Interrupting Anticoagulants for Surgery

Interrupting Anticoagulants for Surgery: Guidelines, Risk Stratification, and Clinical Decision-Making.

Raya Kharboutli PA-S2
University of Texas Medical Branch

Regina Medina Urrutia
Universidad Anahuac Campus Xalapa

Anticoagulants are a class of medications used to prevent and treat thromboembolic events such as stroke, deep vein thrombosis, and pulmonary embolism. These agents are divided into two main categories: antiplatelet agents and anticoagulants that inhibit coagulation factors. Understanding their mechanisms of action is critical for making safe perioperative decisions. 

Antiplatelet agents like aspirin irreversibly inhibit cyclooxygenase (COX-1), preventing the production of thromboxane A₂, a molecule essential for platelet activation. As a result, platelet aggregation is impaired for the lifespan of the platelet, which is approximately 7-9 days (1). Clopidogrel, a P2Y12 receptor inhibitor, irreversibly blocks ADP receptors on the platelet surface, further preventing platelet activation and aggregation. Following discontinuation, platelet function typically returns to baseline within about 5 days (2). Warfarin is a vitamin K antagonist that works by inhibiting vitamin K epoxide reductase, an enzyme required for the activation of clotting factors II, VII, IX, and X. Warfarin has a delayed onset of action, with therapeutic anticoagulation typically achieved within 2 to 3 days. Monitoring is performed using International Normalized Ratio (INR), and full reversal of anticoagulant effect takes approximately 3 to 5 days. This process can be expedited with the administration of vitamin K (3). Direct oral anticoagulants (DOACs) are a newer class of medications with more predictable pharmacokinetics. These include factor Xa inhibitors such as apixaban, rivaroxaban, and edoxaban, which inhibit factor Xa, thereby blocking the conversion of prothrombin to thrombin. Additionally, dabigatran is a direct thrombin inhibitor (Factor IIa), which prevents the conversion of fibrinogen to fibrin, the final step in clot formation (4). 

The type of anticoagulant used plays an important role in how far in advance it should be discontinued:

  • Warfarin should usually be stopped 5 days before surgery to allow the INR to return to a safe range (usually <1.5) (11).
  • Direct oral anticoagulants (DOACs) like apixaban, rivaroxaban, dabigatran, and edoxaban are usually suspended 24–72 hours before surgery, depending on the bleeding risk of the procedure and the patient’s kidney function. For example, dabigatran is mostly eliminated by the kidneys, so patients with renal impairment need to stop it even earlier (11).

This classification and understanding of mechanisms provide a foundation for evaluating how and when these agents should be temporarily discontinued prior to surgical or invasive procedures, based on the individual agent, patient thrombotic risk, and the bleeding risk associated with the procedure

Interrupting anticoagulation before a procedure is often necessary to reduce the risk of excessive bleeding during or after surgery. Anticoagulants and antiplatelet agents impair the body’s ability to form clots, which is beneficial for preventing thrombosis but can lead to significant complications when tissue trauma or vascular injury is expected. The decision to pause these medications is a balance between two major risks: bleeding and thrombosis. For procedures with a high bleeding risk, such as major surgeries, spinal or epidural anesthesia, and certain endoscopic or urologic procedures, continued anticoagulation can increase the chance of uncontrolled bleeding, hematoma formation, or the need for transfusions (5). On the other hand, abruptly stopping antithrombotic therapy, especially in high-risk patients (such as those with recent stroke, atrial fibrillation, or coronary stents), may raise the risk of life-threatening thromboembolic events (7). Therefore, clinicians must evaluate the type of anticoagulant, the patient’s thrombotic risk, and the bleeding risk of the procedure to determine the safest perioperative plan. In many cases, temporary interruption with or without bridging therapy allows for safe procedural outcomes while minimizing harm from both bleeding and clot formation (6). 

