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Nursing management of acute complications following rt-PA in acute ischemic stroke.

Introduction

The NINDS rt-PA stroke trial was a randomized, double-blind, placebo-controlled study, which enrolled a total of 624 patients within three hours of onset of acute ischemic stroke (AIS). Overall, the results demonstrated that patients treated with rt-PA were at least 30% more likely to have minimal or no deficit at three months following their stroke.[16] Despite the overwhelming evidence that those treated with rt-PA improved, this treatment is not without risk. Examining the complications of thrombolytic therapy for AIS guides specific care for this patient population.

Intracranial Hemorrhage

The primary adverse event monitored in the NINDS rt-PA stroke trial was intracranial hemorrhage (ICH). Intracranial hemorrhage was identified by computed tomography WT) scan. Routine follow-up CT scans were obtained at 24 hours, 7 days and 3 months after thrombolysis per study protocol and at other intervals as determined by patient condition. Symptomatic ICH was diagnosed by CT done in response to neurologic deterioration. Asymptomatic ICH was noted on CT scans performed for routine follow-up. A symptomatic ICH rate of 6.4% was observed within the first 36 hours after the treatment (rt-PA n=25, placebo n=5, p [is less than] 0.001).[16] All fatal ICH (rt-PA n=9, placebo n=1) occurred within 24 hours of treatment.[17] Of those fatal hemorrhages eight (rt-PA=7 and placebo=1) occurred within 12 hours.[17]

Prevention of Intracranial Hemorrhage

The highest risk for fatal ICH occurs during treatment and immediately following for 24 hours, Therefore, knowledge of physiology, prevention and recognition of ICH symptoms, and the ability to urgently intervene are essential. Prevention of secondary neurologic injury is always a goal immediately following acute stroke.

Basic critical care considerations of maintaining adequate cardiac output, oxygenation, glucose control and electrolyte balance should not be ignored to prevent secondary neurologic complications. However, before and after thrombolysis, stringent blood pressure (BP) management is the single most important preventive measure. Therefore, frequent blood pressure monitoring is required. In the NINDS rt-PA stroke trial protocol, blood pressure was taken every 15 minutes until 1 hour post infusion. This was followed with vital signs and neuro checks every 30 minutes for 6 hours and then hourly for a total of 24 hours.

Elevated blood pressure often accompanies an acute ischemic event. This occurs as ischemic brain tissue releases catecholamines that raise systemic blood pressure in an attempt to deliver needed oxygen and glucose.[3] For this reason most physicians will not decrease blood pressure of an ischemic stroke patient unless it increases to 220 mm Hg systolic, and/or 120 nun Hg diastolic and above.[7] Guidelines for managing hypertension in acute stroke patients recommend lowering mean arterial pressure (MAP) no more than 10%, in gradual increments.[15] During acute stroke, autoregulation may be impaired. Rapid changes in MAP alter cerebral blood flow (CBF) and may potentiate the ischemic cascade.[13] Therefore, while manipulating the blood pressure, it is critical to monitor the neurologic response to the titration or administration of these medications.

When considering thrombolytic treatment for AIS, blood pressure must be controlled since severe hypertension increases the risk for ICH.[8] In the NINDS rt-PA stroke trial, recommended BP was [is less than] 185 mm. Hg systolic and [is less than] 105 mm Hg diastolic on repeated measurements prior to thrombolytic treatment. Hypertension was treated with labetalol 5-10 mg intravenous push (IVP). The dose was repeated every 10 minutes as often as needed to achieve desired results. If a beta blocker was not indicated, one inch of nitropaste to the chest wall was used to, reduce the blood pressure. If the patient required a continuous IV infusion of antihypertensive medication to manage BP, the patient was considered to have uncontrolled hypertension and was deemed not an appropriate candidate for thrombolytic therapy. Future technology may help determine the patient's cerebral blood flow status, and more readily identify patients at risk for ICH and facilitate specific blood pressure management during the acute post-thrombolytic phase.[9]

The same blood pressure treatment parameter (systolic [is less than] 185 mm/Hg, diastolic [is less than] 105 mm/Hg) was utilized after thrombolysis treatment to reduce ICH risk.[16] Labetalol or nitroprusside continuous IV infusion may be used if needed. Alternatively, calcium channel blockers and other antihypertensives may be used with caution due to the potential for a precipitous drop in BP that would potentiate the ischemic process.

The need for frequent blood pressure measurements required the use of automated cuffs. However, these cuffs contributed to excessive bruising and oozing at the antecubital intravenous site and should be used with caution. One patient in this trial developed excessive bruising below the blood pressure cuff that required surgical aspiration of clot. It is recommended that when the cuff is not inflated, it should be loosened. Also, the cuff site be checked frequently and its position rotated every two hours.

