Anda di halaman 1dari 77

Cedera Kepala

Cedera Medulla Spinalis


(traumatic brain injury & spine injury) dr. Anna Luthfiana SpS
Bagian Ilmu Penyakit Saraf

&

(traumatic brain injury)

Cedera Kepala

setiap perubahan fungsi mental atau fisik yang diakibatkan oleh benturan pada kepala

(traumatic brain injury)


Comotio cerebri = pingsan sejenak, dengan atau tanpa amnesia

Cedera Kepala

retrograd, tanpa defisit neurologis


Contusio cerebri = Perdarahan permukaan otak, berupa bintik perdarahan besar atau kecil, tanpa kerusakan duramater, dengan defisit neurologis yang reversibel

(traumatic brain injury)


mekanisme Tertutup Terbuka / Penetrans severitas Ringan : GCS 13-15 Sedang : GCS 9-12 Berat : GCS <= 8 morfologi

Cedera Kepala

Fraktura tengkorak

Lesi intrakranial

Kalvaria - Linear / Stelata - Depressed / Non-depressed

Basilar

Fokal - Epidural - Subdural - Intraserebral

Difusa - Konkusi ringan - Konkusi klasik - Cedera aksonal difusa

(traumatic brain injury)


mekanisme

Cedera Kepala

(traumatic brain injury)


mekanisme

Cedera Kepala

severitas
LOC 5 ; FND; PTA 30

GCS 13 - 15 GCS 9 - 12 GCS 8

: Mild Traumatic Brain Injury (CKR) : Moderate Traumatic Brain Injury (CKS) : Severe Traumatic Brain Injury (CKB)

(traumatic brain injury)


GCS dan Outcome (Stein, 2000)
GCS at 24 hour 11-15 8-10 5-7 3-4 Good Recovery or moderate disability 91% 59% 28% 13% Vegetative or dead 6% 27% 54% 80%

Cedera Kepala

(traumatic brain injury)


Tanpa memperdulikan nilai GCS, pasien digolongkan sebagai penderita cedera kepala berat bila: 1. Pupil tak ekual 2. Pemeriksaan motor tak ekual 3. Cedera kepala terbuka dengan bocornya CSS atau adanya jaringan otak yang terbuka. 4. Perburukan neurologik. 5. Fraktura tengkorak depressed.

Cedera Kepala

(traumatic brain injury)


morfologi fraktura tengkorak

Cedera Kepala

Nyeri kepala disertai muntah = # linear

# depressed =

indikasi elevasi :

depresi > 8-10 mm (> ketebalan tulang tengkorak), defisit neurologis, bocornya LCS, open depressed

(traumatic brain injury)


morfologi fraktura tengkorak

Cedera Kepala

# basis kranii = LCS otorrhea atau rhinorrhea, hemotympanum atau lacerasi CAE, battles sign, racoons eyes, paresis n.VII-VIII, n.I, n.VI - Hati-hati pemasangan NGT - Harus diberikan antibiotika profilaksis

(traumatic brain injury)


morfologi fraktura tengkorak Standar Foto Kepala Rutin : AP + Lateral Occipital : Towne Orbita : Caldwell Viscerocranium : Waters Zygomaticum : Axial Basis Cranii dan os petrosum : Stanver bilateral

Cedera Kepala

(traumatic brain injury)


morfologi Lesi intrakranial

Cedera Kepala

Hematoma epidural (EDH) =


regio temporal atau temporal-parietal

robeknya pembuluh meningeal media (darah arterial, atau sekunder dari


vena (1/3 kasus) akibat robeknya sinus vena t.u parietal-oksipital fossa posterior) 0.5% dari keseluruhan atau 9% dari pasien koma cedera kepala menegakkan diagnosis harus ditindaklanjuti segera interval lucid kelemahan anggota gerak (& defisit neurologis) yang tidak ekual dilatasi pupil ipsilateral

Outcome langsung bergantung pada status pasien sebelum operasi.


