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DR: MUNIR SUWALEM

Traumatic brain injury

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review of traumatic brain injery

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Page 1: Traumatic brain injury

DR: MUNIR SUWALEM

Page 2: Traumatic brain injury

TBI is caused by a bump, blow or jolt to the head or a penetrating head injury that disrupts the normal

function of the brain.

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There are approximately 1.5 million people in the U.S. who suffer from a traumatic brain injury each year.  50,000 people die from TBI each year and 85,000 people suffer long term disabilities. 

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The top causes of TBI are: MVA Firearms or explosions falls fighting

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Mechanisms of Injury . Open Head InjuryResults from bullet wounds, etc. Largely focal damage Penetration of the skull Effects can be just as serious as closed brain injury . Closed Head InjuryResulting from a slip and fall, motor vehicle crashes,

etc. Focal damage and diffuse damage to axons Effects tend to be broad (diffuse) No penetration to the skull . Deceleration Injuries (Diffuse Axonal Injury)

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Epidural haematomaEpidural haematoma

EDH occurs in the potential space between the dura and the cranium

EDH results from interruption of dural vessels, including branches of the middle meningeal arteries(most common), veins, dural venous sinuses, and skull vessels..

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As many as 10-20% of all patients with head injuries are estimated to have EDH.

Approximately 17% of previously conscious patients and have EDH, deteriorate into coma .

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The most commonly region involved with EDH is the temporal region (70-80%) because the temporal bone is relatively thin and the middle meningeal artery is close to the inner table of the skull. The incidence of EDH in the temporal region is lower in pediatric patients because the middle meningeal artery has not yet formed

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Commonly unilateral and associated with skull fracture .

CT sign include a biconvex hyperdense elliptical collection with sharply defined edge ( mixed density suggests active bleeding )

The haematoma dose not cross suture lines except at falx which may separate it.

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Subdural haematomaSubdural haematoma

Occurs in the subdural space (potential space b/w dura and arachnoid membranes)

85% is unilateral Caused mainly by traumatic

tearing of bridging veins in the subdural space

The skull fracture +/-

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Acute SDH present within 24 hours of injury with decreased level of consciousness or decline mental status

On CT a crescent fluid collection b/w the brain and inner skull

Crosses the suture lines but not dural reflections

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The appearance of SDHs on CT varies with clot age and organization.

Hyper-acute(first hour): appear relatively iso-dense to the adjacent cortex.

Acute: appear as homogenous hyper-dense (HU more 50-60 ).

Sub-acute (3-21 days) the density droping to (30 HU) ; iso-dense.

Chronic ( more than 4 wks ): becomes hypo-dense and reach to (0 HU)

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Subarachnoid Subarachnoid hemorrhagehemorrhage

SAH refers to extravasation of blood into the space b/w the pia and arachniod membranes.

Rapidly progresses to coma. Its complications include

hydrocephalus,cerbral vasospasm leading to infarction and transtentorial herniation secondary to raised ICP.

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Non cotrast CT is sensitive within 4-5 hrs , appears as high density haemorrhage in the corticlal sulci ,basal cisterns, sylvian fissures ,superior cerebrallar cisterns and in the vintricles.

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Brain contusionBrain contusion Brain Contusions are formed in 2

ways :

Direct trauma and acceleration/deceleration injury.

Occur often at the inferior and polar surface of the frontal and temporal lobes .

Contusions develop in surface of grey matter tapering into white matter.

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Non-contrast CT usefull in the early post traumatic period , but the MR is best modality for demonstrating of edema and contusion distribution

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Diffuse axonal injuryDiffuse axonal injury

High speed injury with streching or shearing of brain tissue.

Associated with LOC 50%, and persistent vegetative state.

Mortatility 30-40% , good outcome 20-30%

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DAI typically consists of several focal white-grey matter interface lesions measuring 1-15mm ,as well as in the corpus callosum and brainstem is characteristic finding in the acute setting.

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50-80% demonstrate a normal CT scan upon presentation, and delayed CT may be helpful in demonstrating edema or spots of hemorrhages.

MRI is better to demonstrating the small petechial haemorrhage where not observed through CT scan, but the because the MR is often out of order so the CT is best.

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