Evaluation of Patients in Coma

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APPROACH TO COMA
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What well discuss

• Basic definitions
• Neuroanatomy of consciousness
• Key examination points (CNS General)
• Investigations
• Coma mimics

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Importance of this topic

• Lot of Semantic confusions about the terminology
  related to coma.
• Work up of the patient with coma is often
  complex and always urgent.
• Examination determines the early management,
  urgency with which imaging and CSF studies are
  obtained.

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CONSCIOUSNESS

• Def Awareness of ones own self and his
  environment
• and responsiveness to external and internal
  stimuli.
• Two Dimensions
• Arousal Primitive function, sense of
  wakefulness (Brainstem, Medial thalamus).
• Cognition Cerebral cortex, Subcortical nuclei.
• Cognition depends on arousal, but normal
• arousal does not guarantee normal cognition.

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Severity of altered sensorium

• Alert Confusion
• Drowsiness Delirium.
• Stupor
• Coma

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Definitions

• Drowsiness inability to sustain a wakeful state
  without external stimuli. Pt can be easily
  arousable, but falls asleep when left alone.
• Stupor A state in which the pt can be aroused by
  noxious stimuli only little motor or verbal
  activity once aroused.
• Coma State of complete loss of consciousness.
  The pt appears to be in deep sleep and not
  arousable at all to any kind of stimuli. He wont
  attempt to avoid painful or noxious stimuli. No
  sleep wake cycle.

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Definitons.

• Confusion inability to maintain a coherent
  sequence of thoughts, usually by inattention and
  disorientation
• Delirium a state of disturbed consciousness
  with motor restlessness and disorientation.
  (Confusion Motor agitation)

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Really Simple Neuroanatomy

• Ascending Reticular Activating System (ARAS) in
  the brainstem (Upper pons midbrain).
• Thalamic nuclei receiving fibers from ARAS and
  sending fibers to Cortex.
• Cerebral cortex.

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ARAS
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ARAS

• ARAS acts as a gating system, increasing or
  decreasing thalamic inhibitory influence on the
  cortex.
• Alters effect of sensory stimuli ascending.
• Alters descending cortical stimulation.

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Demands of Arousal

• Function of ARAS-Thalamic-Cortical system depends
  on
• anatomic integrity of structures
• metabolic integrity (circulatory integrity)
• communicative integrity (neurotransmitter
  function)

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Coma Basics

• Coma implies dysfunction of
• ARAS or
• Both hemi-cortices
• Anatomically, this means
• central brainstem structures (bilaterally) from
  caudal medulla to rostral midbrain
• both hemispheres

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Epidemiology of Coma

• Plum and Posner 1982
• 500 consecutive cases of coma
• 326 diffuse or metabolic brain dysfunction (149
  drug intoxication)
• 101 supratentorial (44/101 ICH)
• 65 subtentorial lesions
• (40/65 brainstem infarcts)

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Etiology (Metabolic)

• AEIOU TIPS They affect cortex or brainstem or
  both.
• A- Alcohol, Anoxia, Acidosis
• E- Electrolytes, enviroment
• I - Immunity, insulin
• O-Opiates
• U- Uremia
• T- Trauma, toxins
• I- Infections
• P- Psychogenic, pharmacologic
• S- Shock, sepsis

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Structural causes
Supratentorial 1.Bilateral cerebral
infarct, concussion , contusion,
2.Postical states, hypertensive encephalopathy,
3.Encephalitis, meningitis, Increased ICP,
4.SAH, hemorrhage , tumor , abscess.
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Structural causes ..
Infratentorial 1. Pontine hemorrhage,
Infarct. 2. Cerebellar hemorrhage , 3.
Basilar artery occlusion , 4. Brainstem
tumors, or traumatic Hge.
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Coma Patient Evaluation
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History

• To seek historical data from friends , family ,
  or others.
• The rate of onset of neurologic or behavioral
  changes
• Abrupt onset favors the CNS hemorrhage or
  ischemia ,
• Gradual onset favors a metabolic problem.
• The history of trauma or on ongoing medical
  illness,
• Suicidal ideation , past attempts at self-harm ,
• History of substance abuse.

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First Step

• Assess the ABCs
• Airway gag reflex,
• Breathing pattern and sufficiency,
• Circulation adequacy and hypotension.

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The roles of vital signs

• Bradycardia Increased ICP , hypothyroidism,
  intoxication and cardiac disease .
• Tachycardia Hypovolemia, Infection.
• Hypertension ICP, ICH, HT encephalopathy, Stroke
  and toxins.
• Hypotension Sepsis, Hypovolemia, Wernickes
  encephalopathy, MI.
• Hypothermia sepsis , hypothyroidism , or
  environmental exposure.
• Hyperthermia sepsis , heat stroke ,
  thyrotoxicosis , stroke , toxins.

