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Perioperative Aspirin & POISE-2

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1 Perioperative Aspirin & POISE-2
Neal Gerstein, MD FASE Associate Professor, UNM Department of Anesthesiology Director, UNM Division of Cardiac Anesthesia

2 The active ingredient of Aspirin was first discovered from the bark of the willow tree in 1763 by Edward Stone of Wadham College, Oxford University. diacetylmorphine

3 Disclosures None

4 Objectives Review risks of holding aspirin perioperatively.
To learn when / which procedures aspirin should / should not be held. Review POISE-2 methodology. Examine limitations of POISE-2. Provide recommendations on perioperative aspirin management.

5 Case 70 y.o. male for primary TKA PMH Meds TIA 5 years prior HTN NIDDM
HLD Remote tobacco Meds ASA 81 mg/day Simvastatin Metformin Naproxen prn

6 Background 100,000,000 non-cardiac operations /year worldwide.
~ 40% of these patients have / at risk for CV disease. Mangano, Anesthesiology 1990 In the U.S., cardiovascular disease (CAD, CVD, PVD): Affects >1/3 adults Leading cause of morbidity & mortality. Wolff et al, Ann Int Med 2009 USPTF Ann Int Med 2009 #1 perioperative complication in patients with CV risk factors → M.I. Associated mortality rate of 15 – 25% Peter et al, Thromb Haemost 2011 Kumar et al, J Gen Int Med 2001 Furthermore, even a mildly elevated troponin postoperatively has been shown to be an independent predictor of increased perioperative morbidity and mortality.

7 Aspirin’s Role in CV Disease
platelet aggregation inhibition thrombosis prevention Primary prevention Secondary prevention Know aspirin’s indication in these two contexts Primary prevention = preventing first occurrence of disease Secondary prevention = prevention of recurrence

8 Aspirin in Secondary Prevention
Most recent AHA/ACC/ACCP guidelines: Indefinite rx in virtually all with established CAD or other atherosclerotic disease ‘unless absolutely contraindicated’ PCI: neuro, cardiac 287 study meta-analysis of antiplatelet rx in 135,000 pt’s with CV disease Aspirin #1 studied rx 25% reduction of death from any vascular cause, MI, CVA

9 Primary Prevention Unclear in those without risk factors Diabetics
2010 ADA/AHA/ACCF Aspirin if increased cardiac risk (10-year risk of cardiac event of >10%). Men > 50 years / women > 60 years & one of the following: Tobacco use Hypertension Significant cardiovascular disease family history Hypercholesterolemia Albuminuria The risk-versus-benefit ratio of aspirin therapy for primary prevention, however, is much less clear than for secondary prevention. The Antithrombotic Trialists’ Collaboration has also recently published a meta-analysis of 6 randomized primary prevention trials. They concluded that aspirin reduced the incidence of vascular events (12% proportional reduction or 0.07% per year absolute reduction, P = ), mainly nonfatal myocardial infarction, by a small but statistically significant amount. The largest reduction was for nonfatal myocardial infarction; 23% proportional reduction, P < The proportional reductions in the aggregate of all serious vascular events were similar for both men and women. There was no reduction in vascular-related mortality attributed to aspirin use. In addition, they found that aspirin significantly increased the rate of major gastrointestinal bleeding and also increased the risk of hemorrhagic stroke. The authors therefore concluded that aspirin therapy is of uncertain value for primary cardiovascular prevention and that strong consideration must be given to balancing the reduction in thrombotic events with the risk of major bleeding


11 Aspirin Pharmacology

12 Key Points in Aspirin Pharmacology
2 isoforms of COX: 1 & 2 Aspirin irreversibly inactivates COX 170x affinity for COX-1 vs COX-2 A single dose of 30 mg completely suppresses TXA2 production for 1 week

