Altered Conscious State

An Altered Conscious State can be defined as one that can be recognized by an individual (or group), or by an external observer of that individual (or group) as representing a major difference in behavior and experience from an ordinary baseline state of waking consciousness.

One’s altered state must be fairly stable over time, and involve changes in a number of the subsystems of consciousness. Both dreaming and nondreaming sleep qualify as discrete altered states.

What Is Consciousness?

Consciousness can be defined as a state of awareness of self and the environment.

Changes in consciousness can be brought about by sexual, athletic, and recreational activity as well as by negative conditions like torture or trauma.

The term consciousness derives from the Latin conscire, to know with, or to be cognizant of something. Consciousness in the ordinary waking state reflects the explicit knowledge of one’s situation; it sometimes includes subjective awareness and intentionality, one’s sense of personal existence, and one’s participation in a shared plan. This implies that each individual’s perception is unique, consisting of a moulding of various sensory modalities over time and interpreted within the full range of that individual’s experiences.

It is clear even from this limited description that the definition of consciousness is metaphysical and difficult to quantify. It would also include what is clinically described as mental state, but psychiatric disease and its differentiation from medical pathology is excluded from this discussion as it exceeds the scope of our discussion.

For clinical purposes, the ability of the individual to respond appropriately to environmental stimuli provides a quantifiable definition of consciousness. Pragmatically, consciousness equals responsiveness.


The level of consciousness describes the rousability of the individual, whereas the content of consciousness may be assessed in terms of the appropriateness of the individual’s response. Broadly speaking, the first is a brainstem functioning and the second is an attribute of the forebrain.

The physical portions of the brain involved in consciousness consist of the ascending arousal system that begins with monoaminegic cell groups in the brain stem and culminates in extensive diffuse cortical projections throughout the cerebrum. En route there is input and modulation from both thalamic and hypothalamic nuclei, as well as basal forebrain cell groups.

The integration of the brain stem and the forebrain is illustrated by individuals who have an isolated pontine injury. They remain awake, but the intact forebrain is unable to interact with the external world, hence the aptly named ‘locked-in syndrome’.

At the other end of the spectrum are individuals in a persistent vegetative state who, in spite of extensive forebrain impairment, appear awake but totally lack the content of consciousness. These clinical extremes emphasize the important role of the brain stem in modulating motor and sensory systems through its descending pathways and regulating the wakefulness of the forebrain through its ascending pathways.

Impairment of conscious state implies dysfunction of the ascending arousal system in the paramedian portion of the upper pons and midbrain, its target in the thalamus or hypothalamus, or both cerebral hemispheres. The resultant changes in the conscious state range from awakeness through lethargy and stupor to coma with a progressively depressed response to various stimuli.

Table X1 | The Glasgow Coma Scale
The GCS is scored between 3 and 15, 3 being the worst and 15 the best. It is composed of three parameters: Best Eye Response, Best Verbal Response, Best Motor Response, as given below.
Best eye response (score out of 4)
1 – No eye opening
2 – Eye opening to pain
3 – Eye opening to verbal command
4 – Eyes open spontaneously
Best verbal response (score out of 5)
1 – No verbal response
2 – Incomprehensible sounds
3 – Inappropriate words
4 – Confused
5 – Orientated
Best motor response (score out of 6)
1 – No motor response
2 – Extension to pain
3 – Flexion to pain
4 – Withdrawal from pain
5 – Localizing pain
6 – Obeys commands

Numerous scales have been proposed to define consciousness but the one that has found universal acceptance is the Glasgow Coma (or Responsiveness) Scale (GCS) (see Table X1). Initially described in 1974 for the assessment of traumatic head injuries, 25 years of experience have shown that the scale can also be used in non-traumatic situations to provide a structured assessment of an individual’s conscious state at various points in time, and also to monitor progress.

Trends provided by repeated measurements of the GCS give clinicians an objective measure to monitor a patient’s deterioration or improvement in response to therapy. In quantifying and standardizing the various responses, the GCS has enabled clinicians worldwide to compare data and therapies. In the spectrum from full awareness to unrousable, coma or unconsciousness is arbitrarily defined as a GCS ≤8.

