traumatic brain injury lecture

8/18/2019 Traumatic Brain Injury Lecture

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TRAUMATIC BRAIN INJURY

- Blunt injury

- Penetrating injury

Mechanism of Injury

Nature of the brain makes it susceptible to acceleration and deceleration injury:

- Soft, gel-like in consistency, one part of the brain may move in relation to another.

- Surrounded by S! and vascular compartments make it floats "ithin the skull.

#t the moment of impact, there is sudden deceleration $or acceleration%, that causes

displacement and distortion of the cerebral tissue.

&njury to the brain tissue at the time of impact can be:

- !unctional loss.

- Structural injury to the neurons.

- 'emporary or permanent.

- 'he e(tent of the injury can be generalised or localised.

A) Primary Injury

) &njury to the brain tissue at the time of impact.

- Structural damage: Bruises, oedema, shearing damage to nerve cells,haemorrhage from tearing of small vessels.

- !unctional loss: *eneralised $+oss of consciousness% or localised $focal

neurological deficit%. !unctional loss can be temporary or permanent.- 'erms loosely used to describe brain injury:

o oncussion: generalised, temporary physiological paralysis results in a

transient loss of consciousness. No structural damage.o ontusion: loss of consciousness "ith bruises or oedema of the brain.

o +aceration +, intracerebral bruises and brain surface is torn.

B) Secondary Injury

) &njury caused by processes that are activated subseuent to the primary injury.

Respiraion

o &nadeuate ventilation

o ypercarbia and hypo(ia

o /enous congestion and cerebral oedema.


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Sysemic !"ood pressure and !"ood #o"ume

o Pressure and volume of systemic blood affect blood flo" to the brain.

o &n normal circumstances, cerebral auto regulatory mechanism maintain cerebral

blood flo" despite changes in systemic blood pressure.

o &n brain injury the mechanism is impaired, thus falls in systemic volume orpressure likely result in cerebral ischemia.

Inra#enous f"uid

o +o" plasma osmolality may result in intravascular fluid being dra"n into the brain

tissue and "orsens brain s"elling.o 0isturbance of the blood-brain barrier.

o !luid given must be isotonic.

o

S may cause hyponatremia.

Temperaure

o 1aise in body temperature increases tissue metabolic demand.

o 'his in turn may aggravate cellular failure or aggravate manifestation of poor

function.

Brain s$e""in%

o 'issues $including brain% reacts to insult e.g. ischemic, inflammatory or traumatic,

by s"elling due to oedema.o !luid accumulation is both e(tracellular and intracellular.

o 0isturbance in the permeability of capillary and cellular membrane.

o *eneralised throughout one or both lobes.

o auses increase in intracranial pressure.

Inracrania" haemaoma

&'radura" haemaoma

!racture of the temporal or parietal bone.

#nterior or posterior branch of the middle meningeal artery.

2ore common in children and young adults.

'ypically presents as short +, follo"ed by lucid interval and again drop in

conscious level.


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'he latter is due to gradual enlarging haematoma that causes raised &P and

supratentorial herniation.

Symptoms:

0eterioration in conscious level.

+ucid interval.

Signs:

Bruise or boggy s"elling in the temporal region.

Pupil dilatation on the side of haematoma.

emiparesis on the same side of the haematoma.

Su!dura" haemaoma

&njury to bridging vessels that travel bet"een skull and brain.

oncave or crescent shape.

'he force of injury is more severe.

Inracere!ra" haemaoma


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3(tradural aematoma


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Subdural aematoma


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Subarachnoid aematoma


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&ntracerebral aematoma

Presenaion of Inracrania" haemaoma

- +oss of consciousness

- #ltered conscious level

- #mnesia

- eadache

- /omiting "ithout nausea

- !ocal neurological deficit

- Sei4ure

- +ucid interval


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Raised Inracrania" Pressure

) #n increase in the pressure inside the skull.

Monro-Kellie hypothesis:

- 'he cranium is incompressible thus, any increase in volume of one of the cranial

constituents must be compensated by a decrease in volume of another.

