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Attorneys' Textbook of Medicine (Third Edition)CHAPTER 93 SEQUELAE OF HEAD INJURIES

Excerpt© Copyright 2008, Matthew Bender & Company, Inc., a member of the LexisNexis Group.

P 93.00 NATURE AND SIGNIFICANCE OFHEAD INJURY

The term ''head injury'' generally refers totraumatic injury to the brain and intimatelyassociated cerebrocranial structures, mostprominently the cerebral hemispheres, thebrainstem, the intracranial vasculature and themeningeal membranes that envelope the brain.However, other major types of cranial injury can besustained during acute head trauma, includinglacerations of the scalp, skull fractures, corticalcontusions and lacerations, and intracranialhemorrhage (Evans and Wilberger, 1999). Traumatic head injury is a major cause ofmorbidity and mortality in the United States,especially among the pediatric population andyoung adults (Evans and Wilberger, 1999;MacKenzie, 2000). Physicians who care forpatients suffering an acute head injury mustunderstand the need for timely evaluation andtreatment of head injuries and the possible long-term complications of such injuries. The impact ofthese injuries can be devastating for both thepatient and society, since death or permanentdisability associated with chronic pain syndromescan result (Evans and Wilberger, 1999). Despiteincreased understanding of the pathophysiology ofbrain injury, no new medical treatments have beendeveloped, and supportive care remains themainstay of therapy. Thus, prevention of acutehead injury remains of utmost importance.

P 93.10 ETIOLOGY AND EPIDEMIOLOGY OFHEAD INJURY

Motor vehicle accidents account for the majority ofacute head injuries, but recent mandates forseatbelt use and air bags have reduced theincidence of head injuries caused by car accidents.In contrast, gunshot wounds to the head havebeen increasing, particularly in urban areas, wherethis is the most common cause of head injuryobserved in these communities (Evans andWilberger, 1999). Among children and

adolescents, sports such as diving, gymnasticsand football are a major cause of head and neckinjuries. Approximately 3 to 25 percent of alltraumatic head injuries in this age group arecaused by organized sporting activities (Proctorand Cantu, 2000). For the population as a whole, closed head injuryleads to 500,000 hospitalizations per year,resulting in over 175,000 deaths as well assignificant disability. Current estimates of theincidence of head injury approach 222 in 100,000population per year. (Evans and Wilberger, 1999)The peak incidence occurs in men between 15 to24 years of age and again above 75 years of age. Head trauma is the leading cause of death anddisability in children, accounting for more than 50percent of deaths in this age group. On average,approximately 100,000 to 200,000 head injuriesoccur per year among children, with a rate of 193to 367 per 100,000 (Gedeit, 2001). The incidencepeaks early in childhood and again duringadolescence, mirroring non-accidental andvehicular causes of trauma, respectively.

[93.11] Mortality There has been a significant decline in overallmortality associated with head injuries from themid-30 percent range reported in the 1970s to lessthan 20 percent in the 1990s. (Evans andWilberger, 1999) Improved mortality rates haveresulted from increased understanding of thepathophysiology of brain injury and thedevelopment of aggressive treatment strategies toprevent intracranial pressure elevations andischemia (lack of blood supply). When secondaryinsults of low oxygen saturation (hypoxia) and lowblood pressure (hypotension) are superimposedon severe head injury, mortality is doubled.Similarly, concomitant elevations in intracranialpressure increases morbidity. Hence, timelytreatment to prevent these insults is of paramountimportance.

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[93.12] Principal Risk Factors for Injury Principal risk factors for sustaining head traumainclude age, gender, race, area of residence,socioeconomic status and occupation. Followinginjury, the critical determinant of ultimate outcomeis the nature of secondary sequelae and the extentto which they develop. Adequate control of thesedepends on the quality of medical care the patientreceives. Males tend to be affected more thanfemales, with a ratio of 2 to 4:1 in adolescents; thehighest rate occurring among the lowersocioeconomic classes. Advanced age is also animportant risk factor for traumatic head injury. Among the elderly, the increase in frequency ofthese injuries is related to the increase infrequency of falls (Luukinen, et al., 1999). In ruralareas, farm equipment is a major source of injury,while in urban areas, violence, particularly gunshotwounds to the head, is a predominant cause(Evans and Wilberger, 1999). Agriculture,construction, mining, manufacturing andtransportation are occupations associated with thehighest risk of traumatic injury and death (Evansand Wilberger, 1999).

[93.13] The Cost of Head Injury Head injuries account for nearly 50 percent of allhospitalizations and are the leading cause of deathdue to injury as well as disabilities in children andyoung adults (MacKenzie, 2000). Each year,approximately 80,000 survivors of head injury willincur some disability or require extensive medicaltreatment for their injury. The direct medical costsfor the treatment of traumatic brain injury isestimated to be $48 billion per year, whichincludes the costs of hospitalization for acute careand rehabilitation services (ACHPR, 1999). In thepediatric population, the costs of the head-injuredpatient are even greater. The median costs for achild having a severe head injury is reported to beabout $53,000 dollars, with rehabilitation servicesaccounting for 37 percent of the total costs. Thespecific costs of head injury vary with the severityof the injury. Early diagnosis and treatment ofpatients with mild head injury can significantlyreduce the costs to patients and their families(Cheung and Kharasch, 1999).

P 93.20 DEFINITIONS

Head trauma is classified as mild, moderate or

severe based on neurologic assessment using theGlasgow Coma Score (which is modified for use inchildren), with the range between 1 and 15. Ingeneral, a Glasgow coma score of at least 13defines mild head injury, 8 to 12 moderate headinjury, and 7 or less severe head injury. (Gedeit,2001; Evans and Wilberger, 1999) By definition, aconcussion is a mild head injury associated withconfusion or loss of consciousness (less than oneminute). Concussions are not usually associatedwith structural brain injury or long-term sequelae.The postconcussion syndrome is a distinct entityand will be discussed in detail later on in thischapter. A brain contusion results from direct injuryto the brain, either from blunt trauma from externalcontact forces or from the brain contactingin t racrania l sur faces resu l t ing f romacceleration/deceleration trauma (Gedeit, 2001).

P 93.30 MECHANISMS OF HEAD INJURY

Traumatic brain injury is an insult to the brain byan external force that results in either a transient orpermanent impairment of cognitive, behavioral,emotional, or physical function. Traumatic braininjury encompasses a shearing injury, which canresult from blunt trauma (such as what may occurin a shaken infant), as well as penetrating injuryfrom a foreign body, such as a bullet (Guthrie etal., 1999). The sequelae of head injury can be classified threeways:

(1) with respect to the physical forces thatultimately cause the damage; (2) with respect to the types of pathophysiologicallesions that result within the cranium, and; (3) with respect to the time of injury onset andcourse.

[93.31] Physical Forces An understanding of the following principles arenecessary in order to understand the physicalforces that produce skull and brain injuries. First,a forceful blow to a restful, movable headproduces maximum head injury beneath the pointof impact (this is known as a ''coup'' injury).Second, a moving head which collides against astationary object produces maximum brain injuryopposite to the site of cranial impact (also known

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as ''contrecoup'' injury). Such lesions are mostcommon at the tips and the undersurfaces of thefrontal and temporal lobes. Third, if a skull fractureis present, the first two principles are notapplicable, because the bone itself, whethertransiently (e.g., a linear skull fracture) orpermanently (e.g., a depressed skull fracture)displaced at the time of impact may directly injurebrain tissue (Proctor and Cantu, 2000). There are also three types of stresses that aregenerated by an applied force: compressive,tensile (the opposite of compressive, sometimesreferred to as negative pressure), and shearing(when the applied force is parallel to a surface).Uniform compressive forces are generallytolerated fairly well by the nervous system, butshearing stresses are very poorly tolerated(Proctor and Cantu, 2000). The cerebrospinal fluid (CSF) acts in a mannerconsistent with a shock absorber, protecting thebrain by converting focally applied externalstresses to a more uniform compressive stress.This occurs because the fluid follows the contoursof the sulci of the brain, thus cushioning the brainfrom damaging shearing forces. Despite thepresence of CSF, however, shearing stresses maystill be imparted to the brain. If rotational forces areapplied to the head, for example, shearing forcesmay potentially occur at sites where rotationalgliding is hindered. These areas are characterizedby (1) irregular surface contacts between the brainand skull (which hinder smooth movement); (2)leakage of CSF between the brain and skull, and(3) attachments between the dura mater (tissuethat covers the surface of the brain) and the brainitself, which impedes brain motion (Proctor andCantu, 2000). The first condition is usually most prominent in thefrontal and temporal regions of the brain and is thereason why major brain contusions occur at thesesites. The second condition is most commonlyassociated with the coup and contrecoup injuries.When the head is accelerated before impact (e.g.,what occurs in auto racing), the brain lags towardthe trailing surface, displacing the CSF, allowingthe shearing forces to be maximal at this site.Usually, brain lag thickens the layer of CSF underthe point of impact, preventing coup injury in amoving head injury. In contrast, when the head isstationary before the point of impact, brain lag nora disproportionate distribution of CSF occurs,

which accounts for the absence of contrecoupinjury and the presence of coup injury (Proctor andCantu, 2000). The scalp also provides energy-absorbingproperties. Approximately ten times more force isrequired to produce a skull fracture in a head withthe scalp in place than in one in which the scalphas been removed. In addition, an athlete's headcan sustain large forces without brain injury if theneck muscles are tensed at the moment of impact.In the relaxed state, the mass of the head acts asits own weight as it is propelled forward. However,when the neck is rigidly tensed, the mass of thehead approximates the mass of the body, enablingthe head to sustain the force within minimumimpact (Proctor and Cantu, 2000). In general, the damage done by the variousphysical forces involved in head trauma isproduced through two basic mechanisms:concussive-compressive mechanisms andacceleration-deceleration mechanisms. Most headinjuries involve some combination of the two, andtheir interaction often is complex (Guthrie, et al., 1999).

[1] Concussive-Compressive Injuries--Concussive-compressive injuries are seenfollowing both blunt and penetrating trauma. Suchinjuries often result in brain contusions,lacerations, and hemorrhage in the epidural,subarachnoid, subdural, or intracerebral spaces(Amann, 2000).

[1a] Blunt Trauma-- A concussive-compressivetype of injury usually results from blunt traumacaused by a blow to the head with a heavy object,such as a baseball bat, hammer or pool cue. Asthe object impacts the head, the kinetic energy ofits motion is transmitted first to the scalp, then tothe skull and finally to the brain and surroundingstructures. The scalp and skull offer someprotection to the brain by dissipating a fraction ofthe energy. However, a force greater than theelasticity of the skull can accommodate willproduce a skull fracture, which can cause directmechanical tearing of the blood vessels andlaceration of the brain, depending on the type andseverity of the fracture (Evans and Wilberger,1999; Amann, 2000). Whether the skull is fractured or not, some portionof the kinetic energy of the blow is transmitted tothe brain and other intracranial contents in the

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form of concussive-compressive pressure waves.The force of these waves tends to be concentratedover the area of impact, which usually is relativelysmall (e.g., the size of a hammer head), but theinertia is propagated to some degree throughoutthe entire brain. Consequently, the clinical pictureis one of local contusion (bruising) and diffuseconcussion (jarring shock) (Evans and Wilberger,1999; Amann, 2000). Head injury is frequently associated with skullfracture, and the clinical significance of the fracturedepends on the type of head injury. With severehead injury, linear fractures are largelyinsignificant. However, the presence of a skullfracture with mild head injury increases the risk ofan intracranial abnormality by as much as four-fold. Basilar skull fractures tend to be complicatedby leak of cerebrospinal fluid, infection and cranialnerve palsies. Hence, patients with basilar skullfractures require closer clinical monitoring thanthose with linear skull fracture. In infants andyoung children, linear fractures may becomplicated by leptomeningeal cysts or ''growing''skull fractures. When these lesions occur, a massmay develop in close proximity to the fracture site,as CSF collects from a disruption of the underlyingtissue. Appropriate treatment of a cyst requiressurgery. For this reason, it is important to followchildren for several months for the development ofa possible cyst (Evans and Wilberger, 1999).

[1b] Penetrating Trauma-- Although penetratingtrauma to the brain is not as common as blunttrauma, the incidence of this type of brain injuryhas been increasing (Blank-Reid and Reid, 2000;Peek-Asa, et al., 2001) Penetrating injury from aforeign body, such as a bullet or other projectileproduces the most destructive concussive-compressive injuries. Damage results from boththe transmission of impact forces from the skull tothe brain and the passage of the projectile throughthe brain tissue. Direct structural damage occursas the projectile crushes the tissue in its path(producing a permanent hole), and to a lesserextent as a result of stretching of the surroundingtissue by waves of kinetic energy. The majority ofdamage is caused by the crushing force. Mortalityrates are higher in patients with penetrating braininjuries compared to those with closed brain injury.In one study, patients with penetrating braininjuries were approximately seven times morelikely to die compared to closed brain injuredpatients (Peek-Asa, et al., 2001).

In the case of penetrating trauma to the head,rapid transport to trauma centers where definitivecare can be rendered is essential. Outcome of theinjury depends on the nature of the missile tract,the presenting neurologic status, and the extent oftissue destruction. Neurologic deterioration occursrapidly and outcome results appear to determinethe patient's neurologic status at the time ofsurgery (Blank-Reid and Reid, 2000). Penetratinghead injuries are often difficult to manage since theextensive surgery that is required can result insevere morbidity and mortality (Rao, et al., 1998).

[2] Acceleration-Deceleration Forces--Acceleration-deceleration injury is the type of headinjury which is characteristic of falls or motorvehicle accidents (e.g., contrecoup contusions). Inboth instances, brain tissue is severely injured dueto disruption of axonal fibers by shearing forcesduring acceleration, deceleration and rotation ofthe head. Diffuse injuries usually result fromshearing forces produced by acceleration ordeceleration with angular rotation, whichcommonly occurs when a moving head strikes astationary object. The resulting injury pattern isknown as ''diffuse axonal injury'' and is often seenin patients with concussion. This is the mostcommon mechanism of injury in young childrenwho experience falls from short distances thatimpart a linear force to the head (Amann, 2000). Two case reports in the literature also describe theunusual scenario of patients with cerebralcontusions resulting from falling tree limbs hittingthe head (e.g., blunt force trauma) (Morrison, etal., 1998) The pathogenesis of these contusionsinvolves a forceful impact resulting fromacceleration of the head and brain of a magnitudecomparable with that of a motor vehicle accident orfall. Acceleration or deceleration forces experienced ina motor vehicle accident induce indirect forceeffect lesions, such as subdural hematomas andsubarachnoid hematomas (Richter, et al., 2001)These lesions occur because the collision of avehicle traveling at high speed with another objectbrings the vehicle and its occupant to animmediate standstill. This abrupt change in motionresults in shear forces that severely damage braintissue. While the occupant's body and head arebrought to a stop by impact with the dashboard (forexample), the brain and other intracranial contents

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continue to travel at the original high velocity untilthey are brought to a stop by impact with the innersurface of the skull. In an instant, the brain issubjected to a combination of powerfulacceleration-deceleration shearing forces whichinvolve angular acceleration (twisting), differentialdeceleration of different regions of the brain andrebound forces as the elastic brain tissue snapsback from its traumatic deformation. Thetremendous amounts of kinetic energy thusimparted to the brain, its covering membranes(e.g., the meninges) and its vasculature producewidespread and severe damage (Richter, et al., 2001). Victims of motor vehicle collisions often develop asyndrome consisting of head, neck, and back pain,short-term memory loss, fatigue and a lack ofstamina, poor balance, and personality changes.This syndrome is often referred to as ''the motorvehicle collision injury syndrome'' in the medicalliterature. Although the pathogenesis of thissyndrome is not well understood, it is believed thatthe collision impact results in an inertial straininjury to the anterior regions of the brain,depressing the functions of the frontotemporallobes which in turn impairs sensory input to thebrain. Early intervention that arrests the metaboliccascade caused by head injury may mitigate thesymptoms of this syndrome (Mamelak, 2000).

[3] Combination Injuries and Multiple Trauma--Every head injury involves both concussive-compressive and acceleration-decelerationmechanisms to varying degrees. In addition to therelatively local concussive-compressive forces thatoccur from a blow to the head, the force generatedby the impact of the object also causes the head tomove. When this occurs, the encased brainaccelerates as a result of being pushed by theinner surface of the skull. When the head stopsmoving, the brain decelerates due to the impactwith the interior surface of the skull. The brain andassociated structures are thus subjected to someinertial acceleration-deceleration shearing forces.For example, when the head of the occupant of acrashing vehicle hits the dashboard or other part ofthe vehicle, the brain is subjected to localconcussive-compressive forces emanating fromthe site of impact, as well as acceleration-deceleration forces. Another example of combination head injuries arechildren who are victims of dog attacks. Childrenwho suffer traumatic head and neck injuries from

a dog attack are subject to both the penetratingcomponent of the bite as well as the blunt natureof the bite (which may represent the mostdevastating component of the head injury) (Calkinset al., 2001). In addition to shearing forces, direct mechanicalinjuries may occur as the brain moves across thebony structures of the interior of the skull and therigid dura mater (the outermost meningealmembrane enveloping the brain). The brain maybe contused (bruised) and brain tissue and/orcerebral blood vessels may be lacerated (cut andmangled). Injuries of this type commonly occuralong the sphenoid wing (a wedge-shaped bone)in the base of the skull and along the falx cerebri(the rigid sickle-shaped fold of the dura materwhich extends down into the cleft between theright and left cerebral hemispheres). Bleeding fromtorn vessels can result in a hematoma (a pool ofextravasated blood), which can elevate intracranialpressure (Evans and Wilberger, 1999) Theresultant compression of the brain tissue leads toischemic (lack of blood supply) and hypoxic(insufficient oxygen supply) brain damage and, ifnot relieved, permanent neuropsychologicaldeficits or possibly death.

Intracranial pressure (ICP) also is raised whentraumatic force is applied to the head. Anymechanism that creates elevated intracranialpressure can produce a herniation of the brain,which commonly occurs in the foramen magnum(the large opening in the base of the skull throughwhich the spinal cord enters and joins thebrainstem). Being the path of least resistance inthe otherwise tightly closed cranium, the brainstemwill be forced down into that opening as a meansof relieving acutely elevated intracranial pressure.Since this region of the brain mediates vitalfunctions such as respiration and blood pressure,herniation damage arising from transmission ofshearing forces to the brainstem can produce avariety of systemic insults and possibly death(Evans and Wilberger, 1999).

[93.32] Pathophysiology The primary pathologic feature of traumatic braininjury is axonal injury. Traumatic forces resultingfrom blunt or penetrating trauma or accelerating-decelerating mechanisms produce strains anddistortions within the brain that disrupt axons(nerve fibers) and small blood vessels. As a

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consequence, brain edema (swelling) occurs.Immediate life-threatening complications can resultfrom this axonal disruption, with an alteration orloss of consciousness often being the firstmanifestation of the disruption. If cerebralimpairment is severe, respiratory drive may beaffected, and the patient may hypoventilate orbecome dyspneic (have difficulty breathing) orapneic (stop breathing). If not addressedimmediately, cardiovascular function may also becompromised (Gedeit, 2001). The number of axons injured and the degree ofcerebral edema is directly proportional to theseverity of the traumatic force. While less severe,axonal injury is usually reversible, whereas moresevere injury may be permanent. These forces canalso result in gross tearing of the veins, arteries,and dural sinuses, resulting in subduralhematoma, epidural hematoma, and contusion.Lacerations of the vasculature and associatededema can lead to a rapid rise in the intracranialpressure, resulting in compression and herniationof the brain. In turn, compression can squeeze offthe cerebral blood vessels, producing ischemic(from lack of blood supply) and hypoxic (frominadequate oxygen supply) brain damage.Intravascular blood clots (thrombi), traumaticvascular spasms and various structural changes inthe walls of the blood vessels themselves also cancontribute to ischemic and hypoxic injury (Gedeit,2001). Primary brain injury from direct trauma is oftencomplicated by secondary neuronal injuriesresulting from disturbances in blood flow, capillarypermeability, and inflammation. Rarely is structuralinjury to the brain at the time of impact the soledeterminant of outcome. Traumatic brain injurystarts a cascade of events leading to impairedmetabolism, altered blood flow, and worseningcerebral swelling. Studies have shown thatischemia, abnormalities in glucose metabolism,and abnormal permeability of the blood-brainbarrier are factors which increase brain edema(Gedeit, 2001). Inflammation, free radicalformation, and influx of calcium can also cause celldamage that worsens edema. These responsesinitiate a downward spiral beginning withrespiratory decompensation, hypotension andcardiovascular collapse that may lead to death. Infact, mortality is doubled when these secondaryinsults are superimposed on severe head injury(Gedeit, 2001; Evans and Wilberger, 1999).

