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Blood transfusion is no longer driven by the “10/30 hemoglobin/hematocrit rule,” because as little as one unit of homologous blood transfusion can increase postoperative complications. Therefore, a more restrictive transfusion protocol has become the standard of care.
More than 50 drugs are approved that interfere with either the coagulation cascade or platelet function. Table 84.1 lists many of these drugs and gives useful data on managing these medications. Reversal agents for anticoagulants, where present, are noted in the table.
Autotransfusion of autologous blood scavenged during surgery (“cell-saver”) can lessen the need for homologous blood transfusion.
Patient positioning using dedicated spine operating tables and hypotensive anesthesia techniques, when appropriate, lessen blood loss by reducing venous pressure, resulting in less epidural bleeding and less overall blood loss.
The coagulation cascade can be manipulated by local or systemic agents to lessen surgical blood loss, with transexamic acid being the most commonly used systemic agent.
Potential operative blood loss should be calculated before surgery, blood products should be made available, and communication with the surgical team should include transfusion triggers and the clotting status of the patient. Mass transfusion protocols are available for cases of extreme blood loss.
Minimizing blood loss in spine surgery increases safety and improves patient outcomes. The causes for significant operative blood loss may be divided into two primary categories, which can cascade together, worsening blood loss. These are patient factors (e.g., habitus, epidural vascular anatomy, coagulation characteristics) and technical factors (e.g., number of levels, dissection technique, hemostatic control). Optimal mitigation of patient factors usually occurs before the date of surgery by modifying factors like body weight and normalizing the patient’s coagulation profile (i.e., holding anticoagulants or medications and supplementals that affect bleeding or working with a hematologist to address chronic anemia and/or coagulation deficiencies). Conversely, the impact of technical factors is greatest in the immediate perioperative period. Blood loss and transfusion requirements are significantly affected by surgical technique, including duration of surgery, attention to hemostatic control, patient positioning, anesthetic techniques, and the pharmacological agents used during surgery. Managing blood loss involves rational planning before and throughout the perioperative period, through attentive manipulation of these two primary factors. A well thought-out plan for managing blood loss will incorporate measures to optimize the clotting cascade, minimize intraoperative blood loss, and plan for the replacement of blood products through intraoperative blood salvage or, in some cases, transfusion. This chapter briefly reviews the physiology of hemostasis and then catalogs interventions available to the spine surgeon that can address these patient and technical factors so as to optimize hemostatic management.
Surgical hemostasis is the controlled arrest of bleeding through physiological (i.e., coagulation) and physical methods (i.e., ligation). The primary physiology at play in hemostasis is clot formation, which is a complex pathway of interconnected reactions. Reducing this complex system to its basic steps allows key components to be assessed with an aim toward improved hemostatic control. The first key step in this process is platelet activation, which occurs in response to exposed collagen in injured endothelium, thrombin, thromboxane A2, or adenine diphosphate. The hemostatic plug, which forms in response to platelet activation in areas of endothelial injury, is termed primary hemostasis. Secondary hemostasis refers to the activation of the coagulation cascade, which ultimately produces a fibrin clot. As hemostasis progresses and a fibrin clot is formed, the fibrinolytic system is simultaneously activated to start the process of clot lysis (tertiary hemostasis) and thereby maintain a balance between clot formation and lysis. Critical to surgical hemostasis is the surgeon’s recognition of factors that will inhibit platelet function, thereby decreasing the effectiveness of primary hemostasis, as well as factors that inhibit the coagulation cascade, which in turn decreases secondary hemostasis. In addition, to physiological methods, physical methods in terms of timely vessel ligation, (electro) coagulation or tamponade, and the reduction of hydrostatic pressure in the epidural system are also measures at the control of the surgical team, which can result in less surgical blood loss.
A key component of the patient evaluation for spine surgery is a complete medical history. Special attention should be paid to medication history, as many medications interfere with primary and secondary hemostasis. Likewise, disease states such as renal failure, hematological conditions, collagen disorders, and liver disease also affect hemostasis. These medical conditions should be diagnosed and optimized before surgery if possible. Patients with uncorrectable medical issues may be too ill for elective spine surgery, and clinical judgment will be required to balance the risks versus benefits. A chemistry panel will yield information on renal and hepatic function and may be useful for evaluation in specific patients. In patients with a personal or family history of bleeding disorder or those who report easy bruising, nose bleeds, menorrhagia, multiple miscarriages, or excessive blood loss with prior surgical procedures, a coagulation profile with coagulation times, platelet counts, and, in some instances, platelet function testing or a thromboelastogram should be obtained.
