Consciousness is defined as a state of being aware of both self and environment. It requires the continuous interaction of two intact components:
- awareness (content) mediated by the cerebral cortex and
- arousal (wakefulness) primarily supported by the brainstem structures (ascending reticular activating system [ARAS] and diencephalon). While the cortex is responsible for cognitive functions, the brainstem essentially activates and maintains cerebral responsiveness to the environment. The cortex has no intrinsic mechanism to generate or support arousal.
Unconsciousness may be induced by failure of either or both the brainstem and cortex. Most commonly, acute loss of consciousness is caused by impaired arousal due to an insult to the brainstem. As a result of damage to the ARAS, the cortex persists in a state of inactivity, the patient presents unwakeful and it is impossible to assess his awareness.
Whereas loss of arousal may develop after a small focal affection of brainstem structures, both diffuse and bilateral injury of cerebral hemispheres is required to produce complete unconsciousness, sparing the ARAS. Being able to produce significant neurological deficit, unilateral injury of the cerebral cortex does not result in a coma if the brainstem structures are intact.
Causes of unconsciousness are generally classified as metabolic (systemic) or structural. Systemic affection is commonly attributable to hypoxia (e.g. severe respiratory disturbances, acute hypoperfusion), drug toxicities, infections, glucose and electrolyte imbalances. Due to the increased sensitivity of cortical cells to metabolic changes and toxic substances, systemic injuries would sooner impair the cortex than affect brainstem structures.
Structural disturbances frequently result from stroke (hemorrhagic or ischemic), head trauma (e.g. hematoma, contusion, concussion), tumor or intracranial infection. Causes of unconsciousness can be age-distributed; with predominantly traumatic and toxic etiologies found in youth, whereas stroke, medication changes and infection are more common causes of a comatose state in the elderly.
Commonly used to consider all possible etiologies of various neurological pathologies, the mnemonic «VITAMINS C/D» may be helpful when considering causes of a coma: vascular (ischemic/hemorrhagic brain injury), infection (e.g. meningitis, abscess, subdural empyema), trauma (e.g. concussion, contusion, hematoma), autoimmune/inflammatory, metabolic (e.g. hypoglycemia, hypoxia), medications (e.g. alcohol, narcotics, sedative-hypnotics), migraine (basilar form), intracranial pressure, neoplasms, seizures, cerebrospinal fluid (CSF) disorders (hydrocephalus) and developmental/congenital abnormalities (Hoesch R.E., Geocadin R.G., 2012).
Apart from a truly comatose state, a number of other conditions may mimic a state of unconsciousness, including:
- physiologic sleep — promptly reversible by means of sensory stimulation with persistent vigilance following arousal.
- «locked-in» syndrome (de-efferented state, Monte Cristo syndrome) — due to impairment of the ventral pons, the patient presents with total paralysis except vertical eye movements and/or blinking, with awareness and arousal being intact (since the ARAS is located in the dorsal pons) (Carandang R.A. et al., 2011; Hoesch R.E., Geocadin R.G., 2012). «Locked-in» patients have preserved vision, hearing and are sensitive to external stimuli. Causes of the «locked-in» syndrome include brainstem ischemic stroke resulting from basilar thromboembolism, pontine hemorrhage, neuromuscular disorders (e.g. acute inflammatory demyelinating polyneuropathy, myasthenia gravis, botulism, acute poliomyelitis) and the use of neuromuscular blocking agents (Carandang R.A. et al., 2011; Stübgen J. et al., 2011; Hoesch R.E., Geocadin R.G., 2012). Voluntary upward gaze and blinking must be checked when assessing any seemingly unconscious patient, to exclude a locked-in state. In peripheral neuromuscular disorders, vertical eye movements are not spared (Stübgen J. et al., 2011). Electroencephalography (EEG) may be helpful in diagnosing locked-in syndrome, by demonstrating normal cortical activity.
