Continuing Education Activity
Unconsciousness is generally caused by a temporary or permanent impairment of either the reticular activating system in the brainstem, both cerebral hemispheres, or bilateral thalami. The causes for an unconscious patient can be differentiated into structural pathology local to the brain or systemic pathology. This activity describes the risk factors, evaluation, and management of unconscious patients and highlights the role of the interprofessional team in enhancing care delivery for affected patients.
- Describe the types and frequency of tests that should be done routinely in unconscious patients.
- Outline how to evaluate the unconscious patient.
- Review management considerations for unconscious patients.
- Summarize the importance of improving care coordination, with particular emphasis on communication between interprofessional medical teams, to enhance prompt and thorough delivery of care to unconscious patients.
Consciousness is the awareness of oneself and the environment and the ability to respond to external stimuli. Impaired consciousness can be defined as reduced alertness, the ability to be aroused, or awareness of oneself and the environment. A patient who is initially observed to be unconscious can ultimately manifest a variety of clinical states. Some patients will regain full consciousness without intervention, while others will require intensive management and intricate diagnostic testing. Etiologies of persistent unconsciousness can be reversible or permanent. During unconsciousness, the patient losses all protective reflexes and sensation responses and is prone to aspiration and skin ulcers.
Coma is a profound and occasionally persistent state of unconsciousness. Plum and Posner define a coma as "a state of unresponsiveness in which the patient lies with eyes closed and cannot be aroused to respond appropriately to stimuli even with vigorous stimulation." Coma has also been defined objectively as a Glasgow coma scale (GCS) less than 8.
Unconsciousness is generally caused by a temporary or permanent impairment of either the reticular activating system in the brainstem, both cerebral hemispheres, or bilateral thalamus. The three main mechanisms are structural brain lesions, diffuse neuronal dysfunction secondary to a systemic pathology, and rarely psychiatric causes.
These causes either destroy an area or exert indirect damage by way of compression or increased intracranial pressure. Increased intracranial pressure impairs global cerebral blood flow and can promote tissue distortion and brain herniation.
- Traumatic brain injury (TBI)
- Intracranial, epidural, subdural hemorrhages
- Intracranial tumors
- Venous thrombosis
- Acute hydrocephalus
- Systemic infections (sepsis)
- 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
- Heavy metals (lead poisoning)
- Fungemia (aspergillosis)
- Gases (carbon monoxide)
- Severe depression
- Conversion disorder
The prevalence and relative etiologies for unconsciousness vary by institution and patient population. A high-volume trauma center will likely see a significant amount of unconscious patients related to traumatic brain injury. Overall, the most prevalent etiology of non-traumatic coma was ischemic or hemorrhage stroke (6 to 54%), followed by anoxia injury (3 to 42%), poisoning (1 to 39%), and metabolic (1 to 29%). Despite stroke being the overall most common cause of non-traumatic coma, the total non-structural causes (37 to 75%) tended to slightly outnumber the structural causes (28 to 64%).
Overall mortality is 25-87%. Stroke and anoxic coma had the highest mortality at 60 to 95% and 54 to 89% respectively. The lowest mortality was found in epilepsy and poisoning, which both had rates less than 10%.
The pathophysiology of unconsciousness involves neuronal dysfunction from a decrease in the supply of glucose or oxygen to the brain. Structural lesions of the central nervous system may lead to coma from direct destruction of arousal areas of the brain or from secondary damage from shifting of intracranial structures, vascular compression, or increased intracranial pressure.
The anatomical seat of arousal is the ascending reticular activating system in the brainstem. Neurons of this system originate in the dorsal pons and midbrain, connect in the thalamus, and project to several areas in the cortex. The cortex processes, integrates, and gives context to the information provided to it, thus generating awareness. The reticular activating system receives impulses by the spinal cord and cortex to be aware of the environment.
The many causes for an unconscious patient can be classified as affecting three main areas of the brain:
Bilateral Hemispheric Damage/Effect
Extensive damage to the bilateral cerebral cortex, as can occur with hypoxic-ischemic injury or brain trauma, causes neuronal death and de-innervation of cortical regions. Such patients lose the ability to process and consciously respond to stimuli. The systemic causes of coma can also be placed in this category, as they produce an abnormal physiologic environment that inhibits neuronal function. This type of pattern is generally reversible if the systemic abnormality can be corrected.
Diencephalic (Thalamic) Injury
The thalamus contains relay nuclei that direct afferent input to the cortex; therefore, bilateral thalamic lesions can mimic the result of a bilateral cortical injury.
Upper Brainstem Injury
The dorsal pons and midbrain contain the reticular activating system. Lesions in this area can inhibit consciousness and result in a comatose state.
History and Physical
History regarding an unconscious patient is based on supplementary data. Questioning a person who has good knowledge of the recent history of the patient is preferable. Knowing the patient’s medical history can provide important clues to the diagnosis. A history of chronic cardiopulmonary, hepatic, or renal disease may be contributing. The use of or access to sedative or psychoactive drugs may suggest intoxication.
Abrupt onset of altered mental status points towards drug poisoning or acute structural lesions such as trauma or stroke. Most metabolic disorders and compressive structural injuries have a relatively gradual onset.
