Neurology II 6.04 Traumatic Brain Injury Dr. Tan

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Subject: Neurology II

Topic: Traumatic Brain Injury


Lecturer: Dr. Alfred Tan
Date: March 4, 2016

OUTLINE Table 1.
I. 3 D’s: Management and Approach Meaning Purpose
II. I.D.E.A.S in traumatic brain injury
a. Determine extent of TBI Recognize and
b. Evaluate Neurological Status DEGREE OF differentiate Provide direction and pace of
c. Assess Neurologic Disease (3Cs and D) SEVERITY degrees of severity management
d. 3 R’s
e. Assess the Neurological Diagnosis Determine cause of head Provide specific treatment
III. Types of head injury DIAGNOSIS injury (ex. Dealing with a based
IV. Hematoma
clot, you want to decide on clinical impression
V. Diagnosis 4 concepts of understanding ICP
VI. Traumatic Brain injury in special circumstances
if
VII. Treatment you will evacuate clot or
not)
OBJECTIVES Determine course of Provide further treatment
None were given DECISIONS treatment (whether based
(treatment) patient on course of head injury
References: Lecture, recording, 2016B trans is improving or
deteriorating)
I. 3 D’S: MANAGEMENT AND APPROACH
 There are 3 D’s in management and approach to traumatic brain A. Degree of Severity
injury.  Recognize: Pace, direction
o Degree of severity  Differentiate: Mild, Moderate, Severe
o Diagnosis  Evaluate: Priorities, Extent of Injury, Neurological Status (SPERM-
o Treatment decisions Sensorium, Pupillary size and reaction, Respiratory pattern and
 The general approach is basically knowing the degree of severity, rate, Motor)
coming up with a diagnosis, and coming up with the treatment  Identify Risk Factors (ex. Intracranial Injuries)
decisions. The 3 D’s in management and approach is just a guide. o This means that you need to recognize and differentiate the
 It is focused on what we’re going to do and it is directed to classifications or categories of the patient you’re dealing with
prevent secondary lesions in head injury (whether you’re dealing with mild, moderate or severe). This
 Secondary Lesions in TBI that you want to prevent include: will give you direction and will set your pace on how you will
deal with the problem.
o Hypoxic Injury o If you’re dealing with a mild head injury, then you would have
o Traumatic Ischemia, Infarction time to get more data (comprehensive history taking) and
o Secondary Hemorrhages (e.g. hematoma)- hemorrhage may examine more thoroughly, in contrast to a patient who’s
lead to increased intracranial pressure already in a severe status. Would you still take a
o Diffuse Cerebral Edema or Cerebral Herniation comprehensive history seeing that your patient is already in
distress? Hence, your actions would be different.
 The emphasis of this lecture is to prevent secondary brain changes
 When you evaluate a patient, you have to evaluate as quickly as
because in primary brain injuries, there’s not much we can do. you can.
Most of these patients with primary brain injuries will probably o ABCD: First and foremost, in any trauma whether abdominal,
survive despite your knowledge on his/her condition. This means chest, and so on, you always have to evaluate the Airway,
that the primary brain injury sustained by the patient is not Breathing, Circulation, Disability (currently it is CAB)
significant. However, some of these patients would die even if  MOST IMPORTANT!
expert care is given to them, maybe because the primary brain  The complications you will see later are related to this.
injury is so severe. The patient would probably die within the next o 6B’S: Find out the extent of the injury by evaluating the
24-48 hours Breathing, Blood, Bowel, Bladder, Bone, and Brain (discussed
 Lastly, some patients may die because of iatrogenic causes (that’s later)
you!). o SPERM: You also have to evaluate the neurological status of
 In such cases, the primary injury is not enough to cause death. the patient using the SPERM (Sensorium, Pupillary size and
However, you failed to recognize and address the development of reaction, Respiratory pattern and rate, Motor)
secondary brain changes and associated complications leading to  Prevent secondary lesions!
the patient’s demise.
 Purpose: A Directed Management
o The outcome of your patient will depend on his neurologic
status by the time you intervene.
 Systemic and Intracranial Insults Associated with Impaired
Outcome
o Hypoxia
o Hypotension
o Increased ICP
o Decreased CPP (Cerebral Perfusion Pressure)