Pathophysiology

The pathological impact of ICH is two-fold and the severity is often determined by location of bleeding. ICH causes structural damage to the brain by destroying surrounding brain tissue with expanding clot (Fig 1). The pressure of the clot disrupts blood flow and the surrounding rim of the clot becomes ischemic. The clot may also increase intracranial pressure by acting as a space-occupying lesion, or by causing edema in the surrounding ischemic area. Increased intracranial pressure may further compromise CBF and cause additional cerebral edema. Rebleeding or cerebral edema may become serious enough to cause midline shift, possible herniation and death.[13] In general ICH presents as a gradual and continuous progression of symptoms over minutes to a few hours. Blood pressure is usually elevated. Focal deficits are related to the location of the hemorrhage. As the hematoma extends, the patient may complain of a headache and nausea and vomiting, and have a change in level of consciousness.[8]

[Figure 1 ILLUSTRATION OMITTED]

Clinical Findings

The neurological clinical signs and symptoms of ICH in this trial varied. This was due in part because the location of the hemorrhage was not always in the area of the treated infarction. Signs and symptoms may be the result of an unrelated or undiagnosed space-occupying lesion. A nurse caring for a stroke patient who deteriorates neurologically after thrombolytic treatment must always first consider ICH until proven otherwise. Nursing assessment should focus on the level of consciousness, comparative motor strength, vital sign changes and degree of headache. The most common presenting signs and symptoms among the 22 symptomatic patients were: change in level of consciousness (91%), increased weakness (73%), significant change in vital signs (50%) and headache (41%).[17]

Post-treatment variables such as hypertension, bleeding and all adverse events in the study were examined to determine if there were any associations that predicted ICH. No post-treatment variable was significantly associated with symptomatic hemorrhage within 36 hours among rt-PA-treated patients. However in univariate analysis, gingival or intravenous site oozing, mean systolic BP [is greater than] 185 mm/Hg, mean pulse pressure and number of times pulse pressure exceeded 50 mm Hg up to one hour before hemorrhage were associated (p [is less than] 0.05) with symptomatic or asymptomatic ICH within 36 hours.[17] In multivariate analysis, only oozing (p=0.02) was significantly associated with any ICH.[17] As a result, patients with oozing or systolic blood pressure elevations require particularly cautious management and frequent thorough assessment.

Interventions for Post-thrombolysis Hemorrhage

Once ICH was suspected, the stroke team followed a predetermined algorithm (Table 1).[16] Blood products (cryoprecipitate, fresh frozen plasma or platelets) were given to 13 (51%) of the 22 symptomatic ICH patients. The decision to treat aggressively was jointly made by the treating physician, the medical-surgical consultants and the patient's family. In the NINDS rt-PA stroke trial, only one symptomatic hemorrhage patient was taken for surgical intervention.[17] A critical pathway was designed as a result of the trial to guide nurses in caring for patients with post-thrombolysis ICH (Table 2).

Table 1. Hemorrhage Algorithm(*)
1. If not present, treating physician/investigator was notified of
a change in status

2. If drug infusing, drug was discontinued

3. Facilitate key diagnostic procedures:
 a. Rapid collection of blood samples for stat PT, PTT,
 fibrinogen, CBC with PLT, and type and cross and bleeding
 time
 b. Rapid transport for stat CT of head without contrast

4. Alert hematologic and neurosurgical consults

5. Anticipate possible:
 a. Administration of cryoprecipitate, plts, or RBCs
 b. Repeat CT scan
 c. Surgical intervention




(*) NINDS rt-PA Stroke Trial

[TABULAR DATA 2 NOT REPRODUCIBLE IN ASCII]

If ICH occurs, blood pressure management remains an important clinical factor. Studies of the relationship of hypertension and spontaneous ICH have shown that a reduction in BP is necessary to avoid further bleeding.[4] Extreme fluctuations in BP are also deleterious. Hypotension may produce hypoperfusion causing secondary ischemia.[13] Common complications following ICH are rebleed, hydrocephalus, cerebral edema, sepsis and death.[11] Surgical and medical interventions post ICH will depend upon the patient's condition, the family's wishes and the stroke team's plan of care.

