BAB I

Pendahuluan

A. Background
Trauma is a leading cause of death worldwide. Trauma patients with head
injury (HI) have a 10-fold higher mortality than in those with no HI. Furthermore, HI
accounts for two-thirds of in-hospital trauma deaths. Disability following traumatic
brain injury may require a lengthy rehabilitation, which places a great burden on
national medical resources. The rapid industrialization and tremendous increase in
motorized vehicles in developing countries have led to an increase in the incidence of
HI. Epidemiological studies are essential for strategic planning for health resources
and prevention (Al Kuwaiti, 2012).
Repetitive head trauma may be a risk factor for Alzheimers disease and is
considered the primary cause of chronic traumatic encephalopathy (CTE), a
pathologically characterised neurodegenerative condition with diverse presentations
during life. The potential long-term effects of cumulative head trauma on the brain
have come to public view with the recognition that athletes in contact sports including
American football demonstrated postmortem findings associated with CTE; a few of
these reported cases harbouring very focal lesions have occurred in individuals under
20 years of age. A fundamental question that needs more exploration is the
relationship between the amount, or dose, of head trauma and alteration in brain
structure and function. Previous studies in boxers have reported frequency and

duration of fighting to be associated with cognitive or neurological problems.

Moreover, postmortem studies of CTE have revealed changes in a number of
subcortical and cortical regions. With advances in neuroimaging, segmentation of
these structures can be completed with automated programmes which are widely
available, reproducible, and thus, if these regions prove to be markers of decline with
repetitive traumatic brain injury, they have the potential to become clinically useful
and readily calculated biomarkers. The Professional Fighters Brain Health Study
(PFBHS) is a longitudinal cohort study of boxers and mixed martial arts (MMA)
fighters designed to better understand the effects of repeated blows to the head on
brain structure and function over time. This cross-sectional analysis of participants
baseline evaluation explores the relationship between exposure to repeated blows to
the head and MRI measures of brain structure and function, along with cognitive
performance (Bernick, 2014).

B. Formulation of the Problem

1. How the definition and pathophysiology of head trauma?
2. How the management of head trauma?
3. How the diagnosis in patients with head trauma?
C. The Objective of the Study
1. Know the definition and pathophysiology of head trauma.
2. Knowing management from head trauma.

3. Knowing the diagnosis patients of head trauma.

D. Benefits of Research
1. For this educational institution can add and supports the development of
science education, especially to give an overview of head trauma.
2. For the public as information regarding the management of head trauma.
3. For researchers can figure out the problem head trauma and can definitively
diagnose patients with head trauma.

BAB I I
LITERATURE REVIEW

A. Definition of Head Injury

Head injury is one of the emergency in surgery. Head injuries will often be
found in every region in Indonesia and in the world. As it is known that the head
is one of the important parts of the body that must be protected because the head
has an important role in protecting the vital organs in the human body. In the head
attached to organs such as the brain that has the function helps the body to
activate the muscles and secrete chemicals that allow the body to respond to
external stimuli, self-control, planning, reasoning, and abstract thinking, which
makes human beings are the most intelligent species on earth. It is also embedded
sensing systems such as ear, nose and upper respiratory tract, mouth and upper
digestive tract is very important that everything possessed by humans.
Heegaard and Biros (2013) foud a head injury is any trauma to the scalp,
skull, or brain. The injury may be only a minor bump on the skull or a serious
brain injury. Head injuries are divided into open and closed head injury. A closed
head injury means you received a hard blow to the head from striking an object,
but the object did not break the skull. An open, or penetrating, head injury means
you were hit with an object that broke the skull and entered the brain. This is
more likely to happen when you move at high speed, such as going through the
windshield during a car accident. It can also happen from a gunshot to the head.

Definition involving brain injury it very much. The cause of a lot of

definitions of head injury is the number of studies conducted by experts both in
Indonesia and abroad that the theme of a head injury. Head injuries are divided
into open and closed head injury. This facilitates the sharing of medical personnel
in determining the definition of a head injury that is not wrong in handling.
Richardson (2013) foud a closed head injury is and injury to the head that does
not expose the contents of the skull. Such an injury can be distinguished from an
open head injury in wich the duramater (the membrane that lines the inferior of
the skull) is torn and consequently the contents of the skull are exposed.
Silver and Thomas (2010), A number of clinical classifications have been
developed over the years, with the Glasgow Coma Scale (GCS) being the most
widely used, although this scale is less useful in pediatric assessment and is a poor
discriminatior of mild head injury. In general, mild head injury is a GCS score of
13 15, moderate head injury a score of 9 12, and severe head injury a score of
8 or less. The classification of the type of head injury by GCS is certainly much
easier for doctors to diagnose the severity of the head injury patients.
In addition, there is a classification of the type of head trauma in terms of
severity. Long and Ross (2013) foud there are three categories that must be
determined. One must consider whether the patient has sustained a minor or major
injury and what the possible complications might be. In minor head injuries have
a major scalp injury, but if the scalp only is involved, it is considered a minor
head injury. These include scalp contusions, scalp lacerations and/or avulsions,
and subgaleal hematomas. After that, major head injuries must evaluation the

skull, brain, or blood vessels of the brain are potentially involved, its considered a
major injury. Injuries to the skull include linear fracture, depressed fracture, and
basiliar fracture. Lesions of the brain include cerebral contusion, and cerebral
laceration.

B. Epidemiology of Head Injury

Epidemiological data of the head injury cases in the world are not so clear
and accurate. It is because cases of head injury is high enough in each country as
well as the lack of research that raised the case for every country. Al Kuwaiti et.
al (2012), From March 2003 March 2006 in Al-Ain Hospital (United Arab
Emirates) 589 patients were studied, and 521 were males (88,3%). The median
(range) followed by fall from height (11,9%). Head injury was mild in 88,2% of
patients, moderate in 5,7%, and severe in 12,1%. 20,9% of patients were admitted
to intensive care unit. 35 patients died (overall mortality 5,9%). The study also
did research on the epidemiology of head trauma in children. Proved that in Korea
the number of children suffering from trauma to the head quite high.
Kim., Song., et. al (2012), In Korea, from June 2008 to May 2009, 2,856
children with THI (Traumatic Head Injury) visited the 5 EDs. The average age of
the subjects was 5.6 (SD 4.9) years old, and 1,585 (55.5%) were 0-4 years old.
The male to female ratio was 2.3 to 1 (1,979 vs 877). Consciousness levels of the
subjects were classified according to the Glasgow Coma Scale (GCS), and 99.1%,
0.6%, and 0.4% were determined as mild, moderate, or severe injury, respectively,

