Head Trauma

By Dr/waleed fawzy

Specialist Of General Surgery

Edwin Smith Papyrus

•The Edwin Smith Papyrus is the world's earliest known medical document, written in hieratic around the 17th century BCE.

• It is the ancient textbook on trauma surgery, and describes anatomical observations and the examination,

diagnosis, treatment, and prognosis of numerous injuries in exquisite detail .

•The papyrus contains the first descriptions of the cranial sutures, the meninges, the external surface of the brain ,

the cerebrospinal fluid, and the intracranial pulsations.

Introduction

• 50,000 cases of head injury/year in U.S

10 % die prior to reach hospital.• 100000 RTA /year in saudi Arabia. 4000

death/year.

• RTA costs about 2 billion dollar/year in Saudi Arabia

• One million patients attend A&E each year in UK with head injury

• 80% are minor (GCS 13-15(

• 10% are moderate (GCS 9-12)

• 10% are severe (GCS <8(

• Severe head injuries account for 50% of trauma related deaths

Pathophysiology of brain injury

• Intracranial pressure

• Normal ICP 10 mm Hg (136 mm water)• Pressure > 20 mm Hg considered abnormal.• Pressure > 40 mmHg is sever elevation

Monro-Kellie Doctrine

• The total volume of intracranial content The total volume of intracranial content must remain constant as the cranium is must remain constant as the cranium is non-expansile boxnon-expansile box

Volume-Pressure Curve

0

10

20

30

40

50

60

70

volume of Mass

ICP

(m

m H

g)

ICP

herniation

point of decompensation

Cerebral perfusion pressure

• Perfusion pressure< 70 mm Hg. Is associated with poor outcome

• Maintaining CPP is a very important priority in management of head injury patients

CPP = MAP-ICPCPP = MAP-ICP

CPP

ICPMAP

Cerebral Blood Flow

• Normal CBF 50 ml/100 gm of brain/min.

(10-15% of cardiac output).

• 20-25 ml/100gm brain/min. EEG disappears.

• 5 ml/100gm/min there is cell death.

Primary brain injury

• Damage caused at time of impact

• Can be focal or diffuse

• Diffuse axonal injury is due to deceleration and shearing forces

• Dependent on extent of initial injury

• Difficult to treat

Secondary brain injury

• Insult imposed after initial injury due to: – Hypoxemia – Hypercapnia – Systemic hypotension – Intracranial hematoma – Intracranial hypertension

• Early treatment is aimed at the prevention of secondary injury

• Autoregulation of cerebral blood flow is lost after head injury

Anatomy Of The Head

A-Scalp

• 1-skin

• 2-connective tissue

• 3-aponeurosis (galea)

• 4-loose areolar tissue

• 5-pericranium

Common injury: Subgaleal hematoma

Skull VaultSkull Vault

B-Skull

• Cranial vault (Calvarium):

Thin in the temporal region• The base: irrigular• The floor:

1. Ant.fossa frontal lobes

2. middle fossa temporal lobes

3. Post.fossa lower brain stem & cerebellum

Meninges

1. The Dura Mater tough & fibrous

Not attached to the arachnoid forming a potential space (the Subdural space)

The veins that travel from the brain surface to the SSS Called the bridging veins

These veins may tear and leads to SDH.

• At specific sites the dura splits to enclose large venous sinuses.

• The midline superior sagital sinus drains into the transverse & sigmoid sinuses.

• The sigmoid sinuses are more dominant on the rt. side,if torn can lead to massive Hge.

Meningeal Arteries• Lie between the dura & the internal surface

of the skull (The epidural Space)

• It grooves the inner surface of the skull, laceration of these arteries cause epidural Hematoma (EDH)

2. Arachnoid mater

• Bleeding in this area cause subarachnoid Hge. (usually caused by ruptured aneurysm and Head injury).

• CSF circulates between Pia and Arachnoid

3. pia mater: is firmly attached to the brain

The Brain

• Consists of:– The Cerebrum– The Cerebellum– The brainstem

Brain stem

3rd Ventricle

Cerebellum

Function of Different brain areasFunction of Different brain areas

• The Frontal lobe: emotions& motor

function• The parietal lobe: sensory function &

spatial orientation• The temporal lobe: regulates certain

memory function • The lt temporal lobe: speech in all rt handed and

most of lt handed persons.

