Management of acute stroke. (Featured CME Topic: Stroke).

Abstract: Stroke ranks as the third leading cause of death and the most common cause of permanent disability in adults. Timely recognition and treatment is imperative to reduce stroke-related morbidity and modality. Patients with acute isehemic stroke should be evaluated for administration of intravenous tissue plasminogen activator (t-PA); those who do not qualify for t-PA should receive aspirin therapy in the absence of a contraindication. In all stroke patients, intravenous hydration with normal saline should be administered, hypoxia should be corrected with supplemental oxygen, and hyperglycemia and fever should be treated aggressively. Blood pressure management should be individualized on the basis of stroke pathophysiology and specific treatment plan (e.g., planned thrombolysis) following published guidelines. Evaluation of stroke etiology should be undertaken, and the results should be used to guide secondary stroke prevention efforts.

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An estimated 730,000 strokes and 300,000 transient ischemic attacks (TIAs) occur in the United States each year.' Stroke ranks as the third leading cause of death and the most common cause of permanent disability in adults; approximately half of all stroke survivors return to some form of employment, although this figure declines with age. (2) At any given time, there are about 4.6 million survivors of stroke, and 170,000 individuals die each year in this country as a direct or indirect consequence of stroke. (3) Most recent estimates place the cost of stroke in the United States in excess of $45 billion per year. (3) Timely recognition and treatment are imperative to reduce stroke-related morbidity and mortality.

Clinical Diagnosis

Typical Presentation

By and large, the diagnosis of stroke is not difficult. Symptoms typically begin suddenly and are referable to the region of the brain that is ischemic or afflicted by hemorrhage. Internal carotid artery distribution strokes often produce unilateral numbness or weakness, or both. In addition, there may be signs of cortical dysfunction such as aphasia, apraxia, agnosia, and visual field defects (Table 1). Vertebrobasilar distribution strokes can produce unilateral or bilateral sensorimotor deficits, often accompanied by signs and symptoms more specific for brainstem or cerebellar dysfunction: vertigo, diplopia, disequilibrium, ataxia, and cranial nerve palsies (Table 2). Because the posterior circulation also supplies parts of the thalamus, internal capsule, and temporal and occipital lobes via the posterior cerebral artery, strokes in this distribution may present with some combination of sensorimotor symptoms, memory disturbance, and homonymous visual field impairment. Dysarthria is a nonspecific symptom or sign that may occur with stroke in either the carotid or vertebrobasilar distribution.

Patients with intracranial hemorrhage (ICH) tend to exhibit a smoothly progressive neurologic decline over the initial hours. They also complain of acute headache and exhibit vomiting or early impairment of consciousness more often than patients with ischemic stroke do. Aside from this last feature, there is nothing at physical examination that reliably enables the clinician to distinguish between ischemic stroke and ICH.

The clinical presentation associated with "spontaneous" (ie, nontraumatic) subarachnoid hemorrhage (SAH) typically serves to distinguish this stroke subtype from all others. If a history can be obtained, acute headache almost invariably is reported. When the hemorrhage is extensive, impaired consciousness is present at initial examination, and acute seizure activity may occur. Focal neurologic deficits are absent unless there is also extension of hemorrhage into the brain parenchyma or ischemia due to vasospasm; ischemia is rarely seen in the acute setting.

Stroke Mimickers

There are several disorders that may mimic stroke and thus confound diagnosis (Table 3). Patients experiencing seizures can present with focal neurologic deficits, especially in the immediate postictal period when there may be unilateral weakness (ie, Todd paralysis) or other signs also commonly associated with stroke. Such deficits usually resolve over several hours but may persist as long as a day or more. There may be a history of an established seizure disorder. The patient or an observer may relate the occurrence of involuntary, rhythmic movements, but frequently the patient cannot recall the seizure itself, the seizure is unobserved, or the seizure is nonconvulsive and thus unapparent.

