CVA patients to wrong hospital, may cause legal action

[Connie31079]

A question to everyone out there:

If you're toned out to a chest pain call, and after a 12-lead and history, you determine that your patient is having an MI, do you:

A.) go to the closest hospital that has the ability to administer thrombolytics, before the patient goes to a hospital with cardiac cath capability?

or

B.) go directly to the hospital with cardiac cath capability, even though it's twice as far away as your closest hospital that has the ability to give thrombolytics??

I've been faced with this exact situation many times, and have always made the choice to stop at my closest hospital, get the patient thrombolyzed, and then continue on to the hospital with cardiac cath capabilities. The patient didn't even come off our stretcher at the first hospital we stopped at, bloodwork was done within 2 minutes of us arriving there, it was determined the patient was a candidate for thrombolytics, it was given as a bolus (we use TNKase here), and then we were off to the next hospital with cardiac cath.

[AZCEP]

There has been numerous discussions about the prehospital triage/transport to capable facilities for each of these groups of patients.

The AMI goes to a cath lab, the trauma patient goes to a trauma center, and the stroke patient goes to a neuro center, that simple.

It does no one any good to transport to the "nearest" facility that can not perform the treatment that is needed when we come in the door. These patients have to be identified and transported directly to a facility that can fix the problem. If this means using air resources to justify bypassing then so be it. Very unusual to find medical direction that opposes patients receiving appropriate treatment.

[Guest Beegers]

I suppose I luck out by me, seeing as I have 2 trauma 2 centers equal distance away, and the majority of hospitals in the area here has some form of stroke program. There are only 2 hospitals that I primarily transport my drunks to because, well, that's all they are good for.

[Ace844]

(Stroke. 2006;37:1710.)

© 2006 American Heart Association @ Inc. Original Contributions

Is the ABCD Score Useful for Risk Stratification of Patients With Acute Transient Ischemic Attack?

Brett L. Cucchiara, MD; Steve R. Messe, MD; Robert A. Taylor, MD; James Pacelli, MD; Douglas Maus, MD; Qaisar Shah, MD Scott E. Kasner, MD

From the University of Pennsylvania Medical Center (B.L.C., S.R.M., J.P., D.M., Q.S., S.E.K.), Philadelphia; and the University of Iowa (R.A.T.), Iowa City, Iowa.

Correspondence to Brett Cucchiara, MD, Department of Neurology, University of Pennsylvania Medical Center, 3400 Spruce St, Philadelphia, PA 19104. E-mail cucchiar@mail.med.upenn.edu)

Background and Purpose— A 6-point scoring system (ABCD) was described recently for stratifying risk after transient ischemic attack (TIA). This score incorporates age (A), blood pressure (, clinical features ©, and duration (D) of TIA. A score <4 reportedly indicates minimal short-term stroke risk. We evaluated this scoring system in an independent population.

Methods— This was a prospective study of TIA patients (diagnosed by a neurologist using the classic <24-hour definition) hospitalized <48 hours from symptom onset. The primary outcome assessment consisted of dichotomization of patients into 2 groups. The high-risk group included patients with stroke or death within 90 days, 50% stenosis in a relevant artery, or a cardioembolic source warranting anticoagulation. All others were classified as low risk. Findings on diffusion-weighted MRI (DWI) were also evaluated when performed and patients classified as DWI+ or DWI–.

Results— Over 3 years, 117 patients were enrolled. Median time from symptom onset to enrollment was 25.2 hours (interquartile range 19.8 to 30.2). Overall, 26 patients (22%) were classified as high risk, including 2 strokes, 2 deaths, 15 with 50% stenosis, and 10 with cardioembolic source. The frequency of high-risk patients increased with ABCD score (0 to 1 13%; 2 8%; 3 17%; 4 27%; 5 26%; 6 30%; P for trend=0.11). ABCD scores in the 2 patients with stroke were 3 and 6. Of those who underwent MRI, 15 of 61 (25%) were DWI+, but this correlated poorly with ABCD score (0 to 1 17%; 2 10%; 3 36%; 4 24%; 5 13%; 6 60%; P for trend=0.24).

Conclusions— Although the ABCD score has some predictive value, patients with a score <4 still have a substantial probability of having a high-risk cause of cerebral ischemia or radiographic evidence of acute infarction despite transient symptoms.

(Editorials Is the ABCD Score Truly Useful?

