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Coma (from the Greek κώμα [ko̞ma], meaning deep sleep) is a
state of unconsciousness lasting more than 6 hours, in which a
person cannot be awakened, fails to respond normally to painful
stimuli, light or sound, lacks a normal sleep-wake cycle and does
not initiate voluntary actions.
All unconscious patients should have neurological
examinations to help determine the site and nature of the lesion,
to monitor progress, and to determine prognosis. Neurological
examination is most useful in the well-oxygenated,
normotensive, normoglycemic patient with no sedation, since
hypoxia, hypotension, hypoglycemia and sedating drugs
profoundly affect the signs elicited. Therefore, immediate
therapeutic intervention is a must to correct aberrations of
hypoxia, hypercarbia and hypoglycemia. Medications recently
taken that cause unconsciousness or delirium must be identified
quickly followed by rapid clinical assessment to detect the form
of coma either with or without lateralizing signs, with or without
signs of meningeal irritation, the pattern of breathing, the size
and reactivity of pupils and ocular movements, the motor
state of unconsciousness lasting more than 6 hours, in which a
person cannot be awakened, fails to respond normally to painful
stimuli, light or sound, lacks a normal sleep-wake cycle and does
not initiate voluntary actions.
All unconscious patients should have neurological
examinations to help determine the site and nature of the lesion,
to monitor progress, and to determine prognosis. Neurological
examination is most useful in the well-oxygenated,
normotensive, normoglycemic patient with no sedation, since
hypoxia, hypotension, hypoglycemia and sedating drugs
profoundly affect the signs elicited. Therefore, immediate
therapeutic intervention is a must to correct aberrations of
hypoxia, hypercarbia and hypoglycemia. Medications recently
taken that cause unconsciousness or delirium must be identified
quickly followed by rapid clinical assessment to detect the form
of coma either with or without lateralizing signs, with or without
signs of meningeal irritation, the pattern of breathing, the size
and reactivity of pupils and ocular movements, the motor
response, the airway clearance, the pattern of breathing and
circulation integrity, etc.
Special consideration must be given to neurological causes
which may lead to unconsciousness like status epilepticus (either
convulsive or non-convulsive), locked-in state, persistent
vegetative state and lastly brain stem death. Any disturbances of
thermoregulation must be measured.
Coma may result from a variety of conditions including
intoxication, metabolic abnormalities, central nervous system
diseases, acute neurologic injuries such as stroke, hypoxia or
traumatic injuries including head trauma caused by falls or
vehicle collisions. Looking for the pathogenesis of coma, two
important neurological components must function perfectly that
maintain consciousness. The first is the gray matter covering the
outer layer of the brain and the other is a structure located in
the brainstem called the reticular activating system (RAS or
ARAS), a more primitive structure that is in close connection
with the reticular formation (RF), a critical anatomical structure
needed for maintenance of arousal. It is necessary to investigate
the integrity of the bilateral cerebral cortices and the reticular
activating system (RAS), as a rule. Unilateral hemispheric lesions
do not produce stupor and coma unless they are of a mass
sufficient to compress either the contralateral hemisphere or the
brain stem (Bateman 2001). Metabolic disorders impair
consciousness by diffuse effects on both the reticular formation
and the cerebral cortex. Coma is rarely a permanent state
although less than 10% of patients survive coma without
significant disability (Bateman 2001); for ICU patients with
persistent coma, the outcome is grim.
Maneuvers to be established with an unconscious patient
include cardiopulmonary resuscitation, laboratory
investigations, a radiological examination to recognize brain
edema, as well as any skull, cervical, spinal, chest, and multiple
traumas. Intracranial pressure and neurophysiological
monitoring are important new areas for investigation in the
unconscious patient.
circulation integrity, etc.
Special consideration must be given to neurological causes
which may lead to unconsciousness like status epilepticus (either
convulsive or non-convulsive), locked-in state, persistent
vegetative state and lastly brain stem death. Any disturbances of
thermoregulation must be measured.