Although brain neoplasms more commonly cause gradually progressive symptoms and signs, tumors--primary or metastatic--also may mimic stroke. Acute, strokelike deterioration occurs most often when there is hemorrhage within the tumor or tumor-associated seizure activity but, at times, symptoms related to tumors may resemble those from stroke or TIA for no discernible reason. Systemic infections and toxic-metabolic disturbances may mimic stroke, especially in patients with preexisting focal brain injury. The acute systemic illness can bring to light old, previously subclinical, neurologic deficits. Migrainous aura may be confused with TIA or stroke, especially when it is prolonged and, on rare occasions, ischemic stroke can complicate migraine. With migrainous aura, there is typically a history of prior, similar symptoms that have been associated with headache. Often nausea, vomiting, photophobia, and phonophobia accompany the aura. Hypoglycemia can acutely produce focal neurologic symptoms and signs that reso lve rapidly after administration of glucose or dextrose. This diagnosis should be considered and excluded in any patient with apparent stroke who is receiving hypoglycemic therapy or is otherwise at risk for low blood sugar. Multiple sclerosis may present acutely with signs and symptoms indistinguishable from stroke on clinical grounds, but a careful history and selective diagnostic testing generally serve to establish the correct diagnosis. Intracranial hematomas (subdural and epidural) also may present in a strokelike fashion. With chronic subdural hematoma, a history of recent trauma is far from invariable, and this is especially true in cases involving the elderly or individuals who are administered warfarin or are otherwise at risk for spontaneous bleeding. Even so, in the absence of antecedent severe trauma, patients with subdural hematomas most often present with headache, fluctuating depression of consciousness, and no or minimal focal neurologic deficit. At times, infectious encephalitis may mimic ac ute stroke but fever, seizure activity, alteration of consciousness, and abnormal cerebrospinal fluid findings are likely to be present.

Acute Stroke Management

Initial Management. Once the diagnosis of acute stroke is suspected, the duration of symptom onset must be determined, as time from stroke onset remains the single most important determinant of therapeutic options (Fig. 1). Patients with symptom onset of less than 3 hours should be evaluated for potential treatment with intravenous tissue plasminogen activator (t-PA).

All patients should receive intravenous hydration with normal saline, hypoxia should be corrected with supplemental oxygen, hyperglycemia should be treated with insulin, and fever should be treated aggressively with antipyretics. The head of the bed may be placed in the horizontal position for patients with ischemic stroke and no elevation of intracranial pressure (ICP). (4) An electrocardiogram should be performed and patients should receive continuous cardiac monitoring. Blood should be drawn for a complete blood cell with platelet count, prothrombin time test with international normalized ratio, partial thromboplastin time test, basic chemistries, fasting lipids, and cardiac markers, when appropriate. Additional blood testing may be appropriate on a case-by-case basis. Oral intake should be withheld until the patient passes a swallow test with sips of water.

Patients with hyperacute stroke should undergo emergent brain computed tomography (CT). The major value of acute CT scanning is in differentiating intracerebral hemorrhage from ischemic stroke and other pathologic processes such as subdural hematoma, tumor, and abscess. CT scan may also delineate the extent of ischemia. For all ischemic stroke subtypes, magnetic resonance imaging (MRI) demonstrates evidence of ischemic injury to the brain earlier than does CT, and newer MRI techniques (such as diffusion-weighted imaging) have further increased its sensitivity. The clinical implications of early positive MRI or the significance of mismatches in diffusion-weighted and perfusion defects are as yet unclear, but it is conceivable that these or other noninvasive means of assessing ischemic injury may serve to indicate whether hyperacute interventional therapy is likely to be beneficial.

Management of Blood Pressure. During brain ischemia, cerebral autoregulation is impaired and cerebral blood flow becomes pressure passive (ie, blood flow declines with declining perfusion pressure). Blood pressure should therefore not be treated unless one of the following exists: 1) systolic blood pressure (SBP) exceeds 220 mm Hg or diastolic blood pressure (DBP) exceeds 120 mm Hg after repeated measurements; 2) cardiac ischemia, heart failure, or aortic dissection is present; 3) thrombolytic therapy is planned; or 4) intracerebral hemorrhage is identified. In the latter situation, blood pressure should be maintained below 180/105 mm Hg, with more aggressive control reserved for patients with no prior history of hypertension. (5) Specific treatment recommendations for the management of blood pressure after acute stroke are presented in Tables 4 and 5. (6)

