Head Injury

HEAD INJURYLouis Louis CrevierCrevier

August 31August 31stst, 2005, 2005POS Large Group SessionPOS Large Group Session

MUMC, Room 4E20MUMC, Room 4E20

Mechanisms of Head InjuryThree varieties of Head Trauma:Three varieties of Head Trauma:

1.1. Skull fractures (linear, depressed, basilar)Skull fractures (linear, depressed, basilar)

2.2. Focal injuries:Focal injuries:Contusions (coup, Contusions (coup, contrecoupcontrecoup, intermediate), intermediate)Haematomas (EDH, SDH, ICH)Haematomas (EDH, SDH, ICH)

3.3. Diffuse Injury:Diffuse Injury:ConcussionConcussionDiffuse axonal injuryDiffuse axonal injury

Pathophysiology of Head Injury1.1. Contact (blow to head):Contact (blow to head):

Local Local –– skull fracture, EDH, coup contusionsskull fracture, EDH, coup contusionsRemote Remote –– vault and basilar fracturevault and basilar fractureShock wave injury Shock wave injury –– contrecoupcontrecoup, ICH, ICH

2.2. Acceleration (head motion):Acceleration (head motion):ConcussionConcussionSDH, DAI, SDH, DAI, contrecoupcontrecoup and intermediate and intermediate contusioncontusionICHICH

Skull Fracture - Linear:Linear skull fracture:Linear skull fracture:

Dark black, straight, no branching, thin Dark black, straight, no branching, thin widthwidth

Vessel groove:Vessel groove:Grey, curving, branching, thick widthGrey, curving, branching, thick width

Suture line:Suture line:Grey, suture line, jagged, wideGrey, suture line, jagged, wide

Skull Fracture - Basilar:Usual locations:Usual locations:

PetrousPetrous temporal bone, orbital surface of frontal temporal bone, orbital surface of frontal bone, bone, basiocciputbasiocciput

Clinical signs:Clinical signs:Battle signBattle signCSF CSF otorrhoeaotorrhoea, , rhinorrhoearhinorrhoeaHaemotympanumHaemotympanumRacoon eyesRacoon eyesCN deficitsCN deficits

Skull Fracture – Basilar (cont.):

Skull Fracture – Battle’s Sign:

Petrous Temporal Bone:TransverseTransverse LongitudinalLongitudinal

20%20% 80%80%Disrupts IAC/cochleaDisrupts IAC/cochlea EAC/EAC/ossiclesossicles, TM, TM

FrontalFrontal--occipital, severeoccipital, severe TemporalTemporal--parietal, milderparietal, milderSpread Spread –– foramen magnumforamen magnum Temporal Temporal squamoussquamous

HaemotympanumHaemotympanum CSF/bloody CSF/bloody otorrhoeaotorrhoea (50/50)(50/50)No Battle’s signNo Battle’s sign Battle’s signBattle’s sign

No No ossicleossicle injuryinjury OssiclesOssicles injured injured –– severe fracturesevere fracture3030--50% facial nerve injury50% facial nerve injury 1010--25% facial nerve injury25% facial nerve injury

Skull Fracture - Growing:Fracture line that widens with timeFracture line that widens with timeProgressive displacement of brain through dural defectProgressive displacement of brain through dural defectUsually asymptomatic, most often presents as scalp massUsually asymptomatic, most often presents as scalp massVery rare, usually required a widely separated fracture and Very rare, usually required a widely separated fracture and dural defectdural defectMost < 1yr, 90% < 3yrs of ageMost < 1yr, 90% < 3yrs of ageRarely develops > 6 months postRarely develops > 6 months post--injuryinjuryXX--ray ray –– widening of fracture and scalloping of edgeswidening of fracture and scalloping of edgesTreatment Treatment –– surgery with dural closuresurgery with dural closure

Skull Fracture - Divisions:Perforating fracture Perforating fracture –– small mass moving at high small mass moving at high velocity (i.e. bullet)velocity (i.e. bullet)