Symptoms:

- eadache

- /omiting "ithout nausea

- #ltered level of consciousness

- cular palsies

Signs:

- Pupillary dilatation

- #bducens nerve palsy

- ushing5s triad: igh SBP, "idened pulse pressure, bradycardia and abnormal

breathing.

- #bnormal respiratory pattern: heyne-Stokes respiration is rapid breathing for a

period and then absent for a period, occurs because of injury to the cerebral

hemispheres or diencephalon. yperventilation can occur "hen the brainstem or

tegmentum is damaged.

Fundoscopy:

- Papilledema.

Treatment:

- #deuate o(ygenation

- yperventilation:


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- 1elease of hard collar.

- ead up position.

-

&/ 2annitol

- #nalgesia and sedation.

- 3/0.

- 0ecompressive craniectomy.

Mana%emen

() Primary sur#ey- Primary survey and provide the necessary action.

- ervical collar: #ll patients "ith head injury should be assumed to have a

simultaneous cervical spine injury until proven other"ise. 'hus cervical collar to

all, unless no neck pain, no tenderness, full 12 and no neurological deficit.- 2onitor conscious level, initial and progress every 67 minutes.

- !or *S less than 67, rule out hypoglycaemia, alcohol and drug overdose.

- &ndication for endotracheal intubation.- +ife-threatening e(tracranial injuries e.g. hypotension and hypo(ia al"ays takes

priority over intracranial injuries.- Non-life-threatening, time consuming procedures such as fracture fi(ation should

be postponed if possible.

) Secondary sur#ey- ead injury: Scalp haematoma or laceration 8 S! or blood from nose or ears 8

1accoon eyes 8 Battle sign 8 Sign of raised &P $ushing5s triad% 8 abnormal

respiratory pattern 8 Sign of herniation: pupillary dilatation.- 3(amination of other systems.

*) Ima%in%s- &ndications for skull radiograph.

- &ndications for ' scanning.

+) Specific reamen

Scalp haematoma


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Scalp laceration

Skull fracture

7% 9pon assessment, decide either discharge, observe for ; hours or transfer toneurosurgical unit.

,) Cere!ra" proecion

- #deuate o(ygenation

- yperventilation:

- 1elease of hard collar.

- ead up position.

- &/ 2annitol

- #nalgesia and sedation.

- 3/0.

- 0ecompressive craniectomy.

#ppendi( 6: Primary survey

#ir"ay pen up the air"ay: ead tilt-chin lift, empty the oral cavity, tongue

should not fall back, oropharyngeal $*uedel% tube if necessary.

Breathing +ook for chest e(pansion, percussion, auscultation. &dentify the < life-

threatening chest conditions: #ir"ay obstruction, 'ension

pneumothora(, 2assive haemothora(, pen pneumothora(, !lail chest

and ardiac tamponade.

irculation Pulse $carotid%, blood pressure, stop any bleeding, manage

haemorrhagic shock by large bore cannulae $(%, crystalloid infusion

and arrange for blood.


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0isability onscious level $#/P9 or *S%, pupil si4e and reaction. $#/P9: alert,

verbal stimuli response, painful stimuli response, unresponsive%.

3(posure omplete undress, "arm blanket, maintain privacy.

#ppendi( : *lasgo" coma scale $*S%

Moor funcion

beying commands <

+ocali4ing 7

!le(ion ;

#bnormal fle(ion =

3(tension

None 6

-er!a" response

riented 7

onfused ;

&nappropriate "ords =

&ncomprehensible

None 6

&ye openin%

Spontaneous ;

'o speech =

'o pain

None 6

*S 67 ) 2


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• Persistent headache or vomiting

• Scalp s"elling or laceration

• igh impact injury

Crieria for CT scannin%

• Skull fracture on radiograph

• !ocal neurological deficit

• Sei4ure

• Battle sign $bruising over the mastoid%

• Periorbital haematoma $raccoon or panda eye bruising%

• Subconjunctival haemorrhage "ith no posterior limit

• Blood or S! in ears or nostrils

•

0ifficult assessment in very young, very old or into(ication.

traumatic brain injury lecture

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