the management of head injury and intracranial pressure

Current Anaesthesia & Critical Care (2002) 13,129^137�c 2002 Elsevier Science Ltd. All rights reserved.doi:10.1054/cacc.401, available online at http://www.idealibrary.com on

FOCUSON:NEUROINTENSIVECARE

Themanagement of head injury and intracranialpressureJ.Goh and A.K.Gupta

*Department of Anaesthesia, Addenbrooke’s Hospital,Cambridge,UK and wNeuro-critical care, Addenbrooke’s Hospital,University of Cambridge,Cambridge,UK

KEYWORDScraniocerebral trauma,intracranial pressure,hypertension, intracranial

Summary Severe head injury occurs predominantly in the young population.Although the incidence is decreasing in the United Kingdom, the eventual outcome ofthesepatientshasmajor social andeconomicimplications.Damagetobraintissue duringhead injury is both primary, due to the initial insult, or secondary, which occurs later.Because little can be done about the primary injury, the intensive care management istargeted at reducing the secondary insults whichmay cause further brain damage.Theprevention of secondary injury involves prompt airwaymanagement and treatment ofhypoxia and hypotension. Severe head injury often causes raised intracranial pressure(ICP). The management is focused on maintaining cerebral perfusion pressure, whichshould be maintained above 70mmHg by adequate £uid replacement or by thejudicious use of inotropes.The methods to control ICP include general measures (151headupposition, avoidance of jugular venous obstruction, preventionof hyperthermiaandhypercarbia) andneurospeci¢cmeasures.Theneurospeci¢cmeasures areparticu-larly useful in patients with refractory intracranial hypertension.The patientmay needsedation, paralysis, use of barbiturate coma, osmotherapy, moderate cooling, con-trolled hyperventilation or surgical intervention. This review focuses on the rationalefor theuse ofthese interventions, outlining theirbene¢ts andtheirpitfalls.�c 2002 ElsevierScience Ltd.Allrights reserved.

INTRODUCTIONHead injury occurs frequently, with about1.4 million pa-tients su¡ering a head injury in the UKeach year.1Severehead injury is de¢ned as a patient having a glasgow comascore (GCS) of 8 or less despite adequate non-surgicalresuscitation, or a GCS deteriorating to 8 or less.The outcome is related to both the initial resuscitation

at the scene, and the intensive care management. Pa-tients presenting with features suggestive of poor out-come (Table 1) can bene¢t from early recognition andaggressive intervention.2

Injury to the brain occurs in two phases.The primaryinjury is that which occurs at themoment of impact andis irreversible. Subsequent physiological insults (Table 2)may trigger various pathophysiologicalmechanisms suchas release of excitatory amino acids (EAA), intracellularcalcium overload, free-radical-mediated injury and in-£ammatory responses, which may lead to cellular injury

0953-7112/02/$-see frontmatter

Correspondence to: AKG.Tel.: +441223 217434; Fax: +441223 217223;E-mail: [email protected]

or death if no intervention is made. These mechanismsmay be compounded by changes in global and regionalcerebral blood £ow (CBF),3 speci¢cally a reduction ofCBF in the ¢rst12^24h after injury.In an analysis of 717 patients from the traumatic coma

data bank (TCDB), pre-hospital hypotension (systolicblood pressure o90mmHg) and hypoxia (PaO2o60mmHg)were among the ¢vemostpowerfulpredic-tors of outcome.4 The initial resuscitation of airway con-trol, adequate oxygenation and maintenance of bloodpressure is therefore crucial to the eventual outcome. Inpatients with a GCS of 8 or less, intubation is necessaryto protect the airway from aspiration of gastric contentsand tomaintain gas exchange (Table 3).

INTENSIVECAREMANAGEMENTThe ICUmanagementof patientswith severe head injuryand raised intracranial pressure (ICP) includes the opti-mization of physiology by providing good intensive care,and the prevention or reversal ofmechanisms of second-

Table 1 practical protocol for management of head-injuredpatients in the emergencydepartment

Group A (minimalhead injury GCS=15)K Patient is awake, orientated and without neurologic

de¢cits andrelates accidentK Noloss of consciousnessK NovomitingK Absentorminimal subgaleal swellingThe patient is released into the care of a familymember withwritten instructions.