In cardiology, several invasive procedures carry moderate to high bleeding risk and typically require temporary interruption of anticoagulant or antiplatelet therapy. The decision depends on the type of medication, the procedure’s bleeding risk, and the patient’s thromboembolic risk. For cardiac surgery, such as coronary artery bypass grafting (CABG) or valve replacement, both antiplatelet agents and anticoagulants are usually interrupted. Aspirin is often continued unless bleeding risk is very high but clopidogrel is typically discontinued at least 5-7 days before surgery to minimize perioperative bleeding (8). Warfarin is usually stopped 5 days prior, aiming for an INR of less than 1.5 on the day of the surgery. In patients at high thromboembolic risk such as mechanical valve or atrial fibrillation with prior stroke, bridging with low molecular weight heparin (LMWH) may be considered. Direct oral anticoagulants are typically held for 2-3 days before major cardiac surgery, with the exact timing depending on renal function.

For pacemaker or implantable cardioverter-defibrillator (ICD) insertion, the bleeding risk is considered moderate. Aspirin may be continued in most cases, but clopidogrel should be stopped 5-7 days prior, especially if dual antiplatelet therapy is not mandatory at the time. DOACs are commonly interrupted 24-48 hours before the procedure, depending on renal function and Warfarin is often continued at a therapeutic INR for minor device procedures, but only interrupted in high-bleeding-risk cases (9).  Percutaneous coronary intervention (PCI) presents a unique challenge, especially in patients already on dual antiplatelet therapy (DAPT). These procedures are rarely elective if DAPT is indicated. If non-urgent PCI must be delayed, clopidogrel is held 5-7 days and DOACs for 48-72 hours prior (10). 

Ultimately, the goal is to minimize both bleeding and thrombotic complications by tailoring medication interruption based on the procedure type, medication half-life, and patient risk factors. 

The management of patients going under anesthesia for surgery is a really common challenge due to the decision to suspend or not the anticoagulants the patients are on. Many protocols can be followed to help make the decision. One of these protocols is to evaluate both the risk of bleeding and thromboembolism, and it’s important to know the dosage of the anticoagulant and the reasons why the patient is taking the specific anticoagulant. 

First of all, the risk of bleeding needs to be estimated. One way is the HAS-BLEED score, which will assess the following risk factors such as hypertension, abnormal liver or renal functions, stroke, bleeding, labile INRs, elderly patients (>65 years), and the use of drugs or alcohol. The second step is to estimate the thromboembolic risk, and to do that, age and comorbidities need to be evaluated (12). If the patient has had a recent event of DVT or PE, the decision is based on the diagnosis, but in this scenario, the surgery is delayed as much as possible. Once the two important risks are evaluated, the duration to interrupt the anticoagulant is going to depend on which medication the patient is on. If the patient has low kidney or liver function, we might need additional consideration. In general, almost every procedure, the anticoagulant must be suspended if the risk of bleeding or high thrombotic risk, but if the risk is low isn’t necessarily necessary to stop the medication (12).

There are really selected procedures where we can keep using the anticoagulant, like in a dental extraction, skin biopsy, or a cataract surgery, but also in a procedure like a cardiac implant electronic device, it’s not necessary to stop taking them. The ERHA states that if the patient is going to be under the implantation of a cardiac electronic device like a pacemaker, the patient should continue the anticoagulant perioperatively (13). Unless the patient has a risk of a thromboembolic event and is under warfarin or DOCAs, the medication should be suspended temporarily. In the case of any endovascular procedures like an angioplasty, a meta-analysis randomly shows that patients who were under warfarin and didn’t interrupt while undergoing the procedure were associated with lower risks of complications compared with those who interrupted the warfarin perioperatively (11).

In patients with high thrombotic risk, it may be necessary to use bridging therapy with low-molecular-weight heparin (LMWH) during the time the oral anticoagulant is stopped. However, the BRIDGE trial showed that bridging in patients with non-valvular atrial fibrillation and moderate thrombotic risk increased the risk of bleeding without significantly reducing thromboembolic events (14). Therefore, bridging should only be considered in selected high-risk patients.

When using spinal or epidural anesthesia, anticoagulants increase the risk of spinal hematoma, which can cause permanent paralysis. According to the American Society of Regional Anesthesia (ASRA), anticoagulants such as DOACs should be stopped at least 72 hours before any neuraxial procedures, and specific guidelines should be followed for restarting the medication (15).

Individual characteristics such as renal or liver function, age, history of bleeding, and the use of other medications like antiplatelet agents or NSAIDs, must also be considered when deciding whether to stop anticoagulants before surgery (11). Restarting anticoagulants too soon can lead to postoperative bleeding, while delaying them too long can cause thromboembolism. In general, anticoagulants can be restarted 24–48 hours after surgery if bleeding is under control and the patient is stable (11).  

