STUDENT PROJECT

Management of Traumatic Brain Injury

By :
1. Nindya Nabilah Utami 1402005243
2. Putu Ayu Adi Supraba 1402005056
3. Putu Ayu Larasati 1402005153
4. Putu Diah Saraswati Rahayu 1402005026
5. Raoulian Irfon 1402005100
6. Rebecca Mutia Agustina Silaen 1402005145
7. Saraswati Putri Yogita 1402005208
8. Chika Christianne Moreen N 1402005082
9. Amylyn Rebecca Nathan 1402005182
10. Tan Beng Hong 1402005174
11. Tarvin Jit Singh Gill 1402005168
12. Tham Hong Yuan 1402005166

Faculty of Medicine
Udayana University
2017

i
 PREFACE

The writer would like to acknowledge our countless thanks to the Most Gracious
and the Most Merciful God who always gives us His grace so we could finish our
Student Project entitled “Management of Traumatic Brain Injury” on time. This
review of the literature is compiled in order to fulfil the requirements of The
Emergency block, seventh semester medical education courses in Medical Faculty
of Udayana University. At this opportunity, the writer would like to express our
deepest and most sincere gratitude to all the lecturers in this block, and everyone
who has helped the writer incompleting this student project. The writer also
realizes that this studentproject is still imperfect. Therefore, the writer expects
criticism and suggestions for this studentproject’s improvement. Last but not least,
the writer hopes that this studentproject can be useful for all who read this
literature review.

Denpasar, october 3rd 2017

Writer

ii
 TABLE OF CONTENT

Title .................................................................................................................... i
Preface ............................................................................................................
........ ii
Table of Content.................................................................................................... iii
CHAPTER I Introduction...................................................................................... 1
CHAPTER II Content ...........................................................................................
2.1. Pre Management…………….…......................................................
2.2. Mild Traumatic Brain Injury............................................................
2.3. Moderate Traumatic Brain Injury……..............................

2.3.1 History and Physical Examinations

2.3.2 Management in Emergency Room
2.3.3 Initial Imaging
2.3.4 No Mass Lesion in moderate TBI
2.3.5 Coagulation Profile and Platelet Transfusion
2.3.6 Seizures Prophylaxis
2.3.7 ICP (Intracranial Pressure) Monitoring
2.3.8 Symptomatic Treatment
2.4. Severe Traumatic Brain Injury........................................................
2.4.1 General consideration
2.4.2 Management of Intracranial Hypertension
2.4.3 Another Approach
2.5. Prognosis …………....................
2.6. Monitoring and Follow Up Management of TBI............
2.6.1 Monitoring………………………………
2.6.2 Follow Up……………………………….

CHAPTER III Conclusion .............................................................................

References .....................................................................................................

iii
 Chapter I
INTRODUCTION
Traumatic Brain Injury (TBI) is generally described as an impact,
penetration, or rapid movement of the brain within the skull which leads to brain
damage, altered mental state, and impaired neurologic function, regardless of the
underlying pathophysiologic cause, such as enlarging extra-axial hematoma,
diffuse swelling, ischemia, blossoming contusion, or any other causes.This
condition usually occurs when there is a traumatic event to the brain, most
commonly caused by mechanical force especially blunt force, such as falls
followed by motor vehicle crashes, traffic-related accidents, assaults, or sport-
related concussions.1–3Statistics recorded that a TBI occurs every 15 seconds in
US, resulting in 1.7 million victims per year. Of those, approximately 52.000
people die every year, 275.000 are hospitalized, 80.000 individuals are left with
significant disability, and 1.4 million are evaluated and discharged for emergency
department.1,3–5TBI is also a contributing factor in more than 30% of all injury-
related deaths. Its frequency is currently higher than any other disease, including
complex disease such as breast cancer, AIDS, Parkinson’s diseases, and multiple
sclerosis.3
The event of TBI can be classified as impact or non-impact, depends on
whether the head makes direct contact with an object (impact TBI), or encounters
a non-impact force such as blast waves or rapid acceleration and deceleration
(non-impact TBI).3It is divided into 2 phases : primary injury, defined as an
immediate consequence of the initial traumatic event, and secondary
injuries,which gradually occur as a consequence of ongoing cellular events that
cause further damage. Because the primary injury is immediate, it isnot easily
treatable, even it is nonreversible. 2,5Usually it is formed as a direct damage to
brain parenchymal tissue, causing both neuronal and vascular injuries, and the
brain to be displaced within the skull.2,3The pattern and extent of damage will
depend on the nature, intensity, and duration of the impact. Compression and
shearing forces, or penetrating injury type, may result in skull fracture,
contusions, intra cranial hematoma, cerebral edema, diffuse brain injury, or
superimposed tissue cavitation and possibly richocet injury. Moreover, rotational

4
forces may lead to additional injuries, including diffuse axonal injury which is
shearing of axons in cerebral white matter, causing neurologic deficits such as
encephalopathy. Finally, diffuse microvascular damage occurs and is due to an
early loss of cerebral vascular auto-regulation and a loss of blood-brain barrier
integrity.2,4
Secondary injuries progress over hours to days later as a result of the
inflammatory cascade and neurological injury that process into making vasogenic
fluid accumulation within the brain, causing a raised intracranial pressure, hypo-
perfusion, cerebral ischemia, and resulting in cerebral edema and cell death. Other
further physiological insults such as hypoxemia, hypotension, hyper or hypo-
capnea, anemia, hyper or hypoglycemia, and hyper-thermic, is well recognized as
a leading contributor to secondary brain injury. Injured brain is more susceptible
to these states, with changes in cerebral auto-regulation exacerbating injury.
Finally, posttraumatic vasospasm is thought as a common occurrence and may
worsen ischemic burden.If these conditions are prevented and corrected,
secondary brain injury can be minimized.2,4,5
Age has appeared to be an independent risk factor for poor outcome. The
classic stereotype of TBI patient is a male in his late teens or early twenties, with
the number of falls among the elderly has increased dramatically. However,
unique brain pathologies in each person produce unique cases of TBI too,
meaning that no two TBIs are the same. It affected individuals differently in
degrees of injury, regional patterns of injury, type and location, and also recovery
profiles.1,3,4This uniqueness of TBI is also caused by the neurochemical and
metabolic responses to TBI which is different in personal. TBI gives rise to early
ionic and neurotransmitter perturbations that initiate a cascade of events that
disrupt normal cellular function, including changes in glucose metabolism, free
radical production and mitochondrial dysfunction. Increased in cerebral glucose
metabolism is due to an increased requirement of cellular energy to restore the
ionic balance and neuronal membrane potential. This case is called
hyperglycolysis, stays in acute period for the first 8 days after head injury and
followed by a prolonged period of decreased cerebral glucose metabolism.
Following TBI, there is an increase number of free radical formation that can be

