CONFUSION Texto

5
Altered Mental Status in the Emergency Department

Austin T. Smith, MD1 Jin H. Han, MD, MSc1
1 Department of Emergency Medicine, Vanderbilt University School of Address for correspondence Jin H. Han, MD, MSc, Department of
Medicine, Nashville, Tennessee Emergency Medicine, Vanderbilt University Medical Center, 1313 21st
Avenue, South 312 Oxford House, Nashville, TN 37232-4700
Semin Neurol 2019;39:5–19. (e-mail: jin.h.han@vanderbilt.edu).
Abstract Altered mental status is an umbrella term that covers a broad spectrum of disease
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Keywords processes that vary greatly in chronicity and severity. Causes can be a primary
► altered mental status neurologic insult or a result of a systemic illness resulting in end-organ dysfunction
► confusion of the brain. Acute changes in mental status are more likely than chronic changes
► altered behavior to be immediately life-threatening and are therefore the focus of this review. Given
► generalized weakness the potential time-sensitive nature, acute changes in mental status must be
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► lethargy addressed immediately and with urgency. We recommend a primary survey
► agitation followed by a secondary survey with special attention to immediate life-threatening
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► psychosis reversible causes. We then recommend a systems-based approach searching for any
► disorientation other life-threatening or reversible causes. Because the differential for altered
► inappropriate mental status is broad, a comprehensive emergency department evaluation includ-
behavior ing a detailed history and physical exam as well as laboratory and radiographic
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► hallucination testing is needed.
“Altered mental status” (AMS) describes any change in a The ED must be adept in evaluating and managing patients
patient’s baseline mental status. This term, however, is vague with acute alterations in mental status. Because acute changes
and has several synonyms, including confusion, “not acting
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in mental status are potentially life-threatening, its primary

right,” altered behavior, generalized weakness, lethargy, goal is to rapidly identify those who are critically ill, efficiently
agitation, psychosis, disorientation, inappropriate behavior, diagnose the underlying etiology, and promptly initiate life-
inattention, and hallucinations.1 AMS covers a broad spec- saving therapies. This review will discuss the causes of AMS,
trum of illnesses ranging in acuity and severity. It is a rather the mental status assessment of the patient with AMS, as well
common chief complaint; up to 5 to 10% of emergency as the appropriate diagnostic workup and treatment. Of all the
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department (ED) patients present with AMS, with rates of forms of AMS, delirium is probably the most well studied and
approximately 40% in the elderly population.2–5 will be the focus of this review. However, the concepts
Changes in mental status have variable time courses pertinent to delirium can be generalized to stupor and
and degrees of severity. Acute changes (minutes to days) coma, because there is significant overlap.
are usually secondary to delirium, stupor, and coma, which
are considered forms of acute brain failure.6 These acute

Definitions
changes in mental status can be life-threatening. It can be
caused by a primary neurologic emergency, but more often Coma, stupor, and delirium represent the broad spectrum of
than not, these changes are the sequelae of an underlying acute brain dysfunction (►Fig. 1) and are associated with
acute medical illness (secondary). In general, the more impairment of consciousness. There are two inter-related
acute and significant the change in mental status is, the domains of neurologic function that are related to conscious-
more likely it is to be life-threatening.7 Chronic (months to ness: content and arousal.8 The content of consciousness con-
years) changes in mental status (e.g., dementia) are unlikely sists of cortex level functions such as orientation, perception,
to be immediately life-threatening.7 For these reasons, executive functions, and memory.8 These processes are per-
acute changes in mental status will be the focus of this formed by widespread neuronal networks located in the
review. cortical regions.9 It can be assessed quickly by asking the
Issue Theme Emergency Neurology; Copyright © 2019 by Thieme Medical DOI https://doi.org/
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6 Altered Mental Status in the Emergency Department Smith, Han
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Fig. 1 Spectrum of acute brain dysfunction based on the Richmond and Agitation Sedation Scale (RASS). 23,24 (Image courtesy of Vanderbilt
University, Nashville, TN. Copyright 2012. Used with permission.)
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patient orientation questions such as their name, the date, and It is also important to note that dementia is an important
where they physically are. Arousal is the patient’s wakeful state predisposing factor to delirium, and patients can have both
and responsiveness to surrounding environment and stimuli. It conditions concurrently.17 Delirium and dementia’s clinical
is mediated by the reticular activating system functions, and features can overlap in patients with end-stage dementia or
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dysfunction is described by terms such as lethargy, drowsiness, dementia with Lewy’s bodies.18,19 When these patients
and somnolence. develop delirium, an acute change in mental status is still
A comatose patient is unresponsive to any stimuli. Stupor observed, and any preexisting abnormalities in cognition
describes a state of arousal only with vigorous and contin- and level of consciousness will likely worsen.
uous painful stimulation. Delirium describes an acute dis-
turbance of consciousness that is accompanied by an acute
Assessment of Acute Changes in Altered
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loss of cognition that is not better explained by a preexisting

Mental Status
neurocognitive disorder such as dementia.10 Delirium is a
highly heterogeneous syndrome and is frequently subtyped Several clinical scoring systems are used to grade the degree
by its psychomotor activity.11 of AMS. These systems are used to standardize and facilitate
communication between providers.
1. Hypoactive delirium is characterized by psychomotor
The most common scoring systems are the Glasgow Coma
retardation, and patients can appear to be drowsy or
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Score (GCS) and the AVPU (alert [A], responsive to verbal

somnolent. Because the clinical presentation of hypoac-
stimuli [V], responsive to painful stimuli [P], and unrespon-
tive delirium is subtle and often attributed to other
sive [U]) scale. The GCS assesses the patient’s eye opening,
etiologies such as depression or fatigue,12,13 this subtype
verbal and motor responses to stimuli, and ranges from 3
is often missed by clinicians.14
(comatose) to 15 (normal). It was initially developed to
2. Hyperactive delirium is characterized by a state of restless-
describe the physiologic derangement in acute traumatic

