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Introduction

Once a patient is identified as a candidate for recombinant tissue plasminogen activator (rt-PA) and treatment is initiated, the focus of care shifts from screening and initial assessment to safety and prevention of complications. Nurses should be familiar with safe dosage and administration of rt-PA. Also they should be competent in neurological assessment, including use of the National Institutes of Health Stroke Scale (NIHSS) and able to recognize the risks and complications of thrombolytic treatment and stroke. This article reviews the nurse's role in immediate posttreatment care following rt-PA therapy for an acute stroke with a focus on assessment and prevention of complications.

Final Pretreatment Assessment

Recombinant tissue plasminogen activator (rt-PA) administration starts immediately once the patient has been thoroughly assessed and identified as an appropriate candidate. Baseline assessment includes pertinent medical history, neurological and physical assessment, lab results and a computed tomography (CT) scan. This evaluation must confirm that treatment can be delivered within three hours of symptom onset.

Dosage and Administration

Administration of rt-PA for stroke is clearly different from that of myocardial infarction (Table 1). The dose of rt-PA must be calculated according to body weight (0.9 mg/kg), with a maximum dose of 90 mg. This is a lower dose of rt-PA than the dose used to treat acute myocardial infarction (AMI). This dose was determined through dose escalation trials to minimize the risk of cerebral hemorrhage in the stroke patient.[16] Ten percent of the drug is given as intravenous (IV) bolus over one minute through a peripheral IV site. The remainder of the drug is given by continuous infusion over one hour. Care is taken to administer the entire drug solution. This is managed by a normal saline flush of the entire IV line at the end of the infusion. Failure to follow these dosing instructions could result in underdosing or overdosing the patient. If the patient's condition worsens at any time during drug administration, the infusion should be stopped immediately until further neurologic assessment and possibly a CT scan of the head is completed.

Table 1. rt-PA Treatment for Acute Ischemic Stroke vs Acute Myocardial Infarction

Acute Ischemic Stroke (AIS)

1. Dose: 0.9 mg/kg, 90 mg max,
weight specific

2. Treatment Window:
0-3 hours from symptom onset

3. Concurrent Therapies:
No aspirin, warfarin, heparin for
24 hours following treatment
and an ICH negative CT

4. Diagnostic Reference:
CT to eliminate
intracranial hemorrhage

5. Evaluation of Efficacy:
Neurological Improvement

Acute Myocardial Infarction (AMI)

1. Dose: 100 mg maximum for
weight [is less than or equal to] 67 kg

2. Treatment Window:
0-12 hours
> 12 hours controversial

3. Concurrent Therapies:
Aspirin, warfarin, heparin may
be given

4. Diagnostic Reference:
ECG to confirm AMI

5. Evaluation of Efficacy:
Evidence or reperfusion - No
angina, no ST changes

Monitoring

Thrombolytic stroke treatment must be followed with intensive management of the stroke patient. The patient-to-nurse ratio should be no more than 2:1 for the first 24 hours. Observations should include frequent neurological and vital signs assessment, bleeding assessment and precautions and continuous electrocardiogram (ECG) monitoring (Table 2). Neurologic changes are detected only by direct assessment of the patient, and although patients are carefully screened and selected, they may still have complications with serious consequences. Immediate recognition and quick response to these changes are critical.

Table 2. Acute Care Unit Orders Post rt-PA

Date Physician's Order

----- 1. Continue Emergency Department orders for rt-PA infusion
and monitoring vital signs and neuro checks until two
hours after start of rt-PA infusion.
----- 2. Vital signs (BP, P, R) and neuro checks (LOC and arm/leg
weakness) q 30 min for 6 hrs, then q 60 min for 16 hrs
after start of rt-PA. Temperature q 4 hrs and PRN.
----- 3. Bleeding precautios: check puncture sites for bleeding
or hematomas.
----- Apply digital pressure or pressure dressing to active
compressible bleeding sites. Evaluate urine, stool,
emesis or other secretions for blood. Perform Hemoccult
testing if there is evidence of bleeding.
----- 4. Call Dr. page#
immediately for evidence of bleeding or neurologic
deterioration, or vital signs outside the following
parameters:
----- a) Systolic BP > 185 or Systolic BP < 110

