het craniocerebraal trauma en de anesthesist de anesthesist update 2013 dr. luc veeckman uz leuven...
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Het craniocerebraal trauma
en de anesthesist
Update 2013
Dr. Luc Veeckman
UZ Leuven
Impact van CCT (USA – 2010)
Oorzaken van CCT (USA - 2010)
Traumatisch hersenlijden
• Mild TBI : GCS 15-13
• Moderate TBI : GCS 12-9
• Severe TBI : GCS 8-3
Glasgow coma schaal
Ernstig craniocerebraal trauma
en de anesthesist
Update 2013
Ernstig craniocerebraal trauma
en de anesthesist
Standaard richtlijnen 2012
De standaard richtlijnen
De standaard richtlijnen
2007
Ernstig CCT - mechanismes
Cell death
Primary lesions
Neuronal trauma
Vascular trauma
(micro- and macro-haematomas)
Blunt trauma
Acceleration – deceleration
Rotation - shearing
Coup & contre-coup lesions
Secondary lesions
Hypotension < 90 mmHg
Hypoxia < 60 mmHg
Hyperglycemia > 180 mg/dl
Ernstig CCT - mechanismes
Primary lesions
Neuronal trauma
Vascular trauma
(micro- and macro-haematomas)
Blunt trauma
Acceleration – deceleration
Rotation - shearing
Coup & contre-coup lesions
Secondary lesions
Hypotension < 90 mmHg
Hypoxia < 60 mmHg
Hyperglycemia > 180 mg/dl
Cell death
Ernstig CCT - mechanismes
Primary lesions
Neuronal trauma
Vascular trauma
(micro- and macro-haematomas)
Blunt trauma
Acceleration – deceleration
Rotation - shearing
Coup & contre-coup lesions
Secondary lesions
Hypotension < 90 mmHg
Hypoxia < 60 mmHg
Hyperglycemia > 180 mg/dl
Cell death
Ernstig CCT - mechanismes
Primary lesions
Neuronal trauma
Vascular trauma
(micro- and macro-haematomas)
Blunt trauma
Acceleration – deceleration
Rotation - shearing
Coup & contre-coup lesions
Secondary lesions
Hypotension < 90 mmHg
Hypoxia < 60 mmHg
Hyperglycemia > 180 mg/dl
Cell death
Ernstig CCT - mechanismes
Cell death
Blunt trauma
Apoptotic pathway
Ischemia
Free radicals
Brain herniation
Inflammation
Necrosis pathway
Excitotoxicity Mitochondrial failure
Neuronal trauma
(Diffuse axonal lesions)
Increased ICP Brain edema
Vascular lesions
(haemorrhagic contusions – haematomas)
Perfusion defects
Ernstig CCT - monitoring
• Kliniek (G-LCS, pupil, …).
• Beeldvorming (MRI, CT, …).
• ICP- en CPP meting : gouden standaard.
• SjO2 en NIRS meting.
• PbtO2 meting.
• Processed EEG recording.
• Cerebrale microdialyse.
• Biochemie : S100β, NSE
• SSEP en MEP monitoring.
Ernstig CCT - behandeling
Pre-hospitaal management
In-hospitaal management
Post-kritische revalidatie
Ernstig CCT - prehospitaal
• Chesnut (1993) : SAP < 90 mmHg en
PaO2 < 60 mmHg.
• Salim (2009) : glycemie > 150 mg/dl
• Marion (1995) : no hypocapnia
Chesnut RM, Marshall SB, Piek J et al. – Acta Neurochir. Suppl (Wien) 1993 ; 59 : 121-5. Early and late
systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain
injury in the Traumatic Coma Data Bank.
Salim A, Hadjizacharia P, Duboise J, Brown C, Inaba K, Chan LS, Margulies D. Am.Surg. 2009 ; 75(1) :
25-29.
Marion DW, Firlik A, McLaughlin MR. - New Horiz. 1995 ; 3(3) : 439-47. Hyperventilation therapy for
severe traumatic brain injury.
Ernstig CCT – neuroprotectie
Behandeling Dieren Mensen
Barbituraten + 0 / -
Hypothermie ++ 0 / -
Erythropoietine ++ ?
Statines ++ ?