Group B (minor head injury GCS=15)K Patient is awake, orientated and without neurologic

de¢citsK Transitory loss of consciousnessK AmnesiaK One episode of vomitingK Signi¢cant subgaleal swellingThe patient who has at least one of these characteristics un-dergoes neurologic evaluation and CTscanwhich, if negative,shortens hospital observation. If CTscan is not available, thepatient has skull X-rays and is held for an observation periodofnotless than 6 h.Ifthe skull X-rays arenegative and a subse-quentneurologiccontrolisnormal, thepatientcanbereleasedinto the care of a family member with written instructions. Ifthe X-rays reveal a fracture, the patientundergoes CTscan.

Group C (moderate headinjuryormildheadinjury withcomplicat-ing factors GCS=9^15)K Impaired consciousnessK Uncooperative for various reasonsK RepeatedvomitingK Neurologic de¢citsK Otorrhagia/otorrhoeaK RhinorrhoeaK Signs of basal fractureK SeizuresK Penetrating or perforatingwoundsK Patients in anticoagulant therapy or a¡ected by coagulo-

pathyK Patients who have undergone previous intracranial

operationsK Epilepticor alcoholic patientsThe patient with at least one of these characteristics under-goes a neurologic evaluation and a CT scan. Hospitalizationand repeated scan, if necessary, within 24 h or prior todischarge.

Group D (Severe head injury GCS = 3^8)K Patient is in comaNecessaryresuscitationmanoeuvres followedbyneurologicalevaluation and immediate CTscan (prior to surgical interven-tion).Comamanagement

Reprintedbypermission from?

Table 2 mechanisms of brain injury, initial event: trauma,ischaemia

Primary Secondary Systemic

Tissue destruction Pressure e¡ects HypoxaemiaHaemorrhage Hydrocephalus HypotensionPressure e¡ects Herniation HypercarbiaDi¡use axonal injury Vasospasm Excessive

hypocarbiaReducedmetabolic rate

Hyperthermia

Impairedautoregulation

Anaemia

Secondaryhyperaemia

Electrolytedisturbance

Oedema Hyperglycaemia

Table 3 Indications for intubation and ventilation afterhead injury (printed with permission from Professor DavidMenon)

Indications for intubation andventilation afterheadinjury

ImmediatelyComa (not obeying, not speaking, not eye opening),i.e.GCSo8Loss of protective laryngealre£exesVentilatory insu⁄ciency (as judgedbybloodgases)Hypoxaemia (PaO2o13 kPa on oxygen)Hypercarbia (PaCO246 kPa)

Spontaneoushyperventilation causing PaCO2o3.5 kPaRespiratory arrhythmia

Before the start ofthe journey:DeterioratingconciousnessBilaterally fracturedmandibleCopiousbleeding intomouthseizures

130 CURRENT ANAESTHESIA & CRITICALCARE

ary neuronal injuryby speci¢c neuroprotective interven-tions.Therapy is guidedbydetection of secondary insultsby continuous monitoring and by the use of imagingtechniques.

OPTIMIZINGPHYSIOLOGY

Intracranial pressure

In1783,Monro and Kelliemade observations on the rigidand inextensible cranial cavity with its incompressiblecontents.The components thatmake up the intracranialcontents are brain (80%), blood (5%), and cerebrospinal£uid (15%). The Monro ^Kellie doctrine states thatchanges in any of the three components will necessitatecompensatory changes in the volume of one or more ofthese components to maintain a constant ICP. Furtherexperiments and hypothesis on the pressure ^volumerelationship of the intracranial contents led to the con-clusion that at ¢rst, ICP rises slowly, accommodated bythe shift of cerebrospinal £uid. The rise is then morerapid as exhaustion of this compensatory mechanism

THE MANAGEMENTOF HEAD INJURY 131

occurs. In resting adults, the normal ICP is between 1and 10mmHg. A sustained rise in ICP will com-promise cerebral perfusion leading to cerebral ischaemiaand secondary neuronal injury. Current data suggestthat an upper threshold of 20^25mmHg should beused to initiate intervention to reduce ICP.5 Methodsof monitoring ICP and its interpretation are discussedin the neuromonitoring article which accompanies thisreview.

Cerebral-perfusion-pressure directedtherapy

Cerebral perfusion pressure (CPP) regulates blood £owin the brain as it determines the gradient across the cer-ebrovascular bed. Mean CPP is calculated using the fol-lowing formula:

CPP =Mean Arterial Pressure (MAP) ^ mean ICP.

