The Daily Dose • Monday, April 30

Perioperative Venous Thromboembolism: A Review

By Dr. Michael D. McDonald, from the IARS 2018 Annual Meeting*

During this review session, Dr. Ronald Gordon, MD, PhD, discusses perioperative venous thromboembolism (VTE). The basis of the talk is a review paper he wrote, Perioperative Venous Thromboembolism: A Review, published in Anesthesia & Analgesia in 20171. Through the progression of his lecture, Dr. Gordon reviewed VTE pathophysiology, prevention strategies, and why as anesthesiologists we should care.

In relation to long-term outcomes of surgical intervention, there is only an approximately 1:100,000 – 1:200,000 risk of mortality directly related to anesthesia. This results in approximately 300 deaths per year, yet this is a concern that most anesthesiologists focus on. Compare these figures to all cause mortality in surgical patients at 1 year being 5%, or ~1,000,000 deaths per year. Additionally, VTE results in 10% of all hospital related deaths and 30% of acute surgical deaths. Given these figures, VTE should be a major target for reducing perioperative morbidity and mortality, and VTE is now considered a preventable complication.

The pathophysiology is well established for the formation of VTE, with the valve cusp being implicated in how thrombus formation is initiated. Oxygenation of the venous valvular cusps is achieved via pulsatile blood flow with muscular contraction of the legs. When pulsatile flow ceases, hypoxia results in endothelial activation and the expression of Weibel-Palade bodies, setting in motion the creation of a thrombotic nidus. These changes take place as soon as anesthetic induction is initiated. As such, prophylactic measures must take place prior to induction of anesthesia.

Prophylaxis of VTE can be divided into two main categories: mechanical and pharmacologic prophylaxis. The use of mechanical prophylaxis, or spontaneous compression devices (SCDs), serve to mimic muscle contraction and maintain pulsatile flow and venous valvular oxygenation. For efficient prophylaxis, SCD initiation must take place prior to induction of anesthesia, and should be continued for 2 weeks post-op for optimal prevention through the use of portable SCDs as an outpatient. Pharmacologic prophylaxis includes short-term anticoagulation (often with SQ heparin or LMWH) to prevent thrombus initiation, or aspirin to prevent thrombus propagation. Anticoagulation therapy should be administered at least 30 minutes prior to induction of anesthesia.

There are many risk factors that contribute to VTE provocation through surgery. Surgery itself induces an inflammatory response promoting a pro-coagulable state. The top four include age >75 (Relative Risk 10-100), thrombophilias such as Factor V Leiden (RR 7), Cancer (RR 6.5), and Oral Contraceptive or Hormone Replacement Therapy (RR 4). Risk factors are additive, and as such physicians must be proactive in minimizing VTE development in the surgical patient. Central lines and PICCs lead to the majority of upper extremity VTE, and thus their use should be minimized in high-risk individuals.

As hospitals increasingly work to decrease overhead costs, and with unplanned readmission contributing greatly to costs, VTE is a prime candidate to target. The three top causes for post-operative 30-day readmission are surgical site infections, venous thromboembolism, and postoperative pain. Anesthesiologists can contribute to minimizing all three, and thus can leverage a higher proportion of bundled surgical payments from hospital administration by demonstrating our role and success in decreasing these complications and readmissions.

Resource:

  1. Gordon RJ, Lombard FW. Perioperative Venous Thromboembolism: A Review. Anesth Analg. 2017:125;403-412.

*Coverage of the Review Course Lecture, Perioperative Venous Thromboembolism: A Review

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