Today we're going to talk about brachial plexus injury. I have no relevant disclosures. The learning objectives today are to describe the different degrees of peripheral nerve injury, understand the peripheral nerves response to trauma, understand the basic concepts of neural regeneration following peripheral nerve injury, classification, diagnosis, and treatment of brachial plexus injuries, complications of brachial plexus injuries, and surgical indications and surgical procedures for brachial plexus injuries. Brachial plexus injury occurs approximately in 0.7 per 1,000 live births in the United States. Babies with increased birth weight, multiparous mothers, and shoulder dystocia are at the highest risk for brachial plexus injuries. The most widely described mechanism of action for this is lateral stretch, which is logical secondary to the location of brachial plexus, the high correlation with shoulder dystocia, and the positioning of the mother and infant. It has been stated that between 50 and 95 percent of these infants will recover spontaneously. The goal of treatment is to maximize arm and hand function. Goals are normalization of limb function with optimization of nerve regeneration and mechanical increase of elbow flexion and shoulder stabilization. For any nerve that is injured, classification makes evaluation and comparison clearer. The set-end classification of nerve injury is commonly used. Sutherland's classification is another classification system that can be used. Neuropraxia occurs with no lasting anatomical changes with fibers preserved. An example of this would be a football stinger injury. When a football player is running and gets hit and falls and he gets a stretch of the brachial plexus injury, it can be called a stinger. With the neuropraxic injury, complete resolution is expected. In axotemesis, there is an interruption of neural continuity to some degree. There is an extremely variable level of deficit that is difficult to evaluate and predict the degree of recovery. Neurotemesis is the most severe injury with total disruption of the elements of the nerve. This will not recover. If it is pre-ganglionic or proximal to the dorsal root ganglion, it is called an invulsion. If it is post-ganglionic or distal to the dorsal root ganglion, it is called a rupture. Both of these require surgical intervention for recovery. Common injuries to nerves can be trauma such as sharp lacerations with a knife cut or hand through the glass, blunt lacerations that occur like in a gunshot, crush, stretching, or traction. That's where our neonatal brachial plexus injuries occur. Ischemia due to tourniquet or stricture injury or compression such as compartment syndrome, hematoma, nerve entrapment, carpal tunnel, or a cubital tunnel. So reaction to nerve injuries, there are some reversible lesions. So ischemia-induced conduction block also known as neuropraxia. This can be compression or traction injuries. Ischemia affects fast axoplasmic transport, abnormal ion channel function, you get lack of saltatory, non-saltatory conduction down the axon. This is temporary and reversible effect on conduction. There's no damage to the epineurium, endoneurium, or perineurium. Example, this could be a surgical positioning to the shoulder and or the foot or this is also what happens when your foot falls asleep but it gets reversed very quickly. Also can occur to prolonged pressure-induced conduction block with focal demyelination. So this is due to compression, traction, or crush injuries. Myelin sheath degeneration leads to a prolonged conduction block, can last for days to weeks. Also there's no damage to the epineurium, endoneurium, or perineurium, or axon. Example, a deep hematoma compression. Non-reversible lesions, crush, traction, or laceration injuries that affect the axon, myelin, endoneurium, perineurium, and epineurium to varying degrees. Example, this could be a gunshot or blast wound, knife lacerations, or a neonatal plexus traction injury for brachial plexus injury. Also wallerian degeneration, secondary to axonal injury. This is degeneration of axons and myelin distant to the site of injury. You get disintegration of cytoskeleton and axoplasm distal to injury site. You have an intact Schwann cells and macrophages, clear myelin debris. Clearance begins three to four days post-injury, complete after 14 days. Nerve conduction distal to site, injury ceases at three to five days post-injury. So nerve regeneration begins immediately following an injury. There's multiple levels involved, distal axon, proximal axon, neuron cell body, and end organ. There's a cascade of events. You have the Schwann cells that have increased synthesis of cell surface adhesion molecules, produces neurotropic factors, divide and increase pool of de-differentiated daughter cells for upregulation expression of nerve growth factor. The macrophages upregulate IL-1 and trigger Schwann cell proliferation. And nerve cell body express growth-associated factors, tubulin, actin, and upregulates gene-associated with axonal regeneration. You