Intravenous Thrombolysis. Intravenous thrombolysis with tissue plasminogen activator (t-PA) is indicated for selected patients within 3 hours of ischemic stroke onset. (7,8) It is important to bear in mind that when stroke onset time is unclear (eg, patient awakens with a deficit), onset time is considered to be the time when patients were last known to be in their usual state of health. Inclusion and exclusion criteria for t-PA are listed in Table 6. If blood pressure exceeds 185/110 mm Hg, a single dose of an antihypertensive can be administered; the patient qualifies for therapy if blood pressure declines below this level. Blood pressure should be monitored every 15 minutes for 2 hours after the start of infusion, then every 30 minutes for 6 hours, and then every 60 minutes for 16 hours. Blood pressure must be maintained below 185/110 mm Hg and antithrombotic agents must be avoided for the first 24 hours post-thrombolysis (Table 5).

Other Considerations. Patients with ischemic stroke who do not qualify for intravenous t-PA should be administered aspirin (160-325 mg/d) as it has been shown to modestly reduce the risk of recurrent stroke and death when administered within the first 48 hours poststroke. (9,10) Neurosurgical consultation should be sought for patients with cerebellar hemorrhage or large cerebellar ischemic infarctions. Although currently available data do not support the emergent administration of anticoagulants for most patients with acute ischemic stroke, nonambulatory patients must receive deep vein thrombosis prophylaxis with heparin or low-molecular weight heparins or heparinoids. (10,11) For those who cannot receive antithrombotic drugs, intermittent external compression stockings should be used. Early mobilization is recommended and the use of an indwelling catheter should be avoided, if possible. Fever should be treated aggressively with antipyretics, and antibiotics should be administered for infectious causes. Phys ical, occupational, and speech therapy should be ordered when indicated.

Determining Ischemic Stroke Mechanism

For patients with ischemic stroke, the pathophysiologic process has generated the stroke and the specific etiology that underlies that process should be determined. All ischemic strokes typically result from one of these three primary causes: embolism, large vessel thrombosis, and small vessel thrombosis. Identification of the pathophysiologic mechanism that has generated the stroke under evaluation (eg, cardioembolism) is not synonymous with identification of that stroke's specific etiology (eg, atrial fibrillation). To determine the cause of stroke with any degree of accuracy and without undue expense, one must consider the age and health history of the patient, details of events surrounding the acute stroke, and findings from the bedside evaluation. With these data, the clinician can address those questions that direct the diagnostic management: With which stroke subtype am I dealing? Which specific causes are more likely to to be responsible for this pathophysiologic process? Which tests will enable me to confirm my clinical impression?

Even with intensive neurodiagnostic intervention, a specific cause of ischemic stroke will not be identified in a sizable proportion of patients. This is especially true when a young person has had a stroke and the cause is not immediately apparent from the initial bedside evaluation. In several recent studies of large patient groups with acute ischemic stroke, the incidence of stroke of unknown cause ranged from 18 to 40%. (12,13) Whether such cases will exhibit a response to acute or chronic stroke therapy similar to that observed in patients with stroke from an identifiable cause is unclear.

Complications of Stroke

Neurologic complications of stroke include stroke progression, seen in over 25% of patients, or recurrence, which is less common with a rate dependent on the mechanism of the index event. Seizures can occur in up to 10% of patients at some point after stroke and are more common after subarachnoid oir intracerebral hemorrhage and large lesions involving the cerebral cortex. Stroke-related seizures are usually easily controlled with a single anticonvulsant. Increased ICP is the most lethal poststroke complication and may be a direct effect of a hematoma or brain edema. Brain edema after ischemic stroke (usually cytotoxic) typically becomes symptomatic after 1 to 4 days. Signs and symptoms of raised ICP include depressed level of consciousness, pupillary asymmetry, abducens nerve palsy, papilledema, and periodic breathing. Treatment of raised ICP should include fluid restriction, elevation of the head of the bed, administration of osmotic diuretics, and hyperventilation. Some degree of vascular cognitive impairm ent or frank dementia can occur in up to 33 to 50% of patients. Recent evidence suggests that cholinesterase inhibitors may be of value in treating these patients. (14, 15) Patients should be monitored for poststroke depression, which occurs in up to 60% of patients and is treatable with antidepressants and/or psychotherapy. (16) Medical complications after stroke include cardiac abnormalities (eg, arrhythmia, myocardial infarction), pulmonary embolism, infection (eg, urinary tract, pneumonia), and gastrointestinal bleeding.