Neurological abnormalities or a headache in an unconscious patient point toward a structural lesion. Cranial nerve abnormalities can suggest brainstem involvement. Metabolic disturbances usually cause diffuse forebrain dysfunction manifesting as confusion, delirium, or encephalopathy before unconsciousness or coma.
The initial step in the evaluation of an unconscious patient is to evaluate for the basic signs of life. The American Heart Association recommends examining for a pulse, followed by assessing airway patency and breathing pattern. If the patient does not have a pulse or does not have a regular breathing pattern, basic life support/advanced cardiovascular life support is indicated.
For patients with a pulse, who are breathing adequately, the evaluation shifts to a detailed neurological examination. The neurologic examination would serve to determine the location and nature of the neurological lesion and to determine prognosis. The examination is considered most useful if the patient is well perfused, normothermic, normoglycemic, and without the effects of neurologically active toxins or medications.
The initial step is to evaluate for reactivity using objective measures. Address the patient verbally, progress to light shaking, then progress to more intense mechanical stimulation. Sufficient stimulus to the supraorbital ridge, nail beds, or temporomandibular joint can be painful without risk of tissue injury. Response to these painful stimuli should be graded bilaterally in case of a focal spinal cord lesion. If these measures do not produce a response, vigorously pressing the examiner's knuckles up and down the sternum should arouse any patient who is not deeply comatose.
The best practice for reporting level of responsiveness is to document specifically how the patient reacted to the external stimulus provided for testing. Coma scales such as the Glasgow Coma Scale (GCS) and the Full Outline of Unresponsiveness (FOUR) exist to aid in objectifying results for provider communication, trending, and prognosis. The physical exam should be repeated at least daily, in a sequential fashion, and documented systematically.
Initial eye position and movements should be noted. Nystagmus is uncommonly seen in unconscious patients but may indicate an irritating brain lesion or even occult seizure activity. The size of the pupils (using a pupilometer) and reaction to light should be documented. A strong light should be used, as pupillary responses may be sluggish in unconscious patients.
If available, a funduscopic exam may reveal essential findings such as papilledema or subhyaloid hemorrhage.
Examination of eye movement with oculocephalic or oculovestibular testing can provide information regarding cranial nerves III, IV, VI, and VIII. In general terms, patients with intact brainstem functioning should have a normal response to these maneuvers. Oculovestibular testing via caloric stimulation should be performed in patients who do not have a cleared cervical spine.
The corneal reflex can be established by stimulating the cornea and observing for blinking. Stimulation should elicit both a direct and consensual response and suggests the normal function of CN V and VII nuclei in the brainstem. It is recommended to stimulate the cornea with drops of normal saline to prevent corneal damage. Contact lenses will markedly reduce this reflex.
The gag and cough reflexes suggest normal function of cranial nerves IX and X nuclei in the brainstem.
Motor function is tested by examining muscular tone, movement patterns, and peripheral tendon reflexes. Decerebrate or decorticate postures carry a bad prognosis.
Neuroimaging is extremely valuable in evaluating the unconscious patient as an intracranial insult is important to define as soon as possible. Computed tomographic (CT) scan of the brain is commonly the first study performed and can reveal several key findings, including hemorrhage, infarction, space-occupying lesion, herniation, edema, and hydrocephalus. Magnetic resonance imaging is a worthwhile study in cases that are still unclear after initial neuroimaging.
Serum testing usually includes complete blood counts, serum electrolytes including calcium and glucose, renal/hepatic functions, coagulation panel, and toxicology studies.
Lumbar puncture should be considered if the diagnosis remains unclear after the above testing or if a cerebral infection is suspected. If meningitis is suspected, empiric antibiotics and antivirals should not be delayed by the lumbar puncture procedure. The risk of herniation in patients with supratentorial mass effect is controversial, but a CT should generally still be performed before the lumbar puncture. Cerebrospinal fluid analysis should include opening pressure, cell count, gram stain, glucose, protein, culture, and viral testing.
Glasgow Coma Scale
- 4 = eyes open spontaneously
- 3 = eye-opening to verbal command
- 2 = eye-opening to pain
- 1 = no eye-opening
- 6 = obey commands
- 5 = localizing pain
- 4 = withdrawal from pain
- 3 = flexion response to pain
- 2 = extension response to pain
- 1 = no motor response
- 5 = oriented
- 4 = confused
- 3 = inappropriate words
- 2 = incomprehensible sounds
- 1 = no verbal response
- 4 = eyelids open or opened, tracking, or blinking to command
- 3 = eyelids open but not tracking
- 2 = eyelids closed but open to a loud voice
- 1 = eyelids closed but open to pain
- 0 = eyelids remain closed with pain
- 4 = thumbs-up, fist, or peace sign
- 3 = localizing to pain
- 2 = flexion response to pain
- 1 = extension response to pain
- 0 = no response to pain or generalized myoclonic status
- 4 = pupil and corneal reflexes present
- 3 = one pupil wide and fixed
- 2 = pupil or corneal reflexes absent
- 1 = pupil and corneal reflexes absent
- 0 = absent pupil, corneal, and cough reflex
- 4 = not intubated, regular breathing pattern
- 3 = not intubated, Cheyne-Stokes breathing pattern
- 2 = not intubated, irregular breathing
- 1 = breaths above the ventilator rate
- 0 = breaths at ventilator rate or below
Treatment / Management
Because the etiology of unconsciousness is often initially unclear, initial treatment paradigms occur before full evaluation or diagnostics. Principles of initial management of unconscious patients:
- Ensure oxygenation
- Maintain circulation
- Control glucose
- Lower intracranial pressure
- Stop seizures
- Treat infection
- Restore acid-base balance and electrolyte balance
- Adjust body temperature
- Administer thiamine
- Consider specific antidotes (naloxone, flumazenil)
- Control agitation
If the above goals are completed, management can then be tailored based on the results of diagnostic testing. Patients who are persistently comatose despite initial interventions often require a high level of care, such as an intensive care unit.
