The brachial plexus block (BPB) is a popular technique for providing operative anesthesia and pain control of the upper extremities [1,2,3]. Also subclavian or jugular vein catheterization is widely performed by anesthesiologists [4,5]. However, these procedures are not always safe and may cause various complications including brachial plexus injury (BPI) [6,7,8,9]. Additionally, the axillary arteriography, which has been used if the femoral route is not available, may also cause BPI [10].

Nerve injury is a serious complication. The patient with BPI may suffer only minor transient pain. However, the injury may result in permanent sensory disturbance or motor loss with poor recovery [4,11]. This paper presents literature reviews of BPI as a complication after BPB or vessel puncture including mechanism, clinical course, management and methods for prevention.

A PubMed search was performed from 1950 to 2014 using the search terms brachial plexus, brachial plexus injury, brachial plexus neuropathies, brachial plexus block, nerve block, and different structures relevant to this review including subclavian vein, jugular vein and axillary artery.

The brachial plexus is formed by the union of the anterior primary divisions (ventral rami) of the C5-C8 and T1 spinal nerves with variable contributions from the C4 and T2 nerves. As the nerve roots leave the intervertebral foramina, they form trunks, divisions, cords, branches and terminal nerves, in that order [12]. It is important to understand how the brachial plexus provides sensory and motor innervations to the upper limbs (Table 1) [13,14].

If the BPI is to happen during BPB or vessel puncture, it could be more common in distal nerves to the intraforaminal dorsal root ganglion. A supraclavicular injury usually occurs at the root and trunk levels, while an infraclavicular injury typically occurs at distal to the cord level.

A direct injection into the nerve may result in immediate severe pain radiating distally down the limb and neuromotor/neurosensory dysfunction in the distribution of the nerve [5,11]. The patient may continue to complain of pain, paresthesia or weakness on the affected side even after the removal of needle or catheter [8]. However, if the hematoma is formed by an injury, symptoms may be delayed and the patient may present only after the hematoma has expanded to a size large enough to compress the nerves. It can occur after hours or days [4,11].

After the nerve injury, the patient can complain of only mild numbness and tingling sensation. But pain is present in the majority of cases and may be described as a shooting or burning sensation. It can be exacerbated by physical factors such as pressure or touch. Severe allodynia or paresthesia can be developed with difficulty of motor activity [4,8,38].

If small fibers are involved, neurosensory loss to pin prick, hyperalgesia, hypesthesia, paresthesia and disturbed sympathetic innervation may be found. On the other hand, if large fibers are involved, motor power disturbance and loss of touch/vibration sense can be more common. In general, chemical toxicity leads to injury in small fibers, while excessive pressure leads to injury in large fibers [3].

Neurological symptoms have been reported according to the procedures in a varied distribution spectrum of the brachial plexus. Tsao and Wilbourn [11] noted that an nerve injury following an axillary regional block primarily involved the median nerve alone or in combination with the ulnar nerve and that no other nerve was injured in isolation. Another study reported that motor weakness after axillary angiography was most commonly involved in the median nerve distribution, followed by the ulnar nerve [37]. This could be explained by the medial brachial fascial compartment. Nerves at the level of the upper arm exit the medial brachial fascial compartment in the sequence (from proximal to distal) of musculocutaneous, axillary and radial. However, the median and ulnar nerves travel within the compartment to the elbow level. Therefore, the median and ulnar nerve are preferentially involved if there is a hematoma within this compartment [11]. On the other hand, the lower trunk, especially the ulnar nerve which arises from the lower trunk fibers, is the most vulnerable to be injured during infraclavicular subclavian vein catheterization [4,5]. But the upper trunk of brachial plexus could be injured during subclavian vein catheterization due to anatomical variations [8].

Connective tissue proliferation and scar formation may occur with time. The early sign of axonal regeneration with the reduplication of Schwann cells and axonal sprouting could be seen 1 to 2 weeks after nerve injury and the further regeneration with an improvement of initial symptoms is usually well advanced by 2 months after the injury. However, the regeneration is often inadequate and the initial loss could persist with severe sensory and/or motor disturbances. In such case, it may not be improved without a surgical intervention [39,40].

The past medical history, social habits, a detailed history associated to the nerve injury, and a review of systems should be evaluated in detail. Also it is important to conduct a physical examination about the sensory and motor disturbances including the level and severity of injury and changes of symptoms [39,41].

Electromyography can be used to diagnose BPI [8,11]. Electromyography may show complete or decreased functional loss if the nerve is stimulated proximal to the lesion, while normal response may be shown if the nerve is stimulated distal to the lesion. Classical signs of a denervation may not be detectable for up to 1-2 weeks after acute nerve transection. Therefore, electromyography should be performed at least 3-4 weeks after nerve damage [37]. Nerve conduction study can be helpful to diagnose nerve injuries, too. It is considered to be abnormal if the responses are less than 50% compared with the contralateral side or age-adjusted normal values [11].

Magnetic resonance imaging and ultrasonography are further methods to diagnose BPI. Magnetic resonance imaging can visualize an edematous nerve or a hematoma formation compressing the nerve [4,11,37]. On ultrasonography, normal brachial plexus appears as a hypoechoic mass containing a tubular structure on a transverse scan and a longitudinal hypoechoic structure containing small hyperechoic linings on a longitudinal scan. The injured nerve can be visualized as an enlarged and edematous nerve with loss of the hyperechoic lining or the discontinuity of the nerve [42].

