Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3865_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
15.09.2026
Размер:
11 Мб
Скачать
☆
220 Anticoagulation Therapy
https://t.me/med1917
3. Hylek EM, Regan S, Go AS, et al. Clinical predictors of prolonged delay in return of the international normalized ratio to within the therapeutic range after excessive anticoagulation with warfarin. Ann Intern Med. 2001;135:393-400.
Watson HG, Baglin T, Laidlaw SL, et al. A comparison of the efficacy and rate of
4. response to oral and intravenous vitamin K in reversal of over-anticoagulation with warfarin. Br J Haematol. 2001;115:145-149.
Smythe MA, Trujillo T, Fanikos J. Reversal agents for use with direct and indirect
5. anticoagulants. Am J Health-Syst Pharm. 2016;73(10 Suppl 2):S27-S48.
6.
Dager W, Hellwig T. Current knowledge about measuring the anticoagulant effect
and managing bleeding with direct oral anticoagulants. Am J Health-Syst Pharm. 2016;73(10 Suppl 2):S14-S26.
Schulman S, Bijsterveld NR. Anticoagulants and their reversal. Transfus Med Rev.
7. 2007;21:37-48.
8.
Pollack CV Jr, Reilly PA, van Ryn J, et al. Idarucizumab for dabigatran reversal - full
cohort analysis. N Engl J Med. 2017 [Epub ahead of print].
9. Koster A, Chew D, Gründel M, et al. An assessment of different filter systems for extracorporeal elimination of bivalirudin: an in vitro study. Anesth Analg. 2003;96:1316-1319.
Awad NI, Brunetti L, Juurlink DN. Enhanced elimination of dabigatran through
10. extracorporeal methods. J Med Toxicol. 2015;11:85-95.
11. Galeone A, Rotunno C, Guida P, et al. Monitoring incomplete heparin reversal and heparin rebound after cardiac surgery. J Cardiothorac Vasc Anesth. 2013;27:853-858.
12. Crowther MA, Berry LR, Monagle PT, et al. Mechanisms responsible for the failure of protamine to inactivate low-molecular-weight heparin. Br J Haematol. 2002;116:178-
186.
13.
Bijsterveld NR, Moons AH, Boekholdt M, et al. Ability of recombinant factor VIIa
to reverse the anticoagulant effect of the pentasaccharide fondaparinux in healthy volunteers. Circulation 2002;106:2550-2554.
Lisman T, Bijsterveld NR, Adelmeijer J, et al. Recombinant factor VIIa reverses the in
14. vitro and ex vivo anticoagulant and profibrinolytic effects of fondaparinux. J Thromb Haemost. 2003;1:2368-2373.
15. Young G, Yonekawa KE, Nakagawa PA, et al. Recombinant activated factor VII effectively reverses the anticoagulant effects of heparin, enoxaparin, fondaparinux, argatroban, and bivalirudin ex vivo as measured using thromboelastography. Blood Coagul Fibrinolysis. 2007;18:547-553.
*16. Desmurs.-Clavel H, Huchon C, Chatard B, et al. Reversal of the inhibitory effect
of fondaparinux on thrombin generation by rFVIIa, aPCC and PCC. Thromb Res. 2009;123:796-798.
17. Garcia DA, Baglin TP, Weitz JI, et al. Parenteral anticoagulants: Antithrombotic Therapy and Prevention of Thrombosis. 9th ed. American College of Chest Physicians Evidence-based Clinical Practice Guidelines. Chest. 2012;141(suppl 2):e24S-e43S.
18. Stratmann G, deSilva AM, Tseng EE, et al. Reversal of direct thrombin inhibition after cardiopulmonary bypass in a patient with heparin-induced thrombocytopenia. Anesth Analg. 2004;98:1635-1639.
ANTICOAGULATION REVERSAL: PART II 221
https://t.me/med1917
19. Nagle E, Tsu L, Dager WE. Bivalirudin for anticoagulation during hypothermic cardiopulmonary bypass and recombinant factor VIIa for iatrogenic coagulopathy. Ann Pharmacother 2011;45:e47.
Lessire S, Douxfils J, Baudar J, et al. Is thrombin time useful for the assessment of
20. dabigatran concentrations? An in vitro and ex vivo study. Thromb Res. 2015;136:693-
696.