Trans Group: Martinez, Marzan, Masanga, Matabang Page 1 of 10


Edited By:
Table 2. Degree of severity A. Identify
DEGREE OF SEVERITY
Low Risk Moderate Risk High Risk
MILD MODERATE SEVERE
GCS 14-15 9-13 <8 •No moderate or •Progressive •Penetrating injury
Eye Opening Spontaneous Pain No eye opening high risk criteria headache •Focal neurological
•No scalp injuries •Persistent vomiting deficits
Vocal Response Talks, coos, cry Moaning No response
•Can have dizziness, •Amnesia •Depressed fractures
Diagnosis NSBI/CCN CTN/Clot/DAI Clot/DAI vomiting but not •Extreme of ages •Decreasing
persistent (<2/ >65) sensorium
 Basis for Classification of Severity •Normal •Unreliable history
o Initial manifestation neurological exam •History of loss of
o Mechanism of Injury •Asymptomatic consciousness
o Associated Injuries •Fractures (basilar
fractures), facial
o Neurological Status (GCS) injury
o Neurological Diagnosis
Figure 1. Identifying risk factors and the corresponding risk levels
C. Diagnosis
 Determine cause of head injury  You can identify risk factors that can increase likelihood of patients
 Provide specific treatment (based on clinical impression) to develop complications or secondary lesions (especially
 Example of head injury/ traumatic brain injury intracranial injuries)
o If a patient has a blood clot base on your clinical impression,  In identifying the risk factors, you can categorize the patient into
then you do not just observe the patient. You have to remove low, moderate and high risk group in developing intracranial
the blood clot. injuries. What are the things we need to watch out?
o Low-risk Group
D. Treatment Decisions  May be asymptomatic
 Determine course of treatment  Headache and vomiting (but not persistent)
 After the diagnosis, you must come up with the treatment  Dizziness (but not persistent)
decisions  Scalp injury
o What will you do to the patient? Are you going to just observe  Normal neurologic exam
the patient (OTD- observe ‘til death?)  NO moderate/severe signs and symptoms
 In relation with the diagnosis, you have to determine the course of o Moderate-risk Group
treatment by noting the trend of the patient’s condition  History of loss of consciousness (may use as a reason for
o Improving—This means you have to continue what you are admitting the patient)
doing.  Persistent/Progressive headache and vomiting
o Unchanged – This means you have to watch him more  Seizures
carefully and find out why the patient is not improving despite  Amnesia
giving treatment. Investigate.  Multiple trauma
o Deteriorating  Extremes of ages (very young , <2 and very old, > 65)
 The trend of your patient’s condition in relation with the course of  Unreliable history
your treatment will aid you in coming up with the treatment  Suspected abuse
decisions and providing further treatment to your patient.  Serious facial injury
 Outcome of head injury is dependent to large extent on  Signs of basilar fracture - Patient with fractures especially
anticipation, recognition, and early treatment of secondary vascular fractures
injuries o High-risk Group
 The most important approach is “pre-emptive” rather than  Depressed level of consciousness
“responsive”. Better to anticipate, to monitor secondary brain  Decreasing sensorium or decrease in level of
injury and act on it on time. If you know the patients who are at consciousness (one of the early changes that you see in a
risk, you should be able to anticipate, and recognize if patient with significant brain injury problem) – when the
complications will come in so that you can prevent secondary level of consciousness is decreased, you have to start
brain injury. investigating for possible secondary head injury
 Focal neurologic findings (especially referable to the brain)
II. I.D.E.A.S. IN HEAD INJURY  Penetrating injuries (even if the patient is awake)
 Identify risk factors  Depressed fracture
 Determine extent of traumatic brain injury (TBI)
 Evaluate neurologic status
 Assess neurologic diagnosis
o Suspect TBI in special circumstances
 Start treatment

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B. Determine Extent Of TBI
3. Bladder
BREATHING  CASE: A patient who’s a little bit restless came in. You then read in
his chart that he was given diuretic or mannitol in a different
hospital. With this, think of a distended bladder. If the patient is
BRAIN BLOOD given mannitol or diuretics, there will be an increase in urine
output leading to the distended bladder hence the patient
becomes restless.
 But remember, restlessness is a bad sign so you must look for its
cause. Patient may have a distended bladder or maybe the patient
BONE BLADDER
is already hypoxic.
 Nevertheless, if patient is restless, don’t give Valium right away
because it might just be a distended bladder. By giving Diazepam
BOWEL (Valium) to the patient, you are just adding insult to the injury