according to the GCS categorization. Most injuries occurred at home (51.3%),

and the most common mechanism of injury was collision (43.2%). With regard to
outcome, 2,682 (93.9%) patients were sent home, and 35 (1.2%) were transferred
to another hospital. A total of 133 (4.7%) patients were hospitalized, and 38
(1.3%) underwent surgery. The incidence and characteristics of pediatric THI
(Traumatic Head Injury) in Korea are affected by sex, location and injury
mechanism.
In addition to the United Arab Emirates and Korea, cases of head trauma
is also an increase in the country of Nigeria and Australia. This is also evidenced
by the existence of an epidemiological study related to an increase in such cases.
Oyedele et. al (2015), Findings revealed that 786 cases of head injury were seen
between 2010 and 2013 translating into an average of 197 case per year.
Furthermore it was also found that, 83% of the reported case involved males.
Findings also revealed that one out of every five reported cases resulted in death.
Road traffic accident accounted for more than three quarters of all cases seen.
Over the 6-year period, there were 1489 presentations at the CHW. Of
these, 65% were male and 35% were female. The mean age was 7 years. A total of
93% were classified as mild, 1.5% as moderate and 5.5% as severe. Sports and
recreational injuries accounted for 26% of all TBI presentations, while motor
vehicle accidents (MVAs) accounted for 77% of all TB deaths. Sixty-two percent
of children underwent a CT brain, and of those, 40% were normal. The existence
of epidemiological studies in several countries such as uni emirate Arabic,
Korean, Nigeria and Australia showed that patients with head trauma is very high.

Patients with head trauma can also occur in children - children, adolescents and
adults. It is makes the head trauma including surgical emergency in the world.
C. Etiology of Head Injury
Injury to the head may damage the scalp, skull or brain. The most
important consequence of head trauma is traumatic brain injury. Head injury may
occur either as a closed head injury, such as the head hitting a car's windshield, or
as a penetrating head injury, as when a bullet pierces the skull. Both may cause
damage that ranges from mild to profound. Rivara et. al (2015) foud cause of
head injury is bicycle accident. There were 3854 injured cyclists in the three year
period; 3390 (88%) completed questionnaires were returned. 51% wore helmets at
the time of crash. Only 22.3% of patients had head injuries and 34% had facial
injuries.
Head injuries can also be caused by trauma during exercise. One example
is the sport of Galelic football and hurling in Ireland with frequent physical
impact and head. Blake et. al (2014), Thirty-five football and 28 hurling squads
participated. There were 1188 football players and 914 hurlers in total over the 6
years. Injuries to the head region constituted 3.0% of football injuries and 2.4% of
hurling injuries. The head injury incidence rate was 0.26 per 1000 hours of
football and 0.19 per 1000 hours of hurling overall. Concussion was diagnosed in
0.8% football and 0.8% hurling injuries. Fractures to the nose constituted 0.7%
football injuries and 0.3% hurling injuries. Fractured mandible was reported in
football (0.2% injuries) and fractured maxilla/orbit in hurling (0.08%). Perforated

eardrum was reported in both football (0.08%) and hurling (0.09%). Lacerations
and contusions accounted for 0.9% injuries for football and 0.8% for hurling.
There was an additional retinal bleed (0.09%) and dental injury (0.09%) in
hurling.
Head injuries can also be caused due to the daily activities - day one, hit
by a stone or wood, collisions due to blunt and sharp as well as a result of the
trauma of war. However, the cause of most of the permanent head injuries caused
by traffic accidents and sports. All things related to the trauma of the head
certainly can cause ill-effects of the head and organs in it. The head is the most
vital part of the body and must be maintained in order to avoid injury.

D. Classification of Head Trauma

1. Basilar Skull Fracture
Basilar skull fracture basically is a linier fracture in skull base. These fracture are
often part of a convexity fracture that has extended into skull base, though they also
occur alone. The skull base is prone to fracture at certain anatomical sites like
sphenoid sinus, foramen magnum, petrous temporal ridge, inner potion of sphenoid
wings at skull base. The middle cranial fossa is weakest with thin bones and multiple
foramina which predispose it to fractures. Basilar fractures often traverse foramina
and thereby may damage cranial nerves and blood vessels. Basilar skull fractures
have been attributed to various mechanisms including impacts to the mandible or face

and the cranial vault, or due to inertial loading by the head (whiplash type injury).
Such inertial loading occurs, for example, when the chest of the motorcycle rider
comes to a sudden stop on contact with an object such as a vehicle or guard rail. The
head is then slowed by loading of the neck. Ring fractures may also result from
vertically directed contact forces applied either inferiorly to the crown (compressive
forces) or from superiorly directed forces applied to the occiput or the mandible
(Wani et al., 2013).
A basal skull fracture may lead to loss of cranial nerve functions and incarceration
of the cranial nerves. Clinical signs may be nausea, vomiting, general malaise,
unconsciousness, seizures, loss of neurological functions. At physical examination,
various pathognomonic defects can be found, such as battle's sign, raccoons eyes,
Leakage of cerebrospinal fluid via ear and nose. Mastoid ecchymosis or retroauricular
ecchymosis also known as battle sign, is a clinical indicator of base of the skull
fracture in the posterior cranial fossa. This sign is caused by blunt trauma to the
mastoid or temporal bone resulting in a longitudinal or mixed fracture within the
temporal bone. Raccoon eyes, a clinical sign most commonly associated with basilar
skull fracture, can be seen in unilateral and bilateral orbital fractures. Trauma to the
frontal region of the skull may cause a fracture to the anterior cranial fossa and
rupture of venous structure at its base, leading to bleeding that extravasates to the
regions of the eyelid and orbital adipose tissue (Epperla, Mazza and Yale, 2015).
2. Epidural Hemorrhage
Epidural hematoma (EDH) is defined as the collection of blood between the skull
and dura matter. EDH mostly results from injury of the middle meningeal artery.

