STEP 1 Identifikasi Istilah

1. Muntah Proyektil: Muntah yang kuat dan mendadak, dikarenakan tabrakan maut
sebagai respond dari adanya permasalahan dari pencernaan. Cedera kepala
menyebabkan disfungsi regulasi.
2. KIE: Komunikasi Informasi dan Edukasi, melindungi pasien dari hal-hal yang belum
mereka ketahui.
3. Vulnus Laceratum: Laserasi atau luka robekan pada suatu jaringan yang tidak intak,
merupakan gangguan diskontinuitas dari sebuah jaringan atau robekan jaringan.
4. Pupil Anisokhor: Perbedaan pupil kiri dan kanan biasanya 0,1 mm karena
meningkatnya TIK.
5. Bloody Otorea: Cairan yang keluar bercampur dengan darah dari telinga
STEP 2 Identifikasi Masalah
1. Apa penyebab pupil anisokhor?
2. Apa penyebab muntah proyektil?
3. Apa yang menyebabkan pasien bicara meracau?
4. Apa yang menyebabkan bloody otorea?
5. Mengapa pada pasien terjadi periode apnea?
6. Apa hasil interpretasi dari pemeriksaan yang ada di skenario?
 7. Apa yang menyebabkan peningkatan TD namun penurunan Nadi(HR) dan
pernafasan(RR)?
8. Apa kemungkinan diagnosis dari pasien di skenario?
9. Apa tatalaksana awal pada pasien di skenario?
10. Apa Komplikasi yang mungkin terjadi pada pasien di skenario?
STEP 3 Analisis Masalah
1. Apa penyebab pupil anisokhor?
Bisa karena inflamasi atau peradangan pada otot iris kemudian berdilatasi pupilnya.
Kemudian peningkatan TIK mengganggu nervus okulomotor sehingga terjadi dilatasi
pupil. Karena adanya trauma sehingga terjadi pembengkakan dan peningkatan pada
TIK dan mengganggu nervus okulomotor sehingga menyebabkan pupil anisokhor.
Pupil anisokhor adalah kejadian perbedaan dilatasi pupil pada mata kanan dan kiri.
Ada juga hubungan dengan saraf simpatis dan parasimpatis yang terjadi gangguan
sehingga menyebabkan pupil anisokhor.
2. Apa penyebab muntah proyektil?
Penyebabnya adalah gangguan saraf cranialis vagus yang menyebabkan gangguan
pada pencernaan sehingga terjadi muntah proyektil. Gangguan saraf cranialis vagus
dapat disebabkan oleh cedera, perdarahan, ataupun peningkatan TIK. Peningkatan
TIK merangsang reseptor muntahnya ikut terangsang sehingga merangsang pada
nervus vagus kemudian diteruskan ke pencernaan seperti sphincter esofagus sehingga
terkontraksi dan terbuka sehingga menimbulkan muntah proyektil. Tanpa ada
rangsangan mual sehingga terjadi up flow

3. Apa yang menyebabkan pasien bicara merancau?

Pada pasien terjadi cedera kepala, Bicara merancau merupakan tanda penurunan
kesadaran karena peningkatan TIK menyebabkan gangguan pada ARAS. GCS
E1V3M4. Ada kemungkinan pasien ini pada tingkat derilium

4. Apa yang menyebabkan bloody otorea?

Terjadi karena fraktur pada basis cranii, karena adanya trauma bagian media fossa
cranii sehingga menyebabkan bloody otorea. Perforasi membran timpani akan
menyebabkan pembuluh darah pada bagian tersebut menyebabkan perdarahan.
Kecelakaan menyebabkan fraktur dan perlukaan.
5. Mengapa pada pasien terjadi periode apnea?
Pada pasien ini terjadi fraktur pada basis cranii pada bagian temporal yang dapat
menyebabkan racoon eyes, bettle sign dsb. Basis cranii berdekatan dengan daerah
batang otak yang mengatur pernafasan (medula oblongata) sehingga menyebabkan
disregulasi pada pernafasan karena gangguan batang otak. Fractur Basis cranii dapat
di bagi berdasarkan lokasinya anterior, posterior atau media. Apabila terjadi fraktur
basis cranii di lokasi posterior akan menyebabkan gangguan pernafasan
6. Apa hasil interpretasi dari pemeriksaan yang ada di skenario?
GCS E1V3M4 total hasil GCS 8 bisa jadi delirium atau somnolen
TD Hipertensi
HR penurunan
RR apnea
 7. Apa yang menyebabkan peningkatan TD namun penurunan Nadi(HR) dan
pernafasan(RR)?
Tanda cushing triad yang mengindikasikan terjadinya peningkatan tekanan
intrakranial. Biasanya tekanan sistolnya sangat tinggi dan penurunan HR dan terjadi
penurunan RR. Sindrom cushing merupakan respond sistem tubuh untuk
mempertahankan darah pada otot. Cedera pada SSP dapat menurunkan tekanan darah
dan HR
8. Apa kemungkinan diagnosis dari pasien di skenario?
Fraktur Basis Cranii atau cedera kepala berat dan melihat perdarahannya di bagian
mana seperti epidural atau subdural. Traumatic Brain Injury memiliki gejala yang
mirip dengan pasien di skenario ini.
9. Apa tatalaksana awal pada pasien di skenario?
Pada Setting RS, Pertama dicek BCA nya (breathing, Circulation, Airway), Diberikan
pengganti cairan hipertonis untuk meningkatkan osmosis pada intravaskular namun
membebani ginjal, memosikan head up 30 derajat akan meningkatkan venous return,
antinyeri, kemudian apabila sudah mulai stabil dapat dilakukan pemeriksaan CT Scan.
10. Apa komplikasi yang mungkin terjadi pada pasien di skenario?
Menimbulkan kerusakan yang luas pada cerebrinya, Hidrocephalus, Syok, Meninggal.
Komplikasinya bergantung pada kecepatan penanganan dan keparahan trauma pada
pasien