ness, agitation, or combativeness. This is the easiest to detect,

brain injuries, but the relationship between GCS score and
but the least common subtype encountered in the ED.15
survival is not linear.20 Additionally, it can be difficult to use
3. Mixed-type delirium is a state that presents with features
reliably if not used regularly.21 The AVPU scale is a simple
of both hyperactive and hypoactive delirium.
scale with four possible outcomes. It stands for alert (A),
Though the subtypes are more commonly associated responsive (R) to verbal stimuli, responsive to painful stimuli
with certain etiologies, this is not absolute. The hypoactive (P), and unresponsive (U). While it is easy to remember, it
subtype is more commonly associated with infection or lacks granularity to detect subtle impairments.22
metabolic causes, while alcohol or benzodiazepine with- Because a patient’s level of arousal is often affected with
drawal is more commonly associated with the hyperactive AMS, we recommend using a structured arousal scale such as
subtype.16 the Richmond Agitation and Sedation Scale (RASS;23 ►Fig. 1)
Dementia is a chronic form of AMS and is characterized by a to characterize the degree of AMS. The scale ranges from 5
gradual loss of cognition over a period of months to years. (unresponsive to pain and voice) to þ4 (extreme combative-
While dementia is not an emergency, there are a few reversible ness);23,24 a score of 0 represents normal and alert.
conditions associated with it that clinicians must be aware of. Several delirium assessments have been developed over
These include normal pressure hydrocephalus, hypothyroid- the past two decades and are summarized in ►Table 1. These
ism, vitamin B12 deficiency, and depression. assessments test both arousal and content. The Confusion
Seminars in Neurology Vol. 39 No. 1/2019

Altered Mental Status in the Emergency Department Smith, Han 7
Table 1 Delirium assessments
Delirium scales
Scale Advantage Disadvantage Sensitivitya Specificitya
CAM25,26 Validated in ED setting, widely Takes 5 to 10 min, heavily reliant 86% 93%
used on subjective impression
bCAM27 Takes <2 min to complete. Validated in single center 78–84% 96–97%
Validated in ED setting
CAM-ICU28 Takes <2 min to complete. Validation results mixed in 18–76% 98–99%
Validated in ED setting noncritically ill patients
3D-CAM142 Excellent diagnostic accuracy Takes 3 min to complete, 93% 96%
single-center validation
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4AT143 Takes <2 min to complete Only validated in medical 90% 84%
inpatients from Italy
DDT-Pro144 Validated in noncritically ill Only validated on traumatic brain 100% 94%
patients injury patients
SQiD145 One question test Relies on caregiver, friend, or 80% 71%

family member
mRASS (146) Takes only 10 s, validated in older Moderate inter-rater reliability, 82–84% 85–88%
ED patients heavily reliant on subjective
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impression
Abbreviation: ED, emergency department.

Note: Most of these delirium assessments have only been validated in older patients.
a
Pooled sensitivity and specificity from 12 validation studies.
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Source: Reprinted with permission from Springer Nature: Springer. Neurologic Emergencies: How to Do a Fast, Focused Evaluation of Any Neurologic
Complaint by Latha Ganti, Joshua N. Goldstein. Copyright 2018.
Assessment Method (CAM),25,26 Brief Confusion Assessment Primary Neurologic

Method,27 Confusion Assessment Method for the Intensive
Care Unit,28 and the RASS have been validated in older ED Trauma
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patients. Delirium affects approximately 10% of older ED Patients presenting with AMS after a trauma may have a
patients,29 and is associated with higher mortality,30 pro- subdural hemorrhage, epidural hemorrhage, subarachnoid
longed hospitalizations,31 and accelerated cognitive and hemorrhage, or other types of intracranial hemorrhage. Sheer
functional decline.32–35 More details on delirium in the ED injury or concussion can also present with AMS. Though rare,
and its assessment can be found at www.eddelirium.org. It is delayed presentations of intracranial hemorrhage can occur46
important to note that very few delirium assessments have and meningitis can present later as a result of facial or skull
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been validated in younger patients, especially in the ED fractures.

setting.
Structural
Structural causes include stroke, ruptured aneurysms causing
Differential Diagnosis
subarachnoid hemorrhage, seizures, locked-in syndrome,
In the undifferentiated patient who presents with AMS, a

broad differential diagnosis (►Table 2) must be consid- Table 2 A systematic approach to the differential diagnosis of
ered, as this will guide the evaluation. While a central altered mental status
nervous system etiology should strongly be considered,
AMS is often precipitated by an underlying medical ill- Differential diagnosis of altered mental status
ness. In these cases, AMS represents end-organ damage of Primary neurologic Trauma
the brain. For this reason, it is important to also consider Structural
Infectious
a patient’s vulnerability to developing AMS (►Table 3). Autoimmune/Other
Younger patients and those with little to no vulnerability
Metabolic Toxic
require a highly noxious stimulus, such as severe sepsis, Electrolyte
to develop AMS. Therefore, these patients should be Endocrine
considered to have a life-threatening illness until proven Hepatic
otherwise.36–44 Infectious Central nervous system infections
Given the broad differential of AMS, we recommend a Severe systemic infections
systemic approach (►Table 2) when considering the etiolo- Psychiatric Psychosis
gies. It is important to note that causes often coexist, Catatonia
Mania
particularly in older patients.45

Table 3 Risk factors that increase a patient’s vulnerability to transmitters, release of endogenous neurotransmitters,
developing altered mental status68,69 metabolic derangements, or other physiologic alterations.
Clinical presentations typically depend on the class of toxins,
Vulnerability factors varying from coma (opioids, alcohol, benzodiazepines) to
Older age combativeness (sympathomimetics, anticholinergics). Some
Dementia toxins, such as gamma-hydroxybutyric (GHB) acid, can vary
drastically in their clinical presentation, making it difficult to
Functional impairment
determine the specific toxin on initial presentation. Medica-
Multimorbidity tion reactions such as serotonin syndrome or neuroleptic
Malnutrition malignant syndrome can also present as AMS. Unintentional
Substance abuse and intentional overdose of over-the-counter medications
such as salicylates can also cause deadly poisonings and can
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Source: Reprinted with permission from Springer Nature: Springer. Neu- mimic other conditions such as sepsis, ultimately delaying
rologic Emergencies: How to Do a Fast, Focused Evaluation of Any
the diagnosis and increasing mortality and morbidity.
Neurologic Complaint by Latha Ganti, Joshua N. Goldstein. Copyright 2018.
Electrolyte
hydrocephalus, neoplasm, posterior reversible encephalopa- Several electrolyte derangements can result in AMS and

