CHAPTER 1

A. TRODUCTO

Central nervous system (CNS) trauma is a signiIicant cause oI morbidity and
mortality all over the world. In USA,each year, 500,000 patients with head injury are
seen in the emergency department and oI these more than 50,000 die Irom their
injuries (1). Major cause oI this menace is cerebral ischemia that ensues minutes to
hours aIter the primary head injury. This is commonly known as secondary injury.
Head injury (HI) the so called "silent epidemic" is the leading cause oI death
and dissability in people above 40 years old. It importance regarding soncieconomic
and public health issues has been objet oI analysis and lead to a great number oI
epidemiologica publications |1,2,3,4| mainly in the seventies and eighties.
The objectives embedded in the management oI traumatic brain injury (TBI)
include limiting the primary damage and controlling secondary insults, which are
thrust upon the brain immediately aIter an accident. Applying the recommendations
oI evidencebased guidelines approved by the American Association oI Neurological
Surgeons attains these objectives. At the scene oI accident, airway support,
ventilation and oxygenation are strongly recommended in trying to keep the systolic
blood pressure (SBP) oI the patient at around 100 mmHg (monro )
Following a quick primary and secondary survey and appropriate
resuscitation, we must determine the numerical value oI the GCS score. Mild head
injury: GCS score 1315, moderate head injury: GCS score 912, severe head injury:
GCS score 48, and very severe head injury: GCS score 3.(monro )
Severe traumatic brain injury (TBI, GCS 8) occurs in 60 oI
polytraumatised children aIter car accidents or child abuse, and is associated with
high morbidity and mortality18,19. DiIIuse brain swelling and multiple cerebral
contusions are the most common cause oI death aIter severe head injury in pediatric
patients20. The primary therapeutic aim is to maintain an adequate cerebral blood
Ilow (estimated Irom cerebral perIusion pressure, CPP MAP-ICP, where MAP
1/3 systolic BP2/3 diastolic BP).

. A
O To know and understand about head injury, signs and symptoms, treatment and
complication oI head injury.
O To know and understand about intracerebral hemorrhage.























CASE REPORT

A. DETTY
Name : Tn.G
Age : 57 tahun
#eligion : Katholik
#ace : Dayak
ccupation : -
Address : Kutim
Hospitalized : 07 June 2011; 14.00

. AAESS
Chief complain : weakness in lower limb
History of disease :
Kelemahan anggota gerak bawah telah dirasakan pasien sejak 4,5 tahun
SM#S. Awalnya pasien merasakan nyeri pada daerah pinggang bawah bagian
belakang, yang lama kelamaan semakin meningkat hingga terjadi pembengkakan.
Beberapa bulan setelah itu, pasien mengeluhkan BAK berdarah disertai nyeri hingga
pasien harus dirawat di #S dan menggunakan kateter selama 14 bulan. 7 bulan
setelah keluhan itu, pasien
The patient came to IGD with alteration oI consciousness. Patient had Iallen
down Irom motorcycle and crashed the wall Irom Iront direction since 3 hour beIore
hospitalized. Patient didn`t used helmet. Patient doesn`t remember how he Ielt and in
what position. Patient was unconscious until hospitalized.there is vomit contain Iood
and didn`t spurt. There is otoraghie.

Physical examination :
General condition
Impression : look ill currently
Awarness : GCS E4V5M1

'ital sign
Blood pressure : 150/90 mmHg
Pulse Irequency : 84 x / menit
#espiratory rate : 22 x / menit
Temperature : 36,5
o
C (per axilar)

Generalis status
O Head/neck : normochepali, conjungtiva anemis (/), sklera ikterik (-
/), light reIlex (/), pupil isokor o 3 mm/3 mm, lesion (-).
O Thorax : hemithorax symetris, symmetrical movement oI breath lesion
(-)
Cor : S1 S2 single regular, murmur (-), gallop (-)
Pulmo : Vesikuler, #honki (-/-), Wheezing (-/-)
O Abdomen : Lesion (-), Ilat, soeIl, tympanic, bowel sound () normal
O Ektremitas : edema (-), warm

ocalis status
Lower extremity region :
Look : edeme (-), deIormity (-), muscle atrophy - -
-
Feel : crepitation (-), warm ()
Move : dissability

Genetalia region
Look : edema (-), blood (-), pus (-), hyperemi (), lesion ()
Fell : warm
Move : (-)


aboratory result :
8-6-2011
WBC 8.000
HGB 8,8
HCT 26,4
HCV
MCV
MCH
MCHC
#DW
PLT 484.000
MPV

Blood test
Leukocyt : 18.000
Hemoglobin : 15,5
Hematocryt : 46,9
Trombocyt : 260.000
BT : 2`
CT : 9`
GDS :200 mg/dl

Working diagnose : Multiple cystic meningioma Iornier disease



































1lme lollow up 1herapy
030910 S AlLeraLlon of conclousness
ulzzlness
C L2v2M3 8140/80 mmPg
93x/mlnuLe1382
8832x/mlnuLe llghL refleks
(+/+) pupll anlsokor 3
mm/4mm
C1 conLuslo cerebrl aL sub corLlcal
fronLal basal ganglla sln
8onLgen cervlcal A/LaL fracLure ()
dlslocaslLlon ()
lvlu u3 Z nS 2000 ml/24 hours
ManlLol 3x200cc
CefLrlaxon 2x1 ln[
kuLoln 3x1 ln[
AnLraln 3x1 ln[
8anlLldln 2x1 ln[
8raln acL 2x1 ln[
uleL sonde 6x30 ml
Pead up 30
0

