The axillary nerve innervates all the portions of the deltoid muscle and teres minor muscle. It also provides a sensory branch named the upper lateral cutaneous nerve of the arm that innervates the skin over the lateral aspect of the shoulder.
The deltoid is the largest shoulder muscle, determines the silhouette of the shoulder, and is an essential muscle for shoulder function. Weakness of this muscle is detrimental to the normal function of the shoulder. The deltoid is comprised of three distinct portions, anterior or clavicular, middle or acromial, and posterior or spinal with all portions converging to attach on the deltoid tuberosity on the lateral aspect of the humerus. The deltoids main functions are abduction of the shoulder and stabilization of the humeral head. The posterior portion provides shoulder extension, adduction and external rotation of the shoulder in synergy with the teres minor and infraspinatus. The anterior portion is responsible for shoulder flexion, adduction, and internal rotation of the shoulder in synergy with the pectoralis major, subscapularis, latissimus and teres major. The largest middle portion allows the main function, which is abduction of the shoulder with synergistic action of the supraspinatus muscle during the first 30°.
The axillary nerve originates from the posterior cord of the brachial plexus and contains fibers that originate from C5 and C6 nerve roots that travel via the upper trunk of the brachial plexus and then into the posterior cord. After arising from the posterior cord, the axillary nerve is positioned lateral to the radial nerve and then courses laterally and posteriorly just inferior to the glenohumeral joint. The axillary nerve passes through the quadrilateral space around the posterior and lateral surface of the proximal humerus. The axillary nerve terminates into anterior and posterior muscular branches, both of which innervate the deltoid muscle. The upper lateral cutaneous nerve of the arm arises from the posterior branch. In 65% of cases, the axillary nerve splits into anterior and posterior branches within the quadrangular space, and in the remaining 35% splits within the deltoid muscle. The anterior branch ascends around the surgical neck of humerus with the posterior circumflex humeral artery and its branches distributed anteriorly to the deltoid muscle. In 100% of cases, the posterior branch innervates the teres minor muscle and gives off a branch for the superior lateral brachial cutaneous nerve. The anterior branch innervates the joint capsule and the anterior and middle part of deltoid.
The axillary nerve is one of the most common peripheral nerves injured in athletes who participate in contact sports. It can occur from glenohumeral dislocation, proximal humerus fracture or from a direct blow to the anterolateral deltoid muscle. Compression neuropathy has been reported to occur in quadrilateral space syndrome. Axillary nerve injuries after fracture or dislocation of the shoulder are more commonly present than what is actually appreciated. Concomitant injuries to the joints, bones, or other muscles of the rotator cuff may compromise shoulder motion by itself and axillary nerve injury particularly if they are mild, can go unnoticed.
The relationship to the shoulder joint is the most important factor in reference to the vulnerability of the axillary nerve to traumatic injuries. Glenohumeral dislocation or proximal humeral fractures are likely to traumatize the nerve directly because of the traction during anterior dislocation. Severe blunt trauma to the shoulder particularly during sporting activities such as football, hockey, skiing, volleyball and motorcycle accidents can also injure the axillary nerve. Typically it is due to a direct blow to the anterolateral deltoid muscle, during which compressive force is applied to the axillary nerve. This can be accompanied by traction injury distally to the quadrilateral space. Occasionally gunshot wounds or misplaced intramuscular injections can damage the axillary nerve. The axillary nerve is also at risk during general anesthesia due to positioning, especially with arms raised superiorly above the head. The lesion of the axillary nerve due to traumatic injuries is usually localized at or distally to the quadrilateral space. The axillary nerve is one of the nerves most commonly injured during surgical procedures on the shoulder. Iatrogenic injury to the axillary nerve remains a serious complication of shoulder surgery involving the inferior aspect of the shoulder.
The clinical history is important in evaluating patients with suspected axillary nerve palsy. History of distinct trauma to the shoulder, either blunt trauma, traction injury or penetrating trauma should raise suspicion for an axillary nerve injury. Classically, patients will present with trauma to the shoulder and they will report inability to abduct the shoulder. The patient will also report pain in the shoulder due to the original injury. Loss of deltoid muscle bulk and inability to abduct the shoulder is observed in axillary nerve injuries. Some associated sensory loss over the lateral aspect of the deltoid area can be also present but the sensation may be spared despite significant weakness.
