Indian J Pediatr (2010) 77:1279–1287
DOI 10.1007/s12098-010-0191-1
SYMPOSIUM ON PICU PROTOCOLS OF AIIMS
Approach to the Child with Coma
Suvasini Sharma & Gurpreet Singh Kochar &
Naveen Sankhyan & Sheffali Gulati
Received: 3 August 2010 / Accepted: 18 August 2010 / Published online: 10 September 2010
# Dr. K C Chaudhuri Foundation 2010
Abstract Coma and other states of impaired consciousness
represent a medical emergency. The potential causes are
numerous, and the critical window for diagnosis and
effective intervention is often short. The common causes
of non-traumatic coma include central nervous system
infections, metabolic encephalopathy (hepatic, uremic,
diabetic ketoacidosis etc.), intracranial bleed, stroke and
status epilepticus. The basic principles of management
include 1) Rapid assessment and stabilization, 2) Focussed
clinical evaluation to assess depth of coma, localization of
lesion in the central nervous system and possible clues to
etiology, and 3) Treatment including general and specific
measures. Commonly associated problems such as raised
intracranial pressure and seizures must be recognized and
managed to prevent secondary neurologic injury.
Keywords Altered sensorium . Encephalopathy . Impaired
consciousness . Intracranial pressure
Introduction
Coma is a medical emergency which presents diagnostic as
well as therapeutic challenges. The potential causes of
coma are numerous, and the critical window for diagnosis
and effective intervention (not only to ensure survival but
also to prevent long-term sequelae) is short. Pediatricians in
the emergency services and intensive care units (ICU) have
to frequently manage comatose patients. The incidence of
S. Sharma : G. S. Kochar : N. Sankhyan : S. Gulati (*)
Department of Pediatrics, Child Neurology Division, All India
Institute of Medical Sciences,
New Delhi 110029, India
e-mail: sheffaligulati@gmail.com
non-traumatic coma is 30/100,000 children per yr, and that
of traumatic brain injury is 670/100,000 [1, 2]. Central
nervous system (CNS) infections are the most common
cause of non-traumatic coma in children in our scenario.
This article provides a practical approach to evaluate a child
with non-traumatic coma.
Definitions: Coma and Other States of Impaired
Consciousness
Impaired consciousness implies a significant alteration in
the awareness of self and of the environment, with varying
degrees of wakefulness [3]. Descriptive terms such as
somnolence, stupor, obtundation, and lethargy used to
denote different levels of wakefulness are best avoided,
given the lack of uniformity in the way these states are
defined in the literature.
Coma is characterized by the total absence of arousal
and of awareness. Comatose patients have no eye opening.
As opposed to states of transient unconsciousness such as
syncope or concussion, coma must last for at least 1 h [3].
Vegetative state describes a condition of complete
unawareness of the self and the environment accompanied
by sleep wake cycles with variable preservation of
brainstem functions. The vegetative state is deemed to be
permanent 12 months after traumatic brain injury and
3 months after non-traumatic injury [4]. Minimally con-
scious state is defined as a condition of severely altered
consciousness in which the patient demonstrates minimal
but definite behavioural evidence of self- or environmental
awareness [5]. Brain death is defined as the permanent
absence of all brain functions including those of the
brainstem [6]. Brain-dead patients are irreversibly comatose
and apneic with absent brainstem reflexes.
1280
Etiology (Table 1)
It is clinically useful to categorize the causes of coma into [7]:
1) Coma with focal signs
2) Coma without focal signs and without meningeal
irritation
3) Coma without focal signs and with meningeal irritation
There maybe overlap within these categories. For example, a
child with meningitis may also have focal neurological
deficits. In a study from our center comprising 70 children
aged 5–15 yrs with non-traumatic impairment of conscious-
ness, CNS infections accounted for 33 (50%) of cases (Kochar
