We present our experience of managing patients with iatropathic brachial plexus injury after delayed fixation of a fracture of the clavicle. It is a retrospective cohort study of patients treated at our peripheral nerve injury unit and a single illustrative case report. We identified 21 patients in whom a brachial plexus injury occurred as a direct consequence of fixation of a fracture of the clavicle between September 2000 and September 2011.

The predominant injury involved the C5/C6 nerves, upper trunk, lateral cord and the suprascapular nerve. In all patients, the injured nerve was found to be tethered to the under surface of the clavicle by scar tissue at the site of the fracture and was usually associated with pathognomonic neuropathic pain and paralysis.

Delayed fixation of a fracture of the clavicle, especially between two and four weeks after injury, can result in iatropathic brachial plexus injury. The risk can be reduced by thorough release of the tissues from the inferior surface of the clavicle before mobilisation of the fracture fragments. If features of nerve damage appear post-operatively urgent specialist referral is recommended.

Cite this article: Bone Joint J 2013;95-B:106–10.

The outcomes of 261 nerve injuries in 100 patients were graded good in 173 cases (66%), fair in 70 (26.8%) and poor in 18 (6.9%) at the final review (median 28.4 months (1.3 to 64.2)). The initial grades for the 42 sutures and graft were 11 good, 14 fair and 17 poor. After subsequent revision repairs in seven, neurolyses in 11 and free vascularised fasciocutaneous flaps in 11, the final grades were 15 good, 18 fair and nine poor. Pain was relieved in 30 of 36 patients by nerve repair, revision of repair or neurolysis, and flaps when indicated. The difference in outcome between penetrating missile wounds and those caused by explosions was not statistically significant; in the latter group the onset of recovery from focal conduction block was delayed (mean 4.7 months (2.5 to 10.2) vs 3.8 months (0.6 to 6); p = 0.0001). A total of 42 patients (47 lower limbs) presented with an insensate foot. By final review (mean 27.4 months (20 to 36)) plantar sensation was good in 26 limbs (55%), fair in 16 (34%) and poor in five (11%). Nine patients returned to full military duties, 18 to restricted duties, 30 to sedentary work, and 43 were discharged from military service. Effective rehabilitation must be early, integrated and vigorous. The responsible surgeons must be firmly embedded in the process, at times exerting leadership.

We describe 261 peripheral nerve injuries sustained in war by 100 consecutive service men and women injured in Iraq and Afghanistan. Their mean age was 26.5 years (18.1 to 42.6), the median interval between injury and first review was 4.2 months (mean 8.4 months (0.36 to 48.49)) and median follow-up was 28.4 months (mean 20.5 months (1.3 to 64.2)). The nerve lesions were predominantly focal prolonged conduction block/neurapraxia in 116 (45%), axonotmesis in 92 (35%) and neurotmesis in 53 (20%) and were evenly distributed between the upper and the lower limbs. Explosions accounted for 164 (63%): 213 (82%) nerve injuries were associated with open wounds. Two or more main nerves were injured in 70 patients. The ulnar, common peroneal and tibial nerves were most commonly injured. In 69 patients there was a vascular injury, fracture, or both at the level of the nerve lesion. Major tissue loss was present in 50 patients: amputation of at least one limb was needed in 18. A total of 36 patients continued in severe neuropathic pain.

This paper outlines the methods used in the assessment of these injuries and provides information about the depth and distribution of the nerve lesions, their associated injuries and neuropathic pain syndromes.

We describe 20 patients, aged between 43 and 88 years, with delayed nerve palsy or deepening of an initial palsy caused by arterial injury from low-energy injuries to the shoulder. The onset of palsy ranged from immediately after the injury to four months later. There was progression in all the patients with an initial partial nerve palsy. Pain was severe in 18 patients, in 16 of whom it presented as neurostenalgia and in two as causalgia. Dislocation of the shoulder or fracture of the proximal humerus occurred in 16 patients. There was soft-tissue crushing in two and prolonged unconsciousness from alcoholic intoxication in another two. Decompression of the plexus and repair of the arterial injury brought swift relief from pain in all the patients. Nerve recovery was generally good, but less so in neglected cases. The interval from injury to the repair of the vessels ranged from immediately afterwards to 120 days. Delayed onset of nerve palsy or deepening of a nerve lesion is caused by bleeding and/or impending critical ischaemia and is an overwhelming indication for urgent surgery. There is almost always severe neuropathic pain

We describe a patient with a painful sciatic neuropathy after total hip arthroplasty. Treatment was confined to neuroleptic and analgesic agents until neurolysis at seven years abolished pain and restored function.