- Akinetic mutism — motionless and silent patient appears alert but with little or no evidence of mental activity. Sleep-wake cycles are retained. Whereas response to external stimuli may be lacking, eye opening and visual tracking are intact (Carandang R.A. et al., 2011; Hoesch R.E., Geocadin R.G., 2012). Muscular tone is normal or increased (Stübgen J. et al., 2011). Movements are absent or primitive in response to pain stimulation. Causes of akinetic mutism include bilateral impairment of frontal lobes (basomedial areas) and lesions of paramedian reticular formation in the midbrain and posterior diencephalon (Carandang R.A. et al., 2011; Stübgen J. et al., 2011; Hoesch R.E., Geocadin R.G., 2012).
- Psychogenic coma — a state of functional unresponsiveness, where seemingly comatose patients have normal clinical findings indicative of vigilance. This state may be caused by malingering, psychotic depression, hysterical reaction, catatonic schizophrenia, dissociative state and other psychiatric problems (Carandang R.A. et al., 2011). Examination reveals normal pupillary response, resistance to rapid manual eye opening and closure, nystagmus in oculovestibular test (should be preserved when cortex is intact), normal and symmetrical reflexes, avoidance of self-injury (in the hand drop test), normal EEG findings (Carandang R.A. et al., 2011; Huff J.S., 2011).
- Vegetative state — can be described as a state of wakeful unawareness, when brainstem arousal activity is preserved and patient appears awake but does not demonstrate any cognitive function as a result of extensive bilateral cortical or subcortical white matter injury (Stübgen J. et al., 2011; 2012). Spontaneous eye opening, yawning, rudimentary movements, deep tendon reflexes, decerebrate or decorticate posturing and sleep-wake cycles may be seen (Carandang R.A. et al., 2011; Stübgen J. et al., 2011; Hoesch R.E., Geocadin R.G., 2012). In permanent vegetative state (3 months after nontraumatic brain injury and 12 months after traumatic brain injury), any substantial neurologic recovery is very unlikely (Hoesch R.E., Geocadin R.G., 2012).
- Brain death — a state of irreversible brain destruction confirmed by complete and permanent absence of both cerebral and brainstem functions. EEG shows electrocerebral silence, however spinal reflexes may be preserved in brain dead patients (McIntyre H.B. et al., 2008; Carandang R.A. et al., 2011). Seeing as drug intoxication may sometimes mimic brain death, appropriate neurologic assessment should be postponed until after anticipated resolution of possible toxic effects (Carandang R.A. et al., 2011).
The clinical assessment of a comatose patient should be fast, precise and simultaneously carried out with emergency therapeutic actions. Initial priority should be placed on the evaluation and support of vital functions in accordance with the Advanced Cardiac Life Support protocol. Continuous telemetry monitoring of vital signs should be instituted as soon as practicable.
If possible, rapid neurological examination must be performed prior to any sedation and myoplegia required for endotracheal intubation. The aim of this evaluation is to rapidly determine if unconciousness is caused by focal or diffuse impairment, as well as to identify neurological injuries that demand urgent intervention (e.g. cerebral herniation). Brief neurologic examination should include assessment of consciousness level, pupils (size, asymmetry, reactivity to light) and motor function (Hoesch R.E., Geocadin R.G., 2012).
After stabilization of patient’s condition, a complete head-to-toe physical examination is performed, including inspection of completely undressed patient for signs of trauma, infection, needle marks; measurement of body temperature; evaluation of breath odor (e.g. alcohol, ketones); examination of neck (traumatic deformities, nuchal rigidity, lymphadenopathy); and systematic neurologic assessment (Cooke J.L., 2010; Carandang R.A. et al., 2011).
When examining comatose patient special emphasis should be made on the following assessments:
- Level of consciousness — most commonly assessed using Glasgow Coma Scale (GCS) (Table 1) (Teasdale G., Jennett B., 1974). GCS score for comatose patients is <9. GCS score is annotated with «T» if the patient is unable to demonstrate verbal response due to endotracheal tube (e.g. 5T) (Hoesch R.E., Geocadin R.G., 2012). Despite wide use, the GCS does not allow for assessment of brainstem integrity. For this reason, the Full Outline of UnResponsiveness (FOUR) score has been developed by Wijdicks and colleagues to incorporate the grading of brainstem reflexes and respiration (Table 2) (Wijdicks E.F. et al., 2005).