----- b) Diastolic BP > 105 or Diastolic BP < 60
----- c) Pulse < 50
----- d) respirations > 24
----- e) Decline in neurological status or worsening of
stroke signs.
----- 5. 0.45NS or NS IV to keep open at 50cc/hr x 24 hours.
----- 6. [0.sub.2] at 2/1/min by nasal cannula
----- 7. Continuous cardiac monitoring
----- 8. Measure intake and output.
----- 9. Diet: NPO except meds for 24 hours
----- 10. Bedrest.
----- 11. Medications: acetaminophen 650mg p.o. PRN for pain q 4
to 6 hours.
----- 12. (Patient's regular medications previously prescribed,
if appropriate.)
----- 13. No heparin, warfarin or aspirin for 24 hours.
----- After 24 hours: CT to exclude intracranial hemorrhage
before any anticoagulants.
----- Physician Signature :

The stroke or neurologic intensive care unit may best provide delivery of acute stroke care. However, many hospitals manage these patients in other critical care settings.[2] Nursing staff members best suited to care for stroke patients receiving rt-PA are: 1) familiar with hyperacute stroke treatment, 2) have been trained in appropriate neurological assessment, 3) can provide appropriate blood pressure management of the stroke patient and 4) are familiar with signs of increased intracranial pressure (ICP). Critical care training should provide these competencies to assure care delivery.

Neurological Assessment

Multiple demands of bedside care require nurses to provide a. neurological assessment that is quick, reproducible and sensitive. The National Institutes of Health Stroke Scale (NIHSS) meets all of these criteria. This stroke deficit scale was designed for assessing stroke deficit both during the acute phase and follow-up period by the physician or nurse. The scale can be performed in 5 minutes or less, and has been shown to have good reliability and validity.[3]

A complete baseline NIHSS should be obtained prior to drug administration. After drug initiation, an abbreviated NIHSS should be collected with the vital signs at 15 minute intervals for the first 2 hours, then every half hour for the next 6 hours, and hourly until 24 hours after treatment (Table 3). The abbreviated NIHSS consists of level of consciousness, motor, arm and leg function. After each neurologic evaluation, the patient's scores should be tallied to track improvements or declines. A decline of two points in the total abbreviated NIHSS indicates the need for a complete reassessment and evaluation.[16]
[TABULAR DATA 3 NOT REPRODUCIBLE IN ASCII]

The assessment schedule is strict in the post-thrombolytic therapy period in order to detect or prevent serious complications such as intracerebral hemorrhage (ICH). In the NINDS rt-PA Stroke Trial, all symptomatic ICHs which eventually were fatal occurred within the first 24 hours. Also, all hemorrhage (symptomatic and asymptomatic) occurred most commonly during the first 36 hours in rt-PA treated patients.[16] This justifies the need for intensive monitoring during treatment and the following 24-36 hours.

Vital Signs

Blood pressure, heart rate and respirations are monitored with the neurologic assessment as described above. The most important vital sign in the acute ischemic stroke patient is blood pressure. The majority of acute stoke patients admitted to hospitals have elevated blood pressure or variability in their blood pressure.[1,17] Severe hypertension causes increased cerebral blood volume and may increase intracranial pressure (ICP) in patients with impaired autoregulation. Delays in detection and treatment of hypertension can be critical, especially after the use of a thrombolytic agent.

Conversely, inadequate pressure can compromise the supply of nutrients and oxygen required for cerebral metabolic needs. Blood pressure that is rapidly reduced with antihypertensive treatment to "normal" levels may result in significant reduction in cerebral blood flow and should be avoided.[1,15] Approaches to treatment are controversial. In the NINDS trial, antihypertensive therapy was provided for systolic blood pressure of 185 mm Hg or greater and/or diastolic pressure of 105 mm Hg or greater (Table 4). Labetalol is recommended because it can be easily titrated.[9] Sudden drastic changes in vital signs may indicate new intracerebral hemorrhage or other major systemic bleeding and warrants careful evaluation.