Table X2 | Mnemonics for causes of altered conscious state
T    Trauma
I     Infection
P    Psychogenic
(P)    (Porphyria)
S     Seizure
       Space-occupying lesion
A    Alcohol and other toxins
E    Endocrinopathy
       Electrolyte disturbances
I      Insulin – Diabetes
O    Oxygen: Hypoxia of any cause
U    Uraemia including Hypertension
C erebral
O verdose
M etabolic
A sphyxia and other A ssociations

Differential Diagnoses

As the main diagnostic challenge in a patient with an altered conscious state is to identify the cause, it is reasonable to approach the assessment of the patient armed with a knowledge of the possible differential diagnoses.

There are several well known mnemonics Opens in new window to assist in remembering the rather diverse list. Some are listed in Table X2 . However, the long list of apparently disparate causes can be divided pathophysiologically into structural insults and metabolic insults.

Structural insults are usually focal intracranial lesions that exert direct or indirect pressure on the brain stem and the more caudal portions of the ascending arousal system. They tend to produce lateralizing neurological signs that can assist in pinpointing the level of the lesion. As there is little space in and around the brain stem, any extrinsic or intrinsic compression will rapidly progress through coma to death, unless the pressure on the brain stem is relieved surgically or pharmacologically.

Metabolic insults are usually due to systemic pathology that affects primarily the forebrain, although direct depression of the brain stem may also occur. There are seldom lateralizing signs. The solution to the problem is the correction of the underlying metabolic impairment. Naturally, as in all clinical practice, there are no absolute distinctions. Uncorrected, any of the metabolic causes can eventually cause cerebral oedema and herniation, leading thence to brainstem compression with lateralizing signs and death. Table X3 lists the more common and important causes of an altered conscious state.

Table X3 | Causes of alteration in conscious state
– epidural
– subdural
Cerebral tumor
Cerebral aneurysm
Haemorrhagic CVA

Cerebellar AVM
Pontine haemorrhage
Brainstem tumor
Loss of substrate
Global ischaemia
– hypovolaemia
– cardiogenic
Focal ischaemia
Derangement of normal physiology
Hypo– or hypernatraemia
Addisonian crisis
– status epilepticus
– post-ictal
Hypo– or hyperthyroidism
Cofactor deficiency
Metastatic malignancy
Psychiatric illness
– alcohol
– illicit
– prescription
– subarachnoid blood
– liver failure
– renal failure
– systemic
– meningitis
– encephalitis
– hypothermia/heat exhaustion
– altitude illness/decompression
– envenomations

Clinical Assessment

As in all life-threatening conditions, assessment and management must proceed concurrently. There are two primary considerations, which are not mutually exclusive: identify and correct the primary insult while preventing or minimizing secondary injury, e.g. hypoxia, acidosis, raised intracranial pressure. As in other time-critical situations, the primary and secondary survey approach often proves useful.

Primary Survey

This focuses on attention to the airway, breathing and circulation. It begins the identification of life-threatening problems and allows immediate therapeutic measures such as airway support to be implemented. Supplemental oxygen is indicated, as is frequent monitoring of vital signs and GCS. Endotracheal intubation is required at this stage if the patient is unable to maintain a safe airway or adequate ventilation. This usually corresponds with a GCS of 8 or less. Mild hyperventilation to a PC02 of 30–35 mmHg will help correct underlying acidosis and reduce intracranial pressure. Cervical spine precautions are imperative if trauma is suspected, until clearance of the spine can be obtained.

A bedside glucose determination may identify clinical or biochemical hypoglycaemia, which should be treated with glucose. There is no evidence that 50 mL of intravenous 50% dextrose will cause harm even in an already hyperglycaemic patient, and a case could be made for routinely administering glucose to any patient with an altered conscious state if a bedside glucose estimation is not readily available.

A history of opiate use combined with the clinical signs of pinpoint pupils and hypoventilation may make the administration of naloxone both diagnostic and therapeutic. Parenterally, 0.2–0.4 mg aliquots can be given, to a maximum of 10 mg. The likelihood of serious adverse reactions such as pulmonary oedema is very low. However, in combination overdoses, the negation of the opiate effect may unmask the effects of other toxins, including those with proconvulsant or proarrhythmic tendencies.

Parental administration in uncontrolled situations with a flailing patient is not without its risks to both patient and staff. In particular, there is a risk to staff from needle-stick injuries and bloodborne infections. Intranasal administration of naloxone via an atomixer has entered mainstream pre-hospital practice and eliminate this risk.