Cannabinoiden ++ 0
Steroiden ++ --
Lazaroiden +++ 0
Lidocaine ++ 0
Magnesium ++ 0
Ernstig CCT – opvang op URG
Ernstig CCT – opvang op Oka
• Data for the anesthetic management of CCT are scarce.
Ernstig CCT – opvang op Oka
• Specifieke richtlijnen zijn beperkt.
• Meestal wordt gewerkt met de pre-hospital
guidelines, met zonodig aanpassingen van
zodra ICP of PbtO2 meting beschikbaar is.
• Bij uitgesproken Cushing respons kan
management moeilijk zijn.
• Bij (neurogeen) ARDS kan management
moeilijk zijn.
• Bij CCT + majeur “perifeer” trauma kan
management moeilijk zijn.
Ernstig CCT – opvang op IZ
Haddad & Arabi (see later)
Ernstig craniocerebraal trauma
en de anesthesist
De literatuur van 2011 en 2012
Review articles
Review articles
• Guidelines for the acute medical
management of severe traumatic brain
injury in infants, children and adolescents
– second edition.
Kochaneck PM, Carney N, Adelson PD, Ashwal S, Bell MJ, Bratton S,
Carson S, Chesnut RM, Ghajar J, Goldstein B, Grant GA, Kissoon N,
Peterson K, Selden NR, Tasker RC, Tong KA, Vavilala MS, Wainwright
MS, Warden CR.
Pediatr.Crit.Care Med. 2012 ; Suppl. 1 : S1-82.
Review articles
• Perioperative management of the pediatric
patient with traumatic brain injury.
Bhalla T, Dewhirst E, Sawardekar A Dairo O, Tobias JD
Pediatr.Anesth. 2012 ; 22(7) : 627-40.
This manuscript reviews the current evidence based
medicine regarding the care of pediatric patients with TBI
as it relates to perioperative care of such patients. The
issues reviewed include those related to initial
stabilisation, airway management, intra-operative
mechanical ventilation, hemodynamic support,
administration of blood and blood products, positioning
and the choice of anesthetic technique. The literature is
reviewed regarding fluid management, glucose control,
hyperosmolar therapy, therapeutic hypothermia, …
Review articles
• Perioperative management of traumatic
brain injury.
Curry P, Viernes D, Sharma D.
Int.J.Crit.Illn.Inj.Sci. 2011; 1: 27-35.
For this review, extensive pubmed and Medline search
on various aspects of perioperative management of TBI
was performed, followed by review of research focusing
on the intraoperative and perioperative period. While the
research focusing specifically on the intraoperative and
immediate perioperative TBI management is limited,
clinical management continues to be absed largely on
physiological optimization and recommendations of the
Brain Trauma Foundation guidelines.
Review articles
• Perioperative management of adult
traumatic brain injury.
Sharma D, Vavilala MS.
Anesthesiol.Clin. 2012 ; 30(2) : 333-46.
This article presents an overview of the management of
traumatic brain injury (TBI) as relevant to the practicing
anesthesiologist. Key concepts surroundig the
pathophysiology and anesthetic principles are used to
describe potential ways to reduce secondary insults and
improve outcomes after TBI.
Review articles
• Critical care management of severe
traumatic brain injury in adults.
Haddad SA, Arabi YM.
Scan.J.Trauma Resusc.Emer.Med. 2012 ; 20(12)
In this review, the critical care management of severe
TBI will be discussed with focus on monitoring,
avoidance and minimization of secondary brain insults,
and optimization of cerebral oxygenation and CPP.
Guidelines value
• Acute traumatic brain injury : is current
management evidence based ?
Lei J, Gao G, Jiang J.
J Neurotrauma 2012 (e-published ahead of print).
Based on the above findings, hence, evidence both from
systematic reviews and clinical trials seems lacking the
potential to support current management of acute
traumatic brain injury. Translating from laboratory
success to clinical effect remains an unique challenge. It
might be the time to rethink the way in future practice
and clinical research in TBI.
Trauma and disease impact
Disease impact
• Effect of diabetes mellitus on outcome in
patients with TBI ; a national trauma
database analysis.
Lustenberger T, Talving P, Lam L, Inaba K, Bass M et al.
Brain Injury 2012 (e-published ahead of print).