Also, injury of the middle meningeal vein, diploic veins, and dural venous sinuses
may lead epidural hemorrhage. Early diagnosis and surgical evacuation is the key
point of the management of these hematomas. With the advent of computed
tomography, morbidity and mortality of EDH significantly decreased. EDH may
manifest with many different clinical signs and symptoms (Ak, Yolcu and Balbaloglu,
2013).
3. Subdural Hemorrhage
Acute subdural hematoma is a rare presentation of ruptured aneurysms. The rarity
of the disease makes it difficult to establish reliable clinical guidelines. Rupture of a
cerebral aneurysm normally results in subarachnoid hemorrhage (SAH) and is often
complicated by intracerebral hematoma (ICH), but only on rare occasions does it
cause acute subdural hematoma (aSDH). Diagnosis of aneurysmal SAH can be
difficult in comatose patients in whom loss of conscious due to aneurysm rupture
results in or mimics a traumatic brain injury. The majority of patients with
aneurysmal SAH and coincidental acute subdural bleeding present in a severe clinical
condition, and immediate surgical management is required (Marbacher, Tomasi and
Fandino, 2012).
Subdural hemorrhage (SDH) is the most common pathology associated with
abusive head trauma. The historical teaching describing the origin and location of
subdural hemorrhage has been that the tearing of bridging veins leads to bleeding at
the interface between the inner (meningeal layer)dural margin and the arachnoid
membrane (Hedlund, 2012).
4. Intracerebral Hemorrhage

In most cases primary intracerebral hemorrhages are caused by arterial

hypertension, (in up to 90% of patients) or by amyloid angiopathy. The localisation of
the hematoma is associated with the etiology of hemorrhage. Hypertensive
hemorrhages involve frequently basal ganglia, thalamus or the posterior fossa. The
primary hemorrhages based on amyloid angiopathy may result in lobar hematomas,
typically at the border of the grey and white matter. But cerebral amyloid angiopathy
associated hemorrhages can also involve the subarachnoid space or result in
cerebellar hematomas (Reichart and Frank, 2011).
ICH may cause different neurological deficits. Like in ischemic insults, in ICH
neurological symptoms are developed within minutes to hours. Symptoms of ICH can
be divided into general manifestation and manifestations due to the localisation of
hematoma. Normally, severe headaches are described sometimes in combination with
vomiting, whereas an alteration in level of consciousness also could occur. Symptoms
of lobar ICH are associated with the affected cerebral lobe, so homonyme
hemianopsia, paresis of arm or leg, or aphasia are observed. Small ICH of basal
ganglia could occur without any symptoms, but larger ICH in this region leads to
sensomotoric contralateral hemiparesis, sometimes in combination with aphasic
disorders or homonymous hemianopsia, when the hematoma extends posteriorly and
involves optic radiation (Reichart and Frank, 2011).
5. Minor Head Trauma
a) Concussion
Concussion affects not only cognitive function but also other physiological
systems to include the heart and the autonomic nervous system. Concussed
athletes have exaggerated sympathetic nervous activity and increased heart rates

(HRs) when compared with controls. Cerebral autoregulation (the ability of the
brain to maintain constant perfusion pressure in the face of changing systemic
arterial pressure during exertion) and cerebral blood flow are disturbed after
concussion, which may explain why symptoms reappear or worsen with physical
exertion or other stressors that increase blood pressure (Leddy et al., 2010).
b) Post Concussion Syndrome
The majority of patients with sport-related concussion recover within 7 to 10
days and nonathletes within the first 3 months. There is, however, a significant
minority of athlete and non athlete patients who continue to experience symptoms beyond this, called post-concussion syndrome (PCS). The World Health
Organization defines PCS as persistence of 3 or more of the following after head
injury: headache, dizzi- ness, fatigue, irritability, insomnia, concentration
difficulty, or memory difficulty.The primary forms of PCS treatment have
traditionally

included

rest,

education,

neurocognitive

rehabilitation,

and

antidepressants, with little evidence of success (Leddy et al., 2010)

6. Mayor Head Trauma
a) Contusion
From the focal brain injuries, cerebral contusions (CC) are one of the most
common traumatic finding CC are more common in regions that contact bony
surfaces in the cranial vault during trauma: frontal and temporal poles,
orbitofrontal gyri, perisylvian cortices, and inferolateral temporal lobe surfaces .
Contusions can be characterized by mechanism, anatomic location, or adjacent
injuries caused by the initial mechanical impact, resulting in skull fracture,
cerebral contusion, vascular and parenchymal injury causing intracranial bleed

and ICH. An inflammatory process, edema formation, and excitotoxicity follow,

resulting in further increase in ICP and reduced cerebral perfusion pressure
(Miranda, Cerra and Salazar, 2013).

E. Differential Diagnosis
1. Enchepalopathy
Chronic traumatic encephalopathy (CTE) is a form of neurodegeneration that
is believed to result from repeated head injuries. Originally termed dementia
pugilistica due to its association with boxing, the neuropathology of CTE was first
described by Corsellis in 1973 in a case series of 15 retired boxers. CTE has recently
been found to occur following other causes of repeated head trauma, suggesting that
any repeated blows to the head, such as those that occur due to American football,
hockey, soccer, professional wrestling, and physical abuse, can also lead to
neurodegenerative changes. These changes often include cerebral atrophy, cavum
septum pellucidum with fenestrations, shrinkage of the mammillary bodies, dense tau
immunoreactive inclusions (neurofibrillary tangles, glial tangles, and neuropil
neurites), diffuse axonal injury, and, in some cases, a TDP-43 proteinopathy. In
association with these pathological changes, affected individuals often exhibit
disordered memory and executive functioning, behavioral and personality
disturbances (e.g., apathy, depression, irritability, impulsiveness, suicidality),
parkinsonism, and, occasionally, motor neuron disease. At the present time, there are

no formal clinical or pathological diagnostic criteria for CTE, but the distinctive
neuropathological profile of the disorder lends promise for future research into its
prevention, diagnosis, and treatment. (Brandon, et al., 2011)
It has been understood for decades that participation in certain sporting
activities may increase an athletes risk of developing a neurodegenerative disease
later in life. Not surprisingly, this association was originally noted in boxers, athletes
who receive numerous blows to the head during training and competition. In 1928,
Harrison Martland, a New Jersey pathologist and medical examiner, first described
the clinical spectrum of abnormalities found in "nearly one half of the fighters who
have stayed in the game long enough. Boxers exhibiting cognitive, behavioral, or
motor abnormalities were well known to lay persons, sportswriters, and others within
the boxing community and were referred to by a variety of terms, such as punch
drunk, goofy, and slug-nutty later, the more formal term dementia pugilistica
was introduced in order to lend medical validity to the condition. By the 1970s, a
sufficient number of boxers with dementia pugilistica had been studied pathologically
to support the conclusion that this form of neurodegeneration was similar to, but
distinguishable from, other causes of neurodegenerative disease. As evidence
pertaining to the clinical and neuropathological consequences of repeated mild head
trauma grew, it became clear that this pattern of neurodegeneration was not restricted
to boxers, and the term chronic traumatic encephalopathy (CTE), originally coined by
Miller, became most widely used. (Brandon, et al., 2011)

