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Overview of Coma and Impaired Consciousness

by Kenneth Maiese, MD

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 (see Delirium).


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 Figure: Brain herniation. and Effects of Brain Herniation) contributes to neurologic deterioration because it directly compresses brain tissue, increases ICP, may lead to hydrocephalus, and 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 (see 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 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 Herniation




Compression of ipsilateral 3rd cranial nerve

Unilateral dilated, fixed pupil

Oculomotor paresis

Compression of the posterior cerebral artery

Contralateral homonymous hemianopia

Absence of blinking in response to visual threat in obtunded patients

Compression of the contralateral 3rd cranial nerve and cerebral peduncle (indented by the tentorium to form Kernohan notch)

Contralateral dilated pupil and oculomotor paresis

Ipsilateral hemiparesis

Compression of the ipsilateral cerebral peduncle

Contralateral hemiparesis

Eventually, compression of the upper brain stem and the area in and around the thalamus

Impaired consciousness

Abnormal breathing patterns

Fixed, unequal pupils

Further compromise of the brain stem

Loss of oculocephalic reflex

Loss of oculovestibular reflex

Loss of corneal reflexes

Decerebrate posturing

Subfalcine (cingulate)

Trapping of one or both anterior cerebral arteries, causing infarction of the paramedian cortex

Leg paralysis

Expansion of infarcted area


Increased intracranial pressure

Increased risk of transtentorial herniation, central herniation, or both


Bilateral, more or less symmetric damage to the midbrain

Pupils fixed in midposition

Decerebrate posturing

Many of the same symptoms as transtentorial herniation

Further compromise of the brain stem

Loss of all brain stem reflexes

Disappearance of decerebrate posturing

Cessation of respirations

Brain death

Upward transtentorial

Compression of the posterior 3rd ventricle

Hydrocephalus, which increases intracranial pressure

Distortion of the mesencephalon vasculature

Compression of the veins of Galen and Rosenthal

Superior cerebellar infarction due to occlusion of the superior cerebellar arteries

Early: Nausea, vomiting, occipital headache, ataxia

Later: Somnolence, breathing abnormalities, patchy and progressive loss of brain stem reflexes

Posterior fossa mass (eg, cerebellar hemorrhage)



Increasing somnolence

Respiratory irregularities

Patchy but progressive loss of brain stem reflexes


Compression of the brain stem

Obstruction of CSF flow

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.


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




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


Metabolic and endocrine disorders

Diabetic ketoacidosis

Hepatic encephalopathy










Wernicke encephalopathy





Other disorders

Diffuse axonal injury

Hypertensive encephalopathy

Hyperthermia or hypothermia



CNS stimulants


Other CNS depressants


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). 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*


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 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 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.


  • 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.


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 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, and 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, or Wernicke encephalopathy

  • 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 (see Evaluation of the Neurologic Patient : Neurologic Examination). 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.

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.

Glasgow Coma Scale*

Area Assessed



Eye opening

Open spontaneously; open with blinking at baseline


Open to verbal command, speech, or shout


Open in response to pain applied to the limbs or sternum







Confused conversation but able to answer questions


Inappropriate responses; words discernible


Incomprehensible speech





Obeys commands for movement


Responds to pain with purposeful movement


Withdraws from pain stimuli


Responds to pain with abnormal flexion (decorticate posturing)


Responds to pain with abnormal extension (decerebrate posturing)




*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.

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 (see Anisocoria : Etiology).

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.

In an unresponsive patient, the oculocephalic reflex is tested by the doll’s-eye maneuver: 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-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 and deep tendon reflexes are normal and the doll's-eye reflex is absent, suspect psychogenic unresponsiveness.

Certain patterns of eye abnormalities and other findings may suggest brain herniation (see Figure: Brain herniation. and Effects of Brain Herniation).

Interpretation of Pupillary Response and Eye Movements

Area Assessed




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

Prolonged metabolic depression by drugs or toxins

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

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—see Approach to the Pulmonary Patient:Inspection) 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.


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 Ca 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—see 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 intracranial pressure 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 P co 2 from 40 mm Hg to 30 mm Hg can reduce ICP by about 30%. P co 2 should 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 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 early return of speech (even if incomprehensible), spontaneous eye movements that can track objects, normal resting muscle tone, or the ability to follow commands is considered a favorable prognostic sign. 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 µg/L

If patients were treated with hypothermia, 72 h should be added to the times above because hypothermia slows recovery. If none 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).


  • 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 (see Shock and Fluid Resuscitation:Cardiogenic shock). 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 see Airway Establishment and Control : Tracheal Intubation to prevent aspiration and ensure adequate ventilation:

  • Infrequent, shallow, or stertorous respirations

  • Low O 2 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 CO 2 ) 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 patient’s 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 P co 2 from 40 to 30 mm Hg can reduce ICP about 30%. Hyperventilation that reduces P co 2 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 may be used to control increased ICP (see Increased intracranial pressure).

  • 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 Na, 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.

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.

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