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9 Articles in Volume 10, Issue #4
Chaos (Nonlinear Dynamics) and Migraine
Enhancement of Nerve Regeneration by Therapeutic Laser
Functional Capacity Evaluation (FCE)
Making Practical Sense of Cytochrome P450
Non-pharmacologic Treatment of Shingles
Pain, Neurotechnology, and the Treatment-enhancement Debate
The New Age of Prolotherapy
Treating Myofacial and Other Idiopathic Head and Neck Pain
Treatment of Painful Cutaneous Wounds

Treatment of Painful Cutaneous Wounds

Comprehensive management and pain control are critical for patients with chronic wounds in order to improve outcomes and speed healing.

Chronic cutaneous wounds, such as those caused by pressure, venous insufficiency, neuropathy, or arterial disease, may cause considerable pain and can be challenging to treat. Often severe pain interferes with treatment protocols because patients are unwilling or unable to comply with necessary regimens. For example, compression bandaging, which is necessary for the treatment of venous stasis disease,1 may cause extreme discomfort, and noncompliance that significantly delays wound healing. Additionally, pain activates the sympathetic branch of the autonomic nervous system, triggering a physiological response that slows wound healing.2 Treating wound-related pain is essential for optimal wound healing. In the European Wound Management Position Statement, Briggs, Torra and Bou3 demonstrated the complexity of wound pain and its effect on treatment. The authors stressed the importance of using a combination of techniques that focused not only on physiological factors, but also on psychological and emotional factors. This article reviews the neurology and biochemistry involved in wound pain and discusses treatment options, including noninvasive techniques such as electrical stimulation, ultrasound, and pulsed radio frequency energy.


Cutaneous wounds normally heal in predictable stages: hemostasis and inflammation, granulation, epithelialization, maturation and remodeling. However, when the process is disturbed at any stage, a chronic wound may result.4 A variety of factors can contribute to nonhealing, including infection, inadequate pressure relief, uncontrolled swelling, impaired blood supply, malnutrition and poor glycemic control. In general, if an acute wound fails to heal within four to six weeks, it should be considered chronic. Treatment protocols vary according to the wound cause(s) (see Table 1).4

The most common chronic wounds are pressure (decubital) ulcers, venous insufficiency leg ulcers, arterial insufficiency ulcers, and diabetic foot ulcers (which may be a combination of the previous). Pressure ulcers frequently occur in immobile patients or those with some form of paralysis or orthopedic deformity. Pressure from a bed, footrest, shoe or other device restricts cutaneous blood flow causing tissue breakdown and ulceration. Venous leg ulcers are the result of inadequate venous drainage in the legs. Over time, increased tissue congestion and impaired venous blood flow compromises the skin and leads to overt ulceration. Arterial insufficiency ulcers often result from minor skin trauma in the setting of impaired blood flow. Finally, diabetic foot ulcers occur as a result of the repetitive trauma of walking in the setting of impaired sensation and often abnormal mechanics.

Table 1. Causes of Painful
Chronic Wounds
  • Pressure
  • Diabetic neuropathy
  • Venous insufficiency
  • Acute dermal injury complicated by:
    • infection
    • bleeding
    • poor nutrition
    • smoking
    • anti-inflammatory medication
    • habitual drug use
    • radiation
    • repeated trauma
    • age
    • arterial insufficiency
    • systemic disease
  • Malignancy

Evaluation and treatment of the chronic wound starts with a thorough history and physical examination. Appropriate laboratory and imaging studies should be utilized to help confirm diagnostic suspicions and identify infection. Treatment varies according to the underlying primary etiology but should consider all contributing factors (e.g., diabetic patient with an infected pressure ulcer on the bottom of the foot and concomitant peripheral arterial disease and poor glycemic control; see Table 2). Therapy should be customized for each patient according to his or her own individual needs.

