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APPROACH TO THE PATIENT
 Acute respiratory and cardiovascular problems
should be attended prior to the nuerological
assesment
 In most instances a complete medical
evaluation except for vital signs,fundoscopy
may be deffered until the nuerological
evaluation has established the severity and
nature of coma
HISTORY
 The cirucmstances and rapidity with which
nuerological symptoms developed
 The antecedent symptoms
(confusion,headache,seizures,dizziness,doubl
evision)
 The use of medications,drugs,alcohol
 Chronic liver,kidney,lung,heart or other medical
diseases
General Examination
 Alterations in vital signs (temperature, pulse,
respiratory rate, and blood pressure) are
important in diagnosis
 FEVER-suggests systemic infection,bacterial
meningitis,heatstroke,neurolepticmalignant
syndrome,malignanthyperthermia
 Hypothermia-is observed in patients with
alcohol,barbiturate, sedative,or phenothiazine
intoxication,hypogycemia,peripheral circulatory
failurehdddddddddde important aids in
diagnosis.
 Marked hypertension suggests hypertensive
encephalopathy or cerebral hemorrhage or
headinjury
 Hypotension is characterstic of coma from
alcohol or barbiturate intoxication,internal
hemorrhage,MI,sepsis,profound
hypothyroidism or addissonian crisis
 Pulse:
 Bradycardia-brain tumors,opiates
 Tachycardia-hyperthroidism,uremia
 Patient present with Hypertension with
bradycardia occurs in response to increased
ICP and signs of cerebral herniation
 Multiple bruises (particularly a bruise or boggy
area in the scalp), bleeding, CSF leakage from
an ear or the nose, or periorbital hemorrhage
greatly raises the likelihood of cranial fracture
and intracranial trauma
 Marked pallor suggests internal hemorrhage
 Cutaneous petechiae suggests thrombotic
thrombocytopenic purpura, meningococcemia
or bleeding diathesis assosciated with an
intracerebral hemorrhage
 Cyanosis and reddish or anemic skin
colouration are other indications of an
underlying systemic disease or
carbonmonoxide as responsible for coma
 The odor of the breath may provide a clue to
the etiology of coma.
 The spoiled-fruit odor of diabetic ketoacidotic
coma, the uriniferous odor of uremia, the
musky and slightly fecal fetor of hepatic coma,
and the burnt almond odor of cyanide
poisoning
 Fundoscopic examination can detect sub
arachonoid hemorrhage,hypertensive
encephalopathy,and increased intracranial
pressure
NEUROLOGICAL EXAMINATION
 Tossing about in the bed ,reaching up towards
the
face,crossinglegs,yawning,swallowing,coughin
g, moaning reflect a DROWSY state
 Lack of restlesness movements on one side or
an outturned leg suggests hemiplegia
 Intermittent twitching movements of foot,
finger,or fascial muscle may be only sign of
seizures
 Multifocal myoclonus almost alaways indicates
a metabolic disorder, particularly uemia,anoxia
drug intoxication
 In a drowsy and confused patients bilateral
asterixis is a sign of metabolic
encephalopathy or drug intoxication
 Decorticate rigidity and Decerebrate rigidity, or
"posturing," describe stereotyped arm and leg
movements occurring spontaneously or elicited
by sensory stimulation.
 Flexion of the elbows and wrists and supination
of the arm (decortication) suggests bilateral
damage rostral to the midbrain, whereas
extension of the elbows and wrists with
pronation (decerebration) indicates damage to
motor tracts in the midbrain or caudal
diencephalon.
 The less frequent combination of arm extension
with leg flexion or flaccid legs is associated with
lesions in the pons.
 These concepts have been adapted from animal
work and cannot be applied with precision to
coma in humans.
 In fact, acute and widespread disorders of any
type, regardless of location, frequently cause
limb extension, and almost all extensor posturing
becomes predominantly flexor as time passes.