Over the last several decades, clinical and neuropathological evidence of CTE
has emerged in association with a variety of sports, including American football,
professional wrestling, professional hockey, soccer, as well as other activities
associated with repetitive mild head trauma, such as physical abuse, epileptic
seizures, and head banging (Omalu, et al., 2005; Cajigal, et al., 2007). Although the
incidence and prevalence of CTE is currently unclear, it likely varies by sport,
position, duration of exposure, and age at the time of initial or subsequent head
trauma, as well as with additional variables such as genetic predisposition. To date,
there have been no randomized neuropathological studies of CTE in deceased
athletes, and as such, there is a selection bias in the cases that have come to autopsy.
If one considers the prevalence in deceased professional American football players
who died between February 2008 and June 2010, there were 321 known player deaths
and the brains of 12 of the 321 underwent postmortem neuropathological examination
at Boston University Center for the Study of Traumatic Encephalopathy (BU CSTE).
All 12 examined neuropathologically showed evidence of CTE, suggesting an
estimated lifetime prevalence rate of at least 3.7%. If one assumes that all deceased
players who did not come to autopsy did not have CTE, and that the amount of head
trauma in professional football has remained fairly constant over the past 5 decades, a
prevalence rate of 3.7% would result. Although this represents a conservative
estimate, it suggests a significant public health risk for persons who suffer repetitive
mild traumatic brain injury. (Brandon, et al., 2011)

a. Clinical signs and symptoms of CTE

Whereas concussion and post-concussion syndrome represent temporary
states of neuronal and axonal derangement, CTE is a neurodegenerative disease that
occurs years or decades following recovery from the acute or post-acute effects of
head trauma. The exact relationship between concussion and CTE is not entirely
clear, although repetitive axonal perturbation may initiate a series of metabolic, ionic,
membrane, and cytoskeletal disturbances that trigger the pathological cascade that
leads to CTE in susceptible individuals (Giza, et al., 2001; Yuen, et al., 2009).
The onset of CTE is often in mid-life, usually after the athlete has retired
from his or her sport. In some individuals, the early manifestations of CTE affect
behavior; in particular, individuals with neuropathologically-documented CTE have
been described by family and friends as being more irritable, angry, apathetic, or
having a shorter fuse. Increased suicidality appears to be a particularly salient
symptom caused by CTE (Omalu, et al., 2010). In other cases, cognitive difficulties
may be the first signs to emerge, with poor episodic memory and executive
functioning being two of the most common cognitive dysfunctions reported. Later in
the disease, movement (e.g., parkinsonism), speech, and ocular abnormalities may
emerge in the context of declining cognition and worsening comportment. A minority
of cases with neuropathologically-documented CTE developed dementia before
death; the relative infrequency of dementia in individuals with CTE may be due in
part to the fact that many individuals with CTE have either committed suicide or died

from accidents or drug overdose at an early age (McKee, et al., 2009; Omalu, et al.,
2010).
2. Hydrocephalus
Hydrocephalus is a common complication after TBI. The incidence of
hydrocephalus varies from 5%45%, depending on the severity and the setting (acute
versus post-acute) of the study [Mazzini, et al., 2003]. Tian and colleagues reviewed
the incidence of posttraumatic hydrocephalus in patients with traumatic subarachnoid
hemorrhage and reported that 12% of patients with traumatic subarachnoid
hemorrhage developed hydrocephalus within three months [Tian, et al., 2008].
Kammersgaard and colleagues investigated the incidence of hydrocephalus for
patients (n = 444) requiring rehabilitation in Denmark [Kammersgaard, et al., 2013].
They observed an incidence of 14% with three-quarters occurring during
rehabilitation. Hydrocephalus is defined as an active distention of the ventricular
system of the brain related to inadequate passage of cerebrospinal fluid from its
production within the ventricular system to its point of absorption in the systemic
circulation [Rekate, et al., 2009].
Risk factors for post-traumatic hydrocephalus include advanced age, injury
severity, intraventricular haemorrhage, subarachnoid haemorrhage, meningitis, the
use of decompressive craniotomy, and the duration of coma [Mazzini, et al., 2003;
Ding, et al., 2014]. However, Kammersgaard did not find an increased incidence of

hydrocephalus after decompressive craniotomy [Kammersgaard, et al., 2013].

Patients with post-traumatic hydrocephalus were older, had a higher injury severity
(measured by Glasgow coma scale at admission to rehabilitation) and had a low level
of consciousness.
Post-traumatic hydrocephalus is the most common treatable neurosurgical
complication during rehabilitation [Ding, et al., 2014]. There are two types of
hydrocephalus:

communicating

and

non-communicating

hydrocephalus.

Communicating hydrocephalus is more frequent after TBI, and is caused by

disruption of the absorptive capability of the arachnoid villae. Different portions of
the ventricular system can communicate with each other, and cerebrospinal fluid
may flow from the ventricles to the subarachnoid space. Blood products and/or
inflammatory products impede the flow of the cerebrospinal fluid through the
arachnoid granulations into the blood stream causing a gradual enlargement of the
ventricles. It also known as normal pressure hydrocephalus as the intracranial
pressure is only intermittently elevated, but the enlarged ventricles put increased
pressure on the adjacent cortical tissue [Zolmann, et al., 2011].
Post-traumatic hydrocephalus can cause myriad symptoms in the patient: the
typical clinical triad for normal pressure hydrocephalus is gait ataxia or shortstepping gait, cognitive decline, and urinary incontinence or urge. Usually the onset is
slow, and a high index of suspicion is required of the treating physician. The earliest
indication is often a decline or plateau in functioning and/or subtle mental status

changes [Denes, et al., 2011]. The symptoms of a slow decline or plateau of

functioning are also seen due to neuroendocrine disturbances: e.g., hyponatremia due
to inadequate ADH secretion, anterior pituitary insufficiency. Also the later symptoms
of hydrocephalus, indicative of increased intracranial pressure, such as headache,
nausea, vomiting and lethargy, coincide with symptoms signalling ACTH deficiency .
The diagnosis is not always simple; most physicians rely on a combination of
imaging criteria, other measurements of cerebral spinal fluid dynamics, and clinical
signs.
3. Epilepsy
Characterized by seizures that are unpredictable in frequency, epilepsy is a
common neurological disorder that affects people of all ages, with onset most often
occurring in childhood and older adult- hood. Epilepsy is a spectrum of disorders the
epilepsies with a range of severities, widely differing seizure types and causes, an
array of coexisting conditions, and varying impacts on individuals and their families.
Epilepsy is the fourth most common neurological disorder in the United States after
migraine, stroke, and Alzheimer's disease (Hirtz, et al., 2007), it is estimated that
150,000 new cases are diagnosed in the United States annually (Hirtz, et al., 2007),
and that 1 in 26 individuals will devel- op epilepsy at some point in their lifetime
[Hesdorffer, et al., 2011].
While seizures are well controlled with medications and other treatment

