Guideline in Management of Traumatic

Head Injury

Malang Neurosurgery Team

Dr Saiful Anwar General Hospital
Faculty of Medicine Brawijaya University
Malang
2016
 Neurotrauma Team
Donny Wisnu Wardhana Farhad Bal’afif Tommy A Nazwar

Editor:
Tommy A Nazwar

Malang Neurosurgery Secretariat

Neuro Surgery Division
SMF / Surgery Lab.
Dr Saiful Anwar General Hospital – Faculty of Medicine Brawijaya University
Jl JA Suprapto. Malang
Telp.+62 341 333100
Fax. +62 341 333100
e.mail. bedahsarafmalang@yahoo.com

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 Table of Contents
Neurotrauma Team Members.......................................................................................................... 1
Table of Contents.............................................................................................................................. 5
Table of Figures and Tables............................................................................................................... 7
Abbreviations.................................................................................................................................... 8

CHAPTERS
I. Introduction.............................................................................................................................. 9

II. Forming the Guideline.............................................................................................................. 11

III. GeneralMeasures...................................................................................................................... 14
III.1. Management of head injuries in the Emergency Department Triage............................. 14
III.2. Steps for Management of Head Injury in the Emergency Room..................................... 14
III.2.1. General Precautions............................................................................................. 14
III.2.2. Cardiorespiratory (ABC) System Stabilization and Disability................................ 16
III.2.3. Principles of Management of Head Injury or Head Trauma................................. 17
III.3. Survey Sekunder............................................................................................................. 17
III.3.1. Anamnesis............................................................................................................ 17
III.3.2. Head to Toe Examinations................................................................................... 17
III.3.3. Neurologic Status Examination............................................................................ 18
III.4. Observation..................................................................................................................... 19
III.5. Plain Head Imaging Criteria............................................................................................. 20
III.6. Head CT Scan Imaging Criteria........................................................................................ 20
III.7. Admission Criteria........................................................................................................... 20
III.8. Discharge Criteria for Traumatic Head Injury.................................................................. 21
III.9. Patient Education Following Discharge........................................................................... 21
III.10. High Care Unit (HCU) Admission Criteria......................................................................... 22
III.11. Intensive Care Unit (ICU) Admission Criteria................................................................... 22
III.12. Criteria for Tracheal Intubation....................................................................................... 22

IV. Traumatic Head Injury Management Algorithm....................................................................... 23

IV.1. Mild Head Injury Management Algorithm........................................................................ 23
IV.2. Moderate Head Injury Management Algorithm............................................................... 24
IV.3. Severe Head Injury Management Algorithm.................................................................... 25

V. Medication Treatment Recommendation................................................................................. 26

V.1. Anti-convulsant Recommendation.................................................................................. 26
V.2. Mannitol and Hypertonic Sodium LactateRecommendation..........................................
V.3. Prophylactic Antibiotics in Ventricle Catheter.................................................................
V.4. AnalgesicRecommendation.............................................................................................
V.5. CorticosteroidRecommendation.....................................................................................
V.6. TranquilizerRecommendation.........................................................................................
V.7. NutritionRecommendation.............................................................................................
V.8. GastricMucosalProtector and Acid Suppresor AgentRecommendation .........................
V.9. CiticolineRecommendation.............................................................................................
V.10. PiracetamRecommendation............................................................................................

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 V.11. NeuropeptideRecommendation......................................................................................

VI. Guideline for Surgical Treatment..............................................................................................

VI.1. Surgical Recommendation in Epidural Haemorrhage (EDH).............................................
VI.2. Surgical Recommendation in Subdural Haemorrhage(SDH) ............................................
VI.3. Surgical Recommendation in Intracranial Haemorrhage(ICH) .........................................
VI.4. Surgical Recommendation in Mass Lesion in Fossa Posterior Region...............................
VI.5. Surgical Recommendation in FractureImpression............................................................
VI.6. Surgical Recommendation in FractureBasisCranii.............................................................
VI.7. Surgical Recommendation in DiffuseAxonalInjury (DAI)...................................................

VII. Guideline for Intracranial Pressure Monitoring and Treatment................................................

VII.1. Indications for Intracranial Pressure Monitor Device(Ventrikulostomi)..........................
VII.2. Increased Intracranial Pressure Management.................................................................

VIII. Guideline for Traumatic Head Injury in PediatricSetting...........................................................

VIII.1. Blood Pressure Resuscitation and Oxygenation..............................................................
VIII.2. Indications for Intracranial Pressure Monitor Device.....................................................
VIII.3. Intracranial Pressure Borderline Therapy.......................................................................
VIII.4. Hyperosmolar Therapy to Control Increased Intracranial Pressure................................
VIII.5. Role of LiquorCerebrospinal (LCS) Drainagein Increased Intracranial Pressure Control.
VIII.6. Role of Hyperventilation in Acute Management of Severe Head Injury in Pediatric Setting
VIII.7. Surgery for Increased Intracranial Pressure management in Pediatric Setting...............

IX. Head Injury Related to Sports...................................................................................................

Closing Chapter....................................................................................................................

PS.
Inside Cover : Head Surgery.
Taken from Wilkins RH dan Rengachary SS (Eds). Neurosurgery. 2nd edition. McGraw-Hill. New York, 1996

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 Table of Figure and Tables
Table 1. Traumatic Head Injury Patients in Dr. Saiful Anwar General Hospital Malang from 2010 to
2015.............................................................................................................................. 9
Table 2. Mod. SIGN (Scottish Intercollegiate Guideline Network) 2011 .................................... 12
Table 3. General Precautions..................................................................................................... 15
Table 4. Primary Survey Traumatic Head Injury......................................................................... 16

Evidence Level(EL) andRecommendation Degree (RD)

Table 5. Anti-convulsant Recommendation............................................................................... 26
Table 6. Mannitol and Hypertonic Sodium LactateRecommendation............................................... 29
Table 7. Prophylactic Antibiotics in Ventricle Catheter................................................................... 32
Table 8. Analgesic Recommendation......................................................................................... 34
Table 9. Corticosteroid Recommendation................................................................................. 35
Table 10. Analgesia and Sedation (Tranquilizer) in patients with various acuteneurological
conditions..................................................................................................................... 37

Evidence Level(EL) andRecommendation Degree (RD)

Table 11. Tranquilizer Recommendation......................................................................................
Table 12. Nutrition Recommendation.......................................................................................... 40
Table 13. Gastric Mucosal Protector and Acid Supressor AgentRecommendation.................... 42
Table 14. Citicoline Recommendation......................................................................................... 44
Table 15. Piracetam Recommendation........................................................................................ 46
Table 16. Neuropeptide Recommendation.................................................................................. 48
Table 17. Surgical Recommendation in Epidural Haemorrhage (EDH)........................................ 50
Table 18. Surgical Recommendation in Subdural Haemorrhage(SDH) ....................................... 52
Table 19. Surgical Recommendation in Intracranial Haemorrhage (ICH) ................................... 54
Table 20. Surgical Recommendation in Mass Lesion in Fossa Posterior Region ......................... 56
Table 21. Surgical Recommendation in Fracture Basis Cranii ..................................................... 59
Table 22. Surgical Recommendation in Diffuse Axonal Injury (DAI) ........................................... 60
Table 23. Indications for Intracranial Pressure Monitor Device (Ventrikulostomi) .................... 63
Table 24. Increased Intracranial Pressure Management............................................................. 67
Table 25. Blood Pressure Resuscitation and Oxygenation................................................................. 69
Table 26. Indications for Intracranial Pressure Monitor Device......................................................... 71
Table 27. Intracranial Pressure Borderline Therapy.......................................................................... 74
Table 28. Hyperosmolar Therapy to Control Increased Intracranial Pressure ..................................... 77
Table 29. Role of LiquorCerebrospinal (LCS) Drainagein Increased Intracranial Pressure Control......... 80
Table 30. Role of Hyperventilation in Acute Management of Severe Head Injury in Pediatric Setting... 82
Table 31. Surgery for Increased Intracranial Pressure management in Pediatric Setting ..................... 83
Table 32. Concussion Symptoms.................................................................................................. 89
Table 33. Concussion Degrees according to Cantu System and AAN.......................................... 90
Table 34. Guideline for Athelete to Return to Play (AAN Guideline) .......................................... 90
Table 35. Recommendation for Recurring Concussions in one Competition Season.................. 91

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Figure 1. Neurologic Status Observation Sheet....................................................................... 19

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 Abbreviations

CBF : Cerebral Blood Flow

CMRO2 : Cerebral Metabolic Rate of O2
CPP : Cerebral Perfusion Pressure
CSF : Cerebro Spinal Fluid
CT Scan : Computed Tomography Scanning
EDH : Epidural Hematoma
EVD : External Ventricular Drainage
ER : Emergency Room
GCS : Glasgow Coma Scale
HCU : High Care Unit
ICP : Intracranial Pressure
LCT : Long Chain Triglycerides
LCU : Low Care Unit
MAP : Main Arterial Pressure
MCT : Medium Chain Triglycerides
NSAID : Non Steroidal Anti Inflamatory Drugs
PPI : Proton Pump Inhibitor
RCT : Randomized Control Trial
SDH : Sub Dural Hematoma
SRMD : Stress Related Mucosa Damage
TBI : Traumatic Brain Injury
AAN : American Academy of Neurology

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 CHAPTER I
INTRODUCTION

Traumatic head injury is still a problem that is often faced by neurosurgeons, and in
Indonesia is still a major cause of disability, death and high costs. The development of knowledge
regarding the pathophysiology and management of head injuries, is very rapid in the last decade.
One of the central concepts based on laboratory-based, clinical, biomolecular, and genetic research
is that neurological damage does not only occurs at the moment of impact of an injury, but
develops in the following hours and days. Damage to the nervous system is also affected by the
patient's vulnerability to injury. The development of this pathophysiology has spurred the
development of comprehensive treatment methods, neurorestoration and rehabilitation methods,
in order to improve the outcome of traumatic head injury patients.

Traumatic head injury or often called neurotrauma, is still a serious problem in Indonesia. In
Dr. Saiful Anwar General Hospital Malang, from the data of traumatic head injury patients from
2013 to 2018, a total of patients 5441 people, consisting of mild head injuries 2754 patients
(50,7%), moderate head injuries 1727 patients (31,7%), and severe head injuries 960 patients
(17,6%).

Table 1. Traumatic Head Injury Patients inDr. Saiful Anwar General Hospital Malang from 2010 to
2015
ƩTraumatic ƩSevere Total Death
Total Death
Year Head Injury Head Injury % Number by Severe %
Number
patients Patients Head Injury
2013 1042 143 172 16,5 101 70,1
2014 990 128 195 19,6 113 57,9
2015 1002 148 215 21,3 125 58,1
2016 988 161 226 22,8 136 60,1
2017 1066 219 257 24,1 167 64,9
2018 1014 161 219 21,5 129 58,9
 Death rates at all severity of head injuries range from 10% to 20%. This figure is higher
compared to international literature standards, which ranges from 3-8%.
 Based on the severity, mortality of severe head injury patients is still high, ranging between
15- 25%, with a downward trend. This figure is relatively high compared to the literature
which is 22%.
 The operative management rate ranges from 40- 60% of all head injury patients who come
to ER.
 From these data, the average mortality rate of severe head injury patients is around 74 %
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 The high incidence and mortality of head injury patients requires the need for serious and
comprehensive treatment. Pre-Hospital Care and Hospital Care are very important factors to be
addressed and improved in order to reduce morbidity and mortality.

Improving the management of Pre-Hospital care, is by:

• Introducing guideline for the management of head injuries
• Improving referral system
• Improving the ability of human resources by means of continuing education

Improving the management of Hospital Care, is by:

a. Making clinical practice guidelines for management and actions for each type of head
injury
b. Making an algorithm for head injury management
c. Increased human resource capability (provider)
d. Fulfillment of emergency facilities and infrastructure
e. Fulfillment of high care unit (HCU) care facilities and infrastructure
f. Developing clinical and laboratory research
g. Improving collaboration with other neurotrauma centers and periodic evaluations

The target of achievement is a decrease in mortality and morbidity by 1% per year in Dr.
Saiful Anwar Hospital Malang, so that in the first five years the same morbidity and mortality rates
are achieved with international neurotrauma centers. The initial step is the preparation of these
guidelines.

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 CHAPTER II
FORMING THE GUIDELINE

The process of making guidelines for head injury in Neurosurgery Division of Surgery
Laboratory of Dr. Saiful Anwar General Hospital Malang - Faculty of Medicine, Brawijaya
University Malang is by forming a neurotrauma team consisting of neurosurgeons,
anesthesiologists, resident doctors of Surgery and Anesthesiology as well as paramedics in
Emergency Room and Surgical Inpatient Installation. The neurotrauma team conducted data
collection, problem identification, opinion, practical experience and literature studies and
research related to head injuries.

This guideline consists of two major parts, namely the head injury management algorithm at
Dr. Saiful Anwar General Hospital Malang and recommendations for treatment and therapy both
with surgical intervention and without surgery.

The guideline is based on evidence based medicine by dividing the level of therapy or
intervention into three categories of recommendations namely A, B and C:(Adelson 2003; Mod.
SIGN / Scottish Intercollegiate Guideline Network 2011)
A. Obtained from the level of proof class I, is a method of therapy or intervention / surgery
obtained from prospective randomized controlled trial (RCT) research or meta-analysis of RCT
research. This method is standard (high degree of clinical certainty).
B. Obtained from the level of evidence class II, is a method of therapy or intervention /
surgery obtained from studies that are both prospective and retrospective analysis
(observational studies, cohorts, case-controls, and prevalence studies). This method is a
guideline (moderate clinical certainty).
C. Obtained from the level of evidence class III, is a method of therapy or intervention /
surgery obtained from retrospective research, serial cases, from patient registration data, case
reports, case reviews, and expert opinion (level of evidence IV). This method is an option(unclear
clinical certainty).

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Level of Evidence

Table 2. Mod. SIGN (Scottish Intercollegiate Guideline Network) 2011

Level of
No Evidence Finding
Evidence

Evidence isbased on metaanalysis or systematic review from various randomized

1 I–a
clinical trials with control (Randomized Controlled Trials Study / RCT)

Evidence is based on a minimum of one randomized clinical trials with control

2 I–b
(RCT)

Evidence is based on at least one comparative randomized clinical trials, but

3 II – a
without randomization

4 II – b Evidence is based on at least one quasi-experimental design study

Evidence is based on descriptive non-experimental study (comparative study,

5 III
correlation and case study)

Evidence is based on report of commitee or opinions, or acknowledged clinical

6 IV
experience.

Classification of Recommendation (EBM-HTA), Adelson 2003 (Diagnostic and Treatment)

1. Standard (High degree of clinical certainty)> (I-a, I-B)
Recommendation: A
2. Guidelines (Moderate clinical certainty)> (II-a, II-b)
Recommendation: B
3. Option (Unclear clinical certainty)> (III- IV)
Recommendation: C

The systematics of writing and the contents of the guidelines are such that they are in
accordance with the conditions at RSUD Dr Saiful Anwar Malang as a tertiary type A education
hospital. It is expected that clinicians, consultants, resident doctors and medical students and
paramedics can easily use it.

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 Suggested references and recommendations are obtained from clinical and laboratory
research and exploration of journals or references, which is possible to change according to the
development of science.

Periodically this guideline will be evaluated and supporting research will be carried out so as
to produce references and recommendations with a higher level of clinical certainty.
Editor

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 CHAPTER III
GENERAL MEASURES

III.1. Management of Head Injuries in the Emergency Department Triage

Triage or screening, in charge of checking vital signs and labeling according to gravity, then
the patient is moved to Priority Room 1, 2, or 3 according to the label.

III.2. Steps for Management of Head Injury in the Emergency Room

1. General Precaution
2. Cardiorespiratory System Stabilization (Airway, Breathing, Circulation) by the
Responsible Doctor (DPJP) for P1
At the time of stabilization, the Neurosurgeon Doctor on duty must have been involved
3. Patients in the P2 and P3 emergency categories are directly treated by the
Neurosurgeon on duty
4. Neurological & Secondary Survey Examination (general status examination consists of
history and physical examination of all organs), carried out by the the Neurosurgeon on
duty
5. Determine clinical diagnosis and additional examinations
6. Determine a definitive diagnosis
7. Determine management

III.2.1. General Precaution

General protection consists of:
a. Informed to Consent and Informed Consent
b. Self protection
c. Equipment preparation and service facilities
Before taking action, the doctor is responsible for the completeness and functioning of
the medical equipment and facilities needed for the action to be performed. Before
carrying out medical procedures, the doctor who will take the action must make
preparations and guarantee that the tools and facilities that will be used are complete
and their safety is guaranteed.

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Table 3. General Precautions
(fromGuidelines for Healthcare Facilities with Limited Resources)
No Type of Protection

1 Wash your hands with antiseptics

 after being exposed to blood, bodily fluids, secretions, excretions or
contaminated objects
 immediately after removing the gloves
 between examinations of 2 different patients

2 Wearing gloves
 if it will touch blood, body fluids, secretions, excretions or contaminated
objects
 if in contact with mucosa or skin that is not intact

3 Wearing Masks and Goggles

 to protect the mucosa of the eyes, nose and mouth when dealing with blood or
bodily fluids

4 Wearing protective gowns

 to protect the skin from blood or body fluids
 prevent clothing from getting stained during inspection procedures that
involve contact with blood and bodily fluids

5 Linen
 avoid contact of skin and mucosa with contaminated dirty linen
 Don't wash dirty linen in the patient care area

6 Patient care tools

 avoid contact of skin and mucosa with contaminated equipment and do
not let the clothes worn and the surrounding environment
 tools that have been used must be washed before reuse

7 Environmental Hygiene
 patient care areas must be cleaned regularly using disinfectants

8 Sharp object
 Do not close the syringe that has been used
 Do not remove the used syringe from the syringe
 do not bend, break or manipulate used needles by hand
 Dispose of sharp objects in an impermeable container

9 Patient resuscitation
 avoid mouth-to-mouth resuscitation. Use mouth-pieces, resuscitation bags,
or other ventilation aids

10 Patient placement
 patients who can cause contamination in the environment are placed in a
special room

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III.2.2. Cardiorespiratory (ABC) System Stabilization and Disability
Table 4. Primary SurveyTraumatic Head Injury
Observe, Write down, and
Assessment Evaluation
Manage

A. Airway  Airway patency ...?  Obstruction?

 Additional sounds ...?

