1. Cerebral contusion, or brain bruising, results from blunt trauma to the head and causes bleeding within the brain tissue. 2. CT scans often show patchy areas of bleeding and swelling within the brain that worsen over time as the contusions evolve. 3. Management involves preventing secondary injuries, monitoring for increased intracranial pressure, and surgery in cases of neurological deterioration or large contusions causing mass effect on the brain.

1. CEREBRAL CONTUSION

2. TRAUMATICBRAININJURY
Aninsulttothebrain,notofdegenerativeorcongenitalnature
causedbyanexternalphysicalforcethatmayproducea
diminished oralteredstateofconsciousness,which resultsin
impairmentofcognitiveabilitiesorphysicalfunctioning.Itcan
alsoresultindisturbanceinbehaviororemotionalfunctioning.

3. Highestamongtheadolescents,youngadultsand
Thoseolderthan75.
50%ofmajortraumadeathsareduetoTBI
Vehiclecrashesaretheleadingcauseof braininjury.

4. MECHANISMOFINJURY:
BLUNTINJURY
Motor vehicle injuries
falls
Assaults
PENETRATINGINJURY
Gunshot wounds
Stabbing
Explosions

5. TYPESOFBRAININJURY
CLOSEDINJURY
OPENINJURY

6. CLOSEDINJURY
Of thetwo, closed injuryisfarmore common.
Resulting from fallandmotor vehicle accidents.
Effects aremorebroad(diffuse)
Nopenetration to skull

7. OPENINJURY
Resultsfrombulletswounds.
Largelyfocaldamage
Penetrationofskull
Effectscanbeserious

8. TYPESOFHEADINJURIES
Scalplaceration
Skull fractures
Focalbraininjuries
Diffuse braininjuries

9. Focal
Cerebral contusion
Intracranial hemorrhages
Intracerebral hemorrhages
Diffuse
Concussion
Moderate diffuse axonal injury
Severediffuse axonal injury

10. Pathophysiology
Primayinjury
Atthetimeof trauma.
Irreversible cellularinjuryasadirectresultto injury.

11. Secondaryinjury
Occursafterhoursto weeks afterthe injury.
Includesinjuriesfromedema,ischemia,hypoxemia, vasospasm.

12. CEREBRALCONTUSION
Cereberalcontusionsare
basically”brainbruises”.
Mostofteninvolving thecrown
ofgyrus,theytendtobewedge
shapedwithapexextendinginto
neuralparenchyma.
Cerebralcontusionsarealso
calledgyral“crest”injuries.

13. CLASSIFICATION
COUP
COUNTERCOUP
INTERMEDIATE COUP
GLIDINGCONTUSION
HERNIATIONCONTUSION
FRACTURE CONTUSION

14. COUP
Coup contusion arethose thatoccurbeneath theimmediatearea of
impact.

15. COUNTERCOUP
Countercoupcontusionsarethosethatarethoughttobe
confinedtoareasremotefromandmostoftendirectlyopposite
theimpactsiteontheothersideofbrain.

17. INTERMEDIATECOUP
Intermediate coupoccurswithintheneuralparenchymabetween the
impactsiteandtheopposite sideofbrain.
Trueintermediatecoupcontusions occurinsylvian fissure ,where
frontalandtemporal corties maybeforcibly“slapped” againsteach
other duringthe transmissionofforce fromonesideto other.

18. GLIDINGCONTUSION
Glidingcontusionshasbeendescribed asthose thatoccuratthevertex
ofbrainandareproducedbyrostral tocaudalmovement ofbrainduring
deccelerative injuries.

19. HERNIATIONCONTUSION
They areproducedsuddenforcingofaportionofabrainagainstarigid
opening ,mostoften the incisuraoftentorium .

20. FRACTURECONTUSION
Thefracturecontusiontermis restricted tocontusionlocated
immediately underthefractureline.

21. ETIOLOGY
 Mostcerebralcontusionsresultfromnonmissileorbluntheadinjury.
 Closedheadinjuryinducesabruptchangesinangularmomentumanddeceleration.
 Thebrainissuddenlyandforciblyimpactedagainstanosseousridgeorthe
hard,knife-likeedgeofthefalxcerebriandtentoriumcerebelli.

