Management of Wound Pain

The International Association for the Study of Pain has defined pain as “An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” This definition emphasizes that pain involves two components: physical and emotional. The World Union of Wound Healing Societies defines wound pain as “a noxious symptom or experience directly related to an open skin ulcer.

Wound pain is typically assessed using pain scales, which are one-dimensional and measure only the physical component, intensity of pain. Multidimensional scales, such as the McGill pain questionnaire, that measure both physical and emotional components are used less often. Thus, frequently the clinician or caregiver interprets the patient’s pain experience in accordance with his or her own personal perspectives and biases.

As a result, the patient’s pain experience, especially in the case of chronic wound pain, may be marginalized, and the pain may be poorly controlled.  Wound pain management requires highly individualized, skilled medical care, as well as patience, compassion, and commitment. Pain management experts are not available in most settings, and many clinicians are inadequately prepared to develop pain management plans of care. Clinicians need guidelines on management of acute and chronic wound pain.

The  wound pain experience depends on the interaction and modulation of the biologic and psychosocial characteristics of the individual. Biologic considerations include genetics, sex, and endogenous pain control (e.g., cortisol and endorphins). Psychological characteristics include anxiety, depression,  coping skills, behavior, and cognitive status. Pain is also a consequence of the individual’s history of disease and present disease status. Environmental factors also are part of the individual’s pain responses. Examples of environmental factors are socialization, lifestyle, traumas, and cultural background.

On the positive side, pain is protective and serves as a warning sign of imminent or actual danger and triggers an appropriate response within the body to avoid or minimize injury. Although most of us fear pain and would prefer avoiding the sensation, the inability to feel pain and respond to danger or injury—such as occurs in neuropathy resulting from diabetes, alcoholism, or chemotherapy, or with spinal cord injury or multiple sclerosis—puts the individual at risk for serious bodily harm.

Following injury, the  wound pain signal also initiates the release of chemical mediators, , necessary to start the healing cascade. Another benefit of acute pain in inflamed tissues is that pain provokes hypersensitivity of the injured tissues, causing the individual to guard the damaged tissue while healing occurs. Typically, as healing occurs, pain intensity subsides, as does guarding. Pain can also be a signal of the presence of infection.On the negative side, pain can interfere with the immune response, influence the healing process, and delay wound closure.

Pain is not beneficial when it is “out of control” and triggers an emotional response that includes excessive release of hormones, such as cortisol and epinephrine, which interfere with healing processes. The effects of cortisol and epinephrine Inflammatory mediators and cytokines are helpful following initial injury, but if they are released frequently following repetitive procedures such as sharp or mechanical debridement, or dressing changes, they lower the firing thresholds and decrease the baseline sensitivity of nociceptors (pain receptors) in such a way that they begin to respond to normally innocuous thermal and mechanical stimuli, resulting in hyperalgesia (exaggerated pain response).

 

The pain experience begins as acute pain and over time—3 to 6 months depending on the source—is learned by the nervous system and becomes chronic or persistent pain that can even be prompted by the patient’s expectation of pain

 

Nociceptive pain

Nociceptive pain is when there is excitation of the nociceptor terminals in the skin. Nociceptors are triggered by different stimuli producing three overlapping nociceptive pain patterns: mechanical, ischemic, and inflamatory Mechanical nociception is triggered by mechanical distortion of the tissues such as during repositioning, pressure, or scar  tissue  manipulation.

  • Ischemic nociception occurs when there is interruption of blood flow and resulting alteration of the chemical environment of the tissues. Ischemic tissues become more acidic, are hypoxic, and are rich in nociceptor-sensitizing chemicals: bradykinin, potassium ions, and prostaglandins. An example of ischemic pain is intermittent claudication that occurs during walking and then subsides when the activity ceases.
  • Inflammatory nociception is related to the inflammatory processes following tissue injury and the chemical mediators involved and will reduce as the tissues heal. Inflammatory pain is also the pain called neuritis due to irritation of nociceptive nerve endings, axons, or nerve processing circuits.When peripheral nociceptors are in a continuous inflammatory state, such as occurs with repeated procedural traumas like dressing changes, they become sensitized and release a mixture of endogenous pain and infl ammatory mediators whose presence lowers the threshold for nociceptor fi ring and enhances the response to any further stimulus. This is referred to as peripheral nerve sensitization

