SUBJECT SEMINAR

ON COMA

Presenter : Dr.Mohan.T.Shenoy
Chairperson: Dr.Shivasharanappa
 References
• Nelson Textbook of Pediatrics 18th ed.
• Pediatric Neurology – Kenneth.F.Swaiman 3rd ed.
• Rogers' Textbook of Pediatric Intensive Care, 4th ed.
• Neurology in clinical practice, 4th ed Volume 1 by Walter
George Bradley
• Roberts - Manual of Clinical Problems in Pediatrics 5th ed
• Meherban Singh Pediatric Emergencies 4th ed.
• Pediatric & Neonatal emergencies by Sachdeva
• Fenichel: Clinical Pediatric Neurology, 5th ed.
• Pediatric Practical neurology by Veena Kalra
• Management of Pediatric Traumatic Brain Injury
Anaesthesia Tutorial of the week No.127 MARCH 30 2009
Definitions - Plum & Posner,1982
 Definitions
 Consciousness
State of wakefulness and awareness of self and surroundings.

 Sleep
Biological active state with identifiable behavioral and EEG stages

 Lethargy
State of reduced wakefulness with attention deficits.

 Obtundation
Blunted alertness with decreased interest in environment and
slower than normal reactivity to stimulation.

 Stupor
State of unresponsiveness with little or no spontaneous
movement, resembling deep sleep but differing from coma
because vigorous and repeated stimulation induces temporary
arousal.
 Coma Definition
“state of reduced neuronal activity with altered
consciousness characterized by loss of both
wakefulness (arousal, vigilance) and awareness of the
self and environment”

Sustained, pathologic state

Eyes closed
Unarousable unresponsiveness
Sleep-wake cycles are absent.

Transitory state that can evolve toward

Recovery of consciousness
A minimally conscious state
Vegetative state or
Brain death.
 Various states of consciousness

Conscious
Alert and oriented
state

Drowsy Sleepy but can be woken up

Stupor Unconscious but responds to vigorous stimulation

Coma Unconscious and unresponsive

All cognitive functions lost

Maybe awake
PVS But totally unresponsive
(Persistent 
May last for years
Vegetative
Breathing, circulation and internal
State)
organ functions intact.
 Other Terms
Confusional state:
 Inability to think without customary speed, clarity and coherence,
resulting in inattention and impaired perception or registration of
information
 misinterpretation of stimuli
 difficulty following commands
 disorientation (due to decreased cerebral oxygen consumption 20%
below normal)

Delirium
 confusional state accompanied by hyperactivity or
sympathetic overactivity (diaphoresis, tremor, arterial
hypertension, tachycardia)
Conditions Simulating coma

Akinetic Mutism
Locked in syndrome (pseudocoma)
Psychogenic unresponsiveness
Abulia
Catatonia
Vegetative state (coma vigil)
 Akinetic Mutism
 Coined by Cairns in 1941.

 Characterized by
Severe poverty of movement, speech and thought
No associated arousal disorder or descending
motor tract impairment.
 Apathy, and indifference to painful stimuli

 Hallmark feature
• marked dimunition in drive.
 EXAMPLES

Severe frontal lobe damage -loss of inhibitory control.

Olfactory groove meningioma.

Final stages of Creutzfeldt-Jacob disease.

Acute cases of encephalitis lethargica.

Stroke that affects both anterior cerebral territories.

Ablation of cingulate gyrus as in treatment of psychosis.

 Locked in syndrome
(deafferent or ventral pontine state)
(pseudocoma)
 Patient is awake and alert, but unable to move or speak.

 Pontine lesions affect lateral eye movement and motor

control

 Lesions often spare vertical eye movements and blinking.

