2. • A 5 year old child was brought with history of
fever, progressive lethargy and posturing for 3
days . He had been vomiting several times
since morning. His temperature was 40
degree celsius.
• how will you manage this patient?
5. Impairment of consciousness
states
• Impairment of consciousness with activated
mental state
• Impairment of consciousness with reduced
mental state
• Impairment of consciousness along the
continuum of coma–vegetative state–
minimally conscious state.
6. Impairment of consciousness with
activated mental state
• Confusion: state of impaired ability to think
and reason clearly, resulting in difficulty with
orientation, simple cognitive processing, and
acquisition of new memory.
• Delirium is an activated mental state that may
include disorientation, irritability, fearful-
responses, and sensory misperception.
Patients may be hyperactive and have signs of
increased sympathetic tone.
7. Impairment of consciousness with
reduced mental state
• Drowsiness
• Obtundation arousal is present to stimuli
• Stupor
State Stimulus needed for arousal
Drowsiness Verbal and light touch
Obtundation Deep touch
Stupor Vigorous, painful, or noxious
stimulation
8. • Coma is a “state of deep, unarousable,
sustained pathologic unconsciousness with
the eyes closed that results from dysfunction
of the ascending reticular-activating system in
the brainstem or in both cerebral
hemispheres”
• Patients in coma lack both wakefulness and
awareness.
13. Etiology -cont
C. Nutritional
Thiamine deficiency
Niacin or nicotinic acid
deficiency
Pyridoxine dependency
Folate and B12 deficiency
D. Exogenous Toxins and
Poisons
Alcohol intoxication
Over-the-counter
medications
Prescription medications
(oral and ophthalmic)
Herbal treatments
Heavy-metal poisoning
Mushroom and plant
intoxication
Illegal drugs
Industrial agents
E. Hypertensive
Encephalopathy
F. Burn Encephalopathy
14. PATHOPHYSIOLOGY OF COMA
• Consciousness has two dimensions –
wakefulness and awareness.
• Integral Consciousness requires an intact -
1) RAS
2) Cerebral hemispheres,
3) Healthy projections between the two
systems.
15. ANATOMY AND PHYSIOLOGY - CONSCIOUSNESS
Function Site
Awake – RAS
(Reticular Activating
System)
•Rostral brainstem (midbrain
and upper pontine tegmentum)
to the lower thalamus .
•The hypothalamus.
Awareness
(a higher cognitive
function) =
cognition + affect
Cerebral
hemispheres.
17. • Coma with focal signs
Intracranial hemorrhage
Stroke: arterial ischemic or sinovenous thrombosis
Tumors
Focal infections: brain abscess
Post seizure state: Todd’ paralysis
Acute disseminated encephalomylelitis
18. • Coma without focal signs and with meningeal
irritation:
Meningitis
Encephalitis
Subarachnoid hemorrhage
• Coma without focal signs and without
meningial irritation:
Hypoxic-ischemia: cardiac or pulmonary failure,
shock, near drowning.
20. • Post infectious disorders:
ADEM
Hemorrhagic shock and encephalopathy syndrome
• Post immunisation encephalopathy
Whole cell pertusis vaccine
• Drugs and toxins
• Cerebral malaria
• Rickettsial : lyme disease, rocky mountain spotted
fever
• Hypertensive encephalopathy
• Post seizure states
• Non-convulsive status epilepticus
21. The goals of coma therapy
(a) Adhere to the principles of neuroresuscitation, the A,
B, and Cs
(b) Immediately identify signs of intracranial pathology:
herniation, increased intracranial pressure (ICP), or a
focal neurologic signs, head trauma.
(c) Identify and specifically treat the underlying cause.
(d) Determine prognosis.
(e) Plan appropriate long-term therapy.
22.
23. Rapid assessment and stabilization
• Establish and maintain airway: intubate if
GCS<= 8 ,impaired airway reflexes, abnormal
breathing pattern, signs of raised ICT, oxygen
saturation<92% despite high flow oxygen,
fluid refractory shock.
• Circulation: establish IV access, take samples
(serum electrolytes), fluid bolus if in
circulatory failure (20ml/kg NS), inotropes if
required
• Blood glucose : regent strip testing , if
<50mg/dl give 10% D 2ml/kg.
