Brain injury power point for First Aid to learn more

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1. BRAIN INJURIES
DR. OMAR ARZU

2. NEUROSURGICAL CASE
A 19 yr OLD BOY HAVING THE HISTORY OF FALL FROM
A BIKE ,HITTING THE RIGHT SIDE OF HIS HEAD
FORCEFULLY ON THE ROAD IS BROUGHT TO THE
CASUALTY .ON EXAMINATION HIS PULSE:40/MIN,
B.P :170/110mmHg
ON FUNDOSCOPIC EXAMINATION HE HAS VENOUS
DISTENSION AND ABSENT PULSATIONS OF THE
RETINAL VASCULATURE.ALSO ON SYSTEMIC
EXAMINATION HIS LIMBS ON THE LEFT SIDE ARE
MORE FLACCID THAN THE RIGHT SIDE.
-WHAT MAY BE THE LIKELY DIAGNOSIS?

3. DEFINITION
•ANY INJURY TO THE BRAIN,REGARDLESS OF
THE AGE OF ONSET,WHETHER MECHANICAL
OR INFECTIOUS IN ORIGIN,THE RESULT OF
WHICH MAY BE EXPECTED TO CONTINUE
INDEFINITELY CONSTITUTING A
SUBSTANTIAL HANDICAP TO THE
INDIVIDUAL EITHER OR WHICH MAY
DIRECTLY RESULTING IN SOME SORT OF
NEUROLOGICAL IMPAIRMENT.

5. CLASSIFICATION
•PRIMARY BRAIN INJURY
•SECONDARY BRAIN INJURY

6. PRIMARY BRAIN INJURY
•INJURY CAUSED AT THE TIME OF
IMPACT.
•IRREVERSIBLE
•CLASSIFIED INTO
1.DIFFUSE AXONAL
2.CEREBRAL CONCUSSION
3.CEREBRAL CONTUSION AND
LACERATION

7. DIFFUSE AXONAL INJURY
•DUE TO SHEAR STRESS AT GREY
MATTER-WHITE MATTER JUNCTION.
•ACCELERATION-DECELERATION TYPE
FORCES DUE TO DIFFERENTIAL BRAIN
MOVEMENT.
•WALLERIAN DEGENARATION OF
NEURONS MAY OCCUR AFTER A FEW
WEEKS.

8. Accelerationhappens when
there is aresultant force on an
object, in any direction.
Deceleration takes place when a
resultant force acts on an object
in the direction opposite to the
direction in which it is moving.

9. Resultant force isthe net force
acting on an object due to multiple
forces.

10. Wallerian degeneration is an active
process of degeneration that
results when a nerve fiber is cut or
crushed and the part of the axon
distal to the injury (which in most
cases is farther from the neuron's
cell body) degenerates.

11. CEREBRAL CONCUSSION
•BRIEF LOSS OF CONSCIOUSNESS
FOLLOWED BY PROMPT RECOVERY
AND WITHOUT ANY LOCALISING
NEUROLOGIC SIGNS.
•PERIOD OF AMNESIA IS THE STRIKING
FEATURE.
•POST-CONCUSSION SYNDROME?

12. Persistent post-concussive
symptoms —also called post-
concussionsyndrome —occurs when
symptoms of a mild traumatic brain
injury last longer than expected after
an injury. These symptoms may
include headaches, dizziness, and
problems with concentration and
memory. They can last weeks to
months.

13. C.CONTUSION-LACERATION
•CONTUSION SEEN AS SMALL AREAS OF
HAEMORRHAGES OR MINOR BRUISE IN
THE CEREBRAL PARENCHYMA
•BBB DEFICITS AND CEREBRAL EDEMA
MAY ACCOMPANY THIS.
•LACERATION DUE TO RAPID MOVT.
AND SHEARING OF BRAIN TISSUE.
•PIA AND ARACHNOID MAY BE TORN

14. •The blood–brain barrier (BBB) protects
neurons from factors present in the systemic
circulation and maintains the highly regulated
brain internal milieu, which is required for
proper synaptic and neuronal functioning
•BBB breakdown facilitates entry into the brain
of neurotoxic blood-derived products, cells and
pathogens and is associated with inflammatory
and immune responses, which can initiate
multiple neurodegenerative pathways

15. SECONDARY BRAIN INJURY
•PROGRESSIVE BRAIN DAMAGE
EVOLVING AS A RESULT OF PRIMARY
ONE.
•CLASSIFIED INTO
1.INTRACRANIAL HAEMATOMA
2.CEREBRAL SWELLING
3.CEREBRAL HERNIATION
4.CEREBRAL ISCHAEMIA
5.INFECTIONS AND OTHERS

