Coma

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Coma is from the Greek word koma which means deep sleep. One definition is as follows:

'A state of profound unconsciousness caused by disease, injury, or poison. The patient is unresponsive and cannot be roused.'

It may be a transient phenomenon during acute illness or persist in the long term. Patients in a coma are alive yet unable to perceive or react meaningfully to their external environment. A minority of coma patients may be able to open their eyes occasionally or groan and withdraw limbs from painful stimuli, but those in 'deep' coma do not exhibit these responses.[1]

It is important to remember that being in a coma means being unconscious. However, having a reduced conscious level need not be a comatose state. It could be an intermediate state of consciousness - eg, stupor, drowsiness, etc. Thus, it needs to be distinguished from the following terms:

  • Stupor - similar to coma in that responsiveness is greatly diminished. However, the person can still be partially roused by some stimuli, such as pain.
  • Obtundation - reduced awareness to surroundings. Again the patient can respond to some stimuli - eg, pain.
  • Drowsiness - this is similar to obtundation and probably represents a lesser loss of consciousness.

Glasgow Coma Scale (GCS)

The GCS is used across the world and is a means of scoring a patient's conscious level. It is also useful to monitor progress of the patient. The GCS is determined by assessing three aspects: eye opening (four levels), verbal response (five levels) and motor response (six levels). The best response is taken and a sum of all three elements is decided. Scores are interpreted as follows:

  • 3 - lowest score; indicates deep coma or death.
  • <8 - severe reduction in consciousness and the patient is unlikely to be able to maintain their airway spontaneously, thus should be intubated and ventilated.[2]
  • 15 - highest score; indicates normal conscious level.
Patients with a reduced GCS are at risk of being unable to maintain their airway (especially as GCS approaches 8 or below). Thus, they must be resuscitated fully before going on to determine the cause. This usually includes endotracheal intubation, providing supplemental oxygen and fluid resuscitation.

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AVPU scale

This is also a scale used to measure a patient's conscious level. It is more simple than the GCS and can be used by doctors, nurses, first aiders and ambulance crews. Four elements are tested:

  • Alert - meaning spontaneous eye opening, speaking and intact motor functions - eg,  moving limbs.
  • Voice - responds when spoken to - eg, grunt or actual speech.
  • Pain - responds to pain - eg, sternal rub.
  • Unresponsive - if no response to pain, ie no eye, voice or motor movement.

Ambulance crew usually use AVPU initially and if the patient scores anything other than an 'A', they record a formal GCS. AVPU can also be used by first aiders and it helps them to decide whether an ambulance might need to be called. However, there are some disadvantages to using the AVPU scale:

  • It is not helpful in management of patients with prolonged reduction in consciousness.
  • Although good in cases of poisoning, it is less good in patients under the influence of alcohol.[3]

Priority has to be to resuscitate the patient first, as mentioned above. Once the patient is stable, try to obtain a collateral history if possible - eg, family/friends, witnesses or ambulance crew.

There is need to know the circumstances in which the coma occurred. Is this the predictable progression of an existing disease - eg, brainstem infarction, intracranial mass lesions, subarachnoid haemorrhage? Alternatively, is this an unpredictable event associated with a pre-existing disease - eg, cardiac arrhythmia, systemic sepsis? Is there significant past medical history - eg, history of seizures, trauma, febrile illness or neurological signs? Has there been any recent travel and is there possibility of immunosuppression?[4]

Examination should include the following:[5] 