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General examination

• Look for external injuries.
• Skin needle tracks, rash.
• Breath odour fetor hepaticus, uremia, acetone,
  or alcohol.
• CVS, RS and ABDOMEN.

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Neurologic Exam

• Cornerstone of assessment,
• Descriptive, systematic,
• Reference point for serial assessment.

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Components

• Level of Consciousness
• Breathing pattern
• Pupillary size and reaction
• Extraocular movements
• Corneal reflex
• Motor status

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Breathing

• Abnormalities of respiration can help localize
  but
• almost always in the context of other signs.
• Cheyne-Stokes respiration
• Cycles of Hyperapnea alternating with apnea.
• bilateral dysfunction of the hemispheres or
  diencephalon.
• Apneustic Long inspiratory phase, upper pons
  lesions.
• Cluster high medulla or lower pons.
• Ataxic Erratic shallow and deep breathing,
  medulla.
• Apnea Terminal stage, Medulla.

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Level of consciousness

• GCS (Glasgow Coma Scale)
• Eye Opening (4), Verbal (5), Motor (6)
• 13-15 Mild, 8-12 Moderate, 3-7 Severe Coma.
• The AVPU scale
• A - alert aware
• V - responds to verbal stimuli
• P - responds to painful stimuli
• U - unresponsive

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Cranial Nerve Exam

• Systematic assessment of brainstem function via
  reflexes
• Cranial Nerve Exam
• Pupillary light response (CN 2-3)
• Gaze/Oculocephalic/calorics (CN 3,4,6,8)
• Corneal reflex (CN 5,7)
• Gag refelx (CN 9,10)

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Pupillary Light Responses

• Afferent Limb Optic Nerve.
• Efferent Limb Parasympathetics via oculomotor.
• Midbrain integrity/ tectum.
• Avoid the term PERLA
• State size, before and after light stimulation,
• Specify right and left.
• Be aware of drug effects - Systemic and Local.

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Pupils Localizing Value

• Small, Reactive pupils Metabolic coma.
• Unilateral fixed, dilated pupil uncal
  herniation, PCOM aneurysm.
• Bilateral, Large fixed pupils Midbrain lesion or
  Death.
• Bilateral, midposition, fixed pupils
  Transtentorial herniation.
• Pinpoint pupils Pontine ICH, infarct, Opiate
  poisoning.
• Horners syndrome- sympathetic dysfunction.

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PUPILLARY ABNORMALITIES
Normal
Horners syndrome
Left 3rd CN palsy
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Terminal stage pupil
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Ciliospinal Reflex

• 1-2 mm pupillary dilatation evoked by noxious
  cutaneous stimulation.
• More prominent in sleep or coma than during
  wakefulness.
• Test integrity of symp.pathways in comatose
  patients.
• Not particularly useful in evaluating brainstem
  function.

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Eye Movements

• Eye movements are the cornerstone of the
  neurologic examinations of the comatose patient ,
  as they closely approximate the ARAS
  anatomatically.
• EOM evaluates the cortex, and the MLF in the
  brainstem.

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Eye Movements

• Note resting position of both eyes
• Conjugate Deviation suggests frontal / pontine
  damage.
• Frontal Eyes look toward the side of lesion.
• Pontine - Eyes look away from the side of
  lesion.
• Dysconjugance suggests Cranial Nerve abn.
• Roving eye movts indicate intact brainstem.
• Ocular bobbing Pontine lesion.

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Oculocephalic and Calorics

• Same reflex elicited differently
• Afferent Eighth nerve
• Efferent 3,4,6 via MLF and PPRF
• Oculocephalics may also involve proprioceptive
  afferents from the neck

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Oculocephalic Reflex (Dolls eye)

• Brisk horizontal rotation of head with eyes held
  open and watch for contraversive movements of
  eyes.
• Then flexion of the neck eyes deviate up,
  followed by extension eyes deviate downward
  Vertical gaze.
• If eyes follow movement of head to side, suspect
  brainstem involvement in coma.
• Caution with suspected c-spine injury.

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DOLLS EYE MOVEMENT
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Caloric test(Oculovestibular reflex)

• Ensure TM integrity
• Elevation of head to 30 degrees (so that lateral
  semicircular canal is vertical)
• Instillation of 50 to 120 ml of ice water
• Awake pt deviation toward, nystagmus away
• Comatose deviation toward, no nystagmus.
• (Brainstem intact, Cortex is damaged)
• No Deviation, no nystagmus - (Brainstem is
  damaged)

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Calorics

• COWS Pneumonic.
• Wait for 5 minutes and test the other ear.
• To test vertical eye movements
• Both ears, cold water-downward gaze
• Both ears, warm water-upward gaze

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Caloric test
Normal
Abnormal
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Corneal Reflex

• Afferent Trigeminal Nerve
• Efferent Third Nerve (Bells Phenomenon
• and Facial Nerve (Eye closure)
• Tests dorsal midbrain (Bells) and pontine
  integrity (Eye closure)

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Gag Reflex

• Afferent Glossopharyngeal
• Efferent Vagus
• Taken in context of other findings

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Motor Exam

• Assess tone, presence of asterixis
• Response to painful stimuli
• none
• abnormal flexor
• abnormal extensor
• normal localization/withdrawal
• Focal weakness.

