The Patient with Altered

Consciousness.
2
Basics Anatomy.
Cerebellum.
Co-ordination,
skilful movement
posture and
balance
Cerebrum.
Interpretation of sensory data.
Co-ordination of muscular
movement. Intellectual and
emotional processes.
Meninges.
Hypothalamus.
Controls ANS.
Emotion and
behaviour.
Temperature
control.
Circadian
rhythm
Brain Stem.
3
Basics - The Reticular Activating
System
Scattered throughout most of the length of the Brain Stem
is a group of nuclei collectively called the Reticular
Formation.

These receive axons from a large number of neurons and
especially from nerves that innervate the face.

These axons play an important role in arousing and
maintaining consciousness. The Reticular Formation and
its connections constitute

- the Reticular Activating System (RAS)

It is involved with the Sleep / Wake Cycle.



4
Basics - The Reticular Activating
System
Visual and acoustic stimuli and mental activities can
stimulate the Reticular Activating System to maintain
attention and alertness.

Conversely removal of visual or auditory stimuli may lead
to drowsiness or sleep. Damage to cells of the Reticular
Formation can result in coma.

The RAS is relatively sensitive to certain drugs - General
anaesthetics function by suppressing this system.

Descending Fibres from the Reticular Formation constitute
one of the most important motor pathways. Fibres from the
Reticular Formation are critical in controlling respiratory
and cardiac rhythms and other vital functions.
Consciousness.
6
Definitions.
Consciousness is defined as a general
awareness of oneself and the surrounding
environment. (Hickey 1997) - capable of
responding to sensory stimuli.

It is a dynamic state and can therefore,
change. Eg. Waking from sleep.

In the same way Unconsciousness
incapable of responding to sensory
stimuli .

7
Definitions.
Consciousness is described as having
two parts to it:

Arousal or wakefulness - a function of the
reticular activating system (RAS) located
in the brainstem.

Awareness or cognition - a function of the
cerebral hemispheres.

8
Underlying Mechanisms.
Consciousness is dependent upon the
cerebral hemispheres being intact and
interacting with the ascending RAS.

It is maintained by a constant stream of
impulses that are sent from the brain stem
upwards into the two cerebral
hemispheres.

Loss of consciousness therefore has two
general mechanisms.
9
Underlying Mechanisms.
Cerebral Hemisphere Malfunction.


Altered Consciousness.


Brain Stem Malfunction.
10
Underlying Mechanisms.
Cerebral Hemisphere Malfunction.

Drug and alcohol intoxication.
Hypoxic brain injury.
Stroke.
Metabolic disorders.
Infection.
Post seizure.
11
Underlying Mechanisms.
Brain Stem Damage.

Direct Damage.
Brain Stem Infarct.

Indirect Damage (pressure from above).
Cerebral Mass (clot, tumour, abscess)
Cerebral Oedema (infarct, hypoxia, infection, injury)
12
REMEMBER.

Alterations in conscious level may be slow
and progressive or may be acute.

Loss of consciousness may be brief or
may be prolonged.

Accurate assessment of conscious level
is one of the most important roles of the
health care practitioner.
Altered Consciousness.
14
Pathological Causes of Decreased
Conscious Level. (after Shah 1999 and Gray and Toghill 2001)
Brain Injury /
Irritation.

Increase in Brain
Volume.
Increase in
Cerebral Blood
Volume.
Increase in CSF
Volume.

Metabolic Causes.

Drugs and
Poisoning.

15
Pathological Causes of Decreased
Conscious Level.
Brain Injury /
Irritation.

Cerebral infection -
encephalitis / meningitis.

Brain infarction.

Post seizure.


Increase in Brain
Volume.

Brain tumours.

Cerebral oedema from
head injury.

Cerebral abscess.

16
Pathological Causes of Decreased
Conscious Level.
Increase in
Cerebral Blood
Volume.

Extradural haematoma.

Subdural haematoma.

Subarachnoid
haemorrhage.

Intracerebral haematoma.

Increase in CSF
Volume.

Hydrocephalus.

17
Generalised metabolic or
toxic disorders can
depress brain function.
18
Metabolic Causes.

Major organ failure. (E.g liver or kidney failure)

Metabolic acidosis.