Preoperative anemia with hemoglobin (Hgb) levels less than 12 g/dL are associated with increased blood transfusion requirements and should be addressed if significant surgical blood loss is anticipated. Preoperative anemia may be treated with erythropoietin in combination with iron supplementation therapy and hematologist consultation. Consideration should be given to delaying elective surgical cases until the Hgb level exceeds 12 g/dL.
Tests of the coagulation system include platelet count, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and the thromboelastogram (TEG). Platelet counts, platelet function, PT, and PTT should all be normal before surgery. Platelet function tests are used in special cases where abnormal platelet function is suspected, and they can be useful in timing surgery as they reveal when the antiplatelet effects of drugs have ended. The PTT and the PT measure multiple coagulation factors predicting coagulation deficits. The TEG has been used since the 1940s and became useful in guiding coagulation therapies in liver and aortic surgeries. TEG data are usually available within 30 minutes of draw time. Information on laboratory testing and terms is available in Box 84.1 .
Prothrombin test (PT) measures coagulation factors VII, X, V, II, and I.
Partial thromboplastin time (PTT) measures coagulation factors XII, XI, IX, VIII, X, V, II, and I.
Platelet count measures the number of platelets in blood. Low levels suggest impaired function. Platelet count for spine surgery should be in the normal range listed for the specific lab where the test was completed. Typical counts for spine surgery should range from 150,000 to 400,000.
Platelet function tests evaluate platelet function. Acquired platelet dysfunction from drugs can be monitored to assure normal platelet function before surgery.
Complete blood count measures hemoglobin, hematocrit, and platelet count, as well as several other indices.
Fibrinogen, factor I in the clotting cascade, is converted to fibrin by thrombin. Low fibrinogen levels are indicative of disseminated intravascular coagulation (DIC).
d -dimer indicates clot lysis and will be markedly elevated in cases of DIC.
Thromboelastogram (TEG) evaluates the entire clot formation process from activation of platelets to clot formation, contraction, and fibrinolysis. It yields multiple data values. The r value, measured in minutes, reflects the reaction time delay from the initiation of the clotting process until the production of fibrin. The r value corresponds to the PT and PTT. Kinetic time (k) measures the time from initial fibrin formation to a specific amount of clot stiffness. This is the time in minutes from fibrin appearance at 2-mm thickness until a thickness of 20 mm has been achieved. The rate of fibrin formation is reflected in the alpha angle (alpha). This is measured by drawing a tangent from the zero axis on the graph measuring the r time and is a function of platelet count and fibrin levels because this angle reflects the interaction of activated platelets and fibrin as they form clots with a larger angle, representing faster clot formation. Maximum amplitude refers to the maximum amount of clot formation and is a measurement of clot strength. Maximum angle mirrors platelet count and fibrin concentration, so as in all types of materials thicker is stronger. Fibrinolysis is assessed with a value called lysis-30, which is the amount of clot that has dissolved within 30 minutes of reaching the maximum amplitude. Lysis-30 will reveal if fibrinolysis is occurring at an abnormally rapid rate. Recommendations for component replacement based on TEG values are as follows: for an r time of greater than 15 minutes infuse two units of fresh frozen plasma, for a maximum amplitude of less than 40 mm infuse 10 units of platelets, and for an alpha angle of less than 40 degrees infuse six units of cryoprecipitate. TEG can guide antifibrinolytic therapy, as Amicar or tranexamic acid will be of benefit in cases of hyperfibrinolysis. [Gastroenterol Hepatol. 2012: 8(8):1-12.]
Metabolic panel measures serum chemistries and renal function with the blood urea nitrogen and creatinine. Liver enzymes may also be assessed, indicating abnormal liver function in some cases. Liver dysfunction and renal failure will affect clotting and hemostasis.
Patients with a history of transient ischemic attack, stroke, deep venous thrombosis (DVT), vascular stents, heavy bleeding after minor trauma, alcoholism, hepatic dysfunction, neuromuscular scoliosis, cerebral palsy, and cardiac disease have an increased risk of bleeding, either from the disease state or from pharmacological therapies for their condition.