get proximal nerve stump bending with axonal sprouting. This is our regeneration units. Growth cone at tip of each. Guided interaction with distal stump. You got rate of axon regeneration. You're going to get one millimeter a day average growth or approximately one inch a month. This occurs faster in young patients and in proximal lesions. Slower in surgically repaired lesions. Factors affecting success is muscle fiber atrophy, neuroma development at injury site, and axonal misdirection, pathfinding errors resulting in abnormal innervation. And you can also get co-contraction phenomenon. So some common descriptors going back to brachial plexus injuries. C5 to C6 are an Orbs palsy. It's the most common level of a brachial plexus injury. Adducted and internally rotated shoulder with an extended impronation at the elbow. You can also get a C8 to T1 or a Klumpke's palsy. It's rare and the weakness of the wrist and hand with resulting in a clawed hand deformity. So although there are descriptors for the levels of brachial plexus injuries, the distinction may not be clear-cut in some cases with the babies. You can also have a Horner syndrome which is constricted pupil drooping upper eyelid and local inability to sweat on one side of the face. That may be seen in lower trunk injuries of C8 to T1. So this is a picture of brachial plexus injury that everybody should be familiar with and be able to draw out. So evaluation includes clinical findings, electrodiagnosis, and MRI. There is a debate about which of these is most effective. MRI is expensive and requires sedation to perform on infants. It is found to correlate with surgical findings 70% of the time, EMG 87% of the time, and clinical findings 60% of the time. The correlation was highest when all three of these were used together. So your clinical exam is going to consist of a history and physical exam. History includes birth number of child, birth weight, presence of maternal diabetes, size of previous infants born to mother, was there a traumatic birth, did the baby have shoulder dystocia, were there motor and sensory findings at birth, and any changes in these findings up to the time of the evaluation. You may also want to know if there was use of forceps or vacuum delivery as this may be indicative of a difficult birth. And the most common association we're going to find with a brachial plexus injury is shoulder dystocia at birth. Clinical examination is going to consist of a history and physical. The physical exam with visualization of the arm including the size and bulk. Sensory evaluation is critical to determine areas of involvement. Range of motion both active and passive are important. You're going to want to check the muscle stretch reflexes as they will be decreased or absent in the distribution of the brachial plexus injury. Contractures are commonly seen in shoulder adduction and internal rotation, wrist flexion, forearm pronation, and even at the elbow into flexion in later months and years. A cool temperature or blue colored arm is often noted. The primitive reflexes are also important since the upper plexus has more frequent involvement. The moro reflex which shows shoulder abduction and elbow flexion is valuable in assessing these active movements. Torticollis may also be seen. So role of the EMG and nerve conduction study. EMG has been recommended to be done in the first few days then with a repeat evaluation after several months to more accurately identify cases where there is reinnervation occurring and therefore having earlier determination of the need for surgical intervention. You're going to be looking at subclinical nerve and muscle responses. So sensory nerve action potentials are important as these are the most sensitive to axonal loss. EMG may show activation of motor unit potentials and muscles with no clinical motor activity. Nerves reach developmental maturation by five years of age. Now although EMGs are useful, some practitioners will not do the first EMG which they recommend in the first few days but they are going to wait to see if there's any recovery or not because if it's a neuropraxic injury they're usually going to have full recovery therefore not needing the EMG or surgical evaluation. So it just kind of depends on the practitioner. Imaging of plane x-rays could also be useful as well as clavicle or humerus fracture may mimic a brachial plexus injury. Caveats in nerve trauma with axonal loss can take up to three weeks for evidence of nerve or muscle denervation to appear on EMG, may take up to three to five days for evidence of distal axonal loss or degeneration to be seen on nerve conduction studies. You can have a sensory afferent nerve injury proximal to cell body and have normal nerve conduction study. Normative values for a nerve conduction study and EMG are going to vary with age. Both nerve conduction study and EMG are uncomfortable for infants to have and you must have access to nerves you want to stimulate and muscles you want to put a needle in. You can assess for conduction blocks and axonal