this presentation help to approach a comatose patient when come to an emergency ward.

1. APPROACH TO
COMA
DR. YAGNIK CHHOTALA
R3 MEDICINE

2. OVERVIEW OF DISCUSSION
CONSCIOUSNESS AND ITS COMPONENTS
ANATOMY RELATED TO CONSCIOUSNESS
DISORDERS OF CONSCIOUSNESS
GENERAL CLINICAL APPROACH TO COMA
HISTORY
GENERAL EXAMINATION
NEUROLOGICAL EXAMINATION

3. Introduction
 Coma is among most common and striking problems
in medicine
 Accounts for large number of admissions to emergency
 Requires immediate attention and an organised
approach

4. What is Consciousness?
Perception -
Awareness
of self and
environment
( Sensory
System)
Reaction –
Meaningful
responsiven
ess (Motor
system)
consciousness
Wakefulness
/alert/arous
al – (Sleep
wave cycle)

5. Component of consciousness
Arousal - appearance of wakefulness
controlled by ARAS(ascending
reticular activating system)
Content - the sum of cognitive and
affective function controlled by
cerebral hemispheres

7. Disorders mainly involve alertness & response
Continnum of
states of reduced
alertness
• 3. Coma: deep sleep like state from which
patient can not be aroused
• 2. Stupor: Transiently Arousable pt by
vigorous stimuli accompnied by motor
behaviour that leads to avoidance of
uncomfortable stimuli
• 1. Drowsy/lethargic/light sleep: easily
arousable and persistence of alertness for
brief periods
• Drowsiness and stupor are usually
accompnied by some degree of confusion

8. Disorders mainly involve cognition
 Confusion: a mental and behavioural state of reduced
comprehension, coherence and capacity to reason
 Delirium: acute confusional state
 Dementia: aquired deterioration in cognitive abilities
that impaires successful performance of activities of
daily living

9. Disorders mainly involve affect
 Hallucination: false perception in absence of external
stimuli
 Delusion: false belief despite reasoning
 Illusion: false interpretation of exeternal stimuli

10. Special conditions simulating coma (COMA MIMICS)
vegetative state(awake coma): Awake +
nonresponsive(emerged from coma) +
meaningless eye movements-always
accompnying signs indicating extensive
damage to cerebral hemispheres (decerebrate
or decorticate limb posture & absent response to
visual stimuli) e.g. cardiac arrest with cerebral
hypoperfusion , head trauma
Minimally conscious state(milder form of
vegetative state): awake + some responsive
• e.g. cardiac arrest , head trauma

11. Akinetic mutism : partial/fully
awake + mute & immobile e.g.
damage to medial thalamus
nuclei/frontal lobes or extreme
hydrocephalus
Abulia(milder form of akinetic
mutism) : partial/fully awake +
mute & mental and physical
slowness e.g.damage to medial
thalamus nuclei/frontal lobes
or extreme hydrocephalus
catatonia: same as akinetic
mutism/abulia but no clinical
evidence of cerebral damage
such as babinski signs &
hypertonicity in limbs e.g.
major psychosis usually
schizophrenia or major
depression

12. Locked in state:
 awake +nonresponsive+ meaningful vertical eye
movements
 damage to ventral pons that transects all descending
motor (corticospinal & corticobulbar) pathways,
severe GBS, critical illness neuropathy, pharmacologic
neuromuscular blockade

13.  Brain death:state of irreversible cessation of all cerebral function with
preservation of cardiac activity and maintenance of respiratory and somatic
function by artificial means
1. Widespread cortical destruction reflected by deep coma &
unresponsiveness to all forms of stimulation
2. Global brainstem damage demonstrated by absent pupillary light reaction
and by the loss of oculovestibular and corneal reflexes
3. Destruction of medulla manifested by complete and irreversible apnea
4. Others:
 heart rate is invariant does not accelerate to atropine;
 diabetes insipidus is usually present but may only develop hours or days
after other clinical signs of brain death,;
 pupils are usually midsized but may be enlarged they should not however
be small;
 loss of DTR is not required because spinal cord remains functional;
 babinski signs are generally absent and toe response is instead often flexor.

