HEAD INJURY

Weru
 INTRODUCTION
 Head injury is a major cause of death in
children and adults worldwide
 Many survivors are catastrophically disabled
 Recognizing a severe head injury and
administering prompt and appropriate
treatment is important for all medical
practitioners.
 CAUSES
1) Road traffic incidences
2) Fall from heights
3) Blunt injuries e.g. by physical assaults
4) Penetrating injuries
- Gun shots
- Sharp objects
 CLASSIFICATION OF HEAD INJURY
 Head injury can be classified as follows:
1. Using Glasgow coma scale:
(a) Minor head injury- GCS of 15 with no loss of
consciousness
(b) Mild head injury- GCS of 14-15 with loss of
consciousness
(c) Moderate head injury- GCS of 9-13
(d) Severe head injury- GCS of 3-8
 Cont’d
GLASGOW COMA SCALE
 EYE OPENING
4. Spontaneous
3. To speech/command
2. To pain
1. None
 Cont’d
 BEST VERBAL RESPONSE
5. Oriented
4. Confused conversation
3. Inappropriate words
2. Incomprehensible sounds
1. None
T. For intubated patients
 Cont’d
 BEST MOTOR RESPONSE
6. Obeys command
5. Localizes pain
4. Flexes to pain
3. Abnormal (decorticate) flexion
2. Extends to pain (decerebrate)
1. None
 Classification cont’d
2. Nature of injury:
(a) Blunt/ closed/concussional
(b) Penetrating
 High velocity e.g. gunshot
 Low velocity e.g. stabbing
3. Morphological i.e. according to type of
injury:
(a) Scalp injuries
 Classification cont’d
(b) Skull fractures:
 Vault
- Open of closed
- Linear or comminuted
- Depressed or non-depressed
 Base – may or may not be associated with CSF
ottorrhea or rhinorrhea or cranial nerve
palsies (IX, X and XI)
 Classification cont’d
(c) Intracranial haemorrhages
 Extradural haematoma
 Subdural haematoma
 Subarachnoid haemorrhage
 Intra cerebral haemorrhage
 Intraventricular haemorrhage
 Classification cont’d
(d) Brain injury which can be:
 Primary- It is the direct result of the trauma to
the brain e.g. in penetrating injuries or as a
result of acceleration (coup) and deceleration
( contra-coup) effects
 Secondary- occurs after the initial event as a
result of hypoxia, hypercapnia, hypotension
(ischaemia), intracranial haemorrhage or
meningitis. It is the main cause of in- hospital
motarity after head injury
 CEREBRAL PERFUSSION
 Understanding the mechanisms underlying the
regulation of cerebral perfusion and how these may
be affected in trauma is important in the
management of head injury victims.
SYSTEMIC ARTERIAL PRESSURE
 Cerebral perfusion is normally auto regulated by the
vasoactive cerebral arterioles to maintain constant
cerebral blood flow over a wide range of systemic BP.
 If systemic BP falls, cerebral vasodilatation occurs to
compensate; a further fall may exceed the arterioles
ability to compensate and cerebral ischaemia occurs
 Cont’d
INTRACRANIAL PRESSURE(ICP)
 Since the skull is a closed compartment, a rise in
intracranial pressure(ICP) will reduce the
cerebral perfusion pressure( CPP)
CPP= MAP(BP)- ICP
 The flow of blood to the brain is auto regulated
until the perfusion pressure is around 40mmHg.
 A rise in ICP coupled with hypotension in
trauma victims with head injuries reduces
cerebral blood flow
 SIGNS OF INCREASED INTRACRANIAL
PRESSURE
 Headache
 Nausea
 Vomiting
 Increased blood pressure
 Decreased mental ability
 Confusion
 Double vision
 Pupils that don’t respond to changes in light
 Shallow breathing
 Seizures
 Loss of consciousness
 Coma
 HISTORY TAKING
 Enquire about the mechanism of injury
- Penetrating
- Blunt injuries
- Acceleration
- Acceleration/ deceleration
- Rotational
 Loss of consciousness
 Loss of memory ( Amnesia)
- Ante grade ( after the injury)
- Retrograde ( before the injury)
 Cont’d
 Level of consciousness at the scene and during
transportation
 Seizures/fits
 Pre-existing medical condition
 Medications especially anti-coagulants
 Alcohol /illicit drugs
 EXAMINATION
 Begin with resuscitation and primary survey
- Stabilize the cervical spine
- ABCDE
 Glasgow coma score
 Pupil size and response to light
 Vital signs
 Lateralizing sign- sign that help to localize a
pathology to a particular area in the brain
 Examination cont’d
 Signs of fracture of base of the skull:
- Bilateral periorbital ecchymosis ( Racoon eyes)