Chronic wounds may take months or, in some cases, years to heal. General principles of wound management include: establishment of a clean, healthy wound base (often through surgical debridement), treatment of infection (both topical and parenteral), coverage of the wound with an appropriate dressing, and maintenance of a moist wound environment.4 Severe wounds—or those in patients with multiple medical problems—may require advanced modalities such as skin grafts or flaps. Despite the goal of healing, amputation is sometimes unavoidable, especially in patients with severe arterial insufficiency or comorbid problems.4

Across all wound types, pain management plays a major role in wound healing. Patients with chronic wounds often report a diminished quality of life because of pain. In addition, with repeated and vigorous medical procedures and restricted lifestyles, patients already may suffer from some degree of depression and anxiety.5-7 Increased anxiety has been shown to be a significant predictor of the intensity of pain experienced during treatment.8 Ongoing inflammation and infection may amplify a patient’s pain experience, and discomfort may increase with each wound treatment instituted.8,9 Evidence suggests that stress significantly slows wound healing and multiple cellular and biochemical mechanisms have been identified that link stress and wound healing.10-13 Understanding the different types of pain and the neurobiology of pain pathways is a critical first step in pain management for a patient with a chronic wound.

Neurobiology of Pain

Wound pain may occur as one of two types (or both): nociceptive and neuropathic. Nociceptors are the free nerve endings that respond to tissue injury. These nerve endings are either small myelinated Ad fibers, which conduct pain quickly and produce sharp localized discomfort, or larger unmyelinated C fibers, which conduct pain slowly and are responsible for dull or throbbing pain. Generally, once damaged tissue has healed, nociceptive pain subsides. If nociceptive pain continues for a prolonged period of time and the nerve fibers are in a constant inflammatory state—such as with repeated wound debridement or dressing changes—sensitization of the nerve fibers may lead to hyperalgesia14 (amplified pain) or allodynia (pain from a benign stimulus, such as light touch). Allodynia, which is more characteristic of neuropathic pain,15 may confound evaluation and treatment.12

Neuropathic pain is caused by insult to the actual nerve fibers or central nervous system. It often occurs after prolonged nociceptive pain from an injury, although it may also be caused by inflammation or compression of a nerve by a lesion or scar tissue. Usually it is chronic and described as burning, tingling, or shooting. Unlike nociceptive pain, neuropathic pain often continues even after the tissue has healed because the damaged nerve fibers continue to misfire.12,15

The complex neural connections involved in the processing of pain are difficult to understand. In 1965, Melzak and Wall16 proposed a “gate control” mechanism of pain that occurs in the spinal cord. Their theory asserted that a pain stimulus is first regulated in the peripheral nervous system and spine. The dorsal horn of the spinal cord receives nociceptive or pain stimuli from Ad and C nerve fibers as well as non-nociceptive or sensory stimuli from large Ab fibers. Ab fibers transmit sensory input faster than both Ad and C fibers. Melzak and Wall16 surmised that when Ab nerve fibers are simultaneously stimulated with the smaller pain fibers, signals race ahead of the pain transmissions and, by synapsing with inhibitory and projection neurons, “close the gate” for transmission of pain stimuli to the brain (see Figure 1). This theory would explain why pain is lessened when an injured area is massaged. If only the smaller Ad and C nerve fibers are stimulated or if an abundance of smaller fibers are stimulated, they inactivate the inhibitory and projection neurons and “open the gate” to the brain.16-18

Once nerve fibers have been stimulated, electrical signals are transmitted through the opening and closing of sodium and other ionic channels through the peripheral nerves and ascending pathways and through the spinal cord to the thalamus, hypothalamus, limbic system, and cerebral cortex. Pain transmission of a small Ad nerve fiber is quickly relayed to the thalamus and cerebral cortex19 for an immediate response (withdrawal and pain relief) that occurs through descending pathways. The C nerve fiber travels the same ascending pathway through the spinal cord, only more slowly. In the brain, the signal takes a path through the hypothalamus, which releases certain hormones including those for stress, and the limbic system, which affects emotions. This might explain why chronic back pain often is associated with depression and anxiety.19 Descending pathways originating in the cortex inhibit the ascending pathways in the midbrain and spinal cord, “closing the gate” and diminishing pain perception. Natural opiate neurotransmitters (endorphins, dynorphins and enkephalins) also are released from the hypothalamus and work to alter pain perception.17,19 The pain experience may be changed by anxiety, stress, emotions, and cognition.3 High levels of anxiety and the release of stress hormones may inhibit descending pathways and “open the gate” causing pain perception to intensify. This explains why individuals experience pain differently and why an individual may respond to the same type of pain differently each time it occurs.17 Pain thresholds are largely influenced by previous pain experiences.