Sympathetic Nervous System

SNS is a component of the autonomic nervous system (ANS) that is concerned with glandular secretions, smooth muscle action, and cardiac muscle. SNS responds to all injuries and pain by releasing catecholamines, epinephrine, and norepinephrine from SNS receptors causing increased heart rate, vasoconstriction, increased blood pressure, enhanced pain perception, sweating, and slower wound healing.

PERSISTENT (NEUROPATHIC) PAIN

Persistent pain is clinically referred to as  neuropathic pain. Rather than arising from stimulation of nociceptors, it reflects an abnormal functioning of the peripheral or central nerves themselves. In short, it is a disease of the nervous system, not a symptom.

Neuropathic pain is clinically defined as pain being present for more than 3 months, whether continuous or intermittent. An example is background pain, which is pain at rest, and is often associated with venous ulcers and burns.

Classification of Neuropathic Pain

Clinicians classify neuropathic pain into two categories: in central neuropathic pain, the lesion or dysfunction affects the CNS; in peripheral neuropathic pain, the lesion or dysfunction affects the PNS.

Peripheral neuropathic pain is sometimes further subdivided into stimulus-evoked pain or stimulus-independent pain (spontaneous pain):

  • Stimulus-evoked pain is a heightened reaction to a painful stimulus, as described previously for hyperalgesia and allodynia, that occurs when the peripheral nerve is damaged or altered.
  • Stimulus-independent pain arises from spontaneous activity in the spinal cord, brainstem, or thalamic/cortical areas. It is less common and may have many mechanisms.

Pain related to dressing changes

 

Many patients experience  wound pain on dressing removal or change, which is largely preventable with the use of appropriate products (EWMA, 2002). EWMA (2002) found that:

Dressing removal is considered to be the time of most pain, followed closely by wound cleansing;

Dried out dressings and adherent products are most likely to cause pain and trauma at dressing changes;

Gauze is most likely to cause pain, while products such as hydrogels, hydrofibres, alginates and soft silicone dressings are least likely;

Supporting the surrounding skin during dressing removal is not considered a priority, despite evidence that many adhesive products may lead to skin stripping and potential skin trauma and pain (Dykes et al, 2001);

Health professionals ranked venous leg ulcers as the most painful wounds, and superficial burns ranked second. They ranked infected wounds, pressure ulcers, cuts and abrasions, paediatric wounds, cavity and fungating wounds as less painful wounds

 

Pain management tips

 

  • Assume every wound in painful and that every patient who has a wound is in pain
  • Patients frequently experience pain during dressing changes (dried out dressings, adhesives, debridement, and pressure of exudate), especially around wound edges and in infected or inflamed wounds.
  • Moist wound healing has been demonstrated to result in less pain .Pain reduction attributed to the bathing of the nerve endings in fluid, preventing dehydration of the nerve receptors
  • Handle all wounds gently; flush avoid rubbing when cleaning
  • Avoid unnecessary stimulus to the wound, such as inappropriate bed/chair surfaces, prodding, poking or exposure to drafts
  • Protect wound edges wounds are most painful at edges
  • Allow patients to change their own dressings whenever possible
  • Encourage and allow patients to take a break whenever necessary…a time out
  • Encourage deep breathing exercises during dressing changes…blood flow can be decreased to wound bed if patient is not relaxed
  • Use dressing that are less likely to adhere to the wound example Silicone foam.
  • Avoid aggressive packing…fill don’t pack the wound with open or dead space
  • Select dressings with absorbency that matches exudate levels
  • Reducing anxiety Time invested prior to dressing removal is time well spent. Talking to patients about how much pain they can expect, together with an explanation of whatever measures are in place to minimise their pain will help to reduce the feelings of fear and anxiety.

 

Wound Pain Ladder