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Radial nerve decompression

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Following compression injury to the radial nerve at the lateral humeral intermuscular septum, the expectation is for a full and spontaneous recovery of the radial nerve in 8-12 weeks. This is the typical duration of recovery for the segmental demyelinating conduction block (neurapraxia) following a”Saturday night palsy” but care should be taken when making such a diagnosis of neurapraxia (see Indications section).
The indications and technique for exploration and decompression of the radial nerve are detailed in the following section on radial nerve decompression.

Indications:
Closed high radial nerve palsy with no evidence of recovery by 12 weeks, pain at the site of injury or mapped to the superficial radial nerve territory and a positive Tinel’s sign at the lateral intermuscular septum. These findings are indicative of a prolonged conduction block or axonopathy injury (Sunderland grade 2 or 2+ injury).
Symptoms and examination:
Injury to the radial nerve may result in a neurapraxia , in which spontaneous recovery is expected within 10-12 weeks. The typical neurapraxic injury however effects only large and myelinated axons for fast pain, temperature, light touch perception and for motor function. The smaller unmyelinated autonomic fibres and slow pain (C fibre) functions are preserved and the patient will have some deep pressure awareness as well as normal skin sweating and none of the vasodilation seen when the nerve injury is more complete with loss of automonic unmyelinated fibres as well as the large myelinated fibres.
The patient should be carefully examined including an assessment for a positive Tinel’s sign – parasthesiae in the cutaneous territory of the nerve elicited when tapping gently over the site of potential injury. The presence of a Tinel’s sign is suggestive of a deeper nerve lesion, one with axonopathy (Wallerian degeneration). Persistent entrapment of a swollen and injured nerve at a tight septum may deepen the nerve lesion and result in more axonal death a longer recovery period and poorer final outcome.
Investigations:
Electrophysiological tests may confirm the site and severity of the nerve injury. Evidence of some denervation in the radial nerve innervated muscles on electromyography is evidence of a degenerative axonopathy lesion (at least Sunderland grade 2). Neurophysiology assessment should not replace repeated clinical examination. In the presence of a Tinel’s sign, neuropathic pain, autonomic disturbance and / or degenerative nerve changes on EMG, consideration should be given to urgent decompression of the radial nerve at the site of compression at the lateral intermuscular septum.
Neurophysiological tests and EMGs may help to confirm the site and depth of the nerve lesion however careful clinical examination will frequently provide this information and electrophysiology is not mandatory to proceeding with decompression but should be available intra-operatively for assessing residual function and providing an accurate prognosis.
Imaging of the nerve may be performed using ultrasound. Evidence of extrinsic compression may be seen with hourglass constriction of the nerve. A neuroma at the site of injury may be identified on imaging after 3 months. The decision to operate should be based on clinical assessment.
Non-operative management:
Most high radial nerve palsies associated with closed fractures of the humeral shaft are managed non-operatively with expectation of useful recovery. Many are conduction block (neurapraxic injuries). Low grade degenerative nerve lesions with axonotmesis but physical continuity of the nerve sheath may recover well as long as the surrounding environment is favourable and there is no entrapment of the nerve. Loss of radial nerve function after interventions such as fracture manipulation, splint application or following surgical stabilisation warrants emergent exploration. A decision for observation should be carefully considered and clinical follow up should be planned at regular intervals not longer than 6 weeks. Recovery is usually full and sudden by 3 months in a conduction block (neurapraxic) injury. Recovery is progressive and dictated by the branching anatomy of the radial nerve for recovering axonotmesis injuries. Exploration is indicated when there is deterioration under observation, failure to progress or pain.
The features of a degenerative nerve lesion (Wallerian degeneration) are:
Neuropathic pain
Tinel’s sign at the site of injury
Dry skin from loss of sudomotor function
Red skin from vasomotor paralysis
Flaccid paralysis with loss of deep pressure awareness and slow pain function
Even in a low grade neurapraxia there may be a need for nerve decompression:
Diagnosis
Deepening nerve lesion under observation
Decompression (haematoma or fracture fragments)
Displaced fracture fragments
Doubt
Delay in recovery
Development of dry skin
Debilitating nerve pain
Alternative operative management and contra-indications:
Late presentation with no evidence of recovery can be managed with exploration and neurolysis, however is such cases if there is no preserved function across the site of nerve injury excision and grafting is unlikely to be successful beyond 6- 9 months from injury due to the reinnervation distances involved to distal muscle targets. In such cases consideration should be given to grafting for pain (the sensory area supplied by the superficial radial nerve is not critical to hand function) and distal tendon or motor nerve transfers. Motor nerve transfers use expendable branches from the median nerve to transfer to key radial nerve and posterior interosseus nerve motor targets. Transfer must be accomplished by 9 months to allow reinnervation of these denervated muscles.
Radial nerve reconstruction should not be attempted in the presence of un-united fractures or active infection at the site of the humeral fracture.

