Management of Severe Traumatic

Brain Injury

Dr. Claudiu Zdrehuş MD, PhD

University of Medicine Cluj-Napoca

Romania
CEEA Chişinău 2010
 Traumatic Brain Injury (TBI)
 Disability 5.3 million people in USA

 Death 52,000 die of their injuries

 Economic Costs $4 billion annually in

USA
Traumatic Brain Injury
 Mortality ↓ 50% 35% 25%
1975 2005

30 years
Evidence based protocols
Maintaining adequate cerebral perfusion

Lu J et al. Acta Neurochir 2005; 95: 281-285

Hesdorffer D et al. J Trauma 2002; 52:1202-1209
Fakhy SM et al. J Trauma 2004; 56: 492-493
 Traumatic brain injury (TBI)
represents a relevant pathology in
the ED and still remains the leading
cause of death among people
younger than 25 years of age and the
main single factor in determining
prognosis in the polytraumatised
patient.

 Approximately 200 patients/100.000

inhabitants/year are admitted in the
ED for a TBI; among them 15-20 are
severe TBI (STBI) patients defined as
patients scored with a GCS < 8.
Neurophysiology
 CBF- 50ml/100gr/min; 700ml/min la 70 kg
 CMRO2 – 3.2ml/100gr/min sau 45ml/min
 CBV- 15% CO

 ICP - 5-15 mmHg

 PPC >70mmHg; = MAP - ICP
Neurophysiology
 ICP = 5-15 mmHg

– cerebral tissue 85%

– CSF10%; 150ml; 500-600 ml/day

– CBV 5%; 75% veins; 25% arterioles and arteries

 Severe TBI

• GCS

• GOS
Glasgow Coma Scale
 Speech
• Alert,oriented, and conversant 5
• Confused, disoriented, but conversant 4
• Intelligible words, not conversant 3
• Unintelligible sounds 2
• No verbalization, even with pain 1
 Eye opening
• Spontaneous 4
• To verbal stimuli 3
• To painful stimuli 2
• None, even with painful stimuli 1
 Motor
• Follows commands 6
• Localizes painful stimuli 5
• Withdraws from painful stimuli 4
• Flexor posturing with central pain 3
• Extensor posturing with central pain 2
• No response to painful stimuli 1
TBI
 moderate TBI- GCS 9-12-on
admission, in first 6h – 48h

 severe TBI - GCS< 8

bedside patient

Why ?
pathophysiolgy
biophysical mechanisms
biochemical mechanisms
molelcular mechanisms
iatrogenity
Pathophysiology
 Mechanical injury

 Primary injury
• Scalp injury
• Skull fracture
• Cerebral contusion
• Diffuse axonal injury
• Hemorrhage

 Secondary injury
• Posttraumatic ischemia
• Neurodegeneration
• Astrogliosis
• Edema
• Tissue destruction
 Grade of Concussions
 Colorado Scale
• Gr I: Confusion, no LOC,
PTA<30 min
• Gr II:LOC<5 min, confusion,
PTA 30 min-24 h
• Gr III: LOC>5 min, PTA>24h
 Cantu Scale
• Gr I: PTA<30min; no LOC
• Gr II: LOC<5min, PTA 30min-
24h
• Gr III: LOC>5min, PTA>24h
 AAN Scale
• Gr I: transient confusion, no
LOC, symptoms<15min
• Gr II: transient confusion, no
LOC, symptoms>15min
• Gr III: Any LOC
 Subdural hematomas
• 20-25% of all comatose victims of TBI
 Epidural hematomas
• 8-10% of all comatose victims of TBI
 Cerebral hemorrhage
• Intraparenchymal hematoma
• Subarachnoid hemorrhage
To avoid secondary brain injury,
always look (and think) ahead!
 What are the priorities in the
treatment of severe traumatic brain
injuries?
 Blood pressure
 Oxygenation
 Hyperosmolar Therapy
 Hypothermia
 Infection Prophylaxis
 Deep Vein Thrombosis Prophylaxis
 Intracranial Hypertension
 Intracranial Pressure Monitoring
 Cerebral Perfusion Pressure
 Brain Oxygen Monitoring
 Anaesthetics, Analgesics and Sedatives
 Nutrition
 Antiseizure Prophylaxis
 Hyperventilation
 Steroids
Blood Pressure and Oxygenation
Jones et al., 1994 Prospective analysis of 124 III Mortality is best predicted by
patients≥14 years old admitted to duration of hypotensive (p=0.0064),
single center with a GCS≤12, or >12 hypoxemia (p=0.0244) and pyrexic
and Injury severity score≥16, with (p=0.0137) insults. Morbidity (Good
clinical indications for monitoring. vs Bad outcome) was predicted by
Subgroup analysis performed on 71 hypotensive insults (p=0.0118), and
patients for whom data existed for 8 pupillary response on admission
potential secondary insults (ICP, (p=0.0226)
hypotension, hypertension, pyrexia,
bradycardia, tachycardia)