5
measured with direct measurement and indirectly by quantify lipid peroxidation,
protein nitration, and DNA oxidation. This increased number of free radical
production has a contribution in mitochondrial impairments. Excessive Ca2+ influx
can overwhelm mitochondrial Ca2+ -buffering capacity and the rate of efflux by
the mitochondrial Na+-Ca2+ exchanger, resulting in Ca2+ accumulation that
contributes to mitochondrial membrane-potential collapse. The end result is
impaired mitochondrial function, reduced energy protein,and potential for cell
death.3
There are some classifications used for categorizing TBI. The most common
used in general is classification as mild, moderate, or severe based on the Glasgow
Coma Scale (GCS).1,3,4Patients are scored on the basis of clinical symptoms,
comprise of the sum score of three components : eye, motor, and verbal scale,
resulting the classification as mild with GCS 13-15, moderate with GCS 9-13, and
severe with GCS <9.3,4,5The treatment of TBI is depend on this classification, each
type has its own procedure even thou its goal is still the same for raising the
quality of life and prevent complication. Based on this review, writer wants to
explain more about TBI’s management.

6
 Chapter II
CONTENT

2.1 Pre-Management
First, treat the greatest threat to life and avoid further harm when
administering immediate care. Health care givers, public health literature and
other non-medical sources of advice (for example, St John Ambulance, police
officers) should encourage people who have any concerns following a head injury
to themselves or to another person, regardless of the injury severity, to seek
immediate medical advice.
Base monitoring and exchange of information about individual patients on the
three separate responses on the Glasgow coma score(GCS). If a total score is
recorded or communicated, base it on a sum of 15, and to avoid confusion specify
this denominator (for example, 13/15). Describe the individual components of the
GCS in all communications and every note and ensure that they always
accompany the total score. In the paediatric version of the GCS, include a
'grimace' alternative to the verbal score to facilitate scoring in preverbal children.
In some patients (for example, patients with dementia, underlying chronic
neurological disorders or learning disabilities) the pre-injury baseline GCS may be
less than 15. Establish this where possible, and take it into account during
assessment.
GCS less than 15 on initial assessment by the healthcare professional,neck
pain or tenderness,focal neurological deficit,paraesthesia in the extremities orany
other clinical suspicion of cervical spine injury immediately attempt full cervical
spine immobilisation. Maintain cervical spine immobilisation until full risk
assessment including clinical assessment indicates it is safe to remove the
immobilisation device.
Transport patients who have sustained a head injury directly to a hospital that
has the resources to further resuscitate them and to investigate and initially
manage multiple injuries. 6

7
2.2 Mild Traumatic Brain Injury
In terms of the medical aspectreview pain medications to avoid
medications which can cause dependence or rebound headache.Avoid over the
counter medications that contain caffeine such as Excedrin, Anacin.Gradually
reduce caffeine intake, in particular, for individuals with irritability or sleep
disruption.Consider short-term (90-120 days) utilization of stimulant therapy. This
is particularly useful in cases where speed of processing is demonstrated to be
delayed or slowed. Ritalin can be particularly effective, initiating therapy at 10
mg. at 8:00 a.m. for 3-4 days, progressing to 10 mg. at 8:00 a.m. and 10 mg. at
noon, progressing to 20 mg. at 8:00 a.m. and 10 mg. at noon, progressing to 20
mg. at 8:00 a.m. and 20 mg. at noon for a period of approximately 90 days. The
medication should be tapered in a schedule similar to initiating therapy`7
Anti-anxietals should be systematically weaned. Anti-depressant therapies
can be considered. Preferential response seems related to serotonergic
medications. Consider changing dosage to before bed should undue daytime
sedation occur with serotonergic medications7
Pharmacological assistance to re-establish sleep patterns can be used on a
short-term basis. Medications such as Restoril and Ambien can be used and
should be tapered prior to discontinuation. Total days used should be less than two
weeks7
A program should be initiated for sleep education and return to normal
sleep cycle and pattern. Naps should be tapered when attempting to re-establish a
normal sleep cycle. Regular bedtime and rise-time should be utilized. The
individual should be counseled to remain in bed with the lights off if they awaken
during the night. An individual awakened by dream activity may be advised to
utilize a low sodium diet and ample hydration prior to bed time. Individuals
whose sleep is disrupted for urination can be counseled to restrict fluids two hours
prior to bed time, emptying the bladder prior to retiring. Use an alarm clock to
ensure a consistent and routine rise time should be encouraged7
Exercise in the early portion of the day should be undertaken to increase
physical conditioning. Exercise in the evening hours should be avoided.7

8
 Complaints of parathesias or radiculopathy should be evaluated via
sophisticated imaging of the cervical region or appropriate thoracic/lumbar region.
Headache management should be conducted following careful differentiation of
potential etiologies with appropriate consults for headaches arising from sinusitis,
temporomandibular joint dysfunction, or cervical strain/sprain. Additionally, the
contribution of vestibular hypersensitivity to increased tension in the cervical
musculature should be considered. Long-standing cervical strain/sprain is often
associated with temporomandibular joint dysfunction and headache as a symptom
triad. Consideration should be given to augmenting the above treatments with
relaxation, visual imagery, or hypnotherapy7
Medications for dizziness, such as Antivert, should be avoided wherever
possible. Instead, physical therapy for treatment of vestibular hypersensitivity
should be undertaken with medication provided which is comfort-oriented, such
as for nausea. In extreme cases, utilization of medications such as Antivert may be
necessary and should be used on a tapering basis in conjunction with treatment for
vestibular hypersensitivity7
Careful neuro-ophthalmologic evaluation should be undertaken for
complaints of visual blurring, double vision, difficulty reading, etc. Diplopia
should be measured with documentation of the divergence in prism diopters,
nystagmus should be characterized, oculomotor pursuits should be characterized,
visual fields and visual acuity should be characterized1
Referral should be made to occupational therapy or visual therapy for
addressing oculomotor deficits which result in deficits in saccades, pursuits, or
diplopia. Patching should be avoided. Use of prism lenses, on a graduated basis,
can be helpful. Strabismus repair surgeries should be avoided until at least one
year post injury and until no further progression is seen in resolution of ocular
divergence. Should strabismus repair be undertaken, this is best accomplished
with adjustable sutures. The need to undertake these surgeries is rare in post-
concussion syndrome.Referral should be made to physical therapy to increase
flexibility and mobility, improve strength, improve cardiorespiratory endurance,
improve muscular endurance, improve range of motion, decrease pain, and treat
vestibular hypersensitivity. Physical therapy should carefully evaluate sleep