P 93.40 MAJOR SEQUELAE OF HEAD INJURY

In addition to the aforementioned classifications,head injuries can be classified either as primary orsecondary injuries, according to their appearancein the complex posttraumatic chain of events. Ingeneral, injuries that result directly from the traumaitself are referred to as primary injuries. Theseverity and location of the primary brain injurydetermines the patient's immediate level ofconsciousness and mental status. Currently, thereis no treatment available for primary brain injury.(Savitsky and Votey, 2000; Zink, 2001) Secondary brain injury occurs subsequent to thetrauma causing primary brain injury, and is a resultof a large number of interrelated pathophysiologicprocesses triggered by the primary injury. If leftunchecked, these processes may lead toirreversible damage of brain tissue which waspartially or totally unaffected by the initial traumaticevent. For example, primary brain injury may leadto impaired autoregulation of cerebral blood flow,which in turn contributes to brain swelling. Thisswelling further exacerbates the injury cascade bycausing compression of brain tissue, elevatedintracranial pressure, and subsequent brainherniation and death. Because of its devastatingconsequences, the focus of most current andinvestigational brain injury therapies is aimed atminimizing secondary brain injury. (Savitsky andVotey, 2000; Zink, 2001) There is some overlap between these twocategories in the actual clinical situation. Forexample, although some of the vascular lesions(such as hematomas) may be delayed in theirappearance or effects, they represent the evolutionof a primary injury originating in the traumaticevent, not a secondary complication. In addition, amajor contribution to the secondary sequelae ofhead trauma comes from inadequate medical care.Although no specific therapies have proveneffective in reversing the devastatingconsequences of primary brain injury, theprevention of secondary brain injury is possiblewith emergent resuscitation and acute stabilizationof the severely head injured patient (Biros andHeegarrd, 2001).

[93.41] Primary Injuries Head injury results in different types of primary

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injury which occur at the moment of impactincluding lacerations of the scalp, skull fractures,cortical contusions and lacerations, diffuse axonalinjury, and intracranial hemorrhage. Current dataindicate that diffuse axonal injury may be the majorform of primary brain injury in the posttraumaticpersistent vegetative state (Kampfl, et al., 1998). Types of intracranial hematomas includeextradural, subarachnoid, subdural, andintracerebral (Evans and Wilberger, 1999) Othercerebral vascular lesions include cerebralaneurysm and arteriovenous fistula as well asmeningeal tears.

[1] Concussion-- A concussion, or mild traumaticbrain injury (MTBI) is defined as a clinicalsyndrome characterized by immediate impairmentof neural function such as an alteration inconsciousness, disturbance of vision or balance,and other symptoms due to brainsteminvolvement. More recently, the definition has beenexpanded to include any alteration in mental statusresulting from minor head trauma that may or maynot involve a loss of consciousness. A concussioncan be accompanied by seizure, vomiting,confusion, headache or lethargy. It is important tounderstand what constitutes a concussion, as thediagnosis and management are based on thisdefinition. It is also important to realize that if aconcussion occurs as a result of traumatic headinjury, its symptoms almost always occurimmediately and may persist for variable lengths oftime (e.g., seconds, minutes, hours, or days)(Amann, 2000; Gedeit, 2001).

Caution should be used when describing aconcussion as a ''head injury'', as this impliesinjury to the cranial vault. Although an injury to thecranial vault often occurs simultaneously withconcussion, it is more appropriate to refer to aconcussion as a brain injury, because the neuraltissue itself undergoes trauma and physiologicchange. In general, patients who experience aconcussion are categorized as having a mildimpairment (score of 13 to 15) as measured by theGlasgow Coma Scale (GCS). However, theusefulness of this scale is somewhat limited in thatmany patients with a concussion may have anormal score of 15 and still present with signs andsymptoms of mild traumatic brain injury (Evansand Wilberger, 1999; Amann, 2000).

[1a] Concussion Versus Contusion-- The forcerequired to produce only a concussion withoutcontusion and more severe injury cannot beprecisely quantified (Amann, 2000). Hence, thepopular notion that concussion is a trivial injuryfrom which uneventful recovery always occurs isnot valid. Severe concussion can result inprolonged loss of consciousness, headache,amnesia, irritability, depression, hyperacusis(heightened hearing acuity to the point ofdiscomfort), motor weakness, inability toconcentrate and personality changes. Thesesymptoms may persist for minutes to months ormore. In some cases, concussion can be fatal,such as when the disturbance of brain functionresults in prolonged apnea (cessation ofbreathing). Concussion may occur in isolation or inassociation with contusion, laceration andhemorrhage. In fact, there is a concussivecomponent to all head trauma. Concussion may result from blunt trauma to thetorso or axial skeleton, with the force of the injuryindirectly transmitted to the brain. Mostconcussions, however, occur when the momentumof the head is changed abruptly by either blunttrauma or acceleration-deceleration forces. Inadults and adolescents, concussion usually resultsfrom motor vehicle accidents, falls, assaults, orsports-related activities. For example, the use ofthe head for controlling, passing and shooting asoccer ball, otherwise known as ''heading'' insoccer lingo, and player-to-player contact havereportedly caused concussions in a highpercentage of professional soccer players (Barnes,et al., 1998). In children less than two years ofage, concussions generally result from motorvehicle accidents and falls which impart apredominantly translational (linear) force to thehead (Amann, 2000). Diagnosis of concussion is clinical and treatmentis supportive. Serious changes in cognitive abilityfollowing a traumatic event are the most frequentindication of minor brain injury, with impaireddirected attention being the most commonsymptom. Changes in cognition are often subtleand the patient may appear easily distracted,impulsive and irritable. Early recognition of thesesymptoms leads to early intervention and improvedoutcomes (Brewer and Therrien, 2000).

[1b] Concussion in Children-- In the United

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States, hundreds of thousands of children aretreated in emergency departments of hospitalseach year for head injury, resulting in 100,000hospital admissions. Approximately 90 percent ofthese injuries are due to minor head injury, suchas concussion (Savitsky and Votey, 2000). Fallsand motor vehicle accidents are the most commoncauses of mild head injury in children, followed bypedestrian injuries, assaults, and bicycle injuries.There is also a significant gender differenceamong the pediatric population with regards tohead injury, with boys having a higher incidence oftraumatic head injury than girls (Savitsky andVotey, 2000). Since minor closed head injury is one of the mostfrequent reasons for a physician visit, andconsensus is lacking among the medicalcommunity as to how children with mild head injuryshould be treated, the American Academy ofPediatrics (AAP) developed a practice parameterfor the management of minor closed head injury inchildren. According to these guidelines, childrenwith minor closed head injury and no loss ofconsciousness should undergo a thoroughphysical and neurologic examination as well asobservation for at least 24 hours. The use ofcranial computed tomography (CT) scan, skull x-ray (radiograph), or magnetic resonance imaging(MRI) is not recommended for the child with minorclosed head injury and no loss of consciousness(American Academy of Pediatrics, 1999). For children with minor closed head injury andbrief loss of consciousness (less than one minute),a thorough physical and neurologic exam shouldalso be performed. Observation in the office,emergency department, in the hospital, or at homemay also be used to evaluate children with mildhead injury with brief loss of consciousness. In thisscenario, cranial CT scan may be warranted,especially if the child exhibits signs and symptomsof brain injury, such as amnesia, lethargy,headache or vomiting at the time of evaluation.Some children with brain injury after mild headtrauma do not exhibit any signs or symptoms.Since a delay in diagnosis of intracranialhemorrhage (the major life-threateningcomplication of mild head injury) increasesmorbidity and mortality, a CT scan should beobtained in the child with mild head injury with aloss of consciousness, posttraumatic amnesia, orsigns and symptoms suggestive of brain injury,such as lethargy, altered mental status, headache,

vomiting or seizure (American Academy of Pediatrics,1999).

[2] Contusion-- Contusion is produced by forcesgreater than those that cause concussion. Morespecifically, a contusion is a bruise on the surfaceof the brain which occurs when the brain is directlyinjured (such as in blunt trauma). Areas of focalcortical injury can result from either direct traumafrom external contact forces or from contact of thebrain with intracranial surfaces withacceleration/deceleration forces (Gedeit, 2001). The extent of damage from a contusion rangesfrom mild to severe. Mild contusion may producelocalized subpial hemorrhage (bleeding into thespace beneath the highly vascularized pia mater,the innermost of the three meningeal membranes).In moderate to severe contusion there is typicallymore diffuse structural damage, pulping of thebrain and frank bleeding and seepage of blood intothe cerebrospinal fluid (CSF) space. Contusions are produced when blood vessels inthe parenchyma (underlying brain tissue) aredamaged, resulting in areas of petechialhemorrhage and subsequent edema (swelling ofthe brain due to accumulation of fluid). Contusionsdevelop in the gray matter located on the surfaceof the brain and taper into the white matter. Bloodfrom the subarachnoid space is often foundoverlying the involved gyrus (fold on the surface ofthe brain). Over time the associated hemorrhagesand edema of a contusion become widespreadand can serve as a nidus (source or focal point) forhemorrhage or swelling, producing a local masseffect. Compression of the underlying tissue canresult in areas of ischemia (lack of blood supply toa region) and tissue infarction (obstruction of theblood vessels), if the compression is significantand unrelieved. Eventually, these areas ofischemia become necrotic and cystic cavities formwithin them (Marx, 2002).

[2a] Site and Mechanism-- The clinical effectsand significance of a contusion depend on theregion of the brain involved, which in turn dependson the site of trauma and the mechanism involved.By definition, a coup contusion occurs at the site ofimpact in the absence of a fracture. In contrast, acontrecoup contusion occurs in the braindiametrically opposite the point of impact.Contusions which occur in areas of the cerebralcortex in between, or in the vicinity of the tentoriumcerebellum or falx cerebri (portion of the dura

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mater in the area of the brainstem and betweenthe two cerebral hemispheres, respectively) arecalled intermediate coup. Coup lesions are more common followingconcussive-compressive injuries (where the headis struck), while contrecoup lesions are morecommon following acceleration-decelerationinjuries (when the head strikes an immovableobject).

Temporal lobe contusions often are associatedwith fractures of the skull and manifest behavioralsymptoms that include lethargy, restlessnessand/or belligerence. Neurological manifestationsinclude unilateral motor weakness (hemiparesis)and aphasia (disturbance of the power ofexpression and/or comprehension of speech)when the dominant frontal lobe is involved. Temporal lobe contusion is not life-threateningunless there is herniation with progressivecompression of the brainstem. If neurologicaldeterioration is in progress, it will be most evidenton the third day following injury. If the cause of thedeterioration is in doubt, a CT scan is indicated toidentify the possible formation of a hematoma. Contusion in the parietotemporal region isassociated with visual disturbances, such ashomonymous hemianopsia (blindness or defectivevision in the right or left halves of both eyes);unilateral motor weakness (hemiparesis) orparalysis (hemiplegia); and disorders of expressionor comprehension of language, or both, which maybe mistaken for a reduced level of consciousness. Significant bilateral frontal lobe contusion isassociated with reduced consciousness orchanges in personality. Contusion of thehypothalamus typically results in coma. Contusionof the motor neurons of the frontal cortex mayproduce contralateral motor weakness. Patients with contusion are often delayed in theirpresentation of signs and symptoms. Althoughthey may have sustained a loss of consciousnessfor a brief period of time, the duration of symptomssuch as confusion and obtundation (altered mentalstatus) is usually prolonged. Most patients withsignificant contusions have full recoveries, butcontusions can also cause significant neurologicimpairment, including increased intracranialpressure, seizures, and focal deficits (Marx, 2002).

Surgery for accessible lesions that are greaterthan 25 milliliters may improve the patient's clinicaloutcome. Medical measures to control intracranialhypertension (elevated blood pressure within thecranial vault) should also be instituted (Morris andMarchall, 2000).

[3] Laceration-- Laceration is defined as a ragged,tearing wound. It is generally a more distinct lesionthan a contusion, and involves direct mechanicaldamage to the meningeal membranes, thecerebral vasculature and individual neurons.Laceration is associated with less pulping of thebrain than contusion, and the pattern of clinicallymanifest neurological symptoms that arise from itvaries with the area of the brain involved. Laceration can occur in almost any head injuryscenario. For example, in severe penetrating headinjury, laceration is caused by the projectile and in-driven bone fragments. In blunt traumatic injury ofsufficient force to produce a depressed fracture ofthe skull, laceration results from in-driven bonefragments. In acceleration-deceleration injuries,laceration may be caused by shearing forces andmass movement of the brain over the bony interiorof the skull and the rigid falx cerebri of the dura mater. Scalp lacerations frequently occur after head injuryand are a source of significant bleeding becausehemostasis is difficult to achieve. Laceratinglesions produce the massive intracranial bleedingthat leads to hematoma formation. Stretching andtearing of the axons (the neuronal processeswhich conduct the nerve impulse) may occur evenin the absence of hemorrhage. The resultantdisturbance of nerve conduction produceswidespread neurological dysfunction, which maybe a critical factor in the abrupt rise in intracranialpressure that causes unconsciousness or coma incases of extensive cerebral contusions. Methods to control bleeding from a scalplaceration include direct digital compression of thebleeding vessel against the skull, infiltration of thewound edges with a mixture of lidocaine andepinephrine, or ligation of the identified bleedingvessels. If a deep laceration occurs (e.g., the galeais lacerated), surgical techniques are employed toclose the wound, after proper debridement andirrigation, and are the most effective methods tostop the bleeding and prevent tissue crush injuryshould compression be applied for too long a period.

10

Once hemostasis is achieved, the wound shouldbe irrigated to wash away any debris. Since theperipheral vessels of the scalp drain into the veinsof the skull, which in turn drain into the venoussinuses, contaminated scalp wounds have thepotential to cause serious intracranial infection.Hence, irrigation of the wound to rinse away debrisis extremely important (Marx, 2002).

[4] Vascular Lesions-- The forces that act on theintracranial contents during closed head traumacan produce various types of damage to theintracranial blood vessels. Prominent among theseare tearing with resultant hematoma, thrombosis(clotting of a vessel) and infarction; aneurysm; andarteriovenous fistula. Meningeal arteries areinjured most commonly in head trauma, but anyportion of the cephalic vascular tree may bedamaged (Goetz, 1999; Marx, 2002).

[4a] Hematoma-- A hematoma is a blood clotformed by blood extravasated from a disruptedvessel. Hematomas are space-occupying lesionsthat sometimes grow large enough to displace andlocally compress the brain and cause life-threatening ischemic (marked by lack of bloodsupply) damage (Townsend, 2001). There are three major kinds of hematoma:intracerebral, subdural and epidural. Intracerebralhematomas occur within the brain, subdural andepidural hematomas occur outside the brain.

An intracerebral hematoma is a clot ofextravasated blood which forms deep within thebrain tissue. Intracerebral hematomas may formanywhere within the brain tissue, but are found inthe frontal and temporal lobes in approximately 85percent of cases (Marx, 2002). This type ofhematoma is caused by shearing or tensile forcesthat mechanically stretch and tear deep smallerarterioles as the brain is propelled against irregularsurfaces in the cranial vault. Small petechialhemorrhages that result from this traumasubsequently coalesce to form intracerebralhematomas. They are frequently associated withextraaxial hematomas, and multiple intracerebralhematomas are often present in many patients.Isolated intracerebral hematomas can be detectedin about 12 percent of all patients experiencingsevere head trauma.

The clinical effects of intracerebral hematomadepend on the size and location of the hematoma,and whether or not bleeding has been contained.Intracerebral hematomas have been reported withvarying degrees of severity of head trauma, withmore than 50 percent of patients experiencing lossof consciousness at the time of impact. The levelof consciousness of the patient correlates with theseverity of the impact and the presence of anycoexisting lesions. If a contusion or otherconcurrent lesion is present, an intracerebralhematoma can produce substantial mass effectsand cause a herniation syndrome. Diagnosis is by CT, since cerebral angiographycannot differentiate intracerebral hematoma froma localized contusion. Many patients with anintracerebral hematoma require emergent medicalintervention or surgery to control elevatedintracranial pressure. Mortality is low in patientswho are conscious before surgery. This is not thecase, however, in unconscious patients, in whommortality approaches 45 percent. Intracerebralhematomas which bleed into the ventricles of thebrain or the cerebellum are also associated with ahigh mortality rate (Marx, 2002). A subdural hematoma is a clot of extravasatedblood which forms between the dura (themeningeal covering of the brain) and the brain. Asubdural hematoma results from bleeding fromveins after blunt head trauma (acceleration-deceleration injuries), which precipitatesmovement of the brain within the skull and theshearing off of veins bridging the surface of thebrain with the adjacent dural venous sinuses. Theblood leaks slowly from the veins, forming ahematoma in the subdural space. A subduralhematoma may be reabsorbed spontaneously ormay form an encapsulated hematoma. Afterapproximately two weeks, membranes formaround the hematoma and the center of theencapsulated hematoma liquefies due tocontinuous bleeding from the vascular membrane.Subdural hematomas are more common thanepidural hematomas and occur in approximately30 percent of patients with severe head trauma(Goetz, 1999, Marx, 2002). Subdural hematomas are classified according tothe time signs and symptoms appear. Patients withacute subdural hematomas are symptomatic within24 hours after the initial traumatic event. Theyoften have a decreased level of consciousness

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followed by declining mental status. Patients witha subacute subdural hematoma are symptomaticbetween 24 hours and two weeks after head injury.These patients usually complain of headache,changes in mental functioning, muscle weakness,or frank paralysis. Chronic subdural hematoma isdefined as the appearance of symptoms two ormore weeks after trauma. Patients with chronicsubdural hematoma may experience a very subtleonset of symptoms or nonspecific symptoms.However, approximately 45 percent of patients willcomplain of unilateral weakness (weakness on oneside of the body) or hemiparesis (paralysis on oneside of the body). Approximately 50 percent ofpatients will also present with an altered level ofconsciousness, with some patients unable to recalltheir head injury or describing only a minor injury(Goetz, 1999; Marx, 2002). The diagnostic method of choice is computedtomography (CT). If a subdural hematoma is notdiagnosed early and is left untreated, it may resultin severe neurologic impairment or death.Treatment is by surgical evacuation of thehematoma (Goetz, 1999; Townsend, 2001). Most patients have a good prognosis followingsurgery. In general, the prognosis is related to thedegree of associated brain injury caused by thepressure of the expanding hematoma onunderlying tissue. The overall survival rate is 35percent to 50 percent, with mortality being highestin the elderly, in patients having a measurement ofeight or less on the Glasgow Coma Scale, and inpatients who present with signs of acute herniationsyndrome in the Emergency Department. Overall,the mortality associated with a chronic subduralhematoma approaches 10 percent, with survivaldecreasing in elderly patients (Marx, 2002). An epidural hematoma develops when bloodcollects between the skull and the dura mater (theoutermost of the three meningeal membranes thatcover the brain) as a result of blunt trauma to thehead. Epidural hematomas most commonly occurin the temporal region of the brain, although theymay occur in other locations such as the frontal orparietal regions. They usually develop in patientswith severe head trauma causing a fracture of thetemporal bone and tearing the middle meningealartery. In 85 percent of cases, epidural hematomais associated with a skull fracture (Marx, 2002;Goetz, 1999; Evans and Wilberger, 1999).

The classic presentation of epidural hematoma isa decreased level of consciousness followed by alucid interval (Goetz, 1999; Marx, 2002). There isoften a progressive reduction in the level ofconsciousness as the hematoma enlarges. Thislucid interval, however, is rarely seen as mostpatients are unconscious from the time of injury(Evans and Wilberger, 1999). Only about 30percent of patients with epidural hematomas followthis classical presentation (Marx, 2002). Mostpatients with an epidural hematoma complain of asevere headache, increased sleepiness, dizziness,nausea and vomiting. Signs and symptomsdevelop according to how rapidly the hematoma isexpanding. In some instances, a patient with asmall epidural hematoma may be asymptomatic,but this is usually rare (Marx, 2002). Definitive diagnosis is by CT scan. Epiduralhematomas require immediate surgical evacuation(Evans and Wilberger, 1999; Goetz, 1999). If thepatient's condition appears to be rapidlydecompensating, the patient should be takendirectly to the operating room for a procedure thatis both diagnostic and therapeutic (Goetz, 1999).For a patient who is not in a coma at the time ofdiagnosis, who receives rapid treatment, themortality rate approximates zero percent. Themortality rate increases to about 20 percent if thepatient is in a coma at the time of diagnosis (Marx,2002). The prognosis is excellent when epiduralhematomas are rapidly diagnosed and treatedsurgically. Conversely, severe neurological deficitsor even death can result from delayed diagnosisand treatment (Goetz, 1999). Hematomas may also form in the posterior fossa(the bilateral depression in the posterior floor of theskull) following a wide variety of head injuries.Posterior fossa hematomas are very rare,constituting less than 1 percent of all reportedsubdural hematomas. Patients usually present withsymptoms such as nausea, vomiting, headache,and a decreased level of consciousness. Themass of the lesion can compress the brainstem,resulting in derangement of a number of vitalrespiratory and cardiovascular functions mediatedby that part of the brain. Neurological deteriorationof the patient can occur rapidly and withoutobvious clinical signs. Treatment is by surgicaldecompression and evacuation of the hematoma.The prognosis is poor, with less than a 5 percent

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survival rate (Marx, 2002).

