Patients with chronic wounds are a heterogeneous population with associated comorbidities, resulting in controversy over therapeutic measures that should be undertaken in their best interest. Pain management in these patients is one such area lacking consensus. Although pain management should be integrative to the treatment and positive outcome of care, undiagnosed or undertreated pain remains a major issue for patients with various wound types.
Understanding the mechanisms of pain and how they relate to chronic wounds will help wound care specialists improve their patients’ quality of life. For example, acute and chronic pain may be among the factors contributing to immobility, which could cause a pressure ulcer (PrU) or exacerbate an existing wound. Estimates of the number of patients with PrUs 1,2 suggest that each year, as many as 40,000 Americans could benefit from an intervention to reduce the pain associated with their PrUs. 3
Although numerous studies have analyzed data regarding PrU-related pain or the degree of pain by PrU stage 4, the topic of pain in PrUs should be envisioned as a whole. The purpose of this article is to review pain mechanisms, to correlate them with pathophysiology of PrUs, and to draw on the principles of practice guidelines and evidence-based medicine in suggesting treatment options.
Pain is a symptom associated with actual or potential tissue injury, and awareness of pathophysiology of wound pain is prerequisite to treating it.
Pain is perceived by the patient in relation to its type (nociceptive, neuropathic, or perceptron dysfunction) and its anatomic origin 5 (epidermis, dermis, subcutaneous tissue, underlying muscle, or bone). Management of chronic wound pain should include a thorough evaluation of pain origin, such as therapeutic maneuvers, bacterial colonization, arterial insufficiency, contractures, and peripheral neuropathy. In addition, pain is a multifaceted symptom with contributing influences, including cognitive, psychosocial, and nutritional factors, that further add density to pain characteristics.
Pain originating in the peripheral nervous system is based on the excitation of the nociceptive afferent fibers, which are contained among A-delta fibers and C-fibers from skin, joints, and muscles. 6 (A-delta fibers transmit sharp, acute pain; C-fibers transmit dull, aching pain.) Strong stimuli, which may eventually become destructive, excite nociceptors (neurons that transmit pain messages). The electric impulses resulting from the primary stimuli are transmitted through the peripheral nerves to the spinal cord, and from there, through ascending pathways to the thalamus, hypothalamus, limbic system, cerebral cortex, and/or other structures, such as mesencephalic reticular formation. The complex neural interconnections and diverse structures involved in the input, processing, and perception of pain impede comprehensive understanding of pain mechanisms.
ANATOMY OF PAIN
All axons that end in the epidermis are considered nociceptors. 7 Studying the intraepidermal nerves of normal adult human skin, Johansson et al 8 found 2 types of epidermal nerves: free nerve endings and nerves in the Merkel cell-neurite complex. All of these nerves originate from nerve trunks in the dermis, enter the epidermis, then divide distally to eventually end in small enlargements, near the surface of the skin and in deeper areas. 7 The free nerve endings are distributed to, and terminated in, the strata basale, spinosum, and granulosum of epidermis. 7,9 Nerve density varies in different body areas, decreasing from the trunk to the distal part of the limbs. Small, more dense patches of innervation show up in the epidermis, which was identified as the morphologic and functional terminal unit coming from the same dermal nerve bundle.