options for the majority of people with epilepsy [Kwan, et al., 2000], the impact of
epilepsy goes well beyond the seizures. The challenges facing the estimated 2.2
million people with epilepsy in the United States [Hirtz, et al., 2007] include having
access to high-quality health care, becoming in- formed about and coordinating health
care and community services, and dealing with stigma and common public
misunderstandings. Liv- ing with epilepsy, particularly for people with refractory
seizures, can involve challenges in school, uncertainties about social and employment situations, limitations on driving, and questions about indepen- dent living.
Epilepsy can impose an immense burden on individuals, families, and society; the
estimated annual direct medical cost of ep- ilepsy in the United States is $9.6 billion
[Yoon, et al., 2009], which does not consider community service costs or indirect
costs from losses in quality of life and productivity (these indirect costs are estimated
to constitute the majority of the cost burden of epilepsy [Begley, et al., 2000]. Further,
epilepsy is asso- ciated with substantially higher rates of mortality than experienced
in the population as a whole [Forsgren, et al., 2005], with sudden unexpected death in
epi- lepsy (SUDEP) being the most common cause of epilepsy-related deaths
[Tomson, et al., 2004]. Estimates indicate that 10 years of life are lost for people
whose epilepsy has a known cause and 2 years are lost for people with epilepsy from
an unknown cause [Gaitatzis, et al., 2004]. Additionally, incidence estimates for the
number of people with epilepsy who die of SUDEP range from 1 per 10,000 personyears for those individuals who are newly diagnosed to 9 per 1000 person-years for
those who are candi- dates for epilepsy surgery [Tomson, et al., 2008].

A significant challenge for people with epilepsy, as well as for the epilepsy
field, has been the multitude of ways that epilepsy is perceived and, in many cases,
misperceived. The centuries of misper- ceptions and misinformation about epilepsy
have resulted in people with epilepsy being stigmatized [Bandstra, et al., 2008]. As a
consequence, people with epilepsy and their families may be faced with a lack of
social support from extended family members; feelings of parental guilt; social isolation, embarrassment, and fear; and discrimination. Although efforts are being made
to correct these misconceptions and to better inform people about the epilepsies,
doing so remains a challenge.

Throughout its report, the committee emphasizes the ways in which epilepsy is a
spectrum of disorders. Epilepsy comprises more than 25 syndromes and many types
of seizures that vary in severity [Berg, et al., 2010]. Additionally, people who have
epilepsy span a spectrum that in- cludes men and women of all ages and of all
socioeconomic back- grounds and races/ethnicities, who live in all areas of the United
States and across the globe. The impacts on physical health and quality of life
encompass a spectrum as well, with individuals experienc- ing different health
outcomes and having a range of activities of daily living that may be affected,
including driving, academic achieve- ment, social interactions, and employment. For
some people, epilepsy is a childhood disorder that goes into remission (although the
sei- zures may have lifelong consequences), while for others, it is a life- long burden

or a condition that develops later in life or in response to an injury or other health

conditions. These many complexities of epilepsy make it a challenging health
condition to convey to the gen- eral public and to promote understanding and
alleviate stigma.
4. Sub Dural Emphyema
Complications of head injury such as subdural empyema are rarely seen, have
long-term morbidity if not diagnosed and managed promptly and appropriately
(Mandell, et al., 2010). The frontal region is the most common location, and it is
caused by frontal sinus fracture and chronic frontal sinusitis associated to nasal
polyposis. Meningitis and encephalitis are often the first diagnosis considered in this
case, space-occupying lesions such as abscesses or subdural empyemas must be
considered as well, in particular when there are neurologic deficits, altered mental
status or seizures at presentation. We present a case of an adult male who presented
with fever, headache, had history of cerebrospinal fluid rhinorrhea and head injury 2
years back, with subdural empyema.
Intracranial subdural empyema (ISDE) is a pyogenic infection localized
within the space between the dura and arachnoid mater. It is a rare condition,
accounting for 15%-20% of localized intracranial infections (Mandell, et al., 2010).
Although its incidence is decreasing, ISDE can be difficult to diagnose because of its
nonspecific presentation (Madhugiri, et al., 2010). The most common triad of

symptoms is fever, headache, and vomiting. (De Bonis, et al., 2009). Improving
patient outcomes is critically dependent on rapid diagnosis, prompt initiation of
appropriate antimicrobial therapy, and early surgical drainage. (Ovalioglu, et al.,
2013). ISDE is an important area of practice that constitutes a neurosurgical
emergency and can be associated with significant morbidity and mortality caused by
focal neurology and seizures (Le Roux, 2007). This study provides clinicians with
useful information on the presentation and management of ISDE in Queensland,
Australia.
a. Clinical Features
The most common clinical feature of ISDE was headache, followed by fever
and altered sensorium. This triad of headache, fever, and altered sensorium was
present in 19 (53%) patients. The classic triad of headache, fever, and vomiting was
present in 13 (36%) patients. Altered sensorium was seen in 24 (67%) patients. Of the
patients with altered sensorium, 54% had Modified Glasgow Coma Scale (GCS)
scores between 13-14, 25% had GCS scores between 9-12, and 21% had GCS scores
8 (on a 15- point scale in which 15 indicates full consciousness). A normal level of
consciousness was seen in 12 (33%) patients. Eight patients (22%) presented with
seizures. Focal motor signs were found in 18 (50%) patients. The most common focal
motor sign was contralateral limb weakness.
5. Alzheimer Disease

