Spinal cord injury

 The term ‘spinal cord injury’ refers to damage to the spinal cord resulting from trauma
(e.g. a car crash) or from disease or degeneration (e.g. cancer). (WHO, 2013)
 A spinal cord injury (SCI) is damage to the tight bundle of cells and nerves that sends
and receives signals from the brain to and from the rest of the body. SCI can be caused
by direct injury to the spinal cord itself or from damage to the tissue and bones
(vertebrae) that surround the spinal cord. This damage can result in temporary or
permanent changes in sensation, movement, strength, and body functions below the site
of injury. (NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND
STROKE)
Risk factors
 Gender and age- SCIs do not happen to all genders equally. For male,they are more
likely to experience spinal cord injury than woman. In fact, only close to 20% of
traumatic spinal cord injuries happen to women. Age is also a factor, as people are at a
higher risk of a SCI if they are between 16 and 30 years old. The risk also goes up if they
are over 65 since older people suffer more injuries because of falls. (Howell law firm,
2020)

 Preexisting health conditions- Having an existing health problem can make the person
more likely to suffer a SCI. A problem with walking or balance can increase the risk of
falling. Some people have problems with their bones or joints, like osteoporosis or
arthritis. If they have a bone disorder and suffer a minor injury, the disorder may
compound the problem and lead to serious spinal cord damage. (Howell law firm, 2020)

 Reckless behavior- Some people engage in high risk activities without taking proper
safety precautions. Diving into shallow water may cause a head injury that results in
paralysis. Playing sports without the right safety gear or driving beyond the posted speed
limit can also lead to a SCI. Refraining from ill-advised behavior in sports or on the road
might spare the person from SCI. In addition, acting responsibly may help you in the
event you suffer a serious injury in an auto accident caused by another driver, as it could
prevent the lawyer representing the other driver from having an opening to unfairly
blame you for causing the accident in the first place. (Howell law firm, 2020)
Type/ class/ stages
 An incomplete injury means the spinal cord is still able to trasnmit some messages to and
from the brain to the rest of the body. (NATIONAL INSTITUTE OF
NEUROLOGICAL DISORDERS AND STROKE)
 A complete injury means there is no nerve communication and motor function
(voluntary movement) below the site where the trauma occurred. (NATIONAL
INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE)

SCIs are graded according to the American Spinal Injury Association (ASIA) grading scale,
which describes the severity of the injury. The scale is graded with letters:

ASIA A: injury is complete spinal cord injury with no sensory or motor function preserved.
ASIA B: a sensory incomplete injury with complete motor function loss.
ASIA C: a motor incomplete injury, where there is some movement, but less than half the
muscle groups are anti-gravity (can lift up against the force of gravity with a full range of
motion).
ASIA D: a motor incomplete injury with more than half of the muscle groups are anti-gravity.
ASIA E: normal.

Physical findings vary, depending on the level of injury, degree of spinal shock, and phase
and degree of recovery, but in general, are classified as follows:
  C-1 to C-3: Tetraplegia with total loss of muscular/respiratory function.
 C-4 to C-5: Tetraplegia with impairment, reduced pulmonary capacity, complete
dependency for ADLs.
 C-6 to C-7: Tetraplegia with some arm/hand movement allowing some independence
in ADLs.
 C-7 to T-1: Tetraplegia with limited use of thumb/fingers, increasing independence.
 T-2 to L-1: Paraplegia with intact arm function and varying function of intercostal
and abdominal muscles.
 L-1 to L-2 or below: Mixed motor-sensory loss; bowel and bladder dysfunction.

Standard Symptoms
Signs and symptoms of a spinal cord injury may present immediately or some symptoms may
be delayed as swelling and bleeding occur in or around the spinal cord. One or more of the
following symptoms may occur with a spinal cord injury: 

 Pain and numbness, or burning sensation

 Inability to move the extremities or walk
 Inability to feel pressure, heat, or cold
 Muscle spasms
 Loss of bladder or bowel control
 Difficulty breathing
Symptoms by Region
There are three main areas in which a person may suffer spinal cord injury: cervical, thoracic,
and lumbar. The fourth section of the spine (sacral), does not contain spinal cord tissue.
Consequently, though you may cause damage to the sacral vertebrae or nerves, you will not
damage the cord at that level.

1.
 Cervical (C1-C8) - Damage to the spinal cord in the cervical spine is considered the
most severe because it can be life-threatening. Symptoms of cervical spinal cord
damage may affect the arms, legs, mid-body, and even the ability to breathe on one’s
own. The higher up in the cervical spine the damage occurs, the worse the injury.
Symptoms may be felt on one or both sides of the body.

2.

1.

Thoracic (T1-T12) - Damage to the spinal cord in the thoracic spine typically affects
the legs. Thoracic spinal cord damage high up in the area may affect blood pressure.

2.

1.