Table 4. Guideline for Blood Pressure Management After rt-PA

Blood Pressure Treatment

If systolic BP 180-230 mm Hg Labetalol 10 mg IV over 1-2
and/or diastolic BP 110-120 minutes. Dose may be repeated
mm Hg on 2 readings 5-10 or doubled q 10-12 minutes
minutes apart < 150 mg total dose.

Systolic BP > Labetalol 10 mg IV over 1-2
230 mm Hg and/or diastolic minutes. Dose may be repeated
121-140 mm Hg and/or doubled every 10 minutes
< 150 mg total dose.

Diastolic BP> 140mm Hg Start infusion of sodium
nitroprusside 0.5-10mcg/kg/min

Blood Pressure Assessment

If systolic BP 180-230 mm Hg BP every 15 minutes during
and/or diastolic BP 110-120 treatment

mm Hg on 2 readings 5-10
minutes apart

Systolic BP > BP every 15 minutes during
230 mm Hg and/or diastolic treatment
121-140 mm Hg

Diastolic BP > BP every 15 minutes during
140mm Hg treatment

Blood Pressure Nursing Indication

If systolic BP 180-230 mm Hg Observe for hypotension
and/or diastolic BP 110-120
mm Hg on 2 readings 5-10
minutes apart

Systolic BP > Observe for hypotension
230 mm Hg and/or diastolic
121-140 mm Hg

Diastolic BP > Observe for hypotension
140mm Hg

Adapted from the NINDS rt-PA Stroke Study Group

Bleeding Assessment

The most frequent adverse reaction associated with rt-PA in all approved indications is bleeding.[16] Intracerebral hemorrhage (ICH) is usually accompanied by an acute change in neurologic status and/or vital sign instability. In the NINDS rt-PA Stroke Trial, the most common signs and symptoms were decreased level of consciousness, changes in motor examination, new headache and increases in blood pressure. If ICH is suspected, a CT scan of the head and coagulation studies should be obtained immediately, and the remainder of the hemorrhage treatment algorithm should be initiated (Fig 1).

[Figure 1 ILLUSTRATION OMITTED]

Peripheral bleeding at venipuncture sites, recent abrasions, shaving nicks and gingival oozing are common in patients receiving thrombolytic therapy. These same symptoms may indicate the patient is at increased risk for intracerebral hemorrhage. Assessment of the skin and oral cavity before, during and after infusion is necessary to detect sites of peripheral bleeding. once detected, pressure should be applied and maintained until oozing stops to prevent hematoma formation. Automatic blood pressure cuffs should be used carefully on patients with antecubital venous access to prevent hematoma formation. Mouthwashes or soft sponges should be used for oral care rather than toothbrushes to prevent unnecessary oral trauma within the first 24 hours after receiving rt-PA.

Cardiac Monitoring

Continuous ECG monitoring should be established and continue for a minimum of 24 hours. Cardiac arrhythmias are common in patients with acute stroke. Also life-threatening arrhythmias contributing to the stroke etiology or resulting from the stroke may be detected in the acute treatment period. Ventricular ectopy, tachycardia and atrioventricular block and asystole are among the serious arrhythmias reported in up to 50% of patients early in the course of acute stroke.[13] Arrhythmias cause concern because they may decrease cardiac stroke volume and compromise cerebral blood flow. These acute ECG changes are felt to be related to an interaction between underlying hypertensive and cardiovascular disease and sympathetic hyperactivity and may cause some degree of myocardial injury.[8] Atrial fibrillation may increase the patient's risk of a second stroke.

In the NINDS trial, the incidence of cardiac arrhythmias was the same in the rt-PA treated group (n=80) and the placebo-treated group (n=79). Moreover, acute myocardial ischemia with the initial hospitalization occurred equally in both the rt-PA treated group (n=14), and the placebo group (n=13).[16] Cardiac consultation should be considered since acute myocardial infarction is a leading cause of death following stroke.