Mortalitas dari hematoma epidural sekitar 0% pada pasien tidak
koma, dan 20% pada pasien koma dalam

(traumatic brain injury)


morfologi Lesi intrakranial

Cedera Kepala

Hematoma subdural (SDH) =


Jauh lebih sering dari hematoma epidural,

sekitar 30% penderita dengan CKB


Paling sering akibat robeknya vena bridging antara korteks serebral dan sinus draining., dapat berkaitan dengan laserasi permukaan atau substansi otak. Umumnya lebih berat dan prognosisnya lebih buruk nyeri kepala terus memberat disertai penurunan kesadaran Mortalitas 60%, diperkecil oleh tindakan operasi yang sangat segera dan pengelolaan medis agresif

(traumatic brain injury)

Cedera Kepala

Types of Damage in Brain Injury (Stamp, 2000)

Diffuse Axonal Injury

Shearing injury of axons Deep cerebral cortex, thalamus, basal ganglia Punctate hemorrhage and diffuse cerebral edema

DIFFUSE AXONAL SHEARING


When axons are torn or stretched as a result of the different layers moving at different speeds, this called SHEARING. Shear damage is microscopic This is a common cause of brain damage after TBI

Mild to moderate ischemia

Severe ischemia

Advanced ischemia

Insufficient oxygen and glucose

Influx of water Na+ ClCytotoxic edema

Inadequate energy supply


Failure of neuronal activity Regional brain dysfunction

Influx of Ca2+
Irreversible cellular injury

Loss of function causes accumulation of glutamate and aspartate which bind to NMDA receptors
Influx of water Na+ Ca2+
Destruction of cell components Formation of free radicals, eicosanoids and leukotrienes

Anaerobic metabolism
Accumulation of lactic acid and H+ compromises neuronal integrity

Cellular injury during ischemia - Inadequate energy supply


Ischemia ( O2,glucose)

ATP
Depolarisation
[Na+]
i

Lactic acid
i

[K+]

[Cl-]

Failed homeostatic mechanisms VCR

[H+]

Neurotransmitters
LCR

[Ca2+]

Free Fe2+

NA DA

Glutamate Lipolysis NO synthesis Proteolysis

Free radicals Glial injury

Auto-oxidation

Arachidonic acid Free radicals

IRREVERSIBLE INJURY

Cerebral Blood Flow

39.9 + 11.2 (Schroeder, 1995) 42.5 + 15.8 (Mc Laughlin, 1996)


Vasoreactivity 0.4-9.1%

29.3 + 16.4
Mc Laughlin, 1996 Contusion

Perilesional edema CT-normal tissue

Ischemia
Edema sitotoksik Ggn membran Ggn sintesis protein

Trauma

Fe lepas

Energi turun

Depolarisasi Sel
Disrupsi Ca Glutamat lepas

Radikal bebas

Asidosis

Destruksi sel
Secondary Brain Injury (Cohadon, 1995)

Hipoksia/ Iskemia/ Trauma Pelepasan neurotransmiter Penurunan ATP Kegagalan pompa Ca intrasel naik

Depolarisasi sel

Nekrosis

Pembentukan Reactive Oxygen Species

Ca mitokondria naik
Fx apoptogenik lepas Tranduksi signal abnormal

Apoptosis

Zauner, 2002

Mechanism of Cytotoxic edema in brain injury (Stamp, 2000)

Cerebral Blood Flow


Regulation of Cerebral Vascular Resistance

CBF

Normal 50 100 ml / min

MAP (mmHg)
Normal 60 - 150 mmHg

PaCo2
(mmHg) Normal 30 - 50 mmHg

Adapted from: Rogers (1996) Textbook of Pediatric Intensive Care pp. 648 - 651

Cellular injury during ischemia

Inadequate Energy supply

Deterioration of Ion Gradients

Consequences of calcium overload

(traumatic brain injury)

