UNCONSCIOUS PATIENT

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UNCONSCIOUS
PATIENT
Dr. M. Sofi MD; FRCP (London);
FRCPEdin; FRCSEdin
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.
a) Arousal depends on an intact:
ascending reticular activating
system
b) 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
ASCENDING RETICULAR ACTIVATION SYSTEM - ARAS
• 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
• Clouding of consciousness is a
very mild form of altered
mental status in which the
patient has inattention and
reduced wakefulness.
• Confusional state is a more
profound deficit that includes
disorientation, bewilderment,
and difficulty following
commands.
• Lethargy consists of severe
drowsiness in which the
patient can be aroused by
moderate stimuli and then
drift back to sleep.
• Obtundation is a state similar
to lethargy in which the patient
has a lessened interest in the
environment, slowed
responses to stimulation, and
tends to sleep more than
normal with drowsiness in
between sleep states.
• Stupor means that only
vigorous and repeated stimuli
will arouse the individual, and
when left undisturbed, the
patient will immediately lapse
back to the unresponsive state.
• Coma is a state of unarousable
unresponsiveness.
Grady Coma Scale
Grade
State of awareness
Responds appropriately
to:
Calling Light Deep
name pain pain
I
Confused, drowsy, lethargic, indifferent
and/or uncooperative; does not lapse
into sleep when left undisturbed
Yes
Yes
Yes
II
Stuporous; may be disoriented to time,
place, and person; will lapse into sleep
when not disturbed; or belligerent and
uncooperative
No
Yes
Yes
III
Deep stupor; requires strong pain to
evoke movement
No
No
Yes
IV
Exhibits decorticate or decerebrate
posturing to a deep pain stimulus
No
No
No
V
Does not respond to any stimuli; flaccid
No
No
No
Coma: 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
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
Pupillary Patterns in Comatose Patients
Pattern
Small, reactive
Site of dysfunction
Diencephalon
Large "fixed," with hippus Midbrain tectum
Midposition, "fixed"
Midbrain
Pinpoint, not reactive
Pons
One dilated
Suggests transtentorial
herniation
Pupils: Localizing Value
Pupils: Localizing Value
Horner’s syndrome
Midriasis-sympathetic
stimulation
Eye Movements
Left 6th Nerve Palsy
Left 3rd Nerve Palsy
CLINICAL ASSESSMENT OF COMA
Brainstem Reflexes
Reflex
Pupillary light
reaction
Technique
Shine light on pupil and observe constriction
Localization
Midbrain and
pontine
tegmentum
Corneal response Open lid if necessary; lightly stroke cornea
with cotton wisp; observe for blink
Pons
Oculocephalic
response (doll's
eyes)
Hold lids open with one hand while turning
head side to side with the other hand;
observe rotation of eyes side to side
Pons—vestibular
Oculovestibular;
cold-water
calorics
With head at 30 degrees, irrigate external
auditory canal and tympanic membrane
slowly with up to 120 ml ice water; observe
for conjugate rotation of the eyes toward the
side irrigated
Pons—vestibular
Puppilary light reflex
• 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).
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)
• 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.
Gag reflex
Test for oculocephalic reflex response (Doll’s eyes
phenomena). (B) abnormal response when thee head
is rotated the eyes do not turn in a conjugated
manner.
Vestibulo-cephalic reflex test
Caloric reflex test is a test of the vestibulo-ocular 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.
Some Abnormal Respiratory Patterns Found in Comatose
Patients
Pattern
Description
Site of
dysfunction
Cheyne–Stokes
Periodic breathing in which phases Cerebral
of hyperpnea alternate with
hemispheres;
apnea; the phases alternate every diencephalons
30 to 45 seconds
Central
neurogenic
hyperventilation
Deep, rapid respirations at a rate
of 24 or more/min
Apneustic
A prolonged inspiratory "cramp"; a Pontine
prolonged gasp
tegmentum
Ataxic
Random sequences of shallow and Medulla
deep respiration without pattern
Midbrain;
diencephalons
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.
Abnormal breathing patterns
Assesses patient’s
neurological
condition
Value range 3 -15
 3 totally
comatose
patient

9-12 Moderate
altered conscious
level
15
fully alert
patient
Coma Mimics
•
•
•
•
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
Catatonia
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
Conversion reactions
• 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
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