Patients who take warfarin (Coumadin) may require cessation or acute reversal of anticoagulation. Occasionally, under the guidance of their internist, cardiologist, or hematologist, bridge therapy may be recommended. Patients will be placed on a shorter-acting anticoagulant or antiplatelet agent (commonly subcutaneous injection of low molecular weight heparin) to provide protection during the period of time in which their usual anticoagulant drug therapy is suspended. Bridge therapy substitutes a shorter-acting anticoagulant for one with a longer half-life and thereby lessens risk of vascular misadventure. The shorter-acting agent is suspended shortly before surgery to allow for safe spine surgical intervention, while also minimizing the risk of a thrombotic event. Those rare patients with congenital coagulation deficits typically require consultation with a hematologist and often perioperative selective clotting factor replacement.
Multiple oral anticoagulants called direct-acting oral anticoagulants and antiplatelet drugs are emerging on the marketplace or are now commonly in use. Knowledge of these medications is critical to preoperative planning. Many of these drugs have no known antidote or reversal agent or, where they exist, they can be prohibitively expensive. Platelet function can be impaired by drugs including aspirin (acetylsalicylic acid [ASA]), nonsteroidal antiinflammatory drugs, and specific platelet inhibitors. ASA can be held preoperatively in most patients without deleterious effects. However, patients with known coronary or cerebral vascular disease or significant risk factors for coronary artery disease should remain on ASA at a dose of 75 to 81 mg to lessen the risk of infarction in the perioperative period. Abrupt ASA cessation may cause a rebound effect on platelet aggregation, increasing risk of arterial thrombosis. In cases where ASA should be continued, surgical bleeding can be expected to be 1.5 times greater than normal, but the overall risk to the patient is lessened.
Nutritional supplements and herbs that inhibit platelet function include alfalfa, anise, bilberry, bladderwrack, bromelin, cat’s claw, celery, soleus, Cordyceps, dong quai, evening primrose oil, fenugreek, feverfew, garlic, ginger, ginkgo biloba, ginseng, grape seed, green tea, guggul, horse chestnut seed, horseradish, licorice, prickly ash, red clover, reishi, same, sweet clover, turmeric, and white willow. In general, all supplements should be held for 2 weeks before surgery because their exact ingredients and their physiological effects are highly variable and not well studied.
Table 84.1 contains a listing of medications that interfere with coagulation, and Table 84.2 lists the protein complex concentrates available today as reversal agents for some anticoagulant drugs. The table lists antidotes where known and gives reported guidelines, estimating the amount of time that must pass before the anticoagulant effects of these medications abate. These estimates are based on the time equivalent to three to four drug half-lives and are more restrictive than those published for needle-based procedures. The primary path for drug metabolism is annotated in the table to alert surgeons treating patients with renal failure/insufficiency or liver dysfunction to agents in which the time needed for coagulation to normalize will be increased. The estimated wait times after drug cessation reported in this table are longer than those noted in other surgical literature because spine surgeries are associated with greater blood loss than most other types of surgeries, and this greater blood loss stresses the coagulation system more than small, less invasive procedures. These timelines are recommendations based on experience and synthesis of the limited literature on the topic, as higher-level evidence guiding the optimal perioperative management of anticoagulation medications is lacking.