Cedera Kepala

Monroe-Kellie Principle

Brain CSF

Blood Mass
Bone

(traumatic brain injury)

Cedera Kepala

(traumatic brain injury)

Cedera Kepala

(traumatic brain injury)

Cedera Kepala

Management of Traumatic Head Injury

Decrease intracranial pressure Support circulation / maximize cerebral perfusion pressure Maximize oxygenation and ventilation Decrease cerebral metabolic rate

MANAGEMENT OF HEAD INJURY Goals of resuscitation and treatment is to minimize secondary ischemic brain injury by promoting and preserving cerebral perfusion Prevent or treat post injury hypotension Prevent or treat hypoxemia and reduce oxygen demand of the brain Prevent or treat intracranial hypertension Avoid measures that decrease cerebral perfusion

TREATMENT
GOAL PHARMACOLOGICAL AGENT : TO GAIN PHYSIOLOGICAL CONTROL OF THE PATIENT IN ORDER TO OPTIMIZE SUBSTRATE DELIVERY TO THE BRAIN AND PREVENT PAROXYSMAL INCREASES IN INTRACRANIAL PRESSURE (PARALYTIC, ANALGESICS, PRESSORS) TO PREVENT OR TREAT BRAIN SWELLING (DIURETICS, BARBITURATES) TO DECREASE SECONDARY(OR DELAYED PRIMARY) DAMAGE (STEROID) TO TREAT SYMPTOMS ASSOCIATED WITH BRAIN INJURY (SEDATIVE, STIMULANTS) TO PREVENT OR TO TREAT COMPLICATION OF BRAIN INJURY (ANTIBIOTIC, ANTICONVULSANT, NEUROPROTECTANT)

Monitoring
Serial neurologic examinations Circulation / Respiration Intracranial Pressure Radiologic Studies Laboratory Studies

(traumatic brain injury) Managemen di Unit Gawat Darurat Pemeriksaan Fisik secara umum Tanda vital:
TD, N, RR, temperatur, tipe pernafasan (cheynestokes, cluster, apneustic, ataxic)

Cedera Kepala

Inspeksi kelainan sistemis Inspeksi kranium

Cranio-cervical auscultation

Tanda2 # basis kranii Tanda2 # kranium lain, # facial, dll Periorbital edema, proptosis Bruit a. carotis = diseksi a. carotis Bruit pada mata = fistula traumatis carotis-cavernosus

Tanda-tanda trauma medulla-spinalis Adanya kejang = tunggal, multiple, status

Manajemen dan Terapi


Di Unit Gawat Darurat: Riwayat: jenis dan saat kecelakaan, kehilangan kesadaran, amnesia, nyeri kepala Pemeriksaan umum menyingkirkan cedera sistemik Pemeriksaan neurologis Radiograf tengkorak Radiograf tulang belakang leher dan lain-lain bila ada indikasi Kadar alkohol darah dan skrining toksik dari urin (terutama suspected) Contoh darah untuk penentuan golongan darah Tes darah dasar dan EKG CT scan kepala (bila memungkinkan) Rawat untuk pengamatan bahkan bila CT scan normal

(traumatic brain injury) Managemen di Unit Gawat Darurat Pemeriksaan Neurologis

Cedera Kepala

Status kesadaran:

GCS, tipe pernafasan, pupil, refleks cahaya, refleks kornea, dolls eye phenomena, deviasi conjugae
tanda herniasi

Saraf kranial:

Pemeriksaan motorik Pemeriksaan refleks patologis, clonus, & refleks fisiologis Pemeriksaan sensoris

t.u n.II, III, IV, VI, VII, & funduskopi

(traumatic brain injury) Managemen di Unit Gawat Darurat Cedera Kepala Ringan (CKR)

