Blood loss associated with anticoagulation in patients with replanted digits The incidence of blood loss and blood transfusion in patients receiving one anticoagulant in addition to aspirin (n = 40) was compared with that in patients receiving two or more anticoagulants in addition to aspirin (n = 15). Multiple-agent therapy produced a greater drop in the hematocrit than single-agent therapy (15 % compared with 6% ). Only 2% of the patients receiving a single agent had transfusions, as compared with 53% of the patients receiving multiple agents. We conclude that administration of multiple anticoagulants greatly increases the incidence of blood loss and blood transfusion as compared with the administration of a single agent plus aspirin. The importance of salvaging a replanted digit or digits must be weighed against the risks of a blood transfusion. (J HAND SURC 1992;17A:226-9.)
Heather Harry
J. Fumas, J. Buncke,
MD, Brookline, Mass., William MD,
T
.
From the Division of Plastic Surgery, Beth Israel Hospital and Harvard Medical School, Brookline, Mass., and the Department of Microsurgery, Davies Medical Center, San Francisco, Calif. Dec. 18, 1990; accepted
in revised form
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Reprint requests: Heather J. Fumas, MD, Division of Plastic Surgery, Beth Israel Hospital and Harvard Medical School, 1180 Beacon St., Brookline, MA 02146. 3/l/32661
226
THE JOURNAL OF HAND SURGERY
MD,
and
Sun Francisco, Calif.
he failure rates in replants are much higher after a crush/avulsion injury than after a guillotine type of injury.‘, ’ The higher failure rates reflect the findings of Mitchell et al.,32 who examined the microvasculature of experimentally avulsed rabbit ears. Under the operating microscope, vascular damage was evident within 0.8 cm from the rupture site. Light and electron microscopy, however, revealed intimal and smooth muscle damage as far as 4 cm from the rupture site. Thus if a crushed or avulsed vessel is trimmed only as far as damage is visualized through the operating microscope, a large segment of damaged intima and media remains. Damage to the intima exposes subendothelial collagen, leading to platelet deposition and activation and d&position of fibrin. The final resultthrombosis-can lead to nonviability of the replanted digit. Experimental evidence suggests that patency rates of microvascular repairs increase with the use of anticoagulants 3-5 Heparin significantly improves patency rates in laboratory animals after repairs in cleanly cut,6
Received for publication July 8, 1991.
Lineaweaver,
crushed, and avnlsed vessels’, ’ and after arterial inversion grafts. s Many anticoagulants have been used to prevent thrombosis in microsurgery.9 In our microsurgical unit (Davies Medical Center in San Francisco), aspirin is routinely given to all patients undergoing replantation surgery. In addition, all patients receive a 5-day course of dextran 40 (25 ml per hour), unless the patients are young children or unless anticoagulation is contraindicated. In the event of a crush or avulsion injury, heparin is sometimes administered instead of or in addition to dextran. Leeches are sometimes used in addition to pharmacologic anticoagulation. While possibly salvaging damaged replanted digits, anticoagulation can lead to significant blood loss. Sometimes the amount of blood lost through oozing of the wounds is enough to require a transfusion. To assess the risk of significant blood loss with the use of single and multiple anticoagulants, we studied those patients with digital replantation who had sustained injuries that predisposed their replanted digits to loss due to thrombosis . Materials
and methods
Fifty-five consecutive patients who had undergone digital replantation after complete amputation(s) from a crush or avulsion injury were entered into the study. No patient had any operation other than replantation. In no patient was anticoagulant therapy contraindicated. All patients received 325 mg of aspirin per day. In addition, some patients received either dextran or heparin (single-agent regimen), while others were treated with two or more of the following: heparin, dextran, and leeches (multiple-agent regimen). The agents were
Vol.
17A.