Conclusion : traumatic brain injury in conjunction with
diabetes mellitus is asociated with an almost 1,5-fold
increased mortality while compared to patients with
isolated TBI without diabetes mellitus (22,6 vs. 16,8 %).
Moreover, patients with diabetes mellitus were less
frequently discharged home (38,9 vs. 46,1 %).
Prospective validation of these findings is warranted to
determine the underlying aetiology.
Disease impact
• Mortality and long-term functional outcome
associated with intracranial pressure after
traumatic brain injury.
Badri S, Chen J, Barber J, Temkin NR, Dikmen SS, Chenut RM, Deem S,
Yanez ND, Treggiari MM.
Intensive Care Med. 2012 ; 38(11) : 1800-9.
Conclusion : average ICP in the first 48 h of monitoring
was an independent predictor of mortality (18 %) and of
a composite endpoint of functional and
neuropsychological outcome at 6-month follow-up in
moderate or severe TBI patients. However, there was no
association between average ICP and
neuropsychological function among survivors.
Disease impact
• Influence of age on brain edema
formation, secondary brain damage and
inflammatory response after brain trauma
in mice.
Timaru-Kast R, Luh C, Gotthard P, Huang C, Schäfer MK, Engelhard K,
Thal SC.
J.Neurotrauma 2012 (e-published ahead of print).
Conclusion : the results therefore indicate that old
animals are prone to functional deficits and strong
ipsilateral cerebral inflammation without major
differences in morphological brain damage, compared to
young.
Trauma impact
• Risk factors for posttraumatic vasospasm.
Shahlaie K, Keachie K, Hutchins IM, Rudisill N, Madden LK, Smith KA,
Ko KA, Latchaw RE, Muizelaar JP.
J. Neurosurg. 2011 ; 115(3) : 602-11.
Conclusions : independent risk factors for posttraumatic
vasospasm (PTV) include parenchymal contusions and
fever. These results suggest that diffuse mechanical
injury and activation of inflammatory pathways may be
underlying mechanisms for the development of PTV, and
that a subset of patients with these risk factors may be
an appropriate population for agressive screening.
Further studies are needed to determine if treatments
targeting fever and inflammation may be effective in
reducing the incidence of vasospasm following severe
TBI.
Trauma impact
• Coagulopathy after isolated severe
traumatic brain injury in children.
Talving P, Lustenberger T, Lam L, Inaba K, Mohseni S, Plurad D, Green
DJ, Demetriades D.
J.Trauma 2011 ; 71(5) : 1205-10.
Conclusion : incidence of coagulopathy in children
suffering isolated severe traumatic brain injury (sTBI) is
exceedingly high at 40 % and reflect the head injury
severity. A low GCS, increasing age, ISS > 15 and
intraparenchymal lesions proved to be independently
associated with TBI coagulopathy.
Trauma impact
• Trauma-induced coagulopathy : standard
coagulation tests, biomarkers of
coagulopathy and endothelial damage in
patients with TBI.
Genét F, Johansson PI, Meyer MA, Solbeck S et al.
J.Neurotrauma 2012 (e-published ahead of print).
Conclusion : ISS (Injury Severity Score) rather than the
presence or absence of head/neck injuries determined
the haemostatic and biomarker response to the injruy.
The coagulopathy indentified thus (13 % isolated
head/neck, 47 % head/neck + other sites and 5 % in non-
TBI patients) reflected the severity of injury rather than its
localization.
Neuroprotection
Neuroprotection
• Effects of selective and non-selective
COX-inhibition against neurological deficit
and brain edema following closed-head
injury in mice.
Girgis H, Palmier B, Groci N et al.
Brain Res. 2012 (e-published ahead of print).
Conclusion : the present study yields considerable
evidence that COX-2 may not solely constitute an
interesting target for the treatment of TBI consequences.
Our data point to a potentially deleterious role of COX-1
in the development of neurological impairment in brain-
injured mice. However, the neuroprotective mechanism
of indomethacin remains to be clarified.
Neuroprotection
• The neuroprotective effect of acute
moderate alcohol consumption on
caspase-3 mediated neuro-apoptosis in
TBI : the role of lysosomial cathepsin L
and nitric oxide.
Kambak G, Kartkava K, Ozcelik E, Guvenal AB, Kabay SC et al.
Gene 2013 (e-published ahead of print).
