Control of Pelvic Hemorrhage



Control of Pelvic Hemorrhage


Lindsay M. Kuroki

David G. Mutch





FUNDAMENTAL CONCEPTS OF NORMAL COAGULATION

Every surgeon should understand the basic mechanisms of normal hemostasis that can be applied when surgical injury to tissue is inflicted. Bleeding during gynecologic surgery usually results from cutting or injuring a vessel, but occasionally, it may result from a preexisting condition or defect in the clotting mechanism. The surgeon should be able to quickly recognize when normal hemostasis is interdicted and operate efficiently to correct vascular injuries and coagulopathies and minimize blood loss.

The following is a discussion of the principles and concepts of normal hemostasis, abnormal hemostasis (congenital and acquired), and management techniques. Coagulation is the working interrelation of five aspects of a complex biochemical and vascular system that causes the formation and dissolution of the fibrin platelet plug. These five components are (a) vasculature, (b) platelets, (c) plasma clotting proteins, (d) fibrinolysis and clot inhibition, and (e) the hypercoagulable response. How these five components interrelate in the normal setting must be understood before one can appreciate how they relate to bleeding or abnormal clotting in disease states. For the purposes of this chapter, we will focus on the first three factors.


Vasculature

The vasculature presents an endothelial-lined flexible conduit through which red cells, white cells, platelets, and all of the plasma proteins flow. At the interface between the flowing blood and vessel wall are several inhibitory biochemical systems that prevent the generation of the platelet-thrombin clot. The antiplatelet substance prostacyclin, produced in the vessel wall, inhibits platelet adhesion to the site of injury. The surface antithrombin III-heparin sulfate complex inhibits deposition of thrombin and fibrin.

A tear in the vessel wall removes the endothelial cell layer, exposing the basement membrane, smooth muscle, collagen, and supporting adventitia. These substances are biochemical activators of platelets and have their own thromboplastic activity. This activity initiates fibrin generation and deposition. A disease or medication that interferes with or intensifies this process can cause bleeding or inappropriate clotting, respectively. The vessel wall is diagrammed in Figure 19.1.

Congenital diseases associated with inadequate connective tissue and vascular dysfunction associated with bleeding are rare. The more frequently seen conditions are hereditary hemorrhagic telangiectasia, Ehlers-Danlos syndrome, and Marfan syndrome, which are characterized by defects in collagen, leading to poor clot formation and platelet activation at the injured site.

Acquired diseases associated with bleeding include deficiencies in vitamin C; Cushing syndrome; acute and chronic inflammatory diseases, such as infectious vasculitis and immune vasculitis; pyrogenic purpura; embolic purpura; and anaphylactoid reactions from drugs. Myeloproliferative disorders, such as multiple myeloma and Waldenström macroglobulinemia,
produce abnormal proteins that interfere with vascular function and therefore permit bleeding.






FIGURE 19.1 Vessel cross-section.


Platelet Function

Platelets are disk-shaped fragments of the large multinucleated megakaryocytes released from the bone marrow on a daily basis (normal count is 150 × 103/mL to 400 × 103/mL), with a lifespan between 8 and 10 days (Fig. 19.2). The surface activation of the receptor sites on the platelet results in a biochemical chain reaction, generating thromboxane A2, which in turn causes contraction of the protein thrombosthenin. This triggers platelet release of dense granules with nonmetabolic adenosine diphosphate (ADP). ADP is a potent platelet-aggregating agent that stimulates more platelets and eventually generates a platelet plug.

The congenital diseases associated with poor platelet function are divided into four types of dysfunction: (a) adhesion to collagen, (b) adhesion to subendothelium, (c) release reaction defects, and (d) ADP aggregation defects. Von Willebrand disease (vWD) (Table 19.1) is the most common hereditary coagulation abnormality, although acquired forms have been described. Excessive bleeding results from the absence, decreased production, or abnormal function of von Willebrand factor, a large multimeric protein synthesized by megakaryocytes and vascular endothelium. This protein is responsible for the proper binding of platelets to the exposed collagen surface at the site of vascular injury. Its absence, therefore, prevents formation of the platelet plug necessary for hemostasis. Clinical manifestations of vWD vary in severity and often go unrecognized until some form of vascular trauma occurs or surgery is performed. In addition, such patients are particularly sensitive
to aspirin or other antiplatelet medications, increasing their tendency to bleed more at the time of surgery.






