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Coma is a state of depressed consciousness in which a patient is not aware, is not awake, and does not respond to vigorous stimulation. Consciousness consists of arousal (subcortical) and awareness (cortical).
Damage to the dorsal brainstem, thalamus, axonal projections to the cortex, or extensive injury to bilateral cortices may result in depressed consciousness or coma.
Toxicologic, metabolic, infectious, and other disorders causing diffuse brain injury cause 65% of coma cases; of these, toxins are the most common. Structural brain diseases account for most of the remaining cases.
A patient with depressed consciousness is unlikely to provide a reliable history. Historical information should be elicited from other available sources, such as emergency medical services personnel, family members, the patient’s belongings, or medical records.
An abrupt onset of coma suggests a stroke, seizure, or cardiac event.
The neurologic examination should include an evaluation of level of consciousness, cranial nerves, brainstem reflexes, and motor responses.
Pinpoint pupils may represent a pontine infarct or intoxication from opioids, clonidine, or cholinergic substances.
Nonconvulsive status epilepticus should be suspected in cases of coma of undetermined cause and is diagnosed by electroencephalography.
Hypoglycemia and hypoxia are two easily identified and reversible causes of coma.
An empiric trial of naloxone will lead to rapid reversal of opioid toxicity and other select medication overdoses.
Targeted temperature management is recommended in comatose adult patients with return of spontaneous circulation after cardiac arrest from either a shockable or nonshockable rhythm, with a goal temperature range of 32°C to 36°C. In children who are comatose post arrest, it is reasonable to target a temperature range of 36°C to 37.5°C. Hyperthermia should be strictly avoided for all comatose postarrest patients.
Most patients with coma will require intensive care monitoring. If the cause of coma is not treatable in the initial facility and the patient needs a higher level of specialty care (e.g., structural lesion requiring neurosurgery), then a coordinated transfer should be facilitated.
Coma is a state of depressed consciousness in which a patient is not aware, is not awake, and does not respond to vigorous stimulation. This stands in contrast to stuporous or lethargic patients, who also may have a decreased level of awareness or consciousness but can be aroused with external stimuli.
Most cases of depressed consciousness or coma are the result of a metabolic derangement, usually a glucose disorder, drug overdose, or adverse drug effect, but other common causes include traumatic brain injury, systemic or central nervous system (CNS) infection, ischemic or hemorrhagic stroke, intracranial mass, and, less commonly, a psychiatric illness. Patients with depressed consciousness represent true emergencies because the potential causes are often life-threatening and must be rapidly diagnosed and reversed whenever possible. A review of relevant neuroanatomy and pathophysiology facilitates our understanding of how consciousness is affected in the setting of disease ( Fig. 12.1 ).
To maintain normal consciousness, the brain requires a constant flow of sensory input and the ability to process this information. Visual, auditory, olfactory, gustatory, visceral, and somatosensory inputs are all synthesized and interpreted by the brain simultaneously. Disruption in this flow of information or inability to process it may lead to depressed consciousness.
Consciousness consists of two domains: arousal and awareness. Arousal ranges from fully awake, to arousable with verbal or tactile stimulation, to unarousable. Anatomically, arousal is maintained by the subcortical structures, including the brainstem nuclei, thalamus, basal forebrain, hypothalamus and, most notably, the ascending reticular activating system (ARAS). ARAS neurons are located predominately in the pons and midbrain, connect to the thalamus, and project to the cortex. Awareness consists of the content of consciousness, ranging from self-aware and coherent to confused, inattentive, or perhaps delusional. Awareness is generated by the bilateral cerebral cortices, which control the processing and understanding of sensory input. A patient’s level of arousal may be low enough that the domain of awareness is difficult to assess.
Consequently, damage to the dorsal brainstem, thalamus, axonal projections to the cortex, or extensive injury to bilateral cortices may result in depressed consciousness or coma. The clinical presentation may vary considerably depending on the location of the insult.
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