Head Trauma

Dr. Candy Lauwrenz SpS, MMKes, QIA

Head Trauma
Statistics :
In USA, 150-300 peoples dead due to head injury per
year.
Mortality rate of TBI is about 25 /100.000 pop ulation
annualy
Disability rate are three time
Main dead cause of young productive peoples
Cost : $ 400 billion per year
- Income loss - Medical fee
- Insurance cost - Indirect cost
(Narayan, 2005)
No data in Indonesia

Pathophysiology
Traumatic Brain Injury

Primary vs. Secondary

Injury
Primary

injury - direct
physical injury to neurons and
glial cells
Secondary injury physiological events after the
primary injury further damage.

Primary Injury
Impact

: epidural, subdural,
contusion, intracerebral hemorrhage,
skull fractures

Inertial

injury

: concussion, diffuse axonal

Hypoxic/Ischemic

Secondary Injury
Hypoxic-ischemic

injury
Release of excitatory amino acids
Excess NMDA receptor activity
Concurrent hypotension and
hypoxemia may be present
Inflammatory response

Jenis trauma
:

Ekstrakranial
Luka pada jaringan kulit bisa :
Luka tertutup oleh karena benda
tumpul berupa hematoma.
Luka terbuka akibat benda tajam /
runcing seperti luka sayat, luka
tusuk, terpotong.

11

12

Jenis trauma
:

Fraktur Tengkorak
Fraktur

pada batok kepala :

Linier

fraktur
Depresed fraktur
Comminuted fraktur
Fraktur

pada basis tengkorak

Longitudinal

fraktur
Transversal fraktur
Circular fraktur

13

Depressed Fraktur

14

15

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Jenis trauma
:

Intrakranial
Trauma serebri :
Komotio serebri
(gegar otak)
Kontusio serebri
Laserasi serebri

17

Mekanisme trauma serebri :

Pergeseran,

otak dapat
bergesekan dengan tulang
tengkorak
Tergencet & terjepit oleh jaringan
keras disekitarnya
Mengalami pantulan (counter
coup)
18

Akibat trauma serebri berupa

oedema

serebri
perdarahan subaraknoid, subdural,
epidural
petechia / hematoma intraserebral
laserasi / memar
terpotong

19

Guidelines for the

Management

Initial :
Airway and Oxygenation
Breathing
Blood Pressure Control
Seizures Prevention
Fluid and Nutrition
Body Temperature
Exitation, vomitus, headache
(Fewel et al, 2003)

CONSIDER .
Cerebral

Blood Flow (CBF)

Mean Arterial Pressure (MAP)
Intracranial Pressure (ICP)

PENILAIAN GLASSGOW
COMA SCALE (GCS)
TAMPAKAN

SKALA

NILAI

EYE
OPENING

SPONTAN

DIPANGGIL

RANGSANG NYERI

TIDAK ADA RESPONSE

(DIAM)

22

23

PENILAIAN GLASSGOW
COMA SCALE (GCS)
TAMPAKAN

SKALA

NILAI

VERBAL
RESPONSE

ORIENTASI BAIK

JAWABAN KACAU

KATA-KATA TIDAK
PATUT
(INAPPROPRIATE)
BUNYI TAK BERARTI

INCOMPREHENSIBL
E

TIDAK BERSUARA

1
24

PENILAIAN GLASSGOW
COMA SCALE (GCS)
MOTOR
RESPONSE

SESUAI PERINTAH

LOKALISASI NYERI

REAKSI PADA NYERI

FLEKSI (DEKORTIKASI)

EKSTENSI
(DESEREBRASI)
TIDAK ADA RESPONSE
(DIAM)

2
1
25

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MANAGEMENT OF
INCREASED ICP

Head elevation
Hyperventilation
Osmotic Therapy
Sedation
Cerebrospinal Fluid Drainage ( Ventricular, Subdural
Drainage )
beneficial in treating the hydrocephalus seen in
thalamic hemorrhage with ventricular extension

2003)

(Broderick et al, 1999; Fewel et al.,

ICP MONITORING

Placed in patient with GCS = 9

Cerebral Edema on CT, Multipel Intracranial Lesions
The duration not exceed of 5 days
Patient with suspected elevation ICP and
deteriorating level of conciousness are candidates
for invasive ICP Monitoring
Intraventricular ICP monitoring and
intraparenchymal fiber optic ICP device are two
commonly used methods of monitoring ICP

(Orlando Regional Health Care, 2003)

Pharmacological
Neuroprotection
1.
2.
3.
4.

Glutamate receptor antagonists,

Calcium antagonists
Free radical scavengers, and
Cyclosporin A

1. Glutamate receptor
antagonists
The

amino acid L-glutamate is an

extensively distributed, mostly
excitatory neurotransmitter in the
CNS.
Extracellular glutamate >>
deleterious effects to neurons.
Glutamate receptors : NMDA, AMPA
and Kainate receptors.

2. Calcium Antagonist
Nimodipine
Not

recommended for severely

head injured patients.
Treatment of the TBI patients
without signs of subarachnoid
bleeding is not indicated.

3. Free radical scavengers

TBI

may lead to an increase in intracellular

free radical activity.
Antioxidatives agents:
Tirilazad
No significant positive influence of treatment
with tirilazad on outcome of severely TBI
(phase III)
Polyethylene

glycol-conjugated
superoxide dismutase (PEG-SOD).
Trend towards better outcome
compared placebo (phase III)

4. Cyclosporin A
Cyclosporin

is a cyclic polypeptide,
consisting of 11 amino acids.
Transplantation medicine as an
immunosuppressant
Protective effect on mitochondrial
ultrastructure, and most likely
mitochondrial function, and on cytoskeletal
derangements after TBI (animals study).
No clinical phase II or III trials evaluating
the efficacy of cyclosporin A in the
treatment of human severe TBI

Citicholin
Mechanisms:
Preserving cardiolipin (an exclusive inner
mitochondrial membrane component) and
sphingomyelin;
Preserving the arachidonic acid content of
PtdCho and Ptd-ethanolamine;
Partially restoring PtdCho levels;
Stimulating glutathione synthesis and
glutathione reductase activity;
Attenuating lipid peroxidation; and
Restoring Na/K-ATPase activity.

Conclusions
Pathophysiological

cascades initiated by injury

of brain have many features in common, and
brain ischemia and mitochondria dysfunction
frequently are the common denominator.

The

effort of mitigating brain injury include:

Maintenance of brain perfusion.
Maintenance to adequate oxygen delivery.
Optimizing source of brain energy.
Neuroprotective strategy

Conclusions
Neuroprotective

Strategies:

Non

Pharmalogical (Hypothermia).
Pharmacological Neuroprotetion.
CDP-Choline

is one of
Pharmacological Neuroprotection can
used in the treatment of TBI

Outcome and Mortality depend

on :
Primary

Cerebral damages
Optimal initial care
Neurosurgery consultation procedure
Immediate and percise surgery
Post-operative ICU
Medical rehabilitation