Coma and Related Disorders of Consciousness

Coma and Related Disorders of Consciousness

Dr. Enrique De La Mora GlaskerDr. Enrique De La Mora Glasker

coma

Reduced alertness and responsiveness Reduced alertness and responsiveness represents a continuum that in severest form represents a continuum that in severest form ,, a deep sleeplike state from which the a deep sleeplike state from which the patient cannot be aroused. patient cannot be aroused.

Stupor

LLesser degrees of unarousability in which esser degrees of unarousability in which the patient can be awakened only by the patient can be awakened only by vigorous stimuli, accompanied by motor vigorous stimuli, accompanied by motor behavior that leads to avoidance of behavior that leads to avoidance of uncomfortable or aggravating stimuli.uncomfortable or aggravating stimuli.

Drowsiness

which is familiar to all persons, simulates which is familiar to all persons, simulates light sleep and is characterized by easy light sleep and is characterized by easy arousal and the persistence of alertness for arousal and the persistence of alertness for brief periods.brief periods.

Drowsiness and stupor

are usually attended by some degree of are usually attended by some degree of confusion. confusion.

vegetative state

signifies an awake but unresponsive state. signifies an awake but unresponsive state. Most of these patients were earlier Most of these patients were earlier comatose and after a period of days or comatose and after a period of days or weeks emerge to an unresponsive state in weeks emerge to an unresponsive state in which their eyelids are open, giving the which their eyelids are open, giving the appearance of wakefulness. appearance of wakefulness.

vegetative state

Yawning, grunting, swallowing, limb and Yawning, grunting, swallowing, limb and head movements persist, but there are few, head movements persist, but there are few, if any, meaningful responses to the external if any, meaningful responses to the external and internal environment-in essence, an and internal environment-in essence, an "awake coma.“"awake coma.“

respiratory and autonomic functions are respiratory and autonomic functions are retained retained

vegetative state most common causes

Cardiac arrest Cardiac arrest

head injurieshead injuries

Akinetic mutism

PPartially or fully awake patient who is able to artially or fully awake patient who is able to form impressions and think but remains immobile form impressions and think but remains immobile and mute, particularly when unstimulated. and mute, particularly when unstimulated.

Causes: Causes: damage in the regions of the medial damage in the regions of the medial thalamic nuclei, the frontal lobes (particularly thalamic nuclei, the frontal lobes (particularly situated deeply or on the orbitofrontal surfaces), or situated deeply or on the orbitofrontal surfaces), or from hydrocephalus. from hydrocephalus.

Abulia

MMental and physical slowness and lack of ental and physical slowness and lack of impulse to activity that is in essence a mild impulse to activity that is in essence a mild form of akinetic mutismform of akinetic mutism..

with the same anatomic origins. with the same anatomic origins.

Catatonia

HHypomobile and mute syndrome associated with a ypomobile and mute syndrome associated with a major psychosis. major psychosis.

patients appear awake with eyes open but make no patients appear awake with eyes open but make no voluntary or responsive movements, although they voluntary or responsive movements, although they blink spontaneously, swallow, and may not appear blink spontaneously, swallow, and may not appear distressed. distressed.

EEyes are half-open as if the patient is in a fog or yes are half-open as if the patient is in a fog or light sleep. light sleep.

NO NO clinical evidence of brain damageclinical evidence of brain damage..

Locked-in state

describes a pseudocoma in which an awake describes a pseudocoma in which an awake patient has no means of producing speech patient has no means of producing speech or volitional limb, face, and pharyngeal or volitional limb, face, and pharyngeal movements in order to indicate that he or movements in order to indicate that he or she is awake, but vertical eye movements she is awake, but vertical eye movements and lid elevation remain unimpaired, thus and lid elevation remain unimpaired, thus allowing the patient to signal. Such allowing the patient to signal. Such individuals have written entire treatises individuals have written entire treatises using Morse codeusing Morse code

Locked-in state

Infarction or hemorrhage of the ventral Infarction or hemorrhage of the ventral pons, which transects all descending pons, which transects all descending corticospinal and corticobulbar pathways, is corticospinal and corticobulbar pathways, is the usual causethe usual cause

Anatomy and Physiology of Unconsciousness

CCerebral cortex erebral cortex

neurons located in the upper brainstem neurons located in the upper brainstem and medial thalamusand medial thalamus

RAS, maintains the cerebral cortex in a RAS, maintains the cerebral cortex in a state of wakeful consciousness. state of wakeful consciousness.