LEVEL OF AROUSAL
 A sequence of increasingly intense stimuli is
used to determine the threshhold for arousal
and the motor response of each side of body
 The results of testing may vary from minute to
minute and serial examinations are useful
 Tickling the nostrils with a cotton whisp is
moderate stimulus to arousal-all but deeply
stuporous amd comatose patients will move
the head away and arouse to some degree
 Noxious stimuli such as pressure on
knuckles,bony prominences
,pinprickstimulation, pinching skin to arousal in
further step-abduction avoidance movement of
a limb is usually purposeful and denotes an
intact corticospinal system
 Posturing indicates severe damage to the
cortico spinal system
GLASGOW COMA SCALE
Newer Scales for Prognosis of
Coma:
 FOUR (Full Outline of UnResponsiveness) SCALE
 New Coma Scale is devised in 2005, Four
components (Eye, Motor, Brainstem, Respiration)
 Each component has maximum of score of Four.
 AVPU
 Alertness, response to Verbal stimuli, response
to Painful stimuli, or Unresponsive
 ACDU
 Alertness, Confusion, Drowsiness,
and Unresponsiveness
 Grady Scale
 Scale of I to V along a scale of Confusion, Stupor,
Deep stupor, abnormal Posturing, and Coma.
BRAINSTEM REFLEXES
 Assessment of brainstem function is essential
to localization of the lesion in coma.
 The brainstem reflexes that are conveniently
examined are pupillary size and reaction to
light, spontaneous and elicited eye
movements, corneal responses, and the
respiratory pattern
 As a rule, coma is due to bilateral hemispheral
disease when these brainstem activities are
preserved, particularly the pupillary reactions
and eye movements.
However, the presence of abnormal brainstem
signs does not always indicate that the primary
lesion is in the brainstem because
hemispheral masses can cause secondary
brainstem pathology by transtentorial
herniation.
OCULAR MOVEMENTS
 In light coma of metabolic origin, the eyes rove
conjugately from side to side in seemingly
random fashion, sometimes resting briefly in a
eccentric position. These movements
disappear as coma deepens, and the eyes
then remain motionless and slightly exotropic.
 The eyelids may remain tonically retracted
because of failure of levator inhibition in some
cases of pontine infarction (eyes-open coma)
 There is persistent conjugate deviation of the
eyes to one side—away from the side of the
paralysis with a large cerebral lesion (looking
toward the lesion) and toward the side of the
paralysis with a unilateral pontine lesion
(looking away from the lesion).
 The eyes turn down and inward with
hematomas or ischemic lesions of the
thalamus and upper midbrain
 "Ocular bobbing" describes brisk downward and
slow upward movements of the eyes
associated with loss of horizontal eye
movements and is diagnostic of bilateral
pontine damage, usually from thrombosis of the
basilar artery.
 Ocular dipping" is a slower, arrhythmic
downward movement followed by a faster
upward movement in patients with normal
reflex horizontal gaze; it indicates diffuse
cortical anoxic damage.
OCULOCEPHALIC REFLEX
 Oculocephalic reflexes (doll’s-eye movements)
are elicited by briskly turning or tilting the
head.
 The eye movements in the direction opposite
to the head movement ,depend on the integrity
of ocular motor nuclei and their
interconnecting tracts extend from midbrain to
pons and medulla
 The ability to elicit them therfore reflects both
reduced cortical influence on the brainstem
 Intact brainstem pathways indicating that
lesion is is caused by lesion in cerebral
hemispheres
 An absence of reflex eye movements usually
signifies damage within the brain stem but
can also results from overdoses of certain
drugs
 The test is performed by irrigating the external
auditory canal with cool water in order to
induce convection currents in the labyrinths.
 After a brief latency, the result is tonic
deviation of both eyes to the side of cool-water
irrigation and nystagmus in the opposite
direction.
 Absence of nystagmus with preserved
conjugate deviation: Cerebral hemisphere
damage
 Absence of conjugate movement: Brainstem
lesion
CORNEAL RESPONSES
 By touching the cornea with a whisp of cotton ,
a response consists of brief bilateral lid closure
is usually observed
 The corneal reflex depends on the integrity of
pontine pathways between the 5th and 7th
cranial nerves in conjuction with reflex eye
movements it is useful test to pontine function
RESPIRATORY PATTERNS
 Shallow, slow, but regular breathing
suggests metabolic or drug depression.