Michael D. Hill @ MD, MSc Nicolas U. Weir, MD, MSc

From the University of Calgary, Department of Clinical Neuroscience, Foothills Medical Centre, Calgary, AL, Canada.

Correspondence to Michael D. Hill, MD, University of Calgary, Department of Clinical Neuroscience, Rm 1242A, Foothills Medical Centre, 1403 29th Street NW, Calgary, Al T2N 2T9, Canada. E-mail michael.hill@calgaryhealthregion.ca)

The understanding of transient ischemic attack (TIA) has changed. The high early risk of stroke demands rapid assessment and treatment. Some patients, such as those with TIA attributable to an active carotid artery plaque, appear to be at higher risk than others.1 The direct result of this paradigm shift is the need to develop tools for stratifying patients according to risk. Although some have adopted a strategy of admitting all TIA patients, this approach may not be the most efficient. Clinical prediction rules may be the most helpful in triaging patients. Factors that are risks for early stroke include clinical ones such as age, diabetes mellitus, longer duration TIA, motor or speech symptoms of TIA, and imaging factors such as the presence of carotid artery disease or a diffusion-weighted imaging lesion on MRI.2–4 The clinical imperative is to sort out those patients who need immediate attention and those who do not.

Why must we risk stratify? A large number of TIA patients do not go on to experience an early stroke. These patients do not need to be exposed to potentially risky therapies from which they will derive no benefit, nor do they need to use scarce and high-intensity resources. The corollary is that we need to learn how to identify those patients who truly are at high risk and offer them emergent assessment, imaging and therapies where the benefit clearly outweighs the risk.

The ABCD score, developed in England, is a clinical tool to stratify TIA patients according to their 7-day risk of stroke.5 The score is derived as follows:

Age >60=1 point.

BP >140/90=1 point.

Clinical features: unilateral weakness=2 points; language disturbance without weakness=1 point; Other=0 points.

Duration: >60 minutes=2 points; 10 to 59 minutes=1 point; <10 minutes=0 points.

The score was derived from the OCSP cohort from 2 decades ago and validated in a more recent cohort in Oxfordshire. A score <4 predicted a 0% risk of stroke in the first week.

The present study assessed the ABCD score in a North American series of TIA patients and concluded that the ABCD score is not useful. However, it should be carefully noted that the outcome chosen was a composite one including stroke, death, ipsilateral carotid stenosis >50% or a cardioembolic source warranting anticoagulation. Although this choice of outcome is a pragmatic one, it is different than the stroke or death outcome on which the ABCD score was validated.

In contrast to the risk of stroke of 10% in the Oxfordshire series, the risk of stroke was slightly <2% in this Pennsylvania series, perhaps because some patients with stroke in the first 24 hours were not included in the cohort. Only 2 patients with ABCD scores of 3 and 6 experienced stroke. This observation makes the point that an ABCD score <4 does not imply an absence of risk, but the number of outcomes is too small to comment further.

It is certainly possible that the populations are different. This is the major reason why clinical prediction rules must be cross-validated in different populations of patients. What appears an excellent rule in one population may not be so useful in another because of inherent differences in risk profile. Although the ABCD rule, without a doubt, will work well in the Oxfordshire and perhaps British population, further work is needed on the ABCD rule to assess its global validity.

How best to triage TIA/minor stroke patients? Our view is that it seems likely that the clinical features of longer duration and motor/speech symptoms are the key criteria warranting more urgent assessment. MR diffusion-weighted imaging then provides the natural technique for assessing the presence or absence of true ischemia. At the same time the neurovasculature can be assessed to understand potential mechanisms and identify the need for carotid revascularization.

Acknowledgments

Disclosures

None.

Footnotes

The opinions in this editorial are not necessarily those of the editors or of the American Heart Association.

See related article, pages 1710–1714.

References

Eliasziw M, Kennedy J, Hill MD, Buchan AM, Barnett HJ. Early risk of stroke after a transient ischemic attack in patients with internal carotid artery disease. CMAJ. 2004; 170: 1105–1109.[Abstract/Free Full Text]

Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000; 284: 2901–2906.[Abstract/Free Full Text]

Johnston SC, Sidney S. Validation of a 4-point prediction rule to stratify short-term stroke risk after TIA. Stroke. 2005; 36: 430. Abstract.

