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| INJURIES (Brain) |
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The most widely accepted concept of brain injury divides
the process into primary and secondary events. Primary
brain injury is considered to be more or less complete
at the time of impact, while secondary injury evolves
over a period of hours to days after trauma.
Primary Injuries
Skull fracture: Breaking of the bony skull; in a depressed
skull fracture, these bone fragments exert pressure
on the brain.
Contusions, or bruises, will often occur under the location
of a particular impact. They are also common in the
tips of the frontal temporal lobes, where the force
of the injury can drive the brain against the bony ridges
on the inside of the skull.
Hematomas, or blood clots, result when small blood vessels
are broken by the injury. They can occur between the
skull and the brain (epidural or subdural hematoma),
or inside the substance of the brain itself (intracerebral
hematoma). In either case, if they are sufficiently
large they will compress or shift the brain, damaging
sensitive structures in the brain stem. They can also
raise the pressure inside the skull and eventually shut
off blood supply to the brain. Prompt surgical removal
of such large blood clots is often lifesaving. However,
certain smaller hematomas can be safely allowed to resolve
themselves without surgery.
Lacerations: Tearing of frontal and temporal lobes or
blood vessels caused by brain rotating across ridges
inside skull.
Diffuse Axonal Injury: After a closed brain injury,
the shifting and rotation of the brain inside the skull
will result in shearing injury to the brain's long connecting
nerve fibers or axons. This can be microscopic and potentially
reversible in mild brain injury, but following more
severe brain injury it can be devastating and result
in permanent disability or even prolonged coma. At present,
there is no special treatment for diffuse axonal injury.
However, recent studies have shown that some of the
damage to axons progresses over the first 12 to 24 hours
after the injury. For this reason, there is hope that
it may be possible to prevent this progression in the
future with specific treatments. Because of these recent
findings, diffuse axonal injury is now thought of as
a combination of primary and secondary damage.
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Secondary Injuries
Delayed secondary injury at the cellular level has come
to be recognized as a major contributor to the ultimate
tissue loss that occurs after brain injury. A cascade
of physiologic, vascular, and biochemical events is
set in motion in injured tissue. This process involves
a multitude of systems, including possible changes in
neuropeptides, electrolytes such as calcium and magnesium,
excitatory amino acids, arachidonic acid metabolites
such as the prostaglandins and the leukotrienes, and
the formation of oxygen-free radicals. This secondary
tissue damage is at the root of most of the severe,
long-term deficits a person with brain injury may experience.
Procedures that minimize this damage can be the difference
between recovery to a normal or near-normal condition
or permanent disability.
Diffuse blood vessel damage has been increasingly implicated
as a major component of brain injury. The vascular response
appears to be biphasic. Depending on the severity of
the trauma, early changes include an initial rise in
blood pressure, an early loss of the automatic regulation
of cerebral blood vessels, and a transient breakdown
of the blood-brain barrier. Vascular changes peak at
approximately 6 hours postinjury but can persist for
as long as 6 days. The clinical significance of these
blood vessel changes is still unclear, but may relate
to delayed brain swelling that is often seen, especially
in younger people. Oxygen-free radical scavenger drugs
prevent or reverse these changes experimentally, suggesting
that such drugs may come to play an important role in
the management of brain injury in the near future.
The process by which brain contusions produce brain
necrosis is equally complex and is also prolonged over
a period of hours. Toxic processes include the release
of free oxygen radicals, damage to cell membranes, opening
of ion channels to influx of calcium, release of cytokines
and metabolism of free fatty acids into highly reactive
substances that may cause vascular spasm and ischaemia.
Such processes may also be interruptable by therapeutic
agents such as lipid antioxidants, calcium channel blockers,
and glutamate antagonists. The search for secure evidence
that new classes of drug based on these mechanisms reduce
the morbidity and mortality of brain injury will be
one of the most important efforts of the nineties.
Free radicals are formed at some point in almost every
mechanism of secondary injury. Their primary targets
are the fatty acids of the cell-membrane. A process
known as lipid peroxidation damages neuronal, glial
and vascular cell membranes in a geometrically progressing
fashion. If unchecked, lipid peroxidation spreads over
the surface of the cell membrane and eventually leads
to cell death. Thus free radicals damage endothelial
cells, disrupt the blood-brain barrier, and directly
injure brain cells, causing edema and structural changes
in neurons and glia. Disruption of the blood-brain barrier
is responsible for brain edema and exposure of brain
cells to damaging blood-borne products.
Free iron, as found in contusions and hematomas, is
particularly toxic, probably by catalyzing the formation
of hydroxyl radical (one of the most destructive of
all the free radicals). Hall and Traystman report that
these products may result in progressive secondary injury
to otherwise viable brain tissue through several mechanisms,
for example, by producing further ischemia or altering
vascular reactivity, by producing brain swelling (edema
or hyperemia), by injuring neurons and glia directly,
or activating macrophages that result in such injury,
or in the case of penetrating brain injury, by establishing
conditions favorable to secondary infection. In other
words, much of the ultimate brain loss may be caused
not by the injury itself, but by an uncontrolled vicious
cycle of biochemical events set in motion by the trauma.
