Issue: October 2010
October 01, 2010
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Reducing the need for transfusion following total knee replacement: Part 2

Issue: October 2010
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Introduction

This is the second part of our Round Table discussion related to current concepts of blood management during and following total knee replacement (TKR). In this part, we discuss infection risk, how to identify and treat anemic patients and more peri- and postoperative methods for managing blood loss.

Our goal was to bring our readers the current approaches from multiple surgeons that will stimulate you to evaluate your program. Minimizing blood transfusion is an important aspect of this surgery both for the patient’s recovery and overall outcomes. The one message the different panelists have made known is the need for blood transfusion is minimal if the patient does not enter with preoperative anemia. Part 1 of this roundtable in the September issue was one of the most read articles when it was placed on our website.

Douglas W. Jackson, MD
Moderator

Round Table Participants

Moderator

Douglas W. Jackson, MDDouglas W. Jackson, MD
Long Beach, Calif.

Javad Parvizi, MD, FRCSJavad Parvizi, MD, FRCS
Rothman Institute
Philadelphia, Pa.

Robert T. Trousdale, MDRobert T. Trousdale, MD
Mayo Clinic
Rochester, Minn.

Bernard N. Stulberg, MDBernard N. Stulberg, MD
Cleveland Clinic
Cleveland, Ohio

Douglas W. Jackson, MD: What is your protocol for identifying patients who are anemic in your primary knee replacement population?

Bernard N. Stulberg, MD: All patients are evaluated by hemoglobin and hematocrit (Hgb/Hct) evaluation 3 to 4 weeks prior to scheduled surgery. Our hospital has established a blood management program and all surgeons are encouraged to have patients who are undergoing elective hip and knee replacement procedures be involved. Once these patients are referred, the nurses associated with the program risk-stratify them for likelihood of transfusion and can then determine if preoperative intervention is warranted. This is according to a protocol established by the blood management committee, which is focused on the efficient use of blood management techniques and blood products.

Jackson: What historical information and laboratory studies do you obtain on the patient to establish the cause of their preoperative anemia?

Stulberg: Laboratory measures include Hgb/Hct, reticulocyte count and study of iron stores. Most anemias in our patient population are mild and likely related to iron deficiency. Supplemental iron is given when appropriate, and their primary physician notified. If anemia is significantly severe, less than 10g/dL, we will refer that patient for formal consultation with a hematologist to be certain that the causes of this anemia are clearly understood.

Jackson: What is your protocol for the erythropoiesis treatment?

Stulberg: Patients with anemia in the range of Hgb of 10g/dl to 13g/dl patients are offered Procrit (epoetin alpha) plus iron, starting 1 time-per-week, 3 weeks before the planned surgical intervention. Postoperative anemia is managed primarily by IV iron and transfusion if Hgb is less than 7.0g/dL in healthy individuals and less than 8.0g/dL for elderly or cardiac patients, unless symptoms dictate the need for transfusion sooner. For the Jehovah’s Witness patients, we will use IV iron and Procrit daily.

Jackson: How do you interpret the FDA warning for deep vein thrombosis (DVT) prophylaxis in patients receiving erythropoietin therapy? Do you alter the length of time of your prophylaxis?

Stulberg: We do not alter our prophylactic regimen for patients who have received Procrit, mostly because the administration of the drug has occurred prior to their surgical procedure and doesn’t appear to add to the risk of DVT following the surgery. We have not as yet seen that that has been an issue for our patients.

Jackson: Patients who undergo transfusions following TKR have been reported to have a higher infection rate, and we know that patients who are anemic will most likely need transfusions. How do we compare the greater infection rate in these patients to possible seeding postoperative infections?

Javad Parvizi, MD, FRCS: Transfusion by the virtue of causing immunomodulation does result in a higher incidence of surgical-site infections which includes periprosthetic joint infection. Based on analyses performed at our institution, patients with chronic anemia resultant from diseases such as renal failure are also at a higher risk of infection. Therefore, patients with chronic anemia who require postoperative transfusion would have a much higher risk of infection than patients requiring transfusion for postoperative anemia.

Jackson: Why do transfusions cause an increase in joint replacement infections?

Parvizi: There has been extensive investigation trying to elucidate the mechanism by which transfusion results in a higher incidence of infection. Transfusion Induced Immunomodulation (TRIM) was coined after observations that patients who received blood transfusions were at an increased risk of infections of any type.

The first observations were made when increased renal graft survival was seen in patients receiving allogenic blood transfusion following the transplant. The “immunosuppressive-effect” of blood transfusion was fully exploited to maximize the survival of transplant tissues before introduction of immunosuppressive agents such as cyclosporine. Many other observations such as improvements in autoimmune diseases status such as in Crohn’s disease, a decrease in repetitive spontaneous abortions, and an increase in recurrence of solid tumors have all confirmed the adverse effect of allogenic transfusion on cell mediated immunity.

The exact mechanism by which allogenic transfusion modulates cell mediated immunity is unknown. Initially the presence of leukocytes in transfused whole blood was considered as the culprit and the usage of leuko-depleted products was introduced to abrogate this effect. In recent years, other hypotheses have been proposed. Part of the cellular immunity involves maturation of Th0 cells into TH 1, 2 and 3 with immune activity. It is believed that release of immunosuppressive cytokines occurs following allogenic blood transfusion which suppress cell mediated immunity.