An accurate diagnosis of axillary nerve injury is based on a careful history and physical examination as well as an understanding of the anatomy of the shoulder and the axillary nerve in particular. Careful neurological evaluation should be performed in order to determine whether the patient is experiencing isolated axillary nerve palsy or a more complex neurogenic injury. Inspection, palpation and neurological examination provide the clinical basis for diagnosis.
The comprehensive neurological exam of the patient should include a cranial nerve exam, detailed sensory and motor exam, as well as muscle stretch reflexes. The initial physical assessment should also involve standard testing for active and passive range of movements of the shoulder. Complete motor examination, and not just examination of the symptomatic arm should be performed. Careful assessment of possible deltoid muscle atrophy should be investigated and compared with the contralateral side. If the injury is acute, there will be no atrophy of the deltoid muscle, but after few weeks of significant axillary nerve palsy, atrophy of the deltoid muscle would be expected. Atrophy of the deltoid muscle is usually easily recognized. The patient’s shoulder should be inspected from the front, from the back, and from above. Due to decrease in the muscle bulk, the acromion becomes more visible.
Anterior, middle and posterior deltoid strength should be separately assessed. The strength of the anterior and midportion of the deltoid muscle should be tested with the patient asked to abduct the shoulder in horizontal position as much as possible. Anterior deltoid muscle weakness can be exaggerated if the patient is asked to perform forward flexion of the shoulder. The posterior deltoid is tested with extension of the shoulder by pushing with the abducted arm against resistance backwards. External and internal rotation of the shoulder should be also separately examined and will be affected in axillary neuropathy. In some cases of complete axillary nerve palsy, or most commonly in partial injuries of the axillary nerve, the deltoid weakness might not be obvious on the clinical exam due to compensation from the supraspinatus muscle, which in some cases can be effective in abducting the shoulder alone. Some patients even might be able to continue participate in competitive sport at a high level if they are not throwing athletes. If present, the sensory deficit has better demarcation and is smaller in size, when compared to sensory loss due to C5 radiculopathy. The patient with axillary nerve injury can present with significant deltoid weakness without sensory deficit on the clinical exam.
The diagnostic workup includes electrodiagnostic studies, X rays and MRI of the shoulder. Rarely MRA or conventional angiography is needed when concomitant vascular injuries are suspected. Clinically suspected axillary nerve injuries should be confirmed by electrophysiological testing, including nerve conduction studies and needle electromyography. The nerve conduction study is performed with recording of the compound muscle action potential (CMAP) from the deltoid muscle using surface electrodes. The stimulation is at the Erb’s point. The contralateral side should be also tested with the nerve conduction study for comparison. The needle electromyography of the deltoid muscle will help to evaluate for any preserved motor units, will help to determine the timing of the injury and will also help to determine early reinnervation process, which may not be obvious on the clinical exam.
The nerve conduction study and needle electromyography will be helpful even within the first week following the injury. Recording the CMAP from the deltoid muscle after stimulating the axillary nerve at the Erb’s point and comparison with the contralateral side can confirm the presence of axillary neuropathy immediately after the injury and can be also used in prognostication. Performing comprehensive electrodiagnostic studies of the upper extremities will help to differentiate isolated axillary neuropathy from more complex neurogenic injuries of the upper extremity. Proper use of electrodiagnostic studies in conjunction with the history and clinical exam improves timely identification of appropriate surgical candidates for axillary nerve repair. X rays of the shoulder and MRI of the shoulder would be useful in evaluating the anatomy of the region and evaluation for associated musculoskeletal injuries due to the original trauma.
Many axillary nerve injures are mild and can be subclinical. Most injuries are due to closed trauma and they are probably due to neurapraxia or axonotmesis. Both of these types of injures have good overall prognosis for spontaneous recovery of deltoid muscle function. Most patients with axillary nerve injury will have an excellent response to non-operative treatment. Patients with traumatic axillary nerve injury due to blunt trauma should be observed for a period of at least 3 months after the onset of the symptoms.
