head injury (2)

HEAD INJURIESHEAD INJURIES

Mizan Kidanu April 03/2013

OUTLINEOUTLINE

IntroductionEpidemiology AnatomyCausesClassificationDiagnosisManagementComplication

INTRODUCTIONINTRODUCTION

A head injury head injury is any trauma that leads to injury of the scalp, skull, or brain

The injuries can range from a minor bump on the skull to severe brain injury

EPIDEMIOLOGYEPIDEMIOLOGY

Number one killer in trauma

25% of all trauma deaths

50% of all deaths from MVA

200,000 people in the world live with the

disability caused by these injuries

50% in ages b/n 15 and 35

ANATOMY ANATOMY

Anatomy of the ’’SCALP’’Skin

firmly bound to the 3rd layer by perpendicular fibers

Connective tissuecontain blood vessels of the scalp

Aponeurosis fibrous sheet, found over much of

the vertex attaches occipitalis to frontalis m

Loose connective tissueaccounts for the mobility of the scalpblood tracks freely in this layer bilateral orbital

edema following sever head injury or cranial operation

Periosteum adheres to the suture lines of the skullcollection of blood beneath this layer outlines the

affected bone cephalohematoma (children)

Anatomy of the meningesDura

endosteum and true meningeal layerforms falx, tentorium, diaphragm

Arachinoidvascular membranearachinoid granulations

Pia highly vascular dips into sulci and fissurescarries cortical vessels

CAUSES OF HEAD INJURYCAUSES OF HEAD INJURY

Road traffic accident65% of deaths following severe

head injuryFalls Injuries at work place, during

sport, or at homeAssaults

CLASSIFICATIONS OF HEAD INJURYCLASSIFICATIONS OF HEAD INJURY

1. Blunt Vs Penetrating

2. Primary Vs Secondary

3. Mild, Moderate, or Severe

PRIMARY INJURY TO SCALP PRIMARY INJURY TO SCALP

Hematoma - Usually do not require Rx

- If large aspiration when it liquefies

Wounds Abrasions - Cleaned & exposed

- Dressed - if hemorrhagic or serous

exudates

Lacerations - Cleaned & sutured( LA or GA)

- LA infiltrated into scalp

- Wound closure without tension

PRIMARY INJURY TO SKULLPRIMARY INJURY TO SKULL

Linear fractures - Do not require Rx - At temporal area tear MMAEDH

Depressed #s - Simple Vs OpenSurgery indicated in:ocompression (large plate of bone)ocosmetic areao compound/open wound: wound debridement elevate the depression suture dural laceration

Fractures of the skull base

DiagnosisoHistory - nasal bleeding,…oPhysical examinationRaccoon eyesBattle signRhinorrhea,......

Management:conservative, advise on danger Snclosure of dura - persistent CSF leak

PRIMARY BRAIN INJURY PRIMARY BRAIN INJURY

The damage caused to the brain at the moment of impact

Concussion temporary neuronal dysfunction after blunt head trauma head CT is normal, & deficits resolve over minutes to hours

Contusion/lacerationbruise of the brainbreakdown of small vessels and extravasation

of blood into the brain

Diffuse axonal injurydamage to axons throughout the brainmost frequent finding in patients who die from severe head injury

Mechanisms Mechanisms

Coup & counter-coup injuries

Common sites:-undersurface of frontal lobetip of temporal lobe

SECONDARY BRAIN INJURYSECONDARY BRAIN INJURY

Extracranial hypoxia hypotension

Intracranial hematoma brain edema raised ICP infection

DIAGNOSISDIAGNOSIS

HistoryHistory Age Loss of consciousness Cause, circumstance and mechanism of

injury Presence of headache & vomiting Seizures Anticoagulant use,….

ASSESSMENT OF NEUROLOGICAL FUNCTIONASSESSMENT OF NEUROLOGICAL FUNCTIONAND OF CONCIOUS LEVELAND OF CONCIOUS LEVEL

Glasgow Coma Score

Best Eye Response (4) No eye opening……………………………1 Eye opening to pain..…………………….2Eye opening to verbal command.……...3Eyes open spontaneously…...………….4

Best Verbal Response (5) No verbal response ………………………1Incomprehensible sounds. ……………..2Inappropriate words. …………………….3Confused …………………………………..4Orientated …………………………………5

Best Motor Response (6) No motor response.…………………..…..1Extension to pain.…………………….…..2Flexion to pain.……………………….…...3Withdrawal from pain..……………….…..4Localizing pain.……….…………….……..5Obeys Commands..……………………….6

Classification of head injuryClassification of head injury

Mild: GCS = 13-15

Moderate: GCS = 9-12

Severe: GCS = 3-8

Exclude other causes of depressed Exclude other causes of depressed conscious level (causes of coma)conscious level (causes of coma)

No focal signsdrugs (alcohol, opiate)circulatory collapsehypothermia / hyperthermiaconcussionmeningitis, encephalitissubarachinoid hemorrhage

Focal signs presentcerebral abscess ,infarction, tumorintracranial hemorrhage

InvestigationsInvestigations

Skull radiograph CXR and X-ray of cervical spinesCT-Scan - first line investigation

Indication for CT-scanIndication for CT-scan

GCS<13 at any stageGCS =13 or 14 at 2 hours following injurySuspected open or depressed #Any sign of basal skull #Post-traumatic seizuresFocal neurologic deficitPost-traumatic amnesia of >30 minutesPersistent vomitingCoagulopathy Significant mechanism of injury

GENERAL MANAGEMENT OF HEAD INJURYGENERAL MANAGEMENT OF HEAD INJURY

ABC ruleABC rulestabilization of airway, breathing and circulationIV access - maintain normovolemia

- hypotonic/glucose containing fluids

should not be usedendotracheal intubation (e.g: GCS ≤ 8, hypoxia,…)

Head end elevation - 300

Treat co-existing injurieschest drain - tension pneumothoraxcervical collar - # of cervical spine,….