Penetrating fracture Penetrating fracture –– results from moderately results from moderately high velocity impacthigh velocity impact

Depressed fracture Depressed fracture –– results from slow moving results from slow moving object of high kinetic energyobject of high kinetic energy

CSF Leak / Fistula:

Possible routes of egress:Possible routes of egress:

CribriformCribriform plateplateSphenoid air cellsSphenoid air cellsPetrousPetrous boneboneMastoid air cellsMastoid air cellsFrontal sinusFrontal sinusTraumatic woundTraumatic wound

CSF Leak / Fistula (cont.):

Traumatic vs. Spontaneous:TraumaticTraumatic SpontaneousSpontaneous

2%2% Rare ++Rare ++AnybodyAnybody 2x females, 40’s2x females, 40’s

> 70% stop one week> 70% stop one week Uncommon to stop on ownUncommon to stop on ownUnusual to be profuseUnusual to be profuse Unusual to be profuseUnusual to be profuse

LateralityLaterality No lateralityNo lateralityAir Air –– 20%20% UnusualUnusual

AnosmiaAnosmia –– 80%80% UnusualUnusualHA uncommon / mildHA uncommon / mild Headache common / severeHeadache common / severe

CSF Fistula - Characteristics:Clear, does not cause excoriation within or around Clear, does not cause excoriation within or around nosenoseCheck glucose with Check glucose with dextrostixdextrostixCollect and test for glucose; >30mg%, nasal Collect and test for glucose; >30mg%, nasal secretions <5mg%secretions <5mg%Beta2Beta2--transferrin, present in CSF but absent in transferrin, present in CSF but absent in tears, saliva, nasal exudates and serum; can be tears, saliva, nasal exudates and serum; can be detected by electrophoresisdetected by electrophoresisRing signRing signSalty tasteSalty tasteImagingImaging

Epidural Haematoma:Biomechanics:Biomechanics:

Secondary to contact injurySecondary to contact injuryDural vessels are torn as a fracture propagates Dural vessels are torn as a fracture propagates across the vessel or if there is sufficient skull across the vessel or if there is sufficient skull bendingbendingNot related to head accelerationNot related to head acceleration

Source:Source:Middle Middle meningealmeningeal arteryartery 50%50%Middle Middle meningealmeningeal veinvein 33%33%DiploicDiploic vein / dural sinusvein / dural sinus 17%17%

Epidural Haematoma (cont.):


MRI(less clearly diagnostic)

CT(more clearly diagnostic)

Epidural Haematoma -Presentation:

Classical (<25%):Classical (<25%):Talk, then dieTalk, then dieBrief postBrief post--traumatic LOCtraumatic LOCFollowed by lucid interval for several hoursFollowed by lucid interval for several hoursThen Then obtundationobtundation, contralateral , contralateral hemiparesishemiparesis, ipsilateral , ipsilateral pupil dilationpupil dilation

Signs and symptoms:Signs and symptoms:60% have dilated pupil60% have dilated pupilNo LOC in 60%No LOC in 60%In In paedspaeds, may also present with significant drop in , may also present with significant drop in hcthct


Subarachnoid Haemorrhage:

Most common cause of SAH is traumaticMost common cause of SAH is traumatic

Usually not in basal cisternsUsually not in basal cisterns

Subarachnoid Haemorrhage (cont.):

Subarachnoid Haemorrhage (cont.):

Acute Subdural Haematoma:

Biomechanics:Biomechanics:

1.1. Complicated SDH:Complicated SDH:SDH associated with SDH associated with parenchymalparenchymal or cortical or cortical lacerationlacerationMore likely secondary to contact injuryMore likely secondary to contact injuryMost commonly associated with acute SDHMost commonly associated with acute SDH

Acute Subdural Haematoma (cont.):

