4. Coma is always a symptomatic expression of an
underlying disease
A methodical approach that leaves none of the
common and treatable causes of coma unexplored
History taking , examination , and management go hand
in hand….
Best thing is one person should take history and other
person examine simultaneously along with taking care
of immediate management
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5. When a comatose patient is 1st seen….
ABC
Maintain airway….oropharyngeal… endotracheal….
Breathing… shallow….?........ Aspiration…?
If trauma… check for bleeding
If hypotension… iv fluids, pressors, volume expanders or
blood preferably monitoring central venous pressure
O2 inhalation
Cervical Fracture …?
Injection Thiamine followed by glucose
(After taking blood for basic investigations)
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11. Large blisters
Ifthe patient has been motionless for a time
Acute barbiturate, alcohol, or opiate intoxication
Facial puffiness
CKD
Myxedema, Hypopituitarism
Central obesity, striae
Nail
Splinterhemorrhage
White nail
Half and half nail
Clubbing
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12. Jaundice
Features of chronic liver disease
Fever
Pneumonia, sepsis, meningitis, sepsis
Hyperthermia
Drugs with anticholinergic activity
Heat stroke
Hypothermia
Alcoholic or barbiturate intoxication
Drowning
Exposure to cold
Peripheral circulatory failure
Myxedema
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16. Most important even though limitted
Simple observing of the patient may give valuable
clues
Abnormal posturing of body
Abnormal movement of one side
The state of responsiveness
Vocalization
Grimacing and deft avoidance movements of the
stimulated parts are preserved in light coma
The Glasgow Coma Scale
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17. The Glasgow Coma Scale
Motor Response
6 - Obeys commands fully
Total – 15
5 - Localizes to noxious stimuli
Poor - 3 or 4
4 - Withdraws from noxious stimuli
3 - Abnormal flexion, i.e. decorticate posturing
2 - Extensor response, i.e. decerebrate posturing
1 - No response
Verbal Response
5 - Alert and Oriented
4 - Confused, yet coherent, speech
3 - Inappropriate words, and jarbled phrases consisting of words
2 - Incomprehensible sounds
1 - No sounds
Eye Opening
4 - Spontaneous eye opening
3 - Eyes open to speech
2 - Eyes open to pain
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1 - No eye opening
18. Signs of meningeal irritation
Meningitis
Subarachnoid hemorrhage (after 12-24 hrs in some)
In the infant, bulging of the anterior fontanel better sign
Confused with meningeal irritation
Phenothiazinepoisoning
Temporal lobe or cerebellar herniation
Decerebrate rigidity
Cervical spondylosis
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19. Hemiplegia
Lack of movement on noxious stimuli
Hemiplegic leg lies in a position of external rotation
( // fracture femur)
Thigh
may appear wider and flatter than the
nonhemiplegic one
Inexpiration, the cheek and lips puff out on the
paralyzed side
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21. Eyes are often turned away from the paralyzed side
Opposite may occur with brainstem lesions
Hemiplegia and an accompanying Babinski sign are
indicative of a contralateral hemispheral lesion
( beware of Kernohan-Woltman sign )
A moan or grimace may be provoked by painful stimuli
on one side but not on the other, reflecting the
presence of a hemianesthesia
During grimacing, facial weakness may be noted
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23. Of the various indicators of brainstem function,
the most useful are pupillary size and reactivity,
ocular movements, oculovestibular reflexes, and,
to a lesser extent, the pattern of breathing.