Abulia
not able to use will power or to make decisions, cerebellar vessel
infarction
 Psychogenic unresponsiveness
 The patient, although apparently unconscious, usually shows
some response to external stimuli

 An attempt to elicit the corneal reflex may cause a vigorous

contraction of the orbicularis oculi

 Marked resistance to passive movement of the limbs may be

present, and signs of organic disease are absent

Catatonia
Rigid plastic posture of limbs in schizophrenia.
Vegetative state coma vigil, apallic syndrome
)

“Persistent unresponsive state with complete

unawareness of self and environment accompanied by
intact sleep-wake cycles with either partial or complete
preservation of hypothalamic and brain stem autonomic
functions”

IF COMA PRECEDES

•Re-emergence of eye opening and

•Spontaneous control of autonomic functions.
SUMMARY
Vegetative

Locked-in
PATHOPHYSIOLOGY
 COMA

RAS
(Diencephalon) COMA

(Pons, Medulla)
AROUSAL- the state of consciousness
 Ascending RAS, from the lower border of the pons to
the ventromedial thalamus

• occupy a paramedian area in the brainstem

 Depth of coma - Assess using GCS
Best eye Best verbal Best motor
response (E) response (V) response (M)
4 Eyes opening 5 Oriented 6 Obeys commands
spontaneously

3 Eye opening to 4 Confused 5 Localizes to pain

speech
2 Eye opening in 3 Inappropriate words 4 Withdraws from pain
response to pain
1 No eye opening 2 Incomprehensible 3 Flexion in response to
sounds pain

1 None 2 Extension to pain

1 No motor response
Glasgow Coma Scale (GCS)
z
 Evaluation
of
Comatose Child
 History
 Sudden onset in an otherwise normal,awake child
 Convulsions / Intracranial hemorrhage

 Preceded by sleepiness or unsteadiness

Ingestion of drug/toxin

 Precede by fever

Acute Infectious process which lead to complications

ADEM
Reye's syndrome
Cerebral malaria

 Associated headache
Raised Intracranial pressure (from hydrocephalus / neoplasm)
Migraine syndromes
 Use of unkerosenated stove/heater
Carbon Monoxide posioning

 Lucid Interval
Traumatic brain injury – extradural hematoma

 Underlying previous diseases

Diabetes – hypoglycemia,ketoacidosis
Congenital heart diseases

 Intermittent episodes of coma

Drug overdosage
Toxidromes
Inborn errors of metabolism
 Munchausen syndrome by proxy
•RECURRENT ENCEPHALOPATHY

 Inborn errors of metabolism

 Epilepsy
 Mitochondrial disorders
 Mental disorders
 Migraine
 Substance abuse
 GENERAL PHYSICAL EXAMINATION
Inspection
Head,Scalp
Skin
 Cyanosis
 Icterus
 Extreme pallor
 Cherry-red color
 Rashes
 Hypermelanosis
Needlemarks
Odor
Fruity
 Musty
Ammoniacal
 Alcoholic
 Signs of trauma
Boggy scalp swelling
Battle sign
Raccoon eyes,
Retinal hemorrhages,
Hemotympanum,
Bruises,
hematomas.
 Vital signs
 Hypothermia

Sepsis
Hypothyroidism
Enviromental exposure

 Hyperthermia
CNS infection
Sepsis
Heat stroke
Thyrotoxicosis
Stroke
Drugs - Salicylates,Anticholinergics,Sympathomimetics)
 Hypotension:

•Shock
•Sepsis
•Drugs
•Adrenal insufficiency
•Myocardial injury

 Hypertension :
 ICH
Thyrotoxicosis
Exposure to sympathomimmetic agents

 Bradycardia

↑ ICP
Hypothyroidism
Calcium channel blockers or ß-blockers
 Cheyne-Stokes

Central Neurogenic Hyperventilation

Apneustic

Cluster

Ataxic
NEUROLOGICAL
EXAMINATION
Abnormal Posture in Coma
 Flexion of the elbows and wrists and arm supination
(decortication)
decortication

It is uncommon in children except after head injury

and indicates hemispheric dysfunction with brainstem
integrity above the midbrain

 Extension of the elbows and wrists with pronation

(decerebration)
decerebration

indicate a more severe disturbance and prognosis.

damage to the corticospinal tracts in the midbrain or
caudal diencephalon.
Arm extension with minimal leg flexion or flaccid legs
Metabolic coma, especially after acute hypoxia,
also may produce vigorous spontaneous
extensor rigidity.