If cerebrovascular autoregulation is intact, cerebralblood £ow (CBF) ismaintainedbetween the limits of ap-proximately 50^150mmHg. As mean arterial pressuredecreases between these thresholds, cerebral vasodila-tation occurs. If the compensatory mechanismsmaintaining ICP are exhausted, then the increase in cer-ebral blood volume (CBV) will cause a rise in ICPand further reduce CPP. Conversely, an increase inMAP causes cerebrovascular vasoconstriction, therebydecreasing CBV, resulting in a decrease in ICP andimproving CPP. Manipulation of MAP to enhanceCPP may help to avoid both global and regionalischaemia.In many centres, management of severe head injury is

focused around maintaining CPP. Although the level atwhich CPP is bestmaintained is not determined, severalstudies suggest that 60^70mmHg may be the criticalthreshold. In one of the bigger prospective studies,Rosner reported improved outcomes for 158 patients inwhom CPP was maintained over 70mmHg comparedwith those from theTraumatic Coma Data Bank.6

Maintaining CPP is achieved by optimizing intravascu-lar volume statuswith a CVPof 8^10mmHg, keeping thehaematocrit between 30% and 35%, ensuring normalosmolality and colloid oncotic pressure, and the use ofinotropic agents (Table 4). Dopamine, norepinephrineand phenylephrine are themost commonly used vasoac-tive agents. Although themost appropriate agent to op-timize cerebral perfusion is still not clear, a recent studysuggests that theuse of dopaminemay lead to higher ICPthan norepinephrine.7 The use of inotropes may have tobe guided with a pulmonary artery catheter or someform of cardiac output monitoring.There is evidence toshow that arti¢cially increasing the blood pressure tomaintain the CPP does not cause a signi¢cant increasein ICP and in some cases, actually lowers it.8

Lund therapy

The approach in the‘Lund therapy’ is based on principlesof intracranial blood volume regulation and improve-ment in brain microcirculation. It does so by counteracting transcapillary ¢ltration through a reduction insystemic blood pressure by antihypertensive therapyand constriction of the pre-capillary resistance vessels.9

Further studies are needed before this therapy is gener-ally implemented.

PHARMACOLOGICTHERAPY

Hyperosmolar therapy

Mannitol

Mannitol administration has been one of the key thera-pies in the treatment of raised ICP. It reduces cerebraloedema and raised ICP by two possible methods. Initi-ally, it causes plasma volume expansion and reduction ofblood viscosity thereby improving cerebral perfusionand microcirculatory dynamics. This e¡ect is rapid andoccurs within minutes of giving it. The osmotic e¡ecttakes place after approximately15min, when an osmoticgradient is established, and it lasts for between 90minand 6h. It may also have some antioxidant activityalthough the clinical signi¢cance is questionable.Although the use ofmannitol has notbeenprospectivelycomparedwith placebo, a Canadian trial did compare itsuse against barbiturate therapy.This study reported thatmannitol was superior to barbiturates, improving out-come,CPP and ICP.10

The use of mannitol is not without its hazards. It maytheoretically lead to worsening of cerebral oedema byreversing the osmotic shift, asmannitol can cause‘open-ing’ of the blood brain^barrier.This is more likely to oc-cur with continuous or prolonged infusions, as opposedto giving boluses of mannitol, leading to accumulation inthe brain. A disrupted blood^brain barrier can also al-lowmannitol to leak into cerebral tissue aggravating oe-dema. Rapid infusions of mannitol may lead to £uidoverload. Administration of large doses of mannitol maylead to acute tubular necrosis and renal failure especiallywhen the serum osmolality is greater than 320mOsm/kg, or if other nephrotoxic drugs are being used con-commitantly. Therefore, its use should be discontinuedwhen it no longer produces signi¢cant ICP reduction.

Hypertonic saline

Hypertonic saline has been evaluatedwith some successas the alternative to mannitol in the control of intracra-nial pressure.11,12 The mechanism of action has not beenfully evaluated. It is postulated thathypertonic salinemayact by volume expansion, thereby improving perfusion;