Stocchetti et al.,
1996
A cohort study of 50 trauma patients III 50% of patients were hypoxic
transported from scene by helicopter, (SaO2<90%) and 24% were
which evaluated the incidence and hypotensive. Both hypoxemia and
effect of hypoxemia and hypotension hypotension negatively affect
on outcome. outcome

Manley et al., Prospective cohort of 107 patients

2001 with GCS 13 admitted to a single III
center; primarily evaluating impact of
hypoxic and hypotensive episodes
during initial resuscitation on Early inhospital hypotension but not
mortality. Impact of multiple episodes hypoxia is associated with
of hypoxia or hypotension analyzed increased mortality.

Struchen et al., Cohort of 184 patients with severe

2001 TBI admitted to a single level I III
ICP>25 mmHg, MAP<80 mmHg,
trauma center neurosurgical ICU who CPP<60 mmHg, and SjO2<50% were
received continuous monitoring of associated with worse outcomes
ICP, MAP, CPP, and SjO2
Blood Pressure and Oxygenation
 There are insufficient data to support (Level I recommendation) a treatment
standard for resuscitation of blood pressure and oxygenation
• Rec A

 Hypotension (systolic blood pressure [SBP] <90 mm Hg) or

hypoxia (apnea, cyanosis or an oxygen (O2) saturation <90% in
the field or a PaO2 <60 mm Hg) must be monitored and
scrupulously avoided, if possible, or corrected immediately in
severe traumatic brain injury patients
• Rec B

 The mean arterial blood pressure should be maintained above 90 mm Hg

through the infusion of fluids throughout the patient’s course to attempt to
maintain cerebral perfusion pressure (CPP) greater than 60 mm Hg.
Patients with a Glasgow Coma Scale (GCS) score less than 9, who are
unable to maintain their airway or who remain hypoxemic despite
supplemental O2, require that their airway be secured, preferably by
endotracheal intubation
• Rec C
Hyperosmolar Therapy
Mendelow et al., Effect of mannitol on CBF and III Mannitol consistently improved MAP,
1985 cerebral perfusion pressure in CPP, and CBF, and lowered ICP by
human TBI. Retrospective analysis 10-20 min after infusion; the effect
was greater with diffuse injury, and in
normal hemisphere. CBF increase was
greatest when CPP was 50 mmHg.

Muizelaar et al., Effect of mannitol on ICP and CBF III Mannitol works best on ICP when
1994 and correlation with pressure
autoregulation is intact; suggests
autoregulation in severe TBI
rheologic effect is more importasnt
patients
than osmotic effect

Retrospective analysis comparing

Qureshi et al., continuous administration of 3%
III More penetrating TBI and mass
1999 lesions in HS group. HS group had a
sodium chloride/acetate solution at
higher inhospital mortality. Patients
75-50 ml/h or 2% solution to NS
treated with HS group were more
maintance in 82 TBI patients with
likely to receive barbiturate treatment
GCS≤8
Hyperosmolar Therapy
 Rec A. There are insufficient data to support a treatment
standard for the use of mannitol.

