We reviewed 101 patients with injuries of the terminal branches of the infraclavicular brachial plexus sustained between 1997 and 2009. Four patterns of injury were identified: 1) anterior glenohumeral dislocation (n = 55), in which the axillary and ulnar nerves were most commonly injured, but the axillary nerve was ruptured in only two patients (3.6%); 2) axillary nerve injury, with or without injury to other nerves, in the absence of dislocation of the shoulder (n = 20): these had a similar pattern of nerve involvement to those with a known dislocation, but the axillary nerve was ruptured in 14 patients (70%); 3) displaced proximal humeral fracture (n = 15), in which nerve injury resulted from medial displacement of the humeral shaft: the fracture was surgically reduced in 13 patients; and 4) hyperextension of the arm (n = 11): these were characterised by disruption of the musculocutaneous nerve. There was variable involvement of the median and radial nerves with the ulnar nerve being least affected. Surgical intervention is not needed in most cases of infraclavicular injury associated with dislocation of the shoulder. Early exploration of the nerves should be considered in patients with an axillary nerve palsy without dislocation of the shoulder and for musculocutaneous nerve palsy with median and/or radial nerve palsy. Urgent operation is needed in cases of nerve injury resulting from fracture of the humeral neck to relieve pressure on nerves

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.

Residual muscle weakness in obstetric brachial plexus palsy results in soft-tissue contractures which limit the functional range of movement and lead to progressive glenoid dysplasia and joint instability. We describe the results of surgical treatment in 98 patients (mean age 2.5 years, 0.5 to 9.0) for the correction of active abduction of the shoulder. The patients underwent transfer of the latissimus dorsi and teres major muscles, release of contractures of subscapularis pectoralis major and minor, and axillary nerve decompression and neurolysis (the modified Quad procedure). The transferred muscles were sutured to the teres minor muscle, not to a point of bony insertion. The mean pre-operative active abduction was 45° (20° to 90°). At a mean follow-up of 4.8 years (2.0 to 8.7), the mean active abduction was 162° (100° to 180°) while 77 (78.6%) of the patients had active abduction of 160° or more. No decline in abduction was noted among the 29 patients (29.6%) followed up for six years or more. This procedure involving release of the contracted internal rotators of the shoulder combined with decompression and neurolysis of the axillary nerve greatly improves active abduction in young patients with muscle imbalance secondary to obstetric brachial plexus palsy.