prof., dr. :sherif wadie reticular activating system (ras)

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