 Rec B. Mannitol is effective for control of raised ICP after

severe head injury. Effective doses range from 0.25 g/kg
body weight to 1 g/kg body weight. Arterial hypotension
(SBP<90mmHg) should be avoided

 Rec C
 Restrict use of mannitol prior to ICP monitoring to patients
with signs of transtentorial herniation or progressive
neurological deterioration not attributable to extracranial
explanations. However, hypovolemia should be avoided by
fluid replacement.
 Serum osmolarity should be kept below 320 mOsm
because of concern for renal failure.
 Euvolemia should be maintained by adequate fluid
replacement. A Foley catheter is essential in these patients.
 Intermittent boluses may be more effective than continuous
infusion.
Prophylactic Hypothermia
Abiki et al., 2000 Single–center RCT comparing II 1 patient died in the hypothermia
effect of moderate hypothermia (3- group (6.7%) vs 3 in normothermi
4 days, 32-33°C vs normothermia group (27.3%). Significantly better
on GOS at 6 months post-injury outcomes in hypothermia than
normothermia group (80% vs
36.4%) (p=0.04)
Significantly less mortality on
Single–center RCT comparing
Jiang et al., 2000 effect of long term (3-14 days) mild
II hypothermia than normothermia
group (25.6%vs45.5%).
hypothermia (33-35°C) vs
Significantly better outcomes in
normothermia on mortality and
hypothermia than normothermia
GOS at 1 year post injury
group (46.5% vs 27.3%; p<0.05).
No significant differencebetween
groups in complications

Qiu et al., 2005 Single–center RCT comparing II Significantly less mortality on

effect of mild hypothermia (3-5 hypothermia than normothermia
days, 33-35° vs normothermis on group (25.6%vs51.2%).
mortality and GOS at 2 years post- Significantly better outcomes in
injury hypothermia than normothermia
group (65.1% vs 32.6%; p<0.05).
Significantly more pulmonary
infection in hypothermia than
normoyhermia group (60.5% vs
32.6%) and more
thrombocytopenia in hypothermia
than normothermia group (62.8%
vs 39.5%)
A Review of Selective Hypothermia in the Management of Traumatic
Brain Injury
J of Neurotrauma 02/17/2009
Eisha Christian, B.A.; Gabriel Zada, M.D.; Gene Sung, M.D.; Steven L.
Giannotta, M.D.

 Several investigators have postulated that the administration of

selective, or preferential, cerebral hypothermia following TBI may
confer the same neuroprotective benefits as systemic hypothermia,
while reducing the associated risks.

 The induction time for selective hypothermia may be shorter, thus

providing earlier neuroprotection from secondary injury following TBI.

 Selective methods of cerebral hypothermia remain a viable option for

neuroprotective therapy in patients that have sustained TBI.

 Further prospective research is clearly indicated to delineate the risks

and benefits associated with these new therapies
Prophylactic Hypothermia
 REC A: There are insufficient data to support a Level I
recommendation

 REC B: There are insufficient data to support a Level II

recommendation

 REC C: Prophylactic Hypothermia is not significantly

associated with decreased mortality when compared with
normothermic controls. Greater decrease in mortality risk
is observed when target temperatures are maintained for
more than 48 h. Prophylactic Hypothermia is associated
with significantly higher GOS scores when compared to
scores for normothermic controls
Infection Prophylaxis
Sundbarg et al., Retrospective analysis of 648 III The TBI patients had no incidence of
1996 patients undergoing ventricular definitive infection and in 3.7% rate
catheter placement for ICP positive CSF cultures deemed
monitoring and drainage, 142 of contaminants.
whom had severe TBI. None were
given prophylactic antibiotics, but
76% received antibiotics for other
systemic illnesses
Randomized trial of 62 patients There was no difference in the rate of
Bouderka et al., II
with severe TBI, on fifth hospital mortality or pneumonia between the
2004
day were randomized to early groups. Early tracheostomy group
tracheostomies (n=31) or showed a decrease in the number of
prolonged intubation (n=31) overall mechanical ventilation days,
and mechanical ventilation days after
the diagnosis of pneumonia. ICU days
were not reduced.
Sirvent et al.,
RCT of 100 mechanically II The overall incidence of pneumonia
1997
ventilated ICU patients (86% of was 37%, 24% in Group 1 and 50% in
which were severe TBI) assigned control group. There was no difference
to a treatment group (43TBI) of in mortality. A short course of
cefuroxime 1,5 gr IV for two doses prophylactic cefuroxime was effective
or no treatment group (43 TBI) in decreasing the incidence of
after endotracheal intubation nosocomial pneumonia in mechanical
ventilated patients.
Infection Prophylaxis
 Rec A: There are insufficient data to support a Level I
recommendation
 Rec B: Periprocedural antibiotics for intubation should be
administered to reduce the incidence of pneumonia. It does
not change the length of stay or mortality.
Early tracheostomy should be performed to reduce
mechanical ventilation days. It does not alter mortality or
the rate of nosocomial pneumonia

