Muhammad Azmi Hakim - 1102012170

LI 1. Memahami dan Menjelaskan Trauma Kepala

LO 1.1. Definisi
Cedera kepala didefinsikan sebaga perubahan fungsi fisik atau mental akibat pukulan terhadap kepala. Kehilangan
kesadaran tidak harus terjadi. Derajat keparahan cedera kepala dapat diklasifikasikan pada GCS postresuscitation, yaitu
skor total dari mata, motoric, dan verbal. Umumnya, skor 13-15 menunjukkan cedera kepala ringan, skor 9-12
menunjukkan cedera kepala sedang, dan skor kurang dari 8 menunjukkan cedera kepala berat. Dalam beberapa tahun
terakhir, beberapa penelitian telah memasukkan pasien dengan skor 13 ke dalam cedera kepala sedang, sementara pasien
yang memiliki skor 14-15 masih termasuk dalam cedera kepala ringan. Concussion (gegar otak) dan cedera kepala ringan
umumnya merupaka sinonim.
(http://emedicine.medscape.com/)

LO 1.2. Etiologi

LO 1.3. Epidemiologi
Trauma merupakan penyebab utama kematian pada anak-anak dan dewasa muda, tetapi insidensi kematian dan kecacatan
trauma telah menurun. Penurunan tersebut dikarenakan meningkatnya kewaspadaan pada alat keselamatan, seperti sabuk
pengaman dan helm pada pengendara motor. Namun begitu, trauma masih menjadi penyebab morbiditas dan mortalitas
yang utama dan dapat menyerang pada setiap sistem organ.

LO 1.4. Klasifikasi

LO 1.5. Patofisiologi
Perubahan structural
Perubahan structural yang nyata pada cedera kepala merupakan hal yang biasa terjadi dan sering memiliki
kesamaan baik pada otopsi maupun neuroimaging. Tengkorak dapat fraktur sebagai fraktur linier sederhana atau fraktur
depresi yang jauh lebih rumit, dimana fragmen tulang-tulang mendorong ke dalam calvaria. Pada pasien cedera kepala
ringan, fraktur tengkorak dapat mengakibatkan perubahan tekana intracranial yang mencolok.
Baik luka langsung maupun cedera kontusio (luka memar), dimana menyebabkan otak terdorong ke arah
sebaliknya, dapat mengakibatkan perdarahan fokal di bawah calvaria. Perdarahan dapat disebabkan oleh kontusio fokal
intraserebral (perdarahan ekstraserebral) . perdarahan ekstraserebral merupakan perdarah subdural yang berasal dari vena-
vena di otak yang sobek tetapi perdarahan epidural yang berasal dari robekan arteri meningeal media atau vena diploica.
Kadang-kadang, perdarahn subdural dapat berasal dari gangguan arteri cortical. Pada tipe perdarahann subdural merupaka
tipe perdarahan yang cepat dan progresif serta dapat terjadi setelah cedera kepala yang sangat riingan pada pasien geriatri.
Kerusakan neuronal juga merupakan hal yang penting. Sebuah penelitian patologi menemukan bahwa kerusakan
neuron secara kuantitatif pada thalamus dorsal berhubungan dengan disabilitas berat dan vegetative state pada pasien
cedera kepala dekat.
Cedera aksonal telah dikenali sebagai kerusakan structural lanjut dari cedera otak. Penggunaan pewarnaan
protein prekursor amyloid telah menghasilkan pengenalan pada jenis cedera ini. Menggunakan teknik ini, para
ilmuwan telah dapat mengidentifikasi cedera aksonal pada pasien dengan cedera kepala ringan. Cedera aksonal
yang lebih berat dan difus telah ditemukan korelasinya dengan vegetative state dan onsetnya koma setelah cedera.

Neurochemical changes
After traumatic brain injury, the brain is bathed with potentially toxic neurochemicals. Catecholamine surges have
been documented in the plasma (higher catecholamine levels correlated with worse clinical outcomes) and in the
cerebrospinal fluid (CSF) of patients with head injuries (higher CSF 5-hydroxyindole acetic acid (HIAA), the
serotonin metabolite, correlated with worse outcomes).[20]Head injury causes release of free radicals and breakdown
of membrane lipids. These lipids fragment into mediators of inflammation. The excitotoxic amino acids (ie,
glutamate, aspartate) initiate a cascade of processes culminating in an increase in intraneuronal calcium and cell
death. Researchers using a microdialysis technique have correlated high CSF levels of excitotoxic amino acids with
poor outcomes in head injury.[21]