Conclusion : our results indicate that moderate alcohol
consumption may have protective effects on apoptotic
cell death after TBI. Protective effects of moderate
ethanol consumption might be related to inhibition of
lysosomial protease release and nitric oxide production.
Neuroprotection
• Reduction of brain edema and expression
of aquaporins with acute ethanol treatment
after traumatic brain injury.
Wang G, Chou DY, Ding JY, Frederickson V, Peng C et al.
J.Neurosurg. 2012 (e-published ahead of print).
Conclusion : the present findings suggest that acute
ethanol administration after TBI deceases aquaporin
(AQP) expression, which may lead to reduced cerebral
edema. Ethanol-terated animals additionally showed
improved cognitive and motor outcomes compared with
untreated animals.
Neuroprotection
• Statins in traumatic brain injury.
Wible EF, Laskowitz DT
Neurotherapeutics 2010 ; 7 : 62-73.
Preclinical studies have shown significant benefit of
statins in models of TBI and related disease processes,
including cerebral ischemia, intracerebral hemorrhage,
and subarachnoid hemorrhage. In fact, multiple
mechanisms have been defined by which statins may
exert benefit after acute brain injury. Statins are
currently positioned to be translated into clinical trials in
acute brain injury ad have the potential to improve
outcomes after TBI.
Neuroprotection
• Statins improve outcome in murine models
of intracranial hemorrhage and traumatic
brain injury : a translational approach.
Indraswari F, Wang H, Lei B, James ML, Kernagis D, Warner DS,
Dawson HN, Laskowitz DT.
J.Neurol.Trauma 2012 ; 29(7) : 1388-400.
Following TBI, rosuvastatin 1 mg/kg was associated with
the greatest improvement in functional outcome, best
histological evidence of reduced neuronal degeneration
at 24 h post-TBI and was also associated with
downregulation of inflammatory gene expression in the
brain. …
Neuroprotection
• Experimental studies of erythropoietin
protection following TBI in rats.
Xu F, Yu ZY, Ding L et al.
Exp.Ther.Med. 2012 (e-published ahead of print).
Conclusion : in this rat model of TBI, EPO significantly
decreased the number of apoptotic cells, the expression
of MCP-1, the infiltration of CD68(+) cells as well as
brain edema to protect the brain.
Neuroprotection
• Erythropoiesis-stimulating agent
administration and survival after servere
traumatic brain injury : a prospective study.
Talving P, Lustenberger T, Inaba K, Lam L, Mohseni S, Chan L,
Demetriades D.
Arch.Surg. 2012 ; 147(3) : 251-55.
Conclusion : erythropiesis-stimulating agents
administration demonstrates a significant survival
advantage without an increase in morbidity in patients
with severe TBI.
Neuroprotection
• Effect of glutamate and blood glutamate
scavengers oxaloacetate and pyruvate on
neurological outcome and pathohistology
of the hippocampus after TBI in rats.
Zlotnik A, Sinelnikov I, Gruenbaum SE, Dubilet M, Dubilet E, Leibowitz A,
Ohayon S, Regev A, Boyko M et al.
Anesthesiology 2012 ; 116(1) : 73-83.
Conclusions : the authors demonstrate that the blood
glutamate scavengers oxaloacetate and pyruvate provide
neuroportection after TBI, expressed both by a reduced
neuronal loss in the hippocampus and improved
neurological outcomes. The findings of this study may
bring about new therapeutic possibilities …
Neuroprotection
• Attenuation of brain edema and spatial
learning defects by the inhibition of
NADPH oxydase activity using apocynin
following diffuse TBI in rats.
Song SX, Gao JL, Wang KJ et al.
Mol.Med.Report 2012 (e-published ahead of print).
Conclusion : the results of this study reveal that
treatment with apocynin may provide a new
neuroprotective therapeutic strategy against difuse brain
injury (DBI) by deminishing the upregulation of NOX2
protein and NOX acitivity, and thus reducing the
generation of reactive oxygen species (ROS) and
subsequent development of brain edema.
Neuroprotection
• Effect of citicoline on functional and
cognitive status among patients with TBI ;
the citicoline Brain Injury Treatment Trial
(COBRIT).
Zafonte RD, Bagiella E, Ansel BM et al.
JAMA 2012 ; 308(19) : 1993-2000.