Table 2. Standard Therapy for Painful Chronic Cutaneous Wounds
Type of Wound Standard Therapy
Pressure ulcer Position changes
Pressure relief
Nutritional status maintenance
Topical antibiotics
Wound dressing
Vacuum-assisted closure
Platelet-derived growth factors
Analgesics/anesthetics for pain
Diabetic ulcer Glycemic control
Off-loading of wound
Clean, moist healing environment
Systemic antibiotics for cellulitis
Topical antibiotics
Wound dressing
Platelet-derived growth factors
Analgesics/anesthetics for pain
Venous ulcer Compression dressing
Systemic antibiotic coverage
Topical antibiotics
Clean, moist healing environment
Analgesics/anesthetics for pain

Treatment of Pain in Chronic Cutaneous Wounds

Management of open wounds requires a multifaceted approach that includes pain control and emotional support at the very outset of treatment. It is necessary to determine the underlying pathology causing the pain (see Table 3). Worsening or change in the type or intensity of pain may indicate a deteriorating condition or impending infection.8 Wound pain occurs as chronic, cyclic, and noncyclic pain.20,21 Chronic pain persists throughout the day. Cyclic pain is caused by repetitive treatment, and noncyclic pain is caused by occasional procedures such as debridement. Each of these should be managed at every level of treatment.

Figure 1. Pain pathways.

Once the type, intensity, location, and cause of pain have been assessed, the patient’s physical and emotional well-being should be evaluated. It is important to remember that no two individuals experience pain exactly the same way or in the same intensity and responses to treatment modalities vary as well. Pain management must be individualized.22 Fears and expectations should be discussed openly.17 A consensus statement by the World Union of Wound Healing Societies23 proposed general guidelines for prevention of pain during dressing-related procedures that included: awareness of the current status of the patient’s pain, identification of pain triggers, and use of pain reducers and preventive analgesia whenever necessary. Patients should be encouraged to actively participate in their treatment, especially cleansing and dressing changes. Consistent communication during any procedure is critical.12

The first line of pain treatment in patients with chronic wounds should be nonpharmaceutical. Changes in positioning, gentle wound cleansing, use of different types of dressings, and distraction or relaxation techniques have been shown to ease discomfort of cyclic pain during procedures.14 Nonpharmaceutical methods reduce anxiety and stress, thereby allowing the body to naturally readjust pain perception and raise tolerance to future treatment.

Chronic background pain should be controlled quickly using analgesics. The World Health Organization (WHO) provided guidelines for the treatment of cancer pain in titrating the type and dose of analgesia to the level of pain.24 These guidelines can be applied to wound pain.25 The recommended steps for control of wound pain include 1) nonsteroidal anti-inflammatory drugs and local anesthesia, 2) addition of a mild oral opioid (if possible), and 3) replacement of the mild opioid with a more potent opioid.25 Ideally, analgesics should be fast-acting, easily titrated to required changes and have minimal side effects.3 Anticonvulsants and sodium channel blockers have been shown to be effective in neuropathic as well as nociceptive pain.26,27 The use of gabapentin, a voltage–sensitive sodium and calcium channel blocker, also has been used as a co-analgesic to morphine in a patient with cancer wound dressing pain.28

Table 3. Types of Wound Pain
Cause Description
Venous or arterial insufficiency Patients with venous disease often describe their pain as an aching heaviness.17,55 Pain from arterial disease is often described as leg cramping or spasm with activity. As the disease progresses, pain may occur even at rest.
Pressure ulcer Pain may be caused by inflammation and irritation from friction and shear forces. Increased pain may indicate infection, improper dressing technique, or skin irritation.
Diabetic neuropathy ulcer Patients with diabetic neuropathy may report pain, which is often described as burning, tingling, shooting or stabbing and may be spontaneous, continuous, or intermittent.57
Atrophie blanche8,55,56 Skin disorder seen in patients with chronic venous insufficiency is frequently associated with severe sharp pain. Plaque ulceration is exquisitely painful.

