Coma is defined as a deep state of unarousable unresponsiveness, characterized by a score of 3 points on the GCS. A comatose state can be caused by a multitude of conditions, making the precise epidemiology and prognosis of coma difficult to determine. Diagnosis is made clinically with a thorough neurologic examination, including assessment of the brain stem to evaluate for the presence of brain death. Definitive management depends on the underlying cause.

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  • A deep state of unarousable unresponsiveness
  • Lowest level of responsiveness on the GCS = 3
Table: Glasgow coma scale (GCS)
Points Best eye-opening response Best verbal response Best motor response
6 Spontaneous Oriented Obeys commands
5 Spontaneous Oriented Localizes pain
4 Spontaneous Confused Withdraws from pain
3 To speech Inappropriate Decorticate posturing
2 To pain Incomprehensible Decerebrate posturing
1 None None None


  • Pathologic (due to underlying pathology)
  • Artificial or induced (e.g., by general anesthesia)


Difficult to determine because of:

  • Variation in assessments by different providers
  • Diagnostic coding for the etiology and not coma itself


Table: Causes of coma
Structural Toxic Metabolic
  • Stroke
  • Brain tumor
  • Epidural hemorrhage
  • Subdural hemorrhage
  • Subarachnoid hemorrhage
  • Hydrocephalus
  • Herniation syndromes
  • Intoxication
  • Anesthetics
  • Dissociative agents
  • CO poisoning
  • Toxic alcohols
  • Antidepressants
  • Anticonvulsants
  • Asphyxia
  • Serotonin syndrome
  • Neuroleptic malignant syndrome
  • Clonidine
  • Respiratory failure
  • Dysthermia
  • Hypoglycemia/hyperglycemia
  • Meningitis
  • Encephalitis
  • Hypothyroidism (myxedema)
  • Thiamine deficiency
  • Nonconvulsive status epilepticus
  • Electrolyte disturbances


The specific sequence of events depends on the underlying etiology, but in general terms:

  1. An initial insult to the arousal areas of the brain occurs, which can be direct (trauma, ischemia, mass effect) or indirect (toxic, metabolic).
  2. If the cause of the initial insult is prolonged, secondary CNS damage and neuronal dysfunction follow.
  3. Because arousal areas are compromised, the individual enters a comatose state.

Clinical Presentation


  • First responders, family members, coworkers, or bystanders must be interrogated about the circumstances surrounding the loss of consciousness to determine the most likely etiology.
  • The following should be determined during interrogation:
    • Circumstances and rapidity of development of neurologic symptoms
    • Symptoms prior to loss of consciousness (e.g., headache, fever, seizures, vomiting)
    • Use of medications, illegal drugs, or alcohol
    • Past medical history (e.g., chronic liver disease, ischemic heart disease)

Physical examination

Evaluation and management may occur simultaneously.


  • ABCs:
    • Airway:
      • Obstructed?
      • Compromised?
    • Breathing: 
      • Spontaneous respiratory effort?
      • Maintaining O2 saturation?
    • Circulation:
      • Palpable pulse?
      • Signs of perfusion?
      • Adequate BP?
  • Signs of trauma

Neurologic examination (level of response to stimuli):

  • Saying or yelling the individual’s name (verbal stimulation)
  • Shaking/tapping the individual (tactile stimulation)
  • Pressing on the individual’s nail beds (peripheral painful stimulation)
  • Sternal rub/supraorbital pressure (central painful stimulus)

Brain stem examination (determination of cerebral death): 

  • Pupillary light reflex:
    • Afferent: cranial nerve (CN) II
    • Efferent: CN III (parasympathetic)
    • Performed by shining a light into each pupil and observing the ipsilateral and contralateral pupils for response
    • Normal response is direct and consensual pupillary constriction.
    • Coma response is lack of constriction. 
  • Oculocephalic reflex/cold calorics:
    • Afferent: CN VIII
    • Efferent: CN III, IV, VI
    • Performed by applying cold water stream to each auditory meatus/external canal and observing the eyes for an oculomotor response 
    • Normal response is slow oculomotor ipsilateral gaze to side of cold followed by rapid oculomotor contralateral gaze back to midline.
    • Coma response is absence of rapid oculomotor contralateral gaze back to midline.
  • Corneal reflex:
    • Afferent: CN V (ophthalmic division)
    • Efferent: CN VII
    • Performed by gently touching a soft-tipped swab to the cornea of each eye
    • Normal response is bilateral blink.
    • Coma response is no blink.
  • Gag reflex
    • Afferent: CN IX
    • Efferent: CN X
    • Performed by gently touching a soft-tipped swab to the uvula and/or posterior pharynx
    • Normal response is to gag.
    • Coma response is no gag.