Drug | Class | Mechanism of Action | Half Life | Antidote | Time to Stop Drug before Surgery | Excretion | Metabolism |
---|---|---|---|---|---|---|---|
Abciximab (Repro) | Glycoprotein Iib/IIIa receptor antagonist | 10 minutes | Platelet transfusion | 120 hours | |||
Aggrastat (Tirofiban) | Antiplatelet | Reversibly binds to platelet glycoprotein IIb/Iia receptors reducing aggregation | 2 hours | 8 hours | Urine 65%, feces 25% | Minimal | |
Aggrenox (Aspirin/Dipyradamole) | Antiplatelet | See aspirin and dipyramole | See individual drugs | ||||
Agrylin (Anagrelide) | Antiplatelet | Disrupts megakaryocyte development reducing platelet count | 1.3 hours | Used for thrombocythemia, adjust dose to keep platelet counts below 600,000 | Urine | Liver | |
Angiomax (Bibalirudin) | Anticoagulant | Reversibly inhibits thrombin | 25 minutes | None | 1 hour | Urine | Plasma |
Argatroban | Anticoagulant | Direct thrombin inhibitor | 51 minutes | None | 2 hours | Feces 65%, urine 22% | Liver |
Arixtra (Fondaparinux) | Anticoagulant | Selective factor Xa inhibitor | 21 hours | PCC, rFVIIa | Recommended 24 hours before CABG, 4 days for spinal surgery | Urine | Unknown |
Aspirin (Bayer Aspirin, Bayer Low Dose Aspirin, Bayer Low Dose Women’s Aspirin, Bufferin, Ecotrin, Ecotrin Low Strength, St Joseph, St Joseph Regular Strength) | Antiplatelet, Salicylate | Nonselectively and irreversibly inhibits cyclooxygenase. Irreversibly inhibits platelet for its lifespan | 6 hours | 14 days | Urine | Liver | |
Atryn (Antithrombin) | Anticoagulant | Inhibits thrombin and factor Xa neutralizes coagulant effects | 17 Hours | None | 72 hours | Other | Unknown |
Betrixaban (Bevyzza) | Anticoagulant | Direct factor Xa inhibitor | 24 hours | Andexanet alfa | 4 days | Feces | |
Brilinta (Ticagrelor) | Antiplatelet | Reversibly binds, reducing platelet activation and aggregation | 9 hours | 7 days | Bile | Liver | |
Cangrelor (Kengreal) | Antiplatelet | 3 minutes | Drug cessation | ||||
Celecoxib (Celebrex) | NSAID | Inhibits cyclooxygenase-2 | 11 hours | 5 days | Feces 57%, urine 27% | Liver | |
Cilostazol (Pletal) | Antiplatelet | Reduces platelet aggregation, reversible | 13 hours | 5 days | Urine 74%, feces 20% | Liver | |
Clopidogrel (Plavix) | Antiplatelet | Irreversibly binds to P2Y12 adenosine diphosphate receptors, inhibiting platelet for its lifetime | 8 hours | 24 days | Urine 50%, feces 46% | Liver | |
Coumadin (Warfarin, Jantoven) | Anticoagulant | Inhibits vitamin K–dependent factors II, VII, IX, X, protein C, protein S | Variable 20–60 hours | FFP, vitamin K, PCC | 120 hours | Urine | Liver |
Danaparoid (Orgaran, Organon) | Anticoagulant | Inhibits factors Xa, IIa | 24 hours | rFVIIa 90 mcg/kg IV | 2 days | Renal | |
Diclofenac (Arthrotec, Cambia, Cataflam, Flector, Pennsaid, Voltaren, Zipsor, Zorvolex) | NSAID | Inhibits cyclooxygenase | 2 hours | 5 days | Urine 65%, bile 35% | Liver | |
Diflunisal (Dolobid) | Salicylate | Inhibits prostaglandin synthesis (reversible) | 12 hours | 2 days | Urine | ||
Dipyridamole (Persantine) | Antiplatelet | Inhibits platelet adenosine uptake reducing aggregation | 10 hours | 2 days | Bile | Liver | |
Edoxaban (Savaysa) | Anticoagulant | Factor Xa inhibitor | 10–14 hours | Andexanet alfa | 2 days | Urine 50% | |
Effient (Prasugrel) | Antiplatelet | Irreversibly binds to P2Y12 adenosine diphosphate receptors inhibiting platelet for its lifetime. | 7 hours | Drug cessation, platelet transfusion | 28 hours | Urine 68%, feces 27% | Liver |