GS et al. unpublished data). Out of these, 13 children were
diagnosed to have viral meningo-encephalitis, five had
tuberculous meningitis, five had brain abscess, two children
Table 1 Causes of coma in children
Coma with focal signs
• Intracranial hemorrhage
• Stroke: arterial ischemic or sinovenous thrombosis
• Tumors
• Focal infections-brain abscess
• Post seizure state: Todd’s paralysis
• Acute disseminated encephalomyelitis
Coma without focal signs and without meningeal irritation
• Hypoxia-Ischemia: Cardiac or pulmonary failure, Cardiac
arrest, Shock, Near drowning
• Metabolic disorders: Hypoglycemia Acidosis (e.g. Organic
acidemias, diabetic keto-acidosis) Hyperammonemia (e.g. hepatic
encephalopathy, urea cycle disorders, valproic acid encephalopa-
thy, disorders of fatty acid metabolism, Reye syndrome) Uremia,
Fluid and Electrolyte disturbances (dehydration, hyponatremia,
hypernatremia)
• Systemic Infections: Bacterial: gram-negative sepsis, meningitis,
toxic shock syndrome, cat-scratch disease, Shigella encephalopa-
thy, Enteric encephalopathy
• Post infectious disorders: Acute necrotizing encephalopathy,
ADEM, Hemorrhagic shock and encephalopathy syndrome
• Post immunization encephalopathy: Whole cell pertussis vaccine,
Semple Rabies vaccine
• Drugs and toxins
• Cerebral malaria
• Rickettsial: Lyme disease, Rocky mountain spotted fever
• Hypertensive encephalopathy
• Post seizure states
• Non-convulsive status epilepticus
• Post migraine
Coma without focal signs and with meningeal irritation
• Meningitis
• Encephalitis
• Subarachnoid hemorrhage
Indian J Pediatr (2010) 77:1279–1287
each had pyogenic meningitis, enteric encephalopathy, and
multiple neurocysticercosis, and one child each had cerebral
malaria rabies encephalitis, meningococcemia and dengue
encephalopathy. Among the other 35 children, seven each had
fulminant hepatic failure, or intracranial bleed. Other causes
included hypoxic ischemic encephalopathy following cardiac
arrest (n=4), metabolic encephalopathy (n=4, uremia-3,
DKA-1), hypertensive encephalopathy (n=2), ADEM (n=
3), refractory status epilepticus (n=3), tumor (n=1). No
cause could be ascertained in 3 cases.
Evaluation of the Comatose Child
Coma is a medical and neurological emergency, requir-
ing immediate consideration of key issues including
immediate life support, identification of cause, and
institution of specific therapy. The evaluation (clinical
as well as investigations) and treatment have to proceed
simultaneously (Fig. 1).
Stabilization As in any emergency, initial steps should be
directed to ensuring adequacy of airway, breathing and
circulatory function [8]. Airway management is of para-
mount importance in children with altered states of
consciousness, as their protective reflexes are obtunded
and they are more prone to aspiration. Children with
Glasgow Coma Score less than 8 should preferably be
intubated; mechanical ventilation should be provided in
case the breathing efforts are not adequate. Appropriate
oxygenation should be ensured.
The next most important step is establishment of
vascular access. If there is evidence of circulatory failure,
fluid bolus (20 mL/kg- Normal saline) should be adminsi-
tered. Samples should be drawn for various investigations.
If hypoglycemia is present, intravenous glucose should be
administered. If the child is having seizures, or there is
history of a seizure preceding the encephalopathy, anticon-
vulsant (inj Lorazepam, 0.1 mg/kg followed by phenytoin
loading 20 mg/kg) should be administered. If there are
features of raised intracranial pressure (asymmetric pupils,
tonic posturing, papilledema, evidence of herniation),
measures to decrease intracranial pressure should be rapidly
instituted (hyperventilation, mannitol etc.). Acid base and
electrolyte abnormalities should be corrected. Normothermia
should be maintained (see algorithm).
History
A careful history should be taken with special emphasis on
the events prior to the onset of coma. Presence of fever,
Indian J Pediatr (2010) 77:1279–1287 1281

