Head Injury: What To Do

Head injury is very common accident in all over the world. Any road accident, violence, trauma, fall from height etc may result head injury. It may be serious enough to endanger life.

Head Injury/Brain Trauma RESULTS FROM :

A. IMPACT DAMAGE:
1. Cortical Contusion
2. Cortical Laceration
3. Bone Penetration
4. Diffuse Axonal Injury
5. Primary Brainstem Injury
B. SECONDARY INJURY: Develops subsequent to impact damage
1. Injury from Intracranial Haematomas
2. Brain oedema
3. Hypoxaemia
4. Ischaemia ( due to raised ICP, rarely due to shock )
5. Infections
6. Seizures
IMPACT DAMAGE cannot be influenced so attention should be focused on reducing
SECONDARY INJURIES.
MANAGEMENT
FIRST AID
a. Maintenance of adequate airway, artificial respiration if necessary.
b. Oxygen if necessary.
c. Light occlusive dressing to compound wound- control bleeding
d. First aid to other injuries.
e. Transport to appropriate centre without inflicting a second accident
f. Transportation should be done in a well-equipped ambulance with a trained attendent cum nurse
g. Start i/v fluid therapy if necessary and/or steroids.
ASSESSMENT IN CASUALTY WARD :
HISTORY ( From patient or attendent ) :
1. Nature of injury
2. Condition immediately following injury
3. Time elapsed since injury
4. Progress in the interim
EXAMINATION
I. CONSCIOUS LEVEL
1. Clear conscious : Completely normal mentally, alert and oriented
2. Cloudy conscious : Patient is conscious but confused and disoriented
3. Rousable coma : Patient is conscious but responds purposefully or semipurposefully to painful stimuli
4. Deep coma : No response to painful stimuli

GLASGOW COMA SCALE : TOTAL SCORE = 15

EYE OPENING :

 Spontaneous ——– ——-4
 To command —————-3
 To Painful stimuli ——– 2
 None ———-1
BEST MOTOR RESPONSE :
 Obeys commands————6
 Localizes pain —————5
 Withdraws——————–4
 Flexor response————–3
 Extensor response ———2
 None ————————1
BEST VOCAL RESPONSE :
 Conscious, oriented ——-5
 Conscious, disoriented—–4
 Inappropriate words ——-3
 Incomprehensible sounds–2
 None ——–1
Mild Head Injury GCS 13-15
Moderate Head Injury GCS 9-12
Severe Head Injury GCS 8 and below

NEUROLOGICALLY ORIENTED GENERAL PHYSICAL EXAMINATION FOR HEAD INJURY

1.VISUAL EXAMINATION OF CRANIUM
a. Evidence of Basal Skull fractures
 Racoon’s eye : Periorbital ecchymoses
 Battle’s sign : Postauricular ecchymoses (arround mastoid air sinuses)
 CSF otorrhoea / Rhinorrhoea
 Haemotympanum or laceration of external auditory canal
b.Facial fractures
 LeFort fractures
 Orbital rim fractures
c. Periorbital oedema, Proptosis

2. CRANIO-CERVICAL AUSCULTATION
a. Over Carotids – bruit present in Carotid dissection
b. Over Globe – bruit present in Carotid-cavernous fistula
3.PHYSICAL SIGNS OF TRAUMA TO SPINE
4.PULSE / B.P / RESPIRATION/ TEMP
( As features of rising ICP )
5.NOTE EXTERNAL INJURY TO OTHER PARTS
Example: CHEST, ABDOMEN & LIMBS
”MANY PATIENTS HAD DIED OF SHOCK DUE TO INTERNAL HAEMORRHAGE THAN RAISED ICP”
NEUROLOGICAL EXAMINATION
A.LEVEL OF CONSCIOUSNESS :
GLASGOW COMA SCALE
B.CRANIAL NERVE EXAMINATIONS :
 Optic Nerve
 Pupillary ¨ Size and Reaction to light
 Facial asymmetry ¨ Check for peripheral VII palsy
 Fundoscopy ¨ Papilloedema, Retinal detachment, Retinal Hge
 Other Cranial Nerves
C.MOTOR RESPONSE : As per GCS
D.SENSORY EXAMINATION :
 Co-operative Patients : *Check pinprick sensation in major dermatomes C4, C6, C7, C8, T4, T6, T10, L2, L4, L5, S1, Sacrococcygeal
*Check post. column function : Joint position sense of LEs
 Uncooperative Patients : Central response to painful stimuli
– Vocalization
– grimace
E. REFLEXES Preserved reflexes indicates that a flaccid limb is due to CNS injury and not nerve root injury(and Vice-versa)
 Check plantar response for upgoing toes ( Babinski sign )
In suspected spinal cord injury: the anal wink and bulbocavernosus reflex are checked on the rectal exam.
SPECIAL TESTS:
1. X-ray skull
2. X- ray cervical spine
3. CT scan of the brain
4. Blood grouping and cross-matching
5. Blood sugar, urea, creatinine and electrolytes.
CRITERIA FOR CT SCAN ( any of the following )
 GCS<15 with skull #
 Abnormal neurology with skull #
 Seizure with skull #
 Developing neurological signs
 GCS<15 for more than 8 hours
 Persistent vomiting