14. HOW TO CLINICALLY APPROACH WITH A COMATOSE
PATIENT???
 Prior to neurological assessment, we have to
manage respiratory and cardiovascular problems
 In most instances, a complete medical evaluation,
except for vital signs, fundoscopy and examination for
nuchal rigidity may be defered until the neurological
evaluation has established the severity and nature of
coma
 CIRCULATION AIRWAY  BREATHING

15. HISTORY
 Given by: family member,observer,108, by phone call
 Is there any H/O trauma, drug ingestion??
 Is there any Antecedent symptoms??:
• cofusion, dizziness(e.g.HTN),
• weakness(e.g.CVA),
• headache, vomiting(e.g.SAH,HTN),
• fever(e.g.meningitis),
• seizures(e.g.epilepsy)

16. What is Onset of neurologic symptoms developed??
Sudden onset Subacute onset
trauma preexisting medical/neurological
problem
drug ingestion secondary brain swelling of a mass such
as tumor, cerebral infarction
cerebral hemorrhage
cardiac arrest
epilepsy
basilar artery embolism

17.  What is Past h/o??:
• Does pt use any medication?(e.g.OHA),
• Is there any illicit drugs taken by pt?(e.g.alprax),
• Does pt have any chronic Diseases of
liver,kidney,lung,heart??
 What is personal h/o??:
• Any addiction??: smoking, alcohol

18. General physcical examination
See for vitals
Measure temparature:Hyperthermia & hypothermia
Pt has Fever? Pt Has Hypothermia(<31 C)?
systemic infection Exposure to cold
bacterial meningitis, encephalitis hypoglycemia
heat stroke peripheral circulatory failure
neuroleptic malignant syndrome extreme hypothyroidism
malignant hyperthermia due to anesthetics,
anticholinergic drug intoxication
; alcohol,babiturate,sedative or
phenothiazine intoxication
rarely lesion that has disturbed
hypothalamic temperature regulating
centers(central fever)
convulsions

19.  Take Pulse:
 If Pt Has Bradycardia?: p/o brain tumors, opiates,myxedema.
 If Pt has Tachycardia?:p/o hyperthyroidism, uremia
 Measure Blood Pressure:
 If Pt has Hypertension?: p/o hypertensive encephalopathy, cerebral
hemorrhage or head injuries
 If pt has Hypotension?: p/o alcohol or barbiturate intoxication,internal
hemorrhage, MI, sepsis, profound hypothyroidism, addisonion crisis
 See Respiratory rate:
 Pt is Tachypnic?: p/o systemic acidosis, pneumonia, rarely infiltration of brain
with lymphoma
 What is Cushing`s response ??:
 Pt present with Hypertension with bradycardia
 occur in response to severe increased ICP and signs of
Cerebral Herniation .

20. GENERAL PHYSICAL EXAMINATION
 Head examination:
 Depressed skull
fracture .
 Bruising over
mastoid process .
(Battle`s sign )
 Racoon eyes
 CSF or blood
discharge from nose
or ear.
 Palpation of the
orbital margins
Zygomatic or malar
fracture
Middle fossa fracture
Anterior cranial fossa
fracture
LIFE THREATENING
Basilar skull
fracture

21. GENERAL PHYSICAL EXAMINATION
 Skin examination:
Is there any Injuries, Bruises?:then p/o trauma
If Pt has Dry Skin: p/o DKA, Atropine overdosage
If pt has Moist skin: Hypoglycemic coma
If Cherry-red discoloration: CO poisoning
Is there any Needle marks?: drug addiction or SC insulin
injection
Is there any Rashes?: meningitis , hypersensitivity ,
endocarditis
Any skin discoloration s/o : cyanosis, pallor
Is there any cutaneous petechiae?: Thrombotic
thrompocytopenic purpura,
meningococcemia,or
bleeding diathesis associated with an ICH

