APPROACH TO DISTURBANCE OF CONSCIOUSNESS

Osama RagabM.D Neurology

Consciousness■ consciousness encompasses two main components: arousal and

awareness.

■ Arousal is mainly supported by the brain stem and the thalami.

■ Awareness refers to conscious perception which includes cognition, experiences from the past and the present, and intentions. Is supported by the cerebral cortex.

■ Awareness can be further divided into awareness of the environment and self.

■Awareness of the environment can be defined as the conscious perception of one’s environment through the sensory modalities, also refers to the knowledge of our own social and cultural history .

■Awareness of self is a mental process that does not require external stimuli .

Consciousness

Consciousness

■ If you are awake and aware of external and internal stimuli so you can respond appropriately to these stimuli ( fronto- parietal function).

■So to be conscious= awake + aware + respond appropriately .

■The Content of consciousness is a term used to define awareness.

Consciousness

Please define coma?

Terminology

■ Coma is un-arousable unresponsiveness state in which the patient lies with the eyes closed( no level no content ).

■ Stupor is defined as unresponsiveness from which the subject can be aroused only by vigorous and repeated stimuli. ( minimal level no content ).

■ Drowsy refers to a mild depression in consciousness that can be aroused to full wakefulness through voice.( assisted good level and content ).

■Delirium: acute onset of abnormal mental state, with disturbed consciousness, disorientation, severe motor restlessness, fear, irritability, visual hallucinations.

■ There may be lucid periods with hyperactivity during which the patient is agitated, talkative and irritable.

■There are also hypoactive periods with hypersomnolence and sleep–wake inversion ( mid level abnormal content).

Terminology

Glasgow coma scale

FOUR score (Full Outline of Unresponsiveness).

■Causes of coma?

■ Structural ( brain insult):• symmetrical.• Asymmetrical.■ Non-structural(systemic).• Metabolic.• Infections• Drugs• Toxins.• psychiatric

Causes of coma

Causes of coma

Causes of coma

Clinical approach to Comatose patient

All alterations in arousal constitute acute life-threatening emergencies until vital functions are stabilized, and the underlying cause of the alteration in arousal is understood.

On arrival to ER immediate attention to: • Airway• Breathing• Circulation• establishing IV access• Blood should be withdrawn: estimation of glucose #

other biochemical parameters # drug screening

Clinical approach to Comatose patient

■ Attention is then directed towards:

1. Assessment of the patient

2. Severity of the coma

3. Diagnostic evaluation

■ All possible information from:

1. Relatives

2. Ambulance personnel

3. Bystanders

particularly about the mode of onset

Clinical approach to Comatose patient

■ Urgent and sometimes empirical therapy is given to prevent further brain damage.

■ Potential immediate metabolic needs of the brain are supplied by empirical use of supplemental oxygen, intravenous (IV) thiamine (at least 100 mg), and IV 50% dextrose in water (25 g).

■ A baseline serum glucose level should be obtained before glucose administration.

Clinical approach to Comatose patient

Clinical approach to Comatose patient

■Clinically recommend empirical glucose administration when the cause of coma is unknown. There are two reasons for this approach:

(1) the frequent occurrence of alterations in arousal due to hypoglycemia and the relatively good prognosis for coma.

(2) the potentially permanent consequences if it is not treated.

■Naloxone hydrochloride may be given parenterally, preferably IV, in doses of 0.4 to 2 mg if opiate overdose is the suspected cause of coma.

General ExaminationBlood Pressure Evaluation

Hypotension

Massive external or internal hemorrhage. MI, cardiac tamponade, dissecting aortic aneurysm, intoxication with alcohol or other drugs (especially barbiturates), Addison disease

HypertensionHypertension is the cause of alterations in arousal in hypertensive subarachnoid hemorrhagebrainstem infarctionsThe Kocher-Cushing (or Claude Bernard) reflex is the development of hypertension associated with bradycardia and respiratory irregularity due to increased ICP.

General ExaminationHeart Rate

Bradycardia can result from myocardial conduction blocks, with certain poisonings, and from effects of drugs such as the beta-blockers.

Tachycardia is a result of hypovolemia, hyperthyroidism, fever, anemia, and certain toxins and drugs including cocaine, atropine, and other anticholinergic medications.

General ExaminationRespiration

causes of decreased respiratory rate are toxic, such as carbon dioxide narcosis or drug overdose with central nervous system (CNS) depressants.

Increased respiratory rate can result from hypoxia, hypercapnia, acidosis, hyperthermia, hepatic disease, toxins or drugs (salicylates), sepsis, pulmonary embolism and sometimes is seen in psychogenic unresponsiveness.

General ExaminationTemperature

measured with a rectal probe in a comatose patient.

Any evidence of fever in a comatose patient warrants strong consideration of LP. Absence of an elevated temperature does not rule out infection.Pure neurogenic hyperthermia is rare and usually is due to subarachnoid hemorrhage or diencephalic (hypothalamus) lesions. A clue to brainstem origin is shivering without sweating particularly when unilateral in nature.

General ExaminationTemperature

measured with a rectal probe in a comatose patient.

Hypothermia regardless of cause is anticipated to lead to altered consciousness. Hypothermia associated with coma are hypothyroid coma, hypopituitarism, Wernicke encephalopathy, cold exposure, drugs (barbiturates).Central lesions causing hypothermia are found in the posterior hypothalamus.

