CHAPTER I

PREFACE

Head injury is a major cause of morbidity and mortality in all age groups.
At present, there is no effective treatment to restore the permanent effects of
primary head injury, and treatment is aimed at reducing the secondary effects of
head injuries that can occur as a result of ischemic, hypoxic and increased
intracranial pressure. Understanding the epidemiology of head injuries is useful for
preventive action, planning primary preventative strategies based on population to
improve effective and efficient treatment, including the provision of rehabilitation
facilities for those affected by head injuries.

Neuropathological changes are related to a number of factors, including the

type and severity of the injury, as well as the scars that can occur as a result of blunt
or sharp injuries that can be both thorough or local. The pathology of head injury is
also influenced by patient factors such as age, comorbidities, alcohol, hypoxia,
sepsis, and treatment.

Rapid and accurate clinical management is very crucial. Primary treatment

must always be aimed at the airway (breathing), breathing (breathing) and
circulation (circulation) in accordance with the principles of ATLS. The most
important thing is not only to authenticate life-threatening head injuries but also to
prevent secondary head injuries. The cervical bone must be immobilized because
there is a possibility of injury. The level of consciousness and size and pupillary
response must be checked periodically in patients with this head injury.

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 CHAPTER II

LITERATURE REVIEW

2.1. Definition

Head trauma is a mechanical trauma to the head both directly and

indirectly that causes neurological dysfunction, that is physical, cognitive,
psychosocial function both temporarily and permanently.1

2.2. The Rules Of Monroe-Kellie

The Monroe-Kellie doctrine states that the total volume in the cranium is
always constant because the cranium are not elastic so they cannot expand if
there is additional volume. In normal conditions, the intracranial volume
consists of 80% brain tissue, 10% LCS, and 10% blood. Increasing the volume
of one of these components, or the addition of pathological components (eg
intracranial hematomas), will result in compensation through decreasing the
volume of other components to maintain pressure.2,3

If there is an additional period such as a hematoma, it will cause the CSF

to be displaced through the foramen magnum towards the sub-arachnoid cavity
and the veins will immediately collapse, where the blood will be squeezed out
of the intracranial space through the jugular vein or through the emisaria vein
and scalp. This compensation mechanism only lasts to a certain extent.
However, if this compensation mechanism is exceeded, a slight increase in
volume will cause an increase in intracranial pressure. 2,3

With increased blood flow to the blood vessels of the brain, intracerebral
hemorrhage will increase in volume, so that it can push or suppress the brain
mass. A normal brain has the ability to autoregulate cerebral blood flow.
Autoregulation guarantees constant blood flow through the cerebral vessels
above the perfusion pressure range by changing the diameter of the blood
vessels in response to cerebral perfusion pressure. Factors that change the
ability of cerebral vessels to contract and dilate, such as ischemia, hypoxia,
hypercapnia, and brain trauma can interfere with autoregulation. 2,3

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 Carbon dioxide is the most potential vasodilator in the cerebral vessels,
causing an increase in cerebral blood flow which results in an increase in
intracranial volume, leading to an increase in intracranial pressure. For
autoregulation to function, carbon dioxide levels must be within acceptable
limits and pressures within limits: cerebral perfusion pressure above 60 mmHg,
mean arterial pressure below 160 mmHg and systolic pressure between 60-160
mmHg and, ICT below 30 mmHg. Brain injury can also damage autoregulation.
When autoregulation is damaged, cerebral blood flow fluctuates with regard to
systemic blood pressure. In patients with autoregulatory damage, any activity
that causes blood pressure, such as coughing, suctioning, and anxiety can cause
increased cerebral blood flow which can increase intracranial pressure.2,3

The brain is able to compensate for or accept minimal changes in

intracranial pressure by transferring cerebrospinal fluid into the spinal
subarachnoid space, increased absorption of cerebrospinal fluid, decreased the
cerebrospinal fluid formation and transfer of venous blood out of the cranium.
2,3

Figure 1. Intracranial pressure will remain normal with increasing volume

until the decompensation point is reached. Above this critical volume,
intracranial pressure will increase rapidly

Brain blood flow is normally 50 - 60 mL / 100 gr brain tissue / minute.