Johansson’s work has confirmed the existence of epidermal nerves in normal adult human skin. 8 The difference between densities of epidermal nerves at different body areas implies area-specific functions of the intraepidermal nerve terminals. The observed intraepithelial nerve fibers may have a pain-perceiving role; trophic or immunoregulatory roles cannot be excluded. 10 Besides the axons in the epidermis, the axons from subcutaneous tissue and underlying muscle also play the role of nociceptors in pain pathology associated with PrUs. A deteriorating PrU can become more painful due to more tissue damage, to the point that tissue damage is so severe that injured nerve endings transmit pain signals. 11
Stimulation of pain sensors is manifested in acute nociceptive pain, known as eudynia 5 (pain due to a stimulus that normally provokes pain). This is based on mechanical, thermal, and/or chemical stimulation of normally functioning pain nerves; these nerves detect pain as a signal and indicate impending or active tissue damage. 5 Neuropathic pain is due in principal to damaged and malfunctioning nerve fibers. Damaged fibers could lead to physiologic changes, such as aberrant generation of electrical signals from nerve endings. Perceptron, or perception of pain dysfunction, is the most complex part of the pain pathway. It occurs at the end of the neural pathway—the brain and spinal cord—where these signals are translated. 5 Any malfunction of the central nervous system pathways or biochemical environment could lead to central neurogenic pain (pain due to perceptron dysfunction). 5
In recent years, considerable advances have been made in understanding the mechanisms of pain. Tissue injury in PrUs may result in hyperalgesia (an increased response to a stimulus that is normally painful) at the site of injury and tactile allodynia 5 (pain due to a stimulus that does not normally provoke pain; could be dynamic, static, or thermal) in areas adjacent to the injury site. Hyperalgesia reflects a sensitization of the peripheral terminal and a central facilitation evoked by the persistent small afferent input (continuous stimulation of C-fibers). 12 Allodynia reflects a central sensitization to signals transmitted via the nociceptors (usually C-fibers) from the site of injury, such that gentle stimuli in the surrounding area of the lesion evoke pain. 13 This mechanism seems to be supported by the fact that large-diameter A-beta fibers can activate central nervous system signaling neurons. 14 Furthermore, allodynia may also be considered a confounding factor in pain assessment.
All of the above-described pain mechanisms interrelate and are responsible for the “pain out of proportion to the stimulus” experienced by patients at dressing changes or when the area surrounding the wound is cleansed.
Animal models of pain perception show a clearly defined primary hyperalgesia and secondary off-site tactile allodynia. 15 Although not yet adequately studied, the postinjury pain state in humans clearly possesses the same complexity. 16,17
The development of animal models for tissue injury and hyperalgesia has allowed for major advances in our understanding of persistent pain of cutaneous origin. 16,17 Although it is tempting to generalize these findings to pain of deep tissues, such as muscle and joint, cutaneous and deep pain have some differences. Cutaneous pain is highly localized to the site of stimulation and is described as sharp, stabbing, or pricking. 18–20 Deep pain is diffuse, dull, and harder to be characterized by the patient.
Pathophysiology: The cornerstone for pharmacologic pain management
Inflammation plays a major role in modulation of pain characteristics in chronic wounds in general and PrUs in particular. Endogenous chemical substances that are released during inflammation lower nociceptor threshold and facilitate hyperalgesia. 21,22
Vande Berg and Rudolph 23 described the histopathology of PrUs in humans using surgical biopsy specimens from the ulcer edge, ulcer margin, and adjacent normal, nonulcerated skin, illustrating the inflammatory nature of the pathophysiology of PrUs.
Using a light microscope, they identified morphologic features of PrUs, including a dense fibrin matrix; occluded blood vessels; numerous inflammatory cells (with a predominance of macrophages); and a range of cellular viability, from functional, normal-appearing cells to cells in all stages of necrosis. Electron microscopy revealed numerous inflammatory cells within a dense fibrin matrix at the ulcer surface. Many of the blood vessels displayed hyperemia. Areas of cell necrosis were evident in random regions within the ulcer and ulcer margin.
The histologic depiction allowed the researchers to conclude that a PrU is an inflammatory lesion. 23 This confirmed an animal model that had described the inflammatory characteristics of experimentally induced PrUs. 24
The inflammatory nature of a PrU should be the fundamental basis for pharmacologic pain management. Senecal 25 has suggested several steps for analgesia in wound pain:
- Step 1: Use a nonsteroidal anti-inflammatory drug (NSAID) with or without a local anesthetic.
- Step 2: Add a mild opioid, using an oral medication if possible.
- Step 3: Replace the mild opioid with a potent opioid analgesic.
