Case Reports

Successful Nonoperative Management of HAGL (Humeral Avulsion of Glenohumeral Ligament) Lesion With Concurrent Axillary Nerve Injury in an Active-Duty US Navy SEAL

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Humeral avulsion of the glenohumeral ligament (HAGL) is a lesion that has been recognized as a cause of recurrent shoulder instability. To our knowledge there are no reports of successful return to full function in young, competitive athletes or return to manual labor following nonoperative management of a HAGL lesion. A 26-year-old Navy SEAL was diagnosed with a HAGL injury, and associated traction injury of the axillary nerve as well as a partial tear of the rotator cuff. Operative intervention was recommended; however, due to issues with training and with inability to properly rehab with the axillary nerve injury, surgical plans were delayed. Interestingly, the patient demonstrated both clinical and radiographic magnetic resonance imaging healing of his lesion over an 18-month period. At 18 months the patient had returned to full active duty without pain or instability as a Navy SEAL.


 

References

The humeral avulsion of glenohumeral ligament (HAGL) lesion has been recognized as a cause of recurrent shoulder instability. In 1942, Nicola1 was the first to describe this lesion, in a small case series of avulsions of the anterior band of the inferior glenohumeral ligament from the humeral neck secondary to a dislocation injury. In 1988, Bach and colleagues2 described it in 2 patients with recurrent anterior dislocations. Wolf and colleagues3 were the first to apply the term HAGL to the injury, in 1995.

HAGL lesion incidence ranges from 1% to 9%, but many authors think the lesion is underdiagnosed.3-5 It occurs in isolation or in combination with other injuries, and it is commonly identified on recurrence of instability. Bui-Mansfield and colleagues6 found that 11% of patients with a diagnosis of HAGL lesion previously had surgery on the same shoulder, whereas for 62% the lesion was associated with other, concurrent lesions, including labral tears (18, 25%), rotator cuff tears (16, 23%), and Hill-Sachs deformities (12, 17%).

Most young athletes who undergo nonoperative therapy for a HAGL lesion continue to experience pain and/or instability that then requires surgical intervention.4 To our knowledge, there are no reports of return to full function in young competitive athletes or return to manual labor after nonoperative management of a HAGL lesion.

In this article, we report the case of a US Navy SEAL who sustained a traction injury causing an axillary nerve injury and a HAGL lesion. Successful nonoperative management allowed him to return to full duty. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

An otherwise healthy 26-year-old Navy SEAL presented with pain and significant weakness in the right (dominant) upper extremity after an injury in a training exercise. The shoulder sustained a traction injury when the man’s fast-moving marine attack craft was in a collision and he was trying not to be thrown off. He reported having a sense of dislocation yet never required a reduction.

Physical examination revealed severe weakness with shoulder abduction, external rotation, and forward flexion; inability to contract the deltoid muscle; and complete numbness along the cutaneous distribution of the axillary nerve. On neurovascular examination, the right upper extremity was otherwise intact. The patient had complete passive range of motion (ROM) with apprehension in abduction with external rotation along with anterior laxity and normal posterior stability.

Standard shoulder radiographs showed no bony abnormalities and a concentrically reduced glenohumeral joint. Magnetic resonance imaging (MRI), reviewed by a staff musculoskeletal radiologist and a sports fellowship–trained orthopedic surgeon, showed a greater tuberosity contusion, a partial tear of the infraspinatus, and a HAGL lesion (Figure 1).

The patient was counseled toward surgical intervention to prevent symptoms of recurrent instability. A detailed discussion ensued about whether to proceed with surgery immediately or to pursue temporary nonoperative treatment to allow for assessment and return of deltoid function. Patient and surgeon decided to delay operative intervention because of concerns about the patient’s ability to effectively rehabilitate while still having a compromised axillary nerve after surgery. The recommendation was to delay initial electromyographic (EMG) and nerve conduction velocity testing at least 4 weeks to allow for completion of Wallerian degeneration and more accurate assessment of the axillary nerve.7 Physical therapy for gentle ROM (excluding external rotation) and isometric rotator cuff exercises were initiated.

Five weeks after injury, the patient left the area to attend a 2-month nonphysical training course and continued rehabilitation and orthopedic follow-up at another military medical facility. Six weeks after injury, initial EMG testing revealed the expected axillary neuropraxia. In addition, some marginal improvement in ROM was noted, but deltoid function was still very limited.

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