Eliquis (Apixaban) | Anticoagulant | Factor Xa inhibitor | 12 hours | Andexxa- factor Xa recombinant 400 mg or 800 mg IV bolus. Future (once approved): Ciraparantag | 36 hours | Urine 27%, feces | Liver |
Enoxaparin (Lovenox) | Anticoagulant | Binds to antithrombin III inhibiting factor X and Xa | 7 hours | Protamine 1 mg IV for each mg of Enoxaparin given. Future (once approved): Ciraparantag | 24 hours | Urine 40% | Liver |
Eptifibatide (Integrlin) | Glycoprotein Iib/IIIa receptor antagonist | 3 hours | Drug cessation, platelet transfusion | Renal | |||
Etodolac (Lodine) | NSAID | Reversibly inhibits cyclooxygenase 1 and 2 | 8 hours | 5 days | Urine 73% | ||
Fenoprofen (Naflon) | NSAID | Inhibits cyclooxygenase | 3 hours | 5 days | Urine 90% | Liver | |
Flurbiprofen (Ansaid) | NSAID | Inhibits cyclooxygenase | 8 hours | 5 days | Urine 70%, feces 30% | ||
Fondaparinux | Anticoagulant | Binds to antithrombin III inhibiting factor X and Xa | 21 hours | None | 96 hours | Urine | Unknown |
Fondaparinux (Arixtra) | Pentasaccharide anticoagulant | Selective factor Xa inhibitor | 21 Hours | PCC, rFVIIa | 2 days | ||
Fragmin (Dalteparin) | Anticoagulant | Binds to antithrombin III, inhibiting factors X and Xa | 5 hours | Protamine 1 mg IV for each mg of heparin given. Future (once approved): Ciraparantag, rVIIa. | 24 hours | Urine | Liver |
Heparin | Anticoagulant | Binds to antithrombin III, inactivates X | 1.5 hours | Protamine 1 mg IV for each mg of heparin given. Future (once approved): Ciraparantag, rVIIa. | 6 hours | Urine | Liver |
Ibuprofen (Advil, Motrin, Caldolor, Duexis) | NSAID | Reversibly inhibits cyclooxygenase | 2 hours | 5 days | Urine | Liver | |
Idraparinux | Pentasaccharide anticoagulant | Factor Xa inhibitor | 80 hours | PCC, rFVIIa | |||
Indomethicin (Indocin) | NSAID | Inhibits cyclooxygenase | 12 hours | 5 days | Urine 60%, feces/bile 33% | Liver | |
Inohep (Tinzaprin) | Anticoagulant | Unknown | None | Unknown | Urine | Unknown | |
Integrilin (Eptifibatide) | Antiplatelet | Reversibly binds to platelet glycoprotein IIb/IIIa receptors, reducing platelet aggregation | 2.5 hours | 5 hours | Urine 50% | Minimal | |
Ipravisk (Desirudin) | Anticoagulant | Direct thrombin inhibitor | 2 hours | None | 6 hours | Urine | Kidney |
Ketoprofen | NSAID | Inhibits cyclooxygenase | 2 hours | 5 days | Urine 90% | Liver | |
Ketorolac (Sprix, Toradol) | NSAID | Reversibly inhibits cyclooxygenase 1 and 2 | 2 to 19 hours | 5 days | Urine 92% | ||
Meclofenamate | NSAID | Inhibits cyclooxygenase | 1.3 hours | 5 days | Urine 70%, feces 30% | Liver | |
Mefenamic acid (Ponstel) | NSAID | Inhibits cyclooxygenase | 2 hours | 5 days | Urine 52%, feces 20% | Liver | |
Meloxicam (Mobic) | NSAID | Inhibits cyclooxygenase | 20 hours | 5 days | Urine, feces | Liver | |
Nabumetone (Relafen) | NSAID | Reversibly inhibits cyclooxygenase 1 and 2 | 24 hours | 5 days | Urine 80% | ||
Naproxen (Aleve, Anaprox, Naprosyn, Vimovo, Treximet) | NSAID | Inhibits cyclooxygenase | 17 hours | 5 days | Urine | Liver | |
Oxaprozin (Daypro) | NSAID | Inhibits cyclooxygenase | 22 hours | 5 days | Urine 65%, feces 35% | Liver | |
Piroxicam (Feldene) | NSAID | Inhibits cyclooxygenase | 50 hours | 14 days | Urine, feces | Liver | |
Pradaxa (Dabigatran) | Anticoagulant | Directly reversibly inhibits thrombin | 17 hours | Praxbind (Idarucizamab) 5 g × 1, future (once approved): Ciraparantag | 72 hours | Urine | Liver |
Refludan (Lepirudin) | Anticoagulant | Unknown/drug not available in United States | None | Unknown | Unknown | Unknown | |
