Dr.Agustinus Juhardi,Sp An.,MSc.

Dept. Anesthesiology & Reanimation

Mardi Rahayu Hosp. Kudus
Penyebab utama kematian pada trauma
Usia produktif
Laki dan perempuan 2 : 1
Untuk menyelamatkan pasien ini, apa yang bisa dilakukan di UGD?
 Target terapi

Traumatic Brain Injury

Primary Brain Secondary Brain

Injury Injury
Results from what Physiologic and bio-
has occurred to the chemical events which
brain at the time of follow the primary
the injury. injury.
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SOME of the SECONDARY EVENTS IN TRAUMATIC BRAIN INJURY

diffuse axonal
BBB inflammation injury
disruption apoptosis

necrosis
edema
formation
Brain trauma ischemia

energy failure
cytokines

Eicosanoids
Acetyl polyamines Calcium
endocannabinoids Choline
ROS
Shohami, 2000
Green pathophysiological processes; Yellow various mediators 6
Primary injury Inflammatory
Direct cell and mediators
vascular damage

Ischemia Bleeding and Increased Edema

haematoma CBF formation

Increased intracranial
pressure

Cell death
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 Monro-Kellie Doctrine
Vintracranial vault=Vbrain+Vblood +Vcsf

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Identifikasi dan Evaluasi
Identifikasi
GCS
CKR
CKS
CKB
ATLS trauma evaluation
Group A (minimal head injury GCS = 15
Patient is awake, oriented and without neurologic
deficits and relates accident
No loss of consciousness
No vomiting
Absent or minimal subgaleal swelling

The patient is released into the care of family

member with written instructions.
Group B (minor head injury GCS = 15)
Patient is awake, oriented and without neurologic
deficits
Transitory loss of consciousness
Amnesia
One episode of vomiting
Significant subgaleal swelling

The patient who has at least one of these

characteristic undergoes neurologic evaluation
and CT scan which, if negative, shortens hospital
observation. If CT scan is not available, the
patient has skull X-rays and is held for an
observation period of not less then 6 h. If the
skull X-rays are negative and a subsequent
neurologic control is normal, the patien can be
released into the care of a family member with
written instructions. If the X-rays reveal a
fracture, the patient undergoes CT scan.
Group C (moderate head injury or mild head injury with complicating
factors GCS = 9-15)
Impaired consciousness
Uncooperative for various reasons
Repeated vomiting
Neurologic deficits
Otorrhagia/otorrhoea
Rhinorrhoea
Sign of basal fracture
Seizures
Penetrating or perforating wounds
Patients in anticoagulant therapy or affected by coagulopathy
Patients who have undergone previous intracranial operations
Epileptic or alcoholic patients

The patient with at least one of these characteristics undergoes a

neurologic evaluation and a CT scan. Hospitalization and repeated
scan, if necessary, within 24 h or prior to discharge.
Group D (severe head injury
GCS = 3-8)

Patient is coma

Necessary resuscitation manouvres followed by

neurological evaluation and immediate CT scan (prior
to surgical intervention). Coma management.
Intubasi Endotrakea
1. Semua pasien koma, GCS < 8
2. Hilangnya reflek proteksi jalan nafas
3. Hipoksemia, hipercapnia (PaO2 < 60
mmHg; PaCO2 > 65 mmHg)
4. Hipokapnia (PaCO2 < 25 mmHg)
5. Respiratory aritmia
6. Kejang
7. Trauma jalan nafas dan thorak

Semua pasien dianggap fraktur cervical

In-line stabilization
Ventilasi
Hipokapnia ringan (PaCO2 35-40)
Hindari hiperventilasi pada 24 jam
pertama (PaCO2 < 25 mmHg), bila tidak
ada tanda kenaikan TIK
Analisa Gas Darah
 Resusitasi Cairan
Hipotensi post-trauma (secundary brain injury).
Koreksi hipotensi (sistolik < 90 mmHg)
MAP dipertahankan > 90
 Resusitasi Cairan
Koloid atau kristaloid?
Hipertonik atau isotonik?
Pilihlah cairan hipertonik (NS 3%, 7,5%)
Lebih umum dipakai NaCl 0.9%
Hindari RL, NS 0.45%
Hindari Dextrose.
Apakah hipertensi perlu koreksi?
Respon kompensasi
Ya. Jika MAP diatas limit autoregulasi.
Idealnya alpa-blocker (pentolamine)
Esmolol, propanolol, labetalol.
Manajemen Kenaikan TIK
CPP = MAP ICP
Trias Cushing: bradikardi, hipertensi, bradipnea.
Manajemen Kenaikan TIK
Posisi kepala head-up 30
Hiperventilasi (kontroversi)
Prinsip: normokapnia, jangan PaCO2 < 35 mmHg.
Osmotik diuretik
Manitol 20% 0.25-1 mg/kgBB 15-25 menit.
Atasi hipovolemia sebelumnya
Bolus lebih baik daripada infus kontinyu
Infusnya harus ada filternya
Loop diuretik
Furosemid 0.7 mg/kg iv 15 mnt setelah manitol

Barbiturat
Konsep Lund
 Staircase ICP control algorithm

7 Barbiturate coma

6
Surgical decompression
5
Mild hypothermia

4
Mannitol

3 Ventricular drainage

2 Moderate head-up

1 Intubation, normocapneic ventilation

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 Physiological Basic of the Lund
Management Strategy

Jv = Kf{(Pc-Pi) (p- i)}

Interstitial
Pi i space

Po p Capillary

The Lund strategy is based on knowledge of the forces that govern

transcapillary filtration of fluid.

Jv = transcapillary filtration of fluid; Kf = filtration coefficient; (Pc Pi) = hydrostatic

pressure difference between plasma and interstitial fluid; (p- i) = oncotic pressure
difference between plasma and interstitial fluid.

Robertson, 2001
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Daisy 10 Months After Accident