Intracranial Pressure and Cerebral Edema Neuro-ICU Guide
1. Intracranial Pressure and
Cerebral Edema Neuro-ICU
2009
PJ Papadakos MD FCCM
Director CCM
Professor Anesthesiology, Surgery
and Neurosurgery
Rochester NY USA
3. HOW DO PATIENTS PRESENT ?HOW DO PATIENTS PRESENT ?
• Obvious--motor vehicle accident, car vsObvious--motor vehicle accident, car vs
pedestrian, fall from height, etcpedestrian, fall from height, etc
• Less obvious--sports injuries (football), delayedLess obvious--sports injuries (football), delayed
deterioration (epidural)deterioration (epidural)
• Hidden--shaken baby syndrome, older childHidden--shaken baby syndrome, older child
maltreatmentmaltreatment
• Inter cranial HemorrhageInter cranial Hemorrhage
• StrokeStroke
4.
5. CAVEATS IN BRAIN INJURYCAVEATS IN BRAIN INJURY
• Neurologic examination - the mostNeurologic examination - the most
important information you haveimportant information you have
• Accurate history is often unavailable orAccurate history is often unavailable or
inaccurateinaccurate
• Potential for associated injuries or illnessPotential for associated injuries or illness
(cardiovascular, respiratory,(cardiovascular, respiratory,
cervical spine)cervical spine)
6. CEREBRAL RESUSCITATIONCEREBRAL RESUSCITATION
• Primary survey - airway, breathing, andPrimary survey - airway, breathing, and
circulationcirculation
• Neurologic evaluationNeurologic evaluation
• Secondary survey - “head to toe”Secondary survey - “head to toe”
• Neuroradiologic evaluationNeuroradiologic evaluation
• Ongoing evaluation and transportOngoing evaluation and transport
8. MECHANISMS OF 2MECHANISMS OF 2ndnd
INJURYINJURY
• GlobalGlobal
– Hypoxia and ischemia of brainHypoxia and ischemia of brain
– Decreased cerebral blood flow due toDecreased cerebral blood flow due to
increased intracranial pressureincreased intracranial pressure
• LocalLocal
– impairment of cerebral blood flow or extraimpairment of cerebral blood flow or extra
cellular milieu due to the presence of injuredcellular milieu due to the presence of injured
brainbrain
9. PATHOPHYSIOLOGYPATHOPHYSIOLOGY
• Primary damage – the only treatment is byPrimary damage – the only treatment is by
preventionprevention..
• Secondary damage – multifactorial andSecondary damage – multifactorial and
time dependent.time dependent.
12. HoursHours Days Weeks / Months
Weeks/Month
s
Dynamic Changes Following Brain InjuryDynamic Changes Following Brain Injury
Ca , Na+
Glut, ROS
8hrs 7
Necrosis Apoptosis
Repair
Remodeling
Plasticity
Functional
Recovery
I
N
J
U
R
Y
142
Inflammation
Barone &Feuerstein JCBF, 1999
14. The Lund Concept
• January 1989, Lund
University Hospital
Department of
Neurosurgery
• Protocol aimed at non-
surgical reduction of ICP
• Bedside measurements of
CBF and vasoreactivity
identified subgroup of
patients with severe TBI,
intractable ICP, and 100%
mortality
15. Lund concept
• Volume-targeted therapy
• Reduction of capillary
hydrostatic pressure
• Maintenance of colloid
osmotic pressure and
control of fluid balance
• Reduction of cerebral
blood volume
• Controlled ICP
17. The Lund Concept
• Avoid hyperglycemia and hyperthemia.
• Avoid hypovolemia and stress response: increased
baroreceptor reflex and cathacholamine release
• Avoid hyperosmotic therapy: transient effects with
adverse rebound and renal effects
• Avoid vasopressors: vasoconstriction increases
BP and CPP but may compromise brain
microcirculatory perfusion (esp. pericontusional)
and other organ system perfusion (ARDS)
18. The Lund Concept
• Stress reduction: sedatives midazolam and
thiopental (0.5-3.0 mg/kg/h) combined with alpha-
2 agonism and beta-1 blockade. Avoid propofol.