These functions, like consciousness itself, are to
a large extent dependent on the integrity of
structures in the midbrain and rostral pons
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25. Unilaterally enlarged pupil (>5.5 mm diameter) ipsilateral
3rd nerve compression
With continued compressioncorectopia (oval or pear )
The light-unreactive pupil continues to enlarge to a size of 6
to 9 mm diameter, associated with slight outward deviation
of the globe
In unusual instances, the pupil contralateral to the mass may
enlarge first
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26. As midbrain displacement continues, both pupils dilate
and become unreactive to light
The last step in the evolution of brainstem compression
tends to be a slight reduction in pupillary size, to 5 to 7
mm
Normal pupillary size, shape, and light reflexes indicate
integrity of midbrain structures and a cause of coma
other than a mass lesion
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27. Pontine tegmental lesions cause extremely miotic pupils
(<1 mm in diameter) with only a slight reaction to
strong light
Ciliospinal reflex lost
A Horner syndrome homolateral to a lesion of the
brainstem or hypothalamus or as a sign of dissection of
the internal carotid artery
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28. Pupil is spared in metaboic conditions and intoxications
Exceptions
Morphine extremely pin point
Barbiturate pin point 1cm or more
Atropine
Dilated, non reacting even to physostigmine
Tricyclics
Hippus metabolic encephalopathy
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31. Movements of Eyes and Eyelids and
Corneal Responses
In light coma of metabolic origin, the eyes rove
conjugately from side to side in random fashion,
sometimes resting briefly in an eccentric position
These movements disappear as coma deepens and the
eyes then remain motionless in slightly exotropic
positions
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32. A lateral and slight downward deviation of one eye
suggests the presence of a third nerve palsy
Medial deviation sixth nerve palsy
Away from the side of the paralysis large cerebral
lesion
Toward the side of the paralysis with a unilateral
pontine lesion
“Wrong-way” conjugate deviation thalamic and
upper brainstem lesions
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33. During a one-sided seizure, the eyes turn or jerk toward
the convulsing side
The eyes may be turned down and inward (looking at
the nose) with hematomas or ischemic lesions of the
thalamus and upper midbrain
Retraction and convergence nystagmus lesions in the
tegmentum of the midbrain
Ocular bobbing Pons
Ocular dipping Anoxia and Drug intoxications
(horizontal eye movements are preserved )
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34. The coma-producing structural lesions of the
brainstem abolish most conjugate ocular movements,
whereas metabolic disorders generally do not.
(except for rare instances of hepatic coma and
anticonvulsant drug overdose)
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36. Elicitation of these reflexes in a comatose
patient provides two pieces of information
Evidence of unimpeded function of the
oculomotor nerves and of the midbrain and
pontine tegmental structures that integrate
ocular movements
Loss of the cortical inhibition that normally
holds these movements in check
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37. Sedative or anticonvulsant intoxication serious enough
to cause coma may obliterate the brainstem
mechanisms for oculocephalic reactions
Asymmetry in elicited eye movements remains a
dependable sign of focal brainstem disease
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39. 10 mL of cold water
In comatose patients, the fast “corrective” phase of
nystagmus is lost and the eyes are tonically deflected to
the side irrigated with cold water or away from the side
irrigated with warm water; this position may be held for
2 to 3 min
With brainstem lesions, these vestibulo-ocular reflexes
are lost or disrupted
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40. Corneal reflex
Progressive deterioration in response to corneal touch
are among the most dependable signs of deepening
coma.
A marked asymmetry in corneal responses indicates
either an acute lesion of the opposite hemisphere or,
less often, an ipsilateral lesion in the brainstem.