 Rec C: Routine ventricular catheter exchange or

prophylactic antibiotic use for ventricular catheter
placement is not recommended to reduce infection.
Early extubation in qualified patients can be done without
increasing risk of pneumonia
Deep Vein Thrombosis Prophylaxis
Gerlach et al., Prospective observational study III No clinically apparent VTE was
2003 of 2,823 patienta undergoing identified in patients with TBI. Early
intracranial surgery including 231 initiation of nandroparin after TBI may
patients with TBI treated with be associated with lower rates of DVT
compression stockings plus compared with historical controls;
nadroparin0,3 ml/day within 24 h increased incidence of intracranial
of surgery bleeding may occur.
Kim et al., 2002 Retrospective study of 64 III Rates of DVT were 4% in those whom
patients with severe TBI admitted heparin was begun less than 72 hours
to a Level I trauma center. and 6% in those whom heparin was
Patients were divided into those begun after 72 h
in whom prophylaxis with 5000
units of subcutaneous heparin
was begun less than or greater
than 72 h after admission
Kleindienst et al., Retrospective analysis of 344 III
2003 patients with TBI treated No TBI patients were diagnised with
compression stockings and DVT. 9 TBI patients (3.2%) had
certoparin 18 mg/day within 24 progression of intracranial
hours of admission or surgery hematomas

Norwood et al.,
Prospective, operational study of III
2002
150 TBI patients treated with The rate of hematoma progression
enoxaparin 30 mg twice daily on CT after initiation of enoxaparin
beginning 24 hours after arrival to was 4%. Early initiation of
the ED enoxaparin after TBI may be
associated with lower rates of DVT,
increase incidence of intracranial
bleeding may occur
Deep Vein Thrombosis Prophylaxis
 Rec A: There are insufficient data to support a Level I
recommendation
 Rec B: There are insufficient data to support a Level
II recommendation
 Rec C:
– Graduated compression stockings or intermittent
pneumatic compression (IPC) stockings are
recommended, unless lower extremity injuries prevent
their use. Use should be continued until patients are
ambulatory.
– Low molecular weight heparin or low dose unfractioned
heparin should be used in combination with mechanical
prophylaxis. There is an increased risk for expansion of
intracranial hemorrhage.
– There is insufficient evidence to support
recommendations regarding the preferred agent, dose,
or timing of pharmacologic prophylaxis for DVT
 Intracranial hypertension is a major
cause of posttraumatic neurologic
morbidity and mortality
• Cohen SM, Marion DW. Traumatic brain injury. Crit Care Med 2005, 377-389
Indications for intracranial pressure monitoring

 Which patients are

at high risk for ICH ?
 Which patients are at high risk for ICH ?

Lee et al., ICP and CPP data III Of 2,698 hourly peak ICP
1998 reviewed in 36 severe recording 905 were 20
TBI patients with clinical mmHg
and radiological evidence
of diffuse axonal injury

Miller et al.,
82 severe TBI patients
2004 CT alterations are associated
were retrospectively III
with, but not predictive of
analyzed regarding initial ICH
findings relative to ICP

Diffuse injury Type I – no ICP

Patterns of ICP III elevation
Poca et al., elevations were
correlated with CT Type II – evidence of ICH
1998
diagnostic categories in 27.6%
94 patients with sever Type III – 63.2%
TBI Type IV – 100%
Are ICP data useful ?

Servadei et al., ICP ranges assessed in III ICP monitoring was the first
2002 patients with traumatic indicator of evolving lesions in
SAH to determine if there 20% of patients. In 40% of
were any identifiable patients CT worsening was not
changes predictive of associated with ICP elevations.
worsening CT scan ICP monitoring alone may be
findings inadequate to follow CT
abnormalities
 Does ICP monitoring improve outcome ?

Aarabi et al., 2006 Prospective observational study of III Of the subgroup of 40 the mean ICP
50 severe TBI patients, 40 with decreased after decompression from
intractable ICH whose ICP was 23.9 to 14.4 mmHg (p< 0.001)
measured before craniectomy

Retrospective study with prospective III No significant difference in mortality or

Cremer et al., outcome data collection comparing GOS at 12 months
2005 mortality and 12 month GOS in
severe TBI patients treated in two
hospitals, one with ICP monitoring,
other without.

