Nuro

HEAD INJEURYTROMATIC BRIAN INJEURY

DR.MOHAMMED A. YOUNUS E.M specialist

Demographics

Account for 75% all pediatric trauma hospitalizations80% of trauma related deaths in childrenDomestic falls, MVA’s, recreational injuries and child abuse account for majority of them.Gang and drug related assaults are on a rise.Firearm injuries to brain account for 12% pediatric deaths.

Pathophysiology of Brain Injury

Primary Brain Injury

Cerebral Contusion

Most common Focal brain InjurySites  Impact site/ under skull #Anteroinferior frontalAnterior TemporalOccipital RegionsPetechial hemorrahges  coalesce  Intracerebral Hematomas later on.

DAI

Hallmark of severe traumatic Brain Injury Differential Movement of Adjacent regions of Brain during acceleration and Deceleration. DAI is major cause of prolonged COMA after TBI, probably due to disruption of Ascending Reticular connections to Cortex. Angular forces > Oblique/ Sagital Forces

The shorn Axons retract and are evident histologically as RETRACTION BALLS. Located predominantly in CORPUS CALLOSUM PERIVENTRICULAR WHITE MATTER BASAL GANGLIA BRAIN STEM

Secondary Brain Injury

Biochemical Cascade
Blood Flow changes(Global/regional)
External Compression
AA/Neurotransmitter release
Uncoupling of Substrate delivery and extraction
Intraparenchymal Extraxial (subdural/epidural)
Intracellular Ca++ accumulation and cytoskeletal/ enzymatic breakdown

Pneumocephalus Depressed skull fracture

Extracellular Cytokines and GF
Generation of free radicals

AUTO REGULATION CPP;MAP ICP

Initial Stabilization
Initial assessment and resuscitative efforts proceed concurrently. Few things to watch for, Airway Cervical spine injury Hypotension Hypothermia Neurogenic Hypertension

Neurological Assessment

Rapid Trauma Neurological Examination Level Of Consciousness Pupils Eom Fundi Extremity Movement Response To Pain Deep Tendon Reflexes Plantar Responses Brainstem Reflexes

Level Of Consciousness

Glasgow Coma Scale
Eye Opening
Best Verbal
Best Motor
Spontaneous 4
Oriented 5
Obeys Command 6
To Voice 3
Confused 4
Localizes 5
To Pain 2
Inappropriate 3
Withdraws 4
None 1
Incomprehensible 2
Flexion 3
None 1
Extension 2
None 1

Children's Coma Scale

Ocular response
Verbal response
Motor response
Opens eyes spontaneously 4
Smiles, orientated to sounds, follows objects, interacts. 5
Infant moves spontaneously or purposefully 6
EOMI, reactive pupils ( opens eyes to speech) 3
Cries but consolable, inappropriate interaction 4
Infant withdraws from touch 5
EOM impaired, fixed pupils (opens eyes to painful stimuli) 2
Inconsistently inconsolable, moaning 3
Infant withdraws from pain 4
EOM paralyzed, fixed pupils( doesn’t open eyes) 1 Inconsolable, agitated 2
Abnormal flexion to pain for an infant (decorticate response) 3
No verbal response 1
Extension to pain (decerebrate response) 2
No motor response 1



Pupillary Exam

Pupillary size is balance b/n Sympath and parasympathetic influences. Size, shape and reactivity to light are tested parameters.
Mydriasis
Miosis
3 Cr.N. damage- Mydriasis
Carotid A. injury in neck or skull base
Unilateral mydriasis – Transtentorial ( Uncal) Herniation Horner’s syndrome- Miosis with Ipsilateral ptosis and anhydrosis. Traumatic iridoplegia
Hypothalamic, cervicothoracic or direct orbital injury.
Seizure/ postictal state
Atropine / Sympathomimetics

Neurodiagnostic Evaluation

Skull Radiograph
Controversial usage, costs> benefits
CT Contiguous slices from vertex to foramen Magnum. Extend to C3 if upper spine # suspected Brain, Blood and Bone windows May miss # that run parallel to CT slice and located at vertex.
Indications controversial, a must in Penetrating head trauma basilar/ depressed skull # Posttraumatic seizure Severe head injury In addition anyone with, Altered level of consiousness Focal deficits Persistent headaches/ repeated emesis
MRI
Better than CT in subacute and chronic phases of injury to detect contusions/shearing in white matter/c.callosum Invaluable in spinal cord injury
Cerebral angiography
Carotid/vertebrobasilar dissections/occlusions Pesudoaneurysms