 Rapid, deep(Kussmaul)breathing seen in
metabolic acidosis,pontomesencephalic
lesions.
 Cheyne-Stokes respiration, signifies
bihemispheral damage/bilateral thalamic
lesions or metabolic suppression and
commonly accompanies light coma
 Apneustic breathing is characterized by a long
inspiratory pause, after which the air is
retained for several seconds and then
released. This abnormality appears with
lesions of the lateral tegmentum of the lower
half of the pons.
 Agonal gasps are lower brainstem (medullary)
damage and are well known as the terminal
respiratory pattern of severe brain damage
LABORATORY STUDIES AND
IMAGING
 The studies that are most useful in the
diagnosis of coma are: chemical-toxicologic
analysis of blood and urine, cranial CT or MRI,
EEG, and CSF examination.
 Arterial blood gas analysis is helpful in patients
with lung disease and acid-base disorders
 The metabolic aberrations commonly
encountered in clinical practice require
measurement of electrolytes, glucose, calcium,
osmolarity, and renal (blood urea nitrogen) and
hepatic (NH3) function.
 The availability of CT and MRI has focussed
on attention on cause of coma that are
detectable by imaging (hemmorhage,tumor or
hydrocephalus)
 The notion that a normal CT scan excludes
anatomic lesion as the cause of coma is
erroneous.
 Bilateral hemisphere infarction, acute
brainstem infarction, encephalitis, meningitis,
mechanical shearing of axons as a result of
closed head trauma, sagittal sinus thrombosis,
and subdural hematoma isodense to adjacent
brain are some of the disorders that may not
be detected.
 Nevertheless, if the source of coma remains
unknown, a scan should be obtained.
 The EEG is useful in metabolic or drug-
induced states but is rarely diagnostic.
 It is essential test when coma is due to
clinically unrecognized,non convulsive seizure,
and shows fairly characterstics patterns in
herpesvirus encephalitis, or to prion
(Creutzfeldt-Jakob) disease.
LUMBAR PUNCTURE
 Examination of the CSF remains
indispensable in the diagnosis of meningitis
and encephalitis. For patients with an altered
level of consciousness, it is generally
recommended that an imaging study be
performed prior to lumbar puncture to exclude
a large intracranial mass lesion.

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approach to coma

  • 1. APPROACH TO THE PATIENT
  • 2.  Acute respiratory and cardiovascular problems should be attended prior to the nuerological assesment  In most instances a complete medical evaluation except for vital signs,fundoscopy may be deffered until the nuerological evaluation has established the severity and nature of coma
  • 3. HISTORY  The cirucmstances and rapidity with which nuerological symptoms developed  The antecedent symptoms (confusion,headache,seizures,dizziness,doubl evision)  The use of medications,drugs,alcohol  Chronic liver,kidney,lung,heart or other medical diseases
  • 5.  Alterations in vital signs (temperature, pulse, respiratory rate, and blood pressure) are important in diagnosis  FEVER-suggests systemic infection,bacterial meningitis,heatstroke,neurolepticmalignant syndrome,malignanthyperthermia  Hypothermia-is observed in patients with alcohol,barbiturate, sedative,or phenothiazine intoxication,hypogycemia,peripheral circulatory failurehdddddddddde important aids in diagnosis.
