The document provides information on traumatic brain injury (TBI): - TBI is defined as an insult to the brain from an external force, which can lead to temporary or permanent impairment. It affects over 1.7 million people annually in the US. - Severity is classified using the Glasgow Coma Scale. More severe injuries have higher mortality rates. Predictors of poor outcome include lower GCS, age over 60, abnormal CT findings, and hypotension. - Treatment aims to prevent secondary injury from hypotension, hypoxia, increased ICP, and includes monitoring vital signs, ICP, CPP, and providing interventions like osmotherapy, surgery, and medications to control ICP and maintain

1. Traumatic Brain Injury
Dr.ZIKRULLAH

2. TBI
“Traumatic brain injury is a non degenerative, non
congenital insult to the brain from an external
mechanical force, possibly leading to permanent or
temporary impairment of cognitive, physical, and
psychosocial functions, with an associated
diminished or altered state of consciousness”

3. TBI - Epidemiology
• contributing factor to 30.5% of all injury-related
deaths in the US
• 1.7 million people affected annually
• Of these, 275,000 are hospitalized and 52,000 die
• accounts for 15% of deaths between the ages of 15-
45 years
• Male/female ratio is 2.5:1
Severe traumatic brain injury. http://www.cdc.gov/traumaticbraininjury/severe.html
www.braintrauma.org/pdf/protected/prognosis_guidelines

4. Overview
Injury GCS Death
on arrival
Minor 15 <1%
Mild 13/14 <5%
Moderate 9-12 <10%
Severe 3-8 >35%
Introduced by Teasdale and Jennett in 1974(GCS)
Teasdale GM, J Neurol Neurosurg Psych 1995;58:526-539.

5. • Raised ICP – uncal herniation – Compresses III N – decreases
parasympathetic tone to constrictor muscles and leads to
dilated sluggish pupils
• B/l dilated and fixed – direct brain stem injury , also raised ICP
• Hypoxemia, hypotension and hypothermia to be corrected
first

6. Consequences
• 85% of patients disabled at 1 year
• Only 15% return to work at 5 years
• 50% mild head injuries have moderate to
severe disability at 1 year
• Only 45% of mild head injuries return to full
functional activity

7. BTF
 Challenge is to reduce mortality and improve outcome
 1996- the Brain Trauma Foundation guidelines were
published
 updated in 2000 and 2007

8. Predictors of poor outcome
• Lower admission GCS
• Age >60 years
• Absence of bilateral pupillary response
• presence of hypotension at any point during
critical illness period
• presence of pathology on initial CT scan
– SAH
– compressed or absent basal cisterns,
– midline shift of greater than 0.5mm
– mass effect
www.braintrauma.org/pdf/protected/prognosis_guidelines

9. Pathophysiology of Head Injury
• Primary injury
• Secondary injury

10. General Injury Types
• Subdural
• Epidural
• Intracerebral
• Diffuse Axonal Injury
• Herniation

11. Herniation Syndromes
• Cerebellotonsillar Herniation - Through
Foramen Magnum
• Uncal Herniation -Transtentorial
• Subfalcine Herniatio- Unilateral herniation
under Falx Cerebri

12. Secondary Injury
• In the past two decades, medical research has
demonstrated that all brain damage does not
occur at the moment of impact, but evolves over
the ensuing hours and days. This is referred to as
secondary injury.
• The injured brain is extremely vulnerable to
hypotension, hypoxia, and increased intracranial
pressure which are causes of secondary injury.

13. Physiological Insults
• The following significantly impact on adversely on
outcome:
– Hypotension
– Hypoxia
– Pyrexia
– Intracranial hypertension
– Cerebral perfusion pressure

14. Aims of Treatment
• General intensive care
• Specific neuro-intensive care
• Surgical management
– Removal of haematoma
– Decompressive craniectomy

15. Significant Reductions in Mortality
and Morbidity
• Rapid transport to a trauma care facility
• Prompt resuscitation
• Prompt evacuation of significant intracranial
hematomas
• ICP monitoring and treatment

16. • 1643 trauma patients treated at seven trauma
centers with differing annual volumes of trauma
patients
• Patients taken to a low volume trauma center had
a 30% greater chance of dying.
J. Trauma 30: 1066-1076, 1990
TRAUMA CENTER

17. recent studies focusing on functional outcomes
– early intubation
– maintenance of normocapnia
– advanced neurocritical care
– neurosurgical intervention
Bernard SA, Nguyen V, Cameron P, et al. Prehospital rapid sequence intubation
improves functional outcome for patients with severe traumatic brain injury: a randomized
controlled trial. Ann Surg 2010; 252:959–965
Curley G, Kavanagh BP, Laffey JG. Hypocapnia and the injured brain: more
harm than benefit. Crit Care Med 2010; 38:1348–1359.

