Craniocerebral Trauma

Injuries to the head that result in changes of the

brain
 Basal Skull Fractures and Cranial Nerves Injuries

• Susah untuk di deteksi lewat imaging, diagnosed by clinical signs

• Fracture of petrous pyramid  deformity of external auditory canal or tears of

the tympanic membrane (leakage of CSF or otorrhea), or blood may collect
behind tympanic membrane

• If fracture extends posteriorly and damaging the sigmoid sinus, tissue behind the
ear and over mastoid process becomes boggy and discolored  Battle Sign

• May also cause blood to leak into the periorbital tissues  raccoon eyes sign
 EPIDEMIOLOGI
• Leading cause of death for people before 45 years of age

• Sering terjadi, bisa menyebabkan kematian or disabilitas permanen

 Basal Skull Fractures and Cranial Nerves Injuries

• Also can be indicated by signs of cranial nerve damage.

• Most liable to injury  olfactory, facial, auditory nerves.

• Anosmia and apparent loss of taste (loss of perception of aromatic flavors)  frequent sequelae of head injury

• Fracture near or in the sella may tear the stalk of the pituitary gland  diabetes insipidus

• Fracture of sphenoid bone  lacerate the optic nerve (results in blindness). Pupil unreactive to direct light stimulus
but still reacts to light stimulus of the opposing eye

• oculomotor nerve injury  ptosis, diplopia, divergence of globes with affected eye resting in an abducted and
slightly depressed position, loss of medial and most of the verticaql movements of the eye, and a fixed, dilated
pupil
 Basal Skull Fractures and Cranial Nerves Injuries

• Trochlear nerve injury diplopia that is worse on looking down, compensatory tilting of the head

• Basal fracture across the middle cranial fossa or direct extracranial injury to the branches of nerve  injury to the
ophthalmic and maxillary divisions of the trigeminal nerves  numbness and paresthesia of the skin supplied by
the nerve branch or chronic neuralgia

• Facial nerve may be involved : transverse fractures through the petrous bone (immediate facial palsy, caused by
contusion or transection of the nerve), longitudinal fractures of the petrous bone (facial palsy often being delayed
for several days)

• Injury to the eight cranial nerve (vestibulocochlear) because of petrous fractures  oss of hearing or in postural
vertigo and nystagmus immediately after trauma
Basal Skull Fractures and Cranial Nerves Injuries

• Raccoon Eyes

• Battle Sign
 Carotid – Cavernous Fistula

• Caused by basal fractures through the sphenoid bone that lacerate the internal carotid artery or one of its
intracavernous branches

• Within hours or a day or two  disfiguring pulsating exophthalmos develops (arterial blood enters the sinus and
distends the superior and inferior ophthalmic veins). Orbit feels tight and painful, eye may become partially or
completely immobile

• Sixth nerve is affected most often, third and fourth less often

• Loss of vision (ischemia of the optic nerve and retina)

• Audible bruit over the eye

• 5-10% of fistulas resolve spontaneously, others must be obliterated by interventional radiologic means such as
detachable balloon or direct surgical repair
 Pneumocephalus, Aerocele, Rhinorrhea (CSF Leak)

• If the skin over a skull fracture is lacerated and underlying meninges are torn, or if fracture passes through the
inner wall of a paranasal sinus  bacteria can enter the cranial cavity  meningitis or abscess formation

• CSF that leaks into the sinus  watery discharge from the nose (CSF rhinorrhea)

• Common occurrence following a skull fracture  collection of air in cranial cavity. Pocket of air is apparent by CT
scan in epidural or subdural space over the cerebral convexities or between the hemispheres
 Concussion
• Reversible traumatic paralysis of nervous function (A transient loss of consciousness and amnesia, mild confusion,
incoordination, headache, fatigue)

• Caused by a sudden change of momentum of the head  either movement is imparted to the stationary head by a
blow or movement of the head is arrested by a hard, unyielding surface

• Clinical signs  immediate abolition of consciousness, suppression of supportive reflexes, transient arrest of
respiration, brief period of bradycardia, fall in blood pressure. Vital signs usually return to normal and stabilize
within a few seconds.

• Brief tonic extension of the limbs, clonic convulsive movements and other peculiar movements  may occur
immediately after loss of consciousness

• Patient will wake up after some time, and slowly return to normal. Corneal, pharyngeal, and cutaneous reflexes will
return. Gradually, contact is made with the environment and patients begins to obey simple command. May also
carry conversation, but patient will not remember. Time required to pass these stages  few seconds, minutes,
hours, days.
 Pathologic Changes Associated with Head Injury

• Kalau traumatic brain injury yang serius  brain can be contused, swollen, lacerated, bisa ada hemorrhages, and
hypoxic ischemic lesion.

