Altered mental status and coma

Last updated: June 14, 2023

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Summary

Altered mental status (AMS) is an acute change in cognitive function, psychological function, and/or level of consciousness and can manifest with confusion, behavioral changes, and changes in alertness ranging from hyperalertness to somnolence or even coma. There are many potential causes of altered mental status, including primary CNS processes, general medical conditions, substance use, and psychiatric illness. Initial management includes stabilization (e.g., definitive airway management) and screening for life-threatening acutely reversible causes (e.g., hypoglycemia, opioid overdose). Coma scores are used to assess and monitor the level of neurological dysfunction. Once stabilized, a full diagnostic evaluation should be performed based on the suspected underlying etiology; this may include basic laboratory studies, ECG, head imaging, and lumbar puncture. Treatment is focused on the management of the underlying etiology in addition to providing supportive care and preventing complications.

Etiology

The following are possible causes of AMS and coma. See “Coma mimics” for differential diagnoses in which consciousness is preserved (e.g., locked-in syndrome, akinetic mutism).

Causes of altered mental status and coma ^[2]^[3]^[4]
	Possible causes
Primary CNS dysfunction	Traumatic brain injury (TBI) Vascular insult: e.g., ischemic stroke, SAH, TTP Infections: e.g., meningitis, encephalitis, CNS abscess Autoimmune disease: e.g., vasculitis, ADEM Malignancy: primary or metastatic brain tumors Seizure (e.g., NCSE) or postictal state Posterior reversible encephalopathy syndrome (PRES) Elevated intracranial pressure, e.g., acute hydrocephalus, IIH Cerebral edema Osmotic myelinolysis
Hypoxia and/or hypoperfusion	Hypoxia Hypercarbia Shock Sepsis Anoxic brain injury: e.g., after cardiac arrest Hypertensive encephalopathy
Endocrine and/or metabolic	Hypoglycemia Hyperglycemic crises (DKA, HHS) Hyponatremia, hypernatremia Hypocalcemia, hypercalcemia Hypomagnesemia, hypermagnesemia Acid-base disorders: e.g., metabolic acidosis Uremic encephalopathy Hepatic encephalopathy Wernicke encephalopathy Thyroid disorders: e.g., thyroid storm, myxedema coma Adrenal dysfunction: e.g., Cushing syndrome, adrenal insufficiency Pituitary infarction
Substance-related	Intoxication: e,g., CNS stimulants, CNS depressants Withdrawal: e.g., alcohol withdrawal, opioid withdrawal Poisoning: e.g., CO toxicity Adverse drug events: e.g., anticholinergic overdose, salicylate toxicity, serotonin syndrome, NMS See also “Overview of substance intoxication and withdrawal.” See also “Approach to the poisoned patient.”
Psychiatric	Psychosis Mania Anxiety disorders Major depression Catatonia
Environmental	Hypothermia Hyperthermia, e.g., heatstroke Altitude sickness, high altitude cerebral edema Decompression sickness, gas embolism Severe pain or discomfort (e.g., due to urinary retention)

Causes of altered mental status and coma: AEIOU TIPS (Alcohol, Epilepsy/Electrolytes/Endocrine, Insulin, Overdose/Oxygen, Uremia, Trauma/Temperature, Infection, Poisons/Psychiatric, Stroke/Seizures/Shock) ^[5]

Gradual onset of AMS or coma suggests infection, metabolic processes, or an enlarging space-occupying lesion. ^[2]

Clinical evaluation

Altered mental status can manifest as:
- Hyperalertness
- Somnolence
- Lethargy
- Obtundation
- Stupor
Coma manifests as depressed consciousness with no response to voice, pain, or other stimulation.
Clinical features of underlying AMS etiologies may be present, e.g.:
- CNS causes focal neurological deficits, lateralizing signs, seizures, meningismus
- Overdose or substance use: classic toxidromes
- Respiratory causes: tachypnea or respiratory depression
- Hepatic causes: jaundice, prolonged bleeding, pruritus
- Endocrine causes: clinical features of hypothyroidism, clinical features of thyrotoxicosis
- Clinical features of TBI

Coma scores

General principles

Use coma scores (e.g., GCS, AVPU scale, FOUR score) for a more objective and reproducible assessment.
Document the score upon presentation.
Frequently reassess to detect changes early.

