Coma
Dr Mohamed I. Abunada
Pediatric Neurology
Dr Alrantisi specialized ped
Hospital
Definitions
 Coma is defined as a state of unresponsiveness
and unconsciousness
 Coma from the Greek word "koma,"
meaning deep sleep
 Coma can be a medical emergency
 That requires intervention without always knowing
the cause
 Knowledge of CNS anatomy can give clues to the
cause
Definitions of levels of arousal
(conciousness)
Alert (Conscious) - Appearance of
wakefulness, awareness of the self and
environment
Lethargy - mild reduction in alertness
Obtundation - moderate reduction in
alertness. Increased response time to stimuli.
Delirium -disturbed consciousness with motor
restlessness, disorientation and hallucination
Definitions of levels of arousal
(Consciousness)
Stupor - Deep sleep, patient can be
aroused only by vigorous and repetitive
stimulation. Returns to deep sleep when
not continually stimulated.
Coma (Unconscious) - Sleep like
appearance and behaviorally unresponsive
to all external stimuli (Unarousable
unresponsiveness, eyes closed)
Encephalopathy
 Encephalopathy describes a diffuse
disorder of the brain in which at least
two of the following symptoms are
present:
(1) altered states of consciousness,
(2) altered cognition or personality, and
(3) seizures.
 Encephalitis is an encephalopathy
accompanied by cerebrospinal fluid
(CSF) pleocytosis.
locked-in syndrome

a brainstem disorder in which the
individual can process information
but cannot respond .
Persistent Vegetative State PVS
 PVS is a form of eyes-open permanent
unconsciousness after recovery from coma with loss
of cognitive function and awareness of the
environment but preservation of sleep-wake cycles
and vegetative function.
 Survival is indefinite with good nursing care.
 The usual causes, in order of frequency, are anoxia
and ischemia, metabolic or encephalitic coma, and
head trauma.
 Anoxia-ischemia has the worst prognosis. Children
who remain in a PVS for 3 months do not regain
functional skills.
Glasgow Coma Scale GCS
Developed to define outcome in adult
patients with head injury
Coma: score of 8 or less
There is a modified scale used for infants
and children
Glasgow Score
 Eye opening
 Spontaneous 4
 To command 3
 To pain 2
 None 1
 Verbal
 Oriented 5
 Confused 4
 Inappropriate words 3
 Incomprehensible sounds 2
 None 1
Motor Response
obeys commands 6
localizes pain 5
withdraws to pain 4
abnormal flexion 3
abnormal extension 2
none 1
TOTAL 3-15
MODIFIED GLASGOW COMA
SCORE For Infants
 Eye opening
 spontaneous 4
 To speech
3
 To pain
2
 None
1
 Verbal
 Coos
5
 Irritable cries 4
 Cries to pain 3
 Moans to pain 2
 None
1
Motor
normal
withdraws to touch
withdraws to pain
abnormal flexion
abnormal extension
none
6
5
4
3
2
1
GCS
Individual elements as well as the sum of
the score are important.
 The score is expressed in the form "GCS 9
= E2 V4 M3 at 07:35

Generally, coma is classified as:
 Severe, with GCS ≤ 8
 Moderate, GCS 9 - 12
 Minor, GCS ≥ 13.
Causes of COMA
Causes of Impaired Consciousness
Possible Causes
 Alcohol
 Epilepsy
 Insulin, Intoxication
 Overdose
AEIOU TIPS
Uremia (and other metabolic causes)
 Trauma
 Infection
 Psychiatric
 Stroke, Syncope
Epileptic
Absence status
 Complex partial seizure
 Post epileptic depression

Hypoxia-ischemia
 Shock
 Cardiac or pulmonary failure (Cardiac
arrest, arrhythmia, CHF)
 Near drowning
 Carbon monoxide poisoning
 Strangulation
Hypoxia and Ischemia
 Hypoxia and ischemia usually occur together
 acute anoxia results in immediate loss of
consciousness.