Patient and Caregiver Education

Patients and caregivers should be educated regarding both short- and long-term clinical expectations. Symptoms of post-stroke depression should be reviewed and patients instructed to seek treatment if appropriate. Applicable secondary stroke preventive strategies should be discussed and stroke symptoms should be reviewed. The use of emergency medical services should be encouraged should the patient experience recurrent stroke symptoms.

Emerging Therapies

For patients with ischemic stroke in whom intravenous thrombolysis is not indicated, consideration can be given to the administration of intra-arterial thrombolysis if the appropriate facilities and personnel are available. A prospective, randomized controlled trial of intra-arterial prourokinase (17) showed a treatment benefit for selected patients with middle cerebral artery stroke, but prourokinase is not currently available for use. These data have led to the adoption of protocols for the administration of intra-arterial t-PA at some centers. The safety and efficacy of the combination of a lower dose of intravenous t-PA followed by intra-arterial t-PA are currently under investigation. Other antithrombotic agents under clinical investigation for ischemic stroke include intravenous heparin administered within 12 hours of stroke onset, a platelet glycoprotein IIb/IIIa antagonist (abciximab), and a direct thrombin inhibitor (argatroban).

Various neuroprotective strategies have been under investigation for administration in isolation or in combination with a thrombolytic agent, but unfortunately no agent has proven effective to date. Mild hypothermia is a powerful neuroprotective strategy in preclinical models and pilot studies in stroke (18) and the recent positive trials after cardiac arrest (19,20) have generated significant interest in this strategy. It is likely that no single agent or intervention will be the "magic bullet" for all patients with stroke but that future management will involve combinations of strategies and directed therapies based on stroke subtype, location, and/or diffusion and perfusion MRI findings.

Table 1

Anterior circulations stroke symptoms and signs

More
specific          Less specific                   Uncommon

Aphasia   Unilateral numbness or weakness  Ataxia
Apraxia   Visual field deficit             Vertigo/disequilibrium
Agnosia   Dysarthria                       Nausea/vomiting
          Headache

Table 2

Posterior circulation stroke symptoms and signs

More specific                            Less specific

Ataxia                          Dysarthria
Diplopia                        Headache
Vertigo/disequilibrium          Unilateral numbness or weakness
Bilateral numbness or weakness  Nausea/vomiting
                                Visual field deficit

Table 3

Stroke mimickers

Seizure
Mass lesion
Migraine
Hypoglycemia
Systemic infection
Toxic-metabolic encephalopathy
Multiple sclerosis
Intracranial (eg, subdural or epidural) hematoma

Table 4

Antihypertensive therapy for hemorrhagic stroke (a)

Blood pressure (b)           Treatment

1. SBP >230 or DBP           Sodium nitroprusside (0.5-10
   >120 mm Hg                 [micro]g/kg/min) or nitroglycerine
                              drip (at 10-20 [micro]g/min).

2. SBP >180 or DBP           Consider 10 mg labetalol (c) IVP.
   >105 mm Hg                 May repeat or double labetalol every
                              10 to 20 min to a maximum dose
                              of 300 mg. Alternatively,
                              administer initial labetalol
                              bolus and then start labetalol
                              drip at 2 to 8 mg/min.

3. Hypertension relative to  If prehemorrhage BP is estimated to
   prestroke condition        have been considerably lower (eg,
                             120/80 mm Hg), then antihypertensive
                              therapy may be appropriate to approximate
                              premorbid pressures, particularly
                              in the first hours after
                              subarachnoid hemorrhage.


(a) Reproduced from Advanced Cardiac Life Support Copyright [C] 1997
American Heart Association. (6) DBP, diastolic blood pressure; SBP,
systolic blood pressure; BP, blood pressure; min, minutes; IVP,
Intravenous push.

(b) All initial blood pressures should be verified before treatment by
repeating reading in 5 min.

(c) Labetalol should be avoided in patients with asthma, cardiac
failure, or severe abnormalities in cardiac conduction. For refractory
hypertension, alternative therapy may be considered with sodium
nitroprusside or enalapril.

Table 5

Antihypertensive therapy for acute ischemic stroke (a)

Blood Pressure (b)          Treatment

Nonthrombolytic candidates
 DBP > 140 mm Hg            Sodium nitroprusside
                             (0.5[micro]g/kg/min). Aim for 10
                             to 20% reduction in DBP.