Dager WE, Gosselin RC, Kitchen S, et al. Dabigatran effects on the international
21. normalized ratio, activated partial thromboplastin time, thrombin time, and fibrinogen: a multicenter, in vitro study. Ann Pharmacother. 2012;46:1627-1636.
*22.
Frontera JA, Lewin Iii JJ, Rabinstein AA, et al. Guideline for reversal of antithrombotics
in intracranial hemorrhage: a statement for healthcare professionals from the Neurocritical Care Society and Society of Critical Care Medicine. Neurocrit Care. 2016;24:6-46.
23. Dager WE, Banares L. Reversing the anticoagulation effects of dabigatran. Hosp Pract. 2017;45:29-38.
24. Steele AP, Lee JA, Dager WE. Incomplete dabigatran reversal with idarucizumab. Clin Toxicol (Phila). 2017 [Epub ahead of print].
25. DagerW,RobertsA.DOACreversalwithlow(<20Units/kg)ormoderatedose(≥20
Units/kg) FEIBA in urgent management of major bleeding. Res Pract Thromb Haemost. 2017;1(Suppl. 1) (Abstract 2016):977.
26. Yin EB, Tan B, Nguyen T, et al. Safety and effectiveness of factor VIII inhibitor bypassing activity (FEIBA) and fresh frozen plasma in oral anticoagulant-associated intracranial hemorrhage: a retrospective analysis. Neurocrit Care. 2017 [Epub ahead of Print].
27. Khadzhynov D, Wagner F, Formella S, et al. Effective elimination of dabigatran by haemodialysis. A phase I single-centre study in patients with end-stage renal disease. Thromb Haemost. 2013;109:596-605.
28.
Chiew AL, Khamoudes D, Chan BS. Use of continuous veno-venous haemodiafiltration
therapy in dabigatran overdose. Clin Toxicol (Phila). 2014;52:283-287.
Chang DN, Dager WE, Chin AI. Removal of dabigatran by hemodialysis. Am J Kidney
29. Dis. 2013;61:487-489.
30.
Liesenfeld KH, Staab A, Härtter S, et al. Pharmacometric characterization of
dabigatran hemodialysis. Clin Pharmacokinet. 2013;52:453-462.
31. Lam WW, Reyes MA, Seger JJ. Plasma exchange for urgent apixaban reversal in a case of hemorrhagic tamponade after pacemaker implantation. Tex Heart Inst J. 2015;42:377-380.
*32. Shetty HGM, Backhouse G, Bentley DP, et al. Effective reversal of warfarin-induced
excessive anticoagulation with low dose vitamin k1. Thromb Haemost. 1992;67:13-15.
*33. Tsu LV, Dienes JE, Dager WE. Vitamin K dosing to reverse warfarin based on INR,
route of administration, and home warfarin dose in the acute/critical care setting. Ann Pharmacother. 2012;46:1617-1626.
34. White RH, McKittrick T, Hutchinson R, et al. Temporary discontinuation of warfarin therapy: changes in the international normalized ratio. Ann Intern Med. 1995;122:40-
42.
222 Anticoagulation Therapy
https://t.me/med1917
35. Crowther MA, Ageno W, Garcia D, et al. Oral vitamin K versus placebo to correct excessive anticoagulation in patients receiving warfarin: a randomized trial. Ann Intern Med. 2009;150:293-300.
Wójcik C, Schymik ML, Cure EG. Activated prothrombin complex concentrate
36. factor VIII inhibitor bypassing activity (FEIBA) for the reversal of warfarin induced coagulopathy. Int J Emerg Med. 2009;2:217-225.
Rowe AS, Mahbubani PS, Bucklin MH, et al. Activated prothrombin complex
37. concentrate versus plasma for reversal of warfarin-associated hemorrhage. Pharmacotherapy. 2016;36:1132-1137.
*38.
Leissinger CA, Blatt PM, Hoots K, et al. Role of prothrombin complex concentrates
in reversing warfarin anticoagulation: a review of the literature. Am J. Hematol. 2008;83:137-143.
39.
Goldstein JN, Marrero M, Masrur S, et al. Management of thrombolysis-associated
symptomatic intracerebral hemorrhage. Arch Neurol. 2010;67:965-969.
