Alteration of consciousness and coma

WATUHATAI PAIBOOL, MD

DIVISION OF NEUROLOGY, DEPARTMENT OF PEDIATRICS

KHON KAEN UNIVERSITY

Outline Definition of consciousness & component

Etiology of alternation of consciousness&coma

Clinical evaluation

Investigation

Management

Introduction

One of most common problem in general medicine

Substantial portion of admission to emergency ward

Various etiologies

DefinitionConsciousness is the state of full awareness of the self and one’s

relationship to the environment

Wakefulness Awareness

Component of consciousnessWAKEFULNESS LEVEL

Ascending sensory stimulation

- brainstem

- hypothalamus

- thalamus

- cerebral cortex

Alertness to stimuli

AWARENESS LEVEL

Difficult to localized

- cerebral cortex

- interaction of subcortical nuclei

Awareness of self and environment

Awearness requires wakefulness

Ascending arousal system

Arousal neurotransmitters

- cholinergic system: ACh

- monoamine: noradrenaline

- serotonin(5-HT)

- peptidergic: orexin

- GABA

Alteration of consciousness

Activated mental status

- Confusion

- Hallucination

- Illusions

- Delusions

- Delirium

Reduced mental status - Drowsiness

- Lethargy

- Obtundation

- Stupor

- Coma Along the recovery continumm after

coma- Vegetative state

Activated mental status

Confusion: impaired ability to think and reason, normal development & intellectual

Hallucination: perception of sensory input that are not present

Illusions: misinterpretation of actual sensory stimuli

Delusions: incorrect thoughts or beliefs, do not change by evidence or logical reason

Delirium: activated mental state that include disorientation, irritability, fear, sensory

misperception

Reduced mental status Clouding of consciousness: minimal reduction of wakefulness, difficulty in

maintenance of attention

Drowsiness: dull with sleepiness

Lethargy: difficult to maintain the arousal states

Obtundation: responsive to stimulation other than pain

Stupor: responsive only to pain

Coma: unresponsive to pain (a state of deep, unarousable sustained pathologic unconsciousness with the eyes closed that results from dysfunction of the ascending reticular activating system in the brain stem or in both cerebral hemispheres, persist at least 1 hour to unconsciousness)

EncehalopathyEncephalopathy: a diffuse disorder of the brain in which at least two of the following symptoms are present:

(1) altered states of consciousness

(2) altered cognition or personality

(3) seizures

Brain dysfunction

Encephalitis Encephalitis: an encephalopathy accompanied by inflammation and

usually cerebrospinal fluid pleocytosis.

- infection: mostly virus

- immune: - parainfection: ADEM

- paraneoplasm: Anti NMDAR encephalitis

- autoimmune: SLE, Hashimoto encephalitis

Brain death

Brain death is a clinical diagnosis based on the absence of neurologic function with a known diagnosis that has resulted in irreversiblecoma.

Coma and apnea must coexist to diagnose brain death.

Guidelines for the Determination of Brain Death in In Children; 1987

Etiology

Structural intracranial disordersTrauma: ICH, SAH, hematoma, diffuse axonal injury

Cerebrovascular event: brain infarction/hemorrhage

Infection: meningitis, encephalitis, abscess

Inflammatory process: demyelinating disease

Neoplasm

Hydrocephalus

Toxic or metabolic disordersHypoxic ischemic encephalopathy

Electrolyte or acid-base disorders

- pH disturbance

- hyper/hypoglycemia, Na, Ca

Intoxication

- Medication, drug abuse

- Alcohol

- Heavy metal: lead

- Poisoning

Seizure and postictal state

Organ dysfunction/systemic disorder

- Hepatic encephalopathy

- Uremic encephalopathy

- Hypertensive encephalopathy

- Endocrine disorders

- Inborn error of metabolism

- shock/cardiopulmonary failure

Psychologic conditions

Clinical evaluation Initial management

Identification of cause

History

General physical examination

Neurological examination

Initial management Assure a stable airway, adequate oxygenation, ventilation and circulation