 Prolonged hypoxia causes personality change
first, then loss of consciousness;
 Prolonged hypoxia can result from
 severe anemia (oxygen-carrying capacity reduced by at least half),
 congestive heart failure,
 chronic lung disease, and
 neuromuscular disorders.
Diagnosis.
Cerebral edema is prominent during the first
72 hours after severe hypoxia.
CT during that time shows decreased density
with loss of the differentiation between gray
and white matter.
Severe, generalized loss of density on the CT
scan correlates with a poor outcome.
An EEG that shows a burst-suppression
pattern or absence of activity is associated
with a poor neurological outcome or death.
BURST SUPRESSION
 pattern of burst of slow and mixed waves
often of high amplitude alternating with a
flat baseline.
 It is usually seen after severe brain injury
such as post ischemia or post anoxia
 Maintaining oxygenation, circulation, and blood glucose
concentration is essential.
 (hyperventilation) Regulate intracranial pressure to levels that
allow satisfactory cerebral perfusion
 Anticonvulsant drugs manage seizures
 Anoxia is invariably associated with lactic acidosis. Restoration of
acid-base balance is essential.
 barbiturate coma to slow cerebral metabolism is common
practice .
 Hypothermia prevents brain damage during the time of
hypoxia and ischemia but has questionable value after the
event.
 Corticosteroids do not improve neurological recovery in
patients with global ischemia after cardiac arrest.
Causes of Impaired Consciousness
cont.
STRUCTURAL
 TRAUMA
 NEOPLASMS
 VASCULAR DISEASE
 FOCAL INFARCTION
 HYDROCEPHALUS
Stroke
Infectious Causes of Coma
 Bacterial meningitis
 Brain abscess
 Epidural, subdural empyema
 Fungal meningitis
 Viral encephalitis
 Postinfectious encephalomyelitis ADEM
Viral encephalitis
Enteroviruses and herpes simplex virus (HSV)
are now the most common viral causes of
encephalitis in children.
 Specific viral identification is possible,
however, in only 15% to 20% of cases.
 In addition to viruses that directly infect the
brain and meninges, encephalopathies may
follow systemic viral infections. These
probably result from demyelination caused by
immune-mediated responses of the brain to
infection.

Acute disseminated encephalomyelitis
(ADEM)
 Immune-mediated disease of
brain. It usually occurs
following a viral infection or
vaccination, but it may also
appear spontaneously.
 Abrupt onset and a
monophasic course.
 Symptoms usually begins 1-3
weeks after infection or
vaccination.
 Major symptoms are fever,
headache, drowsiness,
seizures and coma.
BRAIN ABSCESS
Trauma
 Concussion
 Cerebral contusion
 Epidural hematoma
 Subdural hematoma/effusion
 Intracerebral hematoma
Parenchymal haemorrhage
May cause a rapid decline in consciousness,
from
1. Rupture into the ventricles
2. or subsequent herniation and brainstem
compression.
 Cerebellar haemorrhage or infarct with
1. Subsequent oedema
2. Direct brainstem compression, early
decompression can be lifesaving.
Lt frontoprietal intracerebral he (hyperdense)
Massive (midline shift)
Multifocal hematoma , lt fronal & temporal
Hge extending to fourth ventricle
EPIDURAL HEMATOMA
Rt frontoparietal epidural hematoma +cephalohematoma
SUBDURAL HEMATOMA
Subdural
bleeding
due to
tearing of
veins
Hgh in lateral ventricles
+ dilated ventricles
Metabolic Disorders
The inborn errors of metabolism that cause
states of decreased consciousness are usually
associated with hyperammonemia, hypoglycemia, or
organic aciduria.
Neonatal seizures are an early feature in most of
these conditions, but some may not cause
symptoms until infancy or childhood.
