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Overview of Coma and Impaired Consciousness

By

Kenneth Maiese

, MD, National Heart, Lung, and Blood Institute

Last full review/revision Sep 2020| Content last modified Sep 2020
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Coma is unresponsiveness from which the patient cannot be aroused and in which the patient's eyes remain closed. 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 are closed and 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. Patients with delirium may have periods of appropriate attention and cognition alternating with periods of impaired attention and cognition.

Pathophysiology

Maintaining alertness requires intact function of the cerebral hemispheres and preservation of arousal mechanisms in the reticular activating system (RAS—also 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 also figure Brain herniation and table Effects of Herniation) contributes to neurologic deterioration because it does the following:

  • Directly compresses brain tissue

  • Blocks the blood supply to areas of the brain

  • Increases ICP

  • May lead to hydrocephalus by obstructing the cerebral ventricular system

  • 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. Apoptosis has early and late phases that ultimately lead to the destruction of deoxyribonucleic acid (DNA) in cells. In autophagy, components of cell cytoplasm are recycled in an attempt to remove nonfunctional organelles (1).

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

Pathophysiology reference

  • 1. Maiese K, Chong ZZ, Shang YC, Wang S: Targeting disease through novel pathways of apoptosis and autophagy. Expert Opin Ther Targets 16 (12):1203–1214, 2012. doi: 10.1517/14728222.2012.719499. Epub 2012 Aug 27.

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).

Older age increases the risk of impaired consciousness (see Geriatrics Essentials: Coma and Impaired Consciousness)

Table
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Common Causes of Coma or Impaired Consciousness

Cause

Examples

Focal

Structural disorders

Head trauma (eg, concussion, cerebral lacerations or contusions, epidural or subdural hematoma)

Hydrocephalus (acute)

Intraparenchymal hemorrhage

Cortex or upper brain stem infarct or hemorrhage

Nonstructural disorders

Seizures (eg, nonconvulsive status epilepticus) or a postictal state caused by an epileptogenic focus

Diffuse

Metabolic, hypoxic or ischemic, and endocrine disorders

Hypercapnia

Hyperglycemia

Hypocalcemia (rarely)

Hypoxia/ischemia

Uremia

Infections

Other disorders

Diffuse axonal injury

Hypertensive encephalopathy

Drugs

Anesthetics (eg, propofol)

Antipsychotic drugs if they cause neuroleptic malignant syndrome

CNS stimulants (eg, cocaine)

Opioid and related analgesics

Other CNS depressants

Selective serotonin reuptake inhibitors if they cause release of excess serotonin (serotonin syndrome)

Toxins

Carbon monoxide

CNS = central nervous system.

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. However, hypotension may occur if impaired consciousness is caused by severe infection, severe dehydration, major blood loss, or cardiac arrest.

  • 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.

Table
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Findings by Location*

Location

Abnormal Findings

Bilateral hemispheric damage or dysfunction*

Symmetric tone and response (flexor or extensor) to pain

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

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 (upper brain stem) lesion

Pupils locked in midposition, often unequal in size, with loss of light reflexes (due to a structural or metabolic disorder that causes loss of both sympathetic and parasympathetic pupillary tone)

Toxic-metabolic dysfunction*

Spontaneous, conjugate roving eye movements in mild coma

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 electroencephalography (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 (eg, hospital identification card, drugs) may provide clues to the cause. 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

  • Prescription drug history

  • Use of alcohol and other recreational drugs (eg, anesthetics, stimulants, depressants)

  • Previous and concurrent systemic illnesses, including new-onset heart failure, arrhythmias, respiratory disorders, infections, and metabolic, liver, or kidney disorders

  • 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 cerebrospinal fluid (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, severe hypothyroidism, Wernicke encephalopathy, or, in older people, sepsis

  • Hyperthermia: Heatstroke, infection, stimulant drug overdose, or neuroleptic malignant syndrome

  • Fever, petechial or purpuric rash, hypotension, or severe extremity infections (eg, gangrene of one or more toes): Sepsis or central nervous system (CNS) infection

  • Needle marks: Drug overdose (eg, of opioids or insulin)

  • A bitten tongue: Seizure

  • Breath odor: Alcohol, other drug intoxication, or diabetic ketoacidosis

  • Hypotension or pulse abnormalities: Cardiac dysfunction with hypoperfusion

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.

Table
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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 posturing)

3

Responds to pain with abnormal extension (decerebrate posturing)

2

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. Lancet 2:81–84; 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 Movement). 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 (if the drug comes in contact with the eyes).

