This document discusses the evaluation and management of coma. It begins by defining coma as prolonged unresponsiveness. It then describes the anatomy of arousal centered around the ascending reticular activating system. Assessment of coma involves the Glasgow Coma Scale and examining for signs of increased intracranial pressure. Common causes of coma include metabolic derangements, structural lesions of the brainstem or supratentorial regions. Management involves stabilizing ventilation, circulation, controlling seizures, reducing intracranial pressure and maintaining temperature. Detailed neurological examination can help localize lesions through assessment of reflexes, eye movements, respiratory patterns and posture.

1. Evaluation &
management of coma
DR ABDUL RUB
2ND YEAR PG MEM

2. COMA
 Coma is prolonged Unconsciousness Or Unarousable Unresponsiveness

3. DISORDERS OF CONSCIOUNESS

4. Really Simple Neuroanatomy
 Arousal: where is it localized?
 Ascending Reticular Activating System (ARAS) ‘core of the brainstem’
 receives input from numerous somatic afferents
 projects to midline thalamic nuclei (which are in a circuit with cortical structures)
and the limbic system

5. GLASGOW COMA SCALE
Eye opening Best Motor Response
4 – spontaneous 6 – obeys
3 - to speech 5 - localizes
2 - to pain 4 - withdraws
1 – none 3 – abnormal flexion
Verbal Response 2 – abnormal extension
5 – oriented 1 - none
4 - confused conversation
3 - inappropriate words
2 - incomprehensible sounds
1 - none
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The sum obtained in this scale is used to the assess Coma and Impaired consciousness
Mild is 13 through 15 points Moderate is 9 to 12 points Severe 3 through 8 points
Patients with score less than 8 are in Coma

6. Coma - Aetiology
Metabolic:-
 Ischemic hypoxic
 Hypoglycaemic
 Organ failure
 Electrolyte disturbance
 Toxic
Structural:-
 Supratentorial bilateral
 Unilateral large lesion with transtentorial
herniation
 Infratentorial

7. Supratentorial Lesions
 Epidural or Subdural
Hematoma
 Intraparenchymal
haemorrhage
 Large Ischemic Infarction
 Tumour
 Trauma
 Abscess

8. Supra tentorial mass lesion
differential characteristics
Initiating signs usually of focal cerebral
dysfunction
Signs of dysfunction progress rostral to caudal
Neurologic signs at any given time point to
one anatomic area - diencephalon, midbrain,
brainstem
Motor signs are often asymmetrical

9. Infratentorial Lesions
 Basilar artery thrombosis
 Pontine or Cerebellar
Hematoma
 Ischemic Cerebellar
Infarction
 Tumour
 Abscess

10. Infratentorial Mass Lesions
Differential Characteristics
 History of preceding brainstem dysfunction or sudden onset of
coma
 Localizing brainstem signs precede or accompany onset of
coma and always include oculovestibular abnormality
 Cranial nerve palsies usually present
 “Bizarre” respiratory patterns common, usually present at onset of
coma
Plum and Posner, 1982

11. Why coma management?
 Common medical emergency 3-5%
 Large proportion of comatose patient recover
 Untreated coma may lead to further brain damage

12. Emergency treatment
 Maintain ventilation oxygenation
 Maintain circulation
 Control seizure
 Reduce icp
 Maintain temperature
 Control hypoglycemia

13. Maintain ventilation
 Insert oral airway
 Clean oropharyngeal secretion
 Insert cuffed endotracheal tube if apnea, hypoventilation or liable to
aspirate
 Mechanical ventilation if apnea or raised intracranial pressure

14. Maintain circulation
 If hypotenstion ( <90mmHg systolic)
 Replace fluid:
 Saline if hyperglycemia or suspected stroke, diabetes
 Dextrose saline or isolyte if undiagnosed
 Vasopressor if low systolic pressure inspite of fluid
 Hypertension: Betablocker, Nitroglycerine or Nitropruside

15. Reduce intracranial pressure
 Inj Mannitol 20% 1gm/kg IV fast
 Hyperventilatin to bring pCO2 25-30mmHg

16. Control Seizure
 Inj Lorazepam 4mg or Midazolam 5mg IV slowly
 Inj Diazepam 10-20mg iv slowly
 Inj Phenytoin 15-20mg/Kg 50mg/min IV
 Inj Phenobarb 15-20mg/Kg 50mg/min IV
 Inj Sodium valproate 200-400mg IV