 Hypoglycemia
 Acidosis
 Hyperammonemia
 Uremia

Inborn errors with a delayed onset of
encephalopathy include disorders of pyruvate
metabolism and respiratory chain disorders
,glycogen storage diseases , and primary carnitine
deficiency.
DKA ( diabetic Ketoacidosis)
Hepatic coma
Hypernatremia The usual causes
Dehydration or overhydration with hypertonic saline
solutions.
Hypernatremia is a medical emergency and, if not
corrected promptly, may lead to permanent brain
damage and death.
Hyponatremia
 Hyponatremia may result from water retention,
sodium loss, or both.
 The syndrome of inappropriate antidiuretic hormone
secretion (SIADH) is an important cause of water
retention.
 Sodium loss results from renal disease, vomiting,
and diarrhea.
 Permanent brain damage from hyponatremia is
uncommon but may occur in otherwise healthy
children if the serum sodium concentration remains
less than 115 mEq/L for several hours.
Renal coma
 May occur in acute or chronic renal failure
 Raised blood urea alone cannot be
responsible for the loss of consciousness
but the
 Metabolic acidosis, electrolyte disturbances
and Water intoxication due to fluid
retention may be responsible
Toxic Causes
Immunosuppressive drugs
Substance abuse
Toxins
COMA
History and Physical
Examination
History and Physical Examination
Obtain a careful history of the following:
(1) the events leading to the behavioral
change;
(2) drug or toxic exposure (prescription drugs are more

often at fault than substances of abuse, and a medicine
cabinet inspection should be ordered in every home the child
has visited);
a personal or FH of migraine or epilepsy;
(4) recent or concurrent fever, infectious
disease, or systemic illness
(5) a previous personal or family history of
encephalopathy.
(3)
General Physical Exam
The important variables in locating the site of abnormality
are state of consciousness, pattern of breathing,
pupillary size and reactivity, eye movements, and
motor responses.
 The cause of lethargy and obtundation is usually mild
depression of hemispheric function.
 Stupor and coma are characteristic of much more
extensive disturbance of hemispheric function or
involvement of the diencephalon and upper brainstem.
Vital signs
 Fever (may mean infection)
 Very high temperature and dry skin – consider heat stroke
 Hypothermia often seen in drug intoxication
 BP
Skin examination
 Cyanosis
 Cherry red - carbon monoxide (almond odor)
 Café au lait spots - neurofibromatosis
 Shagreen patches - tuberous sclerosis
 Hyperpigmentation - Addison disease
 Petechiae and purpura - meningococcemia
 Signs of trauma – suspicious bruises
NEUROLOGIC EXAM
 Examination of the eyes, in addition to determining
the presence or absence of papilledema, provides
other etiological clues.
 Small or large pupils that respond poorly to light, or
impaired eye movements suggest a drug or toxic
exposure.
 Fixed deviation of the eyes in one lateral direction may
indicate that
(1)The encephalopathy has focal features
(2)Seizures are a cause of the confusional state
(3)Seizures are part of the encephalopathy.
The general and neurological examinations should
specifically include a search for evidence of trauma,
needle marks on the limbs, meningismus, and cardiac
disease.
