Distributive shock
diving, trampoline
Loss of vasomotor tone due to Spinal cord injury,
dissection of the spinal
interference with sympathetic nervous cord; severe
acute pain (this will stimulate the
system function leads to neurogenic shock. vagus
nerve, which will make the heart rate
Different conditions make the vascular drop; when
this happens, not as much blood
space vasodilate. Prior to the vasodilation, is being
pumped out by the heart, so the
there is adequate volume for the size vascular system
thinks it’s in shock). Brain
of the vessels. When vasodilation occurrs, injury,
which alters the vasomotor center in
the vessels become larger. This makes the the
brainstem or sympathetic outflow to
volume seem less to the body, so the body vessels;
hypoxemia
Neurogenic shock
Occurs when the sympathetic nervous system stops
sending signals to the vessel walls, causing the
vessels throughout the body to vasodilate (also called
loss of sympathetic vascular tone) and the blood
pressure to drop. This usually occurs when there is
severe damage to the central nervous system,
specifically the brain and spinal cord. It is most often
seen after acute spinal cord injury due to blunt
trauma—motor vehicle accidents (MVAs), falls, and
sports injuries. The cervical spine area is the most
commonly injured area. The higher the spinal cord
injury, the more severe the neurogenic shock. With
injuries to the brain, the function of the autonomic
nervous system is decreased, which leads to
vasodilation throughout all vessels. In other words,
the spinal nervous system cannot
control the diameter of the blood vessels. When the
vasomotor center of the brain is injured, the
sympathetic nervous system does not function
properly, leading to systemic vasodilation. As a
result, blood pools in the
venous system, the amount of blood returning to the
right side of the heart is decreased, and ultimately
cardiac output drops and hypotension occurs.
SCI
An injury to the spinal cord via trauma by external
force. These injuries
usually occur as a result of motor vehicle crashes,
accidents, etc. The spinal cord is injured when the
cord undergoes
abnormal motions of acceleration and deceleration.
There are several types
of movements that the spinal cord can become
injured by. They include
hyperflexion (bending forward), hyperextension
(bending backward), axial
loading (compression of the cord, as when landing on
your head—ever
heard of a compression fracture?), and rotation
(turning of the head too far
either way). All of this leads to soft-tissue injury,
fractures of bones of the
spinal column, torn ligaments and muscles, or an
actual penetration of the
cord itself.
The injury is identified by the
level of injury and by complete/ incomplete depth of
injury. For example,
level C5 is an injury at the 5th cervical vertebrae.
That is the level. The cord
injury may be complete or incomplete. If it is
complete, motor and sensory
pathways are damaged and/or transected. This will
result in permanent
loss of motor and sensory function below the level of
injury.
PATHOPHY
The initial injury causes damage to the gray matter of
the cord but the
hemorrhaging, edema, and ischemia will extend to
involve a larger area
of injury, eventually affecting the entire gray matter
of the cord. This
explains why the extent of sensory/motor deficits
remains to be seen
right after an injury
Causes Why:
Contusion-Accidents such as car crashes, diving,
falls (commonly related
to trampolines and construction work)
Concussion-Same
Laceration-Same or may be from penetrating object
Transection-Same or may be from penetrating object
Hemorrhage-Bleeding from trauma
Blood vessel damage to vessels that supply the
cord-Related to the trauma
Fractured bones can damage Bone fragments-can
be a penetrating object the cord
Lab Tests:
X-ray, CT, MRI of the spine to locate the injury as
well as the extent of
damage.
EMG (electromyography) may help to locate the
level.
ABGs to determine oxygenation status and/or acid
base balance.
See the TBI section earlier in the chapter for other
tests that may be
performed in the presence of head injury.
Treatments:
Oxygen if injury is at thoracic level.
Methylprednisolone administered within 8 hours of
injury helps to
prevent further ischemia by reducing edema.
Opiate antagonists such as nalmefene might promote
blood flow to
the spinal cord.
Vasopressors to treat bradycardia due to spinal shock.
Muscle relaxant to help with spasms.
Analgesics to reduce pain.
Surgery to stabilize the spine from further injury—
cervical traction
may be initiated using Gardner–Wells tongs and halo
external fixation
device.
Surgery to remove bone fragments or hematoma,
decompression
laminectomy, spinal fusion, metal rods, etc.
H respiratory impairment
2 antagonists to prevent GI stress ulcer.
Anticoagulants to prevent clot formation.
Stool softeners to prevent constipation and to initiate
bowel
program
Signs and symptoms Why
Areflexia (loss of reflex function)—characterized by
low Initial response to spinal cord injury
characterized by
pulse, low BP, paralysis and weakness of muscles,
loss temporary loss of reflex function below the level
of
of sensation/feeling, bowel/bladder dysfunction, loss
injury. The cord does not function at all because it
has
of ability to perspire been separated from
communication with the brain.
Parasympathetic responses including bradycardia and
hypotension will ensue. This will end and some of
the
reflex function may return. This is one reason why
you see clients regain some function months later
after their initial injury
Neurogenic shock resulting in cardiovascular
changes Brainstem cannot regulate reflexes
such as orthostatic hypotension and bradycardia
Respiratory dysfunction Loss of innervation to the
diaphragm (C1–C4 injury)
with the inability to breathe on one’s own
Hypothermia Brainstem not functioning properly
Paralytic ileus Loss of reflex function
Urinary retention, incontinence Loss of reflex
function
Thrombophlebitis Decreased peripheral resistance,
loss of muscle
function/movement
Paralysis with muscle spasms Upper and lower
motor neurons pathways in the brain
Paraplegia: paralysis of the lower portion of the
body are affected
with lower trunk involvement
Quadriplegia: aka tetraplegia, is paralysis or
impaired
function of all four limbs, trunk, and pelvic organs
SCI Pathophy
Complete Cord Transection- Tetraplegia, mm
flaccidity, loss of all reflexes and sensory function
below level of injury, bladder and bowel atony,
paralytic ileus, unstable blood pressure, dry skin,
Incomplete Cord Transection- Motor deficits,
variable degree of bladder dysfunction, sensorimotor
dysfunction.