Table
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Interpretation of Pupillary Response and Eye Movements

Area Assessed

Finding

Interpretation

Pupils

Sluggish light reactivity retained until all other brain stem reflexes are lost

Diffuse cellular cerebral dysfunction (toxic-metabolic encephalopathy)

Unilateral pupillary dilation, pupil unreactive to light

3rd cranial nerve compression (eg, in transtentorial herniation), usually due to an ipsilateral lesion (see Anisocoria)

Pupils fixed in midposition

Midbrain dysfunction due to structural 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 wide)

Massive pontine hemorrhage

Toxicity due to opioids or certain insecticides (eg, organophosphates, carbamates)

Eye movements

Early abnormal pupillary and oculomotor signs

Primary brain stem lesion

Spontaneous, conjugate roving eye movements but intact brain stem reflexes

Early toxic-metabolic encephalopathy

Gaze preference to one side

Brain stem lesion on the opposite 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 loss of retinal venous pulsations, 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 doll’s-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 patient’s 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-second period.

  • If both eyes deviate toward the irrigated ear, the brain stem reflex 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 also figure Brain herniation and table Effects of 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 > 25 breaths/minute may indicate midbrain or upper pontine dysfunction.

  • An inspiratory gasp with respiratory pauses of about 3 seconds 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, blood urea nitrogen [BUN], creatinine, and calcium levels), complete blood count (CBC) with differential and platelets, liver tests, and ammonia level.

Arterial blood gases (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) is also done to check for myocardial infarction and new arrhythmias.

Chest x-ray should be done to check for new lung disease that may affect brain oxygenation.

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). MRI or contrast CT can then be done if noncontrast CT is not diagnostic; it may detect isodense subdural hematomas, multiple metastases, sagittal sinus thrombosis, herpes encephalitis, or other causes missed by noncontrast CT.

Noncontrast Head CT

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 first 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 uncommon.

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, polymerase chain reaction [PCR] for herpes simplex, visual or spectrophotometric analysis for xanthochromia).

If increased ICP is suspected, CSF pressure is measured. If ICP is increased, ICP monitoring is done continuously, and measures to decrease it are taken.

If seizures may be the cause of coma, particularly if nonconvulsive status epilepticus (recurrent seizures without prominent motor symptoms) is being considered, or if the 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. In some patients with nonconvulsive status epilepticus, the EEG shows spikes, sharp waves, or spike and slow complexes. If psychogenic unresponsiveness or seizure activity (pseudoseizure) that results from a behavior disorder is possible, video EEG monitoring is required.

Depending on the destination, recent travel should prompt testing for bacterial, viral, and parasitic infections that may lead to coma.

Clinicians can consider evoked potentials such as brain stem auditory evoked potentials to assess brain stem function or somatosensory evoked potentials to assess the cortex, thalamic, brain stem, and spinal cord pathways (eg after cardiac arrest).

Prognosis

Prognosis for patients with impaired consciousness 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 hours, 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 hours after cardiac arrest

  • No pupillary light reflexes 24 to 72 hours after cardiac arrest

  • No corneal reflexes 72 hours after cardiac arrest

  • Extensor posturing or no response elicited by painful stimuli 72 hours after cardiac arrest

  • No response 20 milliseconds (N20) after stimulation of somatosensory evoked potential (SEP)

  • Serum neuron-specific enolase level of > 33 mcg/L

  • Preexisting disorders such as coronary artery disease, hypertension, and diabetes mellitus

If patients were treated with hypothermia, 72 hours 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 other neurologic and nonneurologic complications, depending on the cause and duration of impaired consciousness. For example, a drug or disorder causing metabolic coma may also cause hypotension, arrhythmias, myocardial infarction, or pulmonary edema. Prolonged hospitalization in an ICU may also result in polyneuropathy, myopathy, and other complications (eg, pulmonary embolism, pressure ulcers, urinary tract infection).

Treatment

  • Immediate stabilization (airway, breathing, circulation, or ABCs)

  • Admission to an intensive care unit (ICU)

  • Supportive measures, including, when necessary, control of ICP

  • Treatment of underlying disorder

Airway, breathing, and circulation must be ensured immediately. Hypotension must be corrected. Patients with impaired consciousness are admitted to the ICU so that respiratory and neurologic status can be monitored. If hypertension is present, blood pressure should be reduced carefully; lowering blood pressure below the patient's usual level can lead to brain ischemia.

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, but only after they have been given thiamin.

If trauma is involved, the neck is immobilized until CT is done to rule out damage to the cervical spine. Some patients in a stupor or coma after head trauma benefit from treatment with drugs that can improve nerve cell function (eg, amantadine). Such treatment lead to improvement in neurologic responsiveness for as long as the drug is continued. However, such treatment may not make any difference in improvement over the long term.

If opioid overdose is suspected, naloxone 2 mg IV is given and repeated as necessary.