Coma may result from a variety of conditions including
intoxication, metabolic abnormalities, central nervous system
diseases, acute neurologic injuries such as stroke, hypoxia or
traumatic injuries including head trauma caused by falls or
vehicle collisions. Looking for the pathogenesis of coma, two
important neurological components must function perfectly that
maintain consciousness. The first is the gray matter covering the
outer layer of the brain and the other is a structure located in
the brainstem called the reticular activating system (RAS or
ARAS), a more primitive structure that is in close connection
with the reticular formation (RF), a critical anatomical structure
needed for maintenance of arousal. It is necessary to investigate
the integrity of the bilateral cerebral cortices and the reticular
activating system (RAS), as a rule. Unilateral hemispheric lesions
do not produce stupor and coma unless they are of a mass
sufficient to compress either the contralateral hemisphere or the
brain stem (Bateman 2001). Metabolic disorders impair
consciousness by diffuse effects on both the reticular formation
and the cerebral cortex. Coma is rarely a permanent state
although less than 10% of patients survive coma without
significant disability (Bateman 2001); for ICU patients with
persistent coma, the outcome is grim.
Maneuvers to be established with an unconscious patient
include cardiopulmonary resuscitation, laboratory
investigations, a radiological examination to recognize brain
edema, as well as any skull, cervical, spinal, chest, and multiple
traumas. Intracranial pressure and neurophysiological
monitoring are important new areas for investigation in the
unconscious patient.
Diagnosis
In the initial assessment of coma, it is common to judge by
spontaneous actions, response to vocal stimuli and response to
painful stimuli; this is known as the AVPU (alert, vocal stimuli,
painful stimuli, unconscious) scale. The most common scales
used for rapid assessment are:
1. The Glasgow Coma Scale (GCS), which aims to record the
conscious state of a person, in initial as well as continuing
assessment. When a patient is assessed and the resulting score is
either 14 (original scale) or 15 (the more widely used modified or
revised scale), this means ‘normal’; while if a patient is unable to
voluntarily open their eyes, does not have a sleep-wake cycle, is
unresponsive in spite of strong sensory (painful) or verbal
stimuli and who generally scores between 3 to 8 on the Glasgow
Coma Scale, (s)he is considered to be in coma.
2. Pediatric Glasgow Coma Scale: The Pediatric Glasgow Coma
Scale (PGCS) is the equivalent of the Glasgow Coma Scale used to
assess the mental state of adult patients. As with the GCS, the
PGCS comprises three tests: eye, verbal and motor responses.
The three values separately as well as their sum are considered
(Holmes 2005). The lowest possible PGCS is 3 (deep coma or
death) whilst the highest is 15 (fully awake and aware) (Holmes
2005).
Diagnosis of coma is simple; but determining the cause of the
underlying pathology may prove to be challenging. As in those
with deep unconsciousness, there is a risk of asphyxiation as
control over the muscles in the face and throat is diminished, so
those in a coma are typically assessed for airway management,
nasopharyngeal airway or endotracheal intubation to safeguard
the airway (Formisano 2004).
Following the previous assessment patients with impaired
consciousness can be classified according to their degree of
consciousness disturbance into lethargic, stuporous or comatose.
Lethargy resembles sleepiness, except that the patient is
incapable of becoming fully alert; these patients are conversant
In the initial assessment of coma, it is common to judge by
spontaneous actions, response to vocal stimuli and response to
painful stimuli; this is known as the AVPU (alert, vocal stimuli,
painful stimuli, unconscious) scale. The most common scales
used for rapid assessment are:
1. The Glasgow Coma Scale (GCS), which aims to record the
conscious state of a person, in initial as well as continuing
assessment. When a patient is assessed and the resulting score is
either 14 (original scale) or 15 (the more widely used modified or
revised scale), this means ‘normal’; while if a patient is unable to
voluntarily open their eyes, does not have a sleep-wake cycle, is
unresponsive in spite of strong sensory (painful) or verbal
stimuli and who generally scores between 3 to 8 on the Glasgow
Coma Scale, (s)he is considered to be in coma.
2. Pediatric Glasgow Coma Scale: The Pediatric Glasgow Coma
Scale (PGCS) is the equivalent of the Glasgow Coma Scale used to
assess the mental state of adult patients. As with the GCS, the
PGCS comprises three tests: eye, verbal and motor responses.
The three values separately as well as their sum are considered
(Holmes 2005). The lowest possible PGCS is 3 (deep coma or
death) whilst the highest is 15 (fully awake and aware) (Holmes
2005).
