Head Injury Pathology

8/3/2019 Head Injury Pathology

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Shuja Tahir, Awais ShujaFaisalabad, Pakistan IR-085

Jan to Mar, 201184 INDEPENDENT REV IEWS

Head injury is trauma to body Usual scalp injuries are following ;

above the neck. It is commonly ! Abrasions.associated with neck injuries. ! Contusions.

Various types of injuries of the head ! Haematomas.include ; ! Lacerations.1. Scalp injuries.2. Skull injuries (bony injuries). ABRASIONS AND CONTUSIONS3. Brain injuries. These are commonly seen minor4. Intracranial vascular injuries. scalp injuries. These bleed heavily

and continuously due to very goodCommonly used term head injury blood supply of the scalp andactually means injuries of head inability of the blood vessels toinvolving brain trauma. contract due to fibrous tissue

adhesiveness.SCALP INJURIESThese are the injuries to the scalp. Management

Local pressure helps in control ofScalp is an essential covering of the bleeding. Satisfactory haemostasisskull. The name is derived as can be achieved by pressurebelow; dressing. Suturing the wound afterS Skin. debridement will also controlC Connective tissue. bleeding.

A Aponeurosis.L Loose areolar tissue. Healing is quicker and satisfactory.P Pericranium. Wound care, tetanus immunization

and analgesia is all that is requiredThe survival of skull is not possible if to treat these injuries.it is uncovered. Scalp must besaved as much as possible. The infection is rare in scalp

wounds.It has four layers. The forth layers isloose enabling all other layers to HAEMATOMAmove over the pericranium ; When the blow to scalp is forceful1. Skin. and skin continuity remains intact,2. Subcutaneous tissue and blood the haemorrhage collects under the

vessels. scalp either in sub-aponeurotic or3. Epicranial aponeurosis. sub-cutaneous space. It is also4. Sub-aponeurotic areolar tissue. called cephal-haematoma.

Head Injury Pathology

Surgical Principle


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It is commonly seen in neonates. If it bone. Skull injuries are fractures.is large, it may lead to lowering of These can be open or closedthe haematocrit and may warrant fractures.blood transfusion. It should not be These are always associated with

aspirated to avoid introduction of the injuries to the scalp and brain.exogenous infection. Occasionally in children, the skull

may not fracture due to its elasticRarely the sub-periosteal type of nature and brain may still be injuredcephal -haematoma may ge t due to the crushing force of injury.calcified. Then it is removedsurgically. 91% of the patients with extradural

haematoma have skull fracture.

LACERATIONSSome of the fractures may not beThese are also quite commonvisible on radiological examina-injuries of the scalp. These maytion, but clinically these can bepresent without any injury to thediagnosed wi th reasonableskull or brain. The blood loss issatisfaction such as fractures of theprofuse in these injuries because ofbase of the skull.inablity of the scalp vessels to

contract.BASE OF SKULL FRACTURES

Everting the cut end of scalp helps These are the fractures of the baseto stop bleeding immediately due to of the skull. Usually these are notfolding of scalp vessel. obvious on routine radiological

examination. But characteristic

Pressure bandage or stitching of the clinical features help in thescalp wound is usually required to diagnosis.stop the bleeding. The healing issatisfactory due to presence of ANTERIOR CRANIAL FOSSAgood blood supply to the scalp. FRACTURE

The anterior cranial fossa fracturesWhen the scalp injuries are severe are very common basilar fractures.such as degloving injuries of thescalp, there may be heavy losses of Injury to the dura matter leads to theblood leading to haemorrhagic leakage of cerebro-spinal-fluidshock. Blood transfusion is required through the nose (CSF-rhinorrhea).

immediately and plastic surgery isrequired to cover the scalp with skin When these fractures are present ingrafts at a later stage. the anterior cranial fossa, bleeding

through nose is indicative ofSKULL INJURIES fracture of the orbital plates.These are the injuries to the skull


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The sub-conjunctival haemorrhage the base of the skull.may also be present without any S o m e t i m e s t h e t y m p a n i cinjury to the eyes. Cerebro-spinal- membrane remains intact andfluid leakage through the nose (CSF blood collects behind the tympanic

rhinorrhoea ) is also indicative of membrane (haemo-tympanum).open (compound) fracture of the The ossicular chain is damagedanterior-cranial-fossa. and conductive type of deafness

occurs.Injury to the venous sinuses leads toperi-orbital haematomas (Raccoon 7th cranial nerve injury leads toor panda sign). paresis or paralysis in 20% of the

patients with such fractures.Blood s tained vomi t ing i ssuggestive of the compound Cerebro-spinal-fluid may collect infracture of the base of the skull. the middle ear cavity and drain via

These fractures may not be seen Eustachian tube and nose. (CSF-radiologically many times. rhinorrhoea).