DELISA
Complete spinal cord lesions also affect the
autonomic
nervous system. Loss of sympathetic cardiac
innervation from
lesions above the sixth thoracic vertebra can limit
maximal
heart rate to 110 to 130 beats per minute (473).
Lesions at the
cervical and thoracic levels can impair control over
regional
blood flow during exercise, causing venous blood
pooling in
the legs and consequently reducing cardiac preload.
As a result,
stroke volume and cardiac output at a given oxygen
uptake
tend to decline in those with spinal cord injury
(474,475).
Furthermore, the loss of sympathetic nervous control
over
vasomotor and sudomotor responses of the insensate
skin
impairs thermoregulation
Spinal cord injury (SCI) results in varying degrees of
weakness
and sensory loss at and below (i.e., caudal to) the site
of injury.
The motor deficits may be represented as muscle
weakness and
limb paralysis, spasticity, lost of normal bladder
control, and
breathing difficulty.
The primary goals for interfacing patients with SCI
with
EMGBF are much the same as those outlined
previously for
stroke patients. First, attempts are made to reduce
hypermotor responses to induced length changes in
spastic muscles.
Such hyperactive behavior of spastic muscles may
occur during spontaneous episodes of clonus or
during induced clonic
seizures, when the lower or upper extremity responds
to various tactile stimuli. Once the patient can reduce
such responses
in supine, sitting, and ultimately standing postures,
efforts are
directed toward recruitment of weak muscles.
In patients with paraparesis following SCI, EMGBF
training at the Emory University enabled many
patients to increase
the speed at which they ambulate and to reduce the
number
of required assistive devices. For patients with
tetraparesis and
obvious residual voluntary movement, feedback
combined with
an exercise program facilitated active range of
motion (ROM)
and improved upper-extremity function. Feedback
may be
beneficial for these patients because the modality
may be easily
incorporated into exercise programs with
immobilized patients
during the acute phase of injury; it provides
immediate information to the patient concerning the
level of voluntary muscle
activity; and, by so doing, this modality may help
patients
obtain spatial and temporal summation of muscle
potentials
leading toward increased contractility, and therefore
preparing
the patient for a more vigorous therapy program.
However, in
cases in which little activity could be observed
among chronic
SCI patients, feedback provided little or no
significant benefit toward restoration of function
(74). Other clinical trials
demonstrate controversial results on the effects of
EMGBF for
patients with chronic, tetraparesis secondary to SCI.
One study
using a pre-post experimental design found that
EMGBF was
helpful in increasing voluntary muscle recruitment in
longterm spinal injured patients (75), while another
similar study
found no significant improvement (76).
Though SCI can be associated with a range of injury
patterns,
motor deficits are generally a prominent feature
(Chapter 47).
At the time of discharge from initial SCI, the most
frequent
neurologic category is incomplete tetraplegia
(31.2%), followed by
complete paraplegia (28.2%), complete tetraplegia
(17.5%), and
incomplete paraplegia (23.1%). Less than 1% of
persons experience complete neurologic recovery by
hospital discharge (341).
Persons with SCI generally show modest
spontaneous
sensory and motor improvement in the first 3 to 6
months
following injury (342,343), although significant
spontaneous
improvement beyond the first year post SCI is
uncommon
(344). Motor deficits are thus common and persistent Widespread
after SCI, abnormalities in the limbic system have also been
and these impact a number of health, quality of life, described
and other (359,360), the full impact of which has yet to be
issues in subjects with SCI (345–347). For example, appreciated.
by 10 years The temporal sequence of brain changes after CNS
after SCI, 68% of persons with paraplegia, and 76% are just
of those beginning to be understood (351). Also, the direct
with tetraplegia, remain unemployed (348). Concerns study of
over spinal cord function and plasticity at the level of the
sexual and bowel/bladder function are also prevalent spinal
(349). cord is an emerging approach that might provide
There has been limited study of the changes in the novel insights
function after SCI and after other forms of SCI (361,362).
of the human CNS after SCI. Some studies have
found a broad
decrease in brain activation (350–352), particularly in
primary
sensorimotor cortex, whereas others have found
supranormal
brain activation (353). The basis for these
discrepancies remains
unclear but could be due to differences in age or
injury pattern
of the population studied, years post SCI at time of
study, or
the nature of the task used to probe motor system
function,
some uncovering deficient processing and others
emphasizing
supranormal efforts to compensate (351,354). A
commonly
described feature is a change in somatotopic
organization
within primary sensorimotor cortex, with
representation of
supralesional body regions expanding at the expense
of infralesional body regions (102,355–358).
Spontaneous changes in
laterality, so prominent in studies of stroke or MS, as
above, are
generally not prominent after SCI, perhaps due in
part to the
fact that injury typically affects the CNS bilaterally
or perhaps
due in part to the fact that SCI spares brain
commisural fibers
whose integrity helps maintain normal hemispheric
balance.
As such, a laterality index is unlikely to be a useful
variable
in brain mapping studies of subjects with SCI.