24. • Identify signs of cerebral herniation or raised
ICT: ( if GCS<8,abnormal pupil size and
reaction, absent dolls eye
movements,abnormal tone or posturing,
hypertension with brdycardia, abnormal
respiratory pattern) Must act immediately
(Elevate the Head end of bed 30 degrees,
short term Hyperventilation, 20% Mannitol
(0.5-1g/kg) or 3% NaCl(if in shock).
25. • If there are seizures: give IV lorazepam
0.1-0.2mg/kg , then phenytoin 20mg/kg
loading.
• Immobilisation of cervical spine in suspected
cases of traumatic coma.
• Manage hypo/hyperthermia accordingly.
26. History ,physical examination and
neurological assesment
• History: age
Infant Child Adolescent
CNS infection
(meningitis,encephalitis)
Ingestion Drug/Alcohol overdose
Systemic infection with shock CNS infection Intentional poisoning
Metabolic disorders Seizure Trauma, seizures
Abuse / Trauma, Abuse / Trauma CNS infection,
Inborn errors of
metabolism,seizures
DKA, Rey’s
syndrome
DKA, , Rey’s syndrome
Post immunisation
encephalopathy, hemorrhagic
shock and encephalopathy
syndrome ,
27. Approach: History
• Onset :
– Sudden onset: vascular catastrophy or a
convulsion
– Acute onset in normal child: ingestion of drug,
toxin, poison.
– Gradual onset : infectious process, metabolic
derangement.
35. Clues to etiology of coma in general examination
Look for if present ,think of
Pallor Cerebral malaria, intracranial bleed, hemolytic uremic
syndrome
Icterus Hepatic encephalopathy, leptospirosis, complicated malaria
Rashes Meningococcemia, dengue , measles, rickettsial diseases,
arboviral diseases
Petechiae Dengue, meningococcemia , hemorrhagic fevers
Head and scalp
hematomas
Traumatic/ non accidental injury
Dysmorphism,
neurocutaneusmarkers
Possibility of seizures
Abnormal odour DKA, hepatic coma
36. Rapid neurogical assesment
• The goal of neurologic examination are:
To determine depth of coma.
To localise the process leading to coma.
• Includes
Level of consciousness
Pupillary responses
Eye movements(spontaneous or induced)
Motor response
Respiratory pattern
37. A.Level of conciousness
• The level of conciousness must be recorded
in the form of an objective scale.
• The Glasgow coma scale is a useful tool for the
grading of the degree of altered consciousness
and the severity of CNS insult.
• Glasgow coma scale is used for adults and
older children and its modification is used in
infants and young children.
38. Glasgow coma scale
ACTIVITY
BEST RESPONSE
Adults/Older Children Infants ( modified GCS ) Score
Eye Opening
( E )
1. Spontaneous
2. To speech
3. To pain
4. None
1. Spontaneous
2. To speech
3. To pain
4. None
4
3
2
1
Verbal
( V )
1. Appropriate speech
2. Confused speech
3. Inappropriate words
4. Incomprehensible or
none specific sounds
5. None
1. Coos, babbles
2. Irritable, cries but
consolable
3. Cries, inconsolable
4. Moans to pain
5. None
5
4
3
2
1
Motor
( M )
1.Obeys commands
2.Localizes pain
3.Withdraws to pain
4.Decorticate to pain
5.Decerebrate to pain
1. Normal spontaneous
movement
2. Withdraws to touch
3. Withdraws to pain
4. Decorticate to pain
5. Decerebrate to pain
6
5
4
3
2
39. Significance of Glasgow coma scores:
• Diagnosis of different grades of altered
consciousness.
• Coma is defined as: No eye opening (1), No
recognizable words uttered (2 ), Not obeying
commands (5), ie, score = 8 or less.
• Fall of GCS of 2 or more – Indicates deterioration and
need of active intervention
• Prediction of prognosis of comatose child:
– GCS >8: Good chances of recovery
– GCS 3-5: Fatal brain damage
40. B. Size and reactivity of pupils
Pupils Lesion/Dysfunction
Pinpoint Pons, opiates, cholinergic intoxication
Mid position –
fixed or irregular
Midbrain lesion
Unilateral , dilated
and fixed
Uncal herniation
Bilateral , dilated
and fixed
Diffuse damage, central herniation, global
hypoxia ischemia, barbiturates, atropine
41.
42. C. Eye movements
• Oculocephalic or Doll’s eye response: Shows Intact
Brainstem.