FIGURE 19.2 Platelet cross-section.








TABLE 19.1 More Commonly Seen Rare Congenital Clotting Disorders





















NAME


INCIDENCE (PER MILLION)


TREATMENT


Factor VIII (classic hemophilia A, sex-linked)


60-80


FVIII concentrate


Factor IX (classic hemophilia B, sex-linked)


15-20


FIX concentrate


von Willebrand disease (dominant, autosomal)


5-10


Cryoprecipitate (DDAVP), factor VIII concentrate with von Willebrand factor


DDAVP, deamino-D-arginine vasopressin. The remainder of the known congenital clotting factors are very rare and occur with such low frequency that their discussion, diagnosis, and management can be found elsewhere (see Harker LA. Hemostasis manual, 2nd ed. Philadelphia, PA: FA Davis, 1974; Corriveau DM, Fritsma GA. Hemostasis and thrombosis. Philadelphia, PA: JB Lippincott Co., 1988; Triplett DA, ed. Laboratory evaluation of coagulation. Chicago, IL: ASCP Press, 1982).







FIGURE 19.3 Coagulation system. Dashed boxes indicate destruction of factors. (APC1, activated protein C1; HMKa, high molecular weight kininogen; PF3, platelet factor 3; TPA, tissue plasminogen activator; TF, tissue factor; TFPI, tissue factor pathway inhibitor.)

Acquired defects in platelet function are much more common and can be classified into two groups: (a) those due to an underlying condition, such as renal failure, myeloproliferative disorders (polycythemia vera, chronic myelogenous leukemia), and increased fibrin split products in consumptive coagulopathies, and (b) those that are iatrogenic, such as defects caused by medications (aspirin, nonsteroidal anti-inflammatory drugs, antibiotics, antihistamines, tricyclic antidepressants, dextran) and cardiopulmonary bypass surgery.

The laboratory assessment of platelet function has been extrapolated from the research laboratory and is now more readily available. The routine analysis of platelet function should begin with a platelet count and platelet function analyzer (PFA-100). However, in special cases, evaluation of platelet adhesion and aggregation and/or biochemical markers for measuring platelet turnover (e.g., platelet factor 4 and β-thromboglobulin assays) may be useful, although not predictive of surgical bleeding.


Plasma Clotting Proteins

Plasma clotting proteins are a group of serine proteases and cofactors that interact in a synergistic system to generate fibrin. The activation of the clotting system can be initiated in two ways: either by contact activation with factor XII or through thromboplastin activation of factor VII. The clotting cascade is diagrammed in Figure 19.3. The most common congenital factor deficiencies associated with bleeding are hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency). Both are seen in males and rarely in female disorders with sexlinked inheritance patterns. The majority of other congenital bleeding disorders have an autosomal recessive inheritance pattern or a dominant pattern with variable penetrance, making them extremely rare and less pertinent to this discussion.

However, acquired factor deficiencies are common. For example, critically ill patients on antibiotics that kill vitamin K-producing bacteria in the intestine and those who are diet restricted to nothing by mouth are at high risk for a coagulopathy due to loss of vitamin K-dependent factors II, VII, IX, and X. Other commonly acquired multifactor deficiencies are seen in acute and chronic liver disease such as viral hepatitis and alcoholic cirrhosis; consumptive coagulopathies, as in sepsis and placenta abruption; washout coagulopathies, seen in patients who require multiple transfusions after severe blood loss anemia; and major trauma.

The laboratory assessment of the plasma clotting factors has traditionally begun with prothrombin time (PT; factors V, VII, and X, prothrombin, and fibrinogen) and activated partial thromboplastin time (APTT; factors VIII, IX, XI, and XII). Specific factor assays also can identify the exact deficiencies. One must remember that a factor deficiency as low as 30% can generate a normal PT and APTT. This relation is important in investigating minimal prolongations of the PT or APTT that appear insignificant but nonetheless could be obscuring a deficiency. The tissue factor pathway inhibitor modulates activated factors × and VIII but is not apparently clinically significant.









