Chemical Thrombolysis Basic Concepts

After a baseline angiogram confirms the presence and location of the vascular occlusion, a microcatheter is navigated over a microwire into the occluded vessel, traversing the thrombus. Once the microcatheter is positioned immediately distal to the clot, thrombolytic infusion begins; the microcatheter is then pulled back through the clot while drug is infused. Dose adjustments and total dose calculations are made depending on the clinical circumstances, pretreatment dose of rt-PA received, degree of recanalization, and relative size and function of the territory at risk.

The neurointerventionalist should limit the number of microcatheter injections performed during the exam, as there is growing evidence that this may increase the chances of hemorrhagic transformation of the infarcted tissue.51 Direct injection of contrast into stagnant vessels, which contains injured glial cells and thus breakdown of the blood-brain barrier, allows for contrast extravasation. Contrast is readily visualized on the immediate post-thrombolysis CT as an area of high attenuation in the parenchyma. In some instances, MRI with susceptibility-weighted sequences may be useful to differentiate contrast extravasation from ICH.52 Such a distinction may be essential in order to establish the optimal postprocedural antithrombotic regimen and blood pressure goals. Successful recanalization should therefore be based on guide catheter injections. The infusion is terminated when adequate antegrade flow is restored, or the predetermined time limit or maximal dose limit is reached. Ominous signs, such as contrast extravasation, should prompt immediate termination of drug infusion, followed by the appropriate management steps as outlined in Table 4.2.

Fibrinolytic agents have several disadvantages. First, although direct infusion maximizes local drug concentrations, dissolution of clot takes an extended period of time, and time is critical in preserving the ischemic penumbra. Second, fibrino-lytics increase the risk of hemorrhage both intracranially and systemically. Lastly, not all thromboembolic occlusions can be adequately treated with thrombolytic drugs. The resistance to enzymatic degradation may be related to excessive cross-linking in mature embolic clots, or to emboli composed of cholesterol, calcium, or other debris from atherosclerotic lesions. In others, the lack of flow may result in decreased delivery of circulating plasminogen, allowing the high concentration of fibrinolytic to quickly deplete the available plasminogen. This local plas-minogen deficiency would result in impaired fibrinolytic activity.53

TABLE 4.2 Management of Symptomatic Intracerebral Hemorrhage after Intra-

arterial Thrombolysis.

STAT head CT

STAT neurosurgery consult

Check CBC, PT, PTT, platelets, fibrinogen and D-dimer. Repeat every 2 hours until bleeding is controlled

Give FFP 2 units every 6 hours for 24 hours after dose

Give cryoprecipitate 20 units. If fibrinogen level < 200 mg/dL at 1 hour, repeat cryoprecipitate dose.

Give platelets 4 units

Give protamine sulfate 1 mg/100 U heparin received in last 3 hours (give initial 10 mg test dose by slow IVP over 10 minutes and observe for anaphylaxis; if stable give entire calculated dose by slow IVP; maximum dose 100 mg)

Institute frequent neuro checks and therapy of acutely elevated ICP, as needed

May give aminocaproic acid (Amicar) 5 g in 250 cm3 NS IV over 1 hour as a last resort

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