Altered Mental Status in the Emergency Department

Austin T. Smith, MD; Jin H. Han, MD, MSc

Disclosures

Semin Neurol. 2019;39(1):5-19. 

In This Article

General Approach to the Patient With Altered Mental Status

Initial Assessment and Management

As with any patient presenting to the ED, the first step is to determine the severity of the patient's illness. The more altered a patient is (particularly stuporous or comatose patients), the higher the suspicion should be for an acute life-threatening illness. The primary and initial assessment should focus on the patient's airway, breathing and circulation. That should quickly be followed by an assessment for hypoglycemia, opioid intoxication, stroke, sepsis, and seizure which can be recalled quickly by remembering "ABCs and 5S's" (Table 4). These conditions are time-sensitive and require immediate treatment.

A finger stick glucose should be obtained, as hypoglycemia is easily reversible but deadly. If the patient is hypoglycemic, one ampule (50 mL) of D50 should be administered through an intravenous or intraosseous line. Alternatively, 2 mg of intramuscular glucagon can be administered if intravenous/intraosseous access is unable to be obtained rapidly.

If Wernicke's encephalopathy is suspected, 500 mg of thiamine should be administered intravenously before glucose.[73] This is due to a theoretical worsening of encephalopathy in those who are thiamine deficient.[74]

Opioid Intoxication. If an opioid overdose is suspected based on miosis and/or bradypnea, naloxone should be considered. The initial dose is not well established, but in practice is typically 0.4 mg intravenously. To prevent acute withdrawal syndromes, naloxone should be diluted in a 10-mL normal saline flush and administered slowly. Doses can be escalated to 2 mg and up to 10 mg. It is important to note that the half-life of naloxone is shorter than most opioids and frequently requires redosing or even an infusion.

Reversing benzodiazepine overdoses with flumazenil is generally not recommended as it may precipitate withdrawal in chronic users which can be life-threatening.

When the patient's airway is deemed stable and immediate causes have been reversed, vital sign abnormalities should be addressed. Potential causes of vital sign abnormalities resulting in AMS are summarized in Table 5.

Acute Stroke Assessment. A neurologic exam, including language, strength, sensation, coordination, and cranial nerves such as extraocular movements, should be performed, as time-limited treatments make early diagnosis of stroke of utmost importance. This is particularly important in patients in whom the onset was abrupt and occurred within 24 hours of arrival. It is important to note that posterior circulation strokes, including basilar artery occlusion, can be very difficult to diagnose. Basilar artery occlusion can present as AMS with either unilateral or bilateral shaking, twitching, jerking, or posturing which can be mistaken for seizures.[75,76] A midbasilar occlusion with bilateral pontine ischemia can result in "locked-in syndrome" in which the patient can be fully conscious with complete paralysis except vertical eye movements.[77,78] The key to assessing for a possible basilar occlusion is to do a rapid assessment for eye movement and pupillary abnormalities, which is imperative. Parietal lobe strokes can present as AMS without focal neurologic findings, especially if the right parietal lobe is affected.[79] Aphasia can mimic AMS; so, it is important to see if patients can name objects, repeat, and follow commands. If a stroke is suspected, a noncontrast head computed tomography (CT) and CT angiography of the head and neck should be obtained along with prompt neurologic consultation.

Acute Sepsis Assessment. If the patient's presentation is concerning for sepsis, blood cultures should be obtained and broad-spectrum antibiotics initiated, as delays in antibiotics are associated with higher mortality.[80,81] A lactate level should be drawn and rapid administration of intravenous crystalloid fluid should be initiated. It is important to note that AMS is an independent predictor of mortality in sepsis, and is used as part of the quick Sequential Organ Failure Assessment (qSOFA) score for identifying high-risk patients for in-hospital mortality.[82,83]

Acute Assessment for Seizure. Seizure-like activity should also be addressed immediately. Treatment should target the underlying cause which may be structural, metabolic, or toxicologic. Structural causes can be from intracranial hemorrhage, metabolic causes from hypoglycemia or hyponatremia, and toxicologic causes from isoniazid use among other causes.

