Chronic post-surgical (neuropathic) pain

Several risk factors have been identified for the development of CPSP, and there is no single dominant factor.⁴ The risk determinants can be classified according to the timing of the surgery, with factors prior to, during and after the operation contributing to the risk of developing CPSP.⁶

One of the leading risk factors for CPSP is the extent of tissue damage during surgery and injury to the nerves during dissection or retraction.⁴ Nerves are at continuous risk of contusion, stretching, division or entrapment from insults such as surgical retraction, diathermy or compression with bones.⁴ It may be possible to reduce the risk by giving consideration to the surgical approach, pain management and psychological predisposition.⁹ Psychological risk factors are another important consideration; negative affective constructs such as anxiety, depression, pain catastrophisation and general psychological distress have been consistently identified as risk factors for CPSP.¹¹

PAIN OUT, an international quality improvement and research network, is conducting research into peri-operative pain management in the clinical routine setting utilising a large registry.¹² Recent data from the project suggest that educational interventions may improve processes.¹²

Risk factors for development of CPSP⁵

Neuroplasticity (spinal sensitisation) following trauma may transform acute pain to chronic pain if not treated in a timely manner.⁴ However, the development of CPSP is thought to be multifactorial, involving the interplay of patient factors (e.g. psychology, genetics, pre-existing pain); the inflammatory response to tissue damage; and the surgical, anaesthetic and analgesic techniques applied.⁸

Main mechanisms causing surgical pain⁶

The signs and symptoms of peri- and post-surgical pain can be diverse because of the highly heterogeneous population and also because the amount of tissue injury and degree of inflammation varies widely by operation type and procedures utilised.³ Nerve injury during surgery has been implicated in the development of CPSP and some (but not all) patients with CPSP will present with evoked and spontaneous symptoms associated with neuropathic pain, such as allodynia and hyperalgesia.⁶ However, any link between nerve damage during surgery and the development of CPSP is complicated. Not all patients with nerve damage develop CPSP, and those who do develop CPSP do not necessarily have neuropathic pain.⁶ Neuropathic pain is associated with greater pain intensity and functional impairment compared to those with non-neuropathic post-surgical pain, and negatively impacts quality of life.^8,14

Symptoms that have been reported include:^5,7

Inflammatory and immune reactions after nerve damage to axons results in the release of neurotransmitters that act locally and in the spinal cord to produce hypersensitivity and ectopic neural activity; this contributes to central sensitisation.^6,15 Central sensitisation occurs when repetitive nociceptive stimuli result in altered dorsal horn activity and amplification of sensory flow. This can lead to persistent nervous system changes, for example, death of inhibitory neurons, their replacement with excitatory afferent neurons, and microglial activation. These changes lead to post-surgical neuropathic pain symptoms.⁶

According to the ICD-11, CPSP is defined as pain that develops in intensity after a surgical procedure and persists beyond the healing process, at least 3 months after the initiating event.² The pain must be localised to the surgical field or area of injury, projected to the innervation territory of a nerve situated in this area or referred to a dermatome or Head’s zone (regions of altered sensation on the skin, at relevant spinal cord segments, after injury/surgery).² Other causes for the pain and the possibility that it might be continuing from the pre-existing problem must be excluded.^2,16

Specific subdiagnoses included in the ICD-11 are chronic pain after amputation, spinal surgery, thoracotomy, breast surgery, herniotomy, hysterectomy, and after arthroplasty.²

Updated Werner and Kongsgaard criteria for diagnosis of CPSP²

1. The pain develops after a surgical procedure or increases in intensity after the surgical procedure.
2. The pain is of at least 3-6 months’ duration and significantly affects quality of life.
3. The pain is a continuation of acute post-surgery pain or develops after an asymptomatic period.
4. The pain is localized to the surgical field, projected to the innervation territory of a nerve situated in the surgical field, or referred to a dermatome.
5. Other causes of the pain should be excluded (e.g. cancer recurrence, infection).

Guidelines and recommendations

Prevention
Currently, there is no definitive way to prevent the occurrence of CPSP,³ and there is no agreed consensus on the prevention of chronification of acute post-surgical pain. Preventive strategies may include modification of surgical technique, good pain control throughout the peri-surgical period, and pre-surgical psychological intervention focusing on psychosocial and cognitive risk factors.³

Management
The International Association for the Study of Pain (IASP) and European Pain Federation (EFIC) recommend three essential strategic components in chronic post-surgical pain management: multimodal analgesia, procedure-specific analgesia and acute rehabilitation after surgery.¹⁷

Evidence-based guidelines support the use of local anaesthesia and peripheral or neuraxial regional analgesia as important techniques within a multimodal approach.¹⁷ Analgesic approaches should also be tailored to the specific surgical procedure as this can impact the type, severity and location of pain.¹⁷ However, analgesia is just one dimension of recovery – it alone is often not enough to support full recovery from surgery. Managing CPSP using a multimodal interdisciplinary approach may improve pain control.⁵

Click here to view the IASP/EFIC fact sheet on current management of post-surgical pain in adults.

Pharmacological treatments

Prevention
There is some evidence supporting the ability of a preventive, multimodal analgesic regimen to influence the development of CPSP; however, anaesthetic-mediated reduction in the incidence of CPSP has not been confirmed by any large, randomised, prospective trials.¹⁵

Management
As CPSP can result from pain from various mechanisms, pharmacological treatment combining various modes of action will result in improved analgesic properties and possibly reduced side effects and decreased use of opioid treatments.17 This is of particular relevance in CPSP, as the type of surgical procedure may result in pain arising from different mechanisms (e.g. musculoskeletal pain after orthopaedic surgery; visceral pain after abdominal surgery).¹⁷

Where warranted, opioids should only be used in carefully selected patients and prescribed at the lowest dose and shortest duration possible, with well-defined treatment goals and continuous evaluation.¹⁵ For further information on the responsible use of opioids, click here.

Systemic analgesics with proven or potential efficacy as components of multimodal analgesia for PDP¹⁴

Systemic analgesics

• Paracetamol/acetaminophen
• Non-selective and COX-2 selective NSAIDs
• Alpha-2-delta modulators
• NMDA-receptor antagonists
• Alpha-2 adrenergic antagonists
• Systemic local anesthetics
• Corticosteroids

^{COX-2: cyclooxygenase-2; NMDA: N-methyl-D-aspartate receptor; NSAID: non-steroidal anti-inflammatory drug, PSP: post-surgical pain.}