1

Traumatic Brain Injury

and Spinal Cord
Injury
Traumatic Brain InJury
Traumatic brain injury (TBI) occurs when the head strikes an
object or an object strikes the head. It can also be an object
penetrates the skull and enters the brain tissue.
Leading causes of TBI include falls, motor vehicle crashes (MVCs),
and gunshot wounds.
Typical mechanisms of injury include:
Acceleration injuries:
a moving object strikes the stationary head
Accelerationdeceleration injuries:
the head in motion strikes a stationary object
Coupcontrecoup injuries:
the brain bounces back and forth within the skull, striking both
sides of the brain
Rotation injuries:
the brain twists within the skull, resulting in stretching and tearing
of blood vessels and shearing of neurons
Penetration injuries:
a sharp object disrupts the integrity of the skull and penetrates
the brain tissue
The resultant injuries range from mild to severe . Many patients
die from their injuries or are left in a coma or persistent
vegetative state. TBI can have a profound and lasting effect on
the patient and family.
For example, emotional and behavioral changes may affect
interpersonal relationships and family roles, or neurologic decits
may affect the patients ability to resume a chosen career or
return to work at all.
Primary Brain Injury
Primary brain injuries are injuries occurring at the time of trauma.
Primary injuries include scalp lacerations, fractures, concussions,
contusions, hematomas, subarachnoid hemorrhage, diffuse
axonal injury (DAI), and cerebrovascular injury.
Scalp Laceration
A scalp laceration frequently causes signicant bleeding (due to
the vascularity of the scalp) and may be associated with
underlying injuries to the skull and brain. The scalp is gently
palpated to assess for deformation of the skull. Scalp lacerations
can be sutured at the bedside or may require surgical repair,

depending on the size and extent of injury. Avulsed areas of the

scalp may require surgical reimplantation.
Skull Fracture
Depressed skull fractures are fractures in which bone fragments
are driven into the underlying meninges and brain tissue. Patients
with depressed skull fractures may require surgery to debride
bone fragments, repair the skull or dura, evacuate a hematoma,
or repair adjacent structures such as sinuses or blood vessels.
Injury to the dura places the patient at risk for meningitis;
therefore, careful monitoring for signs and symptoms of infection
is important.
Basilar skull fractures occur at the base, or oor of the skull,
typically in the areas of the anterior and middle fossae. Clinical
signs of a basilar skull fracture include Battles sign (bruising
behind the ear) or raccoon eyes (periorbital edema and
bruising).
Drainage of cerebrospinal uid (CSF) from the ear (otorrhea) or
nose (rhinorrhea) indicates injury to the dura. Otorrhea typically
signies a fracture in the middle fossa, and rhinorrhea occurs with
a fracture in the anterior fossa.
Dabbing the drainage from the ear or nose with gauze may reveal
the halo sign (layering of uids, with blood on the inside and
CSF in a yellowish ring on the outside).
CSF leaks typically heal spontaneously; however,
a lumbar drain may be used to reduce pressure on the dural tear
and promote healing.
In some cases, the damaged region of dura must be surgically
repaired.
A loose gauze dressing can be applied to the ear or nose to
quantify the amount and character of drainage while allowing
unobstructed drainage of the uid. The skin around the drainage
site is kept clean, and the patient is instructed not to blow his or
her nose.
RED FLAG! In patients with basilar skull fractures, nasogastric and
nasotracheal intubation are contraindicated because of the risk
for passing the tube through the cribriform fracture into the brain.
Concussion
A concussion is a temporary alteration in mental status resulting
from trauma. The patient may or may not lose consciousness.
Often patients are unable to recall events leading up to the
traumatic event, and occasionally short-term memory is affected.
Concussions are not associated with structural abnormalities on
radiographic imaging. Recovery after a concussion is usually
complete; however, some patients develop post concussive

syndrome (headaches, decreased attention span, short-term

memory impairment, dizziness, irritability, emotional lability,
fatigue, visual disturbances, noise and light sensitivity, and
difculties with executive functions). Post concussive syndrome
can last for months and as long as 1 year after the injury.
Contusion
Cerebral contusions result from laceration of the
microvasculature that causes bruising of, or bleeding into, the
brain tissue. Cerebral contusions can range from mild to severe
depending on the location, size, and extent of brain tissue injury.
The diagnosis of cerebral contusion is made using computed
tomography (CT). Complications of a cerebral contusion include
intracerebral hematoma development and cerebral edema.
Cerebral edema peaks 24 to 72 h after injury, causing increased
intracranial pressure (ICP).
Hematoma
Intracranial hematomas may be epidural, subdural, or
intraparenchymal
Epidural Hematoma
An epidural hematoma is a collection of blood between the dura
and inside surface of the skull, often caused by laceration of the
middle meningeal artery. Patients may have a period of lucidity
followed by a loss of consciousness. The rapidly expanding mass
can cause uncal herniation. Prompt recognition and surgical
evacuation of the hematoma is necessary.
Subdural Hematoma
A subdural hematoma is an accumulation of blood below the dura
and above the arachnoid layer covering the brain. Tearing of the
bridging veins (veins that pass from the surface of the brain to
the inner surface of the dura) or disruption of venous sinuses can
cause a subdural hematoma.
Subdural hematomas can be categorized based on the time from
injury to the onset of symptoms:
Acute. Signs and symptoms of increasing ICP (eg,
headache, focal neurological decit, unilateral pupillary
abnormalities, decreasing level of consciousness) manifest
24 to 48 hours after injury. The need for surgical evacuation
is determined based on the size and location of the
hematoma and the degree of neurological dysfunction.
Subacute. Onset of signs and symptoms is delayed (2 days
to 2 weeks after injury). Disruption of smaller blood vessels
may lead to a slower accumulation of blood, causing the
delay in symptom onset. In some cases, cortical atrophy
(often associated with advanced age and alcoholism) may

