Emergency Medicine 4


Emergency Medicine 4

 

Table 4A.1. Primary headache treatment options

Medication Dose

Acetaminophen 325 mg tablets, up to 6 PO

Ibuprofen 200 mg tablets, 1-4 PO

Naproxen sodium 275 mg tablets, 2-3 PO at onset; may repeat 1-2 tabs in 2 h

Ketorolac 15-30 mg IV/IM

Sumatriptan 6 mg SQ; may repeat in 1 h (maximum 2 doses/day)

Prochlorperazine 5-10 mg slow IV push; may be repeated in 30-60 min

Metoclopramide 10 mg PO/IM/IV

Promethazine (Peds) 0.25 mg/kg 6-9 yr, max 25 mg

>9 yr, max 50 mg

DHE 0.5-1 mg IV/IM; may repeat in 1 h, up to 3 doses in 24 h

Pediatric dosing: 0.1-0.15 mg IM (6-9 yr); 0.2 mg IM (9-12 yr);

0.25-0.5 mg IM (12-16 yr)

Prednisone 80 mg PO, rapid taper over 1 wk

Dexamethasone 10 mg IV followed by 4 mg every 6 h; or 20 mg PO, rapid taper

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tried. Patients who suffer from chronic cluster without remissions or episodic

bouts lasting more than a few weeks may benefit from a 7- to 10-day course of

prednisone (60 to 80 mg/day), with a tapering dose the following week.

Secondary Headache

• Patients treated with any of the previously mentioned medications may experience

relief from their headache, despite having significant intracranial pathology as a cause

of their pain. Thus, response to therapy should not be used to distinguish primary

from secondary causes of headache.

• Treatment of secondary headache varies by etiology. Treatment of primarily neurologic

diagnoses will be described here. Management of neurosurgical, infectious, and

other causes is explained elsewhere.

• Giant-Cell Arteritis

• Giant-cell arteritis (temporal arteritis) is typically seen in patients over age 50 (with

a peak incidence in the 70s). The headache is usually in the temporal region (but

may occur anywhere) and variously described as continuous or intermittent, throbbing

or steady, boring, or aching. Associated symptoms include jaw claudication

(virtually pathognomonic, when present), amaurosis, malaise, anorexia, weight loss,

myalgias, arthralgias, fever, neuropathies, TIAs, and stroke. Patients often complain

of scalp tenderness, and examination may reveal a tender, indurated, warm,

temporal artery with reduced or absent pulse. If the diagnosis of temporal arteritis

is suspected, treatment with prednisone (1 mg/kg) should be initiated; improvement

in headache should be observed within 48 h. Intravenous methylprednisolone,

250 mg q6h, is recommended for patients with associated visual loss. Temporal

artery biopsy should be accomplished within 72 h of initiating treatment; however,

immediate treatment with steroids may prevent complications and should not be

delayed pending confirmation of the diagnosis.

• Benign Intracranial Hypertension

• Benign intracranial hypertension (pseudotumor cerebri) refers to a diffuse increase

in intracranial pressure, producing a diffuse headache, papilledema, and visual

changes. MRI or CT scanning reveals slit-like ventricles. Acetazolamide, with or

without a diuretic, may be sufficient for mild cases. Otherwise, prednisone may be

indicated. Refractory cases may require intermittent lumbar puncture or

lumboperitoneal shunting. Maintaining intracranial pressure at relatively normal

levels helps to protect against irreversible vision loss. The disease process is generally

self-limited and resolves within several months.

• Trigeminal Neuralgia

• Trigeminal neuralgia is described as unilateral jabs of lightning-like pain confined

to the areas of the face supplied by the second and third divisions of the trigeminal

nerve. Attacks may be precipitated by tactile or mechanical stimulation (e.g., brushing

the teeth), and last seconds to minutes. Oral carbamazepine is highly effective for

remission of symptoms (often within 24 h) but cannot be loaded; the initial dose is

100 mg PO BID, increased every 2 days by 100-mg increments (max. dose, 1.2 to

2 g/day). An acute attack may be aborted with intravenous phenytoin, 250 mg, and

the patient discharged on 300 mg PO at bedtime. Alternatively, parenteral narcotics

may be required.

• Post-Traumatic Headache

• Patients may experience headache within hours to days following trauma—in the

setting of a normal neurologic exam and CT scan—which may last for several weeks.

When post-traumatic headache is associated with other nonspecific symptoms (e.g.,

dizziness, vertigo, nausea and vomiting, difficulty with concentration, and labile

mood swings), the symptom complex is referred to as post-traumatic headache

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syndrome. NSAIDs are generally used as first-line therapy, with the addition of

sedatives, physiotherapy, psychotherapy, and—as a last resort—narcotics, if necessary.

Symptoms generally resolve within months.

• Post-Lumbar Puncture Headache

• Post-lumbar puncture headache is caused by leakage of CSF through the defect in

the dura caused by the spinal needle. The pain is aggravated by sitting or standing

and relieved with recumbency. Associated symptoms include orthostatic

lightheadedness, tinnitus, photophobia, anorexia, nausea, and vomiting. The incidence

of post-lumbar puncture headache is reduced by use of a small-gauge spinal

needle, as well as minimizing the amount of CSF removed; however, bed rest and

increased fluid intake immediately following the procedure have not been shown to

influence the course or duration of symptoms. Treatment includes rest and analgesics,

and symptoms are generally self-limited. For more severe cases, caffeine (500

mg in 1 L of normal saline administered over 1 h) may be effective. The dose may

be repeated once, if necessary. Finally, in persistent cases, consultation with anesthesiology

for an autologous epidural “blood patch” may be warranted.

Disposition

• Most patients who present to the ED with headache can be discharged home after

adequate pain relief has been achieved.

• Patients with status migrainosus—or any patient whose pain is not adequately controlled

in the ED—should be admitted.

• Patients with documented visual loss and suspected temporal arteritis should be admitted

for intravenous steroid therapy.

• Any patient with new-onset headache should have close follow-up with his/her primary

care provider (PCP) or the appropriate specialist. Patients with migraine or cluster headaches

should be encouraged to follow-up with their PCPs for consideration of prophylaxis.

• All patients should receive instructions on appropriate use of discharge medications

and explicit return precautions.

Part B: Motor Deficits

Anatomy

• Motor deficits can be caused by CNS or peripheral nervous system dysfunction.

• The motor unit is composed of an anterior horn cell, its motor axon, and muscle

fibers. The motor nerve fibers and the muscle fibers make up the presyntaptic and

postsynaptic components of the neuromuscular junction, respectively.

• Muscle contraction involves an action potential at the motor axon, causing an influx

of calcium that releases acetylcholine into the synaptic cleft; this results in an action

potential at the motor end plate, and subsequent depolarization of the postsynaptic

membrane and contraction of the muscle cell.

Scope of the Problem

• Based on the anatomy of the neuromuscular system, peripheral nervous system causes of

motor weakness correlate with involvement at 1 of 4 levels: the anterior horn cells,

peripheral nerve, neuromuscular junction, or the muscle fiber itself.

• Progressive motor weakness may be accompanied by sensory and autonomic dysfunction,

requiring rapid respiratory or hemodynamic stabilization.

Etiology

The following list is not exhaustive, but includes most etiologies encountered on

an emergency basis. The patient may have a known neurologic disease and present

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with an exacerbation or deterioration, or may have new-onset symptoms without a

prior diagnosis.

• CNS

• Multiple sclerosis (MS)

• Motor Neuron

• Amyotrophic lateral sclerosis (ALS)

• Poliomyelitis

• Peripheral Nerve

• Guillain-Barre syndrome (GBS)

• Tick paralysis

• Porphyric polyneuropathy

• Arsenic poisoning

• Paralytic shellfish poisoning

• Hypophosphatemia

• Neuromuscular Junction

• Myasthenia gravis (MG)

• Botulism

• Lambert-Eaton (LEMS)

• Hypermagnesemia

• Muscle

• Myoglobinuric myopathy

• Hypo- or hyperkalemia

• Toxic myopathy

• Dermato- and polymyositis

• Guillain-Barre syndrome is the most common form of acute inflammatory demyelinating

polyradiculoneuropathy (AIDP). The most frequent impairment results from immunologic

reaction against nerve roots, peripheral nerves, and cranial nerves. The typical

clinical manifestation is motor weakness beginning in the legs and ascending to the

arms, with symptoms evolving over a few days. Approximately 14% of patients will

present with symptoms beginning in the cranial nerves or arms, descending to the legs.

• Myasthenia gravis (MG) is characterized by the formation of antibodies to the

acetycholine receptor of the post-synaptic component of the neuromuscular junction.

Weakness and fatiguability are the predominant symptoms, with a predilection for the

ocular muscles. The proximal muscles of the limbs are affected more than distal muscles.

Oropharyngeal muscle involvement may impair speech, swallowing, or chewing. Respiratory

muscles (i.e., intercostals and diaphragm) are affected in one-third of patients,

leading to respiratory failure.

• Multiple sclerosis (MS) is a demyelinating disease of the axons in the CNS. Clinical

symptoms wax and wane and are attributed to discrete lesions in the CNS which are

“scattered in time and space.” In the presence of demyelinated axons, action potentials

are not conducted normally: edema and inflammation may impair action potential propagation

leading to “negative” symptoms (e.g., diplopia from CN VI paresis), while hyperexcitable

demyelinated axons may produce “positive” symptoms (e.g., Lhermitte’s sign).

• Idiopathic dysfunction of both upper and lower motor neurons (in the anterior horn

cells) contributes to the motor weakness seen in patients with amyotrophic lateral

sclerosis (ALS).

Risk Factors

• Two-thirds of patients with GBS recall an antecedent event, approximately 1 to 3

weeks prior to symptom onset. The most common is infectious (e.g., URI, flulike

symptoms, or diarrhea), but immunizations or surgery may predate the disorder.

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• Myasthenic crisis (i.e., exacerbation requiring ventilatory support) is often precipitated

by infection, changes in medications, pregnancy (or just before menses), or surgery.

