Axillary artery injury combined with delayed brachial plexus palsy due to compressive hematoma in a young patient: a case report
© Murata et al. 2008
Received: 04 December 2007
Accepted: 28 March 2008
Published: 28 March 2008
Axillary artery injury in the shoulder region following blunt trauma without association with either shoulder dislocation or fracture of the humeral neck has been previously reported. Axillary artery injury might also be accompanied with brachial plexus injury. However, delayed onset of brachial plexus palsy caused by a compressive hematoma associated with axillary injury after blunt trauma in the shoulder region has been rarely reported. In previous reports, this condition only occurred in old patients with sclerotic vessels. We present a case of a young patient who suffered axillary artery injury associated with brachial plexus palsy that occurred tardily due to compressive hematoma after blunt trauma in the shoulder region without association of either shoulder dislocation or humeral neck fracture.
A 16-year-old male injured his right shoulder in a motorbike accident. On initial physical evaluation, the pulses on the radial and ulnar arteries in the affected arm were palpable. Paralysis developed later from 2 days after the injury. Functions in the right arm became significantly impaired. Angiography showed complete occlusion of the axillary artery. Magnetic resonance imaging demonstrated a mass measuring 4 × 5 cm that was suspected to be a hematoma compressing the brachial plexus in a space between the subscapular muscle and the pectoralis minor muscle. Surgery was performed on the third day after injury. In intraoperative observations, the axillary artery was occluded with thrombus along 5 cm; a subscapular artery was ruptured; the brachial plexus was compressed by the hematoma. After evacuation of the hematoma, neurolysis of the brachial plexus, and revascularization of the axillary artery, the patient had an excellent functional recovery of the affected upper limb, postoperatively.
Surgeons should be aware that axillary artery injuries may even occur in young people after severe blunt trauma in the shoulder region and can be associated with secondary brachial plexus injury due to a hematoma. For treatment in cases with progressive nervous deficit after trauma, not only reconstruction of the injured artery but also immediate evacuation of the hematoma, and exploration of the brachial plexus are necessary to avoid irreversible neurological damage.
Neurovascular injury in the shoulder region following blunt trauma that is not associated with either anterior dislocation of the shoulder or fracture of the humeral neck has been rarely reported [1–6]. Furthermore, revision of the literature showed that there are only a few case reports of delayed onset of brachial plexus palsy due to hematoma or pseudoaneurysm formation following trauma in the shoulder region [7–9]. However, in these reports, this condition only affected old patients who had sclerotic, non-elastic vessels. Here, we report a young patient who suffered axillary artery injury combined with delayed brachial plexus palsy that occurred tardily due to compressive hematoma after blunt trauma to the shoulder. The patient was successfully treated using surgical intervention.
Cases of delayed brachial plexus palsy due to a hematoma from a ruptured subscapular artery without association of either shoulder dislocations or humeral neck fractures have been previously reported [1, 6]. In previous reports, the affected patients were elderly people with non-elastic vessels, and the etiology was advanced arteriosclerosis that can be vulnerable to stretching force in shoulder trauma. However, our present case was only 16 years old. Injuries of the axillary artery and/or its branches can affect young patients who have suffered blunt injuries in the shoulder region even if fractures and/or joint dislocation were not associated.
Axillary artery injury might be accompanied with brachial plexus injury with an incidence rate of 27–44% . The usual mechanisms of brachial plexus injuries involve direct impact or forceful stretch with extreme movement of the neck and/or arm; and symptoms usually occur just after the injury. In the present case, nervous deficits except for those from the axillary nerve injury occurred tardily from the third day after the initial injury. We postulated that the mechanism of nerve injuries in the present case occurred as follows. A hematoma from the ruptured subscapular artery formed, and nerve compression by the hematoma and/or swollen soft tissues promoted nerve palsy. The development of the hematoma was suspected to have led to gradual progressive brachial palsy. Ischemia of the nerves due to axillary artery occlusion might play a subsidiary role in causing brachial palsy. This possible cause of neuropathy after shoulder injury has been reported by Stenning et al. . The intraoperative findings showed that the hematoma was located dorsally to the cords of the brachial plexus; the cords were compressed by the hematoma against the swollen pectralis minor muscle. In the present case, nervous disturbance was more significant in the muscles and sensory territory that were innervated by the posterior cord than the lateral or medial cords. These findings could be supported by the fact that the posterior cord was most closely located to the hematoma; and the posterior cord could be directly compressed by the hematoma. Additionally, in the triangular space formed by the subscapularis muscle, pectoralis minor muscle, and thorax where the cords are located, the medial part of this space had more space than on the lateral part. This might explain the fact that the muscle and sensory territories that were innervated by the medial cord were the least impaired.
According to the critical analysis and intraoperative findings of the present case, the etiology of axillary nerve palsy was more likely the direct stretching of the nerve at the time of injury rather than compression by a posttraumatic hematoma. Hyperabduction of the glenohumeral joint resulted in stretch injury of the axillary nerve. Intraoperative findings of the loosened but continuous axillary nerve supported this speculation. The severity of the injury of the axillary nerve was categorized as Sunderland's grade 3, in which axon continuity is disrupted by the loss of endoneural tubes but the perineurium is preserved. We performed external neurolysis only to promote spontaneous recovery. Reported prognosis and management programs for axillary nerve palsy have been inconsistent. Although Sunderland  stated that most cases of axillary nerve palsy recover spontaneously, Berry et al.  described that axillary nerve palsy following blunt trauma without an associated fracture or dislocation tend to result in poor recovery. In their report, only 2 of 8 patients with initial complete axillary nerve palsy following blunt trauma without associated fracture or dislocation recovered well. In the present patient, however, without additional surgery, the function of the deltoid muscle was recovered considerably. The patient did not wish an additional surgery because he did not feel any significant inconvenience in his daily activities. If his shoulder elevation function had been seriously impaired, we would have scheduled nerve grafting with the sural nerve or neurotization of the axillary nerve using the motor branch to the long head of the triceps muscle as a secondary surgery.
We reported a young male case of axillary artery injury combined with delayed brachial plexus palsy that occurred tardily due to compressive hematoma after blunt trauma to the shoulder. The patient was saved from severe complications by early diagnosis and immediate surgery. Surgeons should thoroughly consider injuries of axillary arteries and/or their branches when dealing with patients with blunt trauma to the shoulder, even in cases with normal or subtle X-ray findings and/or preserved distal pulses at initial assessment to avoid overlooking this condition. Additionally, surgeons should be aware that this condition may even occur in young people or can be associated with secondary brachial plexus injury due to a hematoma. For treatment, not only reconstruction of the injured axillary artery but also immediate exploration of the brachial plexus is required, especially in cases with progressive nervous deficits after trauma to avoid irreversible neurological damage.
The patient and his family were informed that data obtained would be submitted for publication, and written consent was obtained from the patient and their relatives.
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