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What has pain relief to do with acute surgical wound healing?


Ramon Pediani

Former clinical nurse specialist for acute pain
Victoria Hospital Blackpool

Part-time PhD student
University College of St Martin

Published: March 2001
Last updated: March 2001
Revision: 1.0

Keywords: acute wounds; pain and wound healing; surgical wounds.

Key Points

  1. Unrelieved pain has detrimental effects on wound healing.

  2. Tissue damage and inflammation sensitises nerve endings that transmit nerve signals. Repeated stimulation can cause benign sensations to become painful.

  3. Clinicians must adopt a rational therapeutic approach to pain management to help relieve pain and facilitate wound healing and minimise the risk of developing chronic wound pain.

  4. The implementation of guidelines and protocols will raise the basic standard of care whilst the support of acute pain teams will give much needed direction and consistency to strategies for pain management.

  5. Nursing care is the key to safe pain relief and optimal wound healing.


This paper will examine the role that pain control and the proper management of adverse effects can play in allowing patients to physically recover from surgery. The true relationship of pain relief to creating optimal conditions for wounds to heal (reduced stress response, reduced fatigue, improved circulation and oxygenation, early return to oral nutrition, and early ambulation) has only become clear in the past decade, but much of the knowledge was already established 20-30 years ago. It will be argued that this involves far more than simply dispensing set doses of prescribed analgesics. In addition, the implications of inadequate pain relief in the postoperative period on surgical recovery and the development of long-term chronic wound pain will be discussed.


The connections between the relief of pain and the nature of surgical wounds are far from clear. Certainly the relief of suffering is a nursing goal that one would expect to find shared in common with patients, but despite this the problem of inadequate pain control exists on a large scale. A survey of 5150 hospital patients in 1994 found that 61% suffered pain, 87% of whom had severe or moderate pain [1]. Nurses have a unique role due to their close working relationship with the patient [2]. Their ability to fine-tune analgesia rests on a number of foundations including pain assessment skills, their knowledge of practice, degree of empowerment and the wider goals and structure of the nursing care environment.

Pathophysiology of wound pain

Pain has a protective function in nature, warning of damage, and promoting careful treatment of the affected area. However, postoperative pain can be destructive too: by heightening the cellular stress response, the autonomic, somatic and endocrine reflexes are diminished, resulting in protein breakdown, platelet aggregation, nausea, ileus and a suppressed immune system [2][3]. Low oxygen tension and poor perfusion can slow down the deposition of collagen in tissue undergoing repair [4], both of which can be influenced by pain: restricted breathing due to pain can lead to low-grade hypoxia, and severe pain can cause vasoconstriction, both of which ultimately impair wound healing.

An understanding of the implications of unrelieved pain is not new, and Nimmo and Duthie [5] in 1987 highlighted the four major adverse effects of severe pain following surgery:

  1. Decreased respiratory movement especially after upper laparotomy or thoractomy. A decreased functional lung capacity, difficulty in breathing deeply and in coughing all contribute to hypoxia after operation.

  2. Decreased mobility because of pain on movement. Early mobilisation is more difficult and the risk of deep venous thrombosis is increased.

  3. Increased sympathetic activity leads to a release of catecholamines which has adverse effects such as hypertension followed by myocardial ischaemia and decreased blood flow to some tissues.

  4. Hormonal and metabolic activity resulting from surgery and made worse by pain increases protein breakdown and mobilisation of free fatty acids.

By adopting a rational therapeutic approach to pain management the optimal conditions can be created whereby the patient is able to take deep breaths and cough without being limited by pain, mobilise to relieve pressure, and thereby improve circulation and tissue perfusion. Unfortunately, the side effects of some analgesic techniques can cause patients to experience nausea, dizziness, drowsiness and lower limb weakness, all of which can interfere with mobility.

The high degree of variability found in patient responses to surgery, and to analgesics, requires that nurses have a clear understanding of the therapies in order to respond to patient requirements appropriately.

The natural response to pain is to rest and to prevent the provocation of pain on movement. Opioids and non-steriodal anti-inflammatory drugs (NSAIDs), which may provide adequate pain relief at rest, do not prevent the experience of pain on coughing or changing position. Such pain can greatly compromise the patients' ability to return to normal function. Immobility can predispose patients to deep vein thrombosis, chest infections and pressure sore development. It has been shown that the high quality of pain relief afforded by the use of epidural analgesia can be a major factor in reducing the physiological stress response to surgery. When this state is taken advantage of through early ambulation and early oral nutrition, recovery from surgery is rapid [3].

