HEAD INJURY

By
Angelina. A. Joho
Msc, Critical care & Trauma
 Therapeutic Intervention for
patients with severe head injuries
Objectives;
• At the end of this presentation students will be able to
describe therapeutic intervention for pt with severe head
injury on;
– Achieving Adequate Cerebral Perfusion Pressure
– Ventilatory Support and the Use of Hypocapnia for
Intracranial Pressure Reduction
– Fluid Therapy
– Nutrition
– Thromboprophylaxis
– Sedation and Suppression of Cerebral Metabolism
– Analgesia
– Seizure Prophylaxis
– Hypothermia
– Steroids
– Decompressive Craniectomy
 Overview of head injury

Head injury refers to trauma of the head.

This may or may not include injury to the
brain.
The incidence of head injury is 300 of every
100,000 per year (0.3% of the population),
with a mortality rate of 25 per 100,000 in
North America and 9 per 100,000 in Britain.
• Mortality in patients who require intensive
care treatment after acute head injury is high,
with a rate of 23.5% reported in a recent series
of more than 11,000 admissions. A major
contributor to outcome is Hypotension
• The prevention of this secondary damage is
by avoidance, detection, and treatment of
physiologic derangements that is a major focus
of the intensive care management of
neurotrauma
 Causes
Common causes of head injury are:
• motor vehicle traffic collisions,
• home
• occupational accidents,
• falls
• assaults.
• Bicycle accidents are also a cause of head
injury-related death and disability, especially
among children.
 Mechanism of injury
• TBI occur when mechanical force are transmitted to
the brain tissue, mechanism of injury include
penetrating or blunt trauma to the head.

• Penetrating trauma can result from penetration of a

foreign object eg a bullet, that cause direct damage to
the cerebral tissue.

• Blunt trauma be result of deceleration, acceleration or

rotation force.
 Pathophysiology of TBI
• Pathophysiology can be divided into two categories;
primary injury and secondary injury.

• Primary injury occur at the moment of impact as a result

of mechanical force to the brain, this can be localised to
an area or diffuse or widespread throughout the brain.

• Primary injury may occur as a direct damage to the

parenchyma or as injury to the vessels that causes
hemorrhage, compressing nearby structures. Examples of
primary injuries include contusion, laceration, shearing
injuries, and hemorrhage.
• Primary injury may be mild, with little or no
neurological damage, or severe with major tissue injury

• Secondary injury is a biochemical and cellular response

to the initial trauma that can exacerbate the primary
injury and cause loss of brain tissue not originally
damaged.

• Secondary injury can be caused by ischemia,

hypercapnia, hypotension, cerebral edema, sustained
hypertention, calcium toxicity, or metabolic
derangements.
 Common symptoms
• Coma
• Confusion
• Drowsiness
• personality change
• Seizures
• nausea and vomiting
• headache and lucid interval during which a
patient appears conscious only to deteriorate
later.
 Symptoms of skull fracture
can include:
• leaking cerebrospinal fluid from nose, mouth or
ear) may be and is strongly indicative of basilar
skull fracture and the tearing of sheaths
surrounding the brain, which can lead to secondary
brain infection.

• visible deformity or depression in the head or face;

for example a sunken eye can indicate a maxillar
fracture

• an eye that cannot move or is deviated to one side

can indicate that a broken facial bone is pinching a
nerve that innervates eye muscles
• wounds or bruises on the scalp or face.

• Basilar skull fractures, those that occur at the base of the

skull, are associated with Battle's sign, a subcutaneous
bleed over the mastoid, hemotympanum and
cerebrospinal fluid rhinorrhea and otorrhea.

• Because brain injuries can be life threatening, even

people with apparently slight injuries, with no noticeable
signs or complaints, require close observation.

• The caretakers of those patients with mild trauma who

are released from the hospital are frequently advised to
rouse the patient several times during the next 12 to 24
hours to assess for worsening symptoms.
 The severity of TBI
The severity of TBI according to the GCS score
(within 48 h) is as follows:
• Severe TBI = 3-8
• Moderate TBI = 9-12
• Mild TBI = 13-15
Glasgow coma scale

Eye s Opening •Spontaneous opening 4

•To verbal command 3
•To pain 2
•No response 1

Best verbal response • oriented & converses 5

•Disoriented & converses 4
•Inapproriate words 3
•Incomprehensibe sounds 2
•No response 1

Best motor response To command •Obeys commands 6

To pain stimulus
•Localizes pain 5
•Flexion – withdrawal 4
•Flexion – abnormal ( decorticate 3
rigidity )
 Initial management of head trauma
• Support airway, breathing, and circulation (ABCs). A
cervical spine injury should be considered to be present
in any patient with multisystem trauma.
• Intravenous resuscitation solutions should consist of
isotonic Ringer's lactate (LR) or normal saline (NS).
Fluids should be infused until the patient is euvolemic.
• Make an initial assessment of the patient during the
primary survey (alert, voice, pain, unresponsive).
• Perform a mini-neurologic examination and repeat
frequently (GCS, motor/lateralizing signs).
 Initial management of head
trauma cont.
• Examine the skull depressed skull fractures, Battle's
sign (blood in the ear canal or ecchymosis over
mastoid process),

• Raccoon's eyes (periorbital ecchymosis), or

rhinorrhea. If any of these signs are present, the
patient requires admission and a neurosurgical
consult.

