Chapter 32 Reanimation of the Paralysed Elbow
Conditions resulting in paralysis at the elbow
Absent muscle may result either from trauma destroying or damaging the muscle beyond functional restitution, or from congenital abnormalities including arthrogryposis multiplex congenita.1,2 As we examine the treatment of each of these causes of loss of elbow flexion, a number of treatment techniques will emerge and it will become apparent that all techniques have some application in most conditions. Choosing between these techniques will depend partly upon the repertoire of the surgical team and their experience, and upon patient preference influenced by their age, other conditions, and important factors such as appearance. For such a simple motion, elbow flexion can be remarkably difficult to achieve and it is not uncommon in the senior author’s practice for more than one technique to be employed in a single patient.
Prior to reanimating any elbow, consideration must be given to the passive range of motion. This need not be full or normal; indeed following the restoration of elbow flexion, some degree of contracture is desirable to facilitate the initiation of motion (by virtue of the increased moment arm of muscle action at rest). Similarly full active flexion is not always essential even for feeding. Many children with obstetric brachial palsy develop the ‘trumpet’ sign3 by which in order to get the hand to the mouth the humerus is abducted to 90° or more prior to completion of elbow flexion. This activity compensates for the absence of active external rotation at the shoulder but also excludes gravity from the elbow articulation making flexion easier. It also brings the prehensile radial border of the hand to the mouth in full supination, which is important for those children who have lost pronation.
In dealing with restoration of elbow movement it is important not to consider the elbow in isolation. Too often in adult brachial plexus injury the senior author sees patients in whom elbow flexion has been restored without addressing the instability, or lack of active external rotation, at the shoulder. This results in an elbow that flexes up the anterior chest wall to the anterior neck but does not support a hand that can be positioned in space. Whilst this simple function in a badly paralysed limb can be useful for augmenting brachiothoracic grasp, it is important when planning any brachial plexus reconstruction to consider the implications at the shoulder which may itself be managed by either reanimation or arthrodesis;4,5 a topic that is beyond the scope of this chapter. Furthermore, elbow flexion is valuable in the context of positioning a competent hand in space and so its place in the restoration of function of an upper limb whether from brachial plexus palsy, congenital defects or widespread trauma, must be considered at the outset. A coherent programme with6,7 an appropriate timescale should, therefore, be agreed with the patient at the start of reconstruction and rehabilitation.
Specific circumstances of lost elbow flexion and methods of treatment
Acute denervation
Because two nerves supply the three muscles responsible for elbow flexion, complete neurogenic loss of flexion is only usually associated with injuries to the upper trunk of the brachial plexus especially proximal to Erb’s point at the C5–C6 level. Isolated paralysis of the anterior compartment of the arm may result from an injury to the musculocutaneous nerve distally either through traction or more commonly as a result of a penetrating injury including iatrogenic causes. As with any acute denervation of the muscle the underlying principle is early restoration of nerve continuity. Where there has been a penetrating wound the diagnosis is obvious and exploration is mandatory wherever possible. Problems most commonly arise in the closed injury where the temptation is to ‘wait and see’. A full discussion of the indications for brachial plexus surgery is not appropriate here but we make some observations. The principle of ‘wait and see’ rests on the concept that a neurapraxia may be responsible for loss of nerve function and that this may be fully recoverable. Furthermore, some will argue, that even if the injury is a Sunderland Grade II or III8,9 surgical exploration would reveal a nerve in continuity and that given that the prognosis is uncertain, resection and grafting would not be appropriate. This is all well and good, but against this must be considered the fact that loss of nerve continuity even at the axonal level results in distal end-organ decay and proximal central cell death, and that these consequences are inversely related to the period since injury. For these reasons some surgeons set an arbitrary time of 3 months to assess if recovery is occurring. This would be appropriate particularly if one is able to monitor the progression of a Hoffman–Tinel phenomenon or there is strong circumstantial evidence (from history of low kinetic energy transfer or evidence from scans of thecal integrity) that a neurapraxia is likely. Recovery from a true neurapraxia is not sequential from proximal to distal but is sudden and anatomically more random as the functional conduction blocks recover.
In addition to the necessary investigations of electromyography (which can be useful in identifying neurapraxia) and nerve conduction studies10 (which are less useful because of the difficulty in achieving compound nerve axon potentials or sensory nerve axon potentials in the deeply placed musculocutaneous nerve), in the absence of scan evidence of avulsion, exploration of the upper trunk in the acute phase after injury in experienced hands can be invaluable. If the brachial plexus is explored within a week of injury the nature, extent and severity of the damage are immediately apparent. In the rare case that a lesion in continuity is so innocuous as to leave doubt about resection and repair, nothing is lost after a simple exploration and one can revert to a ‘wait and see’ policy. However in the vast majority of cases we have explored in such circumstances, the indication for treatment has been unequivocally apparent.11 This principle of open exploration at an early stage (especially in the first week before fibrosis clouds the picture) has guided us over 20 years in the management of upper trunk injuries and infraclavicular injuries to the brachial plexus. The only exception to this in adults has been the prolonged crush injury resulting from dislocation of the shoulder and delayed relocation where early exploration is unlikely to yield useful information since traction and disruption is not the cause of injury and the consequences of localized compression can be difficult to conclude from direct inspection.