[4b] Thrombosis and Infarction-- In addition tomore massive hematomas, smaller blood clots(thrombi) may form within cerebral blood vessels.When these clots occlude the flow of blood to theregion of the brain supplied by the affectedvessels, they can produce local ischemic andhypoxic damage (infarction) which in turn results infocal neurologic deficits. These lesions may not beapparent for several hours or days, and usually donot produce marked alterations in mental status(Goetz, 1999). Although carotid dissection (dissection of the mainartery supplying blood to the brain) rarely occurswith head injury, it can be the cause of delayeddeterioration, particularly when neck injury isinvolved (Townsend, 2001). In head injuredpatients, traumatic dissection of the carotid arteryis the most frequent cause of infarction, whereasthrombosis of the cerebral artery is extremely rare.An unusual case of posttraumatic thrombosis ofthe middle cerebral artery has been reported in theliterature, in which a teenager suffering blows tothe head and face experienced a partial rupture inthe arterial wall and subsequent thrombosis andinfarction (Bunai, 2001). When either carotiddissection or thrombosis of the middle cerebralartery is suspected, the diagnosis is made byangiography (Townsend, 2001). Ischemic thalamic infarctions and strokes havealso been reported in children suffering headtrauma. The typical clinical presentation of strokein the pediatric patient (ranging 21 months to 15years of age in this series) involves a decreasedlevel of consciousness, hemiparesis (paralysis onone side of the body), and aphasia (difficulty inspeech). Any child suffering blunt head traumapresenting with these symptoms should besuspected of thrombosis of the cerebral artery andischemic thalamic infarction, and be evaluated assuch (Garg and De Myer, 1995). Venous sinus thrombosis is rarely associated withhead trauma, but can easily be an undetectedsequel to head injury. One case report in theliterature describes an adult patient with unilateralhearing loss, tinnitus (ringing in the ears) andheadache two days after suffering a closed headinjury. CT scan revealed a skull fracture and MRIdemonstrated sigmoid and transverse sinusthrombosis (Brors et al., 2001). If the diagnosis of

venous sinus thrombosis is suspected, cerebralangiography should be performed promptly andthe instillation of urokinase should be consideredin any patient with symptomatic occlusion (D'Alise,et al., 1998). In most cases, infarction is caused by thromboticocclusion of a vessel supplying blood to the brain,but also may be caused by traumatic vascularcompression from a swelling brain. Vessels maybe compressed in the cerebral sulci (furrows of thesurface convolutions) between edematous gyri(elevated ridges of the surface convolutions), orbetween the swelling hemispheres of the brain andthe skull (Goetz, 1999).

[4c] Aneurysm-- Traumatic intracranial aneurysm(a balloon-like sac in the wall of a blood vessel dueto weakening and bulging of the wall) is reportedlya rare event, occurring in less than 1 percent ofcases (Tureyen, 2001). This type of aneurysmusually develops after penetrating head trauma orskull fracture, but can occur after blunt trauma aswell. When aneurysms rupture, they usually causedevastating subarachnoid or intracerebralhemorrhage. At least three cases of posteriorfossa subarachnoid hemorrhage from rupturedcerebellar artery aneurysms have been reportedafter blunt head trauma (Schuster, et al., 1999). Although traumatic aneurysms are most commonin young adults, the frequency in the pediatricpopulation is relatively high. One case report in theliterature describes a posttraumatic aneurysm in achild after falling from a significant height whichsubsequently spontaneously thrombosed(Loevner, et al., 1998). Another case reportdescribes a traumatic posterior inferior cerebellarartery (PICA) aneurysm not related to skull fractureor penetrating or blunt trauma, but resultinginstead from a meningeal tear due to decelerationforces (Sure, et al., 1999). Approximately 85 percent of ruptures occur withinthe first three weeks after the trauma (Voelker andOrtiz, 1997). Thus, a high index of suspicion isnecessary to promptly diagnose a traumaticaneurysm. When a patient suffers a penetratinghead injury or fracture at the base of the skull nearmajor arteries, or exhibits symptoms suggestive ofan aneurysm (e.g. a throbbing headache that ispersistent) after blunt trauma, an arteriogram iswarranted. Treatment is by surgical clipping of theaneurysm (Townsend, 2001). When left untreated,

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the mortality rate is between 30 and 70 percent(Tureyen, 2001).

[4d] Arteriovenous Fistula-- An arteriovenousfistula is an abnormal communication between anartery and a vein. The most common site of afistula following cranial trauma is between thecarotid artery and the cavernous sinus (anirregular venous space in the dura mater on eitherside of the sphenoid bone). Usually, the fistulaforms following laceration of the carotid vesselduring basilar skull fracture, and occurs in thepresence of concomitant damage to the nervesthat accompany the carotid artery through thisregion (namely, the oculomotor, trochlear,abducens, and first division of the trigeminalnerve). Traumatic injury of the subclavian arterycan also result in fistula formation between theright subclavian vein and internal jugular vein(Maher et al., 1997). Posttraumatic arteriovenousfistula also may occur in the scalp vasculature. Traumatic carotid-cavernous fistulas areassociated with a large variety of symptoms,including loss of vision, glaucoma, chemosis(excessive swelling of the conjunctival membraneof the eye), exophthalmos (bulging eyeballs), andorbital nerve palsies. In addition, the high pressurein the veins that drain the brain can cause vesselsto enlarge and compress adjacent structures,producing neurologic deficits (Wadlington andTerry, 1999). Symptoms usually appear within onemonth after the traumatic event, but severe headinjury may lead to asymptomatic arteriovenousfistula formation after a long period of time. Onecase report describes a 38-year-old woman whodeveloped an arteriovenous fistula after sufferinghead injury at the age of three (Fukai, et al., 2001)If a false aneurysm develops as a result of thefistula, this is considered a surgical emergency,requiring early diagnosis and prompt surgicalintervention (Maher, et al., 1997). In diagnosis of the fistula, Doppler ultrasound maybe useful because it reveals the vein-arterial bloodflow on the fistula side. CT scan and magneticresonance imaging (MRI) may also suggest thepresence of a fistula. The diagnosis is confirmedby arteriography of the involved artery (usually thecommon carotid artery, although the subclavian orposterior communicating artery may be the primaryartery) (Dowzenko et al., 1997). Surgical occlusionof the abnormal communication is the mode oftherapy for fistulas (Fukaie et al., 2001; Wadlington

and Terry, 1999).

[5] Meningeal Tears-- The meninges, or threemembrane layers that envelop the brain and spinalcord, are the dura mater (outermost), arachnoid(middle) and pia mater (innermost). Cerebrospinalfluid (CSF) circulates within the spaces betweenthese layers. They serve both as a mechanicalshock absorber for the brain and a physical barrieragainst infection.

When the blood vessels which run through themeninges and into the brain are torn, the leakageof blood gives rise to a hematoma. When themeningeal membranes themselves are torn orpunctured, leakage of cerebrospinal fluid may forma CSF cyst (fluid-filled sac) in the arachnoid space.Leakage of CSF following head trauma is difficultto diagnose and is of considerable importance asit may cause fistula formation and meningitis. Inone study, patients with head injuries and subduralhematoma were found to be at greater risk ofdeveloping an unobserved dural tear, with delayedleakage of CSF (Choi and Spann, 1996). In children, the dura mater may be torn by a linearfracture. The resultant traumatic pulsing of theunderlying arachnoid membrane can enlarge thefracture, producing a leptomeningeal cyst (a CSFcyst involving the arachnoid and pia mater). Ifthere is a fracture of the thin bones of the temporalarea or of the floor of the skull in the region of theeyes and nasal cavity, CSF may leak from the ears(otorrhea) or nose (rhinorrhea), respectively. Suchan injury indicates a communication between thecontents of the skull and the outside, whichincreases the risk of intracranial infection (e.g.,meningitis). Any child with serosanguinous(containing CSF fluid) bleeding from the nose orear should be suspected of having a basilar skullfracture with resultant CSF leakage, and should befollowed closely until the dural tear heals or issurgically repaired because of the high risk fordeveloping meningitis (Savitsky and Votey, 2000).

[93.42] Secondary Injuries Secondary injuries occur subsequent to theprimary injury resulting from head trauma and arealmost always preventable and treatable. Amongthe prominent secondary sequelae of head traumaare cerebral edema (brain swelling) and elevatedintracranial pressure (ICP), various brainherniation syndromes, cardiorespiratory

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complications, spasm of the cerebral vessels,clotting defects (coagulopathies), infection andposttraumatic seizures. Common adverse effectsof these secondary complications of cerebralfunction include ischemia (lack of blood supply)and hypoxia (insufficient oxygen supply). The presence of hypoxia or shock is associatedwith a poor outcome, independent of the injuryseverity. Both occur frequently, not only in the pre-hospital phase but also in patients in intensive caresettings. If present, the correction of shock andhypoxia is the first priority of treatment, and anyhead-injured patient exhibiting signs of poorventilation should be urgently placed onmechanical ventilation (Townsend, 2001; Zink, 2001).

[1] Elevated Intracranial Pressure-- The skullcontains three intracranial components: the brain(80 percent of the volume), blood (10 percent ofthe volume) and cerebrospinal fluid (10 percent ofthe volume). Because the skull interior is aneffectively closed and rigid cavity, its contentshave a specific intracranial pressure (ICP). NormalICP is 15 mm of mercury (Hg) or less, and isregulated under normal circumstances bycompensatory changes in the volume of the threeintracranial components. Following head trauma, the normal balance isdisturbed: the limits of the compensatorymechanism are exceeded by the onset of brainswelling or mass lesions such as hematomascaused by intracranial hemorrhaging and poolingof blood. As the traumatic edema or mass lesionincreases in size, the brain and its vasculaturebecome increasingly compressed within theunyielding skull, resulting in ischemic (lack of bloodsupply) and hypoxic (inadequate oxygen supply)brain damage, brain herniation and related insults.Elevated intracranial pressure thus contributessignificantly to morbidity and mortality followinghead trauma. Evaluation of the severely head injured patientduring the acute period following the traumainvolves rigorous neurologic assessment as wellas frequent monitoring of the patient's intracranialpressure. Clinical signs of rising ICP which may bepresent in conscious patients include alterations inthe level of consciousness, changes in vital signs(blood pressure, pulse and respiration) andpapilledema (swelling of the optic disc in the retinaof the eye). There are no reliable clinical signs in

comatose patients (Townsend, 2001). Monitoring of the intracranial pressure is usuallyinitiated after the first CT scan in patients notrequiring urgent evacuation of a mass lesion. If thepatient is taken to the operating room for urgentsurgery, an ICP monitor is usually placed at theend of the operation, since the brain may swelllater on as a complication of surgery. In somehospitals, young patients who are comatose, withhigh Glasgow Coma Scores (e.g., seven or eight)and normal CT scans may not be monitoredimmediately. In other hospitals, all comatosepatients are monitored, regardless of the findingson CT scan. Although the risk of increasedintracranial pressure in a comatose patient with anormal CT scan is lower than that of a patient withan abnormal CT scan (having an estimated risk of10 to 15 percent), it is higher than the risk ofinserting an ICP monitor (Townsend, 2001). Treatment of elevated ICP involves drainage ofventricular fluid by placement of a ventricularcatheter or the use of osmotic agents such asmannitol (Townsend, 2001).

[2] Brain Herniation-- Brain herniation syndromesconsist of compression and shifting of the brainwithin the skull secondary to increased intracranialpressure. Increased intracranial pressure may bethe result of brain swelling, cerebral edema,expansion of a mass lesion, or any combination ofthese three factors. During herniation, the brain isforced over the rigid structures of the dura mater(the tough, outermost meningeal membrane) orskull interior. The brain also may be forced downinto and impacted in the foramen magnum (thelarge opening at the base of the skull where thespinal cord enters and fuses with the brain), theonly outlet in the otherwise closed skull.

Herniation of the brain is also the most seriouscomplication of lumbar puncture. In a head traumapatient with an intracranial mass lesion, a lumbarpuncture can create a pressure gradient betweenthe brain and spinal cord spaces, leading to adownward herniation of the brain through theforamen magnum or the tentorial notch. Thisresults in further neurologic deterioration anddeath (Naik-Tolani et al., 1999). Herniation syndromes are divided into four types:uncal, central, transfalcine and tonsillar. Herniationcan occur within several minutes or days after

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traumatic brain injury. Once the patient exhibitssigns of herniation syndrome, mortalityapproaches 100 percent if temporary emergencymeasures and neurosurgical treatment are notrapidly implemented (Marx, 2002). Definitivediagnosis of tentorial (pertaining to the dura mater)brain herniations is by cerebral angiography,although special techniques are available tovisualize them on CT, MRI and MR angiography.Treatment is by surgical decompression.

[2a] Uncal Herniations-- The uncus (the lowermedial portion of the temporal lobe of thecerebrum) rests on a portion of the tentoriumcerebelli (the tentlike portion of the dura whichcovers the cerebellum). The tentorium separatesthe posterior fossa from the middle cranial fossa.In this region, the brainstem rises through thetentorium by passing through an opening betweenthe tentorium and the sphenoid bone of the skullbase (the tentorial incisura). Below this, thebrainstem joins with the spinal cord as it passesthrough the foramen magnum.

Rising intracranial pressure due to an evolvingmass lesion can force the uncus over the edge ofthe tentorial incisura and into the posterior fossa,resulting in uncal herniation. This is the mostcommon herniation syndrome and is a form oftranstentorial herniation. Uncal herniation isusually associated with epidural or acute subduralhematomas located in the lateral middle fossa orthe temporal lobe of the brain. Initially, as the uncus herniates, it compresses thethird cranial nerve (the oculomotor nerve, whichinnervates various muscles of the eye). Theresulting pressure produces a characteristicconstellation of clinical signs, including ptosis(drooping of the eyelid), a sluggish pupillaryresponse to light and impaired extraocularmovements. This phase may last from minutes tohours, depending on how rapidly the hematoma isexpanding. As the herniation progresses, contralateralhemiparesis (paralysis on the opposite side of thebrain) develops and eventually, bilateraldecerebrate posturing occurs. Direct brainstem compression causes furtheralterations in the patient's level of consciousness,respiration and cardiovascular function. Mentalstatus changes may be subtle in the initial stages,

and the patient will appear agitated, restless, orconfused. Lethargy soon occurs, however, withprogression to frank coma. Continued progressionof a temporal lobe herniation and compression ofthe brainstem may lead to rapid changes in thepatient's blood pressure and cardiac conduction,and ultimately cardiorespiratory arrest and death(Marx, 2002).

[2b] Central Transtentorial Herniations-- Thecentral transtentorial herniation syndrome iscaused by an expanding lesion at the vertex or thefrontal or occipital lobes of the brain. Thissyndrome is less common than uncal herniation.Neurologic and clinical deterioration occurs ascentral pressure is exerted bilaterally on the brainfrom above. Initially, the patient may present witha subtle change in mental status or decreasedlevel of consciousness, muscle weakness andpinpoint pupils. As central herniation progresses,both pupils become midpoint and lose theirresponsiveness to light. The patient's respiratorypattern is also affected and he or she may begin tohyperventilate. The patient may begin to yawn orsigh initially, then develop tachypnea (rapid andquick breaths), followed by a pattern of shallow,slow breaths at irregular intervals before collapsingfrom respiratory arrest (Marx, 2002).

[2c] Transfalcine Herniations-- These lesions areproduced by a mass effect on one side of the brainwhich forces the medial aspect of that cerebralhemisphere beneath the rigid falx cerebri (theridge of the dura extending down into the cleftbetween the hemispheres). There is damage tothe cingulate gyrus (a key part of the limbicsystem, which mediates emotions and variousregulatory functions), and compression of thecerebral arteries leads to ischemic damage to theinvolved hemisphere. A vicious cycle of edemaensues, and may combine with the mass effect toproduce uncal herniation. Clinically, the patientoften presents with an altered level ofconsciousness and profound weakness of thelower extremities.

[2d] Cerebellotonsillar Herniations-- Herniationof the tonsils (lowest pole) of the cerebelluminvolves a shift of the brainstem and cerebellumtoward the foramen magnum due to an evolvingmass effect (e.g., hematoma) in the posteriorfossa. In the process, the medulla oblongata (acrucial regulator of respiration and other vitalfunctions) is compressed, and depressed

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consciousness and respiratory arrest ensue.Pinpoint pupils and flaccid quadriplegia arecharacteristic signs and symptoms of this type ofherniation. Mortality from cerebellar herniation ishigh, approaching 70 percent (Marx, 2002).

[3] Cardiorespiratory Complications-- A numberof respiratory injuries and complications may beseen following head injury (Marx, 2002). Since themajor respiratory centers are in the brainstem,most respiratory problems arise followingacceleration-deceleration injuries (in which thebrainstem is damaged as a result of massmovement and shearing forces).

[3a] Respiratory Problems-- The types ofrespiratory sequelae that must be addressed at thescene of the trauma and in the emergencydepartment differ somewhat from complicationsthat present in the intensive care unit (ICU).Common complications during the acute stage oftrauma include aspiration pneumonia, apnea(cessation of breathing), and neurogenic (causedby nerve dysfunction) pulmonary edema (fluid inthe lungs). Suppression of the gag and cough reflexescombined with the increased possibility of vomitingfollowing head trauma can result in aspiration ofthe stomach contents into the lungs and the onsetof aspiration pneumonia (infection of the lungs byaspirates). Treatment is by organism-specificantibiotics. Apnea is potentially the most disastrous sequelaand may be the leading cause of death at thescene (Marx, 2002). Although patients have madegood recoveries after as long as 8 to 10 minutes ofprolonged apnea, the accumulating hypoxemia(deficient oxygen levels in the blood) andhypercarbia (excessive levels of carbon dioxide inthe blood) that occur before the respiratory centersresume spontaneous functioning frequently lead tovegetative or even fatal outcomes (Marx, 2002).Treatment is by emergency ventilation. Apnea usually results from compression of thebrainstem or injury after trauma and is one of themost common causes of hypoxia. Hypoxia, definedas an oxygen saturation of less than 60 mm Hg, isa common respiratory complication in head injuredpatients. In addition to apnea, causes of hypoxiainclude partial obstruction of the patient's airwaycaused by blood or debris, injury to the chest wall

and penetrating injury to the lungs. It is difficult toestimate the exact incidence of hypoxia in patientswith head trauma, since hypoxia often remainsunnoticed in the out-of-hospital setting. When thepresence of hypoxia is documented, however, themortality due to severe head injury doubles (Marx,2002). Neurogenic pulmonary edema is defined aspulmonary edema resulting from an insult to thecentral nervous system that occurs in the absenceof cardiac or other disease. This phenomenon hasbeen well documented in the literature for almosta century, and was first described in patients withepilepsy, gunshot wounds to the head, andtraumatic intracranial bleeds. More recently,neurogenic pulmonary edema has been reportedin children and adults with seizures, closed headinjury, intracranial hemorrhage, and penetratinghead trauma. At least two case reports describeneurogenic pulmonary edema in young childrenwith inflicted head injuries. The classic presentation of neurogenic pulmonaryedema is one of acute onset, developinginstantaneously within minutes to hours after headtrauma. Infrequently, a delayed-onset ofpulmonary edema can occur hours to days afterthe precipitating event. Recent research suggeststhat subclinical pulmonary edema may develop inpatients with a normal appearing chest x-ray. Infact, many head-injured patients with an elevatedICP exhibit signs of pulmonary dysfunction longbefore they develop overt pulmonary edema.Although the exact mechanism of neurogenicpulmonary edema remains unknown, thisnoncardiac pulmonary edema probably resultsfrom changes in hydrostatic forces and capillarypermeability directly caused by brain injury.Lowering the ICP appears to reverse theneurogenic cause of the edema (Marx, 2002;Rubin et al., 2001). Signs and symptoms of neurogenic pulmonaryedema include tachypnea (rapid and shallowbreathing), dyspnea (difficulty in breathing), chestpain, rales (a wet, bubbly sound characteristic offluid upon listening to the lungs through astethoscope), and frothy pink pulmonarysecretions. If the head injury is severe, pulmonaryedema can be massive, pouring out of the mouthand nose of the patient. Chest x-ray (radiograph)confirms the diagnosis and demonstrates diffuse,butterfly shaped pulmonary infiltrates (Rubin, et al.,

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2001). Common respiratory complications seen in the ICUinclude hypoxia, atelectasis, bacterial pneumonia,barotrauma, adult respiratory distress syndrome(ARDS) and cardiogenic (caused by cardiacdysfunction) pulmonary edema. Agitationfrequently occurs in the head-injured patient in theICU secondary to hypoxia. The agitated patient willoften exhibit continuous movement, characterizedby fidgeting or moving from side to side, appeardisoriented, and may attempt to removeintravenous catheters. Hypoxemia frequentlycontributes to agitation and in the ICUs of mosthospitals there have been numerous incidences inwhich hypoxemia has been misdiagnosed asagitation. Hypotension (low blood pressure) hasalso been linked to agitation and is considered aform of brain injury as a result of hypoperfusion (aninadequate supply of blood and oxygen to thebrain) (Critical Care Med, 2002). Atelectasis (lung collapse) is common followingsevere head injury and results from a number ofdisturbances of normal lung function. It can bereversed by various means, includingadministration of bronchodilator aerosols orbronchoscopic removal of mucous plugs and secretions. Aspiration can be prevented by properendotracheal intubation, even if mechanicalventilation is not necessary. There is always somepossibility of aspiration, even with the bestavailable devices, so routine nasogastric andoropharyngeal suctioning of collected secretions isa necessary adjunct. However, endotrachealsuctioning of head-injured patients can result insignificant increases in ICP. Sedation and the useof short suctioning times may aid in preventing thiscomplication (Naik-Tolani et al., 1999). Of the five types of barotrauma (injury due topositive pressure in the airways as a result ofmechanical ventilation), only pneumothorax (air inthe chest cavity) normally requires intervention(e.g., a thoracostomy tube). Cardiogenic pulmonary edema (fluid collection andswelling in the lungs) is seen in patients withpreexisting heart disease who have receivedposttraumatic fluid volume replacement therapy orsuffered acute kidney failure. In patients with goodkidney function, simple diuretics usually resolvethe problem. In more critically ill patients,

intravascular volume reduction may be necessary.In patients with poor heart and kidney function,administration of a diuretic like mannitoldramatically reduces brain swelling, but alsodramatically increases intravascular volume. Adult respiratory distress syndrome (ARDS, oneform of which is neurogenic pulmonary edema) ischaracterized by diffuse bilateral lung infiltratesand hypoxia that responds poorly to supplementaloxygen. It usually is self-limiting but can be fatal.Treatment is nonspecific, and entails supportivecare with supplemental oxygenation. Specifictreatment is directed at the underlying traumaticcause (e.g., multiple injuries or infection).