• Lambert-Eaton Myasthenic syndrome (LEMS) is an autoimmune disorder affecting

presynaptic nerve terminals. Like myasthenia gravis, the characteristic weakness, fatiguability,

and pain primarily affects proximal muscles; unlike myasthenia gravis, cranial

nerves are only mildly impaired. An underlying malignancy (usually squamous

cell carcinoma of the lung) is present in 75% of male and 25% of female patients.

• First-degree relatives of patients with MS have a 15- to 20-fold greater risk of developing

the disease. Hyperthermia (resulting from underlying infection) may exacerbate

previous neurologic deficits, or precipitate new symptoms.

Diagnosis

History

• Determine the time course and the distribution of symptoms.

• Toxic or metabolic disturbances may have an abrupt onset; neoplastic, infective, or

inflammatory disorders may progress over days to weeks; hereditary, endocrinologic,

degenerative, or other neoplastic processes may cause symptoms which develop

over a period of months to years.

• Proximal muscle weakness causes difficulty getting up from a squatting position,

climbing or descending stairs, or washing or brushing the hair. Distal weakness of

the upper limbs may manifest as clumsiness or loss of fine motor skills (e.g., tying

shoelaces or buttoning).

• Patients with cranial nerve involvement may present with diplopia, dysarthria, or

impaired chewing or swallowing, with nasal regurgitation.

• Does the patient have a preexisting neuromuscular or systemic disorder? Have there

been any recent infections or immunizations?

• Patients with dystrophies may present with clinical deterioration; likewise, ALS

symptoms tend to worsen with concurrent illness (especially pneumonia). In addition,

patients with neuromuscular junction disorders (e.g., myasthenia gravis) suffer

exacerbations with illness or addition of pharmacologic agents. A history of

similar symptoms suggests familial periodic paralysis or myoglobinuria. Finally,

patients with connective tissue disorders are at risk for vasculitic neuropathy.

• The patient’s medications, social history, and recent diet should be ascertained.

• Ingestion of shellfish containing saxitoxin—specifically, mussels and clams from

both U.S. coasts during the summer months—may produce sensory deficits and

ascending paralysis within 30 min. Home-canned goods may contain botulinum

toxin. Symptom onset temporally related to new medications (e.g., oral contraceptives,

anti-epileptic drugs) may suggest porphyria. Patients on diuretics may become

hypokalemic. In the setting of renal insufficiency, a patient with a neuromuscular

junction disorder may experience increasing weakness after ingesting

magnesium-containing antacids. Myotoxicity has been attributed to several medications,

including cholesterol-lowering agents, colchicine, chloroquine, cyclosporine,

and L-tryptophan.

• Determine whether the patient has had any known exposure to toxins, chemicals,

solvents, or tick bites (e.g., in wooded areas).

• Are there any associated symptoms?

• Patients with GBS commonly report dysesthesias in the hands and feet prior to the

onset of weakness. They may also experience transient bladder paralysis (resulting

in urinary retention) and paralytic ileus. Abdominal pain and mental status changes

in the presence of motor weakness suggests porphyric polyneuropathy. Arsenic poisoning

causes an encephalopathy, in addition to systemic signs and symptoms. The

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pure motor weakness attributed to polymyelitis is accompanied by fever and

meningeal signs.

• Is there a family history of neuromuscular disease?

Vital Signs

• Patients with sensory GBS are at increased risk for autonomic nervous system instability,

manifesting as arrhythmias, orthostatic hypotension, and hypertension.

Physical Exam

• Note the patient’s general appearance. Confusion, in a tachypneic patient using accessory

muscles of respiration, suggests impending neuromuscular respiratory failure.

• Neck: The strength of the patient’s neck flexors (and the trapezius, responsible for

shoulder elevation) parallels that of the diaphragm.

• Chest exam may reveal clear breath sounds in a patient in respiratory distress from

motor weakness. A patient’s vital capacity can be grossly measured by asking him to

count as high as possible with one breath (normal >50).

• Paradoxical abdominal movements indicate diaphragm weakness.

• Neurologic Exam

• Upper motor neuron lesions are associated with weakness (or paralysis), spasticity,

increased deep tendon reflexes (DTRs), and a Babinski response. Lower motor neuron

lesions are characterized by weakness (or paralysis), hypotonia, loss of DTRs,

and normal plantar reflexes. Disorders of neuromuscular transmission exhibit normal

or reduced muscle tone; normal or diminished DTRs; and waxing and waning

weakness in a patchy distribution (i.e., not attributed to a single, discrete lesion)

with cranial nerve involvement; there are no sensory deficits. Myopathic processes

typically cause proximal >distal weakness; DTRs are normal until late in the course;

there is no impairment in sensation or sphincter function.

• Patients with GBS generally have symmetric limb weakness, and decreased or absent

deep tendon reflexes. Despite subjective paresthesias, there is minimal objective

sensory loss.

• Patients with myasthenia gravis who have ocular involvement have ptosis and extraocular

muscle weakness. Fatiguability can be measured by asking the patient to

look upwards for 2 min or by repeatedly testing the proximal muscles (e.g., deltoids

and iliopsoas).

• In contrast to myasthenia gravis, patients with LEMS show improvement with repeated

testing. The extraocular muscles are spared.

Evaluation

• Forced vital capacity is recommended to determine a patient’s respiratory status.

• Laboratory

• Arterial blood gas is helpful in determining ventilatory status.

• Urinalysis, BUN, and creatinine may reveal myglobin and renal insufficiency in the

clinical setting of rhabdomyolysis. Likewise, the creatine kinase (CK) may be elevated

in myopathies.

• Electrolytes, including calcium, phosphorus, and magnesium should be obtained.

• Patients with exacerbation of myasthenia gravis or MS should have a urinalysis and

urine culture, as well as a CBC.

• Lumbar puncture (generally not required in the ED) may be helpful in the diagnosis

of GBS. The CSF may be normal in the first 48 h after symptom onset; however,

within 1 wk, elevated CSF protein is noted (without pleocytosis).

• EKG

• EKG may reveal evidence of hypo- or hyperkalemia or an arrhythmia resulting

from the autonomic dysfunction associated with GBS.

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• Radiography

• Chest radiography may show evidence of pneumonia, atelectasis, an elevated

hemidiaphragm (resulting from weakness), or a malignancy. Occult respiratory

infection should be sought in any patient with MG or MS exacerbation.

• Consider head CT in patients with presumed myasthenia gravis (especially patients

with ocular symptoms) to exclude an intracranial mass producing similar

symptoms.

• Tensilon test

• Edrophonium (Tensilon) is a short-acting acetylcholinesterase inhibitor; patients

with myasthenia gravis generally have transient improvement in their motor

strength within minutes.

• Cholinergic side effects of edrophonium include excessive salivation, bradycardia,

and nausea. Cautious use (with atropine at the bedside) is warranted in

patients with heart or lung disease.

• An initial test dose of 2 mg is given intravenously. If the patient tolerates the medication

but shows no improvement over 1 min, an 8 mg dose is given and the

patient is observed for the next 3 to 5 min for a response. Patients in myasthenic

crisis will show improvement, while patients in cholinergic crisis will be worse.

Treatment

A rapid assessment of the patient’s airway, breathing, and circulation is critical in

patients presenting with motor weakness.

• Specific Treatment

• Guillain-Barre syndrome

• Hypotension generally responds to isotonic fluids. Hypertension should only be treated

if severe and persistent. Short-acting, ±-adrenergic blockers are recommended.

• Plasmapheresis and intravenous immune globulin (IVIG) have been shown to

be equally effective, and both are superior to supportive care alone.

• Myasthenia gravis

• Patients with myasthenia gravis may present in cholinergic crisis; in response to

increasing weakness, the patient increases his anticholinesterase medications, which

worsens the weakness. The presence of cholinergic signs—pallor, miosis, sweating,

nausea/vomiting and diarrhea, salivation, and bradycardia—helps to distinguish

cholinergic crisis from myasthenic crisis.

• Patients with mild exacerbation of MG (i.e., no respiratory or oropharyngeal

compromise) may be treated with prednisone, pyridostigmine, and an eye patch

(for diplopia).

• Moderate or severe MG is an indication for plasmapheresis (or IVIG), in addition

to predisone. If the vital capacity is <12 to 15 mL/kg, the patient should be

intubated. A source of infection should be sought and treated.

• Multiple sclerosis

• Any identifiable infection should be aggressively treated; in the presence of infection,

corticosteroids are not warranted. Symptoms will generally resolve when

the fever or infection is treated.

• Clinical deterioration without an identifiable cause (e.g., infection) is an indication

for high-dose corticosteroids (PO or IV). Optic neuritis warrants IV methylprednisolone.

Disposition

• Patients at risk for respiratory compromise should be admitted to the ICU. This includes

patients with vital capacity <35 mL/kg, or other evidence of diaphragmatic

weakness (e.g., weak neck flexors or trapezius muscles).

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• Patients with any other evidence of autonomic nervous system instability should be

admitted to the ICU.

• Patients with worsening symptoms of myasthenia gravis should be observed in the

ICU for respiratory and bulbar difficulties, including nasal regurgitation and choking

on food.

• Patients with MS exacerbations who are unable to tolerate oral medications or liquids,

require parenteral medications (i.e., antibiotics or steroids), or lack home support should

be admitted.

• Patients with mild MS exacerbations who are candidates for oral steroids or do not

require treatment (e.g., viral infections), and those with mild infections amenable to

outpatient management, may be discharged home. This decision should be made in

consult with the patient’s neurologist.

Part C: Altered Level of Consciousness

Scope of the Problem

The term “coma” is broadly used to refer to any alteration in consciousness. Normal

consciousness requires the integration of both wakefulness (or arousal) and

awareness (or cognition).

• The ascending reticular activating system, located in the pons, is primarily responsible

for arousal of the cerebral cortex.

• Impaired cognition is caused by total or near-total dysfunction of both hemispheres of

the cerebral cortex.

