The management of head injury and intracranial pressure

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<ul><li><p>nd</p><p>ei,ac</p><p>prevention of secondary injury involves prompt airwaymanagement and treatment of</p><p>Current Anaesthesia &amp; Critical Care (2002) 13,129^137c 2002 Elsevier Science Ltd. All rights reserved.doi:10.1054/cacc.401, available online at onhypoxia 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) andneurospecicmeasures.Theneurospecicmeasures 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 theirbenets andtheirpitfalls.c 2002 ElsevierScience Ltd.Allrights reserved.</p><p>INTRODUCTIONHead injury occurs frequently, with about1.4 million pa-tients suering a head injury in the UKeach year.1Severehead injury is dened 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</p><p>at the scene, and the intensive care management. Pa-tients presenting with features suggestive of poor out-come (Table 1) can benet from early recognition andaggressive intervention.2</p><p>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</p><p>or death if no intervention is made. These mechanismsmay be compounded by changes in global and regionalcerebral blood ow (CBF),3 specically a reduction ofCBF in the rst12^24h after injury.In an analysis of 717 patients from the traumatic coma</p><p>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).</p><p>INTENSIVECAREMANAGEMENTThe ICUmanagementof patientswith severe head injuryand raised intracranial pressure (ICP) includes the opti-mization of physiology by providing good intensive care,Correspondence to: AKG.Tel.: +441223 217434; Fax: +441223 217223;FOCUSON:NEUROINTENSIVECAR</p><p>Themanagement of head ipressureJ.Goh and A.K.Gupta</p><p>*Department of Anaesthesia, Addenbrookes Hospital,Cambridge,UK anCambridge,UK</p><p>KEYWORDScraniocerebral trauma,intracranial pressure,hypertension, intracranial</p><p>Summary Severe headAlthough the incidence is dthesepatientshasmajor sochead injury is both primaryBecause little can be donetargeted at reducing the se0953-7112/02/$-see frontmatter</p><p>E-mail:</p><p>jury and intracranial</p><p>wNeuro-critical care, Addenbrookes Hospital,University of Cambridge,</p><p>injury occurs predominantly in the young population.creasing in the United Kingdom, the eventual outcome ofal andeconomicimplications.Damagetobraintissue duringdue to the initial insult, or secondary, which occurs later.bout the primary injury, the intensive care management isondary insults whichmay cause further brain damage.Theand the prevention or reversal ofmechanisms of second-</p></li><li><p>Table 1 practical protocol for management of head-injuredpatients in the emergencydepartment</p><p>130ary neuronal injuryby specic neuroprotective interven-tions.Therapy is guidedbydetection of secondary insultsby continuous monitoring and by the use of imagingtechniques.</p><p>Group A (minimalhead injury GCS=15)K Patient is awake, orientated and without neurologic</p><p>decits andrelates accidentK Noloss of consciousnessK NovomitingK Absentorminimal subgaleal swellingThe patient is released into the care of a familymember withwritten instructions.</p><p>Group B (minor head injury GCS=15)K Patient is awake, orientated and without neurologic</p><p>decitsK Transitory loss of consciousnessK AmnesiaK One episode of vomitingK Signicant 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.</p><p>GroupC (moderate headinjuryormildheadinjury withcomplicat-ing factors GCS=9^15)K Impaired consciousnessK Uncooperative for various reasonsK RepeatedvomitingK Neurologic decitsK Otorrhagia/otorrhoeaK RhinorrhoeaK Signs of basal fractureK SeizuresK Penetrating or perforatingwoundsK Patients in anticoagulant therapy or aected by coagulo-</p><p>pathyK Patients who have undergone previous intracranial</p><p>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.