Hypoxia.

Hypo / Hyperglycaemia. (blood sugar < 3 mmol/L = coma
and possible fitting)

Electrolyte imbalance. (E.g disturbances of calcium,
sodium and potassium.)

Pituitary, adrenal and thyroid disease. (E.g
Hypothyroidism)

Cardiac Arrhythmias (E.g fast atrial fibrillation)

Hypothermia.

19
Drugs / Poisoning.

Sedatives - barbiturates, opiates.

Amphetamines - tricyclic antidepressants.

Steroids.

Salicylates.

Anticonvulsants.

Alcohol.

Poisons.
20

Precipitating Factors

Age: The incidence of altered consciousness increases with age.
Cardiovascular status: Disorders that lower cardiac output,
lower perfusion and precipitate arrhythmias.
Pulmonary disorders: Disorders that cause hypoxia and
hypoxaemia.
Drug therapy: Sedation, analgesia, drug toxicity, drug
interactions.
Cerebral disorders: Including expanding lesions and brain
injury.
Surgical factors: Prolonged anesthesia time.
Perceptual / sensory factors: Sleep deprivation, sensory
overload, sensory deprivation.
Metabolic factors: Changes in glucose level, hypermetabolism,
hypometabolism.
Fluid and electrolyte disturbances: Sodium and
potassium imbalances, hypovolaemia.


Assessment and Management.
22
Priorities.
Establish exactly what happened.
Immediate assessment (life threatening
conditions).
General assessment.
Investigations.
Working diagnosis.
Management plan
Continue to monitor.

Where do you fit in?
Blood and Urine.
Drug screen, U and E, glucose,
calcium, LFTs, ABGs, thyroid,
cortisol levels, blood cultures etc.

CT / MRI Scanning.

CSF investigations.
Assessment.
24
Assessment ?
Consciousness cannot be measured
directly and can only be assessed by
observing a person's behaviour in
response to different stimuli.

Assessment of consciousness is difficult
because it can only be implied by an
evaluation of the person's appearance and
behaviour by another person. (Hickey 1997)

25
Why Assess?
3 reasons.
Is the patients condition,

Improving?
Remaining static?
Deteriorating?
26
Assessment.
Vital signs.

Level of consciousness.

Motor function.

Pupillary signs.

27
Vital Signs.
Changes in respiration, in terms of rate
and pattern of breathing, can give a good
idea of the function of the brain stem.

Alterations in temperature may be due
to damage to the hypothalamus.

Rising blood pressure and falling heart
rate may = increasing ICP. (Cushings sign)
Glasgow Coma Score.
Teasdale and Jennett (1974) and (1976).

The most widely used scoring system for
quantifying consciousness.


Allows standardisation of assessment.

29
Glasgow Coma Score.
Consists of three aspects of behavioural
response, each evaluated independently.

Eye opening.
Best verbal response.
Best motor response.

It assesses the two aspects of
consciousness: arousal and cognition.


30
Glasgow Coma Score.
Highest score = 15
Lowest score = 3 (even patients who are brain stem
dead score 3)

The phrase GCS of 10, 12 etc is largely
meaningless and the figure should be
broken down as E3V3M4, E3V4M4 etc.


A patient scoring of eight or less is
considered to be in a deep coma.


31
Eye Opening.


C = eyes closed by swelling.

Spontaneous.
To speech.
To pain.
None.

4
3
2
1

Best Verbal
Response.


T = tracheostomy / ET tube

Orientated speech.
Confused speech.
Words only.
Sounds only.
None.

5
4
3
2
1

Best Motor
Response.

*

Obeys command.
Localises pain.
Flexion to pain.
Abnormal flexion.
Extension.
None.

6
5
4
3
2
1

Brief Aside.
Applying Painful Stimuli.
33
Painful Stimuli?
When performing the GCS, you are
trying to illicit a purposeful and specific
response to painful stimuli (not just a response
to the irritation).

