partnership with the patient and the interprofessional team.

How should pain be assessed? Pain is subjective and it is ‘whatever the experiencing person says it is, existing whenever he says it does’ even if it seems out of proportion to clinical condition (23). Accordingly, the patients’ self‐report is considered the most valid indicator of pain. Pain intensity can be documented using a wide variety of pain scales (Figure 1). The selection of a specific pain scale must take into account the patients’ age, language, educational level, presence of other sensory impairments, developmental stage and cognitive status.

Figure 1.

Common pain measurement tools.

Pain assessment is particularly challenging in people with cognitive impairment (24). Ferrell et al. (25) evaluated five commonly used self‐report pain rating scales, with people residing in nursing homes. Although most subjects (83%) were able to indicate pain using any one of the scales, there was no one tool that was deemed universally appropriate for use by all patients. Studies have shown that the observation of non verbal indicators encompassing a wide range of vocalised signals and bodily movements may provide means of assessing pain (e.g. neonates and cognitively impaired) for patients who are not able to verbalise their pain 26, 27, 28, 29, 30. Many behavioural mannerisms may have idiosyncratic meaning and a sudden alteration may suggest pain (29).

Nevertheless, once a scale has been selected, the same measurement scale should be used for subsequent comparative assessments. Changes in pain levels may indicate a need to reassess the choice and timing of pain management interventions (31). All pain assessments should be well documented to facilitate the continuity of patient care. The key elements of a holistic pain assessment should include

• • the pain type (nociceptive, neuropathic or mixed),
• • duration of pain (chronic versus acute),
• • severity/intensity,
• • patient impact from the pain,
• • expected levels of pain relief and
• • treatment and adverse events identification (32).

Unfortunately, health care providers’ pain documentation remains less than satisfactory (33). Sixty‐six venous ulcer patients had home care nursing records reviewed. Only 15% of the records contained any documentation of pain, and the assessment was far from standardised. Another community audit showed that pain was not part of a regular community nurse leg ulcer assessment in up to 55% of the reviewed records (34).

Cleanse wounds gently with warm saline or water. Avoid the use of abrasive wipes and cold solutions

Dressing removal and wound cleansing are the most painful wound care interventions 35, 36, 37. The application of cold cleaning solutions to wounds can be unpleasant and harmful to wound healing (e.g. fibroblast function and other metabolic activities may be delayed for hours after exposure to a cold environment) 17, 38. To examine the influence of the irrigation solution temperature on pain (39), lacerations were rinsed with both warm (90–100°F) and room temperature (70°F) saline solution in a random order. The majority of the participants expressed a preference for the use of warm over room temperature solutions. Although the result was not statistically significant, pain ratings tended to be lower using warm solutions (P = 0·082).

Strong antiseptics such as iodine solution are often used to deter bacterial growth. They are cytotoxic, may cause stinging and exacerbate pain. The use of saline or water as cleansing solutions or leaving out the cleansing step resulted in similar infection and healing rates (40). Routine wound manipulation using forceps and gauze to wipe the wound surface can cause tissue damage and should be discouraged (41).

Select an appropriate method of wound debridement for each wound and include the potential for causing wound‐related pain

The practice of debridement is a crucial step to remove dead devitalised tissue that acts as a pro‐inflammatory nidus and growth media for bacteria (42). Increased bacterial burden or infection will result in the release of pro‐inflammatory mediators including bacterial and host metalloproteases that can cause further tissue damage. It is common for a chronic wound to have an increase in senescent cells that are less responsive to cellular signalling with a coexistent decrease in growth factors 43, 44 and diminished cellular signalling responses. Debridement can remove senescent cells and may therefore produce an acute wound in a chronic wound, promoting healing in a stalled wound (45). Several research findings corroborate the pivotal value of sharp debridement. In a study on 143 patients by Saap and Falanga (46), the likelihood of achieving wound closure in PWD was predicted by adequate debridement (odds ratio = 2·4, 95% confidence interval = 1·0–5·6). Faglia et al. (47) showed that early surgical debridement of a deep space abscess in PWD may forestall unnecessary amputation. In diabetic neuropathic foot ulcer subjects, inadequate surgical debridement and the application of platelet‐derived growth factor resulted in only 20% healing at week 20, but with active surgical debridement, the rate of healing increased to 83% (48). The authors concluded that ‘wound debridement is a vital adjunct in the care of patients with chronic diabetic (neuropathic) foot ulcers (48). These data were formulated on a post hoc subgroup analysis, and not all experts universally accepted these findings. However, the Cochrane systemic review by Smith (49) on the efficacy of debridement in PWD ulcers concluded that there was insufficient evidence to support the benefits of surgical debridement for healing. In the only trial that was accepted for the systematic review (50), the authors showed a reduced time to complete healing.