This was demonstrated in a study by Bardram et al [6] in which a group of elderly, high-risk patients underwent laparoscopic colon resection. With a planned, accelerated recovery programme, involving epidural analgesia, patients did not experience postoperative pain, fatigue, ileus or nausea, and were able to be discharged after only two days.

Tissue damage or inflammation sensitises nerve endings, termed 'nociceptors', that transmit pain signals. Goodwin [2] terms the complex mix of macrophages and lymphocytes, alongside chemical mediators, such as histamine, serotonin, bradykinin, substance P, prostaglandins and cytokines in the peripheral tissues, as an 'inflammatory soup'. This 'peripheral sensitisation' decreases the firing threshold and increases the responsiveness of A delta and C nerve fibres, which conduct signals at different rates. Their respective signals are perceived differently: A delta fibres conduct rapidly and give rise to a sharp shocking pain; C fibres signal a more diffuse, constant ache.

Once the signals reach the spinal cord they terminate in the dorsal horn, where another 'soup' of chemical mediators, such as N-methyl-D-asparate (NMDA), lead to 'central sensitisation' of spinal neurons and the transmission of the pain signals onward to the brain. Repeated stimulation, such as from a surgical wound, can give rise to a state of 'hyperalgesia' (also known as 'wind-up') where normally benign sensations can now be perceived as being painful [7], and an increased tenderness extends to a wider area around the actual tissue damage [8]. Once established, the enhanced sensitisation can last for up to five days after the cessation of postoperative opioid analgesia [9] and therefore care must be taken to ensure adequate oral analgesia is available into the later postoperative period.

Descending nerve pathways can modulate the incoming pain signals to the spinal cord, but anxiety and depression can inhibit this action. The provision of analgesia is of obvious importance, but so too is the psychological care of the patient to alleviate depression, anxiety and tension [10].

Preemptive analgesia

An understanding of the central sensitisation to pain, induced by surgical trauma, and the role that this plays in increasing postoperative pain and in the development of chronic pain, provides "a rational basis for preoperative and postoperative strategies to reduce the neuronal barrage associated with tissue damage" [11].

It has been suggested that taking steps to minimise the degree of pain before the hypersensitivity that occurs following surgery has developed, is more effective than treating the pain once it has become fully established. Preemptive analgesia, as it has been termed, is controversial, and research continues apace in this field [12], as the method of analgesia, type of surgery and anatomical area appear to influence its reliability [13]. The concept of preemptive analgesia can involve the provision of opioids, NSAIDs, local anaesthetic blocks and NMDA receptor antagonists such as ketamine. It has been shown that analgesia commenced before surgery can depress central sensitisation to pain signals, and enhance central inhibition mechanisms [9]. Aida et al [14] demonstrated that morphine and ketamine can reduce central sensitisation during major gastric surgery, and result in lower pain scores at rest and on movement, and correspondingly lower postoperative analgesic consumption. Dahl et al [15] however, were unable to detect any significant preemptive analgesic effect in women undergoing abdominal hysterectomy surgery, and Adam et al [16] were unable to demonstrate an effect in women undergoing total mastectomy following a single preoperative injection of ketamine.

That ketamine is a powerful NMDA antagonist, and therefore has the potential to disrupt the central sensitisation mechanism was demonstrated by Stubhaug et al [17]. In a study involving patients who had undergone kidney transplant, in which ketamine was given by continuous low-dose infusion during and after the surgery, there was a reduction in hyperalgesia around the surgical wound. It is possible that the concept of preemptive analgesia is correct, but more attention needs to be paid to the techniques employed to minimise the intensity and duration of nociceptive impulses [18].

Development of chronic wound pain

Acute pain is often associated with a distinct disease or injury and the duration of the pain is often wrongly assumed to be limited to the healing time of the damage [19]. Potter [20] defines acute pain as that which is present for less than four weeks, and chronic pain as that which is present for longer than six months. To these arbitrary descriptions, Potter adds a third, mid-way definition of 'pre-chronic' pain that is present between one and six months, as a way of highlighting the window of opportunity for the prevention of chronic pain.