• Majority of patients that remain in coma 24h after head injury  intracerebral hematomas and concussion

• Most frequent type of lesions  contusions of the surface of the brain beneath the point of impact (coup lesion),
extensive lacerations and contusions on the side opposite the site of impact (countrecoup lesion)

• Blows to the front of the head  coup lesions, blows to the back of the head  countrecoup lesion, blows to the
side of the head  either coup or countrecoup lesions or both. Most common site of cerebral contusions are the
frontal and temporal lobes
 Pathologic Changes Associated with Head Injury
• Contused cortex is diffusely
swollen and hemorrhagic,
most of the blood being found
around parenchymal vessels.

• On CT, lesions appear as

edematous regions of cortex.
Leaked blood  subcortical
white matter admixed with
areas of increased density
 Pathologic Changes Associated with Head Injury
• Axonal lesions may also occur at the time of impact or evolve soon afterward. There is an uneven but
diffuse degeneration of the cerebral white matter  diffuse axonal injury. There is also ballooning and
interruption of axis cylinders (cause short survival)

• DAI  main cause of persistent unconsciousness

• In most cases of severe head injury  there is damage to the corpus callosum by impact with falx.
Necrosis and hemorrhage are sometimes visible by CT. there may also be scattered hemorrhages in the
white matter along lines of force from the point of impact to the contralateral side
 Pathologic Changes Associated with Head Injury

• Primary brainstem hemorrhage due to torsion and tearing of tissue at the time of impacts are distinguished
from the secondary hemorrhages that are a result of the effects of downward displacement of the
brainstem

• Closed head injury also induces variable degrees of vasogenic edema that increases during the first 24 to
48 h and Small zones of infarction that have been attributed to vascular spasm caused by subarachnoid
blood surrounding basal vessels

• Presence of intracranial hypertension  higher incidence of infarction

 Cerebral Fat Embolism

• With fracture of large bones, particularly the femur, with or without head injury, after 24 to 72 h there may
be an acute onset of pulmonary symptoms (dyspnea and hyperpnea) followed by coma with or without
focal signs or seizures

• Caused by systemic fat embolism

• Most patients recover spontaneously in 3 or 4 days

• Treatment  respiratory support, supportive treatment

 Approach to Patients with Head Injury
Patients who are conscious or rapidly regaining consciousness (concussion and minor head injury)

• Most frequently encountered

• Patient is only stunned momentarily, “Saw stars”, or was briefly disoriented

• Pstients are liable to a troublesome posttraumatic syndrome like headache, giddiness, lack of mental clarity,
fatigability, insomnia, nervousness

• Brief asessment for mental clarity, weakness, ocular abnormalities, Babinski signs  appropriate

• CT is not really needed

• <7  severe head injury, 8-12 
moderate head injury, >13  mild
head injury
 Approach to Patients with Head Injury
Patients who are conscious or rapidly regaining consciousness (concussion and minor head injury)

• May be followed by worrisome clinical phenomena :

• Drowsiness, headache, confusion  occur most often in children, and suggest the presence of intracranial
hemorrhage. On CT, mild focal edema near the point of impact may be seen. Symptoms may subside after a few
hours

• Transient paraplegia, blindness, migrainous phenomena  caused by falls or blows on top of the head. Both legs may
become temporarily weak and numb, with wavering bilateral Babinski sign and sometimes sphincteric incontinence.
Impact over occipital area may result in blindness. Symptoms disappear after a few hours. Migrainous phenomena is
induced by a blow to the head.

• Delayed hemiplegia  caused by late evolving epidural or subdural hematoma, or intracerebral hemorrhage.
 Approach to Patients with Head Injury
Serious Cerebral Damage Following a Lucid Interval

• Very important and dangerous

• The initial loss of consciousness from concussion lasted only a few minutes

• Caused by late deterioration  caused by expansion of a subdural hematoma, worsening brain edema around
contusion, delayed appearance of epidural clot

• CT scan  midline shift

 Approach to Patients with Head Injury
Patients Who Remain Comatose From The Time of Head Injury

• Usually caused by severe head injuries

• There are evidence of increased ICP and cerebral contusions, subarachnoid hemorrhage, zones of infarction, amd
scattered intracerebral hemorrhage at point og injury and opposite side

• Pertama di stabilize dulu, and then do clinical and imaging assessment, to uncover surgically remediable lesion
Specific Traumatic Cranial Lesions
Acute Epidural Hemorrhage