disruption with three to five days of injury. You should wait for three weeks to assess for a nerve degeneration and re-innervation in the muscle. Treatment focuses on assessment and intervention design with goal of making changes that will improve not just recovery but also patient function. So function is the ability to perform tasks necessary for daily living, leisure activities, vocational pursuits, and social interactions. The major roadblocks to functional recovery that we need to overcome are going to be pain, weakness, muscle atrophy, contractures, and sensory loss. Nerve regeneration won't matter if functional recovery does not occur. So treatment education is initiated upon the first evaluation. Therapy should be started as soon as possible after diagnosis. So positioning instruction begins immediately with range of motion exercises beginning around two weeks. Splinting is commonly done to provide optimal position of the wrist and fingers to prevent wrist drop. Later on splinting can be done to prevent an elbow flexion contracture. Taping may also be used to optimize positioning of the arm. Electrical stimulation can be used though it is frequently not tolerated at a very young age. You must have some degree of motor nerve preservation for electrical stimulation to work and evidence of increased innervation and motor unit numbers following nerve transection and repair and enhanced diameter of myofibers. Botox may be used for the management of co-contraction phenomenon. Some complications. So it is important to monitor for secondary complications such as muscle atrophy and joint contractures. Pain is infrequent after birth brachial plexus injury but not after trauma. However, they can have pain down the road due to complications. The affected arm is frequently shorter and has decreased circumference as well. Joints may be dislocated and scapular winging is commonly seen. There may be a torticollis present. General child development may be infected including lack of awareness of the arm and body image may be affected. Pain not commonly reported with birth-related brachial plexus injuries. However, self mutilation has been reported. In later brachial plexus injuries, whether traumatic or non-traumatic, pain can become a significant problem. It's most commonly described in avulsion injuries as burning and crushing pain, most commonly in the hand. May develop days to months after the injury. So treatment includes transcutaneous nerve stimulation, anti-convulsants, antidepressants, and topical treatments. Nerve surgery is commonly effective in resolving pain. Amputation, however, is not effective in resolving pain. Surgical intervention is commonly recommended for those having less than anti-gravity strength and elbow flexion at six months. Indications for timing of brachial plexus surgery for infants has been controversial. It has been shown that a longer time for recovery leads to a worse shoulder function and that those who regain elbow function after six months of age have worse function than those who regain it between three and six months. Those with recovery by three months have normal function. Those who have had microsurgery at six months did better than those who spontaneously recovered elbow function at five months. Supraclavicular brachial plexus injuries are generally felt to be due to traction of the plexus. For example, in a motor vehicle collision and these have a worse prognosis than infraclavicular injuries. There may be a fracture of the clavicle or cervical transverse process and supraclavicular fossa swelling may be seen. Supraclavicular injuries may also occur to falls, large objects falling on shoulder, skiing or climbing, or during contact sports. Other etiologies include gunshot wounds, stab wounds, lacerations, or animal bites. Those who have ipsilateral Horner's syndrome and persistent pain are going to have a worse prognosis. Infraclavicular brachial plexus injuries are more commonly associated with fractures and dislocations about the shoulder or humerus, occurring more often in older adults. The posterior cord or axillary nerve or musculocutaneous nerve are classically involved. They are less severe and have better outcomes, may also be due to falls, motor vehicle collision, and tumors. For severe injuries later in life, recommendations are for surgical exploration and nerve grafting, most commonly three to four months post-injury. Surgical interventions may be varied. Microsurgical repair yields results months later. Recovery is generally felt to process at the rate of approximately one millimeter a day or one inch a month. Neuroliasis is where scar and fibrotic tissue are removed from the nerve. Direct nerve transfers have the advantage of quick recovery due to short regeneration distance. The serral nerve and great auricle nerve are commonly used as donor nerve fibers for these grafts. This concludes the presentation. These are the resources I used. Thank you for your time.

brachial plexus injuries

classification

diagnosis

treatment

nerve regeneration