• Oculovestibular response: Lost in pontine lesions,
labyrinthitis, Sedatives, Phenytoin induced coma
• Both lost but intact pupillary reflexes present in
metabolic encephalopathy
• Stimulation of cortical centre for gaze e.g. seizure focus
→ conjugate deviation of eye to contralateral side
• Destructive lesion at gaze centre → conjugate deviation
of eye to same side .
• Neuropthalmolgic examination is incomplete without
fundus examination.
43. D. Motor response
• Single best indicator of the depth and severity
of coma
1. Spontaneous movements.
2. Tone and reflexes
3. Induced movements.
44. Motor responses to noxious stimuli. A, Localization of pain
as patient attempts to remove stimulus. B, Decorticate posturing. C,
Decerebrate posturing. D, Flaccid patient with no response.
45. • Decorticate posturing with flexion of the
upper extremities and extension of the lower
extremities suggests involvement of the
cerebral cortex and preservation of brainstem
function.
• Decerebrate posturing with rigid extension of
the arms and legs is indicative of cortical and
brainstem damage.
• The flaccid patient with no response to
painful stimuli has the gravest prognosis with
injury sustained to deep brainstem lesions.
46. E. Respiratory pattern
• Patient breathing pattern is also helpful in
localising area of CNS dysfunction. They are :
• Cheyne-Stokes respiration.
• Central neurogenic hyperventilation.
• Apneustic breathing.
• Cluster breathing.
• Ataxic breathing.
48. Herniation syndromes
• Brain tissue deforms intracranially and moves from
higher to low pressure when there is asymmetric,
unilateral or generalised increase in intracranial
pressure.
• Signs of cerebral herniation
1. Glasgow coma score <8
2. Abnormal pupil size and reaction (unilateral or bilateral)
3. Absent doll’s eye movements
4. Abnormal tone (decerebrate/decorticate posturing,
flaccidity)
5. Hypertension with bradycardia
6. Respiratory abnormalities (hyperventilation, Cheyne-
Stokes breathing, apnea, respiratory arrest)
7. Papilledema
49.
50. • In transtentorial or central herniation, the
diencephalon is displaced through the notch
of the tentorium cerebelli into the posterior
fossa, with progressive rostral - caudal
compression and ischemia of the brainstem.
• In Uncal herniation, medial displacement of
the uncus compresses upon the oculomotor
nerve leading to unilateral dilated fixed pupil
with ptosis.
51. Central vs uncal herniation
Central uncal
•Arousal
•Breathing
•Pupils
•Oculocephalic
responses
•Motor signs
•Impaired early, before other signs
•Sighs , yawns, sometimes
Cheyne-Stokes respirations
•First , small reactive (hypothalamus),
then one or both approach midposition
•Initially sluggish, later tonic conjugate
Early hemiparesis opposite to hemispheric
lesion followed late by ipsilateral motor
paresis and extensor plantar response
•Impaired late, usually with
other signs
•No early change
•Ipsilateral pupil dilates,
followed by somatic third
nerve paralysis
•Unilateral third nerve
paralysis
•Motor signs late, sometimes
ipsilateral to lesion
52. Metabolic vs structural coma
METABOLIC, TOXIC,
INFECTIOUS CAUSES
• Confusion or stupor
precede motor signs
• Pupillary reactions
preserved
• Symmetrical motor
responses
• Asterixis, myoclonus
• Hyper or hypoventilation
STRUCTURAL
• Supratentorial destructive
or mass lesions:
Initial focal signs
Rostral to caudal progression
• Infratentorial destructive or
mass lesions:
Preceding brainstem dysfunction
Sudden onset of coma
Cranial nerve palsies
Early respiratory disturbances
53. Investigations
1. neuroimaging:
• CT scan:Any comatose child or infant in whom
the neurological findings suggest a structural
lesion or in whom the clinical diagnosis is evasive,
done after stabilistion of a patient.
• Magnetic Resonance Imaging (MRI) of brain is
valuable in identifying evidence of herpes simplex
encephalitis or an acute demyelinating process,
such as acute disseminated encephalomyelitis.
62. SPECIFIC THERAPY
• Acute febrile encephalopathy:
In sick children with Acute febrile
encephalopathy, empirical therapy with
antibiotics, acyclovir, antimalarials should be
considered while awaiting for reports.