• Caused by temporal or parietal fracture and laceration of the middle

meningeal artery or vein

• May not have produced coma initially. Patients often regain

consciousness fast. A few hours later, headache of increasing severity
develops, with vomiting, drowsiness, confusion, aphasia, seizures,
hemiparesis with slightly increased tendon reflexes, and Babinski sign.
Pupil may dilate on the side of hematoma

• Heart rate is often bounding (cushing effect)  because of a raise in

systolic blood pressure

• CT, MRI  lens shaped clot with smooth inner margin

• Treatment  surgical
Acute and Chronic Subdural Hematomas

• Acute subdural hematoma  there may be a brief lucid interval between the blow to the head and advent of coma.
Headache, vomiting, pupillary inequality, dysphagia, cranial-nerve palsies, stiff neck, ataxia of the trunk and gait.
Caused by tearing of bridging veins, and symptoms are caused by compression of adjacent brain and of deep
structures.

• Chronic subdural hematoma  etiology less clear. Period of weeks. Symptoms include headache, lightheadedness,
slowness in thinking, apathy an drowsiness, unsteady gait, occasionally seizures.

• CT and MRI are the most reliable diagnostic procedures  acute clot is initially hyperdense but becomes isodense
after a period of 1 or more weeks, then hypodense over 2 to 6 weeks. On MRI, acute clot is hypointense on T2
weighted images, then become hyperintense

• Treatment  place burr holes and drain the clot, craniotomy,

Subdural Hygroma

• Thinly encapsulated collection of clear or slightly xanthochromic fluid in the subdural space, form after injury.

• Presumably caused by a ball-valve effect of an arachnoidal tear that allows cerebrospinal fluid to collect in the space
between the arachnoid and the dura

• Drowsiness, confusion, irritability, low grade fever (in children)

• Aymptomatic (in adults)

Cerebral Contusion and Traumatic Intracerebral Hemorrhage

• Contused area can swell or develop into hematoma during the first several days of injury.

• Can cause delayed clinical deterioration, sometimes abrupt in onset.

• It is thought that the swelling is caused by excessive administration of intravenous fluids

• Intracerebral hemorrhages  may be apparent after head injury, or delayed in its development by several days.
Clinical manifestations include deepening coma eith hemiplegia, dilating pupil, bilateral Babinski signs, stertorous
and irregular respirations.

• Treatment  craniotomy
Acute Traumatic Brain Swelling in Children

• Is seen in the first hours after injury and may prove rapidly fatal

• CT scan  enlargement of both hemispheres and compression of basal cisterns and ventricles.

• Usually no papilledema in early stages, during which the child hyperventilates, vomits and extensor posturing
Shaken Baby Syndrome

• Inciting trauma is typically violent shaking of the body or head of an infant, resulting in rapid acceleration and
deceleration of the cranium

• Diagnosis is suspected from the combination of subdural hematomas and retinal hemorrhages.

• Low initial Glasgow coma scale, retinal hemorrhage, skull fracture  poor outcome
Penetrating Wounds and Blast Injuries

Missiles and Fragments

• Caused by bullets fired from rifle or handguns. The bullets causes a high temperature coagulative lesion that is sterile
and does not require surgery if projectile exits skull. Main considerations are development of infection or CSF leaks,
epilepsy or aneurysm in distal blood vessel

• If brain is penetrated at lower levels of brainstem  instant death

• Patients usually are comatose, depth and duration of coma depend on the degree of cerebral necrosis, edema and
hemorrhage. Recovery may take months.
Penetrating Wounds and Blast Injuries

Blast Injuries

• Caused by shock waves of an explosive device. Can rupture the tympanic membrane. Deafness, tinnitus, and vertigo
are common. Loss of consciousness may also occur.

• Potential modes of conduction of the force of the blast to cranial contents include acceleration and deceleration of the
head as a wave passes by, which essentially results in concussion, skull deformation which squeezes the brain,
indirect passage of shockwave through the lungs, and entry of the wave through the openings of the cranial vault
(acoustic and optic canals and foramen magnum)
 SEQUELAE OF HEAD INJURY
Posttraumatic Epilepsy

• Most common  seizures

• Basis  contusion or laceration of the cortex

• Interval between head injury and seizure varies. It can happen within moments of the injury (brief tonic extension of
the limb, slight shaking movements immediately after concussion, followed by awakening in a mild confusional
state). It can also happen within the first week of injury.

• Posttraumatic epilepsy refers to late epilepsy  usually happens weeks or months after closed head injury (1-3
months)

• They tend to decrease in frequency as years pass.

