Rechenmacher SJ, Fang JC. Bridging Anticoagulation: Primum Non Nocere. J Am Coll Cardiol. 2015 Sep 22;66(12):1392-403.
Full-text for Emory users.
Conclusions: Periprocedural anticoagulation management is a common clinical dilemma with limited evidence (but 1 notable randomized trial) to guide our practices. Although bridging anticoagulation may be necessary for those patients at highest risk for TE, for most patients it produces excessive bleeding, longer length of hospital stay, and other significant morbidities, while providing no clear prevention of TE. Unfortunately, contemporary clinical practice, as noted in physician surveys, continues to favor interruption of OAC and the use of bridging anticoagulation. While awaiting the results of additional randomized trials, physicians should carefully reconsider the practice of routine bridging and whether periprocedural anticoagulation interruption is even necessary.
Central Illustration. Bridging Anticoagulation: Algorithms for Periprocedural Interrupting and Bridging Anticoagulation. Decision trees for periprocedural interruption of chronic oral anticoagulation (top) and for periprocedural bridging anticoagulation (bottom). OAC = oral anticoagulation.
A discussion during a previous conference included the perioperative management of patients with atrial fibrillation receiving a direct oral anticoagulant (DOAC).
Reference: Douketis JD, et al. Perioperative management of patients with atrial fibrillation receiving a direct oral anticoagulant. JAMA Internal Medicine. 2019 Aug 5; doi:10/1001/jamainternmed.2019.2431
Summary: Each year, 1 in 6 patients with AF, or an estimated 6 million patients worldwide, will require perioperative anticoagulant management. When DOAC regimens became available for clinical use in AF, starting in 2010, no studies had been conducted to inform the timing of perioperative DOAC therapy interruption and resumption, whether heparin bridging should be given, and whether preoperative coagulation function testing was needed. Uncertainty about the perioperative management of DOACs may be associated with unsubstantiated practices and increased harm to patients.
One discussion this week involved the treatment for uremic bleeding.
Reference: Hedges SJ, et al. Evidence-based treatment recommendations for uremic bleeding. National Clinical Practice. Nephrology. 2007 Mar;3(3):138-153.
Summary: Hedges et al (2007) provide a review of normal hemostatic and homeostatic mechanisms that operate within the body to prevent unnecessary bleeding, as well as an in-depth discussion of the dysfunctional components that contribute to complications associated with uremic bleeding syndrome. Prevention and treatment options can include one or a combination of the following: dialysis, erythropoietin, cryoprecipitate, desmopressin, and conjugated estrogens.
The article cited is worth a full text read because:
- Treatment options are compared with regard to their mechanism of action, and onset and duration of efficacy.
- An extensive review of the clinical trials that have evaluated each treatment is also presented (Tables 3, 4, 5).
- An evidence-based treatment algorithm to help guide clinicians through most clinical scenarios, and address common questions related to the management of uremic bleeding.
Uremic bleeding in patients with chronic renal failure is extremely complex. One factor contributing to this complexity is the incomplete elucidation of its pathophysiology. Because the mechanisms underlying uremic bleeding are not fully understood, prevention and treatment for many different clinical scenarios are not clearly defined (p.150).
- EPO works to increase the number of red blood cells, allowing platelets to travel in closer proximity to the endothelium.
- Cryoprecipitate and desmopressin work to increase the proportion of normal or functional factors that might be dysfunctional in patients with uremic bleeding.
- Estrogens are thought to work by decreasing NO levels, thereby increasing concentrations of TxA2 and ADP.
Multiple interventions that simultaneously affect different aspects of the pathophysiology of uremic bleeding might most effectively prevent bleeding in high-risk patients and limit active bleeding in those for who cessation of blood loss is more pressing.
By determining which patients are most at risk, clinicians can utilize dialysis and EPO in the early stages of uremic bleeding, and employ desmopressin, cryoprecipitate and/or estrogens prior to a surgical procedure, thereby possibly preventing bleeding secondary to uremic platelet dysfunction.