Rapid assessment and stabilization

Evaluate • Establish and maintain Airway: Intubate if GCS≤8, impaired airway

reflexes, abnormal respiratory pattern, signs of raised ICP, oxygen

saturation <92% despite high flow oxygen, fluid refractory shock

• Ventilation, Oxygenation as indicated

• Circulation: Establish IV access, take samples* (S. Electrolytes, Arterial

Blood gas, lactate, CBC with platelets, MP slide/RDT, LFT, KFT, Blood

culture, urine sugar and ketones)

• Fluid bolus if in circulatory failure (20 ml/kg NS), inotropes if required

• *Blood Glucose: Perform reagent strip testing and and give dextrose

<50mg/dL

• Identify signs of cerebral herniation or raised ICP; If any of following

present, Give 20%mannitol or 3% NS (if patient in shock), intubate &

short term hyperventilation (PaCO2:30-35mmhg): GCS < 8, abnormal

pupil size and reaction, absent doll’s eye movements, abnormal tone

/Posturing, hypertension with bradycardia, abnormal respiratory pattern.

• Temperature: treat fever & hypothermia

History

Examination- see Table- 2 and 3

Neurological assessment

Investigate

• CT: in patients with: f/o raised ICP, focal neurological deficits,

unexplained altered sensorium, features of herniation

• CSF in suspected meningitis/ encephalitis: (if CSF is

delayed/contraindicated, start i/v antibiotics and acyclovir), Cytology,

biochemistry, culture, Latex Agglutination, Duration of illness > 1 wk:

Fig. 1 Step wise approach to child with non-traumatic impairment of consciousness

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), but other disorders in
which encephalopathy maybe preceded by a febrile illness
must also be considered. These include acute disseminated
encephalomyelitis, Reye’s syndrome, mitochondrial and
other inborn errors of metabolism. History of trauma, drug/
toxin exposure, dog bite, seizures, past medical illnesses,
and family history must be elicited.
1282 Indian J Pediatr (2010) 77:1279–1287

AFB stain, PCR for TB,Viral- PCR for Herpes, Jap B IgM

• Investigations as per presentation: Dengue serology, Widal, Serology for

other pathogens; Leptospira, Mycoplasma, Rickettsia

Manage Management (several problems may co-exist)

• Shock- Treat shock as per PALS guidelines

• Sepsis- start broad spectrum antibiotics

• Hypoglycemia- Blood sugar: <50 mg/dl 2 ml/kg 10% D, Then GIR 6-

8mg/kg/min- maintain euglycemia

• Seizures: Lorazepam 0.1 mg/kg, Then Phenytoin 20 mg/kg loading

Ongoing vitals and Neurological monitoring

Raised ICP: Refer to protocol on raised ICP

• Treat dyselectrolytemia and acid-base imbalance

Acute febrile encephalopathy

• Empiric antibiotic therapy- Ceftriaxone ± Vancomycin

• Acyclovir-In sporadic Meningo-encephalitis with or without: focal

neurological findings, behavior changes, aphasia, suggestive CT (fronto-

temporal changes), hemorrhagic CSF

• Steroids-: Meningococcemia with shock, enteric encephalopathy, ADEM,

prior to a/b dose in pyogenic meningitis

• Antimalarials (Quinine/ Artesunate)- Smear positive, RDT positive cases,

Empiric treatment if resident of P.falciparum endemic area#, short history

(<48 hrs),absent meningeal signs, anemia, hypoglycemia, retinal

hemorrhages

Treat as per identified cause

Fig. 1 (continued)
Indian J Pediatr (2010) 77:1279–1287 1283

• Diabetic Ketoacidosis: Fluids, insulin and other measures

• Hypertensive encephalopathy: antihypertensives

• Toxidrome: Opiate overdose-Naloxone, Benzodiazepine overdose-

Flumanezil, Organophosphate poisoning-Atropine, Pralidoxime

• Envenomation: Antivenom

“Be alert to possibility of Child abuse in an infant/toddler with sudden unexplained

altered consciousness”

Further If first line Investigations non-contributory and patient not improving despite

evaluation empirical therapy, consider second-line investigations:

• MRI- to identify stroke, ADEM, HSE (frontotemporal lesions), Japanese B

(thalamic involvement), viral associated encephalopathy, IEM

• EEG- PLED’s in HSE, NCSE as cause of unexplained altered sensorium

• Drug levels (suspected anti-epileptic toxicity)

• Metabolic work-up- NH3, acylcarnitine profile (TMS), urine organic acids

(GCMS)

• urine toxicology screen

• ESR and autoimmune screen (cerebral vasculitis)

• Thyroid function and thyroid autoantibodies (Hashimoto’s

encephalopathy)

(GCS- Glasgow Coma Scale, ICP- Intracranial Pressure, NH3- Ammonia, TMS- Tandem Mass Spectrometry, GCMS- Gas Chromatography
Mass Spectrometry, ESR-Erythrocyte Sedimentation Rate, ADEM- Acute Disseminated Encephalomyelitis, HSE- Herpes Simplex Encephalitis,
IEM- Inborn error of metabolism, PLED- Periodic Lateralized Epileptiform discharges, NCSE- Nonconvulsive status epilepticus, HSE- Herpes
Simplex Encephalitis, IV- intravenous, NS- Normal Saline, PCR-Polymerase Chain Reaction, AFB-Acid Fast Bacilli, GIR-Glucose Infusion
Rate, CBC-Complete Blood Count, RDT-Rapid Diagnostic Test, LFT-Liver Function Tests, KFT-Kidney Function Tests, #Rajasthan,Gujarat,
Orissa, Chattisgarh, Jharkhand, West Bengal, North Eastern states)
Fig. 1 (continued)

