- Coma is a medical emergency in children that requires prompt evaluation and treatment to identify the underlying cause and prevent further neurological damage. - The neurological examination provides important clues about potential causes and localization through assessment of factors like pupil response, brainstem reflexes, motor function, and presence of focal deficits or posturing. - Initial diagnostic workup includes blood tests, imaging like CT scan or MRI, and lumbar puncture depending on clinical suspicion of conditions like infection, trauma, or metabolic derangement. Treatment focuses on stabilization, identifying and reversing any immediate life-threatening conditions, providing supportive care, and administering specific treatments targeted at suspected etiologies.

1. Approach to an unconscious child
Dr. Nishant Yadav
Junior resident -2
Dept. of Paediatrics
LLRM Medical College and Hospital

2. INTRODUCTION
• Coma is a medical emergency which presents diagnostic as well as
therapeutic challenges.
• The incidence of non traumatic coma is 30/1 lakh children per yr* and
traumatic coma is 670/1 lakh children per yr*.
• CNS infections is the most common cause of non traumatic coma in children
for developing countries.
• The potential causes are numerous, and the critical window for diagnosis
and effective intervention is often short.
*AIIMS PICU PROTOCOL 2017

3. Definition of coma and other impaired
consciousness states
• Impaired consciousness state refers to significant alteration in the
awareness of self and the environment, with varying degrees of
wakefulness.
• COMA- total absence of arousal and awareness with loss of sleep wake
cycle and must last for at least one hour.
• Vegetative state- complete unawareness of the self and the
environment ,preserved sleep wake cycle with variable preservation of
brainstem functions. It is permanent if persists for 12 months after
traumatic brain injury and 3 months after non-traumatic injury.

4. • Minimally conscious state - the patient demonstrates minimal but
definite behavioural evidence of self- or environmental awareness.
• Brain death - permanent absence of all brain functions including those
of the brainstem. Brain-dead patients are irreversibly comatose and
apnoeic with absent brainstem reflexes.

5. Causes of coma in children
Coma with focal signs
• Intracranial hemorrhage
• Stroke: arterial ischemic or venous thrombosis
• Tumors
• Focal infections-brain abscess
• Post seizure state: Todd’s paralysis
• Acute disseminated encephalomyelitis
Coma without focal signs and with meningeal irritation
• Meningitis
• Encephalitis
• Subarachnoid hemorrhage

6. • Coma without focal signs and without meningeal irritation
• Hypoxia-Ischemia: Cardiac or pulmonary failure, Cardiac arrest, Shock, Near drowning
• Metabolic disorders:
a. Hypoglycemia
b. Acidosis (e.g. diabetic ketoacidosis, Organic acidemias)
c. Hyperammonemia (e.g. hepatic encephalopathy, urea cycle disorders, disorders of fatty acid metabolism, Reye
syndrome)
d. Uremia
• Fluid and Electrolyte disturbances (dehydration, hyponatremia, hypernatremia)
• Systemic Infections: Bacterial: gram-negative sepsis, meningitis, toxic shock syndrome, cat-scratch disease, Shigella
encephalopathy, Enteric encephalopathy
• Post infectious disorders: Acute necrotizing encephalopathy, ADEM, Hemorrhagic shock and encephalopathy
syndrome
• Drugs and toxins
• Cerebral malaria
• Rickettsial: Lyme disease, Rocky mountain spotted fever
• Hypertensive encephalopathy
• Post seizure states
• Post migraine

7. Evaluation of the Comatose Child

8. History
• A careful history should be taken with special emphasis on the events
prior to the onset of coma.
• Presence of fever, headache, vomiting, irritability, seizures, rash and the
duration of symptoms must be enquired.
• A history of fever or recent illness suggests an acute infectious etiology
(sepsis, meningitis, encephalitis)
• Encephalopathy may be preceded by a febrile illness in acute
disseminated encephalomyelitis(ADEM), Reye’s syndrome, mitochondrial
and other inborn errors of metabolism.
• History of trauma, drug or toxin exposure, dog bite, seizures, past
medical illnesses, and family history.

