Download 64-unconscious-patient

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.
Arousal depends on an intact:
a)
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.
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
THE ABCDE APPROCH TO COMA
A
AIRWAYS
B
BREATHING
C
CIRCULATION
D
DRUGS/DISABILITY
E
EXPOSURE
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
Coma: Initial assessment and evaluation
• Assess level of
consciousness: response to
vocal and painful stimuli;
this is known as
the AVPU (alert, vocal
stimuli, painful stimuli,
unresponsive) scale.
• Make sure the patient is in an
actual comatose state and or
is not in locked-in state
(patient is either able to
voluntarily move their eyes
or blink) or psychogenic
unresponsiveness
• Assess the severity of the
coma with the Glasgow
coma scale
• Take blood for drug screen
• Check for levels of “serum
glucose, calcium, sodium,
potassium, magnesium,
phosphate, urea, and
creatinine”
• Perform CT or MRI scans
• Continue to monitor brain
waves and identify seizures
of patient using EEGs
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.
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 (Pappiloedema/
subhyaloid hemorrhage)
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
Pupil sizes (left eye vs. right eye)
Possible interpretation
Normal eye with two pupils equal in size and
reactive to light. This means that the patient
is probably not in a coma and is probably
lethargic, under influence of a drug.
"Pinpoint" pupils indicate heroin or opiate
overdose, and can be responsible for a
patient's coma. The pinpoint pupils are still
reactive to light, bilaterally (in both eyes, not
just one).
The right eye is dilated, while the left eye is
normal in size). This could mean a damage to
the oculomotor nerve (3, CN III) on the right
side, or possibility of vascular involvement.
Both pupils are dilated and unreactive to
light. This could be due to certain
medications, hypothermia or severe anoxia
(lack of oxygen).
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
"The OCR/doll's eye reflex is movement of
the eyes in the direction opposite that in
which the head is moved. For example, the
reflex is present if the eyes move to the right
when the head is rotated to the left, and vice
versa.
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.
Ataxic (Biot) breathing is
a random sequences of
shallow and deep breaths
interspersed with
irregular pauses –
pontine lesions
Apneustic breathing
A prolonged inspiratory
"cramp"; a prolonged
gasp --pontine disease.
Abnormal breathing patterns
Cheyne-Stokes breathing
is cyclic, crescendodecrescendo pattern
interrupted by apneas –
cerebral hemisphers;
diancephalon
Central neurogenic hyperventilation:
Deep, rapid respirations at a rate of 24
or more/min -- Midbrain;
diencephalons
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 reaction
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