When the brain's blood flow decreases to 20-25 mL / 100gr / minute, the Electro
Encephalographic activity will disappear and at a value of 5 mL / 100gr /
minute, brain cells die and permanent cell damage occurs. In non-traumatized
patients, the phenomenon of autoregulation maintains blood flow at a constant

3
level if the MAP (mean arterial pressure) is in the range of 50-160 mmHg. If
the MAP is below 50 mmHg, cerebral blood flow is greatly reduced and if the
MAP is above 160 mmHg passive dilatation of blood vessels causes blood flow
to increase.3,4

The mechanism of autoregulation is often disrupted in patients with

secondary brain injury due to ischemia due to sudden hypotension. Once the
compensation mechanism does not work will be followed by a steep rise in
intracranial pressure, brain perfusion will be reduced considerably especially in
a state of hypotension. Therefore, if there is an intracranial hematoma, it must
be removed as early as possible and adequate blood pressure must be
maintained.3,4

2.3. Classification

Classification of head injuries based on:

a. Pathology:
 Cerebral Komosio
 Cerebral contusions
 Cerebral laceration
b. Location of the lesion:
 Diffuse lesions
 Vascular damage to the brain
 Focal lesions
i. Contusion and cerebral laceration
ii. Intracranial hematoma:
a) Extradural hematoma (epidural hematoma)
b) Subdural hematoma
c) Intraparenkhimal hematoma (Subarachnoid hematoma,
Intracerebral hematoma, Intraserebellar hematoma)
2.4. Epidemiology

In the United States, the incidence of head injuries every year is estimated
at 500,000 cases. Of these, 10% died before arriving at the hospital. Arriving at

4
the hospital, 80% were classified as minor head injuries, 10% included
moderate head injuries, and the remaining 10% were severe head injuries. The
incidence of head injuries mainly occurs in the productive age group between
15-44 years. Traffic accidents are the cause of 48% -53% of head injury
incidents, another 20% -28% due to falls and another 3% -9% due to acts of
violence, sports, and recreational activities.5

Epidemiological data in Indonesia do not yet exist, but data from one of
the hospitals in Jakarta, Cipto Mangunkusumo Hospital, for inpatients, there are
60% -70% with minor head injuries, 15% -20% moderate head injuries, and
around 10% with a severe head injury. The highest mortality rate is around 35%
-50% due to CKB, 5% -10% CKS, whereas for CKR no one has died.

Surgery in CKB cases is only performed in a small proportion of patients

(<5%) for example in subdural hematomas and epidural hematoma with brain
stem function that is still good.

Head injuries occur at all ages, but the peak is in young adults between
the ages of 15 and 24. Head injuries are the leading cause of death among people
under the age of 24. Men have an incidence of three or four times more often
than women. The main causes of brain injury are different in different parts of
the United States; in all regions, prominent motor vehicle accidents, and in
metropolitan areas violence often occurs.1

The causal relationship between the mechanism of injury and head injury
is complicated, for example, older people who have a higher incidence of falls
than other ages. Maybe the side effects of drugs, hearing, and vision are less,
the slow response to an event, balance, and mobility are the effects of injury.6

2.5. Pathophysiology
2.5.1. Cranial Fracture

Skull fractures can be divided into linear, depressed, or comminuted

types. If the scalp is torn, it is considered an open or compound fracture.
skull fracture is an important marker of serious injury, but rarely has the
potential to cause problems by itself, the prognosis depends more on the

5
nature and severity of the injury to the brain than the severity of the skull
injury.

Sekitar 80% fraktur bersifat linier. Sebagian besar terjadi di daerah

temporoparietal, di mana sisi tengkorak menipis. Deteksi fraktur linear
sering menimbulkan kecurigaan cedera otak serius, tetapi hasil CT-Scan
pada kebanyakan pasien dinyatakan normal. Fraktur tengkorak linier
umumnya tidak memerlukan intervensi bedah dan dapat dikelola secara
konservatif.