14. Neurological Examination
• It gives important information about the potential causes and localization
of brain dysfunction.
• Level of Consciousness
o The child should be inspected for spontaneous body posture, motor
activity, eye opening, or verbalization.
oThe level of consciousness must be recorded in the form of an objective
scale, such as the Glasgow Coma Scale (GCS).
oFull outline of unresponsiveness (FOUR) score is another scoring system
which has better predictive value than GCS in intubated pts and in pts with
very low GCS scores. Decreasing FOUR Score is associated with
worsening level of consciousness.

17. If one pupil is non-reactive to light, one point is subtracted & If both pupils fail to constrict, two points are
subtracted from the total GCS score.
The modification, referred to as GCS-P.

18. Pupillary Abnormalities
• Pupillary size, shape, symmetry and response to light provide valuable clues to
brainstem and third nerve dysfunction.
• Topical administration of mydriatics must be avoided.
• The pupillary light reflex is very resistant to metabolic dysfunction.

19. Brainstem Function
• The presence of oculocephalic (doll’s eye), oculovestibular, corneal, cough and gag
reflexes are indicative of intact brainstem function.
•

20. Motor Response
• The trunk, limb, position, spontaneous movements and response to stimulation
must be observed for any focal deficits (suggestive of post ictal Todd’s palsy or
structural abnormality) and posturing (decerebrate or decorticate).
• Posturing signals a brainstem herniation syndrome.
• Tonic-clonic or other stereotyped movements signals seizures.
• Myoclonic jerks are seen with anoxic and hepatic encephalopathy.
• Dystonias signify extrapyramidal involvement which maybe seen in Japanese B
encephalitis, tubercular meningitis or inborn errors of metabolism.

23. Other Neurological Findings
• Fundus examination to look for papilledema and retinal hemorrhages.
• Signs of meningeal irritation maybe present in meningitis, encephalitis and
subarachnoid hemorrhage.
• Neck rigidity is present in meningitis, tonsillar herniation or craniocervical
trauma.
• The Kernig’s and Brudzinski’s signs are more reliable signs of meningeal irritation

24. Investigations
Basic Investigations
• RBS by reagent strips should be performed to rule out hypoglycemia.
• A complete blood count and blood biochemistry must be obtained. The TLC maybe
raised or depressed in severe infections.
• The blood biochemistry should include glucose, Na+, K+, Ca++, Mg++, KFT, LFT, ABG
and lactate level.
• Urine should also be examined for reducing sugars and ketones.
• Blood and urine cultures should be taken.
• A peripheral blood smear and rapid diagnostic test for malarial parasite should be
obtained.

25. • Ideally in all children with impaired consciousness, a Computed tomography (CT)
scan of the cranium should be obtained. Esp. in patients with features of raised
ICP, focal neurological deficits, unexplained altered sensorium, features of
herniation .
• Exceptions may include a known c/o uncomplicated metabolic toxic cause of
coma, e.g. diabetic ketoacidosis or hypoglycaemia .
• CT is helpful in intracranial hemorrhage , cranial trauma, stroke, herniation and
cerebral edema.
• A contrast study may reveal features of infection in the form of meningeal
enhancement, brain abscess or neurocysticercosis .
• A normal CT does not rule out elevated intracranial pressure.

26. • If a patient is febrile, infection is suspected, or no other etiology can be
determined, then a lumbar puncture should be performed.
• CSF should be tested for cell count, glucose, protein, Gram stain, Z-N stain,
bacterial culture, viral polymerase chain reaction for Herpes Simplex virus, Latex
agglutination test, and additional cultures guided by clinical suspicion (fungal or
tubercular) .
• If clinical or radiologic evidence is present for intracranial hypertension or lumbar
puncture is otherwise contraindicated (thrombocytopenia, shock, local infection),
it should be deferred and treatment should be initiated for possible infections
(bacterial and viral).