Clinical Features In Head Trauma
Scalp Injuries Skull Fractures Depressed Skull Fractures Basilar Skull Fractures Vascular Injuries Penetrating Head Injury Intracranial Hemorrhage Epidural Hematoma Subdural Hematoma Subarachnoid Hemorrhage Intracerebral Hemorrhage

Scalp Injuries

Most are lacerationSimple Linear/ Stellate  ED RxExtensive, Degloving/Avulsion  Repair GAOverlying Depressed Skull#, Infections  Repair+ Elevation Of #Hematomas
Subgaleal
Cephalohematomas
Galeal Apo & Periost
Periost & Skull
Cross Suture Lines
Limited By S.Lines

Hypotension & Anemia(bp,hct)

Calcify And Disfiguring Sx

Skull Fractures

Thin skull #’s common place.Risk of # associated intracranial injuries?CT to R/o Open ClosedLinear (3/4) Comminuted ( multiple branches)DepressedBasilar

Basilar Skull #

Epidural Hematomas (EDH)

Peak incidence in 2nd decade Source  meningeal vessel, Dural venous sinus, diploic vein from skull #H/o minor head injury Viz fall C/f  size, location, rate of accumulationLucid interval (33%), non specificConfusion, lethargy, agitation, focal neurological deficits.

Diagnosis

CT is diagnostic Initial Ct Hyperdense Lentiform collection beneath skullActively bleeding- Untreated EDH imaging

Treatment

Non surgical
Surgical
Minimal / no symptoms
Should be located outside of Temporal or Post fossae
Should be < 40 ml in volume
Should not be associated with intradural lesions
Should be discovered 6 or more hours after the injury

Subdural Hematoma

Common in infants. And eldarlyCause  high velocity impact/ assault/ child abuse/ fall from significant height.Associated with cerebral contusions + DAISource  cortical bridging veins/ Dural venous sinuses. Adults
Child/infants
Cerebral convexities over frontal/ temporal regions
Occipital + Parietal cortex Parafalcine ( post falx cerebri), supratentorial { abuse}



50% are unconscious immediately.Focal deficits commonHemiparesis – 50%Pupillary abnormality- 28-78%Seizures – 6-22%Rx- larger- urgent removalSmall - Small with mass effect/ significant change in conscious/ focal deficits
Removed
Small with significant brain injuries + mass effect out of proportion to size of clot
Non operative approach


SDH’s are High density collections on CT conforming to convex surface of brainCant cross falx cerebri/ tentorium cerebelli { compartmentalized}Can cross beneath suture linesDistorstion of cortical surface/ effacement of ipsilateral ventricle/ shift of midline often noted.

SAH

Trauma is leading cause.Acute from disruption of perforating vessels around circle of Willis in basal cisternDelayed from ruptured pseudo aneurysm. Rx maintain intravascular vol to prevent ischemia from vasospasm. Mortality 39% { national traumatic coma databank}

Intracerebral Bleed

CT- hyperdense/mixed MRI- small petechial bleed+ DAI Rx- small- non operative. Resolve in 2-3 weeks Large- Sx drainage. Repeat CT in small bleeds after 12-24 hr is warranted to r/o coalescence to form large hematoma.
Rare in Peds.60% from small contusions coalesce to form larger hematoma.Rarely , violent angular acceleration bleed in deep white matter, basal ganglia, thalamusTranstentorial Herniation  midbrain bleed ( Duret hemorrhages) Common sitesAnt Temporal and Inf Frontal lobes { impact against lateral sphenoid bone/ floor of ant fossa}

Penetrating Head Injury

CT- localizes bullet and bone fragments MRI- non advised till magnetic properties of bullet known. Rx. Surgical Debridement of entry and exit wounds Remove accessible bullet and bone Control hemorrhage Repair Dural lacerations + closure of wounds. NO ATTEMPT TO REMOVE BULLET OR BONE BEYOND ENTRY AND EXIT WOUNDS.
Infants and children fall on sharp objects with thin skull and open foraminae could predispose for these injuries. R/o child abuseRx Surgical. Entry wound debrided and FB removed with in driven bone fragments.Peri and post op ABXProphylactic anticonvulsantsAdolescents and children  Gun Shot Wounds. ( 12%) and increasing annually.Higher mortality when Low GCS on presentation (3-4)B/L hemispheric /brainstem injury/ intraventricular trackingHemodynamic instability/ apnea/bothUncontrolled ICP.