Reopro (Abciximab) | Antiplatelet | Binds to platelet glycoprotein IIb/IIIa receptors, reducing platelet aggregation | 10 minutes | 1 hour | Urine | Unknown | |
Salsalate | Salicylate | Inhibits prostaglandin synthesis | 16 hours | 5 days | Urine | Liver | |
Sulindac (Clinoril) | NSAID | Inhibits cyclooxygenase | 16 hours | 5 days | Urine 50%, feces 25% | Liver | |
Thrombate III (Antithrombin III) | Anticoagulant | Forms covalent bond with thrombin/only for use in congenital ATIII deficiency | 3 days | None | Hematology consult needed | Other | Unknown |
Ticagrelor (Brilinta) | Antiplatelet | Reversibly binds to ADP receptors | 9 hours | PB2452 pending FDA approval | 2 days | Feces | |
Ticlid (Ticlopidine) | Antiplatelet | Irreversibly binds to P2Y12 adenosine diphosphate receptors, reducing platelet aggregation | 5 days if repeated dosing | 29 days | Urine 60%, feces 23% | Liver | |
Tinzaprin (Innohep) | Anticoagulant | Protamine 1 mg IV for each mg of heparin given. Future (once approved): Ciraparantag, rVIIa | |||||
Tirofiban (Aggrastat) | Glycoprotein Iib/IIIa receptor antagonist | 2 hours | Platelet transfusion | ||||
Tolmetin | NSAID | Inhibits cyclooxegenase | 5 hours | 5 days | Urine | Liver | |
Valproic acid (Depakene) | Antiepileptic | Inhibits platelet function | 16 hours | 72 hours | |||
Vorapaxar (Zontivity) | Antiplatelet | Inhibits PAR-1 | 13 days | No antidote | 52 days | Feces | |
Xarelto (Rivaroxaban) | Anticoagulant | Factor Xa inhibitor | 9 hours | Andexxa- Factor Xa recombinant 400 mg or 800 mg IV bolus. Future (once approved): Ciraparantag | 36 hours | Urine 66% feces 28% | Liver |
Name | Type | Factor II | Factor VII | Factor IX | Factor X | Protein C | Protein S | Protein Z | Antithrombin III | Heparin | Emergent Dose |
---|---|---|---|---|---|---|---|---|---|---|---|
Bebulin | 3 Factor PCC | 100 | <5 | 100 | 100 | 50–60 IU/kg IV | |||||
Preconativ | 3 Factor PCC | 83.3 | 100 | 83.3 | Dose (IU) = body weight (kg) × desired factor IX increase (% of normal or IU/dL) | ||||||
Proplex-T | 3 Factor PCC | 50 | 400 | 100 | 50 | 1.0 unit/kg × body weight (in kg) × desired increase (% of normal | |||||
Prothrombinex-HT | 3 Factor PCC | 100 | Low | 100 | 100 | (25–50 units/kg | |||||
Profilnine SD | 3 Factor PCC | 150 | 35 | 100 | 100 | 1.0 unit/kg × body weight (in kg) × desired increase (% of normal | |||||
Beriplex (Kcentra) | 4 Factor PCC | 106.9 | 55 | 100 | 141.4 | 120.7 | 86.2 | 124.1 | 2.1 | 1.7 | Pharmacy calculation based on weight and INR not to exceed 5000 units |
Cofact | 4 Factor PCC | 56–140 | 28–80 | 100 | 56–140 | Pharmacy calculation based on weight and INR not to exceed 5000 units | |||||
Kaskadil | 4 Factor PCC | 148 | 40 | 100 | 160 | 20 | Not available in United States | ||||
Octaplex | 4 Factor PCC | 50–129 | 50–129 | 100 | 50–129 | 50–129 | 50–129 | 20–48 | Pharmacy calculation based on weight and INR not to exceed 5000 units |
Factors increasing blood loss during spine surgery include tumor, preoperative anemia, increased numbers of levels fused, pulmonary disease, patient habitus and positioning, anticoagulants, and antiplatelet drugs. , , When surgery is contemplated for reconstruction in cases of spinal metastasis from renal cell carcinoma, preoperative embolization has been shown to significantly reduce intraoperative blood loss. Further, embolization should be considered as a preoperative adjunct in all vascular spinal tumors to minimize blood loss.