Lumbar (L1-L5) - Damage to the spinal cord in the lumbar spine typically affects one
or both legs. Patients with lumbar spinal cord damage may also have trouble
controlling their bladder and/or bowel function. 

2.

Tetraplegia or tetraparesis
This is also known as quadriplegia or quadriparesis. The term describes the complete or
partial loss of all movements and/or sensation from the neck downward, affecting all four
extremities and the trunk. It can also include paralysis of the diaphragm.

Paraplegia or paraparesis
This term describes the complete or partial loss of all movements and/or sensation from the
chest downward, affecting the lower limbs only.

Complete spinal cord lesion

Transverse ischaemic necrosis occurs in this type of lesion, resulting in permanent loss of all
voluntary movements and sensation below the level of the lesion.

Incomplete spinal cord lesion

When the lesion is incomplete, there is potential for any oedema to subside, with the
consequent return of some neurological function, as it is possible that some nerve fibres may
have survived.

Examples of incomplete spinal-cord lesions include:

- Anterior cord syndrome: this is the most common form of incomplete lesion and occurs
after high-velocity impact trauma. The lesion develops as a result of physical trauma, bony
compression and ischaemia;

- Posterior cord syndrome: this occurs with posterior impact injury or hyperextension of the
neck. There may be a resultant loss of position (proprioception), vibration and touch sense;

- Brown-S[ap6]quard syndrome: this involves hemisection of the spinal cord, commonly

seen in stabbing or gunshot injuries. There is loss of voluntary motor control on the same side
as the cord damage;

- Central cord syndrome: this type of injury usually occurs in older patients after a
hyperextension trauma to the neck. There may be significant loss of function in the upper
limbs and hands.

Anatomy
The spinal cord is divided into 31 segments, each with a pair of anterior (motor) and dorsal
(sensory) spinal nerve roots. On each side, the anterior and dorsal nerve roots combine to
form the spinal nerve as it exits from the vertebral column through the neuroforamina. The
spinal cord extends from the base of the skull and terminates near the lower margin of the L1
vertebral body. Thereafter, the spinal canal contains the lumbar, sacral, and coccygeal spinal
nerves that comprise the cauda equina. As a result, injuries below L1 are not considered
spinal cord injuries (SCIs), because they involve the segmental spinal nerves and/or cauda
equina. Spinal injuries proximal to L1, above the termination of the spinal cord, often involve
a combination of spinal cord lesions and segmental root or spinal nerve injuries.

Neuropathways
The spinal cord itself is organized into a series of tracts or neuropathways that carry motor
(descending) and sensory (ascending) information. These tracts are organized somatotopically
within the spinal cord. The corticospinal tracts are descending motor pathways located
anteriorly within the spinal cord. Axons extend from the cerebral cortex in the brain as far as
the corresponding segment, where they form synapses with motor neurons in the anterior
(ventral) horn. They decussate (cross over) in the medulla before entering the spinal cord.

The dorsal columns are ascending sensory tracts that transmit light touch, proprioception, and
vibration information to the sensory cortex. They do not decussate until they reach the
medulla. The lateral spinothalamic tracts transmit pain and temperature sensation. These
tracts usually decussate within 3 segments of their origin as they ascend. The anterior
spinothalamic tract transmits light touch. Autonomic function traverses within the anterior
interomedial tract. Sympathetic nervous system fibers exit the spinal cord between C7 and L1,
whereas parasympathetic system pathways exit between S2 and S4.

Injury to the corticospinal tract or dorsal columns, respectively, results in ipsilateral paralysis
or loss of sensation of light touch, proprioception, and vibration. Unlike injuries of the other
tracts, injury to the lateral spinothalamic tract causes contralateral loss of pain and
temperature sensation. Because the anterior spinothalamic tract also transmits light touch
information, injury to the dorsal columns may result in complete loss of vibration sensation
and proprioception but only partial loss of light touch sensation. Anterior cord injury causes
paralysis and incomplete loss of light touch sensation.
Autonomic function is transmitted in the anterior interomedial tract. The sympathetic nervous
system fibers exit from the spinal cord between C7 and L1. The parasympathetic system
nerves exit between S2 and S4. Therefore, progressively higher spinal cord lesions or injury
causes increasing degrees of autonomic dysfunction.

Vascular supply
The blood supply of the spinal cord consists of 1 anterior and 2 posterior spinal arteries. The
anterior spinal artery supplies the anterior two thirds of the cord. Ischemic injury to this vessel
results in dysfunction of the corticospinal, lateral spinothalamic, and autonomic interomedial
pathways. Anterior spinal artery syndrome involves paraplegia, loss of pain and temperature
sensation, and autonomic dysfunction. The posterior spinal arteries primarily supply the
dorsal columns. The anterior and posterior spinal arteries arise from the vertebral arteries in
the neck and descend from the base of the skull. Various radicular arteries branch off the
thoracic and abdominal aorta to provide collateral flow.

