As this is a case report of a single patient, institutional review board approval was not required. The patient provided informed consent for the study.

A 61-year-old woman, who was a motorcyclist, presented with discomfort in her right shoulder after colliding with a vehicle. Initial examinations in the emergency department revealed a mid-shaft clavicle fracture on the right side, along with intracranial injuries, including subdural and subarachnoid hemorrhages. She was admitted to the neurosurgery department for conservative management of her head injuries. The patient had a history of a similar fracture at the same site approximately 16 years earlier, also due to a motorcycle accident, which had been treated conservatively, resulting in union. Radiographs taken during the current admission revealed a deformed mid-clavicle fracture, likely due to the previous injury (Fig. 1).

Two weeks after injury, the patient continued to experience discomfort in her right shoulder and expressed a desire for pain relief and early return to daily activities. Thus, surgical intervention was planned, including open reduction and internal fixation of the fracture with a plate, along with bone grafting using autogenous iliac cancellous bone, following the excision of deformed bone at the previous fracture site (Fig. 2).

The patient was evaluated 2 hours postoperatively and had a good radial pulse as well as a warm, well-perfused extremity, but decreased sensation in the ulnar and median nerve distributions distally. Motor function was graded as 3 of 5 in elbow flexion, wrist extension, thumbs up, finger abduction, metacarpophalangeal joint flexion and extension, and interphalangeal joint extension. Wrist flexion and interphalangeal joint flexion were graded as 2 of 5, and thumb flexion motor was 1 of 5. The patient had severe pain at the surgical site as well as in the shoulder, upper arm, and forearm. There was no evidence of hematoma at the surgical site.

To rule out the recurrence of intracranial injuries, brain computed tomography (CT) and magnetic resonance imaging (MRI) were performed, which showed no evidence of worsening lesions. However, MRI and CT of the brachial plexus suggested possible localized compression by clavicle fragments (Fig. 3). Given the clinical diagnosis of secondary thoracic outlet syndrome due to indirect nerve compression by the reduced clavicle fragments, a revision surgery was performed on the same day.

During the revision surgery the plate was removed, the fracture site was exposed, and a butterfly fragment beneath the clavicle was excised. Each side was held with reduction forceps and the lower half of the fracture surface was excised with a micro-saw and osteotome, creating space for the clavicle to form a smooth arch (arcuate form) when the fracture was reduced. Cancellous bone from the initial surgery was placed beneath the clavicle to act as a cushion between the clavicle and the brachial plexus, while also promoting bone union. The removed metal plate was re-fixed after bending it to create a superior angularity at the fracture site (Fig. 4). Immediately after the surgery, the severe pain at the surgical site showed much improvement, but recovery of strength was not prominent. Subsequently, gradual improvement was noted. Electromyography (EMG) performed 16 days postoperatively confirmed the presence of brachial plexopathy (Table 1).

Continuous rehabilitation led to significant improvement in the hand and upper extremity by 6 months postoperatively, as confirmed by follow-up x-rays showing fracture union (Fig. 5) and near-normal flexion and extension of the fingers (Fig. 6). EMG and nerve conduction studies performed 1 year after complication onset demonstrated significant recovery of motor and sensory functions, with only partial subjective sensory deficits remaining.

The increasing preference for surgical management of clavicle fractures has led to a rise in associated complications. The most common complications include non-union, malunion, delayed union, and neurovascular injuries. Although less frequent, brachial plexus injury can occur either due to direct trauma to the clavicle or secondary to pressure from callus formation. Recent studies have reported cases of brachial plexus injury following surgical treatment of acute or delayed/non-union clavicle fractures. We compiled 11 studies on this topic (Table 2). Except for two studies, all cases involved delayed union or nonunion that occurred more than 3 months after the injury.

Cao et al. [9] reported a case involving a 34-year-old woman who experienced significant reduction in the range of motion of the right elbow, wrist, and fingers following surgery. Conservative treatment with oral methylcobalamin and nerve stimulation led to complete symptom resolution within 60 days, but additional diagnostic tests such as EMG or MRI were not conducted, leaving the exact nature of the injury unclear.

Jeyaseelan et al. [3] analyzed 21 cases of surgically treated acute clavicle fractures and found that midshaft fractures fixed between 2 and 4 weeks after injury carry significant risk of brachial plexus injury. Increased comminution of the fracture and clavicle shortening during fixation are additional risk factors. Among the cases they described, four underwent nerve transfer or nerve graft procedures following nerve exploration, while the remaining cases had good outcomes with neurolysis alone without bone procedures.

Matthew et al. [5], Johnson et al. [8], and Larrota et al. [11] reported good outcomes with conservative treatment. Commonly, these cases involved atrophic forms of delayed or nonunion, with the initial symptoms appearing 2–3 days after surgery. Larrota et al. [11] hypothesized that hypertrophic non-union can lead to plexus involvement due to compressive phenomena (due to insufficiently resected bony callus), and these cases typically present immediately in the recovery room. Their management involves surgical removal of the plate, complete callus resection, and neurolysis. On the other hand, atrophic non-union may cause plexopathy due to traction or elongation of the plexus during clavicle length restoration. They noted that these cases typically present in a subacute fashion between the second and third postoperative day, and that conservative management through clinical observation and rehabilitation appears to be a reasonable approach. In our case, the acute onset of symptoms immediately after surgery, along with the deformity from the previous fracture, suggest that secondary thoracic outlet syndrome likely developed due to compression by bony fragments during the reduction process. In light of existing studies, this scenario indicates that surgical intervention, including osteoplasty, is more appropriate than conservative management.

Rosati et al. [1], Jin et al. [6], and Kim et al. [7] reported cases in which, after surgical treatment of atrophic non-unions, initial symptoms appeared 2 to 5 days later. However, these cases showed progressive patterns, and while removal of internal fixation and debridement or resection of the fracture site led to nerve recovery, fracture union was not achieved. McGillivray et al. [10] suggested that if brachial plexus symptoms occur immediately after clavicle fixation and if combined plastic/vascular surgical procedures are feasible, emergent nerve/vascular exploration and internal fixation should be performed simultaneously. If simultaneous surgery is not possible, they recommend initially emergent removal of metal fixation followed by MRI to identify the compression site and then performing staged internal fixation in conjunction with plastic/vascular surgical consultation.

In our case, both decompression and fracture union could be achieved without direct nerve and vascular exploration by resecting a portion of the lower clavicle in an arch-shaped manner. The metal plate was contoured with superior angularity to restore the thoracic outlet space while preserving fracture contact.