9
positions in cases involving back pain. A routine exercise program to improve
physical conditioning should be undertaken. If sleep problems exist, every effort
should be made to undertake the exercise routine at times other than the evening
hours7
Musculo-skeletel pain should be aggressively managed by modalities such
as mobilization, heat/cold, ultrasound, regional anethesia, hypnotherapy induced
glove anethesia, biofeedback, non-opoid analgesics and muscle relaxants.The
treating physician's goal should be to gradually progress to no long-term
medications, with possible exception of antidepressant or mood-altering
medications (Lithium) in individuals with a pre-injury chronic condition or
anticonvulsants in individuals with a seizure disorder. This does not preclude
long-term use of chronic medications such as antihypertensives, etc., when used
for those conditions. Any hypertensive used for behavioral dyscontrol should be
weaned. Regional anesthesia combined with physical/occupational therapy is
often preferred to avoid iatrogenic complication. Opoid analgesics should only be
used as a last result8
In terms of cognition the individual should be referred to treatment
designed to improve ability to maintain focus of attention, ability to shift focus of
attention, ability to maintain vigilance, perceptual feature identification,
categorization, cognitive rigidity, cognitive flexibility, and speed of processing8
Attempts should be undertaken to understand the relative etiological
contribution to decreased cognitive function of neurological damage versus
psychological/emotional disturbances such as anxiety and depression.8
In terms of the psychosocial aspect psychiatric/psychological diagnoses
should be made carefully, ruling out the influence of medications, sleep
disturbance, complex partial seizure disorders, and pre-injury personality
characteristics. Counseling efforts should be routine for purposes of education and
adjustment to changes in routine, lifestyle, vocation, family, etc. Counseling
should address issues of sexual performance from an educational perspective.
Reduction in male libido is often related to emotional or neuroendocrine issues
while difficulties such as inability to maintain erection may be related to
attentional deficits and/or depression8

10
 The therapist should ensure a gradual return to a normal pre-injury
lifestyle and routine prior to discontinuation of treatment 8. It may be necessary to
undertake hypotherapy, systematic desensitization approaches, relaxation
approaches, hypnotherapies, rational emotive therapy, or biofeedback, in isolation
or in tandem8
Education should be given regarding the cumulative nature of mild
traumatic brain injury and counsel should be given to avoid engaging in activities
which will potentially result in additional injuries8
2.3 Moderate traumatic Brain Injry
Management of moderate TBI patients is case dependentbut will likely be
similar to that of severe TBI. Generally, the patient with a persistent GCS of 13 or
less may require admission and observation. Moderate TBI is defined as an
admission GCS score of 9 to 12.9 A small percentage may worsen from increasing
ICP (intracranial pressure). Moderate TBI may quickly convert to a
severe TBI even in the absence of risk factors.5
2.3.1 History and Physical Examinations
Patient evaluation begins with a brief determination of the events
surrounding the injury. Although such information is often incomplete and
contradictory in the first minutes and hours after injury, it may prove useful for
guiding initial management.The core of the evaluation is the physical
examination. The initial assessment for TBI as other neurologic emergencies is
usually based on the GCS. The 3 components of the GCS are eye opening, verbal
function, and motor examination.The score for each component should be listed
separately and not lumped into a single overall score. For the eye opening and
motor assessments, the right and left sides should be listed separately.1
Pupil size and reactivity are also important and should be noted for each
eye. Dilatation and loss of reactivity may indicate that the pupil-constricting nerve
fibers on the periphery of the third cranial nerve are significantly compressed by
edematous or displaced brain tissue. Ischemia of the midbrain (where the third
nerve arises from the Edinger-Westphal nucleus) may also be a cause. Careful
initial assessment is important as the baseline against which subsequent
improvement or deterioration in neurologic examination will be gauged.1

11
2.3.2 Management in Emergency Room
Approximately 15% of patients with brain injury in the ER have a
moderate injury. They are still able to follow simple commands, but usually are
confused or somnolent and can have focal neurologic deficits such as
hemiparesis.10In the emergency room, the ABC of resuscitation and ATLS
guideline for the assessment of associated injuries, and preventing or correcting
secondary insults, such as hypoxia and hypotension should be emphasized.11
Blood pressure and fluid maintenance is also the overall objective of
hemodynamic therapy in TBI. Cerebral perfusion pressure (CPP) is a measure of
the adequacy of brain perfusion and is calculated by the mean arterial pressure
(MAP) minus ICP. Recommended treatment goals are SBP >90 mmHg and CPP
>60 mmHg with IV fluids. Oxygenation and ventilation goals are established
early to maintain adequate oxygenation with the partial pressure of oxygen in
arterial blood (PaO2) remaining above 60 mmHg, and normocarbia, and also the
oxygen saturation should be less than 90%.12
On admission to the ER, a brief history is obtained, and cardiopulmonary
stability is ensured before neurologic assessment. A CT scan of the head is
obtained, and a neurosurgeon is contacted. All of these patients requireadmission
for observation in an intensive care unit (ICU) or a similar unit capable of close
nursing observation and frequent neurologic reassessment for at least the first 12to
24 hours. A follow-up CT scan within 24 hours is recommended if the initial CT
scan is abnormal or if there is deterioration of the patient’s neurologic status.
Approximately 10% to 20% of these patients deteriorate and lapse into coma,
serial neurologic examinations are needed in these patients.10
2.3.3 Initial Imaging
A head CT scan should be obtained. 11 After the ABCs have been addressed
and an initial evaluation for associated injurieshas been completed, patients are
usually taken for immediate computed tomography (CT) scanning. 1Noncontrast
computed tomography (CT) is the initial diagnostic imaging study of choice. 5CT
scanning is highly sensitive for detecting acute blood, skull fractures, mass effect,
and other traumatic pathologies that may require immediate intervention.
Although MRI scanning may provide more detail about the brain parenchyma, it