• Treatment  OAE
 SEQUELAE OF HEAD INJURY
Autonomic Dysfunction (“Storm”) Syndrome

• Caused by severe head injury. Observed in some comatose patients and particularly in vegetative state

• Syndrome of episodic vigorous extensor posturing, profuse diaphoresis, hypertension, tachycardia lasting minutes to
hours

• Arise spontaneously

• Treatment  bromocriptine
 SEQUELAE OF HEAD INJURY
Extrapyramidal and Cerebellar Disorders Following Cranial Trauma

• Is still controversial.

• Some patients have early symptoms of Parkinson disease after head injury like tremors, which progressed slowly and
does not respond to L-Dopa.

• Cerebellar ataxia is also rare, often unexplained but also in cases complicated by cerebral anoxia.
 SEQUELAE OF HEAD INJURY
Acute Traumatic Encephalopathy

• In almost all patients with cerebral concussive injury, there is a gap in memory (traumatic amnesia). This gap is
permanent. Some degree of impairment of higher cortical function may also persist for weeks.

• The lower the score of GCS and the longer the posttraumatic gap in the formation of new memories, the more likely
the patient is to suffer some permanent cognitive and personality changes

• Mental and behavioral abnormalities are also present.

 SEQUELAE OF HEAD INJURY
Chronic Traumatic Encephalopathy

• Delayed neurodegenerative cerebral disease that follows mild traumatic brain injury after many years

• Developed in years, marked by dysarthric speech, a state of forgetfulness, slowness in thinking, and signs of
dementia. Movements are slow, stiff, and uncertain, especially legs, and there is a shuffling, wide based gait.

• CT scan  ventricular dilatation and sulcal widening and cavum septi pellucidi
 SEQUELAE OF HEAD INJURY
Posttraumatic Hydrocephalus

• Uncommon complication

• Intermittent headache, vomiting, confusion, drowsiness  mental dullness, apathy, psychomotor retardation (by this
time CSF may be normal, normopressure hydrocephalus)

• Early subarachnoid hemorrhage may be involved in the mechanism

• Ventricoperitoneal shunt
 SEQUELAE OF HEAD INJURY
Postconcussion syndrome

• Cranial pain is either generalized or localized to the part that has been struck and is described as aching, throbbing,
punding, stabbing, pressing, band like.

• Intensification of headache by straining, mental, physical effort. Quiet and rest tends to relieve it

• Dizziness  giddiness or lightheadedness

• Resolve in several weeks for some patients

• May complicate head injuries, and may persists for months or years
 TREATMENT OF HEAD INJURY
Patients with Concussion or Transient Symptoms

• Should not be discharged first until decision is made about appropriate examinations and hasilnya negative.

• Also harus di pantau sampai bisa regain memories and di confirm by family members.

• Lalu di edukasi tentang gejala-gejala concussion yang mungkin di alami

• Kalau ada symptoms, kurangi atau jauhkan hal-hal yang bisa memperparah atau precipitate symptoms
 TREATMENT OF HEAD INJURY
Patients with Severe Head Injury

• ABC first (airway, breathing, circulation)

• Assess injury severity

• Pasang iv  normal saline

• Neurologic survey  depth of coma, pupil reflex, etc

• TTV charted every hour

• CT & MRI!!!  to see ada blood clot atau tidak

• ICP monitoring  kalau moderate or severe head injury. To warn of impending deteriorated bcs of edema or
hemorrhage. Use ventricular catheter. Kalau ICP elevated, infuse hyperosmolar or isoosmolar solutions like normal
saline.
 TREATMENT OF HEAD INJURY
Patients with Severe Head Injury

• Hyperosmolar therapy  creation of a gradient of water concentration from the brain to the blood. Mannitol, glycerol
and urea are effective in lowering ICP.

• Hypocarbia  Hypocarbia, induced by mechanical hyperventilation produces alkalosis of the CSF and cerebral
vasoconstriction with a corresponding reduction in cerebral blood volume and ICP.

• Hypothermia  can reduce ICP but jarang dipakai

• Glucocorticoids  not recommended

• Blood pressure management  can be disregarded unless blood pressure elevation is extreme. Diurectic, ace
inhibitors and beta adrenergic blocking agents can be used to lower blood pressure. But ga boleh sembarangan (harus
pikirin cerebral perfusion juga)
 TREATMENT OF HEAD INJURY
Patients with Severe Head Injury

• If coma persists after 48 hours  NGT

• Surgical decompressions  tergantung patient state and findings in imaging

 PROGNOSIS
• Prognosis worsens semakin tinggi usia nya

• The duration of traumatic amnesia also determines the prognosis. Semakin pendek durasi traumatic amnesia nya,
semakin cepat recovery nya

