Approximately 12,000 new spinal cord injuries (SCIs) occur annually. As the population has aged since the 1970s, the median age at injury has increased from 28 to the current median age of 42 years.15 The diagnosis of SCI begins with a detailed history of events surrounding the incident, precise evaluation of sensory and motor function, and radiographic studies of the spine.
Mechanism of Injury
The type of primary injury sustained depends on the mecha-nism of injury. The greatest cause of SCI is MVCs (36.5%), followed by falls (28.5%), violence (14.3%), other or unknown causes (9.2%), and sports (11.4%).15
Hyperflexion. Hyperflexion injury is most often seen in the cervical area, especially at the level of C5 to C6, because this is the most mobile portion of the cervical spine. This type of injury less than 8 and abnormal findings on a head CT scan.13 Brain
tissue oxygen monitoring may also be used.
Nursing Management
Nursing priorities in management of traumatic brain injury focus on 1) ongoing assessments of vital signs and hemody-namics, 2) reducing increased intracranial pressure and maintaining adequate cerebral perfusion pressure
Nursing diagnoses priorities for the patient with TBI are listed in Box 25-5.
Ongoing nursing assessments are the cornerstone of care of the patient with a TBI. These assessments are the primary mechanism for determining secondary brain injury from cerebral edema and increased ICP. If secondary injury is to be prevented, the nurse must respond immediately to hypo-tensive events and, in collaboration with physicians, maxi-mize CPP through reduction of ICP and restoration of an adequate mean arterial pressure.13
All aspects of care, including hemodynamic management, pulmonary care, maintenance of body temperature, fluid volume management and control of the environment, can impact outcome after TBI.13
Arterial blood pressure should be monitored because hypotension in a patient with TBI is uncommon and may indicate additional injuries. Hypotension will reduce blood flow to the brain. CPP should be maintained at a minimum of 60 mm Hg.13 In the absence of cerebral ischemia, aggres-sive attempts to keep CPP above 70 mm Hg with intravenous fluids and vasopressors should be avoided secondary to the risk of ARDS.13
Capnography (monitoring of exhaled carbon dioxide levels) is suggested to prevent inadvertent hypocapnia or hypercapnia.13 Aggressive pulmonary care must be instituted.
However, endotracheal suctioning can elevate ICP. Tech- niques to counter elevation in ICP with suctioning are out-lined in Box 25-6. Cerebral oxygen consumption is increased during periods of increased body temperature, and therefore euthermia (36° to 37° C) may be achieved with early workup and intervention for infection, use of antipyretics, and cooling measures such as evaporative cooling.
From McQuillan KA, Thurman P. Traumatic brain injuries. In:
McQuillan K, et al, eds. Trauma: from Resuscitation Through Rehabilitation. St. Louis: Elsevier; 2009.
• Pass the suction catheter for no longer than 10 seconds.
• Limit the number of suction catheter passes, preferably to no more than two passes per suctioning episode.
• Hyperoxygenate the patient before and after each passage of the suction catheter (e.g., deliver 4 ventilator breaths at 135% of the patient’s tidal volume on 100% FiO2, at a rate of 4 breaths in 20 seconds).
• Minimize airway stimulation (e.g., stabilize endotracheal tube, avoid passing the suction catheter all the way to the carina).
BOX 25-6 Recommendations for Suctioning Patients with Traumatic Brain Injury BOX 25-5 NURSING DIAGNOSES
PRIORITIES: TRAUMATIC BRAIN INJURY
• Ineffective Breathing Pattern related to neuromuscular impairment, p. 598
• Risk for Aspiration: impaired laryngeal sensation or reflex;
impaired pharyngeal peristalsis or tongue function; impaired laryngeal closure or elevation; increased gastric volume;
decreased lower esophageal sphincter pressure, p. 602
• Impaired Gas Exchange related to ventilation–perfusion mismatching, p. 594
• Imbalanced Nutrition: Less Than Body Requirements related to lack of exogenous nutrients and increased meta-bolic demand, p. 593
• Powerlessness related to lack of control over current situ-ation, p. 600
• Decreased Intracranial Adaptive Capacity related to failure of normal compensatory mechanisms, p. 582
• Risk for Ineffective Cerebral Tissue Perfusion, p. 604
most often is caused by sudden deceleration motion, as in head-on collisions. Injury occurs from compression of the cord as a result of fracture fragments or dislocation of the vertebral bodies. Instability of the spinal column occurs because of the rupture or tearing of the posterior muscles and ligaments.