22. Fundoscopic examination
 SAH: subhyaloid hemorrhages
 Hypertensive encephalopathy:
exudates,hemorrhages,vessel crossing changes,
papilloedema
 Increased ICT: papilloedema

23. NEUROLOGICAL EXAMINATION
 Assessment of mental status:
 Cranial nerves:
 Motor system:
 Reflexes:
 Sensory system:
 Coordination:
 Gait:

24. Specific neurological examination in comatose patient
observed without intervention
Posturing
Level of arousal
Brainstem reflexes
Pupillary signs
Occulomotor movements
Corneal response
Respiratory patterns

25. observed without intervention
 Tossing about in the bed,reaching up toward the face,
crossing legs, yawning, swallowing, coughing or
moaning reflect a drowsy state

26.  Lack of restless movements on one side or an
outturned leg suggests a hemiplegia
•The right leg is externally rotated
•The head and eyes are deviated to the
left hemispheric lesion

27.  Intermittent twitching movements of a foot, finger, or
fascial muscle may be the only sign of seizures
 Multifocal myoclonus almost always indicates a
metabolic disorder particularly uremia, anoxia, drug
intoxication(esp with lithium or haloperidol or a prion
disease)
 In a drowsy and confused pt, bilateral asterexis is a
certain sign of metabolic encephalopathy or drug
intoxication

28. Posturing
Decorticate and decerebrate rigidity or posturing
describe steriotyped arm and leg movements occuring
spontaneously or elicited by sensory stimulation.

29.  Decorticate: flexion of elbows and wrists and
supination suggests bilateral damage rostral to the
midbrain

30.  Decerebrate: extention of elbows and wrists with
pronation suggests damage to motor tracts in the
midbrain or caudal diencephalon

31.  Less frequent combination of arm extention with leg
flexion or flaccid legs is asso with lesions in pons
 These concepts have been adapted from animal work
and can not been applied with precision to coma in
humans.
 In fact, acute and widespread disorders of any type,
regardless of location, frequently cause limb extention,
and almost all extensor posturing become
predominantly flexor as time passes

32.  LEVEL OF AROUSAL
 A sequence of increasingly intense stimuli is used to determine the threshold
for arousal and the motor response of each side of the body. The results of
testing may vary from minute to minute and serial examinations are useful.
 Tickling of nostrils with a cotton wisp is a moderate stimulus to arousal-
all but deeply stuporous and comatose pt will move the head away and
arouse to some degree. An even greater degree of responsiveness is present if
the pt uses his hand to remove an offending stimulus.
 Noxious stimuli such as pressure on knuckles bony prominences, pin prick
stimulation, skin pinching to arousal in further step-abduction avoidance
movement of a limb is usually purposeful and denotes and intact
corticospinal system whereas posturing (decorticate or decrebrate) indicates
severe damage to corticospinal tract.
Posturing may also be unilateral and coexist with purposeful limb movements,
reflecting incomplete damage to motor system

33. LEVEL OF AROUSAL
Edinburgh classification
grades level
0 Fully conscious
1 Drowsy/lethargic, respond to verbal command
2 Obtunded, responds to minimal noxious stimulus(Tickling of nostrils
with a cotton wisp)
3 Stupor, responds to strong noxious stimuli(pressure on knuckles bony
prominences, pin prick stimulation, skin pinching)
4 Coma, no response

35. (Alert, Voice, Pain, Unresponsive) is a system by which a first aider, ambulance crew or
health care professional(or as we just student) can measure and record a patient's
responsiveness, indicating their level of consciousness.
The AVPU scale
•Alert - a fully awake (although not necessarily orientated) patient. This patient will have
spontaneously open eyes, will respond to voice (although may be confused) and will have
bodily motor function.
In some EMS protocols, "Alert" can be subdivided into a scale of 1 to 4, in which 1, 2, 3 and 4
correspond to certain attributes, such as time, person, place, and event.
•Voice - the patient makes some kind of response when you talk to them, which could be in
any of the three component measures of Eyes, Voice or Motor - e.g. patient's eyes open on
being asked "are you okay?!". The response could be as little as a grunt, moan, or slight
move of a limb when prompted by the voice of the examinor .
Pain – its done if the patient don’t responde to the upper two methodes :
Sternal rub the rescuers knuckles are firmly rubbed on the breastbone of the patient.
pinching the ear of the patient's and pressing a pen into the bed of the patient's
fingernail.
 A fully conscious patient would normally locate the pain and push it away
 Patient who is not alert likely to exhibit only withdrawal from pain, or even involuntary
flexion or extension of the limbs from the pain stimulus.Ambulance crews may begin with an AVPU assessment, to be followed by a GCS assessment
if the AVPU score is below "A."