The control of this complex cascade of cellular events
remains one of the most important challenges in the
acute management of brain injury. As with diffuse axonal
injury, it offers a potential therapeutic window of
opportunity during which brain swelling and nerve cell
death may be prevented during the first few hours after
an injury has been sustained.
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Secondary Intracranial Insults
In the minutes and hours after a brain injury, a variety
of other damage may occur.
- Hematoma (epidural, subdural and/or intracerebral)
- Brain swelling/edema
- Increased intracranial pressure
- Cerebral vasospasm
- Intracranial infection
- Epilepsy
In one recent survey of 100 individuals with severe,
moderate and minor brain injury associated with other
injuries by Andrews, 92% were found to have one or more
type of intracranial insult occurring for periods of
5 minutes or longer while being managed in a well staffed
and well equipped intensive care unit.
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Secondary Systemic Insults
Secondary systemic insults (outside the brain) that
may lead to further damage to the brain are extremely
common after brain injuries of all grades of severity,
particularly if they are associated with multiple injuries.
Thus people with brain injury may have combinations
of low blood oxygen, blood pressure, heart, and lung
changes, fever, blood coagulation disorders, and other
adverse changes at recurrent intervals in the days following
brain injury. These occur at a time when the normal
regulatory mechanism by which the cerebrovascular vessels
can relax to maintain an adequate supply of oxygen and
blood during such adverse events is impaired as a result
of the original trauma.
Some of the more common forms of secondary systemic
insults are listed below:
- Hypoxemia (Low blood oxygen)
- Arterial hypotension (high or low blood pressure)
- Hypercarbia (carbon dioxide accumulation)
- Severe hypocarbia
- Pyrexia (fever)
- Hyponatremia (low sodium)
- Anemia
- Abnormal blood coagulation
- Lung changes
- Cardiac (heart) changes
- Nutritional (metabolic) changes
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What is coma?
Coma Management and Care
When we hear the word coma, many of us envision a person
in a deep, sleep-like state, completely unaware of the
outside world. In fact, the word coma simply refers
to unconsciousness. This unconsciousness may be very
deep, where no amount of stimulation will cause the
person to respond. In other cases, however, a person
who is in coma may move, make noise, or respond to pain.
The process of recovery from coma is a continuum along
which a person gradually regains consciousness.
Prolonged coma does not necessarily mean a poor prognosis.
All individuals with traumatic brain injury who are
initially in a coma will emerge from the coma. Some
people will progress and ultimately have a good recovery.
Some will emerge but have significant disabilities,
and others will be in what is known as the minimally
conscious state or the vegetative state for years. In
the vegetative state, people may appear to be awake
and may even open their eyes and look about the room,
but are otherwise unresponsive. A variety of treatments
and techniques may be used to care for these people
and prevent complications. This section gives an overview
of the coma management process.
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Evaluation
While a person is in coma, a variety of evaluations
may be conducted. Ongoing evaluations of a person in
a coma are important to assess the person's status,
identify and prevent complications and to adapt medical
treatment. The Glascow Coma Scale is usually administered
upon admission to determine depth of coma and periodically
thereafter to help determine duration of coma more accurately.
Electroencephalograms (EEGs) and Evoked Potentials (EPs)
or Event Related Potentials (ERPs) are frequently used
to monitor neurophysiologic status. Measurements of
cerebral blood flow may also be helpful in evaluating
coma. Brain imaging technologies, particularly computerized
tomography scans (CT-Scans) and magnetic resonance imaging
(MRI) can offer important information about an individual's
status over time.
In addition, many evaluations will be conducted by individual
members of the treatment team. These include range of
motion, respiratory, nutrition, to name a few.
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Medical Management
Medical management may involve sensory stimulation programs,
positioning programs, medications, surgery, nutrition,
hygiene and various other interventions. Professional
staff can include physicians, neurologists, surgeons,
nurses and many others. Seizures, hypertension, hydrocephalus,
aspiration pneumonia, urinary tract infections, hormonal
abnormalities and skin ulcers are some of the potential
problems that a person in a coma may experience. The
medical staff will be prepared to treat these and any
other unexpected difficulties.
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Medication
Medication might be used to treat seizure disorders,
infections, muscle spasticity, hypertension, and swelling,
to name only a few of the possible reasons. In some
cases, medication might be prescribed that has the potential
to increase the coma duration, but decrease the swelling
in the brain, therefore decreasing the overall extent
of damage to the brain tissue.
It has been suggested that people in coma should not
receive a lot of medications that have sedative side
effects. However, they are often used. When this is
the case, physicians will often use the medication for
a short period of time, and attempt to decrease the
dosage. When any medications are prescribed, it can
be important that those who know the person best, such
as family members, be vigilant to observe any deterioration
in functioning.
