Monro-Kellie hypothesis (1850s)
Cranial compartment is rigid.
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.
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.
CPP = MABP - ICP
Normal CPP is 90 – 100 mmHg.
Causes of raised intracranial pressure (RICP)
Tumours, infection, abscess, oedema.
Extradural, subdural, intracerebral, (SOLs) SAH.
Outflow obstruction from SAH, meningitis, tumours.
Increased production, rare choroid plexus papilloma.
Benign intracranial hypertension, often in young obese females.
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)
Severe 8 or less
Causes of primary brain injury
Depressed skull fracture
Diffuse axonal injury
Causes of intracranial secondary brain injury
Causes of extracranial secondary brain injury
Hypoxia – cerebral oedema
Hypercarbia – cerebral oedema
Acidosis – cerebral oedema
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
Decompressive craniotomy or crainiectomy
No role for steroids in TBI
Intubation, sedation, paralysis, ventilation before transfers
Prevent cerebral hypoxia
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
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.
Trachea central? Rib fractures?
Check air entry
Breathing problems common, keep patent airway, suction.
Less than 8, intubate
Arterial blood gases
Scalp and facial wounds, incised, lacerated
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
To look for changes in patients condition, Used after;
head injury, especially if patient was knocked out
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
A tool to objectively measure neurological condition
Uses eye opening, best verbal response and best motor response
Each response is given a score
spontaneous 4 to speech 3 to pain 2 none 1
Best verbal response
orientated 5 confused 4
inappropriate words 3 incomprehensible sounds 2
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.
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.
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.
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.
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
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.
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
Overdose eg. opiates
Gases, eg Carbon Monoxide
Heavy metals eg. Lead, Mercury
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
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
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
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
Suppratentorial Herniation - Tentorial Notch
Infratentorial Herniation - Foramen Magnum.
Classic pre-coneing triad;
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
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
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
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
? Removal of CSF
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.
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
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.
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
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
Vomiting often without nausea Diplopia - blurred vision
Personality and Behaviour Signs
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
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