The administration of 100 mg thiamine is advocated in patients suspected of having hepatic encephalopathy, but its effect is rarely immediate and a delay in its use will not change the course of the initial resuscitation. The old dogma that thiamine should be withheld until hypoglycaemia is corrected to avoid precipitating Wernicke’s encephalopathy is unfounded, as the absorption of thiamine is so much slower than that of glucose as to render the timing irrelevant.

The routine use of the ‘coma cocktail’ consisting of intravenous 50% dextrose, naloxone and thiamine is no longer advocated.

Secondary Survey

After initial resuscitation, it is important to complete the assessment by obtaining a full history, conducting a full examination and performing any adjunctive investigations. This will assist in identifying the cause of the condition and planning further management.


Obtaining a full history can be difficult as the patient may be confused or obtunded. Details have to be garnered from supplemental sources such as ambulance or police officers, relatives or carers, and primary care physicians. Medical records, when obtainable, may provide clues, and patients will occasionally carry cards or wear bracelets with alerts for particular conditions.

It is crucial to establish the events leading up to the presentation with specific questioning about prodromal events, ingestions, i.v. drug usage, trauma, underlying illness, medications, allergies, and associated seizures and abnormal movements. For example, the presence or absence of a headache and its onset and duration might aid in the clinical diagnosis of a subarachnoid haemorrhage, and a history of head injury with loss of consciousness would increase the likelihood of an extra-axial intracranial collection.

Patients who are taking anticoagulants also have an increased risk of intracranial haemorrhage with minimal trauma.

In the elderly, demential, itself a progressive illness, may be exacerbated by delirium caused by an acute illness, and often only a careful, corroborated history from all care providers and the passage of time will allow the two to be distinguished. In these patients it is important to remember that dementia as a cause of altered conscious state is a diagnosis of exclusion.


A general physical examination, bearing in mind the various differential diagnoses, is the next step. Vital signs may suggest sepsis or other causes of shock. A keen sense of smell might detect fetor hepaticus or the sweet breath of ketosis. A bitter almond scent is pathognomonic of cyanide poisoning. Of note, alteration of consciousness can be attributed to alcoholic intoxication only by the process of exclusion. Thus the characteristic odor of alcoholic liquor is indicative but cannot be presumed to be diagnostic. A bedside blood glucose determination is mandatory, as deficits are easily correctable.

Neurological examination clearly must be as comprehensive as possible. There are several obstacles to this. Initial resuscitation measures such as endotracheal intubation will reduce the ability of the patient to cooperate with the examination, and language difficulties will be accentuated as the neurological examination is strongly language oriented. Thus patients who do not share common language and those with dysphasia may be disadvantaged. Also, sensory modalities are difficult to assess in patients with impaired mentation, although these deficits are often paralleled by deficits in the motor system.

The aim of the neurological examination is, primarily, to differentiate structural and non-structural causes; secondly, to identify groups of signs that may indicate specific diagnoses such as meningitis; and finally, to pinpoint the precise location of a structural lesion. Therefore, emphasis needs to be placed on signs of trauma, tone, reflexes, papillary findings and eye signs, as well as serial estimations of GCS. Circumstances permitting, some or all of the neurological examination should be attempted before the patient receives neuromuscular paralyzing agents.

Signs of trauma need to be documented and spinal precautions taken as indicated. Palpation of the soft tissues and bones of the skull may detect deformity or bruising, and a haemotympanum may herald a fracture of the base of the skull.

Hypotonia is common in acute neurological deficits. Specific examination of anal sphincter tone will uncover spinal cord compromise and is crucial in trauma patients with a depressed level of consciousness. An upgoing Babinski response is indicative of pyramidal pathology, and asymmetry of the peripheral limb reflexes may help to ‘side’ a lesion. Conversely, heightened tone in the neck muscles (neck stiffness) may indicate meningitis or subarachnoid haemorrhage.

Pupillary findings and eye signs may also be useful to differentiate metabolic and structural insults, and more importantly to detect incipent uncal herniation. Intact oculocephalic reflexes and preservation of the ‘doll’s eyes’ response indicates an intact medial longitudinal fasciculus and by default an intact brain stem, suggesting a metabolic cause for coma (Table X3 ).

There are four pairs of nuclei governing ocular movements, and they are spread between the superior and inferior midbrain and the pons. The pattern of ocular movement dysfunction can be used to pinpoint the site of a brainstem lesion. Likewise, specific testing of the oculovestibular reflex and the cranial nerve examination can be used to precisely locate a brainstem lesion but is of limited use in the emergency setting except as a predictor of herniation.