Although neuroprotective strategies employing antiexcitotoxic pharmacotherapies were effective in diminishing the
effects of experimental brain injuries in laboratory animals, clinical trials in humans generally have been
disappointing.[22] These failures have prompted development of more complex models of neuronal injury and cell
death. Recently, researchers have demonstrated that although certain types of glutamate antagonists may protect
against acute cell death, they potentiate slowly progressive neuronal injury in experimental rodent models. Still
others have found that low-dose glutamate administered before brain injury is somehow neuroprotective. Such dose
and timing effects are only beginning to be understood.[23]

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Prostaglandins, inflammatory mediators produced by membrane lipid breakdown, are also elevated dramatically in
the plasma of patients with moderate-to-severe head trauma during the first 2 weeks after injury. Patients with
higher prostaglandin levels had significantly worse outcomes than those with more modest elevations. Furthermore,
levels of a thromboxane metabolite, a potent vasoconstricting prostaglandin, were elevated
disproportionately.[24] Such a process may underlie posttraumatic vasospasm, which has been documented in some,
but not all, transcranial Doppler studies of patients with closed head injuries, even in patients without traumatic
subarachnoid bleeds.[25]

Recently, an increase in T cells reactive against myelin antigens was found in 10 patients with severe head injuries.
Although the sample size was limited, those patients with increased T-cell reactivity had improved outcomes
compared with their nonreactive counterparts, and a beneficial autoimmune response was proposed. [26]

In addition to structural and chemical changes, gene expression is altered following closed head injury. Genes
involving growth factors, hormones, toxin-binders, apoptosis (programmed cell death), and inflammation have all
been implicated in rodent models. For example, in a mouse model of head injury, elevated levels of the transcription
factor p53 were found. p53 translocates to the nucleus and initiates apoptosis or programmed cell death. Such a
process could account for the delayed neuronal loss seen in head injuries.[27]

Secondary insults
Hypotension and hypoxia cause the most prominent secondary trauma-induced brain insults. Both hypoxia and
hypotension had adverse impacts on outcomes of 716 patients with severe head injuries from the Traumatic Coma
Data Bank in the United States. Efforts to limit hypoxic injury with in-field intubation have been unsuccessful.
Indeed, a multicenter study of 4098 patients with severe traumatic brain injury found that in-field intubation was
associated with a dramatic increase in death and poor long-term neurologic outcome, even after controlling for
injury severity.[28]

In the Trauma Coma Data Bank study, hypotension was even more significant than hypoxia and, by itself, was
associated with a 150% increase in mortality rate. Systemic hypotension is critical because brain perfusion
diminishes with lower somatic blood pressures. Brain perfusion (ie, cerebral perfusion pressure) is the difference
between the mean arterial pressure and intracranial pressure. The intracranial pressure is increased in head injury
by intracranial bleeding, cell death, and secondary hypoxic and ischemic injuries. Accordingly, another recent study
reported that death and increased disability outcomes correlated with the durations of both systemic hypotension
and elevated intracranial pressures.[29]

Severe anemia is often coexistent with head injuries, but blood transfusions have been recently associated with
increased mortality and complications among 1,250 ICU-admitted patients with brain injuries. This relationship held
even after controlling for the degree of anemia.[30]

Finally, posttraumatic cerebral infarction occurs in up to 12% of patients with moderate and severe head injuries
and is associated with a decreased Glasgow Coma Scale, low blood pressure, and herniation syndromes.[31]

(http://emedicine.medscape.com/)

LO 1.6. Mnaifestasi klinis

The Glasgow Coma Scale (GCS) is the mainstay for rapid neurologic assessment in acute head injury. Following
ascertainment of the GCS score, the examination is focused on signs of external trauma, as follows:

Bruising or bleeding on the head and scalp and blood in the ear canal or behind the tympanic membranes: May
be clues to occult brain injuries
Anosmia: Common; probably caused by the shearing of the olfactory nerves at the cribriform plate [5]
Abnormal postresuscitation pupillary reactivity: Correlates with a poor 1-year outcome
Isolated internuclear ophthalmoplegia secondary to traumatic brainstem injuries: Has a relatively benign
prognosis [6]
Cranial nerve (CN) VI palsy: May indicate raised intracranial pressure
CN VII palsy: May indicate a fracture of the temporal bone, particularly if it occurs in association with decreased
hearing
Hearing loss: Occurs in 20-30% of patients with head injuries [7]
Dysphagia: Raises the risk of aspiration and inadequate nutrition [8]
Focal motor findings: Include flexor or extensor posturing, tremors and dystonia, impairments in sitting balance,
and primitive reflexes; may be manifestations of a localized contusion or an early herniation syndrome
(http://emedicine.medscape.com/)

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LO 1.7. Diagnosis

Bedside cognitive testing

In the acute setting, measurements of the patient's level of consciousness, attention, and orientation are of primary
importance.