Table 4 NCCUhaemodynamics algorithm (printedwith permission from Professor David Menon)


decreasing cerebral oedemaby its osmotic e¡ects; rever-sing vasomotor dysfunction and vasospasm; andby in£u-encing the balance of sodium and glutamate in theinjured brain.13 Animal studies have also shown that hy-pertonic saline may a¡ect prostaglandin production andincrease levels of cortisol and adrenocorticotrophic hor-mone. As severe trauma activates the in£ammatory cas-cade and induces systemic in£ammatory responsesyndrome, some studies have suggested that the immu-nomodulatory e¡ects of hypertonic saline may lowersepsis-related complications.However, theuse of hypertonic saline is related to sev-

eral problems. Hypernatremia can lead to decreased le-vels of consciousness and seizures with sodium levelsabove170mEq/l.With a rapid increase in serum sodium,central pontine myelinosis is a potential risk. So far, the3% and 7.5% solutions have mainly been trialed for smallvolume resuscitation and ICP control, and the 23% solu-tion for treatment of intracranial hypertension refrac-tory to mannitol. A recent Cochrane review ofhypertonic vs isotonic crystalloids for resuscitation ofcritically ill patients concluded that a large, randomizedcontrol trial is requiredusing clinicallyrelevantoutcomessuch asmortality.14

Intravenous anaesthetic and sedative agents

Intravenous anaesthetic drugs are used with or withoutneuromuscular blocking agents for the sedation of pa-tients who are extremely agitated and confused, or re-quiring mechanical ventilation. They may also possesssome neuroprotective properties.

Barbiturates

High dose barbiturates have been proven to be e¡ectivein the reduction of increased ICP refractory to othertherapies15 and protect against focal ischaemia in animalmodels of severe head injury. However, the prophylacticuse of barbiturates has not been shown to have any im-provement in outcome.16

Barbiturates act in several ways. Cerebral metabolicrate for oxygen is reducedby the suppression of synaptictransmission, thereby reducing cerebral blood £ow andblood volume. There is suppression of the EEG activity,starting initially with the fast activity anteriorly, followedby burst suppression. Barbiturates also act by inhibitingfree-radical-mediated lipid peroxidation, reducing cal-cium in£ux and by blocking sodium channels. However,


a study using jugular bulb saturation has shown that itcaused detrimental outcomes in patients whose jugularbulb saturation fell below 45%.17

Barbiturates are not routinely used for sedationbecause of their propensity for accumulation and cardio-vascular instability.

Propofol

Propofol reduces ICP by the suppression of global meta-bolism.There is up to 50% reduction in the cerebralme-tabolic rate for oxygen associated with a reducedcerebral blood £ow, similar to the e¡ects of the barbitu-rates.Vascular reactivity to carbon dioxide, £ow/meta-bolism coupling and cerebrovascular autoregulation ismaintained. Other possible neuroprotective propertiesare free radical scavenging, possible calcium channelblocking, and glutamate antagonism. It has anticonvul-sant properties, although there have been reportsof excitation, choreoathetoid movements and ¢ts withits use.Problems with the use of propofol are: hypotension,

secondary to vasodilatation andmildmyocardial depres-sion which can compromise CPP. Propofol1% has a calo-ric content of 1kcal/ml and together with the high lipidcontent, prolonged continuous infusion has led toproblems with hypertriglyceridaemia. This is morepronounced in patients cooled for the control of raisedICP and regular blood tests may have to be done tomonitor lipid levels.Cessation of propofol during inducedmoderate hypothermia is advisable.The use of the 2%propofol solution limits the volume and total fat caloriesinfused.

Etomidate

Etomidate has similar neuroprotective e¡ects to barbi-turates. Despite its minimal e¡ect on the cardiovascularsystem, it is disadvantaged by the adrenal suppression itcauses. Even a single dose leads to 6^8h of corticoster-oid synthesis suppression. The formulation for the infu-sion of etomidate is not available in the UK.However, inAmerica, etomidate infusions are commonly used incombinationwith additional steroid cover.

Benzodiazepines

Benzodiazepines depress the central nervous system byaugmenting the gamma amino butyric acid inhibition ofneurones within the central nervous system.This in turnreduces cellular metabolism and may lead to a smalldecrease in cerebral metabolic requirement of oxygen,cerebral blood £ow and ICP. They also have sedative,hypnotic, anxiolytic and anticonvulsant properties.Among the various benzodiazepines, midazolam, whichis short acting and not formulated in propylene glycol is

most suitable for intravenous infusion. Prolonged infu-sion can lead to accumulation and delayed awakening.As these drugs are dependent on the liver for meta-bolism and the kidneys for excretion, impairment ofthese organs will lead to an increase in the duration ofaction.