Conclusion : among patients with traumatic brain injury,
the use of citicoline compared with placebo for 90 days
did not result in improvement in functional and cognitive
status.
Neuroprotection
• Neuroprotective effect of (-)-epigallo-
cathechin-3-gallate in rats when
administered pre- or post TBI.
Itoh T, Tabuchi M, Mizugushi N, Imano M et al.
J.Neurol.Trauma 2012 (e-published ahead of print).
Conclusion : these results indicate that EGCG inhibits
free-radical induced neuronal degeneration and apoptotic
death around the area damaged by TBI. Importantly,
continuous and post-TBI access to EGCG improved
cerebral function following TBI. In summary,
consumption of green tea may be an effective therapy in
TBI patients.
Neuroprotection
• Scriptaid, a novel histone deacetylase
inhibitor, protects against TBI via
modulation of PTEN and AKT pathways.
Wang G, Jiang X, Pu H, Zhang W, An C, Hu X, Liou AK-F et al.
Neurotherapeutics 2012 (e-published ahead of print).
As Scriptaid – a new histone deacetylase inhibitor –
offers long-lasting neuronal and behaviour protection,
even when delivered 12 h after controlled cortical impact,
it is an excellent new cadidate for the effective clinical
treatment of TBI.
Therapeutic management
Management options
• Cerebral hemodynamic effects of acute
hyperoxia and hyperventilation after
severe traumatic brain injury.
Rangel-Castilla L, Lara LR, Gopinath S, Swank PR, Valadka A,
Robertson C.
J.Neurotrauma 2010 ; 27(10) : 1853-63
Conclusions : presure autoregulation, as assessed by
dynamic testing, was impaired in these head-injured
patients. Acute hyperoxia significantly improved
pressure autoregulation, although the effect was smaller
than that induced by hyperventilation. The very small
change in paCO2 induced by hyperoxia does not appear
to explain this finding. Rather, the vasoconstriction
induced by acute hyperoxia may allow the cerebral ...
Management options
• Admission oxygenation and ventilation
parameters associated with discharge
survival in severe pediatric TBI.
Ramaiah VK, Sharma D, Ma L, Prathep S, Hoffman NG, Vavilala MS.
Childs Nerv.Syst. 2012 (e-published ahead of print)
Conclusions : discharge survival after severe pediatric
TBI was associated with admission paO2 301-500 mmHg
and paCO2 = 36-45 mmHg. Admission hypocarbia and
hypercarbia were each associated with increased
discharge mortality.
Management options
• Association between early hyperoxia and
worse outcomes after TBI.
Brenner M, Stein D, Hu P, Kufera J, Woodford M, Scalea T.
Arch.Surg. 2012 (e-published ahead of print)
Conclusions : hyperoxia (paO2 > 200 mmHg) within the
firts 24 hours of hospitalisation is associated with worse
short-term functional outcomes and higher mortality after
TBI. Although the mechanism for this has not been
completely elucidated, it may involve hyperoxia-induced
oxygen-free radical toxicity with or without
vasoconstriction. Hyperoxia and hypoxia were found to
be equally detrimental to short-term outcomes in patients
with TBI. A narrower therapuetic window for oxygenation
may improve mortality and functional outcomes.
Management options
• Hyperbaric oxygen therapy for the
adjunctive treatment of TBI.
Bennett MH, Trytko G, Jonker B
Cochrane Datab.Syst.Rev. 2012
Conclusions : in people with TBI, while the addition of
hyperbaric oxygen therapy (HBOT) may reduce the risk
of death, and improve the final GCS, there is little
evidence that the survivors have a good outcome. The
improvement of 2,68 points in GCS is difficult to interpret.
The routine application of HBOT to TBI patients thus
cannot be justified from this review.
Management options
• Inhaled nitric oxide reduces secondary
brain damage after TBI.
Terpalilli NA, Kim SW, Thai SC et al.
J.Cereb.Blood Flow Metab. 2012 (e-published ahead of print).
Conclusion : NO significantly improved CBF and reduced
ICP in male C57 BI/6 mice. Long-term application (24 h
NO inhalation) resulted in reduced lesion volume,
reduced brain edema formatio and less BBB-dysruption,
as well as imporved neurological function. No adverse
efffects eg. on cerebral autoregulation, systemic blood
pressure or oxidative damage were observed. NO
inhalation might therefore be a safe and effective
treatment option in TBI patients.