 SBP > 220, DBP > 120,      10 to 20 mg labetalol (d) IV push
 or MAP (c) > 130 mm Hg      over 1 to 2 min.
                             May repeat or double
                             labetalol every 20 min to
                             a maximum dose of 150 mg.

 SBP < 220, DBP > 120, or   Emergency
 MAP (c) 130 mm Hg           antihypertensive therapy is
                             deferred in the absence of aortic
                             dissection, acute
                             myocardial infarction
                             severe congestive heart failure,
                             or hypertensive encephalopathy.
Thrombolytic candidates
Pretreatment                1 to 2 inches of nitropaste or 1
 SBP > 185 or                to 2 doses of 10 to 20
 DBP > 110 mm Hg             mg labetalol (d) IV push.
                             If BP is not reduced and maintaine
                             to < 185/110 mm Hg, the patient
                             should not be treated with tPA.
During and after treatment
 Monitor BP                 BP is monitored every 15 min for 2
                             hours then every 30 min for 6 hours, and
                             then every 1 hour for 16 hours.
 DBP > 140 mm Hg            Sodium nitroprusside
                             (0.5 [micro]g/kg/min)
 DBP > 230 or DBP           (1) 10 mg labetalol (d) IVP over
 121 to 140 mm Hg            1 to 2 min. May repeat or double
                             labetalol every 10 min to a
                             maximum dose of 150 mg or give
                             the initial labetalol bolus and
                             then start a labetalol drip at
                             2 to 8 mg/min.
                            (2) If BP not controlled by
                             labetalol, consider sodium
                             nitroprusside.
4. SBP 180 to 230 or DBP    10 mg labetalol (d) IVP. May
   105 to 120 mm Hg          repeat or double labetalol every
                             10 to 20 min to maximum dose of
                             150 mg or give initial labetalol
                             bolus and start a labetalol drip
                             at 2 to 8 mg/min.

(a) Reproduced from Advanced Cardiac Life Support Copyright [c] 1997
American Heart Association. (6) DBP, diastolic blood pressure; SBP,
systolic blood pressure, MAP, mean arterial pressure; BP, blood
pressure; min, minutes; tPA. tissue plasminogen activator; IV,
intravenous.

(b) All initial blood pressures should be verified before treatment by
repeating reading in 5 min.

(c) As estimated by one third the sum of systolic and double diastolic
pressure.

(d) Labetalol should be avoided in patients with asthma, cardiac
failure, or severe abnormalities in cardiac conduction. For refractory
hypertension, alternative therapy may be considered with sodium
nitroprusside or enalapril.

Table 6

Inclusion and exclusions criteria for administration of intravenous
tissue plasminogen activator for acute stroke (a)

Inclusion

  Age >18 yr
  Ischemic stroke by clinical assessment
  Persistent neurologie deficit beyond
   sensory defi cit or ataxia
  Cranial computed tomography negative
   for hemorrhage
  Initiation of treatment within 3 hours
   after symptom onset
Exclusion
  Treatment initiated >3 hours after
   symptom onset
  Neurologic deficit that is rapidly
   improving based on history or
   observation
  CT scan shows major early infarct
   signs (eg, substantial edema, mass
   effect, midline shift)
  Patient taking oral anticoagulants
   or with PT >15 seconds (INR > 1.7)
  Patient receiving heparin within the
   preceding 48 hours who has a
   prolonged PTT
  Platelet count <100,000/[mm.sup.3]
  Pretreatment systolic blood pressure
   >185 mm Hg or diastolic pressure >110
   mm Hg or if aggressive treatment is
   required to reduce blood pressure to
   the specified limits before thrombolytic
   therapy
  Prior stroke or any serious head trauma
   in the preceding 3 months
  Major surgery within the preceding 21 days
  Prior intracerebral hemorrhage
  Gastrointestinal or urinary tract
   hemorrhage within the preceding 14 days
  Seizure at the onset of stroke
  Symptoms suggestive of SAH
  Arterial puncture at a noncompressible
   site within the previous 7 days

(a) CT, computed tomographic; PT, prothrombin time; INR, international
normalized ratio; PTT, partial thromboplastin time; SAH, subarachnoid
hemorrhage.