Examination pneumonia, meningitis, encephalitis, or a brain abscess; but

may also indicate heat stroke or abnormality of hypothalamic
Vital Signs The examination of vital signs provides important temperature regulatory mechanisms. Tachycardia maybe a
clues to the status and the possible etiology of coma. The result of fever, hypovolemic or septic shock, heart failure or
presence of fever suggests an infective process e.g. sepsis, arrhythmias. Bradycardia may result from raised intracranial
1284
pressure or a result of myocardial injury (due to myocarditis,
hypoxia, sepsis, or toxins). Tachypnea with other features of
respiratory distress signifying increased work of breathing is
an indicator of lung pathology e.g. pneumonia, pneumotho-
rax, empyema or asthma. Quiet tachypnea is indicative of
acidosis which maybe present in diabetic ketoacidosis,
uremia, or some poisonings (e.g. ethylene glycol). Hyperten-
sion maybe the cause of alteration in sensorium in hyperten-
sive encephalopathy or maybe a compensatory mechanism to
maintain cerebral perfusion in children with increased intracra-
nial pressure or stroke; in the former, there maybe features of
hypertensive retinopathy and findings suggestive of left
ventricular hypertrophy (ECG, Echocardiography). Hypoten-
sion due to sepsis, cardiac dysfunction toxic ingestion, or
adrenal insufficiency, may lead to poor cerebral perfusion,
resulting in diffuse or watershed hypoxic-ischemic injury.
General Physical Examination Examination of skin and
mucous membranes may reveal helpful etiological clues
(Table 2). Cyanosis suggests poor oxygenation, pallor suggests
anemia or shock, and jaundice is indicative of liver dysfunction.
The head and scalp should be examined for evidence of head
trauma, e.g. cephalhematoma, lacerations, echymosis.
Systemic Examination Chest examination is helpful to
detect underlying pneumonia or empyema. Cardiovascular
examination may suggest congenital or rheumatic heart
disease, both of which predispose the patient to endocardi-
tis and subsequent intracranial abscess dissemination.
Abdominal examination is important to detect hepatosple-
nomegaly which maybe present in many infective con-
ditions and liver disease.
Neurological Examination
The neurological examination gives important information
about the potential causes and localization of brain
dysfunction.
Table 2 Clues to etiology of
coma in general physical Look for
examination
Pallor
Icterus
Rashes
Petechiae
Head and scalp hematomas
Dysmorphism, Neurocutaneous
markers
Abnormal Odour of exhaled breath
Indian J Pediatr (2010) 77:1279–1287
Level of Consciousness The child should be inspected for
spontaneous body posture, motor activity, eye opening, or
verbalization. The level of consciousness must be recorded
in the form of an objective scale, such as the Glasgow
Coma Scale (GCS).While the GCS allows efficient,
standardized communication of a child’s state, a more
detailed description of the child’s clinical findings is often
more useful for relaying detailed information and detecting
changes over time.
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, but if done, should be
documented in the case records to avoid confusion in
interpretation. The pupillary light reflex is very resistant to
metabolic dysfunction. Unilateral pupillary dilatation in
the comatose patient should be as considered evidence of
oculomotor nerve compression from ipsilateral uncal
herniation, unless proved otherwise [8].
Brainstem Function The presence of oculocephalic (doll’s
eye), oculovestibular, corneal, cough and gag reflexes are
indicative of intact brainstem function. Abnormalities of
eye position and movement maybe informative. Conjugate
lateral deviation of the eyes is a sign either of an ipsilateral
hemisphere lesion, a contralateral hemisphere seizure focus,
or damage involving the contralateral pontine horizontal
gaze center (parapontine reticular formation) [8]. Lateral
gaze palsy may signal central herniation with compression
of bilateral sixth nerves. Tonic upward gaze has been
associated with bilateral hemispheric damage.
Motor Response The trunk, limb, position, spontaneous
movements, and response to stimulation must be observed
to look for any focal deficits (suggestive of post ictal
Todd’s palsy or structural abnormality), and posturing
(decerebrate or decorticate). Special attention should be
given to posturing because it often signals a brainstem
herniation syndrome [9]. Tonic-clonic or other stereotyped
If present, think of
Cerebral malaria, Intracranial bleed, Hemolytic uremic syndrome
Hepatic encephalopathy, leptospirosis, complicated malaria
Meningococcemia, Dengue, Measles, Rickettsial diseases,
Arboviral diseases
Dengue, Meningococcemia, Hemorrhagic fevers
Traumatic/non-accidental injury
Possibility of seizures
Diabetic ketoacidosis, hepatic coma
Indian J Pediatr (2010) 77:1279–1287
movements signal seizures. Myoclonic jerks are seen with
anoxic and hepatic encephalopathy. Dystonias signify
extrapyramidal involvement which maybe seen in Japanese