Management options
• Volatile anesthetics influence blood brain
barrier integrity by modulation of tight
junction protein expression in traumatic
brain injury.
Thal S, Luh C, Schalble E-V, Timaru-Kast R, Hedrich J, Luhmann HJ,
Engelhard K, Zehendner CM.
PLOSONE 2012 ; 7(12) (e-published ahead of print).
Therefore, selection of anesthetics may influence the
barrier function and introduce a strong bias in
experimental research on pathophysiology of BBB
dysfunction. Future research is required to investigate
adverse or beneficial effects of volatile anesthetics on
patients at risk for cerebral edema.
Management options
• Influence of isoflurane on neuronal death
and outcome in a rat model of TBI.
Hertle D, Beynon C, Zweckberger K, Vienenkötter B, Jung CS, Kiening K,
Unterberg A, Sakowitz OW.
Acta Neurochirurg. Suppl. 2012 ; 114 : 383-6
After controlled cortical impact (CCII), we tested the
outcome at 4 and 48 h using histological methods and a
neurological test. Increased apoptosis was found in
referenced coritcal areas as early as 48 h after trauma.
Along with histological findings, neurological outcome
was worst as indicated by a higher score in the
experimental group with deep sedation. Although blood
pressure was lower with deep sedation, no frank
hypotension occurred. In our experiments, deep …
Management options
• Severe TBI and controlled hemorrhage in
rats : quest for the optimal mean arterial
blood pressure after whole fresh donor
blood resuscitation.
Brotfein E, Leibowitz A, Dar DE et al.
Shock 2012 ; 36(6) : 630-4.
Conclusion : in this study we found that mild resuscitation
with goals of restoring MAP to 80 mmHg (which is lower
than baseline) provided best results when considering
hemodynamic stability, survival and neurological
outcomes. An aggressive resuscitation may be
detrimental, inducing processes that eventually cause a
significant decrease in survival.
Management options
• Impact of arterial hypertension on
polytrauma and traumatic brain injury.
Sellmann T, Miersch D, Kienbaum P, Flohé S, Schneppendahl J, Lefering
R and the DGU Trauma Registry.
Dtsch.Arzteblad Int. 2012.
Conclusion : systolic blood pressure values above 160
mmHg before arrival in the hospital worsen the outcome
of trauma patients with TBI.
Management options
• Albumin resuscitation for traumatic brain
injury : is intracranial hypertension the
cause of increased mortality.
Cooper DJ, Myburgh J, Finfer S et al.
J.Neurotrauma 2012 (e-published ahead of print).
The use of albumin for resuscitation in patients with
severe TBI is associated with increased ICP during the
first week. This is the most likely mechanism of
increased mortality in these patients.
Management options
• Systematic review of head cooling in
adults after traumatic brain injury and
stroke.
Harris B, Andrews PJD, Murray GD, Forbes J, Moseley O.
Health Technol.Assess. 2012 (e-published ahead of print).
Conclusions : whether head cooling improves functional
outcome or has benefits and fewer side-effects
compared with systemic cooling or no cooling could
could not be established. Some methods of head
cooling can reduce intracranial temperature, which is an
important first step in determining effectiveness, but
there is insufficient evidence to recommend its use
outside of research trials. The principal recommendation
for research are that active cooling devices …
Management options
• Goal directed brain tissue oxygen
monitoring vs. conventional management
in TBI : an analysis of in-hospital recovery.
Green JA, Pellegrini DC, Vanderkolk WE et al.
Neurocrit.Care 2012 (e-published ahead of print).
Conclusion : compared with ICP/CPP directed therapy
alone, the addition of PBtO2 monitoring did not provide a
survival or functional status improvement at discharge.
The true clinical benefit of pBtO2 monitoring will require
further study.
Management options
• A trial of intracranial pressure monitoring in
traumatic brain injury.
Chesnut RM, Temkin N, Carney N et al.
NEJM 2012 (e-published ahead of print).
Conclusions : for patients with severe traumatic brain
injury, care focussed on maintaining monitored
intracranial pressure at 20 mmHg or less was not shown
to be superior to care based on imaging and clinical
examination.
Management options
• Hyperosmolar therapy for raised
intracranial pressure.