040910 S unconclousness
CL1v2M48124/39n72x/mnL
8822x/mnL L39 llghL refleks (+/+)
pupll anlsokor 3mm/4mm rho (/)
whez (/)
1ramadol 3xl ln[
1reaLmenL conLlnuaLed
LvaluaLlon Pead C1 scan
1730 Pasll C1 evaluasl lCP basal ganglla
sln 70 cc mldllne shlfL 13 cm

- CranloLomy clLo
- Slo
- J8 3 kolf
- 8eporL Ck
030910 S unconclousness sedacum (+)
CL1vxM38116/6770x/mnL
8822x/mnL L363 pupll anlsokor
2mm/3mm
roduksl draln 600 cc
Pb
CefLrlaxon 2x1 ln[
kalnex 3x 2 gr ln[
AnLraln 3x1 ln[
8anlLldln 2x1 ln[
neuroLam 3x3 gr
uleL sonde 6x30 ml
1omorrow C1 scan
060910


fever (+) selzure ()
CCSL2vxM38173/88137x/mnL
8840x/mnL L39 pupll anlsokor
ConLlnue LreaLmenL
LxLra 8L 1000 ml/24 hours
larmadol 3x1






3mm/3mm ronchl /
k 28
1393
8onLgen Lhorax (+) dexLra
lnferlorlnfllLraL (+)volce of breaLh
Call drMa'rufSp8Sadvlse
Levofloxacln 1x1
Advlse dr8udlSp8S
lvlu u3 Z nS 18 Lpm naCl
09+kCL 13 Lpm
araceLamol 4x300 mg
Check elecLrolyLe Lomorrow
Call radlologl for MS C1 scan
Lrouble wlLh MS C1 scan devlce

070910 S fever (+)Selzure ()vomlLe ()
C L3vxM3 8130/70 97x/mnL
8830x/mnL L387 pupll lsokor
4mm/4mm ronchl +/
A SPl + lCP + nemonla

lvlu u3 Z nS 18 Lpm naCl
09+kCL 13 Lpm
kalbamln 300 mg
ManlLol 4x200 cc
Levofloxacln 1x1
neuroLam 3x3 gr
8anlLldln 2x1
kuLoln 3x1
CMZ 1x1
uleL 6x 30 cc
Medlxon 4x1
Semax 4x6 LLs
220910 S selzure () fever ()
C L4vxM3 mucous
Meronem 3x1
ConLlnued LreaLmenL
SucLlon LracheosLomy
230910 CCS L4vxM3 mucous ConLlnued LreaLmenL
SucLlon LracheosLomy
240910 CCS L4vxM3 CulLure mucous
uloLab 3x2 ml
ConLlnued LreaLmenL

230910 CCS L4vxM3 ConLlnued LreaLmenL








260910 S lever (+)
C 1 388

araceLamol Lab 300 mg
270910 S selzure () fever ()
C CCS L4v2M3 pupll lsokor
3mm/3mm 8130/80 84x/l
8822x/l 1 363
ConLlnued LreaLmenL
ShlLdown exerclse
280910 CCS L4v2M3 pupll lsokor
3mm/3mm 8140/80 84x/l
8822x/l 1 378
ConLlnued LreaLmenL
290910 Coughlng (+)
CCS L4v2M6 pupll lsokor
3mm/3mm 8130/80 80x/l
8820x/l
ConLunued LreaLmenL
300910 Coughlng
CCS L4v2M6 pupll lsokor
3mm/3mm 8130/90 88x/l
8824x/l
ConLlnued LreaLmenL
011010 CCS L4v2M6 pupll lsokor
3mm/3mm 8130/90 88x/l
8824x/l
ConLlnued LreaLmenL



























CHAPTER
COTET

A.Definition
A head injury is any trauma that leads to injury oI the scalp, skull, or brain.
The injuries can range Irom a minor bump on the skull to serious brain injury.
1

.Epidemiology
Head injury remains the leading cause oI death in trauma cases in Europe and
the USA, and accounts Ior a disproportionate amount oI morbidity in trauma
survivors. Worldwide, several million people, mostly children and young adults, are
treated each year Ior severe head injury.
2
In the United States, 1.5 million individuals per year incur a head injury. I
these injuries, 75 are classiIied as mild. Between 1998 and 2000, the incidence oI
mild traumatic brain injury was 503 cases per 100,000 persons, with a doubling oI
this incidence in Native Americans and children. In 2003, elderly persons with head
injuries exhibited a doubling in hospitalizations and deaths compared to the national
average.
3

In 1995, hospitalization Ior brain injuries decreased 50 compared to 1980
data, primarily because oI increased utilization oI outpatient services Ior patients with
minor head injuries.European rates oI hospitalization Ior head injury have ranged
Irom 91 cases per 100,000 persons per year in Spain in 1988 to 313 cases per 100,000
persons per year in Scotland Irom 1974-1976. In New Zealand, 782 cases per 100,000
oI mild head injury were seen in hospitals or emergency rooms in 1986.
3