The circumstances of Narakas12–14 type I and type II obstetric brachial palsies are similarly specific and the restoration of elbow flexion in these children by primary nerve grafting is the subject of considerable debate and at present there is no universally accepted protocol. The senior author’s own practice is to follow the multiple movement scale as developed in Toronto.15 At 12 weeks, if there is a low score then exploration should be undertaken. At this time the parents are told that the first part of the procedure will be simple exploration of the upper trunk or even the whole brachial plexus and that we will only proceed to surgical repair where the appearance indicates a very low probability of spontaneous or substantial recovery. This judgement requires experience.
In some cases of adult brachial plexus injury (and some cases of congenital brachial plexus injury) C5 and C6 roots are avulsed16–19 and no orthotopic restoration is possible. Here in the acute circumstance nerve transfers must be employed. The principle of a nerve transfer is that an undamaged distal nerve stump which is connected to the muscle in the normal way may be reanimated by neurosynthesis with a competent centrally connected proximal stump of a nerve that was serving another purpose. Clearly, as with tendon transfers, the donor nerve (that is the proximally connected one) must have a function that can be spared. Much has been written on this subject since Sir Herbert Seddon20–22 first described this procedure using intercostal nerves, although the indications in elbow flexion are now quite clear. As stated previously in the case of paralysis of the shoulder and elbow a clear decision must be made about the management of the shoulder whether by nerve transfers (such as the accessory nerve to the suprascapular nerve or the radial nerve to the axillary nerve) or by arthrodesis, at the same time that a management plan is made for the elbow. A number of nerve transfers have been advocated for the elbow and the author’s preferences are given below.
Oberlin transfer
In 1994, Dr Christophe Oberlin23 described the transfer of fascicles of the ulnar nerve to the nerve supplying biceps brachialis. The theory was that fascicles of the ulnar nerve in the upper arm could be isolated using a neuro-stimulator in the case of the C5–C6 injury (where the hand remained competent) and that these fibres which originate from C8 or T1 could be transferred to the nerve to biceps brachialis and so reinnervate that muscle (Fig. 32.1). This is indeed the case and this is a most effective transfer. We would, however, make a number of observations. First, we are sceptical that fascicles to individual hypothenar muscles can be isolated in the mid-proximal arm. This does not detract from the value of the transfer but can be confusing for surgeons newly undertaking this procedure. Second, the median or the ulnar nerve can be used for this transfer and it is likely that the radial nerve can also be used under certain circumstances. The appeal of this transfer lies in the fact that the neurosynthesis is conducted close to the hilum of the muscle and reinnervation is prompt, mitigating the effects of distal target organ decay. This is our preferred nerve transfer in the arms of adults where orthotopic nerve repair is not possible and a good hand exists. We have never found a significant donor defect in the hand.
Intercostal nerve transfer
Sir Herbert Seddon made the discovery that intercostal nerves which are both sensory and motor could be transferred onto nerves in the arm with resultant function. This technique subsequently fell into some disrepute, although it has been resurrected in the past 20 years and we have found it extremely valuable in certain cases. The protocol for such transfers was well described by Chuang24,25 and our practice described here is based upon his work.
Once the musculocutaneous nerve in which orthotoptic repair is not possible has been isolated, its distal stump is prepared as far as possible by dissecting the nerve into the apex of the axilla to the retroclavicular portion where it forms the terminal branch of the upper trunk as the lateral head of the median nerve separates from it. Transected at that point, the distal stump of the musculocutaneous nerve can then be delivered into the axilla. Some surgeons have advocated skeletonizing that nerve into its sensory and motor component to avoid pushing motor fibres distally into the sensory territory after neurosynthesis. Dr Julia Terzis has proposed an alternative and ingenious solution which is to connect the lateral cutaneous nerve of the forearm (the terminal branch of the musculocutaneous nerve) to the nerve to brachioradialis making use of such misdirected fibres to reanimate another elbow flexor.7,26 This technique has the advantage that it does not damage the musculocutaneous nerve further.
Other nerve transfers
Other nerves18,27–35 have also been used to reanimate the musculocutaneous nerve or nerve to biceps brachialis. These included the phrenic nerve which (on the right side easily, and on the left side with some more difficulty) may be harvested endoscopically. This nerve should not be used in small children and certainly never below the age of 3 years, as significant and on occasion fatal respiratory difficulties may ensue. We have been reluctant to use the phrenic nerve generally because of the effect on respiration but where other nerves are not available it has been effective and the adult patient has rarely suffered an identifiable deficit. The phrenic nerve may be used at the same time as three intercostal nerves although a respiratory deficit is more likely.
The spinal accessory nerve can also be used. If the shoulder has been arthrodesed the distal spinal accessory nerve may be spared to reanimate the elbow, although this usually requires an interpositional nerve graft with consequent loss of axonal material at each neurosynthesis. Lastly the cross neck C7 nerve transfer has achieved remarkable popularity since first described by Gu36–38 in China in the early 1990s. The senior author was hesitant to undertake nerve transfers from the undamaged opposite C7 root but after examining the cases of other surgeons, began to undertake this transfer a number of years ago.
In our experience, there has been little if any donor defect. We have, however, subsequently abandoned this nerve transfer as in our hands it has resulted in little functional benefit. Almost all reports of function following this nerve transfer are really reports of muscle activity. This has been demonstrated by several authors.29,39,40 The concern here, however, is that none of our patients (who range from the age of 1 year at the time of transfer to mid-forties) have managed to separate the recovered muscle function from activity of the contralateral limb. It has therefore been a transfer that has clearly resulted in muscle activity, although this activity has in our patients never been translated into day-to-day function or integrated into the activity of the patient. This is in stark contrast to the utility of ipsilateral transfers.