The fracture line extendingPOSTERIOR OR MIDDLE CRANIALposteriorly into the sigmoid sinusFOSSA FRACTUREleads to post-auricular haematomaOne of the common type of skullformation (Battle's sign). This is seenfracture is due to blow on thewithin 24-48 hours of injury.temporal area leading to the

fracture of squamous part of theThe trauma, stress and strain maytemporal bone extending into

have occurred to arterial branchespetrous part. serving as feeding perforants tomedulla oblongata causingThis produces deformity of externalunconsciousness due to neuronalauditory canal, rupture of tympanicdeficit1.membrane and leakage of

cerebro-spinal-fluid through theCLOSED (SIMPLE) FRACTURESfracture line in the ear (CSF-These are the skull fractures whichotorrhea).are not open to exterior. The scalpoverlying the fracture is intact.Bleeding through the ears is seen in

open fractures of middle or

posterior-cranial-fossa. OPEN (COMPOUND) FRACTURESThere are the injuries when skull

Cerebro-spinal-fluid leakage fractures are open to the exterior.through the ears (CSF-otorrhoea) is These fractures are obviousindicative of middle or posterior- clinically and radiologically.cranial-fossa compound fracture of

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fracture should be treated just likeopen (compound) fracture of anyDEPRESSED FRACTURESother site.These are the fractures which occur

when blunt weapon hits the skull

Infection of the wound andand a portion of the skull is brokenadjacent tissue is more common inand pushed inwards.these fractures. Staphylococcusaureus is the most commonThese may be simple (closed) orcausative organism and may leadopen (compound). In children,to formation of "Potts puffy" tumour.greenstick depressed fracture of the

skull is also called "ping pong"Following management is carriedfracture.out ;1. Wound care and debridement.These should always be examined2. Tetanus immunization.carefully clinically. The diagnosis3. Antibiotics cover.should be confirmed radiologically.4. Analgesia.The presence of haematoma many

times may be wrongly diagnosed asTRAUMATIC BRAIN INJURYdepressed fracture of the skull.It is the result of on extentmechanical force applied to theLINEAR FRACTUREScranium and the intra cranialThese are the skull fracture when acontents leading to temporary orcrack is present in the skull. Thesepermanent impairments, functionalmay be simple or compound indisabi l i ty or psycho socialnature. These may be single or

maladjustment. It is of two types.multiple.! Primary Injury! Secondary Injury77% of the patients with intracranial

haematomas have linear skullPRIMARY BRAIN TRAUMAfractures.This is the injury to brain which

The risk of intracranial haemorr- occurs at the time of injury orhage in pat ients with linear impact. The damage to the brainfractures is 400 times more. during primary brain trauma is

permanent and cannot be undone.

DIASTASISHead (brain) injuries vary widely inWhen linear fractures run into thetheir etiology, pathophysiology,suture line, the splitting of cranialclinical presentation and optimalsutures occurs, this is calledtreatment strategies.diastasis. It is common in children.

It is very important to assess the An open (compound) linear skull


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extent of primary brain trauma compartments.accurately for adequate mana-gement. DIFFUSE AXONAL INJURIES (DAI)The CT scan may or may not show It is characterized by extensive,

the mass lesion in these patients. generalized damage to whitematter of the brain.

Almost all significant head injuriesare associated with injuries to the It is a common feature of severebrain. There are two main cate- head injury and immediate coma. Itgories of brain injury ; may be associated with wide1. Focal injuries. spectrum of focal lesions such as2. Diffuse axonal injuries. acute subdural haematoma or

2basal ganglia haemotoma etc .

FOCAL INJURIESThese are caused by direct blows to It is caused by sudden movement of

the head and comprise of the head and comprise of briefcontusions, brain lacerations and cerebral concussion and moreh a e m o r r h a g e l e a d i n g t o prolonged post-traumatic coma. Ithaematoma formation in the extra- is commonly known as diffusedural (epi-dural), sub-dural, sub- axonal injury.arachnoid or intra-cerebral


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Primary traumatic effects involve The amnesia may be :neuronal or vascular elements ofthe brain, which can be affected by RETROGRADE AMNESIAdelayed effects such as de- It is loss of memory of the events

afferentation or secondary events before the accident.such as ischaemia, swelling, brainedema and increased intra-cranial ANTEGRADE AMNESIApressure. It is loss of memory of the events

after the accident (concussion).Axonal damage results in excessiveaccumulation of calcium ions. Concussion may be severe orIschaemia also leads to accumula- minor. It can be discussed undertion of calcium ions. four grades2.

