Head injuries Dr.Abdulrahman AL-Shudaifat MD,

Neurosurgery Department.JUH

IntroductionEpidemic in US• 2,000,000 medically attended cases/year• 400,000 hospitalizations/year• 75,000 deaths/year• Major cause of permanent disability• Leading cause of death in 15-40 year old

age group• Changing ratio of blunt vs. penetrating

injury• Importance of prevention• Of These

– 80% mild– 10% moderate– 10% sever

• > 20% of the head injury patients suffervarying degrees of disability

Causes of head injury:• RTA• FALLS • ASSULTS • DOMESTIC ACCIDENTS • SPORTS • WORK • MISSILE INJURIES.

Anatomy• The head can be divided

into the following layers: 1) Scalp. 2) Skull. 3) Meninges. 4) Brain. 5) Cerebrospinal fluid. 6) Tentorium.

Scalp

1. S : skin2. C : connective tissue3. A: aponeurosis (galea)4. L: loose areolar tissue5. P: pericranium

Bleeding from scalp laceration can result in

major blood loss especially in children

Skull● It is composed of Cranial

vault and abase.

● The floor of the cranialcavity is divided into 3parts:

- Anterior fossa → frontallobe

- Middle fossa → temporallobe

- posterior fossa → brainstem and cerebellum

Meninges1. Dura2. Arachnoid3. pia

• Subdural space is a potetial space exist in which hemorrhage can occur• Cerebrospinal fluid circulate between thearachnoid and pia matter in the subarachnoidspace

The brainConsist of:1) Cerebrum:

• Frontal• Parietal• Temporal• occipital

2) Cerebellum.3) Brain stem:

• Midbrain• Pons• medulla

Cerebrospinal Fluid• It is produced at a rate of 20 ml / hour.

Tentorium• Divide the head into:

– Supratentorial:• Anterior fossa• Middle fossa

– Infratentorial:• Posterior fossa

PHYSIOLOGYCerebral blood flow

• Normal CBF is approximately 54ml/100 g ofbrain/min

• If CBF < 20 ml/min the EEG activity will graduallydisappear, and at CBF of 12ml/min → cell death

• In normal person the Autoregulation maintain aconstant CBF between MAP of 50 and 160 (mmHg). In head injured patient its severelydisturbed.– MAP < 50 mm Hg → CBF declines steeply– MAP > 160 mm Hg → passive dilation of the cerebral

vessels → increase in CBF

Intracranial pressure• Several pathological processes that affect the

brain can cause elevation of the intracranialpressure.

• ICP can have consequences that adversely affectbrain function and hence the patient outcome.

• So elevated ICP not only indicate the presence ofa problem but can often contribute to the problem– 10 mm Hg - normal ICP(in adult)– 20 mm Hg – abnormal– 40 mm Hg sever elevation

Cerebral Perfusion Pressure• It can be calculated by: CPP = MAP – ICP

• Perfusion pressure of less than 70 mm Hg isgenerally associated with poor outcomefollowing a head injury.

Pathophysiology of head injury

•Primary tissue injury Tissue injury due to trauma mechanism, egcontusion, tissue shearing•Secondary injury Tissue damage which builds over minutes-hours afterprimary injury Role is becoming increasingly recognized Major target for investigative research and potentialclinical intervention, SOURCES: -ischemia CPP=MAP-ICP -Excitotoxicity

PATHOLOGY• 3. BRAIN DAMAGE

• 1 ry: AT TIME OF IMPACT UNAVOIDABLE • 2 ry: ANYTIME AFTER IMPACT AVOIDABLE

PRIMARY BRAIN DAMAGE(IMPACT DAMAGE)

• CONCUSSION

• CONTUSION AND LACERATION (SITE COUP, COUNTER COUP) • DIFFUSE WHITE MATTER LESIONS

(ACC. DEC. INJ�SHEARING�LOC)

(CUMULATIVE)

SECONDARY BRAIN DAMAGE• HYPOXIA

• HYPOTENSION

• HEMATOMA • CEREBRAL SWELLING

• IMPAIRED VENOUS RETURN (KINK

, INTRATHORACIC, HEAD DOWN)• TENTORIAL, TONSILLAR HERNIATION

Classification of

head injuries

• Head injuries are classified according to:

1) Mechanism of injury. 2) severity of the injury. 3) Morphology of the injury.

1) Mechanism

• This can be :1) Blunt injury which is divided

into: - High velocity(automobile). - Low velocity (fall, assult).

• 2)Penetrating injury e.ggunshot wounds or otherpenetrating wounds.

2) Severity• This classified according to Glasgow coma

Scale into: 1) Mild (GCS score 14-15). 2) Moderate (GCS score 9-13). 3) Severe (GCS score 3-8).

