Locked-in Syndrome

ByKenneth Maiese, MD

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Patient Education

NOTE: This is the Professional Version. CONSUMERS: Click here for the
Consumer Version

Coma and Impaired Consciousness

Overview of Coma and Impaired Consciousness
Vegetative State and Minimally Conscious State
Locked-in Syndrome
Brain Death
Locked-in syndrome is a state of wakefulness and awareness with quadriplegia and paralysis of
the lower cranial nerves, resulting in inability to show facial expression, move, speak, or
communicate, except by coded eye movements.

Locked-in syndrome typically results from a pontine hemorrhage or infarct that causes
quadriplegia and disrupts and damages the lower cranial nerves and the centers that control
horizontal gaze. Other disorders that result in severe widespread motor paralysis (eg,
Guillain-Barr syndrome) and cancers that involve the posterior fossa and the pons are less
common causes.

Patients have intact cognitive function and are awake, with eye opening and normal sleep-
wake cycles. They can hear and see. However, they cannot move their lower face, chew,
swallow, speak, breathe, move their limbs, or move their eyes laterally. Vertical eye
movement is possible; patients can open and close their eyes or blink a specific number of
times to answer questions.

Diagnosis
Clinical evaluation

Diagnosis is primarily clinical. Because patients lack the motor responses (eg, withdrawal from painful stimuli)
usually used to measure responsiveness, they may be mistakenly thought to be unconscious. Thus, all patients who
cannot move should have their comprehension tested by requesting eye blinking or vertical eye movements.

As in vegetative state, neuroimaging is indicated to rule out treatable disorders. Brain imaging with CT or MRI is
done and helps identify the pontine abnormality. PET, SPECT, or functional MRI may be done to further assess
cerebral function if the diagnosis is in doubt.

In patients with locked-in syndrome, EEG shows normal sleep-wake patterns.

Prognosis
 Prognosis depends on the cause and the subsequent level of support provided. For example, locked-in syndrome due
to transient ischemia or a small stroke in the vertebrobasilar artery distribution may resolve completely. When the
cause (eg, Guillain-Barr syndrome) is partly reversible, recovery can occur over months but is seldom complete.

Favorable prognostic features include

Early recovery of lateral eye movements

Early recovery of evoked potentials in response to magnetic stimulation of the motor cortex

Irreversible or progressive disorders (eg, cancers that involve the posterior fossa and the pons) are usually fatal.

Treatment
Supportive care

Supportive care is the mainstay of treatment for patients with locked-in syndrome and should include the following:

Preventing systemic complications due to immobilization (eg, pneumonia, UTI, thromboembolic disease)
Providing good nutrition
Preventing pressure ulcers
Providing physical therapy to prevent limb contractures

There is no specific treatment.

Speech therapists may help establish a communication code using eye blinks or movements.

Because cognitive function is intact and communication is possible, patients should make their own health care
decisions.

Some patients with locked-in syndrome communicate with each other via the Internet using a computer terminal
controlled by eye movements and other means.

Last full review/revision April 2016 by Kenneth Maiese, MD

Vegetative State and Minimally

Conscious State
ByKenneth Maiese, MD

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Patient Education

NOTE: This is the Professional Version. CONSUMERS: Click here for the
Consumer Version

Coma and Impaired Consciousness

Overview of Coma and Impaired Consciousness
 Vegetative State and Minimally Conscious State
Locked-in Syndrome
Brain Death
A vegetative state is absence of responsiveness and awareness due to overwhelming dysfunction
of the cerebral hemispheres, with sufficient sparing of the diencephalon and brain stem to
preserve autonomic and motor reflexes and sleep-wake cycles. Patients may have complex
reflexes, including eye movements, yawning, and involuntary movements to noxious stimuli, but
show no awareness of self or environment. A minimally conscious state, unlike a vegetative
state, is characterized by some evidence of awareness of self and/or the environment, and
patients tend to improve. Diagnosis is clinical. Treatment is mainly supportive. Prognosis for
patients with persistent deficits is typically bleak.

The vegetative state is a chronic condition that preserves the ability to maintain BP,
respiration, and cardiac function, but not cognitive function. Hypothalamic and medullary
brain stem functions remain intact to support cardiorespiratory and autonomic functions and
are sufficient for survival if medical and nursing care is adequate. The cortex is severely
damaged (eliminating cognitive function), but the reticular activating system (RAS) remains
functional (making wakefulness possible). Midbrain or pontine reflexes may or may not be
present. Patients have no awareness of self and interact with the environment only via
reflexes. Seizure activity may be present but not be clinically evident.

Traditionally, a vegetative state that lasts > 1 mo is considered to be a persistent vegetative

state. However, a diagnosis of persistent vegetative state does not imply permanent disability
because in very rare cases (eg, after traumatic brain injury), patients can improve, reaching a
minimally conscious state or a higher level of consciousness.

The most common causes are

Traumatic brain injury

Diffuse cerebral hypoxia

However, any disorder that results in brain damage can cause a vegetative state. Typically, a
vegetative state occurs because the function of the brain stem and diencephalon resumes after
coma, but cortical function does not.

In the minimally conscious state, unlike the vegetative state, there is evidence that patients
are aware of themselves and/or their environment. Patients also tend to improve (ie, gradually
become more conscious), but improvement is limited. This state may be the first indication of
brain damage or may follow a vegetative state as people recover some function. Patients can
transition between the vegetative state and minimally conscious state, sometimes for years
after the original brain damage.

Symptoms and Signs

Vegetative state
Patients show no evidence of awareness of self or environment and cannot interact with other people. Purposeful
responses to external stimuli are absent, as are language comprehension and expression.

Signs of an intact reticular formation (eg, eye opening) and an intact brain stem (eg, reactive pupils, oculocephalic
reflex) are present. Sleep-wake cycles occur but do not necessarily reflect a specific circadian rhythm and are not
associated with the environment. More complex brain stem reflexes, including yawning, chewing, swallowing, and,
uncommonly, guttural vocalizations, are also present. Arousal and startle reflexes may be preserved; eg, loud sounds
or blinking with bright lights may elicit eye opening. Eyes may water and produce tears. Patients may appear to smile
or frown. Spontaneous roving eye movementsusually slow, of constant velocity, and without saccadic jerksmay
be misinterpreted as volitional tracking and can be misinterpreted by family members as evidence of awareness.