[3b] Cardiovascular Problems-- Neurogenichypertension as well as a wide variety of cardiacrhythm abnormalities occur after head injury(Goetz, 1999; Marx, 2002). Cardiac dysfunctioncan potentially be life-threatening and requiresaggressive management. Since the brain isacutely dependent on oxygen, an adequatecardiac output (volume of blood pumped out of theheart upon contraction) is necessary to ensureadequate cerebral perfusion. In head-injuredpatients, brain injury is a primary cause of cardiacdysfunction. Abnormal cardiac rhythms(dysrhythmias) occur in up to 70 percent ofpatients with subarachnoid hemorrhage and inmore than 50 percent of patients with intracranialhemorrhage. Although supraventricular tachycardia is the mostcommon cardiac dysrhythmia observed after headinjury, many other rhythms have been reported.The electrocardiogram (ECG) reveals large,upright or inverted T waves, prolonged QTintervals, ST segment or depression, and thepresence of U waves. The primary goal ofemergency treatment of cardiac dysrhythmias afterhead injury is to maintain adequate tissueperfusion and to avoid hypoxia. Dysrhythmias willoften disappear as the ICP is reduced. Standardadvanced cardiac life support (ACLS) should befollowed after resolution of the dysrhythmia, sincecardiac injury may also be present in patientsexperiencing multiple trauma (Marx, 2002).

[4] Cerebral Vasospasm-- Spasm (involuntarycycles of contraction and relaxation) of the smoothmuscles of the walls of the cerebral arteries occurin 30 to 40 percent of patients with posttraumaticbleeding into the subarachnoid space (the space

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beneath the innermost of the three meningealmembranes) (Zubkov, 1999). A recent study foundthat the development of posttraumatic vasospasmwas correlated with severe subarachnoidhemorrhage detected on the initial CT scan(Zubkov, 2000). Vasospasm also may be seen inthe carotid and vertebral arteries of the neckfollowing head injury. Neither the etiology nor the pathogenic mechanismof vasospasm are understood as yet. Thetraumatic release of serotonin (which inducessmooth muscle contractions) from certain of thewhite blood cells which produce and store it isthought to play a role. When spasm chokes offcerebral vessels, cerebral ischemia (lack of bloodsupply) results. Eventually, this leads todeterioration of the neurons supplied by thevessels in spasm. This in turn leads to delayedneurological deficits, which may progress to comaand paralysis. Cerebral vasospasm is associated with significantmorbidity and mortality. The prognosis afteraneurysmal subarachnoid hemorrhage is good ifthe diagnosis is made in a timely manner andtreatment is aggressive (Corsten, et al., 2001).Surgical treatment of the aneurysm involvesclipping of the aneurysm or the use of microcoils.Angiography is used to confirm the diagnosis ofcerebral vasospasm after surgical treatment foraneurysm. Transcranial Doppler ultrasonographyand transcranial color-coded sonography are alsouseful for accurate monitoring of cerebralvasospasm in the middle cerebral artery (Proust etal., 1999).

[5] Clotting Defects (Coagulopathies)--Traumatic derangement of the hemostaticmechanism (which maintains the balance betweenclotting and circulation of the blood) can producea coagulopathy known as disseminatedintravascular coagulation (DIC). This conditioninvolves both excessive clotting and excessivebleeding; it can occur in as many as 90 percent ofpatients having severe brain injury (Marx, 2002). As a general rule, the degree of DIC that developsdepends on the extent of brain injury and tissuedestruction. The injured brain is a source of tissuethromboplastin (a factor involved in the initiation ofblood coagulation), which activates the extrinsicclotting system. The central factor in thepathogenic mechanism is thought to be the

traumatic release of thromboplastin (a factorinvolved in the initiation of blood coagulation),which is present in large quantities in brain tissue. Disseminated intravascular coagulation (DIC) maydevelop within hours after brain injury. Earlydiagnosis is by laboratory measurement of clottingparameters (prothrombin and part ialthromboplastin times [PT and PTT, respectively],platelets, plasma fibrinogen levels, and fibrindegradation products). Since awaiting the resultsof coagulation studies introduces a delay intreatment that allows worsening of thecoagulopathy, some clinicians advocate empirictreatment for coagulopathy in patients with severeclosed head injuries who present with a GlasgowComa Scale of six or less (May, et al., 1997). DIC not only increases morbidity and mortalityafter severe head trauma, it also increases the riskof delayed intracranial hemorrhage. If a head-injured patient with DIC whose medical conditionis stable suddenly begins to deteriorate, a repeatCT scan should be performed to rule outintracerebral hemorrhage (Marx, 2002). Treatment is medical and directed at theprecipitating condition. If treatment is not promptand aggressive, the probability of serious morbidityor mortality is extremely high.

[6] Syndrome of Inappropriate Secretion ofAntidiuretic Hormone (SIADH)-- The syndromeof inappropriate secretion of antidiuretic hormone(SIADH) is a posttraumatic derangement of fluidbalance that on rare occasions occurs as asequela of closed penetrating head trauma(Robertson, 2001). The mechanism involvestraumatically increased secretion of antidiuretichormone (ADH, also called vasopressin) by theposterior pituitary gland. Normal action of ADHtakes place in the distal tubules of the kidneys,where it promotes water retention. Followingtrauma, the normal balance between ADHsecretion, water retention and sodium excretion isaltered in such a way that sodium is lost from theserum and increased in the urine and water isretained in the cerebral tissues. The net result isan osmotic imbalance between the intravascularserum and the surrounding tissues, which in turnproduces an increase in the intracranial pressuredue to water retention. Diagnosis is by laboratory measurement of serum

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and urine sodium levels and osmolalities, as wellas clinical signs and symptoms. Because sodiumis an essential component for proper neuronalfunction, the hyponatremia (abnormally low serumsodium) presents clinically as neurologicdeterioration, which may manifest as seizures.Depending on the magnitude of sodium depletionand rate of development, hyponatremia may alsocause mild headache, anorexia, confusion, nauseaand vomiting, coma, convulsions and, in the mostsevere cases, death. In the hyponatremia causedby SIADH, edema and signs of heart failure,cirrhosis, nephrosis, or hypovolemia (low bloodvolume) are usually absent, unless the patient hasone of these disease states as an underlyingmedical condition (Robertson, 2001).

[7] Brain Abscess-- Although relativelyuncommon in current clinical practice, brainabscess remains a serious and life-threateningdisease in children and adolescents. Brainabscess results from seeding of microbes into anarea of injured brain tissue following theintroduction of bacteria into the cranium from apenetrating head injury. Retained bone fragmentsfrom a compound skull fracture are associated withan increased risk of abscess formation morefrequently than retained metallic fragments orprojectiles (such as a bullet). Abscess formationmay also complicate anterior cranial fossa ortemporal bone fractures, cerebrospinal fluidfistulae, and meningitis. Patients with brain abscess usually present withsystemic toxicity, raised intracranial pressure (ICP)and focal neurologic deficits. The typical clinicalpresentation is dominated by increased intracranialpressure, with headache occurring early in thecourse of abscess formation. During the acutephase, drowsiness, confusion and vomiting occur,leading to a slowing in mental acuity andeventually coma. Papilledema occurs rarely and isnot a consistent finding on physical examination. Abscess formation classically evolves in threephases: (1) an initial phase, characterized bytemporary malaise (weakness), fever and mildheadache; (2) a latent phase, when the patientusually appears well; and (3) a terminal phase, inwhich the patient presents with worseningheadache and vomiting and develops focalneurologic deficits and cerebral herniation.Seizures occur in approximately 25 percent to 50percent of patients, may be focal or generalized,

and can occur at any time during the course ofabscess formation. Diagnosis of brain abscess is by contrast-enhanced computed tomography (CT). Treatmentis surgical and requires the administration ofintravenous antibiotics (Cochrane, 1999). The prognosis of brain abscess is good, with amortality rate of less than 10 percent, if theabscess is diagnosed early and treatedaggressively. Focal residual deficits may remain insome patients and seizures occur in 40 percent to50 percent of patients following treatment(Cochrane, 1999).

[7a] Bacterial Meningitis-- Bacteria can infectmeningeal membranes through gross penetratingwounds or the more subtle openings in the thinnasal or aural bones of the base of the skullfollowing basilar skull fracture. Posttraumaticmeningitis is caused by a variety ofmicroorganisms, depending on the portal of entryof the bacteria. Definitive treatment is by theadministration of intravenous antibiotics providingadequate coverage against the infectingmicroorganism (Marx, 2002).

[7b] Osteomyelitis-- Cranial osteomyelitis, orinfection of the skull bone, can occur afterpenetrating injury to the skull and is most often alate sequela of head injury. The patient usuallypresents with pain, tenderness, swelling anderythema (localized redness and warmth) at theinfected site. More than 50 percent of cases canbe visualized on plain skull x-ray; technetium bonescans are useful when the skull radiograph isnegative. However, false-positive bone scans mayoccur in patients experiencing previous headtrauma or craniotomy. A gallium scan, when addedto a skull x-ray or bone scan, will aid indifferentiating infection from other causes of apositive technetium scan. Treatment is by surgicaldrainage and antibiotics (Marx, 2002).

[7c] Subdural Empyema-- The subdural spacecan be contaminated by a wide variety ofmicroorganisms, usually as a result of facial orsinus fracture, open head injuries, meningitis orneurosurgical procedures. Subdural empyema isoften characterized by rapid onset of a severeheadache, hemiparesis (paralysis on one side ofthe body), and cerebral herniation. Seizures occurin approximately 30 percent of cases (Cochrane,

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1999). Because of the nonspecific nature of thesesigns, definitive diagnosis must be made bycomputed tomography (CT) or magneticresonance imaging (MRI). Subdural empyemagives rise to brain swelling and rapid rise inintracranial pressure (ICP), in addition to theinfective processes, and thus constitutes a life-threatening emergency which must be treatedpromptly. Treatment is surgical and antibiotics areemployed (Cochrane, 1999).

[8] Posttraumatic Epilepsy-- Posttraumaticseizures are among the most serious sequelae ofhead trauma and are relatively common in theacute or subacute period. The incidence ofposttraumatic epilepsy after mild head trauma inthe pediatric population is 1 percent to 6 percent(Savitsky and Votey, 2000). In general, the moresevere the head injury, the higher the incidence ofposttraumatic seizures. Acute posttraumaticseizures usually last for a short period of time andare most likely caused by temporary mechanicaland neurochemical changes within the brain. Thepatient often exhibits no additional seizure activityafter the acute seizure. In the subacute period (24to 48 hours after trauma), seizures are caused bycerebral edema that progressively worsens, smallhemorrhages, or penetrating injuries. Posttraumatic epilepsy is much more likely tooccur in patients with severe head injury or injuriesresulting in a tear in the dura. High risk injuriesinclude those with intracranial hemorrhage or duralpenetration. Other risk factors for posttraumaticepilepsy include a low Glasgow Coma Scale(GCS) score, early seizures (those occurring in thefirst week after head trauma), and brain CTfindings consistent with single temporal or frontallesions in the acute phase. In addition, an EEGfocus one month after head injury was found inone study to be a risk factor four times higher thanfor patients without this EEG finding (Angeleri,1999). Depressed skull fractures, penetratingtrauma, abscess formation, acute hematomas,prolonged posttraumatic amnesia, prolongedunconsciousness and focal neurologic deficits arealso associated with a significantly increased riskof posttraumatic seizures. Posttraumatic seizures usually are partial (focal)seizures that originate in a site of local braindamage and may either remain confined to thecerebral hemisphere of origin or generalize to bothhemispheres. Although potentially disabling and

very difficult to treat, this type of seizure pattern isnot in itself life-threatening as a rule. Statusepilepticus, on the other hand, represents a life-threatening emergency in adults. When it occurs,it often is seen in the immediate posttraumaticperiod, and consists of a prolonged, repetitivecycle of seizures without the usual resolution andreturn to consciousness characteristic of otherforms of epilepsy. Its occurrence in adults usuallyis associated with the worst prognosis in terms ofdeveloping chronic late epilepsy. However, statusepilepticus has no prognostic significance inchildren (Marx, 2002). Patients who make a good recovery from all otherinjuries may find themselves seriously disabled ifchronic posttraumatic seizures develop. Themortality rate is low and was reported to be 14percent in one study (Barlow, 2000). In addition,neurologic outcome was found to be significantlyworse in those with posttraumatic epilepsy thanthose without (Barlow, 2000).

[93.43] Iatrogenic Injuries Following HeadTrauma The rates of morbidity and mortality for headtrauma are strongly influenced by the quality andavailability of medical care. Despite advances indiagnosis, medical and surgical therapy and basicscientific understanding of neurophysiologicalevents in head trauma, the proportion of poor orfatal outcomes from head injury remainsunacceptably high (Cullen, 2001). The leading causes of posttraumatic morbidity anddeath are secondary complications that have theironset and/or evolution while the patient is undermedical care (Cullen, 2001). As many as half ofthe deaths among all patients who sustain morethan minor head injury can be prevented; amongthe most common preventable causes are delay intreating a hematoma, uncontrolled seizures,hypercarbia (presence of high levels of carbondioxide in circulating blood), coagulopathy,hypotension, meningitis and hypoxia (Zink, 2001). Iatrogenic causes of secondary brain injury includeunderresuscitation of shock, overhyperventilationresulting in cerebral ischemia, the use ofmedications that induce hypotension, and painfulprocedures or endotracheal suctioning that resultin a reflex increase in intracranial pressure (ICP)(Zink, 2001). Other complications of medical

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intervention include the administration of too muchor too little fluid during fluid resucitation; a delay inthe administration of antibiotics, or inadequate paincontrol. Mechanical ventilation of head-injured patients isalso associated with risks of perforation of theesophagus and aspiration pneumonia; prolongedendotracheal intubation with stricture andpneumonia, and barotrauma with ventilator-induced lung injury. Minor procedures such aschest tube insertion can be complicated byperforation and hemorrhage. Prolongedresuscitation and invasive monitoring in the ICUcan cause hypothermia and coagulopathy andinitiate a cascade of events leading to multiorganfailure and Adult Respiratory Distress Syndrome(ARDS) (Cullen, 2001). Although most patients with head trauma improveand make a good recovery in time, those withmoderate to severe injuries are at significant risk ofdisability and death due to late or misseddiagnosis and/or improper treatment. Commonerrors and omissions include delay in performingdiagnostic procedures, inappropriate use orinterpretation of skull x-rays, frank misdiagnosis,failure to recognize impending neurologicaldeterioration, inadequate correction of hypotensiondue to shock and respiratory problems (includingsimple airway obstruction) and failure to monitorand aggressively treat elevated intracranialpressure, perhaps the leading cause of death inpatients with severe head injury (Zink, 2001). Timely and accurate diagnosis and treatment arecrucial for a good outcome. Unfortunately, a majorcontributor to inadequate care is the simple lack ofavailable trauma care centers outside of majormetropolitan areas, with sophisticated diagnosticand monitoring equipment and experiencedneurosurgical staffs.

[ 9 3 . 4 4 ] N e u r o p s y c h o l o g i c a l a n dNeuropsychiatric Sequelae In addition to neurophysiological sequelae of headinjury, numerous neuropsychological andneuropsychiatric sequelae may be seen as well.Although physical diabilities tend to stabilize overtime, mood, cognitive and behavioral changes aremore central to morbidity, because there may belong-term impairments that adversely affect thepatient's quality of life (Rao and Lyketsos, 2002).

Traumatic brain injury is associated with severalpsychiatric disturbances such as cognitive deficitsand mood disorders. Cognitive deficits are verycommon among head-injured patients, withmemory loss being the most common complaint.Almost all moderate to severe head-injuredpatients suffer from some type of cognitive defect.Disturbances of attention are also common inpatients with brain injury, with patients complainingof difficulties with concentration and easydistractibility. In addition, language problems, suchas lack of spontaneity of speech and aphasia, arefrequent in head-injured patients. The two most common mood disorders associatedwith head injury include major depression andbipolar disorder (defined as intermittent periods ofmajor depression and mania). Anxiety is alsocommonly reported after traumatic brain injury,having an overall prevalence of 29 percent.Another neuropsychiatric disorder frequentlyexperienced by head-injured patients is behavioraldyscontrol disorder (referring to a constellation ofcognitive, somatic, and mood symptoms that occursimultaneously) (Rao and Lyketsos, 2002). The term ''postconcussive syndrome'' has beenused to describe a certain clinical presentation, butis confusing and controversial because it is seen inpatients with and without a concussion (Rao andLyketsos, 2002). The ''postconcussive syndrome''refers to a complex of somatic, cognitive, andaffective symptoms such as headache, sleepdisturbance, memory and attention/concentrationproblems, irritability, anxiety and depression. Thirtyto 80 percent of patients suffering mild head injuryreport having this complex of symptoms at threemonths post injury and 15 percent continue tohave these symptoms at one year after injury. Thepercentage of patients reporting symptoms ishigher for patients with moderate and severe headinjury (Jagoda and Riggio, 2000). A complete diagnosis should include the type andseverity of the brain injury, the associatedneuropsychiatric sequelae, other medical illnessesthat may be present, and the patient's currentfunctional capacity. Key components in making thediagnosis include obtaining a detailed history fromthe patient, a review of the patient's old medicalrecords, performing a complete mental status,physical and neurologic examination, as well as abrief test of global cognitive functioning, such as

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the MMSE. The MMSE (Mini-Mental StatusExamination), however, is not particularly sensitivein determining cognitive loss in mild head injury.The patient's stage of recovery and prognosis forcomplete recovery should also be noted (Rao andLyketsos, 2002).

P 93.50 MANAGEMENT OF HEAD INJURY:OVERVIEW

Appropriate management of the head injuredpatient depends on accurate classification of thehead injury. Although a number of classificationschemes are used for assessment of neurologicdamage following head injury, the most reliableand popular scheme is the Glasgow Coma Scale(GCS). Head injury is classified into three groupsbased upon the GCS score: (1) mild head injury(score of 13 to 15), (2) moderate head injury(score of 9-12) and (3) severe head injury (3 to 8).However, the management of head injury iscomplicated by the fact that the GCS score is notalways predictive of the presence of an intracraniallesion, such as a subdural hematoma. Indeed, 10percent to 20 percent of head-injured patients witha GCS score above 12 have positive findings of amass lesion on CT scan of the head (Jagoda andRiggio, 2000; Cheung and Kharasch, 1999). From the emergency physicians' point of view, apatient presenting with a GSC score of less than 9has severe brain injury. Over the past 30 years,mortality from severe head injury has beenreduced by half, from about 50 percent toapproximately 25 percent due to advances inemergency medical care and diagnostic modalities(Zink, 2001). Increased understanding ofsecondary brain injury and its impact on neurologicsequelae after brain injury have also lead toimproved outcomes. The most critical decisionfacing emergency physicians today is whether ornot to order a CT scan in the patient with mildhead trauma (Cheung and Kharasch, 1999).

[93.51] Critical Factors Affecting Outcome Aggressive early management of head injuryimproves outcome significantly. The initialevaluation and stabilization of the head traumapatient begins at the scene with aggressivemanagement of the airway, breathing andcirculation according to ACLS guidelines.Endotracheal intubation in the field also improvessurvival in severely head-injured patients by

preventing secondary injury caused by hypoxiaand ischemia. If the patient has evidence ofincreased ICP (such as pupil asymmetry), ICPtreatment should be initiated as follows: (1) ensureadequate oxygenation, cerebral venous drainage,and pain relief, sedation or paralysis; (2)hyperventilation (as a temporary measure); or (3)the use of an osmotic agent such as mannitol(Dangor and Lam, 1999). Three types of injury can be singled out as beingboth prominent causes of severe disability anddeath and commonly mismanaged: intracranialhematomas, elevated intracranial pressure (ICP)and cervical spine injury. Acute subduralhematomas occur in about 20 percent of patientswith severe head injury, and approximately 50percent of these patients are unconscious from thetime of injury (Evans and Wilberger, 1999) It hasbeen demonstrated that patients with a subduralhematoma who undergo surgery within four hoursof their injury have a mortality rate that is threetimes lower than those who have surgery morethan four hours after their injury (Cheung andKharasch, 1999; Evans and Wilberger, 1999).Hence, a delay in diagnosis and treatment canadversely affect outcome in any head-injuredpatient with an intracranial lesion requiring surgicalintervention.

[93.52] Grading of Head Injuries for Triage andManagement Many physicians consider a systematic protocol fortreatment as likely to provide the most effectivecare. A key element of the overall systematicapproach is prioritization of injuries. Those thatpose the greatest threat to life and limb must betreated first. Toward this end, triage and initialmanagement are based on assignment of patientsto one of four categories according to level ofconsciousness upon arrival in the emergencydepartment (ED) (Meagher and Narayan, 2000):Grade I: Mild Head Injury. Patient is alert, orientedand shows no signs of focal neurological deficits;may have headache, nausea, vomiting, andtransient loss of consciousness (LOC). Grade II: Moderate Head Injury. Patient is alert buthas focal neurological deficit (e.g. hemiparesis oraphasia), or impaired consciousness (lethargic)but is able to follow simple commands (e.g., holdup two fingers).

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Grade III: Severe Head Injury. Patient'sconsciousness is impaired to the degree that he orshe is unable to follow simple commands; mayspeak, but speech will be inappropriate at best;has variable, often flaccid motor responses. Grade IV: Brain Dead. No evidence of brainfunction. (Meagher and Narayan, 2000).

