COMA

BY KAGYENDA FRED
 Content flow
• Definition
• Epidemiology
• pathophysiology
• Etiological classification
• Diagnosis
• Investigations
• Management
• Complications
• Prognosis
 Definition
Coma refers to a state of unconsciousness in which the
patient can not be aroused even with a painful stimuli.
• Coma is an extreme state of altered awareness
without spontaneous eye opening, verbalization or
purposeful response to external stimulation of any
type.ie a sustained state of Glasgow Coma Scale of 8
or less
• Coma is a peadiatric emergency indicating
significant CNS insult requiring a prompt
management
 Consciousness
• Consciousness is the state of awareness of
ones self and environment
Phases
Awake- Aware- Alert
 Grades of consciousness
• Delirium- state of agitation characterized by;
irritability, disorientation, fearful responses
and misperception
• Lethargy- difficult to maintain aroused state
• Obtundation - responsive to stimulation other
than pain
• Stupor- responsive only to pain
• Coma- unresponsive to pain
 Epidemiology
• Cerebral malaria was found to be the leading
cause of coma in children, accounting for
approximately 30% of cases. Bacterial
meningitis and head injuries were also
common causes of coma in pediatric patients.
• In terms of outcomes, children with coma in
Uganda have a poor prognosis, with a high
mortality rate among those with severe brain
injury or infectious causes of coma.
 Pathophysiology of Coma
• Maintaining alertness requires intact function of the cerebral
hemispheres and preservation of arousal mechanisms in the
reticular activating system
• Therefore, the mechanism of impaired consciousness must
involve both cerebral hemispheres or dysfunction of the RAS.
• Any condition that increases intracranial pressure (ICP) may
decrease cerebral perfusion pressure, resulting in secondary
brain ischemia. Secondary brain ischemia may affect the RAS
or both cerebral hemispheres, impairing consciousness.
• Impaired consciousness may progress to coma and ultimately
to brain death.
 continuation
1. Bilateral diffuse cortical lesion impairing all cortical
functions
• Unilateral cerebral hemisphere disorders are not
sufficient, although they may cause severe neurologic
deficits.
• However, rarely, a unilateral massive hemispheric focal
lesion (eg, left middle cerebral artery stroke) impairs
consciousness if the contralateral hemisphere is
already compromised or if it results in compression of
the contralateral hemisphere (eg, by causing edema).
 Continuation
2. Focal brain stem lesion affecting the
reticular activating system (RAS)
Reticular Formation is formed of large
number of neurons present through the
entire brainstem, it extends upward to the
level of the thalamus and downward to be
continuous with the interneurons of the
spinal cord.
 Functions of RAS
Sleep and arousal
• Varying level of consciousness is paralleled by changes in
neuronal activities, which can also be expressed in EEG.
• The ascending activating system (originate from reticular
nuclei to thalamus rather than to whole cerebral) increases
general level of sensory stimulation thus lead to increased
level of neuronal activities and increased arousal level.
• The noradrenergic neurons and histamine secreting neurons
also stimulate arousal level.
• Sleep inducing neurons, like serotonergic neurons of the
raphe nuclei could inhibit thalamus and cerebral function thus
decrease arousal level.
 continuation

Pain
• A descending inhibitory pathway could inhibit
transmission of pain.
• Peptide neurotransmitters (like opiate drugs,
morphine) released at synapses of
periaqueductal gray matter, raphe nuclei, and
dorsal horn of spinal gray matter could block
the pain sensation.
 Etiological classification
Traumatic coma
Non-traumatic coma
NB
Structural and non structural lesions
 Structural cause
• By mechanical force that brings about cellular
damage such as physical pressure or blockage
in neuronal transmission.
• This can be;
Supra-tentorial lesions ( hemispheres)
Infra-tentorial lesions ( Brainstem)
Diffuse axonal brain injury
 Non structural coma
• Common among the pediatric group
• It is limited to abberation of cellular function.
• It causes mild agitation and confusion but
progresses to obtundation, stupor and finally
complete unconsciousness.
Causes includes;
a) Drug intoxication
eg, Barbiturates, opiates and other sedative drugs
b) Metabolic disturbances
-Hypoxia/ anoxia
-diabetes mellitus (DKA)
-Hypoglycemia
-hyponatremia
-uremic encephalopathy in renal failure
-hepatic failure
-hypothermia
c) Infection
Cerebral malaria
-meningitis
-encephalitis
-cerebral abscess
-systemic spesis
d) Endocrine causes
-Hypo/hyperthyroidism
-Hypoadrenalism

e) Others
-epilepsy
-brain tumor
-functional (‘pseudo-coma’)
 Diagnosis of coma
This involves;
-History
-Examination from head to toe
-Detailed neurological examination
 History should include,
• Exact timing of onset of altered mental status
• Circumstances leading to coma
• Associated symptoms eg. convulsions, fever, vomiting, headache
etc
• Important previous medical eg chronic illnesses, malignany and
surgical history
• Previous psychological and neurological conditions including
previous episodes of coma
• History of immediate or recent trauma
• History of ingestion of drugs,toxins and any poisonous substances
• History of any bites and stings
 Physical examination
Vital signs
Heart rate
*Bradycardia -raised ICP
*Tachycardia - V-fib, AF
Blood pressure
*Hypertension - raised ICP, hypertensive
encephalopathy
*Hypotension - Decreased ICP
 Respiratory pattern