Some patients acutely recovering from head trauma demonstrate no ability to retain new information. Mental status
assessments have validated the prognostic value of the duration of posttraumatic amnesia; patients with longer
durations of posttraumatic amnesia have poorer outcomes.[9]

In the long-term setting, the following bedside cognitive tests can be employed:

Mini-Mental State Examination

Luria "fist, chop, slap" sequencing task: To rapidly assess motor regulation
Antisaccade task: Impaired in patients with symptomatic brain injury; the sensitivity of this test in detecting brain
injury has been questioned [10]
Letter and category fluency: To provide information about self-generative frontal processes.
Untimed Trails B test: Allows further qualitative testing of frontal functioning
Laboratory studies

Sodium levels: Alterations in serum sodium levels occur in as many as 50% of comatose patients with head
injuries [11] ; hyponatremia may be due to the syndrome of inappropriate antidiuretic hormone (SIADH) or cerebral
salt wasting; elevated sodium levels in head injury indicate simple dehydration or diabetes insipidus
Magnesium levels: These are depleted in the acute phases of minor and severe head injuries
Coagulation studies: Including prothrombin time (PT), activated partial thromboplastin time (aPTT), and platelet
count; these are important to exclude a coagulopathy
Blood alcohol levels and drug screens: May help to explain subnormal levels of consciousness and cognition in
some patients with head trauma
Renal function tests and creatine kinase levels: To help exclude rhabdomyolysis if a crush injury has occurred or
marked rigidity is present
Neuron-specific enolase and protein S-100 B: Elevated serum levels may correlate with persistent cognitive
impairment at 6 months in patients with severe or mild head injuries [12]
Imaging studies

Computed tomography scanning: The main imaging modality used in the acute setting
Magnetic resonance imaging: Typically reserved for patients who have mental status abnormalities unexplained
by CT scan findings
Electroencephalography

Although certain electroencephalographic patterns may have prognostic significance, considerable interpretation is
needed, and sedative medications and electrical artifacts are confounding. The most useful role of
electroencephalography (EEG) in head injuries may be to assist in the diagnosis of nonconvulsive status
epilepticus.

(http://emedicine.medscape.com/)

LO 1.8. Diagnosis banding

Acute Management of Stroke

Acute Subdural Hematoma

Alzheimer Disease Imaging

Anterior Circulation Stroke

Brain Metastasis

Cerebral Aneurysms

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Confusional States and Acute Memory Disorders

Emergent Management of Subarachnoid Hemorrhage

Epileptic and Epileptiform Encephalopathies

Frontal Lobe Syndromes

Generalized Tonic-Clonic Seizures

Hydrocephalus

Prion-Related Diseases

Psychiatric Disorders Associated With Epilepsy

Subdural Empyema

Temporal Lobe Epilepsy

(http://emedicine.medscape.com/)

LO 1.9. Tatalaksana

Intracranial pressure

If the intracranial pressure rises above 20-25 mm Hg, intravenous mannitol, cerebrospinal fluid drainage, and
hyperventilation can be used. If the intracranial pressure does not respond to these conventional treatments, high-
dose barbiturate therapy is permissible.[13]

Another approach used by some clinicians is to focus primarily on improving cerebral perfusion pressure as
opposed to intracranial pressure in isolation.

Decompressive craniectomies are sometimes advocated for patients with increased intracranial pressure refractory
to conventional medical treatment.

Hypertonicity

Dantrolene, baclofen, diazepam, and tizanidine are current oral medication approaches to hypertonicity. Baclofen
and tizanidine are customarily preferred because of their more favorable side-effect profiles.

Subdural hematomas

Traditionally, the prompt surgical evacuation of subdural hematomas was believed to be a major determinant of an
optimal outcome. However, research indicates that the extent of the original intracranial injury and the generated
intracranial pressures may be more important than the timing of surgery.

(emedicine.medscape.com)

LO 1.10. Komplikasi

LO 1.11. Pencegahan

LI 2. Memahami dan Menjelaskan Fraktrur Basis Kranii

LO 2.1. Definisi
a basilar fracture is a linear fracture at the base of the skull. It is usually associated with a dural tear and is found at
specific points on the skull base.

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LO 2.2. Etiologi

In newborns, "ping-pong" depressed fractures are secondary to the baby's head impinging against the mother's
sacral promontory during uterine contractions.[15]The use of forceps also may cause injury to the skull, but this is
rare.