• Normovolemia: by normalizing plasma oncotic
pressure via RBC infusion to normal S-Hb (125-
140 g/L) and albumin transfusion (20-25%)
• Normalize BP: Clonidine (0.3-1.0 ug/kg X 4-6)
and Metoprolol (0.04-0.08 mg/kg). Refrain from
using vasopressors. Dihydroergotamine induce
venous vasoconstriction with great volume in
venous side. No fixed limits for CPP
20. BRAIN: CEREBRAL EDEMA-VASOGENICBRAIN: CEREBRAL EDEMA-VASOGENIC
(Caused mainly by activation of NMDA receptors by glutamate)(Caused mainly by activation of NMDA receptors by glutamate)
21. BRAIN: CEREBRAL EDEMA-CYTOTOXICBRAIN: CEREBRAL EDEMA-CYTOTOXIC
(Caused mainly by activation of cytokines, ROS and other(Caused mainly by activation of cytokines, ROS and other
pro-inflammatory mediators)pro-inflammatory mediators)
22. o The brain has the abilityThe brain has the ability
to control its bloodto control its blood
supply to match itssupply to match its
metabolic requirementsmetabolic requirements
o Chemical or metabolicChemical or metabolic
byproducts of cerebralbyproducts of cerebral
metabolism can altermetabolism can alter
blood vessel caliber andblood vessel caliber and
behaviorbehavior
BLOOD: CEREBRAL BLOOD FLOWBLOOD: CEREBRAL BLOOD FLOW
24. CSF: CEREBROSPINAL FLUIDCSF: CEREBROSPINAL FLUID
• 10% of intracranial volume10% of intracranial volume
• Initial displacement of CSF from ventriclesInitial displacement of CSF from ventricles
• Ventriculostomy to drain CSFVentriculostomy to drain CSF
25. Intracranial ComplianceIntracranial Compliance
• Calvarium is composed of three fluidCalvarium is composed of three fluid
compartments: Cerebral Blood Volume,compartments: Cerebral Blood Volume,
CSF, and cerebral parenchymaCSF, and cerebral parenchyma
26.
27. GUIDELINES – GENERAL ASPECTSGUIDELINES – GENERAL ASPECTS
• Standards:Standards: accepted principles of patientaccepted principles of patient
management that reflect a high degree ofmanagement that reflect a high degree of
clinical certaintyclinical certainty
• Guidelines:Guidelines: strategies that reflect moderatestrategies that reflect moderate
clinical certaintyclinical certainty
• Options:Options: unclear clinical certaintyunclear clinical certainty
30. PREHOSPITAL AIRWAY MANAGEMENTPREHOSPITAL AIRWAY MANAGEMENT
• Hypoxia must be avoided, and correctHypoxia must be avoided, and correct
immediatelyimmediately . 13%-27%. 13%-27% ↓↓↓↓OO22
• Supplemental oxygen should be administeredSupplemental oxygen should be administered
• No advantage of ETI (ET intubation) Vs. BVMNo advantage of ETI (ET intubation) Vs. BVM
(Bag / valve / mask) ventilation for the(Bag / valve / mask) ventilation for the pre-pre-
hospitalhospital airway in pediatric TBIairway in pediatric TBI
420 TBI; 115 BVM; 177 ETI420 TBI; 115 BVM; 177 ETIno change (no change (Gausche,Gausche,
JAMA 2000JAMA 2000))
• TBI + ETITBI + ETI ETCOETCO22
31. RESUSCITATION OF BP AND ORESUSCITATION OF BP AND O22 AND PREHOSPITAL BRAIN-AND PREHOSPITAL BRAIN-
SPECIFIC TX’S FOR SPTBI PATIENTSSPECIFIC TX’S FOR SPTBI PATIENTS
• Hypotension should be identified and correctedHypotension should be identified and corrected
as rapidly as possible with fluid resuscitation.as rapidly as possible with fluid resuscitation.