Cedera Kepala

BR dengan HOB elevasi 30-45 derajat Pemeriksaan neurologis tiap 2 jam Oksigenasi IVFD isotonik (misal: NS, RL, Assering) Analgetika ringan PO atau PR Anti-emesis (k/p) Lain-lain individual

MANAGEMENT OF MILD HEAD INJURY


HISTORY : NAME, AGE, SEX, RACE, OCCUPATION MECHANISM OF INJURY TIME OF INJURY LOSS OF CONSCIOUSNESS IMMEDIATELY AFTER INJURY SUBSEQUENT LEVEL OF ALERTNESS AMNESIA : RETROGRADE, ANTEROGRADE HEADACHE : MILD, MODERATE, SEVERE SEIZURE

MANAGEMENT OF MILD HEAD INJURY


GENERAL EXAMINATION TO EXCLUDE SYSTEMIC INJURY LIMITED NEUROLOGICAL EXAMINATION CERVICAL SPINE AND OTHER RADIOGRAPHS AS INDICATED BLOOD ALKOHOL LEVEL AND URINE TOXIC SCREEN CT SCAN OF THE HEAD IN ALL PATIENT EXCEPT COMPLETELY ASYMPTOMATIC AND NEUROLOGICALLY NORMAL PATIENT IS IDEAL

MANAGEMENT OF MILD HEAD INJURY


OBSERVE IN/ADMITTED TO HOSPITAL NO CT SCANNER AVAILABLE ABNORMAL CT SCAN ALL PENETRATING HEAD INJURY HISTORY OF LOSS CONSCIUOSNESS DETERIORATING CONSCIOUSNESS MODERATE TO SEVERE HEADACHE SIGNIFICANT ALCOHOLIC/DRUG INTOXICATION SKULL FRAKTURE CSF LEAK RHINORRHEA OR OTORRHEA

MANAGEMENT OF MILD HEAD INJURY


SIGNIFICANT ASSOCIATED INJURIES NO RELIABLE COMPANION AT HOME UNABLE TO RETURN PROMPTLY AMNESIA HISTORY OF LOOS OF CONSCIOUSNESS

MANAGEMENT OF MILD HEAD INJURY


DISCHARGE FROM HOSPITAL : PATIENT DOES NOT MEET ANY OF CRITERIA FOR ADMISSION DISCUSS NEED TO RETURN IF ANY PROBLEMS DEVELOP AND ISSUE AWARNING SHEET SCHEDULE FOLLOW-UP CLINIC VISIT, USSUALY WITHIN 1 WEEK

Peringatan untuk pasien cedera kepala ringan dan sedang

yang terpaksa dipulangkan/ menolak observasi


di rumah sakit:
PADA SAAT INI KAMI BELUM MENEMUKAN KELAINAN YANG MENUNJUKKAN BAHWA CEDERA KEPALA YANG ANDA ALAMI ADALAH SANGAT SERIUS. NAMUN, GEJALA YANG BARU DAN KOMPLIKASI YANG TIDAK DISANGKA-SANGKA DAPAT TIMBUL DALAM BEBERAPA JAM HINGGA BEBERAPA HARI SETELAH CEDERA. 24 JAM PERTAMA ADALAH WAKTU YANG PALING GENTING DAN ANDA HARUS TETAP BERADA DALAM PENGAWASAN KELUARGA ATAU ORANG YANG DAPAT DIPERTANGGUNG-JAWABKAN, PALING TIDAK DALAM PERIODE INI.

