Perioperative management of nerve injury

What is perioperative peripheral nerve injury?

Perioperative peripheral nerve injury (PPNI) is defined as a new neurological deficit, motor, sensory or both, arising in association with surgery and anaesthesia, that was not present before the procedure. The reported incidence varies from 0.03% in large retrospective surgical series to transient paraesthesia rates of up to 8–15% in the days immediately following peripheral nerve blockade, although permanent injury beyond 12 months is rare, occurring in approximately 2–4 per 10,000 blocks [1–3]. General anaesthesia alone poses a risk of PPNI with a reported incidence of 13.8 per 100,000 versus 4.42 per 100,000 in regional anaesthesia alone, highlighting how challenging elucidating the cause can be [4].

Classification of nerve injury

The classification systems described by Seddon (1943) and Sunderland (1951) remain the standard for grading the severity of peripheral nerve injury and guiding prognosis [5, 6]. Seddon described three categories: neurapraxia, axonotmesis and neurotmesis [5]. Sunderland expanded this to five grades based on which anatomical layers, endoneurium, perineurium and epineurium, are disrupted, with a sixth mixed-pattern grade added later by Mackinnon [7]. In perioperative practice, the overwhelming majority of nerve injuries are neurapraxias (Sunderland Grade I), which carry an excellent prognosis (Table 1).

How should this patient be assessed?

The Regional Anaesthesia UK (RA-UK) algorithm for the initial management of postoperative unexpected/persistent neurological dysfunction provides a structured pathway for the management of symptoms following peripheral nerve blocks and surgery and is designed to assist with risk stratification and early recognition of patients requiring urgent attention [8].

Applied to this patient, the algorithm directs the clinician through the following steps:

Step 1: Is neurological dysfunction suspected? Yes. The patient has new-onset paraesthesia in the little finger which was not present before surgery, persisting beyond 18 hours.

Step 2: Review pre-existing neurological symptoms. The patient’s history of bilateral intermittent nocturnal hand tingling should be documented. Compare preoperative and postoperative deficits to determine whether this is genuinely new or an exacerbation of a pre-existing condition.

Step 3: Clinical assessment. Review the medical, anaesthetic and surgical records with the aim of finding a possible mechanism of injury or risk factor contributing to the lesion. Assess all functions of the nerve affected to determine the severity of the lesion and initial prognosis, in this case the ulnar nerve (motor: finger abduction, adduction, Froment’s sign; sensory: little finger and ulnar half of ring finger). Observe the skin for colour changes and swelling. Check distal pulses. Consider loosening bandages, splitting any casts and gentle repositioning of the limb, which can sometimes resolve the symptoms. A thorough examination and documentation are essential to help detect progression or remission of any lesion.

Step 4: Is the distribution consistent with the peripheral nerve block performed? The interscalene block was targeted at C5–C6. The little finger is C8–T1 territory. This suggests the deficit is unlikely to be a direct block-related injury and is more consistent with a positional, surgical or pre-existing cause.

Step 5: Is motor function affected, symptoms progressive or the deficit painful? Motor function is grossly intact, and the deficit is purely sensory and non-progressive. This classifies the lesion as non-urgent [8].

Management of a non-urgent lesion

For a non-urgent lesion as identified by the RA-UK/British Orthopaedic Association (BOA) algorithm, the following management steps are recommended:

Reassurance: The patient should be informed that most perioperative sensory neuropathies are neurapraxias that resolve completely within days to weeks. Follow-up is essential to monitor regression or progression.

Limb protection: Consider a sling or splint if appropriate and advise care for numb areas to prevent inadvertent pressure injury or burns.

Analgesia review: If neuropathic pain is present, consider referral to the acute pain service and initiation of neuropathic analgesic agents (e.g., gabapentin, pregabalin or amitriptyline).

Complex regional pain syndrome (CRPS) screening: Early involvement of the chronic pain team should be considered if allodynia or hyperalgesia is present, to exclude or treat CRPS.

Follow-up in 2–4 weeks: If the deficit persists, neurophysiology studies [nerve conduction studies (NCS) and electromyography (EMG)] and magnetic resonance imaging (MRI) should be considered, followed by referral for neurology consultation or to a nerve injury specialist.

When to seek urgent help

The RA-UK/BOA algorithm directs the clinician to seek urgent senior surgical and neurological consultation if motor function is affected, symptoms are progressive or there is unexplained severe pain and to exclude any reversible causes such as compartment syndrome, haematoma or bone fragment impingement. Urgent imaging (ultrasound or MRI) should be obtained, and surgical decompression may be required. Imaging must not delay surgical decompression when indicated. The differential diagnosis should always include post-surgical inflammatory neuropathy.

Relevance of the little finger

The interscalene block targets the C5–C6 nerve roots, which supply the shoulder and lateral arm (Fig. 1). The C8–T1 dermatomes, which supply the little finger and ulnar border of the hand, are typically spared by interscalene blockade (Fig. 2). Therefore, the new paraesthesia in this patient’s little finger is unlikely to represent a direct consequence of the interscalene block and raises suspicion for an alternative aetiology [11, 12].

Figure 1

Anterior view of the right brachial plexus, showing roots (C5–T1), trunks, divisions, cords and terminal branches. An interscalene block deposits local anaesthetic at the C5–C6 roots and upper trunk, which supplies the shoulder and lateral arm. The ulnar nerve arises from C8 to T1 via the lower trunk and medial cord, supplying the little finger and ulnar border of the hand – territory that lies outside the expected field of an interscalene block. Source: MissMJ, derived from Gray’s anatomy (1918). Public domain, CC0 [9].