(G)(G)
• Hypotension on arrival to ERHypotension on arrival to ER (Pigula, J Ped Surg 1993)(Pigula, J Ped Surg 1993)
18% ER: mortality 61% Vs. 22%,18% ER: mortality 61% Vs. 22%, ↓↓BP+BP+↓↓OO22 ––
mortalitymortality 85% !85% !
• LevineLevine (Neurosurg 1992)(Neurosurg 1992): TBI 0-4y: TBI 0-4y ↓↓BP – 32% poorBP – 32% poor
outcome.outcome.
• LaurssenLaurssen (J Neurosurg 1988)(J Neurosurg 1988)::↑↑BPBP ↓↓EX; WhiteEX; White (CCM(CCM
2001)2001): syst BP > 135: syst BP > 135 X19 in survival !X19 in survival !
32. PREHOSPITAL TREATMENTSPREHOSPITAL TREATMENTS
• No evidence of efficacy: sedation, NMB,No evidence of efficacy: sedation, NMB,
Mannitol, saline 3%, hyperventilation.Mannitol, saline 3%, hyperventilation.
• The prophylactic administration ofThe prophylactic administration of
mannitol is not recommended.mannitol is not recommended.
• Mannitol may be considered for use inMannitol may be considered for use in
euvolemic patients who show signs ofeuvolemic patients who show signs of
cerebral herniation or acute neurologicalcerebral herniation or acute neurological
deterioration.deterioration.
33. PREHOSPITAL TREATMENTSPREHOSPITAL TREATMENTS
• Mild prophylactic hyperventilationMild prophylactic hyperventilation is notis not
recommendedrecommended..
• Hyperventilation may be considered inHyperventilation may be considered in
patients who show signs ofpatients who show signs of
– Imminent cerebral herniation orImminent cerebral herniation or
– acute neurological deteriorationacute neurological deterioration
• After correcting hypotension or hypoxemiaAfter correcting hypotension or hypoxemia
36. Imaging/ Diagnosis of Head Injury
• CT scan remains imaging
of choice
• Regional heterogeneity of
brain metabolism
• Need information on brain
function: CBF, perfusion
and metabolism in TBI
• Xenon-enhanced CT in
the ED setting
37. Need for Portable Imaging
• Transport risk of critical
trauma patients
• Portable CT with helical
scanning capability, low
radiation exposure,
wireless links to imaging
network, user-friendly,
ability to perform
perfusion studies.
39. MRI
• As Field Strength
increases (up to 7T) see
more abnormaities
• Diffusion tensor imaging
(DTI)
• Based on fractional
anisotropic movement of
water molecules
• Non-invasive
measurement of fiber
pathway structure
43. Coup-ContrecoupCoup-Contrecoup
• focal injuryfocal injury
consisting ofconsisting of
contusions andcontusions and
hematoma at thehematoma at the
site of the blow,site of the blow,
opposite side of theopposite side of the
brainbrain
51. INDICATIONS FOR ICP MONITORING IN PATIENTSINDICATIONS FOR ICP MONITORING IN PATIENTS
WITH SEVERE TBIWITH SEVERE TBI
• ↑↑ICPICP ≡≡↓↓Outcome; Aggressive TxOutcome; Aggressive Tx ≡≡↑↑OutcomeOutcome
• Intra-cranial pressure monitoring (ICP) isIntra-cranial pressure monitoring (ICP) is
appropriate in all patients with severe traumaticappropriate in all patients with severe traumatic
brain injury (TBI) (Glasgow Coma [GCS] scorebrain injury (TBI) (Glasgow Coma [GCS] score
≤≤8)8)
• The presence of open fontanels and/or suturesThe presence of open fontanels and/or sutures
in an infant with severe TBI does not precludein an infant with severe TBI does not preclude
the development of intracranial hypertension orthe development of intracranial hypertension or
negate the utility of ICP monitoring.negate the utility of ICP monitoring.
52. INTRACRANIAL PRESSURE MONITORINGINTRACRANIAL PRESSURE MONITORING
• STBI (GCSSTBI (GCS≤≤8) + Abnormal CT8) + Abnormal CT ≡≡ 53-63%53-63% ↑↑ICPICP
(adult data).(adult data).