Alzheimers disease (AD) is the main cause of dementia and accounts for two
thirds of dementia syndromes in people older than 65 years. Memory impairment,
especially impairment of episodic memory, is one of the first symptoms of AD. Due
to public awareness of AD, it is often suspected to be the underlying cause of memory
problems in elderly patients. Since AD is a progressive neurodegenerative disorder
with an untreatable cause and limited therapeutic options, it is highly impor- tant to
carefully establish the correct diagnosis and be aware of medical conditions that may
mimic AD by pres- enting with memory impairment. In clinical research the correct
classification of AD and non-AD is crucial to study disease mechanisms or new
treatment possibilities in homogenous study populations. In this article, we aim to
describe new aspects of the most common differential diagnoses that may clinically
resemble AD, but which have different pathophysiological roots.
a. Memory function
The term memory generally means the ability to reproduce or remember
experienced or learned content. There are different types or constructs of memory,
and the classification of memory categories is still subject to change and discussion.
(Schacter, et al., 2012). Memory may be classified as implicit or explicit: implicit
memory mainly stands for nonverbal habitual memory, such as motor learning (eg,
playing a musical instrument or riding a bicycle); explicit memory contains active or
passive recall of facts or impressions (biographical knowledge, chronological
sequence of experienced events, speech, etc). Another common distinction is between

short-term and long- term memory: short-term memory describes a time span of
seconds or minutes (sometimes also referred to as working memory), and long-term
memory comprises encoding, consolidation, and recall over or after a long period of
time. Memory can also be classified with regard to content: episodic memory, verbal
memory, visual memory, or olfactory memory.
Although there are fewer common syndromic variants of AD, one of its main
and early features is an impair- ment of episodic memorythe capacity to remember
past events together with details about the context in which they occurred (Warren, et
al., 2012). Episodic memory is an essential cognitive function that supports our
ability to form an autobiographical history and helps us to create a concept of the past
and the future.
The hippocampal network, including the parahip- pocampal gyrus,
hippocampus, and neocortical areas, play a major role in the process of memory
consolidation and retrieval. Although its function has not yet fully been understood,
the hippocampus seems to be involved in binding features of an event into a mental
represen- tation, which is important to form episodic memory. Virtually any
neurological, neurodegenerative, toxic, or traumatic damage to brain structures
involved in episodic memory generation, especially the hippocam- pus, may lead to
deficits in episodic memory that may resemble or precede AD (Daulatzai, et al.,
2013), especially in the absence of other neurological or neuropsychological
symptoms or signs indicative of an alternative cause.

F. Management Of Head Trauma

Initial management from head trauma is suitable to The guidelines of

Advanced Trauma Life Support (ATLS) provide a standardized protocol for
approaching the severely injured patient, with special attention to airway, breathing
and circulation (Chowdhury, Kowalski, Arabi, and Dash, 2014).
1. Hypoxemia
The first most important consideration in Trauma Brain Injury is the
maintenance of a clear and unobstructed airway. Hypoxemia is the most
important factors related to worse outcome and therefore needs urgent attention.
In a multicenter prospective study of 150 patients, the mortality was found to be
20% in patients without secondary insults; however, it increased to 37% during
hypoxic episodes. Patients with severe Trauma Brain Injury are to be intubated
by rapid sequence induction by killed personnel. The cervical spine must be
protected and should always be assumed to be injured until definitively cleared
while securing the airway. A randomized controlled trial showed that rapid
sequence intubation (RSI) performed by paramedics was associated with an
increase in the rate of favorable neurologic outcome at 6 months compared with
intubation in the hospital; this highlights the importance of immediate airway
control in cases of severe Trauma Brain Injury (Bernard, Nguyen, Cameron,
Masci, Fitzgerald, and Cooper, 2011).
Similarly, an observational study of 334 patients with pre-hospital
hypothermia (PH) intubations and GCS score 8 and proven Trauma Brain Injury

(on CT scan) revealed a higher rate of overall intubations and was associated
with no increase in mortality over the emergency department intubation
(Vandromme, Melton, Griffin , McGwin , Weinberg, and Minor, 2011). In
addition, the use of RSI with appropriate use of anesthetic agents is of paramount
significance to prevent aspiration-related adverse events and simultaneously
prevent sympathetic surge incited by airway manipulations; however, avoidance
of hypotension should be ensured. The role of lidocaine in cases of RSI is also
controversial; however, a recent retrospective cohort of 101 patients showed that
lidocaine can be used without producing adverse hemodynamic changes (Lin, Yu
JH, Li WC, Weng, and Chen, 2012).
The technique and equipment are also equally important to manage the
pre-hospital intubations, especially by the paramedics. In this regard, the role of
video-laryngoscopes and other difficult intubation kits may certainly give better
chances for airway management and thus would prevent the secondary brain
injuries related to hypoxemia (Bauer, 2012).
In addition, a high incidence of oxygen desaturation during PH
intubations warrants standard monitoring such as pulse oximetry. A study on 87
patients with TBI undergoing RSI by pre-hospital providers revealed that the rate
of SpO2 decline increases as the SpO2 decreases, with an inflection point
occurring around 93%. Intubation attempts below this value are almost always
associated with subsequent desaturation. However, a high incidence of pulse
oximetry failure was also observed with the use of a digital pulse oximetry probe
during pre-hospital RSI. In a retrospective study of 124 patients with severe TBI,

79% of the patients had pulse oximetry failure at the time of RSI. In addition, a
latent period appears to exist in the majority of patients (55%) undergoing
desaturation (Davis, Aguilar, Sonnleitner, Cohen, and Jennings, 2011). Therefore,
caution should be paid to all differential causes of oxygen desaturation, including
pulse oximetry related, while attempting RSI.
2.

Hypercarbia/hypocarbia
The intubated patients should be ventilated so as to maintain
normocarbia (PaCO2 35 and 40 mmHg). Monitoring of oxygen saturation and
capnography is recommended in severely head-injured patients so as to avoid
unrecognized hypoxemia or changes in ventilation. This is best assessed by end
tidal capnography, and generally corresponds to EtCO2 30-35 mmHg. In analysis
of data of 11,000 patients, both hypo- and hypercapnia were associated with
worse outcomes in intubated patients (Davis, Peay, Sise, Kennedy, Simon, and
Tominaga, 2011). In another retrospective review of 77 patients, both hypocarbia
(PaCO2 - <35 mmHg) and hypercarbia (PaCO 2 - >45 mmHg) were associated
with a substantial increase in in-hospital mortality (Dumont, Visioni, Rughani,
Tranmer, and Crookes, 2011). A study on guideline-based management in prehospital ventilation (PaCO2 >29 mmHg) in 100 patients (without herniation
signs) showed that the in-hospital mortality was 29% among those in whom
guideline levels were achieved and 46% (16 of 35) in those in whom guideline
levels were not achieved pre-hospital. Similarly, a retrospective review of 851
patients on targeted ventilation (PaCO2 30-39 mmHg) at the emergency

department also found decreased mortality (21.2% vs. 33.7%) in comparison

with ventilation achieved outside the target range (Caulfield, Dutton, Floccare,
Stansbury, and Scalea, 2011). Therefore, pre-hospital normoventilation should be
ensured. However, in cases with signs of potential brain herniation, transient
hyperventilation may be an option. There is strong evidence that capnography
can affect the outcome. Therefore, continuous capnography is recommended in
all ventilated Trauma Brain Injury patients (Holmes, Peng, and Bair, 2012). As
ETCO2 values may be confounded by low tissue perfusion, long-term ventilation
should be guided by the frequent sampling of blood gases. The frequency of
blood gas sampling is yet to be quantified.
Oxygenation and ventilation can become difficult if there are other
major injuries, particularly chest injuries, aspiration of gastric contents or acute
pulmonary edema. Appropriate positive end expiratory pressure (PEEP) should
be used. There is no evidence that 10 mmHg PEEP impairs cerebral blood flow
or elevates intracranial pressure (ICP) and, indeed, ICP may improve with
improved oxygenation (Chowdhury, Kowalski, Arabi, and Dash, 2014).
3.

