Page 22 - CASA Bulletin of Anesthesiologisy 2022 9(6)-1 (3)
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CASA Bulletin of Anesthesiology


               the P2Y12 platelet receptor inhibitor Clopidogrel. This may be due to either a genetic deficiency
               in the enzyme that converts clopidogrel to its active metabolite or co morbidities such as
               diabetes, renal impairment, drug interactions or tobacco use that share a common metabolic
               pathway. Many neuro interventionists will use the VerifyNow  P2Y12 assay to measure the
                                                                           TM
               efficacy of clopidogrel activity. It measures P2Y12 reaction units (PRU) and a value <194 is
               deemed adequate platelet inhibition. Patients who are deemed inadequate responders can be
               treated with the newer generation thienopyridine class drugs prasugrel and ticaglor that have the
               benefit of faster onset and efficacy but the downside of increased bleeding risk, cost and twice
               daily dosing for ticagrelor.

                   When complications occur in the NIR suite successful management is dependent on effective
               communication between the proceduralist and the Anesthesiologist. Although intra-procedure
               aneurysm rupture is arguably the most feared and devastating complication of an endovascular
               intervention it is intra-arterial thrombus formation and the risk for ischemic complications that
               happens more frequently. When the proceduralist is aware of thrombus formation they will often
               ask for the blood pressure to be raised, more heparin to be given and sometimes glycoprotein IIb-
               IIIa inhibitors are given either locally intra-arterially or systemically intravenously to inhibit
               platelet aggregation. Patients with vasospasm after sub arachnoid may present to the NIR for
               possible interventions including angioplasty and possibly intra-arterial injection of calcium
               antagonists such as verapamil and nicardipine directly into the constricted arteries. This may
               cause profound hypotension and should be anticipated as these patients are at particular risk of
               further brain injury due to cerebral ischemia.

                   When an aneurysm ruptures during an endovascular intervention this will usually elicit a
                             ’                                                                    cranial
               pressure. The proceduralist should be immediately alerted and they will attempt to control the
               bleeding by occluding the artery with a balloon whilst coils are packed into the aneurysm. It will
               often be necessary to reverse any heparin that has been given with protamine and a platelet
               infusion might be necessary if the patient has received DAPT. Whilst the initial reaction to a
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               normal or slightly elevated blood pressure in the setting of a balloon artery occlusion and other
               maneuvers to try and lower intracranial pressure should be considered such as hyperventilation
               to lower paCO2, hyperosmotic therapy and draining CSF (if a ventriculostomy has been placed
               for ruptured aneurysms prior to the procedure). It may be necessary to take the patient
               emergently to the OR following the procedure for a decompressive craniectomy.

               Embolization Procedures

                   Technological advancements in both micro catheters and wires feeding arteries to both
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               Again, it is of paramount importance that the patient remains immobile so that the catheter does
               not migrate on injection into normal arterial branches. The proceduralist may ask for normal or
               lower blood pressure on injection to try and prevent embolization of embolic materials into
               draining veins causing some degree of venous outflow obstruction or even the pulmonary
               circulation which may present as post procedural hypoxemia. When an AVM is embolized
               relative hypotension is often necessary for up to 24hrs as blood is shunted into a chronically
               hypotensive vascular bed that requires time to restore its auto-regulatory capacity.





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