Introduction
Consciousness represents the state of being aware of oneself and the surrounding environment, coupled with the capacity to respond to external stimuli.[1] Impaired consciousness, conversely, is characterized by reduced alertness, decreased wakefulness, and a diminished awareness of both self and surroundings.[1] While some individuals may spontaneously regain full consciousness, others necessitate intensive medical intervention and thorough diagnostic evaluations.
Coma is defined as a profound state of unconsciousness, often prolonged, where an individual lies with eyes closed and cannot be awakened to respond appropriately to stimuli, even with vigorous attempts.[2] The Glasgow Coma Scale (GCS) is a standardized medical tool used to objectively assess the depth of coma. GCS scores are valuable in predicting outcomes for patients with traumatic brain injuries (TBIs), subarachnoid hemorrhages, and bacterial meningitis.
During unconsciousness, patients lose protective reflexes and sensory responses, making them susceptible to complications such as aspiration, anoxic brain injuries, airway obstruction, and pressure ulcers.[1] The underlying causes of persistent unconsciousness can be reversible or irreversible. Damage to the ascending reticular activating system (RAS), cerebral hemispheres, and metabolic or toxic disruptions are potential contributors to impaired consciousness.
This article provides an in-depth exploration of the causes and physiological mechanisms of reduced consciousness. It emphasizes the critical role of an interprofessional healthcare team in the assessment and management of this complex condition, aiming to improve patient outcomes and minimize potential complications.
Etiology of Unconsciousness
The RAS is crucial for initiating and maintaining consciousness. Originating in the upper pons and midbrain, it projects to the thalamus and hypothalamus, ultimately reaching the cerebral cortex. Consciousness can be disrupted by temporary or permanent damage to the RAS in the brainstem, the cerebral hemispheres, or any condition that alters cerebral metabolism. Damage to the cerebral hemispheres is typically diffuse and bilateral; unilateral damage must be extensive enough to affect the opposite hemisphere or brainstem. The primary mechanisms leading to unconsciousness are categorized into structural brain lesions, widespread neuronal dysfunction due to systemic pathology, and, less frequently, psychogenic causes.[1]
Structural causes, such as cerebrovascular accidents (strokes) or TBIs, can directly damage specific brain areas or indirectly cause harm through compression or increased intracranial pressure (ICP). Elevated ICP can impede cerebral blood flow and potentially lead to tissue distortion and brain herniation.[2, 3] Systemic causes, including hypoglycemia or hypothermia, disrupt cerebral metabolism by hindering oxygen or substrate delivery, impairing neuronal function. Psychogenic unresponsiveness is a prolonged dissociative state where the patient is unresponsive or exhibits reduced responses to external stimuli. Clinical signs suggestive of psychogenic unresponsiveness include maintaining a specific posture, nystagmus upon caloric stimulation, or resistance to passive eye-opening. Commonly encountered causes of unconsciousness in emergency settings include stroke, post-anoxic coma, drug toxicity or poisoning, and metabolic disorders such as endocrine or acid-base imbalances.[4]
Epidemiology of Unconsciousness
The prevalence and causes of altered consciousness vary across different healthcare settings and patient populations. Trauma centers, for example, frequently encounter unconscious patients with TBIs. Among non-traumatic causes, hemorrhagic strokes account for 6% to 54%, anoxic brain injuries for 3% to 42%, poisonings for 1% to 39%, and metabolic conditions for 3% to 42% of cases.