Kirkley and colleagues have shown that the transfusion of allogenic blood in total hip arthroplasty results in release of IL 4 and IL10 that in turn results in suppression of Th1 response.

Jackson: What do you advise telling patients who may receive a transfusion about their risks of infection?

Parvizi: First we try to avoid transfusion as much as possible. So we do not have a Hgb trigger for transfusion. Instead we base the need for transfusion on patient symptoms. In addition we implement other strategies such as administration of hematinics (such as iron), erythropoeitin, and so on to treat postoperative anemia. I tell patients that for every unit of blood transfusion received their risk for infection is doubled. That is still a negligible risk as incidence of infection after primary arthroplasty at our institution is less than 0.5%.

Jackson: Do you use re-transfusion systems on patients with knee replacements and what are their risks?

Parvizi: We do not. First and foremost because we do not utilize drains for primary arthroplasty. Then there is the expense that is associated with re-transfusion systems. The literature is divided in terms of the effectiveness of these systems in reducing the need for transfusion.

Jackson: Blood loss during the postoperative period may be minimized by intraoperative approaches. Do you deflate the tourniquet before cementing or closing to directly control bleeding?

Robert T. Trousdale, MD: There are many intraoperative techniques one can utilize to try to minimize perioperative and postoperative bleeding after TKR. Presently I do not use the tourniquet at all during the surgery except for cementation of the components. This, I think, has a handful of advantages:

  • It minimizes local trauma to the musculature, soft tissues and nerve structures in the proximal thigh region;
  • It provides a tourniquet when one needs it, namely during cementation of the components to minimize blood interdigitation into the distal femur and proximal tibia during cementation;
  • It allows one to easily coagulate active bleeding — the lateral geniculate vessels if those are violated or the middle geniculate if one uses a posterior cruciate substituting design and resects the posterior cruciate ligament; and
  • Metabolically, it is probably better for the patient to minimize the amount of time the distal limb is anoxic.

I find with getting hemostasis with the tourniquet down before cementation minimizes postoperative blood loss. The blood loss during the TKR when the knee is flexed is really minimal. If one can do the exposure initially very efficaciously, one finds with the knee flexed that there is little blood loss even without the use of the tourniquet.

Jackson: Do you feel customized jigs or navigation without the placement of the femoral rod minimizes the postoperative bleeding from the femoral canal?

Trousdale: Certainly by not violating the femoral canal or tibial canal, one will potentially decrease blood loss especially in the femur. I still, for the majority of my knees, use a femoral intramedullary rod to facilitate my distal femoral resection. I use an extramedullary alignment rod for the tibia resection. I place a bone block from one of the chamfer cuts where the femoral rod was placed to minimize intraoperative and postoperative bleeding from the intramedullary canal.

Jackson: Do you use any sprays or other applications to minimize postoperative oozing? Is there any evidence these reduce transfusion rates in TKRs?

Trousdale: I presently do not use any sprays in the synovium to minimize postoperative bleeding. The evidence of these modalities, I think, are relatively weak. Studies that have documented a decrease of blood loss using various sprays, I think, are flawed, primarily by the estimation of blood loss during the knee surgery. Historically, articles have used pre- and postoperative hemoglobins and transfusion requirements as the endpoints of blood loss. These are very rough estimates of blood loss. One really needs blood volume measurements which are expensive and tedious both pre- and postoperatively to accurately measure blood loss during surgery.

Pre- and postoperative Hgb is markedly influenced by the hemo-dilution and volume status of the patient. Furthermore, transfusion requirements are extremely variable from center-to-center and from surgeon-to-surgeon.

I use one dose of IV tranexamic acid at the beginning of the case and one dose at the time of closure. It is an inexpensive and safe modality to facilitate a decrease in blood loss.

Jackson: Do you inject epinephrine containing cocktails before closing or use any other specific techniques to reduce postoperative bleeding?

Trousdale: I do not use epinephrine containing cocktails before closing to reduce blood loss. I occasionally use a pain-relief cocktail that includes a narcotic and anti-inflammatory agent and a vaso-constrictor, but I primarily use that for pain relief, not so much to prevent blood loss.

  • Douglas W. Jackson, MD, can be reached at Orthopedics Today, 6900 Grove Road, Thorofare, NJ 08086; e-mail: OT@slackinc.com.
  • Javad Parvizi, MD, FRCS, can be reached at the Rothman Institute, 925 Chestnut St., 5th Floor, Philadelphia, PA 19107; 267-339-3617; e-mail: parvj@aol.com.
  • Bernard N. Stulberg, MD, Cleveland Clinic, ORI, 1730 W. 25th St., Cleveland, OH 44113; 216-363-3300; e-mail: stulbeb@ccf.org.
  • Robert T. Trousdale, MD, can be reached at Mayo Clinic, 200 First St. SW E14B, Rochester, MN 55905; 507-284-3663; e-mail: trousdale.robert@mayo.edu.