March
No. 2 Blood loss associated with anticoagulation
1992
227
Table I. Single agent treatment
Anticoagulants Dextran Heparin Dextran Replaced heparin
by
Total
Table II. Multiple-agent Anticoagulant Dextran and leeches Dextran and heparin Heparin and leeches Heparin, dextran, and leeches Total
No. of patients
Average decrease in hematocrit
No. of patients transfused
Total units transfused
Replant survival (%)
28 8
6 5
0 0
0 0
97 75
4
I
I (25%)
2
70
40
z
i (250/o)
2
lis
Average decrease in hematocrit
No. of patients transfused
Total units transfused
Replant survival
2 7 II 4
13 15 60 100
24
77
treatment No. of patients 5 5 2 3
12 16 16 18
1 3 2 2
T5
15
8 (53%)
chosen by the attending physician. Comparisons were then made between the regimens used, the decreases in hematocrit value, and the incidence of blood transfusion. Results The single-agent regimen (Table I) was associated with an average drop in hematocrit of 6% and an incidence of blood transfusion of 2%. Multiple-agent therapy (Table II) produced an average drop in the hematocrit of 15% and an incidence of blood transfusion of 53%. The higher incidence of blood transfusion is statistically significant (p < 0.0001 by x2). The difference in digit-survival rates (88% in the single-agent group and 77% in the multiple-agent group) is not statistically significant. A comparison of anticoagulant regimens cannot be made, however, since a more aggressive multiple-agent approach was taken in patients who had experienced functionally devastating injuries, such as the loss of a thumb or of multiple digits. Discussion The anticoagulant agents used in our microsurgical center are commonly used in microsurgery. Each offers a unique action as an anticoagulant. In low doses, aspirin inhibits platelet aggregation and decreases thromboxane synthesis.‘, lo Heparin is a mucopolysaccharide that accelerates inactivation of coagulation factors primarily through its interaction with antithrombin III. ’ ’ ” Dextran is a polysaccharide that reduces platelet
(20%) (60%) (100%) (67%)
(%I
aggregation and adhesiveness, reduces the level of factor VIII-Ag (von Willebrand factor), and alters the thrombus structure, thus facilitating lysis of clots. I5The medicinal leech, Hirudo medicinalis, releases a histamine that dilates the host vessels while clotting is inhibited by an antithrombin (hirudin), two fibrinases, and an inhibitor of platelet aggregation. Leech hyaluronidase allows these agents to penetrate the host tissue rapidly. 16.I7 Each of these agents is associated with unique possible complications, and familiarity with an agent is important before it is administered to a patient. Common to all agents, however, is the increased possibility of bleeding. Once the blood loss becomes significant, the patient is faced with the risk of blood transfusion. Approximately 20% of all transfusions result in some type of adverse effect,‘* with viral infection currently receiving the most attention. The history of the transmittance of disease through blood transfusions began with the report of a case in which syphilis was passed on to a patient in such a manner in 19 15. I9 Today the major serious risk is viral hepatitis. Posttransfusion hepatitis can be caused by hepatitis B, non-A, non-B hepatitis (NANBH), cytomegalovirus (CMV). and, rarely, Epstein-Barr virus (EBV). The testing of all blood for hepatitis B surface antigen (HBsAg) has nearly eliminated transfusion-associated hepatitis B. Today transfusion-transmitted NANBH accounts for about 90% of posttransfusion hepatitis.‘” NANBH has been estimated to develop in 1% to 12%
228
The Journal of HAND SURGERY
Furnas et al.