Coutts SB, Simon JE, Eliasziw M, Sohn CH, Hill MD, Barber PA, Palumbo V, Kennedy J, Roy J, Gagnon A, Scott JN, Buchan AM, Demchuk AM. Triaging transient ischemic attack and minor stroke patients using acute magnetic resonance imaging. Ann Neurol. 2005; 57: 848–854.[CrossRef][Medline] [Order article via Infotrieve]

Rothwell PM, Giles MF, Flossmann E, Lovelock CE, Redgrave JN, Warlow CP, Mehta Z. A simple score (ABCD) to identify individuals at high early risk of stroke after transient ischaemic attack. Lancet. 2005; 366: 29–36.[CrossRef][Medline] [Order article via Infotrieve]

Related Article:

Is the ABCD Score Useful for Risk Stratification of Patients With Acute Transient Ischemic Attack?

Brett L. Cucchiara, Steve R. Messe, Robert A. Taylor, James Pacelli, Douglas Maus, Qaisar Shah, and Scott E. Kasner

Stroke 2006 37: 1710-1714. [Abstract] [Full Text]

[Ace844]

Stroke

Early Recurrent Ischemic Stroke in Stroke Patients Undergoing Intravenous Thrombolysis

Dimitrios Georgiadis, MD; Stefan Engelter, MD; Barbara Tettenborn, MD; Hansjörg Hungerbühler, MD; Regina Luethy, MD; Felix Müller, MD; Marcel Arnold, MD; Christian Giambarba, MD; Christian Rainer Baumann, MD; Hans-Christian von Büdingen, MD; Philipp Lyrer, MD; Ralf Werner Baumgartner, MD

From the Departments of Neurology, Universities of Zürich (D.G., C.R.B., H.-C.v.B., R.W.B.) and of Basel (S.E., P.L.); the Departments of Neurology, District Hospitals of St Gallen (B.T.) and of Aarau (H.H., C.B.); the Department of Internal Medicine (R.L.), District Hospital of Triemli; the Department of Neurology (F.M.), District Hospital of Thurgau (Münsterlingen); the Department of Neurology (M.A.), University of Bern; and the Department of Internal Medicine (C.G.), District Hospital of Waid, Switzerland.

Correspondence to D. Georgiadis, MD, Department of Neurology, University of Zürich, Frauenklinikstrasse 26, 8091 Zürich, Switzerland. E-mail Dimitrios.Georgiadis@usz.ch

Received October 25, 2005; revision received April 28, 2006; accepted May 1, 2006.

Abstract

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Background— We assessed the incidence of early recurrent ischemic stroke in stroke patients treated with intravenous tissue-type plasminogen activator (tPA) and the temporal pattern of its occurrence compared with symptomatic intracranial hemorrhage (ICH).

Methods and Results— Prospectively collected, population-based data for 341 consecutive acute stroke patients (62% men; mean age, 66 years) treated with tPA according to the National Institute of Neurological Disorders and Stroke study protocol at 8 medical centers in Switzerland (3 academic and 5 community) between January 2001 and November 2004 were retrospectively analyzed. The primary outcome measure was neurological deterioration 4 points on the National Institutes of Health Stroke Scale occurring within 24 hours of tPA treatment and caused either by recurrent ischemic stroke (defined as the occurrence of new neurological symptoms suggesting involvement of initially unaffected vascular territories and evidence of corresponding ischemic lesions on cranial computed tomography scans, in the absence of ICH) or by ICH. Early recurrent ischemic stroke was diagnosed in 2 patients (0.59%; 95% confidence interval, 0.07% to 2.10%) and symptomatic ICH in 15 patients (4.40%; 95% confidence interval, 2.48% to 7.15%). Both recurrent ischemic strokes occurred during thrombolysis, whereas symptomatic ICHs occurred 2 to 22 hours after termination of tPA infusion.

Conclusions— Recurrent ischemic stroke is a rare cause of early neurological deterioration in acute stroke patients undergoing intravenous thrombolysis, with a different temporal pattern compared with that of symptomatic ICH.

Key Words: cerebral infarction • cerebral ischemia • cerebrovascular disorders • stroke • thrombolysis

Introduction

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Thrombolysis for acute myocardial infarction initially raised concerns that the disintegration of potentially preexisting cardiac thrombus could lead to systemic (and in particular, cerebral) embolism.1 It appears plausible that the same mechanism could apply to patients with cardiac or arterial thrombi who are undergoing intravenous thrombolysis (IVT) for acute ischemic stroke, constituting a further cause of neurological deterioration besides intracranial hemorrhage (ICH) and progressive ischemic stroke.