thy syndrome (PRES), and reversible cerebrovascular vasocon- require emergent treatment. We have included alterations
striction syndrome (RCVS) among other causes. Seizures, in glucose and blood urea nitrogen in this section. Though
though often easy to recognize, can present with subtle not true electrolytes, they are reported with electrolytes and,
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findings or as nonconvulsive status epilepticus (NCSE). The for the sake of recall, have been included in this section.
incidence of NCSE in patients with AMS is as high as 8 to 30%.47 Hypoglycemia can present with AMS ranging from delir-
ium to coma; focal neurological symptoms may not be
Infectious present. Similarly, hyperglycemia can present with AMS.
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Central nervous system infections such as meningitis or Changes in mentation are a diagnostic criterion for hyper-
encephalitis can present with the classic triad of fever, osmolar hyperglycemic state (HHS).52 Diabetic ketoacidosis
nuchal rigidity, and AMS or with unexplained neurologic can also present with changes in mental status, though
deficits or AMS without focality.48,49 usually to less of a degree than with HHS.52
Hyponatremia can also result in alterations in mental
Autoimmune/Other status. It is the most common electrolyte disorder,53 and the
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Other less common neurologic causes of AMS include neu- most common cause of such in the outpatient setting is
ropsychiatric lupus, Behçet’s syndrome, vasculitis, acute thiazide diuretic use.54 Hyponatremia can occur in euvo-
disseminated encephalomyelitis, and autoimmune limbic lemic states (SIADH), hypervolemic states (heart failure,
encephalitis.9 cirrhosis), or hypovolemic states (dehydration with poor
Wernicke’s encephalopathy is a clinical diagnosis that pre- intake). Hypotonic hyponatremia is the most common and
sents with ataxia, ophthalmoplegia, and confusion.50 Thiamine relevant form of the disorder.55 Clinical manifestations are
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(vitamin B1) is an essential nutrient that serves as a cofactor, dependent on the severity and acuteness of the state, but
among several other functions, and is required by neurons and levels less than 120 mEq/L are considered severe.55–59 At
other supporting cells in the nervous system.50 The heart and these levels, AMS can occur secondary to brain swelling and
central nervous system are particularly sensitive to thiamine intracranial hypertension.55 It can progress rapidly to life-
deficiency.50 Thiamine deficiency can result in Wernicke– threatening neurologic conditions including seizures, coma,
Korsakoff syndrome along with multiple other forms of brain and cerebral edema leading to brainstem herniation. Her-

injury.50 Providers should have a high suspicion for thiamine niation can cause respiratory arrest leading to permanent
deficiency in chronic alcoholics, malnourished patients (e.g., brain damage or death.55 These complications typically
anorexia nervosa, hyperemesis gravidarum), and in those with occur in euvolemic hyponatremia, such as with psychogenic
malabsorption syndromes. An important population to con- polydipsia, the postoperative state, intracranial pathology,
sider for being thiamine deficient are those who have had endurance exercise, or from recent use of medications
bariatric surgery, particularly a vertical sleeve gastrectomy.51 including thiazides or oxytocin use, as these conditions
typically cause acute (described arbitrarily as < 48 hours)
Metabolic rather than chronic changes. With acute changes, no intra-
Disruption of normal metabolism can result in end-organ cranial adaptation occurs, making the brain more suscep-
damage to the brain. Given the breadth of this category, we tible to edema.55 Though adaptation is beneficial in this
have separated this into four major subcategories: toxic, sense, the risk of osmotic demyelination in these patients
electrolyte, endocrine, and hepatic. markedly increases.56,57,60 For this reason, extreme caution
should be taken when raising a patient’s serum sodium
Toxic concentration.
Exogenous toxins can cause AMS through a variety of Hypernatremia, though not as common, can also cause
mechanisms including introduction of exogenous neuro- AMS typically from diabetes insipidus or severe dehydration.

Severe acidosis or alkalemia can result in AMS, especially Psychiatric

in patients with acute respiratory acidosis from respiratory A psychiatric cause of AMS is a diagnosis of exclusion. Psychia-
failure and subsequent hypercarbia. tric patients suffer from a high rate of comorbid illnesses which
Disorders in calcium can result in AMS. Hypercalcemia is are largely undiagnosed and untreated.72 Several studies have
classically thought as presenting with “stones, bones, groans, shown increased mortality for psychiatric patients from both
and psychiatric overtones.” The last one refers to changes in natural and unnatural causes.72 In one study, 20% of psychiatric
mentation from hypercalcemia. The most common cause of patients had a medical problem causing or exacerbating their
hypercalcemia in outpatients is hyperparathyroidism; in condition.72 Changes in vision appear to be the most predictive
inpatients, it is malignancy.61 Hypocalcemia can result in of a medical illness causing, or at least contributing to, their
hypotension, cardiac dysrhythmias, or heart failure which symptoms.72 Patients with an abnormal neurologic exam, vital
can also precipitate AMS.62,63 sign abnormalities, no history of a psychiatric disorder (parti-
Uremia usually does not cause changes in mental status cularly if older than 40 years) need a thorough medical
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until levels reach 100 mg/dL or higher.64 At these levels, evaluation before attributing symptoms to a psychiatric cause.
emergent dialysis is indicated if the patient is suffering from It is also important to note that in the elderly, “altered mental
AMS.65,66 status” is strongly indicative of delirium.6
Endocrine
General Approach to the Patient with

Thyroid dysfunction can cause a wide array of symptoms.
Altered Mental Status
Hypothyroidism can present with vague symptoms or as
myxedema coma in its most severe form. It is important to Initial Assessment and Management
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consider hypothyroidism in elderly patients as their symp- As with any patient presenting to the ED, the first step is to
toms are often attributed to normal aging or another cause, determine the severity of the patient’s illness. The more
resulting in missed or delays in diagnosis.67 Similarly, altered a patient is (particularly stuporous or comatose
hyperthyroidism can result in mild symptoms or as severe patients), the higher the suspicion should be for an acute
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as thyroid storm, an endocrinologic emergency. life-threatening illness. The primary and initial assessment
Adrenal insufficiency is unlikely to present as isolated AMS, should focus on the patient’s airway, breathing and circula-
but can present with AMS from hypotension that may be tion. That should quickly be followed by an assessment for
refractory to treatment. Other clues to this diagnosis may hypoglycemia, opioid intoxication, stroke, sepsis, and seizure
include dark skin pigmentation, hyponatremia with hyperka- which can be recalled quickly by remembering “ABCs and
lemia, hypoglycemia, or profound refractory shock. A corti- 5S’s” (►Table 4). These conditions are time-sensitive and
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costeroid-producing (i.e., Cushing’s syndrome) condition may require immediate treatment.

