approach to comatose child

1. APPROACH TO COMATOSE CHILD
Dr G. Venkatesh
Junior resident pediatrics
SVMC, AP

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?

3. contents
 Terminology -States of altered conciousness.
Etiology
Approach
 Rapid assessment & Stabilisation.
 History.
 Examination & Neurological assessment.
 Investigations.
 Treatment.

4. • Consciousness is the state of awareness of self
and environment.

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.

9. • Increased neuronal excitability 
Restless/Confusion Delirium Stupor
Coma
• Decreased neuronal excitability Lethargic
 Obtunded Stupor Coma

10. 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

11. Etiology –cont.
2. Structural
A. Traumatic
 Concussion
 Cerebral contusion
 Epidural hematoma or
effusion
 Intracerebral hematoma
 Diffuse axonal injury
 Abusive head trauma
B. Neoplasms
C. Focal Infection
• Abscess
• Cerebritis
D. Hydrocephalus
E.Vascular Disease
• Cerebral infarction
 Thrombosis
 Embolism
 Venous sinus thrombosis
• Cerebral hemorrhage
 Subarachnoid hemorrhage
 Arteriovenous malformation
 Aneurysm
• Congenital abnormality or
dysplasia of vascular supply
• Trauma to carotid or
vertebral arteries in the
neck

12. Etiology –cont.
3.Metabolic, Nutritional, or
Toxic
A. Hypoxic-Ischemic
Encephalopathy
 Shock
 Cardiac or pulmonary failure
 Near-drowning
 Carbon monoxide poisoning
 Cyanide poisoning
 Strangulation
B. Metabolic Disorders
 Sarcoidosis
 Hypoglycemia
 Fluid and electrolyte
imbalance
 Endocrine disorders
 With acidosis
 Diabetic ketoacidosis
 Aminoacidemias
 Organic acidemias
 With hyperammonemia
 Hepatic encephalopathy
 Urea cycle disorders
 Disorders of fatty acid
metabolism
 Reye’s syndrome
 Valproic acid encephalopathy
 Uremia
 Porphyria
 Mitochondrial disorders
 Leigh’s syndrome

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.

16. Aetio-pathophysiological approach
COMA
Structural lesions Metabolic disorders
 Usually focal  Diffuse and
symmetric
Supratentorial Infratentorial
(Hemispheric) (Brainstem).

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.

19. • 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 syndrome,
enteric encephalopathy, shigella encephlopathy

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.

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.

28. 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

29. 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

30. 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

31. 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)

32. – 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
brainstem), Irregular (medulla involved

33. • 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

34. • CVS: Arrhythmias, Murmurs (Congenital heart
disease, Infective endocarditis)
• Chest: Signs of lung disease
• P/A: Tender hepatomegaly (Hepatitis, Sepsis),
Hepatosplenomegaly- malaria

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

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.

47. 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

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

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.

54. Subdural Hematoma

55. Acute epidural hematoma and midline shift

56. Cerebral Abscess

57. Cerebral edema

58. Biochemical investigations

59. investigations

60. electroencephalography
EEG findings Interpretation
•High voltage slow waves
•Slowing of background
activity
•Triphasic waves
•PLEDS Periodic Lateralised
Epileptiform Discharges
•Underlying supratentorial
lesion
•Metabolic coma
•Hepatic coma
•Herpes encephalitis
EEG findings in coma

61. TREATMENT
• Emergency measures (immediate life
support)
• Specific therapy

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.

67. Management approach-outline

70. Thank you

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

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