Monro-Kellie hypothesis (1850s)



Cranial compartment is rigid.

Brain 80%

Blood 10%

Cerebrospinal fluid 10%


Any increase in volumes within the cranial cavity must be compensated for by a decrease in the volume on another component or ICP will rise.


Compensatory mechanisms may maintain a normal ICP for volume changes of 100-120 mls.




Intracranial pressure

0 - 10 mmHg (normally about 10 mmHg lying flat).

Sustained > 15 mmHg is termed intracranial hypertension.

Areas of focal ischaemia develop if ICP > 20 mmHg.

Global ischaemia if > 50 mmHg.

Usually treat if > 20 mmHg.


Normal CPP is 90 – 100 mmHg.




Causes of raised intracranial pressure (RICP)


Brain causes

Tumours, infection, abscess, oedema.


Blood causes

Extradural, subdural, intracerebral, (SOLs) SAH.


CSF causes

Outflow obstruction from SAH, meningitis, tumours.

Increased production, rare choroid plexus papilloma.

Benign intracranial hypertension, often in young obese females.























Head Injuries



Concussion (MTBI)

Altered mental state with or without loss of consciousness.

Temporary neuronal dysfunction.

Caused by diffuse brain injury.

Fibre shearing in the area of the midbrain.

Confusion, disorientation, headache, dizziness, inability to concentrate, irritability, nausea, possible memory loss.

Effects of repeated episodes include motor dysfunctions, cognitive decline and Parkinsonian.



Traumatic brain injury (TBI)

Mild 15-13

Moderate 12-9

Severe 8 or less



Causes of primary brain injury




Foreign body

Depressed skull fracture


Cerebral contusion



Diffuse axonal injury



Causes of intracranial secondary brain injury

Extradural haematoma

Subdural haematoma

Cerebral oedema

Intracranial hypertension





Causes of extracranial secondary brain injury


Hypoxia – cerebral oedema

Hypercarbia – cerebral oedema

Acidosis – cerebral oedema







Intracranial hypertension



Headache, nausea, vomiting, drowsy, confusion, agitation, seizures, neck stiffness, back pain.



Decreased GCS when ICP goes over 40, focal signs, III nerve compression, Cushing’s reflex triad and irregular respirations.


Herniation is a possible complication

Supratentorial hypertension may result in infratentorial herniation

B.P. increase, widening of pulse pressure, bradycardia


Management in head injured patients



Prevent further injuries


Prevent complications of reduced levels of consciousness


Manage intracranial hypertension






Sedation and paralysis


Bed rest


Decompressive craniotomy or crainiectomy


No role for steroids in TBI


Intubation, sedation, paralysis, ventilation before transfers


Prevent hypotension


Maintain euvolaemia


Fluid restriction?


Prevent cerebral hypoxia






Treat pyrexia


Treat hyperglycaemia


Early enteral or parenteral nutrition


Anticonvulsants (phenytoin) for post-traumatic seizures


Antibiotics for open skull fracture


Motor and cognitive rehabilitation


















Principles in trauma care

Primary survey A, B, C,

Why important, death, brain damage is permanent

ACBC, Airway, Cervical spine, Breathing, Circulation

SCI - Cervical spine

C1 – C7 / T1

Full precautions

Often young people

Information about cause, was patient knocked out, alcohol or drugs involved?

Primary resuscitation, give fluids (plasma expanders) and oxygen

Secondary survey, other chest, abdomen or pelvic injuries may take priority

X Rays, neck, chest pelvis

A, B, C, Haemorrhage, Head injury.

Log role

Trachea central? Rib fractures?

Check air entry

Breathing problems common, keep patent airway, suction.

Less than 8, intubate

O2 saturations

Arterial blood gases

Anaesthetic help

Scalp and facial wounds, incised, lacerated


Head Injuries


Remember - Regard every patient with a head injury as having potential spinal cord injury.


Types of head injury


Blunt, accelleration/decelleration injuries         

Scalp - often bleed a lot

Skull - fractures may occur

Brain - injuries tend to be diffuse and may lead to concussion, ie disturbance or loss of consciousness, associated with variable periods of amnesia.                                                                                                       


Sharp or penetrating                                

Scalp    - May be small puncture wounds with larger underlying injuries

Skull    - often depressed skull fractures

Brain   - usually focal damage

            - little or no concussion

            - effects depend on location and extent

            - in high velocity injuries the shock wave leads to more widespread injury



Neurological observations

To look for changes in patients condition, Used after;

head injury, especially if patient was knocked out

intracranial disease

neuro-surgical procedures

other conditions effecting the brain, eg. overdose, ketoacidosis


10 - 15 minute frequency at first

Reduced to 2 - 4 hourly depending on patients condition

Performed by same nurse, together during handovers

Level of consciousness is a reliable indicator of cerebral function

Changes in conscious level occurs before pupil changes or changes in vital singns


Glasgow coma scale

A tool to objectively measure neurological condition

Uses eye opening, best verbal response and best motor response

Each response is given a score


Eye opening

spontaneous            4                      to speech 3               to pain 2                     none 1


Best verbal response

orientated                              5                      confused       4

inappropriate words             3                      incomprehensible sounds 2

none                                       1


Best motor response

obeys commands                 6                      localises to pain                   5

flexion to pain, (withdrawal) 4                   flexion to pain, (abnormal) 3

extension to pain                 2                      none                                       1


The 3 modes of behaviour are then summated to give an overall score.