4. Bowel
Figure 2. Checklist to determine the extent of injury
 CASE: Ruptured spleen or liver, or ruptured viscus -present as
 When you determine the extent of the injury, you have to go over head injury, hypotension - severe blood loss (but in reality it’s just
a checklist (this is important in improving safety precautions) blood loss from somewhere else which you failed to identify)
 Also determine the needs of the patient.  You undress the patient so that you can examine the abdomen.
Check for scars and tire marks.
 6 B’s is used as checklist to make sure that all vital organs are
covered.
5. Bone
 Establish priority. Among the 6 B’s, blood and breathing are the
most important hence you must establish first the circulatory and  CASE: A patient had severe head injury (which is usually associated
breathing status of the patient (CAB) with cervical fracture, fracture-dislocation or request for both AP
and lateral view x-ray spinal cord injury)
1. Breathing  However, when obtaining lateral x-ray, the technician would
usually just twist the neck of the patient instead of bringing the
 CASE: Example: A patient who is in the early his 20’s, came in with
tube to the lateral side to do full lateral x-ray by twisting/tilting the
a bone fracture. The orthopedic resident examined him, did x-ray,
neck of the patient, you may complete the then partial spinal cord
put a cast and referred him after 1 hour. At that time, he was
injury leading to the paralysis of the patient
already slightly cyanotic and his mouth was full of vomitus. Also,
the pupils were already dilated. Dr. Tan told the resident, “sayang  In severe head injury (like falls), it is better to look at the spine or
naman yang cast mo, ang gandaganda, baka ilibing lang yan,” and neck, if the patient is not breathing it might be due to a cervical
only because that resident failed to do one simple thing: to secure fracture or subluxations rather than the brain injury
the airway (clean the mouth and make sure that the patient can  Suspect for cervical spine fracture. Be careful not to move the
breathe well). head when getting the lateral shot. Just move the tube.
 Evaluating the ABCD of the patient is very important and it
definitely has a bearing on the treatment outcome of the patient. 6. Brain
So when the patient comes to the ER, make sure that you do your  Even if the patient’s brain is exposed, don’t panic and make sure
ABCs first before anything else. You have to secure the airway and that you obtained the vital signs of the patient and evaluated the
make sure the patient is breathing well. CABD

2. Blood
 CASE: A 2-year old kid was brought to a hospital’s emergency
room coming from Bataan. As he was examined, he was already
paper-white. In this case, they should’ve sutured the wound to
prevent severe blood loss since the small boy could only sustain
certain amount of blood; especially that hypotension is already
observed in the patient.
 Based on the history, the boy was still crying after the trauma,
which means that probably the primary head injury was not really
that significant (note: the patient is crying hence he is still
conscious – he’s not yet in the moderate or high risk group of
patients who may develop secondary head injury).
 However, the boy still died because of bleeding/severe blood loss.
The wound was only bandaged, and the bleeding was not
controlled, and by the time it was noticed, the boy already lost a
lot of blood. The cause of death could have been prevented.
Lesson: It is important to always get your vital signs.
 If there are signs of hypotension look for bleeding somewhere

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C. Evaluate Neurological Status  For example, in verbal response, what if the patient is
SPERM (Sensorium, Pupils, EOMs, Respiratory Rate, Muscular intubated or has a massive injury in the mouth area?
movement) You’ll not be able to assess the patient’s verbal response
since the patient cannot talk.
 For eye opening response, what if your patient has
swollen eyes? He would certainly not be able to open his
eyes, so how will you score?
 What if your patient has cervical neck injury with a
complete spinal injury leaving the paralyzed? Your score
would be lower.