Calcium ions accumulation leads

POST CONCLUSIVE SYNDROME3to axonal degeneration . Some patients who have sufferedfrom concussion, continue having

The primary brain trauma may be persistent headache, difficulty inminor or severe and can be concentration, nausea, poordescribed as ; memory, insomnia, depression and1. Concussion. confusion. It is called post2. Contusion. concussive syndrome. No organic3. Laceration. abnormality is seen.

Treatment is symptomatic.CONCUSSION

It is the transient loss of neuronal CONTUSIONfunction without permanent This is the brain injury which is moreneuronal damage. It is the minor severe than concussion. It is alwaysmost brain injury. associated with some residual

neuronal deficit which may beIt is physiological disconnection minor leading to nearly full recoverybetween the cortex and brain stem or severe and fatal.or physiological loss of the conduc-tion leading to temporary loss of The period of unconsciousness lasts

2consciousness (black out) . from few minutes to few hours or

days or until death. There is alwaysThe unconsciousness period lasts some degree of organic neuro-only for few moments and recovery logical damage. The recovery isis complete as there is no organic never complete.neurological damage. Somedegree of amnesia is present. It is associated with a host of

complications such as early

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GRADE-I CONCUSSION1. Minor confusion for

a short while.2. No amnesia.3. Rapid return to

normal consciouslevel.

GRADE-II CONCUSSION

1. Longer period ofconfusion.

2. Some degree ofresidual amnesia butpost traumatic only(antegrade).

GRADE-III CONCUSSION1. Severe initial

confusion.2. Greater degree of

residual amnesiaboth retrograde and

antegrade.

GRADE-IV CONCUSSION1. Brief period of loss of

conscious level.2. Subsequent

confusion.3. Amnesia both

retrograde andantegrade.

Coup Contrecoup

PrimaryImpact

SecondaryImpact


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cerebral edema, neuronal swelling Object)and axonal ballooning within 24-48 hours post injury3. Deceleration injuries are common.

When a passenger of the motor

vehicle suddenly hits the ground orLACERATIONmoving brain hits a stationaryThese are the lacerated injuries ofobject such as road.the brain. These may be minor or

severe injuries. Their effects areSudden deceleration of the brainsimilar to contusion injuries. Theleads to distortion and injury to therecovery is never complete.brain.

COUP AND COUNTER COUPSECONDARY BRAIN INJURYINJURIESThis is the trauma to the brain whichCoup injuries are injuries of the partoccurs some time after injury and is

of the brain which comes into direct often preventable.contact with the impact. (Inner sideof the skull bone).

The cranio-cerebral injury rendersthe brain vulnerable to variety ofCounter coup injuries of the brainsecondary insults which areare injuries exactly to the oppositepreventable before irreversiblepart of the brain than the one inneuronal damage occurs.direct contact with the impact (Inner

side of the skull). The mortality rateThe brain shows changes followingis higher in counter coup injuriesany insult which may be traumatic,with occipital point of impact than

neoplastic, inflammatory ofof frontal10. ischaemic in nature.

ACCELERATION INJURIESHypoxia and ischaemia lead to(Immobile Patient Injured by Mobilesignificant neuronal cell loss. TheseObject)changes occur due to cellular ionicor metabolic alterations4. Acceleration injuries are when

stationary brain is hit by a movingFollowing secondary changes areobject (vehicle, missile, assault ).seen after the head injuries :

The sudden acceleration of theCEREBRAL EDEMAstationary brain leads to distortionThis is seen in response to all sortsinjury to the brain (standing personof brain injuries. The edema may behit by vehicle or by some weapon).insignificant following minor braininjuries. It may be severe and mayDECELERATION INJURIESlead to deterioration of conscious(Mobile Patient Injured by Immobile



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level and even death of the patient. KERNOHAN'S NOTCHThe fluid collection in the brain is It is the triad of following clinicalboth extra and intracellular. It is very symptoms ;severe in diffuse primary brain 1. Deteriorating consciousness

trauma and involves almost whole level.of the brain. It leads to severe rise in 2. Dilation of the pupil on the sideintracranial pressure. of compression.