Anatomy and Physiology of Unconsciousness principal causes of coma principal causes of coma (1) lesions of the RAS(1) lesions of the RAS (2) destruction of large portions of both (2) destruction of large portions of both

cerebral hemispherescerebral hemispheres (3) suppression of thalamocerebral (3) suppression of thalamocerebral

function by drugs, toxins, function by drugs, toxins, metabolic metabolic causes:causes: hypoglycemia, hypoglycemia,

anoxia, azotemia, or hepatic failure.anoxia, azotemia, or hepatic failure.

Anatomy and Physiology of Unconsciousness

Pupillary enlargementPupillary enlargement,, loss of vertical and loss of vertical and adduction movements of the globes suggest upper adduction movements of the globes suggest upper brainstem damagebrainstem damage..

lesions lesions inin one or both cerebral hemispheres do not one or both cerebral hemispheres do not affect RAS, a large mass on one side of the brain affect RAS, a large mass on one side of the brain may cause coma by secondarily compressing the may cause coma by secondarily compressing the upper brainstem and abnormalities of the pupils upper brainstem and abnormalities of the pupils and eye movementsand eye movements ..

Anatomy and Physiology of Unconsciousness Mass effect:Mass effect: most typical of most typical of

cerebral hemorrhages and of cerebral hemorrhages and of rapidly expanding tumors within a rapidly expanding tumors within a cerebral hemisphere. In all cases cerebral hemisphere. In all cases the degree of diminished alertness the degree of diminished alertness also relates to the rapidity of also relates to the rapidity of evolution and the extent of evolution and the extent of compression of the RAS.compression of the RAS.

RAS and the thalamic and cortical areas RAS and the thalamic and cortical areas utilize a variety of neurotransmittors. utilize a variety of neurotransmittors. AcetylcholineAcetylcholine,,biogenic amines Cholinergic biogenic amines Cholinergic fibers connect the midbrain to other areas fibers connect the midbrain to other areas of the upper brainstem, thalamus, and of the upper brainstem, thalamus, and cortex. cortex.

SerotoninSerotonin and and norepinephrine regulation of norepinephrine regulation of the sleep-wake cyclethe sleep-wake cycle..

AAlerting effects of amphetamines are lerting effects of amphetamines are likely to be mediated by catecholamine likely to be mediated by catecholamine release.release.

Herniation

transfalcialtransfalcial (displacement of the (displacement of the cingulate gyrus under the falx and cingulate gyrus under the falx and across the midline), across the midline),

transtentorialtranstentorial (displacement of the (displacement of the medial temporal lobe into the tentorial medial temporal lobe into the tentorial opening), opening),

foraminalforaminal (downward forcing of the (downward forcing of the cerebellar tonsils into the foramen cerebellar tonsils into the foramen magnum.magnum.

Epileptic Coma

metabolic derangements in some way alter metabolic derangements in some way alter neuronal electrophysiologic function, neuronal electrophysiologic function, epilepsy is the only primary excitatory epilepsy is the only primary excitatory disturbance of brain electrical activity that disturbance of brain electrical activity that is encountered in clinical practice.is encountered in clinical practice.

Pharmacologic Coma

Can beCan be reversible and leaves no residual reversible and leaves no residual damagedamage..

Many drugs and toxins are capable of Many drugs and toxins are capable of depressing nervous system function. depressing nervous system function.

Approach to the Patient

The diagnosis and management of coma depend on The diagnosis and management of coma depend on knowledge of its main causesknowledge of its main causes..

interpretation of clinical signs, brainstem interpretation of clinical signs, brainstem reflexes and motor function. reflexes and motor function.