13 Aspirin Mechanism Eur Heart J, Vol 7, May 2005
Key Points in Aspirin Pharmacology 2 isoforms of COX: 1 & 2 Aspirin irreversibly inactivates COX 170x affinity for COX-1 vs COX-2 A single dose of 30 mg completely suppresses TXA2 production for 1 week TXA2 is responsible for activating new platelets, stimulating platelet aggregation, and vasoconstriction—consequently causing thrombosis and hemostasis. Under normal conditions, thrombosis is kept in check by the intact endothelial cell lining that is resistant to interactions with platelets and coagulation factors. When endothelial damage occurs, however, the hemostatic process (including platelet aggregation and activation) is initiated to stop bleeding. If this process becomes exaggerated, excess thrombosis can lead to unwanted vascular occlusion and adverse cardiovascular events. Eur Heart J, Vol 7, May 2005

14 Platelets – more than just hemostasis
ADP, TXA2 Thrombin coagulation cascade Inflammatory mediators Atherosclerosis Thrombogenicity Neutrophil activation Platelets role in hemostasis begins by detecting disrupted vascular endothelium and adhering to the newly exposed extracellular matrix. 2) Adherent platelets aggregate and release platelet-activation mediators such as ADP and TXA2. TXA2 production is largely catalyzed by COX-1. 3) Once activated, platelets generate thrombin and catalyze the coagulation cascade 4) Platelets also induce inflammatory leukocytes, which may initiate atherothrombotic plaques promoting undesirable thrombotic events. Platelet granules store many pro- and anti-inflammatory cytokines that have no apparent role in hemostasis 5) It is well established that platelets promote atherosclerosis through several mechanisms and the platelet’s role and cell signaling is similar for both maintenance of normal hemostasis and pathologic thrombosis development 6) the platelet has been identified as a link between inflammation and thrombogenicity. 7) Platelets have been found to express Toll-like receptors to promote neutrophil activation and store antibacterial proteins called thrombocidins, both aiding in pathogen protection and killing.

15 The ‘Aspirin Withdrawal Syndrome’


17 ‘Aspirin Withdrawal Syndrome’
Aspirin use is not just an on-off switch Complex relationship between platelet: Inhibition It must be kept in mind that alternating between platelet inhibition and restoration of platelet function is not a simple “on-off” phenomenon. Inhibition Hemostasis Inflammation Hemostasis Inflammation

18 Aspirin Withdrawal Platelet rebound phenomenon in setting of acute aspirin withdrawal. This rebound period is characterized by: Increased thromboxane production Decreased fibrinolysis Leading to a resultant clinical prothrombotic state Vial et al, Adv Prostaglandin Thromboxane Leukot Res. 1991 Beving et al, Blood Coagul Fibrinolysis 1996 Fatah et al, Eur Heart J 1996

19 Urine metabolites of TXA2 and PGI2
Before, during, and after cessation of a 1-week aspirin regimen. Metabolites (and hence platelet TXA2) rebound to levels beyond that of study controls. Peaked at 7 to 14 days after aspirin withdrawal.

20 Measured ‘HHT’ to approximate platelet-TXA2 production
32 pts who stop aspirin-rx 2 weeks before CABG 25% of this cohort had 12-HHT levels beyond the normal range 2 weeks after withdrawal. Same investigators, earlier study: 12-HHT/TXA2 rebound in healthy subjects after withdrawal of a 1-week aspirin regimen. Dose dependent more rapid rebound with withdrawal of lower aspirin doses. (12-HHT: a platelet metabolite produced concomitantly in equal amounts to TXA2) 12-L-hydroxy-5,8,10-heptadecatrienoic acid In both studies: observed platelet function rebound.

21 Rebound affects more than primary hemostasis
Increase fibrin strength after withdrawal. Less fibrinolysis when fibrin strength enhanced. Same authors: demonstrated that patients with more rigid fibrin networks were more prone to CV events.