AnticonvulsantsAnticonvulsants

may decrease early posttrauma seizures but

no benefit in long term epilepsy prevention

Phenytoin Loading dose = 18 - 20 mg/kg

Maintenance dose = 100 mg q 8 hrly

Regular observation at half hourly interval:

GCSBP, HR, RR, and Temperature oxygen saturationpupil size & reactivitylimb movement

EPIDURAL HEMATOMAEPIDURAL HEMATOMA

Usually from torn middle meningeal artery and/or vein

Other causes: torn dural sinuses(e.g: saggital sinus)oozing from diploe bone & stripped dura

Uncommon but serious,1- 4% of TBIHighest among adolescents and young adultsSkull fractures in 75-95%

Clinical presentationlucid interval (in 1/3 of cases) associated with

headache vomiting, drowsiness, confusion, aphasia, seizures and hemiparesis

epidural hematoma due to venous bleeding neurologic decline is slower

posterior fossa EDH - elevated ICP

Diagnostic evaluation CT scan - lens shaped collection

- hematoma volume

estimation

Management craniotomy / ?burr hole

Prognosis-mortality -10%

SUBDURAL HEMATOMASUBDURAL HEMATOMA

Pathophysiologyresult from the tearing of bridging veins crossing

the subdural space or hemorrhage from severe cerebral contusions

Spread more diffusely over the hemisphere than extradural and are often associated with diffuse swelling of the underlying hemisphere

Clinical manifestations - depends on type

ACUTE SUBDURAL HEMATOMAACUTE SUBDURAL HEMATOMA

1-2 days after onsetcoma in (56%)lucid interval (12-38%)posterior fossa SDH - signs of increased ICP

Result from: torn bridging veinscortical lacerationstorn dural sinuses

CT SCAN FEATURESclot is bright or mixed-densitycrescent-shaped (lunate)may have a less distinct borderdoes not cross the midline due to

the presence of falx

Signs of mass effect: ventricular compression, midline

shift and reduction in the size of the basal cisterns

SUBACUTE SUBDURAL HEMATOMASUBACUTE SUBDURAL HEMATOMA

After approximately 1-2 weeks the subdural collection become isodense to grey matter

detection may be challenging & recognized when: effacement of cortical sulci deviation of lateral ventricle midline shift

Contrast enhancement will often define cortical-subdural interface

CHRONIC SUBDURAL HEMATOMACHRONIC SUBDURAL HEMATOMA

after 2 weeks usually post trivial injurydue to injury of small bridging veinsheadache, cognitive impairment, apathy,

seizures and focal deficitssymptoms are transient and fluctuating proximal, painless and intermittent

paraparesis

CT featuresCT features

After 2 weeks, hypodense crescentic collections

Acute-on-chronic SDHs can further complicate the images, with hyperdense fresh haemorrhage intermixed, or layering posteriorly, within the chronic collection

Do not cross the midline

ManagementManagement

Acute SDH - Surgery for symptomatic & unstable pt Surgery

burr holecraniotomy

Nonoperative Mxclinically stableclot thickness <10mmno clinical or CT signs of herniationrepeat CT scans 6-8 hrs after initial scan

Chronic SDH

Surgery - burr hole

signs of increased ICPclot thickness >10mmcognitive impairmentmotor impairment

RAISED INTRACRANIAL PRESSURERAISED INTRACRANIAL PRESSURE

The three normal contents of the cranial vault are brain tissue (80%), blood (10%), and CSF (10%)

Normal state - ICP normal4-14 mmHg - normal>20mmHg – abnormal

The Monro-Kellie doctrine states that ’’the cranial vault is a rigid structure, and therefore, the total volume of the contents determines ICP ’’

Cerebral Perfusion Pressure (CPP) can be determined by the following formula:

CPP = MAP – ICP

Symptoms & Signs of increased ICPSymptoms & Signs of increased ICP

Diminishing level of consciousness

Headache, vomiting, seizures

Cushing’s Triad: bradycardia

hypertension

abnormal respiration

Pupillary changes

Papilledema

Effects of raised ICPEffects of raised ICP::

brain herniation1. subfalcine herniation2. uncal herniation3. central transtentorial

herniation4. tonsillar herniation

reduced cerebral perfusion

Management of raised ICPManagement of raised ICP

includes airway protection and adequate ventilation (intubation may be required)

a bolus of Mannitol 0.25-1g/kg causes: free water diuresisincreased serum osmolality and extraction

of water from the brainrequire rapid neurosurgical evaluationventriculostomy or craniotomy may be

needed for definitive decompression

COMPLICATIONS HEAD INJURYCOMPLICATIONS HEAD INJURYMeningitis & brain abscessCSF rhinorrhea and otorrheaEpilepsy - about 80% arise in 2yrsHydrocephalus- usually due to atrophied white

matterAmnesia (PTA)Postconcussional SxPosttraumatic encephalopathyCranial nerve injury - in up to 30% pts

REFERENCESREFERENCES

Mark S. Greenberg: Hand Book of Neurosurgery; 6th ed

Bailey & Love’s: Short Practice of Surgery; 24th ed, 2004

Peter J Morris: Oxford Text Book of Surgery; 2nd ed, 2002

Schwartz's: Principles of Surgery; 9th ed, 2010