• Intra-cranial pressure monitoring is not routinelyIntra-cranial pressure monitoring is not routinely
indicated in infants and children with mild orindicated in infants and children with mild or
moderate head injury.moderate head injury.
• However, a physician may choose to monitorHowever, a physician may choose to monitor
ICP in certain conscious patients withICP in certain conscious patients with
• traumatic mass lesions ortraumatic mass lesions or
– serial neurological examination is precluded byserial neurological examination is precluded by
sedation, neuromuscular blockade, or anesthesia.sedation, neuromuscular blockade, or anesthesia.
53. INTRACRANIAL PRESSURE MONITORINGINTRACRANIAL PRESSURE MONITORING
TECHNOLOGYTECHNOLOGY
• ICP monitoring: a ventricular catheter; externalICP monitoring: a ventricular catheter; external
strain gauge transducer (??); catheter tip pressurestrain gauge transducer (??); catheter tip pressure
transducer devicetransducer device All accurate & reliable (O)All accurate & reliable (O)
• Ventricular cath. device most accurate, reliable,Ventricular cath. device most accurate, reliable,
low cost +low cost + enables therapeutic (CSF) drainageenables therapeutic (CSF) drainage..
• No report of meningitisNo report of meningitis ⇔⇔ ICP monitoring.ICP monitoring.
Jensen: 7% +tip; positive > 7.5 daysJensen: 7% +tip; positive > 7.5 days
54. THRESHOLD FOR TREATMENT OF INTRA-THRESHOLD FOR TREATMENT OF INTRA-
CRANIAL HYPERTENSIONCRANIAL HYPERTENSION
• ICP>20-40mmHgICP>20-40mmHg ≡≡ Mort. 28%; ICP>40mmHgMort. 28%; ICP>40mmHg ≡≡ 100%100%
• Treatment for intracranial hypertension, defined as aTreatment for intracranial hypertension, defined as a
pathologic elevation in intracranial pressure (ICP), shouldpathologic elevation in intracranial pressure (ICP), should
begin at an ICPbegin at an ICP ≥≥20 mm Hg. (O)20 mm Hg. (O)
• Patients may herniate at ICP < 20-25mmHg.Patients may herniate at ICP < 20-25mmHg.
• Is there a lower ICP threshold for younger children ?Is there a lower ICP threshold for younger children ?
• Interpretation and treatment ofInterpretation and treatment of ↑↑ICP based on any ICPICP based on any ICP
threshold should be corroborated by frequentthreshold should be corroborated by frequent
– clinical examinationclinical examination
– monitoring of physiologic variables (CPP, Compliance)monitoring of physiologic variables (CPP, Compliance)
– cranial imaging.cranial imaging.
56. THE ROLE OF CSF DRAINAGETHE ROLE OF CSF DRAINAGE
• Cerebrospinal fluid (CSF) drainage canCerebrospinal fluid (CSF) drainage can
be considered as an option in thebe considered as an option in the
management of elevated ICP Drainage:management of elevated ICP Drainage:
VentriculostomyVentriculostomy ±± Lumber puncture.Lumber puncture.
57. Near-infrared spectroscopy
• Measures complex IV
cytocrome c
• Mito redox state
• Can detect changes in
PO2/ lactate-pyruvate
ratio
• Potential tool for
measuring cerebral
aerobic metabolism
58. EEG/ Bispectral Index Analysis
• Continuous EEG
monitoring shows that
20% of TBI patients
have seizures w/in 2
wks
• EEG Power spectrum
analysis to monitor
sedation and prevent
oversedation
59. Microdialysis
• Measures biochemical
changes in brain tissue
• Increased lactate, EAA,
glycerol
• Decreased glucose,
pyruvate
• Need to collect dialysate
q30 minutes for 5 days
(240 samples)
• Future role in target
delivery of agents
60. Brain Oxygen Tension Monitoring
• Direct measurement of
cerebral oxygen
metabolism
• Interpretation of
PbtO2 threshold 10-20
mmHg
• Placement in
uninjured versus
injured brain
63. Muizelaar JP et al: Mannitol
causes compensatory
cerebral vasoconstriction
and vasodilation in response
to blood viscosity changes. J
Neurosurg 59:822-828, 1983
64. • Mannitol (Mannitol (2 X Class III2 X Class III) Vs. Hypertonic Saline () Vs. Hypertonic Saline (3 X Class II;3 X Class II;
1 X Class III1 X Class III).).
• Mannitol is effective.Mannitol is effective.