40. Levy JH, Tanaka KA, Dietrich W. Perioperative hemostatic management of patients treated with vitamin K antagonists. Anesthesiology. 2008;109:918-926.
41. Dager WE, Regalia R, Williamson D, et al. Reversal of elevated international normalized ratios and bleeding with low-dose recombinant activated factor VIIa in patients receiving warfarin. Pharmacotherapy. 2006;26:1091-1098.
42.
Garcia D, Crowther MA, Ageno W. Practical management of coagulopathy associated
with warfarin. BMJ. 2010;340:c1813.
43. Whitling AM, Bussey HI, Lyons RM. Comparing different routes and doses of phytonadione for reversing excessive anticoagulation. Arch Intern Med. 1998;158:2136-
2140.
Baker RI, Coughlin PB, Gallus AS, et al. Warfarin reversal consensus guidelines
44. on behalf of the Australasian Society of Thrombosis and Haemostasis. Med J Aust. 2004;181:492-497.
*45.
Lubetsky A, Yonath H, Olchovsky D, et al. Comparison of oral vs intravenous
phytonadione (vitamin K1) in patients with excessive anticoagulation: a prospective randomized controlled study. Arch Intern Med. 2003;163:2469-2473.
Crowther MA, Douketis JD, Schnurr T, et al. Oral vitamin K lowers the international
46. normalized ratio more rapidly than subcutaneous vitamin K in the treatment of warfarin-associated coagulopathy. A randomized, controlled trial. Ann Intern Med. 2002;137:251-254.
47. van Aart L, Eijkhout HW, Kamphuis JS, et al. Individualized dosing regimen for prothrombin complex concentrate more effective than standard treatment in the reversal of oral anticoagulant therapy: an open, prospective randomized controlled trial. Thromb Res. 2006;118:313-320.
48. Preston FE, Laidlaw ST, Sampson B, et al. Rapid reversal of oral anticoagulation with warfarin by a prothrombin complex concentrate (Beriplex): efficacy and safety in 42 patients. Br J Haematol. 2002;116:619-624.
*49. Kuramatsu JB, Gerner ST, Schellinger PD et al. Reversal, blood pressure levels, and
anticoagulant resumption in patients with anticoagulation-related intracerebral hemorrhage JAMA. 2015;313:824-836.
50. Qureshi W, Mittal C, Patsias I, et al. Restarting anticoagulation and outcomes after major gastrointestinal bleeding in atrial fibrillation. Am J Cardiol. 2014;113:662-668.
10
https://t.me/med1917
Chapter
TRANSITIONS IN CARE—
PERIPROCEDURAL BRIDGING
AND TRANSITIONS BETWEEN
AGENTS
Jessica Rimsans, Katelyn W. Sylvester, and John Fanikos
INTRODUCTION
Patients receiving long-term antiplatelet (AP) therapy or oral anticoagulation (OAC) with vitamin K antagonists (VKA) or a direct-acting oral anticoagulant (DOAC) commonly transition from the ambulatory setting to the hospital and back again. This clinical scenario often requires antithrombotic therapy changes. Each transition point (hospital admission, procedure, unit transfer, discharge to home, or long­term care) represents an opportunity to assess medication regimens for errors, omissions, and treatment adjustments. Emphasis on abbreviating hospital stay and reducing costs further magnifies the need for seamless conversion between oral and parenteral antithrombotic therapies. As these patients transition, either electively or urgently, the diagnosis and indications for anticoagulant therapy should be evaluated. Surgical and invasive procedures add additional levels of complexity where OAC and AP therapy may be continued, interrupted, or replaced with short-term parenteral or bridge therapy. Since there is not a standardized definition of bridging, most regimens have been developed from observational and retrospective studies, registry data, and more recently a randomized controlled trial. Physician and patient preference will play a role in determining whether therapy is continued, stopped, or replaced with an alternative agent.
PERIPROCEDURAL BRIDGING PRINCIPLES
•
Determine thromboembolism risk with interruption of anticoagulant (AC) and/or AP therapy.
•
Assess bleeding risk associated with:
Parenteral AC/AP therapy Surgical or invasive procedure Continuation of AC/AP therapy
•
Weigh risk versus benefits of bridging
•
Consider patient and physician’s goals and preferences
223
224 Anticoagulation Therapy
https://t.me/med1917
PERIPROCEDURAL THROMBOEMBOLIC RISK ASSESSMENT
•
Patients should undergo a thorough assessment for thromboembolism using a standardized risk stratification evaluation.