Acute respiratory and cardiovascular Acute respiratory and cardiovascular problems problems

complete medical evaluation, vital signs, complete medical evaluation, vital signs, funduscopy, and examination for nuchal funduscopy, and examination for nuchal rigidity, rigidity, (complete (complete neurologic evaluation neurologic evaluation for knowfor know the severity and nature of coma. the severity and nature of coma.

History

trauma, cardiac arrest, or known drug trauma, cardiac arrest, or known drug ingestion. ingestion.

(1) (1) CCircumstances and rapidity with ircumstances and rapidity with which neurologic symptoms developed which neurologic symptoms developed

(2) confusion, weakness, headache, (2) confusion, weakness, headache, fever, seizures, dizziness, double vision, fever, seizures, dizziness, double vision, or vomitingor vomiting

(3) use of medications, illicit drugs, or (3) use of medications, illicit drugs, or alcoholalcohol

(4) chronic liver, kidney, lung, heart, (4) chronic liver, kidney, lung, heart,

History

Direct interrogation or telephone Direct interrogation or telephone calls to family and observers on calls to family and observers on the scene are an important part of the scene are an important part of the initial evaluation. Ambulance the initial evaluation. Ambulance technicians often provide the most technicians often provide the most useful information in an enigmatic useful information in an enigmatic case.case.

General Physical Examination

temperature, pulse, respiratory rate and pattern, temperature, pulse, respiratory rate and pattern, Tachypnea may indicate acidosis or pneumonia Tachypnea may indicate acidosis or pneumonia blood pressureblood pressure..

Fever suggests a systemic infection, bacterial Fever suggests a systemic infection, bacterial meningitis, or encephalitis; only rarely is it meningitis, or encephalitis; only rarely is it attributable to a brain lesion that has disturbed attributable to a brain lesion that has disturbed temperature-regulating centers. temperature-regulating centers.

General Physical Examination

High body temperature, 42 to 44°C, High body temperature, 42 to 44°C, associated with dry skin should arouse the associated with dry skin should arouse the suspicion of heat stroke or anticholinergic suspicion of heat stroke or anticholinergic drug intoxication. drug intoxication.

Hypothermia itself causes coma only when Hypothermia itself causes coma only when the temperature is <31°C. the temperature is <31°C.

General Physical Examination AAlcoholic, barbiturate, sedative, or lcoholic, barbiturate, sedative, or

phenothiazine intoxicationphenothiazine intoxication HHypoglycemiaypoglycemia,, peripheral circulatory peripheral circulatory

failurefailure,, or hypothyroidism or hypothyroidism,etc.,etc.

General Physical Examination FFunduscopic examination is unduscopic examination is

invaluable in detecting invaluable in detecting subarachnoid hemorrhage subarachnoid hemorrhage (subhyaloid hemorrhages), (subhyaloid hemorrhages), hypertensive encephalopathy hypertensive encephalopathy (exudates, hemorrhages, vessel-(exudates, hemorrhages, vessel-crossing changes, papilledema), crossing changes, papilledema), and increased intracranial pressure and increased intracranial pressure (papilledema). (papilledema).

Neurologic Assessment

OObservbservationation first without examiner first without examiner intervention. intervention.

Patients who toss about, reach up toward Patients who toss about, reach up toward the face, cross their legs, yawn, swallow, the face, cross their legs, yawn, swallow, cough, or moan are close to being awake. cough, or moan are close to being awake. Lack of restless movements on one side or Lack of restless movements on one side or an outturned leg at rest suggests a an outturned leg at rest suggests a hemiplegia. hemiplegia.


Multifocal myoclonus almost always Multifocal myoclonus almost always indicates a metabolic disorderindicates a metabolic disorder

In a drowsy and confused patient In a drowsy and confused patient bilateral asterixis is a certain sign bilateral asterixis is a certain sign of metabolic encephalopathy or of metabolic encephalopathy or drug ingestion.drug ingestion.

.