Skull fractures in infants originate from neglect, fall, or abuse. Most of the fractures seen in children are a result of
falls and bicycle accidents. In adults, fractures typically occur from motor vehicle accidents or violence.

(http://emedicine.medscape.com/)

LO 2.3. Epidemiologi

Frequency
Simple linear fracture is by far the most common type of fracture, especially in children younger than 5 years.
Temporal bone fractures represent 15-48% of all skull fractures. Basilar skull fractures represent 19-21% of all skull
fractures. Depressed fractures are frontoparietal (75%), temporal (10%), occipital (5%), and other (10%). Most of
the depressed fractures are open fractures (75-90%).

(http://emedicine.medscape.com/)

LO 2.4. Klasifikasi

(http://emedicine.medscape.com/)

LO 2.5. Patofisiologi

LO 2.6. Manifestasi klinis

Patients with fractures of the petrous temporal bone present with CSF otorrhea and bruising over the mastoids, ie,
Battle sign. Presentation with anterior cranial fossa fractures is with CSF rhinorrhea and bruising around the eyes,

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ie, "raccoon eyes." Loss of consciousness and Glasgow Coma Score may vary depending on an associated
intracranial pathologic condition.

Longitudinal temporal bone fractures result in ossicular chain disruption and conductive deafness of greater than 30
dB that lasts longer than 6-7 weeks. Temporary deafness that resolves in less than 3 weeks is due to
hemotympanum and mucosal edema in the middle ear fossa. Facial palsy, nystagmus, and facial numbness are
secondary to involvement of the VII, VI, and V cranial nerves, respectively. Transverse temporal bone fractures
involve the VIII cranial nerve and the labyrinth, resulting in nystagmus, ataxia, and permanent neural hearing loss.

Occipital condylar fracture is a very rare and serious injury.[16] Most of the patients with occipital condylar fracture,
especially with type III, are in a coma and have other associated cervical spinal injuries. These patients may also
present with other lower cranial nerve injuries and hemiplegia or quadriplegia.

Vernet syndrome or jugular foramen syndrome is involvement of the IX, X, and XI cranial nerves with the fracture.
Patients present with difficulty in phonation and aspiration and ipsilateral motor paralysis of the vocal cord, soft
palate (curtain sign), superior pharyngeal constrictor, sternocleidomastoid, and trapezius.

Collet-Sicard syndrome is occipital condylar fracture with IX, X, XI, and XII cranial nerve involvement. [17, 18, 19]

(http://emedicine.medscape.com/)

LO 2.7. Diagnosis
Laboratory Studies
In addition to a complete neurological examination, baseline laboratory analyses, and tetanus toxoid (where
appropriate, as in open skull fractures), the diagnostic workup for fractures is radiological.

Imaging Studies
In 1987, the skull x-ray referral criteria panel decided that skull films are suboptimal in revealing basilar skull
fractures. Hence, other than a fracture at the vertex that might be missed by CT scan and picked up by a plain film,
skull x-ray is of no benefit when a CT scan is obtained. In one study, skull x-ray missed 19.1% of fractures, whereas
CT scan missed 11.9%.[20]

CT scan is the criterion standard modality for aiding in the diagnosis of skull fractures.[21, 22] Thinly sliced bone
windows of up to 1-1.5 mm thick, with sagittal reconstruction, are useful in assessing injuries. Helical CT scan is
helpful in occipital condylar fractures, but 3-dimensional reconstruction usually is not necessary.[23]

CT scan for skull fractures was found to have a sensitivity of 85.4 % and a specificity of 100% in one study.[24]

MRI or magnetic resonance angiography is of ancillary value for suspected ligamentous and vascular injuries. Bony
injuries are far better visualized using CT scan.

Other Tests
Bleeding from the ear or nose in cases of suspected CSF leak, when dabbed on a tissue paper, shows a clear ring
of wet tissue beyond the blood stain, called a "halo" or "ring" sign. A CSF leak can also be revealed by analyzing
the glucose level and by measuring tau-transferrin.

(http://emedicine.medscape.com/)

LO 2.8. Diagnosis banding

LO 2.9. Tatalaksana

Adults with simple linear fractures who are neurologically intact do not require any intervention and may even be
discharged home safely and asked to return if symptomatic. Infants with simple linear fractures should be admitted
for overnight observation regardless of neurological status.[25] Neurologically intact patients with linear basilar
fractures also are treated conservatively, without antibiotics. Temporal bone fractures are managed conservatively,
at least initially, because tympanic membrane rupture usually heals on its own.