[1] Management of Grade I Head Injuries-- Minorhead injury is defined as brain injury resulting in aGCS score of 13 to 15, with a return to a normallevel of consciousness (LOC) within 24 hours(Morris and Marshall, 2000). The majority ofpatients experiencing minor head injury can betreated on an outpatient basis. If the patient isconsidered to be neurologically stable after acomplete physical and neurologic examination, thepatient can be discharged from the ED to home,where he or she is to be observed frequently by areliable observer. Any change indicating adeterioration in neurologic status, such as an acutechange in mental status, loss of consciousness, aworsening headache, or visual disturbances,should prompt immediate evaluation by a physician.

[1a] Use of X-Rays-- Historically, plainradiographs (x-rays) were used to screen for skullfractures and to identify patients at risk for anintracranial injury. The advent of CT, however, hasnow made the use of x-rays obsolete. Since skullx-rays do not have sufficient sensitivity orspecificity to detect skull fractures or intracraniallesions, they are currently not considered clinicallyuseful (Savitsky and Votey, 2000; Amann, 2000).

[1b] Use of CT Scans-- CT scanning is generallyreserved for the head-injured patient exhibiting aprolonged loss of consciousness, symptoms thatpersist over time, or deterioration in neurologicstatus. In general, CT scanning is the diagnosticmethod of choice in patients with severe headinjuries. Computed tomography (CT) scans aregenerally not recommended for adult patients witha history of mild head trauma who are consideredneurologically stable after diagnostic evaluation(Amann, 2000). Since CT scanning is widelyavailable, it is usually the first diagnostic testperformed to exclude intracranial lesions, such assubdural or epidural hematomas. The use of CT scanning in children is controversial(Savitsky and Votey, 2000). Recent guidelinesregarding the use of CT in children have been

published by the American Academy of Pediatricsin conjunction with the American Academy ofFamily Physicians because of the wide variety oftreatment practices regarding this issue. Accordingto these guidelines, a CT scan is notrecommended for the initial evaluation andmanagement of children with minor head injuryand no LOC. An acute change in neurologic statusupon observation, however, such as vomiting,seizure, lethargy or persistent headache in anysuch child requires a repeat medical evaluationwhich most likely includes a CT scan (Gedeit,2001). Children with minor head injury with briefLOC (less than one minute) may undergo a CTscan, if deemed appropriate by their physician(Coombs and Davis, 2000).

[2] Management of Grade II Head Injuries--Because patients with moderate head injury candeteriorate rapidly to Grade III neurologic status,their management is similar to that of patients withsevere head trauma, albeit somewhat less urgent.Similar to the patient with severe head injury, thepriority in managing the patient with moderatehead injury is to minimize secondary brain injury.To this end, maintenance of adequate oxygenationand hemoperfusion are of critical importance(Gedeit, 2001). Since approximately 10 percent ofpatients with moderate head injury will either haveor develop hematomas, a CT scan is warranted.The presence of a subdural or epidural hematomarequires immediate surgical evacuation to preventsecondary injury. Severe cerebral edema(identified by CT scan) also requires placement ofan intracranial pressure monitor. In addition, apatient exhibiting altered mental status may havesuffered a spinal cord injury that requiresimmobilization. Spinal cord immobilization shouldbe continued until a complete diagnosticevaluation is performed (Gedeit, 2001).

[3] Management of Grade III Head Injuries--Since 1991, there have been significant changesin the management of patients with severe headinjury. Current practices parallel therecommendations of evidence-based guidelines.Specific changes include an increase inintracranial pressure monitoring and a decrease inthe use of hyperventilation and steroids. Mostneurosurgeons agree that patients with severehead injury should also receive treatment at aLevel 1 trauma center (Marion and Spiegel, 2000). In the patient with severe head injury, the ABCs of

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emergency medical treatment apply (that is, theestablishment of an adequate airway, breathing,and circulation is the first priority). In patients witha GCS of 8 or less, or those exhibitinghypoventilation, apnea, or cardiopulmonary arrest,endotracheal intubation and mechanical ventilationshould be performed. It is of utmost importancethat hypoxia and hypercarbia (a high carbondioxide level in the blood) be prevented by usingsupplemental oxygen and controlled ventilation,since these factors can contribute to secondarybrain injury and poor outcomes. Patients who exhibit signs of circulatory shock(e.g., tachycardia [a rapid heart beat] orhypotension), should receive intravenous isotonicfluid to ensure an adequate blood volume in orderto maintain blood flow to the brain. The neurologicstatus of the patient should also be assessedusing the Glasgow Coma Scale to evaluate thepatient's response to therapy. The temporary useof hyperventilation or mannitol for patients withimpending brain herniation is appropriate until theneurologic evaluation is complete and the patient'scondition is stabilized. Seizures are common aftersevere posttraumatic brain injury and should betreated with benzodiazepines, phenytoin, andphenobarbital as necessary (Gedeit, 2001).

P 93.60 DIAGNOSTIC EVALUATION ANDEMERGENCY MANAGEMENT

The diagnosis and treatment of traumatic headinjury is a staged, progressive process. At eachstage, more diagnostic information is accumulatedand further therapy is administered, predicated onthe progress of the patient's evolving clinical course. Damage to the brain that occurs as a result ofhead trauma is essentially of two types, structuraland functional. The location and extent of bothtypes is crucial to emergency management, tomonitoring and therapy in the postacute stage ofinjury and to long-term outcome and rehabilitation(Dangor and Lam, 1999; Cheung and Kharasch, 1999). Computed tomography (CT) and other radiologicaldiagnostic modalities provide a great deal ofinformation about the structural damage caused bya head injury. It, however, provides virtually noinformation about the functional damage to theneurons. The fundamental source of informationabout the functional status of the CNS (centralnervous system) neurons is the neurological

examination. However, the ability to define thelocation and extent of neuronal dysfunctionthrough the neurological exam is limited in patientswho are comatose, uncooperative or confused; itis further compromised by the effects of sedativeor paralytic drugs administered as part of thepatient's treatment. This situation has led to an interest in using thebrain's electrical activity as a more objectivesource of information regarding the patient'sneurological status and any changes that occur init over time. Two commonly used techniques fornoninvasively recording the electrochemicalimpulses from the brain's nerve cells areelectroencephalography (EEG) and sensoryevoked potentials (SEPs). Additional factors ofenormous significance to the functional state of theneurons are cerebral blood flow (CBF), cerebralmetabolism and intracranial pressure (ICP).Various techniques are available for monitoringthese functions. Following severe head trauma, the circulation andmetabolic processes of the brain are compromiseddue to secondary damage such as increasedintracranial pressure, arterial hypoxia (insufficientoxygen in the blood), arterial hypotension (due toblood volume loss, for example) and increasedblood viscosity. A number of techniques can beused to measure circulatory function (Dangor andLam, 1999). The ultimate aim of management is toreestablish and maintain the patient's homeostasisin order to provide the best physiologicalenvironment possible for the recovering neurons. Because numerous sequelae of head injury cancause precipitous deterioration and rapid death,triage (prioritization) of the injuries is essential.This in turn requires that all injuries be identifiedand that the emergency department (ED)physician have a thorough knowledge of the typesof injuries that result from trauma and which aremost likely to pose a threat to the patient's life.Priorities of care are established by evaluating andmanaging the patient in the ED according to thefollowing staged approach: history, primary survey,secondary survey, and definitive care (Cheung andKharasch, 1999; Evans and Wilberger, 1999;Townsend, 2001). Traditionally, the diagnosis oftraumatic brain injury is made by history andphysical examination (Jagoda and Riggio, 2000).

[93.61] History

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The initial evaluation of a patient who has sufferedhead trauma begins with a thorough history. Sincethe patient experiencing a concussion is usuallyunable to give an accurate history, witnesses ofthe event often provide valuable information. Oneimportant aspect of the history is the mechanism ofinjury; e.g., whether a moving object struck astationary head, or a moving head struck astationary object, such as what occurs in a motorvehicle accident. This information often indicatesthe forces involved in the event (Amann, 2000). Based on the mechanism of head injury alone, theemergency physician can usually predict thelikelihood of significant injury. The highestincidence of intracranial injuries results fromunprotected head trauma involving large forces.Pedestrians and bicyclists, for example, have thegreatest potential for suffering a severe intracranialinjury. Motor vehicle occupants, assault victims,and patients injured from falls have comparableincidences of intracranial injury. Even falls fromlow heights can result in significant trauma(Cheung and Kharasch, 1999). Perhaps the most important information to beobtained in the patient suffering blunt head traumais loss of consciousness. Current emergencymedicine practice is to assume that if a patient didnot lose consciousness, he or she does not havean intracranial injury. The incidence of intracraniallesions in victims experiencing loss ofconsciousness ranges from 1.3 to 17.2 percentand rises with increasing time of loss ofconsciousness (Cheung and Kharasch, 1999).Other important information to be elucidated in thehistory include the behavior of the patient after thetraumatic event, a history of prior concussiveepisodes, or existing neurologic deficits (Amann,2000).

[93.62] Primary Survey The chief objective of the primary survey is toidentify those injuries that are immediately life-threatening. The identification and management ofthese injuries should proceed simultaneously, andthe entire primary survey should be completedwithin 5 to 10 minutes. The stages in the primarysurvey, outlined below, begin with the ''ABCs''(airway, breathing and circulation) and arefollowed by a brief neurological exam (Townsend,2001).

[1] Airway, Breathing and Circulation--Establishing an airway so that oxygen can get tothe lungs is of cardinal importance, as the brain isparticularly susceptible to permanent damage fromoxygen deprivation. At the same time, thepossibility of an associated cervical spine fracturemust be appreciated, since inappropriatemanipulation of the patient during establishment ofthe airway can cause further injury. Any patientwith traumatic brain injury should be assumed tohave a cervical spine injury unless provenotherwise, and the patient should be assessed forthe presence of other systemic injuries and toxicdrug ingestion as well (Dangor and Lam, 1999). Once an unobstructed airway is established,adequate oxygenation (movement of air into andout of the lungs) must be assured. Inadequateoxygenation rapidly leads to hypoxia, anaerobicmetabolism and acidosis and is the most commoncause of death in head trauma patients (Dangorand Lam, 1999). Respiratory difficulty is oftenmissed by the physician during the early stage ofcare when attention tends to be focused mostintently on evaluation of the most obvious injuries.Indicators of adequate oxygenation should not beneglected; they include extent of chest expansion,skin color, and respiratory rate. A breathing rateabove 30 per minute is suggestive of the patient'sneed for mechanical assistance in breathing. Arespiratory rate above 40 per minute is a definiteindication for mechanical ventilation. Minimal chestexpansion and cyanosis (blue skin color) are alsoindications of inadequate oxygenation. In addition to a patent (open) airway and effectiverespiration, the patient's cardiac function andcirculation must be returned to normal in order toprevent shock and to assure adequate perfusion ofthe brain and other tissues. Control of bleeding isa major part of this effort (Dangor and Lam, 1999;Townsend, 2001).

[2] Neurologic Exam-- A rapid neurologicassessment includes an evaluation of the patient'slevel of consciousness (using the Glasgow ComaScale), pupillary assessment, brain stem reflexes,and focal or lateralizing neurologic signs (Dangorand Lam, 1999; Townsend, 2001). Currently, theGlasgow Coma Scale (GCS) is the most popularsystem for grading the neurologic status of headtrauma patients. This examination assesses thepatient's ability to respond to pain, to speak, and to

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open the eyes (e.g., motor response, verbalresponse, and eye opening). When performed inconcert with examination of the pupils, the GCSprovides an excellent guide to the severity of theinjury in the pre-hospital setting. Patients who areunable to follow commands, do not open their eyesin response to noxious stimuli, or are unable tomake comprehensible sounds are considered tobe in a coma (GCS<<8). All four limbs should betested for responsiveness, either to verbalcommand or to pain, so that any focal neurologicaldeficits are not missed (Morris and Marshall, 2000). Trauma protocols in various hospitals often use anoptimal GCS as a measure of reassurance, andthis has been deemed as a sufficient reason fordischarging a patient to home without furtherdiagnostic evaluation. However, even a perfectGCS of 15 does not exclude the presence ofsignificant intracranial lesions such as subdural orepidural hematomas. In fact, studies show that theincidence of head injuries detected by CT inpatients with a GCS of 15 varies between 2.5percent and 22.5 percent (Cheung and Kharasch,1999). In addition, up to 6 percent of patients withblunt head trauma and loss of consciousness, aGCS of 15, and normal neurological examinationshave been shown to have significant intracraniallesions (Cheung and Kharasch, 1999). Although aperfect GCS score of 15 does not exclude anintracranial lesion that can be detected by CT, alow GCS score does correlate positively with ahigh incidence of a CT abnormality (Cheung andKharasch, 1999). In addition to the GCS, pupillary findings are usedto indicate the severity of the head injury. Amongthe more serious conditions that may besuggested by pupillary findings is herniation of thetemporal lobe, which can cause rapid neurologicdeterioration and death. When present, the pupilsare mildly dilated and respond sluggishly to light.Associated damage to the oculomotor nerve issuggested by pupils that have been dilated fromthe time of the trauma and weakness of the eyemuscles. Pupils that are bilaterally dilated andfixed suggest insufficient cerebral vascularperfusion itself, or secondary to increasedintracranial pressure causing diminished bloodflow. Bilaterally small pupils (less than 3 mm indiameter) suggest opiate drug overdose.

[93.63] Resuscitation

In a patient with depressed consciousness orcoma, resuscitation is accomplished first andforemost by hyperventilation (as a temporarymeasure) and hyperoxygenation. This can beaccomplished either by simple endotrachealintubation or by mask and ventilator if the patientneeds assistance in breathing. Since hypoxemiaand hypercapnia often occur at the time of initialresuscitation, endotracheal intubation in the field(e.g., outside the hospital, at the scene) has beenshown to improve survival in patients withtraumatic brain injury by preventing secondaryinsults resulting from hypoxia and ischemia(Dangor and Lam, 1999; Townsend, 2001).

[93.64] Secondary Survey Once the quick initial evaluation (primary survey)of the patient's injuries and status has beencompleted and he or she has been stabilized withrespect to cardiopulmonary function, a morecomplete assessment of the patient's injuries isconducted. The essential components of thissecondary survey are: history, physical andneurological examination, laboratory tests,radiological evaluation and any special procedures(Evans and Wilberger, 1999; Townsend, 2001).

[1] History-- During the secondary survey,additional details are added to the basic history ofthe accident and the patient's injuries acquiredduring the primary survey and pre-hospital phase.The key points to cover are summarized in theacronym AMPLE: allergies, medications, pastmedical history, last oral intake, and eventssurrounding the trauma (Townsend, 2001).

[2] Physical and Expanded Neurologic Exam--Once the patient's cardiorespiratory function isstabilized, a physical examination should beperformed in which the patient is quickly butcarefully given a complete body survey. The examshould proceed in an organized fashion and on aregional basis: head, neck, chest, abdomen andextremities. As the examiner proceeds, he or sheshould coordinate the findings and other aspectsof the secondary survey and be constantlyintegrating all the diagnostic information withmanagement possibilities. Immediately upon completion of the physicalexam, an expanded neurologic exam should beginin patients who are awake and alert followingresuscitation. Key components of the exam include

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inspection of the cranium for signs of puncturewounds, hemorrhaging behind the tympanicmembranes (ear drums), leakage of cerebrospinalfluid (CSF) from the ears or nose and other signsof injury. Any laterality to the neurological findings(such as a dilated pupil or hemiparesis) suggestsa focal mass lesion. The cranial nerves mediatingvision and ocular motility, hearing, equilibrium,facial sensation and movement and olfaction(sense of smell) should be assessed, since theseare often stretched, torn or contused. The higherthe GCS score, the more important it is to obtain adetailed mental status examination. Forpenetrating head wounds, such as gunshotwounds, there should be detailed documentationof entry and exit wounds, powder burns, andforeign bodies (Evans and Wilberger, 1999;Townsend, 2001).

[3] Lab Tests-- Baseline laboratory tests includea complete blood count (CBC), electrolytes, anarterial blood gas, a coagulation profile, blood typeand crossmatch, an electrocardiogram, andurinalysis (Dangor and Lam, 1999). Blood glucoselevels should be measured as they can indicate orrule out hypoglycemia (low blood sugar) as acause of depressed consciousness. A toxicologyscreen including a blood alcohol test should alsobe ordered as the blood alcohol concentration mayaffect the GCS score. Studies have shown that alower GCS can not be attributed to alcohol unlessthe patient has a minimal blood alcoholconcentration of 200 mg/dL (Cheung andKharasch, 1999).

[93.65] Radiological Investigation Prior to the introduction of computed tomography(CT) in 1972, radiological investigation ofintracranial injuries following head traumacomprised primarily skull x-rays, ventriculographyand cerebral angiography. These techniques stillhave important specific indications, but theradiological diagnosis of intracranial trauma is nowdominated by CT.

[1] X-Rays-- In a severely injured patient, x-rays ofthe cervical spine should be taken first. Sincemovement of an injured neck can damage thespinal cord and result in permanent paralysis, thepatient's head and neck must remain immobilizedin a hard (Philadelphia) collar until the radiologistor neurosurgeon has read the cervical films. Theone exception to this rule is the patient suffering a

gunshot wound to the head. Indirect spinal cordinjury does not occur in a patient having a gunshotwound to the head and cervical spineimmobilization may compromise airwaymanagement in such a patient (Kaups and Davis,1998). Skull x-rays have been largely supplantedby computed tomography (CT) scans in thediagnostic evaluation of head trauma.

[1a] Cervical Spine X-Rays-- Cervical spine injuryshould be suspected in a head trauma patient whohas suffered a motor vehicle accident (especiallya rear-end collision) or a fall. The cervical spine ismost commonly affected because of its mobility.This is followed by the thoracolumbar spine, whichforms the junction between the rigid thoracic spineand the flexible lumbar spine. Injury to the cervicalspine is caused by flexion, flexion-rotation, verticalcompression extension and lateral flexion forces.Approximately one-third of patients with moderateor severe head injury have cervical spine injury(Lida et al., 1999). In addition, patients with uppercervical spine injury are at greater risk ofsustaining skull fractures and intracranialhematomas than those with injury to the lowercervical spine. Due to the prevalence of this injury,all patients with traumatic brain injury should besuspected of having a cervical spine injury untilproven otherwise (Dangor and Lam, 1999). Cervical spine injuries are one of the mostcommon missed diagnoses having seriousimplications for both the patient and physician. Thediagnosis of subluxations or spinal cord injuries inthe absence of vertebral fractures, especially in thecomatose patient, poses a major challenge for thephysician (Demetriades et al., 2000). In aconscious patient, pain or tenderness in the neckmay alert the physician to the presence of cervicalspine injury. Diagnostic hints in an unconsciouspatient include areflexia (absence of reflexes) andflaccid anal sphincter, diaphragmatic breathing,forearms that can be flexed but not extended,facial grimaces in response to pain above theclavicle (collar bone) only and hypotension in theabsence of another clear etiology. Far moreobjective and reliable evidence, however, must beobtained by x-ray visualization of all seven cervicalvertebrae. Lateral, anteroposterior (AP) and open-mouth views are usually adequate, although a''swimmer's view'' (with the patient's arm extendedabove the head) may sometimes be necessary tovisualize the 6th and 7th vertebrae. Althoughlateral cervical spine radiographs show the cervical

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spine below the level of C7, they do notnecessarily rule out spinal cord injury (Dangor andLam, 1999). If the diagnosis remains in doubtfollowing the cervical films, a definitive diagnosiscan be made by CT, which is superior to plain filmx-rays for visualizing spinal injuries in general(Evans and Wilberger, 1999).

[1b] Plain Skull X-Rays-- The use of skull filmshas dramatically decreased since the advent of theCT scanner. Studies show that skull films areneither sensitive or specific for detectingintracranial injuries. CT is a much better diagnosticmodality for the detection of skull fracture, havinga sensitivity of 94 percent. Although the presenceof a skull fracture increases the likelihood ofhaving an intracranial lesion, approximately 50percent of all intracranial abnormalities resultingfrom head trauma are not associated with skullfracture. For this reason, skull films have becomesuperfluous in the management of blunt headtrauma. Thus, any head-injured patient with asuspected skull fracture should undergo a CT scan(Cheung and Kharasch, 1999).

[2] Computed Tomography (CT)-- Computedtomography (CT) is a noninvasive radiologicaltechnique which allows computer-assisted x-rayvisualization of cross-sections of internal softtissue structures based on subtle differences intheir relative densities. A difference in density of aslittle as 0.5 percent can be revealed on CT(Cheung and Kharasch, 1999). In essence, computed tomography is performed byplacing the patient in the CT scanner and makinga series of 10 to 15 sequential ''cuts'' or ''slices'' of1 cm each along the vertical axis of the head.Each slice takes about two seconds to complete.The resulting CT image, reconstructed bycomputer from the series of contiguous 1 cm cuts,should adequately cover the entire brain as well asthe posterior fossa. Different angles of the x-raybeam and patient positions are used asappropriate, providing cuts along different axes.When planning the study, any associated injuries,especially those of the cervical spine, mut be takeninto account as they will restrict the allowablemaneuvers of the patient. Computed tomography is the initial imagingmodality of choice for traumatic brain and spinalinjuries (Gean, et al., 1995; Bagley, 1999). Majortraumatic lesions identifiable with CT scanning

include fractures and fragments, CSF leakage,edema, contusion, epidural hematoma, subduralhematoma, intracerebral hematoma, subarachnoidhemorrhage, intraventricular hemorrhage,hydrocephalus, posttraumatic infarction and brainabscess. Although CT remains the mainstay of evaluation ofhead trauma, it is not infallible. The incidence ofabnormal findings on CT following head traumavaries considerably in published reports, from 37to 73 percent (Zee and Go, 1998). Accurateinterpretation of posttraumatic CT images thusrequires appreciation of some of the technique'skey limitations and artifacts, most of which can becorrected. Principal limitations include motionartifacts (caused by movement of the patient'shead during the procedure) and the partial volumeeffect (inaccurate interpretation of a findingsituated only partially within a ''slice''). Motionartifacts are particularly severe in the vicinity ofbone, which is where extracerebral hematomasare located. However, CT is superior for analyzingvascular lesions, such as aneurysms,arteriovenous fistulas, and intravascular thrombi.