TABLE 19.2 Pertinent Medical History to Screen for Coagulation Problems

















History of spontaneous bruising or bleeding


History of unusual bruising or excessive bleeding after surgery


Family history of bruising or bleeding after surgery


Medication associated with bruising or bleeding


Current medication within past week


Previous coagulation testing


Current coagulation testing



PREOPERATIVE COAGULATION ASSESSMENT FOR SURGICAL PATIENTS

Preoperative evaluation of any patient may be divided into two general categories: elective versus emergency surgery.


Elective Surgery

The elective gynecologic surgical patient must be evaluated by general medical history and specific nature of the surgery. Table 19.2 highlights the most important positive and negative findings. Preoperative coagulation screening (Table 19.3) should supplement the history and physical and be individualized according to risk factors elicited (e.g., a prior emergency surgical procedure; positive personal or family history of spontaneous bleeding or easy bruising; use of medications that can affect coagulation, such as antiplatelet medication; acquired vitamin K deficiency; and fibrinolytic therapy).

The risks of blood-borne infections and adverse reactions are always present, but the documented need for blood transfusion(s) as a lifesaving measure will validate the decision so long as it is congruent with the patient’s religious and personal beliefs. Standard preoperative orders for blood require knowledge of the specific needs of the patient and the indicated surgery. For the routine gynecologic procedure, such as simple hysterectomy in an otherwise healthy woman, a type and screen is appropriate. If an unexpected antibody is identified, the blood bank should notify the ordering physician and set aside 2 units of antigen-negative, crossmatched, compatible blood. In an emergency, the blood bank can always release universal donor type O-negative blood immediately.

In more complex procedures such as pelvic exenteration for cancer, where there usually is significant blood loss, a type and crossmatch for the average number of units used are appropriate and encouraged. With extremely difficult procedures or other complicating medical conditions, additional blood, fresh frozen plasma, and platelets may be required during the procedure and should be requested preoperatively.


Emergency Surgery

As an emergency procedure proceeds, decisions regarding blood replacement must be made. A direct approach to blood replacement therapy and the complications of such therapy depends on a clear understanding of the following concepts.



  • Transfusion with packed red cells may help compensate for the volume of the estimated blood loss but iatrogenically may cause a bleeding disorder (e.g., thrombocytopenic hemophilia). Therefore, platelets and fresh frozen plasma may also be indicated.


  • The patient’s bleeding potential is dynamic and will change rapidly and frequently with the loss of blood and replacement therapy.


  • Direct monitoring before, during, and after surgery offers the best chance to diagnose and manage bleeding problems. It also allows formulation of plans and adjustment of the replacement therapy.


COMPONENT THERAPY FOR REPLACEMENT BEFORE SURGERY

With surgery planned, the preoperative data can be evaluated. Assuming the patient does not have hemophilia, vWD, severe liver disease, or liver failure, a prolonged PT and APTT may suggest a less common acquired or congenital bleeding disorder. Assistance from a clinical pathologist or hematologist should be requested if an intrinsic bleeding disorder is suspected.








TABLE 19.3 Tests to Indicate Coagulation Status















































TEST


REFERENCE RANGEa


LEVEL OF ALARM


SIGNIFICANCE


Hematocrit (%)


37-47


25


Tissue anoxia


White cell count (mL)


4×103 to 12 × 103


3 × 103 to 25 × 103


Susceptibility to infection, leukemia


Platelet count (mL)


140 × 103 to 400 × 103


100 × 103 to 700 × 103


Bleeding, myeloproliferative disorder


Fibrinogen (mg/dL)


150-400


100


Bleeding, liver disease, intravascular consumption


Prothrombin time (s)


10-13


14


Bleeding factor deficiency


Activated partial thromboplastin time (s)


28-38


40


Bleeding factor deficiency, inhibitor


PFA-100


Collagen-epinephrine


Prolonged closure time


Screen for medication effect


Bleeding time (will not predict surgical bleeding)


a Reference ranges may vary in each laboratory, reflecting method, instrumentation, and reagents.




