Perioperative Management Head Injury

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Journal List Int J Crit Illn Inj Sciv. 1(1); Jan-Jun 2011 PMC3209993

Int J Crit Illn Inj Sci. 2011 Jan-Jun; 1(1): 27 –35.

doi: 10.4103/2229-5151.79279 

Perioperative management of traumatic brain injury

Parichat Curry,1 Darwin Viernes,1 and Deepak Sharma1,2 

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This article has been cited by other articles in PMC.

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Abstract

Traumatic brain injury (TBI) is a major public health problem and theleading cause of death and disability worldwide. Despite the moderndiagnosis and treatment, the prognosis for patients with TBI remainspoor. While severity of primary injury is the major factor determiningthe outcomes, the secondary injury caused by physiological insults suchas hypotension, hypoxemia, hypercarbia, hypocarbia, hyperglycemia andhypoglycemia, etc. that develop over time after the onset of the initialinjury, causes further damage to brain tissue, worsening the outcome inTBI. Perioperative period may be particularly important in the course ofTBI management. While surgery and anesthesia may predispose thepatients to new onset secondary injuries which may contribute adverselyto outcomes, the perioperative period is also an opportunity to detectand correct the undiagnosed pre-existing secondary insults, to preventagainst new secondary insults and is a potential window to initiateinterventions that may improve outcome of TBI. For this review,extensive Pubmed and Medline search on various aspects ofperioperative management of TBI was performed, followed by review of

research focusing on intraoperative and perioperative period. While theresearch focusing specifically on the intraoperative and immediateperioperative TBI management is limited, clinical managementcontinues to be based largely on physiological optimization andrecommendations of Brain Trauma Foundation guidelines. This review isfocused on the perioperative management of TBI, with particularemphasis on recent developments.

Keywords: Anesthesia, perioperative management, traumatic braininjury

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INTRODUCTION

Traumatic brain injury (TBI) is a major publichealth problem and the leading cause of deathand disability worldwide.[1]  Approximately

1.7 million people sustain TBI every year inthe United States, leading to 275,000hospitalizations and 52,000 deaths.[1] TBI is acontributing factor in about 30.5% of allinjury-related deaths in the United States.[1] TBI occurs most often in children aged 0 – 4years, adolescents aged 15 – 19 years andelderly aged 65 years and more.[1]  In all agegroups, males have a higher rate of TBI thanfemales.[1]  Falls and motor vehicle-trafficinjury are the leading causes of TBI in theUnited States.[1]  In the recent years, prehospital and intensive care of patients with

TBI has improved substantially and evidence- based guidelines for management have beendeveloped.[2 – 13]  However, despite themodern diagnosis and treatment, the prognosisfor patients with TBI remains poor,

emphasizing the need for further research andimprovement in care. This review will focus

on the perioperative management of TBI, with particular emphasis on recent developments,and is based on extensive Pubmed and

Medline search on various aspects of perioperative management of TBI, followed by

review of research focusing on intraoperativeand perioperative period.

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PATHOPHYSIOLOGY OF TRAUMATIC

BRAIN INJURY

Pathophysiology of TBI involves primary andsecondary injuries to the brain. Primary injuryis the damage caused by the initial traumainvolving mechanical impact to the braintissue and skull due to acceleration – 

deceleration or rotational forces, resulting inskull fracture, brain contusion, expanding

intracranial hematoma or diffuse axonalinjury.[14]  The primary injury then initiates

inflammatory process, edema formation andexcitotoxicity, resulting in further increase inintracranial pressure (ICP) and reduced

cerebral perfusion pressure (CPP).[14,15] Severity of primary injury is the major factor

determining the outcome of TBI patients.Secondary injury is a consequence of

 physiological insults that develop over timeafter the onset of the initial injury, causingfurther damage to the brain tissue andworsening the outcome in TBI patients.[14,15] Two major factors that cause secondary injuryare hypotension [systolic blood pressure (SBP)< 90 mmHg] and hypoxemia (PaO2 < 60mmHg).[16] 

