Transcript Coma - Selam Higher Clinic

coma
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Coma
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Deep sleeplike state
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Can not be aroused.
Stupor
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Lesser degrees of unarousability.
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Require vigorous stimuli
Drowsiness
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Simulates light sleep
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Easy arousal
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Persistence of alertness for a brief periods.
Vegetative state
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Out come of severe brain injury
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Preserved sleep-wake cycles (normal arousal)
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No meaningful interaction with the environment
(No content)
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Akinetic mutism
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Partially or fully awake
Able to form impressions & think but remains
immobile & mute,particularly when unstimulated.
Locked–in sate
• An awake patient with no means of producing speech or
volitional movement in order to indicate that he is awake
• Vertical eye movement & lid elevation remains unimpaired,
allowing patient to signal.
e. g - Infarction or hemorrhage of ventral pons, GBS
pharmacologic neuromuscular blockade
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The anatomic substrate for consciousness
involves the cerebral hemispheres and the RAS
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Cerebral hemispheres- For all complex waking
behaviors
RAS - maintains the cerebral cortex in a state
of wakeful consciousness (arousal)
Pathophysiology of coma
Structural - Operate by compressing the
brainstem
Metabolic - May affect either region
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structural
supratentorial
Central
infratentorial
Lateral
shift
uncal
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Central
Diencephalic level
Midbrain & upper pons
•Drowsy
•Lapses into coma
•Miotic pupil but
reactive
•Pupils dilate to mid
position & unreactive
to light
•Reflex eye movement
difficult to elicit &
may take the form of
an Inter-nuclear
ophthalmoplegia
•Intact reflex eye
movement
•Babinski signs, grasp
reflexes & decorticate
posturing contralaterally to the mass.
Lower pons & medulla
•Ataxic breathing,
irregular pulse & blood
pressure
•Pupil-remain mid position
& unreactive
•Absent reflex eye
movement
•Decerebrate posturing •Flaccid tone, No
response to deep pain.
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uncal
Early
Mid brain
•Approach normal wakefulness
•Ipsitateral pupil dilatation,
reacts sluggishly
• Pupils mid dilated &
unreactive to light
•Normal eye movement
•Evolution to coma is rapid &
• Subsequent rostro caudal
focal motor signs develop
deterioration merges with that
ipsilateral to the mass with
of central syndrome.
bilateral decerebrate posturing
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Subtentorial lesions
Posterior fossa lesions cause coma in three
ways;
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Intrinsic brain stem process may destroy
RAS
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Extrinsic mass
by compression or upward herniation
through the tentorium cerebelli
Down ward herniation via foramen
magnum.
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lateral shift
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Displacement of deep brain structures by a mass,
with or with out herniation, is adequate to
compress the region of the RAS & result in coma.
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Drowsiness & stupor typically occur with moderate
horizontal shift at the level of diencephalon well
before transtentorial or other hernations are evident.
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Acutely appearing masses are more likely to affect
level of consciousness.
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Metabolic causes
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Many systemic metabolic abnormalities cause coma either;
By interrupting the delivery of energy substrates
eg- hypoxia, ischemia, hypoglycemia
By altering neuronal excitabillity
e.g – drug & alcohol intoxication,anesthesia & epilepsy.
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Conditions such as hypoglycemia, hyponatremia,
hyperosmolarity, hypercapnia, hypercalcemia, and hepatic &
renal failure are associated with a variety of alterations in
neurons & astrocytes.
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The reversible effect of these conditions on the brain are not
understood, but may result from impaired energy supply,
change in ion fluxes across neuronal memberanes, & neuro
transmitter abnormalities
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metabolic cont…
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Coma & seizures are a common accompaniment of any
large shifts in sodium & water balance.
e .g DKA, NHHS, hyponatremia from any
cause ( e. g water intoxication, SIADHS )
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The severity of neurologic changes depends to a
large degree on the rapidity with which the serum
changes occur.
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The pathophysiology of other metabolic encephalopathies
such as hypothtroidism, vitamin B12 deficiency, &
hypothermia are incompletely understood but must also
reflect derangements of CNS biochemistry & memberane
function.