- Battle’s sign ( bruising over mastoid region which
develops a day or two after the injury)
- CSF rhinorrhea or ottorrhea
- Haemotypanum (bleeding from ears)
 Eyes examination
Conjugate gaze paresis( inability to move both eyes in
a single horizontal or vertical direction)- lesion in the
brain stem( mid brain or pons)
Roving eyes movements- suggesting mid brain or brain
stem dysfunction
 Cont’d
 Examine the facial skeleton- orbital ridge,
zygomatic or maxillary fractures
 Full neurological examination
- Sensations
- Muscle tone and power
- Reflexes
 Assess the skeletal system for other
associated fractures.
 INVESTIGATIONS
1. Skull X-ray- reveals fractures of the vault
2. CT SCAN and MRI- Indications include:
 Neurological signs such as:
- Confusion
- Impaired levels of consciousness
- Focal neurological signs and symptoms
- Seizures/fits
 Fractures of the vault with neurological signs
 Depressed skull fracture or suspected penetrating
injury
 GCS of below 13 at any point
 GCS of 13 or 14 at 2hrs
 Cont’d
 Suspected basal skull fracture
 Vomiting of more than one episode
 Open fracture of the skull
3. Laboratory investigations such as:
 Blood for grouping and cross matching
 Random blood sugar
 Blood gas analysis: partial pressures of carbon
dioxide and oxygen
 INDICATIONS FOR ADMISSION
1. Confusion or impaired conscious level (GCS
of less than 15) at the time of examination
2. Skull fracture
3. Neurological symptoms or signs, including
headache and fits
4. Difficulties in assessing patients such as:
- Children
- Those under the influence of alcohol or illicit
drugs
- Pre-existing neurological condition e.g.
Parkinson’s disease
 Cont’d
5. Complicating medical conditions other than
head injury, such as anticoagulant therapy
6. Lack of responsible adult to supervise the
patient or other adverse social conditions
 MANAGEMENT OF MILD HEAD INJURY
(GCS of 14-15)
Discharge the patient after:
 Taking detailed history
 Performing a thorough examination
 Treatment of any minor injury
 Period of observation
Criteria to follow before discharge:
 GCS of 15 with no neurological deficits
 Patient should not be under the influence of
alcohol or other drugs
 Patient must be accompanied by responsible adult
 Cont’d
 Verbal and written head injury advice must be
given to the patient and the accompanying adult
which stipulates the symptoms that will prompt
them to seek medical attention. These include:
- Persistent/worsening headache despite analgesics
- Persistent vomiting
- Drowsiness
- Visual disturbances- double or blurred vision
- Development of weakness or numbness of the
limbs
MANAGEMENT OF MODERATE TO SEVERE
HEAD INJURY
Begins with resuscitation
Aim is to prevent secondary brain injury
especially due to increase ICP
Request for CT Scan/MRI of the head; it
identifies:
- Intracranial haematomas which if evacuated
reduce intra-cerebral pressure
- Intra-cerebral contusions
- Scalp soft tissue injuries
- Skull fractures
 MEDICAL MANAGEMENT OF HEAD INJURY
Aim is to control ICP and prevent any other secondary
occurrence e.g. infection
CONTROL OF ICP
 Position/prop the head at 20°-30°
 Avoid obstruction of venous drainage from the head
by the cervical color
 Sedation with or without muscle relaxant
 Ensure normocapnia- PCO₂ of 4.5-5Pa
 Diuretics (mannitol or frusemide) – temporarily reduce
cerebral oedema and ICP
 Seizure control – give prophylactic anticonvulsants in
the first week (seizures increase brain metabolic rate)
 Cont’d
Maintain normothermia- pyrexia increases the
brain metabolic rate and should be avoided
Maintain fluid and electrolyte balance but
avoid over infusion
- Severely brain injured patient are susceptible
to disturbances of sodium hemostasis such as
diabetes inspidus and syndrome of
inappropriate antidiuretic hormone ( S.I.A.D.H)
 Cont’d
 Administration of barbiturates such as theopentone
which reduce brain metabolic rate and help reduce
ICP.
N.B: Barbiturates are associated with respiratory and
metabolic complications hence dosage should be
guided with electroencephalogram (EEG) monitoring
OTHER TREATMENTS:
- Anti-meningitic antibiotic cover
- Analgesics but avoid opiates e.g. morphine
- Tetanus toxoid
- Skin care to prevent bed sores
 SCALP INJURIES