2.2. Uncomplicated SDH:Uncomplicated SDH:Caused by disruption of surface vessels usually Caused by disruption of surface vessels usually bridging veinsbridging veinsResults from accelerationResults from acceleration--deceleration injurydeceleration injuryHead acceleration that produces shortHead acceleration that produces short--duration, high duration, high strain rate loading most commonly seen in setting of strain rate loading most commonly seen in setting of falls where the head strikes a broad surfacefalls where the head strikes a broad surfaceLittle energy is dissipated by focal injuryLittle energy is dissipated by focal injuryThe deceleration causes tensile and shear strains at The deceleration causes tensile and shear strains at the brainthe brain--skull interfaceskull interfaceCommonly associated with DAI because the Commonly associated with DAI because the mechanism of the two injuries is similar and they mechanism of the two injuries is similar and they often coexistoften coexist



Subacute and Chronic SDH:

Subacute: 3 days to 3 weeksSubacute: 3 days to 3 weeksChronic: present 3 weeks postChronic: present 3 weeks post--injuryinjury

Risk factors:Risk factors:Alcohol abuseAlcohol abuseSeizuresSeizuresCSF shuntsCSF shuntsCoagulopathiesCoagulopathiesNeoplasmsNeoplasms

Subacute and Chronic SDH (cont.):

Subacute and Chronic SDH (cont.):

Contusions:What is a contusion?What is a contusion?

Bruise of the neural parenchymaBruise of the neural parenchymaMost commonly involves the crown of the Most commonly involves the crown of the gyrusgyrusSuperficial foci of Superficial foci of punctatepunctate / linear haemorrhage/ linear haemorrhageCaused by extravasation of Caused by extravasation of RBCsRBCs around small around small lacerated vessels within the parenchymalacerated vessels within the parenchymaThe The piapia--arachnoidarachnoid membrane is intact; if breached it is membrane is intact; if breached it is a lacerationa lacerationWedgeWedge--shaped with apex extending into the neural shaped with apex extending into the neural parenchymaparenchyma

Contusions – Types :

1.1. Coup:Coup:Occurs beneath the immediate area of Occurs beneath the immediate area of impactimpact

2.2. ContrecoupContrecoup::Found remote from and most often in a Found remote from and most often in a straight line with the impact site on the other straight line with the impact site on the other sideside

Contusions – Types (cont.):


3.3. Fracture:Fracture:Occurs at the site of fracture Occurs at the site of fracture

4.4. Intermediate:Intermediate:Occurs within the neural parenchymaOccurs within the neural parenchymaMost commonly occurs in the Most commonly occurs in the sylviansylvian fissure fissure where the temporal and frontal cortices are where the temporal and frontal cortices are slapped against each otherslapped against each other



5.5. Gliding:Gliding:Occurs at the vertexOccurs at the vertexHaemorrhagic lesion affecting the Haemorrhagic lesion affecting the parasagittalparasagittal white white matter in the superior part of the cerebral matter in the superior part of the cerebral hemisphereshemispheresProduced by Produced by rostralrostral to caudal movement of the brain to caudal movement of the brain during deceleration injuriesduring deceleration injuries

6.6. Herniation:Herniation:Temporal lobe and Temporal lobe and cerebellarcerebellar tonsils make contact tonsils make contact against edge of against edge of tentoriumtentorium and foramen magnumand foramen magnum

Contusions – Location:

Most commonly occurs in areas where sudden Most commonly occurs in areas where sudden deceleration causes brain to impact on bony deceleration causes brain to impact on bony prominencesprominencesFrontal polesFrontal polesOrbital surfaces of the frontal lobesOrbital surfaces of the frontal lobesTemporal polesTemporal polesInterior surfaces of temporal lobesInterior surfaces of temporal lobesCortex above and below Cortex above and below sylviansylvian fissurefissure

Contusions – Location (cont.):

Mechanism of Coup Contusion:Caused by strains that arise Caused by strains that arise from skull infrom skull in--bendingbendingInduced by brain striking an Induced by brain striking an osseous ridge or dural foldosseous ridge or dural foldRupture of Rupture of pialpial blood vessels blood vessels occurs because of high occurs because of high tensile strains (suction) that tensile strains (suction) that are produced when the focal are produced when the focal depressed elastic skull depressed elastic skull rapidly returns to its normal rapidly returns to its normal configurationconfiguration

