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Alteration of consciousness2

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  • From clinical data directed to lab test
  • Transcript

    • 1. Alteration of Consciousness
    • 2. Reticular activating system (RAS)
    • 3.
      • Good Consciousness =
      • Alertness + Awareness
    • 4.
      • Diminished alertness =
      • Widespread abnormalities of cerebral hemispheres or reduced activity of reticular activating system (RAS)
    • 5. Definition of Terms
      • Confusion :
        • impaired attention and concentration, manifest disorientation in time, place and person , impersistent thinking, speech and performance, reduced comprehension and capacity to reason
        • Fluctuate in severity, typically worse at night ‘sundowning’
        • Perceptual disturbances and misinterpret voices, common objects and actions of other persons
      • Confusion is also found in dementia (progressive failure of language, memory, and other intellectual functions)
    • 6. Definition of Terms
      • Delirium : confusion and associated agitation, hallucination, convulsion and tremor
      • Amnesia : a loss of past memories and to an ability to form new ones, despite alert and normal attentiveness
    • 7. Level of Consciousness(1)
      • Alert  : normal awake and responsive state
      • Drowsiness : state of apparent sleep, briefly arousal with oral command
      • Lethargic  : resembles sleepiness, but not becoming fully alert, slow verbal response and inattentive. Unable to adequately perform simple concentration task (such as counting 20 to 1)
    • 8. Level of Consciousness (2)
      • Somnolent :  easily aroused by voice or touch; awakens and follows commands; req uired stim ulation to maintain arousal
      • Obtunded/Stuporous  : arousable only with repeated and painful stimulation; verbal output is unintelligible or nil; some purposeful movement to noxious stimulation
      • Comatose : no arousal despite vigorous stim ulation , no purposeful movement- only posturing, brainstem reflexes often absent
    • 9. Dementia VS Confusional state
      • Dementia
        • Longstanding nature
        • Varies little from time to time
        • Memory problem
      • Confusional state
        • Acute
        • Fluctuate
        • Clouding of consciousness
    • 10. Causes of confusional state(1)
      • Medical or surgical disease
      • Metabolic disorders
        • Hepatic
        • Uremic
        • Hypo and hypernatremia
        • Hypercalcemia
        • Hypo and hyperglycemia
        • Hypoxia
        • Hypercapnia
    • 11. Causes of confusional state(2)
      • Infectious illness
        • Pneumonia
        • Endocarditis
        • Urinary tract infection
        • Peritonitis
      • Congestive heart failure
      • Postoperative and posttraumatic states
    • 12. Causes of confusional state(3)
      • Drug intoxication
      • Opiates
      • Barbiturates
      • Other sedatives
    • 13. Causes of confusional state(4)
      • Diseases of nervous system
      • Cerebrovascular disease, tumor, abscess
      • Subdural hematoma
      • Meningitis
      • Encephalitis
      • Cerebral vasculitis
      • Hypertensive encephalopathy
    • 14. Approach
      • History --- emphasizing the patient’s condition before the onset of confusion
      • Clinical examination --- focus on
        • signs of diminished attentiveness, disorientation, and drowsiness and
        • the presence of localizing neurological signs
    • 15. Aim of care in confusion patients
      • Control underlying medical illness
      • Quiet the patient and protect him from injury
      • Discontinue drugs that could possibly be responsible for the acute confusional state : sedating, antianxiety, narcotic, anticholinergic, antispasticity, corticosteroid, L-dopa, metoclopramide, cimetidine, antidepressant, antiarrhythmic,anticonvulsant, antibiotics.
    • 16. Medical management
      • Haloperidol, quetiapine, risperidone are helpful in calming the agitated and hallucinating patient, but should be used in the lowest effective doses
      • In alcohol or sedative withdrawal—chlordiazepoxide is the drug of choice. Chloral hydrate, lorazepam, and diazepam are equally effective
    • 17. COMA
    • 18. GLASGOW COMA SCORE
      • Eye opening:
      • Nil 1
      • To pain (applied to limbs) 2
      • To voice (including command) 3
      • Spontaneous (with blinking ) 4
      • Motor response:
      • Nil 1
      • Arm extension to pain (nail bed pressure) 2
      • Arm flexion to pain (nail bed pressure) 3
      • Arm withdrawal from pain (nail bed pressure)4
      • Hand localizes pain(supraorbital or chest pressure)5
      • Obeys commands 6
      • Verbalize response:
      • NIL 1
      • Groans (no re-cognizable words) 2
      • Inappropriate words (including expletives) 3
      • Confused speech 4 Orientated 5
    • 19. Glasgow Coma Scale : Eye opening (E)
    • 20. Glasgow Coma Scale : Motor response (M)
    • 21. Glasgow Coma Scale : Verbal response (V)
    • 22.
      • Notes
      • scoring from the best response
      • verbal response will not correct in the condition of aphasia, intubation and facial injury