22 Clinically relevant to the Perioperative Period?

23 Thrombotic Risks of Aspirin Withdrawal in the Perioperative Period
Aspirin is clearly beneficial for secondary prevention. 25% RRR in preventing future cardiac or ischemic events. ATC BMJ 2002 Tran et al, JAMA 2004 Still, typical practice for surgeons and preoperative clinics to council aspirin cessation 7-10 days preoperatively. Collet et al, Int J Cardiol 2000

24 Cohort 1358 pts admitted for ACS.
Non-user: n=930 (68.%) Prior-users: n=355 (26.1%) Recent withdrawals: n=73 (5.4%) 2x increase in death rates of ‘withdrawers’ vs prior users / nonusers. Average time b/w cessation-cardiac event = 11.9 days. Scheduled surgery = 64% cases. Multivariate analysis: Antiplatelet cessation Independent predictor of both death and major ischemic events. Non-user: no APA >6mo. Prior-users: ‘continued’ aspirin in 3 weeks pre-trial Recent withdrawers: held aspirin within 3 weeks of admission Despite a similar cardiovascular risk profile, recent withdrawers had higher 30-day rates of death or MI (21.9% versus 12.4%, P0.04) Recent withdrawers of antiplt rx (97% of subjects were aspirin) 11.9 days, consistent with the expected time interval for platelet rebound

25 Meta-analysis of retrospective studies (1970-2004)
n=49590 (14981 on aspirin) CV risks associated with perioperative withdrawal of aspirin vs bleeding risks when continued.

26 Mean timing of event after discontinuation of aspirin:
Withdrawal preceded: 10.2% of acute cardiovascular events. 6.1% of lower limb ischemic events. Mean timing of event after discontinuation of aspirin: 8.5 days for coronary events. 25.8 days for a lower limb event.

27 Retrospective case–control
309 admissions over 2 years with diagnosis of CVA or TIA & use of long-term aspirin before the index event. Compared to 309 age- and sex- matched controls with a history of CVA or TIA on long-term aspirin and no acute event in previous 6 months.

28 Most common reason for aspirin discontinuation:
CVA/TIA: 13 patients vs 4 controls had discontinued aspirin in previous 4 weeks: 4.2% vs 1.3%, P = .03 Odds ratio 3.34 (95% CI: 1.07–10.39) Most common reason for aspirin discontinuation: Surgery Mean interval between aspirin d/c and CVA: 9.5 days

29 One study ( patients) focused on adherence to aspirin therapy in the secondary prevention of CAD, two studies (2594) on aspirin discontinuation in acute CAD, two studies (13 706) on adherence to aspirin therapy before or shortly after coronary artery bypass grafting, and another (2229) on aspirin discontinuation among patients undergoing drug-eluting stenting. Overall, aspirin non-adherence/withdrawal was associated with three-fold higher risk of major adverse cardiac events (OR ¼ 3.14 [1.75–5.61], P ¼ ). This risk was magnified in patients with intracoronary stents, as discontinuation of antiplatelet treatment was associated with an even higher risk of adverse events (OR ¼ [29.90–269.60]).Pooling of the available data showed an average of days (95% CI: 10.25–11.07) between day of discontinuation and thrombotic event. The data indicated that aspirin nonadherence or withdrawal was associated with a threefold higher risk of major cardiac events. Again, the mean time between aspirin withdrawal and thrombotic events was 10 days, which is consistent with the timing of peak thromboxane levels in prior studies. Pooling all these groups yielded a highly significant association between aspirin withdrawal/non-compliance and adverse events (3.14 [1.75–5.61], P for effect=0.0001, P for heterogeneity< , I2=89.8%). Although such meta-analysis may be considered robust as performed according to a random-effect approach, the presence and extent of statistical heterogeneity limits its conclusiveness and leaves it mainly in the hypothesis-generating realm. Moreover, the momentous increase in risk faced by those treated with coronary drug-eluting stents can be easily explained by the highly thrombotic milieau generated by PCI with drug-eluting stent implantation, and its consequent dependence on high-intensity antiplatelet regimens for several months

30 Days elapsed between aspirin d/c and thrombotic events:
10.66 (95% CI 10.25–11.07) “… further confirms the major detrimental impact of aspirin withdrawal across a large spectrum of subjects at risk for de-novo or recurrent cardiovascular events.” Another notable finding of this work is the homogeneity in intervals reported from the several included studies from aspirin discontinuation to thrombotic events. Indeed, the typical average interval of 10 days appears coherent with pathophysiologic data on half platelet population renewal, and has relevant management implications, as in any case of mandatory physician-supervised aspirin withdrawal, the drug should be reinstituted well before these 10 days have elapsed.