18. GLAGOW OUTCOME SCALE

20. Resuscitation of Blood Pressure
& Oxygenation
• Hypotension (SBP < 90 mm Hg) or hypoxia
( PaO2 < 60 mm Hg) must be avoided, if possible, or
corrected immediately.
Level II
• Blood pressure should be monitored and
hypotension (systolic blood pressure 90 mm Hg)
avoided.
Level III
• Oxygenation should be monitored and hypoxia
(PaO2 60 mm Hg or O2 saturation 90%) avoided

21. Initial Management
• The first priority for the head injured patient is
complete and rapid physiologic resuscitation.
No specific treatment should be directed at
intracranial hypertension in the absence of signs of
transtentorial herniation or progressive neurologic
deterioration not attributable to extracranial
explanations

22. Monitoring
• General
– Invasive arterial
pressures
– GCS and pupils
– Arterial blood gases
– Temperature
– Blood sugar
– Endtidal Co2
• Specific
– Intracranial pressure
– Transcranial doppler
– Jugular saturation
– Brain oximetry
– Microdialysis
– Imaging

23. • 207 severely head injured patients who had ICP
monitoring and head CT scans
• Patients with abnormal head CT had a 53%-63% chance of
ICP > 20 mm Hg
• Risk of intracranial hypertension (with normal CT)
increased to 60% if two or more of the following were
noted:
– 1) Age over 40 years
– 2) SBP < 90 mm Hg
– 3) motor posturing
J. Neurosurg 56: 650-659, 1982

24. Which patients need ICP
monitoring??
GCS 3–8 and abnormal CT scan
GCS 3–8 with normal CT and two or more of
the following:
Age > 40 years.
Motor posturing
Systolic blood pressure (SBP) <90 mmHg
GCS 9–15 and CT scan
Mass lesion (extra-axial > 1 cm thick
temporal contusion, intracranial
hemorrhage, or ICH, > 3cm)
Effaced cisterns.
Shift > 5 mm.
Following craniotomy
Neurological examination cannot be followed
(i.e., requires another surgical procedure,
sedation).
Neurocrit Care (2012) 17:S112–S121

25. Normal ICP
Waveform
The normal ICP waveform
contains three phases:
•P1 (percussion wave)
from arterial pulsations
•P2 (rebound wave)
reflects intracranial
compliance
•P3 (dichrotic wave)
represents venous
pulsations
In reduced brain compliance the Dicrotic and Tidal waves
augment exceeding the percussion waves

26. Device / method Risk / benefit
1. Intraventricular catheter Adv- drainage of CSF to reduce ICP
DisAdv- infection/ ventricular compression
leads to inaccuracy
2. subdural/ subarachnoid bolts
( Philadelphia, Leeds, Richmond bolts)
Occlusion of port in device leads to
inaccuracy
3. Fiberoptic cath ( Camino labs) Improved fidelity & longevity
Can be placed Intraparenchymal/
intraventricular/ subdural
Used to drain CSF
Accuracy maintained even with fully
collapsed ventricles
Single cath can be used as long as needed

27. ICP Monitoring Technology
Level II
• ICP should be monitored in all salvageable
patients with a severe TBI and an abnormal CT
scan(hematomas, contusions, swelling,
herniation, or compressed basal cisterns.)
Level III
• ICP monitoring is indicated in patients with severe
TBI with a normal CT scan if two or more of the
following features are noted at admission: age
over 40 years, unilateral or bilateral motor
posturing, or systolic blood pressure (BP) < 90 mm
Hg.
BRAIN TRAUMA FOUNDATION

28. • In the current state of technology, the ventricular catheter
connected to an external strain gauge is the most accurate, low
cost, and reliable method of monitoring ICP. It also allows
therapeutic CSF drainage. It also can be recalibrated in situ
• The optimal ICP monitoring device is one that is accurate, reliable,
cost effective, and causes minimal patient morbidity.
• Parenchymal ICP monitors cannot be recalibrated during
monitoring
• Subarachnoid, subdural, and epidural monitors (fluid coupled or
pneumatic) are less accurate
• ICP transduction via fiberoptic or strain gauge devices placed in
ventricular catheters provide similar benefits but at a higher cost.
• Micro strain gauge or fiberoptic devices are calibrated prior to
intracranial insertion and cannot be recalibrated once inserted,
without an associated ventricular catheter.