In a prospective study of 55 chronic venous leg ulcers, Williams et al. (51) compared the healing rate between sloughy wounds that received sharp debridement and clean wounds that were treated with best clinical practice alone. At 4 weeks, ulcers that received debridement showed a 6 cm² reduction in the mean surface area, while the comparative ulcers only achieved a 1 cm² reduction (P = 0·02). By week 20 post‐debridement, the difference was more dramatic with a 7·4 cm² area reduction in the debrided group versus an area increase of 1·3 cm² in the comparative group (P = 0·008). The data between weeks 8 and 20 post‐debridement showed complete healing in 16% of debrided ulcers versus 4·3% of non debrided ulcers. Furthermore, the retrospective chart review of Jones and Fennie (52) concluded that the lack of appropriate debridement of sloughy chronic wounds was one of the significant factors that diminished the odds of healing. While the relationship between surgical/sharp debridement and chronic wound healing continues to be contentious, it is unequivocal that surgical or sharp debridement is painful unless protective sensation has been lost with neuropathy.

To reduce pain, topical anaesthetics may be suitable for use prior to painful intermittent procedures. The use of an EMLA^® cream (a eutectic mixture of two amide local anaesthetics, lidocaine and prilocaine; AstraZeneca, Sweden) has been studied prior to debridement of venous leg ulcers and showed effective pain relief (53). For extremely painful procedures, for example the debridement of deep ulcers, it may be necessary to consider extensive infiltration of local anaesthetic, local neural blockade, spinal analgesia, general anaesthesia or the use of mixed nitrous oxide and oxygen (54).

Alternative methods of debridement have been described 55, 56, but each method is associated with its own degree of pain and trauma. Mechanical debridement especially the saline wet‐to‐dry technique should be abandoned now that relatively painless and less traumatic methods are available. Autolytic debridement is achievable through the use of moist interactive dressings including hydrogels (49), calcium alginates, hydrocolloids and films. Autolytic debridement removes non viable tissue through promoting the activities of phagocytic cells and endogenous enzymes, whereas enzymatic debridement requires exogenous agents such as proteolytic enzymes including collagenase, papain–urea and plant enzymes (fig and pineapple) 56, 57, 58. Desloughing may be hastened by lowering wound pH, but the use of acids (organic or inorganic) and other chemical agents is discouraged in light of the potential for pain. Biological debridement is gaining some popularity by inoculating larvae that feed on the necrotic tissue and exudate in the wound. Despite the potential benefits of maggot therapy, this therapy is not innocuous and local painful reactions are not uncommon 59, 60. The choice of debridement method should be made bearing in mind the urgency to remove slough and necrosis, expertise available to perform sharp surgical debridement, the potential for uncontrolled bleeding and the procedure‐related pain.

There is emerging evidence that novel debridement methods including ultrasonic technologies and hydrojet therapy (mist) may be relatively pain free, but acceptance is hindered by cost and the potential need for an operating room instead of the ambulatory clinical setting (61).

Choose dressings that minimise trauma/pain with application and removal

Up to 80% of nurses noted that patients experienced the most pain during dressing change especially when the dressing is removed (36). Dried out dressing materials, aggressive adhesives, adherent granulation tissue (capillary loops growing into the product matrix) and the glue‐like nature of dehydrated or crusted exudates are some of the dressing‐ and wound‐related factors that render dressing removal painful.

A recent review of dressings and topical agents for secondary intention healing of post‐surgical wounds has been published (62). Patients experienced more pain with gauze than with any other advanced moisture balance dressings including foam (63), alginate 64, 65 and hydrocolloid (66). Ironically, gauze continues to be one of the most commonly used dressing in clinical practice. The various types of dressings and their relationship to wound‐related pain are summarised in Table 2.

Table 2.

Practical considerations for common dressing adhesives and their alternatives

Dressing adhesives/alternatives	Application	Removal
Acrylates (glue on most adhesive dressings): occasionally, glues may be polyurethane based	Strong adhesion to skin (force increases with time)	May cause a high incidence of pain and trauma (skin stripping)
		Tip: use liquid‐film‐forming barrier on periwound skin
	Can cause allergies (contact allergic or irritant dermatitis)	Can leave residue on the skin
Hydrocolloid adhesives	Need to be moulded to skin surface (local warmth to promote adhesion)	May leave variable residue on skin and in the wound
	Contact allergic dermatitis possible, especially Pentalyn H	May be associated with maceration and skin stripping
	Edges may roll	May cause a high incidence of pain and trauma (skin stripping)
	Adhesive may dissolve in the presence of wound exudate
Soft silicone adhesives (wound contact layers and foams)	Good adhesion without strong bonding	Minimal trauma and pain at dressing change
	Instant tack (sticks immediately to the skin)	Easy to check wound and reapply
Non adhesives (e.g. gauze, hydrofibre, calcium alginates, non adherent foams and pastes)	May be difficult to fix to the skin	May cause local trauma (maceration or drying if moisture balance not maintained)
	Susceptible to local friction and shear
	Selection dependent on wound surface exudate level

