Either decreased mental status or cranial

nerve dysfunction can compromise airway protection.

Check for spontaneous swallowing. Do not test gag reflex

as this may induce vomiting.

Note the patient's vital signs and breathing pattern. Low

blood pressure can mimic stroke symptoms. High blood pressure may be a cause or compensation. If you choose to lower

blood pressure later, it will be important to know the presenting baseline pressure. Cheyne-Stokes or apneustic breathing

may indicate severe brain injury. Hypoxia can cause strokelike symptoms in the absence of a actual vascular occlusion.

Other important questions to answer on the physical

examination include the following. Is the rhythm irregular

(atrial fibrillation)? Are there murmurs to indicate valvular

disease? Is there peripheral evidence of emboli (splinter

hemorrhages in nails, on the retina)? Are carotid pulses

palpable? Is there a bruit, indicating possible dissection or

plaque as a source of emboli?

Is there a fever? CNS infections can be confused with

stroke. Hypotension from sepsis can cause hypoperfusion and

mimic stroke. Is there evidence of head trauma or other injury?

Neurologic examination need not be comprehensive

initially. Tools such as the National Institute of Health

stroke scale (NIHSS) are available to "quantify" the

extent of the stroke and are widely available ( Table 82-2).

Table 82-2. National I nstitute of Health stroke sca le.

Category Patient Response Score

LOC questions Answers both correctly 0

Answers one correctly 1

Answers none correctly 2

LOC commands Obeys both correctly 0

Obeys one correctly 1

Obeys none correctly 2

Beat gaze Normal 0

Partial gaze palsy 1

Forced deviation 2

Best visual No visual loss 0

Partial hemianopsia 1

Complete hemianopsia 2

Bilateral hemianopsia 3

Facial palsy"' Normal 0

Minor facial weakness

Partial facial weakness 2

No facial movement 3

Best motor arm No drift 0

Right Drift <1 0 seconds

Left Falls <1 0 seconds 2

No effort against gravity 3

No movement 4

Best motor leg No drift 0

Right Drift <5 seconds 1

Left Falls <5 seconds 2

No effort against gravity 3

No movement 4

Limb ataxia* Absent 0

Ataxia in 1 limb

Ataxia in 2 limbs 2

Sensory No sensory loss 0

Mild sensory loss 1

Severe sensory loss 2

Neglect Absent 0

Mild 1

Severe 2

Articulation Normal 0

Mild 1

Severe 2

Language Normal 0

Mild aphasia 1

Severe aphasia 2

Mute or global aphasia 3

LOC, level of consciousness.

''Items deleted from the modified N I HSS.

CHAPTER 82

Do not delay imaging to perform the complete examination.

The details can be obtained after the computed tomography (CT). Focus on key components, including:

Level of consciousness. Is the patient alert, lethargic,

obtunded, or stuporous? Rapid decline may indicate

herniation.

Eye exam. Asymmetric pupils may indicate herniation or

midbrain involvement. Papilledema indicates increased

intracranial pressure or hypertensive encephalopathy.

Retinal hemorrhages or pale spots indicate emboli. Is there

a gaze deviation? Is there evidence of nystagmus?

Cranial nerve exam. The brainstem is a tightly packed

area, and it is extremely rare to have a stroke that involves

only one cranial nerve. Cranial nerve palsies on one side of

the body and contralateral motor/sensory findings are a

hallmark of brainstem strokes.

Motor exam. Assess for asymmetric weakness and classify

as normal, weak, or not moving at all. Check to see if the

deficit is greater in the face/arm distribution (MCA) or the

leg (ACA) or both (carotid bifurcation). Checking for pronator drift is a sensitive test for subtle weakness.

Sensory exam. Compare sensation to pain and light touch

bilaterally. The sensory exam is often limited by neglect,

receptive aphasia, or mental status. Subtle sensory deficits

may be uncovered by checking for extinction to bilateral

simultaneous light touch on the arms, legs, and face.

Reflexes. Initially reflexes are decreased in the involved

regions. Hyperreflexia may indicate old strokes. Assess for

asymmetric release reflexes such as a Babinski sign or myoclonic jerking when feet are pushed dorsally.

Cerebellar exam. If safe, have the patient walk. Look for

wide or narrow gait and perform a Romberg test. Check for

smooth controlled finger-to-nose, knee-heel-shin, and

rapid alternating movements to test cerebellar fine motor

control.