General ExaminationGeneral appearance

Vomiting may be a sign of increased ICP, drug overdose, or metabolic or other toxic cause. Urinary or fecal incontinence indicates an epileptic seizure or may result from a generalized autonomic discharge Cachexia suggests cancer, chronic inflammatory disorders, Addison disease, hypothyroid coma, or hyperthyroid crisis.Gynecomastia, spider nevi, testicular atrophy, and decreased axillary and pubic hair are common in the alcoholic with cirrhosis.

General ExaminationHead and Neck Examination

The head and neck must be carefully examined for signs of trauma. Raccoon eyes and Battle sign.Meningismus neck stiffness may be a sign of infectious or carcinomatous meningitis, subarachnoid hemorrhage, or central or tonsillar herniation.

General ExaminationEye examination

Edema of the conjunctiva and eyelids may occur in congestive heart failure.Scleral icterusKayser- Fleischer rings Subhyaloid hemorrhage Papilledema results.

General ExaminationEar examination

Hemotympanum or CSF otorrhea from a basilar skull fracture involving the petrous ridge, as well as infection of the middle ear. Infections of the middle ear, mastoid, and paranasal sinuses constitute the most common source of underlying infection in brain abscess.

General ExaminationOral examination

Alcohol intoxication, diabetic ketoacidosis (acetone odor), uremia, and hepatic encephalopathy (musty odor of fetor hepaticus) may be suspected from the odor of the breath. Pustules on the nose or upper lip may seed the cavernous sinus with bacteria by way of the angular vein. Lacerations on the tongue, whether old or new, suggest seizure disorder.Herpetic vesicle.

General ExaminationSkin examination

Hot, dry skin is a feature of heatstroke. Sweaty skin is seen with hypotension or hypoglycemia. Bullous skin lesions most often are a result of barbiturates but also may be caused by imipramine, phenothiazine, and carbon monoxide. Kaposi sarcoma, anogenital herpetic lesions, or oral candidiasis should suggest the acquired immunodeficiency syndrome (AIDS), with its plethora of CNS abnormalities.

General ExaminationCardiac examination

Abdominal examination

Neurological Examination

Neurological ExaminationState of consciousness

The examiner should start with verbal stimuli, softly and then more loudly. If there is no significant response, more threatening stimuli such as taking the patient’s hand and advancing it toward the patient’s face are appliedFinally, painful stimuli may be needed to arouse the patient.

Neurological ExaminationRespiration

Neurological ExaminationPupil Size and Reactivity

Neurological ExaminationOcular motility

Evaluation of ocular motility consists of (1) observation of the resting position of the eyes, including eye deviation.(2) spontaneous eye movements.(3) testing of reflex ocular movements.

Neurological ExaminationOcular motility

(1) observation of the resting positionConjugate lateral eye deviation . Dysconjugate lateral eye movement may result from a sixth nerve palsy in the abducting eye, a third nerve palsy in the adducting eye, or an internuclear ophthalmoplegia.

Neurological ExaminationOcular motility

(1) observation of the resting positionThalamic and subthalamic lesions produce downward and inward deviation of the eyes. Vermal Hemorrhage and brainstem cause upward eye deviation.Skew deviation usually indicates a posterior fossa lesion.

Neurological ExaminationOcular motility

Spontaneous Eye MovementsRoving eye movements are slow, conjugate, lateral to-and-fro movements is due to a metabolic or toxic cause or bilateral lesions above the brainstem.Nystagmus occurring in comatose patients suggests an irritative or epileptogenic supratentorial focus.

Neurological ExaminationReflex Ocular Movements

Neurological ExaminationReflex Ocular Movements

Neurological ExaminationReflex Ocular Movements

Neurological ExaminationMotor System

postures Decerebrate Bilateral midbrain and deep metabolic encephalopathies responsible for decerebrate posturing. Decorticate it may result from lesions in many locations, although usually above the brainstem.

Distinction of toxic and metabolic coma from structural coma

■History (onset and course).

■Lateralizing signs.

■Occular movement.

■Pupil reaction.

■ involuntary limb movements.

■There is always exceptions.

Lateralizing signs

■ Unequal pupils

■ Deviation of the eyes to one side

■ Facial asymmetry

■ Turning of the head to one side

■ Unilateral hypo-hypertonia

■ Asymmetric deep reflexes

■ Unilateral extensor plantar response (Babinski)

■ Unilateral focal or Jacksonian fits

Remember . ABCs: maintain airway, breathing, circulation. Thorough general and neurologic examination. Intravenous fluids: normal saline.. Manage hypoglycemia with 50 mL of 50% glucose IV. Consider thiamine 100 mg IV before glucose.. Consider naloxone 0.4 to 2.0 mg IV for opiate overdose.. Consider flumazenil 0.2 mg IV for benzodiazepine overdose.. Blood tests: arterial blood gases, glucose, electrolytes, calcium, magnesium, phosphorus, blood urea nitrogen (BUN), creatinine, liver enzymes, ammonia, complete blood cell count, urinalysis, blood and urine toxicology screens, thyroid function (TSH).. If focal neurologic signs, deep coma, or history of head trauma, consider therapy for elevated ICP with hyperventilation and mannitol.. Emergency brain imaging: typically unenhanced cranial computed tomography (CT). Consider lumbar puncture (LP) if suspected central nervous system (CNS) infection or suspected subarachnoid hemorrhage (SAH) with normal findings on CT.. Electroencephalogram (EEG)

Thank you