Head Injury

By
Tony Suharsono

Introduction
Almost 2000 patients per 100.000
population attend an Casualty department
annually with head injury.
Of these, between 200 and 400 will require
admission
Male 70 %
Adult 60 %

Definition
Suatu injuri yang dapat melibatkan
seluruh struktur kepala mulai dari lapisan
kulit kepala atau tingkat yang paling
ringan, tulang tengkorak, duramater,
vaskuler otak sampai dengan jaringan
otak sendiri baik berupa luka tertutup
maupun tembus

Mechanism of head injury

Acceleration
Deceleration
Compression
Coup VS Contra coup

Pathophysiology
Injury can occur to the scalp, scull and brain,
independently or in combination
Damage to the brain can occur directly as a result
of the original injury (primary brain damage) or
indirectly as a result of other factors (secondary
brain damage)
The principles cause of secondary brain damage
are hypoxia, hypovolemia, and increases in
intracranial pressure secondary to cerebral edema
or haematoma formation, and cerebral infection.

Pathophysiology
Contact between the surface of the brain
and the interior skull causes bruising
(contusions).
Distortion of the brain caused by internal
shearing forces leads to stretching and
tearing of axonal tracts within the white
matter

Alcohol and head injury

The ingestion of alcohol can affect the conscious
state, and is also associated with an increased
change of sustaining head injury.
Alcohol can also alter conscious state by inducing
hypoglycemia
Therefore all patients with altered consciousness
must have stix testing of capillary blood

Type of head injury

Scalp Injury
Hemorrhage from scalp-wounds is often brisk,
and occasionally life threatening, particularly in
infant and small children, but adult are also at
risk if the wound is large or bleeding is
prolonged
Be careful with patient with bleeding
tendencies or those on anticoagulant teraphy

Scalp Injury
The scalp wound should be carefully inspected for
foreign bodies, underlying fractures, and
herniating brain
Scalp wounds can be probed gently with the finger
of a sterile gloved hand to determine the depth of
the wound
Hemorrhage from scalp wounds can be controlled
by covered wound with non adherent gauze and
secured with a dressing

Type of Head Injury

Scull fracture
Forces large enough to bruise the scalp may
fracture the scull beneath.
Type scull fracture

Scull fracture
Less common in children than in adult
The close relationship between scull
fracture and intracranial hematoma in adult
makes the detection of a fracture important
A compound depressed fracture result when
a violent sharp blow lacerates the scalp, and
drives bone fragment into the intracranial
cavity, sometimes tearing the durameter

Compound depressed scull fracture

Type of Head Injury

Basilar Scull Fracture
A basilar scull fracture describe a fracture location, not
a type
Most basilar scull fracture are linear
Anterior fossa fracture
Periorbital ecchimosis
Rhinnorrhea

Middle fossa fracture

Battle sign
Hemotympanum
Otorrhea

Basilar Scull Fracture

Posterior fossa fracture
The posterior fossa is formed of thick, smooth
bone that rarely is fracture
A small amount of bleeding into this fossa can
put fatal pressure on the brain stem

Check the presence of CSF with halo test

tony, psik 2007

Type of Head Injury

Brain injury
Primary brain damage occur as a result of the
initial injury
It can be due to direct impact damage from
blunt or penetrating injury and or a result of
rotation forces and contra coup injuries induced
by impact
Movement of the brain after impact causes
surface lesion, and produces contusion of the
brain matter

Brain injury
Intracerebral hematoma, subaracnoid hemorrhage
and brain laceration may occur as direct
consequence of the impact
The degree of primary brain damage correlated
with the period of altered consciousness and post
traumatic amnesia
A deteriorating conscious level with or without
localizing neurological sign is the hallmark of
progressive secondary brain injury

Brain injury
The commonest cause of secondary brain
damage is hypoxia
Hypovolemia is also commonly lead to
secondary brain injury
Alone or in combination, hypoxia,
hypercapnia, poor cerebral perfusion and
cerebral contusion are among the factors
that may lead to raised intracranial pressure

Brain injury
Causes of raised intracranial pressure after
head injury
Haematoma
Focal cerebral oedema
Diffuse oedema
Obstruction of CSF pathway

Brain injury
Factors increasing intracranial pressure
Hypoxia
Hypercapnia
Hypotension
Intracranial hemorrhage
Intracranial infection

Brain injury
About 70% of patient persistently in coma
after severe head injury have raised intra
cranial pressure
As intracranial pressure rises cerebrospinal
fluid is driven out of the intracranial
compartment

Intracranial Haematoma
In the context of multiple injury, intracranial
haematoma must be suspected when coma persist
or develops in spite of adequate airway control,
oxygenation, and appropriate fluid replacement
from other injuries.
Classical sign of an expanding intracranial
haematoma (dilatated ipsilateral pupil and
contralateral hemiparesis) are late and inconsistent
signs and represent establish brain injury

Herniation
Herniation occurs whenever portions of the
brain extend beyond their normal location
and impinge on other areas of brain tissue
Herniation can result from an expanding
hematoma, cerebral edema, and a mass.