16. INTRACRANIAL HAEMATOMAS
•CLASSIFIED INTO
1.EXTRADURAL
2.SUBDURAL
3.SUBARACHNOID
4.INTRACEREBRAL

17. EXTRADURAL HAEMATOMA
•DUE TO LACERATION OR RUPTURE OF
MIDDLE MENINGEAL ARTERY.
•LUCID INTERVAL IS THE NOTABLE
FEATURE

20. SUBDURAL HAEMATOMA
•MOST COMMON INTRACRANIAL MASS
LESIONS ARISING FROM HEAD
TRAUMA.
•CLASSIFIED INTO
1.ACUTE
2.SUBACUTE
3.CHRONIC

21. ACUTE SUBDURAL HAEMATOMA
•LESS THAN THREE DAYS
•TORN-BRIDGING VEINS OR FOCAL
TEARS OF CORTICAL ARTERIES ARE
THE USUAL CAUSES
•BLOOD FOLLOWS SUBDURAL SPACE
OVER THE BRAIN CONVEXITY
•BURST TEMPORAL LOBE?

23. CHRONIC SUBDURAL
HAEMATOMA
•MORE THAN 21 DAYS
•MOST COMMON IN INFANTS AND
ADULTS OVER 60 YRS OF AGE
•MANIFESTED AS PROGRESSIVE
NEUROLOGICAL DEFICITS MORE THAN
3WKS AFTER THE TRAUMA

24. SUBARACHNOID HAEMORRHAGE
•TRAUMATIC ONES ARE
DIFFUSE,USUALLY CONTINUOUS OVER
THE FRONTAL LOBES AND THE TIPS OF
TEMPORAL LOBE
•TRAUMATIC LESIONS ARE USUALLY
ASSOCIATED WITH SUBDURAL H’GE OR
BRAIN LACERATION

25. INTRACEREBRAL HAEMATOMAS
•TRAUMATIC CONTUSIONS ARE JOINED
INTO CONTUSIONAL HAEMATOMA
•DISRUPTED CEREBRAL TISSUE
RELEASES THROMBOPLASTIN WHICH
FURTHER POTENTIATES H’GE
•SWIRL SIGN??

27. CEREBRAL SWELLING
•EITHER FOCALLY OR DIFFUSELY
THROUGH OUT CEREBRUM OR
CEREBELLUM
•USUAL PATHOLOGY IS THE LOSS OF
VASOMOTOR TONE
•CEREBRAL CONTUSION AND
PETECHIAL H’GES ALSO CONTRIBUTE
TO BRAIN SWELLING

29. CEREBRAL ISCHAEMIA
•COMMON AFTER SEVERE HEAD
TRAUMA
•USUALLY CAUSED BY HYPOXIA
,IMPAIRED CEREBRAL PERFUSION OR
BOTH

30. CEREBRAL HERNIATION
•TYPES ARE
1.TRANSTENTORIAL
2.FORAMEN MAGNUM
3.SUBFALCINE
•KERNOHAN’S NOTCH PHENOMENON??
•DURET HAEMORRHAGES??

32. INFECTIONS,SEIZURES
&HYDROCEPHALUS
•PENETRATING SKULL
TRAUMA,DEPRESSED SKULL FRACTURES
&BASE OF SKULL FRACTURES ALL
PROVIDE PORTALS FOR CNS INFECTION
•OBSTRUCTION TO CSF OUTFLOW DUE TO
INTERVENTRICULAR BLOOD OR POST
TRAUMATIC COMMUNICATING
HYDROCEPHALUS
•SEIZURES INCREASES ICT;INCREASED
CHANCE FOR BRAIN INJURY

35. GRADING OF BRAIN INJURIES
•GRADE 1-ALERT &ORIENTED WITHOUT
NEUROLOGICAL DEFICIT
•GRADE 2--IMPAIRED CONSCIOUSNESS BUT
UNABLE TO FOLLOW ATLEAST A SIMPLE
COMMAND OR ALERT WITH A FOCAL
NEUROLOGICAL DEFICIT
•GRADE 3-UNABLE TO FOLLOW EVEN A SINGLE
COMMAND B’COZ OF IMPAIRED
CONSCIOUSNESS
•GRADE 4-NO EVIDENCE OF BRAIN
FUNCTION[BRAIN DEAD]

36. COMPLICATIONS OF HEAD
INJURY
PRIMARY-CONCUSSION,BONE
FRAGMENTATION,BRAINSTEM
CONTUSIONS,CORTICAL
LACERATIONS &DIFFUSE
AXONAL INJURY
SECONDARY-INTRACRANIAL
HAEMATOMAS,CEREBRAL
EDEMA,HYPOXAEMIA,ISCHAEMIA,
INFECTION,EPILEPSY,METABOLIC
OR ENDOCRINE DISTURBANCES