Posturing may coexist with purposeful limb

movements, usually reflecting subtotal damage
to the motor system

Flaccidity with no response to painful stimuli

has gravest prognosis with injury sustained to
deep brain structures
 Ocular and motor responses
Assess the following to help determine whether etiology is
structural or medical. Asymmetry points to a structural
lesion.

 a. Pupillary size. Normal or asymmetric?

 b. Pupillary reflex. Fixed or reactive?

 c. Extraocular movements. Normal, asymmetric, or

absent?

 d. Motor response to pain. Decorticate, decerebrate, or

flaccid?
 Oculocephalic (doll's head) response

 Rotating the head from side to side and

observing the position of the eyes.

If the eyes move conjugately in the opposite

direction to that of head movement, the
response is positive and indicates an intact
pons mediating a normal vestibulo-ocular
reflex
 Reflex movements

•tested by moving the head from side to side or

vertically, first slowly then briskly;
•eye movements are evoked in the opposite direction
to head movement.

 Generated by brainstem mechanisms originating in the

labyrinths and cervical proprioceptors.

 Normally suppressed by visual fixation mediated by

the cerebral hemispheres in awake patients but
appear as the hemispheres become suppressed or
inactive.
 Caloric oculovestibular responses

 Requires intact cerebropontine connections.

 Installation of ice-cold water into the external auditory

meatus, having confirmed that there is no tympanic
rupture.

 Normal response in a conscious patient

• nystagmus with the quick phase away from the

stimulated side.
 Ocular movements
 The position of the eyes at rest

 Presence of spontaneous eye movement

 The reflex responses to oculocephalic and

oculovestibular maneuvers

 Diffuse cerebral involvement but intact brainstem

function, slow roving eye movements can be
observed
 Frontal lobe lesion
• Deviation of the eyes towards the side of the
lesion.
 Lateral pontine lesion
• Conjugate deviation to the opposite side

 Midbrain lesion
• Conjugate deviation downwards

 Structural brainstem lesion disconjugate ocular

deviation
 Signs of lateralization
Unequal pupils
Deviation of the eyes to one side
Facial asymmetry
Turning of the head to one side
Unilateral hypo-hypertonia
Asymmetric deep reflexes
Unilateral extensor plantar response (Babinski)
Unilateral focal or Jacksonian fits
Signs of herniation

Dilated nonreactive pupil

Papilledema,
Posturing

Increased intracranial pressure

Cushing triad -hypertension, bradycardia, irregular

respiration

 If present,

provide controlled mild hyperventilation,

consider administration of mannitol or normal saline,
obtain emergent CT scan of the head and neurosurgical
consultation.
CAUSES
MNEMONIC for causes of COMA
Tips from vowels

T - Trauma, Head injury

I - Intussuception,Insulin,Hypoglycemia,Inborn errors of
metabolism
P – Psychogenic
S – Seizures,Shock, Stroke
A - Alcohol ingestion, Abuse
E – Electrolytes,Encephalopathy
I – Infections
O - Overdose, Ingestion
U - Uremic encephalopathy
 ADEM
 Monophasic autoimmune demyelinating disease of the CNS
following a vaccination
nonspecific upper respiratory tract infections
CENTRAL NERVOUS SYSTEM
INFECTION

Meningitis
Meningoencephalitis
Encephalitis
Subdural or epidural empyema, and
Brain abscess
 Important treatable causes

Bacterial meningitis,
Herpes simplex encephalitis,
Bacterial abscess,
Cerebral toxoplasmosis, and
Tuberculosis meningitis
 Complications
Cerebrovascular infarction
Cerebritis
Cranial nerve compression
Development of hydrocephalus
subdural effusions
cerebral edema
cerebral herniation.
MANAGEMENT
 RAISED
Intracranial
Pressure
 Reference Ranges
 2 mm Hg (27 mm H2O) in neonates

 5 mm Hg (68 mm H2O) in young infants

 6–13 mm Hg (82–177 mm H2O) in 1–7 years of age

 5–15 mm Hg (65–204 mm H2O) in adults.