Mangement of ICP

Goal  to maintain CPP by Reducing ICP, and/orIncreasing MAP { hyper/normo volumia preffered as opposed old school Hypovol}Brief periods of hypotension can double the mortality ratesCPP should be match with cerebral metabolic demand to avoid hypoperfusion / hypeeperfusion.Cerebral OEF is helpful as,Decrease in CBF increase OEF increase AvDo2 fractionAvDo2= diff b/n O2 content of Arterial – jugular mixed venous blood.Considering Ao2 as constant, venous O2 alone can solely be assessed.Normal svJo2 is 65%, a drop to 50-55%  global cerebral ischemia


Hyperdynamic therapy
To maintain CPP of about >70, by increasing MAP{ CPP= MAP-ICP}IVF- crystalloid/colloid PRBC if low HCT(<30%)Pressors as needed ( Dopa, Dobu,Phenylephri)if autoregulation is intact? incres CPP vasoconstriction constant CBFless volume reduction in ICP. Systemic Hypo ? Vice versa

Increasing CPP by reducing ICP

Sedation and pain control
Fentanyl/ midazolam drip Etomidate in initial phase
Quiet envir + min extern stimuli
Pharmacological paralysis if needed
Increase in Pneumonia+ sepsis
IV/ ET lidocaine ( ET > IV)
During intubation, before ET suctioning,ET manipulation
Elevation of head end by 20-30deg
Red venous press ICPCan cause orthostatic changesfall CPP rebound ICP rise Excessive PEEP, tight cervical collar, neck flexion/ rotation
Can rise ICP
Bladder distention  rise Contin drainage
Occult seizures unexplained rise Prophylactic Anticonvulsants
Fever  rise Rx + hypothermia.

Specific measures to reduce ICP

Hyperventilation
Rapid & effective response.Red Paco2/incr pH vasoconstricton Red CBF Disadvantages paco2 < 30 torr red CBF to ischemic levelRegional variation in autoreg  hyperventilation induced reverse vascular steal Current recommendations routine hypervent ( 35 ) not be used in first 24 hrs Chronic hypervent be avoided in absence of documented ICP rise Reserved for deterioration not responding to other measures. When needed with caution, PaCo2 never <30 torr. svJo2 can be used as indicator of extreme ischemia( CBF fall) If used, withdrawn slowly to avoid rebound rise


CSF drainage- effective and safe.Provides gradient for bulk flow of edema fluid from parenchyma of brain to ventricles.Continous – 5-10 torr gradientIntermittent for 1-5 min when needed.

Diuretics

Mannitol – works as osmotic diuretic  extract extra and intra cellular edema fluid from brain Disadv- may preferentially affect normal areas ( intact BBB) vs affected zones ( disrupted BBB)
Additional mech reduces blood viscocity ( by hemodilution) and improves Rheology Increas CBF vasocons decreas volume red ICP. 3 dosing methods intermittant boluses when ICP 15-20 Intermittant Q6 hrly Continous infusion
Risks Repeated dose reduced osmotic gradient Hyperosmolar state ( serum osm>320 mOsm) renal failure, rhabdomyolysis, hemolysis

Steroids – No role currently in TBI Barbiturates- usually last resort med. Pros

Cons
Reduce ICP , CBF, CMRO2Inhibit free lipid peroxidation reduce cellular damage Close ICU monitoring Hypotension Hyponatremia Myocardial depression

POST TRAUMATIC SEIZURES

Complicate 10% pediatric head injuriesImpact seizures  follow minor injury , occur on impactEarly posttraumatic seizures within min to hours of injury. No radiological intracranial injury noted in many casesDo not portend later epilepsy Most do not need RxOutcome good.Late seizure  >24 hrs after injuryVisible intracranial injury.Penetrating injuries/ depressed #/ SDH/ Lower GCS scoreLong term risk of epilespy high- need Rx for 6-12 mo. Seizure prophylaxis Only during first week Or till intracranial hypertension phase is passed. Prolonged usage has cognitive deficits on long term follow ups. Phenytoin commonly used

Thank You