allow for a greater amount of uid to collect before

symptoms of increased ICP manifest. Surgical hematoma
evacuation may be performed electively according to the
degree of neurologic dysfunction.
Chronic.
Chronic subdural hematomas result from a small bleed or
slow capillary leak. Cortical atrophy causes tension on
bridging veins and can increase the risk for chronic subdural
hematoma. The slow accumulation of uids and brain
atrophy accounts for the delayed presentation of signs and
symptoms, which include headache, lethargy, con- fusion,
and seizures. Surgical intervention may include drilling burr
holes into the skull or craniotomy to remove the hematoma.
Drains may be placed intraoperatively to prevent
reaccumulation of uid. The head of the patients bed is kept
at to decrease tension placed on bridging veins. When the
head of the bed is raised, it must be raised slowly to prevent
rebleeding because as the head is elevated, the brain settles
downward.
Intraparenchymal Hematoma
An intraparenchymal hematoma is a collection of blood within the
brain parenchyma.
Traumatic causes of intraparenchymal hematoma include
depressed skull fractures and penetrating injuries. Medical
management aims to manage cerebral edema and promote
adequate cerebral perfusion. Surgical management is indicated in
patients with a deteriorating neurologic examination referable to
the injured region of brain tissue, and in patients with increased
ICP that is uncontrolled with maximal medical therapies.

Subarachnoid Hemorrhage
Traumatic subarachnoid hemorrhage occurs with tearing or
shearing of microvessels in the arachnoidlayer, resulting in
hemorrhage into the subarach- noid space (which contains the
CSF). Blood in the subarachnoid space irritates the brainstem,
causing abnormal activity in the autonomic nervous system that
may produce cardiac dysrhythmias and hyper- tension.
Hydrocephalus may result when blood in the subarachnoid space
impedes reabsorption of CSF. Cerebral vasospasm, a less common
complication, may also occur.
Diffuse Axonal Injury(dai)
DAI is characterized by a direct tearing or shearing of axons,
which worsens during the rst 12 to 24 hours as cerebral edema
develops. DAI is thought to occur with rotational and acceleration
deceleration forces. DAI can be classied as mild, moderate, or
severe:

Mild DAI is associated with a coma lasting no longer than 24

hours.
Moderate DAI is characterized by a coma lasting longer than 24
hours with transient exor or extensor posturing.
Severe DAI is characterized by prolonged coma, fever,
diaphoresis, and severe extensor posturing.
DAI is not easily identied through radiographic imaging;
however, small punctate hemorrhages may be visualized deep in
the white matter. Magnetic resonance imaging (MRI) may be
helpful in identifying neuronal damage after 24 hours.
Cerebrovascular Injury
Carotid or vertebral artery dissection must be considered when a
patient presents with neurological decits unexplained by other
brain injuries. Arterial dissection is caused by shearing of the
innermost (intima) or middle (media) vessel layers the intima can
result in clot formation or an intimal ap, either of which can
occlude the vessel, resulting in stroke. To detect this type of
injury, cerebral angiography may be ordered for patients who
have sustained injury to the neck or have unexplained focal
neurological decits.
RED FLAG! Early identication of cerebrovascular injury, exclusion
of concomitant hemorrhage, and initiation of anticoagulation
therapy (if warranted) can prevent stroke in patients with
cerebrovascular injury.
Secondary Brain Injury
Secondary brain injury occurs after the initial traumatic event
and causes additional brain injury. Secondary processes (eg,
hypoxemia, hypotension, anemia, cerebral edema, cerebral
ischemia, uncontrolled increased ICP, hypercarbia, hyperthermia,
seizures, hyperglycemia, local or systemic infection) can cause or
exacerbate secondary brain injury.
Cerebral edema commonly occurs in patients with TBIs 24 to 48
hours after the primary insult and typically peaks at 72 hours.3 If
cerebral edema is not aggressively treated, herniation may ensue.
Serial neurologic examinations that include evaluation of level of
consciousness and motor and cranial nerve function are
necessary to identify increased ICP and prevent herniation.
Cerebral ischemia, a major cause of morbidity and mortality,
may be a result of direct vascular injury, loss of autoregulation, or
cerebral edema that causes compression or occlusion of blood
vessels within the brain. Several studies have suggested that
cerebral blood ow may decrease up to 50% during the rst 24 to
48 hours after TBI.4 Continuous surveillance of end-tidal carbon
dioxide (ETCO2) or frequent assessment of the arterial carbon
dioxide tension (PaCO2) is important to prevent cerebral ischemia.