12
requires much more time than a CT scan. CT scanning also has few restrictions on
access to an acutely injured patient, unlike MRI scanning.1
Special attention should be given while reading CTfor the presence of
parenchymal abnormalities, such as contusion or edema, as well as skull or facial
fractures. Contusions are often detected in areas of the brain that make contact
with bony prominences, such as the frontal, temporal, and occipital poles. Small
contusions may evolve into hemorrhages,which should be considered if clinical
deterioration occurs because it might lead to herniation. A normal CT scan does
not preclude a severe neurologic injury, if a patient’s neurologic examination is
abnormal, it must be assumed that a severe brain injury has occurred until proved
otherwise. Repeat imaging should be strongly considered with any neurologic
changes.2,13
2.3.4 No Mass Lesionin Moderate TBI
In the setting of no mass lesion, such as contusions, subdural hematoma
(SDH), or epidural hematoma (EDH), supportive care is warranted along with
frequent repeat clinical exams, preferably by the same person. Repeat evaluation
with imaging along with repeating labs for electrolytes or cultures depending on
the context are needed in patients with decline status.13Patients with GCS >8 and
EDH <30 cm3, thickness <15 mm, midline shift <5 mm, and no focal deficits can
be managed non operatively with serial CT scanning and close neurological
observation.11 In the setting of a hematoma, repeat imaging within the appropriate
time interval is warranted, generally 6 hours from the initial CT of head to
monitor for expansion.13
2.3.5 Coagulation Profile and Platelet Transfusion
Coagulation profile (Complete blood count or CBC, Prothrombin
time/International Normalized Ratio or PT/INR, and activated
PartialThromboplastin Time or aPTT) is recommended on admission.It has been
shown that fast correction of a patient’s INR to 1.3 or lower decreases hematoma
growth and improves outcomes.Platelet transfusion is recommended for
thrombocytopenia (platelet count less than 100,000) in the setting of intracranial
hemorrhage.13
2.3.6 Seizures Prophylaxis

13
 Nonconvulsive seizures have been detected in 23% of moderate to severe
TBI patients.2Posttraumatic seizures are classified as either early or late, those
occurring before 7 days are early PTS. Seizures exacerbate secondary brain injury
by increasing ICP, worsening cerebral hypoxia, and increasing metabolic demand.
Nonconvulsive electrographic seizures also occur, and can lead to cerebral
metabolic crisis, a delayed increase in ICP, and worse clinical outcomes. Current
evidence supports the use of antiepileptic drugs (AEDs) to prevent early PTS, but
not late PTS. Risk factors for developing early PTS include penetrating TBI,
depressed skull fractures, cortical contusions, and subdural and epidural
hematomas. At risk patients should be managed with AEDs for seizure
prophylaxis in 7 days.14Hemorrhage on CT, especially subarachnoid hemorrhage
(SAH) warrants up to 1 week of antiepileptic drug (AED) therapy, which is often
levetiracetam or phenytoin. Levetiracetam has similar efficacy as phenytoin,which
is recommended as an agent for the first lineprophylaxis because of its higher
availability and lower cost.5If a person with TBI experiences a seizure, a
prolonged course of AEDs is necessary.13
2.3.7 ICP (Intracranial Pressure) Monitoring
ICP monitoring is considered inmoderate TBI patients who fulfill one or
more of the following criteria:11
 Postoperative period after removal of acute subduralhematoma or multiple
cerebral contusions (CC). Suddenchanges in ICP could signal hemorrhages
due todecompression or reperfusion, new extra-axial collections or
worsening brain swelling.
 GCS of 9–11 and CC (temporal or bifrontal) withoutsurgical intervention.
ICP monitoringcan help recognize progression of the contusions.
 Diffuse injury type III. Due to the high probability ofintracranial
hypertension and poor outcome, ICPmonitoring in these cases is
indispensable.
 General anesthesia for emergency non-cranial surgery.Especially in the
presence of large mass lesions under conservative treatment (epidural,
subdural hematomas,CC). ICP monitoring is indicated in these cases dueto
loss of clinical evaluation and to evaluate effects ofanesthetics on
cerebrovascular autoregulation.

14
  Concomitant severe chest trauma requiring deepsedation, high PEEP
levels, recruitment maneuvers or prone ventilation. In these cases,
monitoringis important because utilization of protectiveventilation with
low tidal volumes can cause hypercapnia,cerebral vasodilation and
increased ICP. Utilization of high levels of PEEP may worsenintracranial
hypertension by hindering adequate cerebral venous return.
 Concomitant intra-abdominal compartment syndrome.This syndrome is
associated with intracranial hypertension.
 Prolonged traumatic shock. These patients haveincreased risk of cerebral
edema.
2.3.8 Symptomatic Treatment
Symptomatic treatment is recommended for common post-moderate TBI
symptoms. The symptoms including headache, nausea, and dizziness. Early
Potentially severe
TBI (Moderate)
consultation of psychiatry, physical and occupational therapy, and speech and
language pathology is recommended to assess for a long-term rehabilitation
Injuries
To avoid
plan.13 secondary
ABC of associated
resuscitation assessment (1st
injuries examination ATLS)

Clinical
stabilization

Cerebral CT scan Other lesions

CT scan of other regions Specific
(thorax, abdomen,
(2nd exam ATLS) neck, pelvis, long Treatmen
bones, etc) t

Normal Abnormal
Surgical
Room-ICU

ICU Admission
Close neurologic
observation Call Neurosurgenon
Serial CT, TCD Consider
examinations neuromonitoring (ICP)
To avoid secondary
insults

Decrease ≥ 2 Mass lesions

points in GCS (EDH, SDH, CC) Yes
Pupillary
alterations Neurologica
New neurologic l worsening
deficit
Seizures No Consider evacuation
CT Scan according guidelines

Detection and Intracranial

treatment of non hypertension
neurologic
causes of
deterioration 15
Intubation
Hyperventilation Specific
Osmotherapy protocol
Call
neurosurgeon
Fig. 1 Algorithm for Moderate TBI management11

