The Patient with Altered Consciousness.

1. The Patient with Altered Consciousness. HECS 2063 Ian Goulden.

2. Learning Outcomes. • Describe the main causes of altered consciousness. • Discuss assessment strategies / tools for the patient with altered consciousness. • Outline the main aspects in the management of the patient with altered consciousness.

3. Anatomy and Physiology

4. Cerebrum. Interpretation of sensory data. Co-ordination of muscular movement. Intellectual and emotional processes. Basics – Anatomy. Meninges. Hypothalamus. Controls ANS. Emotion and behaviour. Temperature control. Circadian rhythm Cerebellum. Co-ordination, skilful movement posture and balance Brain Stem.

5. Basics – Meninges.

6. Basics -The Monro-Kellie Hypothesis. (17th century). • The intracranial volume is fixed, apart from some minimal give due to the meninges and foramina. The intracranial contents are; • Brain and intracellular water. 80 - 85 % • Cerebral blood volume. 3 - 7 % • Cerebrospinal fluid. 5 - 12 % • For practical purposes these volumes are considered as noncompressible. Because pressure is related to volume, any increase in the volume of one of the compartments will have to be buffered by a decrease in the volume of the others. Should such a compensation not occur or be inadequate the Intracranial Pressure will become elevated.

7. Basics – Intracranial Pressure. • Intracranial pressure is a normal phenomenon which can be measured. • It is a reflection of the total intracranial volume against the rigid skull. • The normal value is less than 10 mm Hg (1.3 kPa) this being largely determined by the CSF pressure(the pressure at which CSF production equals the rate of absorption) and the cerebral blood volume. • Fluctuations occur with respect to respiration and arterial waveform and transient rises in are associated with activities such as coughing, straining at stool and sex.

8. Basics - Cerebral Blood Flow. • The brain is only 2 % of the total body mass, it receives however 15 % of the cardiac output and uses 20 % of total blood glucose supply. • Cerebral blood flow is essential for the supply of oxygen and nutrients to the cerebral tissues. • A critical relationship exists between cerebral blood flow and ICP, cerebral blood flow being disadvantaged in the presence of raised ICP.

9. Basics - Cerebral Perfusion Pressure. • Cerebral perfusion pressure (CPP) is the pressure required to maintain an adequate cerebral blood flow. It is defined as the blood pressure gradient across the brain. • This being the difference between; • Mean cerebral arterial and venous blood flow. • Mean cerebral venous pressure approximates ICP and since in the supine position, mean cerebral arterial pressure is equal to mean arterial pressure (MAP). • Cerebral perfusion pressure can be calculated as follows CPP = MAP - ICP An acceptable CPP is above 70 mm Hg. A CPP below 30 mm Hg may lead to cessation of the cerebral blood flow.

10. 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 sources 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.

11. 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.

12. Consciousness.

13. 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 ”.

14. 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.

15. 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.

16. Underlying Mechanisms. Cerebral Hemisphere Malfunction. Altered Consciousness. Brain Stem Malfunction.

17. Underlying Mechanisms. Cerebral Hemisphere Malfunction. • Drug and alcohol intoxication. • Hypoxic brain injury. • Stroke. • Metabolic disorders. • Infection. • Post seizure.

18. 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)

19. 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.

20. Altered Consciousness.

21. Pathological Causes of Decreased Conscious Level. (after Shah 1999 and Gray and Toghill 2001)

22. Brain Injury / Irritation. Cerebral infection - encephalitis / meningitis. Brain infarction. Post seizure. Increase in Brain Volume. Brain tumours. Cerebral oedema from head injury. Cerebral abscess. Pathological Causes of Decreased Conscious Level.

23. Increase in Cerebral Blood Volume. Extradural haematoma. Subdural haematoma. Subarachnoid haemorrhage. Intracerebral haematoma. Increase in CSF Volume. Hydrocephalus. Pathological Causes of Decreased Conscious Level.

24. Generalised metabolic or toxic disorders can depress brain function.

25. 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.

26. Drugs / Poisoning. • Sedatives - barbiturates, opiates. • Amphetamines - tricyclic antidepressants. • Steroids. • Salicylates. • Anticonvulsants. • Alcohol. • Poisons.

27. 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 glucoselevel, hypermetabolism, hypometabolism. • Fluid and electrolyte disturbances:Sodium and potassium imbalances, hypovolaemia.

28. Assessment and Management.

29. 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.

30. Assessment.

31. 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)

32. Why Assess? 3 reasons. Is the patient’s condition, • Improving? • Remaining static? • Deteriorating?

33. Assessment. • Vital signs. • Level of consciousness. • Motor function. • Pupillary signs.

34. 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 temperaturemay be due to damage to the hypothalamus. • Rising blood pressure and falling heart rate may = increasing ICP. (Cushing’s sign)

35. Glasgow Coma Score. Teasdale and Jennett (1974) and (1976). The most widely used scoring system for quantifying consciousness. Allows standardisation of assessment.

36. 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.

37. 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.

38. 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

39. Brief Aside. Applying Painful Stimuli.

40. 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) .

41. 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.

42. Back to the GCS

43. 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. Eye Opening. A patient with flaccid ocular muscles may have their eyes open at all times.

44. 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.

45. Best Motor Response.

46. 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.

47. 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.

48. 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.

49. 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?

50. 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.