[2a] Fractures and Fragments-- The extent ofdepression of a fracture fragment is bestdemonstrated by CT using bone windows. Otherforeign objects, such as bullet fragments, as wellas their hemorrhagic track through the brain alsoare readily identified by CT, as is pneumocephalus(intracranial air).

[2b] Cerebrospinal Fluid (CSF) Leakage-- ACSF leak can be identified by CT scan particularlyusing bone windows with coronal views (Zee andGo, 1998; Townsend, 2001). Common sites forrhinorrhea (CSF leakage from the nose) includethe cribriform plate and the anterior cranial fossa.The common site for otorrhea (CSF leakage fromthe ear) is through the petrous bone (Zee and Go,1998; Townsend, 2001). If sufficient information is not obtained by astandard scan, intrathecal (within the CSF)contrast enhanced CT may be used. In this case,contrast material is injected by lumbar punctureand the scan is performed with the patient tiltedhead downward 10 to 15 degrees. Any fractureswill be revealed as contrast material leaks throughinto the cavity of the nose or ear (Zee and Go,1998; Townsend, 2001).

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For a patient with clinically diagnosed CSFleakage suspected of having a CSF fistula, thecombinat ion of magnet ic resonancecisternography and plain high-resolution CT ishighly accurate in locating the site of the fistula.This combination of imaging modalities representsa noninvasive alternative to CT cisternography inthe diagnosis of CSF fistula (Shetty, et al., 1998).

[2c] Edema-- Edema may be focal, multifocal ordiffuse. An edematous area appears as a zone oflow density on CT scans, with mass effectsmanifested as compression, displacement ordistortion of the cerebral ventricles. Focal andmultifocal lesions can be distinguished bycomparison with the somewhat denser whitematter of the brain since these lesions, whenadjacent to traumatic mass lesions, demonstratedecreased density on CT scans compared withnormal tissue (Marx, 2002). Diffuse edema over the whole brain may bedifficult to identify owing to the lack of any region ofnormal brain density for comparison. In suchcases, however, there usually is obvious bilateralventricular compression. When interpreting the CTscan, it must be kept in mind that the presence ofother low density components in the traumatizedbrain, such as lipids, necrosis or cavitation, can bemistaken for edema or obscure edema that is present.

[2d] Contusion-- Non-contrast-enhanced CT isthe diagnostic tool predominantly used to detectcontusions early in the posttraumatic period.Contusions appear heterogenous and irregular onCT scan because of mixed regions of hemorrhage,necrosis, and infarction. The surroundingedematous tissue also appears hypodense. Bydays three and four, following the initial traumaticevent, the blood located within the contusionbegins to degrade, so that magnetic resonanceimaging (MRI) becomes a more useful diagnostictest (Marx, 2002). Contusions are most commonly located in theanterior frontal and temporal lobes. Contusionsoften produce a mass effect as well, whichmanifests as displacement and distortion of theventricles (although this may be minimal). Sincecerebral contusions may evolve into delayed post-traumatic intracerebral hematomas, they should befollowed carefully by CT scans (Zee and Go, 1998;Baley, 1999).

[2e] Epidural Hematoma-- An acute epiduralhematoma (between the inner surface of the skulland the exterior of the dura mater) generallyappears as a biconvex (lens-shaped) region ofuniformly high density on CT. Epidural hematomas are most often located overthe temporal or temporoparietal region, and formfrom extravasated blood from anterior or posteriorbranches of the middle meningeal vessels that aredamaged due to a linear skull fracture (Goetz,1999). They displace the brain from the midlinemuch more than subdural hematomas do. Thedevelopment of an epidural hematoma also maybe delayed, or may be masked by a large subduralhematoma on the opposite side of the brain.Because an initially hidden epidural hematomamay enlarge rapidly following evacuation of thecontralateral subdural hematoma, a postoperativeCT scan should be obtained. Since approximately20 percent of patients with an epidural hematomahave blood in both the epidural and subduralspaces at surgery (or autopsy), it is not alwayspossible to discriminate between epidural andsubdural hematomas on CT (Goetz, 1999). Occasionally, an epidural hematoma will remainundetected in the first CT, which is usuallyperformed a few hours after injury, but will appearon subsequent CT scans as the patient'sneurologic status rapidly deteriorates and thehematoma evolves. This is known as a ''delayedepidural hematoma'' and is a potential for a misseddiagnosis by emergency physicians. Although theoccurrence of delayed hematoma is rare, 8percent of patients in a large series were found tohave delayed epidural hematoma (Inamasu, et al.,2001). In most of the reported cases, the initial CTscan was taken within 24 hours after the injury andreported to be normal, while the delayed evolutionof the hematoma occurred over the next 24 to 96hours. The progression of symptoms in delayedepidural hematoma are also more gradual ratherthan acute. Hence, even when the initial CT scanis normal, repeated CT scans should be obtainedin patients suffering blunt head trauma withworsening symptoms, to rule out the developmentof delayed epidural hematoma (Inamasu, et al., 2001).

[2f] Subdural Hematoma-- On CT scan, an acutesubdural hematoma appears as a hyperdenselesion over the outer surface of the brain betweenthe inner surface of the skull and dura. Diagnosisis more complex with a subacute subdural

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hematoma, since the hematoma appears isodenserelative to the brain itself. During the acute period,T1-weighted magnetic resonance imaging may bemore useful in detecting a lesion in the subduralspace. A chronic subdural hematoma appears asa hypodense area on the CT scan (Goetz, 1999;Marx, 2002). CT can detect a subdural hematomaat a depth of 5 mm; shallower hematomas may bemissed due to their close proximity to the skull. Arelatively large subdural hematoma also may bemissed due to partial volume artifacts if it is locatedhigh over the brain and beneath the convexity ofthe skull. High subdural hematomas may be detected byscanning perpendicular to the suspected location.Subdural hematomas undergo a decrease indensity over time, as the high-density bloodcomponents in the clot (such as hemoglobin)disintegrate. In addition, there is probably sometransdural migration of cerebrospinal fluid into thehematoma, which also decreases the density ofthe lesion. Eventually, the hematoma may not bevisible. In such cases, major mass effects, such asventricular distortion and brain shift, may be noted.If these are also absent or minimal, other clues tothe presence of a hematoma include obliteration ofthe sulci (furrows) over the convexity of theinvolved side and distortion of the ventricle on theopposite side. Contrast enhancement may be useful. Confusion may exist concerning the classificationof subdural hematomas according to CT density.For example, new bleeding into a chronic subduralhematoma will have the appearance of an acutelesion on CT. An acute subdural hygroma (a fluidfilled sac or cyst) will have the appearance of achronic subdural hematoma. Since managementdecisions can be altered dramatically, informationobtained from the history becomes more important(Goetz, 1999).

[2g] Intracerebral Hematoma-- An intracerebralhematoma may be detected on the first CT scanimmediately following the trauma, but often is notseen for several hours or days. In contrast to acontusion, intracerebral hematomas are usuallylocated deep within the brain tissue and tend tobecome well demarcated over time (Marx, 2002).On CT scan an intracerebral hematoma appearsas a well-defined hyperdense homogenous area ofhemorrhage. Intracerebral hematomas maydevelop in any part of the brain, but are foundmost commonly in the frontal and anterior temporal

lobes of the cerebrum (Goetz, 1999). They may besingular, but consist of multiple foci morecommonly than any other form of posttraumatichematoma. This may help to distinguish them fromhematomas due to other causes, such ashypertension, aneurysms or arteriovenous fistulas. Computed tomography can detect an intracerebralhematoma as small as 0.5 cm in diameter.15 By 3to 4 weeks following the trauma, the density of thelesion may diminish, making it impossible tovisualize except by the use of contrastenhancement. Distortion of the ventricles ordisplacement of the brain from the midline due tothe mass effect of the hematoma also should benoted. The majority of intracerebral hematomasdevelop immediately following trauma, but mayappear later within the first week after injury(Goetz, 1999). On occasion, their developmentmay be delayed for up to 3 weeks.

[2h] Subarachnoid Hemorrhage-- Subarachnoidhemorrhage is detected on the initial CT scan inapproximately 33 percent of patients with severehead injury and has an incidence of 44 percent inall cases of severe head trauma. It is the mostcommon CT scan abnormality seen after traumaticbrain injury (Marx, 2002). Bleeding into thesubarachnoid space (between the arachnoid andpia mater meningeal membranes) appears on CTas high-density linear regions in specific areas ofthe brain. Subarachnoid hemorrhaging typically ispresent for only a few days following trauma andcommonly is associated with a hematoma (eitherintracerebral or extracerebral). It may lead to hydrocephalus.

[2i] Intraventricular Hemorrhage-- Bleeding intothe cerebral ventricles usually is associated withbleeding within the substance of the brain tissue(parenchymal hemorrhage). Since the advent ofCT, traumatic intraventricular hemorrhage hasbeen diagnosed more frequently. In the past, itwas associated with a poor prognosis, butintraventricular hemorrhage by itself is rare,suggesting that other lesions that occurconcomitantly with it may contribute to a pooroutcome (Abraszko, et al., 1995). The uniform highdensity image of the ventricles (due to the bloodtherein) is characteristic of the acute stage.

[2j] Hydrocephalus-- The incidence ofposttraumatic communicating hydrocephalus (anexcessive accumulation of fluid in the ventricles)ranges from less than 1 percent to 29 percent in

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patients with severe head injury. If CT criteria forventriculomegaly are used, the incidencereportedly varies from 30 percent to 86 percent(Guyot and Michael, 2000). The CT scan showsventriculomegaly (enlarged ventricles) within 10 to14 days, and sometimes low-density edemaaround the ventricle borders. Ventriculomegalyafter head injury is a subject of current debate, asthere is presently no definitive manner todistinguish between posttraumatic hydrocephalusfrom cerebral atrophy in its presence. Thediagnosis is established by using a combination ofclinical, neuroimaging results, and physiologicdata. For example, the presence of lateneurological deterioration associated withincreased intracranial pressure confirmed by CTscan findings is more useful in the diagnosis ofposttraumatic hydrocephalus than CT scan alone(Phuenpathom, et al., 1999). CSF dynamics arealso correlated to changes in ventricular massduring the first three months following severe headinjury and are useful in the diagnosis ofposttraumatic hydrocephalus (Marmarou, et al., 1996). Although the diagnosis of hydrocephalus is oftenproblematic, it is most easily made whenventricular dilatation is observed on CT (withminimal dilation of the sulci) and abnormal CSFpressure is present (Townsend, 2001). The returnof the ventricles to normal size followingcompression by edema or hematoma should notbe mistaken for hydrocephalus. The ventricularpathways may also be blocked by a posteriorfossa hematoma, giving rise to an acuteobstructive hydrocephalus, but this is seen lessoften (Townsend, 2001).

[2k] Posttraumatic Brain Atrophy--Posttraumatic brain atrophy is a delayed sequelasometimes seen in a few months to a yearfollowing trauma. A diagnostic sign on CT isenlargement of the ventricles. Posttraumatic brainatrophy can be distinguished from hydrocephalusby the presence of enlarged cortical sulci (fissures)in the former. Late magnetic resonance imaging(MRI) findings after severe head trauma alsoreveal lesions associated with cerebellar atrophyas a consequence of severe head trauma (Soto-Ares, et al., 2001).

[2l] Posttraumatic Infarction-- Mechanical shift ofthe brain and herniation across the falx and/ortentorium is the predominant cause ofposttraumatic cerebral infarction in most head-

injured patients (Server, et al., 2001). Acuteposttraumatic ischemic infarction appears as a lowdensity area surrounded by a normal brain (Gean,et al., 1995; Tyagi, et al., 1995; Server, et al.,2001). Infarction usually is first detectable at about24 hours following the trauma. Sixty percent ofthese lesions can be visualized by 7 days. Anadditional 15 percent of infarctions may bevisualized by contrast enhanced CT over thesubsequent 3-week period, although somecontrast-enhanced infarctions may be detectedwithin the first 24 hours after injury. Infarctionssmaller than 2 cm may not show up on CT (Gean,et al., 1995; Tyagi, et al., 1995; Server, et al., 2001).

[2m] Brain Abscess-- Abscess is an infectioussequela, usually seen following penetrating headtrauma, sinus bone fractures or as a complicationof surgery. In one study, the primary cause of brainabscess was reported to be neglected(undiagnosed and untreated) compounddepressed skull fractures (Stephanov, 1999). Brainabscess appears as an area of low density on theCT image. With contrast enhancement, the low-density area is circumscribed by a bright ringrepresenting edema. If the abscess has developedin the vicinity of the ventricles, ventricularcompression and displacement often is visible.

[3] Ventriculography-- Ventriculography involvesx-ray of the brain following removal ofcerebrospinal fluid from the cerebral ventricles andreplacement with air or other contrast medium.Prior to the introduction of CT, ventriculographywas used to determine the degree of posttraumaticsupratentorial brain shift (the tentorium is thetentlike process of the dura mater that liesbetween the cerebellum and the occipital lobes ofthe cerebrum at the back and base of the brain).Contemporary use of ventriculography isunnecessary since the advent of MRI scans.

[4] Cerebral Angiography-- Despite advances inother imaging techniques, angiography remainsthe radiographic tool of choice for the evaluation oftraumatic vascular lesions (Gaskill-Shipley andTomsick, 1996). The three primary indications forcerebral angiography are: (1) elevated intracranialpressure (ICP) and shifted or slitlike ventricles(due to compression from a mass lesion) on theventriculogram; (2) progressive neurologicaldeterioration in the absence of an apparent cause;and (3) suspected vascular injuries. Angiographyis particularly useful for detecting traumatic

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aneurysms, arteriovenous fistulas and venousocclusions caused by cerebrovascular trauma(Gaskill-Shipley and Tomsick, 1996; Quintana, etal., 1996; Waran and Menon, 2000). Magnetic resonance imaging (MRI) and magneticresonance angiography (MRA) may also aid inselecting those patients with suspected vascularinjuries requiring conventional angiography(James, 1997). In children, MR angiography offersa non-invasive alternative to conventionalangiography for the diagnosis of vascular lesionsand during follow-up evaluation of anticoagulationtherapy (James, et al., 1995).

[4a] Aneurysms-- Enhanced CT (using a contrastmedium) may suggest the presence of a cerebralaneurysm, but precise visualization andlocalization is likely to be impossible without theuse of angiography, especially if the aneurysm isassociated with an extracerebral hematoma(Townsend, 2001). Patients who deteriorateneurologically when no explanation is forthcomingfrom the CT scan should therefore undergoangiography. In addition, any patient with apenetrating head injury or skull base fracture nearthe major arteries should undergo an arteriogram(Townsend, 2001). A new form of angiography,called digital subtraction angiography, is especiallyuseful for studying the extracranial arteries, suchas those in the neck (Kuker and Thron, 1996;Mignon, et al., 1999).

[4b] Thrombosis and Infarction-- Unlikehematomas, the smaller clots that form withincerebral vessels and cause infarctions of thetissue do not show up reliably on CT. When this issuspected, definitive diagnosis can be made withcerebral angiography. Because of the decreaseduse of cerebral angiography following the adventof CT, many of these severely disabling lesionsprobably go undetected (Gean, et al., 1995;Gebara, 1997; Bagley, 1999). For strokes involvingthe spinal cord (e.g., spinal cord infarcts),magnetic resonance imaging (MRI) is the bestmethod to visualize the spinal cord and can revealspinal hemorrhages and infarcts (Gean, et al.,1995; Goetz, 1999; Bagley, 1999). A newtechnique known as diffuse-weighted imaging hasbeen found to be more sensitive than CT indetecting acute ischemia and can be used tovisualize major ischemic change more easily thanCT (Barber et al., 1999).

[4c] Arteriovenous Fistulas-- Selective cerebralangiography is performed on the vessels in theregion of suspected injury in order to define theextent of the lesion. If a carotid-cavernous sinusfistula is suspected, CT or MRI are the initialdiagnostic tests of choice. The final and mostdecisive diagnostic test is cerebral arteriography ofboth the internal and external carotid arteries(Gaskill-Shipley and Tomsick, 1996; Goetz, 1999).

[5] Magnetic Resonance Imaging (MRI)--Magnetic resonance imaging (MRI) is performedby exposing the patient to a magnetic field thataligns the protons in the nucleus of the body'shydrogen atoms along the axis of the magnet.When a pulse of radiofrequency (RF) energy isapplied, the protons resonate, re-transmitting theabsorbed radio waves in the form of an RF ''echo.''These signals are detected by an externalantenna, and a computer then maps their positionand intensity, producing an image of the scannedtissue (Bagley, 1999). Although the techniqueprovides very sharp images, it takes a long time(about 45 minutes), and the patient cannot bemonitored during the procedure. MRI is superior to CT scans for certain types oftraumatic brain injuries, particularly those involvingthe white matter of the brain. MRI is especiallyuseful in the diagnosis of subacute and chronicstages of the neurologic sequelae of head injury(Gean et al., 1995; Bagley, 1999). In one study,MRI identified mass lesions in 80 percent ofpatients, 6 percent of which were not detected byCT (Jagoda and Riggio, 2000). Lesions which canbe identified on MRI range from scattered punctatehyperintensities to the more obvious cerebral hemorrhages. Although MRI is not typically used in theemergency management of severe head injury, itmay provide useful information regardingneurologic outcome. For example, patients withsubcortical white matter lesions or brainstemlesions visualized on early brain MRI usually havea longer duration of coma. Likewise, the presenceof persistent parenchymal lesions correlates withsevere cognitive deficits. Brain MRI performedseveral months after traumatic brain injury has abetter prognostic accuracy than the initial MRIscan (Zink, 2001).

[6] Electroencephalographic (EEG) and EvokedPotential (EP) Monitoring-- Brain Stem AuditoryEvoked Potentials (BAEPs) abnormalities have

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been reported in mild head injury, but findings donot correlate with the severity or prognosis of theinjury. Studies of BAEPs and EEG recordings haveshown changes in the brain's electrical activity upto six weeks after injury, suggesting that mild headinjury can cause both cortical and brainstem injury(Jagoda and Riggio, 2000).

[6a] Electroencephalography (EEG)-- EEGrecords spontaneous electrical activity of the brainnoninvasively through scalp electrodes. The basicpremise on which it functions is that traumaticstructural and functional alterations of the braingive rise to EEG patterns in the damagedstructures which differ from those produced byintact structures (Jordan, 1999; Guerit, 2000).Accurate assessments depend on good technique,an understanding of the situations in which EEG ismost useful and the establishment of acute stagebaseline recordings for comparing subsequentchanges. Continuous EEG monitoring has recentlybeen found to be beneficial for targeting themanagement of acute severe head traumapatients. In comatose patients, it can providediagnostic and prognostic information which isotherwise unobtainable (Jordan, 1999; Guerit, 2000).

[6b] Evoked Potentials (EP)-- While the recordingof EP is more involved than recording of EEG, theEP allows more precise localization of functionaldamage (Guerit, 2000). In essence, the EP is theresponse evoked from selected CNS neurons byan external stimulus applied to them by thetechnician. Sensory stimuli commonly used includevisual (e.g., strobe light flashes), auditory (clicks ortones) and somatesthetic (having to do with thesense of having a body, elicited in EP bydepolarizing cranial or peripheral nerves) (Guerit,2000). Advances in EP technology permit the noninvasiverecording of evoked potentials from scalp and neckelectrodes. Clinical interpretation of EP recordingsis based primarily on three characteristics of thewaveforms: (1) the presence or absence of peaks,(2) the amplitude of peaks, and (3) the latency ofpeaks. Since the interpretation of EP waveforms inhead trauma patients is based on comparison withthe recordings from a normal population, strictstandardization of technique is essential.Moreover, since there is considerable variationbetween laboratories with respect to equipmentand technique, each EP lab must establish its ownnormal baseline.

The absence of a peak is generally an indication offrank structural and/or functional damage to thepathway being stimulated. Other reasons for anabsent peak must be ruled out, however. Bothbarbiturates and seizure activity, for example, cancause the transient loss of EP peak, which returnswhen the drug is withdrawn or the seizure ends(Guerit, 2000). The amplitude of EP peaks is themost sensitive indicator of neuropathologicalchanges, but is also the most variable aspect ofnormal waveforms. Three-modality evoked potentials (TMEPs) havebeen used for many years along with the EEG asboth a diagnostic and prognostic tool for patientswho are comatose. The use of cognitive evokedpotentials is more recent and when used inconjunction with continuous EEG monitoringprovide information about the function of thecerebral cortex. Thus, cognitive evoked potentialscan complement TMEPs as a prognostic tool.Their presence in comatose patients suggests ahigh probability (greater than 90 percent) of acomplete recovery of consciousness (Guerit, 2000).