o Unified Neurological Scale


 It uses the same evaluation criteria as the Glasgow Coma
Scale, but it is unidirectional that deals with the
limitations of Glasgow Coma Scale (There is a hierarchy
amongst criteria – hence you consider the best response
of the patient)
 Monitors overall brain function. For example, the patient
cannot move because of cervical fracture but he is
awake - patient still has a high score despite limitations
on his movement because monitoring sensorium is
basically monitoring the overall brain function not the
specific neurological deficit. This is the advantage of this
Figure 3. SPERM clinical monitoring.
 In Glasgow Coma Scale, if you ask the intern about the
 Sensorium neurological status of the patient, he will just give you
o This is the most important aspect in doing neurological exam. the Glasgow score. Example: Intern told you that the
o Usually called the level of consciousness (LOC). patient’s score is Glasgow 9 but how does a patient with
o To assess the LOC, Glasgow Coma Scale Scoring is used. a Glasgow score of 9 looks like?
o Glasgow Coma Scale Scoring  With Unified Neurological Scale, you describe the best
 *VEM - Verbal, Eye Opening and Motor Response response of the patient and you categorize it based on
 You have a score of 3-15  its level on the unified neurological scale.
 In most books, it’s usually arranged as EMV, but Dr. Tan
preferred VEM because he believes in the hierarchy of
functions. A patient who can talk is definitely better than
all the others. Eye opening is about arousal, while motor
response is very primitive.
 Level of unconsciousness - but sometimes, some patients
are also conscious so we refer to it as level of
responsiveness. There are a lot of clinical monitoring
methods used to evaluate the patients’ level of
unconsciousness but GLASGOW COMA SCALE is still the
one preferred.

Figure 5. Unified Neurological Scale. With this type of monitoring,


you can monitor if the patient is improving or deteriorating over
time since it is unidirectional.

Figure 4. Glasgow Coma Sale (important!)  How can you say that a clinical monitoring is good?
o A good clinical monitoring is what we call RSVP. Reliable and
Degree of Severity: GCS score Reproducible, Simple and Easy, Valid and Effective, and Practical
 Mild Head Injury: 13-15 and has prognostic value
 Moderate Head Injury: 9-12
 Severe Head Injury: < 8

o GCS has certain limitations

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D. 3 R’s
 Resuscitate the patient when he comes in so that the
neurological exam is valid. For example, a patient comes in with a
o If the clinical monitoring has these characteristics then it is Glasgow score of 3 (he’s flaccid and not breathing) then assess
considered to be good. (get the BP), all you need to do is intubate - you would then find
out that the patient would be doing fine – patient was just
 Pupillary size and response hypoxic/hypotensive for a short while (Glasgow scoring is usually
o Normal patients have brisk & reactive pupillary response. done after 6 hours so that you can assess the real status of the
o You always have to do this again and again. patient – you check the real status of the patient after the patient
o When the patient’s pupil is sluggish, this means that there is has been resuscitated)
an underlying problem, especially when the pupil blows  Repeat the neurological exam from time to time for you to know
(meaning it is dilated) – when the pupil blows, you also blow the progress of your patient’s condition or trend (whether he is
your horn (You have to call for help) improving or not)
 For example, patient with sluggish pupil or dilated pupil
 Record – this is very important in referring patients to another
being monitored by a sluggish intern- recipe of disaster!
hospital.
The patient will unfortunately die.  Put the time you see the patient and his status (Referral
slip)
 EOMs/Calorics  For example, a patient came in from a different hospital. It
o Ice water calorics was noted that he was awake when he was evaluated at
 Be careful in doing Doll’s head maneuver in patients with the said hospital. However, when you saw the patient, he
cervical head injury (in fact you should not do that) was already unconscious. This means that the patient was
 Check if the pupils/eyes are moving or not already deteriorating. Knowing this, you don’t just observe
 These are basically done to test brain functions the patient (OTD); instead, you must be able to come up
 Cervical fracture – important to watch out for; you may with the diagnosis right away (i.e. you need to get the CT
complete the spinal cord injury scan immediately).

 Respiratory Rate and Pattern E. Assess Neurologic Diagnosis (3Cs and a D)


o In patients with increased ICP, they usually go into a certain
 This will guide you towards the treatment decision
respiratory pattern (indicating respiratory and cardiac
 Take note of the 3R’s in management of patients with TBI
deterioration) – rostro-caudal deterioration