A study analyzing data from the TraumaticComa Data Bank demonstrated thathypotension and hypoxemia were

independently associated with increasedmorbidity and mortality from severe TBI.[17] A single episode of hypotension wasassociated with increased morbidity andmortality.[17]  A meta-analysis of 8721 patients (IMPACT study) also suggested thathypotension and hypoxia were significantly

associated with unfavorable 6-monthoutcome.[18]  A study on the association between intraoperative hypotension andoutcome demonstrated that patients who hadintraoperative hypotension had over threetimes increased mortality than normotensive patients.[19]  Moreover, the duration ofintraoperative hypotension was also inverselyassociated with functional outcome.[19] Otherfactors implicated in secondary injury include

hypoglycemia, hyperglycemia, hypercarbiaand hypocarbia, and raised ICP.[20 – 25] 

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THE IMPORTANCE OF

PERIOPERATIVE PERIOD

Given the poor outcomes of TBI and impact ofsecondary insults, current TBI management

focuses on prevention of primary injury andavoidance of secondary injuries. Thus, thecornerstones of modern TBI management are

field resuscitation, expeditious triage,emergent surgical evacuation of mass lesions,

control of ICP, and support of CPP,multimodal monitoring and optimization of physiological environment. Perioperative period may be particularly important in thecourse of TBI management for numerousreasons. First, despite the aggressiveinterventions to rapidly correct hypoxemia,hypotension, hypo and hypercarbia, and hypoand hyperglycemia in the emergency

department, it is not unusual for one or moreof these complicating factors to persist orremain undetected as the patient is emergently

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transported to the operating room. Hence, perioperative period may provide anopportunity to either continue ongoingresuscitation or to correct the pre-existingsecondary insults. Secondly, surgery andanesthesia may predispose the patient to newonset secondary injuries (such asintraoperative hypotension due to surgical blood loss or effect of anesthetic agents, newonset hyperglycemia due to stress response,etc.), which may contribute adversely tooutcomes. Since secondary injury is largely preventable/treatable, the perioperative periodmay be a potential window to initiateinterventions that may improve the outcome ofTBI. Perioperative management involves rapidevaluation, continuation of resuscitation

(cerebral and systemic), early surgicalintervention, intensive monitoring and

anesthetic planning.

Initial Assessment and Ongoing

Resuscitation

The initial assessment and stabilization isusually achieved in the emergency departmentand resuscitation initiated before the patient istransported to Computed Tomography (CT)scanner and then to the operating room.

 Nevertheless, it is important for the anesthesiateam to perform another rapid assessment asthe patient is received in the operating room.The assessment should always begin withairway, breathing and circulation, followed bya rapid assessment of neurological status andassociated extracranial injuries and attention tospecific secondary injury mechanisms andongoing treatment thereof. Information abouttime and mechanism of injury can be valuable.Brief neurological assessment is performed byusing Glasgow Coma Scale (GCS)[26]  score

and pupillary responses. Associated thoracic,abdominal, spinal and long bone injuries may be stable or evolve during the perioperative period and must be considered in differentialdiagnosis of new onset hypotension, anemia,hemodynamic instability or hypoxemia duringanesthesia and surgery. As the patient istransported to the operating room, all

resuscitative measures should continue.

Airway Management

Patients with TBI requiring surgery willinvariably require tracheal intubation. In fact,

most patients are likely to arrive in theoperating room already intubated. However,some patients, particularly those withextradural hematoma, may be conscious and breathing spontaneously. The indwellingtracheal tube can possibly migrate duringtransport, leading to endobronchial intubationor even dislodgement, and hence, adequate position of the tube must always be confirmed.In the select patients who may not be alreadyintubated, airway management is complicated by a number of factors, including urgency ofsituation (because of pre-existing/worseninghypoxia), uncertainty of cervical spine status,uncertainty of airway (due to presence of blood, vomitus, debris in the oral cavity or dueto laryngo-pharyngeal injury or skull base

fracture), full stomach, intracranialhypertension and uncertain volume status. All

TBI patients requiring urgent surgery must beconsidered to have full stomach and airwaymanagement must account for possibleunderlying cervical spine injury. Although ithas been reported that patients with

craniocerebral trauma had an incidence ofcervical spine injury (CSI) similar to that ofthe general trauma population,[27]  emergingevidence suggests a higher incidence ofcervical injury in patients who have

experienced craniocerebral trauma, especiallyamong those with increasing severity of

craniocerebral injury as determined by lowGCS score and unconsciousness.[28,29] 