COMPONENT THERAPY FOR REPLACEMENT DURING SURGERY

According to Schifman and Steinbronn, when intraoperative blood loss exceeds 15% of the patient’s estimated blood volume, the surgeon should consider red blood cell transfusion to replace the acute blood loss. As a general rule, 15% of an adult’s blood volume (in milliliters) equals the patient’s weight (in kilograms) times 10. For example, for a 75-kg woman (165 pounds), 15% of blood volume is (75 × 10) 750 mL. When considering the risks and benefits of transfusing blood, the following should be considered: the patient’s estimated blood volume and hemoglobin/hematocrit prior to surgery, the estimated intraoperative blood loss, the anticipated additional blood loss, and the risk of hypoxic and metabolic complications.

When massive blood replacement therapy is under way, intraoperative monitoring of coagulation at 2-hour intervals or after every 10 units of blood transfused is usually sufficient. It is important to remember that a patient bleeding during a surgical procedure has a higher demand for clotting factors and platelets than does a patient at bed rest. The use of blood and blood components in the management of massive bleeding that is due to a major vessel rupture has the following objectives:



  • To maintain sufficient blood volume and circulating red cells to carry enough oxygen to sustain life.


  • To replace blood sufficiently to achieve adequate coagulation and hemostasis, assuming there was extensive loss of plasma clotting factors and platelets.


  • To avoid falling so far behind in replacement that consumptive coagulopathy leads to exacerbated bleeding at the microvascular level due to insufficient clotting factors and platelets.

These objectives require repeated assessment of the patient throughout the surgical procedure and clear communication with anesthesia and the operating room staff.

The following guidelines are recommended for component therapy in clinical situations requiring massive blood replacement to maintain normal hemostasis.

Correction of the deficit in blood volume with crystalloid volume expanders will generally maintain hemodynamic stability, while transfusion of packed red blood cells is used to improve and maintain tissue oxygenation. Each unit of packed cells contains approximately 250 mL of red cells and, in an adult, will raise the hematocrit by roughly 3% unless there is continued bleeding (Table 19.4). Development of massive transfusion protocols has resulted in improved outcomes and decreased mortality. Most protocols focus on delivering a minimum ratio of 2 units (500 mL) of fresh frozen plasma for every 3 units of packed red blood cells and 1 unit of platelets (300 mL) for every 5 units of packed red blood cells. The size and age of the patient affect blood replacement. Posttransfusion labs should include CBC, PT, and APTT.

Platelets should be given when the platelet count falls below 100,000/mL in massive hemorrhage (measurement error of a platelet count can be as high as 62,000/mL in a bleeding patient). When a long surgical procedure is anticipated, or when more than 6 units of blood are given, 6 units of platelets in a volume of 300 mL should be given toward
the end of the surgical procedure or when surgical hemostasis is achieved. This amount should be administered once to provide a maximum bolus effect. Because platelets are often difficult to obtain, their use should be reserved until near the end of the procedure. Pooling and transporting the platelets can take up to an hour, so the blood bank should be given sufficient notice to have them readily available in surgery when needed. In assessing the patient’s coagulation status, it should be remembered that clotting factors are constantly changing.








TABLE 19.4 Blood Products









































BLOOD PRODUCT


VOLUME (ML)


ADDITIONAL FACTORS


EXPECTED RESPONSE


COMMON INDICATIONS


PRBC 1 unit


200-250


Fibrinogen: 10-75 mg


Increase: 1 mg/dL Hgb 3% Hct


ABLA MTP Surgical blood loss


Platelets SDA


300-500


Fibrinogen: 2-4 mg/mL (360-900 mg)


Increase: 30-60 K/mm3


Plt count <10 K MTP


RDPa


50 per unit


Clotting factors: Equivalent of 200-250 mL of plasma “6 pack” of pooled RDP similar to SDP



Bleeding with known qualitative plt defect


FFPb 1 unit


180-300


Fibrinogen: 400 mg


Clotting factors: 1 mL contains 1 active unit of each factor


Decrease: PT/INR PTT


Coagulopathy Warfarin overdose DIC


Cryo 10 pack



Fibrinogen: 1,200-1,500


Clotting factors: VIII, vWF, XII


Decrease: PT/INR PTT Increase: Fibrinogen


vWD


DIC


Hemophilia A


a 4-10 RDP units are pooled prior to transfusion.
b Duration of FFP effect is approximately 6 h.