 Threshold of 20 mm Hg usually accepted for

starting active treatment
 Cerebral perfusion pressure = systemic arterial pressure
– ICP

 Normal cerebral perfusion pressure is between 50 to 55 mm

of Hg.

 A drop below 50 mm is generally associated with ischemic

brain injury

 Increased ICP reduces cerebral blood flow

 CT scan may be normal if ICP elevation occurs acutely.

 Infants develop less ICP due to sutural seperation

 Most patients with non-traumatic encephalopathies have

raised ICP,although papilledema may be absent
Systolic Blood Pressure
 Monro-Kellie doctrine
“Skull is a rigid cavity and that its contents are relatively non-
compressible and consist of the brain parenchyma, intravascular
blood and CSF and Expansion in the volume of any one
compartment is likely to occur at the expense of the other two”

Intracranial volume
brain tissue (70%),
cerebrospinal fluid (10%),
cerebral blood volume (10%)
interstitial water (10%).

 Although the Monro-Kellie doctrine is a useful concept,

it is not as consistently applicable to infants as it is to
adults.
 Monroe- Kellie Principle

Rogers (1996) Textbook of Pediatric Intensive Care p. 646

 Treatment of raised intracranial
pressure
1. Maintain adequate cerebral perfusion pressure and cerebral
perfusion

Treatment of shock
Limitation of excessive hyperventilation

2. Prevent hypoxia and hypercarbia

Tracheal intubation/controlled ventilation

Seizure treatment and prophylaxis

3. Decrease cerebral blood volume

Acute hyperventilation
 Treatment (contd.)
4. Decrease brain tissue volume

Mannitol
Dexamethasone for vasogenic edema

5. Decrease cerebrospinal fluid (CSF) volume

CSF drainage
Acetazolamide

 6. Removal of mass lesion

Surgical removal/decompression
 Complications
 The clinical course of a child in coma largely depends
on the underlying illness and timing of treatment.

 Because the child's neurologic function will evolve

over time, frequent serial examinations may be
essential for diagnosis, identification of complications,
and prognostication.

 Neurologic complications of coma include

autonomic dysfunction,
increased ICP,
cerebral herniation,
seizures, and
metabolic derangements that may prolong the comatose state.
Signs of Herniation / Increased ICP
 Headache, nausea, vomiting
 Decreasing LOC
 Sixth nerve paresis (one or both eyes adducted)
 Decreased respiratory rate
 Cushing reflex
(hypertension/bradycardia/bradynpea)
 Papilledema
 Development of signs of herniation
Fixed and dilated pupil
Contralateral hemiparesis
Posturing
 Clinical Factors Associated with
Cerebral Edema

Prolonged Illness
Severe acidosis - low PA CO2
Severe dehydration
Bicarbonate therapy
Persistent hyponatremia
Excessive fluid admistration
 Core investigations
 A Dextrostix reading should be taking on all children
at the initial evaluation.

Even if results are normal, laboratory glucose testing

should be requested for confirmation, as hypoglycemia
alone may cause coma, and hypoglycemia in association
with other etiologies may worsen outcome.

 Hypoglycemia (capillary glucose <2.6 mmol/L) must

be treated urgently with an IV dextrose infusion.
 Hyperglycemia may occur in diabetic ketoacidosis
(capillary glucose >11 mmol/L, pH <7.3, and urine
ketones).
 Electrolytes should be measured on all patients, as
abnormalities may cause coma or may occur
secondary to intracranial abnormalities.