Before selecting a drug to relieve the patient’s pain, the clinician should balance the risks and benefits of treatment. Pain related to the PrU could impede the patient’s mobility; however, the adverse effects of analgesics—such as respiratory depression, nausea, sedation, and constipation—could negate the beneficial effects on quality of life. Furthermore, pain is a protective function that alerts the clinician to impending tissue damage; pain relief may reduce awareness of new infections at the wound site. On the other hand, providing analgesia may facilitate early ambulation, encourage wound healing and oxygenation, and minimize the risk of developing further complications related to immobility (deep vein thrombosis, pulmonary complications, and new PrUs). Wound care specialists have the mission to break the cycle of pain-immobility-inflammation-pressure ulcers for better patient outcomes.
A chronic wound, such as a PrU, may not need continuous analgesia. Instead, pain relief may be more appropriate at certain times, such as before dressing changes, especially for patients who had previously experienced pain at those times and may become extremely anxious at the prospect of future pain.
The clinician should keep in mind that systemic administration of opioids could cause a myriad of adverse effects and still not control the pain generated by a PrU. Increasing evidence points to the beneficial effects of topically applied opioids, which lack the adverse effects and toxicity of their systemically administered counterparts. Stein and colleagues 26–29 showed in animal and human studies that peripheral opioid receptors exist. Their studies suggest that the presence of inflammation is critical for the recruitment and activation of opioid receptors. Due to the fact that a PrU is an inflammatory lesion, 23 topical opioids (using a hydrogel as a transport media) may be an alternative in management of PrU-related pain. 30
Another safe alternative to systemic opioids is the lidocaine patch 5% (Lidoderm, Endo Pharmaceuticals, Inc, Chadds Ford, PA), a local anesthetic that blocks sodium channels. This product was recently approved by the Food and Drug Administration for the treatment of postherpetic neuralgia. The lidocaine patch reduces peripheral nociceptor sensitization and diminishes central nervous system excitability, making it a suitable option for off-label use in the treatment of chronic neuropathic pain. 31 In terms of safety, insignificant lidocaine serum levels are achieved, even with chronic use. Because it is an amide-type anesthetic, lidocaine has a lower incidence of allergic reactions than the ester-type anesthetics, such as procaine and tetracaine. 31
EMLA cream (eutectic mixture of local anesthetics, consisting of lidocaine 2.5% and prilocaine 2.5%; AstraZeneca, Wilmington, DE) is a viable alternative for local analgesia. In a meta-analysis of clinical trials of pain associated with chronic venous ulcers, 32 EMLA was found to be statistically significant in reducing debridement pain scores. Because local anesthetics might have a vasoactive effect in addition to producing analgesia, a small, prospective, placebo-controlled study attempted to document the effect of EMLA 5% cream on cutaneous circulation. Using video capillaroscopy, laser Doppler flowmetry, and skin temperature, cutaneous circulation was continuously monitored under standardized conditions. The results showed that EMLA cream upregulated nutritive perfusion. No clinically relevant vasoconstrictive effects are expected from an application period of 60 minutes. 33 Further research is warranted to determine the impact of EMLA on wound healing.
Koleshikov et al 34 found consistent anesthetic synergy between a topical opioid and a local anesthetic agent. The combination of low doses of local morphine and lidocaine revealed activity far beyond additive interactions, strongly suggesting synergy between opioids and lidocaine. This fact could provide further insight into the use of topical agents in managing pain in chronic wounds.
Amitriptyline, a tricyclic antidepressant, has potent local anesthetic properties. Haderer et al 35 reported that transdermally applied amitriptyline is more potent than lidocaine in providing cutaneous analgesia in rats. Each test group developed a concentration-dependent cutaneous analgesic block in the areas to which the drugs were applied; however, amitriptyline produced a longer block than lidocaine at the same concentration with an occlusive dressing. The development of amitriptyline as a longer-lasting topical analgesic may improve the ability to treat chronic pain, such as neuropathic pain.