Considering the pharmacodynamic properties of tissue-type plasminogen activator (tPA; half-life of 5 minutes, with only 6.25% of the initial concentration present in plasma 20 minutes after termination of infusion), recurrent ischemic stroke due to tPA should occur early, ie, during or within the first hours after IVT (thus designated as early recurrent ischemic stroke [ERIS] in this study). ICH, on the other hand, would be expected to present a different temporal pattern, as fibrinogen levels only return to normal (within 80% of the initial value) 24 hours after IVT.2 Symptomatic ICH (SICH) was reported in 20 patients treated with tPA in the National Institute of Neurological Disorders and Stroke (NINDS) trial and occurred 2 to 29 hours after IVT initiation; in 95% of cases, symptoms occurred within the first 24 hours.2

Editorial p 187

Clinical Perspective p 241

Recurrent ischemic stroke constituted an end point in the NINDS rt-PA Stroke Study3 but not in the European Cooperative Acute Stroke Study (ECASS) I,4 ECASS II,5 or Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke (ATLANTIS)6 trials or the Standard Treatment with Alteplase to Reverse Stroke (STARS)7 Study. Even in the NINDS trial, recurrent ischemic stroke was reported for the whole follow-up period of 90 days, but specific details about the time point of its occurrence were not provided, making it impossible to differentiate between ERIS and recurrent ischemic stroke due to other causes.

This retrospective, population-based study collected data from all centers of German-speaking Switzerland that perform IVT for acute ischemic stroke to investigate the incidence and time of onset of ERIS and SICH within the first 24 hours after intravenous tPA, administered according to the NINDS study protocol during an observation period of 47 months.

Methods

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We hypothesized that ERIS associated with IVT should occur during or within hours after termination of tPA infusion. Surveillance for ERIS or SICH was limited to 24 hours after IVT, a time window also adopted by the Prolyse in Acute Cerebral Thromboembolism (PROACT) trial.8

Patients with neurological deterioration causing a 4-point worsening on the National Institutes of Health Stroke Scale (NIHSS) were further evaluated. ERIS was defined as the occurrence of new neurological symptoms suggesting the involvement of initially unaffected vascular territories and evidence of corresponding ischemic lesions on cranial computed tomography (CCT) scans, in the absence of ICH. Neurological deterioration and evidence of appropriately located ICH on CCT, magnetic resonance imaging (MRI) scans, or both was diagnosed as SICH.

Data collected included patient age, sex, NIHSS score on admission, latency between symptom onset and initiation of IVT, and latency between initiation of IVT and neurological deterioration.

Patient Population

We retrospectively analyzed prospectively collected data for all acute stroke patients treated with IVT in the Neurological Departments of the University Hospitals of Basel, Bern, and Zürich; the Neurological Departments of the District Hospitals of Aarau, Münsterlingen, and St Gallen; and the Departments of Internal Medicine of the District Hospitals of Triemli and Waid between January 2001 and November 2004. These hospitals have a catchment area of &3 500 000 inhabitants and are the only centers in the German-speaking part of Switzerland that offer IVT.

IVT Protocol

Each hospital involved in this study used its own institutional protocol for tPA administration. Patients were evaluated further only if they fulfilled the criteria applied by the NINDS study.3 All patients treated with IVT were admitted to intermediate- or intensive-care units, where they remained for at least 24 hours. An emergency CCT scan was performed after neurological deterioration.

Statistical Analysis

Normally distributed data were expressed as mean±SD and nonnormally distributed data as median and 95% confidence intervals (CIs).

The authors had full access to the data and take responsibility for its integrity. All authors have read and agree to the manuscript as written.

Results

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A total of 372 patients were treated with IVT during the observation period; 31 of them were excluded for not meeting the NINDS criteria (time window >3 hours); no ERISs and 1 SICH (3.2%) were diagnosed in these patients. Thus, 341 (92%) patients were further evaluated (Aarau, n=52; Basel, n=89; Bern, n=7; Münsterlingen, n=17; St Gallen, n=52; Triemli, n=24; Zürich, n=94; and Waid, n=6). There were 212 men and 129 women, aged 66±15 years (range, 16 to 94 years). NIHSS score on admission was 13 (median; 95% CI, 12 to 14; range, 2 to 25). Latency between symptom onset and initiation of treatment was 153±29 minutes (range, 10 to 180 minutes).