Hemorrhagic Transformation

Not all hemorrhages following ischemic stroke can be attributed to rt-PA therapy. Hemorrhagic transformation (HT), is a natural phenomena in the ischemic stroke population. Hemorrhagic transformation is common in large infarcts and cardioembolic strokes.[7] The absolute incidence of HT is not known. The literature reports a variable incidence of 50-70%.[8] Although the mechanism of HT is not fully understood, the most accepted theory is presented by Fisher and Adams.[6] Following occlusion and infarction of brain tissue, the clot or embolic fragments migrate from the source of occlusion to distal branches. Blood flow may be partially re-established and blood leaks through damaged vessels.[2,6,8] In large infarcts, cerebral edema occludes the nearby small blood vessels. Once the edema subsides reperfusion of the occluded small vessels result in extravasation of blood from the damaged vessels into the brain tissue (Fig 2).[8]

[Figure 2 ILLUSTRATION OMITTED]

There is concern that thrombolytic therapy for AIS may extend the naturally occurring HT, by reperfusing potentially damaged vessels. Two previous rt-PA studies found no difference in the rate of HT between rt-PA treated and placebo groups.[5,12] Hemorrhagic transformation can be diagnosed by CT scan within 7-10 days following the stroke (Fig 2). Before initiating anticoagulation therapy a CT scan must be done to rule out HT.

Major and Minor Systemic Bleeding

All types of systemic bleeding events were significantly more common in the rt-PA group (rt-PA n=168, placebo n=104, p [is less than] 0.001).[17] Life-threatening systemic bleeding events occurred more frequently in the rt-PA treated group than the placebo group, but not at a significantly higher rate. These bleeding events, with the exception of ICH, were consistent with the general safety profile of the drug when used for other indications such as myocardial infarction or pulmonary embolus.[1] Bleeding precautions should be implemented, and nurses must be prepared to intervene when the patient demonstrates signs and symptoms of bleeding. Since gingival or IV site oozing (evidence of systemic lytic state) were significantly associated with ICH, nurses must be vigilant when assessing the rt-PA-treated stroke patient. If oozing is observed, it is prudent to check fibrinogen levels, CBC and platelets, send a type and crossmatch, assess the patient more frequently and immediately notify the physician so that the patient's care plan care be rapidly reevaluated to decrease any potential for ICH.

Reocclusion

In the NIH rt-PA stroke trial, a subgroup of patients experienced neurological improvement following treatment, then deteriorated again. Documented experience with reocclusion following thrombolysis in the AMI population contributed to clinical concerns of reocclusion of the cerebral vessels following clot lysis. The incidence of reocclusion of a cerebral artery following AIS thrombolysis was not documented as cerebral angiography was not obtained before or after treatment. Therefore, reperfusion or reocclusion were not diagnostically confirmed. It was felt that deterioration following improvement (DFI) would indicate reperfusion followed by reocclusion. DFI was defined as an increase of 4 or more points in the NIH Stroke Scale (Table 3) within the first 24 hours following a 4 point decrease in the Stroke Scale score from baseline. On analysis, DFI was found equally among treated (n=80) and placebo (n=72) patients.

Table 3. Quick Screen NIHSS
Test baseline 15 min 30 min 45 min

LOC, 1 1 1 4
Motor arm 1 1 2 4
Motor leg 1 1 2 4
Cardinal sign 1 1 1 2
(motor face)
TOTAL 4 4 6(*) 14




(*) [is greater than or equal to] 2 point change; perform complete NIHSS

New Stroke

The incidence of new stroke is increased in the first year. The risk of recurrent stroke within the first 30 days and long-term risk of recurrence averages 4-14% per year.[14,18] In the NINDS rt-PA stroke study, new stroke was defined as any symptomatic stroke other than baseline in a new vascular territory or in the same vascular territory as a baseline event after hospitalization. The incidence of second The rate of new stroke did not differ between the two groups (rt-Pa group n=18, placebo group n=17). Thrombolytic therapy is not recommended for a second stroke that occurs within 3 months of an initial stroke because of the increased risk of hemorrhage.

Mortality

Despite the higher rate of ICH and potential for systemic bleeding using thrombolytics, there was no significant difference in mortality at 90 days after stroke onset between rt-PA-treated (n=54, 17%) and those receiving placebo (n=64, 21%).[16] Survival after stroke was evaluated over time and at no point did the rt-PA-treated group deaths exceed deaths in the placebo group.

Nursing Management

Acute stroke patients have always challenged neuroscience nurses. Undoubtedly, nurses play a vital role in the outcome of these patients. The results of the NINDS trial provide information to guide nurses in developing practice standards and pathways for AIS patients. As experience increases with these patients, clinicians need to document patient responses to treatment and identify signs and symptoms that may hold predictive value in determining ICH. The NIHSS (a deficit scale) and Barthel (a functional scale) must be incorporated in the routine assessment of these patients. These scales measure the patients' progress and provide outcome data for peer review. The competency level of knowledge and skills in the area of AIS must improve among all nurses. Education of patients, their families and the community is crucial to the awareness, prevention and response to acute stroke.