Simple depressed fractures in neurologically intact infants are treated expectantly. These depressed fractures heal
well and smooth out with time, without elevation. Seizure medications are recommended if the chance of developing

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seizures is higher than 20%. Open fractures, if contaminated, may require antibiotics in addition to tetanus toxoid.
Sulfisoxazole is a common recommendation.

Types I and II occipital condylar fractures are treated conservatively with neck stabilization, which is achieved with a
hard (Philadelphia) collar or halo traction.

Surgical Therapy
The role of surgery is limited in the management of skull fractures. Infants and children with open depressed
fractures require surgical intervention. Most surgeons prefer to elevate depressed skull fractures if the depressed
segment is more than 5 mm below the inner table of adjacent bone. Indications for immediate elevation are gross
contamination, dural tear with pneumocephalus, and an underlying hematoma. At times, craniectomy is performed if
the underlying brain is damaged and swollen. In these instances, cranioplasty is required at a later date. Another
indication for early surgical intervention is an unstable occipital condylar fracture (type III) that requires atlantoaxial
arthrodesis. This can be achieved with inside-outside fixation.[26]

In a retrospective study by Bonfield et al, the majority of pediatric skull fractures were found to be managed
conservatively, and of those requiring surgical intervention, fewer than half of the surgeries were performed solely
for skull fracture repair only. Surgical intervention was more likely in patients who were hit in the head with an object
or were involved in a motor vehicle crash. Frontal bone fractures were more likely to necessitate repair, and those
patients treated for traumatic brain injury had a greater incidence of 2 or 3 bones involved in the fracture. Most of
the complications that occurred were related to the underlying trauma, not the surgery. In addition, none of the
patients who underwent intervention for repair of only skull fracture had a worsening of neurologic status.[27]

Delayed surgical intervention is required in ossicular incongruences resulting from a longitudinal skull base fracture
of the temporal bone. Ossiculoplasty may be needed if hearing loss persists for longer than 3 months or if the
tympanic membrane has not healed on its own. Another indication is persistent CSF leak after a skull base fracture.
This requires precise detection of the site of leak before any surgical intervention is instituted.

(http://emedicine.medscape.com/)

LO 2.10. Komplikasi

The risk of infection is not high, even without routine antibiotics, especially with CSF rhinorrhea. Facial palsy and
ossicular chain disruption associated with basilar fractures are discussed in the Clinical section. However, notably,
facial palsy that starts with a 2- to 3-day delay is secondary to neurapraxia of the VII cranial nerve and is responsive
to steroids, with a good prognosis. A complete and sudden onset of facial palsy at the time of fracture usually is
secondary to nerve transection, with a poor prognosis.

Other cranial nerves also may be involved in basilar fractures. Fracture of the tip of the petrous temporal bone may
involve the gasserian ganglion. An isolated VI cranial nerve injury is not a direct result of fracture, but it may be
affected secondarily because of tension on the nerve. Lower cranial nerves (IX, X, XI, and XII) may be involved in
occipital condylar fractures, as described earlier in Vernet and Collet-Sicard syndromes (vide supra). Sphenoid
bone fracture may affect the III, IV, and VI cranial nerves and also may disrupt the internal carotid artery and
potentially result in pseudoaneurysm formation and caroticocavernous fistula (if it involves venous structures).
Carotid injury is suspected in cases in which the fracture runs through the carotid canal; in these instances, CT-
angiography is recommended. (emedicine.medscape.com)

LO 2.11. Pencegahan

LI 3. Memahami dan Menjelaskan Perdarahan Intrakranial

LO 3.1. Definisi
Intracranial hemorrhage (ie, the pathological accumulation of blood within the cranial vault) may occur within brain
parenchyma or the surrounding meningeal spaces.
(http://emedicine.medscape.com/)

LO 3.2. Etiologi
Possible causes are as follows:

Hypertension[5]
Arteriovenous malformation

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Aneurysmal rupture
Cerebral amyloid angiopathy
Intracranial neoplasm
Coagulopathy
Hemorrhagic transformation of an ischemic infarct
Cerebral venous thrombosis
Sympathomimetic drug abuse
Moyamoya
Sickle cell disease
Eclampsia or postpartum vasculopathy
Infection
Vasculitis
Neonatal intraventricular hemorrhage
Trauma
(http://emedicine.medscape.com/)

LO 3.3. Epidemiologi

Asian countries have a higher incidence of intracerebral hemorrhage than other regions of the world.
(http://emedicine.medscape.com/)

LO 3.4. Klasifikasi

LO 3.5. Patofisiologi

Nontraumatic intracerebral hemorrhage most commonly results from hypertensive damage to blood vessel walls
(eg, hypertension, eclampsia, drug abuse), but it also may be due to autoregulatory dysfunction with excessive
cerebral blood flow (eg, reperfusion injury, hemorrhagic transformation, cold exposure), rupture of an aneurysm or
arteriovenous malformation (AVM), arteriopathy (eg, cerebral amyloid angiopathy, moyamoya), altered hemostasis
(eg, thrombolysis, anticoagulation, bleeding diathesis), hemorrhagic necrosis (eg, tumor, infection), or venous
outflow obstruction (eg, cerebral venous thrombosis).