Reprinted from Klingensmith ME, Abdulhameed A, Bharat A, et al., eds. The Washington manual of surgery, 6th ed. Lippincott Williams & Wilkins, 2012:133, with permission. Copyright © 2011, Lippincott Williams & Wilkins/Wolters Kluwer Health. ABLA, acute blood loss anemia; Cryo, cryoprecipitate; DIC, disseminated intravascular coagulation; FFP, fresh frozen plasma; Hct, hematocrit; Hgb, hemoglobin; MTP, massive transfusion protocol; plt, platelets; PRBC, packed red blood cells; RDP, random donor platelets; SDP, single-donor platelets; vWD, von Willebrand disease, vWF, von Willebrand factor.


When the PT and APTT are prolonged (more than 14 and 40 seconds, respectively) after replacement therapy, intrinsic disease must be considered initially, if only to be ruled out later. A borderline hemophiliac or patient with liver disease may manifest excessive bleeding after stress, trauma, or blood replacement because of the increased coagulation needs. Therefore, administration of fresh frozen plasma in 2 units (500-mL) doses should begin to correct the deficiencies caused by massive red blood cell replacement. If oozing continues despite the rapid transfusion of 6 units of fresh frozen plasma, a clotting problem or other ongoing bleeding disorders should be suspected and additional support sought.

When the fibrinogen level falls below 100 mg/dL, transfusion of 20 units of cryoprecipitate will provide about 150 mg/dL fibrinogen in a 70-kg person. A low fibrinogen level is rare because fibrinogen is stable and present in fresh frozen plasma. Liver disease or intravascular consumption must be suspected if the fibrinogen level is initially less than 100 mg/dL and remains low throughout surgery and recovery. Twenty units of cryoprecipitate will achieve therapeutic levels quickly and permit monitoring over several hours.

The goals of intraoperative monitoring are as follows:



  • To assess changes in the coagulation mechanism resulting from blood loss and replacement therapy.


  • To identify the coagulation components affected and determine the correct components to initiate therapy and achieve the following values: PT less than 14 seconds, APTT less than 40 seconds, fibrinogen more than 100 mg/dL, and platelets more than 80 × 103/mL. Posttransfusion laboratory monitoring should be drawn after 1 to 2 hours to determine the success of replacement.


  • To assess the efficacy of replacement component therapy in an extensive operative procedure.


COMPONENT THERAPY FOR POSTOPERATIVE REPLACEMENT

The presurgical and intraoperative threshold levels for hematocrit, platelet count, PT, APTT, fibrinogen, and clot retraction also apply postoperatively, and a comparison of these values provides an accurate assessment of the bleeding patient. When laboratory values are abnormal, however, further surgery can be delayed until an attempt at aggressive specific component therapy is made. When abnormal coagulation studies exist, the following causes predominate, in order of frequency (most frequent first):



  • Low platelet count owing to transfusion of only packed red cells or fresh frozen plasma.


  • Prolonged PT and APTT due to transfusion of packed red cells without fresh frozen plasma. Careful monitoring of venous and arterial pressure, as well as cardiac output, should be considered in blood component therapy. Often, a slower rate of administration can achieve hemostasis without cardiovascular overload. If nearly normal coagulation values are achieved, but bleeding continues, surgical causes for bleeding should be considered.


  • 3. Low fibrinogen level owing to dilution with plasma expanders or concurrent development of a disseminated intravascular coagulation (DIC).

The goals of postoperative monitoring are as follows:



  • To assess for a coagulopathy and determine possible etiologies, including blood replacement.


  • To determine the effectiveness of specific component therapy and identify the need for additional components.


  • To enable the surgeon to distinguish surgical from nonsurgical bleeding.

Close postoperative monitoring, whether the patient is bleeding or not, will achieve these objectives with the ultimate goal of recognizing and resolving bleeding disorders in a timely manner.