Mechanism of ContrecoupContusion:

Superficial focal areas of vascular disruption and Superficial focal areas of vascular disruption and cortical damage remote from the site of impact; cortical damage remote from the site of impact; occurs principally because of head motionoccurs principally because of head motionCan result from either translational or angular Can result from either translational or angular movements of the headmovements of the headPredominant mechanism for Predominant mechanism for contrecoupcontrecoupcontusions is accelerationcontusions is accelerationOften not exactly opposite the point of impactOften not exactly opposite the point of impact

Mechanism of ContrecoupContusion (cont.):

Contusion – Evolution:Perivascular haemorrhage (hence the linear deposition Perivascular haemorrhage (hence the linear deposition of haemorrhage)of haemorrhage)Blood extends into adjacent cortex where neurons in Blood extends into adjacent cortex where neurons in affected region undergo necrosis by the presence of affected region undergo necrosis by the presence of ischaemic cells changesischaemic cells changesLater proliferation of capillaries, Later proliferation of capillaries, astrocytesastrocytes and and microgliamicrogliaDead tissue is removed and shrunken, Dead tissue is removed and shrunken, glioticglioticfenestrated scar often containing residual fenestrated scar often containing residual haemosiderinhaemosiderin--filled macrophages resultsfilled macrophages resultsOld contusion tends to be triangular in shape, its broad Old contusion tends to be triangular in shape, its broad base being at the crest of a base being at the crest of a gyrusgyrus and apex in white and apex in white mattermatter

Contusion – Evolution (cont.):

Ventral View

Coronal section

Old Contusion:

Intracerebral Haematoma:

Caused by deceleration injuryCaused by deceleration injuryConfluent haemorrhagesConfluent haemorrhagesMost commonly found in frontal and temporal Most commonly found in frontal and temporal lobes (80 lobes (80 –– 90%)90%)Commonly associated with contusions as well as Commonly associated with contusions as well as acute SDH and SAHacute SDH and SAHMay have delayed onsetMay have delayed onsetMultiple in 20%, associated with SDH in 50%Multiple in 20%, associated with SDH in 50%

Intracerebral Haematoma (cont.):

Diffuse Axonal Injury

Caused by deceleration injuryCaused by deceleration injuryConfluent haemorrhagesConfluent haemorrhagesMost commonly found in frontal and temporal Most commonly found in frontal and temporal lobes (80 lobes (80 –– 90%)90%)Commonly associated with contusions as well as Commonly associated with contusions as well as acute SDH and SAHacute SDH and SAHMay have delayed onsetMay have delayed onsetMultiple in 20%, associated with SDH in 50%Multiple in 20%, associated with SDH in 50%

Diffuse Axonal Injury (cont.):

Diffuse Axonal Injury (cont.):Grades:Grades:

1.1. Widespread axonal damage in CC and cerebral Widespread axonal damage in CC and cerebral hemisphere white matterhemisphere white matter

2.2. Grade 1 and focal abnormalities in CC often Grade 1 and focal abnormalities in CC often associated with small haemorrhages called associated with small haemorrhages called tissue tear haemorrhagestissue tear haemorrhages

3.3. Grade 2 and tissue tear haemorrhages in Grade 2 and tissue tear haemorrhages in rostralrostralbrain stembrain stem


Corpus Corpus CallosumCallosum::

Generally inferior part and to one sideGenerally inferior part and to one side

3 3 –– 5 mm across but AP distance several 5 mm across but AP distance several cmscms

Sometimes restricted to Sometimes restricted to spleniumsplenium, where it , where it may be bilateralmay be bilateral



Mechanisms:Mechanisms:

Primary injury of rotational acceleration / Primary injury of rotational acceleration / decelerationdecelerationAxons are injured by shearing and impaired Axons are injured by shearing and impaired transport and organelle accumulationtransport and organelle accumulationDiffuse axonal injury; axonal retraction balls, Diffuse axonal injury; axonal retraction balls, microglialmicroglial scarscarDegeneration of white matter fibre tractsDegeneration of white matter fibre tracts