In 1998 Crombie et al [21] carried out a survey into the factors responsible for causing chronic pain problems in 5130 patients attending outpatient pain clinics. They found that surgery contributed to the pain in 22.5% of patients, and trauma in 18.7%. Such long-term pain after surgery and trauma, it is claimed, is the cause of disability in a substantial number of patients. In a recent study of over 400 patients who had undergone surgery for repair of groin hernia [22], it was found that at one year post surgery 19% still had wound pain, and for 6% this was moderate to severe pain. It was suggested that the likelihood of developing such chronic wound pain could be predicted by the intensity of the acute postoperative pain. Any factor therefore that contributes to the continuing barrage of nociceptive signals may increase the risk of long-term hypersensitivity.

Wound dressings and pain

It is known that the type of wound dressing can play a role in the generation of localised pain [23]. Maintaining a moist wound surface may bathe nerve endings in fluid and reduce their stimulation [24]. If a wound dries out, particularly to the point where the dressing adheres to it, there will be increased sensitivity on movement and greater pain during dressing changes. This is an area where research is on-going, and is highlighting many factors that impact on the patients' experiences. The distinction between discomfort and pain, and what this means to any individual patient is a highly personal thing. For example, for radiotherapy-induced moist desquamation wounds, Mak et al [25] found that while gentian violet was actually better than a moist hydrocolloid dressing at reducing wound size and pain, it was rated significantly lower by the patients for dressing comfort and aesthetic acceptance.

Research by Briggs [26] however has shown that using a film dressing until suture removal, rather than a dry dressing, significantly reduces the duration of wound pain. Other factors besides the dressing impact on the degree of wound pain, for example, the method of wound closure has also been shown to play a role. Ranaboldo and Rowe-Jones [27] found that laparotomy wounds closed with staples were more painful than wounds closed with subcuticular polydioxanone sutures.

In Krasner's [23] model of chronic wound experience, a distinction is made between noncyclic acute wound pain, such as sharp debridement or drain removal, and cyclic wound pain such as daily dressing changes. She advocates the use of 'time-out' periods during painful dressing changes to allow the patient to rest and feel in control. As part of the overall strategy to minimise postoperative pain, each aspect of surgical and nursing care should be assessed and evidence based practices introduced. With the recognition of the potential to develop chronic pain problems, the level of priority afforded to pain management in the scheme of wider postoperative care now needs to be ethically re-evaluated in the light of such knowledge.

Analgesia - a balancing act

Analgesia, while essential, can have both beneficial and detrimental effects. Opioids such as morphine act on opioid receptors in the brain and spinal cord, but can also give rise to a range of adverse effects such as, in extreme cases, respiratory depression and drowsiness, but more commonly, nausea, dizziness and itching. One difficulty in maintaining an optimal environment for wound healing, that of correcting nutritional deficiencies [28], is that opioids directly stimulate the sensation of nausea and delay gastric emptying; this can compromise the patient's ability to return to oral fluids and diet. So that doses of opioid can be titrated to a particular patient's needs, 'patient controlled analgesia' (PCA) delivery systems have been introduced. Although this is only an alternative method of giving unpleasant drugs, it does at least offer patients control over the dose and timing of administration and the ability to respond quickly when in pain. The PCA pump is, however, only the mechanical component of patient controlled analgesia and for this technology to be truly effective, other factors must be taken into consideration and viewed with equal importance. These include the development of organised services, patient-monitoring protocols, pain assessment tools, the development and provision of educational support and clinical guidance.

It follows that once the structures for caring are in place, the machine component may not be strictly necessary; patient controlled oral morphine or the use of an intramuscular (i.m.) or subcutaneous opioid algorithm can also be the means for delivering high quality analgesia, provided the same level of attention is paid to pain assessment, monitoring, staff education and clinical support [29].

Cartwright et al [30] found that under the traditional intramuscular regimes of 735 patients, 80% received 0, 1, or 2 doses only in the postoperative period. The tradition of under-dosing analgesia by effectively restricting injections has meant that when patients are allowed to take increased doses of opioid via PCA, according to their own assessment of its effectiveness, the incidence of side effects may be seen to rise. This is further compounded when coupled with a reduction in the use of prophylactic antiemetics, previously given at the same time as an opioid injection. Using an i.m. protocol that is titrated to the patients' individual analgesic needs through pain assessment overcomes much of the limitations of traditional practice. Rosen et al [31] have shown that under such a regime, there is no difference between PCA and i.m. morphine in terms of pain relief, postoperative nausea and vomiting or satisfaction following major surgery.

