DOI: 10.1097/MBC.0b013e3283432ff3

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PMID: 21455034

Issn Print: 0957-5235

Publication Date: 2011/04/01


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Revisiting unfractionated heparin as a contraindication to acute stroke intravenous thrombolysis

Christopher Chong; Mae Chiang; Leo Chiu

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Author Information: Section of General Internal Medicine, Lakeridge Health Oshawa, Oshawa, Canada

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There is very solid agreement that as opposed to antiplatelet treatment, early anticoagulation offers no additional benefit, increases the risk of bleeding and is, therefore, generally contraindicated in the treatment of acute stroke and transient ischemic attacks (TIAs) [1,2]. However, some experts still do recommend judiciously using early anticoagulation in special circumstances. Specifically, this strategy has not been well studied in the setting of ischemic cerebrovascular events secondary to cervical artery dissection, symptomatic high-grade carotid stenosis prior to surgery or cardiac emboli with a high risk of re-embolization. These situations remain grey areas in which some feel that prompt anticoagulation is quite reasonably indicated [2]. When early anticoagulation is elected, intravenous (i.v.) unfractionated heparin (UFH) is typically chosen as the ability to rapidly monitor and adjust the degree of anticoagulation may offer a safety advantage over other drugs [1,3]. Thus, it is still not entirely uncommon to see patients on i.v. UFH, particularly if their initial event was a high-risk TIA with complete resolution and the goal is to aggressively prevent a frank stroke.
However, what happens if a patient nonetheless suffers an ischemic stroke while on i.v. UFH? If within the appropriate time window, could thrombolysis be considered? Current contraindications to acute stroke thrombolysis include ‘if receiving heparin in previous 48 h, activated partial thromboplastin time (aPTT) must be in normal range’ [1]. Such cases may best be managed with intraarterial thrombolysis [4] and there have been reported cases of successful intraarterial thrombolysis after reversal of warfarin anticoagulation [5]. However, most hospitals do not possess this highly specialized technology that is still trying to find a clearly defined role in general acute stroke care, and delays in trying to access intraarterial thrombolysis may worsen outcomes [1].
What remains unclear is whether a patient on i.v. UFH could still be considered a candidate for much more widely available systemic i.v. thrombolysis if the aPTT can be normalized within an appropriate time window. Anecdotally, we have personally used early anticoagulation in several instances and were recently faced with an instance of a witnessed ischemic stroke, despite a supratherapeutic aPTT. Our hospital is a district stroke centre, but does not have intraarterial thrombolysis capability. Discussions with neurologists in different academic centres failed to reach even an informal consensus regarding the best approach in this scenario. Thus, we discuss three options for management when stroke clinicians may be met with such a dilemma.
Option 1: do not consider i.v. thrombolysis at all.
We believe any patient who is on i.v. UFH would have been automatically excluded from the major previously conducted acute stroke i.v. thrombolysis trials [6]. From a strict evidence-based medicine perspective, there is no data to support using fibrinolytics in this case and certainly a very real potential for harm. Indeed, deviation from protocol is clearly associated with a higher rate of intracranical hemorrhage (ICH) [1]. On the other hand, it is always extremely difficult for clinicians to do nothing, particularly if the stroke is clinically very severe and thus predicts a poor prognosis in the absence of treatment.
Option 2: reverse the heparin with protamine and then use i.v. thrombolysis.
Protamine is a widely available antidote which rapidly neutralizes heparin in approximately 5 min. It is often used in cardiac patients on UFH complicated by bleeding, and its routine administration to facilitate early femoral artery sheath removal after percutaneous coronary intervention does not appear to increase thrombotic risks [7]. Administering protamine could quickly normalize the aPTT without inducing a clinically significant hypercoaguable state, thus, allowing prompt thrombolysis. However, to the best of our knowledge, there are no studies exploring this strategy.

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