There are a number of medications that can increase
central arousal, to include psycho-stimulants and anti-depressants.
These have been used to treat some individuals in coma,
but have not always been found to be effective. Sensory
stimulation is one way that many coma programs attempt
to increase arousal.
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Nursing Care
Nursing involves the monitoring of all body systems.
A nurse attempts to maintain the persons medical status,
anticipate potential complications and work to restore
a persons functioning.
Nursing practice for the person in a coma usually requires
monitoring vital signs and assessing all peripheral
pulses on a regular basis. In addition, circumferential
leg measurements will probably be performed to monitor
for deep-vein thrombosis. A rehabilitation nurse will
frequently take notice of and document skin color and
temperature changes, food and liquid intake, and bowel
and bladder functioning. Cardiovascular, musculoskeletal
and respiratory functioning will also be closely monitored
by the nursing staff.
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Respiratory Care
Because respiratory problems are extremely common in
people with brain injuries, airway control and mechanical
ventilation are often a major focus in early treatment.
Early aggressive control of the airway, adequate ventilation,
and oxygenation have been demonstrated to improve outcome.
The two main objectives of mechanical ventilation are
(1) to provide the person with adequate ventilation
and oxygenation and (2) to avoid or correct respiratory
muscle overload or fatigue. There are several techniques
of mechanical ventilation that can be utilized.
Artificial airways are another way to provide adequate
respiratory care. Pharyngeal "airways" are not really
airways. They are plastic "spacers" that can be inserted
through the mouth to hold the back of the tongue away
from the back of the throat. Tracheostomies are indicated
when prolonged ventilation is anticipated, when airway
control is required to prevent aspiration or to relieve
upper airway obstruction.
Respiratory therapy has various functions for the person
in a coma. Oxygen therapy might be administered if the
person requires it. Chest physiotherapy is used to help
mobilize secretions from the lower respiratory tract.
This involves a combination of percussion, vibration,
postural drainage, and coached coughing. Suctioning
is used to clear secretions from the pharynx, and should
only be performed when needed for people who have endotracheal
tubes or tracheostomy tubes in place.
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Positioning
People with severe alterations in consciousness (commonly
referred to as the vegetative state) present an array
of positional problems requiring special attention to
achieve an effective upright position. Abnormal reflexes
and reactions cause a pathologic increase in muscle
tone and abnormal posturing of the trunk and extremities.
The first goal of positioning the person to a sitting
position is to inhibit the elicitation of the abnormal
reflexes. The second goal is to help prevent the development
of joint contractures. Prolonged positioning in abnormal
rigid postures can increase the likelihood of muscle
and soft tissue contracture. Preventing the adverse
effects of prolonged bedrest by alleviating pressure
on the skin is the third goal. The fourth goal is to
help alleviate the problems of decreased blood flow
to the extremities, decreased systolic blood pressure
and decreased red blood cell formation. The final goal
is to increase the persons level of awareness through
stimulation to the kinesthetic and visual systems.
As positioning programs occur, it can be important that
continuous evaluations be completed in order to assess
how the intervention is affecting the total body position
and the persons behavior. A varying number of devices
may be necessary at different times throughout a positioning
program.
Finally, a positioning program should include education
for the family and other caretakers about the rationale
behind the program and the reasons for the use of each
devise.
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Therapeutic Intervention
Various therapeutic interventions are available to a
person in the vegetative state. Sensory stimulation
programs are based on the rationale that stimulation
will increase the input into the reticular activating
system in the brain, and thereby increase the person's
arousal level. However, the principles of sensory stimulation
have not, for the most part, been established by science.
The main principles of sensory stimulation are to control
the environment so there are few distractions, apply
one stimulation at a time, conduct brief sessions, stimulation
should be attempted in all five senses, and should vary
in nature and intensity. Many reports state that stimulus
that have emotional significance to the person may be
more likely to emit a response. Some programs will use
tape-recorded messages from family and friends.
People in the vegetative state often will have difficulties
with muscle tone, contractures and heterotopic ossification.
Prolonged stretch (including splinting), whirlpool or
hubbard tank treatment, electric stimulation, altered
body positioning and vibration may all facilitate reductions
in muscle tone as well as range of motion exercises.
Some people with increased muscle tone may benefit from
medications.
Contractures are the loss of passive range of motion
due to alterations in the muscle and connective tissue.
Range of motion exercises and prolonged stretch may
be utilized to help prevent this from happening.
Early symptoms of heterotopic ossification include warmth,
swelling and pain response. This usually occurs around
the large joints of spastic extremities, and is the
appearance of bone in the soft tissue. This problem
should be remediated early so as to prevent disfigurement
that could require surgery to correct.
Bowel and bladder treatment is an intervention that
occurs for people in comas. A persons immobility and
liquid diet frequently require a stool softener to be
administered. Bladder incontinence may be the result
of two interacting factors, the first being an inhibited
detrusor reflex (the ability to push down) and depressed
cognition.
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