The patient is under general anaesthesia in the supine position with the arm supported on an arm table. There should be no neuromuscular blockade and no local anaesthetic nerve blocks within the arm. A supraclavicular block will provide a segmental blockade and will not prevent intra-operative nerve stimulation in the distal nerve under test. The whole limb is prepared and draped leaving the shoulder exposed. A sterile tourniquet may be used for the distal exposure but I prefer to undertake the procedure without a tourniquet as the upper release is not possible with the tourniquet in situ and the nerve stimulation is unreliable after 30 minutes due to tourniquet induced nerve ischaemia.

The patient has had internal fixation of a transverse mid shaft fracture of the left humerus through a posterior approach. There was a radial nerve palsy at the time of injury and the nerve was found to be in continuity at surgery. Subsequently there was no recovery, a static Tinel’s sign was noted at the lateral intermuscular septum. There was no motor reinnervation at 6 months post fracture and EMGs confirmed that the muscles supplied by the radial neve demonstrated complete denervation. There were no motor unit potentials and no evidence of polyphasic responses (sign of reinnervation).
It was decided that the nerve should be explored at the site of maximum Tinel to confirm continuity and exclude a neuroma in continuity developing. The patient was consented for exploration, decompression and neurolysis +/- resection of a neuroma in continuity and nerve grafting. The other option for reconstruction is distal median to radial nerve transfers, however the patient wasn’t wiling to consider this option. He was counselled that if a graft didn’t demonstrate regeneration by 12 months he would require later salvage high radial tendon transfers.

The site of maximum Tinel should be marked at the time of the pre-operative assessment. The interval between the mobile wad muscles (Brachioradialis (BR), extensor carpi radialis longus (ECRL) and extensor carpi radialis brevis (ECRB)) and the biceps and brachialis is marked.

The skin is prepped and the left arm draped. The shoulder is positioned to the right and the hand to the left. The skin is incised and haemostasis is achieved using a bipolar diathermy. There is no tourniquet and it is important to maintain a bloodless field to avoid any iatrogenous damage to the radial nerve or its branches.

The interval between brachialis and BR is identified. In this case there is a thin fat streak along the loose fascial plane. Typically there are cutaneous nerves that exit this interval. The nerve branches should be identified and tagged with sloops which can then be used to gently retract the nerves as they are followed into the interval back to the main radial nerve trunk. The first branch usually identified is the posterior cutaneous nerve of the forearm. In this case the blue tag is an anterolateral nerve branch to the skin over the distal lateral arm. Gently pulling on the nerve identifies the point where it enters the dermis with a small distortion of the skin (the tug sign).

The intermuscular plane is developed by releasing the deep fascia. The plane is vascular with small branches passing from the profunda artery to the adjacent muscles. Haemostasis should be maintained at every stage of this procedure.

A – Brachialis
B – Brachioradialis
Within the interval the distal radial nerve is identified and tagged with a red sloop. The self-retaining retractors should be placed with care to avoid direct or traction injury to the radial nerve or any of its branches.

1 – Cutaneous branch of radial nerve passing superficial to brachialis
2 – Radial nerve
3 – Lateral intermuscular septum
The radial nerve is tethered and flattened proximally with external scar at the level of the lateral intermuscular septum. This was the point of maximum Tinel on clinical examination.

Progressive external neurolysis of the radial nerve is performed as the nerve is traced proximally. Extreme care should be used when dissecting from distal to proximal along a branching nerve as it is easy to dissect in the axilla between branch points and the main trunk and inadvertently section a side branch as the dissection proceeds proximally. To avoid this risk any branch identified should be tagged with sloops and then neurolysed separately to the main trunk before proceeding proximally along the main trunk. The nerve to brachialis fron the radial nerve is identified and tagged with a yellow sloop. Accompanying vessels must be cauterised with bipolar diathermy to achieve this exposure. The brachialishas a dual innervation. The medial 2/3 is supplied on the medial side of the armin the interval between biceps and brachialis by the terminal motor branch of the musculocutaneous nerve as it divides to the motor branch to brachialis and the lateral cutaneous nerve of the forearm. The lateral 1/3 of brachialis is supplied through the radial nerve. The internervous plane for the anterolateral approach to the humerus involves splitting the brachialis to preserve its nerve and blood supply.
Blue sloop – Cutaneous nerve
Yellow sloop – Motor branch to brachialis
Red sloop – Main radial nerve trunk

Here the radial nerve is gently lifted in a red sloop to demonstrate the scar tether and flattening of the nerve as it exits the lateral intermuscular septum.

