1) Stupor and coma are states of decreased or absent responsiveness that require evaluation to identify potentially reversible causes and provide emergency treatment. 2) The initial approach involves stabilizing vital functions, treating potentially reversible causes, obtaining history, and performing a full neurological examination. 3) Emergency treatment may include supplemental oxygen, IV thiamine, glucose, and antibiotics depending on suspected causes identified from history and examination.

1. Approach to
stupor and coma
-Dr. Sachin Adukia

2. Definitions
 Stupor
 state of baseline unresponsiveness that requires repeated application of
vigorous stimuli to achieve arousal.
 Coma
 State of complete unresponsiveness to arousal, in which the patient lies
with the eyes closed.

4. Approach principle
 all alterations in arousal constitute acute, life-threatening emergencies until
 vital functions such as BP and oxygenation stabilized,
 potentially reversible causes of coma treated,
 underlying cause understood
 Emergency therapeutic measures, history and exmaination proceed in parallel
 More than half of all cases of coma are due to diffuse and metabolic brain
dysfunction.

7. Emergency Therapy
 quick initial assessment to ensure comatose patient is medically and neurologically stable
 empirical use of supplemental oxygen,
 IV thiamine (at least 100 mg),
 IV 50% dextrose in water (25 g) after a baseline serum glucose
 Use of IV glucose anoxic brain damage is controversial.
 Extra glucose may augment local lactic acid production by anaerobic glycolysis and
may worsen ischemic or anoxic damage.
 empirical glucose is still recommended for two reasons :
 the frequent occurrence of alterations in arousal due to hypoglycemia and the relatively
good prognosis for coma due to hypoglycemia when it is treated expeditiously;
 potentially permanent consequences if it is not treated.
 By comparison, the prognosis for anoxic or ischemic coma
 generally is poor and probably will remain poor regardless of
 glucose supplementation.
 Thiamine to prevent precipitation of Wernicke encephalopathy.

8. Coma usually manifests in one of three ways.
 Most commonly, as an expected or predictable progression of an
underlying illness.
 focal brainstem infarction with extension
 barbiturate overdose when the ingested drug cannot be fully
removed and begins to cause unresponsiveness
 Second, as an unpredictable event in whose prior conditions are known
to the physician.
 Arrhythmia who suffers anoxia after a cardiac arrest.
 sepsis from IV line in a cardiac patient
 or stroke in hypothyroid patient
 patient whose medical history is totally unknown to the physician.eg
RTA wuth head trauma

9. History
 interviewing relatives, friends, bystanders, or present medical personnel
 Telephone calls to family members may be helpful.
 Wallet be checked
 the circumstances in which the patient was found.
 drug paraphernalia or empty medicine bottles  drug overdose.
 OHA or insulin in the medicine cabinet or refrigerator  hypoglycemia.
 Antiarrhythmic agents procainamide or quinidine 
 existing CAD with ? MI
 or unwitnessed arrhythmia may have caused cerebral hypoperfusion,
 Warfarin, (DVT / PTE)  massive ICH
 Post operative setting
 - fat embolism, Addisonian crisis, and hypothyroid coma Wernicke
encephalopathy, iatrogenic overdose of a narcotic analgesic

10. Symptoms before onset of coma
 headache preceding SAH,
 chest pain with aortic dissection or AMI
 shortness of breath from hypoxia,
 stiff neck in meningoencephalitis,
 vertigo in brainstem stroke.
 Nausea and vomiting are common in poisonings, increased ICP.
 h/o head trauma, drug abuse, seizures, or hemiparesis.
 ataxia, dysarthria or aphasia, ptosis, pupillary dilatation, or disconjugate gaze may
help localize structural lesions

11. Examination,
decision on emergency Ix and Rx
 General appearance, T P R BP, breath sounds,
 best response to stimulation,
 Pupil size and responsiveness,
 Posturing or adventitious movements.
 neck stabilized in all instances of trauma until Cx spine fracture is ruled out
 Airway
 immediate therapeutic intervention.
 Hypotension, marked hypertension,
 bradycardia, arrhythmias causing fall in BP,
 Marked hyperthermia, signs of cerebral herniation

