Another video pertaining to my paper and presentation on brain injury.
Thursday, May 31, 2012
Wednesday, May 30, 2012
Craniotomy
A video from YouTube to go with the topic I have written a paper on and am preparing a presentation for. Not for the squeemish!
Neurologic Injury Research Paper
I recently was assigned a research paper on the topic of mechanical ventilation and neurologic injury. I spent approximately 16 hours researching and writing this paper. It was written in APA format (re-formatted for the purpous of this blog post, the copy and paste was not quite as successful as the original formatting) and I've included a list of sources that I drew my information from. I'm a student and don't pretend to be a genius on this subject nor in the mechanics of writing a paper. I did recieve a 100% on this paper based on its meeting all of the assignment criteria. There was absolutely no plagerism intended, so if there's an issue please bring it to my attention so that I may rectify the situation. Happy reading!
Neurologic Injury
The Roll of Mechanical Ventilation
Neurological injuries are commonly known as
traumatic brain injuries, or TBI. In the United States alone TBI is
reported in over 200 cases per 100,000. This means that with the US
population being over 300 million that just about 600,000 cases of
TBI are reported each year. This does not account for those cases not
reported in an Emergency Department, or ED. As can be imagined, each
person is very different, so each case of TBI can vary greatly from
person to person.
There are three stages of brain injury.
Included in these three stages are mild TBI, moderate TBI, and severe
TBI. According to David W Crippen, MD “almost 100% of persons with
severe head injuries and as many as two thirds of those with
moderate head injury will be permanently disabled”. Economically
this means that the cost of TBI is staggering on the public. A mild
TBI is referred to as a concussion sometimes. Most patients
diagnosed with TBI are mild. Losing consciousness briefly after a
concussion is normal as is a general feeling of dizziness, confusion,
and perhaps small losses in memory and physical abilities. The
brains ability to send messages is temporarily blocked when the
trauma occurs. Losing consciousness is the brains way of shutting
down and restarting. Of course not every patient with a concussion
will lose consciousness. Other conditions possibly associated with a
mild TBI are post-traumatic amnesia that is short lasting and a
slightly lower Glasgow Coma Score, or GCS. A moderate TBI has
similar factors as a mild TBI but the symptoms last longer.
Unconsciousness can last up to a full day as can memory loss and
amnesia. A person with a moderate TBI would have a GCS ranging from
9-12. Finally a severe TBI will mean a patient is in a coma. All
symptoms are elongated further and more severely. GCS score is lower
than 8. A patient with a sever TBI will have trouble functioning
normally after the incident. They may have trouble with attention
span, memory and other cognitive problems. These patients could have
loss of senses, like taste, touch, smell, etc and my develop
seizures, pain, and lose some motor functions. The speed of which a
body recovers from a TBI is also indicative of the type (Traumatic
Brain Injury, 2011). A first sign of increasing ICP in a conscious
TBI victim is a change in their level of consciousness. Careful
observation of the pupils is important to see changes in pupillary
mismatch and decreasing reaction to light.
There are many treatments for brain injuries
with increased intracranial pressure. The most critical goal of
managing neurological injury and adjacent intracranial pressure (ICP)
is to reduce brain volume. The practitioner must decrease
cerebrospinal fluid, or CSF, along with blood volume while
maintaining cerebral perfusion in order to reduce ICP (Crippen,
2011). Normal ICP is 0-15 millimeters of mercury (mmHg). ICPs
elevated to 35mmHg for prolonged amounts of time can be potentially
harmful and once pressures increase above 40mmHg it is impossible not
to have sustained some damage. There are three parts that make up
the intracranial space. The brain, or parynchyma, consists of 1400ml
of the space inside the skull while the CSF and blood both make up
another 75ml each. The change in volume of the brain is
interdependent on the change in the volume of either of the other two
parts of the intracranial space (Sharma, 1999). Cerebral perfusion
pressure is measured by taking the mean arterial pressure and
subtracting the intracranial pressure, or CPP=MAP-ICP. According to
Egan's MAP is normal at about 93mmHg if arterial blood pressure is in
a normal range. ICP normally sits at 10mmHg or less. A good range
for CPP is 83-93mmHg. If a bleed is present then MAP may be kept
slightly higher in order to keep perfusion levels where they need to
be. Ischemia, or insufficient blood flow to the brain, is caused by
a decreased CPP in a vicious cycle that can possibly eternilize
itself. If the CPP is reduced the body reacts by raising the blood
pressure which in turn dilates the blood vessels in the brain. By
dilating, or widening, the vessels the venous flow is increased and
the blood volume increases in the brain. According to the CPP
equation this process then increases ICP, which decreases CPP and the
body starts all over with raising the blood pressure and so on
(Tolias et al, 2003). So the higher the ICP the higher the
practitioner has to increase the patient's MAP to prevent herniation, blockages of the ventricles, which
leads to increasing CSF.
