COMA
Definitions
1. Stuporous: The patient is unresponsive except when
subjected to repeated vigorous stimuli
2. Comatose: The patient is unarousable and unable to
respond to external events or inner needs, although reflex
movements and posturing may be present.
Etiology:
Coma is a major complication of serious central nervous
system disorders.
It can result from seizures, hypothermia, metabolic
disturbances, or structural lesions causing bilateral
cerebral hemispheric dysfunction or a disturbance of the
brain stem reticular activating system.
A mass lesion involving one cerebral hemisphere may
cause coma by compression of the brain stem.
Diagnosis
Glasgow Coma Scale
Eye opening response
Spontaneous………………………………………………………4
To speech…………………………………………………………...3
To pain…………………………………………………………………2
None…………………...........................................................1
Verbal response
Oriented………………………………………………………………5
Confused conversation………………………………………4
Inappropriate words…………………………………………..3
Incomprehensible sounds…………………………………..2
None……………………………………………………………………..1
Best upper limb motor response
Obeys…………………………………………………………………..6
Localizes……………………………………………………….……..5
Withdraws……………………………………………………………4
Flexion in response to pain…………………………………3
Extension in response to pain…………………………….2
None………………………………………………………………….…..1
Absence of brainstem function
As defined by the following:
a. Midposition or fully dilated pupils that do not respond to
light. Drugs may influence and invalidate pupillary
assessment.
b. Absence of spontaneous eye movements and those
induced by side-to-side passive head movements
(oculocephalic reflex) and ice water instillation in the
external auditory canal (ice water calorics).
c. Absence of movement of bulbar musculature, including
facial and oropharyngeal muscles. The corneal, gag,
cough, sucking, and rooting reflexes are absent.
d. Absence of respiratory movements when the patient is
off the respirator.
Assessment & Emergency Measures
The diagnostic workup of the comatose patient must
proceed concomitantly with management.
Supportive therapy for respiration or blood pressure is
initiated; in hypothermia, all vital signs may be absent and
all such patients should be rewarmed before the prognosis
is assessed.
The patient can be positioned on one side with the neck
partly extended, dentures removed, and secretions
cleared by suction; if necessary, the patency of the
airways is maintained with an oropharyngeal airway.
Blood is drawn for serum glucose, electrolyte, and calcium
levels; arterial blood gases; liver and renal function tests;
and toxicologic studies as indicated.
Dextrose 50% (25 g), naloxone (0.4-1.2 mg), and thiamine
(50 mg) are given intravenously.
Further details are then obtained from attendants of the
patient's medical history, the circumstances surrounding
the onset of coma, and the time course of subsequent
events.
Abrupt onset of coma suggests subarachnoid hemorrhage,
brain stem stroke, or intracerebral hemorrhage, whereas a
slower onset and progression occur with other structural
or mass lesions.
A metabolic cause is likely with a preceding intoxicated
state or agitated delirium.
On examination, attention is paid to the behavioral
response to painful stimuli, the pupils and their response
to light, the position of the eyes and their movement in
response to passive movement of the head and ice-water
caloric stimulation, and the respiratory pattern.
1. Stupor & Coma Due to Structural Lesions
Supratentorial mass lesions tend to affect brain function in
an orderly way.
There may initially be signs of hemispheric dysfunction,
such as hemiparesis.
As coma develops and deepens, cerebral function
becomes progressively disturbed, producing a predictable
progression of neurologic signs that suggest rostrocaudal
deterioration.
In contrast, a subtentorial (i.e. brain stem) lesion may lead
to an early, sometimes abrupt disturbance of
consciousness without any orderly rostrocaudal
progression of neurologic signs.
A structural lesion is suspected if the findings suggest
focality.
In such circumstances, a CT scan should be performed
before, or instead of, a lumbar puncture in order to avoid
any risk of cerebral herniation.
2. Stupor & Coma Due to Metabolic Disturbances
Patients with a metabolic cause of coma generally have
signs of patchy, diffuse, and symmetric neurologic
involvement that cannot be explained by loss of function
at any single level or in a sequential manner, although
focal or lateralized deficits may occur in hypoglycemia.
Moreover, pupillary reactivity is usually preserved, while
other brain stem functions are often grossly impaired.
3. Brain Death
An individual who has sustained either
a) Irreversible cessation of circulatory and respiratory
functions, or
b) Irreversible cessation of all functions of the entire
brain, including the brainstem
In order to establish brain death, the irreversibly
comatose patient must be shown to have lost all brain
stem reflex responses, including the pupillary, corneal,
oculovestibular, oculocephalic, oropharyngeal, and
respiratory reflexes, and should have been in this
condition for at least 6 hours.
Spinal reflex movements do not exclude the diagnosis, but
ongoing seizure activity or decerebrate or decorticate
posturing is not consistent with brain death.
The apnea test (presence or absence of spontaneous
respiratory activity at a PaCO2 of at least 60 mm Hg)
serves to determine whether the patient is capable of
respiratory activity.
Reversible coma simulating brain death may be seen with
hypothermia (temperature < 32°C) and overdosage with
central nervous system depressant drugs, and these
conditions must be excluded.
4. Persistent Vegetative State
Patients with severe bilateral hemispheric disease may
show some improvement from an initially comatose state,
so that, after a variable interval, they appear to be awake
but lie motionless and without evidence of awareness or
higher mental activity.
This persistent vegetative state has been variously
referred to as akinetic mutism, apallic state, or coma vigil.
Most patients in this persistent vegetative state will die in
months or years, but partial recovery has occasionally
occurred and in rare instances has been sufficient to
permit communication or even independent living.
5. Locked-In Syndrome (De-efferented State)
Acute destructive lesions (e.g. infarction, hemorrhage,
demyelination, encephalitis) involving the ventral pons
and sparing the tegmentum may lead to a mute,
quadriparetic but conscious state in which the patient is
capable of blinking and of voluntary eye movement in the
vertical plane, with preserved pupillary responses to light.
Such a patient can mistakenly be regarded as comatose.
Physicians should recognize that "locked-in" individuals
are fully aware of their surroundings.
The prognosis is variable, but recovery has occasionally
been reported-in some cases including resumption of
independent daily life, though this may take up to 2 or 3
years.
Treatment
Emergency Measures
The ABCs of resuscitation are pertinent:
Airway must be kept open with positioning or even endotracheal intubation.
Breathing and adequate air exchange can be assessed by auscultation; hand bag
respiratory assistance with oxygen may be needed
Circulation must be ensured by assessing pulse and blood pressure.
An intravenous line is always necessary. Fluids, plasma, blood, or even a dopamine drip
(5-20 ug/kg/min) may be required in cases of hypotension
An extremely hypothermic or febrile child may require vigorous cooling or warming to
save life.
The assessment of vital signs may signal the diagnosis.
Slow, insufficient respirations suggest poisoning by hypnotic drugs; apnea may indicate
diphenoxylate hydrochloride poisoning.
Nasogastric suction is initially important.
The bladder should be catheterized for monitoring urine output
and for urinalysis.