Hipotension/Hypertension
Hypotension is a major secondary brain insult and studies have
demonstrated that a single episode of hypotension dramatically worsens the
outcome (Pearson, Ovalle, Jr, Faul, Sasser, 2012). Hypotension should be treated
with fluid resuscitation to euvolaemia and, if necessary, vasopressors are used to
maintain optimum blood pressure. According to BTF, prior to the insertion of an
ICP monitoring, a MAP 80 mmHg is recommended. The rationale for a MAP

80 mmHg is to maintain cerebral perfusion pressure (CPP) 60 mmHg for a

treatment threshold of ICP > 20 mmHg. Following the insertion of an ICP
monitoring, the management of MAP will be directed by the ICP/CPP values
(Berry, Ley, Bukur, Malinoski, Margulies, Mirocha, et al, 2012).
However, recent studies have challenged the lower limit to define
hypotension in patients with isolated head injury (Brenner, Stein, Hu, Aarabi,
Sheth, and Scalea, 2012). In a study of 15,733 patients with moderate to severe
head injury, the value of systolic blood pressure of 110 mmHg or less is
computed as the best fit model for hypotension when mortality was taken as the
outcome measure (Berry, Ley, Bukur, Malinoski, Margulies, Mirocha, et al,
2012). In another study, maintaining a systolic blood pressure of approximately
120 mmHg has been found to be more efficacious to minimize the secondary
brain injury (Brenner, Stein, Hu, Aarabi, Sheth, and Scalea, 2012). Therefore,
further large clinical trials are needed to support these findings. It is
recommended that patients with severe Trauma Brain Injury have arterial and
central venous lines placed as soon as practical.
Hypertension may be a physiological response produced due to
sympathetic surge, and may signify a compromised cerebral perfusion.
Hypertension should not be treated unless a cause has been excluded or treated
and the systolic blood pressure is >180-200 mmHg or the MAP is >110-120
mmHg. Lowering an increased blood pressure, as a compensatory mechanism to
maintain an adequate CPP, exacerbates cerebral ischemia. For the treatment of
hypertension to achieve CPP targets, an infusion of short-acting beta blocker is

very useful, which maintains blood pressure. These agents do not cause cerebral
vasodilatation when compared with nitrates and calcium channel blockers and,
therefore, do not increase the cerebral blood volume and ICP (Haddad, and
Arabi, 2012).
4.

Fluid Resusitation
Further to this, the prompt resuscitation with fluids is of paramount
importance to preserve optimum CPP. However, the choice of fluids is still a
matter of great conflict. Some studies have suggested that hypertonic fluids
might suppress the biomarkers of Trauma Brain Injury and are correlated with
better outcome (Baker, Rhind, Morrison, Black, Crnko, and Shek, 2011). Many
studies have investigated the effect of various fluids on pre-hospital resuscitation.
No studies have reported better survival and functional outcomes over the use of
isotonic crystalloids (Tan, Cincotta, Clavisi, Bragge, Wasiak, and Pattuwage,
2011). Further to this, a multicenter randomized control trial (RCT) of 1087
patients (15 years or older with blunt trauma who did not meet the criteria for
hypovolemic shock) with severe Trauma Brain Injury (GCS 8 or less) showed
that even the initial resuscitation with hypertonic saline or hypertonic
saline/dextran, compared with normal saline, were found to be comparable in
terms of 6-month neurologic outcome or survival (Bulger, May, Brasel,
Schreiber, Kerby, and Tisherman, 2011).
However, this study was terminated by the data and safety monitoring
board after randomization of 1331 patients. On the other hand, post hoc analysis

(460 patients) of a multicenter RCT study titled Saline Albumin Fluid

Resuscitation Trial (SAFE) highlighted that the use of albumin was associated
with the higher mortality data in patients with severe head injury. Among patients
with severe brain injury (GCS 3-8), 41.8% patients died in the albumin group as
compared with 22.2% patients in the saline group; however, among patients with
GCS scores of 912, death occurred in eight of 50 patients in the albumin group
(16.0%) and eight of 37 patients in the saline group (21.6%). Based on these
findings, colloids should not be used as the first choice of fluid, especially in
patients with severe TBI, and isotonic crystalloids seem to be a safer choice and
are cost-effective as well. The role of colloids in mild to moderate severe head
injury is at present inconclusive and therefore needs well-designed RCTs.
5.

PH
Hypothermia has some protective effects in Trauma Brain Injury by
reducing ICP, cerebral metabolic demands, decreasing disruption of the blood
brain barrier and inhibiting the inflammatory cascade. Induced hypothermia is
now an accepted measure to improve outcome following anoxic brain injury
associated with cardiac arrest, but its benefits in TBI are inconclusive at present
(Fox, Vu, Doyle, Brubacher, Abu-Laban, and Hu, 2011). In a systemic review (12
RCTs), data support the use of early prophylactic mild-to-moderate hypothermia
in patients with severe TBI (GCS score 8) to decrease mortality and improve
the rates of good neurologic recovery. However, this review advocates for early
use (emergency department) of therapeutic hypothermia and also recommends a

long-term or goal-directed cooling protocol, in which cooling was continued for

at least 72 h and/or until stable normalization of ICP for at least 24 h was
achieved. On the other hand, in an epidemiological study (level III evidence) of
21,023 patients, 44.6% patients presented with PH (Bukur, Hadjibashi, Ley,
Malinoski, Singer, Barmparas, 2012).
Moreover, hypothermic patients in comparison with normothermic patients
required 26% more fluid resuscitation and 17% more total blood products in the
emergency department. PH was found to be independently associated with
increased adverse events, including need for a transfusion, mortality, incidence of
adult respiratory distress syndrome and pneumonia. Similarly, a retrospective
review of 1281 patients highlighted that presence of hypothermia (<35C) on
Intensive Care Unit (ICU) admission was found to be an independent factor to
increase the mortality. In addition, penetrating injury, Injury Severity Score 25
and exploratory laparotomy before admission were found to be independent risk
factors for the development of hypothermia on ICU admission (Bukur, Kurtovic,
Berry, Tanios, Ley, and Salim, 2012). The impact of preventative measures used
to avoid the development of hypothermia and the effectiveness of measures for
restoring normothermia warrant further investigation.
Therefore it can be conclut that severe Trauma Brain Iinjury patients impose
very high mortality and morbidity and, strikingly, a substantial portion of these bad
outcomes can be prevented by prompt evaluation and pre-hospital as well as early
emergency management of such cases. Based on the evidence, majority of the