Diagnosis of coma is simple; but determining the cause of the
underlying pathology may prove to be challenging. As in those
with deep unconsciousness, there is a risk of asphyxiation as
control over the muscles in the face and throat is diminished, so
those in a coma are typically assessed for airway management,
nasopharyngeal airway or endotracheal intubation to safeguard
the airway (Formisano 2004).
Following the previous assessment patients with impaired
consciousness can be classified according to their degree of
consciousness disturbance into lethargic, stuporous or comatose.
Lethargy resembles sleepiness, except that the patient is
incapable of becoming fully alert; these patients are conversant
and attentive but slow to respond, unable to adequately perform
simple concentration tasks such as counting from 20 to 1, or
reciting the months in reverse.
Stupor means incomplete arousal to painful stimuli, little or no
response to verbal commands, the patient may obey commands
temporarily when aroused by noxious stimuli but more often
only by pain.
Coma is the absence of verbal or complex motor responses to
any stimulus (Stevens 2006).
Basic assessments
1. Pupillary functions may be normal if the lesion is rostral to
the midbrain, while if the injury is diffuse, e.g., global cerebral
anoxia or ischemia, the pupillary abnormality is bilateral. Pupil
size is important as midposition (2-5 mm) fixed or irregular
pupils imply a focal midbrain lesion; pinpoint reactive pupils
occur in global hypoxic ischemic insult with pontine damage, or
poisoning with opiates and cholinergic active materials; and
bilateral fixed and dilated pupils can reflect central herniation
or global hypoxic ischemic or poisoning with barbiturates,
scopolamine, and atropine. Unilateral dilated pupil suggests
compression of the third cranial nerve and midbrain, which
necessitates an immediate search for a potentially correctable
abnormality to avoid irreversible injury. In case of post-cardiac
arrest coma, if pupils remain nonreactive for more than 6-8
hours after resuscitation, the prognosis for neurological
recovery is generally guarded (Stevens 2006).
2. Posturing of the body: decorticate posturing (painful stimuli
provoke abnormal flexion of upper limbs) indicates a lesion at
the thalamus or cortical damage; decerebrate posturing (the
arms and legs extend and pronate in response to pain) denotes
that the injury is localized to the midbrain and upper pons; an
injury of the lower brain stem (medulla) leads to flaccid
extremities.
simple concentration tasks such as counting from 20 to 1, or
reciting the months in reverse.
Stupor means incomplete arousal to painful stimuli, little or no
response to verbal commands, the patient may obey commands
temporarily when aroused by noxious stimuli but more often
only by pain.
Coma is the absence of verbal or complex motor responses to
any stimulus (Stevens 2006).
Basic assessments
1. Pupillary functions may be normal if the lesion is rostral to
the midbrain, while if the injury is diffuse, e.g., global cerebral
anoxia or ischemia, the pupillary abnormality is bilateral. Pupil
size is important as midposition (2-5 mm) fixed or irregular
pupils imply a focal midbrain lesion; pinpoint reactive pupils
occur in global hypoxic ischemic insult with pontine damage, or
poisoning with opiates and cholinergic active materials; and
bilateral fixed and dilated pupils can reflect central herniation
or global hypoxic ischemic or poisoning with barbiturates,
scopolamine, and atropine. Unilateral dilated pupil suggests
compression of the third cranial nerve and midbrain, which
necessitates an immediate search for a potentially correctable
abnormality to avoid irreversible injury. In case of post-cardiac
arrest coma, if pupils remain nonreactive for more than 6-8
hours after resuscitation, the prognosis for neurological
recovery is generally guarded (Stevens 2006).
2. Posturing of the body: decorticate posturing (painful stimuli
provoke abnormal flexion of upper limbs) indicates a lesion at
the thalamus or cortical damage; decerebrate posturing (the
arms and legs extend and pronate in response to pain) denotes
that the injury is localized to the midbrain and upper pons; an
injury of the lower brain stem (medulla) leads to flaccid
extremities.
3. Ocular reflexes: assessment of the brainstem and cortical
functions happen through special reflex tests such as the
oculocephalic reflex test (Doll’s eyes test), oculovestibular reflex
test (cold caloric test), nasal tickle, corneal reflex, and the gag
reflex.