Etiology

Traumatic Subdural, epidural hematoma

Axonal shear injury

Hypovolemic shock

Vascular Hypertensive encephalopathy

Subarachnoid hemorrhage (SAH), intracerebral hemorrhage

Infarction

Venous occlusion

Basilar aneurysm, basilar migraine

Infectious Abscess, meningitis, encephalitis

Septic shock

Metabolic Hypo-, hyperglycemia

Wernicke’s encephalopathy

Hypoxia, CO2 narcosis

Hypo-, hypernatremia

Hypo-, hypercalcemia

Acidosis, alkalosis

Uremia

Hyperammonemia

Environmental Hypo-, hyperthermia

Toxic CO, cyanide, hydrogen sulfite poisoning

Alcohols, narcotics, sedatives

Anticonvulsants

Psychotropics

INH, heavy metals

Endocrine Hyper-, hypothyroidism

Pheochromocytoma

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Hematologic Anemia

Porphyria

Neurologic Neurogenic shock

Seizures, postictal state

Neoplastic CNS tumor

Carcinoid meningitis

Cardiac Cardiogenic shock

Autoimmune Cerebral vasculitis

Allergic Anaphylactic shock

Diagnosis

• History

• The patient is usually unable to give a reliable history. Alternative sources of information

include a purse or wallet, Medic-Alert bracelets or necklaces, prescription bottles,

prehospital personnel, police, family, friends, and neighbors.

• When, and under what circumstances, did the patient lose consciousness? When

was the last time the patient was observed in his usual state of health? Vascular

events frequently evolve over seconds or minutes. Some metabolic processes develop

over minutes to hours, while infectious and other metabolic disorders progress

over hours to days. A CNS tumor, abscess, or chronic subdural hematoma may

result in symptoms developing over days to weeks.

• Were there any preceding symptoms or events? A preceding state of confusion, without

focal neurologic symptoms, usually suggests a metabolic etiology.

• What are the patient’s medications and allergies? Is there a history of drug or alcohol

abuse?

• What is the patient’s medical history?

• Have there been any previous similar episodes?

• Vital Signs

• Rectal temperature is critical in patients with altered mental status. Hypothermia

may be environmental, or accompany alcohol or sedative intoxication, hypoglycemia,

sepsis, Wernicke’s or hepatic encephalopathy, or myxedema. Hyperthermia

may be due to heat stroke, seizures, malignant hyperthermia, anticholinergic intoxication,

pontine hemorrhage, sepsis or thyroid storm.

• The respiratory rate and character may vary but are only occasionally helpful in determining

the pathology responsible for a patient’s alteration in consciousness. Some of

the commonly described respiratory patterns are: (1) hyperventilation—resulting in

reduced pCO2—associated with hypoxia, metabolic acidosis, brainstem herniation,

salicylate overdose, and heptic encephalopathy; (2) hypoventilation—with CNS depressants,

uremia, diabetic coma, and elevated ICP; (3) ataxic breathing—irregular

rate and depth of inspirations and expirations—frequently precedes respiratory arrest;

(4) Cheyne-Stokes—crescendo-decrescendo respiratory rate and depth, alternating

with periods of apnea; and (5) apneustic breathing—bradypnea with a pause

at end-inspiration.

• Blood pressure will vary depending upon etiology and may be very low, normal or

elevated. Likewise, the pulse may also vary. Bradycardia and elevated blood pressure—

referred to as Cushing’s reflex—is seen in patients with elevated ICP.

• Examination

• C-spine immobilization should be maintained in any patient with suspected trauma,

and patients at risk for cervical injury with minor manipulation (e.g., rheumatoid

arthritis).

• The initial exam should focus on the patient’s stability. Is the patient maintaining his

airway? Is the patient’s breathing regular and effective? Does he have palpable pulses?

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Is there any external evidence of life-threatening pathology that needs to be addressed

immediately (e.g., dilated pupil suggesting herniation)?

• General appearance: Note the patient’s posture. Patients with hemispheric dysfunction

generally lie in normal positions. Brainstem lesions tend to be associated with

abnormal postures. The patient’s breath may smell of acetone (in diabetic ketoacidosis)

or alcohol. Completely undress, carefully inspect, and palpate the patient.

• HEENT: Check the scalp for signs of trauma, surgical scars, or a ventricular shunt.

Look at the conjunctivae for icterus or pallor. The ears should be examined for

hemotympanum. Is there a tongue laceration or dental trauma indicating seizure

activity?

• Neck: Listen for bruits. Check range of motion (only if the cervical spine has been

cleared). The absence of rigidity does not exclude the possibility of SAH or meningitis.

Does the patient have a surgical scar, suggesting a thyroidectomy (and possible

incidental removal of parathyroid glands)?

• Chest: Palpate for evidence of trauma. Listen for equal breath sounds throughout

the chest. Is there any evidence of acute or chronic pulmonary disease?

• Cardiac: Is there evidence of cardiogenic shock (e.g., dysrhythmias, murmurs, extra

heart sounds)?

• Abdomen: Palpate for intraperitoneal fluid, organomegaly, and pulsatile masses.

• Extremities: Does the patient have equal pulses bilaterally? Are there “track marks,”

indicating intravenous drug abuse? Range all joints to exclude injuries (e.g., posterior

shoulder dislocation incurred during a seizure).

• Skin: Examination of the skin may reveal evidence of renal failure (uremic frost);

hyperthyroidism (warm, moist, smooth skin); or hypothyroidism (cool, dry skin

with a yellow tint).

• Neurologic: The neurologic exam is limited to the patient’s level of consciousness,

eyes, spontaneous movements, and reflexes.

• The Glasgow Coma Scale was originally designed for use in accurately describing

the best response of a patient who sustained head trauma. However, despite

its limitations, it is widely used in nontrauma settings as well. Scores range from

3 (worst) to 15, with coma defined as a score <8 (unless the patient has spontaneous

eye opening).

Eyes Verbal Motor Score

No opening No sounds No movement 1

Open to noxious stimulus Unintelligible sounds Extensor response 2

Open to verbal stimulus Nonsensical speech Flexor response 3

Open spontaneously Confused Flexion withdrawal 4

Oriented Localizes noxious stimulus 5

Follows commands 6

• Examine the eyes at rest. Disconjugate gaze may localize the lesion to the pons or

cerebellum (vertical, “skew” deviation), CN VI (persistent adduction of one eye),

CN III (persistent abduction of one eye), or diffuse injury (conjugate upward

gaze is seen in anoxic encephalopathy). Note pupil size, symmetry, and reactivity.

Small pupils suggest an interruption of the sympathetic pathway, organophosphate

poisoning, opiate overdose, or a pontine lesion. Dilated pupils indicate

compression of CN III, anticholinergic overdose, or sympathomimetic

intoxication. Pupils that are normal in size but unreactive are seen with brainstem

(midbrain) lesions. Examination of the eyelids may reveal bilateral or unilateral

ptosis. Bilateral ptosis occurs in midbrain lesions (e.g., basilar artery embolism);

unilateral ptosis is seen with Horner’s syndrome and CN III palsy. Extraocular

movements can be assessed by eliciting the oculocephalic or oculovestibular reflex.

The oculocephalic (or doll’s eyes) maneuver should not be performed if the

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patient is at risk for cervical injury; instead, the more sensitive oculovestibular

(or cold-water calorics) reflex should be tested. A normal response (i.e., conjugate,

horizontal eye movements away from the direction of head movement, or

toward the side of the cold-water irrigation) indicates an intact brainstem. Abnormal

responses (e.g., no eye movement or downward deviation of the eyes)

suggest brainstem involvement or sedative drug intoxication.

• Cranial nerves: The corneal reflex involves both the afferent limb of CN V and the

efferent limb of CN VII. The presence or absence of a gag reflex (CN IX and X),

although important for airway protection, has no localizing value.

• Motor: Observe the patient for spontaneous movements. Unilateral movement

may suggest a focal neurologic deficit. The only evidence of nonconvulsive status

epilepticus may be subtle movement. Observe the patient’s response to a

noxious stimulus.

• Reflexes: Hyperreflexia and clonus suggest hemispheric dysfunction. Asymmetry

of reflexes may localize the deficit.

Differential Diagnosis

• Locked-in syndrome: syndrome of intact consciousness, with voluntary movement restricted

to opening and closing the eyes and moving the eyes in the vertical plane.

• Acute psychosis

• Psychogenic unresponsiveness

• Conversion reaction

• Malingering

Evaluation

• Pulse Oximetry

• Rapid assessment of the patient’s oxygenation status can be obtained with pulse

oximetry.

• Labs

• Bedside glucose testing should be done to exclude hypoglycemia, an easily treated

cause of altered mental status.

• An arterial blood gas will provide more information regarding the patient’s ventilatory

(pCO2) and acid-base status (pH, HCO3, and base deficit). In addition, a low

pO2 in the setting of a normal pulse oximetry value, as well as an elevated carboxyhemoglobin

level, are indicative of carbon monoxide poisoning.

• Electrolytes (including calcium), BUN and creatinine are routinely ordered. Serum

osmolarity, serum drug levels, ammonia, and TSH may be indicated based on the

history and physical exam.

• Selective ordering of serum levels of ethanol and other toxic alcohols and toxicology

screening may confirm or exclude intoxication. True coma is rarely caused by

ethanol levels under 250 mg/dL; patients suspected of acute intoxication but with

lower levels require further testing (e.g., head CT, LP) to search for another explanation

for their symptoms.

• Urinalysis and pregnancy testing should routinely be performed.

• Consider blood, urine, and throat cultures in any case where sepsis is a concern.

• Lumbar puncture for analysis of cerebrospinal fluid (CSF) is indicated in any patient

suspected of having a CNS infection or subarachnoid hemorrhage (after negative

head CT). This procedure is deferred when there is clinical evidence of increased

ICP.

• Electrocardiogram

• EKG may reveal a cardiac etiology (especially in the elderly) or evidence of other

pathology: “cerebral” T waves in SAH, Osborne or “J” waves in hypothermia, or

prolonged Q-T interval in hypocalcemia.

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• EEG

• Although not readily available, bedside EEG may be useful in suspected

nonconvulsive status epilepticus.

• Imaging

• Noncontrast head CT is the primary neuroimaging study and will identify intracranial

hemorrhage and some abscesses, tumors, and noninfectious inflammatory disorders.

Contrast-enhanced CT scans are more sensitive for abscess, tumor, and inflammatory

processes; it will also identify infectious or neoplastic meningeal disease.

• Chest radiography is useful in suspected pulmonary infections and malignancy and

is performed after endotracheal intubation for confirmation of adequate tube placement.