More generally, skin examination may reveal needle tracks suggestive of drug use or a meningococcal rash. Mucosal changes such as cyanosis or the cherry-red glow of carbon monoxide poisoning can be diagnostic. Cardiac monitoring and cardiovascular examination should identify rhythm disturbances, the murmurs of endocarditis and valvular disease, or evidence of shock from myocardial ischaemia or infarction. Respiratory patterns may aid in identifying the site of the lesion. Abdominal examination may detect organomegaly, ascites, bruits or pulsatile masses.


Specific laboratory and radiological investigations must be guided by the history and examination, and their timing determined by the priorities of resuscitation.


A full blood examination may reveal anaemia, immunocompromise, thrombocytopenia, inflammation or infection, but is rarely specific. CRP and ESR are non-specific acute-phase reactants and single determinants are not initially useful, although they may later be followed to monitor resolution of the illness or response to therapy. Coagulation profiles are particularly useful in haematological and liver disease, or if patients are taking anticoagulants such as warfarin.


Serum electrolyte levels aid in the differentiation of the various hypo- and hyperelemental causes of coma. Electrolyte imbalances may also be secondary to the causative insult and may not need specific correction. In hypotensive patients, a high to normal sodium and a low potassium suggests primary or secondary addisonian crisis.

Liver, renal and thyroid function tests may confirm focal organ dysfunction. The last may not always be readily available, but hypothermic patient and hyperthyroidism in the presence of tremor and tachyarrhythmias.

A serum glucose provides confirmation of bedside testing. Serum lactate determinations may reveal a metabolic acidosis and reflect the degree of tissue hypoxia, which again may be primary or secondary. Creatinine kinase and myogloginuria are useful to determine the presence and extent of rhabdomyolysis and to predict the likelihood of requiring dialysis. Serum and urine osmolarity may be useful in toxic ingestions such as ethylene glycol.

Blood gas analysis may give important information regarding acid-base balance, and along with the anion gap and the serum electrolytes can help distinguish between the various types and causes of acidosis and alkalosis. Knowledge of the partial pressure of oxygen and carbon dioxide is vital to resuscitative efforts.


Sepsis is a major metabolic cause of conscious state alteration and may present with no localizing symptoms or signs, especially in the elderly. In this case, blood cultures — preferably multiple sets obtained before antibiotic therapy — may be the only means of isolating the causative organism.

Naturally, system-specific specimens such as sputum, urine and cerebrospinal fluid should be collected when clinically indicated. Although as a rule specimens should be obtained prior to therapy, in suspected meningitis or encephalitis the administration of antibiotics or antiviral agents should not be delayed while a lumbar puncture/CT scan is performed.

Specific Laboratory Testing

Based on information from the history and examination, specific drug assays and urine screens may be indicated. These may include prescribed medications such as lithium or theophylline, or drugs of addiction such as amphetamine or opiates. Routine urine drug screens are of very limited value.

Venom detection kits can be used in specific clinical situations, and evidence of systemic envenomation can be screened for with other tests, such as coagulation profiles and creatinine kinase.


A chest X-ray may reveal primary infection or malignancy. In a patient with an altered conscious state and any suspicion of head trauma, a full cervical spine series is mandatory. Inadequate plain films should be supplemented by CT imaging of the rest of the spine and the pelvis should be guided by clinical assessment.

Intracranial imaging is best achieved with a plain CT of the head which, if normal and concern regarding intracranial pathology persists, may be followed by a contrast-enhanced scan or MRI. The latter has a higher sensitivity for encephalitis and cerebral vasculitis, although it may not always be easily accessible from the ED. Also, the technical constraints of MRI require a stable patient. Emergency CT angiography has a role in the delineation of cerebral aneurysms, and interventional angiography can provide therapeutic options, particularly in a patient who is progressing towards herniation.

Other Tests

The 12-lead ECG can highlight rate and rhythm disturbances. Specific changes, such as the U wave of hypokalaemia, the J wave of hypothermia and focal infarction and ischaemic patterns, serve to confirm and offer pointers to the cause of the coma.

It is worth noting that intracranial bleeding such as subarachnoid haemorrhage can be associated with an ischaemic-looking ECG. Care is required in cases of depressed level of consciousness with ECG changes, as the use of thrombolysis or anticoagulation based on the ECG in the presence of intracranial bleeding may well be fatal.

It is clear from the previous discussion that a good history and thorough examination are key to the appropriate choice of investigations.