The differential diagnosis for the causes of unconsciousness is broad.
Some etiologies are straightforward, such as anoxic brain injury, cerebrovascular accidents, seizures, and poisonings, but some categories have a wide differential in and of themselves. For example, metabolic causes of coma may include hepatic encephalopathy, uremia, electrolyte abnormalities, and endocrine disorders. Infections, shock, disorders of temperature regulation, respiratory failure, and trauma can also cause a coma.
When examining an unconscious patient, it is crucial to differentiate organic causes of coma from disorders that cause psychiatric unresponsiveness, such as catatonia, severe depression, conversion disorder, and malingering. Psychogenic unresponsiveness is more likely to include active lid closing, reactive pupils, nystagmus, variable motor tone, eupnea or hyperventilation, the absence of pathologic reflexes, and a normal EEG. Structural brain disorders can also mimic psychiatric illness. Psychogenic coma should be diagnosed only after a thorough medical and neurological assessment.
The prognosis of unconscious patients is variable and highly dependent on the etiology, the severity of brain injury, and individual patient factors. The GCS is used to evaluate outcomes for research purposes.
TBI has been the most studied etiology of coma, likely due to its high prevalence and highly variable outcomes. Estimated mortality in patients in a coma from TBI ranges from 40 to 50%. Predictors linked to outcomes include patient age, motor findings, neuro-ophthalmologic signs, secondary injuries, neuroimaging findings, and duration of coma.
Patients with non-traumatic etiologies that do not recover quickly have an even worse prognosis than the TBI cohort. The mortality rate of non-traumatic coma varied from 25 to 87%. Patients who have a non-traumatic loss of consciousness lasting more than six hours had a one-month mortality rate of 76%. Non-traumatic coma outcomes are quite variable by etiology. Non-traumatic unconsciousness due to depressant overdose, demyelinating disease, seizures, poisoning, or auto-immune encephalitis carries an excellent prognosis with adequate supportive care. Vascular causes such as a large stroke or aneurysmal hemorrhage carry a grave prognosis, as does hypoxic-ischemic injury. Neuro-ophthalmologic signs and motor function are consistent predictors of long-term outcomes.
- Permanent initial brain damage
- Secondary brain injury from anoxia
- Aspiration pneumonia
- Bladder bowel dysfunction
- Skin ulcers
Deterrence and Patient Education
Prevention is preferable to late interventions. Patients need to be educated about their systemic illnesses and how to prevent complications. Some conditions leading to unconsciousness may allow interventions prior to the development of a coma. Closer monitoring and education of patients with poorly controlled diabetes might be an opportunity for prevention. For those patients at risk for drug overdoses or illicit drug use intoxication, early intervention and counseling will prevent many complications. Patients can be educated to establish wishes regarding life decisions in the case that they become unconscious.
Enhancing Healthcare Team Outcomes
Unconsciousness is caused by a temporary or permanent impairment of the bilateral forebrain (thalamus/cerebrum) or reticular activating system of the brainstem. Because of the diverse causes for an unconscious patient, the condition is best managed by an interprofessional team that consists of a neurologist, internist, intensivist, primary care provider, and neurosurgeon. A systematic evaluation of the unconscious patient is recommended. Because many cases of unconsciousness are reversible, the management of unconscious patients necessitates thorough history-taking, patient evaluation, stabilizing treatment, and diagnostic testing occurring simultaneously. The prognosis of persistently unconscious patients is variable but generally poor. The most consistent prognostic exam findings are neuro-ophthalmologic responses and motor function. [Level 5]
The nurse helps the patient with the absent protective reflexes, elimination, skincare, reorientation to the surroundings, and orientation for the family (problem-oriented approach) to improves outcomes. Early communication with the next of kin, family, or appropriate advocate is always necessary. When the prognosis is poor, these interprofessional discussions will include consideration of future withdrawal of treatment and cardiopulmonary resuscitation. It is essential to have an idea of the patient’s state of health before their presentation. Understanding that prognosis in many comatose patients is poor, a pre-morbid condition will inform decisions regarding the escalation of care and appropriateness of cardiopulmonary resuscitation. Decisions have to be consistent with the patient’s established wishes.