31 To date, the only published randomized controlled clinical trial evaluating whether to continue aspirin in the preoperative period was published in 2010 by Oscarsson et al.

32 Randomized double blind placebo-controlled.
220 high-risk patients (PCI excluded). Undergoing intermediate- to high- risk noncardiac surgery. Randomized to: daily low-dose aspirin (75mg) or placebo 7 days before surgery until 3 days post-procedure Aspirin held if needed in placebo group Study was undertaken with the primary aim of assessing the incidence of perioperative myocardial damage in patients with or without low-dose aspirin treatment in the perioperative period. Patients on chronic aspirin rx pre-study (n=196; 90% of the study population): Our hypothesis was that low-dose aspirin reduces the incidence of myocardial damage and major adverse cardiac events (MACEs, defined as acute myocardial infarction, severe arrhythmia, cardiac arrest, or cardiovascular death) without increasing bleeding complications.

33 Inclusion (one of the following) High-risk surgery
CAD Heart failure Renal impairment CVA TIA Insulin-dep DM Exclusion Unstable CAD Decompensated HF Shock Aspirin allergy < 18 yo History of ICH, GIB Rx with warfarin, clopidogrel, mtx Vascular surgery High-risk surgery (large fluid shifts; known cardiac risk >5%) Esophageal Liver Pancreatic Intermediate-risk (cardiac risk 1-5%) Head & neck Intraperitoneal Intrathoracic Major ortho Prostate undergoing vascular surgery were excluded since the Vascular Society in Sweden recommends continuation of aspirin in the perioperative period.

34 Secondary endpoints (any with first 30 days postop):
Primary endpoint Postoperative myocardial damage (TnT) Secondary endpoints (any with first 30 days postop): MACE acute MI cardiac arrest severe arrhythmia CV death Cardio-cerebrovascular complications MACE or stroke/TIA Perioperative blood loss and major bleeding Study endpoints

35 LEFT: Baseline characteristics
RIGHT: Perioperative characteristics.

36 Myocardial damage and cardio-cerebrovascular complications.
Postoperative myocardial damage, defined as a TnT value 0.04 on at least one occasion in the first 48 h after operation period. (MACEs, including acute myocardial infarction, cardiac arrest, severe arrhythmia, or cardiovascular death within the first 30 postoperative days.) Cardiocerebrovascular events: MACE, TIA/stroke, or both. In patients with more than one event, only one event is included in the outcome variable. Statistical analysis was undertaken on an intention-to-treat basis. Patients were assumed not to have had an event when data were missing 1.8% of aspirin-treated patients versus 9.0% of placebotreated patients had a major adverse cardiac event (P = 0.02) within 30 days postoperatively. Aspirin conferred a 7.2% absolute risk reduction, with a RR reduction of 80%, with a number needed to treat of 14 patients. In addition, there was a significantly lower incidence of perioperative CVA or TIA in the aspirin group.

