CHAPTER 80

Temporal Arteritis

Administer oral prednisone 80 mg. The patient should be

discharged home on prednisone 40 mg daily. Close

follow-up for biopsy and definitive diagnosis should

be arranged before the patient is discharged from the ED.

Pseudotumor Cerebri

A normal CT scan should be followed by LP to assess

opening pressure. An opening pressure >25 em H20 suggests the diagnosis. CSF should be removed to bring ICP

into the normal range (usually about 20 mL of CSF). Oral

acetazolamide and steroids may be started in the ED after

consulting with a neurologist.

Carotid or Vertebral Artery Dissection

For patients with only pain and no neurologic signs

suggestive of CVA, head CT scan is often normal. CT

angiography of neck, MRI/MRA, or duplex ultrasound

may show the abnormality in the affected vessel. Treatment

may include aspirin or heparin. Emergent neurologic and

vascular surgery consultation is appropriate.

DISPOSITION

� Admission

Most patients with an emergent secondary headache

should be admitted to the hospital. Patients with meningitis

with AMS, SAH, intracranial hemorrhage, cervical artery

dissection, or tumor with mass effect or signs of increased

ICP should be admitted to an intensive care unit.

� Discharge

Patients with benign headache syndromes whose pain is

well controlled can be discharged home. Patients with sec ­

ondary headaches that are not life- or organ-threatening

(temporal arteritis, pseudotumor cerebri) can be discharged home after close follow-up is arranged. These

patients should be given very specific instructions to

return if headache worsens or they experience any new or

different symptoms, including focal weakness, numbness,

speech or visual problems, or vomiting.

SUGGESTED READING

Denny CJ, Schull MJ. Headache and facial pain. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Clince DM, Cydulka, RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th

ed. New York, NY: McGraw-Hill, 201 1, pp. 1 1 13-11 18.

Edlow JA, Panagos PD, Godwin SA, et a!. Clinical policy: Critical

issues in the evaluation and management of adult patients

presenting to the emergency department with acute headache. Ann Emerg Med. 2008;52:407-436.

Swadron SP. Pitfalls in the management of headache in the

emergency department. Emerg Med Clin North Am.

20 1 0;28:127-147.

Dizziness

Wi lliam B. Lauth, MD

Key Points

• The patient's definition of "dizzi ness" must be clarified

with a careful and explicit history taken by the health

care provider.

• True vertigo must be differentiated from other types of

dizziness.

INTRODUCTION

Dizziness is one of the most common emergency department (ED) presentations and one of the most difficult to

characterize. Dizziness means different things to different

people and crosses language and cultural boundaries. The

precise definition ranges from weakness, giddiness, and

anxiety to true vertigo, presyncope, disequilibrium, or

nonspecific lightheadedness. A very careful history from

the patient, friends, or family is the most important part of

the initial evaluation of the dizzy patient.

Dizziness can be divided into 4 main types: vertigo,

presyncope, disequilibrium, and lightheadedness. Vertigo is

defined as the perception of movement where no move ­

ment exists. Patients often describe feeling the room spinning. It can be further divided into central and peripheral

types. Peripheral vertigo is usually benign and caused by an

inner ear problem, whereas central vertigo is usually serious

and involves pathology within the cerebellum or brainstem.

Presyncope is defined as lightheadedness derived from feeling an impending loss of consciousness. Disequilibrium

refers to a feeling of unsteadiness, imbalance, or a sensation

of floating while walking. Lightheadedness is the most difficult type of dizziness to characterize. Many patients in this

group have vague, poorly defined symptoms, such as j ust

not feeling right, that do not fall into one of the other

categories.

341

• Attempt to distinguish peripheral from central vertigo.

• Consider life-th reatening causes of dizzi ness such as

cardiac syncope and cerebellar infarct or hemorrhage

in all patients, especially the elderly.