Patients cannot react to visual threat and cannot follow commands. The limbs may move, but the only purposeful
motor responses that occur are primitive (eg, grasping an object that contacts the hand). Pain usually elicits a motor
response (typically decorticate or decerebrate posturing) but no purposeful avoidance. Patients have fecal and urinary
incontinence. Cranial nerve and spinal reflexes are typically preserved.

Rarely, brain activity, detected by functional MRI or EEG, indicates a response to questions and commands even
though there is no behavioral response. The extent of patients' actual awareness is not yet known. In most patients
who have such brain activity, the vegetative state resulted from traumatic brain injury, not hypoxic encephalopathy.

Minimally conscious state

Fragments of meaningful interaction with the environment are preserved. Patients may establish eye contact,
purposefully grasp at objects, respond to commands in a stereotypic manner, or answer with the same word.

Diagnosis
Clinical criteria after sufficient observation
Neuroimaging

A vegetative state is suggested by characteristic findings (eg, no purposeful activity or comprehension) plus signs of
an intact reticular formation. Diagnosis is based on clinical criteria. However, neuroimaging is indicated to rule out
treatable disorders.

The vegetative state must be distinguished from the minimally conscious state. Both states can be permanent or
temporary, and the physical examination may not reliably distinguish one from the other. Sufficient observation is
needed. If observation is too brief, evidence of awareness may be overlooked. Some patients with severe Parkinson
disease are misdiagnosed as being in a vegetative state.

CT or MRI can differentiate an ischemic infarct, an intracerebral hemorrhage, and a mass lesion involving the cortex
or the brain stem. MR angiography can be used to visualize the cerebral vasculature after exclusion of a cerebral
hemorrhage. Diffusion-weighted MRI is becoming the preferred imaging modality for following ongoing ischemic
changes in the brain.

PET and SPECT can be used to assess cerebral function (rather than brain anatomy). If the diagnosis of persistent
vegetative state is in doubt, PET or SPECT should be done.

EEG is useful in assessing cortical dysfunction and identifying occult seizure activity.

Prognosis
Vegetative state
Prognosis varies somewhat by cause and duration of the vegetative state. Prognosis may be better if the cause is a
reversible metabolic condition (eg, toxic encephalopathy) than if the cause is neuronal death due to extensive hypoxia
and ischemia or another condition. Also, younger patients may recover more motor function than older patients but
not more cognition, behavior, or speech.

Recovery from a vegetative state is unlikely after 1 mo if brain damage is nontraumatic and after 12 mo if brain
damage is traumatic. Even if some recovery occurs after these intervals, most patients are severely disabled. Rarely,
improvement occurs late; after 5 yr, about 3% of patients recover the ability to communicate and comprehend, but
even fewer can live independently; no patients regain normal function.
If a vegetative state persists, most patients die within 6 mo of the original brain damage. The cause is usually
pulmonary infection, UTI, or multiple organ failure, or death may be sudden and of unknown cause. For most of the
rest, life expectancy is about 2 to 5 yr; only about 25% of patients live > 5 yr. A few patients live for decades.

Minimally conscious state

Most patients tend to recover consciousness but to a limited extent depending on how long the minimally conscious
state has lasted. The longer it has lasted, the less chance of patients recovering higher cortical function. Prognosis may
be better if the cause is traumatic brain injury.

Rarely, patients regain clear but limited awareness after years of coma, called awakenings by the news media.

Treatment
Supportive care

Supportive care is the mainstay of treatment for patients in a vegetative state or minimally conscious state; it should
include the following:

Preventing systemic complications due to immobilization (eg, pneumonia, UTI, thromboembolic disease)
Providing good nutrition
Preventing pressure ulcers
Providing physical therapy to prevent limb contractures

Vegetative state has no specific treatment. Decisions about life-sustaining care should involve social services, the
hospital ethics committee, and family members. Maintaining patients, especially those without advanced directives to
guide decisions about terminating treatment, in a prolonged vegetative state raises ethical and other (eg, resource
utilization) questions.

Most patients in a minimally conscious state do not respond to specific treatments. However, rarely, treatment
with zolpidem can cause dramatic and repeated improvement in neurologic responsiveness for as long as the drug is
continued.

Key Points
Vegetative state is typically characterized by absence of responsiveness and awareness due to overwhelming
dysfunction of the cerebral hemispheres, intact brain stem function, and sometimes the simulation of
awareness despite its absence.
Minimally conscious state differs from vegetative state in that patients have some interaction with the
environment and tend to improve over time.
Diagnosis requires exclusion of other disorders and often prolonged observation, particularly to differentiate
vegetative state, minimally conscious state, and Parkinson disease.
Prognosis tends to be poor, particularly for patients in a vegetative state.
Treatment is mainly supportive.

Last full review/revision April 2016 by Kenneth Maiese, MD

Overview of Coma and Impaired

Consciousness
ByKenneth Maiese, MD
 CLICK HERE FOR

Patient Education

NOTE: This is the Professional Version. CONSUMERS: Click here for the
Consumer Version

Coma and Impaired Consciousness

Overview of Coma and Impaired Consciousness
Vegetative State and Minimally Conscious State
Locked-in Syndrome
Brain Death
Coma is unresponsiveness from which the patient cannot be aroused.Impaired
consciousness refers to similar, less severe disturbances of consciousness; these disturbances are
not considered coma. The mechanism for coma or impaired consciousness involves dysfunction
of both cerebral hemispheres or of the reticular activating system (also known as the ascending
arousal system). Causes may be structural or nonstructural (eg, toxic or metabolic
disturbances). Damage may be focal or diffuse. Diagnosis is clinical; identification of cause
requires laboratory tests and neuroimaging. Treatment is immediate stabilization and specific
management of the cause. For long-term coma, adjunctive treatment includes passive range-of-
motion exercises, enteral feedings, and measures to prevent pressure ulcers.

Decreased or impaired consciousness or alertness refers to decreased responsiveness to

external stimuli. Severe impairment includes

Coma: The patient cannot be aroused, and the eyes do not open in response to any
stimulation.
Stupor: The patient can be awakened only by vigorous physical stimulation.

Less severely impaired levels of consciousness are often labeled as lethargy or, if more
severe, obtundation. However, differentiation between less severely impaired levels is often
imprecise; the label is less important than a precise clinical description (eg, the best level of
response is partial limb withdrawal to nail bed pressure). Delirium differs because cognitive
disturbances (in attention, cognition, and level of consciousness) fluctuate more; also,
delirium is usually reversible.