Cranial Nerve Exam
 I. olfactory-smell
 II. Optic-Visual acuity, visual fields, pupils reaction, color
 III. Oculomotor - eye movement
 IV. Trochlear eye movement
 V. Trigeminal Nerve - facial sensation, corneals,
 VI. Abducens-eye movement
 VII. Facial nerve - motor and sensory to face
 VIII. Acoustic nerve - hearing
 IX. Glossopharyngeal - gag reflex, elevate palate
 X. Vagus - swallowing movement of the cords
 XI. Accessory Nerve - sternocleidomastoid muscle , trapezius
function
 XII. Hypoglossal nerve - tongue movement, fasciculations
Level of lesion
Level of lesion
Motor response
Pupillary
response
Respiratory
Pattern
Cortex
Flexion withdrawal
Small reactive
Normal or cheyne
stokes
Thalamus
Abn. Flexion
( decortication)
Small reactive
Normal or cheyne
stokes
Midbrain
Abn. Extension
(decerebration)
Fixed midposition
Hyperventilation
Pons
No response
pinpoint
Normal or
apneustic
Medulla
No response
Small reactive
irregular
Corneal reflex
 Test the fifth nerve sensory and seventh
nerve motor
 Cotton on cornea and look for a blink or
watch the lower eyelashes move toward
the midline
 Good test for mid and low pontine
dysfunction
Oculocephalic Reflex DOLLs Eye
 Tests-sensory from the eighth nerve
 Motor Part of the 3rd, 4th 6th nerves
 Can only be done in patient with stable
spine
 Turn the head quickly to the side and the
eyes should move to the opposite directions
of the movement
Cold Caloric Response
 Oculovestiublar reflex
 Tests the same pathway as doll’s eyes but can be done in
patient with unstable cervical cord.
 Elevate the head 30 degrees place a catheter in the ear
and inject ice water.
 In an awake patient: nystagmus COWS:
Cold water - fast component opposite
Warm water – Same side
 When supratentorial disease develops
 Due to metabolic depression of cortical function - the fast
component disappears and the eyes move toward the cold
water stimulus
Respiratory Pattern
 Injury location and type of breathing
 Post hyperventilation apnea -bilateral hemispheric
dysfunction or can result from bilateral damage
anywhere along the descending pathway between
the forebrain and upper pons
 Cheyne-stokes breathing (periods of hyperpnea
alternate with periods of apnea)
 Central Neurogenic Hyperventilation (formerly known as
Ondine’s curse) a sustained, rapid, deep
hyperventilation ,loss of involuntary respirationmedulla (Lesions just ventral to the aqueduct or
fourth ventricle)
Flexion of the upper
limb with extension of
the lower limb
(decorticate response)
and
extension of the upper
and lower limb
(decerebrate
response) indicate a
more severe
disturbance and
prognosis.
Infratentorial lesions
 Brainstem symptoms are often seen
initially
 Sudden onset of coma
 Cranial nerve abnormalities
 Alteration of the respiratory pattern
Progression of Lesions
Laboratory Work up
 CBC with diff PT,PTT, INR
 LFT’s
 Toxic screen
 Blood, urine culture
 Chest x-ray
 Urine ketones, glucose
 Electrolytes Ca, Mg, BUN, creatinine
Other Lab work
 Blood ammonia
 Lead levels
 Serum cortisol
 Skeletal survey
 Amino acid profile
 Blood pyruvate and lactate
 Organic acid analysis
Other test to consider
 EEG
 MRI
 Echocardiogram
 Head CT with contrast enhancement
promptly to exclude the possibility of
a mass lesion and herniation.
COMA
Treatment
TREATMENT OF ELEVATED ICP
 INTUBATION
 Hyperventilate for a short period of time
 Keep head elevated
 Midline position to enhance venous drainage into the
chest
 Check electrolytes
 Correct hyponatremia - produces brain swelling
 Restore low BP
Medical Intervention of increased ICP
 Decrease CSF
 Shunt fluid with external ventricultomy tube
 Diamox 25-100 mg/kg/day in 3 doses
 Reduce the size of other compartment
 Mannitol or 3% NaCl
 Mannitol –0.25 to 1.0 gm/ kg
 Infuse over 10 to 15 minutes
 Place foley
 May need to provide NS bolus to maintain BP
3% Na Cl
 Give as 5ml/kg bolus over an hour
 Can be given in peripheral IV
 Sodium movement across the blood
brain barrier is low.
 Therefore works similar to Mannitol
Treatment of elevated ICP
 Progression of treatment
 Mannitol, or 3% NaCl
 Sedation and pain medication
 Fever control
 Intubation
 ICP monitor and drainage of CSF
 Pentobarbital coma
 Surgery for decompression craniotomy
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