Normal would be Glasgow coma scale 15.

Any deterioration must be reported to medical staff at once as it may signify the development of an intracranial lesion.

If changes are noted during the assessment, again they must be reported at once.


Vital signs

Blood pressure, pulse, respiration and temperature.

To check ABC are adequate to prevent secondary brain damage secondary to cerebral hypoxia.

Blood pressure may rise in increased intracranial pressure.               Pulse rate may fall.


Pupillary response

Normal pupils are equal is size and respond to light

+ means the pupil has contracted                        -  means the pupil has not contracted

c means the eye is closed

A pupil will not react to light and may dilate due to pressure on the occulomotor, (third) cranial nerve.


Motor strength

Limb power is measured on both sides to respond to both cerebral hemispheres

/           means normal power on both sides

R         means right                                       L          means left



Nursing management in head injuries



Has patient been knocked out?                            Level of consciousness

Headache                                                                 Vertigo

Temperature                                                             Shock



Airway and breathing - hypoxia and excess CO2 cause cerebral oedema.

Suction, humidified oxygen, semiprone position, intubation.

Observations, bleeding, loss of CSF from nose and ears may indicate base of skull fracture.

Keep safe during periods of agitation, look out for causes of distress.

Convulsions may occur.

Control temperature.

Aid in treatment of cerebral oedema, hyperosmolar solutions, (eg mannitol).

Keep head slightly elevated to reduce cerebral oedema, about 15` or 30` if there is a CSF leak.

Prophylactic antibiotics for open skull fractures.

Care of unconscious patient

Prevention of effects of immobility


Possible complications following a head injury

Amnesia                                                                                personality and behavioural change

inability to formulate words – dysphasia                         inability to concentrate

impaired intelligence                       haemorrhage                        hydrocephalus                                            

raised intracranial pressure           cerebral infarction    infection

meningitis                                         convulsions              visual disturbance

diabetes insipidus                           deafness                   damage to any of the cranial nerves hemiparesis or other paralysis     death



Causes of unconsciousness


Poisons and drugs


General anaesthetics

Overdose eg. opiates

Gases, eg Carbon Monoxide

Heavy metals eg. Lead, Mercury


Vascular causes





Encephalitis (Viral)

Meningitis (Bacterial)



Endocrine causes








Metabolic causes

Diabetes mellitus


Hepatic Coma


Mechanical causes


Hypothermia, Hyperthermia







Description of brain injury



“Bruising” of cerebral tissue

Most commonly affects frontal, occipital and under-surface of temporal lobes

“Coup”             - indicating haemorrhage and oedema immediately under injury site

Contre-coup” - damage occurs directly opposite the injury site due to rapid                          acceleration/deceleration injury.



eg. due to skull fracture



Localised collection of blood

Extradural      - situated or occurring outside the dura mater

Subdural       - between the dura mater and arachnoid mater

Intracerebral - within the brain substance


Diffuse brain injury

No localised brain pathology

Shearing of white matter - causing disruption and tearing of neuronal axon fibres

Features may therefore be focal or global


Intracranal Pressure

The pressure exerted within the cerebral ventricular system.

Adult skull is a rigid box, containing non-compressible components:

Brain (80%)                           Cerebrospinal fluid                          Blood

Normal value: 5 - 12 mmHg.

Transient rises occur with coughing sneezing.

A correlation exists between ICP and conscious level.

ICP increases ------- conscious level decreases.

Initial rise in ICP - compensatory mechanisms

1) Downward displacement of CSF to distendable spinal dural sac.

2) Reduction in blood flow.

As ICP rises, compensation overcome ------- Small rises in volume lead to dramatic rises in ICP.


Causes of RICP

Head injury                                                               Cerebral oedema

Abscess or inflammation                                        Haemorrhage

Tumour                                                                      Cranial surgery

Hydrocephalus                                                         SOL  =   Space occupying lesion

Pathophysiology is explained by modified Monro-Kellie hypothesis, which states: "the skull, a rigid compartment, is filled to capacity with essentially non-compressible contents - brain tissue, intra-vascular blood and cerebrospinal fluid.  if any of these three increases in volume, another must decrease or else intracranial pressure will rise."    (Hickey, 1986).


Signs and symptoms of raised ICP

Headache - early morning, associated with vomiting

Deterioration in conscious level, changes in GCS

Sudden change eg. quietness or restlessness

Contralateral Hemiparesis/Hemiplegia

Deterioration in respiratory pattern

Alteration in pupil size, light reaction. 

Blurring of vision, ocular muscle paresis/ paralysis.

Increase in systolic BP, widening of pulse pressure.

Bradycardia, or pulse changes

Problems with speech, comprehension.