The central nervous system (CNS) coordinates and

interprets sensory inputs from visual, vestibular, and proprioceptive systems. These 3 systems give us the sense of

position in our 3-dimensional universe. The disruption of

any 1 of these 3 can produce vertigo. The most common

forms of vertigo involve dysfunction of the vestibular apparatus and are thus considered peripheral vertigo. By far the

most common cause of vertigo is benign paroxysmal positional vertigo (BPPV), which is caused by a mechanical

disorder of the inner ear. It is due to the accumulation of

floating calcium carbonate particles in either the left or

right semicircular canals. These particles stimulate the labyrinth, causing asymmetric input from the normal and

affected semicircular canals, which produces the sensation

of vertigo. Clinically, BPPV is characterized by vertigo pre ­

cipitated by certain head movements, which aggravate this

unilateral dysfunction. Other causes of peripheral vertigo

include Meniere disease, labyrinthitis, and vestibular neu ­

ronitis. Meniere disease is a disorder in which there is an

increase in volume and pressure of the endolymph of the

inner ear, eventually leading to damage of the endolymphatic system and deafness. The pathophysiology of labyrinthitis is not completely understood, although many cases

are associated with systemic or viral illnesses, which is

thought to cause inflammation in the vestibular apparatus.

Viral infection of the vestibular nerve is believed to be the

most common cause of vestibular neuronitis.

CHAPTER 81

Central vertigo is much less common than peripheral

vertigo and is due to CNS dysfunction. Cerebellar infarct

or hemorrhage, cerebellopontine angle tumors and

schwannomas, and vertebrobasilar insufficiency frequently

cause central vertigo symptoms.

CLINICAL PRESENTATION

� History

The cause of dizziness can be elicited by history alone in

more than half of all cases. Patients with vertigo complain

of a sensation of movement, or "the room spinning"

around them, with associated nausea and vomiting. BPPV

usually has an abrupt onset, lasts < 1 minute, and is pro ­

voked by head movement. ED physicians should be aware

that some causes of central vertigo such as vertebrobasilar

insufficiency (VBI), transient ischemic attack, and cerebellar hemorrhage may also have an acute onset. Meniere

disease is associated with hearing loss and tinnitus, and the

vertigo usually lasts for hours. The vertigo caused by labyrinthitis and vestibular neuronitis usually lasts for a few

days. In contradistinction, the symptoms of central vertigo

are usually less acute, more persistent, and may have asso ­

ciated neurologic symptoms ( Table 81-1).

Patients with presyncope often complain of feeling as

though they are going to pass out. This may be associated

with a stressful event (vasovagal episode), exertion (aortic

stenosis), sudden change in posture (hypovolemia), or

Table 81-1. Differentiating peripheral

from central vertigo.

Peripheral

Onset Sudden

Severity of vertigo Intense spinning

Pattern Paroxysmal, intermittent

Aggravated by Yes

position/movement

Associated nausea/ Frequent

diaphoresis

Nystagmus Rotatory-vertical, horizontal

Fatigue of Yes

symptoms/signs

Hearing loss/tinnitus May occur

Abnormal tympanic May occur

membrane

Central nervous system Absent

symptoms/sign

Central

Sudden or slow

Ill-defined, less

intense

Constant

variable

variable

Vertical

No

Does not occur

Does not occur

Usually present

Reprinted with permission from Goldman B. Chapter 1 64. Vertigo and

Dizziness. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK,

Meckler GO, eds. Tintina/lis Emergency Medicine: A Comprehensive

Study Guide. 7th ed. New York: McGraw-Hill, 201 1.

palpitations (dysrhythmia). Disequilibrium is most often a

complaint of elderly patients. Their sense of loss of balance

is usually worse at night (limited visual acuity is further

impaired) and later in the day (more fatigued). Patients

with lightheadedness usually have vague complaints. Past

medical history and associated chronic medical conditions

should be ascertained in an attempt to find a cause for

their complaints.

� Physical Examination

A complete physical examination should be performed,

paying special attention to a few key areas. Vital signs can

suggest a cause early in the evaluation. Hypotension suggests causes related to decreased cerebral perfusion,

whereas hypertension may point to VBI, stroke, or hemorrhage. Bradycardia or tachycardia may cause presyncope

from impaired cardiac output.

The head, eyes, ears, nose, and throat examination may

reveal a possible cause for vertigo. Ears should be carefully

examined for presence of a ruptured tympanic membrane,

decreased hearing, infection, cerumen impaction, and foreign bodies. The cardiovascular examination should assess

for signs of vascular insufficiency (carotid bruits, decreased

peripheral pulses). Auscultate for any arrhythmia or the

systolic murmur of aortic stenosis.