Herniation

Herniation
Early signs
Decreasing level of consciousness
Ipsilateral pupil dilatation
Cheyne stokes respiration
Contralateral hemiparesis
Positive babinski reflex
Elevated ICP

Herniation
Late signs
Unconsciousness
Bilateral fixed and dilatated pupil
Central neurogenic breathing or other abnormal
respiratory pattern
Flexion or extension posturing
Elevated ICP unresponsive to therapy
Bradicardia

Diagnostic examination techniques

and devices used in head injury
X ray
CT scan
MRI
Angiography
Intracranial pressure monitoring

CT scan
Immediate CT scan
Patient in coma GCS 8 or less
Patients with depression of concious level
GCS 9-13 associated with scull fracture
Patient who deteriorate with a progression to
coma

CT scan
Urgent CT Scan
Patient who are drowsy and/or disorientated
GCS 14-15 and have a scull fracture
Patient with abnormal neurological signs
together with a scull fracture
Patient with depression of conscious level
(GCS 9-13) together with focal neurological
deficit.

Guidelines for CT Scanning

Patient undergoing CT examination must
have
A secure airway
Adequate ventilation
Circulating blood vol devicit corrected
Further haemorrhage controlled

Intracranial pressure monitoring

Is indicated for any patient with severe head
injury (GCS<8) and for those with
abnormal CT Scan findings.
Normal ICP 1-10 mmHg
Cerebral perfusion pressure >70 mmHg
CPP=MAP-ICP

Assessment
Airway
Breathing
Circulation
Disability
Exposure and environment control
Full set of vital sign, Five interventions,
facilitation of family presence

Assessment
Give comfort measures
History (MIVT: mechanism, injuries
suspected, vital sign on scene, treatment
received) and head to toe examination
Inspect the posterior surfaces

Specific examination
GCS
The cranial nerve
Pupillary response
Reflexes
Sensation
Examination of nose and ears for blood,
CSF, Hemotympanum

tony, psik 2007

Pupillary response

Nursing Diagnose
Infective airway clearance
Risk of aspiration
Impaired cerebral perfusion
Ineffective breathing pattern
Risk of infection

Management of patient with head

injury
The to main aim of management patient
with head injury are
Firstly, to provide the best condition for
recovery from any brain damage already
sustained and
Secondly, to prevent or to treat complication
leading to secondary brain damage

Management of patient with head

injury
Airway
Orally intubate patients with a GCS less than or
equal to 8
Insert an oral gastric tube to decompress the
stomach. Avoid nasogastric tube

Breathing
Maintain PaO2 greater than 100 mmHg and
oxygen saturation greater then 95%
Avoid hiperventilation unless signs of
herniation are present
Consider neuromuscular blockade for patient
who are difficult to ventilate

Circulation
Establish normovolemia. Keep MAP 70-90
mmHg
Maintain CPP >70 mmHg
Restore volume as needed with isotonic
fluid and blood product
Insert indwelling urinary catheter. Maintain
an hourly urine output of 0,5-1 mL/Kg

Disability
Perform and document serial neurologic
examination

Facilitate Diagnosis and

Neurosurgical Consultation
Rapidly obtain appropriate diagnostic
studies
Monitor ICP in all patients with a GCS
score of 8 or lower
Facilitate surgical intervention
Admit to a neurologic critical care unit or
transfer to an appropriate facility

Reduce Intracranial pressure

Provide sedation and analgesia
Infuse mannitol 0,25-1 g/Kg in intermitten bolus
Maintain head on a neutral, midline position
Keep the patients head elevated 30 degrees
Minimize external stimulation
Consider ventriculostomy placement for CSF
drainage
Consider surgical decompression

General Care
Assess for and manage other injuries
Immobilize the spine and obtain cervical spine
films
Perform toxicologic or alcohol screening as
indicated
Regulate temperature to maintain normotermia
Treat seizure
Do not use IV dextrose infusion
Do not give dextrose 50% except in hypoglycemia
Do not give steroid
Consider organ donation in patient with a GCS of
less than or equal to 4 who remain unresponsive to
treatment

Thank Qiu

tony, psik 2007