Both blunt and penetrating trauma can cause injuries to the peripheral and central nervous systems. Emergency providers must maintain a high index of suspicion, especially in the setting of polytrauma. There are 2 major classifications of peripheral nerve injuries (PNIs). Some PNIs are classically associated with certain traumatic mechanisms. Most closed PNIs are managed conservatively, whereas sharp nerve transections require specialist consultation for urgent repair. Spinal cord injuries almost universally require computed tomography imaging; some require emergent magnetic resonance imaging. Providers should work to minimize secondary injury. Surgical specialists are needed for closed reduction, surgical decompression, or stabilization.
Injuries to the peripheral nervous system and spinal cord regularly occur during blunt and penetrating trauma.
Other life-threatening injuries should be prioritized in the setting of polytrauma before pursing definitive management of injuries to peripheral nerves or the spinal cord.
Sharply transected peripheral nerve injuries should prompt consultation for immediate repair.
Providers should have a low threshold for intubation during the acute management of spinal cord injuries because lower cervical and even thoracic injuries can result in insufficient airway protection or breathing.
First-line management of neurogenic shock should be intravenous fluids followed by, if necessary, norepinephrine to maintain a mean arterial pressure of at least 85 mm Hg.
All trauma, whether blunt or penetrating, has the potential to cause injury to the nervous system. This includes the brain and spinal cord of the central nervous system and the somatic and autonomic components of the peripheral nervous system (PNS). Traumatic injuries to the PNS are a significant source of morbidity. Peripheral nerve injury (PNI) can result in permanent disability and entail significant health care and patient costs. Acute costs associated with these injuries average nearly $6000 in the emergency department (ED) and $20,000 to $60,000 in inpatient expenses. These costs do not consider the burden of decreased quality of life and long-term health care costs.
Spinal cord injuries (SCIs) similarly can cause significant permanent disability and even death. The financial cost to patients and society from SCIs is significant, accumulating average expenses in the United States between $375,000 and $1,150,000 in the first year alone, depending on severity of injury. Subsequent annual expenses average between $45,000 to $200,000.
Emergency medicine providers play an essential role in the recognition and subsequent management of these patients. Presentations can be subtle and sometimes are missed, risking morbidity and even mortality for patients, and subjecting providers to high medicolegal liability. Prior malpractice suits involving missed cervical injuries in blunt trauma patients, for example, have resulted in multimillion-dollar awards.
This article covers the pathophysiology, clinical assessment, and management of traumatic PNIs and SCIs. The primary population of this review is adult patients. Please see the article “ Neurologic Emergencies at the Extremes of Age ,” by Khoujah and Cobb for further discussion of pediatric and geriatric populations.
Peripheral nerve injury
Traumatic PNI represents a significant burden of disease. PNIs are thought to have an incidence of more than 350,000 per year in the United States. Previous estimates using the National Inpatient Sample and National Emergency Department Sample show widely varying estimates of injuries based on diagnosis codes and likely underestimate the true burden of injury. The overall trend in injuries has been relatively stable, with upper extremity PNI more common than lower extremity PNI. , Among trauma patients evaluated at a level 1 trauma center, 2.8% were identified as having a PNI. European trauma registry data showed PNIs associated with 3.3% of severe upper extremity trauma and 1.8% of severe lower extremity trauma. , PNIs may remain occult in severely injured patients given priorities of resuscitation and concomitant injuries that limit the examination. A previous case series of traumatic brain injury patients identified a 34% incidence of PNIs not recognized on initial evaluation.
Males account for 80% of traumatic PNIs with a mean age of approximately 40 years in registry data. , Blunt mechanisms, including motor vehicle accidents and falls, account for the majority of injuries but disproportionately higher rates of PNIs are observed in penetrating trauma then compared to the overall trauma population. In upper extremity trauma, the ulnar nerve is injured most commonly, followed by the radial and median nerves. The peroneal nerve is the lower extremity nerve most commonly injured followed by the sciatic and tibial nerves. Sports-related acute nerve injury represents less than 1% of all injuries but has been increasing.