 A complete blood count with differential is indicated in

all patients to detect infection, anemia, disseminated
intravascular coagulopathy, lead encephalopathy, or
sickle cell disease.

 A blood gas should be performed on every patient.

 Liver function tests should be performed, as hepatic

encephalopathy may cause coma, and liver injury can
occur in the setting of systemic hypoxic ischemic
injury.
 Blood, urine, and stool cultures should be
obtained in most patients to investigate
infectious etiologies.
 Toxin screens should be performed in all
children and include acetaminophen, salicylate,
and ethanol.
 Specific tests for medications found in the home
should be conducted as necessary.

Ammonia, lactate, and pyruvate tests may be

performed in all patients to screen for metabolic
disorders.
If history is suggestive of metabolic disease,
measurement of organic acids, amino acids, and
acylcarnitine profile may be indicated.
 CT HEAD
 After resuscitation, a head CT should be performed
in all children to detect

 Intracranial hemorrhage,

 Space-occupying lesions (such as tumor or

abscess),

 Edema,

 Focal hypodensities (such as acute disseminated

encephalitis, herpes simplex encephalitis, infarct)

 Hydrocephalus.
 Cerebrospinal fluid
 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, lumbar
puncture should be deferred and treatment
should be initiated for possible infections
(bacterial and viral).
 A normal CT does not rule out elevated ICP.
 Cell count (both the first and last tubes should
be tested to help differentiate true findings in
the case of a traumatic tap), glucose,
protein, Gram stain, bacterial culture, viral
polymerase chain reaction, and additional
cultures when suspected clinically (fungal or
tubercular).
 EEG
Diagnostic as well as a prognostic role in coma

History of seizures
Eyelid blinking
Unexplained nystagmus
Nonconvulsive status epilepticus
 An EEG may detect useful background changes (such as
triphasic waves suggestive of metabolic encephalopathy or
sharp waves associated with herpes simplex encephalitis) and
may identify subclinical seizures.

 EEG may be required to detect subclinical seizures.

 If the cause of coma remains unknown, additional studies may

be directed at uncommon causes of coma in children, such as
Hashimoto encephalitis (thyroid function tests and thyroid
autoantibodies), cerebral vasculitis (erythrocyte sedimentation
rate, ESR; antinuclear antibody, ANA, panel; and possibly
angiography), or paraneoplastic disorders.

 Once the patient has been stabilized and the etiology of coma
remains unclear, a brain MRI may be performed for diagnostic
and prognostic purposes.
EEG findings in some conditions
causing coma
Two Classes of Brain Injury
PRIMARY SECONDARY
 SKULL FRACTURE  BRAIN SWELLING/EDEMA
 INCREASED INTRACRANIAL
 CONTUSION/ BRUISING PRESSURE
OF THE BRAIN  INTRACRANIAL INFECTION
 EPILEPSY
 HYPOXEMIA (LOW BLOOD
 HEMATOMA/BLOOD
OXYGEN)
CLOT ON THE BRAIN
 HIGH OR LOW BLOOD
PRESSURE
 DIFFUSE AXONAL  ANOXIA/HYPOXIA (LACK OF
INJURY OXYGEN TO THE BRAIN)
 Primary Brain Injury
 Occurs at the time of in initial injury

 May result in

 brain contusion,
 laceration,
 haematoma formation
 diffuse axonal injury.

 Younger children are more likely to develop subdural

haematomas and diffuse cerebral oedema without a skull
fracture

 Adolescents more likely to develop skull fractures,

contusions and extradural haematomas are more
common.
 Secondary Brain Injury
 Occurs in the minutes to days after the initial injury

 May be due to hypotension, raised intracranial

pressure or cerebral ischaemia.

 Worsened by hypoxia, hypercarbia, anaemia,

pyrexia, hypoglycaemia or hyperglycaemia.

 May be modified by simple clinical interventions,

avoidance of hypotension and hypoxia.