A complete neurologic examination is essential for all

patients with a complaint of dizziness. Assess for the presence and type of nystagmus. While performing the cranial

nerve examination, pay special attention to cranial nerves

VII, VIII, and IX. Cranial neuropathies associated with eranial nerve VIII suggest brainstem involvement and a central

cause of vertigo. Patients with peripheral vertigo should be

able to ambulate, although they may veer to one side.

Patients with cerebellar infarction or hemorrhage usually

cannot ambulate. A Romberg test can be used to differentiate cerebellar from spinal cord (posterior column) dysfunction. Have the patient stand, with feet together, and then

have them close their eyes. Excessive swaying or imbalance is

a positive test and is seen in patients with significant proprioceptive loss from posterior column dysfunction.

DIAGNOSTIC STUDIES

� Laboratory

No specific laboratory test can aid in the diagnosis of vertigo (Table 81-2). However, older patients on multiple

medications with nonspecific symptoms should have

hemoglobin, electrolytes, and renal function evaluated.

Electrocardiogram (ECG) and serial troponins should be

performed in patients suspected of having a cardiac cause

for their symptoms.

� Imaging

Head computed tomography (CT) scan is indicated in

patients with a suspected central cause for their symptoms

(focal neurologic findings, altered mental status, severe

Table 81-2. Anci llary testing of vertigo and dizziness.

Condition Suggested Tests

Bacterial labyrinthitis CBC, blood cultures, a scan or MRI for

possible abscess, lumbar puncture if

meningitis suspected

Vertigo associated with a scan or MRI

closed head injury

Near-syncope ECG, Holter monitor, CBC, glucose, electrolytes, renal function, table tilt testing

Cardiac dysrhythmias ECG, Holter monitor

Suspected valvular heart ECG, echocardiography

disease

Nonspecific diuiness; CBC, electrolytes, glucose, renal function

disequil ibrium of aging tests

Thyrotoxicosis

Cerebellar hemorrhage,

infarction or tumor

Vertebral artery

dissection

Vertebrobasilar

insufficiency

Thyroid stimulating hormone, triiodothyronine, thyroxine

a or MRI

Cerebral angiogram to include neck

vessels or MRA

ECG, cardiac monitoring, echocardiogram,

carotid Doppler, MRI, MRA

CBC, complete blood count.

Repri nted with permission from Goldman B. Chapter 1 64. Vertigo

and Dizziness. In: Tintina lli JE, Stapczynski JS, Cline OM, Ma OJ, Cydulka

RK, Meckler GO, eds. Tintinolli's Emergency Medicine: A

Comprehensive Study Guide. 7th ed. New York: McGraw-Hill, 201 1.

headache), or significant cerebrovascular accident risk factors (Figure 81-1). Magnetic resonance imaging (MRI)/

magnetic resonance angiography (MRA) may be per ­

formed if vertebral artery dissection or vertebrobasilar

insufficiency is considered.

 

50

30

10

3-8

• Never delay administering antibiotics while wa iting for

a CT scan or lumbar puncture (LP) when considering the

diagnosis of bacterial meningitis.

• When subarachnoid hemorrhage is suspected, follow a

normal CT scan with LP.

sinuses, the dura, cranial nerves, or extracranial sources

(muscle tension). In emergent headaches, pain may

arise from mass effect (tumor or subdural hematoma),

inflammation of the meninges (meningitis and SAH),

vascular inflammation (temporal arteritis), vascular

dissection (carotid and vertebral artery dissection) , or

extracranial sources ( dental caries, otitis media,

sinusitis).

...... Emergent Secondary Headaches

Subarachnoid Hemorrhage

Although SAH represents <1% of headaches in patients

who present to the ED, it occurs in approximately 12% of

patients with a severe sudden headache. Pain is often

maximal at onset, in the occipital region, and may resolve

spontaneously in the ED. The median age at presentation

is 50 years. More than 50% of patients have a normal

neurologic examination. Rupture of an aneurysm is the

most common cause.

Meningitis

Classic triad of headache, fever, and meningismus is often

not present. It is more difficult to diagnose at extremes of

age. Immunosuppression can cause atypical subacute

presentations.

336

Intracranial Bleed

Subdural bleed can occur with minimal or unrecognized

trauma (warfarin use, elderly). Epidural bleed usually

occurs with significant trauma. Intracerebral bleed is often

associated with severe hypertension.

Temporal Arteritis

Occurs in patients older than 50 years and is more fre ­

quent in women. It is caused by a systemic panarteritis.