C.Anatomy
1. The Cerebrum
The cerebrum is the largest part oI the human brain. The cerebrum,
consisting oI Iour paired lobes within two convoluted hemispheres, is concerned
with higher brain Iunctions, including the perception oI sensory impulses, the
instigation oI voluntary movement, the storage oI memory, thought processes,and
reasoning ability. The cerebrum is also concerned with instinctual and limbic
(emotional) Iunctions. The lobes oI cerebrum are Irontal lobe, parietal lobe,
temporal lobe, and occipital lobe.
4



















. The Cerebellum
The cerebellum is the second largest structure oI the brain. It occupies the
inIerior and posterior aspect oI the cranial cavity. The cerebellum is separated
Irom the overlying cerebrum by a transverse Iissure. A portion oI the meninges
called the tentorium cerebella extends into the transverse Iissure.
4
Figure 1. The Cerebrum
Figure 2. The Iunction oI Cerebral Lobes
The cerebellum consists oI two hemispheres and a central constricted area
called the vermis. The Ialx cerebelli is the portion oI the meninges that partially
extends between the hemispheres.
4

The principal Iunction oI the cerebellum is coordinating skeletal muscle
contractions by recruiting precise motor units within the muscles. Impulses Ior
voluntary muscular movement originate in the cerebral cortex and are coordinated
by the cerebellum. The cerebellum constantly initiates impulses to selective motor
units Ior maintaining posture and muscle tone. The cerebellum also processes
incoming impulses Irom proprioceptors within muscles, tendons, joints, and
special sense organs to reIine learned movement patterns. A proprioceptor is a
sensory nerve ending that is sensitive to changes in the tension oI a muscle or
tendon.
4











. Spinal Cord
The spinal cord is 18 in (45 cm)
long. It is continuous above with the medulla
oblongata at the level oI the Ioramen magnum and ends below at the lower level
oI the 1st, or the upper level oI the 2nd lumbar vertebra. InIeriorly, it tapers into
the conus medullaris Irom which a prolongation oI pia mater, the filum terminale,
descends to be attached to the back oI the coccyx.
5
Figure 3. The Cerebellum
In transverse section oI the cord is seen the central canal around which is
the H-shaped grey matter, surrounded in turn by the white matter which contains
the long ascending and descending tracts. Within the posterior horns oI the grey
matter, capped by the substantia gelatinosa, terminate many oI the sensory Iibres
entering Irom the posterior nerve roots. In the large anterior horns lie the motor
cells which give rise to the Iibres oI the anterior roots. In the thoracic and upper
lumbar cord are Iound the lateral horns on each side, containing the cells oI
origin oI the sympathetic system.




Impulses are conducted through the ascending and descending tracts oI
the spinal cord within the columns oI white matter.
5
a. Descending tracts
1. %he pyramidal (lateral cerebrospinal or crossed motor) tract. The motor
transverse section through a thoracic segment. pathway commences at the
pyramidal cells oI the motor cortex, decussates in the medulla, then descends
in the pyramidal tract on the contralateral side oI the cord. At each spinal
Figure 4. Spinal Cord
segment, Iibres enter the anterior horn and connect up with the motor cells
therethe tract thereIore becomes progressively smaller as it descends.
5

. %he direct pyramidal (anterior cerebrospinal or uncrossed motor) tract is a
small tract descending without medullary decussation. At each
segment,however, Iibres pass Irom it to the ventral horn (anterior) motor cells
oI the opposite side.
5


b. Ascending Tracts
1. The posterior and anterior spinocerebellar tracts ascend on the same side oI
the cord and enter the cerebellum through the inIerior and superior cerebellar
peduncles respectively.
5

2. The lateral and anterior spinothalamic tracts. Pain and temperature Iibres
enter the posterior roots, ascend a Iew segments, relay in the substantia
gelatinosa, then cross to the opposite side to ascend in these tracts to the
thalamus, where they are relayed to the sensory cortex.
5

3. The posterior columns comprise a medial and lateral tract, termed respectively
the fasciculus gracilis (of Goll) and fasciculus cuneatus (of Burdach). They
convey 1st order sensory Iibres subserving Iine touch and proprioception
(position sense), mostly uncrossed, to the gracile and cuneate nuclei in the
medulla where, aIter synapse, the 2nd order Iibres decussate, pass to the
thalamus and, aIter Iurther synapse, 3rd order Iibres are relayed to the sensory
cortex. Some Iibres pass Irom the medulla to the cerebellum along the inIerior
cerebellar peduncle.
5



D.Classification of head injury
1. Classification based on severity
Severity oI head injury is classiIied based on Glasgow Coma Scale (GCS).
Since its introduction in 1974, the GCS has been widely used as an initial
measure oI the severity oI brain injury. The scale incorporates neurological
Iindings such as voluntary movements, speech, and eye movements, into a 3- to
15-point scale. GCS allows measurement oI neurological Iindings, and it has been
used to predict immediate and long-term outcome aIter head injury.
2,6
ild head injury
GCS 14 to 15 is a mild head injury
oderate head injury
GCS 9 to 14 is moderate head injury
Severe head injury
GCS 8 to 3 is a severe head injury



Figure 5. Principal Ascending and Descending Tracts oI
Spinal Cord
Figure 6. Principal Ascending and Descending Tracts oI Spinal Cord
GASGOW COA SCAE
Eye Opening
4. spontaneous
3. to verbal command
2. to pain
1. no response
otor Response
6. beys verbal command
5. Localizes pain
4. withdraws to pain
3. Ilexion to pain
2. extension to pain
1. no response
'erbal Response
5. oriented
4. conIused
3. inappropiate words
2. non-spesiIic sounds
1. no response

