Download coma: diagnosis and management

Dr. M.A. Sofi MD;FRCP
(London)FRCPEdin; FRCSEdin
DIAGNOSIS & MANAGEMENT
Coma definition:
A state of unconsciousness
lasting more than six
hours, in which a person:
 cannot be awakened
 fails to respond normally
to painful stimuli, light, or
sound
 lacks a normal sleep-wake
cycle
 does not initiate voluntary
actions.
Consciousness requires:
 An intact pontine
reticular activating
system
 An intact cerebral
hemisphere, or at least
part of a hemisphere
Coma requires: dysfunction
of either the:
 Pontine reticular
activating system, or
 Bihemispheric cerebral
dysfunction
NEUROLOGICAL ASSESSMENT
Consciousness is a state of
awareness of self and the
environment. This state is
determined by two separate
functions:
a) Awareness (content of
consciousness).
b) Arousal (level of
consciousness)
Coma is caused by disordered
arousal rather than
impairment of the content of
consciousness.
 Arousal depends on an intact
ascending reticular activating
system and connections with
diencephalic structures.
Coma is caused by:
 Diffuse bilateral hemisphere
damage.
 Failure of the ascending
reticular activating system, or
both.
Sites and causes of coma.
ARAS



Diffuse mass of
neurons & nerve
fibers that make
the core of the
brain stem.
Fibers run
through medulla
oblongata, pons &
midbrain.
Receives fibers
from the sensory
pathways via long
ascending spinal
tracts.
Ascending ReticularActivating System
It’s believed to be the
center of arousal and
motivation in mammals.
 Alertness, maintenance
of attention and
wakefulness.
 Emotional reactions,
important in learning
processes.

 Identify
causes(s) of a deteriorating conscious
level.
 Stabilize, evaluate, and treat the comatose
patient in the emergency setting.
 Use an organized, sequential, prioritized
approach.
 Use the Glasgow coma scale for assessment
of altered conscious level.
Altered levels of consciousness
 Altered level of

Drowsiness - this is similar to
obtundation and probably
represents a lesser loss of
consciousness

Obtundation: refers to less
than full alertness, typically as a
result of a medical condition or
trauma.

Stupor: Similar to coma in that
responsiveness is greatly
diminished. However, the
person can still be partially
roused by some stimuli, such as
pain
consciousness: Measure of
arousal other than normal.


Level of consciousness (LOC):
Measurement of a person's
arousability and responsiveness
to stimuli from the
environment.
Lethargy: A mildly depressed
level of consciousness or
alertness, can be aroused with
little difficulty.
Causes
I. Head Trauma
Coma may result from significant traumatic injury to the head, such as
from a car accident or fall.
II. Bleeding (Hemorrhage) into the brain or skull
Types of brain/skull hemorrhage include:
a. Intracerebral hemorrhage: bleeding within the brain tissue
b. Epidural hemorrhage: bleeding inside the skull, but outside the
dura, (the covering of the brain)
c. Subdural hemorrhage: bleeding inside the skull, and inside the
dura, but not in the brain tissue itself
d. Subarachnoid hemorrhage: bleeding in the space immediately
adjacent to the brain tissue
Coma: Causes
III. Causes of brain/skull hemorrhage include:
a. High blood pressure (hypertension)
b. Cerebral aneurysm: a weak spot in a blood vessel of the brain
c. Arteriovenous malformation (AVM): an abnormal cluster of
blood vessels
d. Tumors
IV. Swelling of the brain (cerebral edema)
Causes of swelling of the brain:
a. Infections
b. Metabolic imbalances
c. Traumatic injuries
d. Problems with the flow of cerebrospinal fluid (CSF)
Coma: Causes
V. Lack of oxygen to the brain
The most common causes for lack of oxygen to the brain include:
a. Heart arrhythmias
b. Lung disease, including pneumonia, emphysema, or asthma.
c. Anemia (low red blood cell count)
d. Toxins
VI. Poisons
External poisons are those that are ingested or inhaled.
Internal poisons are by-products of the body's normal
metabolism that for some reason cannot be excreted properly.
VII. Endocrine disorders
a. Myxedema coma (hypothyroidism)
b. Diabetes Mellitus: Hypoglycemia or Hyperglycemia
INVESTIGATIONS

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Capillary blood glucose.
Arterial blood gas.
Bloods - FBC, renal function,
LFTs, CK, TFTs, cardiac enzymes.
Urine dipstick and pregnancy
test (especially if seizures have
occurred in a woman of childbearing age).
Urine drug screen.
Paracetamol and salicylate
levels.
Blood cultures.
Thick and thin films for malaria.