4. Vital signs: temperature (rectal is most accurate), blood
pressure, heart rate (pulse), respiratory rate, and oxygen
saturation (Inouye 2006). It is mandatory to evaluate these basic
vital signs quickly and efficiently to gain insight into a patient’s
metabolism, fluid status, heart function, vascular integrity, and
tissue oxygenation status.
5. The respiratory pattern (breathing rhythm) is significant and
should be noted in a comatose patient. Certain stereotypical
patterns of breathing have been identified including Cheyne-
Stokes respiratory pattern, where the patient’s breathing is
described as alternating episodes of hyperventilation and apnea,
a dangerous pattern often seen in pending herniation, extensive
cortical lesions, or brainstem damage. Apneustic breathing is
characterized by sudden pauses of inspiration and is due to
pontine lesion. Ataxic (Biot’s) breathing is an irregular chaotic
pattern and is due to a lesion of the medulla. The first priority in
managing a comatose patient is to stabilize the vital functions,
following the ABC rule (Airway, Breathing, and Circulation).
Once a person in a coma is stable, assessment of the underlying
cause must be done, including imaging (CT scan, CT
angiography, magnetic resonance imaging (MRI), magnetic
resonance angiography (MRA) and magnetic resonance
venography (MRV) if needed ) and special studies, e.g., EEG and
transcranial Doppler.
Coma is a medical emergency, and attention must first be
directed to maintaining the patient’s respiration and circulation
as previously mentioned using intubation and ventilation,
administration of intravenous fluids or blood and other
supportive care as needed. Measurement of electrolytes is a
commonly performed diagnostic procedure, most often sodium
functions happen through special reflex tests such as the
oculocephalic reflex test (Doll’s eyes test), oculovestibular reflex
test (cold caloric test), nasal tickle, corneal reflex, and the gag
reflex.
4. Vital signs: temperature (rectal is most accurate), blood
pressure, heart rate (pulse), respiratory rate, and oxygen
saturation (Inouye 2006). It is mandatory to evaluate these basic
vital signs quickly and efficiently to gain insight into a patient’s
metabolism, fluid status, heart function, vascular integrity, and
tissue oxygenation status.
5. The respiratory pattern (breathing rhythm) is significant and
should be noted in a comatose patient. Certain stereotypical
patterns of breathing have been identified including Cheyne-
Stokes respiratory pattern, where the patient’s breathing is
described as alternating episodes of hyperventilation and apnea,
a dangerous pattern often seen in pending herniation, extensive
cortical lesions, or brainstem damage. Apneustic breathing is
characterized by sudden pauses of inspiration and is due to
pontine lesion. Ataxic (Biot’s) breathing is an irregular chaotic
pattern and is due to a lesion of the medulla. The first priority in
managing a comatose patient is to stabilize the vital functions,
following the ABC rule (Airway, Breathing, and Circulation).
Once a person in a coma is stable, assessment of the underlying
cause must be done, including imaging (CT scan, CT
angiography, magnetic resonance imaging (MRI), magnetic
resonance angiography (MRA) and magnetic resonance
venography (MRV) if needed ) and special studies, e.g., EEG and
transcranial Doppler.
Coma is a medical emergency, and attention must first be
directed to maintaining the patient’s respiration and circulation
as previously mentioned using intubation and ventilation,
administration of intravenous fluids or blood and other
supportive care as needed. Measurement of electrolytes is a
commonly performed diagnostic procedure, most often sodium
and potassium; chloride levels are rarely measured except for
arterial blood gases (Bateman 2001). Once a patient is stable and
no longer in immediate danger, the medical staff should start
parallel work, first investigating the patient to find out any
underlying pathology of his presenting illness, second, managing
the presenting illness symptoms. Infections must be prevented
and a balanced nutrition provided. The nursing staff, to guard
against pressure ulcers, may move the patient every 2–3 hours
from side to side and, depending on the state of consciousness,
sometimes to a chair. Physical therapy may also be used to
prevent contractures and orthopedic deformities that would
limit recovery for those patients who emerge from coma
(Wijdicks 2002).