Brain Areas

Cerebrospinal fluid

• Produced by the choroid plexus 30ml/hr• It is located in the lateral ventricle• CSF comes through foramen of Monro to the 3rd

ventricle and pass through Aqueduct of Sylvius to the 4th ventricle

• It then exit into the subarachnoid space.• It is reabsorbed into the venous circ.through the

arachnoid granulation that project into SSS.

Tentorium

• Tentorium cerebelli divides the head into: 1-supratentorial compartment comprising the anterior and middle cr.fossa 2-Infratentorial compartment containing the post.fossa.• The midbrain connects the cerebral hemisheres to

the rest of the brain stem,and it passes through a large aperture in the tentorium called the tentorial incisura

Facial n.

Falx cerebri Tentorium

Sagital section thrx the Head

Tentorium

• The Oculomotor IIIrd nerve runs along the edge of the tentorium and may become compressed against it during downward brain herniation.

• Parasympathetic fibers that are pupillary constrictors lie on the surface of the IIIrd nerve causes pupillary dilatation due to unopposed sympathetic activity,with further compression of the IIIrd nerve , full Oculomotor paralysis occur causing the eye to deviate “down and out”

• The part of the brain that usually herniates thr tentorial notch is the medial part of the temporal lobe, known as the uncus.

• Uncal Herniation causes compression of the pyramidal tract in the midbrain.

• The motor tract crosses the opposite side at the foramen magnum and compression causes contralateral hemiplegia.

• The ipsilateral pupillary dilatation + contralateral Hemiplegia is called :

classic tentorial Herniation.

The Ipsilateral pupillary dilatation + Ipsilateral Hemiplegia can occur:

Kernohan’”s Notch Syndrome

Dilated Pupil

Classification

– A-Mechanism of injury:A-Mechanism of injury:

Blunt injury: falls, automobile collisions and blunt assault.

Penetrating injury: gunshot and stab wounds

Penetrating injury from low velocity bullet

B.Severity Of Injury

• Mild GCS Score 14-15

• Moderate GCS Score 9-13

• Sever GCS Score 3-8

Assessment AreaScore

Eye opening (E)

Spontaneous

To speech

To pain

None

4

3

2

1

Best Motor Response (M)

Obeys Commands

Localizes Pain

Normal Flexion (withdrawal)

Abnormal Flexion (decorticate)

Extension (decerebrate)

None (flaccid)

6

5

4

3

2

1

Verbal Response (V)

Oriented

Confused conversation

Inappropriate Words

Incomprehensible sounds

None

5

4

3

2

1

C.Morphology Of Injury

1. Skull Fractures.

• Vault Linear vs. Stellate

Depressed/Nondepressed

Open/Closed

• Basilar with/without csf leak

with/without VII nerve palsy

• 2. Intracranial lesions

• Focal Epidural

Subdural

Intracerebral

• Diffuse Mild Concussion

Classic Concussion

Diffuse Axonal Injury

Basal Skull Fracture

Signs:Signs:

• Periorbital Ecchymosis (Raccoon Eyes)

• Retroauricular Ecchymosis (Battle’s Sign)

• CSF Leak : 1-Rhinorrhea or 2- otorrhea

• V11 Nerve Palsy

Epidural hematoma• 0.5% of all head injuries &9% of comatosed• Presents with lucid interval (talk & die)• Biconvex in shape• Most often temporal or tempoparietal• Result from tearing of middle meningeal a.• May be venous in 30% from torn venous

sinuses especially in parietoccipital or post.fossa.

Epidural Hematoma

Subdural Hematoma

• More Common occur due to tear of the bridging veins between the cerebral cortex and draining venous sinus.

• It covers the entire surface of hemisphere

• prognosis much worse than epidural one.

• Needs very rapid surgical intervention.

Subdural Hematoma

The site of hematoma

Contusions & Intracerebral Hematoma

• Pure cerebral contusions are common.

• Always seen with subdural hematoma.

• Contusions can coalesce or evolve to form an intracerebral hematoma.

• Can occur in any part of the brain including cerebellum and brainstem.

