Head Injuries

HEAD INJURIES
STUDY UNIT 1.4.1
DR N SCHEEPERS
LEARNING OUTCOMES: SU 1.7.1
After engaging with the materials and activities in this study unit you should be able to:
• Distinguish between the three main groups of head injuries.
• Explain the clinical manifestations based on the pathophysiology regarding the following:
 Injuries to the scalp
 Injuries to the scull, dome, or base
 Brain injuries
 Secondary bleeding:
 Epidural bleeding or haematoma
 Subdural bleeding or haematoma
 Brain stem injury
 Intra-cerebral bleeding or haematoma
• Explain the emergency treatment of a patient with head injuries.
• Develop a nursing care for a patient with head injuries.
• Explain the late complications of a patient with head injuries.
• Explain the causes of death in a patient with head injuries.
• Diagnose the set of criteria around brain death.
HEAD INJURIES
Any degree of traumatic
injury to the scalp, skull
or brain.
Caused by:
• Falls (35.2 %)
• MVA (17.3 %)
• Trauma caused with
objects (16.5 %)
• Assaults (10%)
SCALP INJURIES
• Most minor injuries
• Bleeds profusely – due vascular structure
Trauma to scalp may result in:
Abrasion
Contusion
Laceration
Hematoma beneath the layers of tissue
Avulsion (tearing away) of scalp – An emergency
injury
•Major complication: Intracranial infection

• Breaks in continuity of skull-
SKULL
caused by forceful trauma
FRACTURE
S • Classified according to type
and location
CLASSIFICATIO
N TO TYPE
1. LINEAR SKULL FRACTURE
• Most common fractures
• Indicates a break in the continuity of the

skull
• In-hospital: for observation

CLASSIFICATION
TO TYPE
2. Depressed skull fractures
• Bones of the skull are forcefully

displaced downward.
• Vary from slight depression, to bones of

the skull being splintered and
embedded within brain tissue.
CLASSIFICATION TO
LOCATION
1. BASILAR FRACTURES
• A fracture of the base of the skull - can be open (tear in
dura matter) or closed (dura is intact).
• Cause tears in the paranasal sinus of frontal bone or the
middle ear located in temporal bone causing signs such as:
• Haemorrhage from the nose, pharynx, ears and conjunctiva
• Battle`s sign (An area of ecchymosis seen over the mastoid)
• CSF ottorhea and rhinorrhoea
• Raccoon eyes
TRAUMATIC BRAIN INJURY (TBI)
CLOSED BRAIN INJURY OPEN BRAIN INJURY
• Sudden trauma to the brain that causes
• Head accelerates and then rapidly Object penetrates the skull, enters the
bleeding, bruising or tearing of nerves. decelerates brain and damages the soft brain
tissue
• Classified as closed brain injury and open

• Collides with another object (e.g
brain injury. wall, dashboard of a car)
• Brain tissue get damaged but

there is no opening through the
skull or dura matter.
TRAUMATIC BRAIN INJURY (TBI)
BRAIN INJURIES
CLASSIFICATION
1. Focal injuries (Contusions and
hematomas)
2. Diffuse (Concussions and diffuse
axonal injuries)
TYPES OF BRAIN INJURIES
1. CONTUSION
2. CONCUSSION
3. DIFFUSE AXONAL
INJURY
4. INTRACRANIAL
HEMORRHAGE
TYPES OF BRAIN INJURY
1. CONTUSION
Clinical manifestations: CONTUSION
- Brain is bruised and damaged in
- Loss of consciousness (stupor and
specific area
confusion)
- Cause: Severe acceleration-
deceleration force / blunt trauma - No hematoma – but brain tissue and
- Moderate to severe TBI neurological changes
- Affects: Frontal, Orbital and Temporal - Brain tissue haemorrhage

lobes. - Effects of injury shows 18 – 36 hours
after injury
CONTUSIO
N
CLINICAL MANIFESTATIONS:
2. CONCUSSION
2.1 GRADE 1 CONCUSSION
- Temporary loss of consciousness - Transient confusion
- No apparent brain structural damage - Conscious
- Resolves: 15 minutes
- Cause: Blunt trauma from an
acceleration-deceleration force, a
2.2 GRADE 2 CONCUSSION
direct blow or a blast injury.
- Transient confusion
- Conscious
- Resolves: >15 minutes