People may emerge from a coma with a combination of
physical, intellectual and psychological difficulties that need
special attention; recovery usually occurs gradually and some
patients acquire more and more ability to respond, others never
progress beyond very basic responses. Regaining consciousness
is not instant in all comatose patients: in the first days, patients
are only awake for a few minutes, the duration of awake time
gradually increases, until they regain full consciousness. The
coma patient awakens sometimes in a profound state of
confusion, not knowing how they got there and sometimes
suffering from dysarthria, the inability to articulate speech, and
other disabilities. Time is the best general predictor of a chance
of recovery: after 4 months of coma caused by brain damage, the
chance of partial recovery is less than 15%, and the chance of full
recovery is very low (Wijdicks 2002). Coma which lasts seconds
to minutes may result in post-traumatic amnesia (PTA) lasting
from hours to days; recovery occurs over days to weeks. Coma
which lasts hours to days may result in PTA lasting from days to
weeks; its recovery occurs over months. Coma which lasts weeks
may result in PTA that lasts months; recovery occurs over
months.
arterial blood gases (Bateman 2001). Once a patient is stable and
no longer in immediate danger, the medical staff should start
parallel work, first investigating the patient to find out any
underlying pathology of his presenting illness, second, managing
the presenting illness symptoms. Infections must be prevented
and a balanced nutrition provided. The nursing staff, to guard
against pressure ulcers, may move the patient every 2–3 hours
from side to side and, depending on the state of consciousness,
sometimes to a chair. Physical therapy may also be used to
prevent contractures and orthopedic deformities that would
limit recovery for those patients who emerge from coma
(Wijdicks 2002).
People may emerge from a coma with a combination of
physical, intellectual and psychological difficulties that need
special attention; recovery usually occurs gradually and some
patients acquire more and more ability to respond, others never
progress beyond very basic responses. Regaining consciousness
is not instant in all comatose patients: in the first days, patients
are only awake for a few minutes, the duration of awake time
gradually increases, until they regain full consciousness. The
coma patient awakens sometimes in a profound state of
confusion, not knowing how they got there and sometimes
suffering from dysarthria, the inability to articulate speech, and
other disabilities. Time is the best general predictor of a chance
of recovery: after 4 months of coma caused by brain damage, the
chance of partial recovery is less than 15%, and the chance of full
recovery is very low (Wijdicks 2002). Coma which lasts seconds
to minutes may result in post-traumatic amnesia (PTA) lasting
from hours to days; recovery occurs over days to weeks. Coma
which lasts hours to days may result in PTA lasting from days to
weeks; its recovery occurs over months. Coma which lasts weeks
may result in PTA that lasts months; recovery occurs over
months.
General Care of the Comatose Patient
1. Airway protection: adequate oxygenation, ventilation and
prevention of aspiration are the most important goals; most
patients will require endotracheal intubation and frequent
orotracheal suctioning.
2. Intravenous hydration: stuporous patients should receive
nothing by mouth; use only isotonic fluids in these patients to
avoid increasing the size of the cerebral edema or increased
intracranial pressure (ICP).
3. Nutrition: enteral feeds via a small bore nasogastric tube.
4. Skin: the patient must be turned every 1-2 hours to prevent
pressure sores; an inflatable or foam mattress and protective
heel pads may also be beneficial.
5. Eyes: prevent corneal abrasion by taping the eyelids shut or
by applying a lubricant.
6. Bowel care: constipation and gastric stress ulcers should be
avoided.
7. Bladder care: indwelling urinary catheters are a common
source of infection and should be used judiciously; intermittent
catheterization every 6 hours when possible.
8. Joint mobility: passive range of motion daily exercises to
prevent contractures.
9. Deep venous thrombosis prophylaxis: subcutaneous
anticoagulants and external pneumatic compression stockings or
both (Upchurch 1995).
To complete this important critical situation, we will discuss
two other categories, the permanent vegetative state and lockedin
syndrome.
Permanent Vegetative State
Permanent vegetative state (PVS) means an irreversible state of
wakefulness without awareness, associated with sleep-wake
cycles and preserved brainstem functions. There are no reliable
1. Airway protection: adequate oxygenation, ventilation and
prevention of aspiration are the most important goals; most
patients will require endotracheal intubation and frequent
orotracheal suctioning.
2. Intravenous hydration: stuporous patients should receive
nothing by mouth; use only isotonic fluids in these patients to
avoid increasing the size of the cerebral edema or increased
intracranial pressure (ICP).
3. Nutrition: enteral feeds via a small bore nasogastric tube.
4. Skin: the patient must be turned every 1-2 hours to prevent
pressure sores; an inflatable or foam mattress and protective
heel pads may also be beneficial.