Nerve conduction study and needle electromyography should be performed to assess the extent of the injury. The electrodiagnosis can be performed immediately after the injury and will still provide valuable information which might not be available on the clinical exam. Physical therapy should be initiated including passive and active range of motion. The physical therapy will help to preserve the maximum range of motion and will help to prevent joint contracture. Excellent functional recovery of the shoulder can be seen even in cases in which only partial reinnervation of the deltoid muscle occurs after significant axillary nerve injury. Shoulder contracture after isolated axillary nerve injuries usually does not occur as the intact muscles of the shoulder are able to maintain active range of motion of the shoulder. When there are concomitant injuries to the joint itself, bones and/or ligaments, shoulder contracture is possible, but can be prevented with physiotherapy. Concomitant injuries to the bones, ligaments, or muscles should be accordingly treated including surgical treatment.
Indications for Surgery
The indication for operative treatment of axillary neuropathy due to trauma will be determined based on the evidence of recovery and nature of the injury. The patient who sustained closed trauma, after being initially evaluated, should be clinically and electrophysiologically followed over the ensuing months. If there is no clinical or electrodiagnostic evidence of recovery by 3 months after the injury, it is a reasonable time frame to consider operative treatment. However, if the cause of the axillary nerve injury is penetrating trauma or other trauma that is highly suspicious for neurotmesis, operative exploration should be performed much sooner if the clinical exam and electrophysiological studies show complete axillary nerve palsy. Electrodiagnostic studies could be performed immediately after the injury, which will help to evaluate for extent of the denervation. If the electrodiagnostic studies demonstrate absent CMAP from the deltoid muscle and active denervation without recruiting motor units, early operative exploration might be considered following penetrating trauma.
The most favorable results of surgical treatment have been documented to occur when the surgery is performed less than 6 months after the injury. The axillary nerve has a proximal monofascicular structure and it is composed of primarily motor fibers and it is of relatively short length and these attributes make the axillary nerve appropriate for surgical intervention when neurotmesis is present. Standard modalities of neurolysis, neurorrhaphy, nerve grafting, and neurotization can be used in treatment of axillary nerve injuries. The choice of the treatment will be determined during the surgical procedure after exploration of the nerve. Neurorrhaphy will be indicated if there is recent injury to the nerve. If the injury occurred several weeks or months prior, retraction with nerve gap and scarring of the nerve ends have occurred already. Mobilization of axillary nerve is not possible in these cases and nerve grafting will be required. Neurolysis can be attempted when the nerve is in continuity and appears intact but shows a scar or is entrapped by fibrous bands. Neurotization procedures have been also used with use of thoracodorsal, phrenic, spinal accessory, medial pectoral, radial motor branch or intercostal nerves. The most commonly performed surgical procedure for axillary nerve injuries is nerve grafting.
If the axillary nerve injury occurred more than 24 months prior to surgical intervention, the results following surgical repair are unpredictable and continued non-operative treatment or lifestyle modifications should be considered. Muscle transfer procedures can also be attempted in the chronic setting.
Surgery is performed under general anesthesia with the patient in lateral decubitus position. This position will enable both anterior and posterior exposure of the shoulder and will enable access for sural nerve harvesting if needed. Modified anterior deltopectoral approach is used with the skin incision more medially. The arm is positioned in adduction and external rotation to increase the distance between the nerve and the operative field. This will enable appropriate surgical exposure, which will be centered more medially under the pectoralis major and pectoralis minor. The muscles that need to be released are short head of the biceps brachii, coracobrachialis, and pectoralis, which release should be done within 1 cm of their osseous origin to avoid injury to the musculocutaneous nerve.