[7] Intracranial Pressure (ICP) Monitoring-- ICPmonitoring can significantly reduce mortality andmorbidity by allowing the administration ofappropriate treatment before clinical deteriorationof the patient becomes apparent (Morris andMarshall, 2000; Zink, 2001). Although monitoringof ICP requires neurosurgical intervention and theavailability of an intensive care unit, it is necessaryto properly manage increased ICP in the severelyhead injured patient with cerebral swelling.Monitoring also allows the clinician to maintain anadequate cerebral perfusion pressure (CPP) bymanipulating the ICP and systemic bloodpressures (Gedeit, 2001). Invasive monitoring isdifficult in patients presenting with a coagulopathy.Three commonly used devices for monitoring ICPinclude an intraventricular catheter (used in directventricular cannulation), a fiberoptic monitor, andthe subarachnoid bolt device (Dangor and Lam,1999; Gedeit, 2001).

[7a] Intraventricular Catheter-- Cannulation ofthe cerebral ventricles using an intraventricularcatheter is the most invasive ICP monitoringprocedure. This is the ideal method of measuringICP because it can be used to measure pressureand drain CSF to reduce pressure (Townsend,2001). Since this procedure is invasive, it is

34

associated with a higher risk of infection. Otherdisadvantages of an intraventricular catheter isthat it is difficult to insert in compressed ventricles,and the procedure may have to be discontinued ifthe ventricle collapses.

[7b] Fiberoptic Monitor-- A fiberoptic cathetercan measure ICP epidurally, subdurally, orintraparenchymally and can be inserted at thebeside. It offers the advantage of a lower risk ofinfection compared to the use of an intraventricularcatheter but does not allow drainage of the CSF(Dangor and Lam, 1999; Gedeit, 2001).

[7c] Subarachnoid Bolt-- The subarachnoid boltcan be inserted at the patient's bedside andutilizes the same monitoring sites as ventricularcannulation. Since the device is inserted into thesubarachnoid space, the dura mater is penetratedbut the cerebral cortex is not. Thus, the rate ofinfection is low (less than 2 percent versus a highof 20 percent for cannulation) (Dangor and Lam,1999) and readings are independent of the size ofthe ventricles. Disadvantages include the lack ofaccess to the CSF and ventricular system, andfalse readings resulting from occlusion of thelumen caused by the surface of the brain (Dangorand Lam, 1999).

[8] Cerebral Perfusion Pressure-- Themaintenance of cerebral perfusion (cerebral bloodflow) and lowering of intracranial pressure are thetwo primary goals of head injury management. Bydefinition, cerebral perfusion pressure (CPP) iscalculated as the difference between the meanarterial pressure and intracranial pressure (ICP).For infants and children, a CPP of 50 mm Hg ormore is usually adequate; for adolescents andadults, the CPP must be maintained at a levelgreater than 60 mm Hg (Gedeit, 2001). Optimization of CPP requires the maintenance ofsystemic hemodynamics and control of ICP. Sincesystemic hypotension (defined by a systolic bloodpressure of less than 90 mm Hg) is associatedwith a poor outcome, aggressive fluidmanagement is necessary to maintain the patient'sintravascular volume. In addition, the presence ofhypotension in the adult head-injured patientshould prompt investigation of other sites of bloodloss. Hypertension may be a compensatorymechanism to maintain CPP and for this reason,moderate increases in the patient's blood pressure(e.g., up to 160-180 mm Hg systolic) should not be

treated. However, severe hypertension should betreated because it may increase cerebral bloodvolume and may lead to vasogenic edema andprecipitate hemorrhage in injured areas of thebrain (Dangor and Lam, 1999).

[9] Lumbar Puncture-- Lumbar puncture iscontraindicated in the acute stage of head trauma.If meningitis is a concern due to the presence ofcerebrospinal fluid leakage from the nose or ears,or a fever, a CT scan should be taken prior toperforming a spinal tap for identification ofpathogens, in order to rule out unsuspected earlyabscess or delayed hemorrhage. Both of theselesions can cause brain herniation and rapiddeterioration following lumbar puncture. If CT isnot available, empiric administration of antibioticsis preferred to the risk of lumbar puncture (Dangorand Lam, 1999).

P 93.70 DEFINITIVE MANAGEMENT

The management of head trauma begins at thescene of injury (prehospital care by emergencymedical technicians) and continues in theemergency department of the hospital. Up to thispoint, management is essentially acute emergencycare, which must be thorough and rapid in order toget the patient into the operating room or theintensive care unit where definitive treatment isprovided. In hospital management is a continuationof prehospital (emergency medical services) andemergency department care (Dangor and Lam, 1999).

[93.71] Surgical Management Surgical treatment of head trauma is typicallyindicated for evacuation of mass lesions, repair ofpenetrating wound damage and debridement forcontrol of infection. Specific lesions thatnecessitate surgery include subdural hematoma,epidural hematoma, large intracerebralhematoma/contusion, posterior fossa hematoma,depressed skull fractures, penetrating wounds andintracranial infection (Dangor and Lam, 1999).

[1] Subdural Hematoma-- Most patients with anacute or subacute subdural hematoma will requiresurgical evacuation of the lesion. A small subduralhematoma, however, may heal spontaneouslywithout surgical intervention (Goetz, 1999).

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The ''golden hour'' in trauma refers to the conceptthat the physician has only a short period of time inwhich to diagnose and treat brain injury beforeserious harm occurs. In applying this concept toclosed head injury, the focus is on early diagnosisof expanding intracranial hematomas, so thatsurgical evacuation can be performed beforesecondary brain injury occurs. Studies show thatearly evacuation of subdural hematoma in adultsleads to a decrease in morbidity and mortalityassociated with head injury (Schutzman andGreenes, 2001). Patients with intracranialhematoma have a better outcome if the hematomais diagnosed and treated early, before neurologicdeterioration begins. An acute subdural hematoma is surgicallyremoved by means of a large trauma craniotomyflap procedure, which involves excising a largeplate of skull bone in the temporal region (side ofthe head above the ear). Owing to their large size,subdural hematomas cannot be evacuatedadequately through burr holes (small holes drilledin the skull to facilitate removal of bone). In many cases the patient will be undergoing suchrapid neurological deterioration that emergencydecompression is mandatory. Since burr holes donot provide adequate decompression of a largesubdural hematoma, rapid temporarydecompression is achieved by opening the incisionthrough the dura as well as the skull along oneside (temporal region), rather than taking the timeto saw and remove the bone plate before openingthe dura. Once the bone plate is removed and thedura fully opened, the clot is gently removed fromthe surface of the brain by a combination ofirrigation, suction, and traction. This should bedone with care to avoid causing further damage tothe brain. A peripheral clot (on the side of thebrain) may be removed using a brain retractor, butno attempt should be made to retrieve smallpieces of the hematoma beneath the dura. A large decompression is advocated for patientswith intractable ICP. The decompression shouldinclude the dura and expansion of the dura shouldbe accomplished by using a graft. However, theopening should be large enough so that the braindoes not herniate through the surgically createdhole, extinguishing its blood supply (Townsend, 2001). If the brain remains swollen after removal of thehematoma, manni to l and increased

hyperventilation should be employed. Contusionson the tips of the frontal and temporal lobes shouldbe resected. Any source of bleeding should besought. When found, the vessel should be repairedwith bipolar coagulation, Surgicel,(R) Gelfoam(R)or Avitene.(R) Control of bleeding should never byattempted by means of injection of saline(physiological sodium chloride solution) into theventricular/cerebrospinal fluid system to causebrain expansion, as this causes further brain damage. Once the evacuation and repairs are completed,the dura is closed and tacked tightly to the edgesand center of the bone, to minimize the chance ofa recurrent hematoma. A second compression ofthe brain under these circumstances is frequentlycatastrophic. The bone plate is replaced andsecured with wire or sutures, and the scalp incisionis closed (Townsend, 2001). Because bleeding within the subdural space mayrecur, a surgical drain should be left in place forseveral days after surgery and the patientmonitored carefully for signs of continued bleeding.(Goetz, 1999) One of the pitfalls of rapid surgical decompressionis extrusion of the brain through the craniotomydefect that occurs in response to acute brainswelling. To avoid this complication, a new surgicaltechnique has been developed, in which multiplefenestrations are created in a mesh-like fashion sothat clots can be removed through small duralopenings. This technique allows for the gradualand gentle release of clots without furtherdisruption of brain tissue (Guilburd and Sviri, 2001). The treatment of chronic subdural hematomasremains controversial. If the patient with a chronicsubdural hematoma becomes symptomatic, mostneurosurgeons believe that surgical evacuation ofthe lesion should be performed (Marx, 2002).

[2] Epidural Hematoma-- In the case of acuteepidural hematomas producing neurologicaldeficits, emergency surgical evacuation is thestandard treatment. Epidural hematomas areevacuated via the large trauma flap craniotomyused for managing subdural hematomas. Onceexposed, the clot is removed and the torn bloodvessel repaired. Bipolar coagulation usuallysuffices. Since additional hematomas not detectedon CT often are discovered beneath the duramater, the dura should be opened when it is made

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taut by the bulging brain below. If an epiduralhematoma is not found on the side where thecraniotomy was made, burr holes should be placedto search for a lesion on the opposite side. Whenthe dura is slack and preoperative CT has notdisclosed additional lesions, it is not necessary toopen the dura. Once all repairs have been made,the craniotomy is carefully closed (Townsend, 2001). One recent study examined whether or notpatients with epidural hematomas can be safelytransported to a neurosurgical unit fordecompression or if surgeons must still beprepared to perform emergency craniotomies. Theauthors of this study found that there is usuallyenough time to safely transfer patients to aneurosurgical unit, if transport is rapid andanesthesiological services are available duringtransport. They also concluded that surgeonswithout training in neurosurgery should not performemergency craniotomies in local hospitals, butshould instead transfer the patient immediately tothe nearest department of neurosurgery (Wester,1999).

[3] Intracerebral Hematoma and Contusion--Hematomas within the tissue of the cortex areevacuated after craniectomy (excision of a portionof the skull) performed as described for subduraland epidural hematomas. Intracerebralhematomas usually are found within the frontaland temporal lobes. Since the surface of the brainover the intracerebral clot may appear normal,exploration with a blunt needle using ultrasoundguidance often is useful. Once located, the clot isevacuated with gentle suction. No bleeding controlis usually required. Deep intracerebral clots shouldnot be evacuated unless they are larger than 1 or2 cm and cause significant mass effects, such asbrain shift, pronounced intracranial pressureelevation or neurological deterioration. Contusions are most often found on the front andlower surface of the frontal and temporal lobes ofthe cerebral cortex. Those larger than 2 cm indiameter should be resected. The lesion isexposed by craniectomy and suction and retractionis applied to identify surrounding normal braintissue. The contusion is removed by resecting fromthe center of the lesion outward, taking care tostay within the area of necrotic (devitalized) tissue.The extent of removal depends on the location ofthe lesion in the cortex. Extreme care must betaken in removing contusions further back and on

top of the temporal lobe, in the parietal or occipitallobes, or in the area of the central sulcus (the deepfissure separating the frontal and parietal lobes),as motor, language and vision functions arelocated in these areas. No excess neurologicaldeficit is sustained by removing these lesions,however, as long as resection is strictly confined tothe contused tissue (Townsend, 2001).

[4] Posterior Fossa Hematoma-- Hematomas inthe posterior cranial fossa (the depression in theback of the base of the skull) are evacuated by astandard suboccipital craniotomy procedure (at thebase of the back of the skull). This operation isbest performed with the patient prone or in the''reclining park bench'' position, as this allowsbetter control of bleeding and prevention of airembolism. In addition, the patient can bemaneuvered more readily if a contrecoup lesion,frequently found in association with posterior fossahematomas, is present in the frontal or temporallobes (Bozbuga, et al., 1999; Townsend, 2001).

[5] Depressed Skull Fractures-- Surgicaltreatment of skull fractures is generally reservedfor depressed fractures in which the bone fragmentis driven into the brain a distance greater than thethickness of the skull itself (about 2 to 6 mm).Depressed fractures are divided into closed orcompound (open) types, depending on whetherthe overlying scalp is intact or has been lacerated.The general objective of surgical repair ofdepressed fractures is to restore the structural andfunctional integrity of the skull. Specific aims areprevention of infection, repair of any dural tearsand intracranial bleeding and elimination ofcosmetic deformities. If laceration of the scalp isextensive in a compound fracture, it may providean adequate opening to the injury. Otherwise ascalp flap is created. Leveling of the fragment mustbe avoided, as it is likely to cause furtherlaceration of the meninges and brain. If the bonefragment has not been devitalized, it may be wiredin place. Otherwise, acrylic cranioplasty may berequired. Dural tears should be repaired andbleeding controlled before closing (Asano et al.,1995; Townsend, 2001). Traditionally, management of compounddepressed skull fractures involved removal of allbone fragments followed by delayed cranioplasty,due to concern over the potential for developinginfection. However, one recent study demonstratedthat immediate replacement of bone fragments

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(within 72 hours of injury) in compound depressedskull fractures is not associated with an increasedrisk of infection (Wylen, et al., 1999).

[6] Penetrating Trauma-- In all penetratingprojectile wounds of the head there is compound(open) fracture of the skull, dural tearing andlaceration of the brain accompanied by bleeding.Consequently, these injuries should be treated assoon as possible to avoid complications fromintracranial hematomas and infection. Following emergency medical care, neurologicalexam and grading of neurological status asdescribed earlier, all patients except those inGrade IV (brain death) should be prepared forimmediate surgical treatment. The emergencydiagnostic method of choice is CT. If the path ofthe projectile passes in the vicinity of a major bloodvessel, however, cerebral angiography (x-ray ofthe blood vessels in the brain) should beperformed if the patient's condition allows. Large intravenous doses of appropriate antibioticsshould be given perioperatively, during theoperation, and for five days postoperatively toguard against the possibility of infection from thecranial wound and from the projectile.17 The use ofantiepileptics prophylactically in patients withpenetrating head injuries for the prevention ofposttraumatic epilepsy is controversial. Mannitolshould be given to control intracranial pressurefrom evolving brain edema and/or hematoma formation. The surgical opening in the skull must be largeenough to allow adequate visualization of the duraltear and lacerated brain beneath it. In virtually allcivilian injuries, a craniotomy procedure may beused, whereby a plate of bone encompassing theentry site of the projectile is removed and allcomminuted (splintered or broken) fragments areremoved. This plate may be replaced later inclosing. In situations where a significant risk frombone infection will persist, primarily among militarycasualties of war, a craniectomy (excision of thebone surrounding the entry site) must be used,followed later by cranioplasty (plastic surgicalcorrection of the defect). Upon opening of the skull, visual inspection willreveal the lacerated dura, pulped brain, clottedblood and bone fragments. After opening andretracting the dura, debris on the surface of thecortex is removed by gentle suction. Next, the

missile tract is debrided. This is the most crucialpart of the surgery. If the entire length and bore ofthe track is debrided of devitalized and necroticbrain tissue (the limits of the debridement beingthe surrounding healthy white matter), the removalof hematomas and bone fragments as well aspulped brain usually can be accomplished. Theprojectile at the end of the tract should be removedas well. The number of bone fragments retrievedshould be counted and compared with the counttaken from the radiological image. If debridementhas been thorough, the missile tract will notcollapse. If the tract does collapse, either furtherremoval of devitalized tissue is necessary, or ahematoma is present. If the projectile has passed completely through thehead, the exit wound is managed in a similarfashion to that of the entry wound. If the projectilehas passed across to the other side of the brain,just short of exiting, the surgeon should not pursueit along the tract. Rather, a separate craniotomyshould be performed nearer the site of lodgement.All easily accessible bullets and metallicfragments, especially those which are copper orcopper-coated, should be removed at the primaryoperation. Large intact bullets should be removedas well, as they have a tendency to migrate overtime. Small metallic fragments deeply embeddedin the brain need not be removed. In all of suchcases, a bullet or fragment can serve as a nucleusfor the formation of an infectious abscess or hematoma. Although the prognosis for nonpenetrating headinjury has improved, the high mortality rate forpatients who are comatose after missile injuryappears to be the same. Non-comatose patientssuffering penetrating head wounds almost alwayssurvive, albeit with neurologic deficits dependingon the path of the bullet. In contrast, the mortalityrate in the comatose patient approximates 90percent in most studies. However, despite this highmortality rate, most trauma centers use the samemedical management as for patients who arecomatose with nonpenetrating injury. For mostpatients with gunshot wounds to the head,operative therapy of the missile tract is stilldebated. The current standard is surgicaldebridement of the first few centimeters of the tractfollowed by a watertight dural closure. Conflictingreports from the Middle East suggest that simpleskin closure of the bullet hole, without anydebridement, is not associated with a worseoutcome (Townsend, 2001).

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[7] Infection-- Surgical management of infection isindicated for osteomyelitis (infection of bone),subdural empyema (accumulation of pus beneaththe dura) and brain abscess, all of which aresequelae of penetrating wounds or basilar skullfractures. For osteomyelitis, treatment entailssurgical debridement and removal of infected boneand the administration of antibiotics. The choice ofantibiotic depends on culture and sensitivityresults. The presence of systemic symptomssuggests that the patient has an underlyingsubdural or epidural empyema. Usually,Staphylococcus species, Streptococcus species orvarious anaerobic pathogens are involved (Marx,2002). Surgical treatment of subdural empyema isby drainage and debridement of the lesion.

Brain abscess is managed medically byintravenous antibiotics or surgically by aspirationand debridement, depending on the size of theabscess. If the brain abscess is relatively small(less than 2 centimeters in diameter), the abscesscan be treated successfully with antibiotics withoutsurgical intervention. The initial choice of antibioticshould be directed to the most likely causativemicroorganism (e.g., S. aureus) and be chosenbased on culture and sensitivity results. Laboratorydiagnosis involves culture of the purulent materialobtained from the abscess and antibiotic sensitivitytesting. Staphylococcus aureus is the mostcommon microorganism causing brain abscessfollowing compound skull fracture and penetratinghead injury. Intravenous antibiotics are usuallyadministered for six to eight weeks. For larger abscesses, surgical aspiration anddebridement of the abscess is usually required(Cochrane, 1999). The initial surgical approach tobrain abscess is drainage through a burr hole(Townsend, 2001). Excision of the abscess bycraniotomy may be necessary in some cases. Although prolonged, pathogen-specific antibiotictherapy is a crucial component in the managementof all these posttraumatic sequelae, antibioticsshould not be given prophylactically in the ICUsetting in patients with leakage of CSF caused bybasilar skull fractures (Marx, 2002).

[8] Aneurysm-- Surgery is the recommendedtreatment, with surgical clipping of the aneurysmand/or endovascular occlusion being the definitivetreatments of choice (Tureyen, 2001, Voekler and

Ortiz, 1997; Schuster et al., 1999).

[9] Arteriovenous Fistula-- Current treatment ofchoice is endovascular closure of the fistula,especially in patients with rapid neurologicdeterioration. Endovascular repair is achieved bypercutaneous endovascular balloonization of thefistula ring, although microcoils are also used. Fordural arteriovenous fistulas involving the superiorsagittal sinus, transarterial intravenous coilembolization is an effective treatment (Fukai, et al.,2001). Surgical closure of the fistula usually resultsin rapid resolution of symptoms with a goodprognosis for complete neurologic recovery(Wadlington and Terry, 1999).

[93.72] Medical Management The majority of head trauma patients requireobservation and medical management followingemergency department evaluation. Those who areinitially treated surgically also require medicalmanagement in the intensive care unit (ICU), onceneurosurgery has been completed. The twoprincipal causes of death from head injury, ingeneral, are (1) uncontrolled elevated intracranialpressure, and (2) massive systemic insults, suchas septicemia (bacterial infection of thebloodstream) and associated septic shock orcardiorespiratory failure (Townsend, 2001).

[1] Elevated Intracranial Pressure (ICP)-- Thefirst line of treatment is drainage of ventricular fluidby placement of a ventricular catheter. If the ICPstill remains elevated, hyperosmotic agents suchas mannitol or diuretics are used. The role ofhyperventilation is controversial, and mostclinicians believe this treatment option should notbe used as it potentially results in widespreadischemia (Zink, 2001; Townsend, 2001; Naik-Tolani, et al., 1999). Optimum therapy is tomaintain the ICP below 20 and the cerebralperfusion pressure (CPP, an index of perfusion,calculated as the difference between the meanarterial pressure and the ICP) above 70 mm Hg.When the ICP remains refractory to treatment, aCT scan should be performed to look for a newlyformed or expanding mass lesion. The presence ofan epidural or an acute subdural hematomarequires emergency surgical decompression(Townsend, 2001).

[2] Thrombosis and Infarction-- Therapy forthese injuries presently is limited. Anticoagulant

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therapy is contraindicated in trauma patients andattempts at surgical removal of thrombi(thrombectomy) usually are futile. Treatment iscurrently directed at control of elevated intracranialpressure, the precipitating factor associated withthrombosis and infarction (Townsend, 2001). Theinstillation of urokinase should be considered inany patient with venous sinus thrombosis andsymptomatic occlusion (D'Alise, et al., 1998).

[3] Clotting Defects-- Therapy for disseminatedintravascular coagulation (DIC) is directed at theunderlying causes of the excessive bleeding orclotting. Excessive bleeding may be managed byinfusion of whole blood, packed red blood cells,crystalloids, fresh frozen plasma or plateletconcentrates. Some clinicians have suggested,however, that the introduction of these bloodcomponents may further aggravate the condition(Townsend, 2001). Excessive clotting activity hasbeen treated with heparin (an anticoagulant), butthis rarely is effective. Moreover, the use ofanticoagulant therapy in a trauma patient is ameasure many clinicians are uncomfortable with(Townsend, 2001).