29. ICP monitoring
• ICP < 20 mmHg
• No evidence directly in favor of ICP monitoring
– but:
severe TBI have high ICP
Poor outcome with intracranial hypertension
Better outcome with protocols for treatment of ICP
Better outcome with succesful ICP lowering therapies
J Neurosurg 56:650-659, 1982
Neurocrit Care (2013) 18:131–142

30. ICP Treatment Threshold
Guideline
• ICP treatment should be initiated at an upper
threshold of 20 - 25 mm Hg.(Level II)
• A combination of ICP values, and clinical and
brain CT findings, should be used to determine
the need for treatment.(Level III)
BRAIN TRAUMA FOUNDATION

32. Cerebral Perfusion Pressure
CPP = MAP - ICP
• Avoid aggressive attempts to maintain CPP >70mmHg
• Avoid CPP of < 50mmHg
Increase MAP: - -volume expansion
-vasoconstriction
-inotropes
Decrease ICP: - -surgery
-drain CSF
-osmotherapy
-decrease metabolism
BRAIN TRAUMA FOUNDATION

33. Level II
• Aggressive attempts to maintain CPP above 70 mm Hg
with fluids and pressors should be avoided because of
the risk of ARDS.
Level III
• CPP of <50 mm Hg should be avoided.
• The CPP value to target lies within the range of 50–70
mm Hg. Patients with intact pressure autoregulation
tolerate higher CPP values.
• Ancillary monitoring of cerebral parameters that
include blood flow, oxygenation, or metabolism
facilitates CPP management.

34. Robertson et al
Crit Care Med 1999;27:2086-2095
• RCT 189 adults with severe TBI
• CPP vs ICP targeted management
– CPP group: CPP > 70mmHg
– ICP group: ICP< 20 mmHg ;CPP >50mmHg
• 6 month outcome
– No difference in outcome
– Five time increase in systemic complications(ARDS) in CPP group(p
0.0007)

35. Optimal CPP
Brain Trauma Foundation, J Neurotrauma 2003,2007
CPP < 70 mmHg
CPP 60 - 70 mmHg
Avoid CPP < 50 mmHg
Intact Autoregulation:
CPP > 70 mmHg
Robertson C, Crit Care Med 1999Robertson et al.,
Contant et al. J Neurosurg 2001 (n=189)
Balestreri et al. Neurocrit Care 2006 (n=429)

36. Raised CPP may help ICP when autoregulation is intact

37. Defective autoregulation

38. Management of CPP
• Traditional ICP approach
• Rosner et al. approach is based on vasodilatory
cascade
• Lund therapy emphasizes reduction in
microvascular pressures to minimize brain
edema formation
Rosner et al; J Neurosurg 1995; 83:949–62

39. Rosner view of cerebral blood flow
assumes intact autoregulation

40. Claudia S. Robertson Anesthesiology 2001; 95:1513–17

41. Claudia S. Robertson Anesthesiology 2001; 95:1513–17
The Lund Protocol
Brain Volume Regulation With Preserved Microcirculation
• Based on Physiological Principles : volume targeted
approach
• Aim to decrease cranial fluid volume
• Maintain cerebral flow

42. Lund Protocol
• Focuses on prevention and reduction of cerebral oedema
• Accepts CPP as low as 50 mmHg
• Lowers MAP with clonidine and b-blocker
• Decreases CBV by reducing hydrostatic pressure with
dihydroergotamine and thiopentone
• Increases plasma oncotic pressure to normal with
albumin, diuretics and blood products.
Claudia S. Robertson
Anesthesiology 2001; 95:1513–17

43. None of these approaches have been demonstrated to improve outcome
after TBI over the traditional ICP management approach
Rosner et al Lund therapy
Claudia S. Robertson
Anesthesiology 2001; 95:1513–17
robertson et al
Crit Care Med 1999;27:2086-2095

