altered loc

The Patient with Altered Consciousness.

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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.

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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.

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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.

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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 ”.

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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.

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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.

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Underlying Mechanisms.

Cerebral Hemisphere Malfunction.

Altered Consciousness.

Brain Stem Malfunction.

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Underlying Mechanisms.

Cerebral Hemisphere Malfunction.

Drug and alcohol intoxication. Hypoxic brain injury. Stroke. Metabolic disorders. Infection. Post seizure.

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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)

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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.

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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.

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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.

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

Extradural haematoma.

Subdural haematoma.

Subarachnoid haemorrhage.

Intracerebral haematoma.

Increase in CSF Volume.

Hydrocephalus.

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Generalised metabolic or toxic disorders can depress brain function.

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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.

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Drugs / Poisoning. Sedatives - barbiturates, opiates.

Amphetamines - tricyclic antidepressants.

Steroids.

Salicylates.

Anticonvulsants.

Alcohol.

Poisons.

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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.

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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, LFT’s, ABG’s, thyroid, cortisol levels, blood cultures etc.

CT / MRI Scanning.

CSF investigations.

Assessment.

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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)

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Why Assess?

3 reasons.Is the patient’s condition,

Improving? Remaining static? Deteriorating?

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Assessment.

Vital signs.

Level of consciousness.

Motor function.

Pupillary signs.

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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. (Cushing’s sign)

Glasgow Coma Score. Teasdale and Jennett (1974) and (1976).

The most widely used scoring system for quantifying consciousness.

Allows standardisation of assessment.

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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.

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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.

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Eye Opening.  C = eyes closed by swelling.

Spontaneous.To speech.To pain.None.

4321

Best Verbal Response.  T = tracheostomy / ET tube

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

54321

Best Motor Response.  *

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

654321

Brief Aside.

Applying Painful Stimuli.

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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) .

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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

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Eye Opening.Spontaneous

4Eyes 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.

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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.

None1

No sounds made at all.

Best Verbal Response.

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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.

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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.

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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.

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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.

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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?

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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.

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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.

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Assessment of the Pupil.

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Assessment of the Pupil.

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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?

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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.

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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.

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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 IV access. Immobility

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

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Management of the Unconscious Patient.

Neurological impairment.

Assessment and monitoring. GCS. Appropriate stimulation. Potential for pain. Positioning. Monitor ICP?

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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 IV in acute event.

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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.

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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.

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Management of the Unconscious Patient.

Rehabilitation.

Support and care of long term carers. Discharge planning.

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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.  

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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.