Pain Management in Pharmacy Practice

Written by Donna Cosgrove PhD MPSI

Donna graduated with a BSc in Pharmacy from the Royal College of Surgeons in Ireland. She then returned to university to complete a MSc in Neuropharmacology. This led to a PhD investigating the genetics of schizophrenia, followed by a postdoctoral research position in the same area. Currently Donna works as a pharmacist in Galway, and as a clinical writer.

Overview

60 Second Summary

60 Second Summary

Pain management represents a major component of community pharmacy practice, with widespread use of OTC analgesics.

Effective management requires distinguishing acute from chronic pain and recognising the biological, psychological, and social factors that influence symptom presentation. Acute pain arises from tissue injury and inflammatory processes, whereas chronic pain reflects persistent nociceptive, neuropathic, or nociplastic mechanisms and is associated with significant functional and psychosocial burden.

Evidence indicates that ibuprofen/paracetamol combinations and fast-acting NSAIDs offer the most effective OTC relief for acute pain, while topical NSAIDs provide comparable efficacy with lower systemic risk. Chronic pain management increasingly emphasises non-opioid pharmacological options and non-pharmacological interventions, including exercise therapy, psychological support, TENS, and acupuncture.

Prescription data show rising analgesic use in Ireland that may be mitigated by increased availability to services that offer non-pharmacological management of pain. Multimodal approaches integrating medication with targeted physical and psychological therapies remain essential for safe, effective pain management.

Introduction

Approximately 47% of EU consumers report using an over-the-counter (OTC) analgesic at least once weekly within the last month,1 positioning pain management as one of the main reasons for consultation within community pharmacy practice.2 An effective OTC analgesic should demonstrate satisfactory analgesic efficacy in a substantial proportion of patients, exhibit a rapid onset of action, and provide an adequate duration of effect. Self-care -pain management undertaken without prescription -remains appropriate for numerous minor, self-limiting conditions such as bruising, viral upper respiratory tract infections, minor wounds, ear pain, fever, headache, dysmenorrhoea, mild musculoskeletal pain, sinusitis or cold/flu symptoms, sprains and strains, and teething or dental discomfort. However, the extensive range of OTC analgesic options frequently complicates patient decision-making.3 Consequently, pharmacy professionals must be equipped to deliver evidence-based recommendations and identify red flags warranting referral for clinical evaluation or escalation to prescription-only analgesia, particularly when pain persists or deteriorates beyond the expected clinical trajectory.

Acute pain is defined as pain lasting less than 12 weeks and

may arise secondary to tissue injury, nerve insult, or surgical intervention. It is commonly associated with inflammatory responses, including swelling and reduced function, and may substantially impair activities of daily living and health-related quality of life.4 A wide range of analgesic interventions are available, including paracetamol, non-steroidal anti-inflammatory drugs (NSAIDs), opioids, complementary therapies, and herbal preparations. Within each class, multiple formulations exist, e.g. rapid-release tablets, effervescent preparations, liquid formulations, and fixed-dose combinations, which may influence onset and extent of analgesic effect.

Chronic pain persists beyond the expected period of tissue healing, typically exceeding 3-6 months, and is associated with considerable functional limitation and psychosocial burden. Established non-modifiable risk factors include female sex, age greater than 65 years, high-intensity acute pain, and lower socioeconomic status. Modifiable psychological risk factors (e.g. elevated pain catastrophising, heightened pain-related fear, and increased symptoms of anxiety, depression, or post-traumatic stress disorder) also contribute to chronic pain development and persistence.5 Chronic pain prevalence across Europe is high, with reported rates ranging from 12% to 48%, and an estimated prevalence of 43.5% in the UK. Selection of appropriate analgesic strategies requires consideration of both the temporal profile of pain (acute versus chronic) and the underlying nociceptive mechanism, including degenerative pathology (e.g. osteoarthritis), traumatic injury, or muscle spasm.4

Table 1. Management considerations based on pain type: acute vs. chronic

Nociception and Types of Pain

Nociception refers to the neural processes encoding actual or potential tissue damage. It arises from the activation of primary afferent nociceptors (unmyelinated C-fibres and thinly myelinated Aδ-fibres) which remain quiescent under normal physiological conditions and fire in response to noxious mechanical, thermal, or chemical stimuli. Once activated, signals are transmitted through peripheral afferents to the dorsal horn of the spinal cord and relayed via ascending pathways to supraspinal centres. Motor and autonomic responses are mediated through descending pathways projecting back to the spinal cord.