present with changes in mood and headaches with AMS. A finger stick glucose should be obtained, as hypoglycemia
is easily reversible but deadly. If the patient is hypoglycemic,
Hepatic one ampule (50 mL) of D50 should be administered through an
Acute liver failure can result in hepatic encephalopathy. intravenous or intraosseous line. Alternatively, 2 mg of intra-
Hepatic encephalopathy is not completely understood, but muscular glucagon can be administered if intravenous/
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ammonia and several other toxins are believed to play a role. intraosseous access is unable to be obtained rapidly.
Acute liver failure can also result in cerebral edema, hypo- If Wernicke’s encephalopathy is suspected, 500 mg of
glycemia, coagulopathy, infection, and acute renal failure, all thiamine should be administered intravenously before glu-
of which can contribute directly or indirectly to AMS. cose.73 This is due to a theoretical worsening of encephalo-
pathy in those who are thiamine deficient.74
Infectious

Both systemic (e.g., pneumonia, pyelonephritis) and central Opioid Intoxication

nervous system infections (e.g., infections described earlier) If an opioid overdose is suspected based on miosis and/or
can result in AMS. In the former case, AMS should be con- bradypnea, naloxone should be considered. The initial dose is
sidered end-organ dysfunction of the brain as a result of the not well established, but in practice is typically 0.4 mg
insult and may be indicative of severe disease. Certain risk intravenously. To prevent acute withdrawal syndromes,
factors make patients more vulnerable to this. Risk factors naloxone should be diluted in a 10-mL normal saline flush
include older age, dementia, functional impairment, medical
comorbidities, malnutrition, and substance abuse68,69 Table 4 The acute assessment of altered mental status
(►Table 3). Patients who have acute changes in mental status
from a systemic infection and have little or no vulnerability The acute assessment of altered mental status: ABCs and
5S’s
factors should be assumed to have a life-threatening condition
such as severe sepsis. It is important to note that AMS in the Airway, Breathing, Circulation
setting of a systemic infection is component of the Sequential Sugar Stroke Sepsis Seizure Sonorous
Organ Failure Assessment (SOFA) score, which has been shown (hypoglycemia) respirations
to be a predictor of prolonged intensive care unit stay and (opioid
intoxication)
hospital mortality.70,71

and administered slowly. Doses can be escalated to 2 mg and initiated, as delays in antibiotics are associated with
up to 10 mg. It is important to note that the half-life of higher mortality.80,81 A lactate level should be drawn and
naloxone is shorter than most opioids and frequently rapid administration of intravenous crystalloid fluid should
requires redosing or even an infusion. be initiated. It is important to note that AMS is an inde-
Reversing benzodiazepine overdoses with flumazenil is pendent predictor of mortality in sepsis, and is used as part
generally not recommended as it may precipitate withdra- of the quick Sequential Organ Failure Assessment (qSOFA)
wal in chronic users which can be life-threatening. score for identifying high-risk patients for in-hospital
When the patient’s airway is deemed stable and immedi- mortality.82,83
ate causes have been reversed, vital sign abnormalities
should be addressed. Potential causes of vital sign abnorm- Acute Assessment for Seizure
alities resulting in AMS are summarized in ►Table 5. Seizure-like activity should also be addressed immediately.
Treatment should target the underlying cause which may be
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Acute Stroke Assessment structural, metabolic, or toxicologic. Structural causes can be
A neurologic exam, including language, strength, sensation, from intracranial hemorrhage, metabolic causes from hypo-
coordination, and cranial nerves such as extraocular move- glycemia or hyponatremia, and toxicologic causes from iso-
ments, should be performed, as time-limited treatments make niazid use among other causes.
early diagnosis of stroke of utmost importance. This is parti- In patients presenting with generalized tonic–clonic sei-

cularly important in patients in whom the onset was abrupt zures of unknown etiology, first-line treatment is a benzo-
and occurred within 24 hours of arrival. It is important to note diazepine. In practice, lorazepam is often the first-line agent
that posterior circulation strokes, including basilar artery and should be administered at a dose of 0.1 mg/kg intrave-
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occlusion, can be very difficult to diagnose. Basilar artery nously.84 If intravenous or intraosseous access is not present,
occlusion can present as AMS with either unilateral or bilateral an alternative is intramuscular midazolam which should be
shaking, twitching, jerking, or posturing which can be mis- given at a dose of 5 mg if body weight is 13 to 40 kg and
taken for seizures.75,76 A midbasilar occlusion with bilateral 10 mg if body weight is greater than 40 kg.85,86
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pontine ischemia can result in “locked-in syndrome” in which If the cause of seizures is hyponatremia, the sodium
the patient can be fully conscious with complete paralysis should be acutely raised.55 This is typically done using
except vertical eye movements.77,78 The key to assessing for a hypertonic saline (3% NaCl). Care should be given to only
possible basilar occlusion is to do a rapid assessment for eye raise the serum sodium at 4 to 6 mEq/L within 4 to 6 hours.
movement and pupillary abnormalities, which is imperative. Though no evidence-based guidelines exist, an infusion of
Parietal lobe strokes can present as AMS without focal neuro- 100 mL over 10 minutes with no more than 300 mL total
logic findings, especially if the right parietal lobe is affected.79
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volume is frequently used to acutely raise the serum

Aphasia can mimic AMS; so, it is important to see if patients sodium. Most experts recommend not exceeding 6 to 8
can name objects, repeat, and follow commands. If a stroke is mEq/L in any 24-hour period regardless of the acuity of the
suspected, a noncontrast head computed tomography (CT) and hyponatremia.55,87 Increasing the serum sodium concen-
CT angiography of the head and neck should be obtained along trations more rapidly can result in osmotic demyelination
with prompt neurologic consultation. syndrome.
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If the cause is isoniazid toxicity, patients should be treated

Acute Sepsis Assessment with high-dose pyridoxine. In general, the dose is 1 g intra-
If the patient’s presentation is concerning for sepsis, blood venously for every gram ingested; if the dose is unknown, 5 g
cultures should be obtained and broad-spectrum antibiotics should be administered intravenously.88–90
Table 5 Causes of altered mental status secondary to vital sign abnormalities

Causes of altered mental status secondary to vital sign abnormalities

Vital sign Abnormality Causes
Temperature Hyperthermia Endocrine, infectious, environmental
Hypothermia Endocrine, infectious, environmental
Pulse Tachycardia Dysrhythmias, infectious, endocrine
Bradycardia Dysrhythmias, infectious, endocrine
Respiratory rate Tachypnea Infectious, toxic causes
Bradypnea Opioid intoxication, increased intracranial pressure
Blood pressure Hypertension Hypertensive encephalopathy, increased intracranial
pressure
Hypotension Shock (distributive, hypovolemic, obstructive, neurogenic,
cardiogenic)
Oxygen saturation Hypoxia Hypoxemia, toxicologic causes