Hyperextension. Hyperextension injuries involve back-ward and downback-ward motion of the head. With this injury, often seen in rear-end collisions or MVCs, the spinal cord is stretched and distorted. Neurologic deficits associated with this injury are often caused by contusion and ischemia of the cord without significant bony involvement. A mild form of hyperextension is the whiplash injury.
Rotation. Rotation injuries often occur in conjunction with a flexion or extension injury. Severe rotation of the neck or body results in tearing of the posterior ligaments and dis-placement (rotation) of the spinal column.
Axial loading. Axial loading, or vertical compression, injuries occur from vertical force along the spinal cord. This most commonly is seen in a fall from a height in which the person lands on the feet or buttocks. Compression injuries cause burst fractures of the vertebral body that often send bony fragments into the spinal canal or directly into the spinal cord (Figure 25-4).
Penetrating injuries. Penetrating injury to the spinal cord can be caused by a bullet, knife, or any other object that pen-etrates the cord. These types of injury cause permanent damage by anatomically transecting the spinal cord.
Pathophysiology
SCIs are the result of a mechanical force that disrupts neuro-logic tissue or its vascular supply, or both. Much like the
FIG 25-4 Spinal Cord Compression Burst Fracture. Com-pression injuries cause burst fractures of the vertebral body that often send bony fragments into the spinal canal or directly into the spinal cord. Include hyperflexion, hyperexten-sion, rotation, axial loading (vertical compression), and missile or penetrating injuries.
pathophysiology of TBI, the injury process includes primary and secondary injury mechanisms. Primary injury is the neu- rologic damage that occurs at the moment of impact. Second-ary injury refers to the complex biochemical processes affecting cellular function. Secondary injury can occur within minutes of injury and can last for days to weeks.
Several events after SCI lead to spinal cord ischemia and loss of neurologic function. A cascade of events is initiated that includes systemic and local vascular changes, electrolyte and biochemical changes, neurotransmitter accumulation, and local edema (Box 25-7). Collectively, these pathophysi-ologic events result in worsening of the injury, potentially extending the level of functional deficit and worsening long- term outcome. Knowledge of the pathophysiology of second-ary processes has led to the development of new medications, which target the cellular changes contributing to injury.
Despite ongoing research efforts at repairing the primary injury, minimizing damage by reducing secondary injury has shown the most promise.
Functional Injury of the Spinal Cord
Functional injury of the spinal cord refers to the degree of disruption of normal spinal cord function. This depends on what specific sensory and motor structures are damaged.
SCIs are classified as complete or incomplete. The most fre- quent categories at hospital discharge are incomplete tetraple-gia (40%) and incomplete paraplequent categories at hospital discharge are incomplete tetraple-gia (18%),15 followed by complete paraplegia (18%) and complete tetraplegia (11%).15 SCI cannot be classified until spinal shock has resolved.
Complete injury. Complete SCI is a complete dissection of the spinal cord that results in a total loss of sensory and motor function below the level of injury.
Tetraplegia. With tetraplegia, the injury occurs from the C1 to T1 level. Residual muscle function depends on the specific cervical segments involved. The potential functional status resulting from different neurologic levels of injury is described in Table 25-5.
Paraplegia. With paraplegia, the injury occurs in the tho-racolumbar region (T2 to L1). Patients with injuries in this area may have full use of the arms and may need a wheelchair, although some may have limited ability to ambulate short distances with crutches and orthoses (custom external support devices). Thoracic L1 and L2 injuries produce para-plegia with variable innervation to intercostal and abdominal muscles.
Incomplete injury. Incomplete SCI results in a mixed loss of voluntary motor activity and sensation below the level of the lesion. Incomplete SCI exists if any function remains below the level of injury. Incomplete injuries can result in a variety of syndromes, which are classified according to the degree of motor and sensory loss below the level of injury.
Brown-séquard syndrome. The Brown-Séquard syn-drome is associated with damage to only one side of the cord.
This produces loss of voluntary motor movement on the same side as the injury, with loss of pain, temperature, and sensa-tion on the opposite side. Functionally, the side of the body with the best motor control has little or no sensation, whereas the side of the body with sensation has little or no motor control.
Central cord syndrome. Central cord syndrome is asso-ciated with cervical hyperextension–hyperflexion injury and hematoma formation in the center of the cervical cord. This
Adapted from Sekhon LHS, Fehlings MG. Epidemiology, demographics, and pathophysiology of acute spinal cord injury.
Spine. 2001: 26(24S):S2.