1. Concussion
 The clinical profile of a patient with cerebral concussion
IMMEDIATELY after trauma:
o The patient may or may not lose consciousness (if
there is loss of consciousness, it must occur immediately
after the trauma)
o They may have neurologic deficits that are secondary to
head injury
Fig 6. Breathing patterns o They will wake up as if nothing happened.
 There are no pathologic changes.
 Increased ICP may lead to anywhere from central
 In some, this may be mild and the patient may develop
neurologic hyperventilation then patient may later
“Posttraumatic syndrome” (dizziness, headache especially
develop Cheyne-Stokes respiration and will eventually
among women)
lead to apneustic breathing or Ataxic breathing - each of
 Violent shaking or jarring of the brain with a resulting transient
this represent level of the lesion as it progresses caudally
functional impairment such as loss of consciousness
until the point in time wherein the patient can no longer
All concussions involve a physical force that imparts motion to
breathe (ataxic or apneustic breathing)
the stationary head or, more commonly, a hard surface that
 Cushing’s triad: When you have increased ICP =
arrests the motion of a moving head, i.e., concussion does not
Hypertension, bradycardia, irregular respiratory pattern
occur if the head is stationary
 Rostro-caudal deterioration
 Clinical signs of concussive brain injury
o Immediate abolition of consciousness, suppression of
 Muscular Movements (Motor)
reflexes (falling to the ground if standing), transient arrest
o Very primitive. Note movement of each extremity to know if
of respiration, brief period of bradycardia, and fall in
there is laterality – this may aid in identifying the location of
blood pressure following a momentary rise at the time of
the lesion.

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impact. o Mild: coma usually last for 6-24hours
o In its mildest form, there is no apparent loss of o Moderate
consciousness or collapse, only a brief period of stunned o Severe
disorientation and amnesia during which the individual  Sometimes, it is difficult to distinguish if it’s mild or
appears outwardly normal severe. In severe DAI, you have brainstem findings,
decerebrate or decorticate (formerly known as brainstem
2. Contusion contusion)
 A bruising of cerebral tissue without interruption of its  With neurologic basis
architecture  Produce changes in the next 15 minutes following
 Focal injury
 May be found on the surface of the brain beneath the
point of impact (coup lesion) and sometimes there may be
more extensive lacerations and contusions on the side
opposite the site of point of impact (contrecoup lesion).
 Example: Given a particular patient where you can see
subarachnoid hemorrhages and contusion changes, but
he hit the back of his head not the front, so this is what
you call contrecoup lesion.
 The petechial hemorrhages on the surface, which is part of
the contusion, can coalesce to form bigger hemorrhages.
Sometimes these hemorrhages can be big enough that
you may need to do some interventions. These are called
contusion hematoma. Fortunately this patient remained Figure 9. Death is usually associated with the severity of DAI: as the
awake and stable and they didn’t need to do any kind of DAI becomes more severe, the mortality increased (refer to the table)
intervention.
 Most common site of cerebral contusion [baps]
o Frontal and temporal lobes

Figure 10. Mild, Moderate, Severe Diffuse Axonal Injury

III. TYPES OF HEAD INJURIES


 Scalp injuries (with foreign bodies)
o Very common
o This may include:
 Abrasions
Figure 7. Natural History of Cerebral contusion (may also be seen in
 Lacerations
diffuse axonal injury). The dip in the curve is the lucid interval which
 Contusions – coup/contre-coup mechanism
may happen for hours to weeks
 Avulsions
o Case: A patient came to you from a different hospital and his
3. Clot wound was already sutured. You admitted him but you were
assured that he’s okay since wound was already sutured. After
few days, you then noticed that the wound was swollen and
infected. You did a CT scan and found that there were stones
and dirt particles, which means that the previous doctor didn’t
clean it before suturing. Lesson: Do not trust other hospitals
when they bring patients that are already sutured. And if you
were the first doctor seen by the patient, be sure to clean the
wound before suturing it.
 Skull fractures (please refer to the sample cases below)
o Linear fracture
Figure 8. You have a clinical picture of a patient who already woke up
o Depressed fracture
but began to deteriorate, which means that there’s a lucid interval.
o Basilar fracture
Until proven otherwise, consider blood clot
o Diastatic fracture
o Ping-pong fracture
4. Diffuse Axonal Injury
o Growing fracture
 Usually sustained from a vehicular accident. May develop
 Penetrating injuries (please refer to the sample cases below)
from acceleration-deceleration type of injury (especially
 Gunshot injuries or wounds
with rotator component), wherein there are sheering
 Hacking injuries
forces that destroy your axons. It can be:

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A. Exposed Cranium parietal. The lesion thus causes a localized bulge, limited by suture
lines. The adherence of the periosteum at the sutures arrests the
spread of the lesion to adjacent bones. A unilateral parietal
hematoma is limited medially by the sagittal suture, frontally by
the coronal suture, and posteriorly by the parieto-occipital
(lambdoidal) suture. The underlying bone sometimes has a
fracture.