CLINICAL MANIFESTATIONS
2.3 GRADE 3 CONCUSSION:
- Loss of consciousness – lasts

from seconds to minutes
3. DIFFUSE AXONAL INJURY (DAI)
- Most severe brain injury
- Results from: widespread shearing

and rotational forces that produce
damage through the brain to axons
in the cerebral hemisphere, corpus
collosum and brain stem.
- Prolonged traumatic coma

CLINICAL MANIFESTATIONS OF DIA
• Comatose
• Decorticate and
decerebrate
posturing
• Global cerebral
oedema
CLINICAL MANIFESTATIONS
4. INTRACRANIAL HEAMORRHAGE
- Loss of consciousness – brief
Bleeding in brain in a form of haematomas - Lucid interval – patient is awake and conversant
(collections of blood in brain) epidural,
- Compensation of expanding haematoma
subdural and intracranial
occurs:
4.1 EPIDURAL HAEMORRHAGE • Rapid absorption of CSF and decreased
 Cause: Skull fracture, causes a rupture or intravascular blood volume – ICP normal ranges
laceration of middle meningeal artery. • When compensation stop- slight increase in

haematoma = increased ICP
 Haemorrhage – cause rapid increased ICP
TYPES OF BRAIN INJURIES EMERGENCY EPIDURAL HEMATOMA MANAGEMENT:
CLINICAL MANIFESTATIONS - Burr holes in skull to remove hematoma in order to
WHEN COMPENSATION STOPS: decrease ICP and control bleeding.
- Restlessness - Craniotomy performed to remove hematoma and

control bleeding.
- Confusion, agitated
- Drain inserted after procedures to prevent re-
- Pupils- fixed and dilated
accumulation of blood.
- Paralysis of an extremity
- Condition deteriorates rapidly
- Herniation can occur

4.2 Subdural hemorrhage
4.3 Intracerebral hemorrhage
•READ IN TEXTBOOK: PG 1999

PATHOPHYSIOLOGY OF TBI
Brain suffers traumatic injury
Cerebral oedema or bleeding increases

intracranial volume
Compensating mechanisms work
Rigid cranial volt allows no expansion of skull in brain to maintain blood flow and
which increases intracranial pressure prevent tissue damage. (CPP =
MAP – ICP) is 70 – 100 mmHg
Decreased cerebral blood flow occurs due to
pressure on blood vessels within the brain
Cerebral hypoxia and ischemia occurs

Cushing triad occurs:
SBP, Bradycardia and
Vasomotor center triggered (Brainstem) causes bradypnea
increase in arterial pressure
Intracranial pressure continues to rise. This Cessation of cerebral blood

may cause herniation flow results in brain death
MANAGEMENT OF HEAD INJURIES
Physical and neurological examinations
Diagnostic tests:
- CT scan
- MRI
- Positron emission tomography (PET) – Biochemical and metabolic function of the brain
Proper patient positioning maintained
Maintain adequate oxygenation – (pCO2 levels, ABGs)
Maintain a MAP above 70mmHg to ensure CPP
Fluid resuscitation
Nutrition
Manage pain and anxiety (Ativan)
Sedated patient (Propofol)

