Disorders of Consciousness
Minimally conscious state
Persistent vegetative state
1. Description of the problem
What every clinician should know
Coma is a condition in which a patient cannot be aroused to consciousness. Coma describes a clinical state that can be due to a variety of etiologies. Comatose patients have a depressed level of consciousness, lacking both arousal and awareness, to the extent that they cannot be aroused to an interactive state.
Neuroanatomically, coma may be a result of damage to the reticular activating system in the brainstem and/or diencephalon, or both cerebral hemispheres (bihemispheric dysfunction). Different terms are applied to persistent/chronic disorders of consciousness such as minimally conscious states (MCS) or persistent vegetative states (PVS). These terms/diagnoses are not used in the acute/subacute care of a comatose patient.
Over time, patients with persistent disorders of consciousness may remain stable or evolve. MCS and PVS are two common entities of persistently perturbed consciousness. These diagnoses are not made in the acute care setting. The goal of caring for the newly comatose patient is rapid assessment and treatment to restore full consciousness and neurologic function. The approach to this task is detailed below. Persistent disorders of consciousness are a different scenario altogether; however, it is useful to discuss them here for the sake of clarity.
MCS is a condition in which a patient has a depressed level of consciousness, with some level of awareness. On the other hand, patients with PVS show limited ability to arouse, with partial preservation of sleep-waking cycle, but lack of awareness. These patients may have roving eye movements, but do not fixate on an object. MCS and PVS are commonly the result of anoxic or traumatic brain injury.
Finally, the syndrome of ‘irreversible coma’ is also known as brain death. Brain death is a state of permanent cessation of brain activity characterized by loss of both cerebral hemisphere and brainstem function. This includes (1) absent cerebral hemispheric function manifested by coma; (2) absent brainstem function manifested by absent brain stem reflexes on neurologic exam; and (3) absent spontaneous respiratory activity manifest by the “apnea test.” Other confirmatory tests can be used and are detailed in the chapter on brain death. This diagnosis should be made only by an appropriately trained physician.
Key management points
Initial assessment of the comatose patient focuses on basic life support: airway, breathing and circulation. Once adequate oxygenation, ventilation and hemodynamic function are confirmed, a neurologic examination is conducted. The patient’s level of arousability is assessed. If the patient cannot be aroused to the point of following simple commands, he/she is considered comatose.
If the patient can be aroused to follow commands, various terms may be used, such as lethargic or obtunded (these terms are not strictly defined or used consistently within the medical field). Various coma scales/scores can be used as part of this neurologic assessment. The most common is the Glasgow Coma Scale, which ranges from 3 to 15. More recently, the FOUR (Full Outline of UnResponsiveness) Score was introduced by Widjicks et al.
Be sure to consider the potential for cervical spine instability in these patients and manage appropriately with cervical immobilization and imaging as dictated by the clinical scenario. In general, patient unarousal to the point of following commands (i.e. comatose; GCS below 9) requires airway protection with an endotracheal tube. This is a useful rule of thumb but is not universal.
Once level of consciousness has been assessed, pupillary size and reactivity are assessed, followed by corneal (usually with a drop of sterile saline into the eye), gag and cough reflexes. Motor response to pain is elicited, usually with a pinch to a skin fold or nail bed. Various reflexive responses (such as decorticate and decerebrate posturing) are assessed. The patient’s history, if available, will guide subsequent studies (motor vehicle accident, cardiac arrest, blast injury, methadone overdose, etc.).
Administration of thiamine and dextrose should be considered. The thiamine is used to avoid precipitating neurologic injury (Wernicke-Korsakoff syndrome) with dextrose in someone who has thiamine deficiency. Keep in mind that there is no high-level evidence to support this, although it remains common practice. Empiric opioid or benzodiazepine reversal is considered in the appropriate clinical context.
Similarly, antidotes for nerve agent intoxication or other toxic exposures (such as methanol) need to be considered, depending on the clinical context. Contact a poison control center for assistance if needed. Finally, comatose survivors of cardiac arrest should be treated with therapeutic hypothermia initiated as soon as possible.