The primary watershed area of the spinal cord is the midthoracic region. Vascular injury may
cause a cord lesion at a level several segments higher than the level of spinal injury. For
example, a lower cervical spine fracture may result in disruption of the vertebral artery that
ascends through the affected vertebra. The resulting vascular injury may cause an ischemic
high cervical cord injury. At any given level of the spinal cord, the central part is a watershed
area. Cervical hyperextension injuries may cause ischemic injury to the central part of the
cord, causing a central cord syndrome.
Pathophysiology
Spinal cord injury (SCI), as with acute stroke, is a dynamic process. In all acute cord
syndromes, the full extent of injury may not be apparent initially. Incomplete cord lesions
may evolve into more complete lesions. More commonly, the injury level rises 1 or 2 spinal
levels during the hours to days after the initial event. A complex cascade of pathophysiologic
events related to free radicals, vasogenic edema, and altered blood flow accounts for this
clinical deterioration. Normal oxygenation, perfusion, and acid-base balance are required to
prevent worsening of the spinal cord injury.

Spinal cord injury can be sustained through different mechanisms, with the following 3
common abnormalities leading to tissue damage:

Destruction from direct trauma

Compression by bone fragments, hematoma, or disk material

Ischemia from damage or impingement on the spinal arteries

Edema could ensue subsequent to any of these types of damage.

Neurogenic shock
Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and
peripheral vasodilation resulting from severe autonomic dysfunction and the interruption of
sympathetic nervous system control in acute spinal cord injury. Hypothermia is also
characteristic. This condition does not usually occur with spinal cord injury below the level of
T6 but is more common in injuries above T6, secondary to the disruption of the sympathetic
outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in vascular resistance,
with the associated vascular dilatation. Neurogenic shock needs to be differentiated from
spinal and hypovolemic shock. Hypovolemic shock tends to be associated with tachycardia.

Spinal shock
Shock associated with a spinal cord injury involving the lower thoracic cord must be
considered hemorrhagic until proven otherwise. In this article, spinal shock is defined as the
complete loss of all neurologic function, including reflexes and rectal tone, below a specific
level that is associated with autonomic dysfunction. That is, spinal shock is a state of transient
physiologic (rather than anatomic) reflex depression of cord function below the level of
injury, with associated loss of all sensorimotor functions.

An initial increase in blood pressure due to the release of catecholamines, followed by

hypotension, is noted. Flaccid paralysis, including of the bowel and bladder, is observed, and
sometimes sustained priapism develops. These symptoms tend to last several hours to days
until the reflex arcs below the level of the injury begin to function again (eg, bulbocavernosus
reflex, muscle stretch reflex [MSR]).

Primary vs secondary SCIs

Spinal cord injuries may be primary or secondary. Primary spinal cord injuries arise from
mechanical disruption, transection, or distraction of neural elements. This injury usually
occurs with fracture and/or dislocation of the spine. However, primary spinal cord injury may
occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or
weapons may also cause primary spinal cord injury. More commonly, displaced bony
fragments cause penetrating spinal cord and/or segmental spinal nerve injuries.

Extradural pathology may also cause a primary spinal cord injury. Spinal epidural hematomas
or abscesses cause acute cord compression and injury. Spinal cord compression from
metastatic disease is a common oncologic emergency.

Longitudinal distraction with or without flexion and/or extension of the vertebral column may
result in primary spinal cord injury without spinal fracture or dislocation. The spinal cord is
tethered more securely than the vertebral column. Longitudinal distraction of the spinal cord
with or without flexion and/or extension of the vertebral column may result in spinal cord
injury without radiologic abnormality (SCIWORA).

SCIWORA was first coined in 1982 by Pang and Wilberger. Originally, it referred to spinal
cord injury without radiographic or computed tomography (CT) scanning evidence of fracture
or dislocation. However with the advent of magnetic resonance imaging (MRI), the term has
become ambiguous. Findings on MRI such as intervertebral disk rupture, spinal epidural
hematoma, cord contusion, and hematomyelia have all been recognized as causing primary or
secondary spinal cord injury. SCIWORA should now be more correctly renamed as "spinal
cord injury without neuroimaging abnormality" and recognize that its prognosis is actually
better than patients with spinal cord injury and radiologic evidence of traumatic injury. [7, 8,
9]

Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or
hypoperfusion due to shock are the major causes of secondary spinal cord injury. Anoxic or
hypoxic effects compound the extent of spinal cord injury.

Complete vs incomplete spinal cord syndrome

One of the goals of the physician is to classify the pattern of the neurologic deficit into one of
the cord syndromes. Spinal cord syndromes may be complete or incomplete. In most clinical
scenarios, physicians should use a best-fit model to classify the spinal cord injury syndrome.