DIAGNOSTIC STUDIES

� Imaging

Noncontrasted head CT is currently the test of choice for

the initial evaluation of stroke patients. Most acute strokes

are not visible on CT. Its role is not to "rule in stroke;' but

rather to rule out other entities that would be a con traindication to fibrinolytic reperfusion therapy. Bleeding is an

obvious contraindication to fibrinolytics. Large strokes

that show early ischemic changes (edema) on the CT scan

are more likely to convert to hemorrhagic strokes and thus

are a relative contraindication to fibrinolytic treatment.

Plain CT is very sensitive for bleeding or mass effects from

other intracranial lesions (Figure 82- 1 and 82-2).

� Laboratory

Important lab studies include rapid blood glucose and coagulation studies (prothrombin time, partial thromboplastin

time). These must be ordered as quickly as possible after

Figure 82-1. CT sca n showing an ischemic

stroke. Note the hypodense area anterior and to

the right of the fourth ventricle (arrow).

Figure 82-2. CT sca ns showing hemorrhagic

stroke (a rrow).

patient arrival. Other common tests include complete blood

count, electrolytes, and renal function. Electrocardiogram

and cardiac enzymes are often ordered to assess for cardiac

causes of the event.

CEREBROVASCULAR ACCIDENT

PROCEDURES

No special procedures are required in stroke patients. It is

important, however, to avoid doing procedures that could

complicate the course of fibrinolytic treatment. Any central

lines should be placed in areas where bleeding can be

monitored and controlled with compression (jugular or

femoral, not subclavian). Peripheral IVs are preferred.

Do not perform a lumbar puncture unless there is a strong

suspicion of subarachnoid hemorrhage or meningitis as

the cause of symptoms.

MEDICAL DECISION MAKING

The first decision that should be considered with an ischernie stroke is eligibility for fibrinolytic reperfusion therapy (Figure 82-3). Critical factors include the following:

1. Is this truly an ischemic stroke (vs hemorrhagic or

other stroke mimic)?

2. Is the time of the onset of symptoms clear?

3. Are there exclusion factors?

4. Is your institution capable of TPA administration, or

do you need to transfer the patient to a stroke center?

History Er physical exam to distinguish typica l

stroke syndromes versus alternative causes

Assess for possibil ity of

thrombolysis

airway

compromise

Admit to general or

telemetry floor

Large infarct with

edema, sh ift and

possibility of ai rway

compromise

Neurosurgical

consultation

Figure 82-3. Cerebrovascu lar accident diagnostic algorithm. BP, blood pressure; CT, computed

tomography; ICU, intensive care unit.

CHAPTER 82

TREATMENT

First, do no harm. Limit further damage by paying attention to the details of supportive care. Intubate if the patient

is unable to protect his or her airway. Provide s upplemental oxygen for hypoxia (generally for 0 2 sats <95%; there is

some evidence that hyperoxia can worsen neuronal damage

by free radical oxidation). In addition, administer IV fluids

if the patient appears hypovolemic or is hypotensive. Aim

for euvolemia; volume overload can worsen cerebral

edema. Severely anemic patients may need blood transfusion to assure good oxygen-carrying capability. Be very

cautious lowering blood pressure, if you lower it at all.

Hypotension is much worse than hypertension. Blood

pressure control for ischemic strokes is not warranted

unless pressures are sustained above 220/120 mmHg.

Blood pressure control for hemorrhagic strokes has less

evidence, but many recommend controlling any blood

pressure over 1 50/90 mmHg.

� Ischemic Strokes

For patients with ischemic strokes or TIA, aspirin (325 mg

orally) helps prevent platelet aggregation. Do not give until

you assure that the patient does not have an intracranial

hemorrhage. If you think the patient might receive fibrinolytics, hold the aspirin for the first 24 hours. Consult a

neurologist and/or stroke team whenever available. If fibrinolytic therapy is administered, the FDA-approved dose is

Reteplase (rTPA) 0.9 mg/kg (max dose 90 mg). Ten percent

should be administered as a bolus, with the remainder of

the infusion over the next hour. Intensive care monitoring

is need for the first 24 hours after treatment. Any worsening of condition should prompt immediate cessation of the

infusion and repeat head CT.

� Hemorrhagic Stroke

Mitigate elevated intracranial pressure by elevating the

head of the bed to 30 degrees. Treat coagulopathy. Patients

on warfarin with high international normalized ratios

should be reversed with fresh-frozen plasma or prothrombin complex concentrate and vitamin K. Do not give

aspmn. Consult neurosurgery. Many intracerebral clots

will benefit from early clot evacuation. Implement seizure

precautions and consider antiepileptic administration in

consultation with the admitting team.