Pain in PrUs can be persistent, permanent, or episodic (occur at dressing changes and/or debridement). Management of this pain goes beyond administering a set dosage of a prescribed analgesic. Objective pain assessment should be done not only during dressing changes, but also before and after the procedure, for an integrative evaluation of the patient’s distress.
Briggs et al 36 have proposed several methods to reduce a patient’s apprehension at dressing removal:
- identify what the patient recognizes as pain triggers and as pain-alleviating factors
- involve the patient in the dressing change if possible, including allowing the patient to remove the dressing himself or herself
- encourage slow, rhythmic breathing during the procedure
- offer the patient the option to call a “time-out” during the procedure.
In a recent large-scale study, 37 the European Wound Management Association found that the most important strategy for avoiding wound damage was the use of nontraumatic dressings. According to recent trends in wound care, dressing choice should be reconsidered if soaking is required for removal or if removal is causing a problem with pain or bleeding/trauma. 37 Dressings that were identified as the least likely to cause trauma were hydrofibers, hydrogels, alginates, and soft silicones. Interestingly, the survey found that the most important factors influencing the clinician’s choice of dressings were financial and reimbursement issues, 37 not the likelihood of reducing pain.
The aforementioned strategies for pain treatment may imply that imposing preemptive analgesia (that is, administrating an analgesic in anticipation of pain) should be the rule of thumb in managing chronic wound pain. It is true that the proper approach to managing patients with painful PrUs will result in increasing functional independence and a better quality of life. However, pain treatment should focus primarily on reversing pathologic mechanisms that cause the pain in the first place, such as PrUs, wound infection, and arterial insufficiency. In addition, further research is needed to increase understanding of pain mechanisms in PrUs and to find efficient interventions for its alleviation.
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7. Oaklander AL. The density of remaining nerve endings in human skin with and without postherpetic neuralgia after shingles. Pain 2001; 92:139–145.
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11. Koay J, Orengo I. Application of local anesthetics in dermatologic surgery. Dermatol Surg 2002; 28:143–8.
12. Lindholm C, Bergsten A, Berglund E. Chronic wounds and nursing care. J Wound Care 1999; 8:5–10.
13. Yaksh TL, Hua X-Y, Kalcheva I, Nozaki-Taguchi N, Marsala M. The spinal biology in humans and animals of pain states generated by persistent small afferent input. Proc Natl Acad Sci USA 1999; 96:7680–6.
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18. Dubner RK, Ren K. Assessing transient and persistent pain in animals. In: Wall PD, and Melzack R, editors. Textbook of Pain. Edinburgh, Scotland: Churchill-Livingstone; 1999. p 359–69.
19. Hargreaves K, Dubner R, Brown F, Flores C, Joris J. A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia. Pain 1988; 32:77–88.
20. Imbe H, Iwata K, Zhou QQ, Zou S, Dubner R, Ren K. Orofacial deep and cutaneous tissue inflammation and trigeminal neuronal activation. Implications for persistent temporomandibular pain. Cells Tissues Organs 2001; 169:238–47.
21. Zimmermann M. Basic concepts of pain and pain therapy. Arzneimittelforschung 1984; 34( 9A):1053–9.
22. Galer BS, Dworkin RH. A Clinical Guide to Neuropathic Pain. McGraw-Hill, Minneapolis. 2000. p154.
23. Vande Berg JS, Rudolph R. Pressure (decubitus) ulcer: variation in histopathology—a light and electron microscope study. Hum Pathol 1995; 26:195–200.
24. Salcido R, Donofrio JC, Fisher SB, et al. Histopathology of pressure ulcers as a result of sequential computer-controlled pressure sessions in a fuzzy rat model. Adv Wound Care 1994; 7( 5):23–40.
25. Senecal SJ. Pain management of wound care. Nurs Clin North Am 1999; 34:847–60.
26. Parsons CG, Czlonkowki A, Stein C, et al. Peripheral opioid receptors mediating antinociception in inflammation. Activation by endogenous opioids and role of the pituitary-adrenal axis. Pain 1990; 41:81–93.