Dressing adhesives may also contribute to trauma and pain. Repeated application and removal of adhesive tapes and dressings mechanically strips the stratum corneum from the underlying epidermal and dermal cells, causing skin damage (67). In severe cases, erythema, oedema and blistering had been observed 68, 69. A study of 4200 wounds in 1891 nursing home residents identified pain and trauma associated with dressing removal as a major concern for both patients and health care providers (69). Dykes and Heggie (70) compared five commonly used dressings including a silicone dressing on the skin of 12 healthy volunteers. The silicone dressing required a low peel force and was shown to be the least damaging to the superficial skin when compared with other tested materials (P < 0·05). Zillmer et al. (71) also reported that soft silicone adhesives did not alter the skin barrier function (transepidermal water loss) or stratum corneum hydration (electrical conductance) documented with the repeated use of hydrocolloid dressings. The removal of the silicone dressing was less painful compared with dressings that required higher peel force in a subsequent study by Dykes and Heggie (n = 24, P < 0·01) (70). Careful dressing selection avoids most of the pain and trauma associated with wound dressing changes. Health care providers considered the use of ‘atraumatic’ dressings as the most important strategy to avoid wound damage and patient stress. Non adherent layers can also be used effectively for reducing adhesion to the wound and preventing damage and pain on removal 68, 69, 72, 73.

Treat infection that may cause wound‐related pain and inhibit healing

Chronic wounds are colonised by polymicrobial flora ranging from 1·6 to 4·4 species per gram of tissue at any time (74), but not all chronic wounds have associated superficial bacterial damage or deep infection that require treatment. Wound deterioration emerges when the bioburden begins to overwhelm host defences causing injury to the tissue. Cutting and Harding (75) originally proposed that the presence of unexpected pain or local tenderness together with other criteria is indicative of bacterial damage in granulating wounds. More recently, an international Delphi panel of 54 members arrived at a consensus that an increase in pain intensity should indeed raise the suspicion of infection in a variety of acute and chronic wounds (76). Gardner et al. (77) evaluated the validity of a checklist of 12 clinical signs and symptoms to identify localised chronic wound infection (n = 36). None of the subjects with non infected wounds exhibited increasing pain. Pain was a useful indicator of infection, with high specificity value (100%) and inter‐rater reliability (κ = 0·73) (77) in this study population.

The mechanism linking infection to pain remains elusive but is thought to be linked to Toll‐like receptors, a family of pattern recognition receptors that mediate innate immune responses from pathogens or endogenous signals. Under various pathological conditions, the central nervous system (CNS) mounts a well‐organised innate immune response, in which glial cells, in particular microglia, are activated. Furthermore, the innate immune system has emerged as a promising target for therapeutic control of development and persistence of chronic pain. Specifically, the microglial cells respond to peripheral infection and injury and initiate a CNS immune activation that may contribute to chronic pain.

However, there is no evidence that any individual sign or symptom is independently reliable to identify wound infection. Sibbald et al. (78) created a mnemonic NERDS© and STONEES© to conceptually separate superficial from deep compartment bacterial damage or infection. Superficial bacterial damage can be documented through the mnemonic NERDS: Non healing, Exudate that has increased, Red friable granulation, Debris on the surface and Smell. Three criteria are very sensitive and specific for this diagnosis with two criteria less sensitive but four criteria more specific. Surface increased bacterial burden may be treated with antibacterial dressings or topical antimicrobial agents, while deeper infection would necessitate systemic antimicrobial therapies. STONEES identifies the criteria for surrounding skin and deep infection: increased wound Size, increased surrounding skin Temperature, the probing or exposed bone (Os), New or satellite areas of breakdown, the two Es (Exudate and the combination of Erythema and/or oEdema) along with Smell. Clinicians need to triangulate looking for two or three signs. Odour and increased exudate are in both clusters of superficial and deep signs (Table 3). Additional criteria are needed to determine if bacterial damage is superficial, deep or both.

Table 3.