While stroke is the most common non-traumatic cause of coma overall, non-structural causes are slightly more prevalent (37% to 75%) than structural causes (28% to 64%).[5]
Overall mortality rates associated with unconsciousness range from 25% to 87%. Strokes and anoxic coma have the highest mortality rates, ranging from 60% to 95% and 54% to 89%, respectively. Conversely, epilepsy and poisoning are associated with lower mortality rates, typically below 10%.[5]
Pathophysiology of Unconsciousness
The underlying pathophysiology of unconsciousness is neuronal dysfunction resulting from a reduced supply of glucose or oxygen to the brain.[6] In cases of structural central nervous system lesions, coma can arise from direct destruction of brain arousal centers or secondary damage due to intracranial structure shifts, vascular compression, or elevated ICP.[6]
The ascending RAS in the brainstem is the primary anatomical site for arousal. Neurons from this system originate in the dorsal pons and midbrain, connect in the thalamus, and project to various cortical regions. The cortex is crucial for processing, integrating, and contextualizing information, ultimately generating awareness.[1] The RAS receives input from the spinal cord and cortex, facilitating awareness of the external environment.[5, 7]
Unconsciousness can result from damage to three primary brain areas:[2]
Bilateral Hemispheric Damage
Extensive damage to the cerebral cortex, due to hypoxic or ischemic injuries or brain trauma, leads to neuronal death and denervation of cortical areas. Consequently, patients lose the ability to process and consciously respond to stimuli. Coma caused by systemic factors also falls into this category, as it creates an abnormal physiological environment inhibiting neuronal function. This pattern is typically reversible if the underlying systemic abnormality is corrected.
Diencephalic (Thalamic) Injury
The thalamus contains relay nuclei that direct afferent input to the cortex. Bilateral thalamic lesions can produce findings similar to those seen in bilateral cortical injury.
Upper Brainstem Injury
The dorsal pons and midbrain house the RAS. Lesions in this area can directly impair consciousness and lead to a comatose state.
History and Physical Examination in Unconscious Patients
Obtaining a comprehensive medical history is crucial when evaluating an unconscious patient. Information from witnesses, family members, or paramedics can provide valuable insights.[3] Reviewing past hospital records and examining personal belongings like wallets or medical alert bracelets may yield additional information. Key historical details include the timeline of altered consciousness, current medications, recent illnesses, prior episodes resembling transient ischemic attacks (TIAs), syncope, or seizures, and symptoms preceding loss of consciousness.
Individual vital signs, respiratory patterns, and skin abnormalities can suggest various diagnoses. However, the eyes are particularly informative. Papilledema can indicate increased ICP, Roth spots may suggest bacterial endocarditis, and pupillary light reflex abnormalities are often due to downward herniation of mesial temporal structures or brainstem lesions. Toxic causes generally do not significantly affect pupil size, except for substances known to cause miosis or mydriasis. Fractures and wounds typically indicate trauma.
A neurological examination helps determine the location and nature of the neurological lesion and assess prognosis. This examination is most valuable when the patient is well-perfused, normothermic, normoglycemic, and free from neurologically active toxins or medications.[8] The GCS assesses coma severity and provides prognostic information. Evaluating spontaneous movements, muscle tone, and reflexes can help identify conditions such as hemiplegia and contralateral cerebral lesions or upper brainstem involvement.
Evaluation of Unconsciousness
Initial Assessment: ABCs
The initial step in evaluating an unconscious patient is to assess vital signs. Following American Heart Association guidelines, check for a pulse, ensure airway patency, and assess breathing pattern. Absent pulse or irregular breathing necessitates immediate basic or advanced cardiovascular life support. For patients with a pulse and effective breathing, the evaluation proceeds to a general physical and neurological examination.