Lane et al., 2000 Retrospective review of the Ontario III ICP monitoring was associated with
Trauma Registry evaluating 541 improve survival.
severely TBI patients with ICP
monitoring

Timofeev et al., Retrospective analysis of outcomes III Of 27 patients for whom pre and post
2006 for severe TBI patients who were surgical ICP was measured, mean ICP
treated for intractable ICH with decreased from 25±6 mmHg to 16±6
decompression craniectomy mmHg (p<0.01)
Indications for intracranial pressure monitoring
 Recommendations BTF 2007
– Rec A: There are insufficient data to support a
treatment standard for this topic
– Rec B: ICP should be monitored in all
salvageable patients with severe TBI, GCS 3-8
after resuscitation and an abnormal CT scan.
An abnormal CT scan of the head is one that
reveals hematomas, contusions, swelling,
herniation or compressed basal cisterns
– Rec C: ICP monitoring is indicated in patients
with severe TBI with a normal CT scan if two or
more of the following features are noted on
admission: age over 40 years, unilateral or
bilateral motor posturing, or systolic
BP<90mmHg
 Intracranial pressure monitoring technology

 AAMI standards of ICP device

• Pressure range 0-100 mmHg

• Accuracy ± 2 mmHg in range of 0 – 20 mmHg
• Maximum error 10% in range of 20 – 100 mmHg
 Intracranial pressure monitoring technology
 Conclusions:
– The ventricular catheter connected to an
external strain gauge is the most
accurate, low-cost, and reliable method of
monitoring ICP

– Subarahnoid, subdural, and epidural

monitors (fluid coupled or pneumatic) are
less accurate
 What is the critical
value of ICP as an
upper threshold
above which
treatment should be
initiated ?
Intracranial pressure thresholds

Chambers 207 adult patients with III It may be inappropriate to

et al., 2001 ICP and CPP set a single target of ICP
monitoring, to as higher values may be
determine if there were tolerated
thresholds for
determination of
outcome

Ratanalert Prospective trial of 27 III

et al., 2004 patients, ICP treatment No difference in outcome
thresholds of 20 or 25
mmHg. Protocols were
similar with
CPP>70mmHg and
SjO2>54%
Intracranial pressure thresholds
 Recommendations
– Rec A: There are insufficient data to
support a standard for this topic
– Rec B: Treatment should be initiated
with ICP threshold above 20 mmHg

– Rec C: A combination of ICP values,

and clinical and brain CT findings,
should be used to determine the need
for treatment
Cerebral perfusion pressure thresholds

Is low CPP harmful ?

Cerebral perfusion pressure

Andews et 1 year outcome for 69 III Low CPP and hypotension

al., 2002 patients with TBI are powerful predictors of
death and poor outcome
Clifton et 393 MRT III
al., 2002 Poor outcome was
associated with CPP<60
mmHg. No benefit of
maintaining CPP>70 mmHg
Cerebral perfusion pressure
 Recommendations
– Rec A: There are insufficient data to
support a standard for this topic
– Rec B: Aggressive attempts to maintain
CPP above 70 mmHg with fluids and
pressors should be avoided because of
the risk of ARDS

– Rec C: CPP of < 50mmHg should be

avoided
Brain Oxygen Monitoring and Thresholds

Van den 101 severe TBI, III Patients with initial

Brink et al., monitoring of brain values of PbrO2
2000 tissue oxygenation. <10mmHg for more than
Outcome- GOS at 6 30 min had higher rates
months postinjury of mortality and worse
outcome

Valadka et
al., 1998 POS of 34 TBI
patients, GOS at 3 III Low PbrO2 values (< 15
months mmHg) and the duration
of time spent with low
PbrO2 are associated
with high mortality
Brain Oxygen Monitoring and Thresholds

 Recommendations
– Rec A: There are insufficient data to
support a standard for this topic
– Rec B: There are insufficient data to
support level II recommendation for this
topic
– Rec C: SjO2 < 50% or PbrO2 < 15mmHg
are treatment thresholds
Anaesthetics, Analgesics, and Sedatives
Recommended dose regimens
 Morphine sulphate  Sufentanil
• 4mg/h cont inf • 10-30mcg/kg test bolus
• Titrate if needed • 0.05-2mcg/kg/h cont inf