The choice of technique for tracheal intubationis determined by urgency, individualexpertise/skills and available resources and

generally incorporates rapid sequenceintubation with cricoid pressure and manualin-line stabilization.[27]  The anterior portionor cervical collar may be removed when

manual in-line stabilization is established toallow greater mouth opening and facilitatelaryngoscopy. Newer airway devises, particularly Glidescope videolaryngoscope,have gained popularity in recent years for use

in trauma victims and may be useful indifficult airway scenarios. However, theintubation time using Glidescope may be

longer due to difficulty in passing the trachealtube through the glottis despite easier

visualization.[30]  Nasal intubation should beavoided in patients with base of skull fracture,

severe facial fractures or bleeding diathesis. Inany case, it is advisable to have a back-up plan

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ready in case of difficult intubation, given thesignificant risk of intracranial hypertensionresulting from increased cerebral bloodvolume (CBV) because of hypoxemia andhypercarbia.

Choice of induction agents and musclerelaxants is important for successfuluncomplicated airway management. Sodiumthiopental, etomidate and propofol arecommonly used to induce anesthesia beforeintubation. All these agents decrease the

systemic hemodynamic response to intubation, blunt increases in ICP, and decrease thecerebral metabolic rate for oxygen (CMRO2).However, propofol and thiopental may causecardiovascular depression leading tohypotension, especially in the presence ofuncorrected hypovolemia. Etomidate may be

advantageous due to little change in blood pressure during induction despite reduction ofCMRO2.[31] However, it may lead to adrenalinsufficiency causing delayed hypotension andrequiring vasopressor use.[32]  Ketamine,which causes limited cardiovascularcompromise, has been associated withincreased cerebral blood flow (CBF) andincreased ICP, and as such, may be relativelycontraindicated for intubating patients with

risk for or pre-existing increased ICP.[33] Thechoice of muscle relaxant for rapid sequenceinduction is between succinylcholine androcuronium.[34]  Succinylcholine maycontribute to increased ICP[35,36]  which can be blunted by administration of an adequatedose of an induction agent such asthiopental.[37] While the clinical significance

of the effect of succinylcholine on ICP isquestionable,[37,38]  increases in ICPsecondary to hypoxia and hypercarbia are welldocumented and much more likely to be

clinically important. Hence, in patients withTBI, clinicians may not avoid usingsuccinylcholine.[38] 

Anesthetic Management

The major goals of anesthetic management ofTBI are to

  maintain CPP;  treat increased ICP;   provide optimal surgical

conditions;

  avoid secondary insults such ashypoxemia, hyper and hypocarbia,hypo and hyperglycemia; and

   provide adequate analgesia andamnesia.

Anesthetic technique

Important pharmacodynamic and pharmacokinetic differences exist between

intravenous and volatile anesthetic agents.Intravenous agents including thiopental,

 propofol and etomidate cause cerebralvasoconstriction and reduce CBF, CBV,CMRO2and ICP.[39]  Opioids have no directeffects on cerebral hemodynamics in the presence of controlled ventilation.[40]  All

volatile anesthetic agents (isoflurane,sevoflurane, desflurane) decrease CMRO2 andmay cause cerebral vasodilation, resulting inincreasing CBF and ICP. But at concentrationless than 1 minimum alveolar concentration(MAC), the cerebral vasodilatory effects areminimal and hence they may be used in lowconcentrations in patients with TBI.[41]  Nitrous oxide can increase CMRO2 and causecerebral vasodialation and increased ICP andshould be avoided.[42] Importantly, the effectsof anesthetic agents (inhalation vs. total

intravenous anesthesia) on outcome of TBIhave not been demonstrated. In the absence ofconclusive evidence, either anesthetictechnique may be employed judiciously.However, more importantly, the principles ofanesthetic management should adhere to thecurrent guidelines for the management ofsevere TBI [Table 1].[2 – 13] 

Table 1 Recommendations from the 2007 guidelinesfor management of severe traumatic braininjury[2 – 13] 

Ventilation

Ventilation should be adjusted to ensureadequate oxygenation and gas exchange.

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Inspired oxygen concentration is adjusted tomaintain PaO2 >60 mmHg.

