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.
It is important to remember that being in a coma means being unconscious but 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 by 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.
The Glasgow Coma Scale (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 (4 levels), verbal response (5 levels) and motor response (6 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.
- 15 - highest score; indicates normal conscious level.
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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:
- A lert - meaning spontaneous eye opening, speaking and intact motor functions, eg moving limbs.
- V oice - responds when spoken to, eg grunt or actual speech.
- P ain - responds to pain, eg sternal rub.
- U nresponsive - 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.
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? Also try to determine about any recent travel and possibility of immunosuppression.
Examination should include the following:
- 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).
- Is there a MedicAlert® or similar bracelet/necklace or 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 'Alert, Voice response, Pain response, Unresponsive' (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:
- 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 suggests 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)
Useful focal indicators of pathology in comatose patients
- 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.
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 (rotate the patient's head from side to side and observe the position of the eyes) - shows doll's eye movement if the brainstem is intact but stays in the mid-position of the head if the brainstem is depressed.
- 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.
- 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
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, liver function tests, CK, thyroid function tests, 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
- CT scan of the brain/MRI scan (especially if there is coma with focal signs)
- EEG and other electroneurophysiological tests (eg event-related potentials) - these can be useful for determining prognosis, eg functional MRI
- Functional neuroimaging is likely to become very important in making decisions regarding outcome
- 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.
- Give intravenous thiamine and glucose to all in whom diagnosis is unclear. Remember to give thiamine first, as glucose may cause Wernicke's encephalopathy in those who are malnourished.
- Trial of naloxone or flumazenil is easily done and response is rapid.
- Treat underlying cause, eg antibiotics if meningitis is suspected, surgery to remove subdural haematoma, anticonvulsants, etc.
- Raised intracranial pressure may require mannitol infusion.
- 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.
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 Glasgow Coma Scale (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 6 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.
- After 1 week - 3% chance of recovery.
- After 7 days - high incidence of death/persistent vegetative state.
- Absence of brainstem reflexes for 24 hours (without sedative drugs) - very little chance of recovery.
Persistent vegetative state
A persistent vegetative state (PVS) 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 non-cognitive brain function and normal or near-normal sleep-wake cycles. Gag, cough, sucking and swallowing reflexes may be preserved. The two conditions exist on a continuum of impaired consciousness.
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.
It is said that vegetative states are rare and that sufficient assessment will often reveal evidence of active cognition, thus eliminating the diagnosis.
For more details, see full separate article Vegetative States.
Further reading & references
- Wijdicks EF; The bare essentials: coma. Pract Neurol. 2010 Feb;10(1):51-60.
- Young GB; Coma. Ann N Y Acad Sci. 2009 Mar;1157:32-47.
- Longmore M, Wilkinson IB and Rajagopalan SR (2004): Oxford Handbook of Clinical Medicine, 6th ed, OUP
- 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.
- Kumar P, Clarke M; Clinical Medicine, 6th Ed, (2005). WB Saunders: London
- Young GB; The EEG in coma. J Clin Neurophysiol. 2000 Sep;17(5):473-85.
- Owen AM, Schiff ND, Laureys S; A new era of coma and consciousness science. Prog Brain Res. 2009;177:399-411.
- Schierhout G, Roberts I; Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev. 2001;(4):CD000173.
- Wakai A, Roberts I, Schierhout G; Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev. 2007 Jan 24;(1):CD001049.
- Perel P, Yanagawa T, Bunn F, et al; Nutritional support for head-injured patients. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD001530.
- Stevens RD, Bhardwaj A; Approach to the comatose patient. Crit Care Med. 2006 Jan;34(1):31-41.
- Manish M, Veenu S; Persistent vegetative state. Neurology. 2007 May 8;68(19):1635.
- Bernat JL; Chronic disorders of consciousness. Lancet. 2006 Apr 8;367(9517):1181-92.
|Original Author: Dr Gurvinder Rull||Current Version: Dr Gurvinder Rull|
|Last Checked: 20/04/2011||Document ID: 1980 Version: 23||© EMIS|
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