Management of Combative Patients With regard to benzodiazepines, midazolam is the most

Very agitated or combative patients (RASS þ3 or þ4) may pose commonly used and best studied for the management of
a significant danger to themselves and to the health care acute agitation. When given intramuscularly (5–10 mg) or
providers caring for them. Additionally, this can impede the intravenously (2–5 mg), it has fast and predictable onset as
diagnostic workup and delay potentially lifesaving care. While well as a short duration of action.97,98 Caution must be
pharmacologic sedation is the mainstay treatment to rapidly undertaken with serial dosing as respiratory depression
calm the patient, the first step should be verbal deescalation. has been reported in 13% if cases, especially in those who
The provider should also attempt to meet patients’ physical are intoxicated with ethanol or opioid medications.98 For-
needs such as providing them with food or environmental tunately, this serious side effect is usually transient.98–100
changes if appropriate. Other initial steps should include Benzodiazepines should be used sparingly, as it may exacer-
dimming or turning off the lights, minimizing auditory stimu- bate delirium, especially in older adults.101,102 Consequently,
lation from monitors or infusion pump alarms, minimizing the the risks of benzodiazepine use must be carefully balanced
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number of providers who interact with the patient, and having with the benefits in this particular patient group.
family members at the patient’s bedside.91,92 Intramuscular ketamine is another agent used frequently
If verbal and environmental attempts to calm the patient for agitation.103 It has been found to have a similar safety
are unsuccessful, physical restraints and pharmacologic profile when compared with antipsychotics and benzodiaze-
sedation may be required. If physical restraints are used, pines.104–107 Ketamine is an N-methyl-D-aspartate (NMDA)

they should be done so for the shortest amount of time antagonist, but also antagonizes neuronal hyperpolarization-
possible. Patients should not be placed in the prone position, activated cationic currents, nicotinic acetyl-choline ion chan-
as this has been associated with increased mortality in both nels, and is a delta- and mu-opioid agonist.108–110 The intra-
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adult and pediatric populations.93,94 muscular dose (4–5 mg/kg) is much higher than the
Pharmacologic sedation should focus on treating the intravenous doses used for sedations (1–2 mg/kg), which
cause of agitation, which is thought to be neurochemical usually requires a higher concentration that is often not
imbalance resulting in excess dopamine and autonomic stocked in hospitals due to concern for potential medication
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hyperactivity.95 Commonly used agents include neuroleptics dosing errors.
and/or benzodiazepines, and are summarized in ►Table 6. Pain can also precipitate agitation and delirium, especially
First-generation antipsychotics such as haloperidol are fre- in older adults. If pain is the suspected cause, scheduled
quently administered with an anticholinergic agent such as nonopioid analgesics, particularly acetaminophen and ibu-
diphenhydramine which reduces dystonic effects and can profen, should be administered, as these can reduce opioid
also provide additional sedation depending on the agent.96 consumption by 30 to 50%.111 Adding gabapentin and/or
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opioids may be necessary for breakthrough pain. Severely

Table 6 Agents for acute undifferentiated agitation in the injured trauma patients may require regional anesthesia by
emergency department use of nerve blocks.
If ethanol or benzodiazepine withdrawal is suspected,
Agent Formulation Dose Onset of Max benzodiazepines and α-2 agonists such as clonidine can be
(mg) action daily administered.
(min) dose
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(mg)
Further Management
Lorazepam IV 2 2–3 12 When the patient’s vital signs and potential time-sensitive
IM 2–4 3–5 12 illnesses (hypoglycemia, stroke, sepsis, seizure, opioid over-
Midazolam IV 2–5 1–5 15 dose, etc.) have been addressed, further history should be
obtained along with a complete physical exam and then further

IM 5 5–10 15
diagnostic evaluation based on the differential diagnosis.
Haloperidol IV 5–10 5–10 20–30
IM 5–10 15–20 20–30
History
Droperidol IV 2.5–5 3–10 15
When the immediately life-threatening conditions have
IM 2.5–10 3–10 15
been excluded or managed, a detailed and accurate history
Olanzapine IM 5–10 15 30
should be obtained. A significant challenge to this goal is that
PO 5–10 30–60 30 patients with AMS are frequently unable to provide an
Ketamine IM 4–5/kg 3–4 1,000 accurate history, even in those with subtle alterations.112
IV 0.5–1/kg 0.5 5/kg For this reason, it is critically important that an accurate
history be obtained from a collateral historian who knows
Abbreviations: IM, intramuscular; IV, intravenous; PO, oral. the patient well and can describe the events that proceeded
Source: Adapted from Vilke GM et al. J Forensic Leg Med 2012; 19:117–121
the changes in mental status. Usually this collateral historian
(147) and Wilson MP et al. West J Emerg Med 2012;13:26–34 (148).
Source: Reprinted with permission from Springer Nature: Springer. Neu-
is a family member, caregiver, or friend. If the patient is from
rologic Emergencies: How to Do a Fast, Focused Evaluation of Any a skilled nursing facility, the patient’s nurse should be
Neurologic Complaint by Latha Ganti, Joshua N. Goldstein. Copyright 2018. contacted by phone.

Timing Social History

Most patients presenting to the ED present with acute Because drug overdoses and withdrawals are frequently a
changes (minutes to days) rather than gradual (months to cause for AMS, a complete social history including substance
years). In general, acute changes are more likely to be life- use should be obtained. While this is a common problem for
threatening, particularly if the changes are abrupt (seconds) younger patients, older adults can also be abusers of ethanol
and/or are associated with profound changes in mental and sedative hypnotics.125,126 A sexual history should also be
status (RASS 2 or þ2).7 An abrupt (seconds) change obtained, as high-risk sexual behavior can result in systemic
in mental status may also suggest a cerebrovascular event, infections or even neurosyphilis and HIV-related illnesses.
especially in the presence of focal neurologic findings.
Medical/Surgical History
Associated Symptoms A patient’s medical history may make them more prone to
Any preceding illnesses, concurrent symptoms, or other illnesses resulting in AMS. Prior CNS pathology, endocrine
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associated symptoms should be determined. Any recent focal system disorders, and malignancies, among other causes, may
neurologic symptoms, even if brief and resolved, should raise make patients susceptible to AMS secondary to exacerbation of
suspicion for stroke, as transient ischemic attacks are a major their disease processes or related processes (paraneoplastic
risk factor for the development of a stroke.113,114 Fevers, syndromes). Similarly, a surgical history is important, as post-
chills, or general weakness should raise suspicion for infec- surgical complications such as infections may result in AMS.

