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The most
likely person to present with a closed-head injury is the male who is
less than 24 year of age. These injuries can be due to [1]
acceleration/deceleration injuries [2] or being struck by a falling
object or during an assault. The damage from the strike is more likely
to result in permanent damage.
A closed- head injury can cause damage by
·
the actual blow causing
contusions and bleeding into the brain, causing pressure on
the adjacent brain tissue
·
the contra-coupe on the
other side of the head as the brain rocks forward and then
back causes contusion on another part of the brain
·
Because the skull is a
closed enclosure, rising intracranial pressure [ICP] any
part of the brain will raise pressure throughout the entire
brain.
·
The blow itself may
result in apnea which leads to anoxic damage if the patient
is not given rescue breaths in a timely manner.
·
the altered LOC can
result in a patient who cannot protect his airway because
his reflex are gone, or he suffers soft-tissue upper airway
obstruction and he might even have a limited reaction to
hypercapnea
On a microscopic level
·
After traumatic brain
injury, the brain is bathed with potentially toxic
neurochemicals such as catecholamine, free radicals and
mediators of inflammation so that cerebral edema results.
·
Tissue hypoxia secondary
to apnea, poor upper airway control or hypoventilation
associated with a head injury causes lactic acidosis from
anaerobic metabolism which cause edema of brain cells.
·
Systemic hypotension
results in decreased cerebral perfusion and if there is
intracranial edema this becomes worse. The pressure gradient
between mean arterial blood pressure [MAP] and ICP equals
the brain perfusion. If the gradient drops because the ICP
rises, there is less perfusion of the brain
S/S of closed-head injury
·
On interview, there will
be a recent history of a trauma or a history of multiple
head trauma such as those seen with professional boxers or
football players.
·
The patient may have
altered LOC
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o
The
Glasgow Coma Score is the mainstay for rapid
neurological assessment in acute head injury and it collates
well with the patient’s outcome.
o
If conscious, the
patient may complain of a headache
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On inspection, look for
the presence of Cerebral Spinal Fluid [CSF] in the nasal
secretions, which implies there is risk of ascending
meningitis because the olfactory nerves were sheared off at
the cribiform plate leaving the brain tissue open in the
nasal cavity
o
If the nasal secretions
or fluid from the ear contain CSF, one might see the dried
droplets on an absorbent filter paper separate into a dark
center of blood and a clear outer ring of CSF. “double ring
sign”
·
Look for blood in the
ear canal or behind the tympanic membranes
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Look for the reaction of
the pupils to light.
o
Bilateral fixed and
dilated pupils especially when accompanied by a Glasgow Coma
Score of 3 or less has a poor prognosis.
o
Remember that if the
patient received Atropine during the advanced life support
to treat bradycardia, this drug will cause the eyes to
dilate and not respond to light
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Look for paralysis,
posturing, seizures or primitive reflexes.
o
primitive reflexes such
as the Babinski reflex are those reflexes that are normal
in babies but are a sign of brain damage in the adult.
o
Flexor or extensor
posturing implies extensive intracranial pathology or raised
intracranial pressure
·
Patient may start having
seizures and abnormal EEG tracing
Treatment of closed-head injury patients
Much of closed-head injury
management involves prevention of diffuse cerebral edema.
Diffuse cerebral edema is present in
39% of patients with closed-head injuries.
Decrease ICP by monitoring the ICP
pressure [normal 4-13 mmH20] with a ‘bolt’ in the head [1]
draining the head of excess water and [2] prevention of adding
more water to the brain than needed
·
mid-line the head to
facilitate drainage of the jugular veins
·
raise the HOB 30-45
degrees to facilitate drainage of the jugular veins which
drain the brain
·
keep the patient sedated
to prevent fighting the ventilator or coughing which raises
the mean airway pressures; barbiturates both sedate and
decrease cerebral edema
·
while fluid restriction
is no longer recommended, we need to adjust the patient’s IV
fluids to keep blood volume at a normal level so that we
will not change hydrostatic and osmotic pressures
·
we avoid letting the
glucose levels rise because glucose can increase lactic
acidosis formation in anaerobic metabolism
·
mild hyperventilation to
the point that PaC02 is around 30 torr for short time-frames
while the ICP
o
If we lower the PaC02
more than this we risk vasoconstriction and increased
resistance to blood flow
o
If we reduce the PaC02
prophetically, the benefits of hyperventilation are lost as
the HC03- drops to compensate the pH for the lower PaC02
o
If hyperventilation is
used we must increase the PaC02 over 24- 48 hours to avoid a
rebound of the ICP
·
Mild hyperoxemia because
we are decreasing blood flow to the head, some advocate
increasing the Fi02 to get a Pa02 of 100-120 torr.
·
Avoid high PEEP unless
absolutely necessary, because this raises intrathoracic
pressures and slows down draining of the head.
·
Avoid unnecessary
suctioning of the airway or any other interruption of the
circuit that would result in sudden airway pressure changes.
These pressure surges will transit to the intrathoracic
pressures and affect the blood flow in the jugular veins and
cause a pressure rise in the ICP-this can be countered by a
short period of hyper-ventilation.
·
CPT in fact, coughing is
contraindicated in this patient because we do not want to
increase ICP
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Mannitol by IV. Mannitol
is an osmotic diuretic that pulls water out of the cerebral
tissue.
·
systemic steroids can
help with inflammation
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Treat seizures
Anoxic encephopathy & long-term
effects of anoxic episodes
Coma and Persistent Vegetative State Information Page: National
Institute of Neurological Disorders and Stroke (NINDS)
NEJM -- Medical Aspects of the Persistent Vegetative State-
First of Two Parts
Once the initial trauma or disease
is over, if it involved the central nervous system [CNS] and the
event resulted in significant anoxia for any amount of time, we
have to assess the patient for s/s of anoxic encephalopathy.
As a general rule, in young people
suffering from drowning, persistent coma after 48 hours is
significant for permanent brain damage
While a tiny number of patients
recover from traumatic coma after 12 months, patient who are
comatose due to metabolic problems such as diabetic coma have no
recovery after only 3 months.
There are levels to brain damage. A
coma is a profound state of unconsciousness in which the patient
does not respond to stimuli.
During the persistent vegetative
state, which sometimes follows a coma, the patient has lost
awareness of his surroundings, but retains non-cognitive
function and even normal sleep patterns. Breathing and
circulation remain relatively intact.
Most patients in PVS will die within
2-5 years and they will usually die of infections such as
pneumonia.
The role of the RCP in these types of patient includes:
·
maintaining a patent
airway by:
o
recommendation of
tracheostomy in a timely manner & keeping it clean
o
hyper-inflation by
bagging or IPPB, and suctioning of secretions if the patient
cannot cough effectively.
o
Turn frequently
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If the patient has an
intact cough reflex, we may simply stimulate the cough with
the suction catheter and use the catheter to collect the
secretions, but be aware that nasotracheal suctioning can
introduce bacteria into the lower airway.
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If he wheezes, start
Beta II agonists.
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Mobilize secretions by
CPT/PD or appropriate adjuncts
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Prevention of infection
by:
o
Use aseptic or sterile
technique as required
o
Suggest Tracheal
Aspirate for gram stain and C&S for increased secretions
and/fever or changes in X-rays
o
Good oral care & keep
the HOB up to minimize aspiration
·
Emotional support for
the family & reinforcement of realistic goals.