• MRI and CT are both insensitive in the first few hours after ischemic stroke.

Diffusion-weighted MRI, however, will detect acute infarction.

Treatment

• Maintain an adequate oxygen saturation. Consider intubation for airway protection

or maintenance of adequate ventilation.

• All patients with altered mental status of unknown etiology should receive thiamine 100

mg IV. Patients with hypoglycemia (also consider in patients with low-normal bedside

results) should receive 25 g of 50% dextrose IV (pediatric dosing: 25% dextrose, 0.5 g/

kg). Although some references recommend empiric administration of naloxone, selective

use guided by the history, vital signs, and physical exam is acceptable.

• Flumazenil is indicated only for acute benzodiazepine overdose. Indiscriminate use

may cause seizures in patients with cocaine or tricyclic toxicity or cause withdrawal

seizures in chronic benzodiazepine users.

• Hypotension should be treated with isotonic fluids and vasopressor agents, as needed.

An appropriate target mean arterial pressure is 90 to 100 mm Hg.

• Determining the etiology of hypertension, malignant hypertension, ischemic stroke,

or response to elevated ICP is crucial to guiding treatment (if any).

• Elevated intracranial pressure should be recognized early and managed with head-of-bed

elevation to 30 degrees (when practical), hyperventilation (target CO2 30-35), mannitol

0.5 g/kg (20% solution) infused over 5-15 min, and furosemide 1 mg/kg IV. Use of

medications will likely be in concert with neurosurgical consultation.

Disposition

• Patients in true coma require admission to an ICU with neurologic or neurosurgical

consultation, as appropriate. Patients with no clear etiology for their altered mental

status should be admitted, even if all symptoms have resolved.

• Patients with hypoglycemia, unrelated to insulin use, should be admitted for evaluation

to determine the cause of the episode (e.g., stroke, MI, sepsis in the elderly).

• Although admission is sometimes recommended for narcotic overdose (because of

the long duration of action of most narcotics compared to that of naloxone), this is

usually not practical. A period of observation in the ED (i.e., 4-6 h) is sufficient to

prevent recurrence of symptoms

• Acute ethanol intoxication requires observation until the patient is able to “walk and

talk.” This allows reassessment for concomitant illness or injury and ensures that the

patient is safe to leave.

• Patients with psychogenic “coma” may be discharged after resolution of symptoms.

Psychiatric consultation is indicated prior to discharge.

• Patients who are discharged home should have follow-up with a primary physician

within 24-48 h.

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Suggested Reading

1. Coma. In: Simon RP, Aminoff MJ, Greenberg DA, eds. Clinical Neurology 4th ed.

Stamford: Appleton and Lange, 1999.

2. Feske SK. Coma and confusional states: Emergency diagnosis and management. Neurol

Clin North Am 1998; 16:2.

3. Hamilton GC: Altered mental status—depressed level of consciousness. In: Hamilton

GC, ed. Presenting Signs and Symptoms in the Emergency Department. Baltimore:

Williams and Wilkins, 1993.

4. Wolfe R, Brown D. Coma. In: Rosen P, Barkin RM, eds. Emergency Medicine: Concepts

and Clinical Practice. 4th ed. St. Louis: Mosby-Year Book Inc., 1996.

Part D: Infections of the Central Nervous System

Basic Anatomy

• The central nervous system (CNS) is encased within three membranous layers, called

meninges. These meninges, from the outermost layer inward, are the dura mater, the

arachnoid, and the pia mater. The dura adheres to the inner surface of the cranium;

the arachnoid attaches to the inner surface of the dura; and the pia is attached to the

brain, following all of its contours. The space between the arachnoid and pia—the

subarachnoid space—is filled with cerebrospinal fluid (CSF).

• The cranial dura extends through the foramen magnum to become the spinal dura

mater. The spinal epidural space is located between the periosteum of the vertebrae

and the dura and is filled with fatty connective tissue and a vertebral venous plexus.

• The spinal arachnoid closely attaches to the inner surface of the dura, creating the subarachnoid

space between itself and the spinal cord that, like the cranial subarachnoid

space, is filled with CSF. The spinal cord ends (i.e., becomes the cauda equina) at about

the level of the disk between the first and second lumbar vertebrae; however, the spinal

dural sheath (and its arachnoid lining) ends at about the second sacral vertebra. The

large subarchnoid cistern, between these two points, is the site at which sampling of CSF

occurs (i.e., lumbar puncture) with relatively little risk of damage to the spinal cord.

Scope of the Problem

• Meningitis

• Meningitis is inflammation of the membranes of the brain or spinal cord, which

may accompany an infectious, neoplastic, toxic, or autoimmune process. Because

the precise etiology may not be evident in the emergency department, empiric treatment

for bacterial meningitis is of utmost importance.

• Despite early and aggressive use of antibiotics, the overall mortality rate remains at

25% for bacterial and fungal meningitis.

• The causative organism varies with the age, immune status, living conditions, travel

history, and overall health of the individual. However, with the decline in frequency

of Haemophilus influenzae meningitis as a result of the H. influenzae type b vaccine, S.

pneumoniae is now the most common cause in adults and children over one month

old. N. meningitidis is the second most common organism isolated in both age groups.

• Antibiotic resistance is a frequently observed trend, with increasing resistance of S.

pneumoniae to penicillin and third-generation cephalosporins.

• Long-term sequelae of bacterial meningitis include cognitive deficits, seizure disorders,

hearing loss, blindness, gait disturbances, focal motor deficits, and hydrocephalus.

• “Aseptic” meningitis refers to conditions in which there is CSF pleocytosis and a

clinical suspicion of meningitis, but with negative bacterial cultures. Typical etiologies

include viral meningitis, fungal infections, and drugs (e.g., NSAIDs, TMP-SMX,

and INH).

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• Encephalitis

• Encephalitis is inflammation of the brain parenchyma. It may coexist with viral

meningitis or it may present as a distinct entity, caused most commonly by arboviruses,

herpes viruses, and rabies. Listeria and cat-scratch disease are rare etiologies.

• Encephalitides caused by certain arboviruses (Japanese, Eastern equine, and St. Louis

encephalitides) are associated with high mortality rates and severe neurologic sequelae.

The death rate from HSV encephalitis has been reduced by acyclovir; however neurologic

deficits—including epilepsy, focal motor deficits, and altered mentation—are common.

• West Nile Virus

• West Nile virus, an arthropod-borne virus (arbovirus), may cause encephalitis, meningitis,

or meningoencephalitis. Patients at highest risk for symptomatic infection

include persons over age 50 and the immunosuppressed. Associated symptoms may

include fever, headache, nausea, vomiting, weakness, altered mental status, stiff

neck, and an erythematous rash. West Nile virus is not cultured from the CSF or

brain tissue, but IgM antibodies may be present in the CSF or serum. Alternatively,

PCR testing of the CSF for West Nile virus RNA may be positive.

• CNS Abscess

• CNS abscess denotes a circumscribed collection of purulent material, or a localized infection,

which may exist within the brain parenchyma (brain abscess); within the meninges

(epidural or subdural empyema); or within or surrounding the spinal cord (intramedullary

or epidural spinal abscess). Complications of intracranial abscess include epilepsy,

focal motor or sensory deficits, and intellectual deficits. Patients with spinal abscesses

may have residual motor or sensory deficits, or bowel or bladder dysfunction.

Risk Factors

• Meningitis

• As mentioned above, the most common pathogens in patients over one month of

age are S. pneumoniae and N. meningitidis; risk factors for other organisms are shown

in Table 4D.1.

• Encephalitis

• The means of access to the CNS varies according to the virus (Table 4D.2).

• CNS Abscess

• CNS abscesses develop as an extension of a contiguous infection (e.g., otitis media,

sinusitis, dental infection), or by hematogenous seeding from a remote site (e.g.,

pulmonary, endocarditis, osteomyelitis). Other risk factors include intravenous drug

abuse, neurosurgical procedures, and penetrating head injury. The causative organisms

vary according to the primary source of the infection and the immune status

of the patient (Table 4D.3).

Diagnosis

History

• The classic triad of fever, nuchal rigidity, and altered mental status is seen in approximately

two-thirds of patients with community-acquired bacterial meningitis.

All patients, however, will likely have at least one of these findings. Other signs and

symptoms which should cause one to suspect meningitis include headache, chills,

vomiting, myalgias/arthralgias, lethargy, malaise, focal neurologic deficits, photophobia,

and seizures. Elderly patients may present with subtle findings, frequently

limited to an altered sensorium. Fungal meningitides present with an atypical

constellation of symptoms, including headache, low-grade fever, weight loss, and

fatigue; similarly, tuberculous meningitis may be associated with fever, weight loss,

night sweats, and malaise, with or without headache and meningismus.

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• Other important historical factors include:

• Duration of symptoms: a fulminant course indicates a bacterial meningitis or aggressive

viral encephalitis, while a subacute presentation suggests a viral, fungal, or

parasitic infection.

Table 4D.1. Organisms causing meningitis

Population Additional Potential Pathogens

Neonate (<1 mo) Group B streptococci, E. coli, Listeria monocytogenes

1 mo to 50 yr H. influenzae (rarely), L. monocytogenes (unlikely)

Adults (over 50 yr), alcoholics, L. monocytogenes, Enterobacteriaceae

other debilitating diseases

Closed head injury with CSF leak S. aureus, Enterobacteriaceae, P. aeruginosa

Recent neurosurgical procedure S. aureus, S. epidermidis, other Streptococcus

or penetrating head injury species, Bacteroides fragilis, Enterobacteriaceae

CSF shunt infection S. epidermidis, S. aureus, Enterobacteriaceae,

diphtheroids, P. acnes

Splenectomy H. influenzae

Chronic otitis media Streptococcus species, Enterobacteriaceae

Bacteroides fragilis

Malignant otitis externa (diabetes) Pseudomonas species

Sickle-cell disease, diabetics Enterobacteriaceae

Immunosuppressed host L. monocytogenes, P. aeruginosa, Enterobac teriaceae,

S. aureus, H. influenzae, Streptococci, anaerobes,

Mycobacterium tuberculosis, Actinobacter spp.,

syphilis, Cryptococcus neoformans, toxoplasmosis,

Herpes simplex, Cytomegalovirus

Table 4D.2. Encephalitis, causative organisms

Virus Route of Entry

Arbovirus Mosquito bite; hematogenous spread

(California, W. Equine, E. Equine,

St. Louis, West Nile)

Herpes virus

Herpes simplex type 1 Skin lesions; retrograde neuronal spread

Varicella zoster Skin lesions; retrograde neuronal spread

E-B virus Mononucleosis

Rabies Animal bite; retrograde neuronal spread

Measles, mumps Post-infectious

Table 4D.3. Etiology of CNS abscess

Source of Infection Likely Pathogen

Local or remote infection

Sinuses, teeth Streptococci

Otitis media, pulmonary infection Bacteroides

Endocarditis S. aureus

Other sources Enterobacteriaceae, Nocardia (rarely)

Neurosurgical procedure, S. aureus, Enterobacteriaceae

penetrating head injury

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• Antecedent infection: recent otitis media, sinusitis, respiratory tract infection, pharyngitis,

or intracranial abscess may suggest recent colonization with, or contiguous

spread of, a particular organism.