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Ethanol levels.
12-lead ECG.
CXR.
CT scan of the brain/MRI scan
(especially with focal signs).
EEG and other
electroneurophysiological
tests. These can be useful for
determining prognosis - eg,
functional MRI.
Functional neuro-imaging is
likely to become very important
in making decisions regarding
outcome.
Other investigations: these will
in part depend on the
suspected cause - eg, lumbar
puncture, autoantibody screen
CLINICAL ASSESSMENT OF COMA
Coma is an acute, life threatening situation and evaluation must be
swift, comprehensive and include:
Resuscitation of CVS and respiratory system.
 Correction of blood glucose and thiamine
 Control of seizures
 Temperature
 Specific treatments— naloxone.
If Indicated
Assessment now should comprise:
1. History—through friend, family or emergency medical personnel
2. General physical examination
3. Neurological assessment—to define the nature of coma
CLINICAL ASSESSMENT OF COMA
The approach to clinical evaluation is used to categories coma into:
A. Coma without focal signs or meningism.
This is the most common form of coma and results from anoxicischaemic, metabolic, toxic, and drug induced insults, infections, and
post-ictal states.
B. Coma without focal signs with meningism.
This results from subarachnoid hemorrhage, meningitis, and
meningoencephalitis.
C. Coma with focal signs.
This results from intracranial haemorrhage, infarction, tumor or
abscess.
THE ABCD2E APPROCH TO COMA
A
AIRWAYS
B
BREATHING
C
CIRCULATION
D
DRUGS/DISABILITY
E
EXPOSURE
CLINICAL ASSESSMENT OF COMA
General examination
Neurological (general)
Skin: rash, anemia, jaundice
Head, neck and eardrum (trauma)
Temperature: (fever infection
hypothermia-drugs/circulatory
failure
Meningism (SAH/meningitis)
Blood pressure (for example,
septicemia/Addison's disease)
Fundoscopy
Breath (fetor hepaticus/alcohol)
Motor response
Cardiovascular (for example,
arrhythmia)
Deep tendon reflexes: Biceps,
Triceps, Brachioradialis, Patellar,
Achilis
Abdomen (organomegaly)
Muscle tone/Planters
CLINICAL ASSESSMENT OF COMA
Brain stem function
Respiratory pattern
Pupillary responses
Cheyne Stokes: hemisphere
Spontaneous eye movements Central neurogenic
hyperventillation:
Oculocephalic responses
rapid/midbrain
Caloric responses
Apneustic: Rapid with
pauses/lower
Corneal responses
pontine
Assesses patient’s
neurological
condition
Value range 3 -15
 3 totally comatose
patient


9-12 Moderate
altered conscious
level
15
fully alert
patient
Abnormalities of
respiration:
• Ataxic (Biot) breathing is
a random pattern of
shallow and deep breaths
interspersed with irregular
pauses – pontine lesions
• Apneustic breathing
involves repetitive gasps,
with pauses at full
inspiration lasting a few
seconds - pontine disease.
• Cheyne-Stokes
respiration is cyclic, with a
crescendo-decrescendo
pattern interrupted by
apneas – brainstem
lesions.
Systematic assessment of brainstem function
via reflexes
 Cranial Nerve Exam

◦ Pupillary light response (CN 2-3)
◦ Occulocephalic/calorics (CN 3,4,6,8)
◦ Caloric reflex test
◦ Corneal reflex (CN 5,7)
◦ Gag refelx (CN 9,10)
•
•
•
•
Pupillary light reflex (PLR) is a
reflex that controls the diameter
of the pupil, in response to the
intensity (luminance) of light.
Controls adaptation to various
levels of lightness/darkness.
A greater intensity of light
causes the pupil to constrict
(miosis).
lower intensity of light causes
the pupil to dilate (mydriasis,
expansion) (allowing more light
in).
Pupils: Localizing Value



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Unilateral pupillary
dilatation with lack of
response to light - suggests
uncal herniation of the
temporal lobe over the
tentorium entrapping the
third nerve.
Pupil fixed in the midposition with loss of light
reflex - typical of midbrain
lesions.
Small pupils with response
to light - lesions in the pons.
Fixed dilatation - suggests
significant damage to the
brainstem.
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

Horner's syndrome occurs
in lesions of the
hypothalamus or brainstem
and in diseases affecting
the wall of the carotid
artery.
Small pupils reacting
briskly to light - metabolic
cause (eg, hepatic or renal
failure).
Corneal reflexes: these are
normally intact until there is
a very deep coma. In drug
intoxication, they may be
absent in a patient
otherwise in a light coma.
Otherwise, loss of corneal
reflex is indicative of a poor
prognosis.
Pupils: Localizing Value
Bilateral pupillary constriction- Opiod toxicity
Dilated Rt.
Pupil & eye
deviated to
right
Normal
size
Lft.pupil &
eye midprimary
position
Pupils: Localizing Value
Horner’s syndrome
Midriasis-sympathetic
stimulation
Pupils: Localizing Value
Corneal Reflex
 Afferent:
Trigeminal Nerve
 Efferent: Third
Nerve (Bell’s
Phenomenon
and Facial Nerve
(Eye closure)
 Tests dorsal
midbrain (Bell’s)
and pontine
integrity (Eye
closure)
Gag Reflex

Definition: The gag reflex evaluates
the integrity of Cranial nerves IX and X

Test procedure: Using a long handle
swab stick (orange swab) gently and
briskly touch the pharyngeal wall
behind the pillars of the fauces.