C. Basal Skull Fracture

Figure 11. Exposed cranium injuries

 In scalp injuries from thermal burns, sometimes you can have


avulsion of the scalp.
 The most important thing to do here is to cover the scalp defect
with moist material. You have to remember that your bones are
not made of plastic, instead they are living tissues, and therefore it
has to be soaked in wet sterile saline. In figure above, it was never
covered so it became infected.
 This patient developed osteomyelitis.

B. Extracranial Hemorrhage/Edema in newborn Figure 13. Observable manifestations in skull base fractures

 Battle’s sign (behind the ear)


o If the fracture extends more posteriorly, damaging the sigmoid
sinus, the tissue behind the ear and over the mastoid process
becomes boggy and discolored.
• Raccoon eyes (black eye)
o Basal fracture of the anterior skull may also cause blood to leak
into the periorbital tissues, imparting a characteristic "raccoon"
or "panda bear" appearance.
• Epistaxis (blood coming from the nose)
• Rhinorrhea (CSF coming from the nose)
• Otorrhea (CSF coming from the ear)
Figure 12. Different bleeding locations in the cranium
• Otorrhagia (blood from the ear)
• Traumatic otorrhagia (blood coming from the ear/ear
 Also known as “bukol” in children hemorrhage)
 This may be caput succedaneum, cephalhematoma or subgaleal o Fracture of the petrous pyramid often deforms the external
hemorrhage auditory canal or tears the tympanic membrane, with resultant
 Difference between cephalhematoma or subgaleal hemorrhage: leakage of CSF (otorrhea); or, blood may collect behind an intact
cephalhematoma is limited by suture line (since it is a tympanic membrane (hemotympanum) and discolor it.
subperiosteal bleeding) o One of the major complications of otorrhagia is that patients
 Some doctors have a tendency to aspirate it right away, but this is could develop facial palsy. If it’s not present, you still have to
unnecessary since sometimes it would resolve by itself. If you advise the relatives or the patient that facial palsy may still
really want to aspirate, make sure you do it aseptically. Otherwise, develop because some are just delayed. Otherwise, they’d
you might introduce bacteria into the blood, which is a very good blame you if it develops later on.
culture medium for bacterial growth (patient may have subgaleal o Note: The presence of any of these signs calls for CT scanning of
abscess after the initial doctor tapped them). the skull base using bone window settings to detect a fracture
 In scalp edema or in the frankly hemorrhagic scalp edema called
caput succedaneum, the infant has a scalp swelling that alters the D. Ping Pong Fractures
head contour smoothly, usually symmetrically, and at the vertex.  These are compound depressed skull fractures
Scalp edema, whether from injury or infiltration of intravenous  Take note of the hair impacted into the wound
fluid, transilluminates readily, but the greater the hemorrhage, the  In compound depressed open skull fractures, foreign materials
more opaque the lesion. (DeMeyer) can go in and you can have skull infections like osteomyelitis,
 In subgaleal hemorrhage, the blood occupies a space between the meningitis, and abscess. The beauty now is that we now have 3D
external periosteum and the galea aponeurotica of the scalp. It reconstructions and you can easily see the skull fracture and its
does not transilluminate. It may cause significant blood loss. extent. In depressed fractures, if you have an ordinary x-ray, your
 In cephalohematoma, blood dissects the external periosteum clue is double density. Double density film suggests compressed
away from one of the large, flat calvarial bones, usually the fracture until proven otherwise.

Page 7 of 10
E. Penetrating Injury B. Subdural Hematoma
Examples:
 ‘Indian pana’ – arrow penetrating the skull
 Patient pricked his head with a pencil and had a seizure afterwards
 Case: A paranoid/psychiatric patient had persecutory auditory
hallucinations. What he did was to drive a nail into his head. It was
not noticed until after 2 weeks and yet he didn’t develop
meningitis. They isolated and removed the nail, and replaced it
with a magic bullet which is stiff enough like a nail. Since the injury
was in midline, it must have hit the sinus and it may be clogged
with blood so if the nail is removed, the patient may bleed
profusely. You may be able to control the bleeding outside but you
cannot control the bleeding inside the sinus and with this, the
patient may die. Fig 15. Left: Normal; Right: Subacute Subdural Hematoma
 The same patient in the previous case, again nailed his head, but
this time it was in front, so they called him “Boy Pako.” If you look
at the angiogram, this time it reached deep beyond the basilar
artery. Again same procedure was done and fortunately, he lived.