Nonpenetrating and penetrating cranial trauma are also common causes of intracerebral hemorrhage.Patients who
experience blunt head trauma and subsequently receive warfarin or clopidogrel are considered at increased risk for
traumatic intracranial hemorrhage. According to one study, patients receiving clopidogrel have a significantly higher
prevalence of immediate traumatic intracranial hemorrhage compared with patients receiving warfarin. Delayed
traumatic intracranial hemorrhage is rare and occurred only in patients receiving warfarin.[1]

Chronic hypertension produces a small vessel vasculopathy characterized by lipohyalinosis, fibrinoid necrosis, and
development of Charcot-Bouchard aneurysms, affecting penetrating arteries throughout the brain including
lenticulostriates, thalamoperforators, paramedian branches of the basilar artery, superior cerebellar arteries, and
anterior inferior cerebellar arteries.

Predilection sites for intracerebral hemorrhage include the basal ganglia (40-50%), lobar regions (20-50%),
thalamus (10-15%), pons (5-12%), cerebellum (5-10%), and other brainstem sites (1-5%).

Intraventricular hemorrhage occurs in one third of intracerebral hemorrhage cases from extension of thalamic
ganglionic bleeding into the ventricular space. Isolated intraventricular hemorrhage frequently arise from
subependymal structures including the germinal matrix, AVMs, and cavernous angiomas.

(http://emedicine.medscape.com/)

LO 3.6. Mnaifestasi klinis

Onset of symptoms of intracerebral hemorrhage is usually during daytime activity, with progressive (ie, minutes to
hours) development of the following:

Alteration in level of consciousness (approximately 50%)

Nausea and vomiting (approximately 40-50%)
Headache (approximately 40%)

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Seizures[4] (approximately 6-7%)

Focal neurological deficits
Lobar hemorrhage due to cerebral amyloid angiopathy may be preceded by prodromal symptoms of focal
numbness, tingling, or weakness.

A history of hypertension, trauma, illicit drug abuse, or a bleeding diathesis may be elicited.

Clinical manifestations of intracerebral hemorrhage are determined by the size and location of hemorrhage, but may
include the following:

Hypertension, fever, or cardiac arrhythmias

Nuchal rigidity
Subhyaloid retinal hemorrhages
Altered level of consciousness
Anisocoria
Focal neurological deficits
o Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis,
homonymous hemianopia, aphasia, neglect, or apraxia
o Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia,
miosis, aphasia, or confusion
o Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous
hemianopia, abulia, aphasia, neglect, or apraxia
o Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion
o Brain stem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing,
miosis, or autonomic instability
o Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze
paresis, skew deviation, miosis, or decreased level of consciousness
(http://emedicine.medscape.com/)

LO 3.7. Diagnosis

Laboratory Studies
See the list below:

Complete blood count (CBC) with platelets: Monitor for infection and assess hematocrit and platelet count to
identify hemorrhagic risk and complications.
Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy.
Serum chemistries including electrolytes and osmolarity: Assess for metabolic derangements, such as
hyponatremia, and monitor osmolarity for guidance of osmotic diuresis.
Toxicology screen and serum alcohol level if illicit drug use or excessive alcohol intake is suspected: Identify
exogenous toxins that can cause intracerebral hemorrhage.
Screening for hematologic, infectious, and vasculitic etiologies in select patients: Selective testing for more
uncommon causes of intracerebral hemorrhage.

CT scan
CT scan readily demonstrates acute hemorrhage as hyperdense signal intensity (see image below). Multifocal
hemorrhages at the frontal, temporal, or occipital poles suggest a traumatic etiology.

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Muhammad Azmi Hakim - 1102012170

Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.

Patients with mild blunt head trauma and preinjury anticoagulant or antiplatelet use are at increased risk of
intracranial hemorrhage and should undergo urgent and liberal CT scanning.[6]

Hematoma volume in cubic centimeters can be approximated by a modified ellipsoid equation: (A x B x C)/2, where
A, B, and C represent the longest linear dimensions in centimeters of the hematoma in each orthogonal plane.

Perihematomal edema and displacement of tissue with herniation also can be appreciated.