63. Specific therapy-Acute febrile encephalopathy:
• Empiric antibiotic therapy: IV ceftriaxone+
amikacin
• Acyclovir - in sporadic meningo-encephalitis
with or without: focal neurological
findings,behaviour changes, aphasia, suggestive
CT(frontotemporal changes), hemorrhagic CSF.
• Antimalarials: (quinine/artesunate)- smear
positive, rapid tests positive , empiric treatment if
short history(<48 hours),P.falciparum endemic
area, absent meningial signs,anemia,
hypoglycemia,retinal hemorrhages.
64. Specific therapy
• Treat dyselectrolytemia and acid-base imbalance
• Space occupying lesions require prompt
neurosurgical management.
• Antihypertensives for hypertensive
encephalopathy.
• Hepatic encephalopathy – Lactulose, systemic
antibiotics, vitamins, protein restriction
• Medical management and Dialysis for ARF, CRF
• Poisoning – Gastric lavage, Antidotes
65. prognosis
• The prognosis for recovery from coma depends
primarily on the cause, rather than on the depth
of coma.
• Coma from drug intoxication and metabolic
causes carry the best prognosis.
• Prolonged coma after a global hypoxic ischemic
insult carries a poor prognosis.
• Infectious encephalopathies have a good
outcome with mild or moderate difficulties only.
• Children who survive traumatic injury have a
better prognosis than children who suffer a global
hypoxic-ischemic injury
66. appropriate long-term therapy
• Early rehabilitation, by a team comprising
doctors, teachers, physiotherapist, occupational
and speech therapist and a psychologist is often
very much rewarding.
• It is essential to test hearing early, particularly
after meningitis.
• Many children, who had seizures acutely, do not
develop epilepsy at follow up and may be
weaned off from their anticonvulsants after three
to six months.
71. Alert: Fully conscious
Lethargic: appear somnolent, but may be able to maintain
arousal
Obtunded: requires touch or voice to maintain arousal
Stuporous: unresponsiveness from which the individual can
be aroused only by painful stimulus
Comatose: State in which the patient is unable to arouse or
respond to noxious stimuli and is completely unaware of self
and surroundings
Levels of Consciousness:
72. • Minimally Conscious State
“a condition of severely altered consciousness
in which the person demonstrates minimal
but definite behavioral evidence of self or
environmental awareness”
73. • Vegetative State
“condition of complete unawareness of the
self and the environment, accompanied by
sleep–wake cycles with either complete or
partial preservation of hypothalamic and
brainstem autonomic functions”
74. Severe Disorders of Consciousness
Condition Self-
Awareness
Pain and
Suffering
Sleep–
Wake
Cycles
Motor Function Respiratory
Function
Coma Absent No Absent No purposeful
movement
Variably
depressed
Vegetative
state
Absent No Intact No purposeful
movement
Normal
Minimally
conscious
State
Very
limited
Yes Intact Severe limitation
of movement
Variably
depressed
75. Causes of Coma
• T Trauma, head injury Shaken baby syndrome: non-specific
history, retinal hemorrhages.
• I Intussusception Mental status changes may precede
abdominal finding
Insulin, Hypoglycemia
Inborn errors of metabolism
• P Psychogenic Common in adolescents
• S Seizures Postictal states, non-convulsive status may
masquerade as undifferentiated coma.
Shock, stroke Coma secondary to poor brain perfusion,
arterial and venous infarcts
Shunt Blocked or infected ventriculo-peritoneal
shunts
76. • A Alcohol ingestion, abuse
• E Electrolytes Disturbances of sodium, calcium,
magnesium
Encephalopathy Hypertensive, Reye syndrome, hepatic
failure, urea cycle defects, lead
encephalopathy
• I Infections Encephalitis, meningitis, malaria
• O Overdose, ingestion Consider with unexplained loss of
consciousness
• U Uremic encephalopathy
77.
78. Apneustic breathing:
• Lesion: Lower pons
• Characterized by inspiratory pause, lasting for 2-
3 sec, often alternating with end expiratory
pauses.
• Pontine infarctions
Anoxic encephalopathy
Central neurogenic hyperventliation:
• Lesion: Mid brain
79. Kussumaul’s breathing:
• Diabetic ketoacidosis
Uremia
• Characterized by rapid, deep respiration
Biot’s breathing:
• Fast & deep respirations with apnoea in between
Ataxic breathing:
• Lesion: Medulla
• Inco-ordination in breathing