 Traumatic Head Injury

ALL-NET Pediatric Critical Care Textbook Source: LifeART EM

Pro (1998) Lippincott Williams & Wilkins.
Cerebral Contusion
oFocal haemorrhage

edema under impact

oSusceptible areas
Gyri in close contact
with the skulllobe
•Frontal
•Temporal lobes
 Cerebral haemorrhage
History of significant head injury

 Extradural haemorrhage may be present

even if lucid afterwards

Subdural haematoma & retinal haemorrhages

 consider non-accidental injury caused by

shaking or direct trauma.
Extradural haemorrhage

Usually associated with

a skull fracture.

Usually following direct

head trauma.

Arterial/venous bleeding
into the extradural
space
Subarachnoid Hemorrhage
 Much more common in adults.

 Presentation is usually with acute onset headache,

neck stiffness and occasionally fever, seizures and
coma may develop.

 Retinal haemorrhage is usually present.

 Haemodynamic stress in the susceptible intracranial

arteries

 Saccular or berry aneurysms

 Polycystic
Kidney disease
Ehlers–Danlos syndrome
 Marfan syndrome
 Onset is unpredictable
 Overall appears to occur at a surprisingly low
rate.
 Likelihood of having multiple intracranial
aneurysms estimated to be around 20%.
 Incidentally discovered unruptured aneurysms
bleed at a rate depending on size.
 Size<1 cm bleed @ 0.05% to 0.5% per year

 Size >1 cm bleed @ 1% to 2%.

About 40% die following the initial hemorrhage

but at a later stage.
 Rebleeding
• Rebleeding is the principal cause of death,
usually by raised ICP
• Occurs with a peak incidence in 1st 24 hours
after the initial event.

If the aneurysm is left unsecured,

• 20% in the first 2 weeks,
• 50% in the first 6 months,

• Thereafter 3% to 4% per year.

Subdural haematoma
Acute subdural

 In neonates by rupture
of the vein of Galen.

Chronic subdural

 Tearing of veins as they

cross the subdural space
between the arachnoid
and pia mater
Subdural haematoma
 Characteristic lesion in
non-accidental injury
caused by shaking or
direct trauma in infants or
toddlers.

 Retinal haemorrhages are

usually present.

 Occasionally seen
following a fall from a
considerable height.
Intracerebral Hemorrhage
MOST common cause:
Hypertensive

•Other causes:

•Traumatic
•Contusion,
•Coup/Contracoup

Rupture of small blood vessels

with bleeding inside parenchyma

Putamen
Cerebellar
Thalamic
Pontine ( 3 P’s)
 In young children

Initial presentation may be with anaemia and shock.

Often a lucid interval until the conscious level deteriorates
Seizures occur due to the enlarging haematoma acting as a
space-occupying lesion.

 Focal neurological signs

dilatation of the ipsilateral pupil,

paresis of the contralateral limbs and
a false localising uni- or bilateral VIth nerve paresis.

 Diagnosis confirmed with a CT scan.

 Management : Correct hypovolaemia.

 Surgical evacuation of the haematoma and arrest of the

bleeding may be required and can be urgent in some situations.
 INVESTIGATIONS
 A CT scan of the head usually identifies blood in the CSF.

 A lumbar puncture in the acute situation is best avoided as

haemorrhage may extend following the release of
intracranial pressure.

 The cause is often an aneurysm or arterio-venous

malformation (AVM). It can be identified on MR
angiography (MRA) or CT or conventional angiography.

 Treatment can be neurosurgical or with interventional

radiography.
CHILD ABUSE
Nonaccidental trauma (NAT), or
Child abuse
 Hypoxia and Ischemia

• Hypoxia = reduced blood oxygen content

• Ischemia = reduced tissue perfusion.

• Often go hand in hand because sustained

changes in tissue oxygenation have
secondary circulatory effects.