Brainstem reflexes and respiration
|Localizing pain stimuli||5|
|Withdrawal from painful stimuli||4|
|Flexor posturing to painful stimuli||3|
|Extensor posturing to painful stimuli||2|
Brainstem reflexes and respiration
|Eyelids open or opened, tracking, or blinking to command||4|
|Eyelids open but not tracking||3|
|Eyelids closed but open to loud voice||2|
|Eyelids closed but open to pain||1|
|Eyelids remained closed with pain||0|
|Thumbs up, fist or peace sign||4|
|Localizing to pain||3|
|Flexion response to pain||2|
|Extension response to pain||1|
|No response to pain or generalized myoclonus||0|
|Pupils and corneals intact||4|
|One pupil wide and fixed||3|
|Pupil or corneal absent||2|
|Pupil and corneal absent||1|
|Absent pupil, corneal and cough reflex||0|
|Not intubated, regular breathing pattern||4|
|Not intubated, Cheyne — Stokes breathing||3|
|Not intubated, irregular breathing||2|
|Breathes above ventilator rate||1|
|Breathes at ventilator rate or apnea||0|
- Size, reactivity to light and equality of pupils. One of the most important tools for differentiating systemic and structural brain impairments is the inspection of pupils. Whereas in toxic-metabolic coma pupillary reactivity is generally preserved, a lack of pupillary response demands further search for a structural lesion (Huff J.S., 2011; Stübgen J. et al., 2011). Disturbances of pupillary reactivity occur because most of structural comas develop as a result of injury to the brainstem where sympathetic fibers and the parasympathetic Edinger — Westphal nucleus which regulates pupillary size are located (McIntyre H.B. et al., 2008). Unilateral dilation of pupil («blown pupil») in most instances indicates the side of possible compression of the third cranial nerve (oculomotor), as a result of lateral tentorial herniation of the temporal lobe. However, some cases of lateral herniation with contralateral third nerve compression may also occur. Compression of the midbrain is demonstrated by fixed midsized (3–5 mm) pupils, showing impairment of both sympathetic and parasympathetic regulation (McIntyre H.B. et al., 2008; Stübgen J. et al., 2011). Pontine lesions are often accompanied by disruption of sympathetic pathways presenting with pinpoint minimally reactive pupils. Although in most metabolic comas, pupillary reactivity is intact owing to sparing of the respective regulatory centers in the brainstem, some cases of drug-related unconsciousness presents with affected pupils (e.g. opioids — pinpoint minimally reactive pupils; barbiturates — relatively fixed pupils of varying size; anticholinergics — significantly dilated and relatively fixed pupils) (Kunschner L.J., Huff J.S., 2003; McIntyre H.B. et al., 2008). While funduscopic examination provides relevant information (e.g. papilledema suggests increased intracranial pressure (ICP), subhyaloid hemorrhage is indicative of subarachnoid hemorrhage), under no circumstances should pupils be intentionally dilated, else, one of the most reliable clinical indicators for neurologic dynamic assessment will be lost (McIntyre H.B. et al., 2008).