Pathophysiology
Maintaining alertness requires intact function of the cerebral hemispheres and preservation of arousal mechanisms in
the reticular activating system (RASalso known as the ascending arousal system)an extensive network of nuclei
and interconnecting fibers in the upper pons, midbrain, and posterior diencephalon. Therefore, the mechanism of
impaired consciousness must involve both cerebral hemispheres or dysfunction of the RAS.

To impair consciousness, cerebral dysfunction must be bilateral; unilateral cerebral hemisphere disorders are not
sufficient, although they may cause severe neurologic deficits. However, rarely, a unilateral massive hemispheric
focal lesion (eg, left middle cerebral artery stroke) impairs consciousness if the contralateral hemisphere is already
compromised or if it results in compression of the contralateral hemisphere (eg, by causing edema).

Usually, RAS dysfunction results from a condition that has diffuse effects, such as toxic or metabolic disturbances
(eg, hypoglycemia, hypoxia, uremia, drug overdose). RAS dysfunction can also be caused by focal ischemia (eg,
certain upper brain stem infarcts), hemorrhage, or direct, mechanical disruption.
Any condition that increases intracranial pressure (ICP) may decrease cerebral perfusion pressure, resulting in
secondary brain ischemia. Secondary brain ischemia may affect the RAS or both cerebral hemispheres, impairing
consciousness.

When brain damage is extensive, brain herniation (see Figure: Brain herniation. and Effects of Brain Herniation)
contributes to neurologic deterioration because it does the following:

Directly compresses brain tissue

Increases ICP
May lead to hydrocephalus
Results in neuronal and vascular cell dysfunction

In addition to the direct effects of increased ICP on neuronal and vascular cells, cellular pathways of apoptosis and
autophagy (which are forms of programmed cell death or destruction) can become activated.

Impaired consciousness may progress to coma and ultimately to brain death.

Brain herniation.
Because the skull is rigid after infancy, intracranial masses or swelling may increase intracranial pressure,
sometimes causing protrusion (herniation) of brain tissue through one of the rigid intracranial barriers
(tentorial notch, falx cerebri, foramen magnum). When intracranial pressure is increased sufficiently,
regardless of the cause, Cushing reflex and other autonomic abnormalities can occur. Cushing reflex
includes systolic hypertension with increased pulse pressure, irregular respirations, and bradycardia. Brain
herniation is life threatening.

Transtentorial herniation: The medial temporal lobe is squeezed by a unilateral mass across and under the
tentlike tentorium that supports the temporal lobe. The herniating lobe compresses the following structures:

Ipsilateral 3rd cranial nerve (often first) and posterior cerebral artery
As herniation progresses, the ipsilateral cerebral peduncle
In about 5% of patients, the contralateral 3rd cranial nerve and cerebral peduncle
Eventually, the upper brain stem and the area in or around the thalamus

Subfalcine herniation: The cingulate gyrus is pushed under the falx cerebri by an expanding mass high in a
cerebral hemisphere. In this process, one or both anterior cerebral arteries become trapped, causing
infarction of the paramedian cortex. As the infarcted area expands, patients are at risk of transtentorial
herniation, central herniation, or both.

Central herniation: Both temporal lobes herniate through the tentorial notch because of bilateral mass
effects or diffuse brain edema. Ultimately, brain death occurs.

Upward transtentorial herniation: This type can occur when an infratentorial mass (eg, tumor, cerebellar
hemorrhage) compresses the brain stem, kinking it and causing patchy brain stem ischemia. The posterior
3rd ventricle becomes compressed. Upward herniation also distorts the mesencephalon vasculature,
compresses the veins of Galen and Rosenthal, and causes superior cerebellar infarction due to occlusion of
the superior cerebellar arteries.

Tonsillar herniation: Usually, the cause is an expanding infratentorial mass (eg, cerebellar hemorrhage).
The cerebellar tonsils, forced through the foramen magnum, compress the brain stem and obstruct CSF
flow.
 Effects of Brain Herniation
Type of
Mechanism*
Herniation
Transtentorial Compression of ipsilateral 3rd
cranial nerve
Compression of the posterior
cerebral artery
Compression of the contralateral 3rd
cranial nerve and cerebral peduncle
(indented by the tentorium to form
Kernohan notch)
Compression of the ipsilateral
cerebral peduncle
Eventually, compression of the upper
brain stem and the area in and
around the thalamus
Further compromise of the brain
stem
Subfalcine Trapping of one or both anterior
(cingulate) cerebral arteries, causing infarction
of the paramedian cortex
Expansion of infarcted area
Central Bilateral, more or less symmetric
damage to the midbrain
Findings
Unilateral dilated, fixed pupil
Oculomotor paresis
Contralateral homonymous
hemianopia
Absence of blinking in
response to visual threat from
the hemianopic side in
obtunded patients
Contralateral dilated pupil and
oculomotor paresis
Ipsilateral hemiparesis
Contralateral hemiparesis
Impaired consciousness
Abnormal breathing patterns
Fixed, unequal pupils
Loss of oculocephalic reflex
Loss of oculovestibular reflex
Loss of corneal reflexes
Decerebrate posturing
Leg paralysis
Edema
Increased intracranial pressure
Increased risk of transtentorial
herniation, central herniation,
or both
Pupils fixed in midposition
Decerebrate posturing
Many of the same symptoms as
transtentorial herniation
Type of
Mechanism* Findings
Herniation
Further compromise of the brain Loss of all brain stem reflexes
stem
Disappearance of decerebrate
posturing

Cessation of respirations

Brain death
Upward Compression of the posterior 3rd Hydrocephalus, which
transtentorial ventricle increases intracranial pressure
Distortion of the mesencephalon Early: Nausea, vomiting,
vasculature occipital headache, ataxia

Compression of the veins of Galen Later: Somnolence, breathing

and Rosenthal abnormalities, patchy and
progressive loss of brain stem
Superior cerebellar infarction due to reflexes
occlusion of the superior cerebellar
arteries
Posterior fossa mass (eg, cerebellar Ataxia, dysarthria
hemorrhage)
Progression Increasing somnolence

Respiratory irregularities

Patchy but progressive loss of

Tonsillar Compression of the brain stem
Obstruction of CSF flow
brain stem reflexes
Acute hydrocephalus (with
impaired consciousness,
headache, vomiting, and
meningismus)

Dysconjugate eye movements

Later, abrupt respiratory and

cardiac arrest
*Not all mechanisms occur in every patient.