Once the axillary, radial, and musculocutaneous nerves are identified, the axillary nerve should be fully exposed and the axillary artery and vein must be identified and protected. The area of the lesion is often localized at or just distal to the quadrilateral space. If the nerve appears in continuity or if there is possible neuroma, nerve stimulator can be used to assess the conductivity of the nerve. If there is activity, then neurolysis should be performed only. If there is no muscle response after the nerve is electrically stimulated proximally to the lesion, the neuroma should be excised and grafted. When primary repair cannot be performed without undue tension to the axillary nerve due to nerve gap, grafting is required. Posterior incision might be needed if the lesion is deep in the quadrilateral space. Nerve repair with autograft is limited when there is insufficient amount of autologous nerves available for large nerve defects.
Traditionally, nerve autografts have been used to reconstruct peripheral nerve defects not amenable to primary repair. Autograft alternatives include allografts and artificial nerve conduits. The cadaveric nerve allograft provides an unlimited graft source without the comorbidities associated with autograft reconstruction while retaining the elements that promote cell migration into the graft. Nerve conduits are effective for short nerve gaps and have a limited role in overcoming major peripheral nerve gaps. Recent advances in allograft tissue processing have rendered them nonimmunogenic and eliminated the need for immunosuppression while their 3-dimensional structure is maintained. Allografts are becoming an attractive alternative to autografts and conduits.
Pearls and Pitfalls of Technique
The motor fascicle for the deltoid muscle is located most superiorly at the level of the quadrilateral space. It is separate from the fascicle for the teres minor and the fascicle for the upper lateral cutaneous nerve of the arm. In surgical repair of the axillary nerve, this motor fascicle should be correctly identified, matched and aligned to ensure proper reinnervation of the deltoid muscle. Primary tensionless end-to-end neurorrhaphy and nerve autografting continue to be the gold standards for nerve repair. Defects that cannot be overcome with mobilization need to be bridged using a conduit, allograft, or autograft. Complete debridement to healthy nerve tissue, nerve approximation without tension, end-to-end fascicular alignment and atraumatic and secure mechanical coaptation of nerve ends are critical to successful nerve reinnervation. Weakness of the posterior deltoid muscle can be compensated for by the latissimus dorsi muscle, however, there is no muscle that can compensate similarly for anterior deltoid muscle weakness. Therefore, restoring the function for the anterior axillary nerve branch will be crucial in the functional recovery of the shoulder. Proper use of intraoperative electrodiagnostic studies is helpful in the surgical decision-making and the surgeon will need to be familiar with their use.
Surgical complications are rare, but possible during the axillary nerve repair. Transient nerve palsies can occur due to partial intraoperative sectioning or excessive intraoperative traction. Musculocutaneous nerve, radial nerve or brachial plexus palsy are potential complications. Axillary nerve can be transected during neurolysis, which will necessitate repair. Recovery is expected over the ensuing months after the operation. Postoperative infections are possible that will require oral or intravenous antibiotic treatment. Intraoperative vascular lesions including the axillary artery or the axillary vein are possible and will require immediate repair. Symptomatic injuries to the tendons or muscles that had been divided for improved exposure might require secondary repair.
Following the surgical axillary nerve repair, the shoulder is immobilized for 3 to 4 weeks. After the immobilization, physical therapy program and home exercise program are initiated including passive and active range of movements and strengthening exercises. When axillary nerve injury is combined by significant musculoskeletal shoulder injuries the functional outcome can be affected despite the return of the axillary nerve function.
Outcomes/Evidence in the Literature
Most of the literature regarding axillary nerve surgery outcomes is based on the functional recovery and manual muscle strength testing.
Gumina, Postacchini. “Anterior dislocation of the shoulder in elderly patients”. Bone Joint Surg Br. vol. 79. 1997. pp. 540-3. (Evaluated consecutive patients with anterior shoulder dislocations, aged 60 years or more after a mean follow-up of 7.1 years. Axillary nerve injuries were seen in 9.3% of the 108 patients, but all recovered completely in 3 to 12 months.)
Artico. “Isolated lesion of the axillary nerve: surgical treatment and outcome in 12 cases”. Neurosurgery. vol. 29. 1991. pp. 697-700. (Treated surgically 12 patients including nerve grafting in six patients and neurolysis in six patients. They reported a 50% good and a 50% excellent result after surgery with no difference when comparing the outcomes of neurolysis and nerve grafting.)