• Recent course of antibiotics: may alter CSF analysis and clinical presentation.

• History of a penetrating or closed head injury, neurosurgical procedure (including

VP shunt placement), or congenital dural defect.

• Living conditions or epidemic exposure: college dormitories, military barracks, and

jails/prisons are typical areas for epidemics of N. meningitidis; exposure in day-care

centers, or to family members with a specific infectious disease (e.g., M. tuberculosis)

may suggest an otherwise atypical causative organism.

• Immune suppression: HIV, malignancy, splenectomy, or other immunologic deficits.

• Social history: alcohol or IV drug abuse, low socioeconomic status.

• Underlying medical conditions: sickle cell disease or thalassemia major, bacterial

endocarditis, cirrhosis, diabetes.

• Barrier disruption: VP shunt, central IV lines, loss of cutaneous integrity (including

prior varicella-zoster infection).

• History of mosquito or tick bite; exposure to animals at risk for rabies infection.

Examination

• Meningitis

• Evaluate the patient’s overall appearance and mental status.

• HEENT exam should include a search for evidence of trauma, surgery, infections

(otitis, mastoiditis, sinusitis, pharyngitis), or pupillary abnormalities. Note that

papilledema takes time to develop, and this finding can be absent in the majority of

patients with bacterial meningitis. In infants <12 mo of age, when meningeal signs

are unreliable, the anterior fontanelle should be evaluated for bulging.

• Test the neck for rigidity: Brudzinski’s sign (if the neck is passively flexed, flexion of

the hips occurs; or, on passive flexion of one hip, flexion of the other hip occurs);

and Kernig’s sign (resistance to passive extension of the knee). Neck stiffness is

often absent at the extremes of age, or in patients with altered levels of consciousness,

immunosuppressed, or partially treated disease.

• Examination of the chest may reveal a concurrent pneumonia.

• A new heart murmur may indicate endocarditis.

• Examination of the abdomen may suggest an infectious process, and thus a source

for bacteremia and meningitis or abscess.

• A complete neurologic exam must be documented, revealing a number of potential

abnormalities: isolated cranial nerve deficits (including ophthalmoplegia); focal motor

or sensory deficits; cerebellar dysfunction; and increased deep tendon reflexes.

Localizing signs are generally absent in bacterial meningitis; their presence suggests

the possibility of a focal infection, such as an abscess. The level of consciousness may

range from confusion or delirium to stupor or coma.

• The skin should be examined for the petechial or hemorrhagic lesions suggestive of

meningococcemia, or a rash characteristic of HSV, herpes zoster, or leptospirosis (purpura

and petechiae on the oral, vaginal, or conjunctival mucosa).

• Arthritis may be associated with N. meningitidis or, less commonly, other bacterial

meningitides.

• Encephalitis

• Clinical suspicion of encephalitis should be raised in the setting of new “psychiatric”

symptoms, cognitive deficits (especially memory disturbances and aphasia), acute confusion,

and movement disorders (e.g., choreoathetosis and parkinsonism).

• Abscess

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• Patients with CNS abscess often experience a delay in diagnosis as a result of nonspecific

presenting complaints.

• While headache is almost universally present, fever is seen approximately half of the

time.

• One-third of patients may have focal neurologic signs, including hemiparesis and

seizures.

• Increased intracranial pressure may cause vomiting, confusion, or altered levels of

consciousness in 50% of patients.

• Meningismus is noted on <50% of exams, while papilledema is present in one-third

of patients.

Evaluation

• Delay in the diagnosis of bacterial meningitis in the elderly, especially with nonspecific

symptoms, is responsible for the high mortality in this population. While urinalysis or

chest X-ray may indicate an infectious process outside the CNS, it is important to remember

that the diagnosis of meningitis still needs to be suspected—and aggressively

pursued—because of the risk of hematogenous spread of the involved organisms.

Laboratory

• Cerebrospinal Fluid

• Lumbar puncture (LP) should be performed whenever meningitis is suspected. If

there will be a delay in performing the LP, blood cultures should be drawn and

antibiotics administered empirically. Immediate LP may be contraindicated in the

following situations:

• Suspected HIV disease

• Focal neurologic exam

• Evidence of increased intracranial pressure

• Hemodynamic instability

• Overlying infection at the LP site

• Suspected coagulopathy

• Suspect subarachnoid hemorrhage

• An opening pressure, if measured, should be performed with the patient fully extended.

Normal adult pressures are 5-19 cm H2O, when the patient is in the lateral recumbent

position. Opening pressure may be elevated in bacterial and fungal meningitis.

• The cerebrospinal fluid is normally clear and colorless. Infection, inflammation, or

bleeding may cause the fluid to be turbid. Note that fluid can be clear even when

several hundred cells are present.

• True CNS bleeding (e.g., a subarachnoid hemorrhage) may be distinguished from a

traumatic tap by the presence of xanthochromia. In addition, RBC count will generally

decrease in sequential tubes with a traumatic tap.

• CSF analysis should include cell count and differential, glucose and protein, stat

gram’s stain and culture, and a fourth tube for special tests as indicated by the

clinical scenario.

• Normal adult CSF contains <6 WBCs/mm3, with no more than one PMN. Early

in the course of bacterial meningitis, lymphocytes may predominate.

• CSF analysis in viral meningitis and encephalitis typically reveals <500 WBCs/

mm3, with almost 100% mononuclear cells (but early presentations may have

PMN pleocytosis).

• Brain abscess and parameningeal infections (e.g., subdural empyema, epidural

abscess) have cell counts and differentials similar to those of viral meningitis.

• The normal ratio of CSF:serum glucose is 0.6 (0-0.4 in the setting of severe hyperglycemia).

CSF glucose may be decreased in bacterial, fungal and tuberculous

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meningitis; carcinomatous meningitis, and (normal or decreased) in subarachnoid

hemorrhage. Mild decreases in CSF glucose may be seen in viral and parameningeal

processes.

• CSF protein levels are normally <45 mg/dl in adults. An elevated protein, usually

>150 mg/dl, is suggestive of bacterial meningitis. Other causes of elevated CSF protein

include any infectious meningitis, viral or parasitic encephalitis, carcinomatous

meningitis, subarachnoid hemorrhage, CNS vasculitis, neurosyphilis, hepatic encephalopathy,

and demyelination syndromes.

• Other tests to consider include viral cultures, acid-fast stain and culture for M. tuberculosis,

India ink and cryptococcal antigen, VDRL, cytology, bacterial antigens for S.

pneumoniae, H. influenzae, and N. meningitidis (especially in patients recently treated

with antibiotics), and Borrelia antibodies in cases of suspected Lyme disease. Other

more specialized tests are rarely ordered in the ED.

• Blood Tests

• Although a CBC with differential may add to the clinical picture in a patient with

suspected meningitis, a normal result does not exclude the diagnosis.

• PT and PTT may be useful to exclude a suspected coagulopathy, or DIC.

• Serum electrolytes, BUN/Cr, and glucose are routinely ordered.

• Blood cultures (two specimens, collected 15 min apart) may identify the organism

in up to 80% of cases depending upon the etiology.

• Imaging

• A CT scan of the head should be performed prior to LP in the following situations:

• Altered mental status

• Focal neurologic exam (excluding ophthalmoplegia)

• Evidence of increased intracranial pressure

• Minimal or absent fever

• Recent-onset seizure

• Suspected subarachnoid hemorrhage or intracranial mass lesions

• Contrast-enhanced CT is the study of choice for evaluation of possible CNS abscess.

Although not readily available, MRI is equally sensitive.

• MRI is the imaging study of choice when cranial epidural abscess or subdural empyema

is suspected.

• A chest X-ray may reveal a concomitant pneumonia, especially in cases of pneumococcal

meningitis.

• EEG

• In the setting of suspected herpes encephalitis, focal or lateralized EEG abnormalities

may help pinpoint the diagnosis.

Treatment

• Meningitis

• Administration of IV antibiotics should begin as soon as the suspicion of bacterial

meningitis is entertained. Empiric therapy should be based on the suspected pathogen,

taking into consideration the patient’s age and risk factors for specific organisms.

An infectious disease consultant may be helpful for information regarding

local drug resistance patterns (Table 4D.4).

• Encephalitis

• Herpes simplex and varicella encephalitis are the only treatable forms of encephalitis.

Acyclovir is dosed at 10mg/kg IV q8 h.

• CNS Abscess

• The mainstay of treatment of CNS abscess is antibiotics. Neurosurgical consultation

is recommended for possible aspiration or excision (Table 4D.5).

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• Specific Treatment

• Meningitis

• Glucocorticoids, based on studies in children with predominantly H. influenzae

type b meningitis, have been shown to reduce the morbidity associated with an

inflammatory reaction to bacteriolysis. Dexamethasone, 0.15 mg/kg IV, may be

considered in children as well as adults, especially in cases with positive Gram’s

stain (indicating a high bacterial load), altered level of consciousness, or increased

intracranial pressure. If dexamethasone is given, benefit is greatest when started

prior to or concurrent with initial antibiotic therapy.