44. The current advice is that a target CPP of 60–70 mm
Hg is better, rather than a rigorous attempt to keep
the value above 70. There is some evidence that
overly aggressive attempts to elevate CPP, usually
through elevation of MAP, may result in potential
harm to the patient
Neurocrit Care (2012) 17:S112–S121

45. Brain Oxygen Monitoring and
Thresholds
Level III
• Jugular venous saturation (<50%) or brain tissue
oxygen tension (<15 mm Hg) are treatment thresholds.
 CBF directly (thermal diffusion probes, trans-cranial
Doppler)
 Adequate delivery of oxygen (jugular venous
saturation monitors, brain tissue oxygen monitors,
near-infrared spectroscopy),
 To assess the metabolic state of the brain (cerebral
microdialysis)

46. HYPEROSMOLAR THERAPY

47. • Currently, osmotic therapy is routinely used in a
wide range of acute conditions. Guidelines
recommend its use in head injury, ischemic stroke
and intracerebral hemorrhage
• no appropriately designed and powered studies
have prospectively addressed the impact of
osmotic therapy on outcome
New trends in hyperosmolar therapy?
Curr Opin Crit Care 2013, 19:77–82

48. • One effect may be an immediate plasma expanding
effect, which reduces the hematocrit, increases the
deformability of erythrocytes, and thereby reduces
blood viscosity, increases CBF, and increases
cerebral oxygen delivery.
• These rheological effects may explain why mannitol
reduces ICP within a few minutes of its
administration, and why its effect on ICP is most
marked in patients with low CPP (<70).

49. Mannitol
 Mannitol(0.5 - 1.5 gm/kg) is effective for control of
raised ICP after severe head injury(L II)
 The indications for the use of mannitol prior to ICP
monitoring are signs of transtentorial herniation or
progressive neurological deterioration not
attributable to systemic pathology.
 However, hypovolemia should be avoided by
fluid replacement
Brain Trauma Foundation, J Neurotrauma 2007

50. Mannitol
 sugar alcohol (C6H14O6)
 excreted unchanged in the urine
 Reduces blood viscosity
 Enhanced flow and cerebral oxygen delivery
 subsequent cerebral vasoconstriction reduce CBV, ICP,
and increase CPP
 Slow osmotic effect over 15-30 min
 Movement of water from the brain to the systemic
circulation. Effect up to 6 h
 May cause hypotension (osmotic diuresis)
 Rebound effect
J Neurosurg. 2008;108:80–7
J Neurotrauma. 2008;25:291–8.

51. Mannitol
• Rebound effect
• Intracellular accumulation of organic and idiogenic osmoles
• The net effect is restoration of cell size with maintenance of
the hyperosmolar state
• Iatrogenic brain edema may occur if a hyperosmolar state is
reversed too rapidly
Neurocrit Care (2013) 18:131–142

52. Mannitol
• Adverse effects
– Renal failure
– Hyponatremia
– hypochloremia
– hyperkalemia
– acidosis
– rebound ICP increases

53. Mannitol
• no evidence to support a S osm (320mos/l) threshold strategy for
guiding mannitol therapy
• osmolar gap (OG)
its elevation correlates well with accumulation
of serum mannitol
An OG threshold of 55 mOsm/ kg has been
suggested for monitoring therapy
Wakai A, Roberts I, Schierhout G. Mannitol for acute traumatic
brain injury. Cochrane Database Syst Rev 2007
J Am Soc Nephrol. 1997;8:1028–33

54. Hypertonic Saline
• 1.5% - 23.4%
• 3% NS
• 513 mmol/l Na+
• Osmolality 1027 mOsm/l
• Osmotic action in the brain
• advantage in hypovolemia
– Restores intravascular volume
– Increase MAP and CPP

55. Hypertonic Saline
• Neurotrauma guidelines task force found
insufficient evidence to support the preferential use
of HTS
• This was primarily due to a paucity of RCTs and to
patient heterogeneity among retrospective studies
• Evidence suggests that HTS may be more favorable
than mannitol for elevated ICP, with a greater and
more durable effect.
Crit Care Med. 2003; 31(6):1683–7
Mortazavi MM, Romeo AK, J Neurosurg. 2011;
Kamel H, Navi BB Crit Care Med. 2011;39(3):554–9.