The patient and family should not be discharged from the hospital without an understanding of the stroke type, cause of their stroke and knowledge that stroke can strike again. Each patient should understand their risk factors and how to modify their risk for secondary stroke prevention, and slow cerebrovascular disease progression.

Summary

rt-PA treatment of AIS offers potential improvement of stroke symptoms as well as risk of ICH. Although there was an increased hemorrhage rate in the rt-PA treated group, the mortality was comparable.[16] Careful screening, management of hypertension and precautions to lessen the risk of hemorrhage are important aspects of nursing care for these patients. Thorough and frequent assessments to detect hemorrhage early are critical to the safe delivery of rt-PA treatment to acute ischemic stroke patients. Response to rt-PA treatment accompanied by expert nursing care is the ideal combination for patient recovery from the devastating sequelae of stroke.

References

[1.] Activase (Alteplase, rt-PA) Package Insert. Genentech, Inc, 1996.

[2.] Adams RD, Victor M: Principles of Neurology, 4th edition. McGraw-Hill, 1989.

[3.] Barch C: Stroke: Acute cerebral infarct and intracerebral hemorrhage. Pages 470-485 in: Manual of Critical Care Nursing, Swearingen P, Keen J (editors). Mosby, 1995.

[4.] Dandapani B, Suzuki S, Kelly R, Reyes-Iglesias Y, Duncan R: Relation between blood pressure and outcome in intracerebral hemorrhage. Stroke 1995; 26(1):21-24.

[5.] del Zoppo G et al: Recombinant tissue plasminogen activator in acute and embolic stroke. Ann Neurol 1992; 32:78-86.

[6.] Fisher CM, Adams RD: Observations on brain embolism with special reference to the mechanism of hemorrhagic infarction. J Neuropathol Exp Neurology 1951; 10:92-94.

[7.] Hund E, Grau A, Hacke W: Neurocritical care for acute ischemic stroke. Neurol Clin 1995; 13(3):511-527.

[8.] Kase C, Caplan L: Intracerebral Hemorrhage. Heinemann, 1994.

[9.] Kaufmann et al: Assessment of acute stroke with xenon cerebral blood flow measurements: Selection guidelines for thrombolytic treatment. J Cerebrovasc Dis 1996; 6:2-14.

[10.] Keller C, Williams A: Cardiac dysrrhythmia associated with central nervous system dysfunction. J Neurosci Nurs 1993; 25(6)349-355.

[11.] Mitchell S, Yates R: Cerebrovascular disease. Pages 593-594 in: Critical Care Nursing: Body-Mind-Spirit, Dossey B, Guzzetta C, Kenner C (editors). JB Lippincott, 1992.

[12.] Mori E, Yoneda Y, Tabuchi M et al: Intravenous recombinant tissue plasminogen activator in acute carotid artery territory stroke. Neurology 1992: 42:976-982.

[13.] Powers W: Acute hypertension after stroke: The scientific basis for treatment decisions. Neurology 1993;43:461-467.

[14.] Sacco RL, Hauser WA, Mohr JP, Foulkes MA: One year outcome after cerebral infarction in whites, blacks and hispanics. Stroke 1991; 22:305-311.

[15.] Shephard T, Fox S: Assessment and management of hypertension in the acute ischemic stroke patient. J Neurosci Nuts 1996; 28(1):5-12.

[16.] The National Institute of Neurological Disorders and Stroke (NINDS) rt-PA Stroke Study Group: Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995; 333:1581-1587.

[17.] The National Institute of Neurological Disorders and Stroke (NINDS) rt-PA Stroke Study Group, Submitted.

[18.] Viitanen M, Eriksson S, Asplund K: Risk of recurrent stroke, myocardial infarction, and epilepsy during long-term follow-up after stroke. Eur Neurol 1988; 29:227-231.

Carol Barch, Judith Spilker, Patty Bratina, Karen Rapp, Sheila Daley, Rosario Donnarumma, Sharion Sailor, Janet Braimah, Gail Kongable and the NINDS rt-PA Stroke Study Group

Questions or comments about this article may be directed to: Carol Barch, MN, RN, CRNP, CNRN, University of Pittsburgh Medical Center, Stroke Institute, 200 Lothrop Street, Suite C-422, Pittsburgh, Pennsylvania 15213.
COPYRIGHT 1997 American Association of Neuroscience Nurses
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 1997 Gale, Cengage Learning. All rights reserved.

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Title Annotation:Special Issue on rt-PA Stroke Treatment; recombinant tissue plasminogen activator
Author:Barch, Carol; Spilker, Judith; Bratina, Patty; Rapp, Karen; Daley, Sheila; Donnarumma, Rosario; Sail
Publication:Journal of Neuroscience Nursing
Date:Dec 1, 1997
Words:2982
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