Iodinated contrast may be injected to increase screening yield for underlying tumor or vascular malformation.

CT angiography "spot sign" may be used to predict growth of intracerebral hematomas.[7]

MRI
The MRI appearance of hemorrhage on conventional T1 and T2 sequences evolves over time because of chemical
and physical changes within and around the hematoma (see Table 1 below).

Conventional T1 and T2 sequences are not highly sensitive to hemorrhage in the first few hours, but newer gradient
refocused echo sequences appear to be able to detect intracerebral hemorrhage reliably within the first 1-2 hours of

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onset (see following images).

Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral
hemorrhage associated with a right frontal arteriovenous malformation.

Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal
intracranial hemorrhage due to sickle cell disease.

AVMs and cavernous angiomas may be identified by the presence of multiple flow voids adjacent to the hematoma.

Paramagnetic contrast may be injected to increase screening yield for underlying tumor or vascular malformation.

Gradient echo sequences may reveal multiple foci of hypointensity attributable to hemosiderin deposition from prior
silent cerebral microbleeds. A multilobar distribution of hypointense foci on gradient echo imaging may provide
supportive evidence of cerebral amyloid angiopathy, while multiple deep foci may suggest an underlying
hypertensive arteriopathy.

MRI studies incorporating gradient echo or susceptibility-weighted sequences may be used as the sole imaging
modality for patients with acute stroke, readily identifying intracranial hemorrhage.

Permeability techniques, including use of source perfusion imaging data, may be used to detect blood-brain
derangements that precede hemorrhagic transformation after thrombolysis.[8]

Vessel imaging
CT angiography permits screening of large and medium-sized vessels for AVMs, vasculitis, and other
arteriopathies.

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MR angiography permits screening of large and medium-sized vessels for AVMs, vasculitis, and other
arteriopathies.

Conventional catheter angiography definitively assesses large, medium-sized, and sizable small vessels for AVMs,
vasculitis, and other arteriopathies.

Consider catheter angiography for young patients, patients with lobar hemorrhage, patients without a history of
hypertension, and patients without a clear cause of hemorrhage who are surgical candidates. Angiography may be
deferred for older patients with suspected hypertensive intracerebral hemorrhage and patients who do not have any
structural abnormalities on CT scan or MRI.

Timing of angiography depends on clinical status and neurosurgical considerations.

Other Tests
ECG frequently identifies cerebrum-induced dysrhythmia or cardiac injury.

(http://emedicine.medscape.com/)

LO 3.8. Diagnosis banding

Acute Management of Stroke

Acute Subdural Hematoma

Anisocoria

Blood Dyscrasias and Stroke

Cardioembolic Stroke

Cerebellar Hemorrhage

Cerebral Amyloid Angiopathy

Cerebral Aneurysms

Cerebral Venous Thrombosis

Dissection Syndromes

Emergent Management of Subarachnoid Hemorrhage

Epidural Hematoma in Emergency Medicine

Head Injury

Herpes Simplex Encephalitis

Hydrocephalus

Lumbar Puncture (CSF Examination)

Magnetic Resonance Imaging in Acute Stroke

Moyamoya Disease

Neonatal Injuries in Child Abuse

Neurologic Effects of Cocaine

Neurological Sequelae of Infectious Endocarditis

Pediatric Status Epilepticus

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 Muhammad Azmi Hakim - 1102012170

Posttraumatic Epilepsy

Reperfusion Injury in Stroke

Secondary CNS Melanomas

Stroke Anticoagulation and Prophylaxis

Subdural Empyema

Thrombolytic Therapy in Stroke

Vascular Surgery for Arteriovenous Malformations

Vein of Galen Malformation

(http://emedicine.medscape.com/)

LO 3.9. Tatalaksana

Medical therapy of intracranial hemorrhage is principally focused on adjunctive measures to minimize injury and to
stabilize individuals in the perioperative phase. Recent clinical trial data suggests that treatment with recombinant
factor VIIa (rFVIIa) within 4 hours after the onset of intracerebral hemorrhage limits the growth of the hematoma,
reduces mortality, and improves functional outcomes at 90 days.[10] However, further study of this medication in a
broader cohort did not result in improved clinical outcomes. This intervention may also result in a small increase in
the frequency of thromboembolic adverse events. The early use of rFVIIa in patients with head injury without
systemic coagulopathy may reduce the occurrence of enlargement of contusions, the requirement of further
operation, and adverse outcome.[11]