•
Identify level of thromboembolism risk based on underlying disease and comor­bidities.
•
Previous literature and current guidelines historically risk stratified patients using Cardiac Failure, Hypertension, Age, Diabetes, and Stroke (doubled) (CHADS however, CHA validated and adopted into clinical practice.
-VASc (vascular disease and sex category) has since been
2DS2
1
2-4
);
2
PERIPROCEDURAL BLEEDING RISK ASSESSMENT
•
Patients should undergo a thorough assessment for bleeding risk.
•
The procedure itself is one of the most important risk factors for bleeding.
•
Consider patient risk factors and comorbidities that may impact oral or paren­teral anticoagulation and increase procedural and postprocedural bleeding risk.
•
Various prognostic and scoring indices for bleeding exist for initiating VKA therapy, in-hospital risk, and postprocedural risk.
•
Consider using an appropriate bleeding index to identify patient’s risk level for bleeding.
5-9
10-13
DETERMINING PROCEDURAL RISK OF HEMORRHAGE
•
Assess the risk of bleeding from the procedure.
•
Incidence of hemorrhage will depend on the procedure and occurs in as many as 11.9% of patients during routine surgery. Published bleeding rates include the following:
Thoracic surgery 33.7% Abdominal surgery 11.4% Other major surgery 14.3%
•
Two thirds of bleeding events will occur within 48 hours after the intervention.
•
Procedures in closed areas or cavities carry a high risk for hemorrhagic compli­cations (Table 10-1), including:
Pericardial region (related to pacemaker/internal cardiac defibril-
lator [ICD] insertion)
Spinal (related to trauma from lumbar puncture or epidural place-
ment)
Urologic procedures (involving the retroperitoneum or bladder
lumen)
•
Assess patient specific risk factors for bleeding (Table 10-2).
5,6
4,7
TRANSITIONS IN CARE 225
https://t.me/med1917
TABLE 10-1: Procedural Risk of Hemorrhage in the Setting of
Perioprocedural Anticoagulation
When assessing the risk of periprocedural bleeding in the setting of anticoagulation, it is im­portant to evaluate the bleeding risk in relation to the dose of anticoagulation (i.e., therapeutic anticoagulation vs. prophylactic doses of anticoagulation).
High Bleeding Risk Invasive Procedure or Surgery
Cardiothoracic
• Thoracic aortic aneurysm repair, heart valve replacement/repair, coronary artery bypass, cardiac biopsy, heart transplantation, coronary angiography +/- PCI
Lung surgery: lobectomy, wedge
• resection, segmentectomy, pneumonectomy
• Implantable cardiodefibrillator device implantation or pacemaker insertion
Urological
• Transurethral prostate resection, prostectomy, prostate surgery/biopsy, bladder resection or tumor ablation, nephrectomy, kidney biopsy/surgery, urogynecological surgery
Gastrointestinal
• Intra-abdominal surgery, appendectomy, bowel resection, intestinal anastomosis, PEG tube placement, cholecystectomy, polypectomy, colonoscopy with biopsy >2 cm
Orthopedic
•
Joint arthroplasty, hip/knee replacement,
other major orthopedic surgery
Vascular
• AAA repair, endarterectomy, carotid bypass surgery, port placement, other major vascular surgery
Cancer
• Urologic, gynecologic, head and neck, colorectal, breast
Neurosurgical
• Intracranial or spinal surgery, laminectomy, other major neurosurgery
1,5-9
1
Low Bleeding Risk Invasive Procedure or Surgery
Abdominal hernia repair Abdominal hysterectomy Axillary node dissection Arthrocentesis Ablation Arthroscopy Biopsy if low vascularity of site (bladder, thyroid, lymph node, pancreas) Bronchoscopy without biopsy Cataract eye surgery Central venous catheter removal Cutaneous surgeries Dental hygiene or extraction (uncomplicated) Dermatologic procedures (minor) Dilation and curettage Electrophysiologic testing Hemorrhoid surgery or hydrocele repair Joint and soft tissue injections/aspirations Non-coronary angiography Gastrointestinal endoscopy or colonoscopy without biopsy Skin cancer excision
(continued)
226 Anticoagulation Therapy
https://t.me/med1917
TABLE 10-1: (Continued)
High Bleeding Risk Invasive Procedure or Surgery
Surgery and procedures/biopsies in highly vascular organs
• Kidney, liver, spleen, breast
Reconstructive plastic surgery with extensive tissue injury
Other
•
Complicated dental surgery (multiple
tooth extractions)
Sternotomy wire removal
•
•
Endoscopy guided fine-needle aspira-
tion
Any major surgery >45 min in duration
•
AAA: abdominal aortic aneurysm, PCI: percutaneous coronary intervention, PEG: percutaneous endoscopic gastrostomy
Low Bleeding Risk Invasive Procedure or Surgery
PERIPROCEDURAL MANAGEMENT OF ANTIPLATELET THERAPY
•
Evidence supporting periprocedural management of AP therapy is limited.
