Head Injury

DR. GAJANAN PANDIT

D. ORTHO; DNB ORTHO

DEEPAK HOSPITAL JALNA

Demographics

• Account for >50 % all trauma hospitalizations• 80% of trauma related deaths in Deepak

Hospital Jalna• Domestic falls, RTA’s, recreational injuries and

Assaults account for majority of them.

Pathophysiology of Brain Injury

Primary Brain Injury

Cerebral Contusion

Most common Focal brain Injury

Sites Impact site/ under skull #

Anteroinferior frontal

Anterior Temporal

Occipital Regions

Petechial 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

1.CORPUS CALLOSUM

2.PERIVENTRICULAR WHITE MATTER

3.BASAL GANGLIA

4.BRAIN STEM

Secondary Brain InjuryBiochemical Cascade Blood Flow

changes(Global/regional)External Compression

AA/Neurotransmitter release

Uncoupling of Substrate delivery and extraction

IntraparenchymalExtraxial (subdural/epidural)

Intracellular Ca++ accumulation and cytoskeletal/ enzymatic breakdown

PneumocephalusDepressed skull fracture

Extracellular Cytokines and GF

Generation of free radicals

CMRoxyCMRglucose

CBF OEF/GEF

Initial Stabilization

• Initial assessment and resuscitative efforts proceed concurrently.

Few things to watch for,1.Airway2.Cervical spine injury3.Hypotension4.Hypothermia5.Neurogenic Hypertension

Cervical Spine X-ray: Lateral view. 1, Vertebral body (TH1). 2, Spinous process of C7. 3, Lamina. 4, Inferior articular process. 5, Superior articular process. 6,Spinous process of C2. 7, Odontoid process. 8, Anterior arch of C1 (Atlas). 9,Trachea.

Neurological Assessment

• Rapid Trauma Neurological Examination1. Level Of Consciousness2. Pupils3. Eom4. Fundi5. Extremity Movement6. Response To Pain7. Deep Tendon Reflexes8. Plantar Responses9. 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

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

Eye Movements

• SO4,LR6, All3Injury location Abnormality

Cavernous sinus/Sup Orbital fissure All 3 Cr.N’s ( 3,4,6) are affected + V1 division

Transtentorial ( Uncal ) herniation 3 Cr.N

Raised ICP ( false localizing sign) Isolated Abducens(6) palsy

Frontal eyes field ( brodman’s area 8) Ipsilateral tonic conjugate deviation

Seizure involving frontal eyes field Conjugate deviation to contralateral side

Occipital lobe injury ( unilateral) Hemianopsia + ipsilateral conjugate gaze preference

Brainstem Reflexes

Facial palsy unilateral 7 N injury- Basilar skull #

Corneal reflex ( V1+V2) Rostral Pontine function

Dolls eye maneuver Vestibuloocular function

Ice water caloric test ( never in awake child)

COWS normal responseComa – same side deviationStuporous/obtunded – nystagmus to contralateral rapid component

Gag and cough reflex 9,10th N + brainstem swallowing centers

Periodic( Cheyne-stokes) b/l hemispheric/diencephalic injury to as caudal as upper pons

Apneustic ( prolonged ispiratory plateau) Mid- caudal pons injury

Ataxic breathing( irregular stuttering resp)

Medullary respiratory generator center.

Deep tendon and superficial reflexes

• DTR’s exaggerated after TBI due to cortical disinhibition

• Decreased / absent after Spinal cord injury• Asymmetric DTR’s unilateral brain/spine injury• Superficial lost/decreased in corticospinal

dysfunction and helpful in localizing lesions• Plantar response

Normal reflex Intact descending corticospinal inhibition

Positive Babinski Interrupted inhibition pathways

Neurodiagnostic Evaluation Skull Radiograph Controversial usage, costs> benefits

CT Contiguous slices from vertex to foramen Magnum.Extend to C3 if upper spine # suspectedBrain, Blood and Bone windowsMay miss # that run parallel to CT slice and located at vertex.

Indications controversial, a must in1.Penetrating head trauma2.basilar/ depressed skull #3.Posttraumatic seizure4.Severe head injuryIn addition anyone with,1.Altered level of consiousness2.Focal deficits3.Persistent headaches/ repeated emesis

MRI Better than CT in subacute and chronic phases of injury to detect contusions/shearing in white matter/c.callosumInvaluable in spinal cord injury

Cerebral angiography Carotid/vertebrobasilar dissections/occlusionsPesudoaneurysms

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 laceration– Simple Linear/ Stellate ED Rx– Extensive, Degloving/Avulsion Repair GA– Overlying 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 1. Open 2. Closed3. Linear (3/4) 4. Comminuted ( multiple branches)5. Diastatic ( edges split apart)<3yrleptomeningeal

cyst, cephalomalacia,6. Depressed7. Basilar

Depressed Skull #

• From focal blow• Closed 10% FND/15% seizures Rx, for

cosmetic reasons• < skull thickness- no elevation• Open/ frontal sinus intracranial wall

elevate and Sx + frontal sinus irrigation• Free floating – remove/replace wrt size and

after soaking in abx

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 wrt size, location, rate of accumulation– Lucid interval (33%), non specific– Confusion, lethargy, agitation, focal neurological

deficits.