  • Baseline observations - BP, PR, temperature (rectal ideally - if hypothermic, consider myxoedema coma), capillary blood glucose and oxygen saturation.
  • Response to external stimuli - usually none present.
  • Primary survey of skin and mucous membranes - any evidence of hyperpigmentation, sepsis, myxoedema, intravenous drug misuse, anaemia, jaundice, purpura, cherry-red discolouration (suggesting carbon monoxide poisoning).
  • Note whether there is a medical emergency identification bracelet or similar or whether there are any clues to previous history in the patient's possessions.
  • Smell the patient's breath for evidence of ketones, solvents, and alcohol.
  • Assess responsiveness and GCS or simpler AVPU scale.
  • Respiratory, abdominal (any chance of intra-abdominal bleeding), cardiovascular and neurological examination.
  • Remember, if the patient is paralysed and ventilated then neurological examination will be limited.
  • Particular aspects to focus on include:
    • Pupils - abnormal movements, size, response to light stimulus.
    • Fundoscopy to look for papilloedema.
    • Corneal reflex.
    • Gag reflex.
    • Respiratory pattern.
    • Response to painful stimuli.
    • Plantars.
    • Doll's head manoeuvre.
    • Any evidence of head injury - eg, bruising behind the ear, or panda eyes.
  • There may be abnormal posturing or seizures.
  • Other clues that can be gained from the examination:
    • Clubbing suggests respiratory disease.
    • Tracheal deviation, chest fluid or lung collapse suggest respiratory cause.
    • Enlarged abdominal organs - hepatic disorder, polycystic kidneys (associated with subarachnoid bleeding), or abnormal haematopoiesis.
    • Note position, posture and any spontaneous movements, and examine the ears and pharynx.
    • Examine the skull and spine and test for neck stiffness and Kernig's sign (if there is no cervical spine trauma).

Brainstem function

  • Brainstem reflexes identify lesions affecting the reticular activating substance and determine prognosis.

Pupillary reactions and corneal reflexes

  • Unilateral pupillary dilatation with lack of response to light - suggests uncal herniation of the temporal lobe over the tentorium entrapping the third nerve.
  • Pupil fixed in the mid-position with loss of light reflex - typical of midbrain lesions.
  • Small pupils with response to light - lesions in the pons.
  • Fixed dilatation - suggests significant damage to the brainstem.
  • Horner's syndrome occurs in lesions of the hypothalamus or brainstem and in diseases affecting the wall of the carotid artery.
  • Small pupils reacting briskly to light - metabolic cause (eg, hepatic or renal failure).
  • Corneal reflexes: these are normally intact until there is a very deep coma. In drug intoxication, they may be absent in a patient otherwise in a light coma. Otherwise, loss of corneal reflex is indicative of a poor prognosis.

Eye movements

Spontaneous eye movements

  • Conjugate deviation of the eyes - possible focal hemispheric or brainstem lesion.
  • Depression of the eyes - lesion in the midbrain at the level of the tectum.
  • Skew deviation of the eyes - lesion at the pontomedullary junction.
  • Unco-ordinated eye movements - a small amount of eye divergence is normal in unconsciousness but more significant inco-ordination suggests damage to the oculomotor or abducent nerves in the brainstem or pathways.
  • Normal roving eye movement - similar to those of sleep - often occurs in light coma, and cannot be faked, so excludes the possibility of psychogenic unresponsiveness (jerky eye movement).

Reflex eye movements

  • Oculocephalic response in which the patient's head is rotated from side to side and the position of the eyes is observed. The eyes will move together in the opposite direction to the head movement - eg, rotate head to the left, the eyes move to the right; this is the normal oculocephalic response (also called doll's eye movement). Where a brainstem lesion is present this eye movement is absent or asymmetric. This procedure should only be done provided there is no neck instability. 
  • Oculovestibular testing (instil 20 ml ice-cold water into the external auditory meatus):
    • Psychogenic coma - nystagmus with quick movement away from water (shows active pons and intact corticopontine connections).
    • Tonic, conjugate movement in the direction of the ear with water - suggests a cause situated above the tentorium with intact pons.
    • Disconjugate/no response - lesion within the brainstem.

Respiratory pattern (if the patient is not on a ventilator)

  • Deep breathing - acidosis.
  • Regular shallow breathing - drug overdose.
  • Long-cycle, Cheyne-Stokes respiration - damage at the diencephalon.
  • Short-cycle, Cheyne-Stokes respiration - damage at the medulla.
  • Central neurogenic hyperventilation - lesions in the low midbrain and upper pons.
  • Yawning, vomiting and hiccupping - brainstem lesions.

