Coma and Related Disorders of Consciousness

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Coma and Related Disorders of Consciousness

• Dr. Enrique De La Mora Glasker

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coma

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

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Stupor

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

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Drowsiness

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

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Drowsiness and stupor

• are usually attended by some degree of confusion.

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vegetative state

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

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vegetative state

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

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vegetative state most common causes

• Cardiac arrest
• head injuries

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Akinetic mutism

• Partially or fully awake patient who is able to
  form impressions and think but remains immobile
  and mute, particularly when unstimulated.
• Causes damage in the regions of the medial
  thalamic nuclei, the frontal lobes (particularly
  situated deeply or on the orbitofrontal
  surfaces), or from hydrocephalus.

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Abulia

• Mental and physical slowness and lack of impulse
  to activity that is in essence a mild form of
  akinetic mutism.
• with the same anatomic origins.

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Catatonia

• Hypomobile and mute syndrome associated with a
  major psychosis.
• patients appear awake with eyes open but make no
  voluntary or responsive movements, although they
  blink spontaneously, swallow, and may not appear
  distressed.
• Eyes are half-open as if the patient is in a fog
  or light sleep.
• NO clinical evidence of brain damage.

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Locked-in state

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

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Locked-in state

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

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Anatomy and Physiology of Unconsciousness

• Cerebral cortex
• neurons located in the upper brainstem and
  medial thalamus
• RAS, maintains the cerebral cortex in a state of
  wakeful consciousness.

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Anatomy and Physiology of Unconsciousness

• principal causes of coma
• (1) lesions of the RAS
• (2) destruction of large portions of both
  cerebral hemispheres
• (3) suppression of thalamocerebral function by
  drugs, toxins,
• metabolic causes hypoglycemia, anoxia, azotemia,
  or hepatic failure.

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Anatomy and Physiology of Unconsciousness

• Pupillary enlargement, loss of vertical and
  adduction movements of the globes suggest upper
  brainstem damage.
• lesions in one or both cerebral hemispheres do
  not affect RAS, a large mass on one side of the
  brain may cause coma by secondarily compressing
  the upper brainstem and abnormalities of the
  pupils and eye movements .

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Anatomy and Physiology of Unconsciousness

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

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• RAS and the thalamic and cortical areas utilize a
  variety of neurotransmittors. Acetylcholine,biogen
  ic amines Cholinergic fibers connect the
  midbrain to other areas of the upper brainstem,
  thalamus, and cortex.
• Serotonin and norepinephrine regulation of the
  sleep-wake cycle.
• Alerting effects of amphetamines are likely to
  be mediated by catecholamine release.

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Herniation

• transfalcial (displacement of the cingulate
  gyrus under the falx and across the midline),
• transtentorial (displacement of the medial
  temporal lobe into the tentorial opening),
• foraminal (downward forcing of the cerebellar
  tonsils into the foramen magnum.

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Epileptic Coma

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

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Pharmacologic Coma

• Can be reversible and leaves no residual damage.
• Many drugs and toxins are capable of depressing
  nervous system function.

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Approach to the Patient

• The diagnosis and management of coma depend on
  knowledge of its main causes.
• interpretation of clinical signs, brainstem
  reflexes and motor function.
• Acute respiratory and cardiovascular problems
• complete medical evaluation, vital signs,
  funduscopy, and examination for nuchal rigidity,
  (complete neurologic evaluation for know the
  severity and nature of coma.

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History

• trauma, cardiac arrest, or known drug ingestion.
• (1) Circumstances and rapidity with which
  neurologic symptoms developed
• (2) confusion, weakness, headache, fever,
  seizures, dizziness, double vision, or vomiting
• (3) use of medications, illicit drugs, or
  alcohol
• (4) chronic liver, kidney, lung, heart,

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History

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

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General Physical Examination

• temperature, pulse, respiratory rate and pattern,
  Tachypnea may indicate acidosis or pneumonia
  blood pressure.
• Fever suggests a systemic infection, bacterial
  meningitis, or encephalitis only rarely is it
  attributable to a brain lesion that has disturbed
  temperature-regulating centers.

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General Physical Examination

• High body temperature, 42 to 44C, associated
  with dry skin should arouse the suspicion of heat
  stroke or anticholinergic drug intoxication.
• Hypothermia itself causes coma only when the
  temperature is lt31C.

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General Physical Examination

• Alcoholic, barbiturate, sedative, or
  phenothiazine intoxication
• Hypoglycemia, peripheral circulatory failure, or
  hypothyroidism,etc.

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General Physical Examination

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

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Neurologic Assessment

• Observation first without examiner intervention.
• Patients who toss about, reach up toward the
  face, cross their legs, yawn, swallow, cough, or
  moan are close to being awake. Lack of restless
  movements on one side or an outturned leg at rest
  suggests a hemiplegia.

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Neurologic Assessment

• Multifocal myoclonus almost always indicates a
  metabolic disorder
• In a drowsy and confused patient bilateral
  asterixis is a certain sign of metabolic
  encephalopathy or drug ingestion.