5. Eyes: prevent corneal abrasion by taping the eyelids shut or
by applying a lubricant.
6. Bowel care: constipation and gastric stress ulcers should be
avoided.
7. Bladder care: indwelling urinary catheters are a common
source of infection and should be used judiciously; intermittent
catheterization every 6 hours when possible.
8. Joint mobility: passive range of motion daily exercises to
prevent contractures.
9. Deep venous thrombosis prophylaxis: subcutaneous
anticoagulants and external pneumatic compression stockings or
both (Upchurch 1995).
To complete this important critical situation, we will discuss
two other categories, the permanent vegetative state and lockedin
syndrome.
Permanent Vegetative State
Permanent vegetative state (PVS) means an irreversible state of
wakefulness without awareness, associated with sleep-wake
cycles and preserved brainstem functions. There are no reliable
set of criteria defining and ensuring diagnosis of PVS in infants
under 3 months old, apart from anencephalics.
There are three major categories of disease in adults and
children that result in PVS, upon which the outcome of PVS
depends:
A. In acute traumatic and nontraumatic brain injury, PVS
usually evolves within 1 month of injury from a state of eyesclosed
coma to a state of wakefulness without awareness with
sleep-wake cycles and preserved brainstem functions.
B. Some degenerative and metabolic disorders of the brain (i.e.,
late stage of dementia of Alzheimer type, end stage of Parkinson
disease, and motor neuron disease, pontine myelinolysis, severe
uncorrected hypoglycaemic coma) inevitably progress toward an
irreversible vegetative state. Patients who are severely impaired
but retain some degree of awareness may lapse briefly into a
vegetative state from the effects of medication, infection,
superimposed illnesses, or decreased fluid and nutritional
intake. Such a temporary encephalopathy must be corrected
before labeling that patient with the diagnosis of PVS.
Consciousness recovery is unlikely if the vegetative state persists
for several months.
C. The third cause is severe developmental malformations of
the nervous system - the developmental vegetative state is a
form of PVS that affects some infants and children with severe
congenital malformations of the nervous system. These children
do not acquire awareness of self or their environment. This
diagnosis can be made at birth only in infants with anencephaly.
For children with other severe malformations who appear
vegetative at birth, observation for 3 to 6 months is
recommended to determine whether these infants acquire
awareness. The majority of such infants who are vegetative at
birth remain vegetative; those who acquire awareness usually
recover only to a severe disability.
under 3 months old, apart from anencephalics.
There are three major categories of disease in adults and
children that result in PVS, upon which the outcome of PVS
depends:
A. In acute traumatic and nontraumatic brain injury, PVS
usually evolves within 1 month of injury from a state of eyesclosed
coma to a state of wakefulness without awareness with
sleep-wake cycles and preserved brainstem functions.
B. Some degenerative and metabolic disorders of the brain (i.e.,
late stage of dementia of Alzheimer type, end stage of Parkinson
disease, and motor neuron disease, pontine myelinolysis, severe
uncorrected hypoglycaemic coma) inevitably progress toward an
irreversible vegetative state. Patients who are severely impaired
but retain some degree of awareness may lapse briefly into a
vegetative state from the effects of medication, infection,
superimposed illnesses, or decreased fluid and nutritional
intake. Such a temporary encephalopathy must be corrected
before labeling that patient with the diagnosis of PVS.
Consciousness recovery is unlikely if the vegetative state persists
for several months.
C. The third cause is severe developmental malformations of
the nervous system - the developmental vegetative state is a
form of PVS that affects some infants and children with severe
congenital malformations of the nervous system. These children
do not acquire awareness of self or their environment. This
diagnosis can be made at birth only in infants with anencephaly.
For children with other severe malformations who appear
vegetative at birth, observation for 3 to 6 months is
recommended to determine whether these infants acquire
awareness. The majority of such infants who are vegetative at
birth remain vegetative; those who acquire awareness usually
recover only to a severe disability.
Diagnosis
The vegetative state is diagnosed, according to its definition, as
being persistent at least for one month. Based upon class II
evidence and consensus that reflects a high degree of clinical
certainty, the following criteria is standard concerning PVS:
– PVS can be judged to be permanent, at 12 months after
traumatic brain injury in adults and children. Special
attention to signs of awareness should be devoted to
children during the first year after traumatic injury.