• In areas with high prevalence of drug-resistant S. pneumoniae, vancomycin is

added empirically.

• In penicillin-allergic patients, trimethoprim-sulfamethoxazole and vancomycin

are recommended.

• Amphotericin B and flucytosine are the drugs of choice for cryptococcal meningitis.

• Initial therapy for tuberculous meningitis should include isoniazid (INH),

rifampin, ethambutol, and pyrazinamide (PZA).

Table 4D.4. Empiric antimicrobial therapy for meningitis

Population Empiric Therapy

Neonate (0-7 days) Ampicillin + Cefotaxime or

Ampicillin + Gentamicin or

Ampicillin + Amikacin

Neonate (8-28 days) Ampicillin + Cefotaxime

1 mo to 50 yr Vancomycin + Ceftriaxone or

Vancomycin + Cefotaxime

Adults (over 50 yr) Ampicillin + Ceftriaxone + Vancomycin or

Ampicillin + Cefotaxime + Vancomycin

Recent neurosurgical procedure, Vancomycin + Ceftazidime

penetrating head injury, CSF leak

CSF shunt infection Peds: Vancomycin + Cefotaxime or

Vancomycin + Ceftriaxone

Adults: Vancomycin + Rifampin

Immunosuppressed host Ampicillin + Ceftazidime +Vancomycin

Suspected HSV 2 meningitis Acyclovir

Table 4D.5. Antibiotic therapy of CNS abscess

Source Empiric Therapy

Otogenic Ceftriaxone + metronidazole or

Cefotaxime + metronidazole

Sinogenic, odontogenic Penicillin G + metronidazole

Remote infection Penicillin G + metronidazole

Post-surgical, head trauma (Cefotaxime or Ceftriaxone) + nafcillin or

(Cefotaxime or Cefotaxime) + oxacillin or

(Cefotaxime or Ceftriaxone) + vancomycin (MRSA)

Unknown source Ceftriaxone + metronidazole or

Cefotaxime + metronidazole

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• If the CSF pressure is >40 cm H2O, consider giving mannitol. Only the CSF in

the manometer should be collected, to reduce the risk of tentorial herniation.

Patients with clinical and CT evidence of increased intracranial pressure also

require appropriate therapy.

• Complications of meningitis should be anticipated and managed including dehydration,

hypotensive shock, hyponatremia, coagulopathies, seizures, cerebral

edema, loss of protective airway reflexes, respiratory failure, and stroke.

• Close contacts of patients diagnosed with H. influenzae type b or N. meningitidis

should receive prophylactic treatment. Health care personnel coming into contact

with respiratory droplets are also candidates for prophylaxis (Table 4D.6).

• Encephalitis

• Post-infectious encephalomyelitis—an acute inflammatory, demyelinating process

preceded by infection or immunization with influenza, measles, and varicella—

is treated with high-dose intravenous methylprednisolone.

• Bacterial causes of encephalitis include Listeria, Lyme disease, Rocky Mountain

Spotted Fever (RMSF), Leptospirosis, and the Ehrlichioses.

• Immunocompromised patients are at increased risk for amebic encephalitis, toxoplasmosis,

and CMV, in addition to the herpes viruses. Empiric therapy of encephalitis—

in addition to acyclovir—is shown in Table 4D.7.

• CNS abscess

• Although not a true abscess, focal lesions in the brain parenchyma attributable

to toxoplasmosis in the immunocompromised patient are treated with

pyrimethamine plus sulfadiazine. Patients with sulfa allergies are treated with

pyrimethamine plus clindamycin. If a fungal abscess is suspected, amphotericin

B should be added to the empiric regimen.

• Treatment of epidural abscess and subdural empyema includes surgical drainage

and intravenous antibiotics, as described above for empiric therapy of CNS abscess.

Table 4D.6. Meningitis prophylaxis

Organism Treatment

H. influenzae type b: Rifampin, 20 mg/kg PO (up to 600 mg) q 12 h for 4 doses

N. meningitidis: Peds: Rifampin 10 mg/kg PO q 12 h for 4 doses or

Ceftriaxone 125 mg IM, single dose

Adults: Rifampin 600 mg PO q 12 h for 4 doses or

Azithromycin 500 mg PO, single dose

Ciprofloxacin 500 mg PO, single dose or

Ceftriaxone 250 mg IM, single dose

Table 4D.7. Encephalitis, empiric therapy

Organism Treatment

Lyme disease Ceftriaxone

RMSF Peds <8 yo: Chloramphenicol

Adults: Doxycycline

Leptospirosis Penicillin G

Ehrlichiosis Doxycycline

Amebae Amphotericin

CMV Gancylcovir or foscarnet (more toxicity)

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Disposition

• All patients with suspected bacterial meningitis, encephalitis, or CNS abscess are admitted.

• Patients definitively diagnosed with viral meningitis, if the social situation permits, may

be discharged if associated symptoms (e.g., pain, vomiting) are controlled.

Suggested Reading

1. Disorders of consciousness approach to diagnosis and acute confusional states. In: Simon

RP, Aminoff MJ, Greenberg DA, eds. Clinical Neurology 4th ed. Stamford, Appleton

and Lange, 1999.

2. Gilbert DN, Moellering RC, Sande MA, eds. The Sanford Guide to Antimicrobial

Therapy. 32nd ed. Hyde Park: Antimicrobial Therapy Inc., 2002.

3. Lavoie FW. Meningitis, Encephalitis, and Central Nervous System Abscess. In: Rosen P,

Barkin RM, eds. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis:

Mosby Year Book Inc., 1996.

4. Pruitt AA. Infections of the Nervous System. Neurol Clin North Am 1998; 16:2

Part E: Cerebrovascular Emergencies

Basic Anatomy

• The anterior circulation, consisting of the paired internal carotid arteries and their

branches (ophthalmic, anterior cerebral, and middle cerebral arteries), supplies most

of the cerebral hemispheres and the deep cortical gray matter.

• The anterior cerebral artery (ACA) supplies the parasagittal cerebral cortex, which

includes portions of the motor and sensory cortex related to the contralateral lower

limb and the so-called bladder inhibitory or micturition center.

• The middle cerebral artery (MCA) supplies most of the remainder of the cerebral

hemisphere, and deep cortical structures.

• The cortical branches of the MCA include the superior division, which supplies

the entire motor and sensory cortical representation of the face, and upper limb;

and the expressive language (Broca’s) area of the dominant hemisphere.

• The inferior division supplies the visual radiations, the region of visual cortex

related to macular vision, and the receptive language (Wernicke’s) area of the

dominant hemisphere.

• Lenticulostriate branches supply the basal ganglia, as well as motor fibers related

to the face, hand, arm, and leg.

• The posterior circulation, consisting of the paired vertebral arteries, the basilar artery,

and their branches—the posterior inferior cerebellar (PICA), anterior inferior cerebellar

(AICA), superior cerebellar, and posterior cerebral arteries—supplies the brainstem,

cerebellum, thalamus, and the medial aspects of the occipital and temporal lobes.

• The anterior and posterior circulations join via the posterior communicating arteries

to form the circle of Willis at the base of the skull.

Clinicoanatomic Correlation

• Anterior Circulation

• Anterior circulation strokes rarely have associated symptoms; neurologic deficits

accompanied by headache, nausea, and vomiting are more suggestive of intracerebral

hemorrhage or posterior circulation stroke.

• Clinical syndrome of ACA occlusion

• Contralateral weakness and sensory loss affecting the lower limb.

• Confusion and impaired cognition.

• Urinary incontinence.

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• Clinical syndrome of MCA occlusion

• Superior division stroke results in contralateral weakness and sensory deficit in

the face and upper limb.

• If the dominant hemisphere is involved, Broca’s aphasia occurs (impaired language

expression with normal comprehension).

• Inferior division stroke results in marked impairment of contralateral cortical

sensory functions, contralateral homonymous hemianopsia, and contralateral

neglect.

• If the dominant hemisphere is involved, Wernicke’s aphasia occurs (impaired

comprehension and recall, with fluent—but often nonsensical—speech).

• An acute confusional state may indicate involvement of the nondominant

hemisphere.

• Occlusion at the bifurcation or trifurcation of the MCA combines the features

of superior and inferior division stroke.

• Posterior Circulation

• Posterior circulation strokes frequently present more of a diagnostic challenge. In

addition, complications of cerebellar infarcts, such as edema compressing brainstem

structures, may cause rapid deterioration (i.e., within hours).

• Symptoms associated with vertebrobasilar infarcts include syncope, vertigo or

lightheadedness, nystagmus, dysphagia, dysarthria, facial sensory disturbance, ataxia,

depressed consciousness or confusion, and incontinence.

• Clinical syndrome of posterior cerebral artery (PCA) occlusion

• Contralateral homonymous hemianopsia.

• Ocular abnormalities (including oculomotor (III) nerve palsy and internuclear

ophthalmoplegia).

• With involvement of the dominant hemisphere, patients may be unable to name

objects or to read but retain the ability to write.

• Clinical syndrome of basilar artery occlusion

• Thrombosis is often incompatible with survival.

• Basilar artery thrombosis affects the pons and may be confused with pontine

hemorrhage.

• Coma is common.

• Hemiplegia or tetraplegia is usually present.

• The pupils are constricted but reactive.

• Involvement of the dorsal portion of the pons (i.e., the tegmentum) produces

unilateral or bilateral abducens (VI) nerve palsy; vertical nystagmus may be

present.

• Infarction of the ventral portion of the pons with sparing of the tegmentum

causes tetraplegia in a patient who remains conscious (referred to as the

locked-in syndrome). Voluntary eye opening, vertical eye movements, and

ocular convergence are preserved.

• Emboli usually stop at the top of the basilar artery, at the bifurcation into the

PCAs.

• Immediate loss of consciousness (or depressed LOC) is caused by impaired

blood flow to the reticular activating system.

• Hemiplegia or tetraplegia with decerebrate or decorticate posturing.

• Ipsilateral or bilateral oculomotor (III) nerve palsies.

• Clinical syndrome of PICA occlusion

• Results in lateral medullary (Wallenburg’s) syndrome

• Symptoms may include vertigo, nausea, vomiting, dysphagia, dysarthria, hoarseness

(due to vocal cord paralysis), and hiccup.