Primary Injury Mechanisms
• Acute compression
• Impact
• Missile
• Distraction
• Laceration
• Shear
Secondary Injury Mechanisms
• Systemic effects
• Heart rate: brief increase, then prolonged bradycardia
• Blood pressure: brief hypertension, then prolonged hypotension
• Decreased
• Peripheral resistance
• Decreased cardiac output
• Increased catecholamines, then decreased
• Hypoxia
• Hyperthermia
• Injudicious movement of the unstable spine leading to wors-ening compression
• Local vascular changes
• Loss of autoregulation
• Systemic hypotension (neurogenic shock)
• Hemorrhage (especially gray matter)
• Loss of microcirculation
• Reduction in blood flow
• Vasospasm
• Thrombosis
• Electrolyte changes
• Increased intracellular calcium
• Increased intracellular sodium
• Increased sodium permeability
• Increased intracellular potassium Biochemical Changes
• Neurotransmitter accumulation
• Catecholamines (e.g., norepinephrine, dopamine)
• Excitotoxic amino acids (e.g., glutamate)
• Arachidonic acid release
• Free radical production
• Eicosanoid production
• Prostaglandins
• Lipid peroxidation
• Endogenous opioids
• Cytokines
• Edema
• Loss of energy metabolism
• Decreased adenosine triphosphate production
• Apoptosis
BOX 25-7 Primary and Secondary Mechanisms of Acute Spinal Cord Injury
NEUROLOGIC LEVEL (VERTEBRAE) OF COMPLETE
INJURY FUNCTIONAL ABILITY
C1-C4 Requires electric wheelchair with breath, head, or shoulder controls
C5 Needs electric wheelchair with hand
control and/or manual wheelchair with rim projections; may require adaptive devices to assist with ADLs
C6 Independent in manual wheelchair on
level surface; may need hand controls; adaptive devices may be needed for ADLs
C7 Requires manual wheelchair on most
surfaces
C8-T1 May need adaptive devices
TABLE 25-5 Quadriplegia Functional Status
ADLs, Activities of daily living.
injury produces a motor and sensory deficit more pronounced in the upper extremities than in the lower extremities. Various degrees of bowel and bladder dysfunction may be present.
Anterior cord syndrome. The anterior cord syndrome is associated with injury to the anterior gray horn cells (motor), the spinothalamic tracts (pain), anterior spinothalamic tract (light touch), and the corticospinal tracts (temperature). The
result is a loss of motor function and loss of the sensations of pain and temperature below the level of injury. However, below the level of injury, position sense and sensations of pressure and vibrations remain intact. Anterior cord syn- drome is commonly caused by flexion injuries or acute her-niation of an intervertebral disk.
Posterior cord syndrome. Posterior cord syndrome is associated with cervical hyperextension injury with damage to the posterior column. This results in the loss of position sense, pressure, and vibration below the level of injury. Motor function and sensation of pain and temperature remain intact. These patients may not be able to ambulate because the loss of position sense impairs spontaneous movement.
Spinal shock. Spinal shock is a condition that can occur shortly after traumatic injury to the spinal cord. Spinal shock is the complete loss of all muscle tone and normal reflex activ-ity below the level of injury.5 Patients with spinal shock may appear completely flaccid, without neurological function below the area of the injury, although all of the area may not necessarily be destroyed.
Neurogenic shock. Neurogenic shock results from injury to the descending sympathetic pathways in the spinal cord.
This results from loss of vasomotor tone and sympathetic innervation to the heart. A relative hypovolemia and hypo-volemic shock ensues, causing hypotension and decreased systemic vascular resistance. Patients with SCI at T6 or above may have profound neurogenic shock as a result of interrup- tion of the sympathetic nervous system and loss of vasocon-strictor response below the level of the injury. Blood vessels cannot constrict, and the heart rate is slow, which results in hypotension, venous pooling, and decreased cardiac output.
Airway. Assessment of ABCs is essential to ensure optimal oxygenation and perfusion to all vital organs, including the spinal cord. Complete cardiovascular and respiratory assess-ments are essential to the patient’s survival and prognosis. The primary assessment begins with an evaluation of airway clear-ance. In an unresponsive person, an oral airway is inserted while the patient’s neck is maintained in a neutral position.
The patient must undergo intubation before severe hypoxia can occur, which could further damage the spinal cord.
Breathing. Assessment of breathing patterns and gas exchange is made after an airway has been secured. The level of injury dictates the degree of altered breathing patterns and gas exchange (Table 25-6). Because complete injuries above the C3 level result in paralysis of the diaphragm, patients with these injuries require ventilatory assistance.