A complete cord syndrome is characterized clinically as complete loss of motor and sensory
function below the level of the traumatic lesion. Incomplete cord syndromes have variable
neurologic findings with partial loss of sensory and/or motor function below the level of
injury; these include the anterior cord syndrome, the Brown-Séquard syndrome, and the
central cord syndrome.
Anterior cord syndrome involves a lesion causing variable loss of motor function and pain
and/or temperature sensation, with preservation of proprioception.

Brown-Séquard syndrome, which is often associated with a hemisection lesion of the cord,
involves a relatively greater ipsilateral loss of proprioception and motor function, with
contralateral loss of pain and temperature sensation.

Central cord syndrome usually involves a cervical lesion, with greater motor weakness in the
upper extremities than in the lower extremities, with sacral sensory sparing. The pattern of
motor weakness shows greater distal involvement in the affected extremity than proximal
muscle weakness. Sensory loss is variable, and the patient is more likely to lose pain and/or
temperature sensation than proprioception and/or vibration. Dysesthesias, especially those in
the upper extremities (eg, sensation of burning in the hands or arms), are common.

Other cord syndromes

The conus medullaris syndrome, cauda equina syndrome, and spinal cord concussion are
briefly discussed below.

Conus medullaris syndrome is a sacral cord injury, with or without involvement of the lumbar
nerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesser
degree, lower limbs, whereas the sacral segments occasionally may show preserved reflexes
(eg, bulbocavernosus and micturition reflexes). Motor and sensory loss in the lower limbs is
variable.

Cauda equina syndrome involves injury to the lumbosacral nerve roots in the spinal canal and
is characterized by an areflexic bowel and/or bladder, with variable motor and sensory loss in
the lower limbs. Because this syndrome is a nerve root injury rather than a true spinal cord
injury, the affected limbs are areflexic. Cauda equina syndrome is usually caused by a central
lumbar disk herniation.

A spinal cord concussion is characterized by a transient neurologic deficit localized to the

spinal cord that fully recovers without any apparent structural damage.

The spinal cord is the central part of the communication system between the brain and body.
It is flexible, nearly an inch in diameter at its widest point, and 18 inches long. It starts below
the base of the brain (in the neck, also known as the cervical spine) and extends downward,
ending near the waist or low back (lumbar spine). The spinal cord and nerve roots comprise
the central nervous system.
The central nervous system enables the body to move (motor nerves) and feel (sensory
nerves). In the brain, there are 12 cranial (skull) nerves. Five are motor, three are sensory, and
four are motor / sensory.

Thirty-one pairs of nerve roots branch off the spinal cord and go beyond the spinal column to
enable the body to move and feel. These nerves form the peripheral nervous system. Below
are the number of pairs of spinal nerves at each level (region) of the spinal column.

Cervical: 8
Thoracic: 12
Lumbar: 5
Sacral: 5
Coccyx (tailbone): 1
Three sheaths or membranes (meninges) surround and protect the spinal cord. Cerebrospinal
fluid, a clear body fluid, circulates between the meninges, brain, and spinal cord. The brain
and spinal cord float in this protective fluid. The three meninges are:
Dura mater: gray outer layer of the spinal cord and nerve roots. It is made of strong
connective tissue.
Arachnoid membrane: resembles a loosely woven fabric of arteries and veins. This layer is
thinner than the dura mater.
Pia mater: innermost layer, a delicate and highly vascular (that means that blood goes to this
layer) membrane that provides blood to the spinal cord and nerve roots.
The design of the spine's vertebrae creates a hollow in the middle of the spinal column. The
spinal cord rests in this protective bony environment.
For spinal cord injury, it's particularly important to understand the autonomic nervous system.
This system of nerves sends sensory impulses to the brain from the arteries, heart, lungs, and
organs in the abdomen and pelvis. These involuntary impulses occur without your conscious
knowledge. The autonomic nerves affect such reactions as reflexes and the body's response to
temperature changes.

There are two types of autonomic nerves: sympathetic and parasympathetic.

Sympathetic system: responds to stress and prepares the body for action
Parasympathetic system: works while the body is at rest
Autonomic nerves influence involuntary body processes such as breathing, heartbeat,
digestion, and blood pressure. The autonomic nervous system works to maintain the body's
homeostasis, or stable internal environment. When a spinal cord injury disrupts one or more
of these involuntary body processes, the outcome can be life-altering.

With regard to laboratory studies, the following may be helpful:

Arterial blood gas (ABG) measurements may be useful to evaluate adequacy of oxygenation
and ventilation

Lactate levels to monitor perfusion status can be helpful in the presence of shock

Hemoglobin and/or hematocrit levels may be measured initially and monitored serially to
detect or monitor sources of blood loss

Urinalysis can be performed to detect any associated genitourinary injury

Diagnostic imaging traditionally begins with the acquisition of standard radiographs of the
affected region of the spine. Investigators have shown that computed tomography (CT)
scanning is exquisitely sensitive for the detection of spinal fractures and is cost effective. In
many centers, CT scanning has supplanted plain radiographs.