 Most scalp injuries are simple penetrating

injuries
 Management:
Debridement and suturing
Antibiotic cover
Tetanus toxoid
Analgesics
 SKULL FRACTURES
 Occur as a result of crushing or other severe
forces
 Site varies with the direction the force came from
PHYSICAL SIGNS OF SKULL FRACTURES
 Anterior fossa
- Nasal bleeding
- Orbital haematoma (Racoon eyes)
- CSF rhinorrhea- fracture of petrous temporal bone
- Cranial nerve palsies- cranial nerves I to VI
 Cont’d
 Middle fossa
- Orbital haematoma
- Bleeding from ears (Haemotypanum)
- CSF ottorrhea(rare)
- Cranial nerve palsies- cranial nerves VII and VIII
 Posterior fossa
- battle’s sign
- Cranial nerve palsies- cranial nerves IX, X and XI
 Cont’d
TREATMENT OF SKULL FRACTURES
1) Linear & slightly comminuted fractures
 Repair the scalp if broken
 Analgesics
 Antibiotic cover
 Follow up
2) Depressed fractures
 Conservative treatment if the depression is less than
the thickness of the skull
 Surgical elevation if the depression is greater than
bone thickness associated with intracranial
haematoma & epileptic focus
 Cont’d
3) Open fractures
 Wound debridement
 Elevation
 Antibiotic cover
 Follow up
INTRACRANIAL HAEMATOMAS
 EXTRADURAL/EPIDURAL HAEMATOMA

It is a neurosurgical emergency

 It is associated with skull fractures and is more
common in young male patients
 Commonest site temporal regions since it is
the thinnest part of the skull and also overlies
the largest meningeal artery (middle
meningeal artery)
 Can also occur in frontal and posterior fossa
 Can also occur due to disruption
 Cont’d
Clinical features
 Initial injury followed by lucid interval when
the patient complains of headache but is fully
alert and oriented with no neurological
deficits
 After minutes or hours a rapid deterioration
occurs with contra lateral hemiparesis,
reduced consciousness levels and ipsilateral
pupillary dilatation as a result of brain
compression and herniation
 Cont’d
NB:
 Early recognition of extradural haematoma
and intervention is likely to result in full
recovery whereas delay can result to
secondary brain injury
 EDH may also occur together with primary
brain injury
 Cont’d
Investigations:
 CT Scan/MRI
- Lenti form ( lens shaped or biconvex) hyper-
dense lesion between the skull and brain
- Associated mass effect on the underlying brain
with or without a midline shift
Treatment
 Immediate surgical evacuation via craniotomy
It has a motarity rate of 18%
EPIDURAL HAEMATOMA
 ACUTE SUBDURAL HAEMATOMA
 Blood accumulates in the space between the
dura and arachnoid
 Occurs as a result of disruption of a cortical
blood vessel or brain laceration
 It is nearly always associated with significant
primary brain injury
Clinical features:
 Presents with impaired levels of consciousness
from the time of injury, but further
deterioration occurs as the haematoma
expands
 Cont’d
Investigations:
CT Scan/MRI
- Hyper dense lesion which may spread across
the surface of the brain margin giving diffuse
and concave appearance
ACUTE SUBDURAL HAEMATOMA
ACUTE SUBDURAL HAEMATOMA
 Cont’d
Treatment:
 Evacuation via craniotomy
 Small haematomas with little effect can may
be managed conservatively in neurological
centers
Motarity rate is 40%
 CHRONIC SUBDURAL HAEMATOMA
 It follows trivial (often forgotten) injury,
usually in elderly patients, sustained weeks or
months before
 There is a small tear in a cerebral vein as it
traverses the subdural space
 Whenever the patient coughs, strains of bends
over, a little blood extravasates
 Cont’d
Clinical features:
Occur as a result of developing intracranial mass
 Mental deterioration
 Headaches
 Vomiting
 Drowsiness which progresses to coma
 Moderate papilloedema is seen in about half of
the cases.
 Cont’d
Investigations:
 CT Scan/MRI- Demonstrates the outline of the
clot
Treatment:
 Evacuation of the clot and fluid through burr-
holes
 SUBARACHNOID HAEMORRHAGE
 Associated with severe head injury
 Presents with features of meningeal irritation:
- Headache
- Neck stiffness
- Positive Kernig’s sign
- Sometimes pyrexia

Treatment:
 Analgesics and bed rest until severe headache
subsides
 Rapid rehabilitation afterwards
INTRACEREBRAL HAEMORRHAGES
 Associated with severe head injuries
 Sometimes may develop within the brain
substance, often in the frontal or temporal
lobes
 If exerting mass effect & high intracranial
pressure, evacuation is performed and the
injured lobe may be removed
 INTRAVENTRICULAR HAEMORRHAGE
 May occur from tearing of choroid plexus at
the time of injury or rupture of an
intracerebral clot into the ventricle
 It occurs particularly in childhood and usually
as part of overwhelming head injury
COMPLICATIONS OF HEAD INJURY
1. EARLY COMPLICATIONS
a) Haemorrhages
- Extradural
- Subdural
- Subarachnoid
- Intracerebral
- Intraventricular
b) Meningitis
 Cont’d
c) Hyperpyrexia
- Occurs as a result of injury to the heat
regulating centre
- It is a serious complication an must be treated
vigorously by means of cooling blankets
 Cont’d
2. LATE COMPLICATIONS
a) Amnesia ( loss of memory)
b) Epilepsy
- Mostly follows penetrating brain injury with
resultant cortical scarring
c) Long term neurological deficits such as:
 Blindness
 Deafness
 Speech defects
 Limbs paresis and plegias
 Vegetative state