Type

Stimulus

TypeofResponse

Points

Eyes

Open

SpontaneouslyToverbalcommandTop

4321

BestMotorResponse

ToverbalcommandTopainfulstim

ObeysLocalizedpainFlexion-withdra

654321

BestVerbalResponse

OrientedandconversesDisorienteda

54321

Lowest score = 3, Highest score =15

3) Morphology

SkullFracture

•Vault

•Basilar

•Linearvs.satellite•Depressed/nond

Intracraniallesions

•Focal •Diffuse

•Epidural•Subdural•Intracerebral •Mil

Management of traumatic braininjury

Prehospital care :•ABC’s (Airway, breathing, circulation).•Fluid resuscitation to reverse shock,hypotension.•Spine precautions: 5-10% of head trauma patients haveunstable spine injury.•An effective EMS and air ambulancesystem can dramatically reduce mortalityfrom head trauma.

Indications for admission:• GCS below 15.• Abnormal CT –scan.• Neurological symp.&signs.• Difficulty of assessing the patient.• Epilepsy.• Other medical conditions.• Social ?

Initial evaluation and resuscitation:

• Initial evaluation and resuscitation; Rapid neurological examination (1-3 minutes)

Assess GCS, pupil function, doll’s eyes, cough, gag, cornealreflex

• Empiric management of elevated ICP; Intubations , ventilation, sedation, mannitol, head elevation• Secondary injury survey; Examine head, ears, eyes, nasopharynx, mouth for injury, facial

fractures C-spine x-rays Evaluate for peripheral injury• STAT head CT scan ; Diagnostic procedure of choice for all patients with suspected

traumatic brain injury• Repeat neurological exam frequently.

• Immediate surgery for evacuation of hematoma,if necessary.

• Monitor ICP with implanted pressure gauge.• Medically manage cerebral edema to maintain

cerebral perfusion pressure > 70 mmHg .• Perform serial head CT scans: 20% of cerebral contusions may enlarge to

surgical hematoma.

Definitive management of traumatic braininjury:

ICP monitoring:

Specific types of head injury

1) Skull fractures• The significance of skull fracture should not be

underestimated since it takes considerableforce to fracture the skull.

• linear vault fracture increase the risk of anintracranial heamatoma by about 400 times ina conscious patient and by 20 in comatosepatient.

• Fragment depressed more than the thicknessof the skull require surgical elevation

• Open or compound skull fracture require earlysurgical repair

Basal skull fractures; • The presence of clinical

signs of basal skullfracture should increasethe index of suspicionand help in itsidentification:– Periorbital

ecchymosis (Raccoon eye)

– Retroauicularecchymosis ( Battle’ssign)

– CSF leakage– 7th nerve palsy.

Management

Scalp wounds

• They are usually tolerated well and cause fewcomplications.

• Shave the hair around the wound and clean thewound before suturing.

• Bleeding from a deep scalp wound usually canbe controlled by applying direct pressurecauterizing or ligating large vesseles.

Depressed skull fractures• Need to be elevated if the

degree of depression isgreater than the thicknessof the adjacent skull.

• Cosmosis can affect thedecision .

• Less significantdepressed fracture cansafely be managed withclosure of the overlyingscalp laceration.

2) Intracranial lesions• These lesions may be classified as focal or

diffuse , although the two forms frequentlycoexist.

• Diffuse brain injury is the most common type ofhead injury .It represent a continuum of braindamage produced by increasing amounts ofacceleration-deceleration forces

• In general they have a normal CT scan butdemonstrate altered sensorium or even deepcoma.

2) Intracranial lesions• Based on the depth and duration of coma ,

diffuse injuries may be classified as mildconcussion ,classic concussion and diffuseaxonal damage.

Mild concussion• Consciousness is preserved

but there is a noticeabledegree of temporaryneurological dysfunction .

• These injuries are commonand, because of their milddegree, often go unnoticed .

• The mildest form ofconcussion results inconfusion and disorientationwithout amnesia (loss ofmemory) .

Classic Cerebral Concussion• There is a loss of consciousness which is

transient and reversible.• This condition always is accompanied by some

degree of severity of posttraumatic amnesia.• The length of amnesia is a good measure of the

severity of the injury.• Many patients with classic cerebral concussion

have no sequale other than amnesia for theevents relating to the injury, but some patientsmay have more long-lasting neurological deficitse.g. memory difficulties and depression.

Diffuse axonal injury• Term used to define prolonged posttraumatic

coma that is not due to mass lesion or ischemicinsult

• These patients are rendered deeply comatoseand remain so for prolonged periods

• They often demonstrate evidence ofdecortication or decerbration and often remainseverely disabled , if they survive

• These patients often exhibit autonomicdysfunction such as Hypertension,Hyperhydrosis, and Hyperpyrexia.