tion. Headaches should raise suspicion for intracranial mass
or encephalitis. A recent trauma involving facial fractures
Physical Exam
should raise suspicion for meningitis.
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In the initial assessment and management section under
Medications general approach to the patient with altered mental status,
Medications are a common cause of AMS, particularly in the initial physical exam should focus on the patient’s airway,
older and vulnerable adults. A complete and accurate med- breathing, and circulation. This should be done in conjunction
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ication list should be obtained in all patients. It is important with a rapid but thorough neurologic exam and evaluation for
to note that medication lists obtained from a chart review or hypoglycemia, stroke, sepsis, seizure activity, and opioid
from triage are often inaccurate.115,116 It may be necessary to intoxication (►Table 4). Once any vital signs, abnormalities,
call the patient’s pharmacy to obtain an accurate medication or immediate life-threatening causes have been addressed, a
list. Any recent changes or additions should be noted and the more thorough physical exam should be performed.
timing of symptoms should be compared with the change.
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Fill dates can also be compared with the number of pills Head, Ears, Nose, and Throat
present. An examination of the head should be performed to look for
The American Geriatrics Society maintains a list of poten- any signs of trauma which may suggest an intracranial
tially inappropriate medications (Beers’ criteria) in older hemorrhage as the cause. The ears should be examined for
adults.117 Commonly used medications that can result in signs of infection, hemotympanum, or Battle’s sign, which
AMS include anticholinergic medications (antihistamines, can be a sign of a skull base fracture.127 The nose and throat
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antispasmodics, tricyclic antidepressants), benzodiazepines should also be examined for trauma or signs of infection.
and nonbenzodiazepine hypnotics, and many skeletal mus-
cle relaxants.117 Eyes
Other rare causes of medication-induced AMS include A thorough examination of the eyes should be performed as
antibiotics which can cause antibiomania. The exact they can be helpful for detecting several different disease
pathophysiology is unknown, but clarithromycin, cipro- processes. Ocular exam findings and the differential diag-

floxacin, and ofloxacin seem to be the most common nosis are summarized on ►Table 7. The pupils should be
causative agents. Though rare, it occurs among all age examined for size and reactivity. Miosis or mydriasis may
groups, with the greatest number of cases occurring in suggest opioid or anticholinergic toxicity, respectively.
those in the 35-year-old group.118 A key diagnostic feature Extraocular movements should be tested even if the patient
is symptom onset soon after initiating the offending is seemingly unconscious, as this may be the only way a
agent.119 Cefepime has also been found to cause AMS. patient can communicate (such as in locked-in syndrome).
The mechanism is unknown but thought to be caused by Ophthalmoplegia may be present in patients with Wer-
Cefepime binding to GABA class A receptors resulting in nicke’s encephalopathy or increased intracranial pressure.
increased central excitation.120,121 Patients who are most Visual fields should be tested to evaluate for deficits which
susceptible appear to be those with conditions that com- may suggest stroke. With the patient at rest, the eyes should
promise the integrity of the blood–brain barrier—inflam- also be examined for nystagmus which may suggest intox-
matory conditions, organic acid accumulation, renal ication or stroke. The eyes should also be examined for the
dysfunction to name a few.120,122,123 Metronidazole can presence of exophthalmos or proptosis, which can
also cause an encephalopathy, but the pathophysiology is be secondary to hyperparathyroidism, infection, or trauma.
thought to be separate than that of antibiomania and A funduscopic exam can also be performed to assess for
cefepime-induced AMS.124 papilledema, which may suggest increased intracranial

Table 7 Ocular exam findings and differential diagnosis Pain out of proportion to the physical exam may suggest
mesenteric ischemia. Hepatosplenomegaly may suggest liver
Ocular exam disease, a hematologic cause or an oncologic cause.
Mydriasis Sympathomimetic
Anticholinergic Neurologic
Miosis Opiate A thorough neurologic exam should assess for focal deficits in
Pontine stroke language strength, sensation, coordination, gait, and cranial
Horizontal Drug intoxication nerve function. Orientation and other high-level cortical
nystagmus Peripheral nervous system Lesion(149) functions should be assessed as well. Deep tendon reflexes
Vertical Central nervous system lesion (149) should be examined for hyperreflexia or hyporeflexia to
nystagmus Wernicke’s encephalopathy evaluate for upper motor neuron lesions or infectious/
demyelinating causes. The patient’s gait should be examined
Rotary nystagmus Drug intoxication
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Central nervous system lesion if possible to assess for ataxia, antalgia, circumduction, or any
other abnormalities. Gait disturbances, while often nonspe-
Exophthalmos Grave’s disease (hyperthyroid)
cific, may suggest Wernicke’s encephalopathy, toxicologic
Ophthalmoplegia Wernicke’s encephalopathy causes, or stroke. Tone, balance, coordination, and position
Increased intracranial pressure
sense should be assessed as well. Increased tone may suggest
Proptosis Retrobulbar hematoma

a hypermetabolic state such as serotonin syndrome, malig-
Orbital cellulitis
nant hyperthermia, or neuromuscular malignant syndrome.
Scleral Icterus Hepatic failure
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Gaze deviation Seizure Genitourinary
Oculogyric crisis The genitourinary region should be inspected for any signs of
Visual field deficit Central retinal artery occlusion infection. Males should be inspected for infection and
Occipital lobe infarct females for infection and vaginal foreign bodies such as
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tampons. A rectal exam should be performed to evaluate
Source: Reprinted with permission from Springer Nature: Springer. Neu-
rologic Emergencies: How to Do a Fast, Focused Evaluation of Any for tone, blood, or pain out of proportion to exam. Decreased
Neurologic Complaint by Latha Ganti, Joshua N. Goldstein. Copyright 2018. tone may suggest spinal cord injury from neoplasm, trauma,
or infection. Pain may suggest prostatitis or an abscess. Blood
or melena may suggest a gastrointestinal bleed.
pressure, or retinal subhyaloid hemorrhages, which may
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suggest subarachnoid hemorrhage. Skin