AVPU scale

An abbreviated scale that helps rapidly classify and communicate a patient's level of consciousness in emergency settings. ^[6]^[7]

A: Alert
V: responsive to Verbal stimuli
P: responsive to Painful stimuli
U: Unresponsive

Glasgow coma scale (GCS) ^[8]

A standardized scale used to assess the level of consciousness and neurological status in multiple settings, e.g., TBI classification. GCS is less useful in intubated patients and does not provide a detailed assessment of brainstem function.

Glasgow coma scale (GCS) ^[9]
Criteria	Response	Score
Eye opening (E)	Spontaneous	4
	To verbal command	3
	To pain	2
	No response	1
	Closed due to local factor (e.g., ocular injury)	Nontestable
Verbal response (V)	Oriented	5
	Confused	4
	Inappropriate words	3
	Incomprehensible sounds	2
	No response	1
	Other factor(s) interfering with communication (e.g., intubation)	Nontestable
Best motor response (M)	Follows instructions	6
	Localizes pain stimulus	5
	Withdraws from pain (normal flexion to pain)	4
	Decorticate posturing (abnormal flexion to pain)	3
	Decerebrate posturing (extension to pain)	2
	No motor response	1
	Preexisting factor(s) causing paralysis	Nontestable
Interpretation GCS 3 (minimum score): deeply comatose or imminent brain death GCS 15 (maximum score): fully conscious

Glasgow Coma Scale (GCS)

Full Outline of UnResponsiveness (FOUR) score ^[8]

The FOUR score is equally useful in nonintubated and intubated patients and is more discriminatory than GCS in patients with very low levels of consciousness ^[10]^[11]

Full Outline of UnResponsiveness (FOUR) score ^[12]
Criteria	Response	Score
Eye response (E)	Tracking or blinking to command	4
	Eyelids open spontaneously or to command	3
	Eyelids closed but open in response to loud voices	2
	Eyelids closed but open in response to pain	1
	Eyelids remained closed in response to pain	0
Motor response (M)	Can make thumbs up, fist, or peace sign	4
	Localizes pain stimulus	3
	Flexion response to pain	2
	Extension response to pain	1
	No response to pain or generalized myoclonus status epilepticus	0
Brainstem reflexes (B)	Pupil and corneal reflexes present	4
	One pupil wide and fixed	3
	Pupil OR corneal reflexes absent	2
	Pupil AND corneal reflexes absent; cough reflex present	1
	Absent pupil, corneal, and cough reflexes	0
Respiration (R)	Not intubated; regular breathing pattern	4
	Not intubated; Cheyne-Stokes breathing pattern	3
	Not intubated; irregular breathing pattern	2
	Intubated; breathing above ventilator rate	1
	Intubated; breathing at ventilator rate or apnea	0

Consider using the FOUR score instead of GCS to assess intubated patients, as it does not rely on verbal responses. ^[8]

FOUR Score

Initial management

The goal of initial management is to identify and treat rapidly reversible and/or time-sensitive critical causes of AMS prior to a full diagnostic evaluation.

Initial evaluation ^[2]^[8]

See also: “Evaluating disability in the ACBDE approach.”

Perform an ABCDE survey.
Identify clinical features of underlying AMS etiologies.
Calculate coma scores (or CAM score for suspected delirium).
Check POC glucose.
Start continuous cardiac monitoring and pulse oximetry.
Obtain IV access and send routine laboratory studies (see “Diagnostics for AMS”).
Plan for early neuroimaging if CNS cause is suspected.
Obtain collateral history from witnesses

Use coma scores to quickly assess and document neurological function at presentation and regularly reassess to detect changes.

In patients with abrupt-onset AMS or coma, consider seizure, stroke, cardiac event, overdose, or intoxication. ^[2]

Managing critical causes of AMS ^[2]^[8]

Perform the following concurrently with the initial evaluation, based on clinical suspicion:

Address rapidly-reversible causes, e.g.:
- Treat respiratory failure with oxygen therapy, bag-mask ventilation, and/or mechanical ventilation.
- Treat shock with immediate hemodynamic support.
- Treat hypoglycemia.
- Manage acute seizures.
- Administer antidotes, e.g., naloxone for opioid overdose.
Initiate protective measures, e.g.:
- Airway protection
  - Basic airway maneuvers for all patients with at-risk airway features
  - Definitive airway for persistently ↓ LOC (e.g., GCS ≤ 8) or signs of complete airway obstruction ^[13]
- C-spine immobilization for trauma
- Neuroprotective measures for CNS injury, including ICP management for cerebral herniation syndromes
Begin time-sensitive management steps: e.g., antibiotics for sepsis, reperfusion therapy for ischemic stroke

Next steps ^[2]^[8]

Once the patient is stabilized, proceed with a full clinical and diagnostic evaluation.
See the following management approaches for specific causes and/or manifestations of AMS:
- ”Management of delirium”
- ”Approach to the agitated or violent patient”
- ”Approach to psychosis”
- ”Approach to the poisoned patient”
- ”Management of ischemic stroke” and “Overview of stroke”
- “Moderate and severe TBI management”

Obtain EEG monitoring for patients with suspected nonconvulsive status epilepticus.