• Asphyxia = impaired gas exchange, as carbon

dioxide accumulates as oxygen falls.
• Longer periods of hypoxia produce cellular
injury.
• Neurons are more vulnerable than glial cells
to hypoxia and hypoglycemia.
• Oligodendrocytes are generally more
vulnerable
than astrocytes
• Factors determining selective vulnerability
of certain neuronal populations still incompletely
understood.
• Neurons in certain areas of the brain such
as the basal ganglia and the hippocampal CA1
pyramidal neurons are particularly vulnerable to
asphyxial injury.
• By contrast, spinal cord neurons tolerate longer
periods of occlusion than do cerebral neurons.
 Encephalopathy
 Encephalopathy from poor or absent cerebral
perfusion (both hypoxia and ischemia) often heralds
a poorer outcome than that from trauma; the
physician has little to offer to improve the outcome.

 Often there is diffuse, global brain injury.

 These children may have experienced a period of

asystole and may have required CPR, such as after
near-drowning episodes, acute life-threatening
events, smoke inhalation, upper or lower airway
obstruction, shock, or electrical injury.
 Severe anaemia

 Apnoea

 Asphyxiation
Carbon monoxide
Drowning

 Respiratory failure

 Shock (adrenal crisis, cardiogenic, septic,

hypovolaemic)

 Cerebrovascular event.
 PROGNOSIS
A poor prognosis is associated with

 Low GCS score (<5)

 Hypotension
 Cerebral edema
 Persistent apnea
 CPR for >25 min
 Persistent loss of cranial nerve reflexes
(gag,corneal)
 Coma for >24 hr
 MANAGEMENT OF
TRAUMATIC BRAIN INJURY
Children with head injury must be
assessed and appropriate management
started immediately.

Delays worsen outcome

particularly hypoxia, hypotension

 Minor head injury
The following signs are worrying and merit
admission of the child to hospital for close
monitoring, including regular neurological
assessments:

 Patients who are not fully alert

 Persistent vomiting
 Severe headache
 Moderate to severe head injury
 All children SHOULD be admitted for rapid assessment.

 The following features in the history and clinical condition indicate

the possibility of a severe head injury:

 History of a fall from a height,

 High-speed road traffic accident,
 Road traffic accident where the child is a pedestrian or a cyclist
 Loss or reduced level of consciousness
 External sign of skull fracture, including base of skull fracture
(‘panda eyes’, blood or CSF in the ear, bruising of the mastoid
process behind the ear)
 A Glasgow coma score of </= 8 or loss of ability to localise pain
on the motor category
 Disturbance of glucose metabolism
Diabetic Ketoacidosis

 Subacute onset with late development of coma.

 Marked ketoacidosis, usually above 40 mmol/l,
together with ketonuria.
 Secondary lactic acidosis (DD severe anoxia or
methyl alcohol or paraldehyde poisoning)
 Patients are dehydrated, rapid, shallow breathing,
occasionally acetone on the breath.
 The plantar responses are usually flexor until coma
supervenes.
 PATHOGENESIS
Glucose Ketones

Hyperglycaemia
Ketoacidosis
Glycosuria
is a state of Acidosis
uncontrolled catabolism
associated with
Osmotic insulin deficiency.
Vomiting
Diuresis
Fluid & Electrolyte
Depletion

Renal Hypoperfusion

Impaired Excretion of
Ketones & Hydrogen ions
Hyperglycaemic non-ketotic diabetic coma

 More commonly seen in the elderly.

 Coma is more common than with ketoacidosis.
 Profound cellular dehydration, risk of
developing cerebral venous thrombosis, which
may contribute to the disturbance of
consciousness.
 It may be induced by drugs, acute pancreatitis,
burns, and heat stroke
 Hypoglycaemic coma
 Much more rapid onset.
 Symptoms appear with blood sugars of less
than 2.5 mmol/l
 Initially autonomic: sweating and pallor, and
then inattention and irritability progressing to
stupor, coma, and frequent seizures.
 May present with a focal onset (hemiparesis)
 Plantar responses are frequently extensor.
 Patients may be hypothermic.
 Diagnosis of Hypoglycemic Coma

 Patient known to be taking insulin.