• Euvolemia + Folly catheterEuvolemia + Folly catheter
• Accepted osmolarity: Mannitol < 320mOsm/L;Accepted osmolarity: Mannitol < 320mOsm/L;
Hyper NS < 360mOsm/LHyper NS < 360mOsm/L
• MannitolMannitol ↓↓blood viscosityblood viscosity ⇒⇒ ↓↓arteriolar diameterarteriolar diameter
andand osmotic effect.osmotic effect.
• Hyper NSHyper NS Osmolar grad; membrane pot.;Osmolar grad; membrane pot.;
cellular volume;cellular volume; ↑↑ANP;ANP; ↓↓Inflammation;Inflammation; ↑↑C.O.C.O.
USE OF HYPEROSMOLAR THERAPYUSE OF HYPEROSMOLAR THERAPY
65. HYPEROSMOLAR THERAPYHYPEROSMOLAR THERAPY
• Hypertonic saline is effective for control ofHypertonic saline is effective for control of
increased ICP after severe head injuryincreased ICP after severe head injury
• Effective doses: cont. infusion of 3% salineEffective doses: cont. infusion of 3% saline
0.1 - 1.0 ml/kg/h, a sliding scale.0.1 - 1.0 ml/kg/h, a sliding scale.
• Goal minimum dose maintain ICP <20Goal minimum dose maintain ICP <20
mmHg.mmHg.
• Mannitol bolus dose: 0.25g/Kg – 1g/Kg.Mannitol bolus dose: 0.25g/Kg – 1g/Kg.
66. Hypertonic saline
• Efficacy in concentrations of 3%-7.5%-
23.4% in lowering ICP
• Therapeutic action more effective (53.9%
vs 35%) and longer lasting than mannitol
• Attenuates microcirculatory disturbances
(prevent secondary cerebral small vessel
diameter increases and aggregation of
WBCs by 90%)
67. Hypertonic saline
• Clinical studies show decreases in mean
number and duration of intracranial
hypertensive episodes
• Vasoregulatory effects: prevents vasospasm
• Lowers rate of clinical failure
• Theoretical concerns of CPM and rapid
brain shrinkage/SDH
68. USE OF HYPERVENTILATION in theUSE OF HYPERVENTILATION in the
ACUTE MANAGEMENTACUTE MANAGEMENT
• Mild or prophylactic hyperventilation (pacoMild or prophylactic hyperventilation (paco22 <35<35
mm hg)mm hg) should be avoidedshould be avoided..
• Mild hyperventilation (pacoMild hyperventilation (paco22 30-35 mm hg) may30-35 mm hg) may
be considered for longer periods for intra-be considered for longer periods for intra-
cranial hypertension refractory tocranial hypertension refractory to
– Sedation and analgesiaSedation and analgesia
– Neuromuscular blockadeNeuromuscular blockade
– Cerebrospinal fluid drainageCerebrospinal fluid drainage
– hyperosmolar therapyhyperosmolar therapy
69. HYPERVENTILATIONHYPERVENTILATION
• Aggressive hyperventilation (PacoAggressive hyperventilation (Paco22 < 30 mm Hg)< 30 mm Hg)
may be considered as a second tier option in themay be considered as a second tier option in the
setting of refractory hypertension (O).setting of refractory hypertension (O).