12.  Hyperthermia or meningismus- LP
 CSF pressure > 500, some recommend leaving the needle in
place to monitor pressure and give IV mannitol
 Can give IV antibiotics and IV steroids pending LP in strong
suspicion of meningitis
 Fundoscopy, CBC, INR, Local c/i- always before LP in
coma
 Blood cultures and throat swabs prior to antibiotic

13.  Hypotension. MAP < 60
 hypovolemia, massive external or internal hemorrhage, myocardial infarction, cardiac
tamponade, dissecting aortic aneurysm,
 intoxication with alcohol or other drugs (especially barbiturates), toxins,
 Wernicke encephalopathy,
 Addison disease, and sepsis may have warm extremities
 Hypertension
 cerebral infarction, in SAH, certain brainstem infarctions, ICP raised.
 Cushing’s reflex- ischemia of the pressor area lying beneath the floor of the fourth
ventricle.
 Heart Rate
 Bradycardia:
 conduction blocks , certain poisionings, Beta blockers
 Tachycardia
 hypovolemia, hyperthyroidism, fever, anemia,
 toxins and drugs, including cocaine, atropine,

14. Temperature in comatose
 Pure neurogenic hyperthermia is rare, is d/t
 SAH or hypothalamus lesions.
 brainstem origin= shivering without sweating.
 particularly when unilateral, may be s/i deep ICH
 heatstroke, thyrotoxic crisis, and drug toxicity
 Hypothermia – reduced cerebral metabolism, EEG silence
 Sepsis, hypothyroid coma, hypopituitarism, Wernicke encephalopathy,
 cold exposure, drugs (barbiturates),
 Central lesions - posterior hypothalamus

15. Others
 Torn clothing
 Cachexia
 ALD
 Fracture skull racoon eyes in ant. Skull #
 Meningismus – infectious or carcinomatous meningitis, SAH, central or tonsillar
herniation
 Funduscopic examination
 Grayish deposits around optic disc in lead poisoning.
 congested and edematous retina in methyl alcohol poisoning, and the disc margin may
be blurred.
 Subhyaloid hemorrhage –consequence of rapid increase in ICP due to subarachnoid
hemorrhage (Terson’s syndrome).
 Papilledema: ICP or hypertensive encephalopathy
 Otoscopic exam-
 hemotympanum or CSF otorrhea from a basilar skull #
 Infections of the middle ear, mastoid, and paranasal sinuses

16. Neurological Examination
 State of Consciousness-
 auditory, visual, noxious stimuli
 Supraorbital pressure evokes a response even if afferent pain pathways lost d/t
spinal cord lesion or periph. neuropathy
 blink response to visual threat need not indicate consciousness.
 apparent coma – ask open or close eyes, look up & down
 To r/o locked-in state
 Purposeful movements indicate a milder alteration
 Vocalization to pain in the early hours of a coma, even if only a grunt light
alteration
 Later, primitive vocalization may be a feature of vegetative state.
 GCS
 FOUR score
 eye response, motor response, brainstem reflexes, respirations

18. Pupil Size and Reactivity
 diencephalic pupils cause small, reactive pupils,
 Thalamic lesions
 toxic-metabolic conditions resulting in coma
 Midbrain lesions produce three types of pupillary abnormality
 midposition pupils, - fixed to light but react to near vision
 Dorsal tectal lesions interrupt the pupillary light reflex,
 fixed, irregular midposition pupils, which may be unequal
 Nuclear midbrain lesions usually affect both sympathetic and
parasympathetic pathways,
 Wide pupillary dilation, unresponsive to light.
 Lesions of 3rd nerve fascicle in brainstem, or after brainstem
 pinpoint pupils- Pontine lesions interrupt sympathetic pathways

19. Asymmetry of pupil size
 may be due to mydriasis of one, such as with 3rd Nr palsy
 Or miosis of the other, as in Horner syndrome.
 differentiated by the pupillary reactivity to light and associated neurological
signs.
 A dilated pupil due to a partial third nerve palsy is less reactive
 a/w extraocular muscle involvement.
 The pupil in Horner syndrome is reactive
 sluggishly reactive pupil  early s/o uncal herniation, f/b dilation of that pupil
and, later, complete 3rd Nr paralysis.
 common misleading c/o unilateral dilated pupil:
 mydriatic administration,
 old ocular trauma or ophthalmic surgery,
 Carotid artery insufficiency.