3. Hemiparesis of the side of theWhen the primary injury to the brain compression.is localized, the cerebral edema isalso localized initially giving rise to Ischaemia whether generalized orthe symptoms similar to local localized produces a sequence ofcompression caused by space intracellular changes leading tooccupying intracranial lesion or increased cell permeability to waterlocalized haematoma. and calcium ions.

The cerebral edema becomes There is loss of cellular integrity anddiffuse and generalized if not function with increased productiontreated adequately and in time. Mid of prostaglandins, free radicals,brain compression or trauma leads acidosis and lactate accumulation.to loss of consciousness. These events may be exacerbated

by glucose infusion.In the earlier lesions, the third Drugs should be used to;cranial nerve is stimulated showing ! Decrease cerebral metabolicpupillary constriction. Later on requirements for

when the third nerve paralysis oxygen.occurs, the dilatation of the pupil is ! Improvement of blood flow tonoted. ischaemic areas preventing

calcium-ion-induced injury.This happens due to the pressure of ! Inhibition of free radicaltemporal lobe on the oculomotor formation,nerve against tentorium cerebelli. ! Lactate removal.

! Inhibition of prostaglandinIn untreated or inadequately synthesis.treated patients, the displacement ! Prevention of complement-of brain stem at tentorial opening mediated leukocyte aggre-

9presses the opposite cruss as well gation .leading to hemiparesis of the side ofintra-cranial haemorrhage. This INTRACRANIAL VASCULARgives rise to triad of symptoms CHANGEScalled "Kernohan's notch". Following pathological changes

are seen secondary to the brain



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injury ; CARDIOVASCULAR ANDMETABOLIC RESPONSE TO

The basic pathological change is SEVERE HEAD INJURYischaemia. The cerebral blood flow Head injury patients show a

is altered which also causes metabolic response similar to thatcerebral ischaemia and deterio- reported for patients with 20-40%rates conscious level and increases body surface area burns.cerebral edema. This in turn leadsto further increase in intracranial A hyperdynamic state is foundpressure, cerebral compression, characterized by;cerebral ischaemia and a vicious

! Increased cardiac output.circle is set up. This also leads to

! Increased cardiac work.coning of the midbrain.

! Moderate hypertension.! Tachycardia.

EXTRACRANIAL FACTORS! Decreased or normal systemic

AFFECTING SECONDARY BRAIN and pulmonary vascularTRAUMA resistance.Following extracranial factors also ! Increased pulmonary shunting.affect the secondary brain trauma ; ! Increased oxygen delivery and

utilization.

HYPOXIAThe magnitude of these changesPatients with head injury are unabledoes not correlate with changes into protect airway and gas exchangeintracranial pressure, Glasgowmay be impaired. It can lead tocoma score or CT scan findings10.hypoxia and respiratory failure.

HYPOTENSIONRespiratory failure leads to cerebralischaemia and worsening of the Normal Cerebral Blood flow isconsciousness level maintained at a constant level via

mechanism cal led cerebral A rise in PCO2 leads to cerebral autoregulation.venous dilatation and congestionleading to worsening of the Hypotension due to intra cranialcerebral ischaemia while low PO2 loss of blood or any other reasonleads to decrease in cerebral blood can cause secondary brain injury.flow and cerebral ischaemia.

Hypotension leads to decreasedIt is best to keep the arterial Po2 (> ce rebral pe rf us ion pres su re8KPa) & PCO2 (4.5-5 Kpa) levels resulting in cerebral ischaemia,within normal range. renal ischaemia and low cardiac

output even when autoregulatorymechanisms are working.

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The vascular volume and blood are injured, these bleed inside thepressure should also be maintained closed cranial cavity. If the bleedingwithin normal range for adequate is severe enough and leads tocerebral oxygenation. intracranial clot formation, it

Hypotension (systemic BP below 90 causes compression of the brain.mm of Hg) and Hypoxia PO2arterial less than 60 mm of Hg or The intracranial haemorrhage mayapn o ea o r c y an o s i s a r e be ;independently associated with 1. Extradural or Epidural.increas e in morbidi t y and 2. Subdural.

11mortality . 3. Sub arachnoid.

