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Correspondence |

Nonstroke Treatment

William M. Landau, MD
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Copyright 2006 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.

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Arch Neurol. 2006;63(10):1506-1506. doi:10.1001/archneur.63.10.1506-a
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The timely review1 regarding tissue plasminogen activator (tPA) use for acute stroke implies that some physicians' reluctance to prescribe tPA is attributable to their unjustified fear of cerebral hemorrhage for patients and litigation and poor pay for themselves. Because the reviewers' earnest premise is that tPA “increases recovery from stroke symptoms by up to 50% with a low serious complication rate,” they imply that choice should be certain. But a fourth factor to consider is that equally conscientious evaluation of the complex database by professional colleagues may be less enthusiastic.

The original 1995 reference2 states that at 3 months, not earlier,

As compared with the placebo group, there was a 12% absolute (32% relative) increase in the number of patients with minimal or no disability (a score of 95 or 100 on the Barthel index) in the tPA group. There was also an 11% absolute (55% relative) increase in the number of patients with an NIHSS [National Institutes of Health Stroke Scale] score of 0 or 1 in this group.

Thus the tPA-treated patient improved her chances of doing very well from the placebo level of 38% to 50%, 1 chance in 8. Her best risk of poorer-quality functional survival also reached 50%. Most important, mortality risks were equivalent: more infarction stroke deaths in the placebo group and more hemorrhage deaths with tPA. “Symptomatic intracerebral hemorrhage” occurred in 7% of tPA patients, most often during the first 36 hours. “At 3 months, 17 of the 28 patients [including 2 placebo, 1 death] with symptomatic hemorrhage (61%) had died.” Thus the 1-in-10 risk (16/168) of sudden tPA complication death counters the 1-in-8 chance for delayed better improvement.

Although informed consent includes the bleeding risk, the family expects to beat the odds, the catastrophic event is often early, and the caring physician must endeavor to provide more than “I told you so” support. Whether the highest-risk patients may be ethically discouraged from treatment remains still to be ascertained. Both experience and education lead many doctors to believe that the decision to treat during the critical 180 minutes should not be a “slam dunk” choice.

AUTHOR INFORMATION

Correspondence: Dr Landau, Department of Neurology, Washington University School of Medicine, Campus Box 8111, 660 S Euclid Ave, St Louis, MO 63110-1093 (landauw@neuro.wustl.edu).

REFERENCES

Bambauer  KZ, Johnston  SC, Bambauer  DE, Zivin  JA. Reasons why few patients with acute stroke receive tissue plasminogen activator. Arch Neurol 2006;63661- 664
PubMed
National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group,  Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;3331581- 1587
PubMed

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Bambauer  KZ, Johnston  SC, Bambauer  DE, Zivin  JA. Reasons why few patients with acute stroke receive tissue plasminogen activator. Arch Neurol 2006;63661- 664
PubMed
National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group,  Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;3331581- 1587
PubMed

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