Neuromuscular blockade

The use of neuromuscular blocking drugs in the neuroin-tensive care unit is controversial. These drugs areuseful in the ventilated head injury patient as they pre-vent coughing and straining against the endotrachealtubewhich lead to sharp rises in the ICP, and they reducethe response to interventions such as suctioning of thetrachea. Paralysing the patient facilitates blood gas ma-nipulation, particularly, during controlled hyperventila-tion and also prevents shivering during inducedhypothermia.Despite the advantages, it can lead to problems such

as prolonged intensive care stay, increased incidence ofpneumonia,myopathy anddelayedrecognition of seizureactivity. Information from the Traumatic Coma DataBank suggests that although thegroup ofpatientsreceiv-ing neuromuscular blocking drugs had lower mortality,they also hadmore complications and the survivors weremore severely disabled.

Steroids. Studies have shown that steroidsmay be use-ful in restoring the disrupted vascular permeability inhead injury, reducing cerebrospinal £uid production andas a free radical scavenger. However, a recent meta-analysis of the use of steroids in head injury has shownno overall improvement in the outcome.18

The use of high-dose steroids is also associated withmany complications, for example, gastrointestinal hae-morrhage, increased rate of infection, impaired woundhealing and hyperglycaemia.

Excitatory amino acid antagonists. It is thought thatthe release of EAA neuro transmitters and the overexci-tation of the corresponding receptors play a role in celldamage and cell death in the injured brain.This has leadto the development of EAA antagonists. There have, asyet, been no successful phase III trials of EAA acidantagonists.19

Tromethamine. (THAM, tris-hydroxymethylamino-methane). Tromethamine is a bu¡ering agent shownto be promising in the control of ICP in both clinicalexperiments and animal studies. Tromethamine actsby entering the cerebrospinal £uid compartmentreducing cerebral acidosis, cerebral lactate and oedema.It may be used to reverse the adverse e¡ects of hyper-ventilation.20


NON-PHARMACOLOGICTHERAPY

Head elevation

Thepatientswithraised ICP arebestnursed15^301 headup.The patient must be adequately £uid resuscitated orthe patients could su¡er from orthostatic hypotension,which may be detrimental to the cerebroperfusionpressure.

Avoiding venous compression in the neck

The head and neck should be optimally positioned toavoid jugular venous congestion. The use of ties aroundthe neck must be checked to ensure it is not excessivelytight thereby obstructing jugular venous out£ow. Careshould be taken to ensure neck collars are not too tightand the neck shouldbe in the neutral position.Rigid neckcollars may cause a small rise in ICP. Therefore, earlyclearance of the neck is necessary, failing which,alternativemethods of neck stabilizationmay have to beconsidered.21

Hypothermia

Moderate hypothermia (32^331C centigrade) has beenshown to improve outcome in animal models of experi-mental head injury and some small clinical studies. In ad-dition to cerebral metabolic suppression, hypothermiahas also been found to modify a number of molecularresponses such as the release of EAA, cytokines, free ra-dicals and in£ammatory mediators.22 However, tem-peratures less than 321C centigrade pose risk of cardiacarrhythmias, myocardial depression, increase in bloodviscosity and possibly a¡ecting vascular perfusion. Rapidrewarming also carries the risk of raising ICP by causinghyperaemia.Based on previous smaller studies, moderate hy-

pothermia has been the cornerstone of therapy forraised ICP for many years, but its use has now becomemore controversial. In a recently published large multi-centred randomized control trial of induced hypother-mia for 48h after injury, no signi¢cant bene¢t inoutcome was demonstrated.23 This has put the use ofprophylactic hypothermia (32^331C) in acute brain in-jury in doubt as a clinical intervention.

Hyperthermia

Elevations inbrain temperaturehavebeen shown to havea detrimental e¡ect on outcome after severe braininjury.24 Increases in temperature may be controlledpharmacologially by the use of paracetamol and the cau-tious use of non-steroidal anti-in£ammatory drugs, e.g.diclofenac.Temperature control can also be achieved by

the use of cooling devices, cold sponging, ice packs andcentral venous cooling.

