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Pain in Chronic Wounds: Mechanism and Management 299
wound-related pain in the background of the disease with 80% scoring their pain as
NRS 4/10 (Numerical Rating Scale) equivalent to mild to moderate in intensity
(Leren et al. 2020).
It is evident that the pain from these chronic wounds is debilitating and affects
not only wound healing but also the patient's quality of life. While patients give
pain alleviation a higher priority in wound management, the primary focus of
healthcare providers revolves around local wound care and wound healing,
thus ignoring pain management and the holistic care of the patient. This apparent
lack of acumen is often the cause of disappointment on both sides, as the patient’s
expectation and the care provider’s treatment goal often fail to match. Eventually, it
is the patient and not the wound that should be the point of attention for care.
According to the International Association for the Study of Pain, the term
chronic pain is used to describe the pain which persists beyond the normal tissue
healing time thereby lacking the warning of acute nociceptive stimuli. Chronic pain
can be broadly classified into two types—neuropathic which is caused by damage
to the nervous tissue and nociceptive which occurs as a consequence of inflamed or
damaged tissue activating receptors called nociceptors. Acute pain primarily serves
to warn of an injury and is nociceptive, only relieved by the decrease in harmful
inputs (Price et al. 2007). This is in contrast to chronic pain which involves both
physical and emotional components and rarely indicates ongoing tissue damage
(Schaible and Richter 2004). A wound represents a loss of skin integrity and cut
nerve fibers and so the ensuing pain is due to a combination of nociceptive pain and
pain caused by nerve damage (neuropathic pain) (Price et al. 2007).
Pain manifestations in a wound can be broadly categorized as the following
(Minimising pain 2004):
(i) The background pain is a continuous or intermittent pain that is felt even at
rest,
(ii) The incident pain, also called breakthrough pain, occurs during day-to-day
activities such as mobilization
(iii) The procedural pain resulting from routine procedures such as dressing
change or wound cleansing and
(iv) The operative pain associated with significant wound intervention, such as
debridement or biopsy.
Chronic wounds are characterized by a hyperinflammatory response that
impedes healing (Bechert and Abraham 2009). They are associated with primary
hyperalgesia, which describes a heightened sensitivity around the wound caused by
a sustained zone of inflammation around the wound. This should be differentiated
from allodynia which is the occurrence of pain in response to a normal,
non-noxious stimulus. Primary hyperalgesia is essentially the consequence of
endogenous inflammation in the wound leading to a lowering of the nociceptive
threshold. However, the pain experienced in chronic wounds is more complex than
what is usually though t of. It is an amalgam of cyclic acute wound pain, non-cyclic
acute wound pain, and chronic wound pain. Cyclic acute wound pain is induced by
300 A. G. Goswami et al.
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regular, repetitive intervention like periodic dressing changes. Non-cyclic acute
wound pain is provoked by procedures that are either one time or occur at infrequent, varia ble intervals, such as wound debridement. Chronic wound pain is the
background pain irrespective of any manipulation and is contributed by the primary
etiology of the wound. It is the continuous pain that is associated with the wound
irrespective of its condition and at times may also be intermittent or cyclic. Since
the usage of such terms as above is often fraught with confusion, the wound pain
management model simplifies the terminology and uses “temporary” and “persistent” pain to differentiate between the temporal pain experiences (Price et al. 2007).
Pathophysiology of Wound-Related Pain
The cause of wound pain can be due to nociceptive or neuropathic stimuli. Chronic
wounds are vulnerable to the recurring noxious stimuli that arise from the infiltration with inflammatory cells, the release of proinflammatory cytokines, and the
formation of a dense fibrin matrix at the wound surface. Furthermore, tissues in
chronic wounds are often arrested in an inflammatory state which releases a wide
range of pro-inflammatory mediators such as prostaglandins, leukotrienes, histamine, serotonin, and substance P. Free nerve endings, originating from the dermis
have nociceptors, which respond to these mediators causing nociceptive pain
(Tracey 2017; Dubin and Patapoutian 2010).