Pain, in contrast, represents the conscious perception of this activity and incorporates sensory, emotional, and cognitive dimensions. The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience

associated with, or resembling that associated with, actual or potential tissue damage.” Pain is inherently subjective and influenced by biological, psychological, and social factors. Notably, pain intensity does not reliably correlate with the extent of nociceptive input or injury severity; psychosocial determinants often account for a greater proportion of variance in pain reports. Early identification of such factors is therefore essential to prevent progression to persistent pain states.

Aδ-and C-fibres terminate in specialised free nerve endings distributed across the skin, musculature, joint capsules, bone, and some visceral organs. Superficial structures are typically innervated by both fibre types, whereas deep somatic tissues such as muscle and joints are predominantly supplied by C-fibres. Acute inflammatory pain is generally sharp, short-lived, and mediated largely by Aδ-fibres. Chronic inflammatory pain, which persists beyond the expected healing period, is primarily C-fibre mediated. Additionally, “silent” nociceptors-abundant in visceral tissues-do not respond to mechanical stimuli under normal conditions but become sensitised during inflammation by locally released chemical mediators.

Neuropathic Pain

Neuropathic pain arises from lesions or diseases affecting the somatosensory nervous system and is frequently associated with allodynia (where pain is caused by a stimulus that does not normally provoke it) and spontaneous pain. Common aetiologies include metabolic disorders (e.g. diabetes), trauma, neurotoxins, malignancy, infectious processes (e.g. herpes zoster), and degenerative neurological disease. Structural injury such as compression or stretch alters axonal neurochemistry and promotes hyperexcitability of affected neurons. During neuropathic pain, nociceptors demonstrate a dynamic expression of ion channels, e.g. sodium channels, which are the major channels involved in neuronal excitability. Neurogenic inflammation occurs when inflammatory mediators, (e.g. substance P, calcitonin gene-related peptide, neurokinin) are released locally by the afferent neurons, which further amplifies peripheral and central sensitisation.

Inflammatory Pain

Inflammatory pain is a natural biological response to harmful stimuli that helps eradicate the necrotic cells and initiate the tissue repairing process. Neutrophils are usually the first respondents

Hyperalgesia and Peripheral Sensitisation

Hyperalgesia refers to an increased pain response to a stimulus that is normally painful. Primary hyperalgesia occurs at the site of injury and is predominantly due to peripheral mechanisms, whereas secondary hyperalgesia and allodynia arise from central sensitisation within the CNS. Prostaglandin E2 (PGE2), generated through COX activation, is a major mediator of these processes.

Repeated noxious stimulation leads to reduced activation thresholds and increased firing of primary afferents. The collective release of inflammatory mediators at the injury site, often described as the “inflammatory soup” (ATP, bradykinin, 5-HT, NE, PGE2, NGF, substance P), drives sustained sensitisation through intracellular signalling cascades (e.g., cAMP/PKA, PKC/DAG). The net effect is heightened nociceptor responsiveness, producing amplified pain perception even when stimulus intensity remains unchanged.