IV. HEMATOMA
A. Epidural Hematoma

Figure 16 Left: showing acute subdural hematoma on right side and


subdural hematoma associated with temporal lobe intra-cerebral
hematoma (“burst” temporal lobe).

 Acute subdural hematoma


o The blood clot is after the dura, hence the brain parenchyma is
also affected. Even if you remove the blood clot, they don’t
usually wake up
Figure 14. Left: normal; Right: epidural hematoma o These blood collections are located between the brain
parenchyma and the dural membranes and are classified by
 In epidural hematoma, you can see fractures in temporal or their temporal profile
parietal area. You will note that this fracture crosses or is o Arachnoid–dura interface (site of subdural hematoma)
perpendicular to the blood vessels in the groove and this caused o Mortality is 70%-80%
the epidural hematoma.  Poorer outcome compared to epidural hematoma
 Development of epidural hematoma can be very fast hence this is  Subacute Subdural hematoma- just drain through a burr hole
one of the few ‘real’ neurosurgery emergencies. You have to  Chronic Subdural Hematoma
remove the blood clot. o Older individuals are at greater risk because as the brain ages,
o Sometimes you talk to patient and he’s okay, after a short there is an innate atrophy of the cerebral cortex. Thus in
while the pupil becomes dilated  deteriorating seniors, as the brain “normally” lessens in volume, an
increasing space develops within their subdural compartment.
 Immediately after the closed head injury, the patient “typically”
In turn this leads to increased stretch on the bridging veins
experiences an initial but relatively brief loss of consciousness
between the skull and the cerebral. When any individual
secondary to the primary concussive injury. This is then followed
sustains direct head trauma, the brain parenchyma
by a lucid interval with return of wakefulness.
accelerates and decelerates in relation to fixed dural
 Subsequently, as the torn vessels leak, an epidural hematoma structures. This leads to a tearing of the now anatomically
develops and enlarges, leading to a rapid lapse into coma. stretched veins that form a “bridge” between the cerebral
Sometimes this entire process may transpire from injury, to cortex and the skull. Similarly concomitant injury to cortical
transient loss of consciousness, and to a brief period of a arteries can also lead to bleeding into the subdural space.
“paradoxically reassuring alertness,” only to have a devastating, (Netter)
often irreversible, coma develop within just 1 hour after the blunt o Often mistaken for “mild stroke” because it is a great
head injury. mimicker
 However, this classic presentation occurs in less than one third of o Suspect child abuse in children with chronic subdural
affected individuals. The actual rate of symptom progression hematoma
depends on the type of associated brain injuries, their etiology, and
the subsequent precise rate of blood accumulation within the Note: Patients do not always present as trauma especially in patients
epidural space >65 years old. (e.g. Chronic subdural hematoma)

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Clinical Presentation and Diagnosis patient was apparently fine afterwards. Unfortunately, he
 The initial severity of the injury determines the patient’s clinical developed infection repeatedly. He became debilitated and
presentation; this varies from neurologically intact, to altered these doctors couldn’t control infection. When he evaluated
mental states, subsequently associated with pupillary inequality the patient, he saw one of the blades in the sinus. As long as
and motor weakness, and eventually becoming comatose with you don’t clean the sinus, infection will always come in.
signs of decorticate or decerebrate posturing. The lucid interval, a  Elevation of Depressed Fracture
classical finding with epidural hematoma, is also commonly seen o Case 3: A baseball bat hit the patient so there’s a depressed
with acute SDH. Brain CT is the initial test of choice for detecting fracture. If the skin is intact, you could elevate the bones.
SDH and concomitant brain injuries. An acute SDH is recognized by Just like a jigsaw puzzle, you collect them all and put them all
its hyperdense crescent-shaped image between the brain and together.
skull. Unlike epidural hematomas, SDHs typically cross skull suture o Use of Double density X-ray
lines, and sometimes extend along the falx cerebri. Note: Indications for surgery should depend on timing and neurologic
status of the patient.
Table 3. Different types of hemorrhages and hematomas.
V. 4 CONCEPTS OF UNDERSTANDING ICP
  Part of head injury is basically knowing intracranial pressures
(ICP). The following concepts are usually associated with
brain trauma:
o Monroe – Kellie hypothesis
o Cerebral Blood Flow and Cerebral Perfusion Pressure
o Autoregulation
o Intracranial Pressure Volume Relationship
Note: some treatment modalities are anchored in ICP directed while
some are anchored in cerebral perfusion pressure (aside from the
hyperventilation method)

Monroe-Kellie Hypothesis
 The sum of the intracranial volumes of:
o Blood
 Normal volume of blood in the intracranial cavity at a
given time = 100 – 150 mL
o CSF
o Brain
 Other components (e.g. tumor or hematoma) are
constant, and that an increase in any one of these must
be offset by an equal decrease in another.