A properly performed lateral radiograph of the cervical spine that includes the C7-T1 junction
can provide sufficient information to allow the multiple trauma victim to proceed emergently
to the operating room if necessary without additional intervention other than maintenance of
full spinal immobilization and a hard cervical collar.

Noncontiguous spinal fractures are defined as spinal fractures separated by at least 1 normal
vertebra. Noncontiguous fractures are common and occur in 10-15% of patients with spinal
cord injury. Therefore, once a spinal fracture is identified, the entire axial skeleton must be
imaged, preferably by CT scanning, to assess for noncontiguous fractures.

Testing & Diagnosis

In the trauma situation, the doctor will check first to make sure the patient has a working
airway, is breathing and has a pulse. The next step in the evaluation is to assess an
individual’s neurologic function. The doctor will do this by testing the patient’s strength and
sensation in his/her arms and legs. If there is obvious weakness or the patient is not fully
awake, the patient is kept in a rigid cervical collar and on a spine board until a full imaging
assessment can be complete.

Radiological Evaluation

Historically, the radiological diagnosis of SCI started with x-rays. However, with the
technological advancements and availability at most hospitals, the entire spine may be imaged
with computerized tomography (CT or CAT scan) as an initial screen to identify fractures and
other bony abnormalities. For patients with known or suspected injuries, MRI is helpful for
looking at the actual spinal cord itself as well as for detecting any blood clots, herniated discs
or other masses that may be compressing the spinal cord.

Treatment
Treatment of SCI begins before the patient is admitted to the hospital. Paramedics or other
emergency medical services personnel carefully immobilize the entire spine at the scene of
the accident. In the emergency department, this immobilization is continued while more
immediate life-threatening problems are identified and addressed. If the patient must undergo
emergency surgery because of trauma to the abdomen, chest or another area, immobilization
and alignment of the spine are maintained during the operation.

Non-Surgical Treatments

If a patient has a SCI, he or she will usually be admitted to an intensive care unit (ICU). For
many injuries of the cervical spine, traction may be indicated to help bring the spine into
proper alignment. Standard ICU care, including maintaining a stable blood pressure,
monitoring cardiovascular function, ensuring adequate ventilation and lung function and
preventing and promptly treating infection and other complications, is essential so that SCI
patients can achieve the best possible outcome.

Surgery

Occasionally, a surgeon may wish to take a patient to the operating room immediately if the
spinal cord appears to be compressed by a herniated disc, blood clot or other lesion. This is
most commonly done for patients with an incomplete SCI or with progressive neurological
deterioration. Even if surgery cannot reverse damage to the spinal cord, surgery may be
needed to stabilize the spine to prevent future pain or deformity. The surgeon will decide
which procedure will provide the greatest benefit to the patient.

 Immobilize initially with C-collar and spinal precautions (log-roll)

Maintain full spinal precautions until cleared by a neurosurgeon. This involves a c-collar to

immobilize the neck, keeping the HOB flat, and using a strict log-roll technique for turning.

Any twist or bend of the spine could cause further damage to the spinal cord.

 Manage and maintain Halo brace, including pin care twice daily
 

Halo brace is used to immobilize the cervical spine with unstable vertebral fractures. Four

pins are inserted into the skull – pin care should be done twice daily to prevent infection at the

pin sites. A wrench should be kept at bedside to remove the vest in the case that chest

compressions are needed.

 Administer medications

o Analgesics

o Muscle Relaxants

Patients may experience pain from the initial trauma as well as neuropathic pain due to the

nerve injuries. Muscle relaxants like cyclobenzaprine and gabapentin can also help ease any

muscle spasms or nerve pain.

 Encourage PT/OT, passive and active ROM

PT and OT can help the patient to maintain whatever functional ability they have. ROM

exercises help to prevent atrophy and contractures.

 Monitor hemodynamics for signs of Autonomic Dysreflexia or Neurogenic Shock

 
Neurogenic shock is a risk within the first 24-72 hours, autonomic dysreflexia is a risk any

time. Both show warm, flushed skin and an elevated temperature. Neurogenic shock shows

hypotension and bradycardia, while autonomic dysreflexia shows hypertension and

bradycardia. Find and treat  cause of A.D. as soon as possible.

 Monitor for and provide interventions to prevent complications of immobility:

o Chest expansion exercises

o DVT prophylaxis

o Pad bony prominences, turn q2h

Immobility can lead to pneumonia, DVT/thrombophlebitis, and pressure ulcers. Monitor for

signs and intervene to prevent them. Assess skin with every turn, monitoring for developing

pressure ulcers (they can develop in as little as 2 hours).  