Seizures during the early stages of TBI can have severe

negative effects on ICP and cerebral metabolic demands.
Evidence-based guidelines sup- port the use of antiseizure
medication in the rst 7 days after TBI.5 Seizures that occur after
this initial period (late posttraumatic seizures) are not prevented
by prophylactic administration of anti- seizure medications.5
Hyperthermia (temperature greater than 00F [37.5C]) in a
patient with severe TBI increases metabolic demands and may
compound secondary brain injury. Inducing hypothermia may be
benecial in improving functional outcome, although further
research is required before this practice is recognized as a
standard.5 Currently, induced hypothermia is used on a case bycase basis.
RED FLAG! Preventing and mitigating secondary brain injury
maximizes the patients chances for positive functional outcomes.
Management
Initial assessment and treatment of the patient with TBI begins
immediately after the insult.
Prehospital management of TBI focuses on rapid systems
assessment and denitive airway management. Airway
management is essential for early correction of hypoxia and
hypercarbia, which exacerbate secondary brain injury and affect
morbidity and mortality in patients with TBI. Following transfer of
the patient to the critical care unit, management continues to
focus on preventing or mitigating secondary brain injury, as well
as providing supportive care, preventing or managing
multisystemic complications, and providing family support. A
collaborative care guide for a patient with TBI is given in Box 231.
Caring for the Patient in a Coma or Persistent Vegetative State
Many patients with TBI will be in a coma or persistent vegetative
state:
Coma is an alteration in consciousness caused by damage to
both hemispheres of the brain or the brainstem. Coma results
from disruption of the reticular activating system (RAS), which is a
physiological region encompassing nuclei from the medulla to the
cerebral cortex. The RAS is responsible for wakefulness,
heightened arousal, and alertness. Consciousness can be placed
on a continuum from full consciousness to coma, and states of
coma can be subdivided into light coma, coma, and deep coma.
The duration of coma depends on the type and severity of brain
injury. The Ranchos Los Amigos Scale (Table 23-2) can be used to
describe the patients level of awareness and ability to interact
with the environment.

Coma (sensory) stimulation (Box 23-2) may increase the patients

level of arousal and attention, and lead to better functional
outcomes.
RED FLAG! Coma stimulation is only appropriate for patients with
stable, normal ICPs.
Persistent vegetative state (irreversible coma, coma vigil) is
characterized by a period of sleep-like coma followed by a return
to the awake state with ;an inability to respond to the
environment. In a persistent vegetative state, higher cortical
functions of the cerebral hemispheres have been damaged
permanently, but the lower functions of the brainstem remain
intact. The patients eyes open spontaneously and may appear as
if they are opening in response to verbal stimuli. Sleepwake
cycles exist, and the patient maintains normal cardiovascular and
respiratory control. Also seen are involuntary lip smacking,
chewing, and roving eye movements. A diagnosis of persistent
vegetative state cannot be made for at least 4 weeks after onset
of TBI and coma.
Preventing and Managing Multisystemic Complications
Sympathetic Storming
Patients with severe TBI may experience sympathetic storming as
a result of an imbalance of the sympathetic and parasympathetic
nervous systems.
Sympathetic storming is characterized by diaphoresis; agitation,
restlessness, or posturing; hyperventilation; tachycardia; and
fever. Stressful events (eg, suctioning, turning, loud noises) can
trigger a storming episode.7 The diagnosis of sympathetic
storming is typically based on the appearance of suggestive signs
and symptoms, and treatment focuses on nding a medication
regimen that suppresses the sympathetic nervous system while
avoiding adverse effects such as hypotension and bradycardia.
Agents commonly used as part of the medication regimen include
-adrenergic blockers, -adrenergic blockers, opiates, sedatives,
-aminobutyric acid agonists, and dopamine agonists.
Disorders of Sodium Imbalance Disorders of sodium imbalance are
common in the patient with TBI (Table 23-3).
Diabetes insipidus occurs as a result of a decrease in
antidiuretic hormone (ADH) secretion, leading to hypovolemia and
hypernatremia.
Syndrome of inappropriate antidiuretic hormone secretion
(SIADH), in which ADH is released in excessive amounts, results in
hemodilution, hypervolemia and hyponatremia.

Cerebral saltwasting syndrome (centrally mediated excessive

renal excretion of sodium and water) may cause hyponatremia in
normovolemia to hypovolemia.
Cardiovascular Complications
Myocardial stunning and a transient decrease in cardiac function
may occur in severe TBI. Serum cardiac enzymes,
electrocardiography, echocardiography, and hemodynamic
monitoring may be used to evaluate myocardial function and
guide therapy in the critical phases of TBI. The release of large
amounts of thromboplastin in response to brain injury can cause
disorders of coagulation, such as disseminated intra- vascular
coagulation (DIC). Immobility can place patients with TBI at risk
for deep venous thrombosis (DVT) and pulmonary embolism.
Pulmonary Complications
Patients with TBI are at increased risk for pneumonia, acute
respiratory distress syndrome (ARDS), pulmonary embolism, and
neurogenic ( ash) pulmonary edema. Neurogenic pulmonary
edema, which has a sudden onset, may result from injury to the
brainstem, increased ICP, or an increase in sympathetic nervous
system that causes a catecholamine surge at the time of trauma.
Treatment of neurogenic pulmonary edema includes the judicious
use of low-dose diuretics. Early mobility is critical for preventing
pulmonary complications such as pulmonary embolism and
pneumonia.
Caring for the Family Bond , surveyed the needs of family
members of patients with severe TBI and identied the following
four needs:
The need for specic, truthful information
The need for information to be consistent
The need to be actively involved in the care of the patient
The need to be able to make sense of the entire experience
Providing emotional support and supporting the family in the
process of gathering information and making decisions are
essential nursing responsibilities. Measures such as providing
accurate and timely information, coordinating available support
services (eg, social care, pastoral support) and seeking to involve
the family in patient care (eg, encouraging family members to
assist in providing sensory stimulation) help to meet the needs of
the family, as well as the patient. A patients condition may be so
severe that brain death is the nal outcome. The concept of brain
death is often confusing for families because death is so
commonly associated with cardiopulmonary death. When
communicating with the family about brain death, the language
used is very important, and care must be taken to assess the
understanding and coping mechanisms of family members. Many

patients who are declared brain dead are candidates for organ
donation. Discussions about brain death should be separated in
time from conversations regarding the opportunities for organ
donation.