4. Intracerebral.

FLUIDS AND ELECTROLYTE1. High risk groupBALANCEIt includes depressed or deter-Abnormal fluid balance also affectsiorating conscious level, focalthe injured brain secondarily.neurological signs. DepressedPreferably isotonic fluids should bepenetrating skull injuries.used as blood brain barrier is

disturbed and the anti-diuretic-2 Moderate risk grouphormone secretion may be

abnormal. It includes patients who showchange in conscious level effect of

In patients with head injury when alcohol, drugs. Victims of multipleautoregulation is impaired, blood trauma. Skull or facial fractures. Essp res su re and haematoc r i t than 2 years of age suspected .

determine cerebral oxygen delivery. Victims of child abuseInjury to blood brain barrier impairsbrain's volume regulation and may 3 Low risk groupcontribute to cerebral edema. Asymptomatic or with minimalIntravenous-fluids should be symptoms. Scalp injuries no

8selected to affect favorably the neurological involvement .blood flow, cerebral oxygendelivery, brain metabolism and INTRACRANIAL HAEMATOMASbrain volume. Rise in temperature These may result following arterialleads to increased metabolic or venous bleeding. The haemo-demands, poor cellular functions rrhage always follows primary brainand deterioration in the conscious trauma. It may be present anylevel. where in the brain such as ;

1. Extradural or Epidural.INTRA CRANIAL VASCULAR 2. Subdural.INJURIES 3. Sub-arachnoid.Whenever the intracranial vessels 4. Intra-cerebral.


EPIDURAL HEMATOMA

Scalp

Skull

Dura mater

Arachnoid mater

SubarachnoidspacePia mater

Brain

Bleeding into the space betweenthe dura mater and the skull

SUBDURAL HEMATOMAScalp

Skull

Dura mater

Arachnoid mater

Subarachnoidspace

Pia mater

Brain

Bleeding into the space betweenthe dura mater and the brain itself

IntracerebralHemorrhage

Bleeding inside the brain

SubarachnoidHemorrhage

Bleeding in thesubarachnoid space


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The deeper hemorrhages lead to This herniation not only compressesedema and necrosis and make the the midbrain but also impedes thesu rg i ca l i n t e r ven t ion l e s s cerebro-spinal-fluid flow leading tosuccessful. further rise in intracranial pressure

and thus making the situation evenThe superficial or extradural worse. It leads to formation ofhemorrhages cause early focal "Kernohn's notch".changes and the surgical treatmentis quite successful. BRAIN NECROSIS

The portion of brain primarily getsThe subdural haematoma may be necrosed due to compression byaspirated percutaneously comple- cerebral edema, rise in intracranialtely in many elderly patients7. pressure, intracerebral haemorr-CONING hage and ischaemia which followsIt is the herniation of the supra- all these changes.tentorial part of the brain throughtentorial hiatus or the herniation of The cerebral necrosis is usuallyinfra-tentorial contents through the liquefactive in nature and theforamen magnum. damage is irreversible.



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8(2)" 367-408, 1992 AprREFERENCES1. Sahuqullo J, Vilalta J. Lamar ca J et al.

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Blunt basal head trauma aspects ofhypothesis [JC: mom] 37(1): 37-9,unconsciousness. Acta Neuro-1992 Jan.chirurgica - supplement. [JC : 19e]55: 25-8. 19923. Cervos - Navarro J. Lafuente JV.

Traumatic brain injuries: structural9. Aoki N Sakai T, Oikawa A: Acutechanges. Journal of Neurological

subdural haematoma successfullysciences. [JC:jbj] 103-suppl: 83-14,treated by percutaneous subdural1991 Jul.tapping in an elderly patient. ActaNeurochirurgica. [JC : 19c] 111(3-4):4. Doberstein CE: Horda DA. Becker DP.132-4 1991.Clinical considerations in the

reduction of secondary brain injury.10. Hein PM. Schulz E. Counter coup Annals of emergency medical [JC:

fractures of anterior cranial fossa : a427] 22(6): 993-7, 1993 Jun.consequence of blunt force caused bya fall. Acta Neurochirurgica [JC : 19c]5. Clifton GL. Robertson CS. Grossman105(1-2): 24-9, 1990.RG. Cardiovascular and metabolic

responses to severe head injury11. Chesnut RM. Marchall LF, Klauber MRneurosurgical review. [JC:nov]

et al. The role of secondary brain12suppl 1:465-73, 1989.injury in determining outcome fromsevere head injury. Journal of trauma6. Sutin KM. Ruskin KT, Kaufman BS.[JC : kaf] 34(2): 216-22, 1993 FebIntravenous fluid therapy in neurologic

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The author :Awais ShujaMRCSis assistant Professor of

surgery at IndependentMedical [email protected]

The author :Muhammad Shuja Tahir

FRCS (Ed), FCPS (Hon)is professor and head of thedepartment of Surgery atI ndependen t Med ica lCollege Faisalabad.

[email protected]

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Head Injury Pathology