of patients who receive transfusions,“. ‘l-23 at a rate of three to six cases per 1000 units transfused.‘g Of those patients who receive more than 5 units of blood, 5% to 18% contract NANBH.24 Almost all cases occur between 5 and 12 weeks after transfusion, but the acute illness is subclinical in the majority of cases. Of the persons infected, 40% to 60% will have cirrhosis, which carries a 53% 5-year mortality rate.‘*. x In the United States, cirrhosis develops in approximately 15,000 to 30,000 patients per year as a direct consequence of posttransfusion NANBH.19 CMV and EBV are closely related viruses of the herpes group. The incidence of symptomatic CMV infection, primarily a mononucleosis-like syndrome, 1 to 3 months after transfusion is less than 4% in healthy persons. ‘OAlthough the EBV virus is harbored by approximately 90% of all blood donors, posttransfusion EBV is relatively uncommon in immunocompetent persons. The risk of transmitting the human immunodeficiency virus (HIV) through blood transfusions receives much attention in the professional and lay literature. Approximately 2% of adults and 12% of children with AIDS contracted their disease through a transfusion of blood or blood products. I9The incidence of transfusiontransmitted HIV infections has recently been estimated by the American Red Cross to be 1 in 153,000 per unit transfused.26 A person receiving the national average number of units transfused (5.4 units) has a 1: 28,000 chance of contracting the HIV virus. HTLV-1 was the first human retrovirus discovered. In approximately 1% of those who are antibody positive for HTLV-1 , a unique form of adult T-cell leukemia/lymphoma will develop. This virus can be transmitted by transfusion, but its clinical significance has yet to be defined.” The list of infectious agents potentially transmitted by blood transfusion is quite large, ranging from Salmonella choleraesuis and Brucella abortus to the organisms that cause malaria and filariasis.“, I9 Certain bacteria can multiply in refrigerated stored blood,“. ” resulting in transfusion-transmitted bacterial infections. Bacteremic and endotoxic shock can develop, sometimes resulting in death.18. “. 24 Immune function can be impaired by blood transfusions. Transfusions performed in rats impair the macrophage’s ability to phagocytose and kill bacteria.*’ Alloimmunization of recipients to red cell, white cell, platelet, and protein antigens can occur, particularly in black patients receiving blood from white donors.**. 29This condition occurs in 4% to 40% of patients with sickle cell anemia and results in difficulty in obtaining compatible blood, de-
layed transfusion reactions, and occasional life-threatening events .29 Other occurrences associated with transfusions include nonhemolytic febrile reactions and allergic reactions. 18.*’ Massive transfusions are associated with iron overload with resultant hemosiderosis, depletion of coagulation proteins and platelets, hypothermia, citrate toxicity, acidosis, and hyperkalemia.“. 22 Death can occur as a result of acute hemolysis if donor red blood cells and recipient plasma are incornpatible. From 1976 through 1985, there were 256 transfusion-associated deaths from causes other than AIDS or hepatitis.24 Fifty-one percent of the patients died of acute hemolysis after the transfusion of ABO-incompatible products. These deaths were due primarily to human error in properly identifying the unit of blood or the recipient. Other causes of death included acute pulmonary injury (15%), bacterial contamination of product (10%). delayed hemolysis (lo%), damaged product (3%), and graft-versus-host disease (0.4%). With today’s keen awareness of the risks associated with blood transfusions, transfusions of whole blood and red cells have declined since 1986.30 Finally crumbling is the surgical mandate that patients with preoperative hemoglobin levels below 10 gmidl must be given transfusions.30. 