STEP 4 Strukturisasi Konsep

Trauma Kepala

Perdarahan Vulnus Laceratum Fraktur Cranial

Fraktur Basis
Peningkatan TIK
Cranii

Herniasi, Gejala:
Muntah Proyektil, Bloody Otorrhea
Pupil Anisokhor

ABC dan
Resusitasi Cairan

Tatalaksana
sesuai Etiologi
STEP 5 Learning Objective
1. Mahasiswa mampu menjelaskan Definisi, Klasifikasi (derajat, lokasi lapisan),
Etiopatofisiologi, Manifestasi Klinis, Diagnosis dan Tatalaksana dari Cedera Kepala.
STEP 6 Belajar Mandiri
STEP 7 Sintesis Masalah
1. Head Injury:
a. Definition
Head injury can be defined as trauma to the brain and/or its coverings from an
externally applied mechanical force, involving the cranium and intracranial
structures. Head injury usually refers to traumatic brain injury (TBI), but is a
broader category because it can involve damage to structures other than the
brain, such as the scalp and skull. The incidence of fatal head wounds has
remained similar throughout history in spite of modern Kevlar helmets.
b. Classification
A. Cranial fracture
A powerful blow that affects a broad area of the cranium can result in
comminuted fractures with multiple
fragments. In contrast, a blow to a relatively narrow area can cause a
depressed fracture, where a single bone
fragment is pushed inward, putting pressure on the brain. Diastatic fractures
that follow the suture lines are more
common in children. Fractures that tear the scalp can increase the risk of
intracranial infection.
Basilar skull fractures can lead to cerebrospinal fluid (CSF) leakage into the
sinuses, causing air-filled spaces called
aeroceles, which can become a source of infection. Basilar skull fractures
along the petrous bone and pituitary fossa
can result in a "hinge fracture," indicating a strong lateral impact
to the head. "Ring fractures" encircling the foramen
magnum are typically caused by extreme neck hyperextension, falls from
heights with landing on the feet, and
frequently occur on the orbital roof due to a "contra-coup injury"
when someone falls backward, with the occiput
hitting a hard surface.
Fraktur midfacial is classified into three patterns: Le Fort I, II, and III.
There are three vertical supporting axes in midfacial injuries: nasofrontal-
maxillary, frontozygomaticomaxillary, and
pterygomaxillary.
There are five fragile horizontal lines: frontal bone, nasal bone, alveolus,
zygomatic arch, and infraorbital region.
Classic signs of midfacial fractures include subconjunctival hemorrhage,
malocclusion, a sensation of thickness in the
midfacial area or hypesthesia (maxillary division of the trigeminal nerve),
facial bruising, ocular signs/symptoms, and
mobility of the maxillary area.
B. Concussion
A concussion is the mildest form of brain injury, characterized by a brief loss
of consciousness and either
retrograde amnesia (memory loss before the accident) or anterograde amnesia
(memory loss after the
traumatic event). It can result from a physiological disconnection between the
cortex and the brainstem.
Based on its neurological dysfunction, concussions are divided into four
grades:
1. Grade I: Temporary confusion followed by a return to normal consciousness
without amnesia.
2. Grade II: More severe confusion and post-traumatic amnesia.
3. Grade III: Severe confusion, post-traumatic amnesia, and retrograde
amnesia.
4. Grade IV: Classic concussion (brief loss of consciousness, varying periods
of confusion, post-traumatic
amnesia, and retrograde amnesia).
C. Contusion
In the case of a contusion, brain injury presents as a region of bleeding in the
central part, mixed with areas
of non-hemorrhagic necrosis, and some areas of the brain experience edema.
Over time, this central
bleeding area mixes with the non-hemorrhagic necrotic region and the brain
areas suffering from edema,
leading to the central bleeding area being surrounded by pericontusional
edema.
D. Laceration
The blood vessel damage that occurs in contusions typically involves capillary
blood vessels. If it involves damage to larger blood vessels, such as the pia-
arachnoid and the cortical layers, it can result in lacerations, and in some
cases, perforation of brain tissue.
Primary Injury

Primary injury includes injury upon the initial impact that causes displacement
of the brain due to direct impact, rapid acceleration-deceleration, or
penetration. These injuries may cause contusions, hematomas, or axonal
injuries.