Hyperventilation

Hyperventilation has been one of the key therapeuticinterventions for raised ICP over the last 20 years. Therationale for its use is based on the fact that hyperventi-lation reduces cerebral blood volume by cerebral vaso-constriction thereby reducing ICP. However, one studyfound that in normal humans, hyperventilation to aPaCO2 of 26mmHg led to a 7.2% reduction in CBV but a30.7% decrease in CBF.25 In the early stages after headinjury, CBF may already be reduced, making the risk ofCBF falling below the ischaemic threshold much morelikely if hypocapnic vasoconstriction is superimposed.Such ischaemia has been documented by imaging techni-ques such as positron emission tomography,26 jugularbulb desaturation below 50%,27 and brain tissueoxygen.28

Prolonged hyperventilation (PaCO2 of 25mmHg)for 5 days was shown to worsen outcome comparedwith a controlled group of head-injured patients.29

With prolonged hyperventilation, adaptation to the hy-pocapnia occurs after several hours due to compensa-tory reductions in cerebral extracellular bicarbonatewhich rapidly restores the pH of extracellular £uid.If rapid normalization of carbon dioxide tension takesplace cerebral hyperaemia can worsen intracranialhypertension.With this large body of evidence, it has become a

standard that in the absence of increased ICP,chronicprolongedhyperventilation(PaCO2o25mmHg),should be avoided after severe head injury, andPaCO2 values below 35mmHg be avoided during the¢rst 24h after severe head injurybecause it can compro-mise cerebral perfusion during a time when CBF isreduced.6

Glucose control and nutrition in head injury

The stress response in severe head injury increases levelsof catecholamines and cortisol, leading to hyperglycae-mia.This is known toworsen neurologic outcome,30 andtight glucose control (plasma glucoseo10mmol/l) is re-commended. Fasting the patient is not feasible becauseof protein energy malnutrition as discussed below. Theessential point is the regularmonitoring of glucose levelsand treating hyperglycaemiawith supplemental insulin.Patients with head injury are hypermetabolic and hyper-catabolic. Although the caloric requirements vary withage, sex and body surface area, in general, 140% ofthe resting metabolism should be replaced in the non-paralysedpatient and100% in the paralysedpatient. Mal-nutrition or weight loss may lead to a poorer outcome


in head-injured patients.The caloric replacement shouldbe started within 72h of the injury if there are nocontraindications. Early enteral nutrition also blunts thehypermetabolic response.The nitrogen loss in the fasting head-injured

patient is two to three times that of the normalperson, and less than 50% of the nitrogen provided isretained by the body. Nitrogen excretion is improvedwith the addition of branched chained aminoacids and arginine, but there is no proof that theuse of these substrates improves the long-termoutcome.

Table 5 Addenbrooke’s NCCUICP/CPP management algorithm

Prophylactic anticonvulsants

After severehead injury, seizures can occur early (before7 days) or late (after 7 days) following trauma. Anticon-vulsants such as phenytoin or carbamazepine reduce theriskof early post-traumatic seizures if the patients are athigh risk. Risk factors include GCSo10, cortical contu-sions, depressed skull fracture, subdural haematoma,epidural haematoma, intracerebral haematoma, pene-trating head wound or seizure within 24h of injury.Prophylactic anticonvulsants are not recommended forpreventing late post traumatic seizures.

(printedwith permission from Professor David Menon)


SURGICALMANAGEMENT

Decompressive craniectomy

Decompressive craniectomy is one of the modalitiesused in themanagement of uncontrolled intracranial hy-pertension. It may be considered when conventionalmedical therapy has failed. There are di¡erences in opi-nion regarding the indications, timing or even the surgi-cal technique.Decompressive craniectomy is thought toreduce ICP, decrease midline shift and increase focalblood £ow to the traumatized brain. However, someanimal studies have suggested that craniectomy maylead to greater cerebral oedema andmore local damage.The use of decompressive craniectomy remains contro-versial. Many studies are retrospective and there isinsu⁄cient evidence to prove that it is superior to con-servative treatment.

Controlled lumbar CSF drainage

A possible way of treating refractory intracranial hyper-tension is by the controlled drainage of lumbar cere-brospinal £uid. However, there is a danger of transtentorial or tonsillar herniation and should only be per-formed if the basilar cisterns are discernable.

SEQUENTIALELEVATIONOFTHERAPYINTHEMANAGEMENTOFSEVEREHEADINJURYThere are many treatment algorithms for the manage-ment of severe head injury. A coherent approach isneeded to treat the diversepathophysiological processesthat occur in severe head injury. The standard protocolillustrated in Table 5 is the ICP/CPP Management algo-rithm used in the neurosciences critical care unit at Ad-denbrookes Hospital.The initial baselinemonitoring andtherapy is universally applied to all patients with or atrisk of intracranial hypertension.The various treatmentmodalities are then targeted to the clinical presentationand results of the physiologicalmonitoring.A recent audit has demonstrated a signi¢cant im-

provement in outcome in patients treated after theinstitution of the above protocol compared withpatients treated before protocol driven management(personal communication from Prof.DKMenon).

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