Ropper AH.
NEJM 2012 ; 367 : 746-52.
Management options
• Reduction of brain edema and expression
of aquaporins with acute ethanol treatment
after TBI.
Wang T, Chou DY, Ding JY et al
J. Neurosurg. 2012.
Conclusions : the present findings suggest that acute
ethanol administration after TBI decreases aquaporin
(AQP) expression, which may lead to reduced cerebral
edema. Ethanol-treated animals additionally showed
improved cognitive and motor outcomes compared with
untreated animals.
Management options
• Barbiturates for acute TBI.
Roberts I, Sydenham E
Cochrane Datab.Syst.Rev. 2012
There is no evidence that barbiturate therapy in patients
with acute severe head injury imporves outcome.
Barbiturate therapy results in a fall in blood pressure in
one in four patients. Thsi hypotensive effect will offset
any ICP lowering effect on cerebral perfusion pressure.
Management options
• Decompressive craniectomy for diffuse
traumatic brain injury.
Cooper DJ, Rosenfeld JV, Murray L, Arabi YM, Davies AR et al. For the
DECRA trial investigators.
NEJM 2011; 364(16) : 1453-502.
Conclusions : In adults with severe diffuse traumatic
brain injury and refractory intracranial hypertension, early
bifrontotemporoparietal decompressive craniectomy
decreased intracranial pressure and the length of stay in
the ICU, but was associated with more unfavorable
outcomes.
Ernstig craniocerebraal trauma
Take home messages
Deel 3
Ernstig CCT - mechanismes
Cell death
Primary lesions
Neuronal trauma
Vascular trauma
(micro- and macro-haematomas)
Blunt trauma
Secondary lesions
Avoid aggravating factors
Te vermijden …
• Bloeddruk :
• SAP < 90 (110 ?)
• SAP > 160 (180-200 ?) mmHg.
• Oxygenatie : PaO2 < 60 en > 200 mmHg ???
• Ventilatie : PaCO2 < 35 mmHg en > 45 mmHg.
• Glycemie : < 60 mg/dl en > 180 mg/dl.
• Temperatuur : < 35,5 °C en > 36,5 °C.
• Natremie : > 142 mEq/l
• Osmolariteit : < 290 mOsm.
• Metabole acidose < 7,35 of alkalose > 7,45
• Hypovolemie.
• Albumine-oplossingen.
Te vermijden …
• Bloeddruk :
• SAP < 90 (110 ?)
• SAP > 160 (180-200 ?) mmHg.
• Oxygenatie : PaO2 < 60 en > 200 mmHg ???
• Ventilatie : PaCO2 < 35 mmHg en > 45 mmHg.
• Glycemie : < 60 mg/dl en > 180 mg/dl.
• Temperatuur : < 35,5 °C en > 36,5 °C.
• Natremie : > 142 mEq/l
• Osmolariteit : < 290 mOsm.
• Metabole acidose < 7,35 of alkalose > 7,45
• Hypovolemie.
• Albumine-oplossingen.
Te gebruiken …
• Erythropoietine
• Rosuvastatine
• Ethanol
• Oxaloacetaat en pyruvaat
• Nitric oxide
• Scriptaid
• Topical head cooling ??
Ernstig CCT - mechanismes
Cell death
Blunt trauma
Apoptotic pathway
Ischemia
Free radicals
Brain herniation
Inflammation
Necrosis pathway
Excitotoxicity Mitochondrial failure
Neuronal trauma
(Diffuse axonal lesions)
Increased ICP Brain edema
Vascular lesions
(haemorrhagic contusions – haematomas)
Perfusion defects
Te gebruiken …
• Erythropoietine
• Rosuvastatine
• Ethanol
• Oxaloacetaat en pyruvaat
• Nitric oxide
• Scriptaid
• Topical head cooling ??
Ethanol neuroprotection ?
• BAC 0,04 % : 1,4 x risk of vehicle accident
• BAC 0,08 % : 11 x risk of motor vehicle accident
• BAC 0,1 % : 48 x risk of motor vehicle accident.
• BAC 0,15 % : 380 x risk of motor vehicle accident.
Einde
Mangat HS. Continuum (Minneap.Minn) 2012 ; 18(3) : 532-46. Severe traumatic brain injury.
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