Neuropathic pain on the other hand arises from dysfunction of sensory axons of
peripheral or central nerves. An increase in the cell membrane expression of
voltage-gated sodium channels in response to the inflammatory mediators leads to
decreased activation threshold and thus causes increased membrane excitability
(Freedman et al. 2004). The release of chemokines such as substance P and
TNF-alpha, besides other neuropeptides, causes activation of A-b and A-d afferent
fibers and contributes to neuronal hyperexcitability and low pain perception
threshold. Due to the ongoing inflammatory process in a chronic wound, high levels
of pro-inflammatory mediators are probably the cause of persistent low pain
threshold and the resultant background persistent pain. The persistent inflammation
and cell injury in chronic wounds are also associated with reduced pain threshold
(allodynia), the spontaneous firing of nociceptors (spontaneous pain), an exaggerated and prolonged response to a noxious stimulus (hyperalgesia), and the spread of
pain perception to uninjured tissue (widened receptive fields). The peripheral nerve
regeneration in chronic wounds has immature sprouts of neurons that have
increased sensitivity to both noxious and non-noxious stimulus and irritation of
these nerve endings are the source of intensified pain (Stechmiller et al. 2019).
A third category, called nociplastic pain, has been described by the international
community of pain researchers (Fitzcharles et al. 2021). It is mechanistically distinct
from inflammation-induced nociceptive pain and nerve injury-induced neuropathic
pain. It is to be noted that the true mechanism underlying this type of pain in chronic
Pain in Chronic Wounds: Mechanism and Management 301
wounds is not fully understood at present. It is believed that diminished spinal
inhibition, spinal cord reorganization and amplified spinal reflex transmission, and
glial cell activation are some of the mechanisms responsible for spinal causes of
nociplastic pain. The supraspinal mechanisms such as decreased pain inhibition
activity in brain, decreased GABAergic transmission while increase in substance P
in cerebrospinal fluid, augmented processing of pain stimuli in the central nervous
system, altered sensory modulation of pain and sensitization are responsible for its
pathogenesis (Ni js et al. 2021). The symptoms include widespread or multifocal pain
of intense nature, disproportionate to the degree and extent of tissue injury or in
absence of tissue injury. Nociplastic pain is often associated with tension headache,
fatigue, and sleep and mood problems. Although it can occur in isolation, often it
may coexist with other types of pain (Freynhagen et al. 2019). Early recognition of
this type of pain is important, as the standard therapies of nociceptive pain may not
be adequate. There is a d ecreased response to peripherally directed therapies such as
non-steroidal anti-inflammatory drugs and opioids. Mood elevators, psychotherapy
and various counselling techniques may help.
The electrical impulse generated in response to noxious stimuli in the wound is
conducted from peripheral receptors through the spinal pathways until the higher
centers in the brain where the pain is perceived. However, pain perception is not a
unilateral, lucid, solitary pathway but an intricate neuronal network that integrates
multiple sensory, cognitive, emotional, endocrine, and autonomic pathways coupled with immune responses modulated by intrinsic neuronal inhibitory inputs. This
modifies the nerve impulses of varying dimensions and culminates in the production of pain percept ion (Bourne et al. 2014). This complex interplay of several
pathways explains why similar noxious stimuli provoke different types and degrees
of pain perception in different individuals under different circumstances.
Pain Pathways
As previously described, chronic pain is of two types—neuropathic and nociceptive. Nociceptive pain is a physiologic response to an injury and serves a protective
role, while neuropathic pain is an inappropriate response from damaged neurons
which causes signals to travel along abnormal pathways (Bechert and Abraham
2009) Nociceptors are free nerve endings found in cutaneous and visceral tissue.