 Spontaneous hypoglycaemia with insulinomas
are usually diagnosed late.
 May be a long history of intermittent symptoms
and in relation to fasting or exercise.
 May also be precipitated by
hepatic disease
alcohol intake
Hypopituitarism
Addison's disease
 Treatment

 Glucose, together with thiamine

 Unless treated promptly, hypoglycaemia results in

irreversible brain damage.

 Cerebellar purkinje cells, cerebral cortex, and particularly

the hippocampus and basal ganglia are affected

 Dementia and a cerebellar ataxia are the clinical sequelae

of inadequately treated hypoglycaemia.
 Hepatic encephalopathy

1. Raise head end

2. IV cefotaxim and cloxacillin
3. IV fluid N/5 in 10% Dextrose
4. KCl added as per serum potassium
5. Lactulose through NG tube
6. Hepatic Coma feed
7. IV Rantidine 12 hrly
8. Mannitol 20% bolus then in maintenence doses
8. IV Vitamin K
 Brain Death
Guidelines suggested by American Academy
of Neurology (1995) are generally accepted.

The Academy urged caution in applying the

criteria to children younger than 5 years old, but
subsequent experience supports the validity of the
standards in newborns and through childhood.

Absence of cerebral blood flow is the earliest

and most definitive proof of brain death.
BRAIN DEATH
 Prognosis in coma
 In general, coma carries a serious prognosis

 Main determinants => Etiology,Duration,Depth

 Poor prognosis: Length of coma and increasing age.

 Brainstem reflexes early in the coma are an important

predictor.

 In general, cardiorespiratory arrest ,absence of pupillary

light and corneal reflexes 6 hours after the onset of coma
is very unlikely to be associated with survival
 RECOVERY PROSPECTS

 Recovery BEST in children due to primary epilepsy

 CNS infections have good survival rates.

 EXCELLENT for Coma due to depressant drugs

carries an provided that resuscitative and supportive
measures are available and anoxia not sustained.

 Metabolic causes, apart from anoxia, carry a better

prognosis than structural lesions and head injury
 POOR OUTCOME

o Shock
o Hypothermia
o GCS < 6
o Flaccidity
o Non-reactive pupils
o Areflexia
o Absent corneal reflexes
o Decerebrate / Decorticate posturing
o Fixed dilated pupils > 2hrs
 CONCLUSION
 Coma describes a state of altered wakefulness and
awareness caused by multiple conditions that affect the
brainstem or cortex diffusely.

 Coma is a medical emergency that requires rapid and

accurate evaluation.

 Management in a PICU with adequate monitoring till child

improves.

 Appropriate investigations required to find out cause which in

turn determines treatment.

 Complications, such as elevated ICP and seizures, must be

recognized and managed to prevent secondary neurologic
injury.
 Herniation Syndromes
 CPP = MAP – ICP: Must keep CPP >60 mm Hg
 Uncal Herniation:
Occurs when unilateral mass pushes the uncus
(temporal lobe) through the tentorial incisa, prersenting
as:
 Ipsilateral pupil dilatation
 Contralateral hemiparesis
 Deepening coma
 Decorticate posturing
 Apnea and death
 Herniation Syndromes
Cerebellar Herniation
Downward displacement of cerebellar tonsils
through the foramen magnum.
Presents as :
Medullary compression
Pinpoint pupils
Flaccid quadriplegia
Apnea and circulatory collapse
 BRAIN INJURY

Congenital brain injury Acquired Brain Injury

Pre-birth During birth After birth process

Traumatic Brain Injury

(external physical force)
Non-traumatic
Brain Injury
Closed Open Head
Head
Injury Injury

Savage, 1991
Neither definition includes “acquired”
brain injuries caused by internal
conditions, such as:

Stroke
Brain Infection
Tumor
Anoxia
Exposure to Toxic Substances