B. Breathing  Is oxygenation effective ...?  Rate and depth

 Chest movement
 Air entry
 Cyanosis

C. Circulation  Is perfusion adequate ...?  Pulse rate and volume

 Skin color
 Capilarry return
 Bleeding
 Blood pressure

D. Disability  Are there neurological  The level of consciousness

disabilities ...? using the GCS system
 Pupils (large, shape, light
reflexes, compare left and
right, and consensual
reflexes)
 Motorc lateralization

E. Exposure  Injury to other life-threatening  Injury, open sores,

organs ...? deformities and limb
movements

III.2.3. Principles of Management of Head Injury or Head Trauma

1. Management of primary head injuries
2. Prevent and treat secondary head injuries
3. Optimization of brain metabolism
4. Rehabilitation

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15
III.3. Secondary Survey
III.3.1. Anamnesis (Autoanamnesis or Heteroanamnesis)
Informations needed are:
 Patient's identity: name, age, sex, ethnicity, religion, occupation, address
 The main complaint
 Trauma mechanism
 Trauma Chronology
 Never faint or wake up after a trauma
 Retrograde amnesia or antegrade, post-traumatic amnesia (PTA)
 Complaints: headache severity, decreased consciousness, convulsions, vertigo
 History of intoxication, alcohol, narcotics, post-operative head
 Comorbid diseases: epilepsy, heart disease, asthma, history of head surgery,
hypertension and diabetes mellitus, and impaired physiology of blood clots

III.3.2. Head to Toe Examination

Inspection by inspection, palpation, percussion, and auscultation, as well as special
examinations to determine pathological abnormalities, by method from head to toe.
Physical examination closely related to head injuries are:
1. Examination of the head, look for signs:
a. The lesions on the head include; sub-cutaneous, sub-galeal hematomas, open
wounds, penetrating wounds and foreign bodies.
b. Cranii base fracture signs, including:
• peri-orbital ecymosis (brill hematoma) and retro-auricular ecymosis (battle sign)
• check leakage liquor with a halo test on bloody-rhinorhoe and bloody-otorhoe
• hemotympanum or auditory canal lesions
• cranial nerve parese
• examination of carotid cavernous fistula signs
c. Facial fracture signs include; maxilla fractures (Lefort), orbital rhyme fractures and
mandible fractures
d. Signs of trauma to the eye include; conjunctival bleeding, front ventricular bleeding,
pupillary damage and other lesions in the eye

2. Examination of the neck and spine

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 Look for signs of spinal cord injury and injury to the spinal cord. Examination includes
complaints, injury, deformity, motor status, sensory, and autonomic.

III.3.3. Neurologic Status Exampination

Neurological status examination consists of:
a. Level of consciusness; based on the Glasgow Coma Scale (GCS)
Head injuries based on GCS, which are assessed after ABC is stable are classified:
GCS 13-15: Mild head injury
GCS 9 - 12: Moderate head injury
GCS 3-8: Severe head injury
b. Cranial nerves; especially nerves I-II-III-IV-VI-VII-VIII
c. Motorist, Sensory, Physiological Reflexes, and Pathological Reflexes
(compare the left and right, up and down looking for lateralization marks)
d. Autonomous; bulbocavernous reflexes, cremaster reflexes, sphincter reflexes, tendon
reflexes, and anal sphincter tone.

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III.4. Observation
Use general observation sheets (vital signs: tension, pulse, respiration, and temperature) and
neurological surgery special observation sheet. An example neurological status observation sheet is
as follows:

Picture 1. Neurological status observation sheet.

The data shows decreased level of consciousness accompanied by dilated pupils and
hemiparesis. GCS decreased from 15 to 5 indicating that there has been a delay in handling.
This data illustrates an example of inappropriate handling

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III.5. Plain Head Imaging Criteria
Indications of plain head examination in the form of patients with GCS 15 with lesions on
the scalp, without indication of CT Head Scan.

III.6. Head CT Scan Imaging Criteria

Head CT Scan imaging criteria :
1. GCS <15 after resuscitation
2. Cushing Sign (bradycardia and hypertension)
3. Complaints of headaches and / or vomiting that persist after adequate medical
administration (based on type, dosage, method of administration, and onset)
4. There are neurological focal signs (lateralization)
5. Neurological detection, both general in nature, such as: decreased GCS by 2 points or
more (not due to extracranial factors) and seizures; or are focal in nature, such as:
lateralization or worsening lateralization.
6. There are signs of fracture or suspected fracture
7. Penetrating trauma or suspicion of penetrating trauma
8. Age <5 years and> 50 years
9. Postoperative evaluation
10. GCS does not improve within 2x24 hours and is extracranial either
11. Multitrauma patients (significant trauma of more than 1 (one) organ)
12. Social indications

III.7. Admission Criteria

Patient will be admitted following these criteria:
1. Confusion or a history of fainting / decreased consciousness
2. Neurologic complaints and symptoms, including persistent headaches and vomiting
3. Difficulties in clinical judgment, for example alcohol, epilepsy
4. Other medical conditions: coagulation disorders, diabetes mellitus
5. Skull fracture
6. CT scan of the head is abnormal
7. No one can be responsible for observations outside the hospital
8. Age of patients over 50 years
9. Children
10. Social indications
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III.8. Discharge Criteria for Traumatic Head Injury
Criteria for head injury patients can be discharged by:
 Conscious and well-oriented, never faints
 There are no neurological symptoms
 Complaints are reduced, vomiting or headache disappears
 There is no head fracture or cranium base
 Someone is watching at home
 Have place to stay in the city

III.9. Patient Education Following Discharge

A Head Trauma patient who will be discharged is given a written warning.
Bring the patient to ER right away if they show these symptoms:
 Frequent vomitting
 Worsening headache or vertigo
 Restlessness-or decreased consciousness
 Seizures
 Paralized

III.10.High Care Unit (HCU) Admission Criteria

A Head Trauma patient needs to be admitted to HCU following these criteria:
 Needs close observation
 After receiving operation
 GCS < 13 with increased intracranial pressure signs
 GCS < 15 with lateralization and/or unstable haemodynamics
 Abnormal findings in Head CT Scan without indications for operation yet
 Neurologic deficit without indications for operation yet

III.11. Intensive Care Unit (ICU) Admission Criteria

Head trauma patients who meet the criteria of HCU admission and need ventilator.

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III.12.Brain Death Criteria
Brain Death criteria:
 GCS 3
 No brainstem reflex:
 Fixed pupils
 No corneal reflex
 No occulovestibular reflex(cold water calorics test)
 No occulocephalic reflex(contraindicated for cervical injury)
 Nogag and cough reflex
 No response to deep central pain
 Vital sign:
 Core Temp > 32C (> 90F)
 SBP > 90 mmHg
 No drugs in the system!
 Apnea test (+)  will be assessed as the last examination

Brain death, defined as the absence of clinical brain function when the proximate cause
is known and demonstrably irreversible, is commonly encountered in the ICU setting
following severe traumatic brain injury, aneurysmal subarachnoid hemorrhage, blunt carotid
injury, hypoxic-ischemic brain insults, fulminant hepatic failure, or severe hypoperfusion.
Brain death occurs when
1. intracranial pressure (ICP) exceeds cerebral perfusion pressure (CPP), resulting in
cessation of cerebral blood flow and oxygen delivery
2. as a result of absent cerebral blood flow secondary to traumatic injury or critical
illness.
Brain death determination is a clinical diagnosis, confirmed by a thorough and well
documented neurologic examination in conjunction with a positive apnea test (lack of
spontaneous respiratory efforts in the presence of an elevated PaCO2).
The diagnosis of brain death requires independent brain death determinations by three
licensed physicians.
In specific clinical situations, confirmatory tests may be indicated.
The determination of brain death should be made by a combination of clinical
neurologic examination and apnea test. Confirmatory tests may be performed at the
discretion of the physicians involved.
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Documentation of brain death should include the following information:
1. Etiology and irreversibility of the patient’s coma and overall clinical condition
2. Absent pupillary light response (pupils fixed in midpoint or dilated position)
3. Absent corneal reflexes
4. Absent oculovestibular reflexes (using oculocephalic / oculovestibular testing)
5. Absent gag reflex
6. Absent motor response or grimace to a noxious pain stimulus
7. Absent spontaneous respiration despite a PaCO2 ≥ 60 mmHg
8. Justification for and result of additional confirmatory test(s)
9. Findings of repeat neurologic examination
Pre-oxygenation as well as correction of hypotension and metabolic acidosis should be
performed prior to during apnea testing.

Clinical Neurologic Examination

The clinical neurologic examination, supplemented in appropriate clinical situations by
performance of one or more confirmatory tests, remains the standard for the determination
of brain death.
Declaration of brain death requires not only a careful clinical examination, but also:
 Establishment of the cause of coma
 Ascertainment of irreversibility
 Resolution of any misleading clinical neurologic signs
 Recognition of possible confounding factors
 Interpretation of neuroimaging studies
 Performance of any confirmatory laboratory tests deemed necessary
A clinical neurologic examination to determine the presence of brain death can only proceed
if the following four prerequisites have been met:
1) Clinical or neuroimaging evidence of an acute central nervous system (CNS) catastrophe
that is compatible with the diagnosis of brain death.
 Typically, computed tomography (CT) of the brain demonstrates a catastrophic brain
injury.
 A normal CT scan should raise doubt as to the diagnosis of brain death and lead to
further imaging studies.
2) Exclusion of complicating medical conditions that may confound clinical assessment such
as:

22
  Severe electrolyte, acid-base or endocrine disorders
 Refractory shock (systolic blood pressure < 90 mmHg)
 Guillain-Barré syndrome
 "Locked-in" syndrome
(A consequence of destruction of the pons, typically due to basilar artery thrombosis,
in which the patient cannot move the limbs, grimace, or swallow, but retains
consciousness, voluntary blinking, and vertical eye movements)
3) Absence of drug intoxication, poisoning, sedative, or neuromuscular blocking agents.
 Drug screens may be needed when appropriate
 Naloxone or flumazenil may be administered to document that no lingering effect of
narcotics or benzodiazepines is present
4) Absence of severe hypothermia, defined as a core temperature < 32°C (90°F).
 Pupillary response to light is lost at core temperatures of 28°- 32°C
 Brainstem reflexes disappear when core temperature drops below 28°C
 A core body temperature of ≥ 36°C is recommended
A comprehensive clinical neurologic examination includes documentation of the presence of
coma, the absence of brainstem reflexes, and apnea. Each of these three components is
described in further detail below:
1) Coma or unresponsiveness
 No cerebral motor response to pain in all extremities (nailbed pressure and
supraorbital pressure)
2) Absence of brainstem reflexes
The examination of brainstem reflexes requires the assessment of reflex pathways in the
mesencephalon, pons, and medulla oblongata. As brain death occurs, patients lose their
brainstem reflexes in a rostral-to-caudal direction with the medulla oblongata being the
last part of the brain to cease function. Complete cessation of all brainstem reflexes may
require several hours to develop.
 Pupils (CN II & III)
 Round or oval pupils measuring 4 to 9 mm with no response to bright light
 Ocular movement (CN III, VI & VIII)
 No oculocephalic movements should be elicited by rapid turning of the head
(performed only when no fracture or instability of the cervical spine is present)
 No deviation of the eyes to cold caloric stimulation

23
 I. Each tympanum should be irrigated with ice water after the head has been
tilted 30 degrees.
II. Allow 1 minute after injection and at least 5 minutes between testing on each
side.
III. The presence of clotted blood or cerumen within the external auditory canal
may diminish the stimulatory response.
IV. There should be no tonic deviation toward the cold stimulus.
 Facial sensation and facial motor response (CN V & VII)
 No corneal reflex to touch of the corneal edge by a swab
 No jaw reflex
 No grimacing to deep pressure on nail bed, supraorbital ridge, or
temporomandibular joint
 Pharyngeal and tracheal reflexes (CN IX & X)
 No response to stimulation of the posterior pharynx with a tongue blade
 No cough response to bronchial suctioning
(moving the endotracheal tube back and forth may not be an adequate stimulus;
current recommendation is to pass a suction catheter several times to the level of
the carina in an attempt to stimulate the patient to cough)
3) Apnea
A patient is considered to meet apnea test criteria for brain death if:
a) No spontaneous respiratory efforts were witnessed during the test (as evidenced by
physical attempts to inspire or documentation of end-tidal carbon dioxide by bedside
waveform analysis)
AND
b) The patient's PaCO2 is in excess of 60 mmHg (or at least 20 mmHg above baseline)

Confirmatory Laboratory Tests

A confirmatory test is not mandatory, but is desirable in patients in whom specific
components of clinical testing cannot be reliably performed or evaluated. The following
confirmatory test findings are listed in order of the most sensitive test first.
1) Conventional angiography
No intracerebral filling at the level of the carotid bifurcation or circle of Willis. The
external carotid circulation is patent, and filling of the superior longitudinal sinus may be
delayed.

24
2) Electroencephalography
No electrical activity during at least 30 minutes of recording that adheres to the minimal
technical criteria for EEG recording in suspected brain death.
3) Transcranial Doppler ultrasonography
Small systolic peaks in early systole without diastolic flow or reverberating flow,
indicating very high vascular resistance associated with greatly increased intracranial
pressure. Ten percent of patients may not have temporal insonation windows precluding
use of this technique for determining brain death.
4) Technetium-99m cerebral blood flow scan
No uptake of isotope in brain parenchyma (“hollow skull phenomenon”).
5) Somatosensory evoked potentials
Bilateral absence of N20-P22 response with median nerve stimulation.

Clinical Conditions That May Interfere with the Diagnosis of Brain Death
The following physical conditions may interfere with the clinical diagnosis of brain death. In
such situations, confirmatory tests are recommended as clinical neurologic examination
alone may not be accurate.
 Severe facial trauma
 Preexisting pupillary abnormalities
 Toxic levels of any sedative drugs, aminoglycosides, tricyclic antidepressants,
anticholinergics, antiepileptic drugs, chemotherapeutic agents, or neuromuscular
blocking agents
 Sleep apnea or severe pulmonary disease resulting in chronic retention of carbon dioxide
(PaCO2)

Clinical Observations Compatible with the Diagnosis of Brain Death

The following physical findings are occasionally seen and should not be misinterpreted as
evidence for brainstem function:
 Spontaneous limb movements other than pathologic flexion or extension response
 Cyclical dilatation and constriction of light-fixed pupils
 Respiratory-like movements (shoulder elevation and adduction, back arching, intercostals
expansion without significant tidal volumes)
 Sweating, blushing, tachycardia

25
 Normal blood pressure without pharmacologic support or sudden increases in blood
pressure
 Absence of diabetes insipidus
 Deep tendon reflexes; superficial abdominal reflexes; triple flexion response
 Babinski reflex

Medical Record Documentation

Following the determination of brain death, appropriate documentation in the patient’s
medical record should be performed.
This documentation should include the following components:
 Etiology and irreversibility of the patient’s coma and overall clinical condition
 Absent pupillary light response (pupils fixed in midpoint or dilated position)
 Absent corneal reflexes
 Absent oculovestibular reflexes (using oculocephalic and oculovestibular testing)
 Absent gag reflex
 Absent motor response or grimace to a noxious pain stimulus
 Absent spontaneous respiration despite a PaCO2 ≥ 60 mmHg (when apnea testing can be
safely or appropriately performed)
 Justification for and result of additional confirmatory tests (if indicated)
 Findings of repeat neurologic examination (performed by three licensed physician)
 Time of death (documented as the time at which the second physician determination of
brain death is completed).

26
III.13. Criteria for Tracheal Intubation
 Inadequate Airway
 GCS  8
 Brain Herniation
 Rapid deterioration
Tracheal intubation must be carried out by competent medical personnel.

27
 CHAPTER IV
Algorithm for the Management of Patients with Head Injury

IV.1. Algorithm for the Management of Minor Head Injury Patients

Patient

1. StabilizationofAirway, Breathing and Circulation

Emergency care installation (ECI)
(ABC)
2. Anamnesis&Physical Diagnostic
3. Radiological examination, according to indications
4. Lab examination
(DL,SE, GDA,FH, &Other labs as indicated)
5. Symptomatic + Antibiotic Therapy according to
Hospitalized in
R. 13/ ü IVSD 0,9 NS 1,5 ml / kg body weight (BW)/ hour
Operation
HCU (child< 2 years: D5 0,25 NS)
ü fasting for 6 hours
ü Symptomatic drug IV or supp
ü Observation closely as a brain injury patient
ICU ü Note the vital state and st. neurological when it
will be sent to the treatment room (R.13/HCU)
ü Handover of patients and complete information
on the patient's condition

VS Stable
St. Stable
Neurology get worse

ü Stabilization
out of ü Resuscitation
hospital
ü Rediagnosis Cito

ICU Operation

28
IV.1. Algorithm for the Management of Patients with Medium Head Injury

Patient
ü Stabilizationof Airway, BreathingandCirculation(ABC)
ü Overcome Hypotension with Isotonic Fluids & Find
the Causes
Emergency care installation (ECI)
ü If the tension is stable, install IVFD 0.9 NS 1.5 ml / kg
body weight (BW)/ hour
ü Laboratory examination
(DL, SE, BGA, GDA, FH, cross match)
ü Give symptomatic medicine IV orSupp
ü Perform Heteroanamnesis, General Physical
Examination and Neurological Status
ü InstallNaso Gastric tube
ü Install Folley Kateter &evaluation of urine production
ü When hemodainamic has stabilized, do it:
 Photo RöLeher Lateral
 Photo Rö Thorak AP
 Other radiological examination for indications
• CT Scan of the Head
Hospitalize ü Doctor in charge of service (DCS) - Doctor-Specialist
Operation Education Program (DSEP) of Neurosurgery reports
d in R. 13/
HCU DCS Senior Neurosurgery


ICU

Improve Get worse

VS Stable
St. StableNeurology
ü Stabilization
ü Resuscitation
out of ü Rediagnosis Cito
hospital
ü

ICU Operation

29
IV.2. Algorithm for the Management of Severe Head Injury Patients (option 1)

Patient ü Resusitazation ofAirway, BreathingandCirculation (ABC)

ü Install the oropharynx or nasopharyngeal tube if necessary.
If there is an acute airway obstruction performed
Emergency care installation (ECI) cricothyrotomy or tracheotomy
ü Installation of Intubation & Ventilation Control
(PCO2 35-40 mmhg, PaO2100 mmHg atau SPO2>97%)
ü installCollar Brace
ü installNaso Gastric Tube
ü If shocked, give isotonic fluid (RL and colloid or blood). Look
for causes, resolve, maintain tension> 90 mmHg.
ü If there are signs of uncal herniation or rapid deterioration
and no hypotension or kidney failure and / or heart failure,
give mannitol 20% 200 ml bolus in 20 minutes or 5 ml / kg
body weight (BW), or 1 gr / kg body weight. If the indicator
of mannitol administration continues, keep blood
osmolality <320 mOsm.
ü If seizures: Diazepam 10 mg iv slowly, can be added until
the seizures stop. Monitor respiratory depression, followed
by phenitoin bolus 10-18 mg / kg BW in 100 cc PZ within 30
minutes, followed by 8 mg / kg BW
ü Perform a Lab examination (DL, BGA, GDA, SGOT/PT, BUN,
SK, SE, FH, cross match)
Operation Hospitalize ü perform Heteroanamnesis
d in
ü perform General Physical Examination and Neurological
R. 13/
Status
HCU
ü Give symptomatic IV drugs or supp and antibiotics as
ICU indicated
ü Install the catheter, note the state and production of urine
ü Observation Vital signs, if hemodynamically stable, do it:
 photo Ro Leher Lat
Improve  photo Ro Thorak AP
 Other radiological examination for indications
VS Stable • CT Scan of the Head
St. Stable Neurologi ü Close observation and simultaneous reporting to the surgeon
ü Doctor in charge of service (DCS) - Doctor-Specialist
Education Program (DSEP) of Neurosurgery reports DCS
out of Senior Neurosurgery
hospital

30
Algorithm for the Management of Severe Head Injury Patients (2nd choice)

Severe head injury

(GCS ≤ 8)

Emergency measures
for Diagnostics and Evaluation based on
Therapy according to ATLS
Indications

 Intubasi endotracheal
 Liquid Resusitasi
 Ventilasi (PaCO2 35mmHg)
 Oxygenation
 Sedation ± Pharmacological Paralysis
(short-term)

Herniation? * ± Hyperventilation *
Deterioration?* ± Manitol (1gr/kg) *

CT Scan of Head Yes

Resolution
without contrast
No

Surgical Yes
Indications?