A skin exam should evaluate for evidence of acute and
Neck chronic disease. Findings of chronic liver disease include
The neck should be examined for masses, nodules, or thyr- jaundice, scleral icterus, and caput medusa, and may suggest
omegaly, which may indicate thyroid dysfunction. The neck hepatic encephalopathy. Dry or doughy skin may suggest
should also be evaluated for meningismus, suggestive of hypothyroidism. Darkened or bronze skin may suggest Addi-
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meningitis or subarachnoid hemorrhage, but the absence son’s disease.

of such does not rule out either condition.49 Acute skin findings such as petechiae or purpura may
suggest hematologic or infectious causes such as bacterial
Cardiac meningitis. The skin should also be assessed for soft-tissue
The cardiac exam should evaluate for general perfusion, infections, particularly in the decubitus regions which are
heart rate, heart rhythm, and any extra heart sounds. A more likely to be missed.

new murmur may suggest endocarditis, which can result Additionally, the skin should be examined for any drug
in bacteremia or septic emboli. It may also represent cardiac patches (e.g., fentanyl or scopolamine) or other potential
shock in a patient who is hypotensive and poorly perfused. A chemical exposures which can result in AMS.
friction rub may suggest cardiac tamponade.
Laboratory Evaluation
Lungs
The pulmonary exam should evaluate for pulmonary edema, As with any complaint, the history and physical exam should
pneumonia, or pneumothorax. This can be done by ausculta- guide laboratory testing. In patients who are unable to provide
tion with a stethoscope or with visualization using bedside a history, a broad approach may be necessary. All patients
ultrasound. presenting to the ED with AMS should have a fingerstick
glucose performed as part of the primary survey to rule out
Abdomen hypoglycemia, which can be reversed immediately.
An abdominal exam should evaluate for tenderness, hepato-
megaly, splenomegaly, and the presence of ascites. Tenderness Complete Blood Count
or rigidity may suggest an acute abdomen from cholecystitis, A complete blood count may reveal profound anemia, throm-
appendicitis, diverticulitis, or volvulus, among other causes. bocytopenia, polycythemia, or thrombocytosis resulting in

inadequate perfusion or hyperviscosity. A leukocytosis or is important for providers to not anchor on a urinary tract
leukopenia may be the result of a malignancy, infection, or an infection given the high rate of asymptomatic bacteriuria. In
immunocompromised state. Thrombocytopenia may result addition to evaluating for infection, a urinalysis can help
in a spontaneous intracranial hemorrhage. Thrombocytosis determine hydration status based on the specific gravity and
may suggest an infectious etiology or malignancy. the presence/absence of ketones. It may also show evidence
of myoglobinuria, which can represent hemolysis or
Basic Metabolic Profile rhabdomyolysis.
A basic metabolic profile (serum sodium, potassium, chloride,
bicarbonate, blood urea nitrogen, and creatinine) can evaluate Toxicologic Evaluation
for electrolyte or other blood chemistry abnormalities. An Like urinalyses, a urine drug screen (UDS) should be inter-
ionized calcium should be obtained to evaluate for hyperpar- preted with caution. Though quick and easy to obtain, they
athyroidism, hypercalcemia of malignancy, or for conditions are prone to both false positives and false negatives. They rely
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associated with a low calcium based on their basic metabolic on multiple factors for detection and the time from ingestion
panel.128 In malnourished patients or those with liver disease to detection varies significantly.133 It is important to note
who have an abnormal serum calcium level, an albumin should that it is often not the drug itself but a metabolite of the drug
be ordered to calculate a corrected calcium level. that is detected on a UDS.
In patients with a toxic overdose in which the substance is

Liver Function Tests unknown or if concern for polysubstance ingestion is pre-
Liver function tests may reveal evidence of liver disease, but sent, a serum osmolality should be drawn to calculate an
normal liver enzymes do not rule out disease. Liver disease osmolar gap to evaluate for toxic alcohols. Serum acetami-
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may be intrinsic (e.g., cirrhosis of the liver, primary scleros- nophen and salicylate levels should be considered in this
ing cholangitis) or extrinsic (e.g., toxins, infection) in nature. patient population as well.
Elevated alkaline phosphatase may represent evidence of
gallbladder disease, but is nonspecific and may represent Lumbar Puncture
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bone breakdown. If stigmata of liver disease is present (e.g., A lumbar puncture can evaluate for several etiologies of AMS,
jaundice, musky odor, varicosities, ascites), an ammonia including subarachnoid hemorrhage, meningitis, and ence-
level should be considered. While an ammonia level should phalitis. A lumbar puncture should be considered in all
not be used for screening, it may be helpful for trending patients with AMS in whom no other etiology has been
when being treated for hepatic encephalopathy.129 Cholan- discovered or if they are immunocompromised. It should
gitis may present with AMS along with right upper quadrant also strongly be considered in patients with a first-time
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pain, jaundice, fever, and shock, known as Reynold’s psychosis if any atypical features are present. Prior to a
pentad.130 lumbar puncture, a head CT should be performed on patients
with AMS due to potential risk of iatrogenic herniation if
Lipase increased intracranial pressure is present.134
A lipase should be considered in patients with upper quad- The basic evaluation of cerebrospinal fluid (CSF) should
rant or midepigastric abdominal pain. Severe acute pancrea- include a total white blood cell count, protein, glucose, and
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titis can even lead to pancreatic encephalopathy, a rare but culture. If concerns for other processes (e.g., Lyme disease,
poorly understood complication of acute pancreatitis.131 neurosyphilis, cryptococcal meningitis, anti-NMDA [N-
methyl-aspartate] encephalitis, etc.) exist, specific antigens
Endocrine Studies should be sent. We also recommend drawing an additional 3
Thyroid function tests (thyroid-stimulating hormone and to 4 mL of CSF to freeze in the event that further testing is
free T4) should be considered in patients with signs and needed after admission.