Medications to Avoid in the First 24 Hours

Unlike the AMI population, anticoagulant (warfarin, heparin) or antiplatelet (aspirin) drugs are not recommended until 24 hours after the initial bolus of rt-PA. Prior to initiating any anticoagulant therapy, a repeat head CT scan should be obtained to rule out ICH. Sedatives and narcotics are also discouraged as they could decrease patient responsiveness and confound the neurologic evaluation.

Management Issues Independent of rt-PA therapy

At most institutions, the standard of care provided to patients with ischemic stroke continues to be prevention of stroke extension and secondary complications. Recent reports on the advantages of critical paths for stroke include these standard treatments and often improve resource utilization when followed.[12,18] This improved resource management is most often related to revision of traditional care delivery systems, eliminating redundant use of resources, minimizing delays in consultation and reducing diagnostic testing that is considered "low yield" in a cost/benefit analysis. Ideally, an aggressive stroke treatment plan is incorporated into a stroke pathway that manages secondary complications as well as resource utilization. Nursing care directives and therapy referrals should include assessment and intervention strategies. Clinical pathways which include these interventions are optimally in place within 24 hours of admission for each stroke patient (Table 5).

Table 5. Acute Ischemic Stroke ICH / Systemic Bleed Clinical Pathway for rt-PA

Suspect ICH if: new complaints of H/A, increased
weakness sudden marked changes in VS, sudden change in
LOC, nausea/vomiting, diaphoresis/pallor, seizure activity,
and/or hiccups.
Suspect systemic bleeding if: decreased LOC, tachycardic,
hypotensive, cool, clammy, diaphoretic and/or pallor.

Admission weight: Admission NIHSS score:

Care Element Suspect ICH/systemic bleed

Consults: Neurosurgery if ICH suspected
Hematology if ICH suspected
General surgery if systemic bleed suspected

Assessments: VS q 15 min.
Neuro exam, cardinal sign q 15 min
Continuous EKG monitoring with interpretation
Check for gingival or IV site oozing

Diagnostics: STAT noncontrast head CT scan
Labs: Stat: PT/PTT, fibrinogen, CBC with PLT,
type and cross and bleeding time
Pulse Oximeter, consider [SVO.sub.2] Brain
Oximeter
Consider ICP monitor
Consider hemodynamic monitoring
Check for occult blood in stool
Treatments: If receiving thrombolytic - stop infusion

Consider continuous drip for BP management
[O.sub.2] PRN
Consider intubation and hyperventilation
Consider mannitol
Consider blood products (cryo, FFP, PLT and/or
PRBCs)
Consider surgery
Apply pressure to compressible sites for
major or minor systemic bleeding

Activity:
Bedrest
Change position q1-2 hrs as tolerated
Nutrition:

NPO

Admission weight: Cardinal sign:

Care Element 2-24 hrs post-ICH

Consults: Same

Assessments: VS q1 hr and PRN
Cardinal sign, neuro exam
GCS/pupil check q1 hr and PRN
Monitor ECG
Monitor [SVO.sub.2,] ICP

Diagnostics: Labs: Na++, osmolality (if on mannitol)
Glucose q6 and PRN (with history of
ABGs [CO.sub.2] 30-35 (hyperventilation)
Pulse [O.sub.2] consider brain oximeter
Consider ICP monitor

Treatments: Keep [PO.sub.2] > 90 mm Hg
Keep [CO.sub.2] 30-35 mm Hg
Consider mannitol 25 gm q4-6hr
Consider BP management
Consider surgery treat DKA HOC with
insulin drip PRN

Activity: Same

Nutrition: Same

Admission weight:

Care Element 24-36 hrs post-ICH

Consults: Same

Assessments: Advance VS as to
Advance neuro, exam
Consider dc ECG

Diagnostics: Consider dc [O.sub.2] monitors

Treatments: Keep [PO.sub.2] > 90 mm Hg
Wean hyperventilation
Wean mannitol
Wean BP gtt, add oral agent