– PVS can be judged to be permanent if it lasts more than 3
months, in case of nontraumatic brain injury in both adults
and children.
– The chance for recovery, after these periods, is exceedingly
low and recovery is almost always to a severe disability.
Management
When a patient has been diagnosed as being in a PVS by a
physician skilled in neurological assessment and diagnosis,
physicians have the responsibility of discussing with the family
or surrogates the probability of the patient’s attaining the
various stages of recovery or remaining in a PVS:
– Patients in PVS should receive appropriate medical, nursing,
or home care to maintain their personal dignity and
hygiene.
– Physicians and the family/surrogates must determine
appropriate levels of treatment relative to the
administration or withdrawal of 1) medications and other
commonly ordered treatments; 2) supplemental oxygen and
use of antibiotics; 3) complex organ-sustaining treatments
such as dialysis; 4) administration of blood products; and 5)
artificial hydration and nutrition.
Recovery from PVS can be defined in terms of recovery of
consciousness and function. Recovery of consciousness can be
confirmed when a patient shows reliable signs of awareness of
The vegetative state is diagnosed, according to its definition, as
being persistent at least for one month. Based upon class II
evidence and consensus that reflects a high degree of clinical
certainty, the following criteria is standard concerning PVS:
– PVS can be judged to be permanent, at 12 months after
traumatic brain injury in adults and children. Special
attention to signs of awareness should be devoted to
children during the first year after traumatic injury.
– PVS can be judged to be permanent if it lasts more than 3
months, in case of nontraumatic brain injury in both adults
and children.
– The chance for recovery, after these periods, is exceedingly
low and recovery is almost always to a severe disability.
Management
When a patient has been diagnosed as being in a PVS by a
physician skilled in neurological assessment and diagnosis,
physicians have the responsibility of discussing with the family
or surrogates the probability of the patient’s attaining the
various stages of recovery or remaining in a PVS:
– Patients in PVS should receive appropriate medical, nursing,
or home care to maintain their personal dignity and
hygiene.
– Physicians and the family/surrogates must determine
appropriate levels of treatment relative to the
administration or withdrawal of 1) medications and other
commonly ordered treatments; 2) supplemental oxygen and
use of antibiotics; 3) complex organ-sustaining treatments
such as dialysis; 4) administration of blood products; and 5)
artificial hydration and nutrition.
Recovery from PVS can be defined in terms of recovery of
consciousness and function. Recovery of consciousness can be
confirmed when a patient shows reliable signs of awareness of
self and their environment, reproducible voluntary behavioral
responses to visual and auditory stimuli, and interaction with
others. Recovery of function occurs when a patient becomes
mobile and is able to communicate, learn, and perform adaptive
skills and self care and participate in recreational or vocational
activities. Using these parameters, recovery of function can be
defined with the Glasgow Outcome Scale.
The life span of adults and children in a PVS proves to be
reduced; for most PVS patients, life expectancy ranges from 2 to
5 years and survival beyond 10 years is unusual. Once PVS is
considered permanent, a “Do not resuscitate (DNR)” order is
appropriate which includes no ventilatory or cardiopulmonary
resuscitation. The decision to implement a DNR order, however,
may be made earlier in the course of the patient’s illness if there
is an advanced directive or agreement by the appropriate
surrogate of the patient and the physicians responsible for the
care of the patient (Plum 2007).
Locked-in Syndrome
Locked-in syndrome usually results in quadriparesis and the
inability to speak in otherwise cognitively intact individuals.
Patients with locked-in syndrome may be able to communicate
with others through coded messages by blinking or moving their
eyes, which are often not affected by the paralysis. Patients with
locked-in syndrome are conscious and aware with no loss of
cognitive functions. They sometimes can retain proprioception
and sensation throughout their body. Some patients with lockedin
syndrome may have the ability to move some muscles of the
face, and some or all of the extraocular eye muscles. Patients
with locked-in syndrome lack coordination between breathing
and voice that restricts them from producing voluntary sounds,
even though the vocal cords themselves are not paralyzed. In
children, the commonest cause is a stroke of the ventral pons.