• Nasogastric and nasotracheal intubation are

contraindicated in patients with significant facial
trauma because a cribriform plate fracture may be
present
 Secondary survey
• Secondary survey is only undertaken when
the patient ABCs are stable. followed with
Continually reassessment of ABCs
• Head to toe assessment is done to rule out any
abnormalities.
• A history, including the mechanism of injury,
past medical history, drug intake, should be
completed.
• And investigation
 Principles of Management
• Mortality in patients who require intensive care
treatment after acute head injury is high, with a
rate of 23.5% reported in a recent series of more
than 11,000 admissions.
• A major contributor to outcome Hypotension It is
prevention of this secondary damage by
avoidance, detection, and treatment of physiologic
derangements that is a major focus of the
intensive care management of neurotrauma.
 Principle of management cont.
• Hypotension (SBP <90 mm Hg) and
hypoxemia (PaO2 <60 mm Hg or 8 kPa)
during the acute to sub- acute phases of brain
injury are associated with a worse outcome.
• Other factors that have been found to
adversely affect outcome include intracranial
hypertension, hyperglycaemia, hyperthermia,
and cerebral perfusion pressure (CPP) less
than 50 mm Hg.
 Monitoring in Acute Neurotrauma

• Continuous pulse oximetry,

• regular arterial blood gas analysis,
• invasive blood pressure monitoring,
• blood glucose levels, and
• core temperature monitoring are all important.
 Intracranial Pressure Monitoring

• Intraventricular devices to monitor ICP are

regarded as the “gold standard” and have the
added advantage that intracranial fluid may be
removed to control intracranial hypertension.
• Intraparenchymal monitors or fiberoptic
probes are often preferentially used because of
a lower risk of infection and hemorrhage, as
well as ease of insertion. Ventricular and
subdural transducers may also be used.
Jugular Venous Oximetry
• Jugular venous oximetry may be used to aid
assessment of cerebral blood flow (CBF) in
neurotrauma. Jugular venous oxygen
saturation (SjvO2) values below 50% have
been associated with a worse outcome
• Normal value
 Therapeutic intervention
1) Achieving Adequate Cerebral Perfusion
Pressure (CPP)
• it is important to ensure that CPP , is
maintained rather than focusing solely on ICP as
a target.
• CPP should be > 60 to 70mmhg
• Targets may be achieved by either decreasing
ICP < 20mmHg, or increasing MAP via volume
expansion, inotropes, and vasopressors.
• medical & Nursing interventions
– Aims ; maintain the ICP < 20mmHg
– Maintaing CPP > 70 mmHg
• Therapy instituted to decrease ICP & then
identify underlying cause
• CPP = Mean Arterial BP - ICP
2) Ventilatory support and the use
of hypocapnia for intracranial
pressure reduction
A Glasgow Coma Scale (GCS) score of 8 or less,
ventilatory failure, central neurogenic
hyperventilation, and recurrent seizures are all
indications for intubation and ventilation.
• Hyperventilation is no longer recommended
as a prophylactic intervention after severe
TBI,33 and hyperventilation to below a PaCO 2
of 25 mm Hg is never indicated.
3) Fluid Therapy
• Fluid management aimed at restoring euvolemia
and preventing hypotension is important in acute
head trauma. However, it may be complicated
by hemorrhage, concealed or continuing, from
associated extracranial trauma
4) Mannitol
• Mannitol is an osmotic agent that can reduce ICP and
improve cerebral blood flow, CPP, and brain
metabolism. It reduces ICP within 30 minutes, and the
effect lasts variably up to 6 to 8 hours. Mannitol expands
plasma volume, initially can reduce hypotension, and can
improve oxygen-carrying capacity.