These receptors remain inactive unless stimulated. They respond, as suggested by
their name, to “noxious ” stimuli which are stimuli that damage or threaten damage
to tissues. Their termination in “free nerve endings” implies that they remain
independent of other cells for signal transduction. In other words, the proteins
which are responsible for signal transduction are intrinsic to the receptor itself
(Choniere 2001). These receptors get activated by either actual injury to the tissue
or changes in the surrounding tissues. The stimulation causes the cellular changes in
the nerve ending to get converted into an electrical impulse that travels to the dorsal
or ventral roots of the spinal cord (Fig. 1). These fibers are referred to as the
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Fig. 1 The pain pathway
Pain in Chronic Wounds: Mechanism and Management 303
first-order neurons and are primarily C- type (small and unmyelinated) and A-delta
type fibers (small and myelinated). Most impulses pass through the dorsal horn of
the spinal cord which is, therefore, a critical site for pain transmission. These
impulses are carried from the primary afferent neuron to a second-order neuron” in
the cord for transmission to the brain through the ascending tracts (spinothalamic
tracts) (Giordano 2002).
Neuropathic pain is caused by nerve dysfunction or damag e to the nervous
system. Neuropathic pain is an inappropriate response, as damaged nerve fibers can
lead to the generation of aberrant electrical signals from the nerve endings (Briggs
2004; Basu et al. 2022) Damage to nerves can result in alteration or amplification of
the pain signal. Neuropathic pain may be the result of a pathological process at any
level in the nervous system, from the nociceptor, distal nerve, plexus level, dorsal
root ganglion, root entry zone, and higher levels in the CNS. Nociceptive pain, in
contrast, usually indicates a proper functioning nervous system and is considered
physiological because it results from the activation of nociceptors (Bechert and
Abraham 2009) On the other hand, neuropathic pain perception occurs in the brain
and spinal cord, with the pathological process anywhere in the nervous system
(Table 1) In nociceptive pain, the perception is still in the brain and spinal cord, but
its origin and intensity is localized at the peripheral nociceptors, at the peripheral
nerve endings (Bechert and Abraham 2009).
Table 1 Comparison between nociceptive and neuropathic pain
Nociceptive pain Neuropathic pain
Definition Physiological activation of pain
Cause Actual/potential tissue damage Primary lesion/dysfunction of nervous
Mechanism Physiological pain transduction Ectopic pain impulse generation
Noxious
stimuli
Origin Nociceptors Nervous system lesions
Pain
pathway
Pain
description
Treatment Analgesics Poorly responsive to conventional
Function Protective/Healing/Pathological Pathological
Pain
threshold
Examples Post-operative pain, sports
receptors
Present Absent
Normal Abnormal
Dull, throbbing, aching,
cramping
High or Low Low
injuries
Lesion/dysfunction of nociceptive
pathways
system (peripheral or central)
Burning, shooting, tingling, stabbing,
electric like
analgesics
Distal polyneuropathy,
Postherpetic/Trigeminal neuralgia,
Complex regional pain syndrome
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Effects of Pain in Patients with Chronic Wounds
Poorly controlled pain in chronic wounds adversely affects the patient not only
psychosocially but also by impairing the wound healing process and affecting the
patient’s recovery and overall wellbeing. This pain profoundly affects the patient's
behaviour, personality and social relationships. Depression, anxiety, chronic fatigue, sleep disturbances are their constant companion which further leads to frustration, fear, helplessness, hopelessness, and anger. This leads to poor quality of life
and increases morbidity (Basu et al. 20 22; AGS Panel on Persistent Pain in Older
Persons 2002).
Broadly speaking, chronic pain may affect poor compliance with treatment. Pain
experienced during dressings and debridement makes adherence to treatment plans
difficult. The vicious cycle of pain and poor wound healing leads to vasoconstriction of blood vessels at the wound bed which reduces tissue perfusion, compromises oxygen and nutrient supply to the already inflicted area thereby halting the
normal wound healing process. The psychological concerns are the most challenging. Chronic wounds are persistent and form an important niche in a person’s
life. Chronic wound pain generates a wide-ranging response from anxiety to
depression. This further worsens the pain which perplexes the wound healing
process. Furthermore, chronic woun ds are detrimental to the q uality of everyday
living. Severe pain prevents patients to perform normal daily activities.
Diagnosis and Assessment
Most of the chronic wounds can be diagnosed clinically, on the basis of the history
given by the patient, the location of the wound and its characteristic features. The
diagnosis of an infection complicating the ulcer is essential and is usually quite
easily made by the typical features that accompany an infection—the presence of
pain in a previously painless wound or an increase in pain, purulent discharge from
the site and the classic signs of inflammation—erythema, warmth, tenderness.