Closed brain traumas can be caused by many
things. Tumors in the brain, falls, accidents, sporting activities,
and blows to the head are the main cause of these types of injuries
(Pillbeam, 1998). Other more specific causes can be shaken baby
syndrome, stroke, intracranial bleeding,
hydrocephalus, Lyme Disease, etc.
In the news recently has been the discovery of
high occurrences of concussions received by elite athletes,
especially football players, over many years of playing.
Statistically a professional athlete's life expectancy is about 1/3
that of the average human being and the average professional football
player will live approximately 20 years shorter than average
(Strength Planet, 2011). This statistic alone is evidence of how
devastating closed head injuries and increased ICP can be. The focus
of this topic is going to be mechanical ventilation and
hyperventilation as a treatment for increased ICP but that will be
discussed later.
There is quite a range of treatments for
increased ICP. Starting with relatively non-invasive treatments for
this disorder patients are put on fluid restriction and specialized
diuretics prescribed by a neurologist. A patient with a closed brain
injury would be on an ordered dietary NPO, or nothing by mouth, and
would not be set up with IV liquids like most patients. A diuretic
like Mannitol is delivered directly to the patient in a continual IV
drip that removes water from the brain and expels it as waste. A
patient with an edematous brain needs to be urinating as much of the
fluid out as possible. Not only does Mannitol expel extra fluid as
waste it also thins out the blood and increases cerebral blood flow
which helps reverse the lowered CPP (Sharma, 1999). Corticosteroids
can also be administered via an IV to decrease cerebral swelling.
Steroids have many side affects and those should be considered when
administering them to any patient.
Another non-invasive treatment for increased
ICP is to raise the the head of the patient's bed 30 degrees to
recruit gravity in helping improve venous drainage into the the
spine. Also by lowering the mean arterial pressure, or MAP, using an
anti-hypertensive, such as calcium channel blockers, the practitioner
can decrease cerebral blood flow thus reducing CPP. Physiological
circumstances that should be avoided or fixed are seizures, high
temperatures, and restlessness. These increase the body's metabolic
pursuit and oxygen consumption. High body temperatures will also
increase vasodilation in the brain and rouse cerebral edema (Sharma,
1999). Keeping a patient sedated will decrease their agitation.
However sedation on a patient with a head injury is done very very
carefully because it is harder to assess cranial activity after
sedation.
Normal laryngeal intubation can be very
agitating on a patient. As stated the practitioner wants to keep the
patient calm so as not to raise the ICPs any more so it is wise to
pre-oxygenate a patient with a closed brain injury so as not to
decrease the oxygenation in the bloodstream. Rapid sequence
intubation, or RSI, is also indicated for this type of patient
because it is quick and the patient is unconscious throughout the
entire procedure thus not agitating and raising ICP levels. A quick
sequence of drugs is given finishing with a paralyzing agent. RSI can
be done within one minute (Lafferty, 2011).
There are much more invasive techniques which
are used to treat increased ICP. A small lumbar puncture can be used
to drain a small amount of CSF out of the spine. This procedure is
helpful with the head of the patient elevated. The catheter inserted
in the lumbar does not remove a lot of CSF but with the help of
gravity any amount of fluid removal is imperative to severe patients.
Both an epidural monitor and subarachnoidal bolts have their place
in successfully draining CSF from the brain as well. Along with
these there are intraventricular catheters which are one of the most
popular devices used to drain CSF. A catheter is inserted directly
into the the ventricle and both CSF draining and monitoring is
possible (Sharma, 1999). Newer fiber optic technology has recently
come out allowing monitoring and draining of CSF by a probe being
surgically implanted in the brain, ventricles, and subdural space. A
transducer is on the tip of the fiber optic to measure pressure and a
catheter is put in place for drainage. The catheter can also be use to for
introduction of medicine (Arbour, 2011).
A more serious increase in ICPs might require
even more invasive procedures. Something called a burr hole can be
drilled in the patients head in the OR or right at bedside. It
creates a space just big enough to place and ICP catheter. If that
small procedure isn't enough a decompressive
craniectomy can be done. This is where part of
the skull is removed to allow the brain to swell without damaging the
parynchyma or causing vessels to be crushed further increasing ICPs.
The skull piece is surgically stored in the patient's abdomen until
they are recovered and it can be put back into place (Egans, 2003).
