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.

Jeremtisky E, Omert L, Dunham CM, Protetch J, Rodriguez A. J.Trauma 2003 ; 4(2) : 312-9. Harbingers of poor

outcome the day after severe brain injury : hypothermia, hypoxia, and hypoperfusion.