Test findings:
◦ A positive gag reflex will produce a
non symmetrical elevation of the
uvula or the fauces.
◦ If there is no movement of the uvula
with the gag reflex and with saying
'ahh' this may signify bilateral
palatal muscle paralysis.
◦ In a normal gag reflex there will be a
symmetrical elevation of the uvula
or the fauces / tonsilar arches.



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Oculocephalic response in which the patient's head
is rotated from side to side and the position of the
eyes is observed.
The eyes will move together in the opposite direction
to the head movement - this is the normal
oculocephalic response (also called doll's eye
movement).
Flexion: eyes deviate up and eyelids open (doll’s
head phenomenon)
Extension: eyes deviate downward
Where a brainstem lesion is present this eye
movement is absent or asymmetric. This procedure
should only be done provided there is no neck
instability
Doll’s Eye reflex movement




Brisk rotation of head
with eyes held open
Watch for contraversive
movements
Flexion: eyes deviate
up and eyelids open
(doll’s head
phenomenon)
Extension: eyes deviate
Abnormalities are caused by lesions of
downward
the inner ear or brainstem, especially
the pons and midbrain.
Vestibulo-occular reflex
Caloric reflex test
caloric reflex test
is a test of the vestibuloocular reflex that
involves irrigating cold
or warm water or air
into the external
auditory canal.
The eyes should move
conjugately in the
direction opposite to
the cold irrigation and
same side to warm
irrigation. An abnormal
response (absent or
asymmetric) implies
brain stem disease.
One mnemonic used to remember the FAST direction of
nystagmus is COWS. COWS: Cold Opposite, Warm Same.
Eye movements: Spontaneous eye movements



Conjugate deviation of
the eyes - possible focal
hemispheric or brainstem
lesion.
Depression of the eyes lesion in the midbrain at
the level of the tectum.
Skew deviation of the
eyes - lesion at the
pontomedullary junction.


Unco-ordinated eye
movements - a small
amount of eye divergence
is normal in
unconsciousness but more
significant inco-ordination
suggests damage to the 3rd
or 6th nerves in the
brainstem or pathways.
Normal roving eye
movement - similar to
those of sleep - often
occurs in light coma, and
cannot be faked, so
excludes the possibility of
psychogenic
unresponsiveness (jerky
eye movement).
 Akinetic
mutism
 ‘Locked-in’ syndrome
 Catatonia
 Conversion reactions
Akinetic Mutism
Silent, immobile but
alert appearing
 Usually due to lesion
in bilateral mesial
frontal lobes, bilateral
thalamic lesions or
lesions in periaqueductal grey
(brainstem)

Many cases of akinetic
mutism have occurred
after a thalamic stroke
“Locked-In’ Syndrome
Infarction of basis
pontis (all descending
motor fibers to body
and face)
 May spare eyemovements
 Often spares eyeopening
 EEG is normal or
shows alpha activity

Bilateral Pontine Infarction
 Symptom
complex associated with
severe psychiatric disease with:
◦ stupor, excitement, mutism, posturing
◦ can also be seen in organic brain
disease: encephalitis, toxic and druginduced psychosis
 Fairly
rare
 Occulocephalics may or may not be
present
 The presence of nystagmus with cold
water calorics indicates the patient is
physiologically awake
 EEG used to confirm normal activity
Management

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Resuscitation - with
intubation and ventilation if
needed and rehydration.
Give intravenous thiamine
and glucose to all in whom
diagnosis is unclear.
Trial of naloxone or
flumazenil is easily done and
response is rapid.
Treat any underlying cause
(eg, antibiotics if meningitis
is suspected, surgery to
remove SD hematoma,
anticonvulsants, etc).



Raised intracranial
pressure may require
mannitol infusion.
If there is a risk that the
patient may have aspirated
then they should be
covered with antibiotics.
Fluid rehydration,
prevention of pressure
sores and adequate
nutrition should also be
focused on.[
Prognosis

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Head injury then prognosis is
directly proportional to the
GCS score
The lack of brainstem and
lateralising signs suggests the
cause is most likely metabolic
and potentially reversible.
Drug overdose - good
prognosis with appropriate
treatment.
Coma not due to head injury
or drug overdose, lasting
longer than six hours - only
10% chance of recovery.

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Subarachnoid haemorrhage
or stroke - <5% chance of
recovery.
Hypoxia or ischaemia (eg,
after cardiac arrest) - ~10%
chance of recovery.
Coma >24 hours - 10%
chance of recovery.
After one week - 3% chance
of recovery.
After seven days - high
incidence of death/persistent
vegetative state (PVS).
Absence of brainstem
reflexes for 24 hours
(without sedative drugs) very little chance of recovery.