2Monitoring arterial

PCO2 is recommended since end-tidalCO2 may not be reliable. Hypercarbia should be avoided but hypocarbia must not be usedindiscriminately.[12]  Excessivehyperventilation may cause cerebralvasoconstriction leading to ischemia.[12] Hence, hyperventilation should be used judiciously for short-term control of ICP andto facilitate surgical exposure duringcraniotomy. Normocarbia should be restored before dural closure to avoid development oftension pneumocephalus. Monitoring cerebraloxygenation is recommended when utilizinghyperventilation for prolonged periods. In theintraoperative period, this may be

accomplished by jugular venousoximetry[9,43] and in the postoperative period

 by brain tissue oxygenation (PbtO2) or CBFmonitoring (e.g. using Transcranial Dopplerultrasonography).[9] 

Monitoring

In additional to standard American Society ofAnesthesiology (ASA) monitors, arterialcatheterization is recommended for beat-to- beat blood pressure monitoring and for blood

gas analysis and blood glucose monitoringduring craniotomy. Central venous pressure(CVP) may be useful, particularly forresuscitation and when vasopressors areadministered. However, it is advisable not todelay surgical evacuation of expandingintracranial hematoma because of institution ofinvasive monitoring. According to the currentguidelines, ICP monitoring is recommended inall salvageable patients with a severe TBI(GCS < 9) and an abnormal CT scan(hematomas, contusions, swelling, herniation

or compressed basal cistern), and in patientswith severe TBI with a normal CT scan if twoor more of the following features are noted atthe admission: age > 40 years, unilateral or bilateral motor posturing, or SBP < 90mmHg.[5] The use of multimodal monitoringfor postoperative and intensive care of patientswith TBI is increasing and monitoring cerebral

oxygenation (global or focal) or CBF andmetabolism parameters may be helpful inmaking important treatment decisions.[9] 

Intravenous Fluids, Blood Pressure

Management and Vasopressor Use

Hypotension following TBI can compromisecerebral hemodynamics and cause cerebralischemia. Therefore, blood pressuremanagement, including choice of fluids andvasopressors, is of paramount importance.Brain Trauma Foundation guidelines for themanagement of TBI recommend avoidinghypotension (SBP < 90 mmHg) andmaintaining CPP between 50 and 70mmHg.[2,8]  Warm, non-glucose containingisotonic crystalloid solution is preferable forTBI patients. The role of colloid iscontroversial. A post-hoc analysis of theSaline versus Albumin Fluid Evaluation(SAFE) study demonstrated that resuscitationwith albumin was associated with highermortality rate and unfavorable neurological

outcome at 24 months.[44]  Hypertonic salinemay be beneficial resuscitation fluid for TBI

 patients because it increases intravascular fluidand decreases ICP. Prehospital hypertonicsaline resuscitation has been shown to beassociated with a reduction in serum biomarker levels (S100B, Neuron Specific

Enolase and Membrane Basic Protein) whichcorrelated with better outcome.[45] However,a double-blind randomized controlled trialcomparing prehospital resuscitation ofhypotensive TBI patients with hypertonic

saline with standard fluid resuscitation protocols found no difference in neurological

outcome at 6 months.[46] 

Vasopressors are commonly administered totreat hypotension or to augment CPP.However, there are only a few studiescomparing the effectiveness of commonly

used vasopressors in TBI and results of thesestudies are conflicting. Human data explicitlycomparing vasopressors are limited to threesmall prospective, randomized, crossover trials

comparing sequential effectiveness betweennorepinephrine and dopamine. Despite there being no differences in mean cerebral flowvelocity[47,48]  and cerebral oxygenation ormetabolism[49] between the two vasopressors,

norepinephrine had more predictable andconsistent effect[48]  while dopamine use ledto higher ICP.[47]  A recent single-center

retrospective study of patients with severe TBIwho received phenylephrine, norepinephrine

or dopamine reported maximum increase inMAP and CPP from baseline with

 phenypephrine use.[50]  There was nodifference in ICP between the treatment

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groups after initiating the vasopressor althoughit was unclear whether improved MAP/CPPwith vasopressor use translated into improvedCBF or oxygenation.[50]  Current evidencedoes not support preference of one vasopressorover the other.