The IVD or Intraventricular Drain has several
names. External Ventricular Drain and ventriculostomy are similar
devices. The IVD is a piece of medical equipment that is used in
closed neurological injuries. It was designed to decrease elevated
ICPs and hydrocephalus when there is something obstructing the normal
flow of CFS around the brain. It is a small, plastic tube that is
surgically inserted in the side of the brain that is blocked to drain
fluids from the ventricles thus reducing ICPs. A ventricular
drainage device is designed to shunt cranial fluid from the brain.
The small plastic tubing is surgically placed in the ventricle where
pressure buildup is taking place using a one-way valve into another
portion of the brain that is not blocked and/or down into the stomach
where the extra fluid would be excreted as waste (Dempsey, 2012).
This type of drain would be internal. The external drains would
drain into a bag at bedside. These types of devices are used quite
commonly in neonates. Babies have the probability of having the
shunt device in their cranium their entire lives, although some may
be able to have them removed eventually. Complications can arise
such as shunt blockage and infection. Like any surgical procedure
infection is highly likely if not cared for properly. Watching for
signs of infection such as swelling, fever, and lack of healing is
important in these patients. Vomiting and seizures are signs to
watch for that indicate the catheter has a blockage. Permanent brain
damage can occur if these things occur (Kakarla et al, 2008).
Now is where the respiratory department can
aid in decreasing a patient's ICPs. The patient will need to be
monitored for clear, patent airways, breathing and oxygenation. A
direct cause of vasodilation is low tissue oxygenation, hypoxia, and
high levels of carbon dioxide, hypercapnia, in the
blood. If the vessels dilate it allows increasing amounts of blood
flow to the brain increasing the
vicious cycle of raising the patient’s ICPs.
Hyperventilating a patient can temporarily reduce cranial swelling.
The brain swells immediately in a patients with TBI. If
hyperventilation is applied quickly for less than 48 hours ICP may be
able to be reduced. Because the body is always trying to balance
itself, or keep itself in homeostasis after 48 hours or more the body
adjusts against the settings and normalizes it's blood gas values.
Reducing cerebral blood flow is important to reduce ICP. Alkalosis
in combination with hypocapnia can help reduce blood flow in the
brain therefore keeping the pressure of arterial carbon dioxide
levels, or PaCO2, between 25-30mm Hg is important.
Of course as all science and technologies the
medical field is constantly advancing and changing. New therapies and
procedures are discovered all the time to improve patient care. So
as new information is received old information is often shelved or
put on a back burner. Such is the case with hyperventilating a
patient in order to decrease ICP. All the advance drains, monitors,
and drugs combined have much less harmful side affects than keep a
person's blood gas levels in a state of alkalosis. Hyperventilation
would be a last ditch effort if none of the other procedures or
therapies worked. This does not mean that the role of the
respiratory therapist is obsolete during this particular trauma. The
respiratory staff will always work side by side with the nursing
staff in care of a patient with a TBI. Monitoring of the oxygen in
the blood would be a main concern for respiratory. Not to mention if
a TBI patient is on a ventilator they would need a respiratory
therapist monitoring that patient.
References
- Kakarla UK, Kim LJ, Chand SW, Theodore N, Spetzler RF (2008). “Safety and accuracy of bedside external ventricular drain placement”. Neurosurgery 63 (1 Suppl 1)
- Crippen DW. 2011. “Head Trauma”.Emedicine.com
- Davis DP, Kimbro TA, Vilke GM. The use of midazolan for prehospital rapid sequence intubation may be associated with dose-related increase in hypotension. Prehospital Emergency Care 2001; 5:163-168.
- Lafferty KA. 2011 “Rapid Sequence Intubation” Emedicine.com
- Tolias C, Sgouros S. 2003 “Initial Evaluation and Management of CNS Injury” Emedicine.com
- Sharma A, (1999). Raised Intracranial Pressure and its Management. Vol 1 No 1
- 15 Facts About World Class Athletes. (2001) Retrieved from: http://strengthplanet.com
- Arbour, R. 2011. “Intracranial Hyptertension Monitoring and Nursing Assessment” ccn.aacnjournals.org
- Traumatic Brain Injuy (2011) The Journey Home. Retrieved from http://www.traumaticbraininjuryatoz.org/
- Pilbeam SP, Cairo JM, (1998). Mechanical Ventilation Physiological and Clinical Applications. St Louis, MO: Mosby, Inc.
- Wilkins RL, Stoller JK, Kacmarek R. (2003). Fundamentals of Respiratory Care. St. Louis, MO: Mosby, Inc.
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