Etiology
Coma or impaired consciousness may result from structural disorders, which typically cause focal damage, or
nonstructural disorders, which most often cause diffuse damage (see Table: Common Causes of Coma or Impaired
Consciousness).

Common Causes of Coma or Impaired Consciousness

Cause Examples
Cause Examples
Focal
Structural disorders Brain abscess

Brain tumor

Head trauma (eg, concussion, cerebral lacerations or

contusions, epidural or subdural hematoma)

Hydrocephalus (acute)

Intraparenchymal hemorrhage

Subarachnoid hemorrhage

Upper brain stem infarct or hemorrhage

Nonstructural disorders Seizures (eg, nonconvulsive status epilepticus) or a postictal
state caused by an epileptogenic focus
Diffuse
Metabolic and endocrine Diabetic ketoacidosis
disorders
Hepatic encephalopathy

Hypercalcemia

Hypercapnia

Hyperglycemia

Hypernatremia

Hypoglycemia

Hyponatremia

Hypoxia

Hypothyroidism

Uremia

Wernicke encephalopathy
Infections Encephalitis

Meningitis

Sepsis
Cause Examples
Other disorders Diffuse axonal injury

Hypertensive encephalopathy

Hyperthermia or hypothermia
Drugs Alcohol

CNS stimulants

Sedatives

Other CNS depressants

Toxins Carbon monoxide
Psychiatric disorders (eg, psychogenic unresponsiveness) can mimic impaired consciousness, are volitional, and can
be distinguished from true impaired consciousness by neurologic examination.

Symptoms and Signs

Consciousness is decreased to varying degrees. Repeated stimuli arouse patients only briefly or not at all.

Depending on the cause, other symptoms develop (see Table: Findings by Location*):

Eye abnormalities: Pupils may be dilated, pinpoint, or unequal. One or both pupils may be fixed in
midposition. Eye movement may be dysconjugate or absent (oculomotor paresis) or involve unusual patterns
(eg, ocular bobbing, ocular dipping, opsoclonus). Homonymous hemianopia may be present. Other
abnormalities include absence of blinking in response to visual threat (almost touching the eye), as well as
loss of the oculocephalic reflex (the eyes do not move in response to head rotation), the oculovestibular
reflex (the eyes do not move in response to caloric stimulation), and corneal reflexes.
Autonomic dysfunction: Patients may have abnormal breathing patterns (Cheyne-Stokes or Biot
respirations), sometimes with hypertension and bradycardia (Cushing reflex). Abrupt respiratory and cardiac
arrest may occur.
Motor dysfunction: Abnormalities include flaccidity, hemiparesis, asterixis, multifocal myoclonus,
decorticate posturing (elbow flexion and shoulder adduction with leg extension), and decerebrate posturing
(limb extension and internal shoulder rotation).
Other symptoms: If the brain stem is compromised, nausea, vomiting, meningismus, occipital headache,
ataxia, and increasing somnolence can occur.

Findings by Location*

Location Abnormal Findings

Bilateral hemispheric Symmetric tone and response (flexor or extensor) to pain
damage or dysfunction*
Myoclonus (possible)

Periodic cycling of breathing

Supratentorial mass
compressing the brain
stem
Ipsilateral 3rd cranial nerve palsy with unilateral dilated,
fixed pupil and oculomotor paresis
Sometimes contralateral homonymous hemianopia and
absent blinking response to visual threat
Location Abnormal Findings
Contralateral hemiparesis
Brain stem lesion Early abnormal pupillary and oculomotor signs

Abnormal oculocephalic reflex

Abnormal oculovestibular reflex

Asymmetrical motor responses

Decorticate rigidity (usually due to an upper brain stem

lesion) or decerebrate rigidity (usually due to a bilateral
midbrain or pontine lesion)

Hyperventilation (due to a midbrain or upper pontine lesion)

Midbrain lesion Pupils locked in midposition with loss of light reflexes (due
to a structural or metabolic disorder that causes loss of both
sympathetic and parasympathetic pupillary tone)
Toxic-metabolic Spontaneous, conjugate roving eye movements in mild coma
dysfunction*
Fixed eye position in deeper coma

Abnormal oculovestibular reflex

Multifocal myoclonus

Asterixis (may be considered a type of negative myoclonus)

Decorticate and decerebrate rigidity or flaccidity

*Not all of the findings occur in all cases. Brain stem reflexes and pupillary light
responses may be intact in patients with bilateral hemispheric damage or dysfunction
or toxic-metabolic dysfunction; however, hypothermia, sedative overdose, or use of an
anesthetic can cause partial loss of brain stem reflexes.

Diagnosis
History
General physical examination
Neurologic examination, including eye examination
Laboratory tests (eg, pulse oximetry, bedside glucose measurement, blood and urine tests)
Immediate neuroimaging
Sometimes measurement of ICP
If diagnosis is unclear, lumbar puncture or EEG

Impaired consciousness is diagnosed if repeated stimuli arouse patients only briefly or not at all. If stimulation triggers
primitive reflex movements (eg, decerebrate or decorticate posturing), impaired consciousness may be deepening into
coma.

Diagnosis and initial stabilization (airway, breathing, and circulation) should occur simultaneously. Temperature is
measured to check for hypothermia or hyperthermia; if either is present, treatment is started immediately. Glucose
levels must be measured at bedside to identify low levels, which should also be corrected immediately. If trauma is
involved, the neck is immobilized until clinical history, physical examination, or imaging tests exclude an unstable
injury and damage to the cervical spine.

History
Medical identification bracelets or the contents of a wallet or purse may provide clues (eg, hospital identification card,
drugs). Relatives, paramedics, police officers, and any witnesses should be questioned about the circumstances and
environment in which the patient was found; containers that may have held food, alcohol, drugs, or poisons should be
examined and saved for identification (eg, drug identification aided by a poison center) and possible chemical
analysis.

Relatives should be asked about the following:

The onset and time course of the problem (eg, whether seizure, headache, vomiting, head trauma, or drug
ingestion was observed; how quickly symptoms appeared; whether the course has been progressive or
waxing and waning)
Baseline mental status
Recent infections and possible exposure to infections
Recent travel
Ingestions of unusual meals
Psychiatric problems and symptoms
Drug history
Alcohol and other substance use
Previous illnesses
The last time the patient was normal
Any hunches they may have about what might be the cause (eg, possible occult overdose, possible occult
head trauma due to recent intoxication)

Medical records should be reviewed if available.