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• Neurologic exam may reveal nystagmus; ipsilateral Horner’s syndrome, paralysis

of the soft palate and posterior pharynx, and limb ataxia; and impaired pain/

temperature sensation in the ipsilateral face and contralateral limbs.

• The motor system is spared.

• Clinical syndrome of AICA occlusion

• Produces ipsilateral facial weakness, gaze palsy, deafness, and tinnitus.

• Clinical syndrome of superior cerebellar artery occlusion

• Hypertropia (deviation of the eyes in opposite directions equally).

• Contralateral sensory disturbance.

• Lacunar Infarction

• These infarcts occur in the deep gray and white matter structures (e.g., basal ganglia

and internal capsule); the onset may be subacute with symptoms developing over

hours or days.

• Headache is absent or minor; there is no impairment in level of consciousness.

• Pure motor hemiparesis: uniformly affects the contralateral face and limbs.

• Pure sensory stroke: contralateral hemisensory loss (may be associated with paresthesia).

• Dysarthria-clumsy hand syndrome: includes dysarthria, dysphagia, and contralateral

facial and hand weakness and clumsiness.

• Ataxic hemiparesis: consists of cerebellar ataxia and leg > arm > face weakness.

Scope of the Problem

• Disruption in the flow of blood to the brain results in ischemia and cell death. The

central area of infarction is surrounded by a region of salvageable tissue, referred to as

the penumbra.

• Mechanisms of ischemia include embolism, thrombosis, and hemorrhage. Identifying

the etiology of the patient’s symptoms is critical for determining therapy.

• Massive cerebral infarcts are typically associated with cerebral edema, which peaks 3 to

5 days after onset. Patients with such swelling are at risk for herniation.

Risk Factors

• Vascular Disorders

• Atherosclerosis

• Diastolic or isolated systolic hypertension

• Hyperlipidemia (hypercholesterolemia)

• Cigarette smoking

• Oral contraceptive use

• Diabetes mellitus

• Hereditary predisposition (i.e., family history of ischemic vascular disease at

age <60)

• Excessive alcohol use

• Physical inactivity

• Age

• Male gender

• Ethnicity

• Carotid or vertebral artery dissection

• Signs and symptoms of carotid dissection may include jaw or neck pain, visual

changes similar to those that accompany migraine headaches, and Horner’s syndrome.

• Vertebral or basilar artery dissection is associated with headache, posterior neck

pain, and acute brainstem dysfunction.

• Venous or sinus thrombosis

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• Patients with this disease process usually have a predisposing condition, such

as contiguous infection (e.g., otitis, sinusitis), hypercoagulable state, or dehydration.

• Clinical manifestations include headache, papilledema, depressed level of consciousness,

seizures, and focal neurologic deficits.

• Inflammatory disorders

• Giant cell arteritis, systemic lupus erythematosis, polyarteritis nodosa, granulomatous

angiitis (primary angiitis of the CNS), syphilitic arteritis, AIDS

• Drug abuse

• Cocaine, amphetamines, and heroin

• Infective endocarditis caused by IV drug abuse may lead to embolic stroke.

• Other forms of drug abuse are postulated to cause vasospasm, vasculitis, or rupture

of preexisting aneurysms or vascular malformations.

• Migraine

• Fibromuscular dysplasia

• Cardiac Disorders

• Mural thrombus

• Generally associated with myocardial infarction (MI) or cardiomyopathy.

• Rheumatic heart disease

• Arrhythmias

• Atrial fibrillation and bradycardia-tachycardia (sick sinus) syndrome

• Endocarditis

• Mitral valve prolapse: small increase in risk of stroke; massive strokes are rare

• Paradoxic embolus

• Embolic material from the systemic circulation may gain access to the brain

through a pathologic communication between right and left sides of heart (e.g.,

ASD, patent foramen ovale).

• Atrial myxoma

• Prosthetic heart valves

• Hematologic Disorders

• Thrombocytosis, polycythemia, sickle cell disease, leukocytosis (i.e., leukemia),

hypercoagulable states

Diagnosis

History

• Attempt to identify, as accurately as possible, the onset, course, and type of symptoms,

as well as the patient’s activity at onset.

• Determine the patient’s stroke risk factors, other potential causes for the patient’s symptoms,

and any contraindications to thrombolytics or other agents.

• Neurologic deficits that occur abruptly, and are maximal at onset, suggest an embolic

stroke. Stepwise, incremental deficits are more indicative of thrombosis.

• Hemorrhagic strokes often have a rapid onset. Maximum deficit may be present immediately

but worsening may occur. Consciousness may be impaired.

• Subarachnoid hemorrhage (SAH) is characterized by symptoms of variable onset and

progression; severe headache and neck stiffness; and often impaired consciousness.

Vital Signs

• Hypotension may be the underlying cause of a stroke; markedly elevated blood pressure

is suggestive but not diagnostic of a hemorrhagic stroke.

• An irregular cardiac rhythm may indicate chronic or new-onset atrial fibrillation and

an embolic source.

• Increased ICP may be accompanied by bradycardia.

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Physical Examination

• Focus on searching for an underlying systemic cause, especially a treatable one.

• HEENT

• Note any signs of trauma. Palpate the temporal arteries.

• Fundoscopic exam may reveal evidence of embolization. Papilledema indicates

increased ICP. Retinal hemorrhages may be noted in SAH.

• Determine patency of the airway and ensure the airway is protected.

• Neck: evaluate the carotid pulses and check for carotid bruits, Neck stiffness may or

may not be present in SAH.

• Cardiac exam: note any arrhythmias or evidence of valvular disease (i.e., murmurs).

• Neurologic exam

• The initial neurologic exam should be a brief search for signs of increased ICP or

impending transtentorial herniation (e.g., dilated pupil, depressed consciousness,

or posturing).

• Neurologic deficits that do not conform to the distribution of any single cerebral

artery suggest a hemorrhagic or mass lesion.

• Assess the level of consciousness and mental status. Determine whether the patient

has aphasia (expressive or receptive?) or dysarthria.

• Evaluate cranial nerve function, with special attention paid to pupils, extraocular

movements, visual fields, facial symmetry, gag reflex and corneal reflex.

• The presence of a gaze palsy may help localize the lesion. A patient with a cerebral

hemispheric stroke will typically gaze toward the side of the insult; a brainstem

infarct will cause the patient to gaze away from the side of the lesion.

• Motor exam: the most sensitive indicator of upper extremity weakness is the

presence of a pronator drift. Whenever possible, lower extremity strength should

be assessed by observing the patient’s gait.

• Sensory exam: peripheral sensation (light touch, pinprick, and vibration/position

sense). Double simultaneous stimulation: assess sensation on both sides of

the body simultaneously; patients with cortical infarcts will only notice the unaffected

side.

• Cerebellar exam: look for nystagmus, ataxia, or poor coordination.

• Reflexes: recent stroke is accompanied by hyporeflexia (and flaccidity). Search

for pathologic reflexes (e.g., presence of a Babinski reflex indicates an upper motor

neuron disorder).

Evaluation

• Pulse Oximetry

• Rapid determination of oxygen saturation may reveal impending respiratory failure

and the need for mechanical ventilation. Supplemental oxygen may suffice.

• Laboratory

• Bedside glucose testing is crucial to exclude hypoglycemia as a cause of focal neurologic

deficits.

• A complete blood count may reveal an underlying hematologic disorder presenting

as a stroke.

• Prothrombin time (PT) and partial thromboplastin time (PTT) are helpful in excluding

coagulopathy.

• Baseline serum electrolytes are recommended.

• An elevated ESR may suggest giant cell arteritis or other vasculitis.

• Blood for type and cross match (patients with SAH)

• Consider a toxicology screen in patients suspected of drug abuse (although the

results seldom change the patient’s acute management).

• Pregnancy test in females of child-bearing age.

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• Lumbar puncture (LP) is indicated when CNS infection or SAH is suspected. In

the case of SAH, LP is performed after a negative CT scan. LP may also suggest a

venous or sinus thrombosis (CSF pressure is typically increased and pleocytosis

may occur), or granulomatous angiitis (CSF pleocytosis occurs).

• EKG

• May detect cardiac ischemia, or cardiac arrhythmias which predispose to stroke

(e.g., atrial fibrillation). In addition, multiple abnormalities are described in patients

with subarachnoid hemorrhage, including peaked or symmetric, deeply inverted

T waves; shortened PR intervals; and tall U waves.

• Chest radiograph

• In selected patients, chest X-ray (CXR) may reveal an infectious process, malignancy,

or evidence of heart failure. In intubated patients, CXR is used to confirm

placement of the endotracheal tube.

• Imaging

• Noncontrast CT scan is the emergency radiologic study of choice when evaluating

patients with suspected stroke, TIA, or SAH. CT is able to distinguish between

ischemic and hemorrhagic strokes, and will detect blood in more than

90% of cases of aneurysmal rupture. In addition, early signs of cerebral edema

are identified with noncontrast CT scanning.

• When available, MRI is useful for early ischemic infarcts. MRI may also be more

sensitive for ischemic strokes in the brainstem or cerebellum, as well as in detecting

thrombotic occlusion of venous sinuses.

• Electroencephalogram (EEG) is rarely useful in the acute evaluation of stroke. It

may, however, help to differentiate between seizure disorder and TIA, or between

lacunar and cortical infarcts.

Differential Diagnosis

• Vascular Disorder

• Intracerebral hemorrhage, SAH

• Subdural or epidural hematoma

• Hypertensive encephalopathy

• Complicated migraine

• Arterial embolism to an extremity

• Air embolism

• Structural Lesion

• Abscess, neoplasm

• Multiple sclerosis

• Metabolic Process

• Hypoglycemia, hyperosmolar nonketotic hyperglycemia

• Infectious Process

• Encephalitis, meningitis

• Peripheral Nerve Disorder

• Bell’s palsy, other peripheral nerve palsies

• Peripheral vertigo

• Other

• Acute angle closure glaucoma

• Seizure with postictal (Todd’s) paralysis

Treatment

• General Management Issues

• As with all emergent conditions, evaluation of the patient with a neurologic deficit

begins with airway, breathing, and circulation. Patients with severely depressed mental

Neurologic Emergencies 107

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status and patients with an unprotected airway may require intubation and mechanical

ventilation.