36. Level of
consciousness
Spontaneous 4
To loud voice 3
To Pain 2
Absent 1
Converses/Oriented 5
Converses/Desoriented
(inappropriate sentence)
4
Inapropriate words 3
Incomprehensible sounds 2
Absent 1
Obeys 6
Localizes Pain 5
Withdraws(flexion) 4
Eyes Open
Verbal
Motor
The sum obtained in this scale is used to the assess
Coma and Impaired consciousness
Mild is 13 to 15 points
Moderate is 9 to 12 points
Severe 3 to 8 points
Patients with score less than 8 are in Coma
GCS

37. Glasgow Coma Scale
The scale was published in 1974 by Graham Teasdale and Bryan J. Jennett, professors
of neurosurgery at the University of Glasgow's Institute of Neurological Sciences at
the city's Southern General Hospital.
oSevere, with GCS ≤ 8
oModerate, GCS 9 - 12
oMinor, GCS ≥ 13.
The score is expressed in the form "GCS 9 = E2 V4 M3 at
07:35" Tracheal intubation and severe facial/eye swelling or damage make it
impossible to test the verbal and eye responses. In these circumstances, the
score is given as 1 with a modifier attached e.g. 'E1c' where 'c' = closed, or 'V1t'
where t = tube. A composite might be 'GCS 5tc'. This would mean, for example,
eyes closed because of swelling = 1, intubated = 1, leaving a motor score of 3
for 'abnormal flexion'. Often the 1 is left out, so the scale reads Ec or Vt.
Don’t
Miss

38. eye response (E)
1.No eye opening
2. Eye opening in response to pain. (Patient
responds to pressure on the patient’s
fingernail bed; if this does not elicit a
response, supraorbital and sternal pressure
or rub may be used.)
3. Eye opening to speech. (Not to be confused
with an awaking of a sleeping person; such
patients receive a score of 4, not 3.)
4. Eyes opening spontaneously
Best verbal response (V)
There are 5 grades starting with the most severe:
1.No verbal response
2.Incomprehensible sounds. (Moaning but no words.)
3.Inappropriate words. (Random or exclamatory
articulated speech, but no conversational exchange)
4.Confused. (The patient responds to questions
coherently but there is some disorientation and
confusion.)
5. Oriented. (Patient responds coherently and
appropriately to questions such as the patient’s
name and age, where they are and why, the year,
month, etc.)
Best motor response (M)
There are 6 grades starting with the most severe:
1.No motor response
2.Extension to pain (adduction of arm, internal rotation of shoulder, pronation of forearm,
extension of wrist, decerebrate response)
3.Abnormal flexion to pain (adduction of arm, internal rotation of shoulder, pronation of
forearm, flexion of wrist, decorticate response)
4.Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when
supra-orbital pressure applied ; pulls part of body away when nailbed pinched)
5.Localizes to pain. (Purposeful movements towards painful stimuli; e.g., hand crosses mid-line
and gets above clavicle when supra-orbital pressure applied.)
6.Obeys commands. (The patient does simple things as asked.)

39. Revised Trauma Score
GCS score + Respiratory score + Systolic BP score =
Revised Trauma Score
•The score range is 0-12.
•A patient with an RTS score of 12 is labeled DELAYED (walking
wounded)
• 11 is URGENT (intervention is required but the patient can wait a
short time)
• 10-3 is IMMEDIATE (immediate intervention is necessary).
•The last possible label is MORGUE which is given to seriously
injured people with an RTS score of 3 or lower. These people should
not receive certain care because they are unlikely to survive.
The reasoning is that diverting scarce resources away from people with a little chance of survival increases the
chances of survival of others who are inherently more likely to survive.