Spinal cord injury

Spinal Cord Injury is most common in young adults between the
ages of 16 and 30 years. Common causes include MVCs, falls,
sports, and acts of violence.
Classication Spinal cord injuries can be classied by mechanism,
type of vertebral injury, or level of injury.
Mechanism of Injury
Spinal cord injuries occur as a result of penetrating injury or blunt
forces.
Typical mechanisms of blunt injury are
Hyperexion injuries are caused by a sudden deceleration of the
head and neck, and are often seen in patients who have sustained
trauma from a head-on MVC or diving accident. The cervical
region is most often involved, especially at the C5C6 level.
Hyperextension injuries can be caused by a fall, a rear-end MVC
(whiplash), or getting hit in the head (eg, during a boxing match).
Hyperextension of the head and neck may cause contusion and
ischemia of the spinal cord without vertebral column damage.
Axial loading (compression) injuries typically occur when a
person lands on the feet, buttocks, or head after falling, jumping,
or diving from a height. Compression of the vertebral column
causes a burst fracture that can result in damage to the spinal
cord.
Rotational injuries result from forces that cause extreme
twisting or lateral exion of the head and neck. Fracture or
dislocation of vertebrae may also occur.
Type of Vertebral Injury Mechanical forces can result in fracture or
dislocation of vertebrae, or both. Box 23-9 presents denitions of
types of fractures and dislocations. A fracture may be considered
unstable if the longitudinal ligaments are torn.
Level of Injury
Spinal cord injuries can also be classied according to the
segment of the spinal cord that is affected:
Upper cervical (C1C2) injuries (atlas fractures, atlantoaxial
subluxation, odontoid fractures, hangmans fractures)
Lower cervical (C3C8) injuries

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Thoracic (T1T12) injuries

Lumbar (L1L5) injuries
Sacral (S1S5) injuries
The degree of functional recovery depends on the location and
extent of the injury. The level of spinal cord injury is determined
by the effect of the injury on sensory and motor function. The
dermatome pathways are used to determine the level of sensory
loss (Fig. 23-8). Retention of all or some of the motor or sensory
function below the level of injury implies that the lesion is
incomplete, whereas total loss of voluntary muscle control and
sensation below the level of injury suggests that the lesion is
complete.

BOX 23-9 Types of Vertebral Fractures and Dislocations

Fractures
Simple fracture: single fracture; alignment of the vertebrae is
intact and neurological decits do not occur
Compression fracture: fracture caused by axial loading and
hyperexion
Wedge compression fracture: a stable fracture that involves
compression of the vertebral body in the cervical area Teardrop
fracture: an unstable fracture that involves a piece of bone
breaking off the vertebra; seen in wedge fractures
Comminuted fracture: the vertebra is shattered into several
pieces; bone fragments may be driven into spinal cord
Dislocations Dislocation: one vertebra overrides another
Subluxation: partial or incomplete dislocation
Fracturedislocation: fracture and dislocation
Pathophysiology
Injury to the spinal cord that occurs at the time of impact is
referred to as the primary injury. The more mobile areas of the
vertebral column (eg, the cervi- cal area) are most frequently
involved. Damage to the spinal cord is most often associated with
damage to the vertebral column and ligaments. The vertebrae
may be fractured, dislocated (subluxed), or compressed. As a
result of the injury to the vertebral column, the spinal cord itself
may be contused, compressed, or dislocated. Equally destructive
is the injury or damage to the spinal cord that continues for hours
after the trauma.
Mechanisms of secondary injury include the following:
During the inammatory response, immune cells release
harmful substances, causing cellular damage.

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Hypoperfusion of the spinal cord from micro- scopic hemorrhage

and edema leads to ischemia
. The release of catecholamines and vasoactive sub- stances
contributes to decreased circulation and perfusion of the spinal
cord.
The release of excess neurotransmitters results in
overexcitation of the nerve cells, which allows high levels of
calcium to enter the cells, causing cellular death.
Clinical Manifestations
Common clinical manifestations include
1. spinal cord syndromes
2. autonomic dysfunction.
Spinal Cord Syndromes Incomplete cord injuries often cause
recognizable neurological syndromes that are classied according
to the area damaged
Central cord syndrome. Damage to the spinal cord is centrally

located. Hyperextension of the cervical spine often is the

mechanism of injury, and the damage is greatest to the cervical
tracts supplying the arms. Clinically, the patient may present with
greater involvement of the upper extremities over the lower.
Damage is located on one side of the spinal cord. On the same
side as the lesion (ipsilaterally), the patient has complete motor
paralysis but maintains sensation of pain, temperature, and
touch. On the opposite side of the lesion (contralaterally), there is
loss of pain, temperature, and touch, but the patient maintains
motor function. Clinically, the patients limb with the best motor
strength has the poorest sensation, and vice versa.
Anterior cord syndrome. The anterior aspect of the spinal cord is
damaged. Clinically, the patient usually has complete motor
paralysis and loss of pain and temperature below the level of
injury, with preservation of light touch, proprioception, and
vibratory sense.
Posterior cord syndrome, which is rarely seen, is usually the
result of a hyperextension injury at the cervical level. Position
sense (proprioception), light touch, and vibratory sense are lost
below the level of the injury.
Autonomic Dysfunction
The autonomic nervous system carries nerve impulses from the
brain and spinal cord to effector organs throughout the body.
Sympathetic nerves exit the spinal cord between C7 and L1, and
parasympathetic nerves exit between S2 and S4. Therefore,
spinal cord injury can result in autonomic nervous system
dysfunction. Common manifestations of this dysfunction include