B encephalitis, tubercular meningitis, inborn errors of
metabolism or metoclopramide toxicity.
Other Neurological Findings xFundus examination must be
performed to look for papilledema and retinal hemorrhages.
Papilledema is very rare in acute encephalopthies. 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 [3].
Herniation Syndromes Brain tissue deforms intracranially and
moves from higher to lower pressure when there is asymmetric,
unilateral or generalized increased intracranial pressure [3].
This gives rise to the various herniation syndromes (Table 3).
Signs of herniation tend to progress in a rostrocaudal manner
[9]. The importance lies in recognition and prompt treatment,
before the damage becomes irreversible.
Investigations
These maybe divided into standard basic investigations
which must be performed in all children presenting with
coma, and second line investigations.
Basic Investigations
Immediate blood glucose by reagent strips should be
performed to rule out hypoglycemia. A complete blood count
and blood biochemistry must be obtained. The total leukocyte
count maybe raised or depressed in severe infections. The
Table 3 Clinical recognition of herniation syndromes
Type of Herniation
Subfalcine herniation (medially of the cingulate gyrus)
Central transtentorial (downward of diencephalic
structures)
Lateral transtentorial (downward and medially of
uncus and parahippocampal gyrus)
Upward Transtentorial (upward of the cerebellar
vermis and midbrain)
Transforaminal (downward of cerebellar tonsils
and medulla)
a
Clinical signs of potentially reversible brain herniation
1285
blood biochemistry should include glucose, sodium, potassi-
um, calcium, magnesium, renal and liver function tests,
arterial blood gas analysis and lactate. Urine should also be
examined for reducing sugars and ketones. Blood and urine
cultures should be taken. A peripheral smear and rapid
diagnostic test for malarial parasite should be obtained.
Ideally in all children with impaired consciousness, a
Computed tomography (CT) scan of the cranium should be
obtained. Exceptions may include a known uncomplicated
metabolic-toxic cause of coma, e.g. diabetic ketoacidosis or
hypoglycemia. CT is helpful in looking for features of
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. If a patient is febrile, infection
is suspected, or no other etiology can be determined, then a
lumbar puncture should be performed. If clinical or radiologic
evidence is present for intracranial hypertension, or lumbar
puncture is otherwise contra-indicated (thrombocytopenia,
shock, local infection), it should be deferred and treatment
should be initiated for possible infections (bacterial and viral).
A normal CT does not rule out elevated intracranial pressure.
Cerebrospinal fluid should be tested for cell count, glucose,
protein, Gram stain, Ziehl-Neelsen stain, bacterial culture,
viral polymerase chain reaction for Herpes Simplex virus,
Latex agglutination test, and additional cultures guided by
clinical suspicion (fungal or tubercular).
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
and stopping feeds. Hyperammonemia maybe caused by
some inborn errors of metabolism, Reye’s syndrome, liver
failure or valproate toxicity.
Clinical manifestations
Impaired consciousness, monoparesis of the contralateral lower extremitya
Impaired consciousness, abnormal respirations, symmetrical small reactivea
or midposition fixed reactive pupils, decorticatea evolving to decerebrate
posturing
Impaired consciousness, abnormal respirations, third nerve palsya
(unilateral dilated pupil, ptosis), hemiparesisa
Prominent brainstem signs, downward gaze deviation, upgaze palsy,
decerebrate posturing
Impaired consciousness, neck rigidity, opisthotonus, decerebrate rigidity,
vomiting, irregular respirations, apnea, bradycardia
1286
Magnetic Resonance Imaging (MRI) Magnetic resonance
imaging (MRI) with Magnetic resonance Angiography is
the preferred modality of investigation if the patient
presents with a stroke. MRI is also invaluable in identifying
evidence of frontotemporal pathology in herpes simplex
encephalitis, thalamic involvement in Japanese B enceph-
alitis, demyelination in ADEM, or necrotizing lesions in
acute necrotizing encephalopathy [10, 11]. MRI is also
useful for prognostication.
Electroencephalogram (EEG) An electroencephalogram is
useful in evaluation of patients with altered sensorium.
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 dis-
charges, suggesting herpes encephalitis [12].
Other Investigations A urine toxicology screen should be
obtained when no cause is obtained on clinical evalua-
tion, or there is a clinical suspicion of poisoning. Other
investigations in unexplained coma include thyroid
function tests and thyroid antibodies (for Hashimoto
encephalopathy) and work-up for central nervous system
vasculitis.
Treatment
Management of a child with coma usually proceeds
simultaneously with the clinical evaluation (Fig. 1). The
goals of treatment are:
& Stabilization of vitals: airway, breathing and circulation
& Identification and treatment of brain herniation and raised
intracranial pressure: hyperventilation, mannitol/3% sa-
line etc. Mannitol is administered as an initial bolus of
0.25–1 g/kg (the higher dose for more urgent reduction of
ICP) followed by 0.25–0.5 g/kg boluses repeated every 2–
6 h as per requirement. Hypertonic saline is administered
as a continuous infusion at 0.1 to 1.0 mL/kg/h, to target a
serum sodium level of 145–155 meq/L.
& 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.
Lorazepam should be given (0.1 mg/kg), followed by
Indian J Pediatr (2010) 77:1279–1287
phenytoin loading (20 mg/kg). 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.
& Treatment of infections. In case of suspected sepsis/
meningitis, broad spectrum antibiotics (ceftriaxone, van-
comycin) should be instituted immediately. If viral
encephalitis is likely, then samples for PCR for herpes
simplex virus should be sent and acyclovir should be
started (dose). Antimalarials (quinine/artesunate) should be
started if there is a clinical suspicion of cerebral malaria.
& Antidotes: Naloxone (0.1 mg/kg) should be used in case
of suspected opiate poisoning. Flumazenil is useful for
benzodiazepine overdosage.
& Steroids are of benefit in acute disseminated encephalo-
myelitis, meningococcemia with shock, enteric encepha-
lopathy, tubercular meningitis, and pyogenic meningitis.
& If metabolic causes have been identified, e.g. diabetic
ketoacidosis, hepatic encephalopathy, uremia or hyper-
ammonemia, these should treated appropriately.
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 (Fig. 1). 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, and speech and motor
disturbances. Nosocomial infections are important com-
plications during hospitalization, and must be prevented
and treated promptly.
Prognosis
The outcome of coma depends on the etiology, depth and
duration of impaired consciousness. In one study, of the
283 episodes of pediatric coma (defined as GCS <12 for at
least 6 h), mortality at 1 yr ranged from 3% (intoxication) to
84% (accident), depending on etiology [1]. Prolonged coma
after a hypoxic-ischemic insult carries a poor prognosis
[13]. Most children surviving infectious encephalopathies
have a comparatively better outcomes, often surviving with
mild or moderate difficulties only [14, 15]. 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 hypoten-
sion [16]. These children should be followed up for early
Indian J Pediatr (2010) 77:1279–1287
identification of developmental disabilities, learning and
behaviour problems, as well as other neurological sequelae
such as motor, visual or hearing deficit and seizure disorder.
References
1. Wong CP, Forsyth RJ, Kelly TP, et al. Incidence, aetiology, and
outcome of non-traumatic coma: a population based study. Arch
Dis Child. 2001;84:193–9.
2. McCarthy ML, Serpi T, Kufera JA, et al. Factors influencing
admission among children with traumatic brain injury. Acad
Emerg Med. 2002;9:684.
3. Taylor DA, Ashwal S. Impairment of consciousness and coma. In:
Swaiman KF, Ashwal S, Ferriero DM, editors. Pediatric neurol-
ogy: principles and practice. 4th ed. Philadelphia: Elsevier
Publications; 2006. p. 1379–400.
4. Multi-Society Task Force on Persistent Vegetative State.
Medical aspects of persistent vegetative state. N Engl J Med.
1994;330:1572–9.
5. Giacino JT, Ashwal S, Childs N, et al. The minimally conscious
state. Neurology. 2002;58:349–53.
6. Task Force for the Determination of Brain Death in Children.
Guidelines for the determination of brain death in children.
Pediatrics. 1987;80:298.
1287
7. Bates D. The management of medical coma. J Neurol Neurosurg
Psychiatry. 1993;56:589–98.
8. Stevens RD, Bhardwaj A. Approach to the comatose patient. Crit
Care Med. 2006;34:31–41.
9. Brazis PW, Masdeu JC, Biller J. Coma. In: Brazis PW, Masdeu
JC, Biller J, editors. Localization in clinical neurology. 4th ed.
Philadelphia: Lippincott Williams and Wilkins; 2001. p. 559–
86.
10. Murthy SNK, Faden HS, Cohen ME, et al. Acute disseminated
encephalomyelitis in children. Pediatrics. 2002;110:e21.
11. Domingues RB, Fink MC, Tsanaclis AM, et al. Diagnosis of
herpes simplex encephalitis by magnetic resonance imaging and
polymerase chain reaction assay of cerebrospinal fluid. J Neurol
Sci. 1998;157:148–53.
12. Misra UK, Kalita J. A comparative study of Japanese and herpes
simplex encephalitides. Electromyogr Clin Neurophysiol.
1998;38:41–6.
13. Kriel RL, Krach LE, Luxenberg MG, et al. Outcome of severe
anoxic/ischemic brain damage in children. Pediatr Neurol.
1994;10:207–12.
14. Grimwood K, Andersen P, Andersen V, et al. Twelve year
outcomes following bacterial meningitis: further evidence for
persisting effects. Arch Dis Child. 2000;83:111–6.
15. Lahat E, Barr J, Barkai J, et al. Long term neurological outcome
of herpes encephalitis. Arch Dis Child. 1999;80:69–71.
16. Johnston B, Seshia SS. Prediction of outcome in nontraumatic
coma in childhood. Acta Neurol Scand. 1984;69:417–27.