56. MANNITOL VS. HYPERTONIC SALINE
• available data are limited by low patient
numbers, limited RCTs, and inconsistent methods
among studies
Class I evidence for this therapy is sparse and most evidence is
derived from either retrospective analyses (Class III) or from case
series (Class IV)

57. MANNITOL VS. HYPERTONIC SALINE
Sakellaridis N, Pavlou E, Karatzas S, et al.. J
Neurosurg 2011; 114:545–548
• prospective comparison between mannitol and
HTS
• equi-osmolar doses(2 ml/kg of 20% mannitol or
0.42 ml/kg of 15% saline)
• In 199 events occurring in 29 patients the mean
decrease in ICP and duration of effect with
mannitol and HTS were similar (change in ICP
7.96mmHg vs. 8.43mmHg; P = 0.586; duration 3h
33 min vs. 4h 17 min; P = 0.40)

58. MANNITOL VS. HYPERTONIC SALINE
Kamel H, Navi BB, Nakagawa K, et al. Crit Care Med
2011; 39:554–559
• a meta-analysis
• 5 trials comprising 112 patients with 184 episodes of
elevated ICP
• RR of ICP control favored HTS[1.16; 95% (CI) 1.00–
1.33], and the difference in ICP was only 2.0mmHg -
questionable clinical significance
authors conclusion
• HTS is more effective than mannitol for the treatment
of elevated ICP and suggest that hypertonic saline
may be superior to the current standard of care

59. MANNITOL VS. HYPERTONIC SALINE
Mortazavi MM, Romeo AK, Deep A, et al. J
Neurosurg 2012; 116:210–221-
• literature review and meta-analysis
• 36 articles selected
• Data suggested that hypertonic saline was more
effective than mannitol in reducing episodes of
elevated ICP
• Limitation: study by Sakellaridis et al was not
included in analysis

60. PROPHYLACTIC ANTIBIOTICS
• Not recommended
• No role for routine ICP catheter exchange
– Minimal manipulation
• Early vs late trache – no change in mortality or
pneumonia rate
– early trache decreases ventilator days
Brain Trauma Foundation, J Neurotrauma 2007
Holloway et al 1996
Bouderka et al 2004

61. Hyperventilation
Level I
• In the absence of increased ICP, chronic prolonged hyperventilation
therapy (PaCO2 of 25 mm Hg or less) should be avoided after severe TBI
Level 2
• The use of prophylactic hyperventilation (PaCO2 < 35 mm Hg) therapy
during the first 24 hours after severe TBI should be avoided because it can
compromise cerebral perfusion during a time when cerebral blood flow
(CBF) is reduced.
Brain Trauma Foundation, J Neurotrauma 2007

62. DVT prophylaxis
( Level III )
• Graduated compression stockings or intermittent
pneumatic compression (IPC) stockings are recommended,
unless lower extremity injuries prevent their use.
• Low molecular weight heparin (LMWH) or low dose
unfractionated heparin should be used in combination
with mechanical prophylaxis.
• Increased risk for expansion of intracranial hemorrhage.
• Insufficient evidence to support recommendations
regarding the preferred agent, dose, or timing of
pharmacologic prophylaxis for deep vein thrombosis
(DVT).

63. Anaesthetics, analgeics and sedatives
High-dose barbiturate therapy may be considered in
hemodynamically stable salvagable severe head injury
patients with intracranial hypertension refractory to
maximal medical and surgical ICP lowering therapy
(Level II)
Both cerebral protective and ICP-lowering effects have
been attributed to barbiturates: alterations in vascular
tone and resistance, suppression of metabolism,
inhibition of free radical-mediated lipid peroxidation
and inhibition of excitotoxicity.
Brain Trauma Foundation, J Neurotrauma 2007

64. • A prospective trial of 73 patients with severe head injury and
medically refractory intracranial hypertension, randomized to receive
either a regimen including high-dose pentobarbital or similar regimen
without pentobarbital.
• The chance of survival for those patients whose ICP decreased(ICP <
20 mm Hg) with barbiturate treatment was 92% compared to 17%
when it did not.
J. Neurosurg 69:15-23, 1988

65. High dose barbiturates
• Sedation/Induced Coma - EEG burst suppression
– Prophylactically not recommended
– Refractory elevated ICP after med management: YES
– Criteria:
• Refractory intracranial hypertension
• Na 145-155 (but < 160), Osm 320-330
• Repeat Head CT without surgically treatable lesion
• Neurosurgeon recommends non surgical treatment
Jiang, Neursurg, 2000