No Operation

ICU

Monitoring
ICP

Test for
Intracranial
hypertension

* If found signs of herniation or progressive neurological deterioration is not due to extracranial

factors

31
 CHAPTER V
Medicamentosa Treatment Management Recommendation

V.1. Recommendation for use of anti-seizure drugs

Standard : No supporting data
Guideline : 1) Effective Anti-seizure prophylaxis is administered in the first week after
trauma. Effective alternative medicines are phenytoin and levetiracetam.
2) Anti-seizure prophylactic treatment should not be routinely carried out after
7 days post-trauma because it does not reduce the risk of late phase of
post-traumatic seizures.
3) Administration of prophylaxis with phenytoin is effective for preventing
early phase of post-traumatic seizures
Option :-

Explanation of recommendations:
The use of anti-seizure drugs is not recommended for the prevention of post-
traumatic late-stage seizures because an epileptic focus has formed. It is permissible to use
anti-seizure drugs as a prophylaxis against the occurrence of early phase of post-traumatic
seizures that occur within 7 days post-trauma (early phase) in patients who are at high risk
for post-traumatic seizures. Phenytoin or Carbamazepine has been proven to be effective for
early phase of post-traumatic seizures because this phase has not formed an epileptic focus.
Torbic’s (2013) study of levetiracetam as a recent anti-epileptic drug shows that
levetiracetam has efficacy comparable to phenytoin as post-traumatic seizure prophylaxis
and compared to phenytoin, levetiracetam has fewer side effects.
Criteria for patients at high risk of post-traumatic seizure:
1. GCS ≤ 10 6. Depressed fracture
2. Immediate seizures 7. Chronic alcoholics
3. Cortical contusions 8. Post traumatic Amnesia> 30 minutes
4. Linear fracture 9. Age ≥ 65 years or ≤15 years
5. Penetrating Head Injury

Dosage and method of administration :

32
 Prophylactic treatment with phenytoin to reduce the risk of early phase of post-
traumatic seizures begins with a loading dose immediately after the trauma.
Loading dose for:
 Adult patient 15-20 mg/kgBW
 Pediatric patient 10-20 mg/kgBW,
in 100 cc NS of 0,9%with a maximum infusion rate of 50 mg/minute, followed by a
maintenance dose of 5 mg/kgBW/day divided into 2-3 doses. The maintenance dose can be
increased up to 10 mg/kgBW/day to reach a serum concentration between 10-20 mcg/ml.
Prophylactic treatment with levetiracetam is carried out by administering a dose of
500 mg per 12 hours for 7 days after head injury without the administration of a loading
dose.

Table 5. Level of Evidence (LOE) and Grade of Recommendation (GOR)

LOE/
No Author Description of Assessment Conclusion
GOR

1 Torbic H Meta-analysis of level I dan II/B Effective anti-seizure

et al., 2013 II studies to determine the
effectiveness of anti-
seizure drugs and the risk
factors
prophylaxis was administered
in the first week post-trauma.
The effective alternative drugs
were phenytoin and
levetiracetam.

2 Chang SB, Meta-analysis of several II/B Prophylactic treatment with

Lowenstein level I and II studies to
DH, 2003 determine the prophylactic
role of anti-epileptic drugs
in patients with severe
head injury
phenytoin which began with a
loading dose immediately post-
trauma was effective in
reducing the risk of earlyphase
of post-traumatic seizures.
Prophylaxis was not effective
for late phase seizures. Risk
factors for seizures: severe
head injury, prolonged amnesia
or unconsciousness,
intracranial hematoma or
cerebral contusion, and
depressed fracture.

3 Temkin Randomized double-blind II/B There were no significant

et al., 1999 study to determine the differences in the occurrence of
effectiveness of phenytoin post-traumatic seizures in

33
 administered for 1 week
compared to valproic acid
administered for 1 or 6
months as post-traumatic
seizure prophylaxis
patients receiving phenytoin
therapy for 1 week compared
with those receiving valproic
acid therapy for 1 or 6 months.

4 Annegers Retrospective study to II/B Significant risk factors:

et al., 1998 determine the  subdural hematoma
characteristics of head  skull factures
injury associated with  amnesia lasting more than
post-traumatic seizures one day
 age> 65 years

5 Golden N, Retrospective study with a
1996 casecontrol study design
to determine the effect of
risk factors on the number
of epilepsy events after
early trauma
II/B Risk factors for early post-
traumatic:
epilepsy
 age< 15 years
 depressed fracture
 intracranial lesion
 focal neurological deficit

6 Temkin Randomized double blind II/B Phenytoin was only effective

etal., study to determine the for preventing early post-
1990 effectiveness of phenytoin traumatic seizures
administration to prevent
post-traumatic seizures
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Algattas H and Huang JH. Traumatic brain injury pathophysiology and treatments: early,
intermediate and late phases post injury. Int. J. Mol. Sci. 2014, 15, 309-41; doi:
10.3390/ijms 15010309.
Annegers JF et al. A Population Based Study of Seizure after Traumatic Brain lnjuries.
TheNEJM 1998
Chang S, Bemard and Lowenstein H Daniel. Practice parameter: Antiepileptic drug
prophylaxis insevere traumatic brain injury : Report of the Qua|ity Standards
Subcommittee of the American Academy of Neurology. Neurotogy 2003; 60:10-6.
Golden N. Pengaruh Faktor Resiko terhadap Angka Kejadian Epilepsi Pasca Trauma Dini di
RSUD Dr Soetomo.Karya Tulis Akhir PPDS I llmu Bedah Saraf, Lab AJPF Bedah Saraf FK
Unair/RSUD Dr Soetomo. 1996
Temkin et al.A randomized double blind study of phenytoin for prevention of post
traumaticseizures. The NEJM 1990; 323 :497-502.
Temkin et al. Valproate therapy for prevention of post traumatic seizures: a randomized
trial. J Neurosurg 1999;91:593–600.
Torbic H et al. Use of antiepileptics for seizure prophylaxis after traumatic brain injury. Am J
Health-Syst Pharm. 2013; 70:759-66

34
V.2. Recommendation for use of mannitol and hypertonic sodium lactate
Standard : Therapy using hyperosmolar sodium lactate solution is more effective in
reducing ICPcompared with mannitol.
Guideline : Mannitol helps reduce ICP in patients with severe head injury. Bolus
administration at a dose of 0.25-1 gr/kgBW is recommended compared to
continuous administration.
Option : 1) Mannitol administration can be carried out prior to ICP Monitor placementin
casethe signs of transtentorial herniation or progressive loss of
consciousness occur. Serum osmolarity must bebelow 320mmol/l to prevent
kidney failure. The patient must be kept in a euvolemicstate and have a
urine catheter installed to monitor urine production.
2) Therapy using hyperosmolar sodium lactate solution is more effective in
reducing ICTcompared with mannitol.

Explanation of recommendations :
Mannitol is very useful in increased ICP therapy. Mannitol can reduce ICP by drawing
fluid into the intra-vascular compartment (if ICP decreases, then CBF and CPP will increase).
Mannitol can significantly reduce “non surgical mass lesion” type severe head injury
mortality if there are no episodes of hypotension or hypoxia during treatment on GCS 3-5 or
CT Scan shows grade III cerebral contusions. The mannitol preparations commonly used are
15 and 20%. The patients are bolus administed mannitol 0.25-1 gr/KgBWin 10-20 minutes
per 4-8 hours. Before administering mannitol, routine blood tests, kidney function, blood
sugar, and blood electrolytes must be carried out. Initial blood osmolarity calculation is
carried before mannitol administration. In addition, a foley catheter must be inserted for the
measurement of diuresis.

Osmolarity = 2(Na+ + K+) + Glucose/18 + BUN/2.8

In using mannitol, close observation must be made to keep the patient in a euvolemic
state and serum osmolarity <320 mmol/l. Euvolemic state is maintained by replacing the
isotonic fluid volume and hypotension (TDS <90 mmHg) must be prevented. The rebound
phenomenon can be reduced by bolus administration, and mannitol can be stopped
gradually.

35
 Hypertonic sodium lactate is administered at a dose of 1.5 ml/kgBW for 15 minutes in
each administration. Hypertonic sodium lactate can be administered in cases with increased
ICP, with hypovolemic or hypotensive state. Sodium lactate can reduce ICP with a smaller
dose of administration, reduce ICP greater and faster.
The complications of hypertonic saline are rebound edema, BBB damage, decreased
level of consciousness due to hypernatremia, and central pontine myelinolysis (CPM).
Hypertonic sodium lactate can provide better patient outcomes with the Glasgow Outcome
Scale (GOS) indicator, Barthel Index, and Karnoffsky Score compared with mannitol and can
be administered to patients with shock.

Table 6. Level of Evidence (LOE) and Grade of Recommendation (GOR)

LOE/
No Author Description of Assessment Conclusion
GOR

1 Wakai et Randomized control trial I/A Mannitol administration was

al., 2013 with mannitol better thanpentobarbital
administration in patients administration and was less
with acute trauma with beneficial compared to
moderate and severe head hypertonic saline fluid
injury administration.

2 Ardyansyah Experimental study with I/A Hypertonic sodium lactate can

A., comparative analysis reduce ICP greater and longer
Wahyuhadi between administration of than mannitol.
J., 2011 hypertonic sodium lactate
and mannitol in reducing
ICP

3 Ichai C, et A prospective open I/A The therapy using

al., 2009 randomized study
compared between
hyperosmolar sodium
lactate therapy and
mannitol in reducing ICP in
cases of head injury
hyperosmolar sodium lactate
solution was more effective in
reducing ICT compared with
mannitol.

4 Faris M., Experimental study with
Wahyuhadi comparative analysis
J., 2009 between administration of
sodium lactate and
mannitol in reducing ICT
I/A Hypertonic sodium lactate and
mannitol were effective and
safe in the treatment of
increased ICT. Hypertonic
sodium lactate was more
effective than mannitol.

36
 5 Qureshi et Literature review on III/C Hypertonic saline indicated
al., 2000 hypertonic saline in the beneficial effect in reducing ICP
treatment of brain edema while maintaining
and intracranial hemodynamics in clinical
hypertension studies and in laboratories

6 Balafif F., A case control study II/B Mannitol significantly reduced

Bajamal compared between non- “non surgical mass lesion” type
A.H., 1999 surgical mass lesion type of severe head injury mortality
of patients with severe if there were no episodes of
head injury who hypotension or hypoxia during
empirically receive treatment on GCS 3-5 or CT
mannitol and without scan indicated grade III
mannitol. contusion.

7 Gemma et A prospective randomized II/B Hypertonic saline was as

al., 1997 clinical study compared effective as mannitol in
the effects of 7.5% reducing brain edema during
hypertonic saline and 20% the process of neurosurgery.
mannitol.

8 Mendelow Assessment of the effect of III/C There was a decrease in ICP,

et al.,1985 intravenous administration and an increase in CBF and CPP.
of 20% mannitol at a dose
of 0.25 – 0.5g/kg on ICP,
CPP and CBF.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Ardyansah A., Wahyuhadi J., Perbandingan Pemberian Dosis Multipel Hipertonik Natrium
Laktat dan Manitol terhadap Penurunan Tekanan Intrakranial pada Penderita Cedera
kepala Berat tanpa Indikasi Operasi dengan Tekanan Intrakranial lebih dari 20 mmHg,
SMF Bedah Saraf RSU Dr Soetomo, 2011
Balafif F., Bajamal A.H., Pengaruh Pemberian Mannitol secara empiris pada penderita cedera
kepala berat tipe Non Surgical Mass Lession di RS dr. Soetomo Surabaya. 1999
Faris M. Wahyuhadi J., Perbandingan Pengaruh Pemberian Hipertonik Sodium Laktat dan
Manitol terhadap Progresifitas Penurunan Tekanan Intrakranial Penderita Cedera kepala
Berat Lesi Non Operatif. SMF Bedah Saraf RSU Dr Soetomo,2009
Gemma M, Cozzi S, Tommasino C, Mungo M, Catvi MR, Cipriani A, Garancini MP. 7.5%
Hypertonic saline versus 20% mannitol during elective neurosurgical supratentorial
procedures, J Neurosurg Anesthesiol, 1997;9(4):329 – 34
Ichai C, Armando G, Orban JC, et al. Sodium Lactate versus Mannitol in The Treatment of
Intracranial Hypertensive Episodes in Severe Traumatic Brain-injured Patients. Intensive
Care Med, 200935:471 – 479
Iskandar J. Cedera Kepala. BIP. 2004
Mendelow AD, et al. Effect of mannitol on cerebral blood flow and cerebral perfusion
pressure in human head injury. J Neurosurg 1985;63:43-9
37
 Reilly P, Selladurai B. Initial Management of Head Injury: a Comprehensive Guide. McGraw
Hill, 2007, p177 – 205
Qureshi AI, Suarez JI, Use of hypertonic saline solutions in treatment of cerebral edema and
intracranial hypertension, Crit Care Med,
http://www.ncbi.nlm.nih.gov/pubmed/11008996 2000;28(9):3301-13
Wakai A, McCabe A, Roberts I and Schierhout G. Mannitol for acute traumatic brain injury.
Cochrane Database Syst Rev. Aug 5, 2013

V.3. Recommendation for use of antibiotic prophylaxis in the placement of

ventricular catheter
Standard : No supporting data
Guideline : No supporting data
Option : 1) Administration of antibiotics in the placement and replacement of
ventricular catheters every 5 days does not reduce the risk of infection.
2) The use of local and systemic antibiotics does not reduce the risk of
infection in the placement of ventricular catheter.

Explanation of recommendations :
In severe traumatic brain injury, the incidence of infection can increase with the
placement of ICP monitors, mechanical ventilation, etc. In general, infections are found in
the first 10 days after ventriculostomy placement. There was no effect between the catheter
being replaced every 5 days or not. Infection had a significant effect on the morbidity,
mortality and length of stay of the patients.
In the placement of long-term ICP monitor, there was an increase in infection rates
up to 27%, whereas the use of short-term ICP monitors has not been shown to increase the
risk of morbidity and mortality. Of all patients with severe head injury, there was no
definitive incidence of CSF infection.
The 3rd and 4th generation of cephalosporin isa recommended type of antibiotics. In
craniocerebral penetration trauma, there was no evidence to support the use of antibiotic
prophylaxis, but experts recommend routine broad-spectrum antibiotics related to the
severity of possible complications and antibiotic selection according to the germ map at the
local hospital.

Table 7. Level of Evidence (LOE) and Grade of Recommendation (GOR)

No Author Description of Assessment LOE/GOR Conclusion

1 Arabi et al., Analysis of incidence of III/C The use of local and systemic

38
 2005 ventroculostomy infection antibiotics does not reduce the
and evaluation of the risk risk of infection in ventricular
factors. catheter placement.

2 Holloway A retrospective analysis of III/C The incidence of infection was

et al.,1996 584 severe head injury
patients related to the
effect of catheter
replacement on the
incidence of infection
found in 61 patients with
venticulostomy. In general,
infections are found in the first
10 days after ventriculostomy
placement. There was no effect
between the catheter being
replaced every 5 days or not.

3 Sunbarg et A retrospective analysis of III/C Of all severe head injury

al.,1996 648 patients using ICT patients,there was no
monitors. 142 patients had definitive incidence of CSF
severe head injury. None infection.
of the patients received
antibioticprophylaxis.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and
Research)

Reference
Arabi Y, Memish ZA, Balkhy HH, Ventriculostomy-associated infections: Insidence and risk
factors. ,Amj Infect Control 2005;33:137-43.
Holloway KL, Barnes T, Choi S. Ventriculostomy infections: the effect of monitoring duration
and catheter exchange in 584 patients. J Neurosurg 1996;85:419–24.
Sundbarg G, Nordstrom C-H, Soderstrom S. Complication due to prolonged ventricular fluid
pressure recording.Br. J Neurosurg 1988;2:485–95.
Yuen, ECP.2004. Theuse of prophylactic antibiotic in trauma. Hong Kong Journal of
Emergency Medicine

V.4. Recommendation for use of analgesics

Standard : No supporting data
Guideline : 1) Ketorolac and acetaminophen can be used in head trauma patients.
Ketorolac should only be administered a maximum of 5 days or the
maximum dose is reached (180 mg).
2) Other NSAIDs such as ibuprofen and naproxen can be administered orally.
3) Ketoprofen supp and acetaminophen supp are useful to reduce pain in
patients with mild head injury.

39
Option : 1) There is no data that allows metamizole to be administered to head trauma
patients (the incidence of agranulocytosis 92% occurred in the first 2 months
of metamizole use)
2) Indomethacin can be beneficial for reducing refractory intracranial pressure
in patients with severe head injuries.

Explanation of recommendations :
Stimulation of pain can trigger an increase in ICT and must be treated. In head injury
patients, there was an increase in level of PG where PG plays a role in the process of pain.
NSAIDs such as ketorolac, metamizole and ketoprofen were useful in reducing pain by
inhibiting PG synthesis through blockade of Cyclooxigenase (COX) enzyme. Acetaminophen is
not classified as NSAID, but has the same mechanism in inhibiting PG synthesis through COX
enzyme blockade. Increased levels of prostaglandins occured in head injury patients.
However, the use of NSAIDs can also cause gastrointestinal bleeding and impaired kidney
function.
Indomethacin is classified as NSAID. It has anti-inflammatory, analgesic and
antipyretic properties through reversible inhibitory effects on the COX enzyme.
Indomethacin can function as an alternative therapy in the management of increased
refractory intracranial pressure in patients with severe head injury. But the mechanism of
action of indomethacin in reducing cerebral blood flow (CBF) and intracranial pressure is not
fully understood.
Ketorolac for adults is administered at a single 30 mg dose intravenously or 30 mg/6
hours intravenously with a maximum dose of 120 mg/day. Metamizole is administered at a
dose of 500-1000mg/6 hours orally, intravenously or perectally.

Table 8. Level of Evidence (LOE) and Grade of Recommendation (GOR)

LOE/
No Author Description of Assessment Conclusion
GOR

1 Prasetya H, Quasi-experimental II/B Ketoprofen and

Bajamal research on the use of acetaminophen were useful in
A.H., 2005 ketoprofen and reducing pain in patients with
acetaminophen on mild head injury.
patients with mild head
injury.

2 Roberts et Review: The role of III/C Indomethacin was considered

40
 al., 2002 indomethacin in the in the management of head
treatment of head injuries injuries with increased ICP
refractory

3 Heden- Retrospective study III/C The incidence of

malm K et discussed case report of agranulocytosis 92% occurred
al., 2002 agranulocytosis due to the in the first 2 months of
use of metamizole metamizole use.

