Syahrul

Department of Neurology
Faculty of Medicine
Syiah Kuala University
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The nervous system is composed of
Brain
Spinal cord
The nervous system is divided into:
Central nervous system (Brain & Spinal Cord)
Peripheral nervous system

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Scalp
Blood supply
Calvaria
Brain
Occupies 80% of
calvarium
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Cerebral Blood Flow (CBF)
Main Arterial Pressure (MAP)
Intracranial Pressure (ICP)
Cerebral Perfusion Pressure (CPP)
CPP = MAP ICP
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Scalp injuries
Skull injuries
Brain injuries
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Scalp has many blood vessels so injury may
bleed profusely.
Control bleeding with direct pressure.
Dont apply pressure when there is possible
skull injury.
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It include fractures to
the cranium and the
face, can be associated
with brain injury.
It is divided into:
Open skull fracture:
cranium is fractures and
scalp is lacerated.
Closed skull fracture:
scalp is lacerated but
cranium is intact.
Basal skull fracture

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Primary (Direct) Brain Injuries
Secondary (Indirect) Injuries
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It occur at the time of original insult
Direct damage done to brain parenchyma
and associated with vascular injuries
Brain tissue can be lacerated, punctured or
bruised by broken bones or foreign bodies
Damage is already done
Irreversible
Damage control (debridement)
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Damage that occurs after the initial insult
(ongoing injury processes)
Expanding mass lesions, swelling or bleeding
quickly overwhelm buffers
End result is increased intracranial pressure
(ICP) and/or herniation
Diagnosis and treatments target minimizing
the effects of these indirect insults
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Usually caused by blunt injuries.
Injuries patient shows transient alteration in
neurologic function
Mild injury usually with no detectable brain
damage.
May have brief loss of consciousness.
Headache grogginess and short memory loss
are common.
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A bruised brain or contusion can occur with
closed head injuries.
Usually caused by blow that causes the brain
to hit inside the skull
Unconsciousness or decreased level of
consciousness can occur
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Is a collection of blood within tissue.
Hematoma inside the cranium is named
according to its location:
Subdural hematoma: blood collection between
brain and dura
Epidural hematoma: blood collection between
dura and the skull
Subarachnoid Hemorrhage:
Intracerebral hematoma: blood collection within
the brain
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Mild injury
0-20 minute loss of consciousness GCS = 13-15
PTA < 24 hours
Moderate injury
20 minutes to 6 hours LOC GCS = 9-12
Severe injury
> 6 hours LOC GCS = 3-8
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primary brain injury causes
variable degrees of neuronal
death
occurs at the time of the injury
focal lesion
diffuse injury
exacerbated by secondary
events that lead to secondary
brain injury
Pathophysiology of brain injury
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structural damage
cerebral ischaemia
reduction in oxygen delivery below critical
thresholds
Pathophysiology of brain injury
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ischaemic insults occur frequently
90% patients have histological evidence of neuronal ischaemia
Graham et al, J Neurol Neurosurg Psychiatr 1989;52:346
antemortem evidence of ischaemia elusive
CBF < 18 ml/100g/min in 30% patients
arterio-venous oxygen differences relatively low
Bouma et al, J Neurosurg 1991;75:685-93
anaerobic glycolysis is not always accompanied by high
OEF values
suggest other/novel pathophysiological mechanisms
Wu et al, Neurosurgery 2004; 55: 1306-15
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structural damage
cerebral ischaemia
reduction in oxygen delivery below critical
thresholds
initiation of complex biochemical
mechanisms
profound energy crisis
mitochondrial impairment/failure &
reduced ATP production
inability to utilise delivered oxygen &
glucose
irreversible axonal & neuronal
damage
Pathophysiology of brain injury
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secondary brain damage
ionic, metabolic, immunological & inflammatory
changes
renders the brain more susceptible to secondary
insults
irreversible neuronal damage or death
secondary insults
systemic & intracranial changes
hypoxaemia, hypotension, hyperthermia
raised intracranial pressure
fatally damage susceptible neurones
Maas et al, Curr Opin Crit Care 2000;6:281
Secondary brain injury
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prevention or treatment of secondary insults to
minimise ischaemic brain injury
likely that specialist neurocritical care, with goal
directed therapy, might improve outcome
Smith, Brit J Anaesth 2004;93:735
management practices undergone extensive revision
longstanding and established practice not as efficacious or
innocuous as believed
Intensive care management
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ICP
Impaired brain metabolism
- Brain tissue hypoxia
- Cell energy dysfunction
Standard Monitoring - Tip of the Iceberg
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Brain Herniation
Four Types
Uncal Transtentorial
Central Transtentorial
Cerebellotonsillar
Upward Posterior Fossa