. Classification based on mechanism
Penetrating trauma: Missiles such as bullets or sharp instruments (such as
knives, screwdrivers, or ice picks) may penetrate the skull. The result is called
a penetrating head injury. Penetrating injuries oIten require surgery to remove
debris Irom the brain tissue. The initial injury itselI may cause immediate
death, especially iI Irom a high-energy missile such as a bullet.
7

lunt head trauma: These injuries may be Irom a direct blow (a club or large
missile) or Irom a rapid deceleration Iorce (a Iall or striking the windshield in
a car accident).
7


. Classification based on orphology
Skull Fractures
inear skull fracture: A common injury, especially in children. A linear
skull Iracture is a simple break in the skull that Iollows a relatively straight
line. It can occur aIter seemingly minor head injuries (Ialls, blows such as
being struck by a rock, stick, or other object; or Irom motor vehicle
accidents). A linear skull Iracture is not a serious injury unless there is an
additional injury to the brain itselI.
7

Depressed skull fractures: These are common aIter IorceIul impact by blunt
objects-most commonly, hammers, rocks, or other heavy but Iairly small
objects. These injuries cause "dents" in the skull bone. II the depth oI a
depressed Iracture is at least equal to the thickness oI the surrounding skull
bone (about 1/4-1/2 inch), surgery is oIten required to elevate the bony pieces
and to inspect the brain Ior evidence oI injury. Minimally depressed Iractures
are less than the thickness oI the bone. ther Iractures are not depressed at all.
They usually do not require surgical treatment unless other injuries are noted.
7

asilar skull fracture: A Iracture oI the bones that Iorm the base (Iloor) oI
the skull and results Irom severe blunt head trauma oI signiIicant Iorce. A
basilar skull Iracture commonly connects to the sinus cavities. This
connection may allow Iluid or air entry into the inside oI the skull and may
cause inIection. Surgery is usually not necessary unless other injuries are also
involved.
7



ntracranial esions
Subdural hematoma: Bleeding between the brain tissue and the dura mater
(a tough Iibrous layer oI tissue between the brain and skull) is called a
subdural hematoma. The stretching and tearing oI "bridging veins" between
the brain and dura mater causes this type oI bleeding. A subdural hematoma
may be acute, developing suddenly aIter the injury, or chronic, slowly
accumulating aIter injury. Chronic subdural hematoma is more common in the
elderly whose bridging veins are oIten brittle and stretched and can more
easily begin to slowly bleed aIter minor injuries. Subdural hematomas are
potentially serious and may require surgery.
7

Epidural hematoma: The skull is made up oI a variety oI bones; the dura,
the thick membrane that wraps around the brain, attaches at the suture lines
where the bones come together. II bleeding occurs in the enclosed space
between the dura and the bone, and a hematoma (blood clot) Iorms, there is
nowhere Ior it to accumulate and pressure within the epidural space can build
quickly. The increasing pressure pushes the hematoma against the brain tissue
and may cause signiIicant damage.
7

Tiny epidural hematomas potentially may be observed without
surgery, but oIten surgery is indicated to removed the hematoma and relieve
the pressure on the brain. The earlier the operation, the better, because the
death rate increases iI the patient is in a coma at the time oI operation.
7

An epidural hematoma may oIten occur with trauma to the temporal
bone located on the side oI the head above the ear. Aside Irom the Iact that the
temporal bone is thinner than the other skull bones (Irontal, parietal,
occipital), it is also the location oI the middle meningeal artery that runs just
beneath the bone. Fracture oI the temporal bone is associated with tearing oI
this artery and may lead to an epidural hematoma.
7
Subarachnoid hemorrhage: Subarachnoid hemorrhage can be caused by
trauma and oIten does not require surgery. Blood accumulates in the space
beneath the arachnoid layer that surrounds the brain. While this can irritate the
brain and cause symptoms oI headache, vomiting, and stiII neck, treatment
may be watchIul waiting without surgery unless symptoms worsen.
7

ntracerebral hemorrhage/cerebral contusion: These terms describe
bleeding into the brain tissue itselI. A contusion is like a bruise to the brain
tissue and usually requires no special intervention, much like a concussion.
Most doctors admit people with cerebral (brain) contusion to the hospital Ior
observation since there may be rare complications such as brain swelling. An
intracerebral hemorrhage is a pool oI blood within the brain tissue. Minor
bleeding may stop without any treatment and cause no serious problems.
More serious or large bleeds usually require surgery.
7


E. Sign and Symptom
Head injury symptoms may also include: vomiting, diIIiculty
tolerating bright lights, leaking CSF Irom the ear or nose, bleeding Irom the
ear , speech diIIiculty, paralysis, diIIiculty swallowing, and numbness oI the
body. ther symptoms may be more subtle and include: nausea, dizziness,
irritability, diIIiculty concentrating and thinking, and amnesia. Late signs oI
signiIicant head injury and raised pressure within the brain and skull include a
dilated pupil, high blood pressure, low pulse rate, and abnormal breathing
pattern. Coma may be present iI the patient doesn't waken completely and is
deIined as a prolonged episode oI loss oI consciousness. There are diIIerent
levels oI coma, and the Glasgow Coma Scale is one way oI measuring its
depth.
7

F. Treatment of head injury
O In the setting oI acute head injury, give priority to the immediate
assessment and stabilization oI the airway, breathing and circulation.
O Following stabilization, direct attention to prevention oI secondary
injury. Keep mean arterial pressures above 90 mm Hg; arterial
saturations should be greater than 90. Urgent CT scanning is a
priority.
O #educing intracranial pressure, since elevated intracranial pressure is
an independent predictor oI poor outcome. II the intracranial pressure
rises above 20-25 mm Hg, intravenous mannitol, CSF drainage, and
hyperventilation can be used. Hypertonic saline has also been used in
lieu oI mannitol to lower intracranial pressure, but more deIinitive
studies are needed.