Assessing Responsiveness
Objectively measure responsiveness, starting with verbal address, progressing to gentle shaking, and then to more intense mechanical stimulation. Painful stimuli can be applied to areas like the supraorbital ridge, nail beds, or temporomandibular joint, ensuring no tissue injury. For focal spinal cord lesions, grade responses to painful stimuli bilaterally. If these measures fail, sternal rub can be used to awaken patients not in a deep coma.[2]
Documenting the patient’s specific reactions to external stimuli is best practice for reporting responsiveness.[2] Standardized coma scales like the GCS and Full Outline of UnResponsiveness (FOUR) score facilitate effective communication among clinicians, track patient progress, and assess prognosis.[9, 10, 11] Daily systematic physical examinations with consistent documentation are crucial.[8]
Glasgow Coma Scale (GCS)
Eye Response:
- 4: Spontaneous eye opening
- 3: Opens eyes to verbal command
- 2: Opens eyes to pain
- 1: No eye opening
Motor Response:
- 6: Obeys commands
- 5: Localizes pain
- 4: Withdraws from pain
- 3: Flexion to pain
- 2: Extension to pain
- 1: No motor response
Verbal Response:
- 5: Oriented
- 4: Confused
- 3: Inappropriate words
- 2: Incomprehensible sounds
- 1: No verbal response
GCS Severity:
- 8 or less: Severe
- 9 to 12: Moderate
- 13 to 15: Mild
FOUR Score Assessment
Eye Response:
- 4: Eyelids open or opened, tracking, or blinking to command
- 3: Eyelids open but not tracking
- 2: Eyelids closed, open to loud voice
- 1: Eyelids closed, open to pain
- 0: Eyelids remain closed with pain
Motor Response:
- 4: Thumbs-up, fist, or peace sign
- 3: Localizing to pain
- 2: Flexion to pain
- 1: Extension to pain
- 0: No response to pain or generalized myoclonic status
Brainstem Reflexes:
- 4: Pupillary and corneal reflexes present
- 3: One pupil wide and fixed
- 2: Pupillary or corneal reflexes absent
- 1: Pupillary and corneal reflexes absent
- 0: Absent pupillary, corneal, and cough reflexes
Respiration:
- 4: Not intubated, regular breathing pattern
- 3: Not intubated, Cheyne-Stokes breathing
- 2: Not intubated, irregular breathing
- 1: Breaths above ventilator rate
- 0: Breaths at or below ventilator rate
Pupillary Examination
Note initial eye position and movements. Nystagmus is uncommon in unconscious patients but may indicate an irritating brain lesion or occult seizure activity. Document pupil size using a pupilometer and assess light responses, as reactions may be sluggish in unconscious patients.[8, 12] Anisocoria, abnormal light reflexes, or irregular pupil sizes may indicate increased ICP.[13]
Cranial Nerve Assessment
Funduscopic examination can reveal papilledema or subhyaloid hemorrhage. Oculocephalic or oculovestibular testing assesses cranial nerves III, IV, VI, and VIII function. Intact brainstem function should elicit normal responses to these maneuvers. Caloric stimulation can be used for oculovestibular testing in patients with cleared cervical spines.
Corneal reflex testing involves stimulating the cornea and observing for a blink response. Normal responses include both direct and consensual blinks, indicating normal cranial nerves V and VII function. Use normal saline drops for corneal stimulation to prevent damage. Contact lenses can diminish this reflex. Gag and cough reflexes indicate normal cranial nerves IX and X function.[2]
Motor Function Assessment
Assess motor function by evaluating muscle tone, movement patterns, and peripheral tendon reflexes. Decorticate posturing (upper-extremity flexion and lower-extremity extension) indicates damage at or below the cerebral cortex. Decerebrate posturing (upper and lower extremity extension) typically indicates brainstem damage below the red nucleus, often from pontine strokes. Both postures are associated with poor prognosis.
Neuroimaging
Neuroimaging is critical for unconscious patients to promptly identify intracranial abnormalities. Brain computed tomography (CT) is usually the initial study, revealing hemorrhage, infarction, space-occupying lesions, herniation, edema, and hydrocephalus. Magnetic resonance imaging (MRI) is a valuable follow-up when initial neuroimaging is inconclusive.[1, 3]
Laboratory Testing
Serum testing includes complete blood count, serum electrolytes (calcium, glucose), renal and hepatic function tests, coagulation panels, arterial blood gas analysis, and toxicology studies.[3] Electrocardiogram (ECG) should also be obtained. Additional tests may include carboxyhemoglobin levels (suspected carbon monoxide poisoning), blood cultures, and adrenal and thyroid function tests, depending on history and physical findings.
Lumbar Puncture
Consider lumbar puncture if the diagnosis remains uncertain or cerebral infection is suspected.[3] In suspected meningitis, do not delay empiric antibiotics and antivirals while awaiting lumbar puncture results. CT scan is essential before lumbar puncture to rule out supratentorial mass effect and herniation risk.[2] Cerebrospinal fluid analysis should include opening pressure, cell count, Gram stain, glucose, protein, culture, and viral testing.[8]
Electroencephalogram (EEG)
EEG is indicated for patients with suspected seizures or when the underlying cause of unconsciousness remains unidentified after other diagnostic tests.