Indicators of chronic wound infection include increased pain, serous exudate,
impaired healing, discoloured granulation tissue, foul odour and wound breakdown.
Infection can also increase the sensitivity of the nociceptors. This emphasizes the
importance of infection control in allaying pain in these patients.
Pain Assessment
The assessment of chronic pain is a tedious task and more often than not, subjective. However, this is one evaluation which must not, at any point of time, be
overlooked or disregarded. Chronic pain affects not only the patient’s physical state
but also his emotional wellbeing. Pain, as described earlier, is an early marker of
Pain in Chronic Wounds: Mechanism and Management 305
certain complications in wounds, whi ch, if left unattended, can have devastating
consequences.
The asses sment of pain should begin with a thorough history taking including
and not limited to the site and duration of pain, and any history of radiation of pain.
Its intensity, quality and aggravating and relieving factors should also be inquired.
Idea about whether it is a new onset pain or an exacerbation of an old pain is
important and probably the most significant area which needs to be explored is how
it affects the activities of the patient’s daily living.
Validated pain scales such as the Visual Analog Scale (which is considered the
gold standard) are commonly used tools for pain assessment (Mani et al. 2016)
Several other assessment tool s have been developed to make the pain assessment
process universal. However, using these tools requires consideration of the patient’s
age and cognitive status.
(A) Pain scales: These help in the quantification of patients’ present pain
intensity.
1. Visual analogue scale (VAS)
2. Numeric Rating Scale (NRS)
3. Verbal Rating Scale (VRS)
4. Wong-Baker pain rating scale: for patients with limited cognitive ability.
(B) Pain Questionnaires: contains verbal descriptions that help patients distin-
guish different types of pain. These are Mc Gill Pain Questionnaire, Brief
Pain Inventory, Neuropathic Pain Questionnaire, and 4-Item Pain Intensity
Measure among many others. However, the ability of patients to answer
these questionnaires is influenced by a multitude of individual and environmental factors and is useful for chronic pain assessment.
(C) Pain assessment in special groups.
1. Cognitively impaired adults: The American Geriatrics Society describes six
domains for pain assessment in this group: (AGS Panel on Persistent Pain in
Older Persons 2002)
• Facial expression
• Negative verbalization, vocalization
• Body movements
• Changes in activity patterns or routines
• Changes in interpersonal interactions
• Mental status changes
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2. Children
(a) Self-reporting: what a child is saying
(b) Behavioural measures: motor/ behavioural response, facial expression
(c) Physiologic measures: change in heart rate, respiration, blood pressure,
oxygen saturation, sweating, neuroendocrine respon ses
(d) Pain scales: like COMFORT pain scale, FLACC, CRIES pain scale
Nevertheless, pain assessment is a continuous process and should be done at
regular intervals in a standardized manner. To simplify the assessment of pain, Fink
et al. proposed a simple guide using the WILDA approach, which is as follows
(Fink 2000):
• Words: patients’ description of pain
• Intensity: quantification of pain intensity
• Location: site of pain
• Duration of pain
• Aggravating/associated factors
Management
Step 1: Identification and initiation of treatment of the underlying cause.
Step 2: Treat local factors causing wound pain—ischaemia, infection, excessive
drying or exudate in the wound.
WHO Pain Management Ladder
The World Health Organisation has designed a three-tier analgesic ladder for the
management of chronic pain (World Health Organization 2018). It’s three main
principles are “by the clock, by the mouth and by the ladder”. That is to say,
analgesia should be provided “round the clock” than just on request, preferably by
the oral route and following the ladder described below.
The first step involves the use of non-opioid medications such as the
non-steroidal anti-inflammatory drugs (NSAID) and tricyclic antidepressants. It is
only when these medications fail to provide relief to the patient the next tier drug
should be used which includes administration of “weak” opioids such as codeine,
tramadol in combination with NSAIDs. The final tier is used when the patient does
not receive relief from the medications used in the first two tiers. It includes
“strong” opioids like morphine, hydromorphone etc., with discontinuation of the
second-tier opioids. Adjuvants like antidepressants, anticonvulsants or corticosteroids may be added at any step of the ladder.