II the intracranial pressure does not respond to
these conventional treatments, high-dose barbiturate therapy is
permissible, despite the Iact that no evidence currently suggests that
barbiturate treatment actually improves outcomes.
O Improving cerebral perIusion pressure as opposed to intracranial
pressure in isolation. ne study reported that 80 oI patients with
severe head injuries experienced recoveries with no or little disability
aIter volume expansion, mannitol, CSF drainage, and vasopressors
were used to maintain a cerebral perIusion pressure oI at least 70 mm
Hg.

ther studies have Iound higher perIusion pressures were
associated with more complications and have recommended
maintaining a cerebral perIusion pressure oI 50-70 mm Hg.


O Head injury induces a hypermetabolic state and early nutritional
interventions may be as critical as cerebral perIusion pressure. Parental
or enteral Ieedings reduced mortality by at least 50 in one study
when given early in the course oI severe head injury.
O Anticonvulsant therapy
O Neuroprotective agents mostly have Iailed to improve the outcomes oI
patients with brain injury.
O For patients with minor head injuries, nothing more may be needed
other than observation and symptom control. Headache may require
pain medication. Nausea and vomiting may require medications to
control these symptoms.
O Intracerebral bleeding or bleeding in the spaces surrounding the brain
are neurosurgical emergencies, although not all bleeding requires an
operation. The decision to operate will be individualized based upon
the injury and the patient's medical status. ne option may include
craniotomy, drilling a hole into the skull or removing part oI one oI the
skull bones to remove or drain a blood clot, and thereby relieve
pressure on brain tissue.
O Supportive care is oIten required Ior those patients with signiIicant
amounts oI bleeding in their brain and who are in coma.
O Intubation to help control breathing and to protect them Irom vomiting
and aspirating vomit into the lungs.

G. ntracerebral Hemorrhage
Intracerebral hemorrhages are composed oI hemorrhagic areas within
the cerebral parenchyma, which may be as small as 1 mm or large enough to
involve the majority oI a cerebral hemisphere. More than 60 oI traumatic
intracerebral hemorrhages coexist with extracerebral hemorrhages, eg,
subdural, epidural, and subarachnoid hemorrhages. n occasion, traumatic
hemorrhages may extend into the subdural space, resulting in concomitant
subdural hemorrhages. The opposite can also occur.
8

















Figure 7. location oI intracerebral hemorrhage

1. Spontaneous ntracerebral Hemorrhage
Spontaneous intracerebral hemorrhage (SICH) is a blood clot that
arises in the brain parenchyma in the absence oI trauma or surgery.
Nontraumatic intracerebral hemorrhage is bleeding into the parenchyma oI the
brain that may extend into the ventricles and, in rare cases, the subarachnoid
space.
9
Advancing age and hypertension are the most important risk Iactors

Ior ICH. ICH occurs slightly more Irequently

among men than women and is
signiIicantly more common among

young and middle-aged blacks than whites
oI similar ages. #eported incidence rates oI ICH among Asian populations

are
also higher than those reported Ior whites in the United

States and Europe.
Pathophysiological change in small arteries

and arterioles due to sustained
hypertension is generally regarded

as the most important cause oI ICH.
Cerebral amyloid

angiopathy is increasingly recognized as a cause oI lobar
ICH in

the elderly.
10
ther causes oI ICH include vascular malIormations,

ruptured
aneurysms, coagulation disorders, use oI anticoagulants

and thrombolytic
agents, hemorrhage into a cerebral inIarct,

bleeding into brain tumors, and
drug abuse.
10

a. Pathologic Process
Intracerebral hemorrhages commonly occur in the cerebral lobes,
basal ganglia, thalamus, brain stem (predominantly the pons), and
cerebellum. Extension into the ventricles occurs in association with deep,
large hematomas. Edematous parenchyma, oIten discolored by
degradation products oI hemoglobin, is visible adjacent to the clot.
Histologic sections are characterized by the presence oI edema, neuronal
damage, macrophages, and neutrophils in the region surrounding the
hematoma. The hemorrhage spreads between planes oI white-matter
cleavage with minimal destruction, leaving nests oI intact neural tissue
within and surrounding the hematoma.This pattern oI spread accounts Ior
the presence oI viable and salvageable neural tissue in the immediate
vicinity oI the hematoma.
9


b. Origin of Hematoma
Intracerebral bleeding results Irom the rupture oI the small
penetrating arteries that originate Irom basilar arteries or the anterior,
middle, or posterior cerebral arteries. Degenerative changes in the vessel
wall induced by chronic hypertension reduce compliance and increase the
likelihood oI spontaneous rupture. In 1868, Charcot and Bouchard
attributed bleeding to rupture at points oI dilatation in the walls oI small
arterioles (microaneurysms). These morphologic entities were later Iound
to be subadventitial hemorrhages or extravascular clots resulting Irom
endothelial damage by the hematoma. Electron-microscopical studies
suggest that most bleeding occurs at or near the biIurcation oI aIIected
arteries, where prominent degeneration oI the media and smooth muscles
can be seen.
9


