A fifty-seven-year-old man, who was right-hand dominant and had no history of problems related to the shoulder, sustained a closed anterior subcoracoid dislocation of the right glenohumeral joint as the result of a fall (Fig. 1). Immediately after the injury, the patient had pain and numbness in the entire hand and forearm and was unable to flex or extend the elbow or to move the digits. On clinical testing, the flexors of the wrist and digits as well as the intrinsic muscles of the hand did not contract. Active flexion of the elbow was possible against gravity but not against manual resistance. There was numbness over the deltoid muscle and no clinical activity of that muscle.
With use of a Kocher maneuver and intravenous sedation, a closed reduction was achieved without difficulty. A large, tense, painful swelling developed in the anterior axillary fold and extended over the cephalad part of the chest. The right arm became edematous, although the radial pulse at the wrist remained palpable. Complete paralysis of flexion and extension of the elbow developed in addition to the neurological deficits noted before the reduction.
Selective axillary angiography was performed, with the patient sedated, approximately one hour after the manipulative reduction. It revealed complete rupture of the posterior circumflex artery as well as active bleeding from the anterior circumflex artery. There was evidence of some antegrade filling of the arcuate artery from the anterior circumflex artery (Fig. 2). The lesions of the circumflex arteries appeared isolated to their point of origin off the axillary artery, and there was no evidence of intimal dissection within the axillary artery.
In the operating room, three hours after the manipulative reduction, an exploration was performed with the patient under general anesthesia. The hematoma was evacuated, and the axillary sheath was explored through a deltopectoral approach with detachment of the short head of the biceps brachii and the pectoralis minor from the coracoid process as well as partial detachment of the insertion of the tendon of the pectoralis major. The anterior and posterior circumflex arteries were both found to be completely ruptured close to their origin from the axillary artery. The infraclavicular brachial plexus was explored, and the components were noted to be bruised but intact. There was a rupture of the supraspinatus tendon, which was thought to be consistent with the trauma as the edges of the tendon were actively bleeding. The tendon was repaired with a transosseous suture technique. A trough was created at the exact transition from the cartilage of the humeral head to the greater tuberosity. The cancellous bone that formed the base of the trough was bleeding but to a lesser degree than is usually observed during standard repairs of the rotator cuff. Because of the age of the patient and the risk of additional operative trauma, a decision was made to ligate the anterior and posterior circumflex arteries rather than to reconstruct them. The potential risk of subsequent avascular necrosis of the humeral head was recognized.
A magnetic resonance image made one month after the operation revealed no findings that were consistent with the development of avascular necrosis of the humeral head. Four months after the injury, standard radiographic assessment of the glenohumeral joint demonstrated osteoporosis of the head and the greater tuberosity, suggestive of vascular perfusion throughout the proximal aspect of the humerus. All signs of the plexopathy resolved by six months after the operation.
Radiographic examination at eighteen months showed the proximal aspect of the humerus to be normal (Fig. 3). Magnetic resonance images made at the same time revealed no signs of avascular disturbance of the humeral head (Figs. 4-A, 4-B, and 4-C). The patient had normal motion of the shoulder, with only mild limitation of strength when he used the right arm behind and above the head.