Wound pain as a result of infection^*

Bacterial relationship	Pain	Clinical characteristics
Colonisation	Not usually related to bacterial damage	Healthy granulation
Local infection (critical colonisation, increased bacterial burden and covert infection)	May be painful	NERDS
		Non healing
		Exudate (increased)
		Red friable granulation tissue
		Debris
		Smell
Deep and surrounding skin infection	Increased pain most reliable symptom and may be clinically more useful than any one individual sign	STONEES
		Size increasing
		Temperature increased (surrounding skin)
		Os (probes or exposed bone)
		New areas of breakdown
		Erythema/oEdema
		Exudate (increased)
		Smell

^* If any three criteria for NERDS and STONEES are present, this is reliable for the association with bacterial damage (103).

Treat local factors that may induce wound‐related pain (e.g. inflammation and trauma)

Other than infection, clinicians must be cognizant of other local factors that may exacerbate wound‐related pain. Many of these stalled chronic wounds show markedly increased activity of inflammatory cells and associated mediators perpetuated by recurring tissue trauma (e.g. pressure, bacterial growth, leucocyte trapping or ischaemic reperfusion injury).

The inflammatory cells are needed to remove non vitalised tissue and to allow regeneration of granulation tissue, but this prolonged and superfluous inflammatory response can be deleterious. Wound healing is stalled with degradation of extracellular matrix and growth factors that occurs more rapidly than their synthesis. This process hinders the wound from progressing towards the proliferative phase and ultimately reepithelialisation. Inflammatory cells secrete cytokines that increase vascular permeability causing local oedema and leading to wound exudation. There is also evidence to suggest that certain cytokines such as interleukin (IL)‐1B, IL‐6 and tumour necrosis factor (TNF)‐alpha are involved in the process of pathologic pain. These pro‐inflammatory cytokines have been shown to activate and sensitise pain receptors. For instance, IL‐1B has been shown to increase the production of substance P and prostaglandins E2 in a number of neuronal and glial cells. Topical application of TNF‐alpha to the peripheral nerve axon in vivo has been shown to activate nociceptive neurons.

Certain inflammatory diseases such as pyoderma gangrenosum and vasculitis are often associated with painful non healing wounds. It is often challenging to differentiate the presence of certain non infectious conditions that produce an inflammatory response from infection. Although swelling, redness, pain and increased temperature may be presented in both scenarios, symptoms are often symmetrical in inflammatory disease. In addition, wounds that are related to inflammatory diseases may be accompanied with palpable purpura, livedo pattern, rolled ulcer margins and satellite lesions.

Select an appropriate dressing to minimise wound‐related pain based on wear time, moisture balance and periwound maceration

Winter (79) showed that partial‐thickness wounds reepithelialised more rapidly in a moist wound environment under occlusive dressings. Since the publication of this seminal work, numerous studies have established that adequate moisture accelerates the reepithelialisation process, facilitates the action of growth factors, increases keratinocyte and fibroblast proliferation, enhances collagen synthesis, promotes angiogenesis and facilitates early wound contraction. Moisture is essential to all phases of healing. To accomplish moisture balance, a plethora of dressings with varying fluid handling and hydrating capacities has been introduced. Foam dressings wick up and lock in wound drainage for highly exudative wounds. Alginates (the fluid is outside the fibres that are bioresorbable) and hydrofibres (the fluid is inside the fibres and not bioresorbable) are both capable of absorbing a high volume of fluid. Desiccated wounds, however, would benefit from a hydrogel (donate moisture) or occlusive dressings (prevent moisture loss). Despite the availability of different classes of dressings, previous systemic reviews of randomised controlled trials have failed to show the benefit of one dressing class over another in various chronic wound types. There were no significant differences between modern advanced moisture controlling dressing and normal saline gauze 80, 81. However, saline gauze usually requires frequent dressing changes to maintain moisture balance, increasing potential trauma, pain and nursing costs. Alternative dressings may remain on the wound for longer periods to avoid frequent removal (82). It is prudent to reconsider the choice of dressing if removal causes pain that may be associated with bleeding or trauma 31, 82. If soaking is required to achieve pain‐free removal, moisture balance has not been maintained and an alternate dressing should be chosen.