</p><p>Group D (Severe head injury GCS = 3^8)K Patient is in comaNecessaryresuscitationmanoeuvres followedbyneurologicalevaluation and immediate CTscan (prior to surgical interven-tion).Comamanagement</p><p>Reprintedbypermission from?Table 2 mechanisms of brain injury, initial event: trauma,ischaemia</p><p>Primary Secondary Systemic</p><p>Tissue destruction Pressure eects HypoxaemiaHaemorrhage Hydrocephalus HypotensionPressure eects Herniation HypercarbiaDiuse axonal injury Vasospasm Excessive</p><p>hypocarbiaReducedmetabolic rate</p><p>Hyperthermia</p><p>Impairedautoregulation</p><p>Anaemia</p><p>Secondaryhyperaemia</p><p>Electrolytedisturbance</p><p>Oedema Hyperglycaemia</p><p>CURRENT ANAESTHESIA &amp; CRITICALCAREOPTIMIZINGPHYSIOLOGY</p><p>Intracranial pressure</p><p>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 cerebrospinaluid (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</p><p>Table 3 Indications for intubation and ventilation afterhead injury (printed with permission from Professor DavidMenon)</p><p>Indications for intubation andventilation afterheadinjury</p><p>ImmediatelyComa (not obeying, not speaking, not eye opening),i.e.GCSo8Loss of protective laryngealreexesVentilatory insuciency (as judgedbybloodgases)Hypoxaemia (PaO2o13 kPa on oxygen)Hypercarbia (PaCO246 kPa)</p><p>Spontaneoushyperventilation causing PaCO2o3.5 kPaRespiratory arrhythmia</p><p>Before the start ofthe journey:DeterioratingconciousnessBilaterally fracturedmandibleCopiousbleeding intomouthseizures</p></li><li><p>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.</p><p>Cerebral-perfusion-pressure directedtherapy</p><p>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:</p><p>CPP =Mean Arterial Pressure (MAP) ^ mean ICP.</p><p>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</p><p>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</p><p>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 articially increasing the blood pressure to</p><p>THE MANAGEMENTOF HEAD INJURYmaintain the CPP does not cause a signicant increasein ICP and in some cases, actually lowers it.8Lund therapy</p><p>The approach in theLund 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</p><p>Further studies are needed before this therapy is gener-ally implemented.</p><p>PHARMACOLOGICTHERAPY</p><p>Hyperosmolar therapy</p><p>Mannitol</p><p>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 eect is rapid andoccurs within minutes of giving it. The osmotic eecttakes place after approximately15min, when an osmoticgradient is established, and it lasts for between 90minand 6h. It may also have some antioxidant activityalthough the clinical signicance 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</p><p>The use of mannitol is not without its hazards. It maytheoretically lead to worsening of cerebral oedema byreversing the osmotic shift, asmannitol can causeopen-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 signicant ICP reduction.</p><p>Hypertonic saline</p><p>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 been</p><p>131fully evaluated. It is postulated thathypertonic salinemayact by volume expansion, thereby improving perfusion;</p></li><li><p>si</p><p>CURRENT ANAESTHESIA &amp; CRITICALCARETable 4 NCCUhaemodynamics algorithm (printedwith permis</p><p>132decreasing cerebral oedemaby its osmotic eects; rever-sing vasomotor dysfunction and vasospasm; andby inu-encing the balance of sodium and glutamate in theinjured brain.13 Animal studies have also shown that hy-pertonic saline may aect prostaglandin production andincrease levels of cortisol and adrenocorticotrophic hor-mone. As severe trauma activates the inammatory cas-cade and induces systemic inammatory responsesyndrome, some studies have suggested that the immu-nomodulatory eects of hypertonic saline may lowersepsis-related complications.However, theuse of hypertonic saline is related to sev-</p><p>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.14on from Professor David Menon)Intravenous anaesthetic and sedative agents</p><p>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.</p><p>Barbiturates</p><p>High dose barbiturates have been proven to be eectivein 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</p><p>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 inux and by blocking sodium channels. However,</p></li><li><p>a study...</p></li></ul>


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