Bilateral contusion & intracerebral hematoma

Diffuse Injuries

• Mild Concussion

• Classic Cerebral Concussion

• Diffuse Axonal Injury

A. Mild Concussion

Consciousness is preserved inspite of temporary neurological dysfunction like confusion , disorientation but no loss of memory

B. Classic Cerebral Concussion

• An injury that results in a L.O.C.• Ass’ post traumatic Amnesia• Length of amnesia is a good measure of the

severity of injury. Amnesia is transient & reversible. and returns to full consciousness by 6 hours.

• Other symptoms: dizziness, nausea, anosmia and depression. this referred as a post-concussion syndrome

C. Diffuse Axonal Injury

Definition: Prolonged post-traumatic coma that is not due to mass lesion or ischemic insults.• These patients are deeply comatosed, and remain so for

prolonged periods.• Often show sign of decerebration or decortication, they

can exhibit autonomic dysfunction , such as HTN, Hyperhydrosis and hyperpyrexia.

• Distinguishing between DAI and Hypoxic Brain Injury is difficult and indeed they may coexist.

Management

Management Of Mild Head Injury

• Def.: Patient is awake & may be oriented

• History: Name, age sex ,occupation

Mech. of Injury ,Time of Injury

L.O.C Immediate post-injury

Subsequent level of consciousness

Amnesia

Headache Seizures

• General exam to exclude systemic injuries

• Limited neurological exam.

• Cervical spine x-ray

• Bl.Alcohol level, urine toxicology screen

• C.T Scan head except completely asymptomatic & neurologically normal

Criteria for admission• No CT Scan Available

• Abnormal CT

• Penetrating head injury

• H/O LOC

• Deteriorating level of Consciousness.

• Moderate to sever headache.

• Significant Alcohol intake

• Skull fracture

• CSF Leak

• Significant associated injury.

• No reliable companion

• Amnesia.

Criteria for discharge from ER

• Does not meet any of the criteria.

• Discuss with the patient to return if any problem or symptom occur.

• F/U within one week.

Management of Moderate Head Injury GCS 9-13

Initial Exam

• Same as for mild head injury plus baseline

Blood workup.

• CT Scan for head

• Admission for Observation.

After Admission• Frequent neurological Checks.• F/U Ct sacn , if condition deteriorates, or

preferably before discharge.• If the patient improves ,discharge with f/u in the

clinic.• If the patient stops following simple commands,

repeat CT scan,and manage as sever head injury

Management of Sever Head InjuryGCS 3-8

Assessment & Management:• ABCs.• 1ry Survey & Resuscitation. With critical trauma you may never get beyond the primary survey• 2ry Survey & AMPLE History.

• A = Allergies• M = Medications• P = Past medical history• L = Last oral intake• E = Events leading up to incident

• Neurological re-evaluation:• Eye opening Pupillary light Reaction• Motor response Occulocephalic Doll’s Eye• Occulo-vestibular Caloric test

Initial Assessment (Primary Survey)

• Airway with C-Spine Control– Return head to neutral position– Stabilize without traction– Noisy breathing is obstructed breathing

• But all obstructed breathing is not noisyBut all obstructed breathing is not noisy

• Airway with C-Spine Control– Anticipate airway problems with

• Decreased level of consciousness• Head trauma• Facial trauma• Neck trauma• Upper thorax trauma• Severe Burns to any of these areas

– Open, Clear, Maintain.

• Breathing

Ask yourself the next questions:– Is oxygen getting to the blood?

• Is air moving?

• Is it moving adequately?

• Is it moving at an adequate rate?

• Breathing

Look

Listen

Feel

• Breathing– Oxygenate immediately if:

• Decreased level of consciousness

• Shock

• Severe hemorrhage

• Chest pain

• Chest trauma

• Dyspnea

• Respiratory distress

• Multi-system trauma

• Breathing

If you think about giving oxygen, GIVE IT!!

• Breathing– Consider assisted ventilations if:

• Respirations < 12

• Respirations > 24

• Tidal volume ↓• Respiratory effort ↑

– If you can’t tell if ventilations are adequate, they aren’t!!

Indications for intubation and ventilation

• GCS less than or equal to 8 • Loss of protective laryngeal reflexes • Ventilatory insufficiency as judged by blood gases

– PaO2 less than 9kPa )67 mm hg)– PaCO2 greater than 6kPa (45 mm hg)

• Spontaneous hyperventilation • Respiratory arrhythmia • Bilateral fractured mandible • Copious bleeding into mouth • Seizures

• Circulation– Is the heart beating?– Is there serious external bleeding?– Is the patient perfusing?