The BPI must be differentiated from those of the original injury, operation or misuse of a tourniquet. Tourniquet injury usually affects the radial nerve with/without the median and ulnar nerves and is correlated with a good outcome in most cases [11].

In general, the management for BPI is similar to that of other nerve lesions. The treatment of BPI should be individualized for each patient depending on the injury site, degree of damage, lag between injury and repair, age, occupation, and so on.

Conservative management is indicated if the lesions in continuity are non-degenerative or if the fascicles are intact. The treatment with medications consists of both opioid and non-opioid analgesics. Other drugs to control acute neuropathic pain include antidepressants (tricyclic antidepressants, serotonin and norepinephrine reuptake inhibitors), antiepileptic drugs (gabapentin, phenytoin, pregabalin), membrane stabilizers (intravenous lidocaine), ketamine and systemic glucocorticoid [43]. In addition, physiotherapy should be immediately initiated to prevent atonia [4,44,45]. Galvanic stimulation to the affected muscles and nerve ganglion blocks has been reported to provide symptom relief [3,46].

If a hematoma forms, its prompt evacuation may significantly reduce symptoms. Chitwood et al. [10] reported a better prognosis (eight-fold) in patients with medial brachial fascial compartment syndrome when a surgical evacuation was conducted within 4 hours of injury compared with after 4 hours from injury. Sensory changes after axillary artery puncture should be considered as an early indicator of developing BPI due to hematoma formation [37].

Lesions should be treated with surgical intervention if sensory or motor disturbances persist with a severe degeneration. An intraoperative examination of the nerve action potential is a useful method for the assessment of the neural function. The presence of nerve action potential beyond an injury indicates a preserved axonal function with good recovery. On the other hand, the absence of nerve action potential means an inadequate regeneration with poor recovery. Preganglionic injuries are usually treated with nerve transfers, while postganglionic lesions are treated with resection and repair, or nerve graft (an excision of the damaged segment and nerve autograft between two nerve ends) (Fig. 1) [39,41,47,48].

Sufficient knowledge of anatomy, understanding of procedure, and adept skills in needle placement are essential for prevention of BPI. Only medical agents that have been proven reliability and safety should be used for nerve block. New agents should be used as cautiously as possible [3].

Nerve blocks should be performed without searching for paresthesia. The paresthesia method for the nerve block may increase the risk of postanesthetic neurological sequelae compared with no paresthesia methods [15], though paresthesia at the time of needle insertion does not always lead to postanesthesia nerve injury [49]. Currently, the paresthesia technique is not widely used for BPB. Instead of it, nerve stimulation has been the standard method for decades. In recent years, ultrasound guided nerve block has become popular with the improvements of ultrasound technology. Ultrasound allows a direct visualization of various peripheral nerves and localization of the local anesthetics. This may increase the success rate, decrease performance time and reduce the volume of local anesthetics [50,51]. However, further studies are needed to clarify the issue if ultrasound guidance could actually reduce the risk of nerve injury.

The type of needle seems to influence nerve penetration. Hirasawa et al. [52] studied the effect of three different types of needles (a short-bevelled, a long-bevelled and a tapered needle) on the degree of nerve injury in rabbits. A tapered needle did not cause any damage or tearing of the nerve fibers and resulted in the lowest level of damage to the perineurium. With both short- and long-bevelled needles, neural damage was reduced when the face of the bevel was inserted parallel to the nerve fibers.

Discovery of complications of BPB may be missed, since BPB is frequently performed as an out-patient procedure. Patients may confuse symptoms of BPI following BPB with symptoms caused by the original injury or operation. A careful observation and follow-up are imperative after the operation as well as during procedures [3,53].

While performing a subclavian catheterization, the interventionist should move the needle parallel to the coronal plane and avoid entering extreme depths [8]. A subclavian venipuncture should not be too laterally or deeply attempted [4]. If a fist attempt is failed, repeated attempts in the same region should be avoided. Multiple attempts could increase the chance of complications, because an anatomical anomaly may be present [8]. Puncturing the subclavian artery may lead to hematoma formation, which may compress the nerves and cause neurologic damage. If the patient has a prolonged bleeding time, coagulopathy should be corrected first before the performance of subclavian venipuncture or extrathoracic veins like the jugular vein should be used for catheterization [4]. The chances of a BPI are really greater when an inexperienced physician is performing a subclavian vein catheterization [4].

Whenever possible, the patient should not be heavily sedated and should be encouraged to immediately inform any experience of numbness/paresthesia during BPB or vessel puncture. If there is any notice, the needle should be withdrawn immediately [4,5,18].

A brachial plexus injury is a potential complication of a nerve block or vessel puncture. With an early recognition of nerve injuries, an appropriate management should be performed in order to reduce neurologic deficits and to maximize recovery. Comprehensive knowledge of anatomy and adept skills are crucial to avoid nerve injuries. Whenever possible, the patient should not be heavily sedated and should be encouraged to immediately inform a practitioner about any experiences of numbness/paresthesia during the nerve block or vessel puncture.