While the analgesics may provide dramatic pain relief and thereby improve the
patient’s standard of living and decrease the risk of immobilisation-induced complications such as deep vein thrombosis, pulmonary embolism, and pressure sores,
Pain in Chronic Wounds: Mechanism and Management 307
these are not without adverse effects of their own. While patients on opioids should
be monitored for sedation, respiratory depression, nausea, and constipation, the
rampant use of NSAIDs may result in duodenal ulcer, duodenal ulcer perforation
and analgesic-induced nephropathy.
Management of Breakthrough Pain
Breakthrough pain is a transitory pain which occurs on a background of relatively
well—controlled baseline pain. This can be managed by both pharmacological
and non-pharmacological means. Prophylactic administration of additional pain
medication in patients in whom breakthrough pain is predictable, such as
movement-induced pain, may prove effective and is usually done around 30 minutes prior to the pain—inducing activity. Pharmacological methods to treat the
breakthrough pain include increasing opioid dose, administration of a short-acting
supplement or reducing the time interval between the doses. The supplemental dose
which is chosen should be adequate to provide pain relief without causing additional side-effects.
Wound Pain Management
Wound pain management model, described by Price et al. (2007) starts with the
assumption that all wounds are painful unless otherwise proven. A complete and
comprehensive assessment of the wound is based on a correct diagnosis of the
pathology of the wound and the source of pain, assessment of which are indispensible in wound management (Fig. 2).
Fig. 2 Summary of wound pain management
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Topical Treatment
Patients with chronic wounds tend to have hypersensitivity around the wound and
so experience excruciating pain during dressing changes. Also, local factors like
tissue trauma, infection and poor moisture balance will add to the patient’s woes
and are quite often responsible for increased pain scores. It is therefore essential to
have a holistic approach to pain management. Systemic analgesics form only a part
of the management. Non-pharmacological and pharmacological local treatment can
sometimes provide dramatic relief to the patient.
Local wound management techniques include autolytic debridement, dressing
application, use of local anaesthetics. Psychosocial therapy can be employed—
asking the patients to organise their day by socialization, participatory events and
exercise (Price et al. 2007).
Regular wound dressing is of paramount importance in wound care. Patients
report excruciating pain during dressing change with the maximum pain at the time
of dressing removal, which causes trauma and pain by stripping the superficial crust
of granulation tissue and newly formed epithelial layer (Briggs 2004; Dykes et al.
2001). A dressing should be selected which maintains adequate moisture balance
without getting adhered to the wound bed. In addition, an ideal dressing should
manage excess exudate, allow for gaseous exchange, provide thermal insulation,
prevent bacterial colonisation, be comfortable and easy to apply and remove, and
importantly, cost-effective (Paschou et al. 2018). It is reported that patients experienced more pain with gauze dressings when compared with advanced
moisture-balanced preparations including foam, alginate, and hydrocolloid dressings (Woo and Sibbald 2008). Use of atraumatic dressings is considered to be
pivotal in prevention of wound injury and pain in the wound during dressing. One
such example would be the soft silicone dressing, which has a low peel strength so
as to minimize trauma during removal. These are now considered the gold—
standard for wound dressing. Hydrofibres and alginate dressings form a gel which is
in contact with the exudate and are excellent non-adherent dressings and provide
sufficient pain relief to the patient. But even these dressings have the tendency to
cause trauma if allowed to dry out.
Management of Infection
Chronic wounds are susceptible to infection by mic roorganisms which colonize
in the wounds after external contamination. Infection of the wound leads to an
inflammatory response with influx of neutrophils at the site. This also leads to the
accumulation of cytolytic enzymes, free radicals and inflammatory mediators. The
eventual tissue hypoxia that ensues promotes a vicious cycle. Pain over a previously
non-painful wound or increasing pain over the wound could be one of the earliest
signs of infection (Alexiadou and Doupis 2012) Detection and treatment of the
infection in the early stages promote healing and thereby, reduce the patient’s pain.
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