• How do we know?

To Determine the cause of Hypotension

D.P.L F.A.S.T C.T.SCAN

Common sites Of Blood Loss

Overtoccult

1-scalp laceration

2-Maxillofacial

3-Open fracture

4-Other soft tissue injury

Intraperitoneal/retroperit.

Hemothorax

Pelvic hematoma

Subgaleal/extradural Hge

Aortic Rupture

• If there is hypotension, this usually not due to the brain injury itself, except in the terminal stage when medullary failure occur.

• Hypotension is a marker of sever blood loss also spinal cord injury, cardiac contusion or tamponade and tension pneumothorax.

• Circulation– No carotid pulse?

• CPR

• PASG

– Survival rate from cardiac arrest secondary to trauma is very low

• Disability (CNS Function)– Level of consciousness = Best brain perfusion

sign– Use GCS initially– Check pupils

• The eyes are the window of the CNS

• Disability

– Decreased Level Of Consciousness ==• Brain injury• Hypoxia• Hypoglycemia• Shock

– NEVER think drugs, alcohol, or personality first

• Expose and Examine

You can’t treat what you don’t find!– If you don’t look , you won’t see!– Remove ALL clothing from critical patients

ASAP– Avoid delaying resuscitation while disrobing

patient– Cover patient with blanket when finished

Primary Resuscitation

• Immobilize C-spine (manual & rigid collar)• Keep airway open• Oxygenate• Rapidly extricate to long board .• Begin assisted ventilation .• Expose & Protect from exposure• Apply and consider inflation of PASG• Consider intubation• Establish IVs

2 ry SurveyTo detect any major systemic injuryRequiring care by other specialties•Long bone & Pelvis Fracture 32%.•Maxillary or Mandibular Fracture 22%•Major chest injury 23%•Abdominal visceral injury 7%•Spinal Injury 2%

Miller Jd,Sweet RC

J.American Medical Association 1978

Neurological Examination

• GCS

• Pupillary light response

• Doll’s Eye Movement (occulocephalic).

• Calorics (occulovestibular)

• Corneal Response.

Important Consideration

• 1-Neurological exam. should be done prior to sedation or paralyzing the patient.

• 2-It is not allowed to use long acting paralytic agents.

• 3-Succinylcholine,vecuronium or very small dose pancuronium are recommended.

• 4-Small repeated doses of i.v morphine (4-6 mg) are used in providing analgesia & sedation that is reversible.

• 5-serial exam. Should be performed because of variability of response over time.

• 6-Early sign of temporal lobe herniation is mild dilatation of pupil and sluggish pupillary response.

• 7-With worsening of herniation there is further dilatation of pupil followed by ptosis & paresis of medial rectus. Down& out position of the eye that is diagnostic of IIIrd Nerve palsy.

Pupillary Light ResponseValadka AB, Narayan 1996

Pupil SizeLight Responseinterpretation

Uni.dilatatationSluggish/fixedIII n. Compress.

=tent.herniation

Bil.dialtationSluggish / fixed▼brain perfusion

Bil. Nerve palsy

Uni.dilatation Cross reactionMarcus-Gun

Optic nerve injury

Bil.ConstrictionDifficult to determine

Drugs/opiates

Pontine lesion

Metabolic

Uni.ConstrictionPreservedInjured symp. pth

Diagnostic procedures

• 1-C.T Scan: • within 30 min after injury should be repeated

whenever there is change in the patient clinical status.• The scalp may demonstrate subgaleal hematoma.• Skull may be seen better on bone window.• The presence of intracranial hematoma, shift of the

midline, the septum pellucidum which lies between the two lateral ventricles,should be in

the midline. An actual shift of 5 mm or more is considered significant and usually indicates surgery.

Indications for CT

• GCS less than 13 at any point since the injury • GCS equal to 13 or 14 at 2 hours after the injury • Suspected open or depressed skull fracture • Any sign of basal skull fracture • Post-traumatic seizure • Focal neurological deficit • More than one episode of vomiting • Amnesia for greater than 30 minutes of events before impact • If LOC in patients older then 65 years, coagulopathy or dangerous

mechanism of injury

• 2-Angiography:

May be done in the absence of C.T in Acute Head Injury. Supratentorial mass lesion usually can be detected by lateral shift of the ant.cerebral artery and vein.