Localising signs, eg Grand Mal, Focal Seizure activity.

Moderately elevated temperature


Pupil change





Process by which tissues in a high pressure compartment is compressed and forced through an available opening into an adjoining low-pressure compartment.


Skull - 2 compartments

Supratentorial                                                           Infratentorial

Suppratentorial Herniation            - Tentorial Notch

Infratentorial Herniation     - Foramen Magnum.


Classic pre-coneing triad;

B.P. increase

Widening of pulse pressure



Care and Management of Client with Closed Head Injury



Preservation of brain homeostasis

Prevention of secondary brain injury

Maintenance of cardiovascular and respiratory function to maintain            cerebral perfusion


Collect information

What time did the accident occur?                       What caused the injury?

What was the direction and force of the blow?  Was there loss of consciousness?

What was the duration of unconsciousness?    Any related post-traumatic amnesia?

Any neurological deficits noted?


Difficulty in maintaining airway due to lowered level of consciousness

CO2 retention  -------  cerebral vasodilation  --------  increase in ICP

Semi-prone position

Head of bed elevated 30 degrees ------- reduces intracranial venous pressure

Pulmonary secretions - suction no longer than 15 seconds, pre-oxygenate 100% 02

Hyperventilation - reduce pCO2 to encourage cerebral vasoconstriction.


Alteration of conscious level and neurological function due to Head Injury

Establish base-line neurological status

Monitor Glasgow Coma Scale, limb and pupil size and reaction, vital signs as indicated.

Report any deterioration immediately.


Increased ICP with risk of brain herniation


Tentorial herniation

The protrusion of brain tissue into the tentorial notch, caused by increased intracranial pressure.

Nurse with head of bed elevated 30 degrees

Maintain head and neck position in neutral position - prevents cerebral venous drainage obstruction.

Avoid valsalva manoeuvre - increases intraabdominal pressure - intrathoracic pressure - ICP

Avoid extreme hip flexion

Control body temperature - 1 degrees centigrade increases metabolic demand of the brain by 10%

Assist in fluid restriction if indicated

Administer cerebral diuretics (hyperosmolar agent) eg. mannitol 20% 100 mls if indicated.

Controlled ventilation, avoid hypoxia

? Hypothermia

? Removal of CSF

Pre-op care


Potential seizure activity

Seizure activity increases metabolic rate, causes hypercapnoea and increases ICP


Potential fluid and electrolyte imbalance

Maintain accurate fluid balance recording

Monitor urine for SG (diabetes insipidus may develop due to hypothalamic/adjacent structural damage)

Potential for altered nutrition due to decreased conscious level


Potential for injury due to altered consciousness, restlessness and confusion

Sedation contra-indicated: may mask deterioration in neurological condition


Need to consider:

Hygiene needs, prevent complications of bed rest eg. pressure sore development, muscle wasting and contractures.



Complications of Head Injury

Cerebro-spinal fluid leakage, CSF rhinorrhoea, otorrhoea due to basal skull fracture

? possibility of meningitis, cerebral abscess.

Post-traumatic epilepsy


Diabetes insipidus.


Intracranial haemorrhage


Subdural haemorrhage

More common than extradural

Signs may be delayed after injury by weeks - blood oozes from veins

Headache, apathy, gradual deterioration in consciousness level - often with lucid periods, localising signs

Craniotomy is required


Subarachnoid haemorrhage  (SAH)

Often hard to differentiate from intracerebral - both are usually spontaneous


Clinical features

Headache - often abrupt onset                             Loss of senses

Feelings of ill-ease in the head                            Increasing headache

Neck stiffness                                                           Vomiting


Caused by trauma and congenital lesions.

Blood in CSF is irritant therefore headache, neck stiffness, photophobia and irritability.


Extradural haemorrhage

Between the Dura and the Skull

70% rupture of middle meningeal vessels

Often a history of being unconscious followed by recovery, followed by changes

Check using CT/MRI

Local signs may present

Always account for after a skull fracture

Pre-op care



Signs of increased intracranial pressure (ICP) in infants and children



Tense, bulging fontanel : lack of normal pulsations         Separated cranial sutures

Irritability                                                                                                                High-pitched cry

Increased occipito-frontal circumference                                           Distended scalp veins

Changes in feeding                                                                                              Cries when held or rocked

“Setting-sun” sign



Headache                                                                                                               Nausea

Vomiting often without nausea                                                            Diplopia - blurred vision



Personality and Behaviour Signs

Irritability,  restlessness

Indifference, drowsiness or lack of interest

Decline in school performance

Diminished physical activity and motor performance

Increased complaints of fatigue, tiredness, increased time devoted to sleep

Significant weight loss possible from anorexia and vomiting

Memory loss if pressure is greatly increased

Inability to follow simple commands

Progression to lethargy and drowsiness


Late Signs

Lowered level of consciousness

Decreased motor response to command

Decreased sensory response to painful stimuli

Alterations in pupil size and reactivity

Sometimes decerebrate or decorticate posturing

Cheyne-Stokes respirations