      • sensory loss may interfere painful stimulation
      • eye opening may be interfered by orbital swelling and 3 rd CN palsy
      • arm movements may be impaired from local trauma or cervical cord lesion
      GLASGOW COMA SCORE
    • 23. Approach to the patient
      • History
        • Circumstances and rapidity with which neurologic symptoms developed
        • Immediately preceding medical and neurologic symptoms
        • Use of medications, illicit drugs, or alcohol
        • Chronic liver, kidney, lung, heart, or other medical disease
    • 24. General physical examination
      • Vital sign
        • Temperature
          • Fever
          • Hypothermia -- <31 °C causes coma
        • Pulse
        • Respiratory rate and pattern
        • Blood pressure
      • Funduscopic examination
      • Cutaneous lesion
    • 25. Neurologic assessment
      • Observe
        • Movement : restless, twitching, multifocal myoclonus, asterixis
        • Decorticate rigidity
        • Suggest severe bilateral damage rostral to midbrain
        • Decerebrate rigidity
        • Indicate damage to motor tracts in the midbrain or caudal diencephalon
    • 26. Decorticate posture results from damage to one or both corticospinal tracts
    • 27. Decerebrate posture results from damage to the upper brain stem
    • 28. Neurologic assessment
      • Level of arousal and elicited movements
      • Brainstem reflexes
        • pupils
        • Ocular movements
        • respiration
    • 29. Pupils in comatose patients
      • DESCRIPTIONS INTERPRETATION
      • Small, reactive Metabolic causes
      • Diencephalic lesion
      • Midposition, fixed Mid brain lesion
      • large, fixed Extensive brain stem lesion
      • A noxia
      • S edative overdose
      • A nticholinergic poisoning or
      • mydriatic eyedrops
      • Pin point Pontine lesion
      • Opiates
      • Unilateral fixed dilated T hird nerve palsy
    • 30.  
    • 31. Doll’s eye maneuver (Oculocephalic reflex) Cold caloric test (Oculovestibular reflex)
    • 32.  
    • 33. Eye movements Condition Awake Cerebral dysfunction, brainstem intact Brain stem lesion Doll’s eyes Negative Positive Negative Condition Awake Cerebral dysfunction, brainstem intact Brain stem lesion Cold calorics Nystagmus, N/V, pain Slow deviation toward water Negative
    • 34. Respiratory patterns
    • 35. Respiratory pattern(1)
      • Cheyne-Stokes respiration : bilateral cortical or bilateral thalamic lesions, metabolic disturbances, incipient transtentorial herniation
      • Hyperventilation : midbrain or pons lesions
      • Apneusis : lateral tegmentum of lower half of pons
      • Cluster : lower pontine or high medullary lesions
      • Ataxic : dorsomedial medulla lesion
    • 36. Respiratory pattern(2)
      • Least useful sign because :
        • Acid-base derangements
        • Hypoxia
        • Cardiac influences
    • 37. Conditions mimic coma
      • Brain death
      • Locked-in syndrome
      • Vegetative state
      • Frontal lobe disease
      • Non-convulsive status epilepticus
      • Psychiatric disorder (catatonia, depression)
    • 38. Vegetative state
      • An awake but unresponsive state
      • Extensive damage in both cerebral hemisphere
      • Retained respiratory and autonomic functions
      • Cardiac arrest and head injury are the most common causes.
    • 39. Locked-in state
      • Awake patient has no means of producing speech or volitional limb, face and pharyngeal movements
      • Vertical eye movement and lid elevation remain unimpaired
      • Infarction or hemorrhage of the ventral pons
    • 40. COMA LOCALIZING SIGN NO LOCALIZING SIGN SUPRATENTORIAL INFRATENTORIAL NO STIFF NECK STIFF NECK - CVD - TUMOUR - ABSCESS STRU C TURAL DAMAGE FUNCTIONAL NEURONAL DEPRESSION - HYPOXIA - CARDIAC ARREST - ENCEPHALITIS - HEPATIC - URAEMIC - POST ICTAL STATE - FLUID ELECTROLYTE IMBALANCE - DRUGS - SAH - MENINGITIS
    • 41. Blood test
      • CBC
      • FBS
      • BUN, Creatinine
      • Electrolyte, calcium
      • LFT
      • Drug screen, toxicology screen
    • 42. Other tests
      • EKG
      • CT or MRI brain
      • CSF exam
      • EEG
    • 43. Prognosis of coma
      • Recovery from coma depends primarily on the causes, rather than on the depth of coma
      • Intoxication and metabolic causes carry the best prognosis
      • Coma from traumatic head injury far better than those with coma from other structural causes
      • Coma from global hypoxic-ischemic carries least favorable prognosis
      • At 3 rd day, no papillary light reflex or GCS < 5 is associated with poor prognosis
    • 44. Brain Herniation
      • Central transtentorial herniation
    • 45.
      • Uncal transtentorial herniation
      Brain Herniation
    • 46. Management of Transtentorial herniation
      • Intubation and hyperventilation (P CO 2 25-30 mmHg)
      • Mannitol (0.5-1 gm/kg body weight or 20 % mannitol 200 cc. infusion 10-20 minutes repeat every 4 hours if necessary
      • Furosemide 20-40 mg IV
      • Dexamethasone 4-10 mg IV q 6 hours decrease perilesional vasogenic cerebral edema. Active at 24-48 hours.
      • Consult surgery

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