BILA ADA DARI TANDA-TANDA DIBAWAH INI TERJADI, SEGERA KEMBALI KE RUMAH-SAKIT: 1. 2. 3. 4. 5. 6. 7. 8. Mengantuk atau semakin sulit membangunkan pasien (Pasien harus dibangunkan setiap 2 jam selama masa tidur). Mual atau muntah. Kejang-kejang atau sawan. Mengalirnya darah atau cairan dari hidung atau telinga. Nyeri kepala hebat. Kelemahan atau kehilangan rasa dari tungkai atau lengan. Bingung atau berkelakuan asing. Satu pupil (bagian hitam dari mata) lebih lebar dari sisi lainnya; gerakan yang tidak biasa dari bola mata, penglihatan ganda atau gangguan penglihatan lainnya. Denyut nadi yang sangat lambat/sangat cepat, atau pola pernafasan yg tidak biasa. Jangan makan sedatif atau penghilang nyeri jenis apapun yang lebih kuat dari parasetamol, paling tidak dalam 24 jam pertama. Jangan gunakan obat-obat yang mengandung asetosal (aspirin).

9.

(traumatic brain injury) Managemen di Unit Gawat Darurat Cedera Kepala Sedang (CKS)

Cedera Kepala

Sama dgn CKR GCS = 9-12 ICU Head CT-scan

CKB Intubasi & Hiperventilasi

MANAGEMENT OF MODERATE HEAD INJURY


INITIAL WORKUP SAME AS FOR MILD INJURY,PLUS BASELINE BLOOD WORK CT SCAN OF THE HEAD OBTAINED IN ALL CASES ADMISSION FOR OBSERVATIONAFTER ADMISSION FREQUENT NEUROLOGICAL CHECKS FOLLOW-UP CT SCAN IF CONDITION DETERIORATES

MANAGEMENT OF MODERATE (CONT)


IF PATIENT IMPROVES (90%) DISCHARGE WHEN APPROPRIATE FOLLOW-UP IN CLINIC IF PATIENT DETERIORATE (10%) IF PATIENT STOPS FOLLOWING SIMPLE COMMANDS, REPEAT CT SCAN AND MANAGE PER SEVERE HEAD INJURY PROTOCOL.

INITIAL MANAGEMENT OF SEVERE HEAD INJURY


ASSESSMENT AND MANAGEMENT ABC PRIMARY SURVEY AND AMPLE HISTORY (ALLERGIES, MEDICATIONS, PAST ILLNESS, LAST MEAL, EVENTS RELATED HEAD INJURY) NEUROLOGICAL REEVALUATION: EYE OPENING MOTOR RESPONSE VERBAL RESPONSE PUPILLARY LIGH REACTIONS DOLLS EYE

INITIAL MANAGEMENT OF SEVERE HEAD INJURY (CONT)

THERAPEUTIC AGENTS MANNITOL ANTICONVULSANT MODERATE HIPERVENTILATION

INDICATION OF SURGERY
EPIDURAL HEMORRHAGE SUBDURAL HEMORRHAGE INTRACEREBRAL HEMORRHAGE DEPRESSED FRAKTURE

SECARA UMUM
A, B, Cs Major early risk is hypotension Adequate fluid resuscitation to restore normal BP does NOT worsen neurologic outcome Avoid hypotonic fluids Emergent airway control for GCS 8 or less GSC 10 or less with abnormal head CT Rapid neurologic deterioration If needed for other injuries

Tanda-tanda klinis IC-HTN


Dilatasi pupil unilateral atau bilateral Refleks cahaya asimetris Deserebrasi atau dekortikasi Deteriorasi neurologis progresif

MANAGEMENT OF INCREASED ICP


Head position Head elevated 30 degrees and midline Sedation and pain control Analgesic + anxiolytic Fentanyl, morphine, or propofol plus a benzodiazepine Continuous infusions or scheduled doses to maintain sedation Watch for and treat hypotension Seizure prophylaxis Phenytoin or phosphenytoin

MANAGEMENT OF INCREASED ICP


Neuromuscular blockade Facilitates mechanical ventilation and control of pCO2 Prevents shivering Use if movement increases ICP Temperature control A rise in temp of 1o C increases cerebral metabolic rate by 10%, increasing ICP by several mm Hg Maintain temp < 37.5 o C Scheduled acetaminophen, body exposure, cooling blanket