Circulation. Assessment of cardiac output and tissue per-fusion is imperative to detect life-threatening injuries and promote recovery of injured spinal cord tissue. The patient with SCI is at high risk for developing alterations in cardiac output and tissue perfusion because the cardiovascular system is subjected to a variety of serious and potential physiologic alterations, including dysrhythmias, cardiac arrest, ortho-static hypotension, emboli, and thrombophlebitis.
The patient with SCI is assessed for adequate tissue perfu-sion by means of invasive and noninvasive hemodynamic monitoring techniques. Cardiac monitoring is required to detect bradycardia and other dysrhythmias that occur in response to reflex vagus activity mediated by the dominant parasympathetic nervous system, as well as changes in ECG rhythm as a result of hypothermia or hypoxia.
Neurologic assessment for spinal cord injury. The initial neurologic assessment may not be an accurate indication of eventual motor and sensory loss. It focuses on the rapid and accurate identification of present, absent, or impaired func-tioning of the motor, sensory, and reflex systems that Cellular oxygenation is threatened as cardiac output declines
because of a decrease in stroke volume (hypovolemia) and heart rate (bradycardia). The duration of this shock state can persist for up to 1 month after injury. Blood pressure support may be required with the use of sympathomimetic medica-tions. Because hypotension is a problem, the nurse must be cautious when adjusting backrest position or when reposi-tioning a patient in bed because orthostatic blood pressure changes can occur (see “Neurogenic Shock” in Chapter 26).
Autonomic dysreflexia. Autonomic dysreflexia is a life-threatening complication that may occur with SCI. This condition is caused by a massive sympathetic response to a noxious stimuli (e.g., full bladder, line insertions, fecal impaction) that results in bradycardia, hypertension, facial flushing, and headache. Immediate intervention is needed to prevent cerebral hemorrhage, seizures, and acute pulmo-nary edema. Treatment is aimed at alleviating the noxious stimuli. A clinical algorithm for treatment of autonomic dys- reflexia is provided in Box 25-8. If symptoms persist, antihy-pertensive agents can be administered to reduce blood pressure. Prevention of autonomic dysreflexia is imperative and can be accomplished through the use of a rehabilitative bowel and bladder program.
Assessment in Spinal Cord Injury
On admission to the critical care unit, attention to the ABCs is imperative in the patient with known or suspected SCI.
Stabilization of the spinal cord is mandatory to prevent further injury, and spinal precautions are maintained until the spine is cleared of injury. Stabilization may include the use of bedrest with log-rolling maneuvers and a hard cervical collar until definitive stabilization is achieved. After the ABCs have been evaluated and interventions for life-threatening complications have been initiated, a full physical assessment is made to determine the extent of injury.
• If patient is supine, immediately sit the patient up.
• Begin frequent vital sign monitoring and perform every 5 minutes.
• Survey for instigating causes; begin with urinary system.
• Loosen clothing, constrictive devices.
• If indwelling catheter is not placed, catheterize the patient.
• Lidocaine jelly may be instilled 5 minutes before cathe-ter insertion.
• If indwelling catheter is present, do the following:
• Check system for kinks and obstructions to flow.
• Irrigate the bladder with small sterile amount of fluid, utilizing strict aseptic technique.
• If not draining, remove the catheter and replace.
• If systolic blood pressure is greater than 150 mm Hg, con-sider rapid-onset, short-duration antihypertensive agent.
• If acute symptoms persist, suspect fecal impaction:
• Instill lidocaine jelly into rectum; wait at least 5 minutes.
• Perform digital examination to check for presence of stool; if present, gently remove. If signs of autonomic dysreflexia persist, stop examination; instill additional lidocaine jelly and wait 20 minutes to reexamine.
• If no stool is found and the abdomen is distended, con-sider administration of laxative.
BOX 25-8 Autonomic Dysreflexia
NEUROLOGIC LEVEL (VERTEBRAE) OF COMPLETE
INJURY RESPIRATORY
FUNCTION COMMENT
C1-C2 Paralysis of
diaphragm
Ventilator-dependent
C3-C5 Various
degrees of diaphragm paralysis
Some diaphragm control; may need ventilatory support; weaning depends on preinjury pulmonary status.