Treatment and Management of Unconsciousness
Initial treatment for unconsciousness is often empiric, initiated before a definitive diagnosis is made.[1, 2]
Oxygenation: Intubation is generally necessary for unconscious patients with oxygen saturation below 90%, GCS score below 8, or weakened cough or gag reflex.
Circulation: Treat mean arterial blood pressure below 70 mm Hg with fluids or vasopressors. Treat mean arterial pressure above 130 mm Hg with intravenous labetalol (5 to 20 mg as needed).
Vital Signs: Obtain vital signs if not already done.
Glucose Administration: Administer 25 g dextrose if the cause of coma is unknown, while awaiting lab results.
Thiamine Administration: Administer 100 mg thiamine with or before glucose in malnourished patients.
Specific Antidotes: Consider naloxone and flumazenil for suspected drug overdose. Gastric lavage and activated charcoal are also options.
Intracranial Pressure Management: For clinically evident or CT-indicated herniation, administer intravenous mannitol (1 g/kg) and hyperventilate.
Seizure Control: Phenytoin or fosphenytoin are preferred for managing seizures in unconscious patients. Non-convulsive seizures may be treated with phenytoin or lorazepam.
Infection Treatment: Administer empiric antibiotics or antivirals for suspected bacterial meningitis or viral encephalitis.
Acid-Base and Electrolyte Balance: Correct acid-base and electrolyte imbalances.
Body Temperature Management: Maintain body temperature below 38.5 °C in ischemic patients using cooling blankets and antipyretics. Hypothermia is neuroprotective after cardiac arrest. Rewarming is generally unnecessary unless temperature falls below 33 °C.
Agitation Control: Tailor management strategies after diagnostic results are available. Persistently comatose patients often require intensive care unit admission.
Differential Diagnosis of Unconsciousness
The differential diagnosis for unconsciousness is broad due to numerous potential causes.[1] While some etiologies like anoxic brain injury, cerebrovascular accidents, seizures, and poisonings are more straightforward, others, such as metabolic causes, have wide differentials including hepatic encephalopathy, uremia, electrolyte abnormalities, and endocrine disorders. Infections, shock, temperature regulation disorders, respiratory failure, and trauma can also induce coma.[14]
Distinguishing between organic and psychogenic causes of unresponsiveness (catatonia, severe depression, conversion disorder, malingering) is crucial.[15, 16] Psychogenic unresponsiveness may present with actively closed eyelids, reactive pupils, nystagmus, variable motor tone, eupnea or hyperventilation, absent pathologic reflexes, and normal EEG.[2] Structural brain disorders can sometimes mimic psychiatric conditions. Psychogenic coma diagnosis should only be considered after thorough medical and neurological evaluation.[1]
Unconsciousness can arise from structural, systemic, and psychogenic causes.
Structural Causes: Stroke, TBIs, intracranial tumors, inflammation, venous thrombosis, acute hydrocephalus, locked-in syndrome, akinetic mutism, intracranial, epidural, and subdural hemorrhages.
Systemic Causes: Hypoglycemia, hyperglycemia, hyponatremia, hypernatremia, hypercalcemia, seizures, systemic infections, meningitis, encephalitis, adrenal crisis, pituitary apoplexy with pituitary hormonal insufficiency, endocrine abnormalities, myxedema coma, medication overdose, illicit drug use, neuroleptic malignant syndrome, excessive alcohol intake, hepatic encephalopathy, uremia, heavy metal poisoning, malaria, aspergillosis, herbicides, carbon monoxide poisoning, and anesthesia.
Psychogenic Causes: Catatonia, severe depression, conversion disorder, and malingering.
Prognosis of Unconsciousness
Prognosis in unconscious patients is highly variable and depends on etiology, brain injury severity, and patient characteristics. GCS is useful for prognosis, but artificial ventilation and sedatives can affect accuracy. GCS assessment upon admission, before interventions, is optimal.[17] FOUR score has comparable sensitivity and specificity but is more complex and less established than GCS.