3’ Autologous transfusions and intraoperative salvage of blood have also contributed to decreasing transfusion rates. The replant patient who has suffered a crush or avulsion injury has a greater thrombogenic potential than the patient who has experienced a sharp cut injury. Evidence’. 3-8suggests that anticoagulation of these patients can increase the survivability of the replanted parts. Our study demonstrates that the patients given a single anticoagulation agent (in addition to aspirin) are at low risk of needing a transfusion. However, patients who are given multiple anticoagulants risk losing significant amounts of blood. Our criteria for transfusion are stringent and take into account the patient’s age and health status, whether the patient has symptoms of acute anemia, and whether the patient is actively losing blood. Nevertheless, a significantly greater proportion of patients receiving multiple anticoagulants needed blood transfusions. Conclusion The importance of attempting to salvage a replanted digit or digits by the administration of two or more anticoagulants must be weighed against the risks of a blood transfusion. A patient who has had multiple finger amputations or who has lost a thumb will have a significant loss of function if replants fail. The risk of a
Vol. 17A, No. 2 March 1992
blood transfusion may therefore be acceptable if there is believed to be a chance of salvaging major function by increasing the number of anticoagulants. On the other hand, failure of a single-finger replant or distalfinger replants is less likely to significantly affect the function of the hand. In these situations the risks of a blood transfusion may outweigh the benefit of salvaging these parts. The clinical situation should be thoroughly discussed with the patient, and all options should be carefully considered. REFERENCES I. Cooley BC, Ruas EJ, Wilgis EFS. Scanning electron microscopy of crushediavulsion arterial trauma: effect of heparin and aspirin administration. Microsurgery 1987;8:1 l-6. 2. Morrison WA, O’Brien B McC, MacLeod AM. Evaluation of digital replantation-a review of 100 cases. Orthop Clin North Am 1977;8:295-308. 3. Kolar L, Wieberdink J, Reneman RS. Anticoagulation in microvascular surgery. Eur Surg Res 1973;5:52-7. 4. Rohrich RJ. Billings E. Handren J, Wolfort B, May JW. Prevention of microvascular thrombosis with human tissue type plasminogen activator. Surg Forum 1986;37: 589-90. 5. Rosenbaum TJ, Sundt TM. Thrombus formation and endothelial alterations in microarterial anastomoses. J Neurosurg 1977 ;47:430-4 1. 6. Vlaston C. Earle AS. Intraoperation heparin in replantation surgery-an experimental study. Ann Plast Surg 1983;10:112-4. 7. Khouri RK, Cooley BC. Kenna DM, Edstrom LE. Thrombosis of microvascular anastomoses in traumatized vessels: fibrin versus platelets. Plast Reconstr Surg 1990:8:110-7. 8. Greenberg BM. Masem M, May JW. Therapeutic value of intravenous heparin in microvascular surgery: an experimental vascular thrombosis study. Plast Reconstr Surg 1988;82:463-70. 9. May JW, Rothkopf DM. Salvage of a failing microvascular free muscle flap by direct continuous intravascular infusion of heparin: a case report. Plast Reconstr Surg lY89;83: 1045-Y. IO. Weiss SC. Platelet physiology and abnormalities of platelet function. N Engl J Med 1975;293:531-41. 11 Moake JL, Levine JD. Thrombotic disorders. Clin Symp lY85;37:27. 12. Cines DB. Heparin: do we understand its antithrombotic actions’? Chest 1986;89:420-6. 13 Wessler S, Gitel SN. Pharmacology of heparin and warfarin. J Am Coil Cardiol 1986;8:10B-20B. 14. Ketchum LD. Pharmacological alterations in the clotting mechanism: use in microvascular surgery. J HAND SURG 1978:3:407-15.