In a depressed fracture from the skull, one or more bone fragments

are depressed, compressing the main part of the brain. In comminuted
fractures, there are some broken bone fragments that may or may not be
compressed inward. In 85% of cases, open depressed fractures can become
infected, or CSF leak occurs. In some patients, depressed skull fractures are
associated with tears, compression, or thrombosis of the underlying dural
sinus veins.

Basilar skull fractures may be linear, depressed, or comminuted

which are often missed by Schedel's Photos and are best identified by CT-
Scan. There may be nerves associated with skull or dural veins that can
cause complications of meningitis if bacteria enter the subarachnoid space.
Signs that lead us to suspect temporal bone fractures include
hemotympanum or tympanic perforation, hearing loss, CSF otorrhea,
peripheral facial nerve weakness, or ecchymosis of the scalp. The state of
lack of smell, bilateral periorbital ecchymosis, and CSF rhinorrhea are likely
sphenoid, frontal, or ethmoid fractures.

2.5.2. Diffuse Axonal Injury

Diffuse Axonal Injury is one of the common and important

pathological conditions in Traumatic Brain Injury (TBI). Axon sensitivity
to mechanical injury seems to be due to its viscoelastic nature and high
pressure in the white matter channel. Although under normal circumstances
axons are flexible but will become fragile if deformations are directly

6
related to brain trauma. Thus, axon travel can rapidly damage the axonal
cytoskeleton which can result in loss of elasticity and a decrease in the value
of axoplasmic transport. Furthermore, swelling of axons occurs in discrete
bulb formations or in elongated varicosities that cause protein buildup.
Calcium that enters the swelling axons causes further damage due to
protease activation. Eventually, swollen axons can break up and contribute
to additional neuropathologic changes in brain tissue. Diffuse Axonal Injury
is largely likely a clinical manifestation of brain trauma.

2.5.3. Coup and Contra Coup Injury

Coup Injury is violence that occurs suddenly that causes the brain to
press quickly forward and hit the side of the skull. Contracoup injury occurs
on the other side when the brain presses rapidly forward and hits the side of
the skull, and then bounces off the other side of the skull. In both cases, the
brain was damaged due to a collision on the inside of the skull.

A bruise on a coup injury will occur at the site of the impact.

Whereas contra coup occurs on the other side, bruises will appear on the
opposite side from the impact site. A brain that experiences a very hard
collision and can suddenly experience a coup and contra coup injury
simultaneously.

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 2.5.4. Cerebral Komosio

If a head injury results in a temporary disruption of cerebral function

in the form of decreased consciousness (syncope/coma, retrograde amnesia)
in the absence of bloody parenchymal lesions in the brain, it is classified as
cerebral comosio. Recent discoveries mention a coma of less than 20
minutes, brief retrograde amnesia, no brain defects, and hospital treatment
of fewer than 48 hours including this group. Usually do not require special
therapy, as long as there are no complications such as hematoma, cerebral
traumatic edema, etc. Patients really need absolute rest, cardiovascular
balance power, respiration, an electrolyte fluid, and calories, and avoid lung
or bladder infections. Mobilization is almost not a problem.11

2.5.5. Cerebral Contusions

If there is a bloody parenchymal lesion, which is characterized by a

longer decreased consciousness. Neurological deficits such as hemiparetic
cerebral nerve paralysis, abnormal reflexes, convulsions, and delirium.

Cerebral contusion is a bruise in the brain tissue due to trauma. Like

bruises in other tissues, cerebral bruises can be associated with several
micro-hemorrhages, resulting from a small PD leakage into brain tissue.
Bruising occurs in 20-30% of cases of severe head injury. This injury is
similar to brain laceration, by definition, where the pia arachnoid membrane
is torn above the site of injury in the laceration and not bruised. This injury
can cause mental function decline in the long term and in an emergency can
cause brain herniation, a life-threatening condition where there is a part of
the brain that presses to the part of the head bone. Therefore treatment aims
to prevent a dangerous increase in intracranial pressure.

