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Coma is a life-threatening process that requires immediate stabilization and a structured approach to diagnosis and management.
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The differential diagnosis for coma is long, but is often divided into structural vs. diffuse neuronal dysfunction; the latter is subdivided into toxic vs. metabolic.
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When available, historical information may be of great use in determining the etiology of coma; in all cases, a focused physical examination can help greatly refine the differential diagnosis.
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The definitive
Initial Diagnosis and Management of Coma
Section snippets
Key points
Pathophysiology
A neuronal network in the dorsal pons and midbrain give rise to the ascending reticular activing system (ARAS), which is responsible for arousal.1 Neurons from these centers run together through the thalamus and then to the bilateral cerebral cortex; the cortex controls sensory processing and understanding, which generates awareness.2, 3 Coma results from an impairment of this axis by a process that affects the brain’s arousal center, consciousness center, the tracts that connect them, or some
Causes
A causal overview of coma is presented in Table 1, categorized based on this logic, and includes coma mimics, which are several disorders that may be easily mistaken for coma but do not involve interruption of the ARAS-thalamic-cortical pathway. For the purposes of this article, the focus is on relatively common entities that may present with coma, rather than those that are uncommon or in which coma is a late finding.
Tumors
Tumors may cause coma by exerting pressure on either a key area (eg, the brainstem) or by causing a diffuse increase in intracranial pressure. More commonly, however, patients with tumors have a slow progression of neurologic findings. Abrupt onset of coma in such patients often results from hemorrhage into an expanding mass. Even small tumors, however, may cause obstructive hydrocephalus or focal infarctions, each of which may in turn lead to the relatively abrupt onset of coma.
Acute Hydrocephalus
There is
Respiratory Insufficiency
Respiratory insufficiency may produce coma in two ways. First, the brain is particularly sensitive to the effects of hypoxia, with coma possible within minutes of acute oxygen deprivation. Second, hypercarbia may cause coma; the exact mechanism is unclear, but may involve an alteration in neurotransmitter levels or changes in intracranial pressure as increases in carbon dioxide levels are associated with increases in cerebral blood flow.
Dysthermia
Extremes of body temperature may accompany other primary
Sedative-Hypnotic Agents
Sedative-hypnotic agents are a broad class of drugs that include ethanol, benzodiazepines, barbiturates, baclofen, gamma-hydroxybutyrate, and others. Most sedative-hypnotic agents act by facilitating the effect of the neurotransmitter gamma-aminobutyric acid (GABA), hyperpolarizing neurons either through an increase in chloride conductance (GABAA)39 or through an increase in potassium conductance (GABAB).40 Ethanol, in addition to interacting with the GABA system,41 also produces some effects
Initial stabilization
The initial stabilization of comatose patients is the same as that for that of all emergency department patients and consists of securing the patients airway (with attention to the cervical spine), breathing, and circulation.
Decisions regarding airway management are often very difficult, driven by gestalt rather than algorithmic decision making, and are based on several factors. Mechanism of coma is important; although a GCS of 8 or less in a trauma patient is often viewed as an indication for
History
Comatose patients by definition cannot give details of their illness, so it is crucial that the provider actively seek alternative sources of information. Emergency medical service responders often provide the most valuable information. They can relay information obtained from family members or bystanders, describe the patient’s initial level of consciousness and how that has changed en route, provide a description of how the patient was found, and contribute important situational information
Physical examination
A complete physical examination will provide clues to the diagnosis of coma and help streamline the patient’s diagnostic evaluation. Crucial physical examination findings, and the important causes of coma associated with them, are listed below.
Pulse
Bradycardia may occur in the context of sympatholytic drugs, such as clonidine; in the setting of sedative hypnotic toxicity, particularly with barbiturates and gamma-hydroxybutyrate; and with increases in intracranial pressure, characteristically accompanied by systemic hypertension. Tachycardia is common with psychotropic drug poisoning, ketamine intoxication, adrenergic hyperactivity from intracranial hemorrhage, and 3,4-methylenedioxymethamphetamine (MDMA) intoxication, which produces coma
Imaging and laboratory testing
Although a thorough history and physical examination will often generate a refined differential diagnosis, imaging studies and laboratory testing play an important role in the diagnosis of coma. Such interventions, however, should serve to refine clinical impressions and should not be ordered indiscriminately as a substitute for thoughtful patient evaluation.
When coma is obviously caused by diffuse neuronal dysfunction, such as hypoglycemia or a known ingestion, CT is rarely if ever necessary.
Grading systems
Grading systems allow providers to quickly convey a general sense of the patient’s condition. This is particularly important when one provider cannot examine the patient, as may occurs in telephone discussions between providers or during emergency medical service communications.
Two major grading systems are used to assess the depths of coma (Table 3). The GCS, first described in 1974,76 is a 15-point composite score of eye, motor, and verbal responses developed to assess patients with head
Treatment
The ultimate treatment of coma depends on the cause. In general, there are three overarching themes regarding the treatment of coma.
First, coma from structural causes may be catastrophic and untreatable. However, when the cause is treatable, it can be treated surgically or with geographically targeted pharmacologic or mechanical intervention. The authors advocate for the early involvement of neurosurgical specialists for patients with coma from intracranial hemorrhage or hydrocephalus because
Summary
Coma represents a true medical emergency. Although drug intoxications are a leading cause of coma in patients who present to the emergency department, other metabolic disturbances and traumatic brain injury are common causes as well. The general emergency department approach to the patient with coma begins with stabilization of airway, breathing, and circulation, followed by a thorough physical examination to generate a limited differential diagnosis that is then refined by focused testing.
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