• Irregular - Brainstem lesion, RICP, Seizures

• Rapid-Acidosis, Aspirin ingestion
• Subdued and slow- Respiratory depression or
sedation.
• Cheyne-stokes - RICP
• Kussmaul - Acidosis
• Apneustic (periodic ) Breathing-Pontine damage,
Central herniation
 General examination
Skin
Ecchymosis - trauma, bleeding disorder
Cyanosis - Congenital cyanotic heart disease
Excess sweating - Hypoglycemia , shock
Decreased skin tugor - Dehydration, hypovolemic shock
Head
Battles sign - basal skull fracture( middle or posterior)
Retinal hemorrhages
Bulging frontanelles
Ears
CSF Otorrhea-fracture of middle base of skull
 Nose
Rhinorrhea - fracture of the anterior base of the
skull
Neck
Nuchal rigidity - meningitis
Pediatric response score
 Neurological examination
This is the most important
• GCS
• Cranial nerves
• sensory system
• Motor system
• Cerebellar signs
• signs of meningeal irritation eg kernig and
Brudzinski sign
• Signs of ICP
Glascow coma scale
 Pupils (Size, shape and reactivity)
•Pupillary reactions preserved - Metabolic cause for coma to be
considered.
•Small, symmetric and reactive - Intact midbrain
•Non reactive - Midbrain dysfunction(structural)
•Unilateral dilated and unresponsive - Ipsilateral 3rd nerve
compression secondary to herniation
•Small pinpoint pupils - Pons lesion, narcotics, barbiturate ingestion
•Mid position dilated - Central herniation, drugs like atropine,
scopolamine
•Large, unreactive dilated pupils - Medullary lesion

• .
 Motor response to painful stimuli
• More severe brain impairment - two typical reflex response to
painful stimuli are described.
• 1) Decorticate posturing - adduction of the arm at the shoulder
with the elbow flexion and leg extension - suggest contralateral
hemispheric or diencephalic damage.
• 2) Decerebrate posturing-arm extension, adduction and
hyperpronation with leg extension -
• Suggests more severe brain damage (upper brain stem
involvement including downward herniation). This is more
ominous sign.
• 3) Complete flaccidity - terminal event with compression of the
medulla.
 Brainstem reflexes
• 1. Oculocephalic reflex /Doll's Eye
• Holding the eyelids open; turn the head
briskly to each side.
• Normal response- Eyes shift to left when head
is turned to right and vice versa. (eyes remain
fixed on distant spot)
• Presence of Doll's eye movement suggest
brain stem damage. (Eyes move in concert
with head movements)
 Brain stem reflexes
• 2. Oculovestibular reflex / caloric test
• Putting ice water sequentially 15 minutes apart
in each ear to chill tympanic membrane
(confirm intactness of tympanic membrane).
• • Normal response -Right ear instillation->
rapid eye movement to the right side and
slowly return to midline. (Indicating intactness
of brainstem function.)
• • Absent response suggest brain stem damage
 Laboratory work up
1.Complete blood count, peripheral smear
2.Urine analysis
3.Blood smear, blood sugar
4.Serum electrolytes
5.Renal function tests
6.Liver function tests
7.Blood gases
8.Screening blood and urine for drugs and toxins
9.ECG/CXR
 Continuation…
10.CT brain - to look for hemorrhage
11.MRI brain - to look for infections,lesions and
masses
12.CSF analysis - to rule out infection, bleed
13.EEG – to rule out nonconvulsive status
epilepticus
 Differential diagnosis
Psychogenic coma – Patient may resist passive
eye opening and avoids passive arm faal over
face
Locked in state - Complete paralysis with
normal cerebral function
 Management
• Initial Stabilization
• 1st priority is stabilization of respiratory and hemodynamic
status (airway, breathing, and circulation management).
• Endotracheal intubation: Often required for airway protection
and adequate oxygenation
• Large bore IV lines should be placed and isotonic fluids
administered as needed to replace intravascular volume and
maintain adequate blood pressure.
• If there is hypoglycemia, give 2-4 mL of 25% dextrose (D25) per
kilogram IV (D10 if young infant).
•Evidence of increased ICP:
•Hyperventilate to decrease blood carbon dioxide
to 25-30 torr and give mannitol (0.5-1 g/kg IV).
•Can also give dexamethasone, 1-2 mg/kg IV
•Fluids given should be isotonic and the volume
limited to maintain adequate perfusion.
•Elevate head to 30 above horizontal to maximize
cerebral venous drainage
• Hospitalization is in the intensive care unit for close
monitoring for changes in respiratory status or signs
of increased ICP.
• IV antibiotics should be given if infection is suspected
• Administer medications to control seizures.
• Gastric aspiration and lavage in suspected poisoning
• Maintenance of normal temperature
• Correction of electrolyte imbalances
 Prognosis
Depends on etiology and duration of coma
• Non structural causes eg Metabolic coma -
better prognosis
• Structural cause of coma - worst prognosis
• longer the duration of coma - worse prognosis
 Complications

• Respiratory failure
• Deep venous thrombosis
• Pneumonia (aspiration and infection)
 REFERENCES
• Nelson s textbook of peadiatrics 20th Edition
2016
• Illustrated textbook of paediatrics ,5th edition.