Patients present with frontotemporal throbbing headache,

jaw claudication, and a nonpulsatile or tender temporal

artery. It may cause visual loss from ischemic optic

neuritis.

Carotid And Vertebral Artery Dissection

Together these entities cause 20% of strokes in patients

younger than 45 years. Carotid dissections occur twice as

often as vertebral dissections. Classically, they present as

acute unilateral headache and/or neck pain, but may present atypically (lower cranial nerve deficits or C5/6 radiculopathy). The median age of onset is 40 years. Sometimes

dissection occurs in association with minor trauma (yawning) or may be spontaneous.

Pseudotumor Cerebri

Benign intracranial hypertension of unclear cause. It has

been linked to the use of oral contraceptives, vitamin A,

tetracyclines, and thyroid disorders. Often occurs in

young, obese females with chronic headaches. Papilledema

is usually the only abnormal examination finding, but

cranial nerve abnormalities, visual field deficits, or

decreased visual acuity may also be present.

Stroke

Although 55% of patients with an intracerebral hemor ­

rhage have a headache, less than 1 7% of ischemic stroke

patients complain of pain. However, cerebellar infarction

often presents as acute pain in the occipital area. Because

of its location in the posterior fossa, there is risk of herniation as surrounding brain edema occurs.

Other

Pituitary apoplexy, acute angle-closure glaucoma, hyper ­

tensive encephalopathy, pheochromocytoma, CO poison ­

ing, preeclampsia, venous sinus thrombosis (often in the

setting of a hypercoagulable state).

� Primary Headaches

Migraine

Abnormal vascular actlvtty is thought to be causal.

Migraines are more common in females, with onset

HEADACHE

usually in teen years, and less commonly after age 40

years. The patient presents with unilateral pulsating

headache that may have an associated aura. The pain usually follows a typical pattern for individual patients and

improves during pregnancy (estrogen excess). Associated

symptoms include nausea and vomiting with photophobia and phonophobia.

Tension

The most common type of primary headache. Often presents with bitemporal nonpulsating pain without associated

nausea, vomiting, photophobia, or phonophobia.

Cluster

Uncommon in the general population, but more common

in men beginning after age 20 years. They present with

acute, severe, unilateral retro-orbital pain with associated

lacrimation, eye injection, and rhinorrhea and usually

occur in "clusters" over days to weeks and resolve spontaneously.

CLINICAL PRESENTATION

� History

A detailed history is most important to make the correct

diagnosis and guide therapy. Headache pattern should be

sought. Patterns that raise concern for a secondary headache

include sudden onset, first ever, or a change in frequency or

intensity from previous. Sudden onset of a severe headache

suggests SAH, but may also be present in venous sinus

thrombosis, cervical artery dissection, cerebellar infarct, and

pituitary apoplexy. A headache that is worse in the mornings

may indicate a tumor, whereas a headache that is worse on

standing is characteristic of a post-lumbar puncture (LP)

headache. Headache location is usually nonspecific.

However, migraines are typically unilateral, tension headaches are bilateral, and SAH is usually occipital or nuchal.

Neck pain with or without neurologic deficits may represent

a carotid or vertebral artery dissection. Headache character

may be pulsatile or throbbing (migraine), squeezing (ten ­

sion), or sharp and acute (cluster and SAH).

Associated symptoms that may point to an emergent

secondary cause include syncope, altered mental status

(AMS), neck pain or stiffness, fever, hypertension, visual

disturbance, weakness, seizures, or trauma. Consider

carbon monoxide poisoning when multiple family

members are concurrently affected during the fall or win ­

ter. Important elements of the past medical history include

immunocompromise, malignancy, coagulopathy

(warfarin), uncontrolled hypertension, aneurysm, connective tissue disease (cervical artery dissection), and cerebrovascular accident (CVA). Family history is also important.

Migraines, SAH, and carotid/vertebral dissections are all

more common if a first-degree relative has been affected.

CHAPTER 80

..... Physical Examination

Vital signs are often normal in patients with headache.

However, fever may indicate meningitis or sinusitis, and

severe hypertension suggests encephalopathy or intracra ­

nial bleed. General appearance should be appreciated and

may aid in diagnosing a life-threatening headache or severe

presentation of a primary headache syndrome. Head and

neck examination should assess for sinus tenderness, dental caries, otitis media or externa, temporal artery tenderness, and meningismus. Eye exam should include visual

acuity, pupil reactivity and funduscopy (papilledema from

increased ICP, subhyaloid hemorrhage from SAH). On the

neurologic examination, include mental status, cranial

nerves, strength, sensation, reflexes, cerebellar and gait if

possible. AMS or focal neurologic deficits often indicate

increased ICP.