[4] Syndrome of Inappropriate Secretion ofAntidiuretic Hormone (SIADH)-- Treatmententails conservative management of waterbalance. Although SIADH is usually an acute self-limited disorder that resolves within two to threeweeks, the condition may be chronic if brain injuryis severe. In general, if the patient has minimalsymptoms, and the SIADH lasts longer than 24 to48 hours, restricting the patient's total fluid intakewill correct the osmotic imbalance and the SIADHwill remit spontaneously. In contrast, if the patienthas severe hyponatremia (low serum sodium) thatis present for less than 24 to 48 hours, which isaccompanied by nausea, vomiting, coma orseizures, the SIADH should be corrected morerapidly by combining fluid restriction with a slowintravenous infusion of hypertonic (3 percent)saline (Robertson, 2001). Whatever treatment is utilized, the patient's urineoutput and serum sodium should be closelymonitored because the SIADH can suddenlyresolve, causing a brisk diuresis that raises theserum sodium more rapidly than what isconsidered safe. The serum sodium should beraised no faster than 24 mEq/L in 24 hours and toa level no greater than 135 mEq/L. Raising theserum sodium faster is associated with acute

osmotic demyelinization, which is characterized bysevere neurologic disturbances, including mutism,seizures and movement disorders (Robertson, 2001).

[5] Infection-- Infection is an infrequentcomplication in head trauma patients as a group.The risk is increased for those with penetratinghead wounds and whose injuries, whetherpenetrating or closed, are severe and require aprolonged stay in the intensive care unit. Generalhospital-acquired infections are treated bystandard antibiotic therapies. The incidence ofinfections directly related to penetratingcraniocerebral wounds has been reduceddramatically by improved diagnostic and surgicalprocedures and the routine use of antibiotics. Bacterial meningitis was a significant cause ofmorbidity and mortality in the past, but has nowbeen practically eliminated by the availability ofmore effective cephalosporin antibiotics. Patientswith a CSF leak that develops from a basilar skullfracture will typically present with early meningitis(occurring within three days of injury) which isusually caused by Streptococcus pneumoniae. Athird-generation cephalosporin such as ceftriaxoneor cefotaxime is the antibiotic of choice, but cultureand sensitivities should be obtained due to theincrease in resistance of these antibiotics topneumococci. If sensitivity data are known and thebacteria are highly resistant to this antibioticregimen, vancomycin should be added. In contrast, meningitis which develops more thanthree days after head trauma is usually caused bygram-negative organisms. In this case, a third-generation cephalosporin should be combined withnafcillin or vancomycin to provide adequatecoverage against Staphylococcus aureus. Inchildren, posttraumatic meningitis is often causedby Haemophilus influenzae (Marx, 2002).

[6] Posttraumatic Epilepsy-- In the emergencydepartment, acute posttraumatic seizureprophylaxis is recommended for head-injuredpatients who will be paralyzed by neuromuscularblocking agents, for purposes of mechanicalventilation, surgery, or transport, because theclinical manifestations of seizures are subdued inthese patients. Phenytoin (15 mg/kg) is theanticonvulsant of choice for seizure prophylaxis.Whether or not the head-injured patient ismaintained on long-term anticonvulsant therapyduring the recovery period depends on the

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patient's subsequent clinical course. Not allpatients who have suffered posttraumatic seizuresin the acute or subacute period require long-termseizure prophylaxis and the role of anticonvulsantsfor this purpose remains unclear (Marx, 2002).

[93.73] Psychological Testing The differential diagnosis for psychologicalsequelae from traumatic head injury must takethree possible considerations into account:

(1) the patient has sustained genuine psychicinjury due to organic brain damage; (2) the psychic injury existed prior to physical insultand has been aggravated by it; or (3) the patient has not sustained psychic injury butfeigns it for the purposes of compensation orsecondary gain (otherwise known as''malingering'').

Every physical injury has emotionalconsequences, but these must be distinguishedfrom severe, incapacitating and permanent psychicdisability. A battery of psychological tests has beendevised to aid in the diagnosis of truepsychopathology as a consequence of physicalinsult. By themselves, these tests are notconsidered diagnostic, but when considered inconjunction with the patient's history, neurologicalexamination, radiological studies and preinjurypsychological test results, they can yield significantinformation useful in the treatment andrehabilitation of the individual with head injury. In the case of traumatic brain injury, the key issueis the proportionality of injury when performing aneuropsychologic assessment. It is wellestablished that mild and most moderate closedhead injuries do not produce alterations in resultsof tests depending on the patient's overall fund ofinformation such as reading and vocabulary. If apatient that has been involved in a motor vehicleaccident claims that he or she has suffered a braininjury, a neuropsychologist can perform tests todetermine whether or not changes in mentalperformance are indeed neurologic. For example,a patient with a Verbal Performance Score whichis significantly lower than what was measuredbefore the accident, has most likely notexperienced this change due to a mild head injury.

In contrast, if the patient is suffering from short-term memory problems, attentional deficits,difficulties in processing information, and cognitivespeed impediments, it is probable that thesechanges were caused by closed head injury (Boll,2000).

[1] Objective Personality Tests-- When used inpsychological testing, the term ''objective'' refers topersonality tests that employ true-false, yes-no ormultiple choice questions that specifically limit thepatient's answering options. In this context,objectivity is understood to mean that differentpersons with similar expertise examining the samepatient data would be able to arrive at similarconclusions regarding the examinee's condition.Objectivity does not mean that the results of thesetests can be proven to be objectively true. Indeed,a drawback of these tests is that they presentpatients with answers that are recognizably moresocially acceptable, allowing fakers andmalingerers to ''fake good'' or ''fake bad.'' Personality assessment is not critical because ofthe widespread availability of validated instrumentsto assess the role of neurological injury in changesin personality. In fact, one may argue that if aperson is neurologically impaired, the results ofpersonality tests may be questionable and mayrequire further assessment using factors for whichthere are no adequate normative data.Nevertheless, personality assessment can providevaluable information on difficulties in cognitivefunctioning, which can result in anxiety anddepression, and other forms of personality change(Boll, 2000).

[1a] The Minnesota Multiphasic PersonalityInventory-- The Minnesota Multiphasic PersonalityInventory (MMPI) is the most useful objectivepersonality test. It consists of 13 test scales: threevalidity scales which are used to identify deliberatefaking, and 10 clinical scales each of which assessa particular behavior or personality characteristics(e.g., depression, hysteria, paranoia). Thesescales are meant to be integrated in such a waythat psychopathology indicated by a deviantanswer in one scale should be reinforced bysimilarly deviant answers on other test scales(e.g., elevations of the schizophrenia scale wouldbe supported by the results of the scales used totest depression, paranoia, hypomania and other symptoms). Of the validity scales, the L scale measures the

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patient's willingness to admit to common humanfrailties such as anger or dislike of others; a highscore often points to intent to fake good. The Fscale measures answers to outrageous or blandand generally accepted statements; a high scoreusually indicates intent to fake bad. The ten clinical scales can be summarized asfollows:Scale 1: assesses a hypochondriacal personalityas determined by responses concerning bodyfunctions and somatic complaints. Scale 2: assesses depressed mood throughanswers to questions regarding vegetativesymptoms and feelings. Scale 3: assesses hysteria as a foundation forsomatic complaints. Scale 4: assesses psychopathic deviance throughquestions concerned with relationships to authorityfigures and family, as well as antisocial activity. Scale 5: assesses whether the patient hastraditional culturally defined masculine or feminineinterests. Scale 6: assesses paranoia through questionsregarding the individual's perceived treatment atthe hands of others. Scale 7: assesses hypaesthenia, or the obsessive-compulsive syndrome. Scale 8: assesses schizophrenia throughquestions regarding how different or isolated theperson feels from others. Scale 9: assesses manic disorder throughquestions that elicit the persons' level ofrestlessness, energy and sense of self-importance. Scale 0: assesses social introversion or shyness.

Scores on all of these scales are synthesized todetermine a personality profile of the examineeand a probable diagnosis of psychopathologybased on that profile. A high score on any onescale is not considered diagnostic of that particularproblem (i.e. a high score on the schizophreniascale should not be interpreted to mean that theperson is schizophrenic).

[1b] Other Objective Personality Tests-- Avariety of other personality tests are used either toaugment the MMPI or arrive at information otherthan possible psychopathology. The CaliforniaPsychological Inventory (CPI) is used to identifypersonality types, particularly among problempopulations such as delinquent students andparolees. The Millon Behavioral Health Inventoryemploys three scales to measure the copingabilities of persons with organic illness. The MillonClinical Multiaxial Inventory uses 175 self-descriptive statements to arrive at the samepersonality profiles as the MMPI.

[2] Projective Personality Tests-- Projectivepersonality tests are open-ended tests that allow apatient to project his or her thoughts onto testmaterial to be interpreted by the examiner. Thus,there is no obvious socially desirable ''answer'' tothese tests. Results of these tests do not meet therequirements of standardization, reliability andvalidity of clinical diagnostic tests, andinterpretation is thus often controversial. The most widely used projective personality test isthe Rorschach Inkblot Test, in which the patient isshown ten cards with inkblot patterns, some inblack and white and some in color, and asked toidentify what the inkblot looks like. The rationalefor the test is based on the assumption that aperson organizes various environmental stimuliaccording to his or her fears, wishes, conflicts,motives and other determinants. Since inkblots areso amorphous in shape, a person's need toorganize his or her perceptions is increased togreater than normal levels when asked to interpretthis material. After the person describes what theinkblots look like the examiner conducts an inquiryto aid in scoring responses. Another widely used projective test, the ThematicApperception Test (TAT) consists of 30 cardsdepicting ambiguous situations, mostly involvingpeople. The individual is asked to make up a storydescribing what led up to the scene, what ishappening, what the people in the picture arethinking or feeling, and how the situation turns out.The TAT provides information on interpersonalrelationships, perception of the environment,personal needs and conflicts. Projective drawing tests include the Draw-APerson Test (DAP), the House-Tree-Person Test(HTP) and the Draw-A-Family Test. As their

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names imply, these tests ask the examinee todraw a particular type of picture. The results areinterpreted to tap into the person's non-verbalizedfeelings regarding what the scenes depict.

[3] Intelligence Tests-- Intelligence tests measurethe capacity of an individual to act purposively andeffectively in dealing with his or her environment.The score arrived at reflects the current functioningof the individual as influenced by such factors ashereditary potential, early learning, culturalbackground, emotional and physical state,motivational level and situational factors operatingat the time of testing. Interpretation involves acareful evaluation of scores for the differentsubsections of the test to assess the degree towhich each of these factors influences currentfunctioning. Intelligence quotient, or I.Q., ismeasured as a percentile rank within a populationor on a scale where a mean score of 100represents normal. The Wechsler Adult Intelligence Scale - Revised(WAIS-R) is the most widely used test ofintelligence among adults. It is comprised of sixverbal subtests: information, comprehension,arithmetic, similarities, digit span and vocabulary,and five performance subtests: digit symbol,picture completion, block design, picturearrangement and object assembly. The testgenerates a verbal I.Q., a performance I.Q. and afull-scale I.Q. A higher verbal than performanceI.Q. sometimes indicates organic brain damage. Ahigher performance than verbal I.Q. may indicateschizophrenia and personality disorders. Other intelligence tests include the Stanford-Binettest and the Shipley-Hartford test. The Stanford-Binet test measures intelligence levels appropriatefor the age of the person. The Shipley-HartfordTest uses 40 vocabulary items and 20 abstractreasoning questions to generate a verbalintelligence score and a conceptual quotientobtained by dividing the abstract reasoning scoreby the vocabulary score and multiplying by a factorof 100. The Shipley-Hartford test is usually usedfor detecting organic brain damage orpsychopathological emotional disorders.

[ 4 ] N e u r o p s y c h o l o g i c a l T e s t s - -Neuropsychological tests assess more subtle andimportant abilities than those measured on mostintelligence tests, and thus are more specific fororganic brain damage. The WAIS-R is sometimes

considered such a test, since organic braindamage interferes with intellectual function, andthus is one potential indicator of brain damage. A number of tests exist to measure sensory andperceptual functioning. For example, manycomplex language tests such as the BostonDiagnostic Aphasia Examination and the WesternAphasia Battery are used to measure difficultieswith language functioning. The Halstead CategoryTest and the Wisconsin Card Sorting Test are twoof the most common tests used to assessnonverbal learning, problem solving and mentalflexibility. For litigation involving head injury, theWisconsin Card Sorting Test is useful in thedetection of malingering in patients suspected offaking a brain injury, having a reported sensitivityof 82 percent and specificity of 93 percent (Suhrand Boyer, 1999). Similarly, the Word MemoryTest, a relatively new computer based test, isuseful in measuring biased responding (e.g.,malingering) in patients with mild head injuriesclaiming they have suffered moderate to severebrain injuries (Green, et al., 1999). In addition to individual tests of cognitive function,a variety of specific battery tests have beendeveloped which provide information across abroad range of known domains of brain behaviorrelationships. These tests represent the mostsc ient i f ica l ly va l idated approach toneuropsychologic evaluation of the head-injuredpatient (Boll, 2000). One such battery is the Halstead-ReitanNeuropsychological Battery, which consists ofseven subtests of ability to categorize, tactileperformance, auditory discrimination and motorspeed. Diffuse brain damage is suggested byimpairment on three of the seven tests andstrongly indicates impairment on four. Whenlocalized damage is present a pattern of deficitsconsistent with clinical examination, history andother test results is usually elicited. The Luria-Nebraska Psychological Battery isanother series of tests composed of 269 itemsc o v e r i n g v a r i o u s c o m p o n e n t s o fneuropsychological investigation: intellectualprocesses, expressive speech, receptive speech,writing, arithmetic, reading, visual functions, motorfunctions, tactile function, rhythmic and pitch skills,memory, etc. Scores help determine whetherpathology is in the left or right brain hemispheres.

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The Bender Gestalt Test is used to determine iforganic brain damage is present, as a projectivepersonality test, and as a test for emotionaldisorder. It consists of nine cards containingsimple designs which the subject is asked toreproduce as accurately as possible on a blanksheet of paper. The resulting drawings are thenscored in terms of accuracy and generalintegration. A number of characteristics in thedrawings of persons with organic brain damagedistinguish their drawings from those of non-braindamaged subjects: perseveration (the subjectresponds in a way beyond what is required),rotation and reversals (the drawing deviates bymore than 45 degrees from the axis of the originalor is drawn in reverse) and concretism (the drawnimage looks more like an actual object than themore abstract designs on the cards). Other neuropsychological tests include theWechsler Memory Scale, in which evidence of amemory quotient lower than the intelligencequotient suggests brain damage, and the Graham-Kendall Memory for Designs, in which a score of12 mistakes or more in accurately reproducing 15simple designs from memory is considered a goodindication of organic brain damage. It is important to keep in mind thatneuropsychological tests were not designed topredict how a head-injured patient is likely tofunction in real-world settings, such as vocationalsettings. Predictions using these tests are muchmore accurate if the tasks used during testingmimic the patient's everyday personal andvocational demands (Sbordone, 2001).

[93.74] Neuropsychological Management andRehabilitation Advances in the medical management of severehead injury have contributed to significantincreases in the survival rate, as well as themedical challenges that people face withdisabilities. Increased awareness of this problemand its consequences for society has led toextensive growth in the rehabilitation industry.Since clinical rehabilitation services vary widely,many clinicians are interested in the effectivenessof rehabilitation for brain injury on patientoutcomes (AJCPR, 1999; Rao and Lyketsos, 2002). It is generally accepted that supportive individual

and family psychotherapy is important for dealingwith the neurobehavioral changes in the head-injured patient. For both patient and family, thepatient's cognitive deficits represent one of thegreatest challenges to coping and adaptation. Thefield of cognitive rehabilitation emerged in the early1980s and has addressed these issues. Since itsintroduction, this field has shown impressivegrowth and application. Cognitive rehabilitationinvolves retraining in various cognitive skills, suchas problem-solving, inductive reasoning, abstractthinking, logical thinking, memory, fine perceptualmotor skills, practical mathematics, spelling andremedial reading. The ultimate goal is to promotecarry-over of these skills to the patient's everydaylife. Since cognitive rehabilitation has grown inpopularity, the Agency for Health Care Policy andResearch (AHCPR) has examined theeffectiveness of cognitive rehabilitation onoutcomes for people who sustain a head injury(AHCPR, 1999). According to their report,compensatory cognitive rehabilitation (CCR)reduces the level of anxiety and improves thepatient's self-concept and interpersonalrelationships. Computer-aided cognitiverehabilitation (CACR) also improves a patient'simmediate recall on neuropsychological testing,but the clinical significance of this finding has notyet been validated (AHCPR, 1999). Other factors that are associated with improvedoutcomes include early rehabilitation in patientswith severe head injury, supported employment inthe vocational setting, and appropriate casemanagement. While case management may onlyhave an indirect effect on the patient's functionaloutcomes such as level of disability, it can directlyaffect family knowledge of the need for rehabilitation, the level of psychosocial anxiety,and the family's ability to cope with a traumaticbrain injury (ACHPR, 1999).

P 93.80 PROGNOSIS

Determining the prognosis following head injury ina given patient is of inestimable value for providingoptimal care for the patient and counseling for thefamily (Zink, 2001). More specifically, prognosticindicators serve three major functions in headtrauma:(1) they allow continuing evaluation of newtreatments by comparison with the outcomes

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expected from standard therapies; (2) in the acute (emergency) stage of evaluationand management, they provide triage guidelineswhich aid physicians in identifying those patientsalmost certain to die or be vegetative, thusavoiding inappropriate and expensive heroicmeasures; and in patients for whom intensive life-saving care is warranted, they aid in charting thepatient's moment by moment course (deteriorationor improvement); and (3) they allow advance counseling and preparationof family and social service agencies with regard tothe kinds of long-term care the patient will need(Zink, 2001).

[93.81] General Considerations and Indicators Some general indicators of prognosis followinghead trauma include the following: Age. The rates for both disability and mortality tendto increase with increasing age. Length of Coma. In general, there is a directcorrelation between the length of coma and theprobability of permanent cognitive deficits. Posttraumatic Amnesia. Posttraumatic amnesialasting less than 1 week is associated with a goodrecovery; amnesia that persists beyond the firstweek is a less favorable sign. Location and Extent of Brain Lesion. Bilaterallesions in the frontal lobes are predictive of markedpersonality changes; bilateral lesions in thetemporal lobes are predictive of permanentcognitive deficits. Blood and CSF Findings. Persistently elevatedlevels of lactic acid in the blood and cerebrospinalfluid is evidence of continued ischemia (lack ofblood supply) and hypoxia (insufficient oxygensupply) of the cerebral tissues, conditions likely toresult in permanent neurological and cognitivedeficits (Zink, 2001). Responsiveness. Movement or other coherentresponse to verbal commands is a favorable sign. Glasgow Coma Scale. Each of the elements of theGlasgow Coma Scale (motor score, eye opening,and verbal score) has a prognostic value in that

lower scores are associated with worse outcomes.Of the GCS components, the motor scorecomponent has the most prognostic value in termsof predicting outcome, based on the eventualscore achieved with the Glasgow Outcome Scale. One study examining early predictors of mortalityand morbidity after severe closed head injuryfound that age was the only important predictor ofoutcome on the Glasgow Outcome Scale, theGlasgow Coma Scale score was the best predictorof neuropsychological function, and pupillaryreactivity was the most predictive factor for qualityof life. Factors important for predicting mortality(such as intracranial pressure, blood glucoselevels, or CT observations) were not correlatedwith morbidity (Lannoo, 2000). Serious head injury in children is associated witha poor prognosis. Of the 10 to 15 percent ofchildren hospitalized for a serious head injury, 33to 50 percent will die. While survivors of severehead injury often have permanent disability,children with mild or moderate head injury are alsoat risk for long-term cognitive and motordysfunction (Gedeit, 2001). To enhance the prognosis in head injury cases,management with ventilation and other supportivemeasures is indicated for patients in chronic coma.Patients who are conscious but paralyzed requirephysical and occupational therapy. Patients whoare conscious and apparently not significantlyimpaired in any way need to receive thoroughintellectual and psychosocial evaluations prior torelease, since many who appear well have in factsustained subtle alterations of personality anddeficits of attention, learning and memorycapabilities. Although poor Glasgow OutcomeScale scores and severe cognitive impairmentsare usually associated with more severe headinjuries, moderate head injuries can cause similarproblems and the needs of these patients shouldnot be overlooked (Hellawell, 1999).

[93.82] Statistical Prognostic Systems An objective and highly accurate means ofestablishing a prognosis for individual patients remains an elusive ideal. Given the complexity ofthe clinical situation in head trauma, it is unlikelythat an infallible system ever will be developed. Despite the difficulties involved, the application of

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various statistical methods to the problem ofassessing a patient's probable outcome is seen asa valuable clinical tool by some authors (Zink,2001). A widely accepted standard system fordescribing the outcome of head injury is theGlasgow Outcome Scale (GOS) (Zink, 2001). Withthe GOS, patients are placed in one of 5categories, ranging from dead to good outcome:

Category Description1 Dead2 Vegetative state3 Severe disability4 Moderate disability5 Good recovery

The GOS score is usually determine at 3, 6, and12 months after the initial posttraumatic injury(Zink, 2001). A number of statistical methods havebeen devised for assigning a patient to a givenoutcome (Zink, 2001). Two of these methods arethe linear logistic regression method (LLRM) andthe discriminant analysis method (Zink, 2001). Twobasic classes of prognostic indicators that may beused in these systems are investigationalindicators (e.g., CT scan, evoked potentials,intracranial pressure) and clinical indicators (e.g.,age, presence of a mass lesion, pupillary lightresponse).