Focal intracranial lesionsIntracranial bleeding• Venous bleeding

– Slow, insidious onset• Arterial bleeding

– Signs and symptoms will be apparent within afew hours

Epidural hematoma

• Lens shaped hematomabetween dura and skull.

• Associated with skullfracture and laceration ofdural artery (eg. middlemeningeal artery).

• Underlying brain is usuallynot injured.

Epidural hematoma.

In traumatic EDH Hematoma formsextremely fast Within 10 – 20minutes after injury.patient may present with externalevidence of head injury such asscalp laceration, cephalohematoma,or contusions. Systemic injuriesmay also be present.Most often the head injury is in thetemporal or temporoparietal region.Patient with epidural hematoma may present with the classical“lucid interval” (20-50% of cases) or“talk and die”.

• The classic Cushing triad involves systemichypertension, bradycardia, and respiratorydepression. This response will be elevated by

the evacuation of the mass

• Imaging :

1.Conservative Therapy • Outcome is directly related to the

neurological status of the patient beforesurgery.

• If a lesion is small and the patient is ingood neurological condition, observing thepatient with frequent neurologicalexaminations is reasonable.

2.Surgical management• Criteria for immediate surgical intervention is

asymptomatic EDH with: 1) Volume greater than 30 ml. 2) Thickness of 10 mm(children 5 mm). 3) A midline shift beyond 5 mm. as most patients with such an EDH experience a

worsening of the conscious state and/or exhibitlateralizing signs.

Surgical management• craniotomy

Position of emergency burr holes

Subdural hematoma

Subdural Hematoma• Much more common

than epidural• Occur most frequently

from tearing of abridging vein betweenthe cerebral cortexand a draining venoussinus

• Also can beassociated witharterial laceration onthe brain surface

Sudural hematoma

• Normally cover theentire surface of thehemisphere

• Prognosis is muchworse than epidural

Subdural hematoma• Crescent shaped hematoma lying between brain

and dura, conforming to brain surface.• Indicative of high acceleration/deceleration injury

with tearing of bridging veins or corticalarterioles.

• Usually associated with severe diffuse injury,immediate deep coma from moment of impact.

• Extreme neurosurgical emergency. • 30% mortality, 30% good outcome.

Subdural hematoma• Its classified to:

1) Acute SDH: <72hrs and appearhyperdense on CT compared to the brain

2)subacute SDH: 3- 20 days and isisodense or hypodense compared to thebain.

3) Chronic SDH: older than 20 days andare hypodense compared to the brain.

Clinically Common neurological findings include :1) Altered level of consciousness2) A dilated pupil ipsilateral to the hematoma3) Failure of the ipsilateral pupil to react to

light.4) Hemiparesis contralateral to the

hematoma

Investigations imaging:

Management

• Conservative:- Small acute SDHs less than 5 mm thick on

axial CT images, without sufficient masseffect to cause midline shift or neurologicalsigns, can be followed clinically

Management• Surgical: Surgery for acute SDH

consists of a largecraniotomy (centeredover the thickest portionof the clot) to decompressthe brain, stop any activesubdural bleeding, andevacuate anyintraparenchymalhematomas in theimmediate vicinity of theacute SDH.

Pathophysiology of chronicsubdural hematoma:

• An SDG begins as a separation in thedura-arachnoid interface, which then isfilled by cerebrospinal fluid (CSF).

• Dural border cells proliferate around thisCSF collection to produce a newmembrane.

Clinically• Usually found in older patients with

cerebral atrophy.• Minor trauma causes small, often

minimally symptomatic subduralhemorrhage. As clot liquifies over next 1-3weeks, the hemorrhage may expand into asignificant mass. Hematoma resemblesdark liquid (old motor oil ).

Clinically• Risk factors for a chronic SDH includes

chronic alcoholism, epilepsy,coagulopathy, arachnoid cysts,anticoagulant therapy (including aspirin),cardiovascular disease,andthrombocytopenia, and diabetes.

Investigation• Lab studies: • Imaging:

Management• Surgical:- Liquefied chronic SDHs commonly can be

treated with drainage through 1-2 burr holes. .- A nonliquified chronic SDH cannot be

decompressed adequately by burr holes andmust be removed by craniotomy.

Cerebral contusion / intracerebralhematoma

• Area of focal tissue injury. Neurological deficit depends onarea injured.

• Commonly occur incoupe/contra coupe pattern

eg. frontal / occipital• 20% of contusions may expand

into surgical hematoma• Observe patients in ICU, repeat

head CT scan within 24 hours.

• ICH

Thank you Early (within a week)

• Hypoxia• I.C. haematoma• Cerebral edema &

Herniation• Early epilepsy• Electrolytes disturbances• Meningitis• Pyrexia

Complications of Head Injuries:

Delayed•Hydrocephalus•Late epilepsy•Post concussionsyndrome• Chronic SDH•Meningitis

THANK YOU ALL………