Diagnosis

• CT is diagnostic • Initial Ct Hyperdense Lentiform collection

beneath skull• Actively bleeding- Mixed densities• Severe anemia- isodense/hypodense• Untreated EDH imaging over days

Hyperdense Isodense Hypodense w.r.t. brain

TreatmentNon 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. • Cause high velocity impact/ assault/ child

abuse/ fall from significant height.• Associated with cerebral contusions + DAI• Source cortical bridging veins/ Dural

venous sinuses.Adults Child/infants

Cerebral convexities over frontal/ temporal regions

Occipital + Parietal cortexParafalcine ( post falx cerebri), supratentorial { abuse}

50% are unconscious immediately.

Focal deficits common

Hemiparesis – 50%

Pupillary abnormality- 28-78%

Seizures – 6-22%

Rx- larger- urgent removal

Small -

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 brain

Cant cross falx cerebri/ tentorium cerebelli { compartmentalized}

Can cross beneath suture lines

Distorstion 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 cistern

• Delayed 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, thalamus

Transtentorial 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 abuse

Rx Surgical.

Entry wound debrided and FB removed with in driven bone fragments.

Peri and post op ABX

Prophylactic anticonvulsants

Adolescents and children Gun Shot Wounds. ( 12%) and increasing annually.

Higher mortality when

1.Low GCS on presentation (3-4)

2.B/L hemispheric /brainstem injury/ intraventricular tracking

3.Hemodynamic instability/ apnea/both

4.Uncontrolled ICP.

Intracranial Hypertension

• Pathophysiology– ICP monitoring & control are cornerstones of

management– Normal ICP

• Adults <10mmhg• Children 3-7mmhg• Infants 1.5- 6mmhg

– When to treat?• Adults > 20• Children >15• Infants >10 { Arbitrary numbers most commonly used,

pending outcome studies}

ICP measurementIntraventricular Cath coupled to ICP transducer is Gold standard.

Which patients need ICP monitoring??

1.TBI + abnormal CT scan who are not following commands ( 50-63%)

2.Comatose + Normal CT had lower risk ( 13%) unless associated with

1. Older age

2. Systemic Hypotension , <90mmhg

3. Motor posturing, with these risk is upto 60%

3.Most clinicians use abnormal CT scan result + low GCS scores ( < 8) as candidates for ICP monitoring

Device / method Risk / benefit

1. Intraventricular catheter Adv- drainage of CSF to reduce ICPDisAdv- infection/ ventricular compression leads to inaccuracy

2. subdural/ subarachnoid bolts( Philadelphia, Leeds, Richmond bolts)

Occlusion of port in device leads to inaccuracy

3. Fiberoptic cath ( Camino labs) Improved fidelity & longevityCan be placed Intraparenchymal/ intraventricular/ subduralUsed to drain CSFAccuracy maintained even with fully collapsed ventriclesSingle cath can be used as long as needed

Non invasive ICP measurement Ultrasonographic tech Pediatr Crit Care Med 2010 Vol. 11, No. 5

Audiological tech- displacement of TM and perilymphatic pressure as a correlate of ICP

Infrared light- thickness of CSF from reflected light as a correlate of ICP

Arterial BP wave contours and blood flow velocity – mathematical model

Changes In optical nerve head with optical coherent tomography

IOP as correlate of ICP With ICP cutoff of 20mmhg it has Specificity of 0.7 and sensitivity of 0.97

Mangement of ICP

• Goal to maintain CPP by – Reducing ICP, and/or– Increasing 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 CBFless volume reduction in ICP.

• Systemic Hypo ? Vice versa

Increasing CPP by reducing ICPSedation 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 changesfall 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 ICPHyperventilation Rapid & effective response.

Red Paco2/incr pH vasoconstricton Red CBF

Disadvantages 1.paco2 < 30 torr red CBF to ischemic level2.Regional variation in autoreg hyperventilation induced reverse vascular steal

Current recommendations1. routine hypervent ( 35 ) not be used in first 24 hrs2.Chronic hypervent be avoided in absence of documented ICP rise3.Reserved for deterioration not responding to other measures.4.When needed with caution, PaCo2 never <30 torr. 5.svJo2 can be used as indicator of extreme ischemia( CBF fall) 6.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 gradient• Intermittent for 1-5 min when needed.

DiureticsMannitol – 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 1. Repeated dose reduced osmotic

gradient 2. Hyperosmolar state ( serum osm>320

mOsm) renal failure, rhabdomyolysis, hemolysis

• Steroids – No role currently in Head Injury • Barbiturates- usually last resort med.

Pros Cons

Reduce ICP , CBF, CMRO2Inhibit free lipid peroxidation reduce cellular damage

Close ICU monitoringHypotensionHyponatremiaMyocardial depression

ALGORITH for treatment of elevated ICP with severe head injury.

Thank You