• If patient remains in vegetative state for > 6 months  will not recover
Spinal Trauma
 Epidemiology

approximately 5 cases per 100,00 population

lebih banyak terjadi pada pria (4:1)

approximately 3500 die because of the injury, 5000 are

left with complete or nearly complete loss of spinal cord
function
MECHANISM OF SPINAL INJURY

3 Types of Vertebral Column Injuries

Fracture- Pure
Dislocations Fractures

Pure
Dislocations
 Mechanism of Spinal Injury

Primer

• biasanya disebabkan adanya kompresi pada

struktur medula spinalis
• bisa juga disebabkan oleh gaya mekanik trauma

Sekunder

• Disebabkan adanya gangguan perfusi pada

tingkat sel  hipoperfusi sistemik
 Gejala dan Tanda Klinis

Derajat Keparahan Defisit Neurologis Renjatan Spinal

(Spinal Shock)
Level cedera • Dapat ditegakkan dalam 72 jam – 7 hari pascacedera
• Dibagi menjadi : komplit (pasien kehilangan fungsi • Hilangnya fungsi sensorik,
• Dapat ditentukan sensorik dan motorik pada level cedera) dan inkomplit motorik dan otonom
melalui pemeriksaan (pasien hanya hilang salah satu saja) sementara
• ASIA Scale • Ditandai dengan hilangnya
sensorik dan motorik aktivitas refleks spinal
• Perbedaan gejala : dibawah lesi dan kelemahan
diatas T1  ekstremitas flaccid
• Ditemukan pada fase akut
tetraplegi, gangguan Sindrom Medulla Spinalis pascacedera
pernapasan, renjatan • Untuk membedakan spinal
neurogenic. Dibawah • Berdasarkan letak lesi/gejalanya, terdapat 4 shock dan injury 
T1  paraplegi dibawah 1 jam masih
sindrom yaitu : Sindrom Brown-Sequard,
dianggap spinal shock,
Anterior cord syndrome, Central Cord selebihnya sudah di anggap
Syndrome, Posterior Cord Syndrome injury
Gejala dan Tanda Klinis
Gejala dan Tanda Klinis
 Diagnosis
Anamnesis Pemeriksaan Fisik Radiologis

• mekanisme trauma • menilai fungsi • Jika alat terbatas,

• riwayat penyakit sensorik dan dapat dilakukan
sebelumnya motorik pasien rontgen terlebih
• AMPLE (Allergy, • sensorik : dahulu, lalu CT.
Medication, Past memberikan • pemeriksaan yang
Illness, Last meal, rangsangan nyeri dapat dilakukan :
Exposure) kepada pasien foto segmen
sesuai pola servikal, foto
dermatom segmen
• motorik : torakolumbal
memeriksa
kekuatan otot
mengikuti pola
miotom
 Treatment
PRE-HOSPITAL

1. Imobilisasi pasien  imobilisasi area servikal (stabilisasi manual, bidai servikal, sandbag atau
towel roll) dan area sepanjang tulang belakang (spine board).
2. Tindakan Resusitasi  penjagaan jalan napas, control perdarahan serta syok.

HOSPITAL

1. Penanganan gawat darurat  imobilisasi, primary survey(ABCD), secondary survey, medikamentosa

(pasien onset < 3 jam diberikan prednisolone 30mg/kgBB IV bolus selama 15 menit for 45 min, lanjut
dengan infus terus menerus selama 23 jam dengan dosis 5,4mg/kgBB/jam. Pasien onset 3-8 jam, caranya
sama namun dilakukan selama 47 jam. >8 jam, tidak dianjurkan)
2. Perawatan intensif
3. Tata laksana operatif  kalau ada fraktur, gambaran neurologis memburuk, herniasi diskus invertebralis
 Treatment
PERAWATAN INTENSIF

• Pasien cedera medulla spinalis bisa mengalami komplikasi akut atau subakut
 Treatment
TATALAKSANA OPERATIF

• Operasi dilakukan kalau terdapat keadaan-keadaan sebagai berikut : ada fraktur dan pecahan tulang
menekan medulla spinalis, gambaran neurologis memburuk, fraktur dan dislokasi tidak stabil,
herniasi diskus intervertebralis yang menekan medulla spinalis

TATALAKSANA REHABILITATIF

• Meningkatkan kualitas individu yang mengalami gangguan secara optimal dalam bidang mental,
fisik, kognitif, dan sosial
• Proses nya : memberikan edukasi mengenai cedera medulla spinalis kepada keluarga pasien,
maksimalkan fungsi mobilisasi dan kemampuan perawatan diri pasien
• Mencegah masalah kesehatan komorbid