Activity: Advance as tol
Nutrition: Consider TPN/enteral feed

Continued monitoring of neurologic condition and vital signs, as well as other standard care practices must be initiated immediately in order to optimize the stroke patient's outcome. These practices include treatment of conditions that would exacerbate newly infarcted brain tissue such as hypoxia, dehydration, hypotension, hyperglycemia, hyperthermia, poor nutrition and interventions to prevent secondary complications. In addition, new conditions may surface in response to the physiologic stress caused by stroke. The general physiologic compromise resulting from stroke may exacerbate preexisting medical conditions that were previously controlled, or secondary complications may further cloud the neurological picture.[3]

Oxygenation is an important concern in the acute ischemic stroke patient. Nursing assessment and intervention should include monitoring oxygen saturation. Many acute stroke patients have obstructive breathing patterns or chronic pulmonary dysfunction which require individualized oxygen management. Pulse oximetry is recommended for monitoring the oxygenation status of the acute stroke patient, and if desaturation occurs, treatment with supplemental oxygen should be initiated.

Adequate hydration without fluid overload may be difficult, particularly in patients with previous cardiopulmonary compromise. Hypovolemia should be corrected in order to optimize cardiac output. Nonglucose containing solutions are recommended. Monitoring of fluid balance through careful measurement of fluid intake and output and treatment of electrolyte disturbances is critical for these patients.
Continued surveillance of blood pressure is important in stabilizing these patients. Antihypertensive treatment should be conservative with doses adjusted as needed to maintain optimum perfusion while controlling high pressures.[14] In an effort to avoid postural hypotension (and potential cerebral ischemia) when patients are first getting out of bed, gradually mobilize the patient, even after short-term bedrest.

Blood glucose should be monitored aggressively and treated appropriately. Serum glucose levels should be targeted at 100mg/dl using sliding scale insulin. The actual range may vary from patient to patient according to the patient's medical history. Patients with elevated blood sugars have been found to develop larger infarctions than those with normal blood sugar levels.[12]

Hyperthermia must be treated immediately. Temperature elevations during ischemia have been found to accelerate and extend pathologic changes in the brain due to increase metabolic needs.[7] Body temperature can be easily monitored, elevated temperatures should be treated with appropriate antipyretic medications and the potential for infection investigated.

Poor nutrition has also been implicated in slower recovery and increased susceptibility to infection in patients with ischemic stroke.[4] Bedside dysphagia testing should be performed within 24 hours of hospital admission or prior to oral feeding or oral medication. This bedside assessment is used to detect the presence of a compromised swallow and assess the risk of aspiration pneumonia. After swallowing has been evaluated, a plan for optimal nutritional therapy can be established.
Patients who have experienced stroke are at risk for developing a wide range of secondary complications which could result in further neurological or medical compromise, or even death. Stroke deficits may include immobility, altered judgement and/or perception or sensory deficits. These deficits lead to complications such as aspiration, falls, systemic infections and venous thrombosis.[10] Medical complications that have been associated with stroke, such as urinary tract infection, pneumonia and sepsis were not significantly different among the treated and placebo groups during the initial hospitalization for stroke.[5] Seizures occurred more often in the rt-PA group and depression occurred more often 3. in the placebo group, however these differences were not statistically significant (p=0.056, p=0.0564. respectively). No differences in medical complications could be detected in the trial patients. However, the rt-PA treated group had a shorter length of stay than the placebo treated group (10.9 days vs. 12.4 days; p=0.02). Also, the rt-PA treated patients were more likely to be discharged to home, (rt-PA=48%, placebo=36%; p=0.04).[6]

Stroke patients are at risk for further neurologic compromise due to cerebral edema and increased 8. intracranial pressure. Brain swelling due to neural cellular (cytogenic) and vascular (vasogenic) disruption is present with all strokes in varying degrees. Massive edema causes increased intracranial pressure, hemispheric shift, brainstem compression and, in extreme cases, herniation and death. Cerebral edema maximizes approximately 24-72 hours following infarction. All stroke patients should be monitored for signs and symptoms of increased intracranial pressure.
Diagnostic evaluation to determine the stroke etiology follows acute treatment as well. Continuous ECG monitoring may detect new onset paroxysmal atrial fibrillation. CT scan, carotid doppler ultrasound and echocardiography are common noninvasive tests used to establish the cause of the stroke. Treatment may include control of risk factors, use of antiplatelet or anticoagulant therapy, surgical and/or interventional neuroradiologic procedures.