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Approach to the patient
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Acute respiratory & cardiovascular problems should be
attended to prior to neurologic assessment.
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Vital signs, funduscopy & examination for nuchal
rigidity
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Neurologic assessment
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Complete medical evaluation
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History
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In many cases, the cause is immediately evident like
trauma, cardiac arrest , or known drug ingestion
In the remainder,certain points are especially useful;
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Circumstances & rapidity with which neurologic
symptoms developed
The antecedent symptoms (confusion, weakness,
headache, fever, seizure, vomiting)
The use of medications , illicit drugs , or alcohol
Chronic liver, kidney, lung, heart , or other
medical disease
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General physical examination
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Hyperthermia -Infection, brain lesion disturbing temperature
regulating center, heat stroke, anticholinergic
drug intoxication
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Hypothermia -alcoholic, barbiturate, phenothiazine intoxication,
hypothyroidism
Hypertension-Hypertensive encephalopathy
Rapid rise in ICP
Hypotension- Alcohol ,barbiturate intoxication
MI , internal hemorrhage, Addisonian crisis.
Funduscopy
Hypertensive encephalopathy (exudates, hemorrhage, AV
nicking, papilledema).
Increased ICP
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Petechiae
TTP , meningococcemia, or a bleeding diathesis
from which an intracerebral hemorrhage arises.
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Respiration
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Less localizing value
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Cheyne-stokes
Bilateral hemispheral damage or metabolic suppression
Commonly accompanied by light coma
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Kussmaul
Usually metabolic acidosis
Also in pontomesencephalic lesion .
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Agonal gasp
Bilateral lower brain stem damage terminal respiratory
pattern of severe brain damage.
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Pupils
Horner’s syndrome
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Lesion in sympathetic efferents originating in
hypothalamus & descending in the brain stem
to the cervical cord produces miosis with ptosis.
 Seen in thalamic & hypothalamic lesions from
cerebral, thalamic hemorrhage or from herniation.
 Bilateral miosis in pontine stroke
 Light reaction is preserved in all cases of
oculosympathetic paralysis.
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Pupil cont…
Unreactive pupils
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Normally reactive & round pupils of mid size
essentially exclude mid brain damage.
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Bilaterally dilated, unreactive
suggest intraxial involvement of third nerve at mid
brain, could be result of stroke, tumor
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Unilaterality implies a peripheral third nerve palsy :
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uncal herniation at the tentorium
nerve compression by PCA
traction at the superior orbital fissure.
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Pupil cont…
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Metabolic Vs structural lesion
 Normally reactive pupils in a comatose patient
strongly support a metabolic process
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Structural causes with reactive pupil
 Early phase of central transtentorial herniation
 Pontine hemorrhage
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Metabolic conditions with unreactive pupil
 Doriden ( gluthetimide )
 Anoxia
 Anticholinergic agents – not respond to 1% pilo
carpine.
 Hypothermia
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Eye movement
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Eyelids
Remain closed in coma.
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Exception – some case of pontine stroke with persistent ,
tonic eyelid retractiion.
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Spontaneous blinking indicates intact pontine reticular
formatiion
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Blinking to light indicates intact functioning visual afferent
pathway but not occipital cortex.
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Corneal reflex
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both metabolic & structural disease of
brain- stem or cortex depress it.
Depth of coma may correlate with the degree of
depression.
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Eye movement cont…
Roving eyes
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Slow, random, usually horizontal movements that
occur spontaneously in coma.
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Can not be duplicated by hysterical patients.
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Indicate intact oculomotor pathways, one parameter
of brain stem function.
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Appear in many metabolic & bilateral hemispheric
structural processes causing coma,
& their presence excludes brain stem structural
lesions.
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Eye movement cont…
Horizontal gaze deviation
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congugate horizontal ocular deviation to one side indicates
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damage to the pons on the opposite side or
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a lesion in the frontal lobe on the same side.
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“the eyes looks toward a hemispheral lesion & away
from a brainstem lesion.”
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epileptic phenomina produce deviation of eyes to the
opposite side of the body.