Recurrent Ischemic Stroke

ERIS was diagnosed in 2 (0.59%; 95% CI, 0.07% to 2.10%) patients. The first was a 72-year-old man with a history of diabetes mellitus and arterial hypertension who was admitted with a dense right hemiparesis, hemihypesthesia, dysarthria, and fixed eye deviation to the left (NIHSS score, 16). Findings from the ECG and baseline CCT were normal. IVT was initiated 170 minutes after symptom onset. Forty minutes later, his level of consciousness rapidly decreased, and the patient became comatose. IVT was discontinued, and CCT performed immediately after neurological deterioration was still unremarkable. The third CCT performed 21 hours after the onset of initial symptoms showed multiple ischemic lesions in the territories of the left middle (with hemorrhagic transformation), anterior cerebral, and anterior choroidal arteries with compression of the left lateral ventricle and temporal horn; a midline shift and trans-tentorial herniation leading to displacement of the pons to the right side and compression of the fourth ventricle; ischemic lesions in the right middle cerebral artery (MCA); and probable ischemic lesions in the medial branch of the right posterior inferior cerebellar artery (Figure). Lesions in the territory of the right MCA and right posterior inferior cerebellar artery were not compatible with the initial symptoms. The patient died 3 days after symptom onset. Necropsy was not permitted.

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Axial CT scan of the brain 12 hours after IVT with tPA in a patient who became comatose 40 minutes after initiation of thrombolytic treatment, showing acute ischemic lesions in the territories of the left middle cerebral, anterior cerebral, anterior choroidal, and right middle cerebral arteries and the medial branch of the right posterior inferior cerebellar arteries.

The second patient was a 78-year-old woman admitted with dysarthria, left-sided weakness, hemihypesthesia, and hemianopia (NIHSS score, 11). The past medical history was unremarkable except for arterial hypertension. The ECG showed no ischemic changes but revealed a first-degree atrioventricular block; mediastinal widening was diagnosed on chest radiography. After normal CCT findings were observed, IVT was initiated 175 minutes after symptom onset. Fifty minutes after IVT initiation, the patient became comatose and developed generalized tonic seizures. IVT was discontinued. Findings on the emergency CCT were normal. CCT performed 6 hours after onset of the presenting stroke revealed an ischemic lesion in the territory of the right MCA and early demarcation of a further ischemic lesion in the territory of the left MCA. Bilateral occlusion of the internal carotid arteries was diagnosed on CCT angiography; this was presumed to be acute, as homogeneous, fresh, mainly hypoechogenic thrombus was visualized in the lumen of both internal carotid arteries on extracranial color duplex sonography. The patient’s presenting symptoms were compatible with the diagnosed ischemic lesion in the territory of the right MCA but not with the second contralateral ischemic lesion. Abdomen and chest CT scans did not confirm the suspected aortic dissection but showed multiple, bilateral, acute kidney infarcts. The patient died on the third day after symptom onset. Necropsy was not permitted.

Symptomatic Intracranial Hemorrhage

SICH occurred in 15 (4.40%; 95% CI, 2.48% to 7.15%) patients (8 of 190 [4.21%] patients treated at the university hospitals and 7 of 151 [4.64%] patients treated in community hospitals). Clinical details of the patients with SICH, the prevalence of vascular risk factors, pretreatment medications, relevant laboratory parameters, and latency between symptom onset and IVT and between IVT and subsequent neurological deterioration are displayed in the Table. None of these patients was treated with anticoagulants, unfractionated or low-molecular-weight heparin, or heparinoids on admission. The international normalized ratio ranged between 0.9 and 1.1, and activated partial thromboplastin time was within the normal range in all cases. Hematomas were located in the infarcted area in 13 patients (space-occupying effect in 5 patients; intraventricular extension in 1 patient). A right pontine hemorrhage occurred in 1 and a left occipital hemorrhage in another patient; initial ischemic lesions were located in the territory of the right MCA in both cases.