.
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Neurologic Assessment

• Decorticate rigidity and decerebrate rigidity, or
  "posturing," describe stereotyped arm and leg
  movements occurring spontaneously or elicited by
  sensory stimulation.

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Brainstem Reflexes

• pupillary responses to light,spontaneous and
  elicited eye movements, corneal responses,
• Respiratory pattern

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A.- PUPILLARY LIGHT RESPONSES Ø     
Simmetrically reactive round pupils Exclude
midbrain damage. (2 to 5
mm )Ø      Enlarged pupil (gt5 mm),
unreactive or poorly reactive Intrinsic
midbrain lesion (ipsilateral) or
by mass effect (contralate
ral).
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• Unilateral pupillary enlargement Ipsilaterall
  mass.
•  
• Oval and slightly eccentric pupils Early
  midbrain third nerve compression.
•  
• Bilaterally dilated and unreactive Severe
  midbrain damage by transtentorial
• pupils herniation or anticholinergic
  drugs toxicity.

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Ø      Reactive bilaterally small but not
pin- point (1 to 2.5 mm) Metabolic en
cephalopathy, deep bilateral
hemispheral lesions as
hydrocephalus or thalamic
hemorrhage Ø      Very small but
reactive pupil Narcotic or barbiturate
overdose or bilateral (Less than 1
mm) pontin damage.   

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Ocular Movements

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

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EYE MOVEMENTS

•  
•       Adducted eye at rest Lateral rectus
  paresis due to VI nerve
• 
  lesion. If is
  bilateral is due to intracraneal
  hypertension.
• Abducted eye at rest, plus ipsi Medial rectus
  paresis due to III nerve
• lateral pupilary enlargement
  dysfunction.
•  
• Vertical separation of the ocular Pontin or
  cerebellar lesion
• Globes. (Skew deviation)
•  
• Coma and spontanous conjugate Midbrain and
  pons intact
• horizontal roving movements
•  

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• Ocular bobbing. Brisk downward
•    and slow upward movement of the
• globes with loss of horizontal eye
•   movements Bilateral pontine damage
•  
•    Ocular dipping. Slower, arrhytmic
• downward followed by a faster upward
• movement with normal reflex horizontal
• gaze Anoxic damage to the
  cerebral cortex.
• Ø   Thalamic and upper midbrain lesions Eyes
  turned down and inward.

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F.- RESPIRATION PATTERNS.

•  
•  
•       Shallow, slow, well-timed regular Suggest
  metabolic or drug depression.
• Breathing
•  
•       Rapid, deep (Kussmaul) breathing Metabolic
  acidosis or ponto-
  mesencephalic lesions.
•  
•       Cheyne-Stokes breathing, with light Mild
  bihemispherical damage or
• Coma metabolic supression.
•  
•      Agonal gasps Bilateral lower
  brainstem damage.
• Terminal respiratory pattern.

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Laboratory Studies and Imaging

• chemical-toxicologic analysis of blood and urine,
  
• cranial CT or MRI, EEG,
• Lumbar puncture and CSF examination (cultures)

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Laboratory Studies and Imaging

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

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 Brain Death

• Neurological examination
• EEG
• Radionuclide brain scanning, cerebral
  angiography, or transcranial Doppler measurements
  may also be used to demonstrate the absence of
  cerebral blood flow

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TREATMENT FOR THE PATIENT IN COMA.

• 1.- The treatment must be instituted inmediately
  even when there is no a certain diagnosis.
• The inmediate goal is the prevention of further
  nervous system damage.
• 2.- Diagnostic procedures and general treatment
  mus be performed simultaneously and to install
  the specific treatment when the etiology is
  known.

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TREATMENT FOR THE PATIENT IN COMA.

• A.- Permeable airway. Oxygen supply through nasal
  fossae to endotraqueal intubation..
• B.- Politrauma patients evaluation. Stabilize
  the neck and the rest of the vertebral colum.
• C.- Establish an intravenous access. Water
  administration carefully monitored.
• D.- Maintain the body temperature the closest to
  the normal values as possible.

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TREATMENT FOR THE PATIENT IN COMA.

• E.- I.V. administration of 50 ml of 50
  glucose.
• F.- Administrate thiamine in malnourished and
  alcoholic patients. 10 mg I.V. and 100 mg
• I.M. /day /3 days.
• G.- Naloxone (0.4 to 0.8 mg) or flumazenil (0.5
  to 1 mg) I.V administration
• H.- Appropriate treatment of intracraneal
  hypertension and seizures.

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TREATMENT FOR THE PATIENT IN COMA.

• ØI.- General measures for the unmovable patient.
  
•       Appropriate nutrition and hydration.
• Ø      Posture changes every two hours.
• Ø      Mobilization of joints.
• Ø      Ocular metilcelulose drops, 1 every 4
  hours.
• Ø      I.V. ranitidine 50 mg every 8 hours, or
  300 mg in 250 ml of 5 dextrose in 24 hours or
  sucralfate 1 g per nasogatric tube every 6 hours.
• Ø      S.C. Heparin, 5000 U every 12 hours.
• Ø      Urinary tract care.
• J.- Etiologic treatment.