17. Maintain Temperature
 Hperthermia: tapid sponging, paracetamol
 Hypothermia: heating blanket

18. HISTORY
 Inquire about-
i. History of diabetes
ii. Hypertension
iii. Head injury
iv. Convulsions
v. Alcohol or drug use
vi. Circumstances in which patient was found
vii. Medications in hospitalized patient like anesthetics, sedatives,
antiepileptic, opiates, antidepressants, antipsychotics.
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19. GENERAL EXAMINATION
1. SIGNS OF TRAUMA- a) Racoon eyes
b) Battle`s sign
c) CSF rhinorrhea or otorrhea
2. BLOOD PRESSURE- Hypertension suggests-
a) Hypertensive encephalopathy
b) Intracerebral haemorrhage
Hypotension suggests-a) Myocardial infarction
b) Septicemia
c) Addison disease
d) Alcohol or barbiturate intoxication
e) Internal haemorrhage.
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20. 3. PULSE- Bradycardia with periodic breathing and hypertension (CUSHING REFLEX) suggests
raised ICP.
4. TEMPERATURE- Hypothermia suggests-
a) Alcohol or barbiturate intoxication
b) Myxedema
c) Advanced tubercular meningitis
d) Peripheral circulatory failure
Hyperthemia suggests- a) Systemic infection
b) Meningoencephalitis
c) Heat stroke
d) Anticholinergic drugs abuse
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21. 5. SIGNS OF MENINGEAL IRRITATION-
a) Meningitis
b) SAH
6. FUNDUS- a) Raised ICP (Papilledema)
b) SAH ( retinal haemorrhages,disc swelling)
c) Hypertensive encephalopathy
7. SKIN INSPECTION- a) Rash suggests menigococcemia, staphylocoocal
endocarditis, typhus, RMSF
b) Excessive sweating suggest hypoglycemia or shock
c) Diffuse petechiae suggest TTP, DIC, fat embolism
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22. NEUROLOGICAL ASSESMENT
 Observation first without examiner intervention.
 Simply watch posture of limbs and body, position of head and eyes, presence
or absence of spontaneous movements on one side, rate and depth of
respiration.
 Yawning and spontaneous shifting of body position indicates minimal degree
of unresponsiveness.
 Multifocal myoclonus almost always indicate metabolic disorder.
 Assess responsiveness by noting patient`s reaction to calling his name, or to
noxious stimuli such as supraorbital or sternal pressure.
 Glasgow coma scale allows rapid assessment and allows to track neurological
changes over time.
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23. POSTURE IN COMATOSE PATIENT
 Decerebrate rigidity: consists of opisthotonus, clenching of jaws, stiff
extension of limbs with internal rotation of arms & plantar flexion of feet.
 Precise correlation between extensor posturing & level of lesion is rarely
possible because extensor posturing arises in variety of settings: midbrain
compression, cerebellar lesions, metabolic, drug intoxication etc.
 Decorticate rigidity: arms in flexion and adduction and legs extended
signify lesion rostral to midbrain.
 Extensor posture of arms with weak flexor responses of legs is seen with
lesions at level of vestibular nuclei (medulla)
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24. REFLEXES