Motor function

  • Abnormalities on one side indicate the probability of a focal cause (sometimes seen in hepatic encephalopathy) and hypoglycaemia.
  • Seizures - hemispheric damage.
  • Multifocal myoclonus - metabolic or anoxia causing diffuse cortical irritation.

There are a number of potential causes for coma and these can be divided in many different ways - eg, reversible/irreversible, according to systems, duration of onset, etc. The following table divides the causes into systems.

Causes of comatose states
Trauma
Toxic
  • Ethanol.
  • Drug overdose - eg, opiates, benzodiazepines, neuroleptics.
  • Sedatives.
  • Recreational drugs - eg:
    • Gamma-hydroxybutyrate[6]
    • Ecstasy
    • Cocaine
  • Poisons- eg, carbon monoxide, solvents.
Metabolic
Neurological
Ischaemic
  • Cerebral hypoperfusion - eg, impaired cardiac output.
  • Cerebrovascular accident.
  • Intracerebral bleed.
  • Hypertensive encephalopathy.
Infective
Auto-immune
  • Vasculitis.
Structural lesions
  • Space-occupying lesions with raised intracranial pressure.
Others
  • Hypothyroidism or hyperthyroidism.

This depends partly on the cause but the following should be done at presentation in all (once the patient has been resuscitated):

  • Capillary blood glucose.
  • Arterial blood gas.
  • Bloods - FBC, renal function, LFTs, CK, TFTs, cardiac enzymes.
  • Urine dipstick and pregnancy test (especially if seizures have occurred in a woman of child-bearing age).
  • Urine drug screen.
  • Paracetamol and salicylate levels.
  • Blood cultures.
  • Thick and thin films for malaria.
  • Ethanol levels.
  • 12-lead ECG.
  • CXR.
  • CT scan of the brain/MRI scan (especially if there is coma with focal signs).
  • EEG and other electroneurophysiological tests (eg, event-related potentials).[8] These can be useful for determining prognosis - eg, functional MRI.[1]
  • Functional neuro-imaging is likely to become very important in making decisions regarding outcome.[9][10]
  • Other investigations: these will in part depend on the suspected cause - eg, lumbar puncture, autoantibody screen
  • Resuscitation - with intubation and ventilation if needed and rehydration.[1]
  • Give intravenous thiamine and glucose to all in whom diagnosis is unclear. Traditionally it was taught to give thiamine first, as glucose may cause Wernicke's encephalopathy in those who are malnourished; however, the evidence does not support this and glucose should be given first if the patient is hypoglycaemic.[11][12] 
  • Trial of naloxone or flumazenil is easily done and response is rapid.
  • Treat any underlying cause (eg, antibiotics if meningitis is suspected, surgery to remove subdural haematoma, anticonvulsants, etc).[13]
  • Raised intracranial pressure may require mannitol infusion.[14] 
  • If there is a risk that the patient may have aspirated then they should be covered with antibiotics.
  • Fluid rehydration, prevention of pressure sores and adequate nutrition should also be focused on.[15]

This depends on the underlying cause and upon the depth, duration and which clinical signs are present. However, if the cause is a head injury then prognosis is directly proportional to the GCS score, ie those with a score less than 8 having a very poor prognosis. The lack of brainstem and lateralising signs suggests the cause is most likely metabolic and potentially reversible. The following is a general guide to prognosis relating to other causes:

  • Drug overdose - good prognosis with appropriate treatment.
  • Coma not due to head injury or drug overdose, lasting longer than six hours - only 10% chance of recovery.
  • Subarachnoid haemorrhage or stroke - <5% chance of recovery.
  • Hypoxia or ischaemia (eg, after cardiac arrest) - ~10% chance of recovery.
  • Coma >24 hours - 10% chance of recovery.[16]
  • After one week - 3% chance of recovery.
  • After seven days - high incidence of death/persistent vegetative state (PVS).
  • Absence of brainstem reflexes for 24 hours (without sedative drugs) - very little chance of recovery.