Alnot. “Surgical repair of the axillary nerve. Apropos of 37 cases”. Int Orthop. vol. 15. 1991. pp. 7-11. (Described the surgical treatment in a series of patients with axillary nerve injuries of which 23 of 25 achieved grade 4/5 or 5/5 strength postoperatively. Majority were treated with grafting.)
Coene, Narakas. “Operative management of lesions of the axillary nerve, isolated or combined with other nerve lesions”. Clin Neurol Neurosurg. vol. 94. 1992. pp. S64-6. (In a series of 66 patients with axillary neuropathy, 27 patients underwent surgical exploration and grafting within 6 months of injury. Nine patient recovered to grade 5/5 strength, and other nine recovered to grade 4/5 strength. Another 10 patients achieved strength graded 4/5 or 5/5 of thirteen patient treated with neurolysis. Of six patients who underwent surgery more than one year after the injury only one patient achieved strength graded 4/5.)
Petrucci. “Axillary nerve injuries–21 cases treated by nerve graft and neurolysis”. J Hand Surg Am. vol. 7. 1982. pp. 271-8. (Presented the results in 15 patients who underwent sural nerve grafting an average of 5.8 months after injury. All but one of the patients achieved a muscle strength grade of 4/5 or 5/5.)
Chuang. “Restoration of shoulder abduction by nerve transfer in avulsed brachial plexus injury: evaluation of 99 patients with various nerve transfers”. Plast Reconstr Surg. vol. 96. 1995. pp. 122-8. (Reported on neurotization with the use of the phrenic or spinal accessory nerve, which requires intercalary sural nerve grafting with either donor nerve. The results were similar with the two nerves. The 23 patients who underwent spinal accessory neurotization with bridging sural nerve grafts had an average of 45 degrees of improvement in abduction.)
Okazaki, M.. “Outcome of axillary nerve injuries treated with nerve grafts”. J Hand Surg Eur Vol. vol. 36. 2011. pp. 535-40. (Evaluated the outcome of axillary nerve injuries treated with nerve grafting with mean interval from injury to surgery of 6.5 months. The deltoid bulk was almost symmetrical in nine of 34 cases, good in 22 and atrophied in three. Grade 4/5 or 5/5 was achieved in 30 of 35 for abduction and in 32 of 35 for retropulsion. Deltoid bulk continued to improve with a longer follow-up after surgery.)
Dahlin, Lars B.. “Axillary nerve injury in young adults–an overlooked diagnosis? Early results of nerve reconstruction and nerve transfers”. J Plast Surg Hand Surg. vol. 46. 2012. pp. 257-61. (Studied the outcome of a group of operatively and non-operatively treated ten young adults with axillary nerve injuries caused by motorcycle accidents, with median age at trauma 13 years, (range 9-24). The axillary nerve was explored and reconstructed at a median of 8 months (range 1-22 months) after trauma in eight patients. Two patients were treated non-operatively. In four cases, a reconstruction with sural nerve graft was performed, in one case only exploration of the nerve was made and in three cases a radial nerve branch transfer to the axillary nerve was performed. Functional recovery was observed in 9/10 cases (median follow up 11 months, range 7-64) with EMG signs of reinnervation in seven patients.)
If the clinical and electrophysiological assessment show that the axillary nerve injury is partial, then non-operative management in the form of rehabilitation is all that is required. If the axillary nerve injury is complete based on the clinical exam and supported by the electrodiagnostic studies, the patient should be followed and re-examined monthly. The axillary nerve is relatively short and the distance from the injury to the deltoid muscle is a short distance and some recovery should be expected in 3 – 4 months. If at 2 months, the EMG shows signs of persistent denervation and no evidence of reinnervation, grafting of the axillary nerve should be considered and planned within the third month. The associated musculoskeletal injuries of the shoulder should be repaired before or at the same time. The axillary nerve is primarily composed of motor fibers and travels only a short distance from its origin to its muscle insertion; it has a good prognosis for recovery after surgical repair and grafting.
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