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spinal shock, neurogenic shock, orthostatic hypotension, and

autonomic dysreexia.
Spinal shock (Fig. 23-10) occurs immediately or within several
hours of a spinal cord injury and is caused by primary and
secondary injury to the spinal cord. Clinically, the patient exhibits
the loss of motor, sensory, reex, and autonomic function below
the level of the injury, with resultant accid paralysis. Loss of
bowel and bladder function and the bodys ability to control
temperature (poikilothermia) occur. There is no treatment, and
the duration of spinal shock depends on the severity of the insult
and the presence of other complications. The return of perianal
reex activity signals the end of the period of spinal shock
. Neurogenic shock, a form of distributive shock, is seen in
patients with severe cervical and upper thoracic injuries. It is
caused by the loss of sympathetic control of the heart and
vasculature, resulting in vasodilation and bradycardia. Signs and
symptoms include hypotension, severe bradycardia, and loss of
the ability to sweat below the level of injury. The hypotension is
managed with IV uid resuscitation. Symptomatic bradycardia
may require temporary external pacing.
Orthostatic hypotension may occur in a patient with a spinal
cord injury because the body is unable to compensate for
changes in position. The cord injury prevents the vasoconstriction
message from the medulla from reaching the blood vessels.
Autonomic dysreexia (hyperreexia) is a medical emergency
that can occur after the resolution of spinal shock in patients with
a spinal cord lesion at T7 or above. The syndrome presents
quickly and can precipitate hypertensive crisis and death. In
autonomic dysreexia, a stimulus below the level of injury (Box
23-10) produces a sympathetic discharge that causes reex
vasoconstriction, leading to extreme hypertension and a
throbbing head- ache. The body attempts to reduce the
hypertension through supercial vasodilation of vessels above the
spinal cord injury, leading to ushing, blurred vision, and nasal
congestion. Other signs and symptoms include bradycardia,
profuse sweating above the level of the injury, piloerection below
the level of injury, pupil dilation, and nausea. Management entails
identication and removal of the stimulus. Nursing interventions
for managing autonomic dysreexia are given in Box 23-11.
Management
Prehospital Management
A spinal cord injury is suspected at the scene of an accident any
time the patient has decreased or absent movement or sensation.
An unconscious patient or one with a head injury is treated as
though a spinal cord injury has occurred until proved otherwise.
Airway patency is assessed, and the cervical spine is immobilized

13

and stabilized. A cervical collar increases the level of stability but

does not provide complete immobilization, especially in the case
of complete ligamentous disruption.
In-Hospital Management
Early Management In the emergency department, the primary
and secondary surveys are completed. Management priorities
include:
Assessment and management of the patients air- way
and breathing. Hypoventilation or respiratory failure from
inadequate innervation of the respiratory muscles and diaphragm
is a common problem after spinal cord injury, particularly in
patients with high cervical injuries. In addition, spinal cord edema
can act like an ascending lesion and compromise function of the
diaphragm. Preexisting pulmonary disease or coexistent chest,
laryngeal, tracheal, or esophageal injuries can further
compromise respiratory function. If the patient requires
ventilatory assistance, elective intubation and mechanical
ventilation are followed by a chest radiograph.
Assessment and management of the patients
circulatory status. Hypotension may be due to neurogenic
shock or hemorrhagic shock (second- ary to associated injuries).
Fluid resuscitation is accomplished by the use of crystalloids or
blood. Early administration of blood enhances oxygen- ation and
may minimize secondary ischemic injury to the spinal cord.
Completion of a thorough neurological assessment,
including
spine x-rays. A digital rectal examination is performed to
determine whether the injury is incomplete or complete. The
lesion is incomplete if the patient can feel the palpating nger or
can contract the perianal muscles around the nger voluntarily.
Sensation usually accompanies voluntary motor activity, and may
be present in the absence of voluntary motor activity. In either
case, the prognosis for further motor and sensory return is good.
Rectal tone by itself, with- out the presence of voluntary perianal
muscle contraction or rectal sensation, is not evidence of an
incomplete cord injury.
Assessment for associated injuries. TBI, intra- thoracic
injuries, intra-abdominal injuries, retro- peritoneal injuries, and
fractures of the pelvis or long bones are often seen in association
with spinal cord injury,
When the patient is stabilized, frequent assessment of
neurological status is necessary to determine the extent of the
spinal cord injury and monitor for changes in level of
consciousness that may occur secondary to TBI. Most facilities
use a specialized ow sheet (eg, the Standard Neurological

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Classication of Spinal Cord Injury ow sheet) to assess and