2.6. Sign and Symtomps

The symptoms of bruising on the brain depend on the severity of the

injury, from mild to severe. Individuals may experience headaches, confusion,
drowsiness, dizziness, loss of consciousness, nausea and vomiting, seizures, and
difficulties with coordination and movement. They also may have difficulty

8
with memory, vision, speech, hearing, managing emotions, and thinking
processes.5

Bruises sign that depends on locations in the brain. Cerebral contusion is

very common in the frontal and temporal lobes, although it also occurs in every
part of the brain, including the brain stem and cerebellum. Cerebral contusions
can occur within a few days or hours of evolution to form intracerebral
hemorrhage. If the lesion is widespread and further neurologist deviations
occur.

2.7. Diagnosis
2.7.1. Anamnesis

The state of the accident and the patient's clinical condition before
entering the emergency room must be ascertained from the patient (if
possible), and eyewitnesses. The strength and location of the head injury
must be determined as precisely as possible. Specific questions must also be
made regarding concussions; because the patient is amnestic during a
concussion, only an eyewitness can accurately measure the duration of loss
of consciousness. History includes; capitis trauma with / or without
impaired consciousness or with lucid intervals, bleeding/otorrhea/
rhinorrhea and traumatic amnesia. 1,7

A. Mild Head Injury: 1.9

a. GCS 13-15
b. Syncope <10 minutes
c. Neurological deficits (-) only functional disorders
d. Normal CT scan
B. Moderate Head Injury
a. GCS 9-12
b. Syncope> 10 minutes to <6 hours
c. Neurological deficits (+)
d. CT scan is abnormal

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C. Severe Head Injury
a. GCS 3-8
b. Syncope> 6 hours
c. Neurological deficits (+)

d. CT scan is abnormal

iii. Physical and Clinical Neurological Inspection

General physical examination from head to foot. Abnormalities can

be found according to the impact of the injury on the brain. The skull must
be palpated for 13 fractures, hematomas and wounds. The patient must be
thoroughly examined for external signs of neck, chest, back, stomach and
limb trauma. bleeding from the nose or ears may indicate CSF leak; Bloody
CSF can be distinguished from the blood through a positive halo test (ie, a
CSF circle in the form of blood when it falls on a piece of white cloth). If
there is no blood mixture, CSF can be distinguished from nasal secretions
because the CSF glucose concentration is 30 mg / dL or more, whereas
lacrimal secretions and nasal mucus usually contain less than 5 mg / dL
glucose.

After determining the level of awareness. Special attention must be

paid to the ability to focus, concentrate (for example, count down from 20
to 1, or read in reverse), orientation, and memory. Eye movements, pupil
size and shape, and reactions to light must be noted. Reactive or dilated
pupils show transtentorial herniation with third cranial nerve compression.
Pupillary mid-position, less reactive, irregular can occur due to injury to the
oculomotor nucleus in the midbrain tegmentum. Nystagmus often occurs
concussion. In comatose patients, the oculocephalic and oculovestibular
reflexes must be tested. The motoric examination must focus on identifying
weaknesses, asymmetries or attitudes. Spontaneous movements must be
assessed to assess the specific use of limbs on one side. If the patient is not
fully cooperative, weakness can be detected by assessment of the
asymmetry of the tone or tendon reflex, or by an arm shift, the response of
special localization by rubbing the sternum, or plantar reflex extensors.

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 Jika kerusakan terjadi di lobus frontal, fungsi intelektual,
kepribadian, dan kelemahan otot akan berkurang. Lobus temporal
mengalami masalah bicara, pendengaran dan memori. Jika lobus parietal
terganggu, pasien akan mengalami gangguan sensibilitas. Jika kerusakan
pada lobus oksipital pasien akan mengeluh gangguan penglihatan dan
batang otak adalah tempat untuk mengatur denyut nadi, pernapasan, dan
tekanan darah.