Blood loss for any operation should be estimated and plans generated to ensure that blood can be replaced if needed. An estimate of 200 mL of blood lost per fused segment can be made preoperatively to plan if and how much blood will be required for replacement. Patients can usually tolerate a loss of 15% of the blood volume before transfusion. In a 70-kg patient, estimating 70 mL blood/kg body weight, a volume of 735 mL would reflect a 15% blood loss. Table 84.3 outlines the calculations used to determine percentage blood loss and amount of blood loss required to reach a specified Hgb level. Where blood loss is greater, transfusion thresholds have shifted to be more restrictive over time. The volume of blood lost or preplanned Hgb transfusion trigger should be calculated before the start of the procedure and communicated to the anesthesia provider. Although higher (“liberal”) trigger points (Hgb 9–10 g/dL) have been used historically, more recent study demonstrates that lower thresholds provide better outcomes, especially in healthy patients. Recent guidelines published in 2016 by the AABB (formerly the American Association of Blood Banks) and the Journal of the American Medical Association recommend a restrictive red blood cell (RBC) transfusion policy, with transfusion recommended for patients undergoing orthopedic procedures who have a Hgb of 8 g/dL in the postoperative period. A Hgb as low as 7 g/dL can be used as a transfusion trigger for healthy patients undergoing surgical procedures who are no longer bleeding acutely, whereas unhealthy patients with known coronary artery disease or cancer may require a higher threshold (Hgb >9 g/dL) ( Box 84.2 ).
Parameter | Class I | Class II (Mild) | Class III (Moderate) | Class IV (Severe) |
---|---|---|---|---|
Approximate blood loss | <15% | 15%‒30% | 31%‒40% | >40% |
Heart rate | ↔ | ↔/↑ | ↑ | ↑/↑↑ |
Blood pressure | ↔ | ↔ | ↔/↓ | ↓ |
Pulse pressure | ↔ | ↓ | ↓ | ↓ |
Respiratory rate | ↔ | ↔ | ↔/↑ | ↑ |
Urine output | ↔ | ↔ | ↓ | ↓↓ |
Glasgow Coma Scale score | ↔ | ↔ | ↓ | ↓ |
Base deficit a | 0 to ‒2 mEq/L | ‒2 to ‒6 mEq/L | ‒6 to ‒10 mEq/L | ‒10 mEq/L or less |
Need for blood products | Monitor | Possible | Yes | Massive transfusion protocol |
a Base excess is the quality of base (HCO 3– , in mEq/L) that is above or below the normal range in the body. A negative number is called a base deficit and indicates metabolic acidosis.
Cherry solution of liquid clotter: one jar of Codman Spongostan mixed with 8 mL of thrombin containing 1000 units of thrombin per mL of saline. Mix together in a 20-mL syringe with a 12-G Angiocath as a directional nozzle. Apply directly to bleeding tissue.
Fibrin glue: two syringes. First syringe contains fresh-frozen plasma; second syringe contains 1 ampule of calcium chloride and thrombin 10,000 to 20,000 units, and can contain antibiotics. Inject the contents of the syringes simultaneously to form fibrin glue.
FloSeal: commercial product.
Autologous blood donation, although previously a more common strategy, has lost favor in recent years, especially preoperative donation, as it does not appear to significantly reduce the need for allogenic transfusion. A review of the National Inpatient Sample database (2004‒2009) demonstrated that preoperative autologous donation was actually a significant predictor of allogenic transfusion after spine surgery, especially following fusion of the thoracolumbar spine. That said, in certain patients where the estimated blood loss exceeds 15% to 30% of the blood volume, autologous blood donation remains an option in the perioperative blood management program.
Autologous blood can be obtained in three ways: preoperative donation, intraoperative salvage, and postoperative salvage. The benefits (in terms of decreased allogenic transfusion rates) of salvage techniques are greater, and the costs and risks are lower than preoperative donation, thus they are still commonly used, especially in cases in which higher blood loss is predicted, like posterior deformity surgery. Although preoperative donation is expensive, a reduction in the potential for allogenic transfusion-related morbidities, like transfusion reaction and infection transmission, may offset the cost. Nevertheless, there are risks to autologous blood transfusions, which include septicemia from bacterial contamination of the unit, nonimmune hemolytic transfusion reactions (HTRs), febrile reactions, and volume overload, with the most common still being clerical error.
One unit of blood can be predonated per week if the hematocrit (Hct) remains above 34%. Other guidelines for autologous donation include a patient age range of 12 to 70 years and a Hgb of at least 11 mg/dL. Full units can be taken from patients weighing more than 50 kg, and half units from those between 25 and 50 kg. Supplemental iron is recommended. In some instances, recombinant erythropoietin can be administered to facilitate increased blood volume for autologous donation. , This has been shown to increase blood production significantly in both animal and clinical studies.
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