Blood loss associuted with anticoagulation
229
15. Ljunstrom KG. The antithrombotic efficacy of dextran. Acta Chir Stand Suppl 1980;543:26-30. 16. Lent CM. New medical and scientific uses of the leech. Nature 1986;323:494. 17. Sawyer RT. Feeding and digestive system. In: Sawyer RT. Leech biology and behaviour. vol 2. Oxford: Clarendon Press, 1986:467. 18. Walker RH. Special report: transfusion viral infections. Transplant Proc 1988;59:7-55. 19. Rubin RH, Tolkoff-Rubin NE. Post transfusion viral infections. Transplant Proc 1988:20:1112-7. 20. Mattsson L. Chronic non-A. non-B hepatitis. Stand J Infect Dis Suppl 1989;59:7-55. 21. U.S. Department of Health and Human Services. Public Health Service, National Institute of Health. Transfusion alert: indications for the use of red blood cells, platelets. and fresh frozen plasma. NIH Publication No. 89-2974. 1989. 22. American Association of Blood Banks and Council of Community Blood Centers. Circular of information for the use of human blood and blood components. ARC 1751, 1986. 23. Iwarson S. Transfusion transmitted non-A. non-B hepatitis. Acta Anaesth Stand 1988;32tSuppl 38):13-5. 24. Sazama K. Reports of 355 transfusion-associated deaths: 1976-1985. Transfusion 1990;30:583-90. 25. Lashner BA, Jones RB, Tang HS, Evans AA, Ozeran SE, Baker AL. Chronic hepatitis: disease factors at diagnosis predictive of morality. Am J Med lY88;85:60914. 26. Cumming PD, Wallace EL, Schorr JB. Dodd RY. Exposure of patients to human immunodeficiency virus through the transfusion of blood components that test antibody-negative. N Engl J Med lY89;321:Y41-6. 27. Cover TL, Aber RC. Yersinia enterocolitica. N Engl J Med 1989;321:16-24. 28. Waymack JP, Yurt RW. The effect of blood transfusion on immune function. V. The effect of the inflammatory response to bacteria1 infections. J Surg Res 1990;48: 147. 53. 29. Vichinsky EP, Earles A, Johnson RA, Hoag MS, Williams A. Lubin B. Alloimmunization in sickle cell anemia and transfusion of racially unmated blood. N Engl J Med 1990;332:1617-21. 30. Surgenor DM, Wallace EL, Hao SHS. Chapman RH. Collection and transfusion of blood in the United States, 1982-1988. N Engl J Med 1990;322:1646-51. 31. Spence RK. Carson JA, Poses R, et al. Elective surgery without transfusion: influence of preoperative hemoglobin level and blood loss on mortality. Am J Surg 1990;159:320-4. 32. Mitchell GM, Morrison WA, Papadopoulos A, O’Brien BM. A study of the extent and pathology of experimental avulsion injury in rabbit arteries and veins. Br J Plast Surg 1985;38:278-87.
Heather Harry
J. Fumas, J. Buncke,
MD, Brookline, Mass., William MD,
T
.
From the Division of Plastic Surgery, Beth Israel Hospital and Harvard Medical School, Brookline, Mass., and the Department of Microsurgery, Davies Medical Center, San Francisco, Calif. Dec. 18, 1990; accepted
in revised form
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Reprint requests: Heather J. Fumas, MD, Division of Plastic Surgery, Beth Israel Hospital and Harvard Medical School, 1180 Beacon St., Brookline, MA 02146. 3/l/32661
226
THE JOURNAL OF HAND SURGERY
MD,
and
Sun Francisco, Calif.
he failure rates in replants are much higher after a crush/avulsion injury than after a guillotine type of injury.‘, ’ The higher failure rates reflect the findings of Mitchell et al.,32 who examined the microvasculature of experimentally avulsed rabbit ears. Under the operating microscope, vascular damage was evident within 0.8 cm from the rupture site. Light and electron microscopy, however, revealed intimal and smooth muscle damage as far as 4 cm from the rupture site. Thus if a crushed or avulsed vessel is trimmed only as far as damage is visualized through the operating microscope, a large segment of damaged intima and media remains. Damage to the intima exposes subendothelial collagen, leading to platelet deposition and activation and d&position of fibrin. The final resultthrombosis-can lead to nonviability of the replanted digit. Experimental evidence suggests that patency rates of microvascular repairs increase with the use of anticoagulants 3-5 Heparin significantly improves patency rates in laboratory animals after repairs in cleanly cut,6
Received for publication July 8, 1991.