- Ocular movements are mediated by the brainstem structures positioned adjacent to the areas responsible for arousal. Assessment of the oculomotor system should start from observation of eye movements at rest. Eyes may symmetrically deviate toward the side of lesion in the motor cortex, or away from the affected side in pontine lesions. Thalamic hemorrhage, compression of the midbrain and hepatic encephalopathy may produce tonic downward deviation, while tonic upward deviation may be seen after anoxia (Carandang R.A. et al., 2011). Midbrain lesions can also present with retraction nystagmus or conversion nystagmus (Hoesch R.E., Geocadin R.G., 2012). Whereas symmetric eye deviations from side to side (roving movements) in comatose patients indicate bilateral impairment of hemispheres with possibly unaffected brainstem structures, disconjugate eye positions may suggest paralysis of cranial nerves III (persistently abducted eye), IV or VI (persistently adducted eye) (Kunschner L.J., Huff J.S., 2003). A vertical disconjugate gaze indicates an impairment of pontine or cerebellar structures (Cooke J.L., 2010). Rapid conjugate downbeat with subsequent slow upward drift (ocular bobbing) may also suggest a pontine lesion. In addition to the observation of spontaneous tonic eye movements, oculocephalic («doll’s eyes») and oculovestibular (caloric) tests are helpful when assessing brainstem integrity. If negative, these tests make structural causes of coma very unlikely (Cooke J.L., 2010). Note that the oculocephalic test should never be performed if cervical spine injury is suspected. Holding the patient’s eyelids open, head should be rotated from side to side and from flexion to extension. Symmetrical smooth deviation of eyes contralateral to the direction of head turning is normal and observed in comatose patients with intact brainstem structures. If oculocephalic test shows abnormal eye movements (eyes remain in fixed position or deviate in the direction of head turn), oculovestibular test should be performed. The latter is more sensitive for brainstem impairment and overcomes voluntary resistance of conscious patient to oculovestibular testing by gaze fixation on a distant object (Cooke J.L., 2010; Hoesch R.E., Geocadin R.G., 2012). To perform this test patient’s head should be elevated to 30 degrees (reverse Trendelenburg position may be useful if cervical spine integrity concerns exist) (Cooke J.L., 2010). Examination of tympanic membrane is also obligatory to exclude any injury (Carandang R.A. et al., 2011). Ice-cold water (up to 120 ml) is slowly and continuously instilled into the external auditory meatus using syringe with catheter (Carandang R.A. et al., 2011). During and several minutes after infusion, the eyes are observed for movements. The other ear is tested after 5 minutes to allow rewarming (Hoesch R.E., Geocadin R.G., 2012). Whereas nystagmus with rapid movement away from cold stimulation is the normal response in an awake individual, suppression of tonic activity by tympanic membrane cooling in comatose patient with bilateral impairment of hemispheres and intact brainstem causes movement of eyes toward the irrigated ear (Cooke J.L., 2010; Carandang R.A. et al., 2011; Hoesch R.E., Geocadin R.G., 2012). Brainstem dysfunction shows defective response. Considering the relative time-consuming nature of this test, oculovestibular assessment should not delay acute lifesaving measures.
- Corneal reflex. Normally, unilateral stimulation of the cornea by touching it with a wisp of cotton or placing a drop of normal saline, causes bilateral blinking, confirming intact pons, ipsilateral trigeminal nerve and bilateral facial nerves (Hoesch R.E., Geocadin R.G., 2012). Corneal reflex is frequently blunted and of low diagnostic value in persons who wear contact lenses (Carandang R.A. et al., 2011).
- Motor response. Brief assessment of motor function is included in the GCS and FOUR score (see above). Assessment of motor function in unconscious patients should start from passive observation of spontaneous movements (if any) with subsequent assessment of response to painful stimuli (Hoesch R.E., Geocadin R.G., 2012). Asymmetric response is indicative of a focal lesion. Lateral cortical impairment presents with contralateral deficit of motor function (Kunschner L.J., Huff J.S., 2003). Focal motor deficit generally suggests primary brain lesions, while in pure toxic-metabolic coma, focal findings are missing (McIntyre H.B. et al., 2008). Posturing or absence of any movements in extremities in response to stimuli suggests severe impairment with poor neurological outcome (Hoesch R.E., Geocadin R.G., 2012). Flexor (decorticate) posturing appears as flexion and internal rotation of the arms with extension of the legs, which is seen in hemispheric cortical impairment. Extensor (decerebrate) posturing (extension and adduction of upper and lower extremities) indicates brainstem injury (Kunschner L.J., Huff J.S., 2003; Carandang R.A. et al., 2011).
- Pattern of breathing may be helpful in localizing site of impairment. Cheyne — Stokes breathing (gradual increase followed by decrease in depth and sometimes in rate of respirations resulting in brief periods of apnea) commonly occur in bilateral cortical hemispheric dysfunction, bilateral thalamic injury or metabolic impairment (Kunschner L.J., Huff J.S., 2003; Hoesch R.E., Geocadin R.G., 2012). Apneustic breathing is characterized by long end-inspiratory pauses and suggests midcaudal pontine lesions. Affection of both cerebral hemispheres, midbrain or pontine structures can produce compensatory central neurogenic hyperventilation. However, this pattern may also occur in acidosis, increased ICP and pulmonary congestion. Irregular respiratory clusters alternated by pauses of various duration (cluster breathing) may present with bilateral hemispheric injuries, pontine and medullary damage. Completely irregular breathing — ataxic respiration (also known as «atrial fibrillation» of respiratory patterns) indicates medullary impairment (Kunschner L.J., Huff J.S., 2003; Hoesch R.E., Geocadin R.G., 2012).