Accepted November 7, 2002.

References

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(2.) Black-Schaffer RM, Osberg JS. Return to work after stroke: Development of a predictive model. Arch Phys Med Rehabil 2002;71:285-290.

(3.) American Heart Association. Targeting the Facts. Dallas, American Heart Association, 2002 (pamphlet).

(4.) Schwarz S, Georgiadis D, Aschoff A, Schwab S. Effects of body position on intracranial pressure and cerebral perfusion in patients with large hemispheric stroke. Stroke 2002;33:497-501.

(5.) Broderick JP, Adams HP Jr, Barsan W, Feinberg W, Feldmann E, Grotta J, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 1999;30:905-915.

(6.) Cummins RO (ed). Acute stroke, in Textbook of Advanced Cardiac Life Support. Dallas, American Heart Association, 1997, pp 10-1-10-28.

(7.) Quality Standards Subcommittee, American Academy of Neurology. Practice advisory: Thrombolytic therapy for acute ischemic stroke: Summary statement. Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 1996;47:835-839.

(8.) Adams HP, Brott TG, Furlan AJ, Gomez CR, Grotta J, Helgasan CM, et al. Guidelines for thrombolytic therapy for acute stroke: A supplement to the guidelines for the management of patients with acute isehemic stroke--A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Circulation 1996;94:1167-1174.

(9.) Chen Z, Sandercock P, Pan H, Counsell C, Collins R, Liu L, et al. Indications for early aspirin use in acute ischemic stroke: A combined analysis of 40,000 randomized patients from the Chinese Acute Stroke Trial and the International Stroke Trial. Stroke 2000;31:1240-1249.

(10.) Coull BM, Williams LS, Goldstein LB, Meschia JF, Heitzman D, Chaturvedi S, et al. Anticoagulants and antiplatelet agents in acute isehemic stroke: Report of the Joint Stroke Guideline Development Committee of the American Academy of Neurology and the American Stroke Association (a Division of the American Heart Association). Neurology 2002;59:13-22.

(11.) Adams HP Jr. Emergent Use of anticoagulation for treatment of patients with ischemic stroke. Stroke 2002;33:856-861.

(12.) Frey JL, Jahnke HK, Bulfinch EW. Differences in stroke between white, Hispanic, and Native American patients: The Barrow Neurological Institute Stroke Database. Stroke 1998;29:29-33.

(13.) Sacco RL, Ellenberg JH, Mohr JP, Tatemichi TK, Hier DB, Price TR, et al. Infarcts of undetermined cause: The NINCDS Stroke Data Bank. Ann Neural 1989;25:382-390.

(14.) Erkinjuntti T, Kurz A, Gauthier S, Bullock R, Lilienfeld S, Rao C, et al. Efficacy of galanthamine in probable vascular dementia and Alzheimer's disease combined with cerebrovascular disease: A randomized trial. Lancet 2002;359:1283-1290.

(15.) Moretti R, Torre P, Antonello RM, Cazzato G. Rivastigmine in subcortical vascular dementia: A comparison trial on efficacy and tolerability for 12 months follow-up. Eur J Neurol 2001;8:361-362.

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RELATED ARTICLE: Key Points

* Timely recognition and treatment are imperative to reduce stroke-related morbidity and mortality.

* Patients with acute ischemic stroke should be evaluated for the administration of intravenous tissue plasminogen activator (t-PA); those who do not qualify for t-PA should receive aspirin therapy in the absence of a contraindication.

* In all stroke patients, intravenous hydration with normal saline should be administered, hypoxia should be corrected with supplemental oxygen, and hyperglycemia and fever should be treated aggressively.

* Blood pressure management should be individualized on the basis of stroke pathophysiology and specific treatment plan (e.g., planned thrombolysis) following published guidelines.

* Evaluation of stroke etiology should be undertaken and used to guide secondary stroke prevention efforts.

From the Stroke Center, University of South Alabama College of Medicine, Mobile, AL.

Reprint requests to Richard M. Zweifler, MD, Stroke Center, University of South Alabama College of Medicine, 2451 Fillingim Street, Mobile, AL 36617. Email: [e-mail]

Copyright [c] 2003 by The Southern Medical Association 0038-4348-03/9604-0380