• Cerebral blood flow (CBF), jugular venous oxygenCerebral blood flow (CBF), jugular venous oxygen
saturation, or brain tissue oxygen monitoring issaturation, or brain tissue oxygen monitoring is
suggested to help identify cerebral ischemia in thissuggested to help identify cerebral ischemia in this
setting.setting.
• Aggressive hyperventilation therapy titrated toAggressive hyperventilation therapy titrated to
clinical effect may be necessary for BRIEFclinical effect may be necessary for BRIEF
PERIODS in cases of cerebral herniation orPERIODS in cases of cerebral herniation or
acute neurologic deterioration.acute neurologic deterioration.
70. High dose barbiturate therapy
• For refractory intracranial hypertension
• Lower cerebral metabolic rate for O2 and
modulate vascular tone
• Membrane stabilization and reduced lipid
peroxidation
• Controversial evidence as to efficacy in
severe TBI
• Differential effects noted between
thiopental, methohexital and pentobarbital
71. THE USE of BARBITURATES in the CONTROL ofTHE USE of BARBITURATES in the CONTROL of
INTRA-CRANIAL HYPERTENSIONINTRA-CRANIAL HYPERTENSION
• High-dose barbiturate therapy may be consideredHigh-dose barbiturate therapy may be considered
in hemodynamically stable patients within hemodynamically stable patients with
salvageable severe head injurysalvageable severe head injury andand refractoryrefractory
intracranial hypertension.intracranial hypertension.
• If high-dose barbiturate therapy is used, thenIf high-dose barbiturate therapy is used, then
appropriate hemodynamic monitoring (CVP, Swan-appropriate hemodynamic monitoring (CVP, Swan-
Ganz, repeated ECHOs) and cardiovascularGanz, repeated ECHOs) and cardiovascular
support (Dopamine, Adrenaline) are essential.support (Dopamine, Adrenaline) are essential.
72. THE USE of BARBITURATES in the CONTROL ofTHE USE of BARBITURATES in the CONTROL of
INTRA-CRANIAL HYPERTENSIONINTRA-CRANIAL HYPERTENSION
• Gold standard – continuous EEG to achieveGold standard – continuous EEG to achieve
a state of burst suppression.a state of burst suppression.
• Serum barbiturate levels are NOT GOOD forSerum barbiturate levels are NOT GOOD for
monitoring that therapy.monitoring that therapy.
• Prophylactic therapy is not recommendedProphylactic therapy is not recommended
(side effects).(side effects).
73. Neuromuscular blockade
• For mechanically ventilated to prevent
cough reflex in initial 24-48 hours
• Muscle relaxants cross BBB and can
activate cerebral Ach receptors causing
autonomic dysfunction, weakness and
seizures
• Resistance due to receptor up-regulation
often present so need monitoring with
peripheral nerve stimulator
77. Brain Thermo-Pooling Phenomenon
• Brain thermo-pooling (elevation of brain tissue
temperature) with damage of blood-brain barrier
(BBB).
• Risk: Blood temperature higher than 38.C.,
systolic blood pressure lower than 90-100mmHg,
and cerebral perfusion pressure (CPP) lower than
70mmHg hinders washout of brain tissue
temperature by cerebral blood flow.
• Recorded brain tissue temperature of 40-44
degrees Celsius.