2.7.2 Supporting Inspection

a. Laboratorium
Laboratory tests carried out when the patient first enters the hospital
and when monitoring is like a blood test; Hemoglobin, leukocytes, platelets
to determine ballast factors that accompany bleeding. Ureum, creatinine to
determine liver function due to bleeding or to interfere with drugs that will
be excreted through the kidneys. Blood sugar while also needed to
determine the factors that can exacerbate the impact of injury or presence of
comorbid disease. Blood Gas and electrolyte analysis should also be

11
checked to assess the presence of acidosis or alkalosis which can occur due
to the impact of injury, hypoventilation for example.

b. Radiology
i. Schedel X-Ray
Schedel X-Ray with various positions such as AP, lateral is useful
to see the skull fracture but does not show soft tissue in the
head.1,7

ii. CT-Scan and MRI

CT is the emergency imaging method of choice for head injuries.

CT is more informative than standard skull radiographs and
provides sensitivity for detecting intracranial blood. In general,
all patients with head injuries must have CT, except for those
classified as low risk (for example, without a concussion, without
neurological abnormalities on examination, and without evidence
or suspicion of a skull fracture, alcohol or drug poisoning, or
moderate risk criteria other). The possibility of detecting intra-
cerebral hemorrhage by CT in these patients is only 1 in 10,000.

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MRI is better for detecting subtle brain injuries, especially for
focal lesions, but is generally not used for emergency evaluation
unless quickly and easily available. CT images should be assessed
for evidence of epidural or subdural hematoma, subarachnoid or
intraventricular, parenchymal bruising and bleeding, brain
edema, and bruising associated with diffuse axonal injury. 1,6,7,8

Figure 2.1. CT-Scan of the epidural hematoma

Figure 2.1. Epidural CT Scan

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 Figure 2.1. CT Scan of Arachnoid Hematoma

2.8 Classification of Glassglow Coma Scale

Visual
1 Open spontaneously
2 With verbal commands
3 With pain
4 No response
Verbal
1 Good orientation
2 Disorientation is not good
3 Inappropriate words, just crying
4 Groaning
5 No response
Motoric
1 According to the order
2 Can localize pain
3 Flexion to pain
4 Abnormal flexion (decortication)
5 Extension (deserebration)
6 No response

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2.9 Treatment
Emergency treatment according to the severity of capitis trauma (mild,
moderate, severe) based on the order:
2.9.1 Primary Survey
a. Airways
Free the airway by checking the mouth, if there is a secret or
foreign object immediately removed by suction or swab. If
necessary, intubation can be used to maintain airway patronization.
Beware if there is a cervical fracture.
b. Breathing
Ensure adequate breathing, pay attention to the frequency, the
pattern of breathing and chest or abdominal breathing and the
equality of right and left chest development. If there are respiratory
disorders immediately find the cause, interference occurs at the
central or peripheral. If necessary, give oxygen as needed. Maintain
oxygen saturation O¬2> 92%
c. Circulation
If the patient shows signs of hemodynamic instability, the IV line
must be installed immediately. Because autoregulation of cerebral
blood flow is often disrupted in acute head injuries, it must be
constantly monitored to avoid hypotension which can cause
ischemic brain or hypertension which can worsen cerebral edema.
Maintain systolic BP> 90 mmHg, avoid using hypotonic fluid.
Short-acting vasopressors (for example, phenylephrine and
norepinephrine) and antihypertensive agents (for example, labetalol
and nicardipine) are better because of their ability to stabilize blood
pressure in a narrow therapeutic range. Nitroprusside sodium must
be avoided because it can dilate the cerebral vessels and increase
ICP.1,7