Lineaweaver,
crushed, and avnlsed vessels’, ’ and after arterial inversion grafts. s Many anticoagulants have been used to prevent thrombosis in microsurgery.9 In our microsurgical unit (Davies Medical Center in San Francisco), aspirin is routinely given to all patients undergoing replantation surgery. In addition, all patients receive a 5-day course of dextran 40 (25 ml per hour), unless the patients are young children or unless anticoagulation is contraindicated. In the event of a crush or avulsion injury, heparin is sometimes administered instead of or in addition to dextran. Leeches are sometimes used in addition to pharmacologic anticoagulation. While possibly salvaging damaged replanted digits, anticoagulation can lead to significant blood loss. Sometimes the amount of blood lost through oozing of the wounds is enough to require a transfusion. To assess the risk of significant blood loss with the use of single and multiple anticoagulants, we studied those patients with digital replantation who had sustained injuries that predisposed their replanted digits to loss due to thrombosis . Materials
and methods
Fifty-five consecutive patients who had undergone digital replantation after complete amputation(s) from a crush or avulsion injury were entered into the study. No patient had any operation other than replantation. In no patient was anticoagulant therapy contraindicated. All patients received 325 mg of aspirin per day. In addition, some patients received either dextran or heparin (single-agent regimen), while others were treated with two or more of the following: heparin, dextran, and leeches (multiple-agent regimen). The agents were
Vol.
17A.
March
No. 2 Blood loss associated with anticoagulation
1992
227
Table I. Single agent treatment
Anticoagulants Dextran Heparin Dextran Replaced heparin
by
Total
Table II. Multiple-agent Anticoagulant Dextran and leeches Dextran and heparin Heparin and leeches Heparin, dextran, and leeches Total
No. of patients
Average decrease in hematocrit
No. of patients transfused
Total units transfused
Replant survival (%)
28 8
6 5
0 0
0 0
97 75
4
I
I (25%)
2
70
40
z
i (250/o)
2
lis
Average decrease in hematocrit
No. of patients transfused
Total units transfused
Replant survival
2 7 II 4
13 15 60 100
24
77
treatment No. of patients 5 5 2 3
12 16 16 18
1 3 2 2
T5
15
8 (53%)
chosen by the attending physician. Comparisons were then made between the regimens used, the decreases in hematocrit value, and the incidence of blood transfusion. Results The single-agent regimen (Table I) was associated with an average drop in hematocrit of 6% and an incidence of blood transfusion of 2%. Multiple-agent therapy (Table II) produced an average drop in the hematocrit of 15% and an incidence of blood transfusion of 53%. The higher incidence of blood transfusion is statistically significant (p < 0.0001 by x2). The difference in digit-survival rates (88% in the single-agent group and 77% in the multiple-agent group) is not statistically significant. A comparison of anticoagulant regimens cannot be made, however, since a more aggressive multiple-agent approach was taken in patients who had experienced functionally devastating injuries, such as the loss of a thumb or of multiple digits. Discussion The anticoagulant agents used in our microsurgical center are commonly used in microsurgery. Each offers a unique action as an anticoagulant. In low doses, aspirin inhibits platelet aggregation and decreases thromboxane synthesis.‘, lo Heparin is a mucopolysaccharide that accelerates inactivation of coagulation factors primarily through its interaction with antithrombin III. ’ ’ ” Dextran is a polysaccharide that reduces platelet
(20%) (60%) (100%) (67%)
(%I
aggregation and adhesiveness, reduces the level of factor VIII-Ag (von Willebrand factor), and alters the thrombus structure, thus facilitating lysis of clots. I5The medicinal leech, Hirudo medicinalis, releases a histamine that dilates the host vessels while clotting is inhibited by an antithrombin (hirudin), two fibrinases, and an inhibitor of platelet aggregation. Leech hyaluronidase allows these agents to penetrate the host tissue rapidly. 16.I7 Each of these agents is associated with unique possible complications, and familiarity with an agent is important before it is administered to a patient. Common to all agents, however, is the increased possibility of bleeding. Once the blood loss becomes significant, the patient is faced with the risk of blood transfusion. Approximately 20% of all transfusions result in some type of adverse effect,‘* with viral infection currently receiving the most attention. The history of the transmittance of disease through blood transfusions began with the report of a case in which syphilis was passed on to a patient in such a manner in 19 15. I9 Today the major serious risk is viral hepatitis. Posttransfusion hepatitis can be caused by hepatitis B, non-A, non-B hepatitis (NANBH), cytomegalovirus (CMV). and, rarely, Epstein-Barr virus (EBV). The testing of all blood for hepatitis B surface antigen (HBsAg) has nearly eliminated transfusion-associated hepatitis B. Today transfusion-transmitted NANBH accounts for about 90% of posttransfusion hepatitis.‘” NANBH has been estimated to develop in 1% to 12%
228
The Journal of HAND SURGERY
Furnas et al.