Most Effective OTC Analgesia

A Cochrane review examining the efficacy of OTC analgesics in acute pain4 concluded that simple, inexpensive, and widely

accessible analgesics provide clinically meaningful pain relief for many patients presenting with conditions such as dental pain, sprains, and strains. This is frequently described by the Number Needed to Treat (NNT), which is the average number of patients who need to be treated with a particular therapy for one additional person to achieve a defined beneficial outcome compared with a control (usually placebo). A lower NNT indicates a more effective treatment, e.g. an NNT of 2 means that for every two people treated, one will experience meaningful benefit who would not have benefited with placebo. Among OTC products available in Ireland, the most effective options for acute pain were combination ibuprofen/paracetamol formulations (400 mg/1,000 mg and 200 mg/500 mg), which relieved pain in approximately 70% of patients and demonstrated an NNT of <2. Fast-acting ibuprofen formulations were also highly effective, achieving pain relief in over 50% of patients with an NNT of 2-3. Paracetamol was less effective comparatively, benefiting around 40% of patients with an NNT between 3 and 5. Notably, the review found no evidence supporting the efficacy of low-dose codeine-containing products for acute pain.

The common advisory to take ibuprofen or other NSAIDs with food was also challenged in this review. NSAIDs are absorbed more rapidly on an empty stomach, which may enhance their analgesic effect. This has been reflected in updates to some product information leaflets: for example, the PIL for Nurofen Express Maximum Strength Tablets now advises administration with water only, without reference to food.9

Topical NSAIDs were also shown to provide substantial pain relief in acute conditions such as sprains, strains, and overuse injuries, with efficacy likely comparable to oral NSAIDs.10 A 2020 guideline developed by the American College of Physicians and the American Academy of Family Physicians11 similarly identified topical NSAIDs as among the most effective therapeutic options for acute, non-low back musculoskeletal pain in adults. Importantly, topical formulations did not demonstrate a significant increase in adverse effects. Diclofenac, ibuprofen, and ketoprofen gels achieved

significantly higher rates of ≥50% pain reduction than placebo, with diclofenac Emulgel showing the most favourable NNT (1.8). Diclofenac medicated plasters also performed well (NNT 3.2), while ibuprofen gel demonstrated an NNT of 3.9 based on marked improvement or complete symptom remission.10 Oral NSAIDs and paracetamol both offered pain reduction; however, the guidelines noted that oral NSAIDs were associated with increased gastrointestinal risk.11

Mechanisms of Action of Analgesics

A range of pharmacological classes are used in the management of acute and chronic pain, each acting through distinct molecular pathways that modulate nociceptive processing and inflammatory responses.

Paracetamol reduces prostaglandin (PG) synthesis from arachidonic acid through COX-1 and COX-2 inhibition and is thought to exert its primary analgesic effects centrally. Owing to its favourable tolerability and modest efficacy, it is widely used alone or in combination with NSAIDs.12

NSAIDs remain foundational in the treatment of many painful conditions, including osteoarthritis and chronic low back pain. They inhibit the COX-1 and COX-2 enzymes, which convert arachidonic acid into prostaglandins and thromboxanes. Their use is limited by gastrointestinal, renal, and cardiovascular risks, necessitating appropriate patient counselling and monitoring.

COX-2 selective inhibitors (e.g. celecoxib, etoricoxib) provide analgesia comparable to traditional NSAIDs with fewer gastrointestinal adverse effects but may increase cardiovascular risk with long-term use. COX-2 is expressed in inflammatory cells, damaged tissue, synovium, vascular endothelium, and the CNS.

Topical NSAIDs (e.g. diclofenac) are effective for localised chronic or acute musculoskeletal pain and are preferred when oral formulations are contraindicated because systemic exposure is significantly lower.

Opioids act as agonists at μ, δ, and κ receptors in the brain, spinal cord, and peripheral tissues. Key adverse effects include respiratory depression, sedation, nausea,

vomiting, and constipation. They are no longer recommended as first-line therapy for chronic primary pain; short-to medium-term use may be appropriate in certain patients.13 Among patients with chronic pain receiving opioids, estimated rates of misuse range from 21-29%, and addiction from 12-18%.