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 d. Disability (to find out lateralization and general and neurological
conditions)
Observation:
 Vital signs: blood pressure, pulse. Temperature, and
breathing
 GCS
 Pupils: the size, shape, and reflex of the light
 Rapid neurological examination: hemiparesis, pathological
reflex
 Injuries
 History: AMPLE (allergies, Medication, Past Illness, Last
Meal, event/environment related to the injury)
2.9.2 Secondary Survey
 Laboratorium
- Blood test: hemoglobin, leukocytes, platelets, creatinine
urea, blood sugar at a time, blood gas analysis and
electrolytes
- Urine test: bleeding
 Radiology
- Head X-Ray
- Head CT scan
- Other X-Ray as indicated
 Treatment Management
- Prepare for surgery on patients who have an indication
- Prepare an intensive room
- Wound Management

- Provision of drugs as needed

2.9.2.1 Mild Head Injury Treatment Management

A. Examination of general status and neurology
B. Wound care

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 C. The patient is discharged with close supervision by the family for
48 hours. If during the house there are things as follows:
a. Patients tend to be sleepy
b. Increasingly severe headaches
c. Projectile vomiting
Then the patient must be brought back to the hospital immediately
D. Patients need to be treated if there are any of the following:
a. Orientation disorder (time and place)
b. Headache and vomiting
c. No one is watching at home

d. The location of the house is far away or difficult to return

to the hospital

2.9.2.2 Moderate dan Severe Head Injury Treatment Management

A. Continue handling ABC
B. Monitor vital signs (temperature, pulse, breathing, blood
pressure), GCS pupils, limb movements, until the patient is
conscious
C. monitoring is carried out every 4 hours
D. monitoring time is up to GCS 15.
Special attention is intended to prevent hypotension.
Traumatic Coma Data Bank Data (TCDB) shows that
hypotension in patients with severe craniocerebral trauma will
increase mortality from 27% - 50% (Wilkins, 1996). Traditional
management which includes limitation of fluid in reducing the
occurrence of brain edema is likely to be dangerous for patients,
especially in patients who have had a lot of fluid loss.
E. Avoid the following conditions:
a. Systolic blood pressure <90 mm Hg
b. Temperature> 38°C
c. Breathing frequency> 20 x / minute
F. Prevent the possibility of intracranial high pressure
a. The head is raised 30°C

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 b. If necessary, can be given 20% Manitol. The initial dose
is 1 gr/kg BW, give in 1/2 - 1 hour, fast drip. Continue
giving at a dose of 0.5 gr/kg body weight fast, 1/2 - 1
hour.
c. Provide analgesics, and if necessary short-term sedation
can be given
d. Overcome complications such as seizures by
prophylactic OAE for 7 days to prevent immediate and
early seizures
i. In cases of the high risk of infection due to basis
cranii fracture / open fracture give antibiotic
prophylaxis, according to the dose of intracranial
infection for 10-14 days.
ii. Gastrointestinal - gastric bleeding
iii. Fever
iv. DIC: patients with closed capitis trauma tend to
experience acute coagulopathy.
v. Adequate fluids and nutrition

vi. Roboransia, neuroprotectant (citicoline),

nootropic as indicated

2.9.3 Operation Indication

A. EDH (epidural hematoma)
a. 40 cc + midline shifting on temporal / frontal / parietal
with brain stem function is still good
b. > 30 cc in the posterior fossa with signs of brain stem
suppression or hydrocephalus with brain stem function is
still good
c. Progressive EDH
d. Slight EDH with decreased awareness is not an indication
of surgery.

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B. SDH (Subdural Hematoma)
a. Expansive SDH (> 40 cc /> 5 mm) with GCS> 6, brain
stem function is still good
b. Thin SDH with decreased awareness is not an indication
of surgery
c. SDH with cerebral edema / cerebral contusions
accompanied by midline shifts with good brain stem
function
C. ICH (Intracerebral Hematoma)
a. Progressive decreased awareness
b. Hypertension and bradycardia and signs of breathing
problems (Cushing reflex)
c. Worsening focal neurological deficits
D. Cranial fracture with cerebral laceration
E. Opened cranial fracture (prevention of intracranial infection)
F. Severe cerebral edema accompanied by signs of increased ICP
considered decompression surgery

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