Remainder of the physical examination is guided by clinical suspicion of the underlying etiology. For example, if meningitis is suspected, testing for signs of meningeal irritation is warranted. 

Examination of brain reflexes

Pupillary light reflexes

Image by Lecturio.


Diagnosis of coma is strictly clinical and relies on a robust neurologic examination. Further investigation (imaging and labs) are carried out to determine etiology. 


The laboratory studies to be requested depend on the suspected underlying etiology. Some routine analyses include: 

  • Electrolytes
  • CBC
  • Arterial or venous blood gas analysis
  • Toxicology studies
  • CSF analysis: urgent evaluation of suspected infection


CT/MRI to evaluate for:

  • Cerebral perfusion abnormalities
  • Intracerebral aneurysm or hemorrhage
  • Cerebral edema
  • Intracranial mass


Initial (ABCs)

  • Airway intubation:
    • Persons with coma are incapable of protecting their own airway.
    • Trauma patients may have a compromised airway.
  • Breathing:
    • Even with an established airway, persons with coma may have respiratory failure.
    • Oxygen saturation should be maintained at  > 90%.
    • Mechanical ventilatory support may be required.
  • Circulation:
    • Persons with coma may be in shock from a variety of etiologies:
      • Cardiogenic causes
      • Sepsis
      • Hypovolemia
    • Adequate vascular access should be established:
      • Peripheral IV
      • Central venous catheter
      • Arterial line 
    • Chemical and/or mechanical circulatory support may be required:
      • CPR/advanced cardiac life support (ACLS) protocols
      • Chemical vasopressors
      • Intraaortic balloon pump

Continued management

  • ICU admission
  • Continuous monitoring
  • Supportive care
  • Management targeted at underlying etiology:
    • For example, naloxone should be considered in cases of opioid overdose.
    • Antibiotics should be started for suspected meningitis.


Recovery is defined as the return of the ability to convincingly and consistently follow commands.


  • Brain death: irreversible cessation of all brain and brain stem functions, regardless of the cause
  • Persistent vegetative state: a state of wakefulness without awareness, where vegetative functions are preserved but cognition is lost because of irreversible damage to the cerebral cortex
  • Apallic syndrome: After awakening, the brain stem, the interbrain, and the spinal cord maintain vegetative functions, while the higher mental processes are no longer present. 


  • The comatose state itself can last for an indefinite period of time.
  • Outcomes depend on the underlying etiology and interpatient variability.
  • Effects of diffuse neuronal injury may linger for the remainder of the individual’s lifetime.

Clinical Relevance

Potential underlying etiologies of coma

  • Loss of cardiac output (e.g., massive pulmonary embolism (PE), cardiac arrhythmia, massive MI)
  • Cerebrovascular accident (e.g., hemorrhagic stroke, ischemic stroke)
  • Severe hypovolemia (e.g., hemorrhage, sepsis)
  • Overdose or toxic exposure (e.g., poisons, drugs, alcohol)
  • Trauma (e.g., fall, motor vehicle accident, electrocution)

Differential diagnosis of coma

  • Locked-in syndrome: neurologic condition characterized by quadriplegia and bulbar palsy as a consequence of injury to the brain stem.
  • Akinetic mutism: rare condition characterized by pathologically slowed or nonexistent bodily movement (akinesia) and loss of speech (mutism)
  • Psychogenic unresponsiveness: also called psychogenic coma. Psychogenic unresponsiveness is the complete lack of responsiveness of psychiatric etiology with no organic cause.
  • Neuromuscular paralysis: characterized by acute-onset neuromuscular weakness progressing to paralysis over days to weeks (< 1 month). Bulbar and respiratory muscle involvement is variable.
  • Syncope: brief loss of consciousness followed by an immediate return to complete alertness.


  1. Huff JS, Tadi P. (2021). Coma. StatPearls. 
  2. Josephson S, Ropper AH, Hauser SL (2018). Coma. IN: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J (Eds.), Harrison’s Principles of Internal Medicine, 20th ed. McGraw-Hill. 
  3. Young GB. (2021). Stupor and coma in adults. UpToDate. Retrieved June 20, 2021, from
  4. Mayer  MD, FCCM, S. A., & Marshall  MD, MS, R. S. (2021). Stupor and coma (S. A. Mayer  MD, FCCM & R. S. Marshall  MD, MS (eds.); pp. 68–87). 

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