APPROACH TO COMATOSE CHILD

Dr G.Venkatesh
 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?
 contents
Terminology -States of altered
conciousness.
Etiology
Approach
Rapid assessment & Stabilisation.
History.
Examination & Neurological assessment.
Investigations.
Treatment.
 Consciousness is the state of
awareness of self and environment.
 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 comavegetative
stateminimally conscious state.
 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.
 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
 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.
 Increased neuronal excitability
Restless/Confusion Delirium
Stupor Coma

Decreased neuronal
excitability Lethargic
Obtunded Stupor Coma
 Etiologies of Impaired
Consciousness and Coma
1.Infectious or Inflammatory
A. Infectious
Bacterial meningitis
Viral encephalitis
Rickettsial infection
Protozoan infection
Helminth infestation
B. Inflammatory
Sepsis-associated encephalopathy
Vasculitis, collagen vascular disorders
Demyelination
Acute disseminated encephalomyelitis
Multiple sclerosis
 Etiology cont.
2. Structural
A. Traumatic E.Vascular Disease
Concussion Cerebral infarction
Cerebral contusion Thrombosis
Epidural hematoma or Embolism
Venous sinus thrombosis
effusion
Intracerebral hematoma Cerebral hemorrhage
Subarachnoid hemorrhage
Diffuse axonal injury
Arteriovenous malformation
Abusive head trauma Aneurysm
B. Neoplasms Congenital abnormality or
C. Focal Infection dysplasia of vascular supply
Abscess Trauma to carotid or
Cerebritis vertebral arteries in the
neck
D. Hydrocephalus
 Etiology cont.
3.Metabolic, Nutritional,
or Toxic With acidosis
A. Hypoxic-Ischemic Diabetic ketoacidosis
Encephalopathy Aminoacidemias
Shock Organic acidemias
Cardiac or pulmonary With hyperammonemia
failure Hepatic encephalopathy
Near-drowning Urea cycle disorders
Carbon monoxide poisoning Disorders of fatty acid
Cyanide poisoning metabolism
Strangulation Reyes syndrome
B. Metabolic Disorders Valproic acid encephalopathy
Hypoglycemia Uremia
Fluid and electrolyte Porphyria
imbalance Mitochondrial disorders
Endocrine disorders
Leighs syndrome
Sarcoidosis
 Etiology -cont
C. Nutritional
Thiamine deficiency
Niacin or nicotinic acid
deficiency
Herbal treatments
Pyridoxine dependency
Heavy-metal poisoning
Folate and B12 deficiency
Mushroom and plant
intoxication
D. Exogenous Toxins and Illegal drugs
Poisons Industrial agents
Alcohol intoxication
Over-the-counter
E. Hypertensive
medications
Prescription medications
Encephalopathy
(oral and ophthalmic)
F. Burn Encephalopathy
 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.
 ANATOMY AND PHYSIOLOGY -
CONSCIOUSNESS
Function Site
Awake RAS Rostral brainstem
(Reticular (midbrain and upper
Activating pontine tegmentum) to
System) the lower thalamus .
The hypothalamus.
Awareness Cerebral
(a higher hemispheres.
cognitive
function) =
cognition +
affect
Aetio-pathophysiological approach
COMA

Structural lesions
Metabolic disorders
Usually focal Diffuse and
symmetric

Supratentorial Infratentorial
(Hemispheric) (Brainstem).
 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
 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.
 Metabolic disorders:
Hypoglycemia
Acidosis: Diabetic ketoacidsis, organic
acidemis
Hyperammonemia: hepatic
encephalopathy, urea cycle disorders,
valproic acid encephlopathy, Reyes
syndrome.
Uremia
Fluid and electrolyte disturbance
(dehydration, hyponatremia,
hypernatremia)
Systemic infections :
Gram negative sepsis, toxic shock
 Drugs and toxins
Cerebral malaria
Rickettsial : lyme disease, rocky
mountain spotted fever
Hypertensive encephalopathy
Post seizure states
Non-convulsive status epilepticus
 The goals of coma therapy
(a)Adhere to the principles of resuscitation, 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.