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• Decorticate posturing in comatose patient
• Lesion above the red nucleus
• Lower limbs extend, upper limbs flex following
  stimulus
• Activity in the brainstem flexor center, the red
  nucleus

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• Decerebrate posturing in comatose patient
• Upper and lower limbs extend following stimulus
• Lesion between red nucleus and vestibular
  nucleus.
• Overactivity of Lateral vestibular nucleus.

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Clinical Value

• Decorticate posturing indicates a higher level of
  brainstem injury than decerebrate posturing (a
  good thing)
• Comatose patients who go from decerebrate to
  decorticate (ascending progression of impaired
  area) have a better prognosis than those that go
  from decorticate to decerebrate (descending
  progression of impaired area).
• Descending impairment will be fatal if medullary
  respiratory and cardiovascular centers are
  damaged.

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Reflexes

• Deep tendon
• Biceps, brachioradialis, triceps
• Patellar, Achilles
• Plantar Responses
• Superficial skin
• Abdominal, cremasteric
• Meningeal signs.

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Goals in Emergency

• Primary Neurological Process?
• evidence of raised ICP,
• focal findings, especially that implicate
  brainstem structures.
• Secondary Processes?
• signs of infection, toxic/metabolic processes
• relative lack of focality.

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Coma classification after examination

• Diseases with no focal or lateralizing signs.
• Diseases with focal brainstem or lateralizing
  cerebral signs.
• Diseases with meninigitic syndromes.

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Diseases with no focal or lateralizing signs.

• Symmetrical examination, small reactive pupil,
  normal eye movements.
• Predominantly metabolic, toxic or septic
• Bilateral cerebral hemispheres or brainstem or
  both are affected.

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Diseases with focal brainstem or lateralizing
cerebral signs.

• Focal lesion in the brainstem directly affect
  the ARAS.
• Focal lesion in the cortex leading to herniation
  and indirectly affecting the ARAS.
• Bilateral cortical lesion can directly cause
  coma.

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Uncal herniaiton

• Expanding lesions in lateral middle fossa.
• Compression of hippocampal gyrus over free edge
  of tentorium.
• Ipsilateral dilated nonreactive pupil.
• Ipsilateral hemiparesis due to compression of
  opposite CST by the midbrain (Kernohan waltman
  sign).

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Uncal herniation
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Transtentorial herniation

• Large midline mass
• Small symmetric pupil or midposition, unreactive
  pupil.
• Decorticate posturing.
• Durets hemorrhages in the midbrain.

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Transtentorial herniation
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Tonsillar herniation

• Posterior fossa lesions
• Herniated tonsils compress the medullary vital
  centers.
• Decerebrate rigidity, apnea, bradycardia
• Neck rigidity, opisthotonus.

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Tonsillar herniation
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Investigations

• Blood glucose, urea, electrolytes, ABG etc
• Non contrast head CT
• Acute blood
• Space occupying lesion
• MRI
• Posterior fossa
• Early infarct
• LP
• Xanothochromia
• Infection
• EEG Non convulsive status epilepticus.

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Coma Mimics

• Akinetic mutism
• Locked-in syndrome
• Persistent Vegetative state
• Conversion reactions

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Akinetic Mutism

• Silent, immobile but alert appearing
• Usually due to lesion in bilateral mesial frontal
  lobes, bilateral thalamic lesions or lesions in
  peri-aqueductal grey (brainstem)

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Persitent Vegetative state

• No evidence of awareness of self or environment
  and an inability to interact with others
• Bowel bladder incontinence
• Hypothalamic brain stem autonomic function
  preservation to permit survival with medical
  nursing care
• Maintainence of intermittent wakefulness and
  sleep-wake cycles
• No evidence of language comprehension or
  expression
• No response to visual,auditory,noxious,or tactile
  stimuli
• Possible preservation of cranial nerves spinal
  cord reflexes

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Locked-In Syndrome

• Infarction of basis pontis (all descending motor
  fibers to body and face)
• May spare eye-movements
• Often spares eye-opening
• EEG is normal or shows alpha activity

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Conversion reactions

• Fairly rare
• Oculocephalics may or may not be present.
• The presence of nystagmus with cold water
  calorics indicates the patient is physiologically
  awake
• EEG used to confirm normal activity

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Thank You