Contusion (bruise on the brain parenchyma)

Hematoma (subdural, epidural, intraparenchymal, intraventricular, and
subarachnoid)
Diffuse axonal injury (stress or damage to axons)
Secondary Injury/Secondary Neurotoxic Cascade
 Secondary injury consists of the changes that occur after the initial insult. It
can be due to:

Systemic hypotension
Hypoxia
Increase in ICP
After a primary brain injury, a cascade of cellular and biochemical events
occurs which include the release of glutamate into the presynaptic space
resulting in ionic shift may activate cytoplasmic and nuclear enzymes,
resulting in mitochondrial damage, and cell death and necrosis.

c. Etiopathophysiology
In general, head injuries occur due to trauma or impact
caused by external mechanical forces. The most serious cause of head injury
or most often due to collisions or accidents such as falling from a vehicle
motorbikes, falls from heights, and due to attacks from outside.
-Direct blow Can cause brain damage on the side of the blow (coup injury) or
on the opposite side of the blow when the brain moves inside the skull and hits
the opposite wall (contrecoup injury)
-Rotation/deceleration Flexion, extension, or rotation of the neck produces
attacks on the brain that strike bony points within the skull (e.g. on the wings
of the sphenoid bone). Violent rotation also causes traumatic lacerations within
the white matter of the brain and brainstem, causing axonal injury and
intracerebral hemorrhage spots;
-Collision The brain is often spared from direct trauma unless it is severe
(especially in elastic children);
-Bullets Tend to cause tissue loss along with trauma. Brain swelling is a
problem resulting from disruption. A skull that will automatically press on the
brain;
-By objects/bone fragments that penetrate brain tissue, for example accidents,
being hit and falling;
-Trauma at birth, for example when birth is assisted with forceps or a vacuum;
-The effect of force or energy transmitted to the brain; h. Effects of
acceleration and deceleration (acceleration-deceleration) on the brain.
d. Clinical Manifestation
1. Epidural Bleeding
a. Hemiparese
b. Babinsky Reflex
c. Fracture in temporal region
d. Dilatation of pupil

2. Epidural hemorage
a. Fracture
b. Isokhor pupil
c. CT Scan show hiperdent in bone skull
3. Subdural Hemmorage
a. CT Scan show hiperdent cresent moon
b. Headache
c. Seizure
d. Increased ICP
e. Abnormal Reflex
4. Increassed ICP
a. Hipertention
b. Bradycardi
c. Apnea
5. Fracture bassis cranii
a. Anterior
i. Anosmia
b. Media
i. Otorea
ii. Vestibulococlear distruption
c. Posterior
i. Bettle Sign
d. Intracerebral Hematoma
i. Headache
ii. Vomiting
iii. Seizure
iv. Altered Mental Status
e. Main Clinical Manifestation
i. Altered Mental Status
1. Mild: GCS Score 13 to 15
a. Loss of consiusness
b. Vomiting
c. Mostly stable
2. Moderate: GCS Score 9 to 12
a. Two Episode Vomiting
b. Persistent Headache
3. Severe: GCS Score 3 to 8
a. Loss of Consiusness
b. Contucions
c. Hematoma/cerbral hematoma
d. Otorhea
e. Increassed ICP

f. Diagnosis
i. Determine by Evaluation and history
1. History(Anamnesis) and physical evaluation
a. Symptoms
i. Pupil Isokhor
ii. Otorea
 iii. Rhinorea
iv. Altered Mental Status (decreasing on
GCS Score)
v. Headache
vi. History of the head injury
vii. Loss of consiusness of the patient
must be monitored
viii. Post traumatic Amnesia
ix. Increassed ICP
x. Other Neurological Symptoms
xi. History of the patient drugs and life
style of the patient
b. Determine the GCS
c. Evaluate the head structure, seek for fracture
d. Babinsky Reflex
2. MRI
3. CT Scan (pneumocephalus is air on inside the brain)
4. Laboratory Examination (elevated sodium indicate
dehydration, depletion of the magnesium)
g. Management
i. Managament of head injury classified non surgey and
surgery
ii. Differentiate the GCS, to know the severity for head trauma
iii. If the patient showing symptoms bring the patient to
hospital
iv. Stabilize the Airway, Breathing, Circulation of the patient to
avoid the brain ischemic
v. Using Prophylaxis Seizure the first week of the trauma
Fenitoin (depressed the glutamate, secretion happen in
hepar) using the fenitoin must show at least an episode of
seizure or the patient have big surgery like craniotomy.
Because we do not know when to stop the prophylaxis.The
using the prophylaxis is still on controvertion
vi. Neurological Examination
vii. Determine the management of the etiology
viii. Consult to the brain surgeon, the principal of the surgery is
to remove the etiological factor like blood (hematoma) or
herniation to lowering the ICP
ix. Agresively Resusitate ariway (using OPA to oxygnate the
pation to avoid ischemic), the fluid of the patient.