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41. Restless movements of both arms and both legs and
grasping and picking movements intact corticospinal
tracts
The occurrence of focal motor epilepsy usually indicates
that the corresponding corticospinal pathway is intact
Massive destruction of a cerebral hemisphere focal
seizures are seldom seen on the paralyzed side
Definite choreic, athetotic, or hemiballistic movements
indicate a disorder of the basal ganglionic and subthalamic
structures, just as they do in the alert patient
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43. The decerebrate ‘State’
Brainstem at the intercollicular level
In a variety of conditions
Midbrain compression due to a hemispheral mass
with cerebellar or other posterior fossa lesions
Anoxia and hypoglycemia;
Rarely with hepatic coma and profound intoxication
Ipsilateral
to a one-sided lesion, hence not due
to involvement of the corticospinal tracts
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44. Decorticate rigidity
Lesions at a higher level—in the cerebral white matter
or internal capsule and thalamus
Bilateral decorticate rigidity is essentially a bilateral
spastic hemiplegia
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45. Diagonal postures, e.g., flexion of one arm and
extension of the opposite arm and leg, usually indicate a
supratentorial lesion
Forceful extensor postures of the arms and weak flexor
responses of the legs are probably due to lesions at
about the level of the vestibular nuclei
Lesions below this level lead to flaccidity and abolition
of all postures and movements. The coma is then
usually profound and often progresses to brain death
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46. Only in the most advanced forms of intoxication and
metabolic coma, as might occur with anoxic necrosis of
neurons throughout the entire brain, are coughing,
swallowing, hiccoughing, and spontaneous respiration
all abolished
Tendon reflexes are usually preserved until the late
stages of coma due to metabolic disturbances and
intoxications
Plantar flexor responses, succeeding extensor
responses, signify ether a return to normalcy or, in the
context of deepening coma, a transition to brain death
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49. Breathing patterns
Cheyne-Stokes
Massive supratentorial lesion
Bilateral deep-seated cerebral lesions
Metabolic disturbances
Presence of CSR signifies bilateral dysfunction of cerebral
structures, usually those deep in the hemispheres or diencephalon,
and is seen with states of drowsiness or stupor
Coma with CSR is usually due to intoxication or a severe metabolic
derangement and occasionally to bilateral lesions, such as subdural
hematomas
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50. Central neurogenic hyperventilation
Lesions of the lower midbrain–upper pontine
tegmentum, either primary or secondary to a
tentorial herniation
Tumors of the medulla, lower pons, and midbrain
Primarybrain lymphoma without brainstem
involvement
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51. Apneustic breathing Low pontine lesions, usually
due to basilar artery occlusion
Biot breathing (chaotic) lesions of the dorsomedial
part of the medulla
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52. Signs of Increased Intracranial Pressure
Headache before the onset of coma
Recurrent vomiting
Severe hypertension beyond the patient's static level
Subhyaloid retinal hemorrhages
Papilledema develops within 12 to 24 h in cases of
brain trauma and hemorrhage, but if it is pronounced, it
usually signifies brain tumor or abscess—i.e., a lesion of
longer duration
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54. Case 1
15 yr old girl, recent weight loss and polydipsia
presenting with a comatose state. She is dehydrated and
in shock. Examination showed tachypnea and sweet
odour
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55. Case 2
A middle aged man brought in a comatose state by
some passengers who got him from the pavement.
There was smell of alcohol in his breath, and had
dilated right pupil and left extensor plantar.
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56. Case 3
A 10 yr old boy with h/o Fallot’s tetrology was brought
by his parents with h/o headache and fever for 2
weeks, severe vomiting and progression into coma. He
had left hemiplegia and lateral rectus palsy and b/l
papilledema
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57. Case 4
35 yr old lady who was on insulin for diabetic ketotic
coma. Her sugar values and blood acetone improved,
but she persisted in the comatose state. She had 3
episodes of GTCS. On examination she had b/l
extensor plantar response and b/l papilledema.
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58. Case 5
60 yr old lady presented with comatose state to the
casualty. She had developed sudden onset of left sided
weakness along with headache and vomiting. She had
left hemiplegia, and bilateral papilledema. Her BP was
normal. She had mild numbness in the left upper and
lower limbs for last 1 month.
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59. Case 6
21 yr old primi in 9th month of gestation presented with
severe vomiting, headache and GTCS. She had mild
fever also.She didn’t have any hypertension or edema
during pregnancy. Examination showed normal BP and
bilteral papilledema. There was no meningeal signs.
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60. Case 7
56 yr old chronic alcoholic presented in comatose state
to the gastroenterology department. He had mild
abdominal pain for last 5 days. Examination showed b/
l extensor plantar response.
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61. Case 8
65 yr old lady was admitted in a comatose state. She
had received an injection for chest pain from a local
hospital. Her skin was dry, she had low temperature.
She had excessive day time somnolence for last 1
month
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