- Ineffective airway clearance and impaired gas exchange
NURSING related to brain injury
MANAGEMENT - Ineffective cerebral tissue perfusion related to increased
OF TBI ICP, decreased CPP and possible seizures
- Insufficient fluid volume related to decreased LOC
- Imbalance nutrition related to increased metabolic

demands/fluid restriction and inadequate intake
- Imbalance body temperature related to damaged thermo-

relating mechanisms in brain due to brain injury
- Risk for impaired skin integrity related to bedrest,

immobility/
COMPLICATIONS OF TBI
• Decreased cerebral perfusion
• Cerebral edema and herniation
• Impaired oxygenation and ventilation
• Impaired fluid, electrolyte and nutritional balance
• Risk of posttraumatic seizures

BRAIN DEATH TESTS DONE BY NEUROLOGIST:
•When a patient has sustained a sever head injury •Pupil reaction – fixed and dilated
incompatible with life, the patient is a potential organ •the eye, which is usually very sensitive, is stroked with a
tissue or piece of cotton wool to see if it reacts

donor.
•pressure is applied to the forehead and the nose is
Criteria indicating brain death:
pinched to see if there's any movement in response
-Comatose
•ice-cold water is inserted into each ear, which would
-Absence of brain stem reflexes
usually cause the eyes to move
-Apnea
•a thin plastic tube is placed down the windpipe to see if
Diagnostic tests done:
it provokes gagging or coughing
-An EEG •the person is disconnected from the ventilator for a short
-Brain stem auditory evoked potential period of time to see if they make any attempt to breathe
-Transcranial Doppler on their own

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HEAD INJURIES

STUDY UNIT 1.4.1

• Bleeds profusely – due vascular structure

Trauma to scalp may result in:

Hematoma beneath the layers of tissue

Avulsion (tearing away) of scalp – An emergency

•Major complication: Intracranial infection

• Most common fractures

• Indicates a break in the continuity of the

• In-hospital: for observation

• Bones of the skull are forcefully

• Vary from slight depression, to bones of

• A fracture of the base of the skull - can be open (tear in

dura matter) or closed (dura is intact).

• Cause tears in the paranasal sinus of frontal bone or the

middle ear located in temporal bone causing signs such as:

• Haemorrhage from the nose, pharynx, ears and conjunctiva

• Battle`s sign (An area of ecchymosis seen over the mastoid)

• CSF ottorhea and rhinorrhoea

• Classified as closed brain injury and open

• Brain tissue get damaged but

- Moderate to severe TBI neurological changes

- Affects: Frontal, Orbital and Temporal - Brain tissue haemorrhage

- No apparent brain structural damage - Conscious

- Resolves: >15 minutes

2.3 GRADE 3 CONCUSSION:

- Loss of consciousness – lasts

3. DIFFUSE AXONAL INJURY (DAI)

- Most severe brain injury

- Results from: widespread shearing

- Prolonged traumatic coma

laceration of middle meningeal artery. • When compensation stop- slight increase in

CLINICAL MANIFESTATIONS - Burr holes in skull to remove hematoma in order to

WHEN COMPENSATION STOPS: decrease ICP and control bleeding.

- Restlessness - Craniotomy performed to remove hematoma and

- Condition deteriorates rapidly

- Herniation can occur

4.2 Subdural hemorrhage

4.3 Intracerebral hemorrhage

•READ IN TEXTBOOK: PG 1999

Cerebral oedema or bleeding increases

Cerebral hypoxia and ischemia occurs

Intracranial pressure continues to rise. This Cessation of cerebral blood

Proper patient positioning maintained

Maintain adequate oxygenation – (pCO2 levels, ABGs)

Maintain a MAP above 70mmHg to ensure CPP

Manage pain and anxiety (Ativan)

Sedated patient (Propofol)

MANAGEMENT - Ineffective cerebral tissue perfusion related to increased

OF TBI ICP, decreased CPP and possible seizures

- Insufficient fluid volume related to decreased LOC

- Imbalance nutrition related to increased metabolic

- Imbalance body temperature related to damaged thermo-

- Risk for impaired skin integrity related to bedrest,

• Cerebral edema and herniation

• Impaired oxygenation and ventilation

• Impaired fluid, electrolyte and nutritional balance

• Risk of posttraumatic seizures