Key Anatomy and Pathophysiology
The terms, peripheral nerve and PNS , encompass nervous tissue and supporting structures between the central nervous system and target tissues or sensory areas. These include cranial nerves (except for the optic nerves) and the autonomic nervous system, in addition to motor and sensory branches originating in the spinal cord. Peripheral nerves have several specialized connective tissues: the endoneurium, the perineurium, and the epineurium ( Fig. 1 ). These define the structure of the nerve and are critical for regeneration.
Most PNIs can be attributed to a combination of mechanisms including traction or stretch, contusion, transection, and compression. Other mechanisms of traumatic injury include ischemia, burns, and electrical injuries. Nerves are vulnerable to different mechanisms along their length due to the changing composition of the nerves and regional anatomy. Nerve roots, for instance, lack both epineurium and perineurium and are relatively tethered to the spinal cord, making them vulnerable to traction and compression. Proximity to bone makes nerves vulnerable to injury from fractures, whereas superficial nerves may be more easily contused or lacerated.
Nerve stretching can be part of normal function with changes in length as nerves cross over joints and at extremes of physiologic movement. Extremes of stretching overwhelm the ability of the connective tissue to compensate and result in injuries with associated hematomas and scarring. Avulsion is an extreme stretch or traction injury causing mechanical failure and disruption of the nerve, often occurring at nerve roots and is associated with significant morbidity.
Compression can cause ischemic injury from direct or indirect pressure (eg, associated compartment syndrome). A classic example is compression of the radial nerve against the humerus as it travels in the radial groove, producing a Saturday night palsy. Hydrostatic forces from penetrating injury also can cause nerve injury or disruption. Crush injuries can occur directly or via entrapment from dislocation-relocation or associated fractures. Laceration or transection mechanisms can be divided into sharp and blunt.
Classification of Peripheral Nerve Injuries
In 1942, Seddon proposed a classification scheme that is still in primary use today for grading nerve injuries based on severity of disruption to the nerve and supporting structures. Seddon divided injuries as neurapraxia, axonotmesis, and neurotmesis ( Fig. 2 ). Sunderland later expanded this to 5 degrees of injury ( Table 1 ).
|Seddon||Sunderland||Clinical Correlate||Pathologic Correlate||Prognosis for Spontaneous Recovery||Surgical Intervention|
|Axonotmesis||2||Ischemia, crush, percussion||Axon degeneration||Good to fair||Usually unnecessary|
|3||Endoneural injury||Intermediate||May be required|
|4||Perineural injury||Poor||May be required|
|Neurotmesis||5||Avulsion, transection||Epineural Injury||Poor||Required|
Presentation and Examination of Peripheral Nerve Injuries
Traumatic PNI initially is a clinical diagnosis and, because PNIs by themselves typically are not life threatening, other more dangerous and time-sensitive causes and associated injuries must be considered. In the trauma patient, prompt global assessment and resuscitation should be undertaken prior to detailed investigation for nerve injury. All sensory or motor abnormalities should be evaluated for alternative causes, especially central causes, such as intracranial hemorrhage and SCIs. An evolving deficit should prompt evaluation for a dynamic process like progressive edema, hematoma formation, pseudoaneurysm formation, or shifting of fractures.
Evidence of nerve injury should prompt consideration of associated fractures, hematomas, compartment syndrome, and arterial injuries. Because nerves typically travel along the neurovascular bundles, and blood vessels are vulnerable to the same forces, approximately 13% of upper extremity PNIs from civilian trauma have an associated vascular injury. , Injuries associated with warfare and penetrating injury have an even higher association between PNIs and vascular injuries, with arterial injuries present in 48 of 119 patients in a case series of PNIs from the Balkan conflict. Traumatic injuries typically present with maximal deficits.
It is critical to determine open versus closed injuries because this significantly alters management. Exploration of an open wound and assessment of the wound mechanism can help identify an associated clinical nerve injury. A clean, sharp transection versus a blunt, ragged transection can affect the urgency of repair. , , Providers should use motor grading and sensory testing to determine the severity and likely anatomic location(s) of injury ( Fig. 3 for sensory distribution of major peripheral nerves). Two-point discrimination is the preferred mode of testing for sensory injury with a recent case series of hand injuries, demonstrating 98.6% sensitivity for detecting nerve injury with a 2-point discrimination tool compared to 82.5% for dry gauze. , Tinel sign also may be present acutely at the area of injury with advancing location and increased pain present in regenerating injuries and developing neuromas, respectively.