Neurolysis is continued in a proximal direction. The epineurium is fibrotic and oedematous suggesting there has been significant trauma with bleeding and fibrosis both around and within the nerve at the time of injury. The lateral intermuscular septum is released. Accompanying veins are engorged at this point suggestive of proximal compression. The veins are cauterised with bipolar diathermy. Bipolar is used at the lowest possible setting to prevent any stimulation of the nerve.

The lateral intermuscular septum is being released. A small section of the fascia is excised to triceps muscle so that there are no residual compression sites.
P – The edge of the humeral plate is visible. The nerve is compressed against it by the intermuscular septum.
S – Intermuscular septum.

Cautery of accompanying veins and branches from the profunda artery.

Excision of the septum.

Releasing scar deep the radial nerve as if contacts the humerus at the distal spiral groove.

The nerve is free at the septum. A Mixter is passed deep to the nerve demonstrating no compression.

A microsurgical background is placed behind the radial nerve and its branches to demonstrate the anatomy. The blue sloop is a cutaneous nerve, the yellow sloop a motor branch to brachialis and the red is around the main radial nerve trunk.
Nerve stimulation should be performed to assess for residual function. Prior to neurolysis there was no stimulation in the motor radial nerve from 0.2mA (normal threshold) to 5mA.
Following the neurolysis and decompression the brachialis stimulated at 0.2mA, BR at 0.2mA, ECRL at 0.4mA and ECRB at 1mA.

The stimulation thresholds suggest that there is some continuity of themotor component of that there has been some regeneration and the neurolysis has enabled a residual conduction block to these fascicles to be reversed. Further regeneration to the digital extensors is now possible and the patient will be monitored in clinic. There is no neuroma to resect. If the outcome remains poor, tendon transfers are still available as a salvage procedure after 12 months.

The deep wound is closed with interrupted absorbable sutures.

A subcuticular absorbable suture is used to close the skin.

Local anaesthesia is administered. If the surgeon wants to asses motor function immediately post-operatively I would advise that the skin adges are infiltrated with local anaesthesia and an indwelling nerve catheter is placed as the nerve exits the spiral groove. A bolus of local anaesthetic can then be place deep around the nerve after assessment in the recovery room.

The wound is supported by steristrips and an occlusive dressing is applied. A supportive wool and crepe bandage provides moderate compression to prevent haematoma formation.

The patient can be discharged the same day with dressing reduction and wound inspection at 1 week. Further clinical review at 6 weeks should assess any motor or sensory Tinel and a progression of Tinel’s sign may be obvious at this stage.

failure of progression and muscle strengthening can be managed with salvage tendon transfers after 12 months. The standard transfers I use are pronator teres for wrist extension (ECRB), flexor carpi radialis to finger extensors and palmaris longus to the extensor pollicis longus.

The decision to explore this nerve was because of the doubt about the diagnosis, the need for decompression, delay in recovery and the worry that the nerve lesion might be deepening (axonal injury, recovering but no clinical recovery due to extrinsic scar). Further delay would most likely result in no functional recovery and nerve death. traditional teaching suggests that all low energy radial nerve palsies recover well. I would advise that the radial nerve should be explored in the following situations:
Saturday night palsy with pain, Tinel’s sign or autonomic disturbance in the radial nerve territory
Low energy humeral fractures where the palsy develops after fracture manipulation or application of a cast
Low energy humeral fractures where the nerve is not recovering in line with expectation
Onset of radial palsy after surgical exposure for plating of the humerus
High energy injuries at the time of internal fixation
I would caution against nailing of the humerus as part of poly trauma management. I have seen cases where the nerve was interposed in the fracture site and has been reamed. Care must also be taken when positioning an external fixator in damage limitation major trauma surgery as the anatomy is often distorted and I would advise that the distal pins are inserted with a mini-open technique where the lateral supracondylar ridge is exposed prior to pin placement to avoid injury to the radial nerve or its branches.

References:
Bishop J, Ring D. management of radial nerve palsy associated with humeral shaft fracture: A decision analysis model. J Hand Surg Am. 2009 Jul-Aug;34(6):991-6.e1. doi: 10.1016/j.jhsa.2008.12.029. Epub 2009 Apr 10
Ray W, Mackinnon S. Clinical outcomes following medial to radial nerve transfer. J Hand Surg Am. 2011; 36: 201-208


Reference

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