(Usually it is the CSF that is displaced first. CSF can be displaced to


the ventricles and subarachnoid spaces when there is an increase
in ICP).

Management of Skull Injuries


 First: do no harm: “Primum non nocere”
o Case 1: The patient, Mr. Clean, had a blood clot due to head
injury and was operated in a provincial hospital. He did fine
and made it. Unfortunately, the doctor, obviously not a
neurosurgeon, did something wrong when doing a
cranioplasty. The patient spent a lot of money because of
continuous infection. When Dr. Tan saw him, he found out
that the metal placed in his head was not anchored well so it Figure 16. Monroe – Kellie doctrine
moves and the edges were wounded leading to continuous
infection. Cerebral Blood Flow
o It’s better to refer the patient to another doctor. That  CBF = CPP/CVR
doesn’t make you less of a doctor. Your interest is always  Cerebral blood flow = cerebral perfusion pressure/ cerebral
what’s best for your patient. vascular resistance
 Frontal Sinus Exenteration  CBF = 800 ml/min or 1/5 total cardiac output
o Case 2: This is something similar to Mr. Clean. This patient o Gray matter = 65-75ml/100gm/min
had a vehicular accident. He also had a subepidural o White matter = 15-20ml/100gm/min
hematoma and he was operated by a general surgeon and
an orthopedic surgeon. They did the operation and the

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Cerebral Perfusion Pressure  Specific – Surgery
 CPP = MAP – ICP  Mild TBI guidelines (checkout www.acepnow.com) – for adults
 Cerebral perfusion pressure = Mean arterial pressure–  For pediatric patients, it is important to know when to do a
intracranial pressure scan – PECARN (Pediatric Emergency Care Applied Research
 Normal adult CPP = 70mmHg Network) may help in assessing (www.mdcalc.com/pecarn-
 Some schools of thought whose main treatment for head injury pediatric-head-injury-trauma-algorithm )
is directed on CPPs. But keeping CPPs very high gives a lot of  Pingpong Fracture – like a greenstick fracture; make a small hole
complications (e.g. ARDS) and then elevate
 Compound Depressed Fracture – when there is air inside,
Autoregulation infection may develop like brain abscess and meningitis,
 The brain ordinarily can maintain a constant CBF when the MAP osteomyelitis
is between 40 and 140 torr by modifying the intracranial
vascular resistance (CVR). This is called Autoregulation.
Hear me, O Lord, when I cry out!
Sometimes in severe brain injury, autoregulation does not work
Have mercy on me and answer me!
making it difficult to maintain CBF or cerebral perfusion. My heart tells me to pray to you,
and I do pray to you, O Lord.
VI. SUSPECTING TRAUMATIC BRAIN INJURIES IN SPECIAL The Lord delivers and vindicates me!
CIRCUMSTANCES I fear no one!
The Lord protects my life!
I am afraid of no one!

(Excerpts from Psalm 27)

We’re almost there! One more trans to read!

Figure 17. Traumatic brain injuries in special circumstances

 Chronic Subdural Hematoma


o This is usually associated with patients who are diagnosed
with mild stroke which can’t be treated and is associated
with progressive headache. Look for a history of head injury
that is very minor hence was ignored. When you examine
them, you may find chronic subdural hematoma. This is
usually for the very old or very young.
o In younger patients, you can also see them in alcoholics.
They would usually deny history of trauma because they
were too drunk at that time and couldn’t remember
anything.
o It can also be seen in infants and toddlers who are
abused, especially those with bilateral hematomas. Red
flags of child abuse are multiple rib fractures, cigarette
burns on the skin and retinal hemorrhages.
o In newborns, they are usually associated with birth
injuries and with prolonged labor or use of forceps
(depressed skull fractures are observed).

VII. TREATMENT
 Symptomatic Treatment
 Supportive Treatment

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