78. Temperature Control in TBI
• Systemic and cerebral
hyperthermia is
detrimental to outcome
• Up to 80% of TBI patients
in ICU setting with
reactive hyperthermia
• Monitoring of core
temperature, pyrexia
identified and treated
• In refractory cases
electrical surface cooling
blankets to prevent brain
hyperthermia
79. Temperature Control in TBI
• Surface cooling is
problematic: access,
time constraints,
imprecision
• Multi-trauma patients
with splinting
• Shivering increases
O2 consumption and
increases ICP
81. Alsius Cooling Catheter
• Saline-filled
Polyethylene balloon
catheter
• Combines cooling
capabilities with
central venous access
• Products may be used
with femoral,
subclavian or jugular
access
82. InnerCool Catheters
• Metallic coil heating
element
• Very Rapid rate of
cooling (6 degrees
Celsius per hour)
• FDA approval for
Neurosurgical ICU
and recovery
83. Radiant Cooling Catheter
• Triple-helical coil
design
• Expandable to 27 Fr in
IVC to increase heat
exchange
• 37 to 33 degrees
Celsius in less than 1
hour
86. Therapeutic Hypothermia
• Hypothermia neuroprotective in TBI
models by decreasing EAAs, augment
antioxidant activity and reduction of
inflammatory markers
• Randomized controlled trials have shown
conflicting results
• Clifton et al., showed possible outcome
benefit with mild hypothermia in patients
with GCS of 5-7
87. Therapeutic Hypothermia
• NABIS H1 (National Acute Brain Injury Study:
Hypothermia): 492 patients at 5 Centers
• Failed to show beneficial outcome
• Intercenter variability in treatment, delay in
reaching target core temp, inconsistent fluid
therapy
• Subgroup analysis showed beneficial effects in
patients age 16-45, normotensive, GCS>4 with
initial core body temp less than 35 degrees Celsius
and maintained core temperature
92. Calcium Channel blockersCalcium Channel blockers
• May be membrane protectiveMay be membrane protective
• Affect VasospasmAffect Vasospasm
93. Coronary/Cerebral StealCoronary/Cerebral Steal
The detrimental redistribution of blood
flow in patients with atherosclerotic
disease from underperfused areas toward
better perfused areas
Before Vasodilator
Stenosis
After Vasodilator
94. Dexabinol
• Cannabinoid and non-competitive NMDA-
receptor antagonist
• Safely decreases mean time of ICP
elevation above 25 mmHg and MAP <90
• Also acts as antioxidant and cytokine
inhibitor
• Phase III trials promising
100. DECOMPRESSIVE CRANIECTOMYDECOMPRESSIVE CRANIECTOMY
• Decompressive craniectomy appears to beDecompressive craniectomy appears to be lessless
effectiveeffective in patients who have experiencedin patients who have experienced
extensive secondary brain insultsextensive secondary brain insults
• Patients who experiencePatients who experience
– Secondary deterioration on the Glasgow coma scaleSecondary deterioration on the Glasgow coma scale
(GCS) and/or evolving cerebral herniation syndrome(GCS) and/or evolving cerebral herniation syndrome
within the first 48 hrs after injury may represent awithin the first 48 hrs after injury may represent a
favorable groupfavorable group
– Unimproved GCS of 3 may represent anUnimproved GCS of 3 may represent an unfavorableunfavorable
groupgroup
101. THE USE OF CORTICOSTEROIDS IN THETHE USE OF CORTICOSTEROIDS IN THE
TREATMENT TBITREATMENT TBI
• With the lack of sufficient evidence forWith the lack of sufficient evidence for
beneficial effect and the potential forbeneficial effect and the potential for
increased complications and suppressionincreased complications and suppression
of adrenal production of cortisol, the routineof adrenal production of cortisol, the routine
use of steroids is not recommendeduse of steroids is not recommended forfor
patients following severe traumatic brainpatients following severe traumatic brain
injury.injury.
102. NUTRITIONAL SUPPORTNUTRITIONAL SUPPORT
• Replace 130-160% of resting metabolismReplace 130-160% of resting metabolism
expenditure after TBI in patients. Weight-expenditure after TBI in patients. Weight-
specific resting metabolic expenditurespecific resting metabolic expenditure
guidelines can be found in Talbot's tables.guidelines can be found in Talbot's tables.
• Based on the adult guidelines, nutritionalBased on the adult guidelines, nutritional
support shouldsupport should
– begin by 72 hrsbegin by 72 hrs
– with full replacement by 7 days.with full replacement by 7 days.
103. THE ROLE of ANTI-SEIZURE PROPHYLAXISTHE ROLE of ANTI-SEIZURE PROPHYLAXIS
FOLLOWING STBIFOLLOWING STBI
• Prophylactic anti-seizure therapy may beProphylactic anti-seizure therapy may be
considered as a treatment option toconsidered as a treatment option to
prevent increased oxygen utilizationprevent increased oxygen utilization