. Traumatic ntracerebral Hemorrhage
Patients with head trauma Irequently have soIt-tissue injuries at the
site oI impact. ther signs oI signiIicant head trauma include periorbital and
postauricular ecchymoses, hemotympanum, CSF otorrhea or rhinorrhea, and
Iacial Iractures. Associated injury to the spine and spinal cord may be
present.
8
Traumatic intracerebral hemorrhage is bleeding into the tissue oI the
brain caused by trauma to the head. This type oI bleeding can cause a
hematoma which expands inside the brain, pushing aside adjacent brain
tissue and compressing it. The term intracerebral basically means "within the
brain tissue"

a. Signs and symptoms
Clinical signs and symptoms oI intracerebral hemorrhage depend on
its size and anatomic location. Anterior Irontal cortical hemorrhages,
particularly on the nondominant side, may Iail to produce Iocal symptoms.
Cortical lesions located posteriorly, or large anterior lesions, produce Iocal
motor, and possibly sensory, deIicits on the contralateral side oI the body,
speech dysIunction, or contralateral visual Iield deIicits. Patients with
dominant temporal lobe lesions may present with speech dysIunction.
Bilateral hemispheric lesions can cause depression oI consciousness.
8
Signs and symptoms oI basal ganglia hemorrhage depend on the
extent and location oI subcortical damage and may include contralateral
motor and sensory deIicits.
8
Cerebellar hemorrhages present with nausea, vertigo, ataxia,
dysmetria, horizontal nystagmus, dysdiadochokinesia, or loss oI
consciousness secondary to tonsillar herniation with brainstem compression
or acute hydrocephalus Irom compression oI the Iourth ventricle.
Hydrocephalus is present in 16 oI patients with posterior Iossa traumatic
hemorrhage.
8
Patients with traumatic brain injury may initially have a good
neurologic exam but may deteriorate several hours to days aIter the initial
injury, as delayed or progressive intracerebral hemorrhage develops.
Adjacent contusions, edema, extracranial blood collections, or acute
hydrocephalus may contribute to the clinical deterioration.
8
b. eurologic findings: herniation and brainstem compression.
Acute traumatic hemispheric intracerebral hemorrhages rarely
present with transtentorial herniation . However, subsequent enlargement oI
the hemorrhage or an increase in the surrounding edema may produce
additional mass eIIect, with Iurther depression oI the level oI consciousness,
worsening oI motor or speech deIicits, and eventually ipsilateral
compression oI the midbrain and third nerve (maniIested by a nonreactive
dilated pupil) via temporal lobe herniation (uncal herniation). Temporal
hemorrhages greater than 30 cc in volume have a greater risk oI brainstem
compression than Irontal or parieto-occipital hemorrhages.
8



























ulSCuSSlCn

Aoomoesls
Case 1heory
O Chlef complaln of Lhls paLlenL ls back
paln weakness ln lower llmb and
splnchLer dlsLurbance slnce Lhree
years ago
O ln Lhls case Lhe Lumor ls locaLed ln Lhe
lnLradural exLramedullary space
O 1he Lumor occurred ln Lhe Lhoraclc
reglon (18 110)
O Male (42 years old)





aLlenLs Lyplcally presenL wlLh paln
sensory loss weakness and splnchLer
dlsLurbances
1yplcally locaLed ln Lhe lnLradular
exLramedullary space grow slowly and
spread laLerally ln Lhe subarachnold
space unLll Lhey lnduce sympLomps
MosL frequenLly occured ln Lhe Lhoraclc
reglon
Mlddleaged woman
lemale male raLlo 34 1



Anamnesa lornler
Case 1heory
O redlsposlng facLors are
O 1he paLlenL has a hlsLory used
Lhe caLeLher unLll 14 monLhs
redlsposlng facLors lncludes dlabeLes
melllLus local Lrauma paraphymosls
perlureLral exLravasaLlon perlrecLal or
O Swollen and eryLhemaLous ln Lhe
scroLum
O aln ln Lhe geneLalla reglon
O lever
perlanal lnfecLlon surgery such as
clrcumclLlon or hernloraphy
PlsLory perlneal Lrauma
lnsLrumenLaLlon ureLhral sLrlcLure
assoclaLed wlLh S1u ureLhral cuLaneus
flsLula
Larly phase swollen eryLhemaLous
and Lender as Lhe lnfecLlon beglns Lo
lnvolve Lhe deep fascla
aln and fever

lnLracerebral hemorrhages are composed of hemorrhaglc areas wlLhln Lhe cerebral
parenchyma whlch may be as small as 1 mm or large enough Lo lnvolve Lhe ma[orlLy of a
cerebral hemlsphere More Lhan 60 of LraumaLlc lnLracerebral hemorrhages coexlsL wlLh
exLracerebral hemorrhages eg subdural epldural and subarachnold hemorrhages Cn
occaslon LraumaLlc hemorrhages may exLend lnLo Lhe subdural space resulLlng ln
concomlLanL subdural hemorrhages 1he opposlLe can also occur