25. BRAINSTEM REFLEXES
 Pupillary size and reactivity
 Ocular movements
 Corneal responses
 Ocular-vestibular reflexes
 Pattern of breathing
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26.  AS A RULE, WHEN THESE BRAINSTEM ACTIVITIES ARE PRESERVED,
PARTICULARLY THE PUPIL REACTIONS AND EYE MOVEMENTS, COMA MUST BE
ASCRIBED TO BILATERAL HEMISPHERAL DISEASE. THE CONVERSE, HOWEVER,
IS NOT ALWAYS TRUE, AS A MASS IN THE HEMISPHERES MAY BE THE
UNDERLYING CAUSE OF COMA BUT NONETHELESS PRODUCE BRAINSTEM
SIGNS BY INDUCING TRANSTENTORIAL HERNIATION.
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27. PUPILLARY REACTIONS
 Symmetrically reactive round pupils: Exclude midbrain damage.
 Enlarged and unreactive pupil (>5 mm): Intrinsic midbrain lesion (ipsilateral) or
by ipsilateral mass.
 Oval and slightly eccentric pupils: Early midbrain or third nerve compression.
 Bilateral dilated and unreactive pupils: Severe midbrain damage by
transtentorial herniation or anticholinergic drugs toxicity (atropine, TCA).
 Reactive bilaterally small but not pin point (1-2.5 mm): Metabolic
encephalopathies or thalamic haemorrhages.
 Very small but reactive pupil (less than 1 mm) : Opioid or barbtiturate
overdose or bilateral pontine haemorrhage.
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28. EYE MOVEMENTS
 In light coma of metabolic origin, eyes rove conjugately from side to side in
random fashion. These movements disappear as coma deepens.
 Adducted eye at rest: 6th nerve palsy. If it is bilateral it is due to raised ICT.
 Abducted eye at rest: 3rd nerve palsy.
 Downward and inward deviation of eyes: Lesions of thalamus and upper
midbrain.
 Eyes turn toward convulsing side in focal seizures.
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29.  OCULAR BOBBING: Brisk downward and slow upward movements of the
eyes associated with loss of horizontal eye movements is diagnostic of
lesions in midbrain and pons.
 OCULAR DIPPING: Slow downward followed by faster upward movement
in patients with normal horizontal gaze and it indicates diffuse cortical
anoxic damage and drug intoxication.
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30. OCULO-CEPHALIC REFLEX
 Also called Doll`s-eye movement.
 Elicited by briskly turning or tilting the head.
 Response in coma of metabolic origin or that due to bihemispheral structural
lesions consist of conjugate movements of eyes in the opposite direction.
 Positive response indicates-
i. Oculomotor, abducent, midbrain and pons are intact.
ii. There is loss of cortical inhibition on brainstem that normally holds these
movements in check.
Absent reflex indicates damage within brainstem but also can be due to
profound overdose of sedatives or anticonvulsants.
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31. RESPIRATORY PATTERNS
 Slow, shallow, regular breathing: metabolic or drug depression.
 Cheyne-Stokes respiration: Massive supratentorial lesions, B/L
cerebral lesions & mild metabolic disturbance.
 Central neurogenic hyperventilation: Lesions of lower midbrain &
upper pons either primary or secondary to transtentorial herniation.
 Apneustic breathing: Lower pontine lesions.
 Biot`s or ataxic breathing: Lesions of dorsomedial part of medulla.
 Agonal gasps: B/L lower brainstem damage & terminal respiratory
pattern.
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32. PATHOLOGICAL ANATOMY OF COMA
 Only if cerebral lesions are bilateral and extensive, then consciousness will
be impaired.
 Unilateral mass lesions like infarct or hemorrhage if are causing coma, it
means compression of midbrain and subthalamic region of RAS has
occurred.
 Either lateral displacement or herniation of temporal lobe can cause their
compression.
 Even small lesions in upper brainstem and thalamus are sufficient to cause
coma.
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33.  Onset of coma-
i. Sudden onset- vascular origin especially brainstem stoke or SAH.
ii. Rapid progression from hemispheric signs to coma- intracerebral
haemorrhage.
iii. Protracted course- tumor, abscess, chronic SDH.
iv. Coma preceded by confusional or agitated state & without lateralizing signs-
metabolic cause.
v. REMEMBER FRONTAL AND OCCIPITAL HEMORRHAGES ARE LESS LIKELY TO
DISPLACE DEEP STRUCTURES AND TO CAUSE COMA THAN ARE CLOTS OF
EQUIVALENT SIZE IN THE PARIETAL OR TEMPORAL LOBES
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34. LABORATORY STUDIES AND IMAGING
 Complete blood count
 Random blood sugar
 RFT, LFT
 Serum electrolytes
 Urine examination for specific gravity, glucose, acetone & protein content.
 ABG analysis
 Chest X-Ray
 ECG
 CT or MRI Scan
 Lumbar Puncture
 EEG
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35. TAKE HOME MESSAGE
 Remember clinical analysis of comatose patient is urgency.
 Evaluate for airway, breathing & circulation.
 History & systematic general and neurological assessment will help a lot.
 Presence or absence of brainstem reflexes helps to localize the lesion.
 Evaluate for imminent herniation.
 Implement rapid & systematic investigation and take prompt therapeutic
action.
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36. THANKS
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