27. Hassan AHS, Ableitner A, Stein C, et al. Inflammation of the rat paw enhances axonal transport of opioid receptors in the sciatic nerve and increases their density in the inflamed tissue. Neurosci 1993; 55:185–95.
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29. Stein C, Hassan AHS, Lehrberger K, et al. Local analgesic effect of endogenous opioid peptides. Lancet 1993; 342:321–4.
30. Flock P. Pilot study to determine the effectiveness of diamorphine gel to control pressure ulcer pain. J Pain Symptom Manage 2003; 25:547–54.
31. Argoff CE. New analgesics for neuropathic pain: the lidocaine patch. Clin J Pain 2000; 16(2 Suppl):S62–6.
32. Cochrane Database Syst Rev 2003;(1):CD001177.
33. Hafner HM, Thomma SR, Eichner M, Steins A, Junger M. The influence of Emla cream on cutaneous microcirculation. Clin Hemorheol Microcirc 2003; 28:121–8.
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36. Briggs M, Torra JE, Bou I. Pain at wound dressing changes: a guide to management. In: Pain at Wound Dressing Changes, European Wound Management Association Position Document, Spring 2002. Available at http://www.Tendra.com/Files/Tendra/safetac/ENGLISH.pdf
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Assessment of Wound Pain
Pain is a subjective phenomenon, challenging both the patient and the clinician to describe it accurately. Several methods have been proposed to bridge the gap between what the patient perceives (subjective) and what the clinician can diagnose (objective).
Using reliable, valid, and consistent pain assessment tools is essential in achieving standardized pain management in chronic wounds. 1 Ideally, pain assessment should be performed before, during, and after treatment of the wound, as well as in between treatments. Although pain scales are currently the gold standard for pain assessment, wound care specialist should be cognizant of the complex changes in psychomotor and cognitive functions that are part of the process of aging, which may interfere with accuracy of these measurements. Three methods have recently been identified 1 as being the most frequently utilized in assessing pain related to chronic wounds and venous leg ulcers: the visual analogue scale, the verbal descriptor scale, and the short-form McGill Pain Questionnaire. None of these have been validated in patients with venous leg ulcers, however.
Therefore, it is difficult to recommend a universal pain evaluation tool for chronic wounds. It has been suggested that a multistep pain assessment process may be the most practical. 1 The first step could be to determine the presence or absence and level of pain by numerical rating scale, which measures pain intensity and offers an alternative to individuals unable to complete more complicated tests, such as the visual analogue scale. If pain is present, the more-detailed short-form McGill Pain Questionnaire or the visual analogue test could further assess the pain.
Still, the typical pain evaluation is usually limited to a univariate assessment (eg, visual analogue score or postoperative opioid consumption). Although clinically practical, such limited surveys may obscure the benefits or actions of a drug that influences 1 of the components of the pain state. 2
Besides pain assessment scales and questionnaires, clinicians should observe patients for nonverbal clues to pain (such as restlessness, guarding, and dilated pupils), especially in patients who are unable to communicate verbally.
The following mnemonic 3 — PQRST —may assist in assessing pain:
- P = Palliative/provocative factors
- What makes the pain worse?
- What makes it better?
- Q = Quality of pain
- What kind of pain are your experiencing?
- Would you describe it as sore, aching, deep, cramping, burning, shooting, or sensitive (or any combination thereof)?
- Do you have other symptoms with the pain, such as fever, chills, nausea, or vomiting?
- R = Region and radiation of pain
- Where is the pain?
- Where does it radiate?
- S = Severity of pain
- Would you describe your pain as none, mild, moderate, severe, or excruciating?
- Rate your pain on a scale from 0 to 10, with 0 representing “no pain” and 10 being “the worst imaginable pain.”
- What is the pain intensity at its worst, best, and now?