 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.
 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).
 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.
 History ,physical examination and
neurological assesment
History: age
Infant Child Adolescent
CNS infection Ingestion Drug/Alcohol
(meningitis,encephalitis) overdose
Systemic infection with CNS infection Intentional
shock poisoning
Metabolic disorders Seizure Trauma, seizures
Abuse / Trauma, Abuse / CNS infection,
Trauma
Inborn errors of DKA, Reys DKA, , Reys
metabolism,seizures syndrome syndrome

Post immunisation
encephalopathy,
hemorrhagic shock and
encephalopathy syndrome
 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.
 Approach: History
Associated symptoms of CNS causes:
Fever Infections
Headache, Vomiting, Diplopia Increased
ICP
Neck stiffness Meningitis, SAH
Rash - Meningococcemia
H/o excess cry, irritability, enlarging head
in infants Meningitis, Hydrocephalus
H/o Trauma (Severity, Bleeding from
ear/nose)
Seizures ICH, ICSOL, Epilepsy, Post-ictal
 Approach: History
Recurrent episodes: Epilepsy, Inborn errors of
metabolism

H/o recent infectious diseases eg. Mumps

(Parotid swelling), measles (rash)

Failure to thrive, vomiting, peculiar skin odour

Metabolic cause

Jaundice, abdominal distension, hematemesis,

melena, bleeding - Hepatic encephalopathy

Urine output, swelling, periorbital puffiness,

Nausea, vomiting, loss of appetite Uremic
encephalopathy
 Approach: History
H/o loose stools- HUS, Hypovolemia ,Ingestion
of toxins/poisons, medications

H/o Immunocompromised state (Cryptococcal

meningitis, TBM), malignancy

Family h/o TB, migraine, epilepsy

Birth H/o: Birth asphyxia, h/o recurrent

hypoglycemia

Developmental delay or regression

h/o envenomation
 Physical examination
Vital signs:

HR: Bradycardia ( ICT, myocardial injury

due to hypoxia, sepsis), Tachycardia
(Shock, Infections, Atropine); Irregular
(Arrhythmia).

BP: (HTN in ICP, HTN encephalopathy),

Hypotension (shock, barbiturates,
adrenal insufficiency)
 Temp: Fever in Infections, Hyperpyrexia,
Hypothalamic lesion or pontine
hemorrhage, atropine poisoning,
Hypothermia in Sepsis, shock, alcohol,
barbiturate poisoning, hypoglycemia

RR: Bradypnea/ Apnea (Drug

intoxication, septicemia), Tachypnea
(Metabolic Acidosis, Brainstem lesions,
Pneumonia), Cheyne-Stoke breathing
(B/L cortical damage with intact
 Any signs of trauma (Scalp
laceration/swelling/fracture, ENT Bleeding)

Pallor - hypoxia, bleeding disorders

Icterus Hepatic encephalopathy, Sepsis

Cyanosis Cyanotic congenital heart disease, Hypoxia

Oedema CHF, Renal failure

Dehydration Hypovolemic shock, HUS

Skin- Meningococcal rash, Petechiae

Signs of meningeal irritation

 CVS: Arrhythmias, Murmurs
(Congenital heart disease, Infective
endocarditis)
Chest: Signs of lung disease
P/A: Tender hepatomegaly (Hepatitis,
Sepsis), Hepatosplenomegaly-
malaria
 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 Traumatic/ non accidental injury
hematomas
Dysmorphism, Possibility of seizures
neurocutaneusmark
ers
Abnormal odour DKA, hepatic coma
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
 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.
 Glasgow coma scale
BEST RESPONSE
ACTIVITY
Adults/Older Children Infants ( modified GCS ) Score
1. Spontaneous 1. Spontaneous 4
Eye Opening 2. To speech 2. To speech 3
(E) 3. To pain 3. To pain 2
4. None 4. None 1

1. Appropriate speech 1. Coos, babbles 5

2. Confused speech 2. Irritable, cries 4
3. Inappropriate words 3. Cries to pain 3
Verbal
4. Incomprehensible or 4. Moans to pain 2
(V)
non specific sounds
5. None 5. None 1

1.Obeys commands 1. Normal spontaneous 6

movement
2.Localizes pain 2. Withdraws to touch 5
Motor 3.Withdraws to pain 3. Withdraws to pain 4
(M) 4.Decorticate to pain 4. Decorticate to pain 3
5.Decerebrate to pain 5. Decerebrate to pain 2
6.None 1
6. None
 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
 B. Size and reactivity of
pupils
Pupils Lesion/Dysfunction

Pinpoint Pons, opiates, cholinergic

intoxication

Mid position Midbrain lesion

fixed or
irregular
Unilateral , Uncal herniation
dilated and
fixed
Bilateral , Diffuse damage, central herniation,
dilated and global hypoxia ischemia,
fixed barbiturates, atropine
 C. Eye movements
Oculocephalic or Dolls 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.
 D. Motor response
Single best indicator of the depth and
severity of coma
1. Spontaneous movements.
2. Tone and reflexes
3. Induced movements.
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.
 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.
 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.
A.Cheyne-Stokes respiration-bilateral cerebral
/diencephalon dysfunction , preceding to
transtentorial herniation