management strategies comprise of rapid correction of hypoxemia and hypotension,

the two most important predictors for mortality. However, there is still a need to
define the goals for the management of hypotension and inclusion of newer difficult
airway carts as well as proper monitoring devices for ensuring better intubation and
ventilatory management. Isotonic saline should be used as the first choice for fluid
resuscitation. The PH has more adverse effects and should therefore be avoided.
Other supportive treatments according to Zhang XY, Yang ZJ, Wang QX,
Fan HR, (2011) :
1. Early extraventricular drainage of CSF is sometimes of value in controlling brain
edema if there is a suspicion that the ventricles will progressively diminish in size
because edema cannot be cannulated from a burr hole.
2. Coughing and straining increase venous pressure, restricting drainage and backing
up blood into the head, thereby increasing ICP. Neuromuscular paralysis may
decrease ICP by preventing sudden changes related to coughing or straining and
by promoting systemic venous pooling that increases venous drainage from the
head. Any other restrictions to jugular blood drainage, such as a kinked neck from
positioning in bed, increase ICP by retarding jugular drainage, transmitting
pressure back into the brain.
3. Trying to differentiate a drug-induced coma from an increased ICPinduced coma
with a trial of naloxone (Narcan) is contraindicated, as it invariably induces
agitation if the stupor is narcotic induced. Agitation increases catecholamine
response, increases cardiac output, and increases blood flow to the head, thereby
increasing hydrostatic pressure and ICP.

4. Use of positive end-expiratory pressure (PEEP) for mechanical ventilation is

controversial in TBI patients with acute lung injury/acute respiratory distress
syndrome. Zhang et al found that PEEP can have a varied impact on blood,
intracranial, and cerebral perfusion pressure in patients with cerebral injury. When
applying this technique, mean arterial and intracranial pressure monitoring appears
beneficial.

G. Prognosis
The outcome of TBI is dependent on number of factors in addition to the
severity of brain injury. The initial GCS score continues to have utility providing both
a description of the initial neurologic condition, and to a lesser extent mortality
prediction. A recently analyzed cohort of 2,808 TBI patients across multiple centers
found a total GCS of 8 or less to be associated with a mortality of 28.7% by two
weeks following injury (Timmons, Bee, Webb, Diaz-Arrastia, and Hesdorffer, 2011).
Out of the three components of the GCS score, the motor portion is most predictive of
outcome. Compared to patients with a GCS motor score of 6, there was a 2.2 fold
increased risk mortality at two weeks with a motor score of 5 ranging to a 17 fold
increased risk with a motor score of 1.
Advanced age is also an important negative prognostic factor. An
examination of the Crash Injury Research Engineering Network database found a
significantly higher mortality rate among elderly motor vehicle accident victims (age
>60 years) compared to their younger counterparts (Richmond, Aldaghlas, Burke,

Rizzo, Griffen, and Pullarkat, 2011). Even mild TBI has been associated with a
greater risk of death with elderly patients having a 1.25 fold greater risk compared to
the general population after controlling for age and medical comorbidities (Cheng,
Lin, Lee, Hsu, Lee, and Su, 2014).
In addition to low initial GCS and advanced age other negative prognostic
factors have been identified including pupillary size and response, and the
development of hypoxia, pyrexia, and high intracranial pressure following initial
presentation. These factors have also been associated with poor initial and long-term
outcomes.
In a retrospective series of 846 patients with severe Trauma Brain Injury
(GCS of 8 or less) reported by Jiang et. al. one-third of patients had either died or
remained in a persistent vegetative state at one year following their injury. However,
31.56% of individuals still experienced a good recovery defined as the ability to live
independently and return to work or school. These data highlight the difficulty with
accurate prediction of individual patient prognosis in Trauma Brain Injury.
In an attempt to assist with clinical decision making numerous predictive
scoring systems have been developed including the recent International Mission on
Prognosis and Analysis of Clinical trials in Traumatic brain injury database (IMPACT
models) and the Corticosteroid Randomization After Significant Head Injury trial
data (CRASH models). These systems have examined large data sets and undergone
external validation with favorable results. However, as with most predictive scoring
systems they are generalizable to the populations they are validated in and are not

reliably generalizable to most patients (Cheng, Lin, Lee, Hsu, Lee, and Su, 2014).
Therefore, initial aggressive treatment of severe TBI will continue to be prudent until
an accurate, fully generalizable means of prediction is available.

H. Complications
Functional deficits resulting from TBI are common and can be divided into
2 categories, as follows: systemic complications and neurologic complications. The
systemic complications of TBI are typical of any severe injury and depend on the
types of intensive treatments used. Be aware of the complications of intensive care
treatment when considering systemic complications of head injury.
One of the most feared systemic complication of TBI is venous
thromboembolism (VTE). Valle and colleagues investigated whether polytrauma
patients with TBI had higher rates of VTE than polytrauma patients without TBI.
While the patients with TBI had worse Injury Severity Scores, longer ICU lengths of
stay and more hypercoagulable thomboelastogram values on admission, they did not
have higher rates of VTE (Valle, Van Haren, Allen, Jouria, Bullock, and Schulman,
2014). The timing of when to initiate chemical thromboprophylaxis in patients with
intracranial hemorrhage has not been fully elucidated. Farooqui and colleagues
initiated chemoprophylaxis for TBI patients 24 hours after a stable head CT was
obtained. This intervention was associated with a lower DVT rate in patients started
on chemoprophylaxis. There was no significant difference in pulmonary embolism
rates. Of note, there was no increase in intracranial hemorrhage in patient's following

the protocol when compared with patients who did not recieve routine
chemoprophylaxis for VTE (Farooqui, Hiser, Barnes, and Litofsky, 2013).
The neurologic complications of TBI include focal neurologic deficits,
global neurologic deficits, seizures, CSF fistulae, hydrocephalus, vascular injuries,
infections, and brain death.