27. Second-Line Investigations
• Metabolic Testing - In cases of unexplained or recurrent encephalopathy, blood
ammonia, urine and blood samples for amino and organic acid disorders, free fatty
acid and carnitine levels should be obtained before starting treatment.
• Hyperammonemia may be caused by some inborn errors of metabolism, Reye’s
syndrome, liver failure or valproate toxicity.
• Magnetic resonance imaging (MRI) with MRA is the preferred modality of
investigation for stroke. It is also useful in identifying
i. frontotemporal pathology in herpes simplex encephalitis
ii. thalamic involvement in Japanese B encephalitis
iii. demyelination in ADEM
iv. necrotizing lesions in acute necrotizing encephalopathy
• MRI is also useful for determining prognosis.

28. • Electroencephalogram (EEG)
• Diffuse theta and delta activity, absence of faster frequencies, and intermittent
rhythmic delta activity are characteristic of severe encephalopathies.
• Specific abnormalities may include epileptiform activity consistent with absence or
complex partial status; triphasic waves indicating hepatic or uremic encephalopathy;
and periodic lateralizing epileptiform discharges, suggesting herpes encephalitis.
Other Investigations
• A urine toxicology screen should be obtained when no cause is obtained on clinical
evaluation, or there is a clinical suspicion of poisoning.
• Other investigations in unexplained coma include thyroid function tests and thyroid
antibodies (for Hashimoto encephalopathy)

29. Treatment
• Management of a child with coma usually proceeds simultaneously with the
clinical evaluation. The goals of treatment are:
 Stabilization of vitals: airway, breathing and circulation
Identify and treat hypoglycemia with intravenous dextrose (2 ml/kg 10% D, Then
glucose infusion rate of 6–8 mg/kg/min).
Identification and treatment of seizures - If the child is having tonic-clonic
movements, tonic deviation of eyes or nystagmus, or there is history of a seizure
preceding the encephalopathy, anticonvulsant should be administered. Non
convulsive status epilepticus (NCSE) maybe seen in comatose children, and should
be looked for in all children with unexplained encephalopathy.
Maintenance of normothermia
Acid base and electrolyte abnormalities should be corrected.
Identification and treatment of brain herniation and raised intracranial pressure
-hyperventilation, mannitol / 3% saline etc.

30. • In case of suspected sepsis/ meningitis- broad spectrum antibiotics
(ceftriaxone+ vancomycin) should be started. If viral encephalitis is likely,
then samples for PCR for HSV should be sent and acyclovir is given.
• Antimalarials (quinine/artesunate)- started if there is a clinical suspicion of
cerebral malaria . For eg. Smear positive, RDT positive cases,if resident of P.
falciparum endemic area, short history (<48 hrs), absent meningeal signs,
anemia, hypoglycemia, retinal hemorrhages.
• Antidotes: Naloxone (0.1 mg/kg) in case of suspected opiate poisoning,
Flumazenil for benzodiazepine overdose and Atropine for organophosphate
poisoning.
• Steroids are given in ADEM , tubercular meningitis, meningococcemia with
shock, enteric encephalopathy and pyogenic meningitis.
• If metabolic causes have been identified, e.g. diabetic ketoacidosis, hepatic
encephalopathy, uremia or hyperammonemia, these should treated
appropriately.

31. • In sick children with acute febrile encephalopathy, empirical therapy with
antibiotics, acyclovir and anti-malarial agents should be considered while the
results of investigations are awaited .
• The clinical course of the child should be monitored closely and documented on a
daily basis.
• Particular attention should be paid to changing level of consciousness, fever,
seizures, autonomic nervous system dysfunction, increased intracranial pressure,
speech and motor disturbances.
• Nosocomial infections are important complications during hospitalization, and
must be prevented and treated promptly.

32. Prognosis
• The outcome of coma depends on the etiology, depth and duration of impaired
consciousness.
• Prolonged coma after a hypoxic-ischemic insult carries a poor prognosis .
• Most children surviving infectious encephalopathies have a comparatively better
outcomes, often surviving with only mild or moderate difficulties.
• Outcome has been shown to be worse for patients who were younger, had a lower
GCS score on presentation, or had absent brainstem reflexes, worse motor
responses, hypothermia, or hypotension.
• These children should be followed up for early identification of developmental
disabilities, learning and behaviour problems, as well as other neurological sequelae
such as motor, visual or hearing deficit and seizure disorder.

33. THANK YOU