• All patients should be placed on continuous pulse oximetry and cardiac monitoring,

and have peripheral intravenous access established.

• Patients noted to have signs of increased ICP should be aggressively managed.

• Oxygen

• Supplemental oxygen may be required to maintain oxygen saturation >95%. However,

in the absence of hypoxia, supplemental oxygen has not been shown to affect

outcome.

• Blood Pressure Control

• In the first few hours following acute stroke, mild to moderate hypertension is

commonly observed. Over the next few hours to days, the blood pressure generally

declines spontaneously. The ischemic penumbra may be dependent upon a moderately

increased blood pressure for adequate perfusion; thus, use of antihypertensive

agents may exacerbate the patient’s condition.

• Cautious blood pressure control—with easily titratable, short-acting parenteral medications—

is recommended in the following situations: (1) hypertensive encephalopathy;

(2) cardiac ischemia or aortic dissection; (3) intracerebral hemorrhage; (4) when

thrombolytic therapy is considered (see exclusion criteria below); and (5) the mean

arterial pressure (MAP) is >130, or the SBP is >220.

• Anticoagulants

• Heparin has been shown to benefit patients at risk for cardioembolic stroke (especially

patients with ischemic or rheumatic heart disease). In addition, patients with

venous sinus occlusion benefit from heparin use.

• Antiplatelet Agents

• Aspirin has been shown to reduce the rate of nonfatal recurrent stroke and death

after acute stroke (versus placebo). Aspirin is recommended in patients who are not

candidates for thrombolytics or other anticoagulants.

• Ticlopidine inhibits the ADP pathway of platelet aggregation; it also reduces blood

fibrinogen levels. In patients with TIA or minor stroke, ticlopidine results in significant

risk reduction in stroke recurrence or death versus aspirin. However, the hematologic

side effects (TTP, thrombocytopenia, and neutropenia) have limited its recommended

use to patients who have a contraindication to aspirin and who can be

closely monitored in this setting; clopidogrel is preferred by many practitioners.

• Clopidogrel is similar in action and effect to ticlopidine. It is recommended for

aspirin-intolerant patients and has a significantly lower rate of TTP than ticlopidine.

Specific Treatment

Acute Ischemic Stroke

• Intravenous Thrombolytics (IV rt-PA)

• In the NINDS rt-PA stroke study, patients treated with rt-PA within 3 h of symptom

onset were at least 30% more likely (than patients given placebo) to have minimal or

no disability at 3 mo on various clinical scales. However, 6.4% of patients in the

treatment arm had a symptomatic ICH within 36 h of stroke onset, compared with

0.6% of patients given placebo. Mortality was similar in both groups. Based on these

results, the FDA approved the use of IV rt-PA in acute ischemic stroke within 3 h of

symptom onset. In addition, the AHA and the American Academy of Neurology

have issued practice guidelines recommending the use of intravenous thrombolysis.

• Other studies have failed to show improvement in outcome over placebo. For this

reason, the use of thrombolytics in stroke remains controversial. However, because

this modality is now being described by certain groups as the standard of care, the

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inclusion and exclusion criteria are included here. It is important to note that both

ACEP and ABEM have developed position statements which indicate that further

studies are necessary before thrombolytics become a community standard of care.

• Dosing for IV rt-PA is as follows: 0.9 mg/kg total dose, with 10% given over 1 min

as a bolus; the remainder is infused over 1 h.

• Consultation with a neurologist is strongly recommended prior to the initiation of

IV rt-PA. Patients with very severe deficits, as well as those over age 75, are probably

at increased risk for ICH. Accurate informed consent is critical.

• Inclusion criteria

• Age >18 yr

• Ischemic stroke with a clearly defined time of onset within 3 h of initiation of

treatment

• Neurologic deficit measurable on the NIHSS

• Baseline CT scan of the brain with no evidence of intracranial hemorrhage

• Exclusion criteria

• Patient history

• Stroke or serious head trauma within the preceding 3 mo

• Major surgery (or biopsy of a parenchymal organ) within the past 14 days

• Prior intracranial hemorrhage; history of CNS neoplasm, aneurysm, or AVM

• Arterial puncture at a noncompressible site within the past 7 days

• Gastrointestinal or urinary tract hemorrhage within the previous 21 days

• Lumbar puncture within the past 7 days

• Recent myocardial infarction

• History of known hereditary or acquired abnormal hemostasis

• Pregnant or lactating female

• Clinical features

• Systolic BP >185 mm Hg or diastolic BP >110 mm Hg, or aggressive treatment

is required to reduce blood pressure to the specified limits

• Rapidly improving or minor symptoms

• Symptoms suggestive of subarachnoid hemorrhage (SAH)

• Seizure at the onset of stroke

• Clinical presentation consistent with acute MI or post-MI pericarditis

• Diagnostic studies

• Major hypodensity or effacement of cerebral sulci in more than one-third of

the territory of the MCA

• Received heparin within 48 h of stroke onset, with elevated PTT

• Prothrombin time (PT) >15 seconds

• Platelet count <100,000/mm3

• 50 > glucose >400 mg/dL

TIA

• In the past, patients with neurologic symptoms that resolved within 24 h were said to

have had a transient ischemic attack (TIA). However, recent evidence indicates that

evidence of infarction is seen on CT of patients whose symptoms last more than 1 h.

For this reason, many neurologists are describing symptoms that persist for more than

1 h as an acute stroke. In addition, the majority of TIAs resolve within minutes.

• Patients with TIAs are at increased risk for subsequent stroke and death.

• Aspirin, ticlopidine, and clopidogrel have all been shown to reduce the risk of future

TIAs, strokes, and death.

• Anticoagulation is recommended for patients with cardiac embolus as a cause of their

TIA symptoms.

Neurologic Emergencies 109

4 Hemorrhagic Stroke

• Cautious blood pressure control is recommended. Various guidelines exist, ranging

from keeping the diastolic blood pressure at approximately 100 mm Hg to basing the

target systolic and diastolic levels on the patient’s premorbid blood pressure.

• Look for and aggressively treat early signs of increased ICP with head-of-bed elevation,

diuretics (furosemide, mannitol), and hyperventilation.

• Although most cases of ICH are not amenable to neurosurgical intervention, some

patients benefit from surgical drainage. Potential surgical candidates are those with

neurologic deterioration, superficial cerebral hemorrhages causing mass effect, and

cerebellar hematomas. Neurosurgical consultation is recommended in all patients with

intracerebral hemorrhage.

Subarachnoid Hemorrhage

• SAH frequently results from rupture of an aneurysm or AVM. Preventing rerupture,

by maintaining adequate blood pressure control, is the mainstay of treatment. Elevation

of the head of the bed, mild sedation, and analgesics (for headache) may suffice.

The blood pressure should be reduced to approximately 160/100 mm Hg, using rapidly

titratable, parenteral medications if necessary.

• Nimodipine, a calcium channel blocker, is indicated for the prevention of cerebral vasospasm

in order to prevent subsequent ischemia; the dose is 60 mg enterally every 4 h.

• A prophylactic anticonvulsant is recommended; consider corticosteroids.

• Prompt neurosurgical consultation is recommended. The timing and outcome of surgical

intervention are determined by the patient’s clinical grade and medical stability,

among other factors.

• Grading of patients with SAH (Table 4E.1).

Disposition

• Acute Stroke Syndromes

• Patients with acute intracerebral hemorrhage require admission to an ICU or

step-down unit for close monitoring.

• All patients with acute ischemic strokes should be hospitalized for medical stabilization

and evaluation of their functional independence as well as their rehabilitation potential.

Patients who receive thrombolytics should be admitted to the ICU within 3 h.

• Patients with multiple previous strokes may not require admission if they are medically

stable and social support is adequate.

• TIA

• Current recommendations are that patients with new TIAs be admitted for workup

and initiation of treatment.

Suggested Reading

1. Barsan WG, Kothari R. Stroke. In: Rosen P, Barkin RM, eds. Emergency Medicine:

Concepts and Clinical Practice. 4th ed. St. Louis: Mosby-Year Book, Inc., 1996.

Table 4E.1. Grading of patients with subarachnoid hemorrhage

Grade Mental Status Neurologic Deficits Surgical Candidate

I Normal None Yes

II Mildly altered Minimal, focal Yes

III Confused Mild, focal Yes

IV Stuporous Moderate to severe No

V Coma Decerebrate posturing No

110 Emergency Medicine

4

2. Baumlin KM, Richardson LD. Stroke syndromes. Emerg Med Clin North Am 1997;

15:3.

3. Brott T et al. Measurements of acute cerebral infarction: A clinical examination scale.

Stroke 1989; 20:864-870.

4. Headache and Facial Pain. In: Simon RP, Aminoff MJ, Greenberg DA, eds. Clinical

Neurology. 4th ed. Stamford: Appleton and Lange, 1999.

5. Henneman PL, Lewis RJ. Is admission medically justified for all patients with acute

stroke or transient ischemic attack? Ann Em Med 1995; 25:458-463.

6. Hickenbottom SL, Barsan WG. Acute ischemic stroke therapy. Neurol Clin 2000; 19:2.

7. Kasner SE, Grotta JC. Ischemic stroke. Neurol Clin North Am 1998; 16:2.

8. Llinas R, Caplan LR. Evidence-based treatment of patients with ischemic cerebrovascular

disease. Neurol Clin 2001; 19:1.

9. Stieg PE, Kase CS. Intracranial hemorrhage: Diagnosis and emergency management.

Neurol Clin North Am 1998; 16:2.

10. Stroke. In: Simon RP, Aminoff MJ, Greenberg DA, eds. Clinical Neurology. 4th ed.

Stamford, Appleton and Lange, 1999.

11. The National Institute of Neurological Disorders and Stroke. rt-PA Stroke Study Group.

Tissue plaminongen activator for acute ischemic stroke. N Engl J Med 1995;

333:1581-1587.

12. Younger JG, Barsan WG. Cerebrovascular emergencies. In: Howell JM, ed. Emergency

Medicine. Philadelphia: WB Saunders Company, 1998.

 

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