When the drainage volume exceeds the fluid handling capacity of a dressing, enzyme‐rich and caustic exudate may spill over to the wound margins, causing pain, maceration or tissue erosion (loss of part of the epidermis but maintaining an epidermal base) (83). In a recent study, 28 patients with chronic ulcers were randomised to one of the two foam dressings (Mepilex Border Mölulycke, Gotherburg, Sweden or Allevyn Adhesive, Smith and Nephew, Hull, UK) for 2 weeks, followed by crossover to the alternate dressing for another 2 weeks. Pain was assessed by a visual analogue scale before, during and after dressing change. At the second dressing change, 22% of the patients treated with Mepilex Border developed maceration in the periwound skin compared with 57% of those treated with Allevyn Adhesive. Patients were prone to experience increased pain with associated wound margin maceration. This periwound irritation may explain why patients reported higher pre‐dressing change pain levels in the Allevyn group compared with the Mepilex group before dressing change. To circumvent periwound maceration, clinicians should consider appropriate skin barrier products with a shorter dressing wear time to meet the needs of the patient (84). As a general guide, wear time should be ‘calculated’ according to the previous dressing change parameters including

• • exudate levels,
• • viscosity of the exudate,
• • the current periwound skin condition and
• • fluid handling characteristics of the selected dressing(s).

There is often a temptation to overestimate wear time, and this will increase the risks of periwound maceration, leakage and strikethrough. These changes are also associated with increased risk of infection. All these complications can compromise wound healing (85).

Evaluate each patient’s need for pharmacological (topical/systemic agents) and non pharmacological strategies to minimise wound‐related pain

The World Health Organization advocates prompt pain management by following a three‐step analgesic ladder starting from non opioids, including aspirin and acetaminophen, for mild symptoms, progressing to weak opioids (codeine) for moderate pain and finally strong opioids such as morphine for severe pain. Depending on the severity of the initial pain, the regimen is based on the implementation of drugs in increasing potency, both alone and in combination with adjuvant therapies. The medication is then titrated with pain reduction for acceptable pain control. Adjuvant therapies (tricyclic antidepressants and anticonvulsants) could be considered at any step to address neuropathic pain. To minimise systemic side‐effects, the topical use of anti‐inflammatory agents and capsaicin has shown promising results. Two randomised controlled trials were conducted to evaluate the effectiveness of ibuprofen‐releasing foam for the treatment of wound pain 86, 87. The study subjects experienced a significant reduction of local wound‐associated pain the first evening after dressing application. The investigational use of topical morphine has also shown positive results in several studies; however, this formulation is not commercially available, and the lack of pharmacokinetic data has precluded the use of these compounds in current routine clinical use.

In addition to medication, pain management should also address other personal and situation factors (e.g. anxiety and depression) that may account for the variability of pain perception. Techniques to address psychological factors are targeted at reduction of anxiety and stress and the improvement of personal coping skills (Figure 2). These wound pain reduction techniques include relaxation exercises, music therapy 88, 89, 90, 91, touch therapy (92), visual stimulation (93), hypnosis, stress reducing strategies (94), guided imagery (95) and behavioural and cognitive therapy, along with distraction 91, 96. However, the evidence to support their relative effectiveness is lacking (97). Other adjunctive therapies for pain control include transcutaneous electrical nerve stimulation, acupuncture, laser and thermal therapy. The clinical utility of these techniques in the management of wound‐related pain requires further investigations. The authors advocate new trials of rigorous research design before revising current evidence‐based recommendations (98).

Figure 2.

Toolkit of wound‐related pain‐relieving strategies.

Involve and empower patients to optimise pain control

Patients with chronic wounds often express feeling of powerlessness, depression and social isolation. In one study, 105 venous leg ulcer patients were randomised to a nurse‐managed leg club or standard treatment alone. Subjects with the social stimulation from the leg club achieved a 76·8% reduction in mean ulcer size (mean 10·3–2·39 cm²), with a significant reduction in pain levels over 12 weeks (P = 0·001) (99). Education is another strategy to empower patients to improve wound‐related pain control. In a pilot study (100), five chronic wound patients found dressing pain more manageable after receiving educational information about the dressing change procedure and the availability of pain relief strategies that they could initiate.

Health care providers should ensure wound‐related pain control for every patient

There has been an increased recognition of wound‐related pain, but even if the pain is identified, pain treatment has often been less than ideal. The ‘Heal Not Hurt’ pain assessment initiative, started in the United Kingdom in 2006, is intended to aid the implementation of the existing pain guidelines 15, 16 by providing the practitioner with a framework to document and guide care (101). This programme has been piloted in the United Kingdom (102) with excellent feedback from clinicians. The programme improved the assessment and documentation of wound‐related pain. Many previous best practice documents for better wound‐related pain control stop with the establishment of the consensus statement. The critical implementation stage is often forgotten that links the recommendations to improved chronic wound‐related pain control.

Conclusion

It is important to consider wound‐related pain control holistically from local wound bed factors and dressing selection to patient‐centred concerns and the treatment of the wound cause. This article provides ten concise statements to facilitate improved pain control for persons with chronic wounds.