66. Pentobarbital Coma Protocol
• 10mg/kg bolus over 30 minutes
• 5mg/kg/hr continuous infusion x 3 hours
• Then 1mg/kg/hr
• Titrate based on EEG burst suppression (2-5/min)
• Continue for at least 72 hours, then wean to keep ICP<20
J. Neurosurg 69:15-23, 1988

67. Steroids
Level 1
• The use of steroids is not recommended for
improving outcome or reducing intracranial
pressure in patients with severe head injury.
Brain Trauma Foundation, J Neurotrauma 2007

68. • Prospective randomized trial in 300 patients
receiving dexamethasone (total IV dose within
51 hours of injury = 2.3 grams IV) versus placebo.
• No difference in outcome examined serially within
one year after treatment.
Zentralbl Neurochir 55:135-143, 1994

69. Antiseizure Prophylaxis
Level II
• Prophylactic use of phenytoin, carbamazepine, phenobarbital or valproate
is not recommended for preventing late post-traumatic seizures.
• Anticonvulsants are indicated to decrease the incidence of early PTS
(within 7 days of injury).
Risk factors include the following:
• GCS < 10
• Cortical contusion
• Depressed skull fracture
• Subdural hematoma
• Epidural hematoma
• Intracerebral hematoma
• Penetrating head wound
• Seizure within 24 h of injury
Brain Trauma Foundation, J Neurotrauma 2007

70. Nutrition
• Replacement of 140% of Resting Metabolic
Expenditure in non-paralyzed patients and
100% Resting Metabolic Expenditure in
paralyzed patients using enteral or parenteral
formulas containing at least 15% of calories as
protein by the seventh day after injury.
(Level II)
Brain Trauma Foundation, J Neurotrauma 2007

71. Is hyperglycemia detrimental?
• Hyperglycemia is associated with high brain lactate levels and
possibly greater cerebral cellular injury, particularly in the
early phases of brain injury
– Recommendation: Avoid hyperglycemia, particularly
during the early stages of brain injury. Consider the use of
intravenous solutions that do not contain dextrose for
early fluid and electrolyte management.
Chopp et al., (1988). Stroke, 19.
Lanier et al., (1987). Anesthesiology, 66.
Ljunggren et al. (1974). Brain Research, 77.
Myers et al., (1976). Journal of Neuropathology and Experiemental
Neurology, 35.
Smith et al. (1986). Journal of Cerebral Blood Flow and Metabolism, 6.
Natale et al. (1990). Resuscitation, 19.

72. PROPHYLACTIC HYPOTHERMIA
• Hypothermia associated with fewer seizures but no
outcome difference (Level III)
• Hypothermia is associated with higher Pulmonary infection
(60.5% vs 32.6%) and thrombocytopenia (62.8% vs 39.5%)
compared to normothermia.
• Prophylactic hypothermia is associated with significantly
higher Glasgow Outcome Scale (GOS) scores when
compared to scores for normothermic controls.
Brain Trauma Foundation, J Neurotrauma 2007

73. National Acute Brain Injury Study
• RCT, MULTICENTRIC
• 52 in the hypothermia
group and 45 in the
normothermia group
• This trial did not confirm
the utility of
hypothermia as a
primary neuroprotective
strategy in patients with
severe traumatic brain
injury.
Lancet Neurol 2011; 10: 131–39

74. Decompressive Craniectomy
• Indications: elevated ICP
refractory to medical
management
•Aims to decrease ICP / increase
perfusion, by opening a closed
system, allowing room for
swelling /expansion
Conclusion : decrease ICP, decreased LOS
mortality and unfavourable outcomes were not reduced.
DECRA Trial Investigators
N Engl J Med 2011;364:1493-502.

80. Thank you all

81. following craniectomy for traumatic
brain injury

82. • Prolonged hyperventilation worsens outcome and
significantly reduces cerebral blood flow based on
jugular venous oxygen saturation monitoring.
• Prophylactic paralysis increases pneumonia and
ICU stay.
• Barbiturates have a significant risk of hypotension
and prophylactic administration is not
recommended.
• Mannitol has a variable ICP response in both
extent of ICP decrease and duration

83. Conclusions
• Avoid a head injury
• Pay attention to rapid resuscitation avoiding
hypotension and hypoxia
• Early transfer to specialist centre