 Provide resources for community support, refer to social worker for home care

resources
Spinal cord injury patients often require many resources in the community and in their home
for care, including wheelchairs, assistive devices, shower chairs, hospital beds, etc. The social
worker can help to set these things up for the patient.

 Acute Pain related to physical injury as manifested by Burning pain below level of
injury, Muscle spasm/spasticity and verblization
 Impaired Physical Mobility related to Immobilization by traction as manifested by
Inability to purposefully move

 Risk for Ineffective Breathing Pattern related to Impairment of innervation of
diaphragm

Herniated nucleus pulposus is prolapse of an intervertebral disk through a tear in the
surrounding annulus fibrosus. The tear causes pain due to irritation of sensory nerves in the
disk, and when the disk impinges on an adjacent nerve root, a segmental radiculopathy with
paresthesias and weakness in the distribution of the affected root results.

Anatomy
The back, or spine, is made up of many parts. the backbone, also called your vertebral
column, provides support and protection. It consists of 33 vertebrae (bones). There are discs
between each of the vertebra that act like pads or shock absorbers. Each disc is made up of a
tire-like outer band called the annulus fibrosus and a gel-like inner substance called the
nucleus pulposus.
Together, the vertebrae and the discs provide a protective tunnel (the spinal canal) to house
the spinal cord and spinal nerves. These nerves run down the center of the vertebrae and exit
to various parts of the body.

Your back also has muscles, ligaments, tendons, and blood vessels. Muscles are strands of
tissues that act as the source of power for movement. Ligaments are the strong, flexible bands
of fibrous tissue that link the bones together, and tendons connect muscles to bones and discs.
Blood vessels provide nourishment. These parts all work together to help you move about.

A herniated disc most often occurs in the lumbar region (low back). This is because the
lumbar spine carries most of the body's weight. Sometimes the herniation can press on a
nerve, causing pain that spreads or radiates to other parts of the body. The amount of pain
associated with a disc rupture often depends on the amount of material that breaks through the
annulus fibrosus and whether it compresses a nerve.

Pathophysiology
herniated nucleus pulposus is a combination of increase in local inflammatory chemokines
and mechanical compression of nerves due to bulging of the nucleus pulposus. It has been
noted that the incidence of herniation is more common in posterolateral area, due to the
anatomy there (thin annulus fibrosus with poor support from anterior-posterior longitudinal
ligaments). Posterolateral herniation may cause compression of the nerve root leading to
 radiculopathy. Spinal cord compression may cause myelopathy secondary to herniation of
midline disc. Back pain is caused due to localized inflammation and herniated disc pressure
over longitudinal ligament.

Diagnosis of Herniated Nucleus Pulposus

MRI or CT
MRI or CT can identify the cause and precise level of the lesion. Rarely (ie, when MRI is
contraindicated and CT is inconclusive), CT myelography is necessary. Electrodiagnostic
testing may help identify the involved root.

Because an asymptomatic herniated disk is common, the clinician must carefully correlate
symptoms with MRI abnormalities before invasive procedures are considered.

Factors that can increase your risk of a herniated disk include:

 Weight. Excess body weight causes extra stress on the disks in your lower back.
 Occupation. People with physically demanding jobs have a greater risk of back
problems. Repetitive lifting, pulling, pushing, bending sideways and twisting also can
increase your risk of a herniated disk.
 Genetics. Some people inherit a predisposition to developing a herniated disk.
 Smoking. It's thought that smoking lessens the oxygen supply to the disk, causing it
to break down more quickly.

DIAGNOSTIC TESTS

 Tests done may include: 

 Spine MRI or spine CT may be done to show where the herniated disk is pressing on
the spinal canal.
 Electromyography (EMG) may be done to determine the exact nerve root that is
involved.
 Myelogram may be done to determine the size and location of disk herniation.
 Nerve conduction velocity test may also be done.
 Spine x-ray may be done to rule out other causes of back or neck pain. It can look at
how healthy your bone is and also look for how much room there is for your spinal nerves to
travel out of the spinal cord. However, it is not possible to diagnose a herniated disk by a
spine x-ray

Diagnosis and Treatment of Herniated Nucleus Pulposus

Diagnosis of herniated nucleus pulposus is done by an experienced orthopedist. A detailed

case history is obtained followed by physical examination of the back.

Confirmatory tests such as X-ray, MRI or CT scan are often helpful in ruling out other

conditions and reaching a correct diagnosis.(1) Advanced technology such as pain mapping

technologies are often used in these conditions. Based on the findings, treatment is planned.

The available treatment options are:

Medications to Treat Herniated Nucleus Pulposus: A large number of over-the-counter

medications are available in the market, for local application as well as for oral ingestion.

(1) These medications control inflammation and pain, and it also helps in starting physical

therapy without excessive discomfort. Prescription medications such as local injection of pain

relieving agents are also available for severe cases. Some of these medications are effective

for up to 6 months after a single shot.