TRANSITIONING FROM VKA TO PARENTERAL THERAPY
•
There are limited high quality data to guide clinicians on how to devise a bridge strategy, if necessary, based on thromboembolism and bleeding risk (Table
1
10-3).
•
Optimal bridge therapy for temporary warfarin interruption for invasive proce­dures has been shown to increase the risk of bleeding in atrial fibrillation patients without a corresponding decrease in thromboembolism risk (BRIDGE trial); it is also associated with an increased risk of bleeding, without a corresponding decrease in thromboembolism risk in patients receiving VKA for prior venous thromboembolism (VTE).
•
In patients on VKA, low dose vitamin K 1 mg orally can be given to normalize INR the day before surgery without conferring warfarin resistance postoperative.
BRIDGING WITH LOW MOLECULAR WEIGHT HEPARIN
•
Registry data suggests bridging may be unnecessary for the vast majority of patients in an anticoagulation management service even with interruptions in warfarin therapy (continued, lower-intensity, or interrupted).
14-19
20
19-25
TRANSITIONS IN CARE 227
https://t.me/med1917
TABLE 10-2: Major Patient Risk Factors and Comorbidities
Increasing Bleeding Risk with Anticoagulation
Risk Factor or Comorbidity
Increasing age Risk increases as age increases >55 years
History of bleeding Higher risk with more recent bleeding event (e.g., gastrointestinal,
Vascular disease Prior stroke or peripheral vascular disease
Renal dysfunction Creatinine clearance
Hepatic dysfunction Associated with altered coagulation function and a higher risk of
Congestive heart failure
Anemia Hematocrit <30% or hemoglobin <13 g/dL males, <12 g/dL females is
Cancer Bleeding risk correlates with the type and extent of cancer
Hypotension Systolic blood pressure <100 mm of Hg
Hypertension Systolic blood pressure >200 mm of Hg
Female Predictor of higher risk; exact mechanism is unknown
Explanation
intraocular, hematuria)
a
associated with higher risk
bleeding with worsening liver function
Exacerbations may alter anticoagulant response and pharmacodynamics
associated with higher risk
<90 mL/min or serum creatinine >1.2 mg/dL
4–7
Diabetes mellitus Impacts many risk factors that increase bleeding risk
Labile INRs Poorly controlled INR, <60% time in therapeutic range
Alcohol consumption
Concomitant drugs Antiplatelet agents and nonsteroidal anti-inflammatory agents
a
Calculated using Cockcroft-Gault formula.
INR: international normalized ratio
•
Low molecular weight heparin (LMWH) prophylactic doses have never been studied in the arena of preventing thromboembolism. Thus, when bridging for atrial fibrillation and mechanical heart valves, therapeutic dosing is usually preferred.
•
There is no randomized controlled trial in patients with atrial fibrillation or heart valves that shows therapeutic LMWH has any benefit in reduction in stroke risk.
•
Standardized LMWH “bridge” regimens often result in significant residual anticoagulant activity shortly before surgery.
•
Patients with impaired renal function are likely to have delayed LMWH clearance.
•
Residual LMWH activity, as measured by anti-factor Xa testing, can last 24 hours after a dose.
≥8 units alcoholic consumption per week
26
228 Anticoagulation Therapy
https://t.me/med1917
•
Duration of LMWH bridging may be significantly longer (12 days) than is reported in clinical trials.