Oral medications may be supplemented with topical anesthetic preparations, although they should be used with caution in open wounds because of increased absorption. Topical preparations include: Eutectic Mixture of Local Anesthetics (EMLA®; Astra Pharmaceutics, Wayne, Pa.) applied 30 to 60 minutes before debridement under occlusion with a film dressing (not approved by the Food and Drug Administration for use in open wounds in the United States)12,15,28; 4% lidocaine solution; 2% lidocaine gel; 1% lidocaine solution; 5% lidocaine patch (Lidoderm®, Endo Pharmaceuticals, Chadds Ford, Pa.); topical diclofenac patch; and morphine topical gel.15,29

Regional or epidural nerve blocks are used primarily in patients with neuropathic pain. Hooshmand et al30 reported that epidural blocks containing Depo-Medrol® (Pfizer, New York, N.Y.) were successful in 89% of patients, whereas regional blocks had a 32% success rate. Ironically, both types of nerve blocks have been associated with development of heel ulcers in patients after knee and hip replacements.31,32,33

In addition to pain reduction, lumbar sympathectomy has been used as a vasodilator to increase blood supply to the legs in patients with ischemic peripheral arterial disease. It has been noted to improve tissue oxygenation and ulcer healing, and decrease pain by interrupting sympathetic-nociceptive pairing.34 Decreases in pain between 35% and 85% have been noted six months after lumbar sympathectomy.34 A recent study found that most physicians in the United Kingdom believe that lumbar sympathectomy is an effective, inexpensive and safe procedure for the treatment of lower extremity ischemia.35 Chemical lumbar sympathectomy has been shown to be an effective alternative to surgical sympathectomy.36,37 Successful results have been reported in two patients after basic fibroblast growth factor injection therapy into the ischemic limb.38

Transcutaneous electrical nerve stimulation (TENS) has been used as a noninvasive, nonpharmacologic adjuvant treatment modality for chronic ischemic pain.14,39,40

Electrodes stimulate non-nociceptive fibers to decrease pain.12 Although new findings on the effectiveness of TENS were nonspecific,41 “lasting” reduction of pain with the use of low-frequency pulsed current (Dermapulse®, Staodyn, Long-mont, Co.) has been shown in patients with recalcitrant venous leg ulcers.42

Noncontact ultrasound has long been reported to decrease the mean healing time of chronic lower-extremity wounds.43,44,45 Significant reduction in pain has been noted after using noncontact ultrasound for control of painful wounds.46,47

Pulsed radio frequency energy (Provant Therapy System®, Regenesis Biomedical, Scottsdale, Az.) has been used as an adjuvant treatment in the healing of diabetic foot and pressure ulcers.48,49 It also has shown benefit in controlling chronic spinal radicular pain and pain associated with lumbosacral spondylosis.50,51 The mechanism by which pulsed radio frequency energy alleviates pain is largely unknown. It has been demonstrated to increase the expression of cytokines (interleukin-related genes) and tumor necrosis factor-related genes that help to potentiate an initial inflammatory response necessary for healing of any type of wound.52,53 However, it may also augment the production of anti-inflammatory cytokines (interleukin 10) as well as heme oxygenase 1,2 (an off-switch for inflammation) which results in the release of potent antioxidants, anti-apoptotic, and anti-inflammatory agents.54

Pulsed radio frequency energy (PRFE) treatment is done usually at home by the patient or caretaker with an applicator pad placed directly over the wound dressing. The applicator pad delivers regulated, nonthermal radiofrequency energy at 27.12 MHz consisting of 42 microsecond pulses delivered 1000 times per second. Treatments last 30 minutes and are performed twice daily. Skilled nursing supervision is not necessary.

Treatment Guidelines for Chronic

  • Controlling pain at every level of treatment will aid in wound healing. Pain triggers should be identified promptly and avoided. Analgesics, anesthetics and other pain reduction modalities should be used to control pain during procedures.
  • Patients should be encouraged to actively participate in their treatment.
  • The primary etiology, size, depth and extent of a wound help guide treatment.
  • All contributing factors to chronic wounds should be identified and treated (e.g. ischemia, uncontrolled edema, or poor glycemic control).
  • Control of infection and bacterial colonization is crucial.
  • Principles of wound care should be followed, including: appropriate debridement, dressing selection, and maintenance of moisture balance.
  • Adjunctive therapies should be considered if appropriate conservative measures fail.


Disabling pain in patients with chronic wounds is a common concern and challenge for healthcare providers. Considerable advances have been made in the understanding of pain mechanisms with resultant new and innovative techniques to reduce discomfort and suffering. A wide range of topical anesth-etics, oral analgesics, and other modalities are available. Noninvasive therapies such as electrical stimulation, ultrasound, and pulsed radio frequency energy14,40-48,51,52 have all shown benefit in managing chronic pain. Comprehensive management and pain control are critical for patients with chronic wounds in order to improve outcomes and speed healing.

Last updated on: January 5, 2012
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