For neuropathic pain, preferred therapies include certain antidepressants, antiepileptics, topical lidocaine, and topical capsaicin. In nociplastic pain (e.g. fibromyalgia), non-pharmacological approaches are prioritised, though TCAs, SNRIs, and gabapentinoids may provide benefit.4

Anticonvulsants (e.g. gabapentin, pregabalin, carbamazepine) are used for neuropathic pain conditions including diabetic neuropathy, post-herpetic neuralgia, and spinal cord injury pain.12 Gabapentinoids bind to the α2δ subunit of voltage-gated calcium channels, reducing calcium influx in hyperexcitable neurons. Carbamazepine is thought to act by binding to and stabilising inactive sodium ion channels, and modulating the release of glutamate and GABA.

Tricyclic antidepressants (e.g. amitriptyline, nortriptyline) exhibit analgesic effects independent of antidepressant activity, believed to stem from presynaptic inhibition of serotonin and noradrenaline reuptake.

SNRIs (e.g. duloxetine) are effective in diabetic neuropathy, fibromyalgia, osteoarthritis, and low back pain. SSRIs may be considered in fibromyalgia but generally lack evidence of efficacy in neuropathic pain.

Musculoskeletal agents such as baclofen and tizanidine are commonly used adjuncts. Baclofen, a GABA-B agonist, likely exerts its effects through inhibition of spinal reflexes, though the mechanism is not fully defined. Tizanidine (and clonidine) act as central α2-adrenergic agonists producing muscle relaxation via presynaptic inhibition. This reduces dorsal horn neuronal activity and inhibits substance P release, producing analgesia and sedation.

Anxiolytics, particularly benzodiazepines, may help manage anxiety associated with acute pain flares but should be used only short-term;

longer-term anxiety management should shift to safer agents such as antidepressants.

Topical lidocaine patches (applied 12 hours on/12 hours off) are useful for localised nociceptive pain, neuropathic pain, and post-herpetic neuralgia.

Ketamine, an NMDA receptor antagonist, provides analgesia at sub-anaesthetic doses by reducing central sensitisation and attenuating excitatory pain signalling.14 Evidence for its use in chronic or neuropathic pain remains limited. An RCT in cancer-related neuropathic pain found ketamine to be comparable with placebo, though subgroups-particularly those with features of central sensitisation-may benefit.15

Glucocorticoids (e.g. prednisolone) are potent anti-inflammatory agents that suppress gene transcription of pro-inflammatory mediators while promoting transcription of anti-inflammatory proteins. These effects are mediated by glucocorticoid receptor binding and nuclear translocation.16

Trends in Prescription Analgesia

A cross-sectional study from England and Ireland examined trends in prescription analgesic use between 2014 and 2022.17 Prescribing data for England were obtained from NHS sources, while Irish data were derived from the Primary Care Reimbursement Service (PCRS) for items dispensed under the General Medical Services (GMS) scheme. The analysis included opioids, systemic NSAIDs, paracetamol, topical analgesics, antimigraine medicines, and agents used for neuropathic pain.

In Ireland, analgesic dispensings per 1,000 GMS population increased from 3,388.6 in 2014 to 4,316 in 2022. Most individual opioids showed increased dispensing (with the exception of hydromorphone, dihydrocodeine, and tramadol). Use of topical analgesics, low-dose amitriptyline, gabapentin, pregabalin, and paracetamol also rose. In contrast, NHS data demonstrated a reduction in analgesic dispensings per 1,000 population over the same period. Despite these divergent trends, the proportional distribution of analgesic classes remained relatively stable across both settings. Codeine was the most commonly dispensed opioid in

England (48% of opioid items) and Ireland (45%), primarily for analgesic rather than antitussive use.