Local anaesthetics can totally block all sensory input to the spinal cord, and can therefore prevent the central sensitisation that takes place. Studies have shown that establishing a regional local anaesthetic block preoperatively can lead to a reduced requirement for opioid analgesia postoperatively [32][33]. The gold standard of pain relief currently is the epidural blockade of sensory nerves, and in a meta-analysis of randomised controlled trials, Ballantyne et al [34] in 1998 provided convincing evidence that postoperative epidural analgesia can significantly decrease pulmonary morbidity.

An alternative to epidural blockade is the instillation of local anaesthetic into the thoracic paravertebral space. This has been shown to achieve pain relief over several thoracic dermatomes in patients with respiratory compromise secondary to thoracic or upper abdominal injury [35]. Coveney et al [36] demonstrated that it is possible to carry out breast surgery without general anaesthesia through use of a paravertebral block. Postoperatively it was found that opioid requirements and the incidence of nausea and vomiting were reduced, and patients were able to be discharged sooner from hospital. A paravertebral infusion of bupivacaine following thoracic surgery is superior to intermittent paravertebral bolus administration in offering pain relief at rest and on movement, and it is claimed that the plasma bupivacaine concentrations are safe [37]. However, a recent prospective randomised study [38] comparing epidural and paravertebral techniques following thoracic surgery found that whilst the paravertebral technique provided superior pain relief and had a greater effect on reducing the cortisol response to surgery compared to the epidural technique, the total dose of bupivacaine was nearly doubled in the paravertebral group. It was reported that occasional episodes of confusion arose in three patients, and though this was attributed to bupivacaine accumulation, it was felt that the paravertebral route could be used safely and routinely. It has previously been shown that plasma local anaesthetic levels are acceptable and that no mortality has been reported from this technique [39].

No analgesia technique should cause the patient to come to any harm, but ironically, epidural analgesia, which can deliver the most profound analgesia, presents an increased risk factor towards the development of pressure sores. Many surgical patients are already at high risk through factors such as age, immobility and dehydration, but the epidural block can further reduce blood pressure, cause motor block of the lower limbs, and block the sensory signals that warn of local tissue pressure damage. Even fit and active patients undergoing routine surgery can fall victim to this. Punt et al [40] describe the development of heel pressure sores in two women in their thirties; they and others [41][42][43] warn of the need for increased vigilance using evidence based pressure sore prevention techniques and adherence to hospital protocols. Provided the level of basic monitoring, education and staff support are well managed, continuous epidural analgesia has been shown to be a safe therapy [44], and is suitable to for use on general surgical wards [45].

A third approach to pain control is through the use of non-steroidal anti-inflammatory drugs (NSAIDs), which work peripherally by inhibiting the enzyme cyclo-oxygenase (COX), which converts arachidonic acid into inflammatory prostaglandins. They may also play a role in preventing central sensitisation [2]. They do not give rise to the same side effects as opioids with no evidence of respiratory depression, sedation or constipation. However, their wide anti-prostaglandin effect can lead to gastric ulceration, renal failure and a prolonged bleeding time due to impaired coagulation [46].

Recent developments in this field have led to the COX-2 specific NSAIDs that do not inhibit all prostaglandin synthesis, but are selective for the type that is involved in pain transmission. Even with this improvement, NSAIDs would not be sufficient to control severe pain, or pain on movement.

The concept of balanced, multimodal analgesia therefore opens up exciting possibilities for pain relief, and can take place in a number of ways. The elderly in particular can benefit from this approach, as reliance on a single analgesic agent may be more likely to give rise to serious adverse effects in this population [6][11]. By combining therapies that work on different parts of the pain pathway, the overall pain relief can be greatly improved. Many hospitals now have formalised the balanced analgesia approach into their prescribing guidelines.

An organised approach to pain management

Max [47] suggested that a number of background factors need to be addressed before improvements in pain control can take place. He recommended routine pain assessment, encouraging patients to talk about their pain, reviewing quality assurance treatment regimes and selectively modifying opioid regulatory practices. The Joint Colleges' 1990 report into pain after surgery [48] summarised the historical inadequacy of acute pain management and made recommendations for change. The report specifically identified the need for a named clinician to be responsible for education, protocol development, supervising the introduction of modern techniques and purposeful clinical audit.