4 Jacobi J et Literature review in II/B Ketorolac and acetaminophen

al., 2002 Medline search 1994-2001 may be used in head trauma
for the preparation of patients
guidelines with a review of
meta-analysis and
evidence tables
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Hedenmalm K et al. Agranulocytosis and other blood dyscrasias associated with dipyrone
(metamizole). Eur J Clin Pharmacol 2002;58(4):265-74.
Jacobi J et al. Clinical practice guidelines for the sustained use of sedatives and analgesics in
the critically ill adult. Am J Health Syst Pharm 2002;59(2):150-78
Prasetya H, Bajamal A.H. Perbandingan Efek Analgetika antara Pemberian Paracetamol 650
mg Suppositoria denganKetoprofen 100 mg Suppositoria terhadap Nyeri Kepala pada
Penderita Cedera kepala Ringan. Karya Akhir, 2005.
Roberts R, Redman J. Indomethacin - A Review of its Role in the Management of Traumatic
Brain Injury. Critical Care and Resuscitation 2002; 4: 271- 280.

41
V.5. Recommendation for use of corticosteroids
Standard : The use of glucocorticoids is not recommended for patients with severe head
injury. Glucocorticoids do not increase output and decrease ICP in patients with
severe head injury.
Guideline : Statistically, the results of therapy with and without corticosteroids in patients
with cerebral contusion were not significantly different.
Option : There was no reduction in mortality rate by administeringmethylprednisolone
in 2 weeks after head injury.

Explanation of recommendations :
Head injury can cause death of some brain cells and damage to corticosteroid
receptors. Head injury also causes an increase in corticosteroid levels or increases the use of
protein receptors and hence the use of corticosteroids is ineffective because of the limited
number of existing protein receptors and some corticosteroid receptors are damaged so that
the formation of lipocortin is also limited. This causes impaired corticosteroid tolerance.
In some cases, it has been reported that the side effects of corticosteroid use can
cause gastrointestinal bleeding and infection. Due to an increase in mortality and lack of
benefits in the use of corticosteroids in several studies,It has been considered not to
administer corticosteroids to patients with head injuries.

Table9. Level of Evidence (LOE) and Grade of Recommendation (GOR)

LOE/
No Author Description of Assessment Conclusion
GOR

1 Alderson The Randomized I/A The study concluded that there

P., 2005 Controlled Trials to assess
the quantity of
effectiveness and safety
regarding corticosteroid
use in head injury
was an increase in mortality
with the use of corticosteroid.
This study suggested that
corticosteroid should no longer
be used routinely in patients
with head injury.

2 CRASH trial Reduction in mortality III/C There was no reduction in

collabo- rates by administering mortality rates by
rators, methylprednisolone within administering
2004 2 weeks after head injury methylprednisolone within 2
weeks after head injury

3 Aiderson Randomized Controlled I/A Systemic review of the RCT for

P., 1997 Trials to assess the corticosteroids in acute head

42
 quantity of effectiveness injuries indicated unclear
and safety regarding effects.
corticosteroid use in head
trauma

4 Kasan U., A comparative prospective II/B Statistically, the therapy

1994 study with and without outcomes with and without
corticosteroid use in head corticosteroids in patients with
injury patients cerebral contusion were not
significantly different.

(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Alderson P, Roberts I. Corticosteroid for acute traumatic brain injury, 2005
CRASH trial collaborators, Effect of intravenous corticosteroids on deathwithin 14 days in 10
008 adults with clinically significant head injury (MRC CRASH trial): randomized placebo-
controlled trial Lancet 2004; 364: 1321–28
Alderson P. Corticosteroids in acute traumatic brain injury: systemic review of randomized
controlled trials, BMJ 1997.
Kasan U. Penatalaksanaan Penderita Memar Otak Penelitian Prospektif Komparatif dengan
dan tanpa penggunaan Kortikosteroid, disertasi 1994.

V.6. Recommendation for use of sedatives (tranquilizer)

Standard : Both propofol and midazolam, or a combination of both, are declared safe for
patients with head injury.
Guideline : 1) Midazolam reduces CBF, so that it tends to be safe and effective for
anesthesia and sedation in patients with increased ICP.
2) Propofol provides good sedation and facilitates early neurological
evaluation.
3) Dexmedetomidine is a sedation without neurological effects and has brain
protective effect.

43
Option :-

44
Explanation of the recommendation :
Sedative is an important component in the management of patients with head
injuries. It can facilitate therapeutic intervention, control ICP, and ensure patient comfort.
This can be seen in the table below, choose sedative according to GCS and whether or not
there is a mechanical ventilatory support.
The ideal sedative agents should:
(i) decrease CMRO2 while maintaining oxygen supply to the brain
(ii) reduce ICP without reducing CPP
(iii) maintaincerebral autoregulation and vascular reactivity to CO2
(iv) have a rapid onset
(v) be easy to control in depth and duration of the sedation.
(vi) have a therapeutic window for evaluating neurological status and detecting neurological
complications. Sedative administration can be used as a tertiary management of ICP
control.
Propofol loading dose is administered at 1-2 mg/kgBW and maintenance dose is
administered at 1-3 mg/kgBW/hour. Midazolam loading dose is administered at 0.03-
0.3mg/kg in 20 minutes; and maintenance dose is administered at 0.03-0.2mg/kg/hour.
Penthotal loading dose is administered at 5-10 mg/kgBW in 10 minutes, and a maintenance
dose is administered at 2-4 mg/kgBW/hour. Phenobarbital: Bolus of 2-5 mg/kgBW or
Thiopenthal of 2-10 mg/kgBWis followed by an infusion of siringe pump (0.3-7.5
mg/kgBW/hour) or thiopental of 1-6 mg/kg/day. Dexmedetomidine is administered with a
loading dose of 0.5-1 mcg/KgBW for 10 minutes, followed by a maintenance dose of 0.2-0.3
mcg/KgBW/hour.

Table 10. Analgesia and Sedation Strategies in Patients with Various Acute Neurological
Conditions
Head injury, Head injury, Cerebrovascul Hepatic Alcohol
mechanical spontaneus ar accident encelophat withdrawl
ventilation, GCS breathing GCS y syndrome
≤8 >8
Analgesia Opioids NSAID - - -
Sedation Midazolam Lightsedation: Lightsedation: Isofluranef Midazolam
Propofol propofol& propofol& or Other
Barbiturates midazolam midazolam shortperio benzodiazepines
(Uncontrolled Neuroleptic Neuroleptic ds Clonidine
ICP) Phenothiazine Phenothiazine Neuroleptics

45
 Clomethiazole
Antagonist No No No? Yes Yes

Monitoring Vitalfunctions, Vitalfunctions, Vitalfunctions, Vitalfunctio Vitalfunctions,

invasive neurologial neurologial ns, neurological
haemodinamic functions functions neurologial function
monitoring, functions,li
ICPSjO2 ver
functiontes
ts
GCS,Glasgowcomascore;ICP,intracranialpressure;NSAID,non-steoidalanti-inflamatorydrugs;
SjO2,oxygensaturationofthejugularvein

Table11. Level of Evidence (LOE) and Grade of Recommendation (GOR)

No Author Description of Assessment LOE/GOR Conclusion

1 Shigemori Consideration for the use II/B Diazepam can be used in the
M et al., of sedation case of epilepsy, but itwas not
2012 suitable for evaluating the level
of consciousness. Midazolam
reduced CBF, so thatit tended
to be safe and effective for
anesthesia and sedation in
patients with increased ICP.
Propofol provided good
sedation and facilitated early
neurological evaluation.
Dexmedetomidine is a sedation
without neurological effects
and has brain protective effect.

2 Chen HI et Examining the use of III/C The use of barbiturates can

al., 2008 barbiturate for the increase brain tissue
intractable pain of oxygenation in patients with
increased ICP when the increased ICP after trauma.
use of sedation therapy
and osmotic therapy fails

3 Karabinis et Examining the safety and I/A Neurological examination can

al., 2004 efficacy of sedation based be faster and easier to predict
on analgesia using using ramifentanil than using
ramifentanil, combination fentanyl or morphine.
of midazolam and propofol

46
 compared with fentanyl,
morphin combined with
midazolam and propofol in
the neurointensive care
unit.

4 Sanchezet Examining the safety and I/A Both propofol and midazolam,
al., 1998 efficacy of the use of or a combination of both is
propofol; midazolam or a declared safe for patients with
combination of propofol head injury.
and midazolam in head
injury patients
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Chen HI, Malhotra NR, Oddo M, Heuer GG, Levine JM, LeRoux PD. Barbiturate infusion for
intractable intracranial hypertension and its effect on brain oxygenation. Neurosurgery.
2008 Nov;63(5):880-6; discussion 886-7. doi: 10.1227/01.NEU.0000327882.10629.06.
Ederoth P et al. Blood-brain barrier transport of morphine in patients with severe brain
trauma. Br J Clin Pharmacol.2004;57(4):427-35
Karabinis A et al. Safety and efficacy of Analgesia-based regimens in intensive care unit
patients with brain injuries: a randomized, controlled trial. Crit Care.2004;8(4): 268 - 80.
Rivier MC, Cholero R, and Ravussin P. Sedation and Analgesia for the Brain- Failure Patient.
In: Sedation and Analgesia in the Critically Ill. Ed. By Park GR and Sladen RN. Blackwell
Science 1995. pp 130-144
Sanchez-Izquierdo-Riera JA et al. Propofol versus Midazolam: safety and efficacy for sedating
the severe trauma patient. Anesth Analg. 1998;86(6):1219-24.
Shigemori M et al. Guidelines for management severe head injury 2nd Edition. Guidelines
from the guidline committee on the managemnt of severe head injury in Japan Society
of Neurotraumatology. Neurol. Med. Chir (Tokyo) 52, 1 – 30, 2012.

V.7. Recommendation for nutrient administration

Standard : Early administration of nutrient
Guideline : 1) Nutrient is administered progressively and total needs must be achieved
within 7 days after trauma.
2) Nutritional requirement of paralyzed head injury patients is 140% of basal
requirement, while nutritional requirement of non-paralyzed head injury
patients is 100% of basal requirement.
3) Nutrient can be administered enterally and parenterally.
4) At least 15% of energy intake must contain protein.
5) Administration of fat should be a combination of Long-Chain Triglyserides
(LCT) and Medium-ChainTriglyserides (MCT)

47
Option : Administration through gastrojejunostomy to avoid gastric emptying problems
and facilitate administration and avoid being pulled when the patient is
nervous because it is placed far from the patient’s face.

Explanation of the recommendation :

Head injury increases the body’s metabolic and catabolic responses and thus requires
adequate nutrient. Adequate early feeding is recommended because it provides better
survival and disability outcomes for patients with head injuries. There are no studies
indicating the best method of administration.
The study found that the combination of LCT and MCT may have a beneficial effect
on protein metabolism in post traumatic viscera. The study indicated that late feeding(more
than 1 week after trauma) is associated with large amount of nitrogen loss followed by
weight loss of 15% per week. To achieve nutritional fulfillment on the 7th day, nutrient
administration should be initiated no later than 72 hours after trauma or injury.

Table 12. Level of Evidence (LOE) and Grade of Recommendation (GOR)

LOE/
No Author Description of Assessment Conclusion
GOR

1 Roger Hartl A retrospective study in III/C The amount of nutrient was

et al., 2008 patients with severe head associated with mortality.
injury and their nutritional
administration

2 Aaron M. Article review III/C Nutritional therapy included

Cook et al., proper administration of fluids
2008 and strict electrolyte
monitoring to prevent excess
fluid, electrolyte or glucose
which can be detrimental to
the patients.

3 Krakau K et Systematic review of I/A The results of the review

al., 2006 metabolic status and indicated an increase in
nutritional therapy in metabolic rate,
patients with moderate- hypercatabolism, and
severe head injuries. gastrointestinal intolerance for
up to 2 weeks after trauma.
The morbidity and mortality
tended to decrease in patients

48
 who received early feeding.

4 Sarafzadeh The study measured II/A Hyperventilation had the

et al.,2003 metabolic changes in
patients with impending or
manifest hypoxia in head
injury patients. The study
examined the safety and
efficacy of the use of
propofol and midazolam in
head injury patients.
potential side effect of cerebral
metabolism. The state of
anaerobic cerebral metabolism
depended on the degree and
duration of hypoxic episodes.

5 Calon B et The study examined the II/B MCT had a beneficial effect on
al.,1990 metabolic values of MCT post-traumatic visceral protein
and LCT in patients with metabolism.
head injury.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Aaron M. Cook et al. Nutrition Considerations in Traumatic Brain Injury.2008 Calon B et al.
Long-chain versus medium and long-chain triglyceride-based fatemulsion in parental
nutrition of severe head trauma patients. Infusiontherapie.1990;17(5):246-8.
Krakau K et al. Metabolism and nutrition in patients with moderate and severe traumatic
brain injury:A systemic review. Brain Inj.2006;20(4):345-67.
Roger Hartl et al. Effect of early nutrition on deaths due to severe traumatic brain injury.
2008.
Sarrafzadeh AS et al. Metabolic changes during impending and manifest cerebral hypoxia in
traumatic brain injury. Br J Neurosurg. 2003;17 (4): 340-6.

49
V.8. Recommendation for use of gastric mucosal protector and acid supressor aget
Standard : Administration of prophylactic pharmacological treatment with acid-supressive
agents with H2 blockers, proton pump inhibitors (PPIs), and gastric mucosal
protectors can help reduce the incidence of gastrointestinal bleeding and stress
related mucosal damage (SRMD). Proton pump inhibitor (PPI) is more
recommended because they it better mechanism of actionand duration of
action than H2 Blockers and gastric mucosal protectors.
Guideline :-
Option :-

50
Explanation of recommendations :
Administration of prophylactic regimens of acid suppressor agents can reduce the
incidence of gastrointestinal bleeding caused by stress ulcers by regulating pH of gastric acid.
PPI has an advantage over other regimens because its mechanism of action blocks the final
pathway of gastric acid production and has a longer duration of action. Recommended
dosage of omeprazole was 40 mg/12 hours iv or 40 mg/day orally or through NGT (Messori
et al., 2000., Michelle et al., David C. Metz, 2005).
Ranitidine was administered at a dose of 150 mg/12 hours orally or through NGT, 50
mg/6-8 hours intravenously or can be administered continuously through intravenous
perinfusion at a dose of 6.25 mg/hour. While Sucralfate as a mucosal protector was
administeredat a dose of 1 gr/6 hours.

Table13. Level of Evidence (LOE) and Grade of Recommendation (GOR)

LOE/
No Author Description of Assessment Conclusion
GOR

1 David C. Meta-analysis of I/A Administration of acid

Metz,2005 Randomized Controlled
Trialson the use of acid
suppressive agents for the
prevention of SRMD and
stress ulcers
suppressive agent regimen can
prevent SRMD and stress ulcers
by maintaining gastric acidity.

2 Michelle E, Meta-analysis of I/A Administration of prophylactic

Allen, 2004 randomized controlled
trials of prophylactic
therapy for stress ulcers.
drug for the prevention of
gastrointestinal bleeding
caused by stress ulcers
provided a slightly significant
result in reducing the incidence
of gastrointestinal bleeding.

3 S Trippoli et Meta-analysis of study on I/A Administration of ranitidine

al., 2000 the use of ranitidine versus and sucralfat was not effective
sucralfate in the in preventing gastrointestinal
prevention of stress ulcers bleeding caused by stress
ulcers.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
David C. Metz. Preventing the Gastrointestinal Consequences of Stress- Related Mucosal
Disease.Medscape. 2005

51
 Michelle E. Allen; Brian J. Kopp; Brian L. Erstad. American Society of Health- System
Pharmacists.ASHP therapeutic guidelines on stress ulcer prophylaxis. Am J Health-Syst
Pharm. 1999;56:347-79.
S Trippoli, M Valani, M Govini, A Corrado. Bleeding and pneumonia in intensive care patients
given ranitidine and sucralfate for prevention of stress ulcer: meta-analysis of
randomized controlled trials. BMJ 2000;321:1103-07

V.9. Recommendation for use of citicolin

Standard : Citicolin did not provide a significant improvement in functional outcome
compared to the placebo group.
Guideline : 1) In the administration of citicolin in patients with post concussion syndrome,
memory improvement and reduction in post-commotio symptoms were
found.
2) Assessment with the Glasgow Outcome Scale in 3 months after injury
indicated a significant improvement.
Option : Administration of Citicolin in the long term after a head injury can provide
increased cognitive abilities.

Explanation of recommendations :
Citicoline (Cytidine 5-diphosphocholine or CDP-Choline) has a function to activate
biosynthesis of neuronal cell membrane phospholipid structure, increase brain metabolism
and increase levels of neurotransmitters including acetylcolin and dopamine. Citicoline also
has a function to improve the activity of mitochondrial ATPase and Na/K ATPase enzyme and
inhibit phospholipase A2 enzyme.
Citicoline can be administered to patients with head injury shortly after the event or
in the long term and the results indicated improvements in the reduction of symptoms of
post concussion syndrome, improvement in the Glasgow Outcome Scale and its cognitive
function. It can be administered at a dose of 1 gram/day orally orthrough injection. The
results of the study indicated that:
a) Citicoline did not provide a significant improvement in functional outcome compared to
the placebo group.
b) There was an improvement in memory function in patients with citicoline administration
than without citicoline administration.
c) There were improvements in motor, cognitive function and psychological functionsand
there was a shortening of the length of stays in patients with citicoline administration.

52
Table14. Level of Evidence (LOE) and Grade of Recommendation (GOR)
Description of LOE/
No Author Conclusion
Assessment GOR

1 Zafonte et al, CORBIT (The Citicoline I/A Citicoline did not provide a
2009 Brain Injury Treatment), a significant outcome
large-scale RCT assessed improvement compared to
the effectiveness of the placebo group.
citicoline administration
on the functional
outcomes of patients with
head injury.

2 Spiers A case report of 2 III/B Citicoline resulted in

PA,Hochanadel patients with citicoline improved cognitive function
G, 1999 administration for 1.5 to 4 after moderate and severe
years after head injury. head injury.

3 Calatayud MV, A single blind randomized II/B Results: there was an

Perez JB, Aso study on 216 moderate improvement in the motor,
Escario J., 1991 and severe head injury cognitive and psychological
patients receiving
functions and there was a
citicoline treatment.
shortening of the length of
stay in patients with
citicoline administration.

4 Levin HS, 1991 Double blind placebo- II/B Results: there was an
control study to assess improvement in memory
the efficacy of citicoline function in patients with
by administering 1 gram citicoline administration
of tablet for 1 month to compared with no citicoline
14 patients for the administration (p <0.02).
treatment of signs and
symptoms of post
concussionsyndrome
after minor and moderate
head injuries
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Levin HS.Treatment of postconcussional symptoms with CDP-coline. J Neurology
Science.103: 539-42, 1991.
Maldonado VC ef aI.Effects of CDP-coline on the recovery of patients with head injury.
JNeurologyScience. 103: 515-18, 1991.

53
 Spiers PA, Hochanadel G: Citicoline for traumatic brain injury: report of two cases,
includingmy own. J lnt Neuropsychol Soc. 5:260-2&+, 1999.
Zafonte R, et al. The Citicoline Brain Injury Treatment (COBRIT) Trial. Journal of Neurotrauma
26:2207–2216 (December 2009).