of patients who receive transfusions,“. ‘l-23 at a rate of three to six cases per 1000 units transfused.‘g Of those patients who receive more than 5 units of blood, 5% to 18% contract NANBH.24 Almost all cases occur between 5 and 12 weeks after transfusion, but the acute illness is subclinical in the majority of cases. Of the persons infected, 40% to 60% will have cirrhosis, which carries a 53% 5-year mortality rate.‘*. x In the United States, cirrhosis develops in approximately 15,000 to 30,000 patients per year as a direct consequence of posttransfusion NANBH.19 CMV and EBV are closely related viruses of the herpes group. The incidence of symptomatic CMV infection, primarily a mononucleosis-like syndrome, 1 to 3 months after transfusion is less than 4% in healthy persons. ‘OAlthough the EBV virus is harbored by approximately 90% of all blood donors, posttransfusion EBV is relatively uncommon in immunocompetent persons. The risk of transmitting the human immunodeficiency virus (HIV) through blood transfusions receives much attention in the professional and lay literature. Approximately 2% of adults and 12% of children with AIDS contracted their disease through a transfusion of blood or blood products. I9The incidence of transfusiontransmitted HIV infections has recently been estimated by the American Red Cross to be 1 in 153,000 per unit transfused.26 A person receiving the national average number of units transfused (5.4 units) has a 1: 28,000 chance of contracting the HIV virus. HTLV-1 was the first human retrovirus discovered. In approximately 1% of those who are antibody positive for HTLV-1 , a unique form of adult T-cell leukemia/lymphoma will develop. This virus can be transmitted by transfusion, but its clinical significance has yet to be defined.” The list of infectious agents potentially transmitted by blood transfusion is quite large, ranging from Salmonella choleraesuis and Brucella abortus to the organisms that cause malaria and filariasis.“, I9 Certain bacteria can multiply in refrigerated stored blood,“. ” resulting in transfusion-transmitted bacterial infections. Bacteremic and endotoxic shock can develop, sometimes resulting in death.18. “. 24 Immune function can be impaired by blood transfusions. Transfusions performed in rats impair the macrophage’s ability to phagocytose and kill bacteria.*’ Alloimmunization of recipients to red cell, white cell, platelet, and protein antigens can occur, particularly in black patients receiving blood from white donors.**. 29This condition occurs in 4% to 40% of patients with sickle cell anemia and results in difficulty in obtaining compatible blood, de-
layed transfusion reactions, and occasional life-threatening events .29 Other occurrences associated with transfusions include nonhemolytic febrile reactions and allergic reactions. 18.*’ Massive transfusions are associated with iron overload with resultant hemosiderosis, depletion of coagulation proteins and platelets, hypothermia, citrate toxicity, acidosis, and hyperkalemia.“. 22 Death can occur as a result of acute hemolysis if donor red blood cells and recipient plasma are incornpatible. From 1976 through 1985, there were 256 transfusion-associated deaths from causes other than AIDS or hepatitis.24 Fifty-one percent of the patients died of acute hemolysis after the transfusion of ABO-incompatible products. These deaths were due primarily to human error in properly identifying the unit of blood or the recipient. Other causes of death included acute pulmonary injury (15%), bacterial contamination of product (10%). delayed hemolysis (lo%), damaged product (3%), and graft-versus-host disease (0.4%). With today’s keen awareness of the risks associated with blood transfusions, transfusions of whole blood and red cells have declined since 1986.30 Finally crumbling is the surgical mandate that patients with preoperative hemoglobin levels below 10 gmidl must be given transfusions.30. 