DIAGNOSTIC STUDIES

..... Laboratory

General laboratory studies (complete blood count, chemistry

panel, urinalysis) add little to the diagnosis of emergent

headaches. Elevated white blood cell (WBC) count may

point to an infection; elevated erythrocyte sedimentation

rate (>50 mm/h) is present in cases of temporal arteritis.

Figure 80-1. Noncontrast head CT scan showi ng

SAH. Note the blood (white areas) in the basal cisterns

and interhemispheric fissure. This is referred to as the

"star sign" (arrow).

.... Imaging

Noncontrast head computed tomography (CT) scan is the

test of choice when evaluating emergent causes of head ­

ache. It can assess for acute SAH (sensitivity 98o/o within 12

hours, 93o/o within 24 hours); acute intracerebral, subdural,

and epidural hematomas; and lesions causing mass effect

(Figure 80-1). Intravenous (IV) contrast is added in

patients with immunocompromise, or when subacute or

chronic subdural, venous sinus thrombosis, or central nervous system infections are suspected. CT scan does not

diagnose idiopathic intracranial hypertension, meningitis,

and some cases of venous sinus thrombosis. When considering carotid or vertebral dissection, CT angiogram of the

neck, duplex ultrasonography, or magnetic resonance

imaging (MRI)/magnetic resonance angiogram (MRA) of

the neck should be performed.

PROCEDURES

LP should be performed when considering meningitis or

SAH (if the head CT scan is nondiagnostic). It can also be

performed to check the opening pressure (normal <20

em H2

0) in patients with suspected pseudotumor cerebri. Opening pressure should also be assessed for

suspected SAH; two thirds of patients will have elevated

pressure. CT should be performed before LP for patients

with any of the following: age >60 years, AMS, focal

neurologic deficit, signs of increased ICP (papilledema),

seizures, immunocompromise, or meningeal signs.

Cerebrospinal fluid ( CSF) findings in acute meningitis

and SAH are listed in Table 80-2. Interpreting CSF results

in the face of a traumatic LP can be difficult. A decrease in

red blood cells (RBCs) to near zero from tubes 1-4 suggests that the blood in tube 1 was from LP-induced trauma,

not SAH. In general, there will be 1 WBC in the CSF for

every 700 RBCs when from a traumatic LP. Xanthochromia

(due to lysis of erythrocytes in CSF), when present, is

indicative of SAH.

Table 80-2. CSF findings in mening itis and SAH.

CSF Normal Bacterial Viral SAH

Cells <5 WBCs 200·5,000 <1,000 1 oos-million

PMN monocytes RBCs

CSF/serum glu- 0.6 Low Normal Normal

cose ratio

Protein 1 5-45 High High Normal to

mg/dl increased

Gram stain Negative Positive Negative Negative

Xanthochromia* Negative Negative Negative Positive

'''Usually present 12 hours after SAH bleed and lasts 2-3 weeks,

MEDICAL DECISION MAKING

History and physical examination may be sufficient to

arrive at a benign diagnosis (tension, migraine, cluster

headache). However, when serious secondary headaches

are considered, CT imaging ± lumbar puncture should be

performed. Treatment of possible meningitis should not be

delayed by CT or LP (Figure 80-2).

TREATMENT

For patients with a presumed benign headache, oral pain

medications (nonsteroidal anti-inflammatory drug,

acetaminophen, hydrocodone) may be sufficient to relieve

pain. For more severe pain, especially when a migraine is s uspected, N antiemetics (prochlorperazine 5-10 mg N) often

provide relief. Sensory stimuli should be decreased (dark quiet

room). N opioids may be used for continued pain.

Patients with a presumed emergent headache usually

require IV medications for pain relief concurrently with

diagnostic tests (CT ± LP) and other treatments (N

antibiotics for meningitis). In general, N antiemetics and

opioids are safe for emergent headaches.

HEADACHE

Subarachnoid Hemorrhage

Emergent neurosurgical consultation is required for

aneurysm clipping or coiling. Nimodipine ( 60 mg by

mouth [PO]) is often given to reduce subsequent vasospasm.