 Midazolam
• 2mg test dose  Propofol
• 2-4mg/h cont inf
• 0.5mg test bolus
• 20-75mcg/kg/min cont inf
• Not to exceed 5 mg/kg/h
 Fentanyl
• 2mcg/kg test dose  Barbiturates
• 2-5mcg/kg/h
• Loading dose 10mg/kg
over 30 min; 5mg/kg every
hour x 3 doses
• 1mg/kg/h
Anaesthetics, Analgesics, and Sedatives

Kelly et al., RCT of propofol vs II ICP lower in day 3

1999 morphine in 42 TBI (p<0.05) in patients
pat (23 propofol,19 received propofol. There
morphine) was no effect on
mortality or GOS
outcomes
Anaesthetics, Analgesics, and Sedatives
 Recommendations

– Rec A: There are insufficient data to support a Level I

recommendations for this topic

– Rec B: Prophylactic administration of barbiturates to

induce burst suppression EEG is not recommended

– Rec C:
High dose barbiturates are recommended for control
ICH refractory to maximum standard medical and
surgical treatment.
Hemodynamic stability is essential before and during
barbiturate therapy
Propofol is rec for the control of ICP, but not for
improvement in mortality or 6 months outcome
High dose propofol can produce significant morbidity
Nutrition
 15-17 g N/day or 0.3-0.5 g N/kg/day

 Proteins 15-20% of caloric composition of a 50 kcal/kg/day

feeding protocol

 Class III st found 111/114 (97%) patients tolerated intragastric

feeding 25 ml/h and increased by 25 ml/h every 12 h until target
was reached
» Borzotta AP et al. J Trauma 1994; 37: 459-468

 Hyperglycemia has been associated with worsened outcome

» Cherian L et al. Crit Care Med 1997; 25: 1378-1383
Nutrition
 Recommendations

– Rec A: There are insufficient data to

support a standard for this topic

– Rec B: patients should be fed to obtain

full caloric replacement by day 7 post
injury
Antiseizure Prophylaxis
 Risk factors for PTS
• GCS< 10

• Cortical contusion

• Depressed skull fractures

• Subdural hematoma

• Epidural hematoma

• Intracerebral hematoma

• Penetrating head wound

Antiseizure Prophylaxis
 Temkin et al. J Neurosurg 1999; 91: 593-560

– RDB parallel group clinical trial of 380 patients with high risk
of PTS
• 1 week phenytoin
• 1 month valproate
• 6 month valproate
– II
– Similar rates of early PTS
– No significant diff in late PTS
Antiseizure Prophylaxis
 Recommendations

– Rec A:
• There are insufficient data to support a Level I
recommendations for this topic
– Rec B:
• Prophylactic use of phenytoin or valproate is
not recommended for preventing the late
PTS
• Anticonvulsivants are indicated to decrease
the incidence of early PTS (within 7 days of
injury)
Hyperventilation- CBF early after severe TBI
 Bouma et al. J Neurosurg 1992; 77:360-368 Level III
– CBF less than 18ml/100g/min in first 24 h in 31.4% of patients

 Marion et al. J Neurosurg 1991; 74: 407-414 Level III

– CBF always lowest during the first 12-24 hours after injury

 Siontos et al. Neurosurgery 1995; 36: 943-949 Level III

– 33% of patients had a CBF less than 28 ml/100g/min during the first
24/48 h after injury
Hyperventilation – Cerebral Oxygen Extraction

 Inberti et al. J Neurosurg 2002; 96: 97-102

– Hyperventilation was the second most common cause for SjO2
desaturation

 Oertel et al. J Neurosurg 2002; 97: 1045-1053

– Reduction of PaCO2 from 35 to 27 mmHg led to a decrease in the
SjO2 from 73 to 67%
Hyperventilation
 Recommendations BTF 2007
– Rec A:
• There are insufficient data to support a Level I
recommendations for this topic
– Rec B:
• Prophylactic hyperventilation (PaCO2 ≤ 25 mmHg) is
not recommended
– Rec C:
• Hyperventilation should be avoided during the first
24 h after injury when CBF is often critically reduced
• If hyperventilation is used, SjO2 or PbrO2
measurements are recommended to monitor oxygen
delivery
Steroids

 Recommendations BTF 2007

• A:
– the use of steroids is not recommended for
improving outcome in patients with moderate
and severe TBI

– High-dose methylprednisolone is associated with

increase mortality and is contraindicated
Thank you for your attention!
THE END