document the patients level of functioning.
Diagnostic studies may be ordered, including radiographs of the
spine, chest, and other structures as clinically indicated; CT and
MRI (to evaluate soft tissue and ligament injuries). Flexion
extension views are obtained to assess for ligament involvement
in patients who are conscious and can follow commands, even
when plain radiographs and CT are negative for bony injury. If the
patient is unconscious or unable to tell the examiner if there is
pain on exion, then an MRI is required to rule out ligament
injuries. A cervical collar is kept on until the MRI results are
obtained or the patient regains consciousness and is able to
cooperate with the studies. The administration of high-dose
steroids (eg, methylprednisolone) in the emergency department
to reduce swelling and minimize secondary injury is controversial.
Some studies have found improvement in function in blunt,
incomplete cord injuries. However, steroid use has also been
associated with severe pneumonia and sepsis. Stabilization of the
Spine
The goals of ongoing management are to stabilize and realign
the spine to prevent further neurological deterioration. This can
be accomplished through closed reduction or surgical techniques.
Closed reduction of an unstable cervical fracture or subluxation
often involves skeletal traction. Short-term cervical traction can
be achieved using Gardner Wells, Vinke, or Crutch eld tongs;
long-term cervical traction entails the use of a halo vest. Stable
fractures can be immobilized using a Miami J or Aspen collar
(cervical fractures), a Minerva brace (cervicothoracic fractures), or
a Jewett brace (thora columbosacral injuries). For some patients,
surgery may be necessary to stabilize and support the spine. The
risks of surgery must be balanced against the possible benets.
Rod placement, laminectomy and fusion, and anterior fusion are
techniques used for surgical stabilization. Bone for fusion usually
comes from the patients iliac crest, tibia, or ribs; alternatively,
bone can be obtained from a tissue bank. After surgery, the
patient receives routine postoperative care. The nurse monitors
the patients motor and sensory status at least every hour for the
rst 24 hours, and then every 4 hours after that. The physician is
notied immediately if any deterioration in neurological status
occurs. The nurse also monitors for complications (eg, spinal uid
stulas, infections, wound dehiscence). Older patients and those
with preexisting comorbidities who have open wounds, injuries to
the thoracolumbar spine, or complete injuries are at particularly
high risk for postoperative infection.
Supportive Care
Supportive care focuses on preventing complications, and
initiating prompt interventions to treat any complications that do

15

occur. A collaborative care guide for the patient with a spinal cord
injury is given in Box 23-12.
Prevention of respiratory compromise.
Patients with a spinal cord injury, especially injuries above T6, are
at risk for respiratory compromise. Respiratory failure is
anticipated if the patients vital capacity is less than 15 to 20
mL/kg and the respiratory rate is greater than 30 breaths/min. If
the oxygen saturation value is less than 90% or if the PaCO2 is
greater than 45 mm Hg, intubation may be required. Routine
bronchial hygiene therapy (BHT) and kinetic therapy using a
specialty bed that rotates a minimum of 40 degrees on a
continuous basis helps prevent pulmonary complications.
RED FLAG! Respiratory complications are the leading cause of
death in the acute and chronic phases of spinal cord injury,
especially in patients with higher-level injuries.
Prevention of cardiovascular compromise. The patient is at risk
for bradycardia, hypotension, and dysrhythmias because of
disruption in the autonomic nervous system. When the blood
pressure is not high enough to sustain vital organ perfusion, lowdose dopamine may be administered after adequate uid
resuscitation. Symptomatic bradycardia may require the
administration of atropine or the use of a transcutaneous or
transvenous pacemaker. Left ventricular dysfunction may occur
secondary to the release of -endorphins; cardiac enzymes should
be obtained if there are ECG changes.
Pain management. Pain management is essential in caring for
patients with spinal cord injuries. It is not unusual for the patient
to report pain, frequently severe pain. The source of the pain may
be neuropathic, musculoskeletal, central, or visceral. Abnormal
sensation may occur at the level of the lesion in injuries caused
by nerve root damage.
Thermoregulation. Ineffective thermoregulation is common in
patients with spinal cord injuries above the thoracolumbar area.
Interruption of the sympathetic nervous system inhibits thalamic
thermoregulatory mechanisms. As a result, the patient cannot
sweat to get rid of body heat, and there is an absence of
vasoconstriction, result- ing in an inability to shiver to increase
body heat. Hypothermia is usually managed by using warmed
blankets, and the room temperature is adjusted to maintain
patient comfort. The goal is to stabilize the patients temperature
above 96.5F (35.8C).
Mobilization and positioning. Attention to mobilization and
positioning is important to pre- vent complications of immobility. A
turn schedule for the patient is important, even if the patient has
not had stabilizing surgery. It may take three staff members to

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accomplish turning safely, particu- larly in patients with cervical

injuries. One per- son stabilizes the neck, and the other two ex
the hips, knees, and ankles and hold the feet at on the bed
surface while turning the patients trunk. Foam wedges, pillows,
or air- lled rolls are used to maintain alighnment
Urinary management. Initially, an indwelling uri- nary catheter is
placed to prevent the bladder from becoming distended
secondary to atony, and to allow for hourly measurement of
urinary output. As soon as spinal shock has resolved, the indwelling catheter is removed and bladder training (eg, with
intermittent catheterization) begins.
Bowel management. Measures to prevent constipation and
begin progress toward bowel continence include maintenance of
appropriate intake; daily administration of stool softeners and a
suppository; and development of a consistent schedule for bowel
elimination. The timing of the program is usually designed to
coincide with the peristalsis that occurs after meals to move food
through the gastrointestinal tract. Rectal stimulation may be
necessary to trigger defecation.
Psychological support. As soon as the patient is medically
stable, the nurse begins to focus on the psychosocial issues that
are of concern to the patient and family (eg, long-term prognosis,
sexual functioning, body image). The nurse answers questions to
the best of his or her knowledge; encourages the patient and
family to express concerns; and focuses on the patients abilities
with- out minimizing the patients disabilities
. Management for TBI/SPINAL CORD INJURY
C O L L A B O R AT I V E C A R E G U I D E for the Patient With a Traumatic Brain
Injury (TBI)
OUTCOMES

INTERVENTIONS

Oxygenation/Ventilation

A patent airway is maintained. Lungs are clear to auscultation.

Arterial pH, PaO2, and SaO2 are maintained within normal limits.
ETCO2 or PCO2 is maintained within prescribed range.
There is no evidence of atelectasis or pneumonia on chest x-ray.

Auscultate breath sounds q24h and PRN.