As such stimuli that causes the patient
to respond purposefully are favoured
(across the midline and up) .
34
Painful Stimuli?
Trapezius pinch?
Supraorbital ridge? (Not in facial #)
Jaw margin? (Not in facial #)
Lateral aspect of fingers?
Sternal rub?
Inflicting a painful stimulus may not
always be needed, as the patient may find
objects such as nasogastric tubes and
oxygen masks irritating, and may localise
spontaneously to such sources of
irritation.

Back to the GCS
36
Eye Opening.
Spontaneous
4
Eyes are open without any active
stimulation by the observer.

To speech.
3
Initially using a normal voice increasing to
loud. No touch should take place.

To pain.
2
Begin with touch. Apply painful stimuli if
required.

NB. No residual discomfort / damage.

No response.
1
Self explanatory, but is dependent on
degree of stimulus as above.

A patient with flaccid ocular muscles may have their eyes open at all times.
37
Orientated
speech.
5

Orientated in time and place. Name /
whereabouts / month / year.
Confused speech.
4

Incorrect answers to one or more of the
above, but is able to formulate full sentences.

Words only.
3


Usually inappropriate words. To
distinguish from above consider - In this
category, conversational exchange is absent,
patients will tend to use single words rather
than sentences and replies are given in
response to physical rather than verbal
stimulation.

Sounds only.
2

Sounds that cannot be identified as words.
i/e. mumbling, screaming, groaning etc.

None
1

No sounds made at all.

Best Verbal Response.
38
Best Motor Response.
Obeys
command.
6
- move your toes, lift up your arms, raise your eyebrows

"Squeeze my fingers" - best not used as it may only
stimulate a grasp reflex. (can do squeeze and release and repeat)
Localises
pain.
5
Moves hand to remove a source of irritation. (with purpose)

Eg. Supra-orbital ridge - patients hand must reach
beyond the level of the chin, and must cross the midline.
Flexion to
pain. 4
Normal response to pain as if touching a hot object, but
no localising. (not purposeful, may be reflex)
Abnormal
flexion. 3
Slower than above, characterised by adduction of the
shoulder and flexion of the elbow, possibly with flexion of
the wrist.
Extension.
2
Patient will straighten and internally rotate the elbow
joint, adduct and internally rotate the shoulder and flex
the wrist. NB: Posturing.
None. 1 No movement at all. NB: Spinal reflexes.
39
Posturing.
Decorticate:

The upper
extremities are
flexed at the elbows
and wrists. The legs
may also be flexed.

Consider lesion in a
mesencephalic (mid-
brain) region of the
brain.

40
Posturing.
Decerebrate:

The arms are extended
and internally rotated.
The legs are extended
with the feet in forced
plantar flexion.

Consider compression
of the brain stem at a
low level.
41
Best Motor Response.
No need to record left and right
differences. (GCS is not a full neurological
assessment).

Best not to measure leg responses as
these may be spinal rather than brain
initiated.

Assessing for Pupillary Changes.
Assessment of the pupils looks at the
function of two cranial nerves.

Cranial nerve III (oculomotor) constricts
the pupil?

Cranial nerve II (optic) reacts to light
being shone into the eye?
43
Pupillary Changes.
Not a true component of GCS.

Pupils are assessed for their reaction to
light, size and shape.

A change in pupil response to light and
size indicates raised ICP and / or
compression of the cranial nerve that
controls pupil constriction.
44
Assessment of the Pupil.
NB. Pre-existing irregularities.
Look at the resting size of both pupils -
the average size is 2 to 5 mm.
Look at the shape of the pupil - normally
pupils are round.
Abnormal shapes are oval or irregular.
Look to see if both pupils are equal in
size.
Look to see if both pupils react to light -
consensual reaction.

Brisk reaction / some or sluggish reaction / no reaction.

45
Assessment of the Pupil.
46
Assessment of the Pupil.

47
Assessment of the Pupil.
Tricyclic antidepressant OD = bilateral
fixed and dilated pupils.

Opiate and benzodiazepine OD = bilateral
fixed and constricted pupils.

