head injury (2)

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Head Injury: Clinical Evaluation & Management

By S. O. ARIGBABU; FRCSEd, FWACS, FMCS

Professor & HeadNeurosurgical Unit, Dept of Surgery,Lagos University Teaching Hospital,

Idi-araba, Lagos

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Head Injury: Introduction

• A fairly common clinical condition of great importance

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Definition

• Head injury may be defined as any pathological change occurring in the head and/or its contents as a result of application of an external force

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Epidemiology of Head Injury

• Occurs worldwide• Incidence varies with geographical

location and level of development• Major cause of permanent disability• Leading cause of death in the 15–40

year old age group• Commoner in males than females

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Epidemiology of Head Injury

• There are no documented figures of national incidence in Nigeria

• Morbidity and mortality are high in underdeveloped world

• Prevention is of great importance

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Causes of Head Injury

• Road Traffic Accidents

• Domestic accidents

• Assaults and Civilian violence (matrimonial, gunshots and stab injuries)

• Industrial accidents

• Sports and Recreational activities

• Others

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Causes of head injury in Children

• Before or during birth– Labour induced/intrauterine depressed skull

fracture– Cephal haematoma– Subgaleal haematoma– Injuries from forceps, vacuum etc– Injuries as a result of precipitous labour

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Causes of head injury in C hildren

• Infants (up to age of 1year)– Fall from parent’s bed– Fall down the stairway– Falls from back of mother or elder sister

(usually 6-8 years)– Crawling to head injury– Barbaric fights– RTA in company of mother– Baby battering by househelp

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Causes of head injury in C hildren

• Older children– Fall from heights

• Balconies • Stairs• Construction sites• Playgrounds

– RTA on the way to/from school– Assault

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Classification of Head Injury

• Anatomical classification– Scalp Injuries

– Bony (cranial injury) = Fractures

– Traumatic Brain Injury (TBI)

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• By mechanism of injury– Blunt vs penetrating head injury

– Open vs closed head injury

– Focal (contusion, haemorrhage) or diffuse (lead to global dysfunction –LOC, cognitive, memory)

– Heamorrhagic vs non-haemmorrhagic

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• According to severity (Glasgow Coma Scale)– Mild (GCS 13 – 15)

– Moderate (GCS 9 – 12)

– Severe ( GCS 3 – 8)

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Cranial Injuries

• Scalp injuries– Abrasions– Contussion– Lacerations– Subgaleal Haematoma

• Skull Fractures– Open or closed– Linear– Depressed/elevated

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Types of Skull Fracture

• Linear– Most common

– Crack in skull

– Detected only on x-ray

• Comminuted– Multiple cracks

radiate from impact point

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Types of Skull Fracture

• Depressed– Bone fragments pressed

inward

– Places pressure on brain

• Fracture Base of skull– Fractures in floor of skull

– Signs and symptoms

• Periorbial ecchymosis (Raccoon eyes)

• Battle’s sign

• CSF drainage from nose, ears

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Injuries to Brain

Primary brain injury

Secondary brain injury

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Injuries to the Brain

• Primary brain injury– Injury due to direct impact of the

trauma to the brain

– Includes brain concussion, brain contusion, and brain laceration

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• Secondary injury– Brain damage which is a result of

complications resulting from the impact of the injury

– Usually a result of brain compression due to either intracranial haematomas or brain swelling

– Role is becoming increasingly recognized– Major target for investigative research and

potential clinical intervention

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– Ischaemia (cerebral perfusion is compromised by systemic hypotension or by elevated intracrainial pressure from brain compression. CPP=MAP-ICP

– ExcitotoxicityTissue injury and ischemia cause release of glutamate, aspartate & potassium, and intraneuronal accumulation of calcium. Result is a wave of spreading depolarization, hypermetabolism and worsening tissue ischemia

– Mainstay of therapy is to optimize cerebral perfusion. Newer therapies utilize sedation and hypothermia to decrease tissue metabolism. Glutamate or calcium antagonists are also used.