CT scan (noncontrast) is emergently performed. A CT angiogram can be added to this study in the patient thought to have a potential vascular etiology for the comatose state, such as basilar artery thrombosis. Alternately, emergent MRI may be performed but is not available in the same time frame as a stat head CT in most medical centers.
Emergent laboratory studies include serum levels of glucose, sodium, calcium, BUN, creatinine and osmolality; arterial or venous blood gases to evaluate pH, po2 and pco2; as well as blood and urine toxicology testing. Co-oximetry analysis should be included in the emergency room assessment to investigate carbon monoxide poisoning. Blood and CSF should be cultured if infection is suspected.
If the history, physical exam, initial head CT and laboratory studies do not reveal the etiology of coma further studies are pursued.
Magnetic resonance imaging provides higher-resolution anatomic imaging. Neurology consultation is usually obtained by this point in the work-up. Electroencephalography (EEG) may distinguish coma from locked-in syndrome or psychic unresponsiveness and can detect subclinical status epilepticus (non-convulsive seizures). Other studies may be used at this point but are beyond the scope of this chapter.
2. Emergency Management
Coma is a medical emergency. Rapid clinical, radiologic and laboratory assessment must proceed immediately to rule out acutely life-threatening correctable conditions or injuries.
The degree of coma can be assessed by the Glasgow Coma Scale. It correlates with prognosis in patients with a traumatic etiology of coma.
To sound/voice 3
To pain 2
Inappropriate words 3
Incomprehensible sounds 2
Obeys commands 6
Localizes to pain 5
Withdraws to pain 4
Abnormal flexion (decorticate) 3
Abnormal extension (decerebrate) 2
There are numerous potential etiologies for coma that go far beyond this discussion. The intensivist should consider general categories of pathologic states that can lead to coma. This obviously occurs once the patient is confirmed to have adequate oxygenation, ventilation, and hemodynamic function (i.e., the patient is not pulseless!). Categories in the differential diagnosis of coma include:
Pharmacologic (such as anesthesia or opioid induced).
Toxic (such as alcohol, methanol, etc.).
Metabolic (hyponatremia, hyperammonemia, hypoglycemia).
Traumatic (head trauma).
Vascular (stroke, subarachnoid hemorrhage).
Hydrocephalus (usually acute rather than chronic).
Infectious/inflammatory (meningitis or encephalitis).
Neoplastic (carcinomatous meningitis, brain tumor causing mass effect).
Seizure (post-ictal state or ongoing non-convulsive seizures).
Pseudo-coma (residual neuromuscular blockade, psychogenic coma, locked-in syndrome). The locked-in syndrome is another condition that resembles coma. It usually results from ventral pontine damage with sparing of the reticular activating system and cerebral hemispheres. In this condition patients are quadraparetic but are conscious and typically retain the ability of upgaze and/or downgaze. The syndrome is assessed at the bedside by asking the patient to move his/her eyes to command.
Neurodegenerative (such as advanced Alzheimer’s dementia).
Coma is very common, as can be ascertained from the various etiologic entities.
Special considerations for nursing and allied health professionals.
What's the evidence?
Hakimi, R, McDonagh, DL. “Unconsciousness in the intensive care unit: a practical approach”. Int Anesthesiol Clin. vol. 46. 2008. pp. 342-58.
Teasdale, G, Jennett, B, Murray, L, Murray, G. “Glasgow Coma Scale: to sum or not to sum”. Lancet. vol. 2. 1983. pp. 678
Wijdicks, EFM, Bamlet, WR, Maramattom, BV. “Validation of a new coma scale: the FOUR Score”. Ann Neurol. vol. 58. 2005. pp. 585-93.
Virgile, RS. “Locked-in syndrome: case and literature review”. Clinical Neurol Neurosurg. vol. 86. 1984. pp. 275-9.
Wijdicks, EF. “The diagnosis of brain death”. N Eng J Med. vol. 344. 2001. pp. 1215-21.
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