View this table:

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Clinical Details, Prevalence of Vascular Risk Factors, Laboratory Parameters, and Latency Between Symptom Onset and IVT and Between IVT and Subsequent Neurological Deterioration in 15 Stroke Patients Who Experienced an ICH After IVT

Discussion

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Introduction

Methods

Results

Discussion

References

The present study is the first report of ERIS in patients with acute ischemic stroke treated with IVT; furthermore, the size of the present study and the fact that it presents population-based data from patients receiving tPA under a predefined protocol allow valid conclusions concerning its incidence. Although recurrent ischemic stroke was assessed in the NINDS trial, the time point of neurological deterioration was not specified, and the pathophysiological mechanism proposed in the present study was not postulated.

The diagnosis of ischemic lesions in multiple cerebral vascular territories in 1 patient and in both MCA territories and both kidneys in the second patient are highly suggestive of the disintegration and subsequent scattering of cardiac or aortic thrombi as the underlying etiology of ERIS. Obviously, disintegration of thrombi can occur spontaneously and is not necessarily associated with tPA administration. Still, the fact that neurological deterioration occurred 40 to 50 minutes after tPA initiation in both cases strongly argues for a causative role of tPA. The only possible means for resolving this issue would be a randomized study comparing the incidence of ERIS between stroke patients treated with IVT and controls; still, such a study would not be ethical, taking into account that IVT constitutes a treatment of proven efficacy for patients with acute ischemic stroke. A registry of patients with ERIS after IVT could provide more information on this intriguing issue.

Unfortunately, no necropsy was performed in the 2 patients; the same was true for echocardiography, which was withheld owing to the lack of therapeutic consequences. We can thus provide no evidence of underlying cardiac or aortic disease to support our hypothesis. Considering that the cause of ERIS both from the clinical and the imaging viewpoint was clearly embolic, it is questionable whether this information would be of great assistance, the basic unanswered question being the causative role of tPA rather than the source of embolic material.

Previous coronary thrombolysis trials reported a 0.49 to 0.7%10 incidence of ischemic stroke until hospital discharge or for the following 30 to 35 days. Only 1 study described the incidence of ischemic stroke within the first 6 hours after thrombolysis, which was 0.13%.10 Comparison of these results with those of the present study is inconclusive, owing to differences in treatment protocols with regard to the dose and duration of tPA infusion and the concomitant use of aspirin, heparin, or both. Furthermore, CCT scans were not always part of the diagnostic work-up for presumed stroke in coronary trials, rendering the determination of true ischemic stroke prevalence impossible.

Obviously, the incidence of ERIS is far too low to justify delay of IVT initiation, considering the demonstrated higher benefit associated with earlier IVT treatment.11 Furthermore, transesophageal echocardiography, the sole method capable of excluding the possibility of intracardiac or aortic thrombi, can barely be performed within the 3-hour window and is not available on a 24-hour basis. We must point out, however, that the true incidence of ERIS was potentially underestimated in this study, because we evaluated only those patients with a deterioration 4 points on the NIHSS.

Although the differences in temporal occurrence of ERIS and SICH are intriguing, they obviously do not allow a definite distinction between these 2 entities in an individual patient. Thus, neurological deterioration should prompt discontinuation of IVT and performance of an urgent CCT scan. Our findings should alert treating physicians to the possibility that deterioration during IVT is not necessarily due to ICH but can also be caused by ERIS. We propose that patients with ERIS should undergo urgent diffusion- and perfusion-weighted MRI to estimate the extent of both the ischemic lesions and the associated penumbra. The results of these MRI studies will be helpful to guide patient management, in particular, to resolve the question of whether further therapeutic regimes such as local intra-arterial or mechanical thrombolysis should be taken into consideration. Exclusion of SICH in these cases should by no means prompt a wait-and-see attitude.

Acknowledgments

Disclosures

None.