CRITERIA FOR URGENT NEUROSURGICAL CONSULTATION
( any of the following )
 Coma ( GCS<8 )
 Rising BP, falling pulse rate
 GCS<15 for more than 8 hours
 Abnormal CT scan of the brain
 Compound skull #
 Depressed skull #
 Fall in GCS despite resuscitation
 CSF leak

CLINICAL CATEGORIZATION OF RISK FOR INTRACRANIAL INJURY/ HEAD INJURY

A.Findings with low risk of ICI
 Asymtomatic
 Headache
 Dizziness
 Scalp haematoma, laceration, contusion or abrasion
 No moderate nor high risk criteria
B.Findings with moderate risk of ICI
 Progressive headache
 EtOH or drug intoxication
 Posttraumatic seizure
 Unreliable or inadequate history
 Age <2yrs ( Unless trivial injury )
 Repeated vomiting
 H/O change or loss of consciousness on or after injury
 Posttraumatic amnesia
 Signs of basal skull fractures
 Multiple trauma
 Serious facial injury
 Suspected child abuse
C.Findings with high risk of ICI
 Depressed level of consciousness not clearly due to EtOH, drugs, metabolic abnormalities, postictal, etc
 Focal neurological deficits : Anisocoria, Hemiparesis
 Decreasing level of consciousness
 Penetrating skull injury or depressed fracture

DEFINITE TREATMENT OF HEAD INJURY

A.ALLOWED HOME
 Conscious, alert and oriented, no skull fracture
 Responsible person to look after the patient at home over next 24 hrs
 To return to hospital immediately if
1. a change in level of consciousness
2. ( including difficulty in awakening )
3. abnormal behaviour
4. severe headache
5. slurred speech
6. difficulty in using arms or legs
7. persistent vomiting
8. seizures
B.OBSERVED IN CASUALTY

 Mild impairment of consciousness, no skull fracture
 Reassessed after 4 hrs to decide whether sufficient improvement has occured to allow home or admit into ward
C.TRANSFER TO THEATRE

 Rapid progressive deterioration of clinical state
 Severe scalp haemorrhage
D.ADMITTED TO WARD

 Unconscious or stuporose
 Focal neurological deficits – hemiparesis
 Skull fractures present
 No responsible domestic supervisor
MAINSTAY OF MANAGEMENT IS CONSTANT FREQUENT EXAMINATION FOR EARLY DETECTION OF SIGNS OF CEREBRAL COMPRESSION

SIGNS OF CEREBRAL COMPRESSION:

 Deterioration of conscious level
 Pupillary changes – Initial constriction followed by dilatation and fixity
 Progressive hemiparesis
 Slowing of pulse
 Elevation of blood pressure
 Irregularity of respiration

CARE OF THE UNCONSCIOUS PATIENT OF HEAD INJURY

A.AIRWAY MAINTAINENCE
 Posture
 Endotracheal intubation
 Tracheostomy
 Artificial ventilation

B. FLUID, ELECTROLYTES, NUTRITION
 Underhydration better than overhydration
 Nasogastric intubation for initial gastric decompression, then for feeding

C.BLADDER AND BOWEL CARE
D.SKIN CARE
 Keeping patient clean and dry
 Change of posture 2 hourly to prevent pressure sores
 Use of air-cushions
E.TEMPERATURE CONTROL

 Hyperpyrexia following loss of thermoregulator — fever upto 420C, no sweating,
 pilo-erection, tachypnoea, circulatory collapse
 Treatment— Expose to fan, Ice cold sponge, Ice packs, cold blankets

TREATMENT OF COMPLICATIONS OF HEAD INJURY

A. INTRACRANIAL HAEMORRHAGE
: Evacuation of haematoma and securing haemostasis

B. CEREBRAL OEDEMA :
1. Dexamethasone: 5 mg i/v 6 hrly
2. 20% mannitol infusion – with caution
3. Frusemide – 40mg i/v – with caution

C.INFECTIONS:
1. Surgical closure of defects
2. Antibiotics

D.SKULL FRACTURES : SURGERY FOR
1. All compound depressed fractures
2. Most simple depressed fractures
3. Growing fractures in children

E.POST CONCUSSION SYNDROME :
With headache,dizziness and memory difficulties being the most frequent. No specific treatment, other than psychological counselling, is helpful

F.POST TRAUMATIC EPILEPSY :
Risk 10% with post-traumatic amnesia of over 24 hrs, 30% with intracerebral haematoma and 50% with cortical lacerations. Prophylactic anticonvulsant therapy with above risk factors.

courtesy:

Dr.  Ekramullah, PhD
Associate professor, Neurology