Summary

Acute stroke treatment with rt-PA requires intensive care Management of the acute stroke patient. Management decisions such as assessment methods, staffing patterns, patient placement and resource allocations must be adjusted to these changing care requirements. The risks of ICH and the need for vigilance and rapid intervention make it clear that effective nursing care is crucial. Only direct observation and neurological assessment will detect these changes. Nurses must safely, effectively and appropriately manage these patients who are at risk for rapid and serious deterioration. With rt-PA being a proven treatment for acute ischemic stroke, nurses' ability to rapidly identify patients, facilitate treatment and deliver effective post-treatment care can reduce disabilities and death due to acute ischemic stroke.

References

[1.] Brott T, MacCarthy EP: Antihypertensive therapy in stroke. Med Therapy Acute Stroke 1989; 8:117-141.

[2.] Brott T, Reed RL: Intensive care for acute stroke in the community hospital setting. Curr Concept Cerebrovasc Dis Stroke 1989; 20(5):694-697.

[3.] Censori B, Camerlingo M, Casto L et al: Prognostic factors in first-ever stroke in the carotid artery territory seen within 6 hours after onset. Stroke 1993; 24:532-535.

[4.] Davalos A, Ricart W, Gonzalez-Huix F et al: Effect of malnutrition after acute stroke on clinical outcome. Stroke 1996; 27:1028-1032.

[5.] Davenport RJ, Dennis MS, Wellwood L, Warlow CP: Complications after acute stroke. Stroke 1996; 27:415-420.

[6.] Fagan SC, Morgenstern LB, Pettita A et al: t-PA reduces length of stay and improves disposition following stroke. Stroke 1997; 28:272.

[7.] Ginsberg MD, Sternau L, Globus MY-T, Dietrich WD, Busto R: Therapeutic modulation of brain temperature: Relevance to ischemic brain injury. Cerebr Brain Metab Rev 1992; 4:189-225.

[8.] Goldstein DS: The electrocardiogram in stroke: Relationship to pathophysiological type and comparison with prior tracings. Stroke 1979; 10(3):253-259.

[9.] Guidelines for the Management of Patients With Acute Ischemic Stroke. A Statement for Healthcare Professionals, from a special writing group of the stroke council. American Heart Association, 1994.

[10.] Henon H, Godefroy 0, Leys D et al: Early predictors of death and disability after acute cerebral ischemic event. Stroke 1995; 26:392-398.

[11.] Lyden PD, Brott T, Tilley B et al: Improved reliability of the NIH Stroke Scale using video training. Stroke 1994; 25:2220-2226.

[12.] Matchar DB, Divine GW, Heyman A et al: The influence of hyperglycemia on outcome of cerebral infarction. Ann Intern Med 1992-1 117:449-456.

[13.] Mikolich JR, Jacob WC, Fletcher GF: Cardiac arrhythmias in patients with acute cerebrovascular accidents. JAMA 1981; 246:1314-1317.

[14.] Shepherd TJ, Fox SW: Assessment and management of hypertension in the acute ischemic patient. J Neurosci Nurs 1996; 28(1):5-12.

[15.] Strandgaard S, Paulson OB: Cerebral autoregulation. Stroke 1984; 15:413-416.

[16.] The National Institute of Neurological Diseases and Stroke rt-PA Stroke Trial Group: Tissue plasminogen activator for acute ischemic stroke. New Eng J Med 1996; 333:1581-1587.

[17.] Wallace JD, Levy LL: Blood pressure after stroke. JAMA 1981; 246:2177-2180.

[18.] Wentworth DA, Atkinson RP: Implementation of an acute stroke program decreases hospitalization cost and length of stay. Stroke 1996; 27:1040-1043.

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