References:

  1. Haut, E. R., Pronovost, P. J., & Owings, J. T. (2016). Thromboembolic complications in trauma patients. Trauma Surgery & Acute Care Open, 1(1), e000022. https://doi.org/10.1136/tsaco-2015-000022
  2. Pannucci, C. J., & Dresher, M. (2017). Postoperative venous thromboembolism: Risk factors and prevention. International Journal of Environmental Research and Public Health, 14(3), 301. https://doi.org/10.3390/ijerph14030301
  3. Hirsh, J., Guyatt, G., Albers, G. W., Harrington, R., & Schünemann, H. J. (2008). Antithrombotic and thrombolytic therapy: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Circulation, 107, 1692–1700. https://doi.org/10.1161/01.CIR.0000063575.17904.4E
  4. Zareba, W. (2020). Perioperative management of patients receiving anticoagulants. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK557590/
  5. Guyatt, G. H., Akl, E. A., Hirsh, J., Crowther, M., Gutterman, D. D., & Schünemann, H. J. (2022). American College of Chest Physicians Antithrombotic Guidelines. Chest, 161(5), 1272–1302. https://doi.org/10.1016/j.chest.2022.01.032
  6. Nasser, M., Jaffer, A. K., Milani, R. V., & Lavie, C. J. (2021). Perioperative management of anticoagulants in patients undergoing elective procedures. Perioperative Medicine, 10(1), 1–9. https://doi.org/10.1186/s13741-020-00170-4
  7. National Library of Medicine. (n.d.). Bethesda Statement on Open Access Publishing. PubMed. https://pubmed.ncbi.nlm.nih.gov/static-page/down_bethesda.html
  8. Kakar, T. S., Elbaroni, M., & Kang, N. (2020). Bridging anticoagulation therapy in patients undergoing procedures: A literature review. Cardiology Research, 11(5), 328–334. https://doi.org/10.14740/cr1110
  9. Douketis, J. D., Spyropoulos, A. C., Duncan, J., Carrier, M., Le Gal, G., & Tafur, A. J. (2021). Perioperative management of anticoagulant and antiplatelet therapy. Thrombosis Journal, 19(1), 29. https://doi.org/10.1186/s12959-021-00279-6
  10. Douketis, J. D., Spyropoulos, A. C., Kaatz, S., Becker, R. C., Caprini, J. A., Dunn, A. S., … & Schulman, S. (2015). Perioperative bridging anticoagulation in patients with atrial fibrillation. New England Journal of Medicine, 373(9), 823–833. https://doi.org/10.1056/NEJMoa1302946
  11. Kaicker, J., Mokrzycki, M. H., & Salvador, D. (2024). Bleeding risk assessment and anticoagulant management during surgery. PubMed. https://pubmed.ncbi.nlm.nih.gov/38320132/
  12. UpToDate. (2024). Perioperative management of patients receiving anticoagulants. UpToDate. https://www.uptodate.com/contents/perioperative-management-of-patients-receiving-anticoagulants
  13. UpToDate. (2024). Periprocedural management of antithrombotic therapy in patients receiving long-term oral anticoagulation and undergoing percutaneous coronary intervention. UpToDate. https://www.uptodate.com/contents/periprocedural-management-of-antithrombotic-therapy-in-patients-receiving-long-term-oral-anticoagulation-and-undergoing-percutaneous-coronary-intervention/print
  14. Heidbuchel, H., Verhamme, P., Alings, M., Antz, M., Hacke, W., Oldgren, J., … & Lip, G. Y. H. (2015). Updated European Heart Rhythm Association practical guide on the use of non-vitamin K antagonist anticoagulants in patients with non-valvular atrial fibrillation. Europace, 17(10), 1467–1507. https://doi.org/10.1093/europace/euv309
  15. Macedo, A. F., Bell, J., McCarron, C., & Fahey, T. (2018). Interventions to improve appropriate prescribing of anticoagulants in atrial fibrillation: A systematic review. BMC Cardiovascular Disorders, 18(1), 24. https://doi.org/10.1186/s12872-018-0762-1

Bacterial Endocarditis Prophylaxis

Dr. Pakeeza Saif
King Edward Medical College, Lahore, Pakistan


Amin H. Karim MD

Houston Methodist Academic Institute
and Weill Medical College of


Dear Dentist: My Murmur Doesn’t Need Meds Anymore!