•
In those patients undergoing pacemaker or ICD placement, a strategy of contin­ued warfarin reduced the incidence of clinically significant pocket hematoma compared with those being bridged with intravenous unfractionated heparin (IV UFH).
27
16
RE-INITIATION OF VKA
•
Patients receiving higher weekly warfarin doses are likely to eliminate the drug faster and return to baseline INR earlier than those patients on lower weekly warfarin doses.
•
Consider any events during the intraoperative and immediate postoperative period (excessive bleeding or bleeding vessels which required intervention) that may impact reinitiating anticoagulation.
•
The decision to restart anticoagulation after a procedure must be made in consultation with the surgeon or proceduralist, taking into account procedure, presence of neuraxial anesthesia, and risk of bleeding/thromboembolism.
•
When warfarin is restarted, often the maintenance dose is reinitiated. When there is a desire for earlier “measured” INR response, another option is to start with an increased dose for the initial 2 days (≈50-100% increase in the maintenance dose), then follow with the usual maintenance dose.
28,29
TRANSITIONING BETWEEN DIRECT­ACTING ORAL ANTICOAGULATION OR TO PARENTERAL THERAPY
•
DOACs have a fast onset and offset. The use of a pre-operative parenteral bridging agent is not needed. Use of a parenteral bridging (generally IV UFH) may be necessary after surgery in high bleeding risk situations due to its short duration and ability to reverse.
•
For low bleeding risk procedures (i.e., dental, ophthalmology, superficial surger­ies) in patients with normal renal function, the DOAC may be continued uninter­rupted at the discretion of the interventionalist.
•
When a DOAC is restarted, renal function, procedure, presence of neuraxial anesthesia, risk of bleeding/thromboembolism, and onset of the agent should be taken into account.
•
The effect of the DOAC on the UFH monitoring strategy (aPTT, anti-factor Xa testing) must be considered; alternative monitoring strategies could be needed to avoid lags in anticoagulation (Table 10-6).
•
In some situations (high bleeding risk/low thrombosis risk, delayed DOAC clear­ance due to acute kidney injury), heparin initiation may be delayed beyond standard recommendations until the DOAC has largely cleared; appropriate laboratory measures may help guide when to initiate UFH (Table 10-6).
30-33
18
30
bridging group and 0.3% in the bridging group (CI 0.6–0.8,
https://t.me/med1917
P = 0.01 for noninferiority)
group and 3.2% in the bridging group (CI 0.2 to 0.78, P =
0.005 for superiority)
12 of 343 patients (3.5%) in the continued warfarin group,
compared with 54 out of 338 (16%) in the heparin-bridging
group (RR 0.19 P <0.001)
significantly
• Incidence of arterial thromboembolism was 0.4% in the no-
• Incidence of major bleeding was 1.3% in the no-bridging
• Clinically significant device pocket hematoma occurred in
• Major surgical and TE complications did not differ
TRANSITIONS IN CARE 229
(continued)
0.2% in bridge vs. no bridge (CI 3.9–75.1)
vs. 3.9% clinically relevant bleeding events
procedural complications and 33.3% were directly related to
the bridging agent
groups (P = 0.56)
30 day rates of clinically relevant bleeding were 2.7% and
For therapeutic and prophylactic LMWH, there were 2.2%
Of the 15 bleeding events in the bridge cohort, 52.9% were
•
•
•
• Recurrent VTE were not significantly different between
Dalteparin 100 IU/kg SQ
AF patients (n = 1,884)
Randomized
Trial Study Design Population Intervention Outcome
TABLE 10-3: Summary of Evidence from Bridging Trials
BRIDGE trial
BID vs placebo 1-3 days
before procedure to 24 hr
before then 5–10 days post
procedure
Warfarin continued through
procedure vs. IV UFH or
LMWH before and/or after
-VASc 2–3,
2
DS
2
<10% with stroke/TIA
Majority CHA
controlled trials
)
15
(Douketis et
al.
Pacemaker or ICD
placement (n = 643), annual
risk of TE >5% or more
Randomized
controlled trial
trial (Birnie et
BRUISE
CONTROL
procedure
)
16
al.
Use of bridge vs. no bridge
during warfarin interruption
Therapeutic LMWH (89%)
and heparin (11%)
History of VTE (n = 1,178),
majority >12 months prior,
low recurrent VTE risk
category
Retrospective
cohort
14
Clark et al.