B.Central
neurogenic hyperventilation.- midbrain

C, Apneusis-pons

D, Cluster breathing.-lower
pons,cerebellum

E, Ataxic breathing-medullary lesion

 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 dolls 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
 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.
 CENTRAL VS UNCAL
CentralHERNIATIONuncal
Arousal Impaired early, before other Impaired late,
signs usually with other
Breathing signs
Sighs , yawns, sometimes No early change
Cheyne-Stokes respirations
Pupils
First , small reactive Ipsilateral pupil
(hypothalamus), then one or dilates, followed by
Oculocephal both approach midposition somatic third nerve
ic responses paralysis
Initially sluggish, later tonic Unilateral third
Motor signs conjugate nerve paralysis

Motor signs late,

Early hemiparesis opposite to sometimes ipsilateral
hemispheric lesion followed to lesion
late by ipsilateral motor
paresis and extensor plantar
response
Metabolic vs structural
coma
METABOLIC, TOXIC, STRUCTURAL
INFECTIOUS CAUSES
Supratentorial
destructive or mass
Confusion or stupor lesions:
precede motor signs Initial focal signs
Pupillary reactions Rostral to caudal progression
preserved
Symmetrical motor Infratentorial
responses destructive or mass
lesions:
Asterixis, myoclonus Preceding brainstem
Hyper or dysfunction
hypoventilation Sudden onset of coma
Cranial nerve palsies
Early respiratory disturbances
 INVESTIGATIONS
First line investigations:
Blood sugar
BUN, serum creatinine to assess the renal
function
Serum electrolytes, calcium.
CBC
Arterial blood gas analysis
Urine analysis.
LFT if jaundice, bleeding manifestations
noted.
 Suspected infections
CSF anlysis
Blood culture
Smear for malarial parasite
Rapid diagnostic test for malaria
 Suspected metabolic cause:
Urine and plasma amino acids level.
Carnitine levels
Serum ammonia levels
Thyroid function tests
Serum cortisol levels.
Urine porphyrines.
 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.
Subdural Hematoma
Acute epidural hematoma and
midline shift
Cerebral Abscess
Cerebral edema
 electroencephalography
EEG findings in coma
EEG findings Interpretation

High voltage slow Underlying

waves supratentorial lesion
Metabolic coma
Slowing of background
activity Hepatic coma
Triphasic waves
PLEDS Periodic Herpes encephalitis
Lateralised
Epileptiform Discharges
 TREATMENT
Emergency measures (immediate
life support)

Specific therapy
 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.
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.
 Specific therapy
Treat dyselectrolytemia and acid-base imbalance
Fluid therapy: avoid hypotonic fluids.
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
 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
 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.
Management approach-outline
 Reference.
PRINCIPLES OF PEDIATRIC AND NEONATAL
EMERGENCIES-3rd EDITION.
PEDIATRIC INTENSIVE CARE PROTOCOLS OF AIIMS.
IJPP 2005;7(1):38- APPROCH TO UNCONCIOUS
CHILD
IJPP 2011;13(2):193- APPROACH TO CHILD WITH
FEVER AND ALTERED SENSORIUM
PRACTICAL STRATEGIES IN PEDIATRIC DIAGNOSIS
AND THERAPY. 2nd EDITION.
NELSON TEXTBOOK OF PEDIATRICS, NINETEENTH
EDITION
SWAIMANS PEDIATRIC NEUROLOGY FIFTH
EDITION
Thank you
 Levels of Consciousness:
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
 Minimally Conscious State
a condition of severely altered
consciousness in which the person
demonstrates minimal but definite
behavioral evidence of self or
environmental awareness
 Vegetative State
condition of complete unawareness
of the self and the environment,
accompanied by sleepwake cycles
with either complete or partial
preservation of hypothalamic and
brainstem autonomic functions
 Severe Disorders of
Consciousness
Conditi Self- Pain Sleep Motor Respirat
on Awaren and Function ory
ess Sufferi Wake Functio
ng Cycle n
s
Coma Absent No Absen No purposeful Variably
t movement depresse
d
Vegetati Absent No Intact No purposeful Normal
ve movement
state
Minimall Very Yes Intact Severe Variably
y limited limitation of depresse
consciou movement d
s
 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
 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
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
Kussumauls breathing:
Diabetic ketoacidosis
Uremia
Characterized by rapid, deep respiration
Biots breathing:
Fast & deep respirations with apnoea in
between
Ataxic breathing:
Lesion: Medulla
Inco-ordination in breathing
GLASGOW COMA SCALE