General physical examination

Physical examination should be focused and efficient and should include thorough examination of the head and face,
skin, and extremities. Signs of head trauma include periorbital ecchymosis (raccoon eyes), ecchymosis behind the ear
(Battle sign), hemotympanum, instability of the maxilla, and CSF rhinorrhea and otorrhea. Scalp contusions and small
bullet holes can be missed unless the head is carefully inspected.

If unstable injury and cervical spine damage have been excluded, passive neck flexion is done; stiffness suggests
subarachnoid hemorrhage or meningitis.

Findings may suggest a cause:

Hypothermia: Environmental exposure, near-drowning, sedative overdose, Wernicke encephalopathy, or, in

the elderly, sepsis
Hyperthermia: Heatstroke
Fever, petechial or purpuric rash, hypotension, or severe extremity infections (eg, gangrene of one or more
toes): Sepsis or CNS infection
Needle marks: Drug overdose (eg, of opioids or insulin)
A bitten tongue: Seizure
Breath odor: Alcohol, other drug intoxication, or diabetic ketoacidosis

Neurologic examination
The neurologic examination determines whether the brain stem is intact and where the lesion is located within the
CNS. The examination focuses on the following:

Level of consciousness
Eyes
 Motor function
Deep tendon reflexes

Level of consciousness is evaluated by attempting to wake patients first with verbal commands, then with nonnoxious
stimuli, and finally with noxious stimuli (eg, pressure to the supraorbital ridge, nail bed, or sternum).

The Glasgow Coma Scale (see Table: Glasgow Coma Scale*) was developed to assess patients with head trauma. For
head trauma, the score assigned by the scale is valuable prognostically. For coma or impaired consciousness of any
cause, the scale is used because it is a relatively reliable, objective measure of the severity of unresponsiveness and
can be used serially for monitoring. The scale assigns points based on responses to stimuli.

Eye opening, facial grimacing, and purposeful withdrawal of limbs from a noxious stimulus indicate that
consciousness is not greatly impaired. Asymmetric motor responses to pain or deep tendon reflexes may indicate a
focal hemispheric lesion.

Clinical Calculator: Glasgow Coma Scale

Glasgow Coma Scale*

Area Assessed Response Points

Eye opening Open spontaneously; open with blinking at baseline 4
Open to verbal command, speech, or shout 3
Open in response to pain applied to the limbs or sternum 2
None 1
Verbal Oriented 5
Confused conversation but able to answer questions 4
Inappropriate responses; words discernible 3
Incomprehensible speech 2
None 1
Motor Obeys commands for movement 6
Responds to pain with purposeful movement 5
Withdraws from pain stimuli 4
Responds to pain with abnormal flexion (decorticate 3
posturing)
Responds to pain with abnormal extension (decerebrate 2
posturing)
None 1
*Combined scores < 8 are typically regarded as coma.

Adapted from Teasdale G, Jennett B: Assessment of coma and impaired consciousness.

A practical scale. Lancet2:8184; 1974.
As impaired consciousness deepens into coma, noxious stimuli may trigger stereotypic reflex posturing.

Decorticate posturing can occur in structural or metabolic disorders and indicates hemispheric damage with
preservation of motor centers in the upper portion of the brain stem (eg, rubrospinal tract).
Decerebrate posturing indicates that the upper brain stem motor centers, which facilitate flexion, have been
structurally damaged and that only the lower brain stem centers (eg, vestibulospinal tract, reticulospinal
tract), which facilitate extension, are responding to sensory stimuli.

Decerebrate posturing may also occur, although less often, in diffuse disorders such as anoxic encephalopathy.
Flaccidity without movement indicates that the lower brain stem is not affecting movement, regardless of whether the
spinal cord is damaged. It is the worst possible motor response.

Asterixis and multifocal myoclonus suggest metabolic disorders such as uremia, hepatic encephalopathy, hypoxic
encephalopathy, and drug toxicity.

Psychogenic unresponsiveness can be differentiated because although voluntary motor response is typically absent,
muscle tone and deep tendon reflexes remain normal, and all brain stem reflexes are preserved. Vital signs are usually
not affected.

Eye examination
The following are evaluated:

Pupillary responses
Extraocular movements
Fundi
Other neuro-ophthalmic reflexes

Pupillary responses and extraocular movements provide information about brain stem function (see
Table: Interpretation of Pupillary Response and Eye Movements). One or both pupils usually become fixed early in
coma due to structural lesions, but pupillary responses are often preserved until very late when coma is due to diffuse
metabolic disorders (called toxic-metabolic encephalopathy), although responses may be sluggish. If one pupil is
dilated, other causes of anisocoria should be considered; they include past ocular trauma, certain headaches, and use
of a scopolamine patch.

Interpretation of Pupillary Response and Eye Movements

Area
Finding Interpretation
Assessed
Pupils Sluggish light reactivity Diffuse cellular cerebral dysfunction (toxic-
retained until all other metabolic encephalopathy)
brain stem reflexes are
lost
Unilateral pupillary 3rd cranial nerve compression (eg, in
dilation, pupil unreactive transtentorial herniation), usually due to an
to light ipsilateral lesion (see Anisocoria)
Pupils fixed in Midbrain dysfunction due to structural
midposition damage (eg, infarction, hemorrhage)

Central herniation

Severe metabolic depression by drugs or

toxins (all other brain stem reflexes are also
absent)
Constricted pupils (1 mm Massive pontine hemorrhage
wide)
Toxicity due to opioids or certain insecticides
(eg, organophosphates, carbamates)
Eye Early abnormal pupillary Primary brain stem lesion
movements and oculomotor signs
Spontaneous, conjugate Early toxic-metabolic encephalopathy
 Area
Finding Interpretation
Assessed
roving eye movements
but intact brain stem
reflexes
Gaze preference to one Brain stem lesion on the opposite side
side
Cerebral hemisphere lesion on the same side
Absent eye movements Further testing required (eg, oculocephalic
and oculovestibular reflexes)

Possibly toxicity due

to phenobarbital or phenytoin, Wernicke
encephalopathy, botulism, or brain death
The fundi should be examined. Papilledema may indicate increased ICP but may take many hours to appear.
Increased ICP can cause earlier changes in the fundi, such as disk hypermia, dilated capillaries, blurring of the medial
disk margins, and sometimes hemorrhages. Subhyaloid hemorrhage may indicate subarachnoid hemorrhage.