Physical Therapy or Exercise for Herniated Nucleus Pulposus: Excessive bed rest in not

beneficial for patients suffering from herniated nucleus pulposus. Physical therapy and

specifically designed exercises, helps in combating this issue by strengthening abdominal

muscles, increasing flexibility, losing excess pounds etc. They help is removing excess strain

over the spine and promotes rapid healing,

Lifestyle Changes and Alternative Ways to Treat Herniated Nucleus

Pulposus: Additional treatments such as lifestyle modification, ergonomic education,

acupuncture, therapeutic massages, wearing appropriate footwear often help in management

of the symptoms.

Surgical Intervention for Herniated Nucleus Pulposus: If conventional treatment does not

relieve symptoms, surgical intervention is considered to treat herniated nucleus pulposus.

Surgery aims at repairing the damages discs or replacing them with artificial spacers. Minimal

invasive laparoscopic surgery is popularly used as a surgical option for herniated nucleus

pulposus.

Treatment

Herniated nucleus pulposus is prolapse of an intervertebral disk through a tear in the

surrounding annulus fibrosus. The tear causes pain due to irritation of sensory nerves in the
disk, and when the disk impinges on an adjacent nerve root, a segmental radiculopathy with
paresthesias and weakness in the distribution of the affected root results. Diagnosis is usually
by MRI or CT. Treatment of mild cases is with analgesics, activity modification, and physical
therapy. Bed rest is rarely indicated. Patients with progressive or severe neurologic deficits,
intractable pain, conservative treatment failure, or cauda equina syndrome with associated
sphincter dysfunction may require immediate or later elective surgery (eg, diskectomy,
laminectomy).
Spinal vertebrae are separated by fibrocartilaginous disks consisting of an outer annulus
fibrosus and an inner nucleus pulposus. When degenerative changes (with or without trauma)
result in protrusion or rupture of the nucleus through the annulus fibrosus in the lumbosacral
or cervical area, the nucleus is displaced posterolaterally or posteriorly into the extradural
space.

Radiculopathy occurs when the herniated nucleus compresses or irritates the nerve root.
Posterior protrusion may compress the cord in the cervical, thoracic, or upper lumbar spine or
the cauda equina, especially in a congenitally narrow spinal canal (spinal stenosis). In the
lumbar area, > 80% of disk ruptures affect L5 or S1 nerve roots; in the cervical area, C6 and
C7 are most commonly affected.

Herniated disks are common.

Symptoms and Signs of Herniated Nucleus Pulposus

Herniated disks often cause no symptoms, or they may cause symptoms and signs in the
distribution of affected nerve roots. Pain usually develops suddenly, and back pain is typically
relieved by bed rest. In contrast, nerve root pain caused by an epidural tumor or abscess
begins more insidiously, and back pain is worsened by bed rest.

Cauda equina compression often results in urine retention or incontinence due to loss of
sphincter function.

In patients with lumbosacral herniation, straight-leg raises stretch the lower lumbar roots and
exacerbate back or leg pain (bilateral if disk herniation is central); straightening the knee
while sitting also causes pain.

Cervical herniation causes pain during neck flexion or tilting.

Diagnosis of Herniated Nucleus Pulposus

MRI or CT
MRI or CT can identify the cause and precise level of the lesion. Rarely (ie, when MRI is
contraindicated and CT is inconclusive), CT myelography is necessary. Electrodiagnostic
testing may help identify the involved root.

Because an asymptomatic herniated disk is common, the clinician must carefully correlate
symptoms with MRI abnormalities before invasive procedures are considered.

Treatment of Herniated Nucleus Pulposus

Conservative treatment initially
Invasive procedures, sometimes including surgery, if neurologic deficits are progressive or
severe
Because a herniated disk desiccates and shrinks over time, symptoms tend to abate regardless
of treatment. Up to 85% of patients with back pain—regardless of cause—recover without
surgery within 6 weeks.

Conservative treatment
Treatment of a herniated disk should be conservative, unless neurologic deficits are
progressive or severe. Heavy or vigorous physical activity is restricted, but ambulation and
light activity (eg, lifting objects < 2.5 to 5 kg [about 5 to 10 lb] using correct techniques) are
permitted as tolerated; prolonged bed rest (including traction) is no longer indicated.

Acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), or other analgesics should

be used as needed to relieve pain. If symptoms are not relieved with nonopioid analgesics,
corticosteroids can be given systemically or as an epidural injection; however, analgesia tends
to be modest and temporary. Oral methylprednisolone may be given, tapered over 6 days,
starting with 24 mg daily and decreased by 4 mg a day.

Physical therapy and home exercises can improve posture and strengthen back muscles and
thus reduce spinal movements that further irritate or compress the nerve root.