  • 6.  Marked hypertension suggests hypertensive encephalopathy or cerebral hemorrhage or headinjury  Hypotension is characterstic of coma from alcohol or barbiturate intoxication,internal hemorrhage,MI,sepsis,profound hypothyroidism or addissonian crisis
  • 7.  Pulse:  Bradycardia-brain tumors,opiates  Tachycardia-hyperthroidism,uremia  Patient present with Hypertension with bradycardia occurs in response to increased ICP and signs of cerebral herniation
  • 8.  Multiple bruises (particularly a bruise or boggy area in the scalp), bleeding, CSF leakage from an ear or the nose, or periorbital hemorrhage greatly raises the likelihood of cranial fracture and intracranial trauma  Marked pallor suggests internal hemorrhage  Cutaneous petechiae suggests thrombotic thrombocytopenic purpura, meningococcemia or bleeding diathesis assosciated with an intracerebral hemorrhage
  • 9.  Cyanosis and reddish or anemic skin colouration are other indications of an underlying systemic disease or carbonmonoxide as responsible for coma
  • 10.  The odor of the breath may provide a clue to the etiology of coma.  The spoiled-fruit odor of diabetic ketoacidotic coma, the uriniferous odor of uremia, the musky and slightly fecal fetor of hepatic coma, and the burnt almond odor of cyanide poisoning
  • 11.  Fundoscopic examination can detect sub arachonoid hemorrhage,hypertensive encephalopathy,and increased intracranial pressure
  • 13.  Tossing about in the bed ,reaching up towards the face,crossinglegs,yawning,swallowing,coughin g, moaning reflect a DROWSY state  Lack of restlesness movements on one side or an outturned leg suggests hemiplegia
  • 14.  Intermittent twitching movements of foot, finger,or fascial muscle may be only sign of seizures  Multifocal myoclonus almost alaways indicates a metabolic disorder, particularly uemia,anoxia drug intoxication  In a drowsy and confused patients bilateral asterixis is a sign of metabolic encephalopathy or drug intoxication
  • 15.  Decorticate rigidity and Decerebrate rigidity, or "posturing," describe stereotyped arm and leg movements occurring spontaneously or elicited by sensory stimulation.  Flexion of the elbows and wrists and supination of the arm (decortication) suggests bilateral damage rostral to the midbrain, whereas extension of the elbows and wrists with pronation (decerebration) indicates damage to motor tracts in the midbrain or caudal diencephalon.
  • 16.
  • 17.  The less frequent combination of arm extension with leg flexion or flaccid legs is associated with lesions in the pons.  These concepts have been adapted from animal work and cannot be applied with precision to coma in humans.  In fact, acute and widespread disorders of any type, regardless of location, frequently cause limb extension, and almost all extensor posturing becomes predominantly flexor as time passes.
  • 18. LEVEL OF AROUSAL  A sequence of increasingly intense stimuli is used to determine the threshhold for arousal and the motor response of each side of body  The results of testing may vary from minute to minute and serial examinations are useful  Tickling the nostrils with a cotton whisp is moderate stimulus to arousal-all but deeply stuporous amd comatose patients will move the head away and arouse to some degree
  • 19.  Noxious stimuli such as pressure on knuckles,bony prominences ,pinprickstimulation, pinching skin to arousal in further step-abduction avoidance movement of a limb is usually purposeful and denotes an intact corticospinal system  Posturing indicates severe damage to the cortico spinal system
  • 21. Newer Scales for Prognosis of Coma:  FOUR (Full Outline of UnResponsiveness) SCALE  New Coma Scale is devised in 2005, Four components (Eye, Motor, Brainstem, Respiration)  Each component has maximum of score of Four.  AVPU  Alertness, response to Verbal stimuli, response to Painful stimuli, or Unresponsive  ACDU  Alertness, Confusion, Drowsiness, and Unresponsiveness  Grady Scale  Scale of I to V along a scale of Confusion, Stupor, Deep stupor, abnormal Posturing, and Coma.
  • 22. BRAINSTEM REFLEXES  Assessment of brainstem function is essential to localization of the lesion in coma.  The brainstem reflexes that are conveniently examined are pupillary size and reaction to light, spontaneous and elicited eye movements, corneal responses, and the respiratory pattern
  • 23.  As a rule, coma is due to bilateral hemispheral disease when these brainstem activities are preserved, particularly the pupillary reactions and eye movements. However, the presence of abnormal brainstem signs does not always indicate that the primary lesion is in the brainstem because hemispheral masses can cause secondary brainstem pathology by transtentorial herniation.
  • 24.
  • 25. OCULAR MOVEMENTS  In light coma of metabolic origin, the eyes rove conjugately from side to side in seemingly random fashion, sometimes resting briefly in a eccentric position. These movements disappear as coma deepens, and the eyes then remain motionless and slightly exotropic.  The eyelids may remain tonically retracted because of failure of levator inhibition in some cases of pontine infarction (eyes-open coma)
  • 26.  There is persistent conjugate deviation of the eyes to one side—away from the side of the paralysis with a large cerebral lesion (looking toward the lesion) and toward the side of the paralysis with a unilateral pontine lesion (looking away from the lesion).  The eyes turn down and inward with hematomas or ischemic lesions of the thalamus and upper midbrain
  • 27.  "Ocular bobbing" describes brisk downward and slow upward movements of the eyes associated with loss of horizontal eye movements and is diagnostic of bilateral pontine damage, usually from thrombosis of the basilar artery.