Perform endotracheal intubation for patients with decreased level of consciousness and poor airway protection.
Cautiously lower blood pressure to a mean arterial pressure (MAP) less than 130 mm Hg, but avoid excessive
hypotension. Early treatment in patients presenting with spontaneous intracerebral hemorrhage is important as it
may decrease hematoma enlargement and lead to better neurologic outcome.[12]
Rapidly stabilize vital signs, and simultaneously acquire emergent CT scan.
Intubate and hyperventilate if intracranial pressure is increased; initiate administration of mannitol for further
control.
Maintain euvolemia, using normotonic rather than hypotonic fluids, to maintain brain perfusion without
exacerbating brain edema.
Avoid hyperthermia.
Correct any identifiable coagulopathy with fresh frozen plasma, vitamin K, protamine, or platelet transfusions.
Initiate fosphenytoin or other anticonvulsant definitely for seizure activity or lobar hemorrhage, and optionally in
other patients.Levetiracetam has shown efficacy in children for prophylaxis of early posthemorrhagic
seizures.[13]Additional data suggest that levetiracetam is more effective than phenytoin for seizure prophylaxis
without suppression of cognitive abilities in patients with ICH.[14]
Facilitate transfer to the operating room or ICU.
While reducing SBP with intravenous nicardipine hydrochloride does not significantly reduce hematoma
expansion in patients with ICH, the Antihypertensive Treatment of Acute Cerebral Hemorrhage study supports
further studies to evaluate the efficacy of aggressive pharmacologic SBP reduction. [15]

Surgical Care
See the list below:

Consider nonsurgical management for patients with minimal neurological deficits or with intracerebral hemorrhage
volumes less than 10 mL.
Consider surgery for patients with cerebellar hemorrhage greater than 3 cm, for patients with intracerebral
hemorrhage associated with a structural vascular lesion, and for young patients with lobar hemorrhage. The
common hypertensive hemorrhages in the basal ganglia have not been shown clearly to benefit from surgery,
although case series with favorable outcomes after stereotactic needle evacuation or endoscopic drainage have
been reported. In the past, standard craniotomy with evacuation of the hematoma did not appear to improve
outcomes.
Other surgical considerations include the following:

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 Muhammad Azmi Hakim - 1102012170

o
Clinical course and timing
o
Patient's age and comorbid conditions
o
Etiology
o
Location of the hematoma
o
Mass effect and drainage patterns
Surgical approaches include the following:
o Craniotomy and clot evacuation under direct visual guidance
o Stereotactic aspiration with thrombolytic agents
o Endoscopic evacuation

Medication Summary
Antihypertensive agents reduce blood pressure to prevent exacerbation of intracerebral hemorrhage. Osmotic
diuretics, such as mannitol, may be used to decrease intracranial pressure.

As hyperthermia may exacerbate neurological injury, acetaminophen may be given to reduce fever and to relieve
headache.

Anticonvulsants are used routinely to avoid seizures that may be induced by cortical damage. Levetiracetam has
shown efficacy in children for prophylaxis of early posthemorrhagic seizures.[13] Additional data suggest that
levetiracetam is more effective than phenytoin for seizure prophylaxis without suppression of cognitive abilities in
patients with ICH.[14] Vitamin K and protamine may be used to restore normal coagulation parameters. Antacids are
used to prevent gastric ulcers associated with intracerebral hemorrhage.

Accumulating data suggest that statins have neuroprotective effects; however, their association with intracerebral
hemorrhage outcome has been inconsistent.[16]Antecedent use of statins prior to intracerebral hemorrhage is
associated with favorable outcome and reduced mortality after intracerebral hemorrhage. This phenomenon
appears to be a class effect of statins.

(http://emedicine.medscape.com/)

LO 3.10. Komplikasi

Neurological deficits or death

Seizures
Hydrocephalus
Spasticity
Urinary complications
Aspiration pneumonia
Neuropathic pain
Deep venous thrombosis
Pulmonary emboli
Cerebral herniation
(http://emedicine.medscape.com/)

LO 3.11. Pencegahan

LI 4. Memahami dan Menjelaskan Trias Cushing

In 1903, Cushing described what is now widely known as the "Cushing Triad" as a clinical tool for recognizing the
presence of elevated ICP. The triad consists of a widening pulse pressure (rising systolic, declining diastolic), irregular
respirations, and bradycardia.[24] In 1922, Jackson noted that the pulse, respiration, and blood pressure are affected
only once the medulla is compressed, and some patients with clinical signs of brain compression had normal lumbar
CSF pressures.[25] Cushing quantified the Monro-Kelly doctrine, writing that the sum of the volume of the brain plus
the CSF volume plus the intracranial blood volume is constant. Therefore, an increase in one should reduce one or
both of the others.[26]
(http://emedicine.medscape.com/)

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