As soon as is possible efforts must be made to meticulously interview family members, friends, caregivers, bystanders or paramedics about relevant medical history, especially pertaining to possible causes and evolution of unconsciousness. In particular, timing and course of coma, recent and past medical history (e.g. head trauma, epilepsy, hypertension, infection, diabetes), access to drugs and psychiatric history should be questioned (Huff J.S., 2011; Stübgen J. et al., 2011).
Choice of ancillary tests generally depends upon obtained medical history and results of systematic physical examination. Completion of the following general tests should be also considered as first-line investigations in the unconscious patient: blood glucose, hemoglobin and hematocrit, arterial blood gases, pulseoximetry, urea and creatinine, electrolytes, urinalysis, electrocardiography. Additionally, essential diagnostic data may be obtained by means of head computerized tomography (CT), analysis of CSF, EEG, chest x-ray, complete blood count, blood and urine cultures, liver and thyroid function tests and toxicologic screen (Kunschner L.J., Huff J.S., 2003; Simon B., Nobay F., 2005; Cooke J.L., 2010; Stübgen J. et al., 2011).
When medical history and physical examination may suggest possible structural causes of unconsciousness (focal neurologic signs), neuro-imaging should be considered (Kunschner L.J., Huff J.S., 2003; Cooke J.L., 2010). However, imaging studies should not delay treatment of promptly reversible comatose states. Non-contrast CT is considered to be a preliminary imaging method of choice for comatose patients, because it can readily visualize most hemorrhagic events which may cause unconsciousness, as well as signs of cerebral edema, ischemia and mass effect. Magnetic resonance imaging (MRI) may be more helpful in visualization of early ischemia (determined several minutes after onset as compared to several hours when using CT) and structural lesions in posterior fossa (Kunschner L.J., Huff J.S., 2003; Cooke J.L., 2010). Indications for additional imaging studies (e.g. angiography) are determined based on the results of non-contrast CT scan.
Lumbar puncture with subsequent analysis of CSF is necessary for diagnosis of meningitis or if subarachnoid hemorrhage is suspected when CT scan shows negative result (Kunschner L.J., Huff J.S., 2003; Carandang R.A. et al., 2011).
Although not routinely used, EEG is the only method that provides accurate diagnosis of nonconvulsive status epilepticus (Kunschner L.J., Huff J.S., 2003). Furthermore it may be helpful in psychogenic coma and confirmation of brain death based on electrocerebral silence (Carandang R.A. et al., 2011). Continuous EEG monitoring allows assessment of dynamics for a comatose patient who requires uninterrupted neuromuscular blockade (e.g. in status epilepticus) (Cooke J.L., 2010).
Absolute priority must be given to support vital functions. Immediate attention must be given to airways, ventilation and circulation.
Endotracheal intubation should be considered with low threshold for comatose patients in order to provide sustained airway opening and to prevent aspiration. Cervical spine precautions are needed if severe neck trauma is suspected. Adequate ventilation is required to maintain normal oxygenation, as well as to regulate ICP — while hypocapnia can reduce ICP due to cerebral vasoconstriction, hypercapnia can increase ICP as a result of vascular dilation. Ideally, the partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2) in arterial blood should be greater than 100 mmHg and in the range of 35–37 mmHg, respectively. It is recommended to avoid hyperventilation (PaCO2 <35 mmHg) unless herniation is suspected (Stübgen J. et al., 2011). In patients with increased ICP, positive end-expiratory pressure should be avoided as well.