37. MANAGEMENT
•THE KEY ASPECTS IN MANAGEMENT ARE
1.ABCDERULES OF TRAUMA
MANAGEMENT [ATLS]
2.ACCURATE CLINICAL
ASSESSMENT
3.IDENTIFY THE PATHOLOGICAL
PROCESS INVOLVED
4.RADIOLOGICAL ASSESSMENT [X-
RAY SKULL,CT SCAN ,MRI]
5.OTHER NEWER OPTIONS

38. SUMMARY OF MANAGEMENT
NO CONCUSSION
CONCUSSION
NEUROLOGIC EXAM. & X-RAY NEUROLOGIC EXAM. & X-RAY
NORMAL ABNORMAL ABNORMAL NORMAL
SEND HOME
OBSERVE FOR 24hrs
SEND HOME IF NORMAL
ADMIT TO NMCH
Patient withCLOSED HEAD INJURY

39. POST ADMISSION
After Admission
CT or MRI BRAIN SCAN
NORMAL BLOOD CLOT
OBSERVE FOR 24 hrs
SUBDURAL OR
EPIDURAL CLOT
INTRACEREBRAL CLOT
CLOT LARGE OR
NEUROLOGIC SIGNS PRESENT
SURGICAL EVACUATION
CONSULT NS
Sx INDICATED AT TIMES

41. NON-ACCIDENTAL HEAD
INJURIES
•INFANTILE CHRONIC SUBDURAL
HAEMATOMA OR EFFUSION
•BIRTH TRAUMA IS A FREQUENT CAUSE
•FUNDOSCOPY,CT,MRI

42. MISSILE INJURIES
•CAUSES CEREBRAL DAMAGE BY,
1.MECHANICAL LACERATION OF
BRAIN TISSUE
2.SHOCK WAVE PROMULGATED
AHEAD OF THE MISSILE
3.CAVITATION IN THE WAKE OF
MISSILE
•HIGH VELOCITYINJURY,TRANSVENTRICULAR
WOUNDS & A LOW GLASGOW COMA SCALE
ARE ASSO. WITH FATAL OUTCOME

43. DELAYED EFFECTS OF HEAD
INJURY
•POST-TRAUMATIC EPILEPSY
•CEREBRO SPINAL FLUID FISTULA
•POST-CONCUSSIONAL SYMPTOMS
•CUMULATIVE BRAIN DAMAGE
•NEUROLOGICAL
&NEUROPSYCHOLOGICAL DEFICITS
•NEUROENDOCRINE &METABOLIC
DISTURBANCES

44. NEUROSURGICAL CASE
A 19 yr OLD BOY HAVING THE HISTORY OF FALL FROM
A BIKE ,HITTING THE RIGHT SIDE OF HIS HEAD
FORCEFULLY ON THE ROAD IS BROUGHT TO THE
CASUALTY .ON EXAMINATION HIS PULSE:40/MIN,
B.P :170/110mmHg
ON FUNDOSCOPIC EXAMINATION HE HAS VENOUS
DISTENSION AND ABSENT PULSATIONS OF THE
RETINAL VASCULATURE.ALSO ON SYSTEMIC
EXAMINATION HIS LIMBS ON THE LEFT SIDE ARE
MORE FLACCID THAN THE RIGHT SIDE.
-WHAT MAY BE THE LIKELY DIAGNOSIS?

45. NEUROSURGICAL CASE
+VE FINDINGS
A 19 yr OLD BOY HAVING THE HISTORY OF FALL FROM
A BIKE ,HITTING THE RIGHT SIDE OF HIS HEAD
FORCEFULLY ON THE ROAD IS BROUGHT TO THE
CASUALTY .ON EXAMINATION HIS PULSE:40/MIN,
B.P :170/110mmHg
ON FUNDOSCOPIC EXAMINATION HE HAS VENOUS
DISTENSION AND ABSENT PULSATIONS OF THE
RETINAL VASCULATURE.ALSO ON SYSTEMIC
EXAMINATION HIS LIMBS ON THELEFT SIDE ARE
MORE FLACCIDTHAN THE RIGHT SIDE.
-WHAT MAY BE THE LIKELY DIAGNOSIS?

47. PATHOPHYSIOLOGY

50. NO HEAD INJURY IS TOO SEVERE
TO DESPAIR OF,NOR TOO
TRIVIAL TO IGNORE
-HIPPOCRATES
PRESENTATION:VINAYAK NARAYAN
EFFECTS:NISHANTH

51. Thank You…
Forever Yours
Vinayak
Narayan.