References

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Abstract

Introduction

Methods

Results

Discussion

References

Stafford PJ, Strachan CJ, Vincent R, Chamberlain DA. Multiple microemboli after disintegration of clot during thrombolysis for acute myocardial infarction. BMJ. 1989; 299: 1310–1312.[Medline] [Order article via Infotrieve]

The NINDS t-PA Stroke Study Group. Intracerebral hemorrhage after intravenous t-PA therapy for ischemic stroke. Stroke. 1997; 28: 2109–2118.[Abstract/Free Full Text]

The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995; 333: 1581–1587.[Abstract/Free Full Text]

Hacke W, Kaste M, Fieschi C, Toni D, Lesaffre E, von Kummer R, Boysen G, Bluhmki E, Hoxter G, Mahagne MH, Hennerici M. Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. The European Cooperative Acute Stroke Study. JAMA. 1995; 274: 1017–1025.[Abstract]

Hacke W, Kaste M, Fieschi C, von Kummer R, Davalos A, Meier D, Larrue V, Bluhmki E, Davis S, Donnan G, Schneider D, Diez-Tejedor E, Trouillas P. Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II). Second European-Australasian Acute Stroke Study Investigators. Lancet. 1998; 352: 1245–1251.[CrossRef][Medline] [Order article via Infotrieve]

Clark WM, Wissman S, Albers GW, Jhamandas JH, Madden KP, Hamilton S. Recombinant tissue-type plasminogen activator (Alteplase) for ischemic stroke 3 to 5 hours after symptom onset: the ATLANTIS Study: a randomized controlled trial. Alteplase Thrombolysis for Acute Noninterventional Therapy in Ischemic Stroke. JAMA. 1999; 282: 2019–2026.[Abstract/Free Full Text]

Albers GW, Bates VE, Clark WM, Bell R, Verro P, Hamilton SA. Intravenous tissue-type plasminogen activator for treatment of acute stroke: the Standard Treatment with Alteplase to Reverse Stroke (STARS) study. JAMA. 2000; 283: 1145–1150.[Abstract/Free Full Text]

Furlan A, Higashida R, Wechsler L, Gent M, Rowley H, Kase C, Pessin M, Ahuja A, Callahan F, Clark WM, Silver F, Rivera F. Intra-arterial prourokinase for acute ischemic stroke: the PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA. 1999; 282: 2003–2011.[Abstract/Free Full Text]

GISSI-2: a factorial randomised trial of alteplase versus streptokinase and heparin versus no heparin among 12,490 patients with acute myocardial infarction. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico. Lancet. 1990; 336: 65–71.[Medline] [Order article via Infotrieve]

Sloan MA, Price TR, Terrin ML, Forman S, Gore JM, Chaitman BR, Hodges M, Mueller H, Rogers WJ, Knatterud GL, Braunwald E. Ischemic cerebral infarction after rt-PA and heparin therapy for acute myocardial infarction: the TIMI-II pilot and randomized clinical trial combined experience. Stroke. 1997; 28: 1107–1114.[Abstract/Free Full Text]

Marler JR, Tilley BC, Lu M, Brott TG, Lyden PC, Grotta JC, Broderick JP, Levine SR, Frankel MP, Horowitz SH, Haley EC Jr, Lewandowski CA, Kwiatkowski TP. Early stroke treatment associated with better outcome: the NINDS rt-PA stroke study. Neurology. 2000; 55: 1649–1655.[Abstract/Free Full Text]

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CLINICAL PERSPECTIVE

The present study provides the first description of early recurrent ischemic stroke (ERIS) as the cause of neurological deterioration in acute stroke patients who are undergoing intravenous thrombolysis. Prospectively collected, population-based data for 341 consecutive acute stroke patients treated with tissue-type plasminogen activator (tPA) at 8 medical centers in Switzerland were retrospectively analyzed. ERIS was defined as neurological deterioration 4 points on the National Institutes of Health Stroke Scale that occurred within 24 hours of tPA treatment, suggesting the involvement of initially unaffected vascular territories and evidence of corresponding ischemic lesions on cranial computed tomography scans, in the absence of intracranial hemorrhage (ICH). The incidence of this complication was low, as it occurred in only 2 of 341 patients (prevalence, 0.59%; 95% confidence interval, 0.07% to 2.10%). The diagnosis of multiple ischemic lesions in both patients suggests the disintegration and subsequent scattering of cardiac or aortic thrombi as the underlying etiology. Furthermore, we observed a different temporal pattern compared with that for ICH, with both ERISs occurring during thrombolysis and all 15 symptomatic ICHs occurring 2 to 22 hours after termination of tPA infusion. These findings should alert treating physicians to the possibility that deterioration during intravenous thrombolysis is not necessarily due to ICH but can also be caused by ERIS. Exclusion of ICH in these cases should by no means prompt a wait-and-see attitude but rather should lead to urgent magnetic resonance imaging studies and, potentially, additional therapeutic interventions such as local thrombolysis.