Unilateral dilation of a pupil with loss of
light reflex may = uncal herniation.
(herniation of temporal lobe)

Glasgow Coma Score -
Problems?
49
Glasgow Coma Score - Problems?
Paralysed / sedated patient?
Spinal cord injury?
Artificial airway?
Children?
Cultural barriers?
Frequency of testing?
Observer error?
- Variability / technique / interpretation.

Management of the
Unconscious Patient.
ABC.

SAFETY.
51
Management of the Unconscious
Patient.
Inadequate airway /
poor gag reflex.
Positioning.
Artificial airways.
(NB Cervical spine)
Ineffective clearance of
secretions / poor cough
reflex.

Assessment.
Use of suction.
Physiotherapy.
Positioning.

Poor respiratory
pattern / altered gas
exchange.

Physiotherapy.
Positioning.
Oxygen therapy.
Monitoring.



52
Management of the Unconscious
Patient.
Potential for alteration
in cardiac status.
Assessment and
monitoring of vital signs.
(including lying and standing BP, 12
lead ECG)
Secure I V access.
Immobility

Waterlow.
Repositioning.
Appropriate aids / tools.
Anti-embolic stockings.
Heparin type drugs









53
Management of the Unconscious
Patient.
Neurological
impairment.
Assessment and
monitoring.
GCS.
Appropriate stimulation.
Potential for pain.
Positioning.
Monitor I CP?












54
Management of the Unconscious
Patient.
Hydration and
Nutrition.
Monitor and Manage
blood sugar. Monitor
input /output.
Assess skin / urine
colour, specific gravity
etc.
Safe administration of
fluids / prescribed
therapy / nutrition.
Enteral is best option for
long term, but I V in
acute event.












55
Management of the Unconscious
Patient.
Potential for
seizure activity.
Observation. Management.
Safety. Medication as
prescribed.
Maintenance of
hygiene .

Appropriate care of skin, eyes,
mouth etc.

Elimination.





Assessment.
Catheter care / bowel care.





56
Management of the Unconscious
Patient.
Sensory /
Perceptual
alterations.
Provide appropriate
sensory input.
Orientation. Family.
TV, radio, tapes etc.

Potential for hospital
acquired infection.

Appropriate precautions.
Handwashing.
Observation and
monitoring.
Appropraite
interventions.




57
Management of the Unconscious
Patient.

Rehabilitation.


Support and care of long
term carers.
Discharge planning.





58
References / Suggested Reading.
Addison C and Crawford B (1999). Not bad, just misunderstood.
Nursing Times. 95:43:52-53.

Fairley D and Cosgrove J (1999). Glasgow Coma Scale: improving
nursing practice through clinical effectiveness.
Nursing in Critical Care. 4:6:276-279.

Fielding K and Rowley G (1990). Reliability of assessment by skilled
observers using the Glasgow coma scale. Aust J of Ad Nursing. 7:4:13-17.

Gray D and Toghill P (2001). An Introduction to the Symptoms and Signs
of Clinical Medicine. London. Arnold.

Hickey JV (2002) The Clinical Practice of Neurological and Neurosurgical
Nursing. 5th edition. New York. Lippincott

Lowry M (1999). The Glasgow Coma Scale in clinical practice: a critique.
Nursing Times. 95:22:40-42.



59
References / Suggested Reading.
Price TE (1996). An evaluation of neuro-assessment tools in the intensive
care unit. Nursing in Critical Care. 1:2:72-77.
Rowley G and Fielding K (1991). Reliability and accuracy of the Glasgow
coma scale with experienced and inexperienced users.
Lancet. 337:535-538.
Shah S (1999). Neurological Assessment. Nursing Standard. 13:22:49-56.
Teasdale G and Jennett B (1974). Assessment of coma and impaired
consciousness, a practical scale. Lancet. 2: 81-84.
Teasdale G and Jennett B (1976). Assessment and prognosis of coma after
head injury. Acta Neurochir. 34:45-55..
Teasdale G, Knill-Jones R, Van der Sande J (1978). Observer variability
in assessing impaired consciousness and coma. Journal of Neurology,
Neurosurgery and Psychiatry. 41:7:603-610.
Watson M and Horn S (1992). Searching for signs of revival. Uses and
abuses of the Glasgow Coma Scale. Professional Nurse. 7:10:670-673.