Critical management steps by cause

Critical causes include potentially rapidly reversible etiologies and conditions that may pose an imminent threat to life.

Critical causes of AMS or coma and their immediate management
Condition	Suggestive features	Immediate intervention
Hypoxic respiratory failure	↓ SpO₂ Dyspnea	Start oxygen therapy. Manage the underlying cause, e.g., acute heart failure.
Hypercapnic respiratory failure	PaCO₂ > 45 mm Hg Dyspnea or hypopnea	Manage the underlying cause, e.g., AECOPD. Consider mechanical ventilation.
Hypoglycemia	Serum or fingerstick glucose ≤ 70 mg/dL (≤ 3.9 mmol/L)	Treat hypoglycemia with oral glucose or IV dextrose.
Opioid overdose	Miosis (often pinpoint pupils) Bradypnea, bradycardia, hypotension Decreased bowel sounds	Administer IV naloxone for respiratory depression. ^[2]^[14]
Carbon monoxide poisoning	Prodrome of headache, nausea, and fatigue Possible history of smoke inhalation Sick household members	Start supplemental O₂ via NRB. Consider HBOT. See also “Management of CO poisoning.”
Cyanide poisoning	Exposure to fire (e.g., burning plastic) Skin flushing, nausea, vomiting, seizures, dyspnea Lactic acidosis	Start supplemental O₂ irrespective of SpO₂ Administer antidote, e.g., hydroxocobalamin, as soon as possible.
Hypothermia	Core body temperature < 35.0°C (95.0°F)	Initiate rewarming therapy as indicated. See ”Management of hypothermia.”
Hyperthermia	Elevated body temperature Environmental exposure and/or excessive physical activity Clinical features of drug-induced hyperthermia	Initiate cooling measures. Discontinue potentially offending drugs. See “Treatment” in “Heatstroke” and in “Drug-induced hyperthermia.”
Shock	Clinical features of shock History of trauma, bleeding, diarrhea, vomiting, and/or reduced oral intake	Provide immediate hemodynamic support. Consider IV hydrocortisone for patients with risk factors for adrenal crisis
Sepsis and/or meningitis	Symptoms of infection ≥ 2 positive SIRS or qSOFA criteria Meningococcal rash may be present	Obtain serum lactate and blood cultures, and consider LP. Begin fluid resuscitation. Consider antibiotic therapy for sepsis or antibiotic therapy for meningitis.
Seizure	History of seizure disorder Generalized seizures or complex partial seizures Postictal state Lactic acidosis	Treat acute seizures, e.g., with IV benzodiazepines Consider treatment for alcohol withdrawal for at-risk patients.
Hypertensive encephalopathy	Elevated blood pressure Headache, vomiting, blurred vision Other clinical features of hypertensive crises	Treat hypertensive crisis with IV antihypertensives.
Imminent brain herniation	Signs of elevated ICP Evidence of cerebral herniation syndromes	Initiate ICP management, e.g., mannitol or hypertonic saline, short-term hyperventilation See ”Hyperosmolar therapy for ICP management” for agents and doses.

Diagnostics

Perform diagnostic studies based on clinical evaluation in tandem with the initial management of AMS and coma. More thorough targeted diagnostics can be obtained once the patient is stabilized.

Routine laboratory studies ^[3]^[8]^[15]

CBC: to evaluate for signs of infection, e.g., leukocytosis
BMP: to evaluate for electrolyte imbalances, acidosis, and renal dysfunction
Blood gases: to evaluate for hypercarbia, hypoxia, and acid-base imbalances
Liver chemistries, albumin, INR: if hepatic encephalopathy is suspected
Blood cultures: if infection is suspected
Urine analysis: Consider including urine toxicology screen.
Consider serum drug levels: e.g., acetaminophen, salicylates, ethanol.