40. Revised Trauma Score
 Glasgow Coma
Scale
 0 = 1 - 3 GCS
 1 = 4 - 5 GCS
 2 = 6 - 8 GCS
 3 = 9 - 12 GCS
 4 = 13 - 15 GCS
• Respiratory Rate
 0 = 0 Respirations
 1 = 1 to 5
Respirations
 2 = 6 to 9
Respirations
 3 = 10 to 29
Respirations
 4 = >29 Respirations
• Systolic BP
• 0 = 0
• 1 = 1 to 49
• 2 = 50 to
75
• 3 = 76 to
89
• 4 = >89
GCS score + Respiratory score + Systolic BP score =
Revised Trauma Score

41. BRAINSTEM REFLEXES
 Essential to localise lesion in coma
 Reflexes
 Pupillary size and reaction to light to see the midbrain function
 Spontaneous or elicited eye movements
 Corneal responses
 Respiratory and pharyngeal responses to see the medullary function
 General rule
 Bilateral hemisphere disease preserves these brainstem activities,
particularly pupillary reaction and eye movements.
 However presence of abnormal brainstem signs does not always
indicate that primary lesion in brainstem because hemisphere
masses can cause secondary brainstem damage by transtentorial
herniations.

43. Pupillary signs
 Examined with bright and diffuse light (preferably not
an ophthalmoscope, which illuminates only limited
part of retina)
 Reactive and round pupils of midsize(2.5-5mm)
• essentially exclude midbrain damage, either primary
or secondary to compression.
• Suggests p/o metabolic disorder

44.  unilateral enlarged and poorly reactive pupil(>6mm)
signifies compression or stretching of third nerve from the
effects of ipsilateral cerebral mass. Less frequently Enlargement
of pupil contralateral to a hemispheral mass may occur. an oval
and slightly eccentric pupil is transient sign that accompnies
early midbrain third nerve compression.
 Bilateral dilated and unreactive(>6mm) indicates severe
midbrain damage usually from compression by a
supratentorial mass
 Other misleading causes of pupillary enlargement
 Intoxication of drugs with anticholinergic activity
 Use of Mydriatic eye drops
 Direct ocular trauma

45.  Unilateral miosis(<2.5mm) occur in dysfunction of sympathetic
afferents originating in the posterior hypothalamus and descending in
tegmentum of brainstem to the cervical cord. Therefore limited
localising value but is an occasional finding in pt with large cerebral
haemorrhage that affects thalamus.
 Reactive and bilaterally small (1-2.5mm) but not pinpoint are seen
in
 Metabolic encephalopathies
 Deep bilateral hemispheral lesions such as hydrocephalus or thalamic
hemorrhage
 Pinpoint reactive pupils (<1mm) seen in
 Narcotic or barbiturate overdoses
 Extensive pontine hemorrhage
(response to naloxone and presence of eye movements assist in
distinguishing between these)

47. Ocular movements
 Observed by elevating lids and observing resting
position and spontaneous eye movements
 Lid tone
 Tested by lifting eyelids and resistance to opening and
speed of closure
 Progressively reduce as unresponsiveness progresses
 Horizontal divergence of eyes at rest is normal in
drowsiness. As coma deepens, the ocular axes may
become parallel again

48.  Resting position of eyes
 Conjugate horizontal deviation to one side indicates:
 Damage to pons on opposite side or
 Damage to frontal lobe on same side
(maxim: eyes look toward a hemisphere lesion and away
from a brainstem lesion)
 Seizures also drives eyes to one side but usually with
superimposed clonic movements of the globes
 Wrong way eyes: eyes may occasionally turn paradoxically
away from side of a deep hemispheral lesion
 Downward and inward eyes: with thalamic and upper
midbrain lesions

49. Corticospinal posture
The head and eyes are deviated to the left hemispheric lesion.
The right arm is pronated with an adducted thumb. The left arm
is supinated with an adducted thumb. The right leg is externally
rotated.