Assessment and management are also inextricably linked and must take place concurrently. The clinical findings on assessment guide management, and the response to treatment may further aid assessment and diagnosis.

Following initial resuscitation, it is important to identify patients in whom trauma is known or suspected. These have a higher risk of skull fractures and focal intracranial pathology, and are more likely to have increased intracranial pressure requiring urgent imaging and subsequent neurosurgical consultation and definitive management. The same pathway is required for patients who have a non-traumatic cause for coma but who have lateralizing signs suggesting a focal intracranial lesion.

Evidence of brainstem herniation is a neurosurgical emergency. A CT scan is helpful in diagnosing the cause of cerebral herniation and should be obtained expeditiously. Neurosurgical consultation can be arranged concurrently so as not to impede smooth transit to theatre for those requiring urgent craniotomy. Cerebral resuscitation is continued concurrently, with relative hyperventilation to maintain a PCO2 of 30–35 mmHg. The role of mannitol is still controversial, but it may be used in consultation with the neurosurgical team. The diuretic effect may, however, add to haemodynamic compromise and secondary neurological embarrassment.

Should there be no lateralizing signs, then a metabolic cause needs to be sought. A metabolic screen and, if indicated, a toxicological screen, is performed. If a cause is found, it is further specifically investigated and definitely managed. If no cause is identified or suggested on initial or other first-line specific investigation, a brain CT scan is performed. Thereafter, patients with identified causes are stabilized and referred for appropriate continuing care. Depending on the pathology, prophylactic anticonvulsants and corticosteroids may be considered.

A normal CT scan does not completely exclude treatable intracranial infection or subarachnoid haemorrhage. Therefore, depending upon the patient’s conscious state and the level of clinical suspicion, a lumbar puncture may further assist with diagnosis. However, it must be emphasized that, in suspected intracranial infection, an obtunded patient should be treated empirically with appropriate antiviral agents and antibiotics, and the lumbar puncture deferred till the risk of herniation is minimized.

In the absence of any identifiable cause, supportive care is provided until specific investigation or the natural evolution of the disease process points to the diagnosis.

Self-limiting causes for altered conscious states, such as seizures Opens in new window and vasovagal syncope Opens in new window, have not been addressed here as they are covered elsewhere.


Patients with continuing altered consciousness should be admitted to a hospital with the range of services and clinical disciplines to manage the primary diagnosis. The level of care required will depend on the state of the patient on presentation and their subsequent response to treatment. Patient wishes, premorbid status and prognosis may also temper treatment choices and pathways.


Discussion of prognosis is difficult, as it depends on the cause and patient-specific factors. Effective cerebral resuscitation with optimal oxygenation and minimization of intracerebral hypercarbia and acidosis will promote the best recovery potential while addressing the underlying disease process. Prognosis is naturally dependent on the degree of irreversible cellular damage and the ability to correct the primary insult while minimizing secondary brain injury.

You Might Also Like:
    Adapted from: Textbook of Adult Emergency Medicine E-Book. Authored By Peter Cameron, George Jelinek, Anne-Maree Kelly, Lindsay Murray, Anthony F. T. Brown. References as cited include:
  1. Hasbun R. Abrahams J, Jekel J, Quagliarello VJ. Computed tomography of the head before lumbar puncture in adults with suspected meningitis. New England Journal of Medicine 2001; 345: 24: 1727–1732.
  2. Hoffman JR, Schriger DL, Luo JS. The empiric use of nalloxone in patients with altered mental status: A reappraisal. Annals of Emergency Medicine 1991; 20:246–252.
  3. Hoffman JR. Schriger DL, Votey SR, et al. The empiric use of hypertonic glucose in patients with status: A reappraisal. Annals of Emergency Medicine 1992; 21: 20–24.
  4. Hoffman DS, Goldfrank LR. The poisoned patient with altered consciousness: Controversies in the use of a ‘coma cocktail’. Journal of the American Medical Association 1995; 274: 562–569.
  5. Kelly AM, Kerr D, Dietze P, et al. A randomized trial of intranasal versus intramuscular naloxone in prehospital treatment for suspected opioid overdose. Medical Journal Association 2005; 182: 24–27.
  6. Teasdale G. Jennett B. Assessment of coma and impaired consciousness: A practical scale. Lancet 1974; 2: 81–84.
  7. Teassdale G, Jennett B. Aspects of coma after head injury. Lancet 1977; 1: 878–881.