37 Absolute risk reduction = 7.2% [95% CI 1.3–13%]
Aspirin use: Absolute risk reduction = 7.2% [95% CI 1.3–13%] NNT = 14 [95% CI 7.6–78] Majority of patients having MACE had it early postop. 1 in aspirin group and 8 in the placebo group had MACE within: 1st 3 postop days (P=0.02). Patients on chronic aspirin rx pre-study (n=196; 90% of the study population): MACE+ : 10 in placebo vs 1 receiving aspirin (P=0.03). ASA use … for postoperative cardiovascular events within the first 30 days after surgery. There was no MACE in the subgroup of patients who had undergone PCI. ARR=CER (control group’s event rate) – EER (experimental group’s event rate) RRR= ARR/CER NNT= 1/NNT Relative risk reduction = 80% [95% CI 9.2–95%] The relative risk reduction can be more useful than the absolute risk reduction in determining an appropriate treatment plan, because it accounts not only for the effectiveness of a proposed treatment, but also for the relative likelihood of an incident (positive or negative) occurring in the absence of treatment.

38 What about increased EBL?!

39 Prospective blinded placebo-control
To evaluate risk of recurrent bleeding with low-dose aspirin in pts with actively bleeding peptic ulcers (PU). Eligible: active PU bleed & cont. need for aspirin. Exclusion: Unsuccessful endoscopic hemostasis Sensitivity to PPI Dual antiplatelet agent needed Randomized post-EGD to aspirin or placebo for 8 weeks.

40 The 30-day incidence of recurrent bleeding was 10
The 30-day incidence of recurrent bleeding was 10.3% in the aspirin group versus 5.4% in placebo group, but the all-cause mortality at 8 weeks was significantly lower in the aspirin group than in the placebo (1.3% vs 12.9%, 95% CI for the difference: 3.7%–19.5%). This difference persisted even when they excluded deaths due to gastrointestinal complications. The authors assert that continuous aspirin therapy for secondary prevention, even in the setting of active bleeding PU disease, may reduce mortality rates because of the reduced risk of cardiovascular and cerebral vascular events. Ann Intern Med. 2010;152(1):1-9

41 41 studies - 49,590 patients (14,981 on aspirin)
12 retrospective obs., 19 prospective obs., 10 randomized Dental, biopsies, multi-level spine, THA, major vascular/CEA, ENT, neurosurg, and TURP’s. No change in bleeding complications, except: TURP/Prostate procedures aspirin users: 0.4–5.0 units of red blood cells, VS control patients 0.3–1.7 units

42 Randomized double blind placebo-controlled
220 high-risk CAD patients Undergoing intermediate- to high- risk noncardiac surgery. Randomized to: daily low-dose aspirin or placebo

43 Two patients (2%) in the aspirin group versus none in the placebo group (p=0.24) had bleeding which necessitated reoperation in the perioperative period. Both had urologic procedures (TURP, open prostatectomy). There were no significant differences in the amount of: Intraoperative EBL (aspirin 300 mL vs placebo 300 mL, p=0.61) postoperative bleeding between the 2 groups surgeon’s assessment of intraoperative bleeding No statistically significant differences between the groups: Crystalloids Packed red blood cells Plasma

44 Dermatologic Chu et al, J Am Acad Dermatol 2011
Alcalay et al, Dermatol Surg 2004 Reviewed bleeding complications: biopsies, excisions, and Mohs procedures while on aspirin No significant events; do not stop aspirin Cook-Norris et al, J Am Acad Dermatol 2011 Retrospective analysis, 220 patients, 363 procedures on DUAL anti-platelet rx (aspirin + clopidogrel) There were significant wound-related complications none life-threatening Attributed majority of problems to combination or the clopidogrel

45 Rosenbaum et al, Ann Vasc Surg 2010
Vascular Rosenbaum et al, Ann Vasc Surg 2010 Retrospective review of various antiplatelet regimes in CEA 260 patients, 171 continued aspirin perioperatively Neck hematoma – no difference Other bleeding complications – no difference Burdess et al, Ann Surg 2010 Prospective; lower extremity vascular All on aspirin ± clopidogrel No statistical difference in major or minor bleeding on dual APA Aspirin alone did not impact bleeding-related issues Burdess:

46 Vascular - Lindblad et al, Stroke 1993
Vascular surgeons blinded to aspirin use in CEA: Could not differentiate patients on aspirin from patients off aspirin just from bleeding behavior

47 Urologic - Renal transplantation
Eng et al, Clin Transplant 2011 Retrospective 59 on aspirin preop vs 213 no anti-platelet agent No significant differences in: Transfusion requirements Change in hemoglobin Hospital LOS (5.1% vs 1.4% for no preoperative therapy, RR = 3.61, P = 0.12). Because of the limited number of patients, the 95% CI for the RR was very wide (0.84–15.21).