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Blood beneath the
dura, overlying the
brain and arachnoid,
resulting from tears
to bridging vessels
Crescent shaped
density that may run
length of skull
Very common in the
elderly
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Blood between
inner table of the
skull and the dura
Lens shaped
hematomas that
do not cross suture
lines on CT
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Focal areas of
hemorrhage
within the
parenchyma
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Bleeding beneath the
arachnoid membrane
on the surface of the
brain.

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Karakteristik CK Tertutup CK Terbuka
Etiologi Trauma Lalu Lintas,
Pukulan-Benturan
Luka Bacok,
Tembak,
Trauma Lalu
Lintas
Klinis CK Ringan,
CK Sedang,
CK Berat
Terdapat
hubungan
intrakranial
dengan dunia luar
(keluar LCS)
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No GCS Diagnosis Klinis
1 GCS = 13 15
Kesadaran Menurun <30; PTA <30
Cedera Kranioserebral Ringan
PA. Komosio Serebri
2 GCS = 9 12
Kesadaran Menurun 30-6 jam
Cedera KranioserebralSedang
PA. Kontusio Serebri Sedang
3 GCS = 3 8
Kesadaran Menurun >6jam
Cedera KranioserebralBerat
PA. Kontusio Serebri Berat

Catatan : Diagnosis klinis akan berubah menjadi Cedera
Kranioserebral Berat, jika pada CT scan kepala ditemukan
perdarahan.
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Akselerasi
Deselerasi
Rotasi
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Eye Opening E
Spontaneous 4
To loud voice 3
To pain 2
None 1
Verbal Response V
Oriented 5
Confused, Disoriented 4
Inappropriate words 3
Incomprehensible words 2
None 1
Motor Response M
Obeys commands 6
Localizes pain 5
Withdraws from pain 4
Abnormal flexion posturing 3
Extensor posturing 2
None 1
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GCS : E4M6V5 = 15
GCS : E1M1V1 = 3

Perhatikan :
GCS : E brill hematoma
M tetraparesis/tetraplegia
V afasia
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GEJALA DAN TANDA
Patofisiologi : terputusnya arteri
meningea media (tersering)
Riwayat truma kepala
Terdapat kesadaran menurun,
PTA
Lucid interval
Hemiparesis masif
Reflek patologi satu sisi atau dua
sisi
Pupil anisokor
Bradikardi relatif
Penunjang : Foto kepala dan CT
Scan kepala
Tatalaksana :
ABC
Operatif : luas perdarahan, lokasi
perdarahan
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Mortality/Morbidity
Reported mortality rates range from 5-43%.
Higher rates are associated with the following:
Advanced age
Intradural lesions
Temporal location
Increased hematoma volume
Rapid clinical progression
Pupillary abnormalities
Increased intracranial pressure (ICP)
Lower Glasgow coma scale (GCS)

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Fewer than 20% of patients demonstrate the classic presentation
of a lucid interval between the initial trauma and subsequent
neurological deterioration. Following injury, the patient may or
may not lose consciousness. If he or she becomes unconscious,
the patient may awaken or remain unconscious.