DISPOSITION

� Admission

All stroke patients should be admitted to the hospital.

Patients with large strokes, evidence of edema on CT scan,

or decreases in mental status are at high risk for decompensation and should be admitted to an intensive care unit

(ICU). All patients who receive fibrinolytic therapy should

be monitored in the ICU for the first 24 hours after treatment. Patients with evidence of arrhythmias or other car ­

diac causes for the stroke should be admitted to a

monitored setting. Patients with hemorrhagic strokes

should be admitted to an ICU setting with neurosurgical

consultation. In many hospitals, this will mean transfer to

a facility with higher levels of care. Patients with TIA

symptoms should be admitted to the hospital for an expedited evaluation.

� Discharge

Stable patients with obvious nonstroke etiologies may be

discharged home if other medical conditions do not war ­

rant admission. Ensure that the patient has a safe social

situation and appropriate follow-up.

SUGGESTED READING

G o S , Worman DJ. Stroke, transient ischemic attack and cervical

artery dissection. 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, 20 1 1, pp. 1 122-1 135.

Hoffman JR, Schriger DL. A graphic reanalysis of the NINDS

Trial. Ann Emerg Med. 2009;54:329-336.e35.

Tissue plasminogen activator for acute ischemic stroke. The

National Institute of Neurological Disorders and Stroke r t-PA

Stroke Study Group. N Eng! J Med. 1 995;333: 1581-1 588.

Seizu res and Status

Epilepticus

Amer Zia Aldeen, MD

Alison R. Foster, MD

Key Points

• Always check a bedside glucose level in seizure

patients.

• Monitor airway, breathing, and circulation in actively

seizing patients and intervene when needed.

INTRODUCTION

A seizure is an episode of abnormal neurologic function

caused by inappropriate, excessive activation of neurons in

the brain. Seizures account for up to 2% of emergency department (ED) visits and affect approximately 4 million people in

the United States. The incidence of seizures is highest among

those <20 and >60 years of age. Status epilepticus is continuous or intermittent seizure activity for more than 5 minutes

without recovery of consciousness. It has a mortality rate of

up to 20%. Half of all patients presenting to the ED in status

epilepticus have no prior history of seizures. ED management

of seizures should focus on cessation of seizure activity.

Seizures result from abnormal excitation or lack of inhibition of neurons in the brain. The cause may be primary

(idiopathic) or secondary, with an underlying etiology that

may be treatable such as hypoglycemia. In patients with a

known seizure disorder, the most common cause of recurrent seizures includes medication noncompliance, sleep

deprivation, alcohol or substance withdrawal, and infection. Secondary causes of seizures include head trauma,

stroke, intracranial infection or mass, electrolyte abnormalities, alcohol withdrawal, drug overdose, and eclampsia.

Seizures are classified as generalized or partial.

Generalized seizures are characterized by excitation of the

entire cerebral cortex and always cause alteration of mental

status. Generalized seizures can manifest as a staring spell

• Intravenous lorazepam is the drug of choice for actively

seizing patients.

• Search for a secondary cause of seizures in first-time

seizure patients and those with a known seizure

disorder who have new or different features.

(absence or petit mal), diffuse motor activity (tonic-clonic

or grand mal), or drop attacks (myoclonic, tonic, clonic, or

atonic). The postictal period refers to the time (lasting up

to 1 hour) after a generalized seizure when the patient

gradually returns to baseline mental status. The postictal

period often distinguishes generalized seizures from other

causes of sudden altered mental status such as syncope.

Partial seizures are caused by localized neuronal activation

that may remain localized or spread to involve other areas of

the brain (referred to as partial seizure with secondary generalization). Patients with simple partial seizures experience

brief focal motor or sensory symptoms without altered

mental status. Complex partial seizures are characterized by

altered consciousness with autonomic, sensory, motor, and/

or psychological manifestations (Table 83-1).

CLINICAL PRESENTATION

� History

While the history is performed, obtain a blood glucose level

in all patients with altered mental status, including those

suspected of having had a seizure. Hypoglycemic seizures

are easily treated with dextrose and do not respond to standard antiepileptic drugs. To determine whether a seizure

actually occurred, gather a complete and detailed history

from witnesses, emergency medical service, and the patient.

353