Blood Transfusion

Anemia is associated with increased in-

hospital mortality[51]  and poor outcome inTBI.[52,53]  Yet, there is little evidence to

support packed red blood cell (PRBC)transfusion practice standards to correctanemia in TBI. While some have suggestedthat patients with TBI may not benefit from ahigher transfusion threshold than other

critically ill patients,[52] others have cautionedagainst the liberal use of blood transfusion inTBI.[53]  Potential mechanisms of cerebralinjury due to anemia include tissue hypoxia,injury caused by reactive oxygen species,inflammation, disruption of blood-brain barrier(BBB) function, vascular thrombosis andanemic cerebral hyperemia.[54]  However, anumber of cerebroprotective physiologicalmechanisms become effective with anemiawhich include aortic chemoreceptor activation,increased sympathetic activity leading to

increased heart rate, stroke volume and cardiacindex, reduced systemic vascular resistance,and enhanced oxygen extraction. Moreover, anumber of cellular mechanisms of cerebral protection become effective in acute anemia.These include Hypoxia Inducible Factor (HIF),increased nitric oxide synthetase and nitricoxide in the brain (nNOS/NO), erythropoietinand vascular endothelial growth factor(VEGF) mediated angiogenesis and vascularrepair.[54]  Although increase in CBF duringacute anemia can improve oxygen delivery,

high hematocrit after PRBC transfusion may potentially decrease CBF and increase the riskof cerebral ischemia.[55]  However, anemiadue to hemodilution may impair cerebralautoregulation.[56]  The overall effects ofanemia on the brain might, therefore, dependon the relative balance between thesecompeting protective and harmful factors of

anemia and PRBC transfusion, and it isunclear whether transfusion trigger in patientswith TBI should be any different from othercritically ill patients and whether the injured brain is more susceptible to deleterious effectsof anemia.

In the absence of defined optimal hemoglobin(Hb) levels, it has been suggested thatneurophysiologic criteria for RBC transfusionmay be more rational and may progressivelyreplace arbitrary Hb-based transfusion triggersin neurocritical care.[57] RBC transfusion mayinfluence cerebral oxygenation through anumber of potential mechanisms in patientswith TBI. Besides increasing the oxygen-carrier capacity of blood, RBC transfusionincreases the circulating volume and canincrease CBF in patients with impairedcerebral autoregulation secondary to the TBI.Transfusion also increases the blood viscosityto which the circulatory network responds withthe release of nitric oxide, leading tovasodilatation and increasing functional

capillary density (which quantifies capillary perfusion).[58] In recent years, there has been

growing interest in the effect of RBCtransfusion on brain tissue oxygenation(PbtO2) in patients with TBI and it seems aninteresting possibility that PbtO2 values may be developed into potential transfusion

triggers. However, most studies evaluating theeffect of transfusion on PbtO2 in neurosurgical patients are limited by small sample size andhave failed to demonstrate a consistentresponse to transfusion or elucidate predictors

of PbtO2  response to transfusion.[59,60]  The potential role of brain tissue oxygenation in

deciding transfusion thresholds has beendiscussed elsewhere.[61,62] 

Existing evidence suggests that both anemiaand RBC transfusion are associated with poorneurological outcome in TBI.[52,53]  While

anemia is associated with increased in-hospitalmortality[51]  and lower hospital dischargeGCS score, discharge Glasgow outcome scoreand Ranchos Los Amigos scores,[52]  RBC

transfusion is associated with acute lunginjury, longer intensive care unit and hospitalstay, and mortality.[63 – 65]  The optimal Hblevel in TBI patients is still unclear but there isno benefit of a liberal transfusion strategy

(transfusion when Hb

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under anesthesia even in non-diabetic patients,[81]  it is possible that added stressduring general anesthesia and surgery mayworsen hyperglycemia and contribute to pooroutcome. Moreover, individual anestheticagents have been shown to have differentialeffects on blood and brain glucoselevels.[82,83] The only perioperative study inchildren with TBI demonstrated thatintraoperative hyperglycemia is common,hypoglycemia in the absence of insulintreatment is not rare, and TBI severity and the presence of subdural hematoma (SDH) predictintraoperative hyperglycemia.[73]  In theauthor's experience in adult patientsundergoing craniotomy for TBI, intraoperativehyperglycemia (glucose > 200 mg/dl) was

common (15%) and hypoglycemia (glucose

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