Meningitis

Do not delay antibiotics for CT scan or LP ( ceftriaxone

+ vancomycin). Perform CT scan before LP if the patient

meets criteria as listed previously. N steroids should be

given empirically to adult patients in whom meningitis is

strongly suspected.

Intracranial Bleed

Emergent neurosurgical consultation is required for evacuation of subdural or epidural bleed. Fresh-frozen plasma

should be administered if the patient is coagulopathic.

Severe uncontrolled hypertension should be treated.

General recommendations include reduction of the mean

arterial pressure by 25% or to < 150/90.

Complaint of

headache

History & physical exam

Red flags present?

Benign headache

Treat symptoms

and refer

A. Figure 80-2. Headache Diagnostic algorithm. CT, computed

tomography; ESR, erythrocyte sedimentation rate; LP, lumbar puncture.

 

 These patients require admission.

� Discharge

Most patients with dental trauma can be discharged to

follow-up with a dentist. Patients with minor odontogenic

abscesses can be discharged after incision and drainage by

either the treating emergency physician or a consulting

oral surgeon. These patients will require oral antibiotics

and follow-up.

SUGGESTED READING

Beaudreau RW. Oral and dental emergencies. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 201 1, pp. 1 572-1583.

Costain N, Marrie TJ. Ludwig's angina. Am J Med. 20 1 1;124:

1 1 5-1 1 7.

Douglass AB, Douglass JM. Common dental emergencies. Am

Pam Physician. 2003;67:5 1 1-5 16.

Nguyen DH, Martin JT. Common dental infections in the

primary care setting. Am Pam Physician. 2008;77:797-802.

Altered Mental Status

Moses S. Lee, MD

Key Points

• Do not delay bedside glucose determination, administration of glucose, and naloxone, if indicated. These

interventions may prevent the need for endotracheal

intubation.

• Ta lk to the paramedics and fami ly; they can often

identify the cause of altered mental status (AMS).

INTRODUCTION

Altered mental status (AMS) may have an organic (ie,

structural, biochemical, pharmacologic) or functional (ie,

psychiatric) cause. AMS accounts for So/o of emergency

department (ED) visits. About 80% of patients with AMS

have a systemic or metabolic cause, and about l So/o have a

structural lesion.

Consciousness has 2 main components: arousal and

cognition. Arousal is controlled by the ascending reticular

activating system (ARAS) in the brainstem. Cognition is

controlled by the cerebral cortex. Lethargy, stupor, obtun ­

dation, and coma are imprecise terms used to describe

alterations of arousal. A description of the patient's arousal

level (eg, opens eyes to voice) is preferable. Delirium is an

alteration of both arousal and cognition. Patients exhibit

restlessness, agitation, and disorientation. Dementia is an

alteration of cognition, not arousal.

ARAS is a complex system of nuclei in the brainstem. It

may be impaired by small structural lesions in the brain -

stem such as ischemic or hemorrhagic stroke, shear forces

from head trauma, or external compression from brain

herniation. Severe toxic and/or metabolic derangements

( eg, hypoxia, hypothermia, drugs) can also cause impairment. Bilateral cerebral cortex dysfunction must occur to

cause decreased levels of arousal or profound AMS. This is

• Identify level of AMS, systemic conditions, and any focal

deficits with the physical examination.

• Re-examine your patients frequently and note any

cha nges in condition and response to therapy.

usually caused by toxic/metabolic derangements, infection,

seizures, subarachnoid hemorrhage (SAH), or increased

intracranial pressure (ICP). Unilateral lesions such as

stroke do not by themselves cause profound AMS.

CLINICAL PRESENTATION

� History

AMS represents a spectrum of disease presentations from

profoundly depressed arousal requiring emergent intubation to severe agitation and confusion requiring restraint

and sedation. Initial stabilizing measures are often needed

before a complete history and physical examination can be

performed.

If the patient is unable to give a coherent history, alternate sources of history should be sought. Prehospital providers should be questioned about the patient's condition

in the field, therapies given and the response, and the

condition of the home environment ( eg, pill bottles, sui ­

cide note). Family members should be contacted to ascertain past history of similar episodes, medical history,

trauma, substance abuse, and the last time the patient was

seen in a normal state. The patient's belongings should be

searched for medical identification bracelets, pill bottles,

phone numbers, or other potential sources of information.