DDecorticate rigidityecorticate rigidity and and decerebrate decerebrate rigidityrigidity, or "posturing," describe , or "posturing," describe stereotyped arm and leg movements stereotyped arm and leg movements occurring spontaneously or elicited by occurring spontaneously or elicited by sensory stimulation. sensory stimulation.

Brainstem Reflexes

pupillary responses to light,pupillary responses to light,sspontaneous and pontaneous and elicited eye movements, corneal responses, elicited eye movements, corneal responses,

RRespiratory pattern espiratory pattern

A.- PUPILLARY LIGHT RESPONSES: Simmetrically reactive round pupils: Exclude

midbrain damage.(2 to 5 mm )

Enlarged pupil (>5 mm), unreactive or poorly reactive: Intrinsic

midbrain lesion (ipsilateral) or by mass effect (contralateral).

Unilateral pupillary enlargement:Unilateral pupillary enlargement: Ipsilaterall Ipsilaterall mass.mass.

Oval and slightly eccentric pupils:Oval and slightly eccentric pupils: EarlyEarly m midbrain idbrain

thirdthird nerve nerve compression.compression.

Bilaterally dilated and unreactiveBilaterally dilated and unreactive Severe Severe

midbrain midbrain damage damage by by transtentorial transtentorial

pupils:pupils: herniation or herniation or anticholinergic anticholinergic drugsdrugs toxicity. toxicity.

Reactive bilaterally small but not pin-point (1 to 2.5 mm): Metabolic

encephalopathy, deep bilateral hemispheral lesions as hydrocephalus or thalamic hemorrhage

Very small but reactive pupil Narcotic or barbiturate overdose or bilateral

(Less than 1 mm): pontin damage.

Ocular Movements

Eye movements are the second sign of Eye movements are the second sign of importance in determining if the brainstem importance in determining if the brainstem has been damaged. has been damaged.

EYE MOVEMENTS Adducted eye at rest:Adducted eye at rest: Lateral rectus paresis Lateral rectus paresis

due to VI nerve due to VI nerve lesion. If is bilateral is lesion. If is bilateral is

due to intracraneal due to intracraneal hypertension.hypertension.

Abducted eye at rest, plus ipsiAbducted eye at rest, plus ipsi Medial rectus paresis Medial rectus paresis due to III nervedue to III nerve

lateral pupilary enlargementlateral pupilary enlargement : : dysfunction.dysfunction.

Vertical separation of the ocularVertical separation of the ocular Pontin or cerebellar Pontin or cerebellar lesionlesion

Globes. (Skew deviation)Globes. (Skew deviation) : : Coma and spontanous conjugateComa and spontanous conjugate Midbrain and Midbrain and

pons intactpons intact horizontal roving movements horizontal roving movements ::

““Ocular bobbing”. Brisk downward Ocular bobbing”. Brisk downward and slow upward movement of the and slow upward movement of the

globes with loss of horizontal eyeglobes with loss of horizontal eye movements :movements : BBilateral pontine ilateral pontine

damagedamage

““Ocular dipping”. Slower, arrhytmic Ocular dipping”. Slower, arrhytmic

downward followed by a faster upward downward followed by a faster upward

movement with normal reflex horizontal movement with normal reflex horizontal

gaze :gaze : Anoxic Anoxic damage to the cerebraldamage to the cerebral

cortex.cortex.

Thalamic and upper midbrain lesions: Thalamic and upper midbrain lesions: EEyes turned down yes turned down and inward.and inward.

F.- RESPIRATION PATTERNS.

Shallow, slow, well-timed regularShallow, slow, well-timed regular Suggest metabolic or Suggest metabolic or

drug depression.drug depression. Breathing:Breathing:

Rapid, deep (Kussmaul) breathing:Rapid, deep (Kussmaul) breathing: Metabolic acidosis Metabolic acidosis

or ponto- or ponto- mesencephalic mesencephalic lesions.lesions.

Cheyne-Stokes breathing, with lightCheyne-Stokes breathing, with light Mild bihemispherical Mild bihemispherical

damage or damage or Coma:Coma: metabolic metabolic supression.supression.