Keep nomothermia and avoid hypoxemia, hypercapnia

Recognize and correct hypoglycemia

Consider specific antedotes for medical overdose

Monitor & treat increased intracranial pressure

Evaluate for seizure and stop

Treat suspected infection

Correct electrolyte and acid-base disturbance

HistoryThe events leading to the behavioral change

Drug or toxic exposure

A personal or family history of migraine or epilepsy

Recurrent or concurrent fever, infection disease or systemic illness

A previous personal or family history of encephalopathy

Clues from historySudden onset in normal child: convulsion or hemorrhage

Sleepiness in normal child: ingestion of drug or toxin

Fever: infection

Hx of fever: demyelinating disease-ADEM

Headache: increased ICP, migraine

Trauma: intracranial hemorrhage

DM: hypoglycemia, DKA

Congenital heart disease: infarction, abscess

Intermittent coma: drug, inborn error of metabolism

Salicylate with influenza or chickenpox: Reye syndrome

Behavioral change, sleep disturbance, movement disorder: Anti NMDAR encephalitis

General physical examinationVital signs

- Fever/hypothermia

- Hyper/hypotension

- RR, pattern of respiration

- PR, regular?, full?

General examination: systemic disease

Neurological examinationLevel of consciousness

Pupil, deviation of eyes

Papilledema, retinal hemorrhage

Meningeal signs

Breathing pattern

Cranial nerve examination

Motor response

Pupil size and reactions

Respiratory pattern

Cheyne-Stokes

Central neurogenic hyperventilation

Apneusis

Cluster breathing and ataxic breathing

Apnea

Cranial nerve examination Systematic assessment of brainstem function via reflexes

CN examination

- Papillary light reflex (CN II-III)

- Oculocephalic/calorics (CN III,IV,VI,VIII)

- Corneal reflex (CN V-VII)

- Gag reflex (CNIX-X)

Papillary light reflex (CN II-III)

Oculocephalic reflex (Doll’s eye reflex)

Proprioceptive head-turning lesion

C-spine injury must be excluded before exam

Normal alert person Absent

Coma with intact brainstem function

Conjugated eye movement in opposite direction of head-turning

Brainstem dysfunction Absent

Oculovesibular test (Caloric test)

Cold water with 30° head elevation

Normal person Nystagmus with fast phase away from tested side

Coma with intact brainstem function

Tonic deviation of both eyes toward tested side

Brainstem lesion No response

Motor response

Left hemiparesis

Decorticate posture

Decerebrate posture

Investigation

InvestigationTest Etiology

Blood glucose Hypoglycemia, DKA

CBC Infection/sepsis

Electrolyte include Calcium Hypo/hypernatremia, hypo/hypercalcemia

LFT, ammonia Hepatic encephalopathy

Renal function test (BUN/Cr) Uremia

Thyroid function test Myxedema coma

Urine toxicology screening Intoxication

Arterial blood gas Hypoxia, hypercapnia

Lactate Lactic acidosis

Investigation Lumbar puncture

if suspected CNS infection

Brain imaging (CT, MRI)

if positive focal neurological deficit, sign of increased ICP

; HSV, JE encephalitis, mass, intracranial hemorrhage

EEG

if suspected seizure (subclinical or NCSE), degree of encephalopathy

Management Initial management : ABC , maintain vital sign

Investigate and treat cause

Prevent & intervene anticipation of complication & sequelae

- Brain edema & increased ICP

- Infection: pneumonia, pressure ulcer, etc.

- Joint contracture

- Deep vein thrombosis

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2. Ropper AH. Coma. In: Longo DL, Fauci AS, Braunwald E, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison’s principles of internal medicine.18th ed. McGraw Hill: NY; 2011. p. 2247-53.

3. Posner JB, Saper CB, Schiff ND, Plum F. Plum and Posner’s diagnosis of stupor and coma, 4th ed. New York: Oxford University Press; 2007.

4. สมศกด ลพธกลธรรม. ภาวะโคมา. ใน: รงโรจน พทยศร, ธรธร พลเกษม,กนกรรณ บญญพสฏฐ, สมบต มงทวพงษา, บรรณาธการ. ต าราประสาทวทยาคลนก. กรงเทพฯ: สมาคมประสาทวทยาแหงประเทศไทย; 2556. หนา 112-31.

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