Prof., Dr. :sherif wadie
Reticular activating system (RAS)
Good Consciousness = Alertness + Awareness
Diminished alertness =
Widespread abnormalities of cerebral
hemispheres or reduced activity of
reticular activating system (RAS)
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)
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
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)
Somnolent : easily aroused by voice or tou ch; awakens and follows commands;
required stimulation 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 stimulation - , no purposeful movement only po
sturing, brainstem reflexes often absent
Dementia Longstanding
nature
Varies little from time to time
Memory problem
Confusional state Acute
Fluctuate
Clouding of consciousness
Medical or surgical disease Metabolic disorders
Hepatic Uremic Hypo and hypernatremia Hypercalcemia Hypo and hyperglycemia Hypoxia Hypercapnia
Infectious illness Pneumonia Endocarditis Urinary tract infection Peritonitis
Congestive heart failure Postoperative and posttraumatic states
Drug intoxication
Opiates Barbiturates Other sedatives
Diseases of nervous system Cerebrovascular disease, tumor, abscess Subdural hematoma Meningitis Encephalitis Cerebral vasculitis Hypertensive encephalopathy
•Alcoholism.•Depression.•Diabetes.•Drug overdose•Head injuries•Encephalitis•Epilepsy•Stroke
causes of confusional state (5)
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
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.
- 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
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
Verbal response:
NIL 1 - Groans (no re cognizable words) 2
Inappropriate words (including expletives) 3 Confused speech
4 Orientated 5
Glasgow Coma Scale : Eye opening (E)
Glasgow Coma Scale : Motor response (M)
Glasgow Coma Scale : Verbal response (V)
Notes1. scoring from the best response 2. verbal response will not correct in the
condition of aphasia, intubation and facialinjury
3. sensory loss may interfere painful stimulation
4. eye opening may be interfered by orbital swelling and 3rd CN palsy
5. arm movements may be impaired from local trauma or cervical cord lesion
GLASGOW COMA SCOREGLASGOW COMA SCORE
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
Vital sign Temperature
Fever Hypothermia -- <31°C causes coma
Pulse Respiratory rate and pattern Blood pressure
Funduscopic examination Cutaneous lesion
Observe Movement : restless, twitching, multifocal
myoclonus, asterisks Decorticate rigidity Suggest severe bilateral damage rostral to
midbrain Decerebrate rigidity Indicate damage to motor tracts in the midbrain
or caudal diencephalon
Level of arousal and elicited movements Brainstem reflexes
pupils Ocular movements respiration
DESCRIPTIONS INTERPRETATION Small, reactive Metabolic causes
Diencephalic lesion
Midposition, fixed Mid brain lesion
large, fixed Extensive brain stem lesion
AnoxiaS edative overdose
A nticholinergic poisoning or mydriatic eyedrops
Pin point Pontine lesion Opiates
Unilateral fixed dilated T hird nerve palsy
Doll’s eye Doll’s eye maneuver maneuver
(Oculocephalic (Oculocephalic reflex)reflex)
Cold caloric test Cold caloric test (Oculovestibular (Oculovestibular
reflex) reflex)
ConditionCondition
AwakeAwake
Cerebral dysfunction, Cerebral dysfunction, brainstem intactbrainstem intact
Brain stem lesionBrain stem lesion
Doll’s eyesDoll’s eyes
NegativeNegative
Positive Positive
NegativeNegative
ConditionCondition
AwakeAwake
Cerebral dysfunction, Cerebral dysfunction, brainstem intactbrainstem intact
Brain stem lesionBrain stem lesion
Cold caloricsCold calorics
Nystagmus, N/V, painNystagmus, N/V, pain
Slow deviation toward Slow deviation toward waterwater
NegativeNegative
Respiratory patterns
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
Least useful sign because :Acid-base derangementsHypoxiaCardiac influences
Brain death Locked-in syndrome Vegetative state Frontal lobe disease Non-convulsive status epilepticus Psychiatric disorder (catatonia,
depression)
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.
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
COMACOMA
LOCALIZING SIGN NO LOCALIZING SIGN
SUPRATENTORIAL INFRATENTORIAL
NO STIFF NECK
STIFF NECK
- CVD- TUMOUR- ABSCESS
STRUCTURAL DAMAGE FUNCTIONAL NEURONAL DEPRESSION
- HYPOXIA
- CARDIAC ARREST
- ENCEPHALITIS
- HEPATIC- URAEMIC- POST ICTAL STATE- FLUID ELECTROLYTE IMBALANCE- DRUGS
- SAH
- MENINGITIS
CBC FBS BUN, Creatinine Electrolyte, calcium LFT Drug screen, toxicology screen
EKG CT or MRI brain CSF exam EEG
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 3rd day, no papillary light reflex or GCS < 5 is associated with poor prognosis
Central transtentorial herniation
Uncal Uncal transtentorial transtentorial herniationherniation
Brain HerniationBrain Herniation
Intubation and hyperventilation (PCO2 25-
30 mmHg) Mannitol (0.5-1 gm/kg body weight or 2
0 % mannitol 200 cc. infusion 10-20 minutes repeat every 4 hours if necessary
Furosemide -2040 mg IV Dexamethasone 4-10 mg IV q 6 hours
decrease perilesional vasogenic cerebral edema. Active at 24-48 hours.
Consult surgery