|Nerves||Example Mechanism(s)||Major Deficits||Pathologic Correlate|
|Brachial plexus||Stinger/burner |
|Variable; typically, C5-C6 or C8-T1, depending on direction of forces |
Autonomic deficits (eg, Horner syndrome) in C8-T1 lesions
|Neuropraxia, nerve avulsion in severe trauma|
|Axillary||Shoulder dislocation |
Surgical neck fracture of humerus
|Sensory: deltoid area |
Motor: shoulder flexion and abduction
|Radial||Midshaft humerus fracture |
Saturday night palsy
|Sensory: dorsal medial hand |
Motor: wrist extension, finger extension
|Ulnar (proximal)||Elbow dislocation |
Medial epicondyle fracture
|Sensory: ulnar hand |
Motor: grip strength, fourth and fifth digits flexion (proximal)
|Median||Supracondylar fracture of humerus |
Laceration (typically distal)
|Sensory: palmar radial hand |
Motor: thumb opposition, second and third digits flexion
|Long thoracic nerve||Penetrating chest, axilla, or supraclavicular trauma||Motor: scapular protraction (may significantly impair upper extremity function)||Neurotmesis|
|Nerves||Example Mechanism(s)||Major Deficits||Pathologic Correlate|
|Sciatic||Posterior hip dislocation |
|Sensory: posterior and lateral leg, dorsal and plantar foot |
Motor: knee flexion, ankle dorsiflexion and plantarflexion
|Peroneal||Knee dislocation |
|Sensory: dorsal foot |
Motor: ankle dorsiflexion and eversion
|Inferior gluteal||Posterior hip dislocation||Sensory: none |
Motor: hip extension and extension of the flexed thigh
|Tibial||Tibial fracture |
|Sensory: plantar foot |
Motor: ankle plantarflexion
Diagnostic Evaluation of Peripheral Nerve Injuries
Clinical examination combined with potential surgical exploration, electromyography, and nerve conduction studies is important for overall assessment of PNIs. Additional diagnostics during acute presentations in the ED are largely supplements to the clinical examination and evaluate primarily for associated injuries and alternative causes.
X-ray and computed tomography evaluation
Peripheral nerves are not imaged by plain radiographs and are poorly imaged with computed tomography (CT). These images can evaluate for associated injuries. Individual nerve injuries may prompt specific radiographs to identify commonly associated fractures or dislocations (eg, hook of hamate fracture in distal ulnar nerve injury or evaluation for a Bankart or Hill-Sachs lesion suggestive of previous dislocation in axillary nerve dysfunction). Although CT is inadequate for direct evaluation of nerve injury, it has added utility for evaluating soft tissue lesions and vascular structures CT myelography is sensitive and specific for brachial plexus injury and nerve root avulsion in later phases of injury.
Magnetic resonance imaging
Magnetic resonance imaging (MRI), also called magnetic resonance neurography, is superior to CT for PNIs due to significantly improved contrast resolution, ability to assess nerve edema, and evolving use of sequences to assess nerve integrity. , , The utility of MRI in the immediate or early evaluation of suspected injury is unclear, because there are no established guidelines and because of typically conservative overall management strategy of closed nerve injuries. Given the limitations of electrodiagnostic testing in the acute phase, there may be select cases of MRI that allow for earlier intervention.
Ultrasonography, along with MRI, is the other preferred imaging technique for nerve injury. Ultrasound offers high spatial resolution, the ability to perform dynamic maneuvers, and comparatively low cost but with limited contrast resolution, limited ability to image deeper structures, and significant operator dependence. , Nerves are imaged best with a high-frequency linear array and have a characteristic echotexture due to bundles of nerve fibers or fascicles.