48 Urologic – Prostate Surgery - 1
Aspirin may cause significant bleeding complications in TURP procedures. vascular bed endogenous urokinase 2 studies from 1990’s: Increased bleeding and need for significant more blood products in TURP patients on aspirin. Wierod et al, Scand J Urol Nephrol 1998 Thurston et al, Br J Urol 1993

49 Urologic – Prostate Surgery - 2
Ala-Opas et al, Scand J Urol Nephrol 1996 Chronic - 250mg/day TURP No greater EBL than nonusers aspirin users: 358 mL vs nonusers: 478 mL Nielsen : RECENT study

50 Urologic – Prostate Surgery - 3
Nielsen et al, Scand J Urol Nephrol 2000 Prospective, randomized, double-blind, placebo-controlled. 150 mg continued perioperatively. Intraop blood loss: no difference Postop blood loss: aspirin group (n=26) significantly higher vs placebo (n=27) median 284ml vs median 144ml, P=0.011 No significant differences in: Foley catheter removal LOS Transfusion requirements Their group recommended holding aspirin for 10 days preoperatively.

51 General / Trauma Surgery
Ferraris et al, Surg Gyn Obst 1983 Small (n=52) observational study ‘Unplanned’ appendectomy & cholecystectomy No impact on bleeding-related complications No additional need for transfusion

52 General / Trauma Surgery
Ott et al, J Trauma 2010 Retrospective, 212 patients adm to L-1 trauma center (excluding head injuries) 67 on aspirin, clopidogrel, warfarin, or combo Total LOS - increased 11.5 days vs 8.8 days, P = 0.04 ICU LOS – no difference 4.7 days vs 3.9 days, P = 0.5 Injury Severity Score – no difference 21.4 vs 21.0, P = 0.76 Mortality – no difference 13.4% users vs 9.7% nonusers, P = 0.41. Although this study was not on patients undergoing an elective surgical procedure, it is germane to the trauma surgical population.

53 Orthopedic Surgery - Hip fracture / Femoral neck fractures
Thaler et al, J Trauma 2010 Used PFA in 98 patients on chronic aspirin rx 64 (65%) had true impaired platelet function Mortality, major bleeding, red blood cell requirement, and drainage blood loss did not correlate with platelet aggregation inhibitor intake or platelet function. collagen/epinephrine closure time (CEPI-CT) has been shown to reflect platelet inhibition by aspirin and clopidogrel

54 Neurosurgery Meningioma with neuro sx’s dx’ed 3 months after placement of DES: dual APA Embolization, admitted/telemetry, plavix stopped / ASA continued / bridged with eptifibatide (Integrillin) until 8 hours preop. no unusual surgical bleeding was noted. The patient was discharged on postoperative day 3 with satisfactory recovery

55 POISE-2 – PeriOperative Ischemic Evaluation
Perioperative Ischemic Evaluation 2 (POISE-2)

56 POISE-2 Evaluation of the effect of ‘low-dose’ aspirin vs placebo
Non-cardiac surgery July Dec 2013 135 hospitals / 23 countries Primary endpoint: 30-day composite risk of death & nonfatal MI Randomized, controlled multicenter trial conducted from

57 POISE-2 - Methods Initiation - 200mg ASA just before surgery & continued 100mg for 30-days post-op. Continuation (daily ASA use pre-op for 4/6 weeks) - stopped aspirin for at least 3 days pre-op - ‘placebo group’ to preop ASA dose after 7-days - ‘aspirin group’ restarted with 100mg postop Continuation group: prior users of aspirin Initiation group: not prior users of aspirin The 30-day follow-up was complete for 99.9% of the patients