Figure 2

Cutaneous innervation of the upper limb, anterior and posterior views, showing dermatomes of the peripheral nerves. The little finger and ulnar border of the hand are supplied by the ulnar nerve (C8–T1) – territory outside the C5–C6 field of an interscalene block. Source: Mikael Häggström, compiled from Gray’s anatomy (1918), plates 812 and 814. Public domain, CC0 [10].

Positional injury: The beach-chair position used for shoulder surgery can cause traction or compression of the ulnar nerve at the elbow or wrist, particularly if the forearm is flexed or the arm is positioned against a hard surface. The ulnar nerve is the most frequently injured peripheral nerve in the perioperative setting [13, 14].

Pre-existing subclinical neuropathy unmasked by surgery (double-crush phenomenon): This patient has diabetes mellitus and reports intermittent nocturnal hand tingling bilaterally, raising the possibility of a pre-existing subclinical ulnar neuropathy or carpal tunnel syndrome. The double-crush hypothesis holds that a nerve already compromised at one level is more vulnerable to a second insult at a distant site. Diabetes increases the risk of perioperative nerve injury by up to tenfold [11, 14].

Surgical factors: Direct or indirect surgical stretch or traction on the brachial plexus during shoulder manipulation, particularly during arthroscopic procedures with traction on the arm, may contribute to nerve injury [1, 11]. Shoulder surgery holds the highest risk of nerve injury with arthroscopic procedures contributing up to 10% of nerve injuries often related to surgical traction or port insertion [15].

Post-surgical inflammatory neuropathy: An increasingly recognised immune-mediated process triggered by the surgical stress response that can mimic other causes of PPNI and must be considered in the differential diagnosis [11].

Neurophysiological investigation

NCS and EMG are the principal diagnostic tools for characterising the location, severity and prognosis of peripheral nerve injuries. NCS assess electrical conduction along a nerve and can localise the site of the conduction block, while EMG examines the electrical activity within muscles to determine the pattern of denervation [11].

A key consideration is the timing of these investigations. Following axonal disruption, Wallerian degeneration is not complete for approximately two to three weeks. Neurophysiology studies performed within this window may give inaccurate results, as the distal nerve segment has not yet degenerated. Studies are therefore typically deferred for at least two to three weeks after the suspected injury [1, 11]. However, early studies can still be informative: the presence of pre-existing EMG abnormalities (e.g., from diabetic neuropathy or subclinical cubital tunnel syndrome) may help establish that the deficit was not caused by the anaesthetic or surgical intervention [11].

In this patient, if symptoms persist at two to four weeks, NCS across the ulnar nerve at the elbow and wrist, together with EMG of the intrinsic hand muscles, would be appropriate initial investigations. MRI of the elbow may be considered if a structural lesion such as a haematoma or ganglion cyst is suspected. Blood tests including glycated haemoglobin, vitamin B12, thyroid function and inflammatory markers should be checked to screen for systemic causes of neuropathy [1, 8].

Prevention strategies

Effective prevention of PPNI requires a systematic approach across the perioperative pathway:

Preoperative assessment: The American Society of Anesthesiologists (ASA) Practice Advisory for the Prevention of Perioperative Peripheral Neuropathies (2018) recommends identifying risk factors including diabetes mellitus, pre-existing neuropathy, peripheral vascular disease, alcohol dependency, obesity and male sex (for ulnar neuropathy) [13]. Furthermore, chemotherapy induced peripheral nerve injury has a prevalence of 68% in the first month after chemotherapy, 60% at three months and 30% at six months or more [16]. Patients should be assessed for their ability to tolerate the anticipated operative position, and pre-existing neurological deficits should be documented [13].

Intraoperative positioning: In the beach-chair position, the ASA advises limiting arm abduction to 90 degrees, positioning the upper extremity to minimise pressure on the postcondylar groove, and using padded supports. Periodic repositioning checks during prolonged procedures are recommended [13]. All positioning measures should be documented.

Safe regional anaesthesia practice: RA-UK, the American Society of Regional Anesthesia (ASRA) and the Royal College of Anaesthetists (RCoA) recommend ultrasound guidance as the primary imaging modality, avoidance of deliberate needle-to-nerve contact and intraneural injection, low pressure injection and adherence to maximum local anaesthetic dose recommendations [11, 12, 17]. The ‘Stop Before You Block’ campaign reduces wrong-sided block risk [17, 18]. Consent for regional anaesthesia should be individualised to the patient’s specific risk profile, particularly in those with pre-existing neuropathy [12]. There is also variation in the incidence of PPNI depending on the block performed with interscalene having the highest [19, 20].

Tourniquet management: Where applicable, inflation times should be minimised, and pressures individualised based on limb occlusion pressure [13].

Documentation and medicolegal considerations

Peripheral nerve injury is one of the most common causes of anaesthesia-related litigation regardless of mode of anaesthesia, and thorough documentation is essential for both patient safety and medicolegal protection [1, 13]. The clinical record should include the preoperative neurological assessment and any pre-existing deficits, the informed consent discussion with individualised risk, the regional anaesthesia technique (guidance modality, needle type, local anaesthetic agent and volume, patient response, ultrasound findings), intraoperative positioning details, and the timeline of all postoperative assessments and management steps taken [1, 11, 13].

Clear, honest and empathetic communication with the patient is a cornerstone of good management. Under the duty of candour, the patient should be informed of the suspected nerve injury, the likely causes, the anticipated course of recovery and the planned investigations. Involvement of the hospital’s clinical governance and risk management teams is advisable when significant nerve injury is identified [11].

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This narrative article is based on a fictional clinical vignette and does not describe a real patient or clinical encounter so consent for publication is not necessary. Images are used solely for illustrative purposes and are not related to the vignette. Where real patient images are included, the authors confirm that written informed consent for publication has been obtained for this purpose in accordance with the journal’s patient consent requirements.