Maintenance of circulation is essential for adequate cerebral perfusion and prevention of further hypoxic injury. Shock should be treated with fluid resuscitation, transfusion of blood components, administration of vasopressors and inotropic agents as appropriate based on its etiology and pathogenesis. Goals for blood pressure (BP) correction largely depend on the nature of neurological injury. Whereas a higher BP is frequently needed to support perfusion in ischemic areas, management of hemorrhagic cerebral catastrophes demands lower BP values to prevent further complications (Hoesch R.E., Geocadin R.G., 2012). Mean BP of 100 mmHg is generally considered safe for the majority of patients, and hypertension does not require treatment unless systolic BP is >160 mmHg (Stübgen J. et al., 2011). If antihypertensive treatment is deemed necessary, priority should be given to hypotensive agents that do not cause significant rise in ICP due to cerebral vasodilation. Hydralazine and labetalol are preferable to manage severe systemic hypertension, whereas use of nitrates and sodium nitroprusside should be avoided (Stübgen J. et al., 2011; Hoesch R.E., Geocadin R.G., 2012). Continuous measurement of urine output (should be ≥0.5 ml/kg/h) is essential to assess adequacy of renal perfusion.
If rapid neurological examination shows signs of severe intracranial hypertension, emergency measures of «brain code» should be instituted, including: raising of head to 30º, elimination of any neck vein compression (e.g. bandages, excessive head turn), hyperventilation (to support PaCO2 of 28–32 mmHg), intravenous (IV) mannitol (1–2 g/kg) and hypertonic sodium chloride (2–23.4% solution; through central vein if >2%) (Hoesch R.E., Geocadin R.G., 2012). Additionally, ICP monitoring is recommended to support cerebral perfusion pressure (difference between mean arterial pressure and ICP) >60 mmHg. If clinical suspicion of intracranial hypertension exists while monitoring is absent, ICP of ≥20 mmHg should be assumed (Hoesch R.E., Geocadin R.G., 2012). When rise in ICP is caused by neoplastic brain edema, steroids (dexamethasone 10 mg IV) may be helpful (Huff J.S., 2011). Refractory intracranial hypertension may require a craniectomy (Hoesch R.E., Geocadin R.G., 2012).
In cases with unclear etiology of coma and signs of focal neurological impairment signs are absent, empirical IV administration of the following agents are to be considered (Kunschner L.J., Huff J.S., 2003; Simon B., Nobay F., 2005):
- Dextrose (50%, 50 ml) — to resolve hypoglycemia. A determination of blood glucose levels should precede dextrose administration (Simon B., Nobay F., 2005).
- Thiamine (100 mg) — to address Wernicke’s encephalopathy. Apart from alcoholism, thiamine deficiency may be caused by malnutrition (e.g. bulimia or anorexia), pregnancy and malignant tumors (Simon B., Nobay F., 2005; Stübgen J. et al., 2011).
- Naloxone (2 mg) — if opioid intoxication is suspected. Treatment of intoxication caused by some synthetic opioids may need higher dosages of naloxone (up to 10 mg) (Simon B., Nobay F., 2005). In chronic narcotic users naloxone may provoke acute withdrawal syndrome (Kunschner L.J., Huff J.S., 2003; Stübgen J. et al., 2011).
- Flumazenil acts as a competitive antagonist of benzodiazepines. While not recommended for routine administration due to the risk of causing generalized seizures (e.g. withdrawal in patients addicted to benzodiazepines), flumazenil (0.2–1.0 mg IV) still can be used by gradually titrating the dose when benzodiazepines are suspected as a cause of comatose state (Simon B., Nobay F., 2005; Stübgen J. et al., 2011).
- Physostigmine (0.5–2.0 mg IV) may be helpful in coma induced by drugs with anticholinergic effects. Extreme caution for physostigmine use should be exercised if intoxication is caused by agents with myocardial depressant properties (e.g. tricyclic antidepressants) given the increased risk of cardiac arrest (Simon B., Nobay F., 2005; Stübgen J. et al., 2011).
Consciousness requires the continuous interaction of both intact awareness and arousal mediated by the cerebral cortex and brainstem structures, respectively.
Being able to produce significant neurological deficit, unilateral injury of the cerebral cortex does not result in a coma if the brainstem structures are intact.
Rapid neurological examination (assessment of consciousness level, pupils and motor function) must be performed prior to any sedation and myoplegia to identify neurological injuries that demand urgent intervention.