9slcol xomlootloo
Case 1heory
O
O aLlenL came wlLh blood pressure
120/80 mmPg and pulse frequency
104 x / menlL 8lood pressure became
147/76 mmPg 98x/mnL
O aLlenL had CCS 14 aL 1400 pm CCS 8
aL 1630 pm CCS 6 aL 1800 pm
O upll lsocor 4mm aL 1400 pm pupll
anlsokor 3mm/3mm aL 1630 pm
aLlenLs may have exLernal evldence of
head ln[urles such as scalp laceraLlons
skull fracLures cephalohemaLoma or
conLuslons
JlLh severe lnLracranlal hyperLenslon a
Cushlng response may occur 1he classlc
Cushlng Lrlad lnvolves sysLemlc
hyperLenslon bradycardla and
resplraLory depresslon
AlLeraLlon ln level of consclousness (le
Clasgow Coma Scale score)
Anlsocorla (eg lpsllaLeral dllaLlon of Lhe
pupll due Lo uncal hernlaLlon wlLh
compresslon of Lhe oculomoLor nerve)

1he cllnlcal varlablllLy assoclaLed wlLh epldural hemorrhage ls remarkable 8arely epldural
hemaLomas may be asympLomaLlc MosL presenL wlLh nonspeclflc slgns and sympLoms
referable Lo an lnLracranlal mass leslon 1he mode of presenLaLlon may be correlaLed wlLh
Lhe slze and slLe of Lhe hemaLoma Lhe raLe of expanslon and Lhe presence of assoclaLed
lnLradural paLhology Lpldural hemaLomas lnvolvlng Lhe Lemporal lobe may cause a more
preclplLous decllne Lhan hemaLomas aL oLher slLes due Lo Lhelr proxlmlLy Lo Lhe bralnsLem
llnally concomlLanL lnLradural leslons Lend Lo lnduce elevaLed lnLracranlal pressure and
Lhus creaLe addlLlonal neurologlc morbldlLy
AlLeraLlon ln consclousness ls a hallmark of epldural hemaLoma buL can be varlable ln
exLenL and duraLlon lorLy percenL of paLlenLs wlLh epldural hemorrhage presenL wlLh a
Clasgow Coma Score of 14 or 13 (Cook eL al 1988) 1he cllnlcal course may follow one of flve
paLLerns (1) consclous LhroughouL (2) unconsclous LhroughouL (3) lnlLlally unconsclous
Lhen consclous (4) lnlLlally consclous Lhen unconsclous and (3) lnlLlally unconsclous
followed by recovery (Lhe socalled lucld lnLerval) followed by reLurn Lo Lhe unconsclous
sLaLe 1he frequency of each of Lhese scenarlos varles slgnlflcanLly among publlshed serles
Powever Lhe classlc lucld lnLerval (paLLern 3) occurs ln less Lhan oneLhlrd of paLlenLs
and Lhus ls noL a senslLlve dlagnosLlc Lool lurLhermore Lhls lucld lnLerval may occur ln
con[uncLlon wlLh expandlng lnLracranlal mass leslons oLher Lhan epldural hemaLoma
Cllnlcal manlfesLaLlons oLher Lhan lmpalred level of consclousness may be encounLered
wlLh epldural hemorrhage alLhough Lhese are Lyplcally laLe flndlngs AbnormallLles ln
puplllary funcLlon may occur as Lhe leslon evolves due Lo lmplngemenL of Lhe oculomoLor
nerve agalnsL Lhe LenLorlal lnclsura Anlsocorla ls noLed ln 30 Lo 73 of paLlenLs wlLh
epldural hemaLoma prlor Lo operaLlon ln approxlmaLely 83 of Lhese mydrlasls ls found
lpsllaLeral Lo Lhe slde of hemorrhage 8llaLeral puplllary dllaLaLlon ls a relaLlvely unusual and
ofLen preLermlnal evenL LaLerallzed moLor deflclLs are found ln roughly oneLhlrd of
paLlenLs (range 23 Lo 37) when presenL hemlparesls ls conLralaLeral Lo Lhe slde of
hemorrhage ln Lhe vasL ma[orlLy of cases buL rarely may be lpsllaLeral or bllaLeral
vegeLaLlve moLor posLurlng (decorLlcaLlon decerebraLlon) ls ldenLlfled ln less Lhan one flfLh
ulsLurbances of cardlovascular funcLlon and venLllaLory drlve occur ln approxlmaLely 13



9efeeJ xomlootloo
Case 1heory

- C1 Scan 1here ls lCP

















lnLracerebral hemorrhages mosL commonly lnvolve
cerebral lobes orlglnaLlng from peneLraLlng corLlcal
branches of Lhe anLerlor
mlddle or posLerlor cerebral arLerles (A) basal
ganglla orlglnaLlng from ascendlng lenLlculosLrlaLe
branches of Lhe mlddle cerebral
arLery (8) Lhe Lhalamus orlglnaLlng from ascendlng
LhalmogenlculaLe branches of Lhe posLerlor cerebral
arLery (C) Lhe pons orlglnaLlng
from paramedlan branches of Lhe basllar arLery (u)
and Lhe cerebellum orlglnaLlng from peneLraLlng
branches of Lhe posLerlor
lnferlor anLerlor lnferlor or superlor cerebellar
arLerles (L)