2.4 Severe Traumatic Brain injury

2.4.1 General consideration

16
 Management of severe traumatic brain injury is a dynamic process that
start from the pre hospital management, entering the emergency department,
transferring to intensive care unit, and continuous with monitoring and evaluation
the clinical progress.1 Management of severe traumatic brain injury is specially
focusing on prevention and manage in secondary brain insult:1
- Hypotension ( systolic pressure < 90 mmHg)
- Hypoxemia (PaO2< 60 mmHg ; O2 saturation < 90%)
- Hypocapnia ( PaCO2< 35 mmHg)
- Hypertension (SBP >160 mmHg or MAP > 110 mmHg)
- Anemia ( Hb<100 g/L, or Hct<0,30)
- Hyponatremia ( Serum Na <142 mEq/L)
- Hyperglycemia (Blood sugar > 10 mmol/L)
- Hypoglicemia (Blood sugar < 4.6 mmol/L)
- Acid-base disorder ( Acidemia : Ph< 7.35 ; Alkalemia : Ph> 7.45)
- Fever (>36o C)
- Hypothermia (<35.5o C)
- Hypo-osmolality (P Osm<290 mOsm/Kg H2O)

All the traumatic brain patients should have a pre hospital management,
stabilize Airway, Breathing, Circulation (ABC), enter to the emergency
department and assessing the GCS and neurological status and have an imaging if
they’re indicated.1 If the initial assessment have made and classify the patient with
severe traumatic brain injury, the patient should be transferred to intensive care
unit.4
Patient with ,moderate – high cranial / brain injury should be
recommended to get imaging examination. CT scan is highly sensitive for
detecting acute blood, skull fracture, mass effect that requires immediate
intervention. MRI is take a longer time, complex procedure and may not suitable
with a patient that use ferromagnetic therapeutics and monitoring
equipment.Severe traumatic brain injury patients are recommended to have
several CT examination for interval few hours after injury to 24 h after injury or
longer. Typically CT are obtain for head and cervical spine, but also may include
thorax, abdomen, pelvis, and thoracix-lumbar spine if indicated 1,15
The indication for immediate CT scan are : 4
- GCS , 13 on initial assessment in the emergency department

17
- GCS , 15 at 2 h after injury on assessment in the emergency
department
- Suspected open or depressed skull fracture
- Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes,
cerebrospinal fluid
leakage from the ear or nose, Battle’s sign)
- Post-traumatic seizure
- Focal neurological deficit
- More than one episode of vomiting
- Amnesia for events .30 min before impact
- Adult patients who have experienced some loss of consciousness or
amnesia since the injury and:
- Age . 65 yr
- Coagulopathy (history of bleeding, clotting disorder, current
treatment with
warfarin)
- Dangerous mechanism of injury (a pedestrian or cyclist struck
by a motor vehicle,an occupant ejected from a motor vehicle or
a fall from a height of > 1 m.
All of the severe TBI patient should be placed in to rigid cervical
collar , it’s aim to protect the cervical spine and also optimizing the
cerebral venous drainage. Optimum cerebral venous drainage is useful to
reduce risk of exacerbation of intracranial hypertension. The patient head
of bed should be maintained at 30o to optimize the cerebral venous
drainage. 15
All the severe TBI patient are recommend to the endotracheal
intubation placement. Placement of endotracheal intubation may induce
sympathetic reflex that will lead to increase the intra cranial pressure, so
rapid sequence intubation in more preferable because it may blunting the
sympathetic reflex. Another way to prevent the sympathetic reflex is by
administerlidocaine or single dose of opioid such as fentanyl and
sufentanyl but it may worsen the hypotension and lead to premature
respiratory depression. Portable chest radiography should be obtained after
the intubation to evaluate the endotracheal tube placement and sign of

18
aspiration. Aspiration will lead to poor oxygenation and acute respiratory
distress syndrome.
Positive End Expiratory Pressure (PEEP) should be re considered
or be used judicious in severe TBI patient, because it will decrease venous
return and increase the intracranial pressure. If needed, PEEP may be used
in the lowest level around 5 – 8 mmHg to prevent lung collapse and
maintain adequate oxygenation.15
Placing central catheter are recommended if there are suspicious
of increasing intravascular volume state. It will used to measure the
intracranial pressure and also to deliver the hyperosmolar solution and
vasopressor. The preferable access is subclavian route. In additional, radial
artery catheter is recommended to optimize the cerebral blood flow
perfusion and to collect the blood sample. 15
Hypotension in severe TBI may be the manifestation of blood loss
or the spinal cord injury that will lead to sympathetic tone compromise.
Using of crystalloid, normal saline for fluid resuscitation is recommended,
and glucose containing fluid should be avoided. If there is increase of ICP,
hypertonic saline infusion may be considered. The hypotension should be
managed by lowering agents like Labetalol, nicardipine, and enalaprilat.
These agents are not increasing the ICP.15
Laboratory work up also should be done in severe TBI patient.
Complete Blood Count, electrolytes, glucose, coagulation parameters,
urine toxicology or urinalysis, an pregnancy test when appropriate.
Electroencephalography (EEG) intermittent or continuous are
recommended due the association of moderate-severe TBI with
hypocampal atrophy. 15

Parameters Goals
Cerebral Perfusion Pressure ≥ 60 mmHg (50 – 70 mmHg)
Glucose 80 = 180 mg/dL
Haemoglobin ≥ 7 g/dL
Intracranial Pressure 20 – 25 mmHg
International Normalize Ratio ≤ 1.4
PaCO2 35 – 45 mmHg

19
PaO2 ≥100 mmHg / 11 kPa
PbtO2 ≥ 15 mmHg
pH 7.35 – 7.45
Platelets ≥ 75.000
Pulse Oxymetri ≥95%
Sistolyc Blood Pressure ≥ 100 mmHg
Serum Sodium 125 – 145 mEq/L
Temprature 36 – 38 o C

After the severe TBI patient resuscitated and stabilize, patient will
be delivered to intensive care unit. The aims of intensive care unit :16
1. Prevention of intracranial hypertension
2. Maintain and stabilize the cerebral perfusion rate
3. Stabilize the patient
4. Prevent the systemic effect , secondary brain insult
5. Optimize the cerebral hemodynamic and oxygenation.