Absolute priority must be given to support vital functions with immediate attention given to airways, ventilation and circulation.
If rapid neurological examination shows signs of severe intracranial hypertension, emergency measures of «brain code» should be instituted.
Carandang R.A., Hayward L.J., Drachman D.A. (2011) Evaluating the patient with altered consciousness in the intensive care unit. In: Irwin and Rippe’s Intensive Care Medicine. 7th ed. Irwin R.S., Rippe J.M. (Eds.). Philadelphia, Lippincott Williams & Wilkins, p. 1751–1760.
Cooke J.L. (2010) Depressed consciousness and coma. In: Rosen’s Emergency Medicine: Concepts and Clinical Practice. 7th ed. Marx J.A. (Ed.). Philadelphia, Mosby, p. 106–112.
Hoesch R.E., Geocadin R.G. (2012) Coma and brain death. In: Emergency Neurology. Roos K.L. (Ed.). New York, Springer, p. 327–349.
Huff J.S. (2011) Altered mental status and coma. In: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. Tintinalli J.E. (Ed.). New York, McGraw-Hill, p. 1390–1397.
Kunschner L.J., Huff J.S. (2003) Altered mental status. In: Principles and Practice of Emergency Neurology. Shah S.M., Kelly K.M. (Eds). Cambridge, Cambridge University Press, p. 43–51.
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Simon B., Nobay F. (2005) Altered mental status. In: An Introduction to Clinical Emergency Medicine. Mahadevan S.V., Garmel G.M. (Eds). Cambridge, Cambridge University Press, 179–191.
Stübgen J., Plum F., Kochanek P. (2011) Coma. In: Vincent J., Abraham E., Kochanek P., Moore F.A., Fink M.P. (Eds). Textbook of Critical Care. 6th ed. Philadelphia, Saunders, p. 153–165.
Teasdale G., Jennett B. (1974) Assessment of coma and impaired consciousness. A practical scale. Lancet, 2(7872): 81–84.
Wijdicks E.F., Bamlet W.R., Maramattom B.V. et al. (2005) Validation of a new coma scale: the FOUR score. Ann. Neurol., 58(4): 585–593.
Резюме. Непритомні пацієнти уособлюють одну з найбільш розповсюджених та складних проблем для фахівців, медицини невідкладних станів та інтенсивної терапії. Кому — стан із повністю відсутньою реакцією на зовнішні та внутрішні стимули — у світі виявляють у ≈⅓ пацієнтів, які надходять до відділень інтенсивної терапії клінік загального профілю. Кома — важливий предиктор смертності та наслідків різних неврологічних розладів. Враховуючи, що непритомний стан тісно пов’язаний із недостатністю функції життєво важливих органів, усі випадки коми необхідно розглядати як потенційно життєзагрозливі критичні стани. У статті описані основні принципи діагностики та лікування, що є запорукою успіху при наданні невідкладної допомоги непритомним пацієнтам.
Ключеві слова: кома, свідомість, оцінка за шкалою FOUR, смерть мозку, кора, стовбур мозку.
Резюме. Пациенты без сознания представляют одну из наиболее распространенных и сложных проблем для специалистов медицины неотложных состояний и интенсивной терапии. Кому — состояние с полностью отсутствующей реакцией на внешние и внутренние стимулы — выявляют в мире у ≈⅓ пациентов, поступающих в отделения интенсивной терапии клиник общего профиля. Кома является важным предиктором смертности и исхода различных неврологических расстройств. Учитывая, что бессознательное состояние тесно связано с недостаточностью функции жизненно важных органов, все случаи комы необходимо рассматривать как потенциально жизнеугрожающие критические состояния. В статье описаны основные принципы диагностики и лечения, которые являются залогом успеха при оказании неотложной помощи пациентам без сознания.
Ключевые слова: кома, сознание, оценка по шкале FOUR, смерть мозга, кора, ствол мозга.
Contact for correspondence:
295006, Simferopol, Lenin blvd, 5/7
Crimean State Medical University
named after S. I. Georgievsky,
Department of Emergency
Medicine and Anesthesiology
E-mail: [email protected]