The oculocephalic reflex is tested by the dolls-eye maneuver in unresponsive patients: The eyes are observed while
the head is passively rotated from side to side or flexed and extended. This maneuver should not be attempted if
cervical spine instability is suspected.

If the reflex is present, the maneuver causes the eyes to move in the opposite direction of head rotation,
flexion, or extension, indicating that the oculovestibular pathways in the brain stem are intact. Thus, in a
supine patient, the eyes continue to look straight up when the head is turned side to side.
If the reflex is absent, the eyes do not move and thus point in whatever direction the head is turned,
indicating the oculovestibular pathways are disrupted. The reflex is also absent in most patients with
psychogenic unresponsiveness because visual fixation is conscious.

If the patient is unconscious and the oculocephalic reflex is absent or the neck is immobilized, oculovestibular (cold
caloric) testing is done. After integrity of the tympanic membrane is confirmed, the patients head is elevated 30, and
with a syringe connected to a flexible catheter, the examiner irrigates the external auditory canal with 50 mL of ice
water over a 30-sec period.

If both eyes deviate toward the irrigated ear, the brain stem is functioning normally, suggesting mildly
impaired consciousness.
If nystagmus away from the irrigated ear also occurs, the patient is conscious and psychogenic
unresponsiveness is likely. In conscious patients, 1 mL of ice water is often enough to induce ocular
deviation and nystagmus. Thus, if psychogenic unresponsiveness is suspected, a small amount of water
should be used (or caloric testing should not be done) because cold caloric testing can induce severe vertigo,
nausea, and vomiting in conscious patients.
If the eyes do not move or movement is dysconjugate after irrigation, the integrity of the brain stem is
uncertain and the coma is deeper. Prognosis may be less favorable.

Pearls & Pitfalls

If muscle tone, deep tendon reflexes, and the response to the doll's-eye maneuver are
normal, suspect psychogenic unresponsiveness.

Certain patterns of eye abnormalities and other findings may suggest brain herniation (see Figure: Brain
herniation. and Effects of Brain Herniation).
 Respiratory patterns
The spontaneous respiratory rate and pattern should be documented unless emergency airway intervention is required.
It may suggest a cause.

Periodic cycling of breathing (Cheyne-Stokes or Biot respiration) may indicate dysfunction of both
hemispheres or of the diencephalon.
Hyperventilation (central neurogenic hyperventilation) with respiratory rates of > 40 breaths/min may
indicate midbrain or upper pontine dysfunction.
An inspiratory gasp with respiratory pauses of about 3 sec after full inspiration (apneustic breathing)
typically indicates pontine or medullary lesions; this type of breathing often progresses to respiratory arrest.

Testing
Initially, pulse oximetry, fingerstick plasma glucose measurements, and cardiac monitoring are done.

Blood tests should include a comprehensive metabolic panel (including at least serum electrolytes, BUN, creatinine,
and calcium levels), CBC with differential and platelets, liver function tests, and ammonia level.

ABGs are measured, and if carbon monoxide toxicity is suspected, carboxyhemoglobin level is measured.

Blood and urine should be obtained for culture and routine toxicology screening; serum ethanol level is also
measured. Other toxicology screening panels and additional toxicology tests (eg, serum drug levels) are done based on
clinical suspicion.

ECG (12-lead) should be done.

If the cause is not immediately apparent, noncontrast head CT should be done as soon as possible to check for masses,
hemorrhage, edema, evidence of bone trauma, and hydrocephalus. Initially, noncontrast CT rather than contrast CT is
preferred to rule out brain hemorrhage. MRI can be done instead if immediately available, but it is not as quick as
newer-generation CT scanners and may not be as sensitive for traumatic bone injuries (eg, skull fractures). Contrast
CT can then be done if noncontrast CT is not diagnostic. MRI or contrast CT may detect isodense subdural
hematomas, multiple metastases, sagittal sinus thrombosis, herpes encephalitis, or other causes missed by noncontrast
CT. A chest x-ray should also be taken.

If coma is unexplained after MRI or CT and other tests, lumbar puncture (spinal tap) is done to check opening
pressure and to exclude infection, subarachnoid hemorrhage, and other abnormalities. However, MRI or CT images
should also be reviewed for intracranial masses, obstructive hydrocephalus, and other abnormalities that could
obstruct CSF flow or the ventricular system and thus significantly increase ICP. Such abnormalities contraindicate
lumbar puncture. Suddenly lowering CSF pressure, as can occur during lumbar puncture, in patients with increased
ICP could trigger brain herniation; however, this outcome is rare.

CSF analysis includes cell and differential counts, protein, glucose, Gram staining, cultures, and sometimes, based on
clinical suspicion, specific tests (eg, cryptococcal antigen test, cytology, measurement of tumor markers, Venereal
Disease Research Laboratory [VDRL] tests, PCR for herpes simplex, visual or spectrophotometric determination of
xanthochromia).

If increased ICP is suspected, pressure is measured. Hyperventilation, managed by an ICU specialist, should be
considered. Hyperventilation causes hypocapnia, which in turn decreases cerebral blood flow globally through
vasoconstriction. Reduction in PCO2 from 40 mm Hg to 30 mm Hg can reduce ICP by about 30%. PCO2should be
maintained at 25 mm Hg to 30 mm Hg, but aggressive hyperventilation to < 25 mm Hg should be avoided because
this approach may reduce cerebral blood flow excessively and result in cerebral ischemia.

If pressure is increased, it is monitored continuously (see Monitoring and Testing the Critical Care Patient :
Intracranial Pressure Monitoring).

If diagnosis remains uncertain, EEG may be done. In most comatose patients, EEG shows slowing and reductions in
wave amplitude that are nonspecific but often occur in toxic-metabolic encephalopathy. However, EEG monitoring
(eg, in the ICU) is increasingly identifying nonconvulsive status epilepticus. In such cases, the EEG may show spikes,
sharp waves, or spike and slow complexes.

Prognosis
Prognosis depends on the cause, duration, and depth of the impairment of consciousness. For example, absent brain
stem reflexes indicates a poor prognosis after cardiac arrest, but not always after a sedative overdose. In general, if
unresponsiveness lasts < 6 h, prognosis is more favorable.