1eotmeot
Case 1heory
O aLlenL came wlLh 1890 cc LuP
wlLhouL mldllne shlfL wlLhouL focal
neurologlcal deflclL and CCS 13
(1213) So Lhe paLlenL LreaLed
conservaLlvely
O aLlenL dldn'L observaLed half hourly
O aLlenL had a focal neurologlcal deflclL
and CCS became decrease (1630)
Lmergency head C1SCAn (1906)
hemorrhage 13676 cc and mldllne
shlfL 14 cm
O AfLer C1scan paLlenL wenL Lo lCu
O aLlenL wlll be LreaLed wlLh surglcal
Lherapy buL paLlenL dle ln Ck






aLlenLs who exhlblL an LuP LhaL ls less
Lhan 30 mL less Lhan 13mm Lhlck and
less Lhan 3mm mldllne shlfL wlLhouL a
focal neurologlcal deflclL and CCS greaLer
Lhan 8 can be LreaLed nonoperaLlvely
1x drSp8S (lCu)
lvlu naCl 098L 31 20 dpm
ManlLol 3x100cc
AnLraln 3x1 amp lv
CefLrlaxon 1x1 gr lv
kalnex
8raln acL
vlLal slgn observaLlon
lf condlLlon were down lCu
Larly followup scannlng should be used
Lo assess a furLher lncrease ln hemaLoma
slze prlor Lo deLerloraLlon uelayed
epldural formaLlon has been reporLed lf
a rapld slze lncrease ls noLed and/or Lhe
paLlenL develops anlsocorla or a
neurologlcal deflclL Lhen surgery ls
lndlcaLed

CCS 9 14 Jl1PCu1 lCCAL SlCnS 8u1
l8AC1u8L Cn SkuLL x8A?
AcLlon
Palf hourly neuro observaLlon for 6 hours
lf decreased CCS develops or focal slgns
go Lo A above
lf CCS sLable aL 6 hours hourly observaLlon
for 12 hours Lhen 4Lh hourly for 8 hours
AL 24 hours lf CCS 13 and lf home
envlronmenL supervlsed dlscharge wlLh
head ln[ury card

CCS 8 C8 LLSS
AcLlon Call neurosurgeon
SedaLe paralyse and lnLubaLe paLlenL
venLllaLe (CC2 abouL 30 mm Pg)
MannlLol 20 lg/kg lv sLaL
ergency C1 scan as soon as posslble

Sulllvan ln 1999 reporLed LhaL LuP enlargemenL was found on followup C1 scans ln nearly
one fourLh (23) of paLlenLs wlLh conservaLlvely managed LuP LuP enlargemenL occurred
early deLecLed on average wlLhln 8 hours of ln[ury and wlLhln 3 hours of lnlLlal dlagnosls
aLlenLs wlLh LuP rehemorrhage reporLed a worsenlng of Lhelr cllnlcal condlLlon more
frequenLly and underwenL subsequenL surglcal evacuaLlon Lwlce as ofLen as Lhose wlLh
sLable LuP buL Lhey dld noL experlence a worse neurologlc ouLcome as measured by
dlsposlLlon aL dlscharge
Slgns and sympLoms referable Lo epldural hemorrhage generally evolve rapldly afLer head
Lrauma nearly Lwo Lhlrds of paLlenLs exhlblL promlnenL flndlngs prompLlng surgery wlLhln 6
hours of ln[ury 83 declare Lhemselves wlLhln 24 hours (8rlcolo and asuL 1984) 1he
remalnder consLlLuLe (1) Lhose wlLh small occulL leslons LhaL remaln asympLomaLlc (2)
Lhose wlLh slowly accumulaLlng cloLs LhaL become sympLomaLlc afLer 24 hours and (3)
Lhose whose hemaLomas develop ln delayed fashlon 1he Lhlrd phenomenon ls noL as rare
as once LhoughL among headln[ury paLlenLs AlLhough mosL paLlenLs demonsLraLe
radlographlc evldence of epldural hemorrhage on Lhelr lnlLlal C1 examlnaLlon a small subseL
develop hemaLoma collecLlons from 2 Lo 120 hours (medlan 12 hours) afLer presenLaLlon
usually afLer LreaLmenL of elevaLed lnLracranlal pressure by medlcal or surglcal means (oon
eL al 1992) 1hus lnLense survelllance ls requlred Lo deLecL cllnlcal deLerloraLlon ln paLlenLs
wlLh lnlLlally unremarkable C1 scans obLalned soon afLer ln[ury because such a decllne may
lndlcaLe Lhe delayed accumulaLlon of an epldural hemaLoma











CHAPTE# V
SUMMA#

1. Severe traumatic brain injury (TBI, GCS 8-3) is associated with high
morbidity and mortality.
2. Intracerebral hemorrhages are composed oI hemorrhagic areas within the
cerebral parenchyma, which may be as small as 1 mm or large enough to
involve the majority oI a cerebral hemisphere.
3. Pneumonia is an important cause oI morbidity Iollowing severe traumatic
brain injury (TBI). Hospitalized patients may have many risk Iactors Ior
pneumonia, including mechanlcal venLllaLlon, prolonged malnuLrlLlon,
underlying hearL and lung diseases, decreased amounts oI stomach acid, and
immune disturbances.
4. Tracheostomy is a surgical procedure in which an opening is made into the
trachea and maintained with a tube in order to establish direct communication
with the external environment.







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. lson BA. . Beau Injuiy.
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