Invasive procedures
Invasive procedures should be considered for the following:

Persistent or worsening neurologic deficits, particularly objective deficits (eg, weakness,

reflex deficits) due to cervical or lumbar radiculopathies
Acute compression of the spinal cord or cauda equina syndrome
Severe, intractable nerve root pain or sensory deficits
Immediate surgical evaluation is needed if clinical findings of spinal cord compression
correlate with MRI abnormalities.

Microscopic diskectomy and laminectomy with surgical removal of herniated material are
usually the procedures of choice. Percutaneous approaches to remove bulging disk material
are still being evaluated.

Dissolving herniated disk material with local injections of the enzyme chymopapain is not
recommended.

Lesions acutely compressing the spinal cord or cauda equina (eg, causing urine retention or
incontinence) require immediate surgical evaluation (see diagnosis of spinal cord
compression ).

If cervical radiculopathies are accompanied by signs of spinal cord compression, surgical

decompression is needed immediately; otherwise, it is done electively when nonsurgical
treatments are ineffective.

Acute Pain related to nerve compression, muscle spasm as manifested by complaints of pain
at the lumbar back part, pain scale of 6/10 and vebalization

Impaired physical mobility related to pain as manifested by verbalization of haan ko kayat

unay agkuti kasi lalo agsakit nukwa

Anxiety related to ineffective individual coping

Preoperative
1. Describe the surgical procedure to patient and family.
2. Informed consent obtained by surgeon.
3. Describe the expected outcomes, both postoperative and long term.
4. Arrange for required preoperative testing.
5. Advise patient to discontinue medications such as herbal products, NSAIDs,
anticoagulants, aspirin, warfarin, and clopidogrel bisulfate.
6. Encourage patient to anticipate and arrange for perioperative and postoperative care
needs.
Perioperative
1. Explain to patient where and when to arrive, as well as surgery time.
2. Instruct patient as to eating and drinking restrictions.
3. Instruct patient about medications to be taken the morning of surgery with a sip of
water.
4. Remind patient to wear comfortable clothing and to leave jewelry and valuables at
home.
5. Tell patient to remove dentures, partial plates, eyeglasses, contact lenses, nail polish,
and sculptured nails.
Intraoperative
1. “Time Out”—right patient, right surgery, right site
2. Proper patient positioning
a. Table options are surgeon specific.
b. If patient is obese, consider using a Jackson table.
3. Intraoperative needs anticipation
a. Equipment
b. Patient-specific needs (e.g., latex allergy)
Postoperative
1. Neurological assessment
a. Strength and sensation assessment, as compared with preoperative status.
b. Special attention to neurological assessment and correlation with the
operative intervention.
2. Mobility
a. Patient should mobilize quickly unless ordered differently due to
complication (e.g., CSF leak).
b. Instruct and help patient to roll to side and bring legs down while
simultaneously rising up with the torso from the bed. This minimizes twisting at the
waist.
c. Instruct and help patient to rise from a chair using the legs, rather than
pushing off with the back.
3. Pain control
a. The degree of pain varies considerably.
b. Intravenous hydromorphone or morphine sulfate may be used as needed until
the patient is able to take oral medications.
c. Codeine, hydrocodone, or oxycodone, with or without acetaminophen, may
be prescribed as needed when the patient is able to take oral medications.
d. NSAIDs, as needed, can be very beneficial.
e. Neuropathic pain medications (e.g., gabapentin) may be beneficial.
f. Antispasmodics may be prescribed if muscle spasms are present.
g. Heat may be applied for spasms and muscular tension.
h. Ice may be applied for radicular pain for no more than 20 minutes per hour.
i. Gentle massage may be used away from the incision.
j. Have patient change positions frequently.
k. Modest activity may be conducted as tolerated.
4. Constipation prevention
a. Consider initiating techniques preoperatively.
b. Ensure adequate water intake.
c. Diet should include adequate fresh fruits, vegetables, and fiber.
d. Stool softener (e.g., docusate) may be used two to three times per day.
e. Motility agents (e.g., senna) should be used only as needed.
5. Urination
a. Urinary hesitancy, especially immediately postoperative, is usually transient.
b. Assess urinary output, frequency, and volume.
 c. Assess to be sure there is adequate emptying. Bladder scanning or
intermittent bladder catheterization may be necessary to assess for retention or
incomplete emptying.
6. Discharge planning
a. Discharge planning should be initiated preoperatively.
b. Reinforce the following: no lifting, bending, or twisting; no sitting for long
periods of time.
c. Remind patient to change positions frequently.
d. Remind patient not to drive while using narcotic pain medications.
e. Explain to patient that sexual activity may be resumed 2 weeks after surgery
and when it is comfortable.
f. Ensure the patient is aware of return-towork and activity recommendations.
7. Reinforce alternative planning and problem solving for practical everyday activities
(e.g., vacuuming, doing laundry, and performing child care).
8. Incision care varies with the type of closure.
9. Ensure the patient is aware of postoperative follow-up recommendations.