ECG findings ^[3]^[8]^[15]

Arrhythmia, including toxin-induced rhythm and conduction abnormalities
ECG features of underlying structural heart disease
ECG signs of elevated ICP

Neuroimaging ^[3]^[8]^[15]

Indications
- Focal neurological deficits
- History of head injury
- Unclear etiology of AMS or coma
- Persistent AMS despite treatment or resolution of the suspected cause
Initial modality: CT head without contrast ^[8]
Advanced imaging: consider based on clinical suspicion
- Acute ischemic stroke: CT or MR angiography
- CNS infection, abscess, or tumor: CT head with and without contrast
- Posterior fossa pathology: MRI brain ^[8]

Additional studies

May be indicated based on the clinical presentation and the suspected underlying etiology. For further information, see:

“Symptom-based diagnostic workup for delirium”
”Toxicological risk assessment”
“Diagnostics in TBI”
“Diagnostic studies for secondary psychosis”
“Diagnostics in agitated or violent patients.”

Supportive care

Symptomatic therapy
- Bladder catheterization for urinary retention ^[16]
- Regular oral care
Prevention of coma complications
- Maintenance fluids as needed
- Prevention of decubitus ulcers
- NG tube placement for enteral nutrition and medication
  - Conscious patients with unsuccessful bedside swallow assessment: Establish NPO status and insert an NG tube.
  - Unconscious patients: Insert an NG tube if the underlying cause is not rapidly reversible.
- Stress ulcer prophylaxis
- VTE prophylaxis
- Corneal protective measures for incomplete eyelid closure (e.g., taping, lubricant). ^[17]
Prevention of iatrogenic complications
Other: Initiate discussions of goals of care and/or end-of-life counseling with the surrogate decision-maker, if appropriate.

Disposition

Depends on the site of initial assessment (e.g., ED vs. ward), clinical stability, expected course, and individual patient factors. ^[2]

Consider ICU admission for patients requiring frequent monitoring, hemodynamic stabilization, and/or respiratory support.
Consider urgent interfacility transfer for neurosurgical intervention if not available locally.
Consider discharge home in patients with all of the following:
- Identified and treated acute and reversible causes (e.g., hypoglycemia, opiate overdose)
- Return to baseline mental status
- Stability on observation
- No other medical issues requiring inpatient treatment

In patients with altered mental status due to long-acting agents (e.g., opioid overdose from methadone, hypoglycemia from sulfonylureas), consider admission for observation even if the mental status has returned to baseline.

Acute management checklist

Perform an ABCDE assessment including a rapid neurological assessment (e.g., using GCS, AVPU, FOUR score).
Identify and treat rapidly reversible critical causes of altered mental status.
Implement immediate protective measures (e.g., definitive airway, C-spine immobilization, neuroprotective measures).
Perform basic diagnostic studies (e.g., CBC, BMP, toxicology screen, ECG).
Obtain head imaging (e.g., CT, MRI) if there is a history of head trauma or concern for a structural CNS process.
Perform further diagnostics (e.g., EEG, LP) based on clinical suspicion.
Review the patient's medications for possible contributing drugs or withdrawal.
Treat the underlying cause.
Start supportive care to prevent the development of complications.
Consider transfer to the ICU or neurosurgical care unit.
Monitor with serial GCS or FOUR score assessments.

Differential diagnoses

The following conditions can mimic coma. See “Causes of AMS and coma” for underlying etiologies.

Conditions in which consciousness is preserved but the patient cannot produce voluntary movements or motor responses ^[4]
- Locked-in syndrome
- Neuromuscular paralysis: e.g., secondary to paralytic medications, botulism, or snake bites
- Akinetic mutism
Psychogenic unresponsiveness: an unresponsive state caused by an underlying psychiatric disorder ^[18]
- Etiologies include mood disorders, psychotic disorders, factitious disorder, malingering
- Clinical features include:
  - Stupor
  - Coma
  - Catatonia
  - Dissociation
  - Psychogenic nonepileptic seizures
- Diagnosis based on typical examination findings, e.g.: ^[15]
  - Active resistance to eye opening
  - Purposeful diversion of the arm when held above the face and dropped

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$Contributor Disclosures - Altered mental status and coma. All of the relevant financial relationships listed for the following individuals have been mitigated: Alexandra Willis (copyeditor, was previously employed by OPEN Health Communications). None of the other individuals in control of the content for this article reported relevant financial relationships with ineligible companies. For details, please review our full conflict of interest (COI) policy:.
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