Infective endocarditis (IE) is a serious infection of the heart’s inner lining, affecting 3 to 10 people per 100,000 annually. It carries a significant risk, with mortality reaching up to 30% within the first 30 days 1 . Staphylococcus aureus was the most frequently identified pathogen, accounting for 31% of cases. The mitral valve was the most commonly affected, involved in forty-one percent of infections, while the aortic valve was affected in thirty-eight percent of cases 2. The diagnosis of IE is primarily clinical and is based on the modified Duke criteria, which include a combination of major and minor clinical, microbiological, and echocardiographic findings.

Guntheroth et al. observed that bacteremia was present in 40% of 2,403 cases following tooth extraction, 38% of individuals during routine mastication, and 11% of those with oral sepsis in the absence of any dental intervention 3. This issue has long concerned both dentists and cardiologists, driven in part by a preference for commission bias—favoring action over inaction—when considering prophylactic antibiotic use.

American Heart Association revised the guidelines on infective endocarditis prophylaxis in 2007 (full guidelines available at http://circ.ahajournals.org ) to promote the judicious use of antibiotics, particularly in clinical scenarios where the anticipated benefits are outweighed by the risks, such as the emergence of antibiotic resistance and the potential for adverse drug reactions. The present revised document was not based on the results of a single study but rather on the collective body of evidence published in numerous studies over the past two decades. The following points were used as a rationale by AHA for updating the guideline4.

  1. IE is much more likely to result from frequent exposure to random bacteremia associated with daily activities such as chewing food, tooth brushing, flossing, use of toothpicks, use of water irrigation devices, and other activities than from bacteremia caused by a dental, gastrointestinal (GI) tract or genitourinary (GU) tract procedure.
  2. Prophylaxis prevents only an exceedingly small number of cases of IE, if any, in individuals who undergo a dental, GI tract, or GU tract procedure.
  3. The risk of antibiotic-associated adverse events exceeds the benefit, if any, from prophylactic antibiotic therapy except in very high-risk situations.
  4. Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities and thus the risk of IE and is more important than the use of prophylactic antibiotics for dental procedures 4.

Several studies have demonstrated that the lifetime risk of infective endocarditis (IE) varies significantly depending on the underlying cardiac condition. In the general population without known heart disease, the risk is approximately 5 cases per 100,000 patient-years. Patients with rheumatic heart disease (RHD) face a substantially higher risk, ranging from 380 to 440 cases per 100,000 patient-years, which is comparable to the risk observed in individuals with mechanical or bioprosthetic heart valves (308 to 383 cases per 100,000 patient-years)5 .

The greatest risks are observed in the following groups:

  • 630 cases per 100,000 patient-years following cardiac valve replacement for native valve IE
  • 740 cases per 100,000 patient-years in patients with a history of previous IE
  • 2,160 cases per 100,000 patient-years in patients undergoing prosthetic valve replacement due to prosthetic valve endocarditis

These variations in risk highlight the importance of tailoring preventive measures to individual patient profiles.

Further research indicates that even with perfect effectiveness, antibiotic prophylaxis would prevent only a negligible number of infective endocarditis cases—given that the estimated absolute risk after a dental procedure is about 1 in 1.1 million for mitral valve prolapse, 1 in 475 000 for congenital heart disease, 1 in 142 000 for rheumatic heart disease, 1 in 114 000 for prosthetic heart valves, and 1 in 95 000 for those with a history of endocarditis6 7 .

Cardiac Conditions Associated with the Highest Risk of Adverse Outcome from Endocarditis for Which Prophylaxis Is Reasonable

  • Prosthetic cardiac valve or prosthetic material used for cardiac valve repair
  • Previous Infective Endocarditis
  • Cardiac transplantation recipients who develop cardiac valvulopathy
  • Congenital heart disease (CHD)
  • Unrepaired cyanotic CHD, including palliative shunts and conduits
  • Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure
  • Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device.

Guidelines also clearly stated that antibiotic prophylaxis is no longer recommended for any other form of congenital heart disease which explicitly includesheart murmurs, valvular regurgitation, or stenosis without prosthetic material or prior endocarditis 4.