Persistent disorders of consciousness can sometimes follow a coma. In such states, which are not always entirely persistent, patients appear to have lost cognition and external awareness, but retain noncognitive brain function and normal or near-normal sleep-wake cycles. Gag, cough, sucking and swallowing reflexes may be preserved.[17]  

Classification and diagnosis can be difficult and require expert repeated multidisciplinary neurological/neurosurgical assessment and input of family, friends and carers to be sure of the state in a given patient. It is thought that misdiagnosis is a common problem. Given the ethical, legal and prognostic ramifications of making these diagnoses, great care must be taken and the potential for a change in the patient's situation accepted with an open mind.[18]

For more details, see separate article Vegetative States.

Further reading & references

  1. Young GB; Coma. Ann N Y Acad Sci. 2009 Mar;1157:32-47.
  2. Longmore M, Wilkinson IB and Rajagopalan SR (2004): Oxford Handbook of Clinical Medicine, 6th ed, OUP
  3. Kelly CA, Upex A, Bateman DN; Comparison of consciousness level assessment in the poisoned patient using the alert/verbal/painful/unresponsive scale and the Glasgow Coma Scale. Ann Emerg Med. 2004 Aug;44(2):108-13.
  4. Kumar P, Clarke M; Clinical Medicine, 6th Ed, (2005). WB Saunders: London
  5. Edlow JA, Rabinstein A, Traub SJ, et al; Diagnosis of reversible causes of coma. Lancet. 2014 Apr 17. pii: S0140-6736(13)62184-4. doi: 10.1016/S0140-6736(13)62184-4.
  6. Thomas G, Bonner S, Gascoigne A; Coma induced by abuse of gamma-hydroxybutyrate (GBH or liquid ecstasy): a case report. BMJ. 1997 Jan 4;314(7073):35-6.
  7. Chaudhari D, Gangadharan V, Forrest T; Heart failure presenting as myxedema coma: case report and review article. Tenn Med. 2014 Feb;107(2):39-41.
  8. Young GB; The EEG in coma. J Clin Neurophysiol. 2000 Sep;17(5):473-85.
  9. Owen AM, Schiff ND, Laureys S; A new era of coma and consciousness science. Prog Brain Res. 2009;177:399-411.
  10. Edlow BL, Giacino JT, Wu O; Functional MRI and outcome in traumatic coma. Curr Neurol Neurosci Rep. 2013 Sep;13(9):375. doi: 10.1007/s11910-013-0375-y.
  11. Hack JB, Hoffman RS; Thiamine before glucose to prevent Wernicke encephalopathy: examining the conventional wisdom. JAMA. 1998 Feb 25;279(8):583-4.
  12. Donnino MW, Vega J, Miller J, et al; Myths and misconceptions of Wernicke's encephalopathy: what every emergency physician should know. Ann Emerg Med. 2007 Dec;50(6):715-21. Epub 2007 Aug 3.
  13. Schierhout G, Roberts I; Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev. 2001;(4):CD000173.
  14. Wakai A, McCabe A, Roberts I, et al; Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev. 2013 Aug 5;8:CD001049. doi: 10.1002/14651858.CD001049.pub5.
  15. Perel P, Yanagawa T, Bunn F, et al; Nutritional support for head-injured patients. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD001530.
  16. Stevens RD, Bhardwaj A; Approach to the comatose patient. Crit Care Med. 2006 Jan;34(1):31-41.
  17. Prolonged Disorders of Consciousness - National Clinical Guideline; Royal College of Physicians (2013)
  18. Manish M, Veenu S; Persistent vegetative state. Neurology. 2007 May 8;68(19):1635.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Gurvinder Rull
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Last Checked:
20/08/2014
Document ID:
1980 (v24)
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