Superficial nerves are well visualized and can be traced along their course to evaluate for swelling, size, or echotexture changes (eg, loss of internal architecture) that may indicate neuropraxia, axonotmesis/neurotmesis, and disruption of nerve continuity. These can be accentuated by dynamic maneuvers. Ultrasound is able to characterize much of the course of the most commonly injured nerves and can identify areas of nerve entrapment. , ,
The role of ultrasound in the ED is evolving but has been shown in some cases to be superior to MRI in evaluation of nerve lesions. Ultrasound evaluation changes management in as many as 58% of cases, including decisions on immediate versus delayed surgery, identification of complete nerve disruption, detection of foreign bodies, and detection of multiple areas of injury. ,
Electrodiagnostic testing is the interrogation of nerve function using electrical impulses and is widely used for evaluation of nerve function, including in traumatic injuries. This technique does not have a role in the acute setting because electromyography and nerve conduction studies cannot differentiate between neuropraxia, axonotmesis, and neurotmesis immediately after injury. , Neuropraxia and higher-grade injuries can be differentiated by 1 week postinjury. PNI features are variable between injury areas and type, and serial evaluations over time are used to help gauge recovery and plan interventions.
Management of Peripheral Nerve Injuries
Disposition and follow-up
Treatment can vary widely after initial evaluation of possible nerve injury because, depending on the type of injury, it may be supportive or surgical. Smith and colleagues outlined a proposed approach to management of nerve injury building on the approach of Grant and colleagues ( Fig. 4 ). ,
The rule of 3s can be helpful in considering the appropriate timing of follow-up and intervention in subspecialty care. Sharp nerve transections are best explored and repaired within 3 days. Open injuries that are ragged or contused may be best explored for repair after 3 weeks to allow demarcation and healing of associated injuries as healthy nerve ends are needed for repair. Closed injuries typically are considered for surgery after 3 months postinjury.
After stabilization and assessment, sharply transected PNIs should prompt consultation for immediate repair or transfer. Transections without cleanly incised ends for anastomosis should still prompt discussion with specialty care and should have urgent follow-up. Closed injuries also should have urgent referral to specialty care not only for possible surgery but also because such patients benefit from comprehensive rehabilitation services.
Wound management in the ED in part is driven by need for specialty care or transfer. Wounds should be decontaminated, explored, and assessed for foreign bodies, tetanus status updated, and pain addressed. Closure should be done in consultation with a specialist if the patient is not a candidate for immediate evaluation or transfer and if within the scope of the emergency provider’s practice. Nerve ends can be tagged with suture to local structures to maintain nerve length, which facilitates better identification of nerves and preserves nerve length on re-exploration.
Spinal cord injury
SCI affects approximately 300,000 individuals in the United States, with approximately 17,810 new cases occurring per year. Like most trauma patients, these individuals tend to be younger and male. Overall, there is an almost 4:1 male predominance among new SCIs in the United States. Paralleling the aging population of the United States, the mean age of patients with acute traumatic SCI has risen gradually from 29 years to 43 years. The most common age at the time of injury for the past several years is 19 years, and more than a quarter (25.61%) of all cases occur between the ages of 16 years and 22 years. Non-Hispanic blacks make up approximately 24% of new cases despite representing approximately only 13% of the US population.
The most common cause of SCIs varies with age and other factors, such as gender and race. Notably, the top 3 causes for both genders are the same: auto accidents, followed by falls and gunshot wounds ( Table 4 ). Over the age of 45 years, falls become the leading cause of SCIs in the United States. The proportion of SCIs from vehicular accidents, acts of violence, and sports-related injuries have been declining from their peaks, while the proportion of SCIs from falls and medical/surgical complications have been increasing.
|Rank||Cause of Spinal Cord Injuries Among Men (% of Total Cases)||Cause of Spinal Cord Injuries Among Women (% of Total Cases)|
|1||Auto accident (28.6)||Auto accident (46.6)|
|2||Fall (22.8)||Fall (23.1)|
|3||Gunshot wound (16.6)||Gunshot wound (9.3)|
|4||Motorcycle accident (7.1)||Medical/surgical complication (5.4)|
|5||Diving (6.5)||Diving (2.4)|
|6||Hit by falling/flying object (3.2)||Motorcycle accident (2.2)|
|7||Medical/surgical complication (2.3)||Pedestrian (2.0)|
|8||Bicycle (1.9)||Horseback riding (1.2)|
|9||Pedestrian (1.4)||Person-to-person contact (1.1)|
|10||Person-to-person contact (1.0)||Bicycle (1.0)|
Globally, approximately 750,000 traumatic SCIs occur each year. Etiologies and consequences of SCIs vary in other countries. Higher-income countries tend to have older populations and see a bimodal distribution of traumatic SCIs, with peaks between the ages of 18 years and 32 years and at ages greater than 65 years. These older populations also see higher rates of tetraplegia with falls. Work-related falls in younger patients are more common in low-income countries.