If a recent (within about 1 hour) 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 as needed 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 oxygen 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 minutes 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 blood pressure; 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 or rocuronium 1 mg/kg IV is typically used as a paralytic. Paralytics should be used only when they are deemed necessary for intubation and needed to avoid further increases in ICP. Otherwise, paralytics should be avoided because rarely, drugs such as succinylcholine can lead to malignant hyperthermia and 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.

Intracranial pressure control

If intracranial pressure (ICP) is increased, clinicians should monitor intracranial and cerebral perfusion pressure, 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. ICP is usually lower in children than in adults. In neonates, ICP can be below the atmospheric pressure. Thus, children are evaluated independently from adult guidelines.

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/hour by continuous IV infusion, titrated gradually up to 3 mg/kg/hour 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; oxygen is used instead.

  • Hyperventilation: Hyperventilation causes hypocapnia, which causes vasoconstriction, thus decreasing cerebral blood flow globally. Reduction in PCO2 from 40 mm Hg 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 minutes 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/hour. The rate can be increased or decreased based on serum sodium, 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 (eg, those with acute brain herniation) 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 minutes, then given as often as needed (usually every 6 to 8 hours) 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.

  • Blood pressure (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/hour, increased by 2.5 mg every 5 minutes to a maximum of 15 mg/hour) or by boluses of labetalol (10 mg IV over 1 to 2 minutes, repeated every 10 minutes to a maximum of 150 mg).

  • Corticosteroids: Corticosteroids are useful for treating vasogenic brain edema. Vasogenic edema results from disruption of the blood-brain barrier, which may occur in patients with a brain tumor. Cytotoxic edema results from cell death and breakdown, which may occur in patients with stroke, cerebral hemorrhage, or trauma; it may also occur after hypoxic brain damage due to cardiac arrest. Treatment with corticosteroids is effective only for tumors and sometimes abscesses of the brain when vasogenic edema is present. Corticosteroids are ineffective for cytotoxic edema and can increase plasma glucose, exacerbating cerebral ischemia and complicating management of diabetes mellitus. For patients without brain ischemia, an initial dose of dexamethasone 20 to 100 mg, followed by 4 mg once a day appears to be effective while minimizing adverse effects. Dexamethasone can be given IV or orally.

  • Removal of cerebrospinal fluid (CSF): CSF can be slowly removed through a shunt inserted into the ventricles to help lower increased ICP. CSF is removed at a rate of 1 to 2 mL/minute for 2 to 3 minutes. Continuous drainage of CSF (eg, through a lumbar drain) should be avoided because it may lead to brain herniation.

  • Position: Positioning the patient to maximize venous outflow from the head can help minimize increases in ICP. The head of the bed can be elevated to 30° (with the head above the heart) as long as cerebral perfusion pressure remains at the desired range. The patient’s head should be kept in a midline position, and neck rotation and flexion should be minimized. Tracheal suctioning, which can increase ICP, should be limited.

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

  • Titrated hypothermia: When ICP is increased after head trauma or cardiac arrest, hypothermia in the range of 32 to 35° C has been used to reduce ICP to < 20 mm Hg. However, use of hypothermia to lower ICP is controversial; some evidence (1) suggests that this treatment may not effectively lower ICP in adults or children and may have adverse effects.

  • 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 hyperventilation and hyperosmolar therapy, pentobarbital can improve functional outcome. Coma is induced by giving pentobarbital 10 mg/kg IV over 30 minutes, followed by 5 mg/kg/hour for 3 hours, then 1 mg/kg/hour. 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, and it may lead to complications such as hydrocephalus in some patients (2). It may be most useful for large cerebral infarcts with impending herniation, particularly in patients < 50 years.

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. Patients require frequent turning and position changes to prevent pressure ulcers. Sometimes special air mattresses are necessary to manage 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. Initiating physical therapy early can improve functional outcome in patients with polyneuropathy and myopathy.

Treatment references

  • 1. Moler FW, Silverstein FS, Holubkov R, et al: Therapeutic hypothermia after in-hospital cardiac arrest in children. N Engl J Med 376 (4):318-329, 2017. doi: 10.1056/NEJMoa1610493.

  • 2. Su TM, Lan CM, Lee TH, et al: Risk factors for the development of posttraumatic hydrocephalus after unilateral decompressive craniectomy in patients with traumatic brain injury. J Clin Neurosci 63:62–67, 2019. doi: 10.1016/j.jocn.2019.02.006. Epub 2019 Mar 1.

Geriatrics Essentials: Coma and Impaired Consciousness

Older 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 and elimination

  • Higher risk of incorrect drug dosing due to polypharmacy with complex dosing regimens

  • Presence of comorbid disorders (eg, diabetes mellitus, hypertension, renal disease)

Relatively minor problems, such as dehydration and urinary tract infections, can alter consciousness in older people.

In older patients, mental status and communications skills may 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.

  • Treat the cause.

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