“ wrong way eyes”- the eyes may turn paradoxically away
from the side of a deep hemispheral lesion.
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Eye movement cont…
oculocephalic testing
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Depend on the integrity of the oculomotor nuclei & their
interconnecting tracts that extend from the mid brain to the pons &
the medulla.
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Are normally suppressed in the awake patient by visual fixation.
Their presence indicate reduced cortical influence on the brain stem.
oculovestibular testing
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Assess virtually the same brain stem reflex as oculocephalic test.
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Tonic deviation of both eyes to the side of cool water irrigation &
nystagmus in the opposite direction.
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Absent cold water calories usually suggest structural posterior fossa
lesion or drug intoxication.
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pupillary reactivity preserved in drug induced coma.
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Eye movement cont…
ocular bobbing
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A brisk down ward & slow upward movement of the eyes.
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Associated with loss of horizontal eye movements.
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Diagnostic of bilateral pontine damage usually from
thrombosis of basilary artery
ocular dipping
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A slower , arrhythmic down ward movement followed by a
faster upward movement
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In patients with normal reflex horizontal gaze.
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Indicates diffuse cortical anoxic damage.
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Motor signs
postures
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Primitive non purposeful reflex, which may occur spontaneously
In response to sensory stimuli (pain)
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Lesions producing flexion tend to be more rostral & those producing
extension more caudal.
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Acute destructive lesions tend to induce the extensor posture,
whereas evolution over time results more in a chronic flexor position.
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Distinction of weak flexor posturing from purposeful with drawal can
be made by noting the response to a painful stimulus applied to the
medial upper arm.
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Adduction is a reflex response
Abduction suggests a high level (with drawal) response.
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posture cont…
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In assymmetric /mismatched posturing, the more
abnormal posture points to the opposite side of the
brain as the more compromised.
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Lack of restless movements on one side or an out
turned leg suggests a hemiplegia.
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Abnormal postural responses do have some relation to
out come , extensor tends to fare worse, probably as
a function of the acuity and depth of the lesion
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Motor signs cont…
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Multifocal myoclonus almost always indicates a metabolic
disorder (uremia, anoxia, drug intoxication)
Frontal release phenomena
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Constitute forced grasping, perioral primitive reflexes
( e.g suck, snout, root ) paratonic rigidity
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Unduly marked in a patient who appears awake but
immobile- akinetic mutism a disturbance principally of
motivation.
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Assymetry of a grasp phenomena suggests a
hemiparesis on the side of weaker response.
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Psychogenic unresponsiveness
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May mimic real coma
In coma, the release of eyelids opened by the examiner produces
gradual, incomplete closure, this can not be voluntarily duplicated
In psychogenic cases, the lids may voluntarily resist opening , &
close too rapidly or in a fluttering manner
Presence of roving eye movements strongly mitigates against a
psychogenic state.
Truly comatose patients can not stop their arm from being dropped
on their face.
Demonestration of unambiguous full, uninhibited oculocephalic
response or complete paralysis of this response during passive head
movement strongly supports a diagnosis of nonpsyohogenic coma.
Presence of caloric-evoked nystagmus defines ‘’ coma ‘’ as
psychogenic.
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In clinical practice , the pain of the procedure most often terminates the
‘’unconsciousness.’’
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Brain death
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The criteria endorsed by the American Academy of
neurology include :
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documentation of both cessation of brain function
and the irreversibility of such cessation.
Cessation
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Hemispheric function
unreceptivity & unresponsivity.
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Brain stem function
Absence of pupillary light, corneal, oculocephalic ,
oculovestibular, oropharyngeal, & respiratory reflexes.
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Brain death cont…
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Irreversiblity
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The absence of reversible causes of coma must be
documented, like hypothermia (<32.3 ºc ), sedative drugs,
neuromuscular blockade , & shock.
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Duration of observation
The cessation of brain function must persist for ‘’an
approprate period of observation’’
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6 hours when confirmatory EEG documentation is available.
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12 hours in the absence of confirmatory test
For ischemic brain damage , 24 hours is suggested, in the
absence of EEG confirmation.
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