Hyperoxygenate before and after each suction pass
Avoid suction passes >10 s.
Monitor ICP and CPP during suctioning and chest physiotherapy.
Provide meticulous oral hygiene.
Monitor for signs of aspiration.
Encourage nonintubated patients to use incentive spirometer, cough, and
deep breathe q4h and PRN.
Turn side-to-side q2h.
Move patient out of bed to chair one to two times per day when ICP has
been controlled.

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Circulation/Perfusion

Patient exhibits normal sinus rhythm without ectopy or ischemic changes.

Patient does not experience thromboembolic complications.

Monitor for myocardial ischemia and dysrhythmias due to sympathetic

activation and catecholamine surges.
Prevent DVT with the use of pneumatic compression devices, compression
hose, and subcutaneous heparin.
Implement early mobilization. Facilitate moving to a chair one to two times
per day.
Monitor blood pressure continuously by arterial line or fre- quently by
noninvasive cuff.
Monitor oxygen delivery (hemoglobin, SaO2, cardiac output).
Administer RBCs, inotropes, IV uids as indicated.
Cerebral Perfusion/Intracranial Pressure

CPP > 60 mm Hg. ICP < 20 mm Hg.

Patient does not experience seizure activity.
Monitor ICP and CPP q1h.
Make neurological checks q12h.
Elevate the head of bed to 30 degrees unless contraindicated
Maintain proper body alignment, keeping the head in a neutral position, and
avoiding sharp hip exion.
Maintain normothermia.
Maintain a quiet environment, cluster care, and provide rest periods.
Provide sedation as necessary and as prescribed.
Administer prophylactic antiepileptic agents as prescribed to prevent
seizure activity.
Fluids/Electrolytes

Serum electrolytes are within normal limits. Serum osmolality remains within
prescribed range.

Maintain strict documentation of I&O; consider insensible losses due to

intubation, fever, and the like.
Monitor serum electrolytes, glucose, and osmolality as ordered.
Consider need for electrolyte replacement therapy and adminis- ter per
physician order or protocol.
Mobility/Safety
There are minimal and transient changes in ICP/CPP during treatments or
patient care activities, and ICP/CPP returns to baseline within 5 min.
Patient does not experience complications related to prolonged
immobilization (eg, DVT, pneumonia, ankylosis).
Patient does not harm self by dislodging medical equipment or falling.
Provide range of motion and functional splinting for paralyzed limbs or
patients in a coma.
Relieve pressure on pressure points (by repositioning) at least q2h.
Consider use of a specialty mattress based on skin and risk factor
assessments. Keep bed rails in the upright position.
Provide restraints if necessary to prevent dislodgment of medical devices
per facility protocol.

Ranchos Los Amigos Scale

Level Guidelines for Interacting With Patient
1. No response to any stimuli occurs.
2. Generalized response. Stimulus response is incoherent, limited, and
nonpurposeful with random movements or incomprehensible sounds.
3. Localized response. Stimulus response is specic but inconsistent; patient may
withdraw or push away, may make sounds, may follow some simple commands, or
may respond to certain family members.

18
Assume that the patient can understand all that is said. Converse with, not
about, the patient.
Do not overwhelm the patient with talking. Leave some moments of silence
between verbal stimuli.
Manage the environment to provide only one source of stimulation at a
time. If talking is taking place, the radio or television should be turned off.
Provide short, random periods of sensory input that are meaningful to the
patient. A favorite television program or tape recording or 30 min of music
from the patients favorite radio station will provide more meaningful
stimulation than constant radio accompaniment, which becomes as
meaningless as the continual bleep of the cardiac monitor.
4. Confusedagitated. Stimulus response is primarily to internal confusion with
increased state of activity; behavior may be bizarre or aggressive; patient may
attempt to remove tubes or restraints or crawl out of bed; verbalization is
incoherent or inappropriate; patient shows minimal awareness of environment and
absent short-term memory.
Be calm and soothing when handling the patient. Approach with gentle
touch to decrease the occurrence of defensive emotional and motor reexes.
Watch for early signs that the patient is becoming agitated (eg, increased
movement, vocal loudness, resistance to activity).
When the patient becomes upset, do not try to reason with him or her or
talk him or her out of it. Talking will be an additional external stimulus that
the patient cannot handle.
If the patient remains upset, either remove him or her from the situation or
remove the situation from him or her.
5. Confused, inappropriatenonagitated. Patient is alert and responds consistently to
simple commands; however, patient has a short attention span and is easily
distracted; memory is impaired and patient exhibits confusion of past and present
events; patient can perform previously learned tasks with maximal structure but is
unable to learn new information; may wander off with vague intention of going
home.
Present the patient with only one task at a time. Allow time to complete it
before giving further instructions.
Make sure that you have the patients attention by placing yourself in view
and touching the patient before talking.
If the patient becomes confused or resistant, stop talking. Wait until he or
she appears relaxed before continuing with instruction or activity.
6. Confusedappropriate. Patient shows goal- directed behavior but still needs
external direction; can understand simple directions and reasoning; follows simple
directions consistently and requires less supervision for previously learned tasks;
has improved past memory depth and detail and basic awareness of self and
surroundings.
Use gestures, demonstrations, and only the most necessary words when
giving instructions.
Maintain the same sequence in routine activities and tasks. Describe these
routines to the patient and relate them to time of day.
7. Automaticappropriate. Patient is able to complete daily routines in structured
environment; has increased awareness of self and surroundings but lacks insight,
judgment, and problem-solving ability.
Supervision is still necessary for continued learning and safety.
Reinforce the patients memory of routines and schedules with clocks,
calendars, and a written log of activities.