V.10.Recommendation for use of piracetam

Standard : No supporting data
Guideline : 1) The administration of piracetam at a dose of 24-30 g/day can significantly
improve neurological symptoms in head injury patients.
2) After 8 weeks of piracetam treatment at a dose of 4800 mg, it was found
that there was a reduction in signs and symptoms of post concussion
syndrome such as vertigo, headache, fatigue, disorder of consciousness,
increased sweating and other symptoms.
3) Doses of 40-50 mg/kg (1600 - 2400 mg/day) provided positive result to
improve the patient’s condition which can be seen in the parameters of the
ability of cognitive function (memory, attention) and motor coordination
function.
Option : A high dose of piracetam (24-30 g/day) can improve the patient’s condition if
the treatment is started immediately after the injury.

Explanation of recommendations :
Piracetam improved brain metabolism by promoting oxidative catabolism, increasing
ATP breakdown, increasing cAMP levels, improving phospholipid metabolism and protein
bio-synthesis. Piracetam also improved the function of oxygen and glucose use by the brain
and increased local perfusion → it can be seen in the parameters of partial oxygen pressure
(oxygen therapy) and blood glucose level.
Piracetam can be administered to patients with head injury and postinjurywith
symptoms of post-concussion syndrome and it had the effect of improving neurological
symptoms and consciousness. The dose administered after head injury was 24-30 g/day
eitherorally or through injection, and the maintenance dose administered was 4.8 g/day
orally.

54
Table15. Level of Evidence (LOE) and Grade of Recommendation (GOR)
No Author Description of Assessment LOE/GOR Conclusion

1 Zavadenko A prospective case/control II/B Results: Doses of 40-50 mg/kg

NN, et al., study to determine the (1600-2400 mg/day) gave a
2008 effectiveness of positive result to improve the
administration of patients’ condition which can
piracetam in 42 mild- be seen in the parameters of
severe closed head injury the ability of cognitive function
patients (memory, attention) and motor
coordination function.

2 Goscinski l, Observational study III/C Result: high dose of piracetam

et al., 1999 conducted in 1995-1996 (24-30 g/day) can improve the
with 100 patients to patient’s condition if treatment
determine the effect of is started immediately after
piracetam on head injury.
injuries.

3 Goscinski l A prospective case-control II/B Result: A dose of 24-30 g/day

et al., 1998 study to determine the gave a positive result to
effectiveness of improve the patient’s
administration of
condition which can be seen in
piracetam in 100 patients
the parameters: partial oxygen
with moderate and severe
head injuries. pressure and blood glucose
level.

4 Hakkaraine Double-blind study with 60 II/B Result: after 8 weeks of

n H., patients with post treatment, it was found a
Hakamies concussion syndrome reduction in signs and
L., 1978 administered with a dose symptoms of post-concussion
of 4800 mg per dayfor 2- syndrome such as vertigo,
12 months headache, fatigue, disorder of
consciousness, increased
sweating and other symptoms.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Hakkrainen, H. & Hakamies, L. Piracetam in the treatment of post- concussional syndrome.
Eur Neurol 17, 50-55, 1978
Goscinski l, Sliwonik S, SondejT, KwiatkowskiS, Moskala M, CichonskiJ, Wegrzyn D, Uhl H,
Piracetam in severe cranio-cerebral injuries. Neurol Neurochir Pol Sep-Oct;32(5):1't 89-
97, 1 998
Goscinski l, Moskala M, Cichonski J, Polak J, Krupa M, Sliwonik S, Sondej T, Clinical
observations conceming piracetam treatment of patients after craniocerebral injury,
Przegl Lek;56(2):1 19-20, 1999

55
 Zavadenko NN, Guzilova LS, The consequences of closed traumatic brain injury and
piracetam efficacy in their treatment in adolescents.Neurosci Behav Physiol; 108(3):43-
8, 2008.

V.11.Recommendation for use of neuropeptides

Standard : No supporting data
Guideline : No supporting data
Option : Neuroprotection in traumatic brain injury prevents and reduces secondary
injuries, and improves the recovery process from injuries. Neuroprotection is
targeted to reduce brain damage and provide good prospect in cases of head
injury and stroke.

Explanation of recommendations :
The main goal of neuroprotection in traumatic brain injury is to prevent and reduce
secondary injury, as well as in the process of recovery from injury, while the goal of
neuroprotection in stroke is to prevent nerve cell death in the penumbra region. There are
absolute and relative neuroprotective processes. Relative mechanisms include: calcium
channel modulation, sodium channel modulation, NMDA receptor antagonist modulation,
GABA receptor antagonist modulation, antioxidants, anti free radicals, molecular adhesion,
adenosine agonists and antagonists. Absolute mechanisms include: neurotrophic factors,
neurotrophic factor-like molecules, and cytokines.

Neurotropic factors play a role in: ontogenetic development that plays a role in the
control of cell proliferation and differentiation (expression of mediator phenotypes, ion
channels, neurite growth), promotion of neuronal survival (if any,does not damage agents)
throughout life and maintaining phenotypes, increasing neuronal cell endurance due to
damaging agents (hypoxia, ischemia, hypoglycemia, eksitotoxicity, toxic substances, and
trauma), as well as neuroprotection, neuroplasticity and synaptic activity in the learning
process.

56
Table16. Level of Evidence (LOE) and Grade of Recommendation (GOR)
LOE/
No Author Description of Assessment Conclusion
GOR

1 Muresanu Review,neuroprotection in III/C Neuroprotection increases the

et al., 2007 traumatic brain injury is to
prevent and reduce
secondary injuries, as well
as in the recovery process
from injuries.
endurance of neurons due to
damaging agents (hypoxia,
ischemia, hypoglycemia,
excitotoxicity, toxic substances,
and trauma).

2 Teasdale, Review, neuroprotection is III/C The concept of

G.M et al., targeted to reduce brain neuroprotection has been
1997 damage and provide good widely known by providing
prospect in cases of head therapy as early as possible
injury and stroke. and many new things are
known to play a role in the
mechanism of head injury and
neuroprotective drugs with
specific targets are widely
developed.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Muresanu FD, et al. Neuroprotection and Neuroplasticity in Craniocerebral
Trauma.Romanian Journal of Neurology 2007. Vol VI, No. 4. Page: 154-165
Teasdale, G.M & Bannan, P. E. 1997.Neuroprotection in Head Injury.In Head
Injury.Pathophysiology and Management of Severe Closed Injury.Editor : Reilly, P;
Bullock, R. Page : 423-436. Chapman & Hall Medicaal. London. UK.

57
 BAB VI
Surgical Reference Management Recommendations
(Guideline for Surgical Treatment)

VI.1. Surgical recommendations for epidural bleeding (EDH)

Standard : There is no data to support this
Guideline : There is no data to support this
Option : Operative or non-operative decision making based on clinical and radiological
conditions of the patient. An indication of surgery or mass evacuation is done
if there is a mass effect and progressive decline in neurological function

Surgical Indications:
1) 1) EDH patients without seeing GCS with a volume> 30 cc, or thickness> 15 mm, or midline
shifts> 5 mm, or
2) Acute EDH patients (GCS <9) and anisochorous pupils (uncal herniation)
Time :
Acute EDH patients with coma (GCS <9) and anisochoric pupils (uncal herniation) are
performed surgically or evacuated

Method:
There is not enough data to support a surgical method, however craniotomy provides better
evacuation possibilities

Explanation of Recommendations:
The thickness, hematoma volume, and midline shift (MLS) structure on the initial CT
scan of the head affect the outcome. Head CT scan evaluation in non-operative patients is
carried out 6-8 hours after trauma. EDH patients with volumes> 30 cc, or thickness> 15 mm,
or midline shifts> 5 mm without looking at GCS, surgery is performed because of the
significant mass effect. EDH patients with volume <30 cc and GCS <9 accompanied by
anisochoric pupils as soon as possible to evacuate. EDH patients with volume <30 cc,
thickness <15 mm, midline shift <5 mm without seeing GCS without anisochoric pupils
performed aggressive non-operative management and close observation.
If the GCS does not improve within 2x24 hours and the extracranial factor is good,
then a repeat CT scan be performed.
Table17. Level of Proof (LP) and Degree of Recommendation (DR)
58
 No Author Rating Description LP/DR Conclution

1 Bullock et Management of epidural III/C Mass evacuation if there is a

al., 2006 hematoma surgery mass effect and progressive
decline in neurological function

2 Mitesh V, Retrospective analysis of III/C Operative or non-operative

1998 221 EDH patients decision making based on the
radiological and clinical
condition of the patient
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

References:
Bullock etal.Surgical Management ofAcuteEpiduralHematomas.Neurosurgery 2006;58:7-
15
Cooper PR, (ed), 1993, Head Injury, 3rd Ed, William & Wilkins Baltimore, Maryland,
USA.Mitesh V. American Journal of Neuroradiology 1998;20:115-6
Narayan RK, Wilberger JE Jr, Povlishock JT (Eds) 1996. Neurotrauma, MC Graw Hill Co. New
York.
Patil PG, Radtke RA, Friedman AH, 2002 Contemp. Neurosurgery 24 (22): 1-6. Wilkins RH and
Rengachary SS (Eds), Neurosurgery Vol. II, 2nd ed. MC Graw Hill Co. New York.

VI.2. Surgical recommendations for subdural bleeding (SDH)

Standard : There is no data to support this
Guideline : 1) Reducing intracranial pressure (ICP) with transventricular LCS drainage and
ICT monitoring, both of which are more important than decompression
operations on thin SDH (tebal 10mm thick)
2) There was no statistically significant difference between operative and
conservative measures in patients with severe head injuries with thin
traumatic acute subdural hematomas.
Option : The indications for surgery in acute SDH are in accordance with the
recommendations.
With the indication of surgery as follows:
A) SDH Acute
1) SDH patients without seeing GCS:
a. With thickness> 10 mm
b. Or midline shift (MLS) > 5 mm at CT-Scan
2) All of SDH patient with GCS < 9 monitoring must be carried out of ICP
3) Patient SDH with GCS < 9 :

59
 a. Thickness of SDH <10 mm and shift in midline structure, if the GCS decreases by more
than 2 points or more between the time of the incident and when you enter the
hospital
b. And or if asymmetry or fixed pupils are dilated
c. And/orICP> 20 mmHg
B) SDH acute
1) There are clinical symptoms of increased ICP (eg, headache & or projectile vomiting),
decreased consciousness or focal neurological deficiencies or seizures
2) Thickness of the lesion> 1cm

Time:
In Patient
a) acute SDH with an indication of surgery, surgery is done as soon as possible (CITO). The
ability to control ICTs is more important than hematoma evacuation.
b) chronic SDH with an indication of surgery then surgery is performed urgently.

Method :
a) Acute SDH with trepanation, evacuation of SDH, and bone decompression and or
duramatter
b) SDH acute with burrhole drainage

Explanation of Recommendations:
severe head injury (SHI) patients with acute SDH complications are the main cause of
death in CKB with intracranial mass lesions where the mortality rate reaches 42% - 90%.
Brain damage that occurs is more severe due to the mechanism of severe trauma, extensive
brain parenchymal damage and cerebral edema. Pathophysiologically, the effect of primary
head injury that occurs on the outcome is more important than the effect of SDH itself so
that the ability to control ICP is more important than the action of hematoma evacuation.
Transventricular LCS drainage action is better than hematoma evacuation surgery and
decompression in thin acute SDH.

60
Table18. Level of Proof (LP) and Degree of Recommendation (DR)
No Author Rating Description LP/DR Conclution
1 Thohari K, Prospective observational II/B Transventricular CSF drainage
Bajamal study to determine the action is better than hematoma
A.H., 2006 difference in outcome evacuation and decompression
between hematoma surgery.
evacuation surgery and
decompression with
transventricular CSF
drainage in patients with
severe head injuries with
subdural hematoma
complications of less than 1
cm and mass effects of
more than 5 mm.
2 Hartanto, Prospective analytic study II/B Surgery (hematoma evacuation
Kasan U, of hematoma evacuation and decompression) is better
2003 and decompression than conservative treatment.
compared to conservative
management in patients
with severe head injuries
with complications of
subdural hematoma less
than 1cm and a mass effect
of more than 5 mm.
3 Widodo, Prospective experimental II/B There is no statistically
Kasan U, research to determine the significant difference between
1999 difference between the operative and conservative
outcome of surgery and measures in patients with
conservative action in severe head injury and thin
patients with severe head acute traumatic subdural
injury with thin acute hematomas.
traumatic subdural
hematoma.
4 Wilberger Retrospective analytic II/B The ability to control ICP is more
et al.,1991 research to find out influential on the final outcome
whether surgery performed than the time of hematoma
less than 4 hours after evacuation
trauma gives a better
outcome
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)
Reference:

61
 Cooper PR, (Ed), 1993, HEAD INJURY, 3rd Ed, William & Wilkins Beltimore, Maryland, USA
Greenberg, MS, 2010, Handbook of Neurosurgery, 7th eds, Thieme, New York.
Hartanto RA, Kasan U, 2003, Operasi Dekompresi dan Evakuasi hematom subdural akut tipis
pada cedera kepalaberat. Karya Tulis Akhir PPDS I Ilmu Bedah Saraf, Lab/UPF Bedah
Saraf FK Unair/RSUDDr Soetomo.
Narayan RK, Wilberger JE Jr, Povlishock JT (Eds), 1996, Neurotrauma, MC Grow Hill Comp,
New York.
Palmer JD, 1997, Head trauma in Manual of Neurosurgery Churchil Livingstone, New York.
pp. 499-580
Patil PG, Radtke RA, Friedman AH, 2002, Contemp. Neurosurgery 24 (22): 1-6. Thohari K.,
Bajamal A.H., Penatalaksanaan Perdarahan Subdural Akut Tipis pada Penderita Cedera
kepala Berat.Karya Tulis Akhir PPDS I Ilmu Bedah Saraf, Lab/UPF Bedah Saraf FK
Unair/RSU Dr. Soetomo. 2006
Valadka AB, Andrews BT, 2005, Neurotrauma: Evidence-Based Answers to Common
Questions, Thieme, New York, Stuttgart.
Widodo J., Kasan U., 1999, Perbandingan tindakan operasi dan konservatif penderita dengan
komplikasihematoma subdural akut traumatika tipis pada cedera kepala berat. Karya
Tulis Akhir PPDS IIlmu Bedah Saraf, Lab/UPF Bedah Saraf FK Unair/RSUD Dr Soetomo.
Wilberger JE Jr, Harris M, Diamond DL, 1991, Acute subdural hematoma: Morbidity,
mortality, andoperative timing. J Neurosurg;74:212-8.

VI.3. Surgical recommendations for cerebral parenchymal bleeding (ICH)

Standard : There is no data to support this
Guideline : There is no data to support this
Option : Indications, time, and surgical method

Surgical Indications:
1) Patients with GCS ≤ 14 have cerebral parenchymal hemorrhage with bleeding volume> 30
cc and shift in midline structure> 5 mm.
2) Patients with GCS <8 have cerebral parenchymal bleeding with bleeding volume <30 cc,
midline shift <5 mm and / or compression of the cysterna.
3) Patients with cerebral parenchymal bleeding and signs of progressive neurological
deterioration according to the lesion, intracranial hypertension that is refractory to
medicals, or signs of a mass effect on CT scan.

62
 Time and Method :
Craniotomy and evacuation of mass lesions are recommended in patients with focal
lesions and with the above surgical indications. Bifrontal decompression craniectomy as
soon as possible (CITO) since trauma is the treatment of choice for patients with diffuse
cerebral edema and stubborn intracranial hypertension with treatment.
Decompression procedures including subtemporal decompression, temporal
lobectomy and hemisphere decompression craniectomy, are the treatment of choice for
patients with persistent intracranial hypertension and diffuse parenchymal trauma with
clinical and radiological presence of transtentorial herniation impending
Table19. Level of Proof (LP) and Degree of Recommendation (DR)
No Author Rating description LP/DR Conclution

1 Bullock et Surgical management of III/C Mass evacuation is immediately

al., 2006 cerebral parenchymal carried out if there is a mass effect
bleeding and decreased progressive
neurological function

2 De Luca et The author's experience IV/C Decompression operations for

al, 2000 handling patients with increasing ICP should be carried
increased intracranial out as soon as possible, before an
pressure irreversible condition occurs

3 Soloniuk et Management and indication III/C An indication of the operation is

al, 1986 of trauma ICH surgery made based on data from existing
and when to evacuate.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference:
Bullock et al., 2006, Surgical management of posteriorfossa mass
lesions.Neurosurgery;58:47– 55.
Cooper PR (ed), 1993, Head Injury, 3rd ed, William & Wilkins Baltimore, Maryland, USA.
De Luca GP, Volpin L, Fornezza U, et al., 2000, The role of decompressive craniectomy
in the treatment ofuncontrollablepost-traumatic intracranial hypertension. Acta
Neurochir Suppl;76:401-4.
Narayan RK, Wilberger JE Jr, Povlishock JT (Eds) , 1996, Neurotrauma, MC Graw Hill
Comp, New York.
Palmer JD., 1997, Head Trauma in Manual of Neurosurgery Churchill Livingstone,New York,
pp 499-580
Patil PG, Radtke RA, Friedman AH, 2002, Contemp. Neurosurgery 24 (22): 1-6.
Soloniuk D, Pitts LH, Lovely M et al., 1986, Traumatic intracerebral hematomas: timing of
appearance and indications for operative removal. J Trauma; 26:787-94.
Wilkins RH and Rengachary SS (eds), Neurosurgery Vol. II, 2nd ed MC Graw Hill Comp New
York.

VI.4. Surgical recommendations for mass lesions in the posterior fossa area

63
Standard : There is no data to support this
Guideline : There is no data to support this
Option : Indications, time and method of surgery

Surgical Indications:
1) 1) Patients with mass effects on head CT scan.
Mass effects are indicated by:
a. compression or obliteration of Ventricular IV
b. b. Compression or loss of the basal cysterna, or
c. c. Obstructive hydrocephalus
Patients with neurological deficits
Time :
Patients with indications for surgery, evacuation should be done immediately (CITO) if there
is a mass effect and a progressive decline in neurological function and patients with GCS> 8
have a better prognosis / outcome
Method :
Suboccipital craniectomy is a widely used method and is recommended for evacuation of
posterior fossa mass lesions
Explanation of Recommendations:
Trauma resulting in a mass lesion in the posterior fossa is only around 3% of all head injuries.
However, most patients with posterior fossa mass lesions are found to have progressive loss
of consciousness due to limited posterior fossa space and direct emphasis on the brain stem.

Appropriate surgical procedures and can immediately give a good outcome. Conservative
therapy can be done selectively in cases of SDH posterior fossa Patients with cerebellum
hemorrhage with a diameter <3cm, or no neurological deficits, but CT scans have mass
effects, can be treated conservatively with close observation and serial CT scans.