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Injuries to the brain

• Early detection of increased intracranial pressure is critical

• If pressure inside skull exceeds average blood pressure, blood flow to brain stops

• Increasing intracranial pressure can force part of the brain to herniate through the tentorial hiatus or the foramen magnum, as the case may be.

• Commonest part of the brain affected is the uncus giving rise to uncal herniation

• Such herniation will lead to damage of the brain stem affecting the vital centers

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Associated injuries

• Nose• Maxillofacial• Ears• Eyes• Mouth• Long bones• Spinal• Chest• Abdominal

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Clinical FeaturesNeurosurgical symptoms

• Blood loss• Loss of consciousness• Drowsiness• Confusion• Headache• Vomiting• CSF Otorrhea• CSF Rhinorrhea

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Clinical featuresNeurosurgical signs: Pupils

• Inspection – Normal – Dilated – pinpoint

• Pupillary Light reflex– normal– Unequal/asymmetrical reaction– Bilaterally fixed , dilated

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Clinical FeaturesNeurosurgical signs: Others

• Paresis

• Paralysis

• Speech difficulties

• Seizures

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Assessment of Head Injury

• Level of consciousness is BEST indicator of patient’s condition– This can be assessed using the Glasgow

coma scale

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Glasgow Coma Scale (GCS)*There are modifications for paediatric patients

• Eye Opening– Spontaneous = 4

– To Voice = 3

– To Pain = 2

– None = 1

• Verbal Response– Oriented = 5

– Confused = 4

– Inappropriate Words = 3

– Incomprehensible Sounds = 2

– None = 1

• Motor Response– Follows

Commands = 6

– Localizes Pain = 5

– Withdraws = 4

– Flexion = 3

– Extension = 2

– None = 1

Score each response then total scores

Maximum Score = 15 Minimum Score = 3

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• Vital Signs– Body responds to increasing

intracranial pressure by raising BP

– Increased BP moves blood into brain against rising ICP

– Heart rate falls in response to rising BP

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Vital Signs

Isolated head injury does not cause hypotension or tachycardia!

Signs of hypovolaemic shock in head injured patient indicate that other injuries

are present!

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• Other Indicators of Increased ICP– Headache

– Nausea

– Vomiting (often projectile)

– Seizures

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Management of Head Injury:Prehospital Care

• ABCs with C-spine control• Fluid resuscitation to reverse shock and hypotension• Spine precautions: C-collar, long board, sand bags

If there is significant head injury assume that there is associated neck injury until proven otherwise

• Ensure adequate oxygenation• Effective Emergency medical services and air ambulance

can dramatically reduce mortality of head injury

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Management of Head Injury:General Measures

• Controlled hyperventilation– Lowers blood carbon dioxide levels– Causes constriction of blood vessels in brain– As vessels constrict brain shrinks– As brain shrinks intracranial pressure drops

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Initial evaluation and resuscitation

• Rapid neurological examination (1 - 3 minutes) – Assess GCS, pupil function, cough, gag, corneal

reflex

• Empiric management of elevated ICP– Intubaton, ventilation, sedation, mannitol, head

elevation

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• Secondary injury survey– Examine head, ears, eyes, nasopharynx,

mouth for injury, facial fractures– C-spine x-rays, maxillofacial views (Le-forte) – Evaluate for peripheral injury– Evaluate for other associated extra-cranial

injuries – X-rays of chest, pelvis and limbs as indicated

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• CT brain scan – Diagnostic procedure of choice for all patients with

suspected traumatic brain injury– Skull X-ray may be useful in the absence of CT

facilities. Remember the C-spine and other structures

– Other investigations/tests as required

• Establish baseline• Repeat neurological exam frequently

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Management

• Immediate surgery for evacuation of hematoma, if necessary

• Replace lost fluids– Dextrose/saline, blood transfusion

• Manage cerebral edema to maintain cerebral perfusion pressure > 70 mmHg– *steroids, mannitol, frusemide, glycerol, fluid

management, keep head elevated etc• Other drugs

– Analgesics, antibiotics, antitetanus, vitamin B complex, vitamin C

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Specific types of head injury

• Concussion– Brief loss of consciousness with normal head CT

scan, normal neuro exam– Patient may have mild lethargy and/or confusion– Treatment: observation– Recovery not beyond 24 hours– In sports, avoid any risk of re-injury until symptoms

have completely resolved.– Second impact before full recovery may be fatal.