19
8. Purposefulappropriate. Patient is alert, oriented, and able to recall and integrate
past and recent events; responds appropriately to environment; still has decreased
ability in abstract reasoning, stress tolerance, and judgment in emergencies or
unusual situations.
The patient should be able to function without supervision.
Consideration should be given to job retraining or a return to school.

C O L L A B O R AT I V E C A R E G U I D E for the Patient With Spinal Cord Injury

OUTCOMES

INTERVENTIONS

Oxygenation/Ventilation

ABGs are within normal limits. Airway patency is maintained. The patient
does not aspirate.
The patient does not develop pulmonary complications (eg, infection,
atelectasis).

Monitor respiratory rate, arterial oxygen saturation, and pulmonary function

test results, and auscultate breath sounds.
Assess need for mechanical ventilation.
Provide for deep breathing, assistive coughing, and incentive spirometer
exercises.
Turn frequently; mobilize out of bed to chair when able.
Apply abdominal binder when out of bed.
Consult pulmonology as needed.
Circulation/Perfusion

There is no evidence of neurogenic (spinal) shock (T10 injuries and higher).

Blood pressure is adequate to maintain vital organ function.
There is no development of DVT or pulmonary embolism.
Monitor for bradycardia, vasodilation, and hypotension.
Assess for dysrhythmias.
Prepare to administer intravascular volume, vasopressors, and positive
chronotropic agents
Begin DVT prophylaxis on admission (eg, external compression device, lowdose heparin or LMWH).
Measure calf and thigh circumference daily and at same location; report
increase.
Apply compression hose to lower extremities before mobilizing out of bed.
There is no evidence of orthostatic hypotension.
Monitor for orthostatic hypotension when raising head of bed and getting
out of bed. Allow patient to dangle before mobilizing out of bed.
Consult cardiology as needed.
Neurological

There is no evidence of deterioration in neurological status.

Perform neurological checks and spinal cord function checks q24h.

Monitor for deterioration in neurological status and report to the physician.
The vertebral column is maintained in a neutral position and in proper
alignment.
For patients with cervical traction: check the orthopedic frame, traction,
and tongs daily to be sure that they are secure. Ensure that traction weights
hang freely.
For patients with a halo vest: Ensure that the pins on the halo ring are
secure and tight.
Fluids/Electrolytes

Serum electrolytes are within normal limits.

Monitor laboratory studies as indicated by patients condition.

Assess for dehydration.
Administer mineral/electrolyte replacement as ordered.

20

Fluid balance is maintained as evidenced by stable weight, absence of

edema, normal skin turgor.

Monitor gastrointestinal and insensible uid loss.

Make accurate daily uid intake and output measurements.
Weigh weekly.
Monitor results of laboratory studies, particularly albumin and electrolyte

levels.
Mobility/Safety
Joint range of motion is maintained and contractures prevented.
Muscle tone is maintained. The patient ambulates in a safe manner to
the best of his or her ability.
Position in correct alignment.
Begin range-of-motion exercises early after admission.
Maintain splint, brace, and adaptive device schedule; check for pressure
ulcers q4h or more often if indicated.
Consult with physical and occupational therapy.
Skin Integrity

Patient is without evidence of skin breakdown.

Consult with wound care specialist to determine correct type of bed.

Reposition patient at least q2h while in bed.
Position patient to prevent pressure on bony prominences.
Use upright, straight-backed chair when patient is out of bed (not a reclining
chair). Use felt pad on chair seat.
Reposition/shift weight q1h when sitting upright.
Use Braden scale to monitor risk for skin breakdown.
Skin integrity is maintained under or around stabilization devices (eg,
cervical collar, halo vest).
Monitor skin underneath stabilization devices and around pins.
Use meticulous skin care underneath stabilization devices and around pins.
Ensure proper t of vest-like stabilization devices by sliding a nger
between the vest and skin.
Nutrition
Protein, carbohydrate, fat, and calorie intake meet minimal daily
requirements.
The patient has a uid intake of up to 3000 mL daily.
Aspiration is prevented.
Consult dietitian.
Encourage uids, high-ber diet.
Monitor uid I&O, calorie count.
Administer parenteral and enteral nutrition as appropriate.
Assist with feeding/feed as needed. Encourage the patient to take small
bites and chew well.
Elimination

Postvoid residuals < 100 mL. Pattern of bowel evacuation every 12 d

is established.

Institute bowel and bladder training programs.

Record the frequency and consistency of stool.
If the patient is voiding independently, monitor postvoid residuals.
Comfort/Pain

Pain < 4 on visual analog scale.

Assess and differentiate pain from anxiety or stress response.

Administer appropriate analgesic or sedative to relieve pain and monitor
patient response.
Use nonpharmacological pain relief techniques (eg, distraction, music,
relaxation therapies).
Psychosocial

21

Patient adapts to loss of motor and sensory function, and maintains a

positive body image.

Provide emotional support by encouraging expression of concerns,

arranging for support services (eg, social services, clergy, neuropsychologist, support groups), and so on.

Integration is made into prior social role.

Provide patient/family counseling regarding stages of grief, sexual function

and management techniques, social services and community resources.
Teaching/Discharge

Planning Complications associated with loss of bowel or bladder control

are prevented.

Teach patient/family:
Bowel program and training
Dietary habits to maintain bowel function
Bladder training/intermittent catheterization
Prevention of, and signs/symptoms of autonomic dysre exia
Complications of immobility are prevented.

Teach patient/family:
Positioning to prevent skin breakdown
Physical therapy exercises
BHT
Patient is discharged to appropriate postacute setting.

Consult rehabilitation/discharge planner/social services early after

admission to initiate placement arrangements.