20
Figure 1.Neuromonitoring of Severe TBI patient30

2.4.2 Management of Intracranial Hypertension

Intracranial hypertension is defined as high of intracranial pressure ≥20
mmHg. ICP threshold are varies depend on age, 18 mmHg in older patients and
22 mmHg in young patient. It will develop in some of traumatic brain injury
patient. Monitoring of intracranial pressure is recommended for severe TBI
because it is associated reduce in-hospital and 2 weeks – post injury mortality. It is
also recommended for all severe TBI with abnormal CT scan and severe TBI
patient with normal CT Scan if age > 40, unilateral or bilateral motor posturing, or
SBP < 90 mmHg.(4) Intracranial pressure measured by placing device in to the
brain, it could be ventricular or intra parenchymal probes that connected to the
monitor. External ventricular drainage tends to be the preferred method given the
potential for cerebrospinal fluid (CSF) drainage as a means to control ICP (3,6).
- Prevention of high ICP : avoidance pyrexia, sedation,
intubation, normocapnic ventilation
- Active treatment in high ICP : hyperosmolar therapy, CBF
drainage
- Aggressive treatment in high ICP : metabolic suppression,
decompressivecraniectomy, hypocapnia, hypothermia. (4)
Some of care procedure and management lead to pain and discomfort
sensation.1Narcotic such as morphin, fentanyl, remifentanyl are probably to be

21
considered to be used. It havea analgesic, mild sedation, and depress the airway
reflex that required when placing the endotracheal intubation. Mild sedation can
give anxiolisis, limiting ICP elevation related to agitation, discomfort or pain,
decrease O2 consumption, CMRO2 , and CO2 production. 16
Hyperventilation therapy may reduce the ICP by brain autoregulation
effect.4 Reduce in PaCO2 may lead to brain vasoconstriction and reduce in ICP.
But, prolong of hyperventilation may lead to ischemia due to the low perfusion. 16
Hyperventilation therapy only recommended for temporizing measure to reduce
an elevated ICP. SjVO2 or PbtO2 should be measure to monitor cerebral
oxygenation and prevent cerebral ischemia.17
Hypothermia 32 – 34o C may reduce cerebral metabolism and CBV,
decrease ICP and increase CPP.(2) Early (within 2.5 h), short-term (48 h post-
injury), prophylactic hypothermia is not recommended toimprove outcomes in
patients with diffuse injury.17
Drugs grouped under analgesia and sedation were commonly used for pain
control or decreasing consciousness, anxiety and agitation;18 but for severe TBI
with patient under GSC score of equal or lesser than 6 which is mostly in coma or
vegetated state hence these group of drugs serve extra purpose in prescription
other than their main function.16,17 They function were mainly regard effects on the
cerebral metabolic rate of oxygen consumption, cerebral blood flow, control
intracranial pressure, and seizure suppression. Few of those commonly used will
be state below. Those drugs that required specific knowladge, involve argument or
not frequent in use in TBI cases such as Ketamine etc. is left out.
o Barbiturate reduce cerebral metabolism, reduce ICP and increase
CPP. But it have some side effects like : hypotension, especially in
volume depleted patients; and immunosuppression with an increase
infection rate . The used of prophylaxis barbiturate may induce burst
suppression EEG. 10 mg/kg Pentobarbital over 30 min, followed by 5
mg/kg/h for 3 hours, then1 mg/kg/h. Sodium thiopental also can be
used.16
Propofol :GABA-R agonist that have rapid onset and short duration of action
reduce ICP, CBF and CMRO2 which mainly related to preservation of

22
carbon dioxide reactivity and cerebral autoregulation.19
o In large dose it handle EEG burst reading that indicating the lower of
brain electrical activities however it might significantly decrease the
cerebral perfusion pressure and mean arterial pressure, causing
Propofol infusion syndrome. Patient can grow tolerance and
tachyphylaxis over time. 18–20
o Narcotics :Opioid narcotis bind to opioid receptor in brain which
majorly contain 3 subtype, μ, κ, δ (mu, kappa, and delta). They are
mainly prescribe for their analgesic property in other cases but in TBI
they can be prescribe for sedative by given together with the drug
mention above such as propofol and midazolam to increase the
analgesic effect and reduce dosages of opioid required.Intravenous
opioids used include tramadol, morphine, fentanyl, sufentanil, and
more recently remifentanil.18
- Tramado]:The usual dose is 50 or 100mg 4-6 hourly.
Intravenous or intramuscular route. Intravenous
injections must be given slowly over 2-3 minutes.
 For post-operative pain administer an initial bolus
of 100mg.
 During the 60 minutes following the initial bolus,
further doses of 50mg may be given every 10-20
minutes, up to a total dose of 250mg including the
initial bolus. Subsequent doses should be
50mg or 100mg 4-6 hourly up to a total daily dose
of 400mg.
 Children below 12 years old shall be given
minimum effective dosage.

23
 Figure 2.Mangementalgorythm of high ICP 4

24
2.4.3 Another Approach
- Infection prophylaxis in Severe TBI
Patient with severe traumatic brain injuries either with open or closed trauma
are going to face high risk of hospital acquired infection due to the long period of
treatment and use of certain equitment (example, ventilator,parentel nutrition and
invasive monitoring), environment factor, immunosuppression
condition(example: hypothemia), complication and etc.16 Ventilator associated
pneumonia (VAP) and central line-associated bacteremias are increased in all
17
critically ill patients. VAP is highly associated with machanical ventilation
which is almost compulsory in severe TBI patient and external ventricular drain
which help to module ICP create opening for cerebral infection.
However, with correct pratice of existing standard operating procedure given
by world health organization(WHO) or respective hospital regarding all the aspect
under infection control standard precaution should be restricted the transmission
of pathogens that is not air-bond. Other than SOP for prevent of infection during
handle patient extra precaution like antimicrobial-impregnated catheters may be
considered to prevent catheter-related infections during external ventricular
drainage17. Pre-surgical antibiotic prophylaxis with width spectrum antibiotic can
be given to patient. Prefred drug are cephalosporin. There is not evidence shown
that it help in lowering the infection rate instead might create regarded antibiotic
resistance bacterial.21 Hence, antibiotic should not be given under condition
without indication of bacterial infection. As antiviral prophylaxis can be given to
patient with complication or manifestation that might induce immunocomprmise
condition.
- Seizure Prophylaxis

