Decreased level of
consciousness
Ali Shoeibi MD, assistant professor of neurology, Mashhad
University of Medical Sciences
Consciousness
State of awareness
of self
and surroundings
Types
• Level of arousal
• Cognitive and affective function
– dementia
– delusions
– Confusion
– inattention
APPROACH TO THE PATIENT IN
COMA
•
Stabilize vital functions such as blood pressure and oxygenation
(A,B,C)
•
Brief history & examination
•
I.V. line & sampling
•
Treat reversible causes of coma
1. supplemental oxygen
2. intravenous thiamine (at least 100 mg)
3. intravenous 50% dextrose in water (25 g)
4. Naloxone hydrochloride may be given parenterally, preferably
intravenously, in doses of 0.4 to 2.0 mg
APPROACH TO THE PATIENT IN
COMA
• Comprehensive history & examination
• The neck should be stabilized in all instances of trauma
until cervical spine fracture or subluxation can be ruled
out
• in unconscious patients with a history of trauma,
peritoneal lavage by an experienced surgeon may be
warranted
Causes of Coma
Causes of Coma
More than half of all cases of coma are due to
metabolic brain dysfunction (Almost half of
these are drug poisonings)
Differentiating Toxic-Metabolic Coma
from Structural Coma
• When the history is available, the patient's underlying
illnesses and medications, or the setting in which they
are found, often help guide the physician to the
appropriate cause
• The time course of the illness resulting in coma can be
helpful. Generally, structural lesions have a more abrupt
onset, whereas metabolic or toxic causes are more
slowly progressive
• The response to initial emergency therapy may help
differentiate metabolic or toxic causes of coma
• In general, structural lesions have focal features or at
least notable asymmetry on neurological examination.
Toxic, metabolic, and psychiatric diseases are
characterized by their symmetry
State of consciousness
• Patients with metabolic problems often have
milder alterations in arousal, typically with
waxing and waning of the behavioral state
• Patients with acute structural lesions tend to stay
at the same level of arousal or progressively
deteriorate
• Toxins may also cause progressive decline in
level of arousal
Respiration
Deep, frequent respiration most commonly
is due to metabolic abnormalities, though
rarely it is caused by pontine lesions or by
neurogenic pulmonary edema secondary
to acute structural lesions
Funduscopic examination
• Subhyaloid hemorrhage or papilledema are
almost pathognomonic of structural lesions
• Papilledema due to increased ICP may be
indicative of an intracranial mass lesion or
hypertensive encephalopathy
• Papilledema does not occur in metabolic
diseases except hypoparathyroidism, lead
intoxication, and malignant hypertension
Pupil size
• The pupils usually are symmetrical in coma from toxicmetabolic causes.
• Patients with metabolic or toxic encephalopathies often
have small pupils with preserved reactivity.
• Exceptions
– methyl alcohol poisoning, which may produce dilated and
unreactive pupils
– late in the course of toxic or metabolic coma if hypoxia or other
permanent brain damage has occurred. In terminal asphyxia the
pupils dilate initially and then become fixed at midposition within
30 minutes
Pupil reactivity
• Pupillary reactivity is relatively resistant to
metabolic insult and usually is spared in coma
from drug intoxication or metabolic causes, even
when other brainstem reflexes are absent.
• Exceptions
– Hypothermia may fix pupils
– severe barbiturate intoxication may fix pupils
– neuromuscular blocking agents produce midposition
or small pupils
– glutethimide and atropine dilate pupils
common mistakes
• the use of insufficient illumination
• preexisting ocular or neurological injury may fix
the pupils or result in pupillary asymmetry
• Seizures may cause transient anisocoria
• Local and systemic medications may affect
pupillary function
Pupil Size and Reactivity
Ocular motility
Asymmetry in oculomotor function
typically is a feature of structural lesions
Spontaneous and reflex eye
movements
• Roving eye movements with full excursion are
most often indicative of metabolic or toxic
abnormalities
• Reflex eye movements normally are intact in
toxic-metabolic coma
• Exceptions:
– rarely in phenobarbital or phenytoin intoxication
– rarely deep metabolic coma from other causes
Doll's eye phenomenon
Muscle tone
• Muscle tone usually is symmetrical and normal or
decreased in metabolic coma
• Structural lesions cause asymmetrical muscle tone.
Tone may be increased,normal, or decreased by
structural lesions
• Any toxic-metabolic cause of coma may be associated
with focal features; however, such features most often
are observed with
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barbiturate or lead poisoning
Hypoglycemia
hepatic encephalopathy
hyponatremia
Differentiating Psychiatric Coma
from Metabolic or Structural Coma
• In the patient with true stupor or coma, passive eyelid opening is
easily performed and is followed by slow, gradual eyelid closure.
– The malingering or hysterical patient often gives active resistance to
passive eye opening and may even hold the eyes tightly closed.
– It is nearly impossible for the psychiatric or malingering patient to mimic
the slow, gradual eyelid closure.
• The pupils normally constrict in sleep or (eyes-closed-type) coma
but dilate with the eyes closed in the awake state. Passive eye
opening in a sleeping person or a truly comatose patient (if pupillary
reflexes are spared) results in pupillary dilation.
– Opening the eyes of an awake person produces constriction.
Differentiating Psychiatric Coma
from Metabolic or Structural Coma
• Roving eye movements cannot be mimicked and
thus also are a good sign of true coma
• during cold caloric testing, the eyes do not
tonically deviate to the side of the caloric
instillation, and the fast phases are preserved,
stupor or true coma is essentially ruled out
• Blinking also increases in psychiatric and
malingering patients but decreases in patients in
true stupor.
PROGNOSIS
• outcome in any comatose patient cannot be predicted
with 100% certainty unless that patient meets the criteria
for brain death
• subcategories:
– drug-induced
– Nontraumatic
– traumatic coma
• Drug-induced coma usually is reversible unless the
patient has not had appropriate systemic support whiIe
comatose and has sustained secondary injury from
hypoperfusion, hypoxia, or lack of other necessary
metabolic substrates
Nontraumatic Coma
• Only about 15% of patients in nontraumatic coma make a
satisfactory recovery
• Functional recovery is related to the cause of coma.
– Diseases causing structural damage, such as cerebrovascular disease
including subarachnoid hemorrhage, carry the worst prognosis
– coma from hypoxia-ischemia due to such causes as cardiac arrest has
an intermediate prognosis
– coma due to hepatic encephalopathy and other metabolic causes has
the best ultimate outcome
• Age does not appear to be predictive of recovery
• The longer a coma lasts, the less likely the patient is to regain
independent functioning.
Nontraumatic Coma
• patients with nontraumatic coma who have not
regained awareness by the end of 1 month are
unlikely to do so. Even if they do regain
consciousness, they have practically no chance
of achieving an independent existence
• poor neurological outcome: within 3 days of
coma
– The absence of pupillary light responses
– The absence of motor responses to pain
– low Glasgow Coma scores (less than 5)
Traumatic Coma
• The prognosis for traumatic coma differs from
that for nontraumatic coma in many ways
– First, many patients with head trauma are young
– Second, prolonged coma of up to several months
does not preclude a satisfactory outcome in traumatic
coma
– Third, in relationship to their initial degree of
neurological abnormality, traumatic coma patients do
better than nontraumatic coma patients
Traumatic Coma
• early predictors of the outcome of posttraumatic coma
include
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patient's age
motor response
pupillary reactivity
depth and duration of coma
• The prognosis worsens with increasing age
• little influence on the outcome
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Cause of injury
skull fracture
lateralization of damage to one hemisphere
extracranial injury