Unlike persistent vegetative state, locked-in syndrome is caused
by damage of the lower brain and brainstem without damage to
the upper brain (Leon Carrion 2002). Possible causes of locked-in
syndrome include: traumatic brain injury, diseases of the
circulatory system, overdose of certain drugs, various causes
which lead to damage to the nerve cells, particularly destruction
of the myelin sheath, e.g., central pontine myelinolysis
secondary to rapid correction of hyponatremia and basilar
artery (ischemic or hemorrhagic) stroke.
There is neither a standard treatment for locked-in syndrome,
nor is there a cure, but stimulation of muscle reflexes with
electrodes (NMES) has been known to help patients regain some
muscle function. Assistive computer interface technologies in
combination with eye tracking may be used to help patients
communicate. Direct brain stimulation research developed a
technique that allows locked-in patients to communicate via
sniffing (Leon Carrion 2002). It is extremely rare for any
significant motor function to return and the majority of lockedin
syndrome patients do not regain motor control, but devices
are available to help patients communicate. 90% die within the
first four months after onset. However, some patients continue
to live for much longer periods of time (Bateman 2001).
Brain Death
After exclusion of the previous syndromes, and in the absence
of brain stem reflexes, brain death in deeply comatose patients
should be established through the following criteria:
1. Irreversible coma
2. Absence of brain stem reflexes
3. Absence of spontaneous respiration (Wood 2004)
responses to visual and auditory stimuli, and interaction with
others. Recovery of function occurs when a patient becomes
mobile and is able to communicate, learn, and perform adaptive
skills and self care and participate in recreational or vocational
activities. Using these parameters, recovery of function can be
defined with the Glasgow Outcome Scale.
The life span of adults and children in a PVS proves to be
reduced; for most PVS patients, life expectancy ranges from 2 to
5 years and survival beyond 10 years is unusual. Once PVS is
considered permanent, a “Do not resuscitate (DNR)” order is
appropriate which includes no ventilatory or cardiopulmonary
resuscitation. The decision to implement a DNR order, however,
may be made earlier in the course of the patient’s illness if there
is an advanced directive or agreement by the appropriate
surrogate of the patient and the physicians responsible for the
care of the patient (Plum 2007).
Locked-in Syndrome
Locked-in syndrome usually results in quadriparesis and the
inability to speak in otherwise cognitively intact individuals.
Patients with locked-in syndrome may be able to communicate
with others through coded messages by blinking or moving their
eyes, which are often not affected by the paralysis. Patients with
locked-in syndrome are conscious and aware with no loss of
cognitive functions. They sometimes can retain proprioception
and sensation throughout their body. Some patients with lockedin
syndrome may have the ability to move some muscles of the
face, and some or all of the extraocular eye muscles. Patients
with locked-in syndrome lack coordination between breathing
and voice that restricts them from producing voluntary sounds,
even though the vocal cords themselves are not paralyzed. In
children, the commonest cause is a stroke of the ventral pons.
Unlike persistent vegetative state, locked-in syndrome is caused
by damage of the lower brain and brainstem without damage to
the upper brain (Leon Carrion 2002). Possible causes of locked-in
syndrome include: traumatic brain injury, diseases of the
circulatory system, overdose of certain drugs, various causes
which lead to damage to the nerve cells, particularly destruction
of the myelin sheath, e.g., central pontine myelinolysis
secondary to rapid correction of hyponatremia and basilar
artery (ischemic or hemorrhagic) stroke.
There is neither a standard treatment for locked-in syndrome,
nor is there a cure, but stimulation of muscle reflexes with
electrodes (NMES) has been known to help patients regain some
muscle function. Assistive computer interface technologies in
combination with eye tracking may be used to help patients
communicate. Direct brain stimulation research developed a
technique that allows locked-in patients to communicate via
sniffing (Leon Carrion 2002). It is extremely rare for any
significant motor function to return and the majority of lockedin
syndrome patients do not regain motor control, but devices
are available to help patients communicate. 90% die within the
first four months after onset. However, some patients continue
to live for much longer periods of time (Bateman 2001).
Brain Death
After exclusion of the previous syndromes, and in the absence
of brain stem reflexes, brain death in deeply comatose patients
should be established through the following criteria:
1. Irreversible coma
2. Absence of brain stem reflexes
3. Absence of spontaneous respiration (Wood 2004)
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