- T = Temporal aspects of pain
- Is the pain better or worse at any particular time of the day or night?
- When does it start or when does it stop?
- Is it intermittent or constant, or does it occur only when you’re moving?
The following additional elements should be included in the initial assessment plan and treatment:
- detailed history consisting of medication usage, treatment history, previous surgeries and injuries, and impact on quality of life and activities of daily living.
- physical examination, emphasizing the body system involved in the pain complaint (for example, the musculoskeletal or neurologic system)
- psychosocial assessment, including family history of depression or chronic pain
- appropriate diagnostic workup to determine the cause of pain and to rule out any contributing, treatable causes.
A thorough pain assessment enables the clinician to develop a pain treatment regimen and evaluate its effectiveness.
1. Nemeth KA, Graham ID, Harrison, MB. The measurement of leg ulcer pain: identification and appraisal of pain assessment tools. Adv Skin Wound Care 2003; 16:260–7.
2. Yaksh TL, Hua X-Y, Kalcheva I, Nozaki-Taguchi N, Marsala M. The spinal biology in humans and animals of pain states generated by persistent small afferent input. Proc Natl Acad Sci USA 1999; 96:7680–6.
3. Dallam LE, Barkauskus C, Ayello EA, Baranoski S. Pain management and wounds. In: Barnoski S, Ayello EA, editors. Wound Care Essentials: Practice Principles. Springhouse, PA: Lippincott Williams & Wilkins; 2004. p 217–38.
Interventions for wound pain
- Administer topical anesthetics.
- Consider operating room procedure under general anesthesia rather than bedside debridement for large, deep ulcers.
- Administer opioids and nonsteroidal anti-inflammatory drugs before and after procedures.
- Assess and reassess for pain during and after procedures.
- Perform interventions at a time of day when the patient is less fatigued.
- Provide analgesia 30 minutes prior to dressing change.
- Assess the patient for pain during and after dressing changes.
- Provide analgesia 30 minutes prior to whirlpool.
- If the patient’s dressing has dried out, thoroughly soak the wound – especially the edges.
- Observe the wound for signs of local infection.
- Gently and thoroughly irrigate the wound to remove debris and reduce the bacterial bioburden, which can cause contaminated wounds to become infected. Infection will increase the inflammation and pain at the wound site.
- Avoid using cytotoxic topical agents.
- Avoid aggressive packing.
- Avoid drying out the wound bed and wound edges.
- Protect the periwound area with sealants, ointments, or moisture barriers.
- Minimize the number of daily dressing changes.
- Select pain-reducing dressings.
- Avoid using tape on fragile skin.
- Splint or immobilize the wounded area as needed.
- Utilize pressure-reducing devices in bed or chair.
- Provide analgesia as needed to allow positioning of patient.
- Avoid trauma (shearing and tear injuries) to fragile skin when transferring, positioning, or holding a patient.
- Utilize all of the interventions listed for noncyclic and cyclic wound pain.
- Control edema.
- Control infection.
- Monitor wound pain while the patient is at rest (at times when no dressing change is taking place).
- Control pain to allow healing and positioning.
- Provide regularly scheduled analgesia, including opioids, patient-controlled analgesia, and topical preparations such as lidocaine gel 2%, depending on the severity of pain.
- Attend to nonwound pain from comorbid pain syndromes such as contractures and diabetes, and iatrogenically induced pain from central lines, venipunctures, catheters, feeding tubes, blood gas drawing, or other equipment or procedures.
- Address the emotional component of the pain or the patient’s suffering. For example, find out what the wound represents to the patient, what the pain means, whether there are associated losses of function, and whether the wound has altered the patient’s body image. In addition, determine whether mental status or behavior has changed related to unrelieved pain.
Source: Dallam LE, Barkauskus C, Ayello EA, Baranoski S. Pain management and wounds. In: Barnoski S, Ayello EA, editors. Wound Care Essentials: Practice Principles. Springhouse, PA: Lippincott Williams & Wilkins; 2004. p 217–38.