3’ Autologous transfusions and intraoperative salvage of blood have also contributed to decreasing transfusion rates. The replant patient who has suffered a crush or avulsion injury has a greater thrombogenic potential than the patient who has experienced a sharp cut injury. Evidence’. 3-8suggests that anticoagulation of these patients can increase the survivability of the replanted parts. Our study demonstrates that the patients given a single anticoagulation agent (in addition to aspirin) are at low risk of needing a transfusion. However, patients who are given multiple anticoagulants risk losing significant amounts of blood. Our criteria for transfusion are stringent and take into account the patient’s age and health status, whether the patient has symptoms of acute anemia, and whether the patient is actively losing blood. Nevertheless, a significantly greater proportion of patients receiving multiple anticoagulants needed blood transfusions. Conclusion The importance of attempting to salvage a replanted digit or digits by the administration of two or more anticoagulants must be weighed against the risks of a blood transfusion. A patient who has had multiple finger amputations or who has lost a thumb will have a significant loss of function if replants fail. The risk of a
Vol. 17A, No. 2 March 1992
blood transfusion may therefore be acceptable if there is believed to be a chance of salvaging major function by increasing the number of anticoagulants. On the other hand, failure of a single-finger replant or distalfinger replants is less likely to significantly affect the function of the hand. In these situations the risks of a blood transfusion may outweigh the benefit of salvaging these parts. The clinical situation should be thoroughly discussed with the patient, and all options should be carefully considered. REFERENCES I. Cooley BC, Ruas EJ, Wilgis EFS. Scanning electron microscopy of crushediavulsion arterial trauma: effect of heparin and aspirin administration. Microsurgery 1987;8:1 l-6. 2. Morrison WA, O’Brien B McC, MacLeod AM. Evaluation of digital replantation-a review of 100 cases. Orthop Clin North Am 1977;8:295-308. 3. Kolar L, Wieberdink J, Reneman RS. Anticoagulation in microvascular surgery. Eur Surg Res 1973;5:52-7. 4. Rohrich RJ. Billings E. Handren J, Wolfort B, May JW. Prevention of microvascular thrombosis with human tissue type plasminogen activator. Surg Forum 1986;37: 589-90. 5. Rosenbaum TJ, Sundt TM. Thrombus formation and endothelial alterations in microarterial anastomoses. J Neurosurg 1977 ;47:430-4 1. 6. Vlaston C. Earle AS. Intraoperation heparin in replantation surgery-an experimental study. Ann Plast Surg 1983;10:112-4. 7. Khouri RK, Cooley BC. Kenna DM, Edstrom LE. Thrombosis of microvascular anastomoses in traumatized vessels: fibrin versus platelets. Plast Reconstr Surg 1990:8:110-7. 8. Greenberg BM. Masem M, May JW. Therapeutic value of intravenous heparin in microvascular surgery: an experimental vascular thrombosis study. Plast Reconstr Surg 1988;82:463-70. 9. May JW, Rothkopf DM. Salvage of a failing microvascular free muscle flap by direct continuous intravascular infusion of heparin: a case report. Plast Reconstr Surg lY89;83: 1045-Y. IO. Weiss SC. Platelet physiology and abnormalities of platelet function. N Engl J Med 1975;293:531-41. 11 Moake JL, Levine JD. Thrombotic disorders. Clin Symp lY85;37:27. 12. Cines DB. Heparin: do we understand its antithrombotic actions’? Chest 1986;89:420-6. 13 Wessler S, Gitel SN. Pharmacology of heparin and warfarin. J Am Coil Cardiol 1986;8:10B-20B. 14. Ketchum LD. Pharmacological alterations in the clotting mechanism: use in microvascular surgery. J HAND SURG 1978:3:407-15.
Blood loss associuted with anticoagulation
229
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