Table 20. Level of Proof (LP) and Degree of Recommendation (DR)

No Author Rating Description LP/DR Conclution

1 Bullock et Surgical management of III/C Immediate mass evacuation when

al., 2006 posterior fossae lesions from there is a mass effect and
24 medline document decreased progressive neurological
analyzes in a systematic function
review

2 Avella et Case report of 24 SDH III/C Patients with GCS> 8 who

al., 2003 patients with posterior fossa immediately undergo surgery have
trauma a better outcome

64
 3 Kizikilc et Case reports of SDH patients III/C Conservative therapy can be done
al., 2003 with posterior fossa trauma selectively in cases of posterior
with arachnoid cysts Case fossa SDH
reports of 24 SDH patients
with posterior fossa trauma
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference:
Avellaetal., 2003, Traumatic SubduralHematomas ofposteriorfossa: Clinicoradiological
analysis of 24 patients.
Bullock et al., 2006, Surgical management of Posterior fossa mass
lession.Neurosurgery;58:47-55
Cooper PR, (ed), 1993, Head Injury, 3rd Ed, William & Wilkins Baltimore, Maryland, USA
Kizikilc et al., 2003, Traumatic Posterior Fossa Subdural Hemorraghe Associated with an
Arachnoid Cyst in a Pediatric Patient. Eur J of Trauma; 29: 242-6
Narayan RK, Wilberger JE Jr, Povlishock JT (Eds), 1996, Neurotrauma, MC Graw Hill Co. New
York.
Patil PG, Radtke RA, Friedman AH, 2002, Contemp. Neurosurgery 24 (22): 1-6.
Wilkins RH and Rengachary SS (Eds), Neurosurgery Vol. II, 2nd Ed. MC Graw Hill Co. New York.

65
VI.5. Surgical recommendations for cranii base fracture
Standard :There is no data to support this
Guideline : Prophylactic antibiotics for the prevention of meningitis in cranii base fractures
are insignificant compared to placebo
Option : Management Base cranii fractures consist of conservative care and or surgical
treatment

Surgical Indications:
1) Kcerebrospinal fluid leakage after trauma accompanied by meningitis.
2) Pneumocephalus or LCS leak for more than five days

Time:
There is no consensus regarding the timing of operations. The final recommendation states
that surgery is expected to be carried out within 5 days of the LCS fistula being isolated.
Immediate surgery is recommended to reduce the incidence of infection

Method :
Surgical procedures for otorrhea include craniotomy of the media fossa or posterior fossa,
tracing the bone to see exposure to the dura covering the petrosus bone. A primary closure is
attempted, but if it is not possible, a fascia lata or fat or muscle graft can be used to cover the
defect. Surgical measures for Rhinorrhea are adjusted to the location of the leak known by
the radiological diagnostic measures.

Explanation of Recommendations:
Conservative treatment is carried out if there is no persistent CSF leak, temporal bone
fracture, facial muscle paralysis, hearing loss, or blindness.
Conservative therapy involves giving intravenous empirical antibiotics for 5 days to
provide a chance of healing dura tears. The latest data recommends giving PNC 1-2 million
units / day in cases of LCS leakage. Nasal and throat cultures were immediately taken, and
antibiotics were chosen according to the culture. The patient is kept in a total bed rest
position with elevation of the head of bed position, to reduce the flow of LCS.
If the liquid leakage does not decrease within 72 hours with conservative therapy,
lumbar drain installation is performed to drain 150 ml of LCS per day for 3-4 days. LCS
diversion from dura leakage can help with spontaneous closure.

66
 Table 21. Level of Proof (LP) and Degree of Recommendation (DR)

No Author Rating Description LP/DR Conclusion

1 Bachli H. et Review several studies on the III/C Significant surgical treatment of

al., 2009 severity of cranii base cranial base fractures can be based
fractures on the severity (CMF-ISS)

2 Katzen T. et Review several studies of skull III/C Treatment of skull base

al., 2007 base fractures fractures can be done
conservatively if no indication is
obtained
surgery

3 Turchan A, Prospective case control for II/B The administration of antibiotic

1995 the incidence of meningitis in prophylaxis for the prevention
the administration of
antibiotics in skull base
of meningitis in skull base
fractures fractures is insignificant
compared to placebo.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference:
Bachli H. et al., 2009, Skull base and maxillofacial fractures: Two centre study with
correlation ofclinical findings with a comprehensive craniofacial classification system.
Journal of Cranio-Maxilofacial Surgery.;37: 305-311
Cooper PR, (Ed), 1993, HEAD INJURY, 3rd Ed, William & Wilkins Beltimore, Maryland, USA.
Greenberg, Mark S, 2010, Handbook of NeuroSurgery 7th Ed. Thieme Publishers, pp 887-
889.
Katzen T., Janahy R, Eby JB, Mathiasen RA., Margulies DM, Shahinian HK., 2007, Craniofacial
and Skull Base Trauma.Available at \AMM/. Skull Base lnstitute'
Kaye AH., 2005, Essential Neurosurgery.Blackwell Publishing, Ltd. Massachusetts.pp 50-51
Narayan RK, Wilberger JE Jr, Povlishock JT (Eds), 1996, NEUROTRAUMA, MC Grow Hill Comp,
New York.
Turchan A, Kasan U., 1995, Penggunaan Kloksasilin Dibandingkan Plasebo Dalam Hal
Mencegah Komplikasi Meningitis Bakteri Pada Penderita Patah Tulang Dasar
Tengkorak.Laboratorium llmu Bedah RSUD Dr Soetomo. Fakultas Kedokteran
UniversitasAirlangga.
Wahyuhadi J, dkk., 2007, Pedoman Tatalaksana Cedera kepala. Tim Neurotrauma RSUD Dr
Soetomo. Fakultas Kedokteran Universitas Airlangga. pp 5, 31-32

67
VI.6. Surgical recommendations for diffuse axonal injury (DAI)
Standard : There is no data to support this
Guideline : 1) Patients with DAI obtained normal head CT scans and GCS <8
2) Nimodipine improves the prognosis of patients with diffuse axonal injury
and decreases vasospasm.
Option :-

Explanation of Recommendations:
Severe head injury patients with diffuse axonal injury without mass lesions must be
intubated or tracheostomy for protection of the airway, and given oxygen by monitoring
oxygen saturation on an ongoing basis. Patients should get ventilator support if breathing
conditions are found or clinical patients are experiencing worsening. Light sedation can be
given with midazolam i.v alone or in combination with morphine.
Nimodipine improves the prognosis of patients with diffuse axonal injury and decreases
vasospasm. Nimodipine is given at a dose of 60 mg every 4 hours immediately after the
patient is admitted to the hospital.

Table 22. Level of Proof (LP) and Degree of Recommendation (DR)

No Penulis RatingDescription LP/DR Conclusion

1 Liew B et The outcome of severe head
al., 2009 injury patients with diffuse
axonal injury treated with ICP-
CPP management compared
to conservative therapy at the
hospital. Sultanah Aminah,
Johor Bahru
II/B Patients with DAI without mass
lesions have normal intracranial
pressure so that ICP monitor
installation is not necessary when
compared with other forms of
severe head injury. The outcome of
patients with diffuse axonal injury
that is treated conservatively is
better in terms of length of stay in
the hospital / ICU and GCS
improvement

2 Farhaoudi Effects of nimodipine on II/B Nimodipine improves the

M. et al., cerebral hemodynamics, prognosis of patients with diffuse
vasospasm and short-term axonal injury and decreases
2007 prognosis of patients with vasospasm.
diffuse axonal injury
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference:
Farhoudi M et all.,2007, Effects of nimodipine on cerebral hemodynamics, and prognosis of
diffuse axonal injury patients. Neurosciences; Vol. 12 (4)
Liew B et al., 2009, Severe Traumatic Brain Injury: Outcome in Patients withDiffuse Axonal
Injury Managed Conservatively in Hospital Sultanah Aminah, Johor Bahru – An
Observational Study. Med J Malaysia;64;4.December

68
 CHAPTER VII
Reference Recommendations for Intracranial Pressure Control
(Guideline for Intracranial Pressure Monitoring and Treatment)

VIII.1. VIII.1. Indications for intracranial pressure monitoring (ventryculostomy)

Standard : There is no data to support this
Guideline : Patients with severe head injuries with intra-cranial pressure ≥ 20 mmHg can
provide significantly better outcomes, judged by cognitive status.
Option :Indications and methods of mounting the monitor ICP

Surgical Indications:
1) Installation of an ICP monitor needs to be done in severe head injury (SHI)severe
head injurysevere head injuryCGS
2) patients (GCS 3-8) after resuscitation) with an abnormal CT-scan of the head
(hematoma, contusio, cerebral edema, or narrowing of the basal cysterna).
3) ICP monitors are also installed in severe head injury (SHI) patients with a normal
CT-scan of head if 2 or more of the following are obtained:
a. age> 40 year
b. TDS < 90 mmHg
c. Postural bilateral or unilateral

Method:
The method of monitoring ICP is to install intraventricular drainage, with the location of
insertion at the kocher point.

Explanation of Recommendations:
The main objective of the Intensive Management Protocol is to maintain adequate
brain perfusion and oxygenation to avoid secondary head injuries. Decreased brain
perfusion and poor outcomes are associated with systemic hypotension and intracranial
hypertension. The only way to determine CPP is to monitor ICP and systemic blood pressure
continuously.
  Patients with severe head injuries with intracranial pressure of 20 mmHg or lower
give a significant outcome assessed in terms of cognitive status.

Table23. Level of Proof (LP) and Degree of Recommendation (DR)

69
 No Autor Rating Description LP/DR conclution

1 Randall M. Intra-cranial pressure II/B Patients with severe head

et al., 2012 monitoring is considered as injuries with intracranial
standard therapy for pressure of 20 mm Hg or lower
patients with severe head give a significant outcome
injury assessed in terms of cognitive
status.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Referensi
Cooper PR, (Ed), 1993, HEAD INJURY, 3rd Ed, William & Wilkins Beltimore, Maryland, USA.
Narayan RK, Wilberger JE Jr, Povlishock JT (Eds), 1996, NEUROTRAUMA, MC Grow Hill Comp,
New York.
Palmer JD., 1997, Head Trauma in Manual of Neurosurgery Churchil Livingstone, New York.
pp 499-580
Patil PG, Radtke RA, Friedman AH, 2002, Contemp. Neurosurgery 24 (22): 1-6. Randall M,
Chesnut, M.D, Temkin N, A trial of Intravranial-Pressure Monitoring in Traumatic brain
injury. J Neurotrauma 2012; 367; 26; 2471-81.
Wilkins RH and Rengachary SS (Eds), Neurosurgery Vol. II, 2nd Ed MC Graw Hill Comp New
York.

VIII.2. VIII.2. Management of increased intracranial pressure

Standard : There is no data to support this
Guideline : monitoring of Intracranial pressure (IP) is required in patients with:
 severe head injury (SHI) accompanied by abnormalities of CT-scan of
head, in the form of hematoma, contusion, edema, or compression
of the basal cysterna
 severe head injury (SHI) with a normal CT-scan of head accompanied
by ≥ 2 of the following criteria:
• age, more than 40 years
• bodily weakness one or two sides
• systolic blood pressure <90mmHg
Option : ICP monitoring is not routinely indicated for CKR and CKS. However, a
monitor can be installed in the case of traumatic mass lesions.

Explanation of Recommendations:
In a number of journals, guidelines have been made to address the improvement of ICTs
along with a number of choices obtained from research:
• Elevation head of bed 30
70
• Maintain normovolemia, provide isotonic fluid, maintain electrolyte balance
• To prevent seizures, diphenylhydantoin (DPH) should be used if there is no DPH,
intravenous diazepam can be given until the seizure stops
• Use of sedation and analgesics in the form of intramuscular 25 mg chlorpamasine can be
considered
• Avoid anemia
• Installation of ICP Monitors
• keepTPO/CPP>70 mmHg
• Drainage of Cerebrospinal Fluid (CSF)
• Manitol 0,25 - 1,0 gr/KgBW
• Maintain optimal oxygenation and ventilation (Hyperventilation PaCO2 30-35 mmHg)
• Tertiary therapy: high-dose barbiturates, hyperventilation PaCo2<30mmHg, Hypothermia,
Decompressive Craniecktomy.

71
Management algorithm for increasing intracranial pressure (ICP) Option 1

Installation
ICP Monitor

keep
CPP > 70mmHg

Yes HypertensionICP ? No

Yes

Drainase Intraventrikel
(f possible)

Yes No
HypertensionICP ?

Yes

Consider for Manitol * Attention to Therapeutic

CT Scanof Head Reset 0,25-1,0 gr/KgBw i.v. Reactions of ICP

Yes HypertensionICP ? No

Yes

Hypertension until
PaCO2 30-35 mmHg

Yes No
HypertensionICP?

Ya

Tertiary Therapy **
ICP Handling

* Can be given again, if the levels of osmolaritas serum < 320mOsm/L & Pt Euvolemi
** High-dose barbiturate therapy; Hyper-affiliation with PaCO2 <30mmHg (Monitoring SjO2,
AVDO2, and or CBF Recommendations
Citation from:Guidelines fot the Management of Severe Head Injury (Journal of Neurotrauma,
November 1996)

72
Algorithm for Improving ICP Options 2

Sedation and Analgesics

Use of a Ventilator
(PaCO2 30-35mmHg ; PEEP until 10cmH20)

Head Up 30with a
Basic Therapy straight neck

Advanced Therapy
Manitol
0,25-1,0 gr/KgBw

Hypertonic liquid THAM

Drainage of CSF

Decompressive
Craniectomy

Comma with
Barbiturates

Citation from:Valadka AB, Andrew BT. 2004. Neurotrauma Evidence-Based Answer to

Common Questions.

73
 Algorithm for Improving ICP Options 3

Sedation

Drainage of CSF

Manitol
0,25-1,0 gr/KgBW

Mild Hiperventilasi -
Hipothermi

Komma with
Barbiturates

Citation from: Peter Reilly. 1997. Head Injury Pathophysiology and Management of Severe
Closed Injury.

74
Table 24. Level of Proof (LP) and Degree of Recommendation (DR)
No Author Rating Description LP/DR Conclution

1 Valadka et Algorithm, ICP handling III/C According to scheme II,

al., 2004 administration of mannitol after
that CSF drainage

2 Peter Reilly, Algorithm, ICP handling III/C Scheme III, CSF drainage first
1997 and then administration of
mannitol

3 Bullock et The critical path for III/C According to scheme I, CSF

al., 1996 handling ICP drainage after that mannitol
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Reference
Bullock RM, Povlishock JT, 1996, Guidelines for the management of Severe Head Injury,
Journal of Neurotrauma,November.
Reilly P, 1997, Head Injury : Pathophysiology and management of Severe Closed Injury.
Valadka, 2004, Neurotrauma Evidence-Based Answer to Common Question.

75
 CHAPTER VIII
Guidelines for the Management of Traumatic Head Injury in Children

VIII.1. Blood pressure fluid resuscitationand oxygenation

Standard : There is not enough data
Guideline : Hypotension must be treated immediately with fluid resuscitation
Option : Control of the airway must be done in children with GCS≤ 8

Explanation of Recommendations:
In children, hypotension is defined as a decrease in blood pressure below 5
percentile according to age or showing signs of shock. The lower limit of systolic blood
pressure (fifth percentile) according to age can be estimated by formula: 70 mmHg + (2 x
Age in years). Oxygenation and ventilation are closely monitored with pulse oxymetry and
End-tidal CO2 monitoring or regular BGA testing. Hypoxia is defined as: apnea, cyanosis,
PaO2 <60-65 mmHg, or 90% oxygen saturation. Central cyanosis is not an early and
appropriate indicator of hypoxia in children.
Hypoventilation is defined as an inadequate breathing according to age, irregular
and shallow breathing, frequent apneic episodes, or signs of hypercarbia. Hypoventilation is
an indication for airway control and assisted ventilation with 100% oxygen.
In children, fluid resuscitation is an indication if there are signs of decreased
perfusion even though blood pressure is adequate. Shock is usually not caused by head
injury itself, an evaluation of spinal injuries or other injuries must be done. Fluid restriction
to limit brain edema is contraindicated in the treatment of head injuries. If peripheral
vascular access is difficult to obtain, intraosseous infusion and medication must be
performed.
Mortality in children is lower than in adults. In children, only hypotension is
associated with a higher mortality rate, while in adults the factors are hypotension and
hypertension. Poor outcomes are associated with: GCS <8, pupillary abnormalities, motoric
deficits, hypoxia, hypotension and extracranial injuries. Hypotension with or without
hypoxia significantly increases mortality.

76
Table25. Level of Evidence (LE) and Grade of Recommendations (GR)
No Author(s) Assessment description
1 Sakellaridis Prospective study to
et al., 2011 compare the effects of
mannitol and hypertonic
saline on intracranial
hypertension in patients
with severe head injury
2 Simma et An open random
al., 2000 prospective study
comparing the use of
hypertonic saline (598
mOsm / L) with ringer’s
lactate given more than 3
days in 35 children with
severe head injury
3 Peterson et Retrospective research to
al., 2000 determine the effect of 3%
hypertonicsaline in reducing
ICP
4 Khanna et Prospective study of the use
al., 2000 of 3% hypertonicsaline
(1025mOsm / L)
5 Fisher et al, The double-blind crossover
1992 study compared the use of
3% saline fluid (1025
mOsm / L) and 0.9% (308
mOsm / L) in children with
severe head injury
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)
References
Fisher B, Thomas D, Peterson B. 1992. Hypertonic saline lowers raised intracranial pressure
in children after head trauma. J Neurosurg Anesthesiol; 4 : 4-10.
LE/GR Conclusion
II/B There was no difference
between the two therapies in
terms of decreased ICP and
duration of action
III/C Patients treated with hypertonic
saline require fewer additional
interventions compared to the
patients with ringer’s lactate-
administered in managing ICP.
Groups with hypertonic saline
have shorter ICU stay, shorter
use of mechanical ventilation,
fewer complications than using
ringer’s lactate
III/C 3% Hypertonic saline is effective
in reducing ICP
III/C Significant decrease in ICP and
increase in CPP during 3% saline
administration. The emergence
of hypernatremia and
hyperosmolerance can be safely
tolerated in pediatric patients
III/C 3% hypertonic salinesolution can
reduce ICP and other
interventions (thiopental and
hyperventilation). Serum sodium
levels increase by about 7 mEq /
L after administration of 3%
saline
77
 Khanna S, Davis D, Peterson B, et al. 2000. Use of hypertonic saline in the treatment of
severe refractory posttraumatic intracranial hypertension in pediatric traumatic brain
injury. Crit Care Med; 28 : 1144-1151.
Peterson B, Kanna S, Fisher B, et al. 2000. Prolonged hypernatremia controls elevated
intracranial pressure in head injured pediatric patients. Crit Care Med; 28 : 1136 -1143.
Sakellaridis N, Pavlou E, Karatzas S, et al 2011. Comparison of mannitol and hypertonic saline
in the treatment of severe brain injury. J Neurosurg; 114 : 545-548.
Simma B, Burger R, Falk M, et al 1998.A prospective, randomized and controlled study of
fluid management in children with severe head injury : Lactated Ringer’s solution versus
hypertonic saline. Crit Care Med; 26 : 1265-1270.