  • 28.  Ocular dipping" is a slower, arrhythmic downward movement followed by a faster upward movement in patients with normal reflex horizontal gaze; it indicates diffuse cortical anoxic damage.
  • 30.  Oculocephalic reflexes (doll’s-eye movements) are elicited by briskly turning or tilting the head.  The eye movements in the direction opposite to the head movement ,depend on the integrity of ocular motor nuclei and their interconnecting tracts extend from midbrain to pons and medulla
  • 31.  The ability to elicit them therfore reflects both reduced cortical influence on the brainstem  Intact brainstem pathways indicating that lesion is is caused by lesion in cerebral hemispheres  An absence of reflex eye movements usually signifies damage within the brain stem but can also results from overdoses of certain drugs
  • 32.
  • 33.  The test is performed by irrigating the external auditory canal with cool water in order to induce convection currents in the labyrinths.  After a brief latency, the result is tonic deviation of both eyes to the side of cool-water irrigation and nystagmus in the opposite direction.
  • 34.  Absence of nystagmus with preserved conjugate deviation: Cerebral hemisphere damage  Absence of conjugate movement: Brainstem lesion
  • 35. CORNEAL RESPONSES  By touching the cornea with a whisp of cotton , a response consists of brief bilateral lid closure is usually observed  The corneal reflex depends on the integrity of pontine pathways between the 5th and 7th cranial nerves in conjuction with reflex eye movements it is useful test to pontine function
  • 36. RESPIRATORY PATTERNS  Shallow, slow, but regular breathing suggests metabolic or drug depression.  Rapid, deep(Kussmaul)breathing seen in metabolic acidosis,pontomesencephalic lesions.  Cheyne-Stokes respiration, signifies bihemispheral damage/bilateral thalamic lesions or metabolic suppression and commonly accompanies light coma
  • 37.  Apneustic breathing is characterized by a long inspiratory pause, after which the air is retained for several seconds and then released. This abnormality appears with lesions of the lateral tegmentum of the lower half of the pons.  Agonal gasps are lower brainstem (medullary) damage and are well known as the terminal respiratory pattern of severe brain damage
  • 38. LABORATORY STUDIES AND IMAGING  The studies that are most useful in the diagnosis of coma are: chemical-toxicologic analysis of blood and urine, cranial CT or MRI, EEG, and CSF examination.  Arterial blood gas analysis is helpful in patients with lung disease and acid-base disorders
  • 39.  The metabolic aberrations commonly encountered in clinical practice require measurement of electrolytes, glucose, calcium, osmolarity, and renal (blood urea nitrogen) and hepatic (NH3) function.
  • 40.  The availability of CT and MRI has focussed on attention on cause of coma that are detectable by imaging (hemmorhage,tumor or hydrocephalus)  The notion that a normal CT scan excludes anatomic lesion as the cause of coma is erroneous.
  • 41.  Bilateral hemisphere infarction, acute brainstem infarction, encephalitis, meningitis, mechanical shearing of axons as a result of closed head trauma, sagittal sinus thrombosis, and subdural hematoma isodense to adjacent brain are some of the disorders that may not be detected.  Nevertheless, if the source of coma remains unknown, a scan should be obtained.
  • 42.  The EEG is useful in metabolic or drug- induced states but is rarely diagnostic.  It is essential test when coma is due to clinically unrecognized,non convulsive seizure, and shows fairly characterstics patterns in herpesvirus encephalitis, or to prion (Creutzfeldt-Jakob) disease.
  • 43. LUMBAR PUNCTURE  Examination of the CSF remains indispensable in the diagnosis of meningitis and encephalitis. For patients with an altered level of consciousness, it is generally recommended that an imaging study be performed prior to lumbar puncture to exclude a large intracranial mass lesion.