Although acute SCIs may involve any part of the spine, certain regions are more common. The needed flexibility of the cervical spine for flexion, extension, and rotation makes this region highly vulnerable to injury. The cervical spine is the most common site of injury in motor vehicle accidents and falls. Complete and incomplete tetraplegia consequently has made up approximately 60% of acute traumatic SCI cases since 2015.
Key Anatomy and Pathophysiology
The spinal cord exits the foramen magnum and travels the length of the spine to the conus medullaris. The anterior-posterior diameter remains relatively constant, with transverse enlargements occurring in cervical and lumbar spine, around C5 and L3, respectively. The bony boundaries of the spinal canal are relatively wide in the upper cervical spine, which can help protect the spinal cord from potentially devasting injuries in this area. The relative area of the cervical canal compared to the cord gets progressively smaller, increasing the chance of SCI in the lower cervical spine.
The spinal cord contains several important paired nerve tracts:
Corticospinal tracts—located both anteriorly/medially and posteriorly/laterally. These are the major descending motor pathways.
Spinothalamic tracts—located anteriorly/laterally. These ascending pathways communicate light touch, temperature, and pain to the brain.
Dorsal columns—located posteriorly/medially. These ascending pathways communicate deep touch, proprioception, and vibration to the brain.
The spinal cord branches into 31 pairs of spinal nerves, named for the anatomic location of their origin. This includes 8 cervical nerves (C1–C8) that exit the spinal column above their associated vertebra except for the C8 spinal nerve, which exits between the seventh cervical and first thoracic vertebra. The thoracic, lumbar, and sacral spinal nerves all exit below their associated vertebra.
Although SCI can occur in isolation, it frequently is associated with injuries of the vertebral column. Any underlying spinal disease can significantly increase the risk of injury to the bony spine and consequently the spinal cord. Many examples are associated with aging (like cervical spondylosis and osteoporosis). Spinal arthropathies like ankylosing spondylitis or rheumatoid arthritis may affect younger patients as well. , Additionally, congenital conditions like the atlantoaxial instability seen in Down syndrome and medication side effects like corticosteroid-induced osteoporosis may place patients at increased risk.
The mechanism of any traumatic neurologic injury may be classified broadly as blunt versus penetrating. Blunt mechanisms are the leading cause of trauma in general and can cause SCI through excessive flexion/extension, rotational movements, shearing, or compressive forces. Penetrating injuries may be due to bullets, knives, or other missiles (like shrapnel) related to the traumatic event. This mechanism classically produces a transection injury of the spinal cord or vertebral fractures with associated SCIs. In rare cases, indirect damage to the spinal cord may occur. High-velocity missiles may cause contusion of the spinal cord as their kinetic energy dissipates despite never physically violating the spinal axis. Case reports describe this phenomenon also occurring with low-velocity bullets.
Classification of Spinal Cord Injuries
The source of SCIs may be primary or secondary. Primary injury encompasses all the initial mechanical insults (eg, compression, shearing, and laceration) affecting nerves at the time of injury. Secondary injury occurs over the following minutes to hours and causes further damage to the spinal cord through edema and additional cellular death. Secondary injury is a complex and poorly understood collection of processes like hypoxia, inflammation, and ischemia but represents an important therapeutic target for emergency physicians and spinal cord specialists.
The degree of injury is classified broadly as complete or incomplete. A complete injury causes total loss of sensation and motor function below the level of injury. Incomplete injuries are highly variable with symptoms that may range from relatively minor to near-complete paralysis. The most widely accepted scale for classifying SCI severity is the American Spinal Injury Association (ASIA) Scale. Grade A is assigned to patients with a complete cord injury, whereas grades B, C, and D identify progressively less severe degrees of incomplete injury. ED providers should be familiar with the ASIA International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI) worksheet ( Fig. 5 ). Its use allows for a rapid and accurate assessment of a patient’s deficits, clear communication with specialists, and longitudinal assessment of the patient.