MRI

Methods of monitoring neurological function

• Methods of monitoring intracranial pressure – Intraventricular catheter – Fibreoptic devices – Strain gauge microtransducer systems

• Methods of monitoring cerebral blood flow – Transcranial doppler

• Methods of monitoring cerebral oxygenation – Jugular venous oxygen saturation – Near-infrared spectroscopy – Brain oxygen tension

• Methods of monitoring function – Clinical neurological assessment – Glasgow coma scale – Electroencephalogram (EEG(– Electromyography

Medical therapy Of Head Injury

• I.C.U can▼ Mortality from 50% in 1970 to 36% 1997.

• The aim of I.C.U To prevent 2ry damage.

Hyperventilation Mannitol LasixI.V.F

Intravenous Fluids

• It is especially critical in head injury not to use hypotonic fluids. The use of glucose containing fluids can result in hyperglycemia which is harmful to the injured brain.

• Normal saline or Ringer’s lactate should be used for resuscitation.

• Na+ level should be carefully monitored in these cases. Hyponatremia is associated with brain edema.

Hyperventilation

• It causes ↓ Pco2 → Cerebral vasoconstriction.• This reduction in intra cranial volume helps

↓ I.C.P.

• Aggressive & prolonged hyperventilation can produce cerebral ischemia. This occur if Pco2 ↓<25 mm Hg

The current concept

• Is to use hyperventilation in moderation and for limited periods.

• It is preferred to keep Pco2 at 30 mm Hg.

• Levels of Pco2 between 25-30 mm Hg are acceptable in presence of ↑ I.C.P

Mannitol• Mannitol 20% is used widely to ↓ ICP.• 1 gm/kg i.v bolus over 5 minutes.• It should not be given to hypotensive patient, as it

aggravates hypovolemia.• The clear indication for use:The clear indication for use:1. Comatose patient who initially has normal,reactive

pupil but develops pupillary dilatation with or éout hemiparesis.The patient then transferred urgently to C.T or OR.

2. Bil.Dilated & non reactive pupil who is not hypotensive.

Furosemide (Lasix)

• Dose: 0.3-0.5 mg/kg i.v

• Combined with mannitol after consulting neurosurgeon

E. Steroids

• It is not recommended in management of Acute Head injury.

F. Barbiturates

• It ↓ ICP. Not used in Presence of Hypotension.• Dosage: Adult: loading 10-12 mg/kg 3 divided

doses . Maintx :1-3 mg/kg/24h i.m or i.v. Pedia.:load 15-20 mg/kg in 2 doses

then maintx 3-5 mg/kg/24h

G. Anticonvulsants

• Post traumatic epilepsy occur in 5% of all patients admitted to the hospital, and in 15% of sever head injury cases.

• Phenytoin is used for the 1st week .• Dosage:

Loadx : 15-20 mg/kg (25mg/min).

Maintx: 200 mg p.o or i.v bid.

Pediax: loadx the same. Mainx 4-7 mg/kg/24h

Surgical Management

• A-Scalp Wounds:• Inspection carefully, attention should be given to

trivial injuries in children by pencils as it can cause penetrating injury with bad sequel if not noticed.

• Adequate cleansing and debridement• Blood loss can be extensive , especially in children• Presence of csf means dural tear

B-Depressed skull fracture

• Needs elevation if the degree of depression is greater than the thickness of adjacent skull. CT is mandatory to r/o intracranial hematoma or depression.

Curvilinear depressed fracture

Depressed fracture

C-Intracranial Mass Lesion

• Early transfer of the patient to a hospital with a neurosurgeon.

• In Rural Areas:

Burr holes may be considered, the purpose of it to is to preserve life by partially evacuating a life threatening intracranial hematoma.

Indications for referral to neurosurgeon

• Persistent coma (GCS<8) after initial resuscitation

• Unexplained confusion persisting for › 4 hours • Deterioration in GCS after admission • A seizure without full recovery • Progressive focal neurological signs • Definite or suspected penetrating injury • CSF leak

Emergency Burr Holes

• Should be considered in the contest of the following:

• The majority of comatosed patients do not have hematoma

• A burr hole placed as little as 2 cm away from hematoma may not locate it.

• Only a small portion of epidural or subdural hematoma can be adequately evacuated, as blood is often clotted.

• A burr hole itself can cause brain damage or Hge.