symptoms of hypothyroidism or hyperthyroidism. As men-

tioned earlier, it is important to consider hypothyroidism in
Imaging
elderly patients with unexplained vague symptoms, as these
symptoms are often attributed to the normal aging Radiography
process.67 Imaging should be guided by history, physical exam, and
A random cortisol should be considered in patients with laboratory analysis. In patients who are unable to provide
signs and symptoms of adrenal insufficiency such as refrac- history, a broader approach may be necessary. A chest X-ray
tory shock, hyperkalemia with hyponatremia, and bronze- should be considered in undifferentiated patients with AMS
colored skin. Though far from a definitive test, a random to evaluate for an infectious infiltrate. It may also identify a
cortisol level may help with the diagnosis. pneumothorax, neoplasm, pulmonary edema, or a pleural
effusion. In patients with abdominal pain, careful attention
Urinalysis should be paid to the hemidiaphragms evaluating for free
A urinalysis should be considered in patients with AMS, air which can suggest a perforated viscous. An abdominal X-
particularly in elderly patients. Results, however, should be ray should also be considered in patients with abdominal
interpreted carefully as asymptomatic bacteriuria is com- pain, though they are much less sensitive than abdominal
mon among all age groups and is frequently overtreated.132 It CT. Plain abdominal films should be evaluated for free air,

an obstructive bowel gas pattern, presence of a volvulus, no etiology of AMS has been discovered, as the incidence of
and pneumointestinalis. NCSE in patients with AMS is as high as 8 to 30%.47,142
Further imaging should be performed based on history,
physical exam, and laboratory analysis, though clinicians Electrocardiogram
should have a low threshold for advanced imaging in patients An electrocardiogram (ECG) should be considered in patients
who are unable to provide history. with AMS, especially if their pulse rate is bradycardic or
tachycardic; it may reveal ECG changes secondary to toxic or
metabolic causes. An ECG can also be considered in patients
Neurologic Imaging
who are highly vulnerable to developing AMS or delirium.
Noncontrast Head Computed Tomography The ECG should be evaluated for rate, rhythm, intervals, and
The most common neuroimaging test ordered in the ED is a presence of ischemia. Patients with any concerning findings
noncontrast head CT due to its speed and availability. It can should be monitored on telemetry in the ED.
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rapidly evaluate for hemorrhage, infarction, cerebral edema,
and bony injury.135 If the clinician is concerned about any of
Disposition
those, a head CT is indicated.
Controversy exists regarding the use of noncontrast head The disposition for patients with AMS depends on the cause,
CT in patients with undifferentiated AMS. In general, older stability, and reversibility of the underlying condition. Stupor-

patients, those with seizures, those with signs/symptoms ous or comatose patients likely require intensive care.
concerning for stroke or trauma, or those with sudden onset Patients with a stroke should be admitted to a stroke unit
of impaired consciousness should undergo a noncontrast if possible, as this has been associated with improved mor-
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head CT.37,136,137 tality and outcomes.143 Patients with large vessel occlusions
may be best served at a comprehensive stroke center where
Computed Tomography Angiography thrombectomies are performed.144
If concern for stroke, carotid artery dissection, or subarachnoid If the cause of AMS is from a toxic etiology, disposition
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hemorrhage exists, CT angiography of the head and neck should be decided in conjunction with a poison center (1–
should be considered. CT angiography is highly sensitive for 800–222–1222). Many ingestions, particularly those invol-
detecting stenosis of vessels, aneurysms, and dissections. ving delayed-release drug formulations, require 24-hour
Additionally, angiography can be used to estimate perfusion monitoring even with a reassuring evaluation.
of the brain parenchyma and may detect large vessel occlu- For delirious patients, there is very little evidence-based
sions, including of the vertebral and basilar arteries.135 Venous literature regarding disposition. There is, however, evidence
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phase angiography can detect dural venous thromboses. that delirious patients discharged from the ED have higher
rates of mortality than those without delirium, particularly if
Magnetic Resonance Imaging the diagnosis is missed in the ED.145
Magnetic resonance imaging (MRI) is not available in all If the cause of AMS, however, is determined and symp-
centers and is more time consuming, but is superior at toms are rapidly reversed, observation or discharge home
detecting ischemic change,138 visualizing the posterior with close supervision can be considered. If a patient without
fossa,139 and visualizing intracranial masses. An MRI can
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a known neurologic disorder becomes delirious from a

be considered if no other etiologies for the patient’s AMS are seemingly benign insult, outpatient follow-up with a neu-
found, and is usually done as an inpatient. If an MRI is rologist should be arranged, as they have essentially failed a
unavailable or a contraindication to such exists, a contrast- “stress test for the brain.”9
enhanced CT may be indicated.
It is important to note that several diseases are largely Disclosures

clinical diagnoses. For example, initial imaging in locked-in J.H.H. is supported by the Veteran Affairs Geriatric
syndrome such as CT can be poorly sensitive,140 although CTA Research, Education, and Clinical Center (GRECC). The
should be utilized to assess for this when suspicion exists. MRI content is solely the responsibility of the authors and
has a higher sensitivity for brainstem strokes, but can still does not necessarily represent the official views of Veter-
result in false negatives within the first 24 hours.141 Similarly, ans Affairs.
MRI findings for central pontine myelinolysis are often not
present for 2 or more weeks after the initial neurologic Conflict of Interest
symptoms.55 A normal MRI does not indicate absence of disease. J.H.H. reports grants from Veteran Affairs Geriatric
Research, Education, and Clinical Center (GRECC), during
the conduct of the study.
Other Studies
Electroencephalogram
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5

Altered Mental Status in the Emergency Department

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in mental status are potentially life-threatening, its primary

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loss of cognition that is not better explained by a preexisting

Score (GCS) and the AVPU (alert [A], responsive to verbal

ness, agitation, or combativeness. This is the easiest to detect,

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Table 1 Delirium assessments

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Abbreviation: ED, emergency department.

Assessment Method (CAM),25,26 Brief Confusion Assessment Primary Neurologic

been validated in younger patients, especially in the ED fractures.

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Severe acidosis or alkalemia can result in AMS, especially Psychiatric

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costeroid-producing (i.e., Cushing’s syndrome) condition may require immediate treatment.

Both systemic (e.g., pneumonia, pyelonephritis) and central Opioid Intoxication

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volume is frequently used to acutely raise the serum

If the cause is isoniazid toxicity, patients should be treated

Table 5 Causes of altered mental status secondary to vital sign abnormalities

Causes of altered mental status secondary to vital sign abnormalities

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Management of Combative Patients With regard to benzodiazepines, midazolam is the most

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opioids may be necessary for breakthrough pain. Severely

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Timing Social History

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suggest subarachnoid hemorrhage. Skin

meningitis or subarachnoid hemorrhage, but the absence son’s disease.

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symptoms of hypothyroidism or hyperthyroidism. As men-

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a known neurologic disorder becomes delirious from a

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mechanistic considerations. Metab Brain Dis 2010;25(01):97–106 JAMA 2017;317(03):301–308

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