TBIs are the most studied etiology of coma due to their prevalence and variable outcomes. Mortality in TBI-induced coma ranges from 40% to 50%.[18] Prognostic factors include age, motor assessments, neuro-ophthalmological signs, secondary injuries, and coma duration.[2]
Non-traumatic coma patients who do not recover quickly generally have a poorer prognosis than TBI patients. Mortality in non-traumatic coma ranges from 25% to 87%.[4, 19] Non-traumatic unconsciousness lasting over 6 hours has a 1-month mortality of 76%.[20] Outcomes vary significantly depending on the underlying cause. Non-traumatic unconsciousness due to depressant overdose, demyelinating disease, seizures, poisoning, or autoimmune encephalitis often has a favorable prognosis with supportive care. Vascular causes like significant stroke or aneurysmal hemorrhage, and hypoxic-ischemic injury, carry a grave prognosis. Neuro-ophthalmological signs and motor function are consistent predictors of long-term outcomes.[20]
Complications of Unconsciousness
Complications are influenced by the cause, circumstances, and duration of unconsciousness. They may include permanent brain damage, secondary brain injury from anoxia, coma, aspiration pneumonia, bladder or bowel dysfunction, skin ulcers, trauma from falls, secondary infections from indwelling catheters, malnutrition, death, fractured ribs from CPR, limb weakness, executive dysfunction, emotional and behavioral changes, pituitary hormonal imbalances, memory difficulties, and visual, speech, and language difficulties.
Deterrence and Patient Education for Unconsciousness
Unconsciousness is a state of lost awareness of self and environment, resembling sleep but without response to verbal or external stimuli, including pain. Causes include brain structure damage (stroke, hemorrhage, tumors, head injuries), seizures, low blood sugar, electrolyte imbalances, and drug overdoses.
Healthcare professionals thoroughly review medical history and medications. Assessment focuses on motor function, responsiveness to stimuli, and pupillary response. Brain imaging (CT or MRI) and blood tests (infection, low blood sugar, electrolyte imbalances) are common. ECG rules out myocardial infarction. EEG assesses brain electrical activity for suspected seizures. Lumbar puncture may be performed to assess for meningitis.
Treatment and duration of unconsciousness depend on the cause. Some patients may require mechanical ventilation, blood pressure regulation medications, and nutritional support (IV or gastric tube).
Enhancing Healthcare Team Outcomes in Unconsciousness Management
Effective management of unconsciousness, with its diverse causes, requires interprofessional collaboration for systematic evaluation and comprehensive treatment planning. The team obtains medical history, performs evaluations, provides stabilization, and conducts diagnostics concurrently. Professionals from emergency medicine, nursing, pharmacy, dietary, cardiology, neurology, endocrinology, palliative care, occupational and physical therapy, addiction medicine, orthopedics, and neurosurgery may be involved. Assisting with elimination, skin care, reorientation, and family guidance improves patient outcomes.[17] Clear communication is paramount given the team size.
While many cases are reversible, prognosis for persistent unconsciousness is variable and often unfavorable. Neuro-ophthalmological responses and motor function are reliable prognostic indicators.[17] Early communication with family is crucial, especially in unfavorable prognoses. Interprofessional discussions are vital for future treatment withdrawal and cardiopulmonary resuscitation considerations.[17] Understanding patient pre-existing conditions is key for these discussions and decisions aligning with patient preferences. Effective team communication is essential for a unified approach.
Prevention is key. Patient education on systemic illnesses and complication prevention allows for early intervention. For poorly controlled diabetes, monitoring and education are preventative. Patients at risk of overdose benefit from early intervention and counseling. Encourage patients to document healthcare preferences. Patient education, monitoring, and interprofessional communication enhance outcomes for unconscious patients.
Review Questions
(Link to review questions is in the original article and is kept as a link)
References
(References are kept as in the original article)
Disclosure: Zaith Bauer declares no relevant financial relationships with ineligible companies.
Disclosure: Orlando De Jesus declares no relevant financial relationships with ineligible companies.
Disclosure: Jessica Bunin declares no relevant financial relationships with ineligible companies.
This rewritten article aims to be more comprehensive and SEO-optimized for an English-speaking audience, focusing on the topic of unconsciousness. It maintains the original article’s information while enhancing its structure and readability.