(second Impact Syndrome)

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• Skull fracture– May or may not have associated underlying

brain injury– Linear or non-depressed - observe– Open or compound - irrigate, close, antibiotic

coverage– Depressed - require surgical repair– Any associated dural tear or brain laceration

requires surgical repair. Children may go on to develop growing skull fracture

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• Basilar skull fracture – – fracture around orbital roof, sphenoid bone,

or petrous or mastoid portion of temporal bone.

– Battle’s or Racoon’s eye signs– May be associated with injury to cranial

nerves 2, 7 or 8, or CSF leak into nose (rhinorhea) or ear (otorhea)- these require special attention. Seldom life threatening

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• Cerebral contusion / intracerebral haematoma:– Area of focal tissue injury. Neurological

deficit depends on area injured.– Commonly occur in coupe/contra coupe

pattern eg. frontal / occipital

– Observe patients in ICU, repeat head CT scan as necessary

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• Epidural Haematoma - EDH– Lens shaped hematoma between dura and skull.– Associated with skull fracture and laceration of dural artery

(eg. middle meningeal artery).– Underlying brain is usually not injured– Arterialized bleeding results in rapid expansion of haematoma

and neurological decline– Often presents with brief loss consciousness, followed by lucid

interval of minutes to hours, before rapid neurological decline into coma.

– Extreme neurosurgical emergency. – Timely diagnosis and surgery is often followed by excellent

recovery.

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• Subdural haematoma – SDH– Crescent shaped hematoma lying

between brain and dura, conforming to brain surface.

– Neurosurgical emergency. – It may be acute, subacute or chronic.– Surgical evacuation is usually

required.

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• Chronic subdural hematoma– Usually found in older patients with cerebral atrophy.– Minor trauma causes small, often minimally symptomatic subdural

hemorrhage. As clot liquifies over next 1-3 weeks, the hemorrhage may expand into a significant mass.

– Hematoma resembles dark liquid crankcase oil.– CT appearance, hypodense crescent shaped mass between dura and

brain.– Presenting symptoms: elevated ICP often associated with

hemiparesis. – May also cause TIA-like episodes or seizures.– Treatment consists of surgical drainage of hematoma via burr holes

and irritation. – Most patients make excellent recovery.

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Complications of Head Injury

• Cerebral oedema• Infections: Meningitis, cerebral abscess• Cranial nerve injuries• Subarachnoid and intracerebral haematoma• Post traumatic epilepsy (Early & Late)• Metabolic disorders• Pulmonary or Fat embolism• Carotico-cavernous fistula/aneurysm• Post concussion syndrome (headaches etc)• Craniofacial deformities including keloids• Permanent psychosocial disabilities (speech, memory impairment

etc)

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Prognosis of head Injuries

• The following factors affect prognosis– Severity of injury

– Intervention time and facilities available for management presence or otherwise, of concomitant injuries like chest injuries, pulmonary embolism

– Psychosocial support available

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Head injury : Summary

• Head injury comes in a bewildering variety of types;– Each has its own special management

considerations and prognostic implications– Clinical examination and Neuro-imaging

procedures are the primary ways to differentiate between the various types of head injury. Take special care to identify or rule out associated injuries.

– Holistic and multidisciplinary management approach should be adopted. When in doubt, invite the specialist.

– Prevetion and emergency medical services will improve prognosis

head injury (2)

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