MANAGEMENT OF INCREASED ICP Osmotherapy with mannitol Decreases extracellular fluid in brain Intermittent doses for ICP spikes or scheduled if elevated ICP is persistent Adverse effects: Hypernatremia, hypokalemia Hyperosmolality Hemodilution and drop in hematocrit Hypotension Follow serum osmolality and Na Hold mannitol if serum osm > 320 mOsm/l

MANAGEMENT OF INCREASED ICP Drainage of CSF Possible if ventricular catheter is in place CSF drainage pressure usually set at 20 cm H2O CSF drains when ICP exceeds drainage pressure Ventricular catheters cannot be placed if cerebral edema has obliterated or significantly compressed ventricles

MANAGEMENT OF INCREASED ICP


Second tier therapies for intracranial hypertension refractory to sedation, muscle relaxation, osmotherapy, and moderate hypothermia: barbiturate coma induced hypertension decompressive craniotomy hypothermia

MANAGEMENT OF INCREASED ICP


Barbiturate coma ICP control is the principal endpoint EEG burst suppression is a useful guide to optimal barbiturate dosage Pentobarbital 10mg/kg followed by infusion at 1 mg/kg/hr, titrated to effect May give additional boluses during infusion for acute spikes in ICP Moderate doses cause sluggishly reactive pupils while large doses may cause mid position to 5 mm nonreacting pupils Watch for hypotension

MANAGEMENT OF INCREASED ICP


Induced hypertension Inotropes to increase MAP, even beyond normal for age, to achieve an optimal CPP Dopamine Norepineprine Rise in ICP in tandem with a rise in MAP implies total loss of autoregulation and is a poor prognostic sign Decompressive craniotomy Large portion of cranium removed to allow room for brain to swell and minimize ischemia Dura must be opened as well

MANAGEMENT OF INCREASED ICP Hypothermia Core body temp of 32o to 33o C Reduced cerebral metabolic activity, reducing ICP Also has cytoprotective effects Adverse effects Arrythmias Coagulopathies Hypokalemia Increased risk of infection

MANAGEMENT OF OTHER SYSTEMS


Respiratory Maintain normocapnia Hyperventilation only appropriate during early diagnosis and management or if herniation is impending Maintain oxygenation pO2 > 100 is optimal PEEP to maintain alveolar recruitment ARDS, neurogenic pulmonary edema frequent complications Hypoxemia has more deleterious effects on brain than modest venous congestion caused by PEEP PEEP of 5 to 10 cm H2O not shown to have detrimental effect on neurologic outcome

MANAGEMENT OF OTHER SYSTEMS


Cardiovascular Maintain normal blood pressure Hypotension significantly reduces CPP Inotropes if necessary to maintain normal BP Induced hypertension if necessary

Gastrointestinal Stress gastritis prophylaxis with H2 blocker Jejunal feeds to maintain healthy intestinal mucosa and prevent bacterial translocation from gut

MANAGEMENT OF OTHER SYSTEMS


Fluids, Electrolytes, Nutrition Goal is NORMOVOLEMIA Total fluid intake should be @ 100% maintenance Bolus as necessary to achieve normal CVP Avoid hypotonic fluids Lactated Ringers and 0.9% saline w/ 20 mEq KCl/l are good choices for maintenance fluids Follow electrolytes closely Avoid hyponatremia Mannitol can cause electrolyte abnormalities Watch for SIADH, diabetes insipidus, cerebral salt wasting

MANAGEMENT OF OTHER SYSTEMS


Fluids, electrolytes, nutrition Provide calories to meet metabolic demands of patient Increased metabolic demands during acute phase of injury Heavily sedated, relaxed, cooled patient has decreased metabolic demands Enteral feedings via nasojejunal catheter preferable to TPN if gut deemed to be healthy Avoid hyperglycemia Associated with poor neurologic outcome Watch serum glucose closely if dextrose containing fluids used