In patients presenting with generalized tonic–clonic seizures of unknown etiology, first-line treatment is a benzodiazepine. In practice, lorazepam is often the first-line agent and should be administered at a dose of 0.1 mg/kg intravenously.[84] If intravenous or intraosseous access is not present, an alternative is intramuscular midazolam which should be given at a dose of 5 mg if body weight is 13 to 40 kg and 10 mg if body weight is greater than 40 kg.[85,86]

If the cause of seizures is hyponatremia, the sodium should be acutely raised.[55] This is typically done using hypertonic saline (3% NaCl). Care should be given to only raise the serum sodium at 4 to 6 mEq/L within 4 to 6 hours. Though no evidence-based guidelines exist, an infusion of 100 mL over 10 minutes with no more than 300 mL total volume is frequently used to acutely raise the serum sodium. Most experts recommend not exceeding 6 to 8 mEq/L in any 24-hour period regardless of the acuity of the hyponatremia.[55,87] Increasing the serum sodium concentrations more rapidly can result in osmotic demyelination syndrome.

If the cause is isoniazid toxicity, patients should be treated with high-dose pyridoxine. In general, the dose is 1 g intravenously for every gram ingested; if the dose is unknown, 5 g should be administered intravenously.[88–90]

Management of Combative Patients

Very agitated or combative patients (RASS +3 or +4) may pose a significant danger to themselves and to the health care providers caring for them. Additionally, this can impede the diagnostic workup and delay potentially lifesaving care. While pharmacologic sedation is the mainstay treatment to rapidly calm the patient, the first step should be verbal deescalation. The provider should also attempt to meet patients' physical needs such as providing them with food or environmental changes if appropriate. Other initial steps should include dimming or turning off the lights, minimizing auditory stimulation from monitors or infusion pump alarms, minimizing the number of providers who interact with the patient, and having family members at the patient's bedside.[91,92]

If verbal and environmental attempts to calm the patient are unsuccessful, physical restraints and pharmacologic sedation may be required. If physical restraints are used, they should be done so for the shortest amount of time possible. Patients should not be placed in the prone position, as this has been associated with increased mortality in both adult and pediatric populations.[93,94]

Pharmacologic sedation should focus on treating the cause of agitation, which is thought to be neurochemical imbalance resulting in excess dopamine and autonomic hyperactivity.[95] Commonly used agents include neuroleptics and/or benzodiazepines, and are summarized in Table 6. First-generation antipsychotics such as haloperidol are frequently administered with an anticholinergic agent such as diphenhydramine which reduces dystonic effects and can also provide additional sedation depending on the agent.[96]

With regard to benzodiazepines, midazolam is the most commonly used and best studied for the management of acute agitation. When given intramuscularly (5–10 mg) or intravenously (2–5 mg), it has fast and predictable onset as well as a short duration of action.[97,98] Caution must be undertaken with serial dosing as respiratory depression has been reported in 13% if cases, especially in those who are intoxicated with ethanol or opioid medications.[98] Fortunately, this serious side effect is usually transient.[98–100] Benzodiazepines should be used sparingly, as it may exacerbate delirium, especially in older adults.[101,102] Consequently, the risks of benzodiazepine use must be carefully balanced with the benefits in this particular patient group.

Intramuscular ketamine is another agent used frequently for agitation.[103] It has been found to have a similar safety profile when compared with antipsychotics and benzodiazepines.[104–107] Ketamine is an N-methyl-D-aspartate (NMDA) antagonist, but also antagonizes neuronal hyperpolarization-activated cationic currents, nicotinic acetyl-choline ion channels, and is a delta- and mu-opioid agonist.[108–110] The intramuscular dose (4–5 mg/kg) is much higher than the intravenous doses used for sedations (1–2 mg/kg), which usually requires a higher concentration that is often not stocked in hospitals due to concern for potential medication dosing errors.

Pain can also precipitate agitation and delirium, especially in older adults. If pain is the suspected cause, scheduled nonopioid analgesics, particularly acetaminophen and ibuprofen, should be administered, as these can reduce opioid consumption by 30 to 50%.[111] Adding gabapentin and/or opioids may be necessary for breakthrough pain. Severely injured trauma patients may require regional anesthesia by use of nerve blocks.

If ethanol or benzodiazepine withdrawal is suspected, benzodiazepines and α-2 agonists such as clonidine can be administered.

Further Management

When the patient's vital signs and potential time-sensitive illnesses (hypoglycemia, stroke, sepsis, seizure, opioid overdose, etc.) have been addressed, further history should be obtained along with a complete physical exam and then further diagnostic evaluation based on the differential diagnosis.

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