332

ALTERED MENTAL STATUS

Patients presenting to the ED with AMS often include

the elderly, who are more prone to infection, have comorbid illnesses, and take multiple medications; substance

abusers ( eg, heroin, cocaine, alcohol withdrawal, and liver

failure); and psychiatric patients who may be on moodstabilizing drugs, which, when taken in excess, have t oxic

effects that cause abnormal arousal or cognition.

.... Physical Examination

Vital signs; airway, breathing, and circulation (ABCs);

pulse oximetry; and bedside glucose should be assessed,

looking for immediate life threats and treatable causes of

AMS (ie, hypoglycemia, hypoxia or abnormal respiratory

pattern, hyper- or hypotension, hyper- or hypothermia).

Naloxone (Narcan), glucose, and thiamine should be

administered, as dictated by history and examination.

A "head-to-toe" examination should follow, looking for

systemic causes of AMS and focal neurologic deficits. The

head should be examined for any signs of trauma. Pupil size,

symmetry, and reactivity should be assessed. Pinpoint pupils

are a sign of opiate overdose or pontine hemorrhage. An

asymmetrically dilated "blown" pupil is a sign of uncal herniation. Fundi should be assessed for the presence of papilledema or subhyaloid hemorrhage associated with SAH.

Neck stiffness indicates meningeal irritation caused by either

SAH or infection. Cardiovascular exam should assess for

dysrhythmias (atrial fibrillation), murmurs (endocarditis),

or rubs (pericarditis). Lung exam should assess for symmetric breath sounds, respiratory rate, wheezes, rhonchi, and

rales. Abdominal exam should assess for masses and organomegaly (alcoholic liver disease, splenic sequestration in

sickle cell disease). Skin exam should assess for color, turgor

(dehydration), rashes (petechiae, purpura suggesting thrombotic thrombocytopenic purpura or meningococcemia),

and infection (cellulitis, fasciitis). If the neurologic examination cannot be completed because of the patient's mental

status, document what you are able to do and how the

patient appears. Mental status assessment should include

AVPU (alert, responds to voice, responds to pain, unresponsive). If the patient responds to voice, the appropriateness

and coherence of the response should be documented. The

cranial nerves, motor, deep tendon reflexes (including

Babinski or plantar reflex), cerebellar, and sensory examinations should be included if possible.

DIAGNOSTIC STUDIES

.... Laboratory

Multiple laboratory tests are obtained in an attempt to gain

more information, although a cause can usually be

ascertained from a thorough history and physical

examination. Initial laboratory tests should include complete blood count (leukocytosis, anemia, and

thrombocytopenia); chemistry (electrolyte abnormalities,

acidosis, and renal failure); urine (pregnancy test,

toxicology screen, infection); coagulation and liver studies

(liver failure, coagulopathy); blood cultures (if infection

suspected); arterial blood gas (hypoxia, hypercarbia, acidosis, and lactate); alcohol level; and serum t oxicology screen.

.... Imaging

Head computed tomography ( CT) scans should be performed to assess for mass lesion, hydrocephalus, and

intracerebral or subarachnoid bleed. Include a chest x-ray if

hypoxia, abnormal respirations, or evidence of pulmonary

infection is present. Electrocardiogram should be performed on all patients, looking for ischemia, QT or QRS

prolongation, or changes consistent with electrolyte

abnormalities.

PROCEDURES

A lumbar puncture may be indicated when considering a

central nervous system infection or bleeding after a

negative head CT scan.

MEDICAL DECISION MAKING

A systematic approach to the altered mental status patient

and the recognition oftreatable causes (mnemonicAEIOUTIPS) will provide optimal management (Figure 79-1 and

Table 79- 1). History, physical examination, and initial

laboratory and imaging tests will often reveal the cause of

mental status change.

TREATMENT

ED patients withAMS should be treated for any life-threatening

abnormalities while ongoing patient assessment continues.

Hypoglycemia, a common cause of AMS, should be treated

with intravenous (N) dextrose: adults: 1 amp DSO (50% glucose solution), pediatrics: 2-4 mL/kg D25 (25% glucose solution). Hypoxic patients should receive oxygen therapy

(administer 100% 02, mechanical ventilation as needed) while

searching for a potential cause (pneumonia, congestive heart

failure, pneumothorax, pulmonary embolism). Patients with

Table 79-1. AEIOU TIPS differential diag nosis

of patients with AMS.