Preventing Infective Endocarditis: Procedures Requiring Antimicrobial Prophylaxis

High-Risk Procedures Requiring Antibiotic Prophylaxis

  • Dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa
  • Respiratory tract procedure with incision and biopsy such as tonsillectomy and adenoidectomy
  • Gastrointestinal or genitourinary procedures in setting of active infection
  • Surgery on infected skin, skin structure, or musculoskeletal tissue

Low-Risk Procedures Not Requiring Antibiotic Prophylaxis

  • Gastrointestinal or Genitourinary procedure in the absence of infection
  • Most Vaginal deliveries or Caesarian deliveries
  • Left atrial appendage occlusion device placement (e.g., Watchman) in the absence of infection — associated with a very low incidence of infective endocarditis, with long-term studies showing no device-related infections over extended follow-up. A single center, 14 year study of 181 patients found no device-related infections over more than 500 patient years of follow up8 .
  • Stable cardiac implantable electronic devices (CIEDs) such as pacemakers and ICDs — antibiotic prophylaxis is not recommended for dental or mucosal procedures solely due to the presence of a CIED in the absence of other high-risk cardiac conditions9 .
  • Atrial septal defect (ASD) closure devices beyond 6 months post-implantation — prophylaxis is not indicated once the device is fully endothelialized and no residual shunt remains10 .

Infective Endocarditis Prophylaxis: Antibiotic Recommendations

  • First line: 2 g amoxicillin orally (or 50 mg/kg kids) 30–60 minutes before the procedure.
  • If allergic to penicillin, 600 mg clindamycin orally (or 20 mg/kg kids).
  • Alternatives include 500 mg azithromycin or clarithromycin orally (15 mg/kg kids)
  • If you can’t take pills, get 2 g ampicillin IM/IV (or 50 mg/kg kids)

Considering rising antimicrobial resistance and the potential for Clostridioides difficile infection linked to antibiotic use, it is advised against relying on the outdated “better safe than sorry” approach to prophylactic antibiotic use, as it may cause more harm than benefit to patients.

References

1. Mostaghim AS, Lo HYA, Khardori N. A retrospective epidemiologic study to define risk factors, microbiology, and clinical outcomes of infective endocarditis in a large tertiary-care teaching hospital. SAGE Open Med. 2017;5. doi:10.1177/2050312117741772

2. Murdoch DR. Clinical Presentation, Etiology, and Outcome of Infective Endocarditis in the 21st Century. Arch Intern Med. 2009;169(5):463. doi:10.1001/archinternmed.2008.603

3. Guntheroth WG. How important are dental procedures as a cause of infective endocarditis? Am J Cardiol. 1984;54(7):797-801. doi:10.1016/S0002-9149(84)80211-8

4. Wilson W, Taubert KA, Gewitz M, et al. Prevention of Infective Endocarditis. Circulation. 2007;116(15):1736-1754. doi:10.1161/CIRCULATIONAHA.106.183095

5. Steckelberg JM; WWR. Risk factors for infective endocarditis. Infectious disease clinics of North America. 1993;7(1):9-19.

6. Pallasch TJ, Wahl MJ. Focal infection: new age or ancient history? Endod Topics. 2003;4(1):32-45. doi:10.1034/j.1601-1546.2003.00002.x

7. Pallasch TJ. Antibiotic prophylaxis: problems in paradise. Dent Clin North Am. 2003;47(4):665-679. doi:10.1016/S0011-8532(03)00037-5

8. Ward RC, McGill T, Adel F, et al. Infection Rate and Outcomes of Watchman Devices: Results from a Single-Center 14-Year Experience. Biomed Hub. 2021;6(2):59-62. doi:10.1159/000516400

9. Canpolat U. Tailored antibiotic prophylaxis in patients undergoing CIED implantation: One size does not fit all the principle. Pacing and Clinical Electrophysiology. 2019;42(4):483-483. doi:10.1111/pace.13624

10. Tanabe Y, Sato Y, Izumo M, et al. Endothelialization of an Amplatzer Septal Occluder Device 6 Months Post Implantation: Is This Enough Time? An In Vivo Angioscopic Assessment. Journal of Invasive Cardiology. 2019;31(2). doi:10.25270/jic/18.00206