VIII.2. Indications for intracranial pressure monitoring

Standard : There is not enough data
Guidelines : There is not enough data
Option : ICP Monitor can be performed on infants and children with severe headinjury

Explanation of Recommendations:
ICP monitor is indicated in patients with severe head injury with an abnormal CT
scan. Severe head injurypatients with normal CT scan are mounted with ICP monitors if they
have at least 2 of the following conditions:
1) Motor posturing
2) Systemic hypotension
Major fontanelle and or sutures that are still open in infants cannot rule out the
possibility of high ICP or eliminate the use of ICP monitors.ICP monitors are not
recommended routinely in moderate and mild brain injury. There is no RCT research to
evaluate the final results of the effect of severe head injurymanagement with or without the
installation of ICP monitors. ICP> 20 mmHg are associated with an increased risk of death.
ICP> 35 mmHg and CPP <55 mmHg (adults) and 45 mmHg (children) are predictive factors
for poor outcome.
Children with brain stem injury with ICP > 40 mmHg are associated with high
mortality and vegetative state. The goals of therapy for pediatric patients with severe head
injury are normalization of ICP (<20 mmHg), optimization of CPP and CBF, prevent secondary
brain injury and avoid complications related to varying therapeutic modalities.

78
Table 26. Level of Evidence (LE) and Grade of Recommendations (GR)
No Author(s) Assessment description
1 Jaganna- Observational study on ICP
than et al, insertion therapy in
2008 conjunction with
decompressive
craniectomy in pediatric
patients
2 Grinkevi- One-centered
ciute et al, observational study of the
2008 relationship of several high
ICP therapies in pediatric
patients
3 Stiefel M, Retrospective study in
et al, 2006 pediatric patients who
performed the installation
of ICP monitors and PO2 in
tissues
4 Wahlstrom Observational study on ICP
et al, 2005 monitoring therapy using
the Lund protocol in
pediatric patients
5 Adelson et A rondomized controlled
al, 2005 trial of hyptothermic and
normothermic therapy in
the treatment of increased
ICP in pediatric patients
6 Pfenninger, Retrospective study on the
Santi, 2002 relationship of ICP
measurement and
monitoring of jugular
venous pressure with
outcomes in pediatric
patients
7 Cruz et al., Retrospective study on the
2002 effects of ICP monitor
placement on pediatric
patients
LE/GR Conclusion
III/C A good outcome is associated
with good ICP management
III/C In this study there were no
differences in outcomes
between groups with mean ICP
pressure (22.2mmHg) and
badICP pressure (24.6mmHg)
III/C Installation of tissue PO2
monitor is a useful and safe
addition to an ICP monitor
installation
III/C In this study, no significant
relationship was found
between ICP value and patient
outcome
III/C ICP > 20 is a bad predictor for
the most sensitive prognosis. A
low ICP rate is associated with a
good prognosis
III/C Intracranial hypertension is
proportional to a poor
prognosis
III/C ICP that is high on the first 1-5
days, is associated with
decreased brain oxygen
extraction and a poor
prognosis
79
 8 White et Retrospective and
al., 2001 observational studies of
136 patients at NICU and
PICU with ICP monitors
III/C 14% survivors on
group 1 and 41% nonsurvivor in
group 2 had ICP> 20mmHg in
the first 72 hours.
Low ICP in the first 6 hours, 12
hours and 24 hours is
significantly associated with
good outcomes

9 Chambers Observational study in III/C ICP> 35 mm is a predictive

et al., 2001 children and adults who factor for poor outcomes in
have ICP and CPP children and adults
monitoring

10 Downard et A retrospective study of III/C ICP> 20 mmHg associated with

al., 2000 children undergoing ICP an increased risk of death
monitor installation

11 Peterson et Retrospective study to III/C Hypertonic Saline 3% is

al., 2000 determine the effect of 3% effective in reducing ICP
hypertonicsalinesolution in
reducing ICP

12 Eder et al., Retrospective study in III/C Children with brainstem injury

2000 children with severe head and ICP> 40mm are associated
injury. with high mortality and
Compares several factors vegetative conditions
and ICP monitor against the
outcomes
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

80
References
Adelson PD, Ragheb J, Kanev P, et al: Phase II clinical trial of moderate hypothermia after
severe traumatic brain injury in children. Neurosurgery 2005; 56:740 –754; discussion
740 –754
Chambers IR, Treadwell L, Mendelow AD : Determination of treshold levels of cerebral
perfusionpressure and intracranial pressure in severe brain injury by using receiver
operatingcharacteristic curves : An observational study in 291 patients. J Neurosurg
2000; 94 :412-416
Cruz J, Nakayama P, Imamura JH, et al: Cerebral extraction of oxygen and intracranial
hypertension in severe, acute, pediatric brain trauma: Preliminary novel management
strategies. Neurosurgery 2002; 50: 774–779; discussion 779 –780
Downard C, Hulka F, Mullins R, et al : Relationship of cerebral perfusion pressure and survival
in pediatric brain-injured patients. J Trauma 2000; 49: 654-659
Elder HG, Legat JA, gruber W : Traumatic brain stem lesion in children. Childs Nerv Syst
2000;16: 21-24
Grinkeviciute DE, Kevalas R, Matukevicius A, et al: Significance of intracranial pressure and
cerebral perfusion pressure in severe pe- diatric traumatic brain injury. Medicina
(Kaunas, Lithuania) 2008; 44:119 –125
Jagannathan J, Okonkwo DO, Yeoh HK, et al: Long-term outcomes and prognostic factors in
pediatric patients with severe traumatic brain injury and elevated intracranial pressure. J
Neurosurg Pediatr 2008; 2:240 –249
Peterson B, Kanna S, Fisher B, et al : Prolonged hypernatremia controls elevated
intracranialpressure in head injured pediatric patients. Crit Care Med 2000; 28 : 1136 -
1143
Pfenninger J, Santi A: Severe traumatic brain injury in children—Are the results improving?
Swiss Med Wkly 2002; 132:116 –120
Stiefel M, Joshua D, Storm P, et al : Brain tissue oxygen monitoring in pediatric patients with
severe traumatic brain injury. J Neurosurg 2006; 105:281-286
White JR, Farukhi Z, Bull C, et al: Predictors of outcome in severely head- injured children.
Crit Care Med 2001; 29:534 –540
Wahlstrom MR, Olivecrona M, Koskinen LO, et al: Severe traumatic brain injury in pediatric
patients: Treatment and outcome using an intracranial pressure targeted therapy— The
Lund concept. Intensive Care Med 2005; 31:832– 839

81
VIII.3. Therapeutic threshold for intracranial hypertension
Standard : There is not enough data
Guidelines : There is not enough data
Option : 1. Intracranial hypertension is defined as a pathological increase in ICP
2. Management starts immediately if ICP ≥ 20 mmHg
3. Interpretation and treatment of intracranial hypertension is based on ICP
critical points associated with: clinical examination, monitoring of
physiological variables such as CPP and serial photographs

Explanation of Recommendations:
The effect of intracranial hypertension or pathological increase in ICP on severe
head injury outcomes in children is related to the peak value of ICP and the duration of the
increase. Poor outcomes when ICP> 30mmHg compared to ICP <20mmHg. Certain limits on
ICP for starting treatment in children with severe head injuryis not be determined.
Table 27. Level of Evidence (LE) and Grade of Recommendations (GR)
No Author(s) Assessment description LE/GR Conclusion

1 Grinkevi- One-centered III/C There were no differences in

ciute et al., observational study of the outcomes in groups with a
2008 relationship of several high mean (22.2mmHg) and bad
ICP therapies in pediatric (24.6mmHg) ICP pressure
patients

2 Kan et al., Prospective study to III/C Patients undergoing

2006 determine mortality and decompressive craniectomy
morbidity in pediatric only for increased ICP have a
patients with severe head high mortality
injury who performed
decompressive
craniectomy

3 Adelson et A randomized-controlled III/C The mean ICP in children with a

al., 2005 trial of hypothermic and
normothermic therapy in
the treatment of increased
ICP in pediatric patients
good prognosis (11.9 ± 4.7 mm
Hg) vs poor prognosis (24.9 ±
26.3 mm Hg).
ICP value > 20 mmHg is
proportional to a poor
prognosis

4 Pfenninger, Retrospective study on the III/C Intracranial hypertension with a

Santi, 2002 relationship of ICP high> 20mmHg is proportional

82
 measurement and
monitoring of jugular
venous pressure with
outcomes in pediatric
patients
5 Cruz et al., Prospective study of ICP
2002 monitoring therapy in
pediatric patients
6 White et Retrospective and
al., 2001 observational study of 136
patients at NICU and PICU
with ICP monitors
7 Sharples et Prospective study. Know
al., 1995 the relationship between
CBF and ICP
8 Cho et al., Retrospective study of
1995 shaken baby syndrome in
patients <2 years, who
were installed with ICP
monitor / undergo surgery.
9 Shapiro and Non-random prospective
Marmarou, study determine the
1982 relationship between ICP
and PVI (Pressure Volume
Index)
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)
References
Adelson PD, Ragheb J, Kanev P, et al: Phase II clinical trial of moderate hypothermia after
severe traumatic brain injury in children. Neurosurgery 2005; 56:740 –754; discussion
740 –754
to a poor prognosis.
III/C A mean ICP of 15-21mmHg on
days 2-5 was found in the group
of patients with good outcomes.
A mean ICP of 19-26mmHg on
days 2-5 was found in the group
of patients with poor outcomes.
III/C 14% survivors and 41%
nonsurvivors had ICP> 20mmHg
in the first 72 hours. Low ICP in
the first 6 hours, 12 hours and
24 hours was significantly
associated with good outcomes.
III/C CBF isinversely proportional to
ICP
III/C Poor outcomes when ICP
>30mmHg compared to ICP
<20mmHg
III/C Increased ICP> 20mmHg
inversely proportional to PVI
(Pressure Volume Index)
83
 Cho D, Wang Y, Chi C : Decompressive craniotomy for acute shaken/impact baby syndrome.
Pediatr Neurosurg 1995; 23: 192-198
Cruz J, Nakayama P, Imamura JH, et al: Cerebral extraction of oxygen and intracranial
hypertension in severe, acute, pediatric brain trauma: Preliminary novel management
strategies. Neurosurgery 2002; 50: 774–779; discussion 779 –780
Grinkeviciute DE, Kevalas R, Matukevicius A, et al: Significance of intracranial pressure and
cerebral perfusion pressure in severe pe- diatric traumatic brain injury. Medicina
(Kaunas, Lithuania) 2008; 44:119 –125
Kan P, Amini A, Hansen K, et al : Outcome after decompressive craniectomy for severe
traumatic brain injury in children. Journal Neurosurgery: Pediatrics 2006; 105:337-342
Pfenninger J, Santi A: Severe traumatic brain injury in children—Are the results improving? .
Swiss Med Wkly 2002; 132:116 –120
Shapiro K, Marmarou A : Clinical applications of the pressure-volume index on treatment of
pediatric head injuries. J Neurosurg 1982; 56 : 819- 825
Sharples PM, Stuart AG, Matthews Ds, et al : Cerebral blood flow and metabolism in children
with severe head injury. Part I : Relation to age, Glasgow Coma Score, outcome,
intracranial pressure, and time after injury. JNNP 1995; 58 : 145 -152
White JR, Farukhi Z, Bull C, et al: Predictors of outcome in severely head- injured children.
Crit Care Med 2001; 29:534 –540

VIII.4. Use of hyperosmolar therapy to control intracranial hypertension

Standard : Administration of mannitol is better than administering pentobarbital and less
beneficial compared to administering hypertonic saline solution.
Guidelines : There was no difference between mannitol and hypertonic saline against
intracranial hypertension in patients with severe head injury in terms of
decreased ICP and duration of action.
Option : Hypertonic saline (3% NaCl)solution and mannitol can be used to control ICP
Explanation of Recommendations:
Mannitol is an option in the management of increased ICP and brain injury. Mannitol
can reduce ICP through two mechanisms:
1. Reduce ICP by increasing blood viscosity by reducing resultant diameter of blood vessels
→ Decrease in cerebral blood volume and ICP (temporary <75 min)
2. Osmotic effects that develop slowly by 15-30 minutes, following the gradual movement
of water from the parenchyma (ICF) to circulation (IVF) → the effect occur > 6 hours and
require an intact Blood Brain Barrier.
Mannitol is effective in bolus doses 0.25 gr / kgBW - 1 gr / kgBW. Terms of use
mannitol:
1. Euvolemia must be maintained with fluid therapy
2. Urethral catheter placement is required to prevent bladder rupture
3. Serum osmolality is maintained below 320 mOsm / L

84
 Hypertonic (3%) saline is effective in reducing ICP and reducing other interventions
(Thiopental and hyperventilation) → ↓ ICP and ↑ CPP. Groups with hypertonic saline have
a shorter ICU stay, shorter use of mechanical ventilation, and fewer complications than RL
use. The effective dose in a continuous infusion of 3% saline is 0.1-1.0 ml / kg / hour. Serum
osmolality is maintained at 320 mOsm / L. Serum sodium levels increase by about 7 mEq / L
after 3% saline. The onset of hypernatremia and hyperosmolar can be safely tolerated in
pediatric patients.
Table 28. Level of Evidence (LE) and Grade of Recommendations (GR)
No Author(s) Assessment description LE/GR Conclusion

1 Sakellaridis Prospective study to II/B There was no difference

et al., 2011 compare the effects of
mannitol and hypertonic
saline on intracranial
hypertension in patients
with severe head injury
between the two therapies in
terms of decreased ICP and
duration of action

2 Wakai, A randomized-controlled I/A Mannitol administration is

2013 trial with mannitol
administration in patients
with acute trauma of
moderate and severe head
injury
better than pentobarbital
administration and less
beneficial compared with
administration of hypertonic
saline solution

3 Simma et An open random III/C Patients treated with hypertonic

al., 2000 prospective study
comparing the use of
hypertonic saline (598
mOsm / L) with
ringerlactate given more
than 3 days in 35 children
with severe head injury
saline require fewer additional
interventions compared tothe
administration of ringer lactate
in managing ICP. Groups with
hypertonic saline have a shorter
ICU stay, shorter use of
mechanical ventilation, fewer
complications compared to use
of ringer lactate

4 Peterson et Retrospective study to III/C 3% Hypertonic saline is effective

al., 2000 determine the effect of 3% in reducing ICP
hypertonicsalinesolution in
reducing ICP

5 Khanna et Prospective study of the III/C Significant reduction in ICP and

al., 2000 use of hypertonic saline an increase in CPP during 3%
solution 3% (1025mOsm / saline administration. The
L) emergence of hypernatremia

85
 and hyperosmolerance can be
safely tolerated in pediatric
patients.

6 Fisher et The double-blind crossover III/C Hypertonic saline 3% can reduce

al., 1992 study compared the use of ICP and reduce other
3% saline fluid (1025 mOsm interventions (thiopental and
/ L) and 0.9% (308 mOsm / hyperventilation).
L) in children with severe Serum sodium levels increase by
head injury. about 7 mEq / L after
administration of 3% saline
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

References
Fisher B, Thomas D, Peterson B ; Hypertonic saline lowers raised intracranial pressure in
childrenafter head trauma. J Neurosurg Anesthesiol 1992; 4: 4-10
Khanna S, Davis D, Peterson B, et al : Use of hypertonic saline in the treatment of
severerefractory posttraumatic intracranial hypertension in pediatric traumatic brain
injury.Crit Care Med 2000; 28 : 1144-1151
Peterson B, Kanna S, Fisher B, et al : Prolonged hypernatremia controls elevated
intracranialpressure in head injured pediatric patients. Crit Care Med 2000; 28 : 1136 -
1143
Sakellaridis N, Pavlou E, Karatzas S, et al : Comparison of mannitol and hypertonic saline in
the treatment of severe brain injury. J Neurosurg 2011; 114 : 545-548
Simma B, Burger R, Falk M, et al : A prospective, randomized and controlled study of
fluidmanagement in children with severe head injury : Lactated
Ringer’s solution versushypertonic saline. Crit Care Med 1998; 26: 1265-1270

VIII.5. The role of cerebrospinal fluid (CSF) drainage in controlling intracranial

pressure (ICP)
Standard : There is not enough data
Guidelines : Drainage of cerebrospinal fluid (3 ml) significantly reduces ICP and increases
CPP for at least 10 minutes.
Option : Removal or drainage can be done through a ventriculostomy catheter or in
combination with lumbar drainage

Explanation of Recommendations:
Class III studies were found in children with the use of ventricular drainage in
traumatic brain injury (TBI). Sahpiro and marmarou conducted a retrospective study in
children with severe TBI, obtained a score ≤ 8 on the Glasgow Coma Scale (GCS), which all of

86
them were under ventricular drainage. Measurable variables include ICP, pressure-volume
index, and mortality.
CSF drainage will increase the Pressure Volume Index (PVI) and decrease ICP, death
only occurs in patients with uncontrolled or refractory intracranial hypertension. CSF
drainage is not limited to the ventricular route. Lumbar drainage as a combination needs to
be considered in cases of:
1) Stubborn intracranial hypertension after pairing with a functioning ventriculostomy
catheter
2) An open basal cistern
3) And there are no features of large mass lesions or compartment shifts in the
radiologyphotograph

87
Table 29. Level of Evidence (LE) and Grade of Recommendations (GR)
No Author(s) Assessment description LE/GR Conclusion

1 Kerr E Case control, to determine II/B Drainage of cerebrospinal fluid

Mary, et the effect of CSF drainage (3 ml) significantly reduces ICP
al., 2001 on the ICP monitor against and increases CPP for at least 10
brain perfusion minutes.

2 Levy et al., Retrospective study, 16 III/C From 16 patients, two patients

1995 patients with lumbar drain died due to uncontrolled ICP

3 Baldwin Clinical serial report, five III/C Three out of five survived after
and rekate, patients with lumbar drain ICP reduced
1991- 1992

4 Shapiro, In a retrospective study, 22 III/C Drainage increases PVI,

Marmaron, patients with EVD were decreases ICP, high mortality
1982 determined to ICP / PVI only in patients with
uncontrolled ICP
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

References
Baldwin HZ, Rekate HL : Preliminary experience wih controlled external lumbar drainage in
diffuse pediatric head injury. Pediatry Neurosurg 1991-2; 17: 115-120
Kerr ME, et al : Dose response to cerebrospinal fluid drainage on cerebral perfusion in
traumatic brain-injured adult, Neurosurg Focus 11 (4):Article 1; 1-6. 2001
Levy DI, Rekate HL, Cherny WB, et al : Controlled lumbar drainage in pediatric head injury. J
Neurosurg 1995; 83 : 452-460.
Shapiro K, Marmarou A : Clinical application of the pressure-volume index on treatment of
pediatric head injuries. J Neurosurg 1982; 56 : 819- 825

88
VIII.6. The role of hyperventilation in acute management of pediatric patients with
severe head injury
Standard : There is not enough data
Guidelines : There is not enough data
Option : Mild or prophylactic hyperventilation (PaCO2 <35 mmHg) should be avoided in
children

Explanation of Recommendations:
Hyperventilation → Hypocapnia (PaCO2 ↓) → brain vasoconstriction→ decreased
CSF → decreasedbrain blood volume → decreased ICP. Hyperventilation shows advantages
in head injurywith various mechanisms:
1) Decreased brain acidosis
2) Increased brain metabolism
3) Improved blood pressure from brain blood flow Hyperventilation → ↓ ICP and ↑ CPP
4) Increased perfusion in ischemic brain areas
Mild hyperventilation (PaCO2 30-35 mmHg) can be considered in conditions of
intracranial hypertension that do not reduce with:
1. Sedation and analgesics
2. Neuromuscular blocker
3. CSF drainage
4. Hyperosmolar therapy
Aggressive hyperventilation (PaCO2 <30 mmHg) can be considered as second-level
therapy for refractory intracranial hypertension. CSF, jugular venous SaO2, or brain tissue
oxygen monitoring are recommended to help identify ischemia in this condition. Brief
aggressive hyperventilation can be considered in cases of brain herniation or decreased
neurological conditions. Hyperventilation is associated with a risk of iatrogenic ischemia.
Hypocapnia (respiratory alkalosis) causes a leftward shift of the Hb-O2 dissociation curve →
interferes with oxygen delivery to injured and intact brain tissue.There is no evidence that
moderate hyperventilation (PaCO2 25-30mmHg) at onset of head injury can cause global or
regional ischemia. Although safe, temporary hyperventilation benefits are still doubtful.