C6-T11 Various
degrees of impaired intercostal muscles and abdominal muscles
Compromised respiratory function; reduced inspiratory ability;
paradoxical breathing patterns;
ineffective cough, sneeze
TABLE 25-6 Effects of Spinal Cord Injury on Ventilatory Functions
5. Active movement against maximal resistance 4. Active movement through range of motion against
resistance
3. Active movement through range of motion against gravity
2. Active movement through range of motion with gravity eliminated
1. Visible or palpable muscle contraction 0. No contraction; total paralysis
TABLE 25-7 Muscle Strength Scale
TRAUMA PATIENT POPULATION RECOMMENDATION Trauma patients that are awake, alert, not
intoxicated, neurologically normal, no complaints of neck pain or tenderness with full range of motion of the cervical spine
Neck is palpated in all directions for tenderness or pain.
If physical examination is negative for pain or tenderness, CT imaging of the cervical spine is not required, and the cervical collar may be removed.
All other trauma patients with suspected cervical injury must be radiologically evaluated. This includes patients with neck pain or tenderness, whether alert or with altered mental status/neurological deficit, or distracting injury.
Axial CT from occiput to T1 with sagittal and coronal reconstructions If CT is positive for injury, continue cervical collar, obtain spine
consultation, and obtain MRI.
In the neurologically intact awake patient with neck pain, if the CT is negative (no injury seen), MRI is negative, and adequate flexion/extension films are negative, discontinue cervical collar.
Trauma patients that are obtunded with gross motor function of extremities
Axial CT from occiput to T1 with sagittal and coronal reconstructions If the CT is negative (no injury seen), the risk/benefit of an additional MRI
must be determined in each hospital.
Options are
A. Continue cervical collar until a clinical exam can be performed.
B. Remove the cervical collar on the basis of negative CT alone.
C. Obtain MRI.
If MRI is negative, collar can be safely removed.
Flexion/extension radiography should not be performed.
TABLE 25-8 East Guidelines for Cervical Spine Clearance
CT, Computed tomography; EAST, Eastern Association of Surgeons in Trauma; MRI, magnetic resonance imaging.
From Como, et al. Practice management guidelines for identification of cervical spine injuries following trauma: update from the Eastern Association for the Surgery of Trauma Practice Management Guidelines Committee. J Trauma. 2009: 67(3):651.
coordinate and regulate vital functions. A detailed motor and sensory examination includes the assessment of all 32 spinal nerves for evidence of dysfunction. Carefully mapped path- ways for the sensory portion of the spinal nerves, called der-matomes, can assist in localizing the functional sensory level of injury. Muscle strength may be graded on a 6-point scale (Table 25-7). Initial assessment must be performed correctly and findings documented in detail so that subsequent serial assessments can rapidly identify deterioration. The American Spinal Injury Association (ASIA) has developed a form that outlines the required assessments for initial and ongoing clas- sification of SCIs (Figure 25-5). Ongoing spinal cord assess-ments must be documented during the critical care phase.
Diagnostic procedures. Diagnostic radiographic evalua-tions can identify the severity of damage to the spinal cord.
Initial evaluation includes anteroposterior and lateral views for all areas of the spinal cord. CT scan of all seven cervical vertebrae and the top of T1 must be obtained to rule out cervicothoracic junction injury. Flexion and extension views can identify subtle ligament injuries. CT, tomography, myelography, and MRI also may be used.
Screening for spinal cord injury. Screening of the spinal cord for injury becomes an integral part of the assessment for all trauma patients. The degree of trauma, alteration in men-tation, intoxication, and distracting injuries dictate the type and extent of examination required to clear the cervical spine.
The Eastern Association of Surgeons in Trauma (EAST) has published guidelines for the clearance of the cervical spine (Table 25-8).16 In these guidelines CT scan has replaced plain radiography as the principal modality for cervical spine assessment following trauma.16 On admission, the spine is palpated for obvious deformity, and the patient is assessed for the subjective response of pain to palpation.16 If the patient has distracting injuries, such as rib fractures, is intoxicated, or has received analgesics, examination of the spinal cord may be deferred.16 MRI may be warranted to diagnose SCI definitively when the patient’s hemodynamic condition is stabilized.16
Medical Management
After assessment and diagnosis of the SCI, medical manage-ment begins. The primary treatAfter assessment and diagnosis of the SCI, medical manage-ment goal is to preserve remaining neurologic function with pharmacologic, surgical, and nonsurgical interventions.
Pharmacologic management. Previously methylprednis-olone was administered in the first 8 hours after SCI,17 However, per current guidelines, this medication is no longer recommended.18
Surgical management. Surgical intervention provides spinal column stability in the presence of an unstable injury.
Unstable injuries include disrupted ligaments and tendons and a vertebral column that cannot maintain normal align-ment. Identification and immobilization of unstable injuries are particularly important for the patient with incomplete neurologic deficit. Without adequate stabilization, movement and dislocation of the vertebral column may cause a complete