20. Ocular movement examination
 Unilateral 3rd Nr palsy - downward and laterally
 6th Nr palsy  inward deviation- but Poor localisation
 fourth nerve palsy- subtle deficit, difficult to detect in coma
 Extraocular nerve palsies often become more apparent with the “doll’s eye maneuver” or
cold caloric testing
 Conjugate lateral eye deviation – d/t ipsilateral lesion in the frontal eye fields
 Dysconjugate lateral eye movement may result from a sixth nerve palsy in the abducting
eye, a third nerve palsy in the adducting eye, or INO
 Downward deviation- Brainstem lesions- MC is tetctal compression
 Thalamic and subthalamic lesions produce downward and inward deviation of the eyes-
looking at the tip of the nose
 upward eye deviation-
 Sleep, seizure, syncope, apnea of Cheyne–Stokes respiration,
 hemorrhage into the vermis, and brainstem ischemia
 encephalitis
 Skew deviation: posterior fossa lesion (brainstem or cerebellar)

21. Spontaneous Eye Movements
 Roving eye movements- Brainstem intact
 Nystagmus in comatose  irritative or epileptogenic supratentorial focus
 ocular bobbing- classical not pathognomic of pontine lesions
 Monocular or paretic bobbing – coexisting ocular motor palsy
 Ocular dipping, also known as inverse ocular bobbing- diffuse cerebral damage
 Reflex eye movements
 oculocephalic reflex (doll’s eye phenomenon)
 caloric (thermal) testing.

22. Motor examination in coma
 Head and eye deviation to one side, with contralateral hemiparesis, suggests a
supratentorial lesion,
 Ipsilateral paralysis - probable brainstem lesion.
 Decerebrate posturing-
 Bilateral midbrain or pontine lesions
 Less commonly, deep metabolic encephalopathies or bilateral supratentorial lesions
involving the motor pathways
 Decorticate posturing
 occurs with relatively reversible lesions.
 Unilateral decerebrate or decorticate postures
 Anywhere in the motor system from cortex to brainstem

23. Adventitious movements in the comatose
 Tonic clonic or other stereotyped movements seizure may be cause of decreased
alertness.
 Myoclonic jerking, - anoxic encephalopathy or metabolic comas, such as hepatic
encephalopathy.
 Rhythmic myoclonus- brainstem injury.
 Tetany occurs with hypocalcemia.
 Cerebellar fits of Hughlings Jackson”
 result from intermittent tonsillar herniation
 characterized by deterioration of level of arousal, opisthotonos, respiratory rate
slowing and irregularity, and pupillary dilatation.

24. Toxic- Metabolic Structural
•Milder alterations in arousal
•waxing and waning of the behavioral state
Same level of arousal or progressively
deteriorate
•Deep, frequent respiration - metabolic
abnormalities
•Papilledema may occur in metabolic:
hypoparathyroidism, lead intoxication,
malignant Hypertension
Subhyaloid hemorrhage or papilledema are
almost pathognomonic
•Symmetrical, small, reactive pupils
•Except methyl alcohol poisoning,
- dilated and unreactive pupils
- and hyothermia- fixed pupils
Asymmetry in oculomotor function
•Roving eye movements with full excursion
•Reflex eye movements normally are intact in
toxic-metabolic coma, except rarely in
phenobarbital or phenytoin intoxication
•Myoclonic jerking
•Muscle tone symmetrical and normal or
decreased
asymmetrical muscle tone. Tone - increased,
normal or decreased

26. Other investigatons
 ECG
 EEG- esp in metaolic encephalopahties
 Also to confirm catatonia, pseudocoma, the locked-in syndrome, PVS, brain
death
 CT or if feasible MRI
 Evoked potentials
 Absence of evoked potentials in response to somatosensory stimuli also is
highly predictive ofbnonawakening from coma.
 Intracranial Pressure Monitoring
 use in treating intracranial HTN following TBI significantly lowers mortality

29. Thank You