The Anesthesiology Consultant

    Tourniquet Use in Sickle Cell Anemia

    Tourniquet Use in Sickle Cell Anemia">
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    The use of a tourniquet in orthopedic surgery or other procedures provides the benefits of producing a bloodless field, reducing blood loss, and decreasing time of surgery. At the same time, prolonged tourniquet use can cause hemostasis, acidosis, and hypoxia, factors known to increase the chances of sickling in patients with sickle cell disease and rarely trait.

    Whether tourniquet use actually increases the chances of complications is a question inadequately answered by the available literature, which primarily consists of retrospective case reports and case series. In a recent review, the incidence of postoperative complications with tourniquet use in patients with sickle cell disease or trait was 12.5% (South Med J 2010 103(11):1156-60). These complications included extremity swelling, severe pain, infection, pulmonary embolus, and DVT. Some of these patients had sickle cell trait as well as disease. Without controlled studies, however, it is unclear whether this rate represents an increase from what is already likely a higher rate of postoperative complications among sickle cell patients.

    Recommendations to prevent sickling with tourniquet use include hyperoxygenation, hyperventilation, adequate hydration, avoiding acidosis, and extremity exanguination. All are uproven. Equally unproven is preoperative use of hydroxyurea to increase hemoglobin F production, a process that takes 8 weeks to occur.

    The bottom line is while many authors have argued against the use of a tourniquet in patients with sickle cell disease or trait, whether it increases the rate of postoperative complications is unproven, and tourniquets can and have been used safely. Their use is not contraindicated.

    Side Note on the Molecular Basis of Sickling

    The hemoglobin molecule consists of 2 alpha- and 2 beta-hemoglobin chains. Hemoglobin S is characterized by a substitution of a valine for a glutamic acid in the beta-chain, increasing the chances of intermolecular hydrogen bonding between hemoglobin molecules. This leads hemoglobin polymerization, RBC deformation and impaired deformability, and acute and long-term organ dysfunction.

    Many factors are thought to promote sickling, especially hypoxia below 30-40 mm Hg O2, which induces a conformational hemoglobin change that facilitates polymerization. In addition, polymerization becomes more likely with a higher concentration of hemoglobin within the RBC, such as what occurs with cellular dehydration. Acidosis activates a K/Cl co-transport pump within the RBC membrane, increasing the chances of RBC dehydration and, therefore, sickling. Acidosis also leads to sickling at lower O2 tensions. Venous stasis also produces a risk because hemoglobin polymerization is a timed-dependent phenomenon, usually occurring after at least 15 seconds of hypoxia. This is unlikely with normal circulation of blood through the lungs, but is more likely with tourniquet use.

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