The growth in acute pain services, and in numbers of acute pain nurses has been gradual over the past 10 years. Cambitzi [49], in 1996, specifically researched the role of the acute pain nurse, and found that there were 88 nurses carrying out all the activities described in the Joint Colleges' report. The recent Clinical Standards Advisory Group (CSAG) report into services for patients with pain [50] identified 220 acute pain services, and of the 144 studied in detail, 81% had an acute pain nurse working for the team. The influence of a dedicated pain nurse as part of an acute pain team has been shown to positively affect patient outcomes [51][52].

Guidelines and protocols are intended to raise the basic standard of care and provide consistency. Protocols prescribe methods of care in a less flexible way than guidelines [53], but neither are a substitute for personal knowledge and their thoughtful application is essential if they are to be safe and effective. Over the past 10 years a distinct body of 'acute pain' research evidence has become available, and there have been moves to disseminate knowledge through organisations such as the Pain Society and Pain Network. Grimshaw et al [54] noted that for guidelines to be valid they must be based on systematic reviews, national or regional development groups and have explicit links between their recommendations and scientific evidence. In the CSAG report [50], it was found that out of the many hospital guidelines produced by acute pain services in the UK, the breadth and quality of a number of these were inadequate. When properly designed and introduced, however, the use of prescribing protocols and treatment algorithms have been shown to decrease the level of pain on movement and on deep inspiration [55].


All nurses have a role to play in minimising pain and promoting health. The support of acute pain teams can now give much needed direction and consistency to strategies for pain management, and to continually research and develop new ones, but it is the daily contact that patients have with nurses that enables individual needs to be taken into account. The purpose of analgesia is not simply to make patients feel better, but to facilitate early ambulation, adequate oxygenation and nutrition and in doing so to reduce the stress response to surgery, encourage wound healing, and minimise the risk of developing chronic wound pain. Nursing care is the key to safe pain relief and therefore to optimal wound healing.

Glossary of pain terms

Acute pain team
A hospital based team consisting in the main of a consultant anaesthetist and clinical nurse specialist, supported by a clinical pharmacist, who take responsibility for developing pain management protocols, providing multidisciplinary education and training, conduct research and clinical audit to underpin developments in practice, and provide a clinical support service to all health care professionals and patients.
Balanced analgesia
The rational mix of analgesic drugs working on different parts of the pain pathway, to give maximum pain relief with minimal side effects from any particular drug.
The N-methyl-D-aspartate (NMDA) receptors in the dorsal horn of the spinal cord are an important part of the pain transmission pathway, and are implicated in the development of central sensitisation. Blocking the pathway at this point is possible with NMDA antagonist drugs such as ketamine.
A free nerve ending which detects noxious stimuli - chemical, mechanical and thermal. When tissue is damaged a variety of chemicals are released or synthesised, including histamine, potassium ions, bradykinin and prostaglandins. The body's own chemicals thereby stimulate these receptors in response to actual or potential damage, and this can be perceived as pain.
Non-steriodal anti-inflammatory drugs target cyclo-oxygenase, a key enzyme involved in the conversion of arachidonic acid into inflammatory prostaglandins. More recently, NSAIDs have been developed that specifically target a sub type, COX - 2, thereby reducing pain with fewer NSAID side effects.
A broad term encompassing natural and synthetic morphine-like compounds, known to inhibit the transmission of pain signals in the spinal cord and brain through their action at opioid receptor sites.
Preemptive analgesia
The practice of administering some form of analgesic prior to the stimulation of pain, in the anticipation of dampening the body's natural response to injury and the increased sensitivity to pain that follows.
Primary secondary hyperalgesia (Wind up)
Increasing sensitivity of neurons to a repeated stimulus can lead to a small stimulus being perceived as painful, resulting in 'primary hyperalgesia'. This can be accompanied by a secondary increase in sensitivity to stimulation in nearby tissues (i.e. uninjured tissue) that is perceived as being painful. Peripheral sensitisation results from the 'soup' of chemicals released from damaged tissues lowering the firing threshold of the nociceptors. Central sensitisation results from alterations in the processing of information from the periphery by the 'soup' of excitatory chemicals in the spinal cord released in response to continued pain. Untreated pain can result in permanent alterations in the central nervous system, giving rise to chronic pain problems in the apparent absence of peripheral tissue damage.


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