22. PATHOLOGY
LOCATIONS
 Theyoccurinverycharacteristic,highlypredictablelocations.Nearlyhalf involve
thetemporallobes.Thetemporaltips,aswellasthelateraland inferiorsurfaces
andtheperisylviangyri,aremostcommonlyaffected.
 Theinferior(orbital)surfacesofthefrontallobesarealsofrequently affected

23.  Convexitygyri,thedorsalcorpuscallosumbody,dorsolateralmidbrain,and
cerebellumarelesscommonsitesofcerebralcontusions.
 Theoccipitalpolesarerarelyinvolved,evenwithrelativelysevereclosed
headinjury.

25. MICROSCOPICFEATURES
 Perivascularmicrohemorrhagesrapidlyformandcoalesceovertimeintomore
confluenthematomas.Edemasurrounding thehemorrhagesdevelops.Activation
andproliferationof astrocytestogetherwithmacrophageinfiltrationensue.
 Necrosiswithneuronallossandastrogliosisaswellashemosiderin-laden
macrophagesarepresentin subacuteandchroniclesions.

26. SYMPTOMS
 Vomiting
 Lethargy
 Headache
 Confusion
 Paralysis
 Lossofconsciousness
 Lossofmemory

27. Alteration ofmental state
Speech difficulties
Seizures
Focalneurologicaldeficits

28. IMAGING
CTSCANFINDINGS:
 ACUTE:
 Themostfrequentabnormalityisthepresenceof petechialhemorrhagesalonggyralcrests
immediatelyadjacenttothecalvaria.Amixturepatchyhyperdensehemorrhagicfoci surroundedby
ill-definedhypodenseareasofedemais common.(saltandpepperappearance)

29.  Lesion"blooming"overtimeisfrequentandisseenwithprogressiveincreasein
hemorrhage,edema,andmasseffect .Smalllesionsmaycoalesce,forminglarger
focalhematomas.Developmentof newlesions thatwerenotpresentoninitial
imagingisalsocommon.

32. CHRONIC:
Haemorrhagicfociturnsisodenceandthenhypodense.
Eventuallytheareasbecameencephalomalacicwithvolumelossandthereis hypodensityoftheinvolved
parenchyma.

33. MultipleCTimagesovertimedemonstrate
theevolution ofa hemorrhagicparenchymal
contusioninatypicallocationoverthe
petrous ridgeofthetemporalbone.The
hematomaisnotvisibleonday1(top row
left),butappears and enlargesoverthenext
fewdays (top rowrightandmiddlerow left),
atypical courseforcontusion.Atday 17
(middlerowright), allthatremainsis a
hypodensehematomathat hasalready
begunto involute.1yearfromtheinitial
trauma, theprevious hematomahasevolved
intoa smallamount ofencephalomalacia
(bottom row).

34. MRI
 MRIismuchmoresensitivethanCTindetectingcerebralcontusionsbutisrarely
obtainedintheacutestageof traumaticbraininjury.

35. T1scansmayshowonlymild
inhomogeneous
isointensities andmasseffect.

36. T2scansshowpatchyhyperintense
areas(edema)surroundinghypointense
fociofhemorrhage.

37. FLAIRscansaremostsensitive for
detectingcorticaledemaand
associatedtSAH,bothofwhichappear
ashyperintense

38. MANANGEMENT
Prevention ofsecondary injury.
Hypoxemia
Hypotension
Anemia
Hyperglycemia

39. INDICATIONFORICPMONITORING
 Severeheadinjury(gcs<8) withabnormalct.
 Severeheadinjurywithnormalct and2offollowing:
Age>40
SBP<90
Decerebrateordecorticateposturing.

40. INVASIVE SYSTEMS:
Intraventicular
Intraparenchymal
Subarachnoid
Epidural.
NONINVASIVE SYSTEMS:
TCD
Tissueresonanceanalysis
Ocularsonography
Intraocularpressure

41. THERAPYFORINTRACRANIALHYPERTENSION
FIRSTTIER:
Positioning
Ventriculardrainage
Osmoticdiuresis
Hyperventilation

42. SECOND TIER:
Sedation
Neuromuscularblockade
Hypothermia
Barbiturate.
 Decompressioncraniectomy
 Evacuatonof contusedbrain

43. SURGICALINDICATION:
 Progressiveneurologicaldeterioration,refracatoryintracranialhypertension,signs
ofmasseffecton ct
 Volume>50ml
 Gcs6-8withfrontalortemporalcontusionvolume>20mlwithmidlineshift>5mm.

44. COMPLICATION
 POSTtraumaticamnesia
 Postconcussionsyndrome
 Posttraumaticepilepsy
 Infections
 Metabolicabnormalities
 Vascularabnormalities.