Prophylactic therapy (phenytoin, carbamazepine, or phenobarbital) is not

recommended for preventing late post-traumatic seizures .16 But prophylaxis
therapy to prevent early post-traumatic seizure in TBI patients who are at high risk
for seizures is recommended 17.
Phenytoin can be use for the prophylaxis of early post-traumatic seizures. A
loading dose of 15 to 20 mg/kg administered intravenously (I.V.) over 30 minutes

25
followed by 100 mg, I.V., every 8 hours, titrated to plasma level, for 7 days. 22
Phenytoin Dose for Seizure Prophylaxis During or Following Neurosurgery
Oral Administration :
- Initial dose: 5 mg/kg/day orally in 2 or 3 equally divided doses, with
subsequent dosage individualized to a maximum of 300 mg orally daily
- Maintenance dose: 4 to 8 mg/kg. Children over 6 years old and adolescents
may require the minimum adult dose (300 mg/day)

Parenteral Administration :
- Loading dose: Do not exceed an infusion rate of 1 to 3 mg/kg/min (or 50
mg per minute, whichever is slower) in pediatric patients

Patients receiving antiseizures prophylaxis should be monitored for potential

side effects as it may be in dizziness, drowsiness, confusion, nervousness; nausea,
vomiting, constipation;tremors, slurred speech, loss of balance or coordination;
rash; abnormal eye movement; headache; sleep problems (insomnia).22
-Steroid

“Guidelines for Management of Severe TBI 4th Edition”17 stated that there
is no beneficial prove of using steroid in TBI patient. However, corticosteroid like
methylprednisolone can reduce post-traumatic neuronal degeneration after injury
in animals, maximize with 30 mg/kg body weight. There are some article that
state that if corticosteroid is given in high dose at the early state of treatment can
serve beneficial effects due to its anti-inflammatory properties but perlong dosing
will bring negative side effect such as osteoporosis.
-Nutrition:

The patient of severe TBI were in condition of altered gastro-intestine funtion

due to the affected conscious hence artificial feeding is needed. Enternal or
parenteral nutrition can both be use in these cases but most of the journal
suggested that enternal nutrition intragastric or intrajejunum16 (pyloric) shall be
the main method since it is cheaper and reduce infection chances as stated in the
journal Critical care management of severe traumatic brain injury in adults, “ The
potential advantages of enteral feeding include stimulation of all gastro-intestinal

26
tract functions, preservation of the immunological gut barrier function and
intestinal mucosal integrity, and reduction of infections and septic
complications.”16
In compare of two method in enternal nutrition transpyloric is prefered due to
it benefits of avoids gastric intolerance, allows higher caloric and nitrogen intake,
lesser gastro residual and has lower risks of ventilator-associated pneumonia.16,23
Parenteral nutrition is suggested only to be given under the contraindication of the
enteral nutrition16 in most of the journal but some said otherwise as parenteral
nutrition serve different purpose or achieving different goal.
Calories replacement intragastric shall be given to the patient within 5 to
7days post injuries to reduce two weeks mortality and within 24-48 hours to
achieve greater endocronologic factor after TBI under the condition of patient that
17
there is no dysfunction in any part of G.I tract. As for glycemic control, around
140% of resting metabolic expenditure in non-paralyzed patients and 100% in
paralyzed patients to be replaced. Tight glucose control is not suggested in severer
TBI patient and moderate glucose control may be the best choice which mean
110–150 mg/dL.23 Intensive insulin treatment can be companion to certain cases to
improve glycemic control.
As for supplement nutrient antioxidants and Immune-Enhancing formulas
like arginine, glutamine, nucleic acid, omega-3 fatty acids, and antioxidants
(vitamin E) is recommended but avoid severer spesis patient.Vitamin B1,5,6,12
shall be given to prevent certain acute nurologic syndrome.24
- Neuromuscular blockade

Neuromuscular blockade, a failure in neuromuscular transmission that can be

induced pharmacologically or result from any of various disturbances at the
myoneural junction. It is often used in intubate/ventilated patients to prevent
reflex and irregular movement of trachea. There are teories about usage of
sedative and neuromuscular blockade to save energy expenditure in severe head
injury patient25 but it is still unclear. It use in ICU is still remaining controversial.It
can also to be use in lowering intracranial pressure but continue use is discouraged
as known that certain neuromuscular blockade agent can travel through blood
brain barrier and potentially cause seizure.26

27
 Table Sedatives Analgesics and Neuromuscular Blockade in the ICU 26

- Deep Vein Thrombosis Prophylaxis

Severe TBI patient also high risk to develop deep vein thrombosis and
pulmonary embolism. Graduated compression stocking and sequential
compression device as mechanical thrombophylaxis are recommended. Low
molecular weight heparin can be used combination with mechanical support, but it
may have side effect like increase the risk of expansion intracranial hemorrhage.
Pharmacologic prophylaxis can be initiated 48 – 72 hours in the absence of
contraindication. Screening with duplex ultrasonography may be helpful to
prevent and evaluate DVT.26

28
2.5 Prognosis
Outcome after severe TBI is poor; about one in three patients dies and most
survivors are left with severe lifelong disabilities. Furthermore, survivors of severe
TBI face prolonged rehabilitation times, causing significant patient and family
suffering as well as enormous economic costs. In the pre-hospital period,
approximately one in five TBI patients suffer from some form of secondary insult.
TBI patients are subject to several secondary insults, of which hypoxia and
hypotension are the most frequently encountered and also most deleterious. There are
also some strong significant predictors of outcome after TBI.27
Ethnic origin and gender may be associated with outcome in TBI patients. A
meta-analysis found slightly poorer quality of life in female compared to male TBI
survivors and found that black patients have poorer outcomes compared to Caucasian
and Asian patients, probably due to genetic differences. Thus, it is still controversial
and there is certainly a multifaceted age-gender-ethnic relationship affecting outcome
after TBI.2 Level of consciousness after injury is a major determinant of TBI severity
and often assessed by the Glasgow Coma Score (GCS). An acute dilation of the pupil
and unresponsiveness to light is considered a neurological emergency and is strongly
associated with poor prognosis that may be associated wih third cranial nerve
compression and subsequent brain stem compression, uncal herniation (transtentorial
herniation of the medial temporal lobe), or reduced blood fl ow to the brain stem.27,28
Magnetic Resonance Spectroscopy (MRS) gives information about the
mtabolism of the brain. The numbers generated from this scan provide a general
prognsosis about the patient’s ability to recover from the injury. 27 Lesions seen with
this are most strongly associated with poor outcome after TBI which includes
bleeding type, status of basal cisterns, midline shift, and tSAH, with tSAH and
complete obliteration of the basal cisterns having the worst prognosis.28 Lastly,
several laboratory variables associate with outcome after TBI, among them blood
glucose levels, hemoglobin concentrations, sodium levels, and markers of
coagulation. Hyperglycemia, low hemoglobin levels, hyponatremia and