MANAGEMENT OF OTHER SYSTEMS


Renal Place foley for strict Is and Os Hematologic Coagulopathy common with head injuries Brain derived thromboplastin activator substances released Follow PT/PTT or DIC screens Blood component replacement if evidence of active bleeding or if surgical intervention anticipated Maintain normal hematocrit to optimize oxygen delivery

MANAGEMENT OF OTHER SYSTEMS


Endocrine DIABETES INSIPIDUS Complete or partial failure of ADH secretion from shearing of pituitary stalk Polyuria, hypernatremia, urine osm < plasma osm Treatment: Run maintenance fluids @ 100% Replace urine output cc for cc with dextrose-containing fluids Continuous vasopressin infusion or DDAVP (subQ or intranasal) q 12 to 24 hrs

MANAGEMENT OF OTHER SYSTEMS


Endocrine CEREBRAL SALT-WASTING ANP-like substance released from brain, inducing natriuresis and diuresis SIADH Elevated level of ADH inappropriate for prevailing osmotic or volume stimuli Hyponatremia, hypo-osmolality, urine osm > plasma osm, high urine Na Treatment is water restriction

SUMMARY
Identify and treat primary brain injury Rule out neurosurgical emergency Minimize secondary ischemic brain injury by promoting cerebral perfusion Maintain normovolemia and adequate BP Maintain normal electrolytes and euglycemia Maintain normocapnia and adequate oxygenation Avoid factors that increase ICP Treat intracranial hypertension

Summary of Recommended Practices


Serial neurologic assessments and physical examination Continuous cardio-respiratory, ICP, and CPP monitoring, +/- cerebral metabolism monitoring adjuncts Maximize Oxygenation and Ventilation Maximize oxygenation (cautious use of PEEP / keep PEEP < 10 to prevent inhibited venous return / individualize according to patient response) Normoventilate Support circulation / maximize cerebral perfusion pressure Maintain mean arterial blood pressure and maintain CPP (goal > 60)

Summary of Recommended Practices


Decrease intracranial pressure Evacuate mass occupying hemorrhages Consider draining CSF with ventriculostomy when possible Hyperosmolar therapy, +/- diuresis (cautious use to avoid hypovolemia and decreased BP) Mid-line neck, elevated head of bead (some research supports elevation not > 30 degrees) Treat pain and agitation - consider premedication for nursing activities, +/neuromuscular blockade (only when needed) Careful monitoring of ICP during nursing care, cluster nursing activities and limit handling when possible Suction only as needed, limit passes, preoxygenate / +/- pre-hyperventilate (PaCo2 not < 30) / use lidocaine IV or IT when possible After careful preparation of visitors, allow calm contact

Summary of Recommended Practices


Decrease Cerebral Metabolic Rate Prevent seizures Reserve pentobarbital for refractory conditions Avoid hyperthermia, +/- hypothermia Avoid hyperglycemia (early)

Late complications from head injury

Post-traumatic seizures Communicating hydrocephalus Post-traumatic syndrome

Hypogonadotropic hypogonadism Chronic traumatic encephalopathy Alzheimers disease

(or post-concussive syndrome)

Prediction of post-traumatic complaints after mild traumatic brain injury

Conclusions: The presence of headache,

dizziness, or nausea in the ER after MTBI is strongly associated with the severity of most PTC after six months. Identifying MTBI patients in the ER without headache, dizziness, nausea, or increased serum marker concentrations may be a promising strategy for predicting a good outcome.
specific serum markers S-100B and neurone specific enolase (NSE)

NSE and S-100B in serum and cerebrospinal fluid have been reported to be markers of cell damage in the human central nervous system

Condition with increased risk of post-traumatic seizures after traumatic brain injury

EDH, SDH, ICH # depressed terbuka dg cedera parenkim otak Kejang dalam 24 jam pertama GCS < 10 Cedera kepala terbuka Riwayat penggunaan alkohol Contusio cerebri

Terima Kasih