58 200 mg preop >>> 100 mg/d x 30 days post-op No aspirin 3 days preop >>> 200 mg preop >>> 100 mg/d postop x 7 days >>> Usual dose for balance No aspirin No aspirin 3 days preop >>> Placebo x 7 days postop >>> Usual dose for balance



61 Problem 1 – High-risk Population?
Participants requiring aspirin for either primary or secondary prevention made up no more than 36.3% of all pts assigned to aspirin group It is unclear from risk criteria whether any addt’l pts met AHA guidelines for aspirin Also, unclear how many CS pts were taking aspirin for a guideline recommendation

62 Problem 2 – Placebo Group really Placebo?
2821 IS patients received no aspirin during study period 2191 CS returned to usual aspirin dose within 7 days Hence, 44% (2191 / ( )) of Placebo Group was actually on aspirin for 23 of 30 day follow-up

63 Problem 3 – Additional Anticoagulants
P2Y12 inhibitors (clopidogrel, cangrelor, and ticagrelor)

64 Bleeding – 1/7 ‘Safety Outcomes’
Major bleed A major bleed was defined as a bleeding event that was not specified under life- threatening bleeding and resulted in any one of the following: 1. a hemoglobin ≤70 g/L and the patient received a transfusion of ≥2 units of red blood cells; 2. a hemoglobin drop of ≥50 g/L and the patient received a transfusion of ≥2 units of red blood cells; 3. the patient received a transfusion of ≥4 units of red blood cells within a 24 hour period; 4. any one of the following interventions (i.e., embolization, superficial vascular repair, nasal packing); or 5. retroperitoneal, intraspinal, or intraocular (confirmed clinically or on imaging) bleeding.


66 * the second composite outcome was a composite of mortality, nonfatal myocardial infarction, cardiac revascularization procedure, nonfatal pulmonary embolism, or nonfatal deep venous thrombosis. Major bleed A major bleed was defined as a bleeding event that was not specified under life- threatening bleeding and resulted in any one of the following: 1. a hemoglobin ≤70 g/L and the patient received a transfusion of ≥2 units of red blood cells; 2. a hemoglobin drop of ≥50 g/L and the patient received a transfusion of ≥2 units of red blood cells; 3. the patient received a transfusion of ≥4 units of red blood cells within a 24 hour period; 4. any one of the following interventions (i.e., embolization, superficial vascular repair, nasal packing); or 5. retroperitoneal, intraspinal, or intraocular (confirmed clinically or on imaging) bleeding.

67 POISE-2 … far from final word

68 POISE-2 Issues Only ~1/3 aspirin-patients were on appropriate indications. 4-4.5% in each group received therapeutic anti-coagulant. 1.2% in each group received P2Y12 inhibitors. Safety of aspirin withdrawal in pts with prior percutaneous coronary interventions not fully elucidated. Placebo (?) vs aspirin.




72 Summary Temporary cessation of aspirin rx should only be considered for procedures: risk of bleeding > > risk of a major adverse CV event 2 major groups of procedures to consider when contemplating aspirin cessation: 1) Additional / excessive EBL would lead to worse outcomes: intracranial surgery spinal canal procedures posterior chamber eye surgery middle ear surgery possibly prostate surgery Korinth M, Acta Neurochir 2006 Chassot et al, BJA 2007 Korinth et al, Eur Spine 2007 2) Procedures in which an increase in surgical blood loss to have minimal consequences: no change in transfusion requirements or no increase in major morbidity or mortality. Samana et al, Can J Anes 2002 However, it is important to note that most of the information on the risks of continuing aspirin in the perioperative period is observational and retrospective. - weighing the increased risk of bleeding with aspirin continuation versus the thrombotic risk associated with aspirin cessation. The perioperative management of aspirin should be based on an optimal risk–benefit assessment


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