Toros and his colleagues (2009) offer a method of clinical examination which may prove decisively important in the early detection of divided nerves, particularly for those ruptured in closed injuries. Amongst the 29 patients studied there were nine cases of radial nerve palsy, in five of these the nerves had been damaged by a compression plate or wire. Toros and his colleagues acknowledge the difficulty in examining a nerve which lies deeper than 3cm from the skin but the possibility of overcoming this limitation by further technical improvement is set out. These workers acknowledge the work of Gruber and his colleagues with the use of ultrasonography for the analysis of closed traction lesions of the brachial plexus.
Nerves are injured by damage to the adjacent skeleton by: traction from displacement which commonly ends in rupture; laceration by a fragment of bone; entrapment within the dislocated joint or in a fracture; late entrapment and compression from callus. On the whole, dislocations are more damaging and the outlook is worse for nerves injured by skeletal injury in the lower limb. The increase in the number of iatropathic injuries to nerves incurred during the treatment of skeletal injury must be a matter of grave concern for orthopaedic surgeons. If a surgeon elects to convert a closed fracture to an open one by whatever technique, then the lesion of the nerve should be exposed. The nerve, indeed the nerve with the adjacent artery, may be in the fracture or in the joint and both will certainly be displaced from their normal position. Lesions of the sciatic, the tibial and the common peroneal nerves are usually associated with high energy injuries. The likelihood of recovery in the untreated case is generally bad. If these nerves are injured it is wise, always, to expose them during operation for fracture or dislocation. Seddon1 had this comment to make when speaking about nerves injured in the arm and at the elbow by closed fracture dislocation; recovery could be awaited if two conditions were met: “the first is reasonable apposition of the bony fragments and the other complete certainty that there is no threat of ischaemia of the forearm muscles” (original italics). Yet it seems that the view that injured nerves can be neglected for three months seems to be growing, presumably to “see what happens”. Uncritical application of this policy is baleful, indeed it is deplorable. Each patient should be considered as an individual and not subject to the rote of an algorithm. In most cases clinical examination will answer the following questions: is this lesion to the nerve complete or incomplete? Is the lesion one of conduction block or is it one of Wallerian degeneration? Repeated examination during the ensuing four to six weeks will usually distinguish between those nerve palsies which are showing signs of recovery from those which are not. Bowden and Scholl2 in a remarkably thorough investigation found that the mean interval between injury and the detection of activity in the appropriate muscle was 64 days for lesions in continuity and 96 days after suture. Shah and Batti3 studied 56 cases of radial palsy in fractures of humerus and recorded evidence of clinical recovery in 10 in the first week, in 12 between one week and one month and in 13 more between the first and the third month. Operation was performed in 22 of the 56 cases; three nerves were ruptured and 10 were entrapped. Shaw and Sakellarides4 observed the onset of recovery in as short a time as two weeks in partial lesions and in five weeks in complete lesions. Ring et al5 saw signs of recovery at seven weeks in their cases of lesions in continuity.
Lambert’s6 further opinion on the subject of radial nerve palsy associated with fractures of the shaft of the humerus offers clinicians insights which extend well beyond his theme. He identifies three important features: first is “anatomical fixity” so that nerves are injured more readily at or near zones of tethering of the nerve; next is the fracture pattern, so that those fractures in which some intermuscular septum is torn and the fracture inherently unstable are associated with a high incidence of radial palsy; the third element is the blood supply to the nerve. The radial nerve may become relatively ischaemic because of compression by the intermuscular septum.
Rupture or severance of a nerve leads to changes both centrally and peripherally. These changes are progressive and ultimately irreversible. The central effect is manifested by the death of cells in the dorsal root ganglion and in the anterior horn of the spinal cord. The extent of loss of the central neurones is worse in more proximal and more violent injuries, and in the immature nervous system. The changes in the distal stump are, in the first weeks, conducive to regeneration of axons but this receptivity falls away. There is of course, the well known atrophy and fibrosis within the distal stump of the nerve and also the atrophy of the target organs but there is too a material change in the ability of the Schwann cells to foster and sustain axonal regrowth, a change which occurs at no later than eight weeks from injury.7
Whilst it is usually possible for a clinician to come to a pretty clear view about the extent of injury and about the likelihood of recovery for such nerves as the radial and the common peroneal which have been damaged in closed injuries it must be admitted that the circumflex nerve is much more difficult to examine. It is rarely possible to elicit a Tinel sign let alone monitor its progression. The early promise of microneurography has yet to be fulfilled. Too many fracture services are not adequately supported by radiological and neurophysiological services. Toros et al say that resolution ultrasonography is faster, more cost effective, non invasive and safer than magnetic resonance imaging. There is the added advantage that the interested clinician in the fracture service may be able to liberate him or herself from the tyranny of a target driven Department of Radiology. This paper represents an important and valuable contribution towards the diagnosis of nerve injuries and application of the method may ease some of the difficulties facing the clinician in analysis of the lesion in closed fractures, reduce the risks of damage during operation for that fracture, and remind the clinician to treat the patient as a whole and not as a radiograph.
1. Seddon HJ. Neurovascular injury. In: Surgical Disorders of Peripheral Nerves. Second ed. Edinburgh:Churchill Livingstone 1957:89-111.
2. Bowden REM, Scholl DH. Recovery of nerves. In: Peripheral Nerve Injuries. Medical Research Council, Special report series No. 282, Chapter1, part 2 1954:16-24.
3. Shah JJ, Bhatti NA. Radial nerve paralysis associated with fractures of the humerus. Clin Orth 1983;172:171-6.
4. Shaw JL, Sakellarides H. Radial nerve paralysis. J. Bone Joint Surg [Am] 1967;49-A:899-902.
5. Ring D, Chin K, Jupiter JB, Boston MA. Radial nerve palsy associated with high-energy humeral shaft fractures. J. Hand Surg 2004;29A:144-7.
6. Lambert SM. Further opinion. http://www.jbjs.org.uk/cgi/content/full/87-B/12/1647/DC1 (date last accessed 24 July 2009).
7. Hall S. The response to injury in the peripheral nervous system. J.Bone Joint. Surg [Br] 2005;87-B:1309-19.
Birch R, MChir, FRCS
London, United Kingdom