Other symptoms include the following:
Severe headache
Vomiting
Seizure
Patients with posterior fossa epidural hematoma may have a
dramatic delayed deterioration. The patient can be conscious and
talking and a minute later apneic, comatose, and minutes from
death.




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Physical
Cushing response, consisting of the following, can indicate increased ICP:
Hypertension
Bradycardia
Bradypnea
Level of consciousness may be decreased, with decreased or fluctuating
GCS.
Contusion, laceration, or bony step-off may be observed in the area of
injury.
Dilated, sluggish, or fixed pupil(s), bilateral or ipsilateral to injury,
suggest increased ICP or herniation.
Classic triad indicating transtentorial herniation consists of the following:
Coma
Fixed and dilated pupil(s)
Decerebrate posturing
Hemiplegia contralateral to injury with herniation may be observed.

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Symptoms
Certain symptoms suggest a fracture at the base of
the skull:
Cerebrospinal fluidthe clear fluid that flows over the
surface of the brain between the meningesmay leak
from the nose (rhinorrhea) or ears (otorrhea).
Blood may collect behind the eardrum, or if the
eardrum is ruptured, blood may drain from the ear.
Bruises may develop behind the ear (Battle's sign) or
around the eyes (Raccoon's eyes).
Blood may collect in the sinuses, which may also be
fractured.

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Diffuse axonal injury is widespread injury to
axons, a part of the nerve cells in the brain.
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A new classification of head injury based primarily on information gleaned from the initial
computerized tomography (CT) scan is described. It utilizes the status of the mesencephalic cisterns,
the degree of midline shift in millimeters, and the presence or absence of one or more surgical
masses. The term diffuse head injury is divided into four subgroups, defined as follows: Diffuse
Injury I includes all diffuse head injuries where there is no visible pathology; Diffuse Injury II includes all
diffuse injuries in which the cisterns are present, the midline shift is less than 5 mm, and/or there is no
high- or mixed-density lesion of more than 25 cc; Diffuse Injury III includes diffuse injuries with
swelling where the cisterns are compressed or absent and the midline shift is 0 to 5 mm with no high-
or mixed-density lesion of more than 25 cc; and Diffuse Injury IV includes diffuse injuries with a midline
shift of more than 5 mm and with no high- or mixed-density lesion of more than 25 cc. There is a direct
relationship between these four diagnostic categories and the mortality rate. Patients suffering
diffuse injury with no visible pathology (Diffuse Injury I) have the lowest mortality rate (10%), while the
mortality rate in patients suffering diffuse injury with a midline shift (Diffuse Injury IV) is greater than
50%. When used in conjunction with the traditional division of intracranial hemorrhages (extradural,
subdural, or intracerebral), this categorization allows a much better assessment of the risk of
intracranial hypertension and of a fatal or nonfatal outcome. This more accurate categorization of
diffuse head injury, based primarily on the result of the initial CT scan, permits specific subsets of
patients to be targeted for specific types of therapy. Patients who would appear to be at low risk
based on a clinical examination, but who are known from the CT scan diagnosis to be at high risk, can
now be identified.
Key Words Traumatic Coma Data Bank head injury coma intracranial pressure computerized
tomography grading system

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Category Definition Diffuse Injury
Diffuse Injury I
no visible intracranial pathology seen on (no visible CT scan
pathology)
Diffuse Injury II
cisterns are present with midline shift 05 mm and/or: lesion
densities present no high- or mixed-density lesion > 25 cc may
include bone fragments and foreign bodies
Diffuse Injury III
cisterns compressed or absent with midline (swelling) shift 05 mm,
no high- or mixed-density lesion > 25 cc
Diffuse Injury IV
midline shift > 5 mm, no high- or mixed-density (shift) lesion > 25 cc
evacuated mass lesionany lesion surgically evacuated non evacuated
masshigh- or mixed-density lesion > 25 cc, not lesion surgically
evacuated.

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