The World Health Organization defines the Defined Daily Dose (DDD) as the assumed average maintenance adult dose for a drug’s principal indication. Using this metric, Irish DDDs for all analgesics increased from 116 to 147.6 per 1,000 GMS population per day between 2014 and 2022; opioid DDDs alone increased from 33 to 40.3. The largest relative growth was observed for tapentadol (389%) and low-dose amitriptyline (194%). In England, DDDs declined from 97 to 80.6 per 1,000 population per day over the same timeframe. Subgroup analysis of English data showed substantially higher analgesic dispensing in areas of greater socioeconomic deprivation.

Some of the observed differences between countries reflect differences in the underlying populations sampled. Irish GMS data disproportionately represent older adults and individuals with socioeconomic disadvantage, i.e. two demographic groups known to experience higher rates of pain, whereas NHS data encompass a broader demographic. Evidence-based NICE guidance for chronic pain recommends first-line non-pharmacological interventions such as structured exercise, psychological therapies, acupuncture, and TENS. While these services are available within the NHS, access for GMS patients

in Ireland is often more limited, and waiting times can be prolonged, potentially contributing to higher reliance on prescribed analgesics.

The Organisation for Economic Co-operation and Development (OECD) incorporates opioid and NSAID prescribing within its 11 quality indicators for prescribing in primary care.18 Despite increasing opioid prescribing in Ireland, a recent study examining prescription drug-related harms from 2010 to 2020 found that opioid-related harm remained relatively stable over time.

OTC sales of low-dose codeine preparations are also substantial: an international comparison ranked Ireland and England second and fourth highest, respectively, among 31 countries.19

NICE guidelines for chronic pain management20 include the following recommendations:

 A person-centred assessment -including biological, psychological and social contributors.

 Non-pharmacological first-line therapies for chronic primary pain, such as supervised exercise programmes, psychological therapy (e.g. CBT), and, in some cases, acupuncture.

 Cautious use of medications -with careful consideration of benefits vs harms, especially for opioids or long-term pharmacotherapy.

 Importance of a shared care plan, ongoing re-evaluation, and involving patients in decision-making.

Non Pharmacological Pain Interventions

Multimodal analgesia, i.e. using more than one analgesic class in combination with non-pharmacological strategies, can enhance pain control while limiting reliance on any single agent and reducing the adverse-effect burden associated with higher doses of individual drugs.5 This synergistic approach is particularly valuable when addressing complex or persistent pain.

Musculoskeletal pain is frequently driven by muscle spasm. Thermal therapies can reduce muscle shortening associated with trauma or underlying neuromuscular or skeletal conditions.8 However, evidence supporting these modalities remains limited due to a lack of large, high-quality clinical trials.

Cryotherapy decreases bleeding, vasodilation, inflammation, oedema formation, and pain perception. The PRICE protocol (protection, rest, ice, compression, elevation) is commonly applied for acute sports injuries and some chronic presentations.

Heat therapy increases collagen extensibility, blood flow, metabolic rate, and facilitates resolution of subacute or chronic inflammation. Heat combined with stretching can reduce muscle contraction, joint

Acupuncture, an invasive technique involving insertion of fine needles at defined points, must be performed by trained practitioners. While evidence does not show superiority over NSAIDs for certain pain conditions, acupuncture may benefit individuals with back or neck pain, knee pain associated with osteoarthritis, postoperative pain, and arthralgia related to aromatase inhibitor therapy.

Therapeutic exercise, including passive mobilisations, active or assisted movements, stretching, and relaxation techniques, can complement other pain management strategies. Early management of musculoskeletal pain prioritises immobilisation, compression, and cryotherapy. As pain subsides, gradual mobilisation prevents chronic muscle shortening and secondary pain generation.

Psychological factors significantly influence pain perception. Interventions such as cognitive behavioural therapy (CBT), education, reassurance, stress-reduction training, and counselling can improve coping and reduce symptom burden. CBT, including digital/online formats, has demonstrated benefit in pain relief. Meta-analyses show that music therapy reduces anxiety and improves sleep in chronic illness, with additional evidence of pain reduction and decreased opioid requirements.5 Similarly, systematic reviews of aromatherapy report anxiolytic and analgesic effects.

References available on request