50. Brainstem hemiparetic posture.
The head and eyes are deviated to the right, the same side as the
hemiparesis as noted from the adducted thumb

51.  Spontaneous eye movements
 Conjugate horizontal roving: excludes damage in
midbrain and pons and p/o metabolic disorder
 Ocular bobbing: brisk downward and slow upward
movement of eyes associated with loss of horizontal eye
movements
 Diagnostic of bilateral pontine damage usually from
thrombosis of basillar artery
 Ocular dipping: slower arrhythmic downward movement
followed by faster upward movement with normal reflex
horizontal gaze
 Indicates diffuse cortical anoxic damage

52.  Reflex eye movements
 Oculocephalic reflex
 Elicited by moving head from side to side or vertically and observing eye
movements in direction opposite to head movement depend on the integrity
of ocular motor nuclei and their interconnecting tracts that extend from
midbrain to pons and medulla
 Doll’s eyes: reflex elevation of eyelids with flexion of neck
 Normally suppressed in awake pt
 Reflects reduced cortical influence on the brainstem and intact brainstem
pathways indicating that coma is caused by lesion or dysfunction in cerebral
hemespheres
 Absence of reflex eye movements:
 Damage within brainstem
 Overdosage of certain drugs
( normal pupillay size and light reaction distiguishes most drug induced comas
from structural brain damage)

53.  Oculovestibular response:
 Thermal or caloric stimulation of vestibular apparatus
provides more intense stimulus for oculocephalic reflex but
provides essentially same information
 Irrigating external auditory canal with cool water in order to
induce invection currents in the labyrinths.
 After the brief latency, result is tonic deviation of both eyes to
side of cool water irrigation and nystagmus in the opposite
direction (acronym COWS to remind direction of nystagmus)
 Loss of induced conjugate ocular movements indicates
brainstem damage
 The presence of corrective nystagmus indicates that the
frontal lobes are functioning and connected to brainstem thus
catatonia or hysterical coma is likely

55.  Corneal reflex
 By touching cornea with wisp of cotton
 Response:consisting of brief bilateral lid closure
 Depends on integrity of pontine pathways between
fifth(afferent) and both seventh(efferent) cranial nerves
 In conjunction with reflex eye movements it is useful test of
pontine function
 CNS depressant drugs diminish or eliminate corneal
responses soon after reflex eye movements are paralysed
but before the pupil become unreactive to light
 Corneal (and pharyngeal) response may be lost for a time
on the side of an acute hemiplegia

56. RESPIRATORY PATTERNS
Less localizing value in compare to other brainstem
signs
Types of breathing
 Shallow, slow but regular:
 metabolic or drug depression
 Cheyne stokes:
 Typical cyclic form ending with abrief apneic period
 Bihemispherial damage or metabolic suppression

57.  Kussmaul (rapid,deep): (central neurogenic
hyperventilation)
 Metabolic acidosis(e.g. DKA,lactic acidosis) or
pontomesencephalic lesions
Apneustic breathing:Prolonged inspiratory gasp
followed by a pause and then expiration
Seen in pontine damage

58.  Agonal gasps:(ataxic breathing)
 Medullary damage
 Terminal respiratory pattern of severe brain damage

59. Summary of neurological examination in comatose
patient
CAUSE PUPILS ABNORMAL
BRAINSTEM
REFLEX
RESPIRATORY
PATTERN
CEREBRAL LESION Small,reactive
(thalamic)
variable Cheyne stoke
MIDBRAIN LESION Dilated,fixed pupillary kussmaul
PONS LESION Pinpoint,reactive Occulomotor,
corneal
Apneustic,
kussmaul
MEDULLARY
LESION
Small,reactive Cough,gag Ataxic
METABOLIC Small,reactive variable Cheyne stoke,
kussmaul

60. References
 Harrison’s priciples of internal medicine 19th edition
 Alagappan
 Dejong
 Vakil golwala
 www.slideshare.net
 Other many internet sites