• Mannitol is administered by repetitive bolus (0.25

gram/kg to 1 gram/kg), Mannitol results in a net
intravascular volume loss because of its diuretic effect,
so monitor input and output to maintain euvolemia.
5) Nutrition
• Early feeding may be associated with a trend
toward improved survival and decreased
disability. If enteral feeding cannot be
achieved, parenteral feeding with gastric stress
ulcer prophylaxis and good glycemic control
should be considered.
6) Thromboprophylaxis
• Neurotrauma patients, particularly those with
extracranial injuries, are at increased risk for the
development of venous thromboembolism.
Prophylactic doses of heparin may be safe from
the second to third day after injury.
• Reasonable but unproven alternatives include the
nonpharmacologic methods of elastic stockings eg
Tedd stocking or pneumatic compression devices
7) Sedation and Suppression of Cerebral
Metabolism
propofol are preferred, can induce both
hypotension and a decrease in CPP, especially
in volume-depleted patients.
Midazolam is an alternative, but its
accumulation means that propofol is often
preferable if rapid emergence is required.
8) Analgesia
• Effective analgesia for these patients, who
often have multiple injuries, is important to
reduce the autonomic responses to stimulation.
Opioids have minimal effect on cerebral
metabolism, blood flow, and ICP, as long as
ventilation and normotension are preserved.
9) Seizure Prophylaxis
• Risk factors for the development of post-
traumatic seizures include GCS scores lower
than 10, cortical contusion, intracranial
hematoma, depressed skull fracture, or a
penetrating injury. There is some evidence to
support prophylaxis in these patients to prevent
early (within 7 days of injury) seizures, but
anticonvulsants appear to be less useful in
preventing the occurrence of late seizures
10) Hypothermia
• Hypothermia reduces cerebral metabolism
with a concurrent reduction in ICP
11) Steroids
• The routine use of corticosteroids in head
injury to reduce edema is not currently
recommended.
Position
• The patient head should be elevated to about
30degrees to reduce ICP
 Take note
• Care must be taken to evaluate blood pressure
in response to head elevation
• Raising the head of the bed may ↓se MAP →
↓sing of CPP
• Hemodynamically unstable pts may need to be
cared for in a flat position
• Pt can be turned from side to side
• However , during positioning & elevating the
head of the bed , monitor and asses patient’s
cerebral & hemodynamic response
 Note cont;
• If the ICP does not return to the baseline with
5 min after change of position , pt must return
to the position that maximised CPP
• Suctioning – ass’d with hypoxemia ; Pt is
preoxygenated with 100% oxygen before &
btn suction attempts , & for I min after the
procedure
• Each suction attempt is limited to < 10 Sec
with no more than 2 suction passes
• Head maintained in neutral position during
suction procedure
 Visitors
• Presence of family member has shown to
increase ICP
• Family members – cautioned to avoid excess
stimulation of the pt or unpleasant
conversation s that can emotionally stimulate
the pt ( discussing prognosis , condition
deficits , restraints ) → ↑ICP
• Assessing pt’s physiological response to
visitors – an important nursing function
• Nursing care plan

• Medical Management
– Adequate oxygenation & ventilation
– Euvolemic fluid administration
– ↓ sing metabolic demands
• Monitor vital signs closely.

• (a) Accurately assess and document

neurological status

• (b) Evaluation of alterations of consciousness

is crucial since symptoms progress rapidly.
 Maintain patent airway
• (a) Intubation and hyperventilation may be
indicated to provide adequate cerebral
perfusion of oxygenated blood and decrease
carbon dioxide induced vascular spasm.
• (b) If patient is not intubated, position the
patient on his side to decrease the possibility
of airway occlusion; use oral or
nasopharyngeal airway, prn.
• Be aware that stimulation of coughing when
suctioning increases intracranial pressure and
may precipitate seizure activity.
• Administer medications as ordered.
• (a) Mannital (osmotic diuretic, to decrease
cerebral edema).
• (b) Corticosteroids (to reduce cerebral edema).
• (c) Dilantin (as a precautionary measure to
prevent seizure activity
• ABCs
• Elevate head of bed (30º).
• (a) Promotes return of venous blood.
• (b) Under no circumstances should patient's head be
lower than the body
• Administer hypertonic I.V. solutions as ordered.
• (a) Dextrose in water (hypotonic) crosses the blood-
brain barrier and increase cerebral edema and
intracranial pressure.
• (b) Fluids will be restricted to reduce intracranial
pressure.
• (c) Accurate intake and output records must be kept.
Protect patient from injury should seizures occur.
• (a) Pad side rails.
• (b) Secure a tongue blade to the head of the bed for
easy access.
• Maintain normal body temperature.
• (a) Intracranial bleeding is frequently accompanied
by increases in body temperature that are resistant to
antipyretic agents.
• (b) Monitor rectal temperature frequently.
• (c) Place patient on hypothermia blanket
• Patient Education. Family members of patients who
return home following injury to the head should be
instructed to return the patient to the hospital if any of
the following problems occur
• Fever greater than 100ºF.
• Pulse less than 50 beats per minute.
• Vomiting.
• Slurred speech.
• Dizziness.
• Blurred or double vision.
• Unequal pupil size.
• Blood or fluid discharge from ears or nose.
• Increased sleepiness.
• Inability to move extremities.
• Convulsions.
• Unconsciousness
 Psycho social support
• Nurses must support the family by providing
information & psychosocial support to
families to reduce their anxiety
•Thanks for listening
 References;
• 1) Primary trauma care Authors are Douglas A
Wilkinson and Marcus W Skinner
• 2) Intensive Care Management of Acute Head
Injury by Virginia Newcombe, David K. Menon
• 3) Tintinalli's Emergency Medicine
• 4) Evidence-Based Practice of Critical Care How
Should Traumatic Brain Injury Be
• Managed?
• Larami MacKenzie, W. Andrew Kofke
•