29
hypernatremia, and coagulopathy are accordingly strongly predictive of poor
outcome.27,28
2.6 Monitoring and Follow Up Management of Traumatic Brain Injury
The outcome of management in traumatic brain injury depends on the severity
of the injury, age, how it is treated, and the complications that might occur. 29 Those
are leading to the need of monitoring for optimizing the therapy. 16 The evaluation is
divided into two, such as:
2.6.1 Monitoring
a. General Monitoring
There are several parameters that need to be evaluated after the
management of traumatic brain injury, wether it was mild, moderate, or
severe brain injury. Those parameters are vital signs (blood pressure, pulse
rate, respiratory rate, temperature, and pain), oxygen saturation, urine output,
blood gases, and serum electrolytes.16 Maintaining Systolic Blood Pressure at
≥100 mmHg for patients with severe TBI 50 to 69 years old or at ≥110
mmHg or above for patients 15 to 49 or >70 years old may be considered to
decrease mortality and improve outcomes.17 Also keeping those parameters in
normal limit would help to minimize the secondary brain insult and
optimalize oxygenation to the brain.16
b. Neuromonitoring
The neuromonitoring mostly for severe traumatic brain injury consist
of Intracranial pressure (ICP) monitoring, electrophysiological (EEG)
monitoring, cerebral perfusion pressure and advance cerebral monitoring16,17
The ICP should be monitored in all patients (GCS 3-8 after
resuscitation) with an abnormal CT scan (the one that reveals hematomas,
contusions, swelling, herniation, or compressed basal cisterns). ICP
monitoring is also indicated in patients with severe TBI with a normal CT
scan if two or more of the following features are noted at admission: age 40
years, SBP less than 90 mmHg, or unilateral or bilateral motor posturing. The
ICP monitoring value should not more that 22 mmHg as it increase mortality
rate and the ICP information is also recommended to reduce inhospital and 2-
week post-injury mortality.16,17

30
 Cerebral perfusion pressure (CPP) and advance cerebral monitoring
information is needed to decrease two-week mortality in severe TBI patients.
The recommended target CPP value for survival and favorable outcomes is
between 60 and 70 mmHg depends on the patients autoregulatory status.
Maintain the CPP threshold with fluid and pressors may be considered
because the risk of respiratory failure in adult. And for the advance cerebral
monitoring such as jugular venous saturation less than 50% may be a
threshold to reduce mortality and improve the outcomes at 3 and 6 month
post-injury.17
Also the continous EEG has been suggested in diagnosing post
traumatic seizure (PTS), especially in those who receive neuromuscular
blockades.16
2.6.2 Follow Up
Follow up management of the patient is needed in order to predict
outcome after TBI. A study shows that relatively simple prognostic model
using seven predictive baseline characteristics, consist of age, motor score,
pupillary reactivity, hypotension, hypoxia, computed tomography
classification, and traumatic subarachnoid hemorrhage has accurately predict
6-month outcome in patients with severe or moderate TBI.16

Chapter III
CONCLUSION

Traumatic Brain Injury (TBI) is generally described as an impact, penetration,

or rapid movement of the brain within the skull which leads to brain damage, altered
mental state, and impaired neurologic function, regardless of the underlying
pathophysiologic cause, such as enlarging extra-axial hematoma, diffuse swelling,
ischemia, blossoming contusion, or any other causes. TBI divided into 2 phases :
primary injury, defined as an immediate consequence of the initial traumatic event,

31
and secondary injuries,which gradually occur as a consequence of ongoing cellular
events that cause further damage.
The most common used in general is classification as mild, moderate, or
severe based on the Glasgow Coma Scale (GCS). Patients are scored on the basis of
clinical symptoms, comprise of the sum score of three components : eye, motor, and
verbal scale, resulting the classification as mild with GCS 13-15, moderate with GCS
9-13, and severe with GCS <9. The treatment of TBI is depend on this classification.
For pre management and GCS less than 15 on initial assessment by the
healthcare professional,neck pain or tenderness,focal neurological deficit,paraesthesia
in the extremities orany other clinical suspicion of cervical spine injury immediately
attempt full cervical spine immobilization. All the traumatic brain patients should
have a pre hospital management, stabilize Airway, Breathing, Circulation (ABC),
enter to the emergency department and assessing the GCS and neurological status and
have an imaging if they’re indicated.
For mild TBI the management generally supportive treatment. The
therapist should ensure a gradual return to a normal pre-injury lifestyle and routine
prior to discontinuation of treatment.
Management of moderate TBI patients is case dependentbut will likely be
similar to that of severe TBI. Blood pressure and fluid maintenance, Recommended
treatment goals are SBP >90 mmHg and CPP >60 mmHg with IV fluids. After the
ABCs have been addressed and an initial evaluation for associated injurieshas been
completed, patients are usually taken for immediate computed tomography (CT)
scanning.
Management of severe traumatic brain injury is specially focusing on
prevention and manage in secondary brain insult. All the severe TBI patient are
recommend to the endotracheal intubation placement, Positive End Expiratory
Pressure (PEEP) should be re considered or be used judicious in severe TBI patient,
Placing central catheter are recommended if there are suspicious of increasing
intravascular volume state. Laboratory work up also should be done in severe TBI
patient.

32
 There are several parameters that need to be evaluated after the management
of traumatic brain injury, Those parameters are vital signs (blood pressure, pulse rate,
respiratory rate, temperature, and pain), oxygen saturation, urine output, blood
gases, serum electrolytes , neuromonitoring and EEG (especially for severe TBI) .
Outcome after severe TBI is poor; about one in three patients dies and most survivors
are left with severe lifelong disabilities.

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