Agonal gasps:Agonal gasps: Bilateral Bilateral lower brainstem lower brainstem damage.damage.

Terminal respiratory Terminal respiratory pattern.pattern.

Laboratory Studies and Imaging

chemical-toxicologic analysis of blood and chemical-toxicologic analysis of blood and urine, urine,

cranial CT or MRI, EEG, cranial CT or MRI, EEG, Lumbar puncture andLumbar puncture and CSF examination CSF examination

(cultures)(cultures)

Laboratory Studies and Imaging

Arterial blood-gas analysis is helpful in Arterial blood-gas analysis is helpful in patients with lung disease and acid-base patients with lung disease and acid-base disorders. disorders.

Toxicologic analysis Toxicologic analysis

Brain Death

Neurological examinationNeurological examination EEGEEG Radionuclide brain scanning, cerebral Radionuclide brain scanning, cerebral

angiography, or transcranial Doppler angiography, or transcranial Doppler measurements may also be used to measurements may also be used to demonstrate the absence of cerebral blood demonstrate the absence of cerebral blood flowflow

TREATMENT FOR THE PATIENT IN COMA.

1.- The treatment must be instituted 1.- The treatment must be instituted inmediately even when there is no a certain inmediately even when there is no a certain diagnosis.diagnosis.

The inmediate goal is the prevention of The inmediate goal is the prevention of further nervous system damage.further nervous system damage.

2.- Diagnostic procedures and general 2.- Diagnostic procedures and general treatment mus be performed simultaneously treatment mus be performed simultaneously and to install the specific treatment when the and to install the specific treatment when the etiology is known.etiology is known.


A.- Permeable airway. Oxygen supply through A.- Permeable airway. Oxygen supply through nasal fossae to endotraqueal intubation..nasal fossae to endotraqueal intubation..

B.- Politrauma patient’s evaluation. Stabilize the neck B.- Politrauma patient’s evaluation. Stabilize the neck and the rest of the vertebral colum.and the rest of the vertebral colum.

C.- Establish an intravenous access. Water C.- Establish an intravenous access. Water administration carefully monitored.administration carefully monitored.

D.- Maintain the body temperature the closest to the D.- Maintain the body temperature the closest to the normal values as possible.normal values as possible.


E.- I.V. administration of 50 ml of 50% E.- I.V. administration of 50 ml of 50% glucose.glucose.

F.- Administrate thiamine in malnourished and F.- Administrate thiamine in malnourished and alcoholic patients. 10 mg I.V. and 100 mgalcoholic patients. 10 mg I.V. and 100 mg

I.M. /day /3 days.I.M. /day /3 days. G.- Naloxone (0.4 to 0.8 mg) or flumazenil (0.5 G.- Naloxone (0.4 to 0.8 mg) or flumazenil (0.5

to 1 mg) I.V administrationto 1 mg) I.V administration H.- Appropriate treatment of intracraneal H.- Appropriate treatment of intracraneal

hypertension and seizures.hypertension and seizures.


I.- General measures for the unmovable patient. I.- General measures for the unmovable patient. Appropriate nutrition and hydration.Appropriate nutrition and hydration. Posture changes every two hours.Posture changes every two hours. Mobilization of joints.Mobilization of joints. Ocular metilcelulose drops, 1 every 4 hours.Ocular metilcelulose drops, 1 every 4 hours. I.V. ranitidine 50 mg every 8 hours, or 300 mg in I.V. ranitidine 50 mg every 8 hours, or 300 mg in

250 ml of 5% dextrose in 24 hours; or sucralfate 1 g 250 ml of 5% dextrose in 24 hours; or sucralfate 1 g per nasogatric tube every 6 hours.per nasogatric tube every 6 hours.

S.C. Heparin, 5000 U every 12 hours.S.C. Heparin, 5000 U every 12 hours. Urinary tract care.Urinary tract care. J.- Etiologic treatment.J.- Etiologic treatment.

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Coma and Related Disorders of Consciousness