89
 Table 30. Level of Evidence (LE) and Grade of Recommendations (GR)
No Author(s) Assessment description LE/GR Conclusion

1 Diringer et Prospective cohort study, II/B Hyperventilation at the onset of

al.,2002 13 patients with severe a head injury has not been
head injury, divided into 2 proven to cause ischemia
groups, comparing groups
treated with moderate and
severe hyperventilation

2 Skippen et Prospective cohort study, II/B When PaCO2 falls, ICP will
al.,1997 23 children with head decrease and CPP increases
injury, GCS <8. Age 3-16
year, average 11 year.
PaCO2 was maintained at>
35, 25-35 and <25 degrees

3 Stringer et Non-random serial study II/B Ischemia due to

al.,1993 for CBF measurements. hyperventilation occurs and
Measured ICT, CPP, MAP, affects injured and intact brain
ETCO2, XeCT, CBF tissue.
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

References
Diringer MN, Videen TO, Yundt K, et al. Regional Cerebrovascular and Metabolic Effects of
Hyperventilation after Severe Traumatic Brain Injury. J Neurosurg 2002;96:103-108
Skippen P, Seear M, Poskitt K, et al. Effect of hyperventilation on regional cerebral blood
flow inhead-injured children. Crit Care Med 1997; 25: 1402-1409
Stringer WA, Hasso AN, Thompson JR, et al. Hyperventialtion-induced cerebral ischemia
inpatients with acute brain lesions: Demonstration by Xenon -enhanced CT.AJNR
1993;14: 475-484

VIII.7. Surgery for management of increased intracranial pressure in pediatrics

Standard : There is not enough data
Guidelines : There is not enough data
Option : 1. Decompressive craniectomy needs to be considered in pediatric patients
with:
a. Severe head injury
b. Cerebral Edema (brain swelling)
c. Intracranial hypertension that persists against intensive medical therapy
d. Severe head injury with intracranial hypertension which seems to be
experiencing improvement from head injury.

90
 2. Decompressive craniectomy is less effective in patients with severe
secondary head injury
3. A good outcome can be expected in cases of decreased secondary GCS and /
or brain herniation syndrome that are still in process within the first 48
hours after injury
4. Patients with GCS 3 and who did not improve were the groups with poor
outcomes

Explanation of Recommendations:
Surgical management generally aimsto control severe intracranial hypertension.
Decompressive craniectomy for cases of traumatic brain injury in children significantly
reduces ICP (average decrease of 9mmHg). A good outcome is obtained at: young age,
earlier surgery and ICP never> 40mmHg.

Table31. Level of Evidence (LE) and Grade of Recommendations (GR)

No Author(s) Assessment description LE/GR Conclusion

1 Ellis JA et Retrospective study of 10 III/C Internal cranial expansion is a

al., 2012 patients who underwent 5 safe and effective surgery for
years of internal cranial patients with refractory
expansion surgery intracerebral hypertension

2 Jaganna- Serial case study of 23 III/C High ICP is proportional to

than et al., patients with a mean age of mortality, a survival rate of 70%
2007 1.9 years who underwent with mortality is found,
decompressive especially in patients with
craniectomy post head multitrauma
injury.

3 Skoglund et Pediatric patients with GCS III/C 3 patients had a GCS score of 5
al., 2006 3-15, history of during 1 year of monitoring, 1
deterioration, herniation patient with GCS 4, 3 patients
and increased ICP with GSC 3 and 1 patient died
performed unilateral or
bilateral decompressive
craniectomy

4 Rutgliano Retrospective case study in III/C 5 out of 6 patients dont have a

et al, 2006 6 patients with an age high ICP. 1 patient experienced
range below 20 years who an increase in ICP, after the
underwent decompressive second operation the ICP

91
 craniectomy returned to normal

5 Kan et al., Serial case study of 6 III/C 5 of 6 patients died.

2006 pediatric patients with a 3 of 4 patients had ICP
mean GCS score of 4. <20mmHg
6 performed
decompressive
craniectomy

6 Ruf et al., Serial case study in 6 cases III/C 3 patients experienced

2003 with GCS score of 3-7, age complete improvement, 2
range 5-11 years, which patients had disability during
was performed by monitoring for 6 months.
unilateral and bilateral Postoperative ICP is regulated
decompressive below 20mmHg
craniectomy.

7 Figaji et al., A study of 5 cases of III/C All patients experienced

2003 pediatric patients improvement and a GCS score
undergoing neurological of 4-5 at 14-40 months of
deterioration (GCS <8) monitoring
performed craniectomy

8 Hejazi et A retrospective study of 7 III/C All patients experienced

al., 2002 serial cases in pediatric complete improvement in
patients who had brain monitoring for 8 months
swelling with initial ICP> postoperative
45mmHg had
decompressive
craniectomy.

9 Taylor et Single center PRCT, 27 III/C Decompressive craniotomy

al., 2001 severe head injury in significantly decreases ICP
children with intracranial within 48 hours after
hypertension that not randomization and the results
effective with medical are not very significant in
therapy and random clinical improvement
ventricular drainage
between bitemporal
decompressive craniotomy
vs without surgery

10 Polin et al., Case control study, 35 III/C Good outcomes are obtained at
1997 patients with severe head a young age, early surgery and
injury who performed ICP never> 40 mmHg

92
 decompressive
craniectomy with pre and
post operative ICP monitors
and medical therapy

11 Cho et al., Retrospective study on III/C Patients who underwent

1995 children with shaken Baby surgeryhave a better survival
syndrome who performed than those who only received
decompressive surgery or medical therapy
medical therapy
(Scottish Intercollegiate Guideline Network: US Agency for Health Care Policy and Research)

Review between Pediatric and Adult head injury:

Comparison between injury in children and adults according to the "National
Pediatric Trauma Registry" shows that the proportion of children who experience traumatic
head injury is greater than adults.But because of the difficulty in assessing therapy in
children with a wide range of age groups and differences in the level of development in each
phase, there are still not many studies that meet the requirements to be standardized for
treatment in the acute phase untill rehabilitation.The assumption is not correctedthat
"children are miniature of adults", it is inappropriate to equate and apply the research
literature to adults or apply the guidelines available for adults in children. Efforts to
recognize specific aspects of children are reviewed and the guidelines that has been
arrangedbecome as a guide to the existing guidelines for adults. The guidelines compiled are
largely the result of a joint consensus.
Pediatric or child is defined as those who are less than 18 years old. Traumatic head
injuries, hereinafter referred to as "head injury" only, are primary or secondary injury
resulting from trauma to the brain.Brain injury due to abuse (abusive head injury) including
abuse, torture, neglect and shaken baby syndrome are included in this category of head
injury. Injuries due to birth trauma, drowning, and brain blood vessel disorders were not
included in this group.
Epidemiologically, head injury in children cause death in 40% of cases of children
aged 1 to 4 years and 70% of deaths in children aged 5 to 19 years. The pattern and
principles of head injury management in children are almost the same as in adults but there
are important differences. This relates to the level of development of the child, anatomical
variation in the head and in general and the child's brain response to traumatic injury.The
related matters are: in children, it is not possible to do a GCS examination like in an adult.

93
Scale modification adopted for children and infants. More response fluctuations in children
and recorded separately on monitoring cards are often misleading. It is often difficult to
decide whether there is a decrease in consciousness at the time of the impact.Concussions
can be very brief and cannot be assessed by observation of blunt trauma to the child's head.
It can occur in a short time with the development of acute brain edema. This condition can
occur in head trauma that appears to be mild and is indicated by a rapid and deep decline in
consciousness status. This condition can be diagnosed only after the diagnosis of mass lesion
is discardedby CT scan.
A sudden decrease in consciousness followed by conditions such as a confused
episode mark the severity of a head injury. Such patients must undergo a CT scan to ensure
there is no intracranial bleeding. Early seizures within one hour of trauma are not as risky as
post-traumatic epilepsy in adults. In general, children improve and recover fully after the
attack, there is no indication of anti-convulsant administration. The thinness of scalp and
calvaria in young children increases the risk of brain damage by penetrating objects which in
adults cannot be penetrated. Some stab wounds to the child's head must be treated as if
there had been direct trauma to the brain.Incoming injuries must be examined carefully to
look for signs of fracture, discharge of CSF or brain tissue. If still in doubt, a CT scan can be
used to assess the extent of damage to that side. Referral to a neurosurgeon is needed to
repair the damage. Impression fractures, both simple and complex, are generally associated
with local damage to the underlying brain. The impact energy can be substantially absorbed
on the trauma side and the acceleration effect on the brain is minimized. The absence of a
history of loss of consciousness does not eliminate the presence of severe focal injury.Plain
head photographs, especially tangential views, can state the extent of bone injury although
CT scans can show more clearly the same aspects, and can add to show whether or not
there is a head injury underneath. Because of its elasticity, the calvaria of a child can change
shape after impact without a fracture. This deformity can be related to local trauma to the
brain or trauma to the meningen that results in the emergence of extradural hematomas.
The absence of a fracture does not eliminate this type of bleeding in a child. Blood loss is an
important consideration as a concern for assessing head injury in children including infants.
A sudden decrease in circulating blood volume can result from bleeding from
wounds, scalp (sub galeal) hematomas and / or intracranial hematomas. In small infants,
because the mechanism of intracranial hematoma compensation can be very large. In
particular, it is important to state that blood pressure can be maintained as a reflection of
increased intracranial pressure and distortion. At surgery, blood pressure can reduce

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quickly. This is important for children if they plan to have surgery as a consideration for
giving blood transfusions immediately. In conditions of emergency, negative O blood can be
given.A child's brain is most likely to develop edema after blunt trauma and it is very
important not to put excessive fluid in a patient with this condition. As in adults, intravenous
fluids are not needed except to replace estimates of blood loss as indicated. Slow brain
edema can cause unexpected changes and observation in young children in hospital for 24
hours after minor injury is recommended.
The fontanelle is most useful in assessing the presence or absence of increased
intracranial pressure in infants. In the presence of retinal bleeding, bilateral skull fractures
indicate a non-accidental trauma. Restlessnessin a child's head injury will interrupt the
process of CT scan. Anesthesia or sedation can be given in this condition.
Recommendations or guidelines for the management of severe head injury in
children according to Guidelines for The Acute Medical Management of Severe Traumatic
Brain Injury in Infants, Children, and Adolescent (Pediatric Critical Care Medicine, 4(3), 2003

(Rainer Gedeit.Head Injury. Pediatrics in Review Vol.22 No.4 April 2001)

(Rainer Gedeit.Head Injury. Pediatrics in Review Vol.22 No.4 April 2001)

References

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Cho DY, Wang YC, Chi CS: Decompressive craniotomy for acute shaken/impact
syndrome.Pediatr Neurosurg 1995; 23:192–198
Ellis JA et al. Internal cranial expansion surgery for the treatment of refractory idiopathic
intracranial hypertension. 2012
Figaji AA, Fieggen AG, Peter JC: Early decompressive craniotomy in children with severe
traumatic brain injury. Childs Nerv Syst 2003; 19:666 – 673
Hejazi N, Witzmann A, Fae P: Unilateral decompressive craniectomy for children with severe
brain injury. Report of seven cases and review of the relevant literature. Eur J Pedi- atr
2002; 161:99–104
Jagannathan J, Okonkwo DO, Dumont AS, et al: Outcome following decompressive craniec-
tomy in children with severe traumatic brain injury: A 10-year single-center experience
with long-term follow up. J Neurosurg 2007; 106: 268 –275
Kan P, Amini A, Hansen K, et al: Outcomes after decompressive craniectomy for severe
traumatic brain injury in children. J Neuro- surg 2006; 105:337–342
Polin RS, Shaffrey ME, Bogaev CA, et al: Decompressive bifrontal craniectomy in the
treatment of severe refractory posttraumatic cerebral edema. Neurosurgery 1997;
41:84–94
Ruf B, Heckmann M, Schroth I, et al: Early decompressive craniectomy and duraplasty for
refractory intracranial hypertension in children: results of a pilot study. Crit Care 2003;
7:R133–R138
Rutigliano D, Egnor MR, Priebe CJ, et al: Decompressive craniectomy in pediatric pa- tients
with traumatic brain injury with intractable elevated intracranial pressure. J Pe- diatr
Surg 2006; 41:83– 87; discussion 83-87
Skoglund TS, Eriksson-Ritzen C, Jensen C, et al: Aspects on decompressive craniectomy in
patients with traumatic head injuries. J Neurotrauma 2006; 23:1502–1509
Taylor A, Warwick B, Rosenfeld J, et al: A randomized trial of very early decompressive
craniectomy in children with traumatic brain injury and sustained intracranial
hypertension. Childs Nerv Syst 2001; 17:154–162

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IX. Sports-related head injury
Head injury is a clinical diagnosis of head injury with neurological dysfunction which
can be in the form of acute symptoms of cognitive dysfunction. There are an estimated 1.7-3.8
million head injury events each year in the US, 10% of them are related to sports trauma. In
general, head injury can heal itself with improvement of symptoms in one week but can also
be a sequel of mild head injuryin the form of headaches and severe head injuryuntildeath
occurs. Proper diagnosis and treatment according to standard guidelines are very important
when treating athletes who have head injury and the possibility of increasing long-term
disorders.
Concussion due to sports trauma
Symptoms of concussion due to sports trauma are classified in 4 groups: physical,
cognitive, emotional and sleep disorders.

Table 32. Symptoms ofconcussion

Physical disorders Cognitive disorders Emotional disorders Sleep disorders

 Headache  Feeling mentally  Irritability  Drowsiness

 Nausea foggy  Sadness  Sleeping more than
 Equilibrium  Feeling of being  More emotional usual
disorder slow and nervous  Trouble falling
 Fatigue  Difficulty asleep
 Visual acuity concentrating
disturbance  Difficulty
 Sensitive to light remembering
 Sensitive to noise  Repeating
 Paresthesia questions
 Tingling sensation  Answering
questions slowly

Table 33. Concussion grading based on Cantu and AAN systems

Grade Cantu System AAN System
Mild 1) Posttraumatic amnesia less than 30 1) Confusion
minutes in duration 2) No loss of consciousness
2) No loss of consciousness 3) Symptoms resolve in less than 15
minutes
Moderat 1) Loss of consciousness less than 5 Symptoms like in mild concussion but the
e minutes in duration symptoms last more than 15 minutes
or
2) Posttraumatic amnesia more than
30 minutes
Severe 1) Loss of consciousness more than 5 Any loss of consciousness

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 minutes in duration
or
2) Posttraumatic amnesia ≥ 24 hours

Contraindications for returning to play sports that require physical contact:

1. Persistent post concussion symptoms
2. Persistent remaining symptoms of head trauma in the central nervous system (organic
dementia, hemiplegia, homonym hemianopsia)
3. Hydrocephalus
4. Spontaneous SAH
5. Abnormal symptoms of foramen magnum (chiari malformations)

Table 34. Guidelines for athletes can get back to play(AAN Guideline)
Grade Recommendations for management of concussion in sports

Mild  Remove from contest

 Check every 5 minutes for symptoms of amnesia and post concussion
 May return to play if symptoms disappear within 15 minutes

Moderat  Remove from contest

e  Not recommended to return to play that day
 Evaluate regularly for signs of developing intracranial disorders
 Check back in the next day
 CT or MRI can be performed if headache or other symptoms worsen or last
more than 1 week
 Return to exercise after 1 week free of symptoms

Severe  Transport with ambulance from field to hospital emergency room if unconscious
(install C-Spine stabilizers)
 Do a neurological examination immediately
 Appropriate neuroimaging
 Can return home with the instructions "head injury" if there are no
abnormalities in the examination
 Immediately go to the hospital when there are signs of abnormalities or mental
status that is sustainable.
 Check neurological status every day until all symptoms improve or stabilize
 There is a prolonged loss of consciousness, persistent mental status change,
worsening of post concussion symptoms or abnormal neurological examination
immediate neurosurgical evaluation or transfer to trauma center
 After loss of consciousness <1 minute at the 3rd degree concussion, do not
return to exercise until symptoms are disappear for one week
 After loss of consciousness> 1 minute at the 3rd degree concussion, do not
return to exercise until symptoms are disappear for two weeks
 CT scan or MRI can be performed if headache or symptom worsens or lasts for

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 more than two weeks

Recurrent concussion over a short period of time is a potentially dangerous condition.

The need for neuroimaging tests (e.g. CT scan) in athletes with improved symptoms is
controversial and depends on the judgment of the doctor. Suggested indications for
neuroimaging are:
1. Severe concussion
2. Persistent symptom > 1 week, although mild symptom
3. Before return to compete after the second and third concussions in the same season of
competition

Table 35. Recommendations for recurring concussion in one season competition

Concussion
No Guide before returning to play
(Severity level)

1 Mild 1 week*
Moderate or severe 1 month* with normal head CT scan or MRI

2 Mild Not recommended to play again on this season, head CT Scan or

MRI**

3 Moderate Not recommended to play again on this seasonand avoid sports

Severe that require physical contact
* without symptoms at rest and activity
** if acute abnormalities are seen on head CT / head MRI (end the season of competition)
Consider not participating in sports that require physical contact

References
Bradley, et al. 2013. Sport related concussion. Division of pediatric sports medicine rainbow
babies and children hospital. Elsevier. Vol 14 : 4
Victoroff, et al. 2012. Diagnosis dan treatment of sport related traumatic brain injury.
Psychiatric annals. 42 : 10
Sahler, et al. 2012. Traumatic brain injury in sports : A review. Hindawi rehabilitation research
and practice.
Greenberg, Mark. 2010. Handbook of neurosurgery 7 ed. Thieme : Hal 850.

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Closing
This guideline will always be periodically evaluated and systematically carried out supporting
studies, so as to get the highest level of clinical certainty, namely standards. Basicallythis guideline
can be used as a reference or recommendation, both for medical treatment and surgical
intervention in the field of head injury.
We hope to perfect this guideline by getting suggestions and criticisms that come from
anywhere and anyone, especially those who are involved in service, education, and research in the
field of neurotrauma.
It seems there is no ivory that is not cracked. Perfection is always beour hope, but various
limitations prevent us from being able to compile this guideline perfectly, so there are always
deficiencies and inaccurancies.

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