A-Alcohol

E-Epilepsy, Electrolytes, Encephalopathy (HTN and hepatic)

1-lnsulin (hypo- and hyperglycemia), Intussusception (peds)

0-Qpiates, Overdose

U-Uremia

T-Trauma, Temperature (hypo- and hyperthermia)

1-lnfection, Intracerebral hemorrhage

P-Psychiatric, Poison

S-Shock

CHAPTER 79

ABCs

Bedside glucose

naloxone/th iamine

IV /0/monitor

History

Improvement with

naloxone or glucose, treat t-- ll>f underlying hypog lycemia

or opiate overdose

From patient, paramedics,

friends, family

Physical exam

· Abnorma l vita l signs (fever,

hypotension)

• Foca l neurologic finding

• Hypoxia, abnormal respirations

Head CT, lab studies,

CXR, ECG, LP 1-----l�

Etiology determined

Admit and treat

Etiology undetermined

Admit for further testing

Figure 79-1. Altered mental status diag nostic algorithm. ABCs, airway, breathing, and

circu lation; CT, computed tomography; CXR, chest x-ray; ECG, electroca rd iogram; GCS, Glasgow

coma scale; LP, lumbar puncture.

suspected opiate overdose (history or pupillary examination)

should be treated presumptively: adults: naloxone 2-4 mg N

given in 0.2- to 0.4-mg increments to avoid precipitating opiate withdrawal in chronic abusers. In a nonemergent setting,

administer naloxone 2-4 mg in a nebulizer with 3 mL of saline.

Pediatric patients should receive naloxone 0.01-0.1 mglkg N.

Actively seizing patients should receive N benwdiazepines:

diazepam 0.1-0.2 mglkg N (or 0.5 mg!kg per rectum) or

lorazepam 0.1 mg!kg N. Patients with suspected meningitis or

sepsis should receive N fluid resuscitation and broadspectrum antibiotic coverage. If hypertensive encephalopathy

is a suspected cause for AMS, the mean arterial pressure should

be reduced by 25% in 30 minutes with N antihypertensive

medications.

DISPOSITION

..... Admission

Most patients with AMS who are not immediately treatable

require admission to the hospital for further work-up, therapies, and observation. The level of admission (observation

unit, floor, telemetry, intensive care unit) should be guided

by the patient's vital signs, reassessments in mental status,

abnormalities identified, and comorbid illnesses.

ALTERED MENTAL STATUS

..... Discharge

Patients with hypoglycemia caused by insulin, who are able

to eat and remain normoglycemic after a period of obser ­

vation, may be safely discharged. If on long-acting oral

hypoglycemics, patients require admission for observation.

For patients with narcotic overdose, discharge is appropriate if the patient improves with naloxone and remains

stable after the duration of action of naloxone has elapsed

(ie, 1-4 hours).

SUGGESTED READING

Huff JS. Altered mental status and coma. In: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 201 1, pp. 1135-1 1 42.

Lehman RK, Mink J. Altered mental status. Clin Pediatr Emerg

Med. 2008;9:68-75.

William K, Brady WJ, HuffJS, et al. Altered mental status: Evaluation

and etiology in the ED. Am ! Emerg Med. 2002;20:613-617.

Headache

joseph M. Weber, MD

Key Points

• Consider emergent causes of headache first.

• Have a low threshold to perform a computed

tomography (CT) scan on patients with a possible

emergent cause for their headache.

INTRODUCTION

Headache is the presenting complaint in 3-5% of all visits

to the emergency department (ED). Headaches are classically divided into primary headache syndromes (migraine,

tension, cluster) and secondary causes, which can range

from benign (sinusitis) to emergent (subarachnoid hemorrhage [SAH], meningitis, tumor with increased intracranial pressure [ICP]). In clinical practice, the emergency

physician attempts to classify a patient's headache as emergent or benign. The majority of headaches in patients

presenting to the ED have a benign etiology; however,

5-10% of patients have a serious or potentially life-threatening cause for their headache (Table 80- 1).

Brain tissue is insensate. In benign headache syndromes, pain originates from blood vessels, venous

Table 80-1 . Headache classification by incidence.

Type of Headache

Tension

Unknown cause

Migraine

Serious secondary cause

Life· threatening

Incidence (%)