After coma, the following prognostic signs are considered favorable:

Early return of speech (even if incomprehensible)

Spontaneous eye movements that can track objects
Normal resting muscle tone
Ability to follow commands

If the cause is a reversible condition (eg, sedative overdose, some metabolic disorders such as uremia), patients may
lose all brain stem reflexes and all motor response and yet recover fully. After trauma, a Glasgow Coma Scale score of
3 to 5 may indicate fatal brain damage, especially if pupils are fixed or oculovestibular reflexes are absent.

After cardiac arrest, clinicians must exclude major confounders of coma, including sedatives, neuromuscular
blockade, hypothermia, metabolic derangements, and severe liver or kidney failure. If brain stem reflexes are absent at
day 1 or lost later, testing for brain death is indicated. Prognosis is poor if patients have any of the following:

Myoclonic status epilepticus (bilaterally synchronous twitching of axial structures, often with eye opening
and upward deviation of the eyes) that occurs within 24 to 48 h after cardiac arrest
No pupillary light reflexes 24 to 72 h after cardiac arrest
No corneal reflexes 72 h after cardiac arrest
Extensor posturing or no response elicited by painful stimuli 72 h after cardiac arrest
No N20 on somatosensory evoked potentials (SEP) or a serum neuron-specific enolase level of > 33 g/L

If patients were treated with hypothermia, 72 h should be added to the times above because hypothermia slows
recovery. If any of the above criteria is met, outcome is usually (but not always) poor; thus, whether to withdraw life
support may be a difficult decision.

Patients may also have nonneurologic complications, depending on the cause of impaired consciousness. For example,
a drug or disorder causing metabolic coma may also cause hypotension, arrhythmias, MI, or pulmonary edema.
Prolonged immobilization may also result in complications (eg, pulmonary embolism, pressure ulcers, UTI).

Treatment
Immediate stabilization (airway, breathing, circulation, or ABCs)
Supportive measures, including, when necessary, control of ICP
Admission to an ICU
Treatment of underlying disorder

Airway, breathing, and circulation must be ensured immediately. Hypotension must be corrected. Patients are
admitted to the ICU so that respiratory and neurologic status can be monitored.

Because some patients in coma are undernourished and susceptible to Wernicke encephalopathy, thiamin 100 mg IV
or IM should be given routinely. If plasma glucose is low, patients should be given 50 mL of 50% dextrose IV.

If opioid overdose is suspected, naloxone 2 mg IV is given.

If trauma is involved, the neck is immobilized until damage to the cervical spine is ruled out.

If a recent (within about 1 h) drug overdose is possible, gastric lavage can be done through a large-bore orogastric
tube (eg, 32 Fr) after endotracheal intubation. Activated charcoal can then be given via the orogastric tube.
Coexisting disorders and abnormalities are treated as indicated. For example, metabolic abnormalities are corrected.
Core body temperature may need to be corrected (eg, cooling for severe hyperthermia, warming for hypothermia).

Endotracheal intubation
Patients with any of the following require endotracheal intubation to prevent aspiration and ensure adequate
ventilation:

Infrequent, shallow, or stertorous respirations

Low O2 saturation (determined by pulse oximetry or ABG measurements)
Impaired airway reflexes
Severe unresponsiveness (including most patients with a Glasgow Coma Scale score 8)

If increased ICP is suspected, intubation should be done via rapid-sequence oral intubation (using a paralytic drug)
rather than via nasotracheal intubation; nasotracheal intubation in a patient who is breathing spontaneously causes
more coughing and gagging, thus increasing ICP, which is already increased because of intracranial abnormalities.

To minimize the increase in ICP that may occur when the airway is manipulated, some clinicians recommend
giving lidocaine 1.5 mg/kg IV 1 to 2 min before giving the paralytic. Patients are sedated before the paralytic is
given. Etomidate is a good choice in hypotensive or trauma patients because it has minimal effects on BP; IV dose is
0.3 mg/kg for adults (or 20 mg for an average-sized adult) and 0.2 to 0.3 mg/kg for children. Alternatively, if
hypotension is absent and unlikely and if propofol is readily available, propofol 0.2 to 1.5 mg/kg may be
used. Succinylcholine 1.5 mg/kg IV is typically used as a paralytic. However, use of paralytics is minimized and,
whenever possible, avoided because they can mask neurologic findings and changes.

Pulse oximetry and ABGs (if possible, end-tidal CO2) should be used to assess adequacy of oxygenation and
ventilation.

ICP control
If ICP is increased, intracranial and cerebral perfusion pressure should be monitored (see Monitoring and Testing the
Critical Care Patient : Intracranial Pressure Monitoring), and pressures should be controlled. The goal is to maintain
ICP at 20 mm Hg and cerebral perfusion pressure at 50 to 70 mm Hg. Cerebral venous drainage can be enhanced
(thus lowering ICP) by elevating the head of the bed to 30 and by keeping the patients head in a midline position.

Control of increased ICP involves several strategies:

Sedation: Sedatives may be necessary to control agitation, excessive muscular activity (eg, due to delirium),
or pain, which can increase ICP. Propofol is often used in adults (contraindicated in children) because onset
and duration of action are quick; dose is 0.3 mg/kg/h by continuous IV infusion, titrated gradually up to 3
mg/kg/h as needed. An initial bolus is not used. The most common adverse effect is hypotension. Prolonged
use at high doses can cause pancreatitis. Benzodiazepines (eg, midazolam, lorazepam) can also be used.
Because sedatives can mask neurologic findings and changes, their use should be minimized and, whenever
possible, avoided. Antipsychotics should be avoided if possible because they can delay recovery. Sedatives
are not used to treat agitation and delirium due to hypoxia; O 2 is used instead.
Hyperventilation: Hyperventilation causes hypocapnia, which causes vasoconstriction, thus decreasing
cerebral blood flow globally. Reduction in PCO2 from 40 to 30 mm Hg can reduce ICP about 30%.
Hyperventilation that reduces PCO2 to 28 to 33 mm Hg decreases ICP for only about 30 min and is used by
some clinicians as a temporary measure until other treatments take effect. Aggressive hyperventilation
to < 25 mm Hg should be avoided because it may reduce cerebral blood flow excessively and result in
cerebral ischemia. Other measures to control increased ICP may be used.
Hydration: Isotonic fluids are used. Providing free water through IV fluids (eg, 5% dextrose, 0.45% saline)
can aggravate cerebral edema and should be avoided. Fluids may be restricted to some degree, but patients
should be kept euvolemic. If patients have no signs of dehydration or fluid overload, IV fluids with normal
saline can be started at 50 to 75 mL/h. The rate can be increased or decreased based on serum Na,
osmolality, urine output, and signs of fluid retention (eg, edema).
Diuretics: Serum osmolality should be kept at 295 to 320 mOsm/kg. Osmotic diuretics (eg, mannitol) may
be given IV to lower ICP and maintain serum osmolality. These drugs do not cross the blood-brain barrier.
They pull water from brain tissue across an osmotic gradient into plasma, eventually leading to equilibrium.
Effectiveness of these drugs decreases after a few hours. Thus, they should be reserved for patients whose
 condition is deteriorating or used preoperatively for patients with hematomas. Mannitol 20% solution is
given 0.5 to 1 g/kg IV (2.5 to 5 mL/kg) over 15 to 30 min, then given as often as needed (usually q 6 to 8 h)
in a dose ranging from 0.25 to 0.5 g/kg (1.25 to 2.5 mL/kg). Mannitol must be used cautiously in patients
with severe coronary artery disease, heart failure, renal insufficiency, or pulmonary vascular congestion
because mannitol rapidly expands intravascular volume. Because osmotic diuretics increase renal excretion
of water relative to sodium, prolonged use of mannitol may result in water depletion and
hypernatremia. Furosemide 1 mg/kg IV can decrease total body water, particularly when transient
hypervolemia associated with mannitol is to be avoided. Fluid and electrolyte balance should be monitored
closely while osmotic diuretics are used. A 3% saline solution is another potential osmotic agent to control
ICP.
BP control: Systemic antihypertensives are needed only when hypertension is severe (> 180/95 mm Hg).
How much BP is reduced depends on the clinical context. Systemic BP needs to be high enough to maintain
cerebral perfusion pressure even when ICP increases. Hypertension can be managed by titrating
a nicardipine drip (5 mg/h, increased by 2.5 mg q 5 min to a maximum of 15 mg/h) or by boluses
of labetalol (10 mg IV over 1 to 2 min, repeated q 10 min to a maximum of 150 mg).
Corticosteroids: These drugs are usually helpful for patients with a brain tumor or brain abscess, but they
are ineffective for patients with head trauma, cerebral hemorrhage, ischemic stroke, or hypoxic brain damage
after cardiac arrest. Corticosteroids increase plasma glucose; this increase may worsen the effects of cerebral
ischemia and complicate management of diabetes mellitus. After an initial dose of dexamethasone 20 to 100
mg, 4 mg once/day appears to be effective while minimizing adverse effects. Dexamethasone can be given
IV or po.

If ICP continues to increase despite other measures to control it, the following may be used:

Pentobarbital coma: Pentobarbital can reduce cerebral blood flow and metabolic demands. However, its
use is controversial because the effect on clinical outcome is not consistently beneficial, and treatment
with pentobarbital can lead to complications (eg, hypotension). In some patients with refractory intracranial
hypertension that does not respond to standard hypercapnia and hyperosmolar therapy, pentobarbital can
improve functional outcome. Coma is induced by giving pentobarbital 10 mg/kg IV over 30 min, followed
by 5 mg/kg/h for 3 h, then 1 mg/kg/h. The dose may be adjusted to suppress bursts of EEG activity, which is
continuously monitored. Hypotension is common and is managed by giving fluids and, if necessary,
vasopressors. Other possible adverse effects include arrhythmias, myocardial depression, and impaired
uptake or release of glutamate.
Decompressive craniotomy: Craniotomy with duraplasty can be done to provide room for brain swelling.
This procedure can prevent deaths, but overall functional outcome may not improve much. It may be most
useful for large cerebral infarcts with impending herniation, particularly in patients < 50 yr.

Long-term care
Patients require meticulous long-term care. Stimulants, sedatives, and opioids should be avoided.

Enteral feeding is started with precautions to prevent aspiration (eg, elevation of the head of the bed); a percutaneous
endoscopic jejunostomy tube is placed if necessary.

Early, vigilant attention to skin care, including checking for breakdown especially at pressure points, is required to
prevent pressure ulcers. Topical ointments to prevent desiccation of the eyes are beneficial.

Passive range-of-motion exercises done by physical therapists and taping or dynamic flexion splitting of the
extremities may prevent contractures. Measures are also taken to prevent UTIs and deep venous thrombosis.

Geriatric Essentials
Elderly patients may be more susceptible to coma, altered consciousness, and delirium because of many factors,
including the following:

Less cognitive reserve due to age-related brain effects and/or preexisting brain disorders
Higher risk of drug interactions affecting the brain due to polypharmacy
Higher risk of drug accumulation and drug effects on the brain due to age-related decreased function of
organs responsible for drug metabolism
Higher risk of incorrect drug dosing due to polypharmacy with complex dosing regimens
Relatively minor problems, such as dehydration and UTIs, can alter consciousness in the elderly.

In elderly patients, mental status and communications skills are more likely to be compromised, making lethargy and
obtundation harder to recognize.

Age-related decreases in cognitive reserve and neuroplasticity can impair recovery from brain injury.

Key Points
Coma and impaired consciousness require dysfunction of both cerebral hemispheres or dysfunction of the
reticular activating system.
Manifestations include abnormalities of the eyes (eg, abnormal conjugate gaze, pupillary responses, and/or
oculocephalic or oculovestibular reflexes), vital signs (eg, abnormal respirations), and motor function (eg,
flaccidity, hemiparesis, asterixis, multifocal myoclonus, decorticate or decerebrate posturing).
Taking a complete history of prior events is critical; ask witnesses and relatives about the time course for the
change in mental status and about possible causes (eg, recent travel, ingestion of unusual meals, exposure to
possible infections, drug or alcohol use, possible trauma).
Do a general physical examination, including thorough examination of the head and face, skin, and
extremities and a complete neurologic examination (focusing on level of consciousness, the eyes, motor
function, and deep tendon reflexes), followed by appropriate blood and urine tests, toxicology screening, and
fingerstick plasma glucose measurements.
Do noncontrast CT as soon as the patient has been stabilized.
Ensure adequate airway, breathing, and circulation.
Give IV or IM thiamin and IV glucose if plasma glucose is low and IV naloxone if opioid overdose is
suspected.
Control ICP using various strategies, which may include sedatives (as needed) to control agitation,
temporary hyperventilation, fluids and diuretics to maintain euvolemia, and antihypertensives to control BP.

Last full review/revision April 2016 by Kenneth Maiese, MD