Almost all cases of DAI, especially if severe, arise Almost all cases of DAI, especially if severe, arise from vehicular injuryfrom vehicular injuryImpact to dashboard, resilient windshields, Impact to dashboard, resilient windshields, energyenergy--absorbing steering columns in which absorbing steering columns in which acceleration is longacceleration is longConversely, most SDH occur because of falls or Conversely, most SDH occur because of falls or assaults in which the impact duration is short and assaults in which the impact duration is short and angular, and acceleration is abruptangular, and acceleration is abruptProlonged rotational accelerationProlonged rotational acceleration


Axonal damage:Axonal damage:

ParasagittalParasagittal white matter of cerebral white matter of cerebral hemisphereshemispheresCCCCMedial Medial lemniscuslemniscusCTTCTTCSTCSTFornixFornix, IC, EC, IC, EC


Concussion

Alteration in consciousness, not necessarily LOCAlteration in consciousness, not necessarily LOC

In general, no gross / microscopic abnormalityIn general, no gross / microscopic abnormality

Minimal or no change CT / MRMinimal or no change CT / MR

Increased metabolismIncreased metabolism

Susceptible to secondary impact syndromeSusceptible to secondary impact syndrome

Concussion (cont.):

Non-Accidental Head Injury in Children

Trauma is the most common cause of death in childhood Trauma is the most common cause of death in childhood and inflicted head injury is the most common cause of and inflicted head injury is the most common cause of traumatic death in infancytraumatic death in infancy

Most common age group for child abuse:Most common age group for child abuse:Shaken impact syndrome is largely restricted to Shaken impact syndrome is largely restricted to children less than 3 yrs, with the majority occurring children less than 3 yrs, with the majority occurring from 0 from 0 –– 1 yrs1 yrs

Main risk factors for nonMain risk factors for non--accidental injuries in kids:accidental injuries in kids:Young parents, unstable family situations, low SES, Young parents, unstable family situations, low SES, disability or prematurity of childdisability or prematurity of child

Non-Accidental Head Injury in Children (cont.):


Common symptoms in children:Common symptoms in children:Lethargy, irritability, seizures, tone changes, Lethargy, irritability, seizures, tone changes, vomiting, poor feeding, breathing vomiting, poor feeding, breathing abnormalitiesabnormalities

Main findings on physical examination:Main findings on physical examination:Decreased LOC, Decreased LOC, opisthoclonusopisthoclonus, full , full fontanellefontanelle, , Seizures 40 Seizures 40 –– 70%, retinal haemorrhages 65 70%, retinal haemorrhages 65 ––95%95%


Mechanism of injury / death in shakenMechanism of injury / death in shaken--infant infant syndrome:syndrome:

Sudden deceleration associated with striking Sudden deceleration associated with striking head against surface; responsible for most if head against surface; responsible for most if not all severe inflicted injuriesnot all severe inflicted injuriesRotational forces about centre of gravity Rotational forces about centre of gravity ––DAI and SDHDAI and SDHTranslational forces less harmful, i.e. Translational forces less harmful, i.e. household falls; rotational or angular household falls; rotational or angular deceleration very uncommondeceleration very uncommon


6 mos old boy with Shaken Impact Syndrome


It is the sudden angular deceleration experienced by It is the sudden angular deceleration experienced by the brain and cerebral vessels, not the specific contact the brain and cerebral vessels, not the specific contact forces applied to the surface of the head that results in forces applied to the surface of the head that results in the damagethe damageThis angular force is distinct from the forces generated This angular force is distinct from the forces generated in most cases of accidental trauma in infantsin most cases of accidental trauma in infantsMore accurate to call it “Shaken Impact Syndrome”More accurate to call it “Shaken Impact Syndrome”Whether shaking alone can cause the constellation of Whether shaking alone can cause the constellation of findings associated with the syndrome is still debatedfindings associated with the syndrome is still debated

Head Injury

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