RISKS OF BLOOD TRANSFUSION

Transfusions of whole blood were given sporadically before 1900, usually to treat specific diseases rather than to replace lost blood volume. It was not until the work of Cannon and Bayliss in 1919, and of Blalock in 1930, that it was proven that the important factors in shock were the loss of circulating blood volume and the decreased return of venous blood to the right heart. Eventually, banking and storage of donated blood became possible with refrigeration and the addition of sugar and later sodium citrate as an anticoagulant.

Homologous blood must be collected from carefully selected volunteer donors and properly matched to the potential recipient. The risks of red blood cell transfusion were reviewed by a National Institutes of Health and Food and Drug Administration Consensus Development Conference on Perioperative Red Cell Transfusion and published in 1988. The following excerpt is taken directly from their report.

In deciding whether to use red blood cell transfusion in the perioperative period, the need for possibly improved oxygenation must be weighed against the risks of adverse consequences, both short term and long term. The disadvantages are of two general types (Table 19.5): transmission of infection and adverse effects attributable to immune mechanisms. In addition, massive transfusion, defined as the replacement by transfusion of more than 50% of a patient’s blood volume in 12 to 24 hours, may be associated with a number of hemostatic and metabolic complications (e.g., ionized calcium, potassium, and acid-base disturbances).

In modern blood banking practice, bacterial contamination of red blood cell units is rare. For practical purposes, the transmissible agents of greatest concern are viruses.



  • Cytomegalovirus infection occurs with moderate frequency among those recipients without prior infection. Most of these infections are asymptomatic, except among immunocompromised people. The use of the newer leukocyte reduction filters (<5 × 106) is under extensive clinical study and application as an alternative to cytomegalovirus-negative blood.


  • Human T-cell lymphotropic viruses occur with low but not negligible frequency among donor populations in the United States. It is not known whether transfusion-transmitted infection with these viruses results in T-cell leukemia/lymphoma and/or neurologic disease several to many years later.


  • On rare occasions, other microbial agents—including parvoviruses, malaria, Toxoplasma, Epstein-Barr virus, and Babesia—cause infection and disease.









TABLE 19.5 Blood Transfusion Risks
























































DISEASE OR SITUATION


RISK


Viral infection



HIV


1:1.9 million



HTLV


1:250,000-1:2.0 million



Hepatitis B


1:180,000



Hepatitis C


1:1.6 million


Bacterial contamination



Platelet packs (stored at room temperature)


1:12,000



Packed or whole red blood cells


1:5 million



Fatal red cell hemolytic reaction


1:250,000-1:1.1 million



Delayed red cell hemolytic reaction


1:1,000-1:1,500


TRALI


1:5,000


Febrile red cell nonhemolytic reaction


1:100


Allergic (urticarial reaction)


1:100


Anaphylactic reaction


1:150,000


HIV, human immunodeficiency virus; HTLV, human T-cell lymphotropic virus; TRALI, transfusion-related acute lung injury.


From Zoon KC. Ten years after: what has been achieved by Consent Decrees: the FDA view. Paper presented at: Fifth Annual FDA and the Changing Paradigm for Blood Regulation; January 16-18, 2002; New Orleans, LA, 2002; Schreiber GB, Busch MP, Kleinman SH, et al. The risk of transfusiontransmitted viral infections: the retrovirus epidemiology donor study. N Engl J Med 1996;334:1685; Dziecxkowski JS, Anderson KC. Transfusion biology and therapy. In: Fauci AS, Martin JB, Braunwald E, et al., eds. Harrison’s principles of internal medicine. 14th ed. New York, NY: McGraw-Hill, 1998:718; Goodnough LT, Breacher ME, Kanter MH, et al. Transfusion medicine: first of two parts—blood transfusion. N Engl J Med 1999;340:438.


It is known that the incidence of hepatitis transmission increases with the number of donor exposures. This relationship is probably true for other transfusion-transmitted infections. HIV presently poses only a remote hazard because of strict donor selection and laboratory screening procedures. The consequences of HIV infection are rarely seen until 2 or many more years have elapsed, but ultimately, morbidity and mortality are extremely high.

Immunologic consequences also complicate homologous red blood cell transfusion. Hemolytic and nonhemolytic reactions are largely caused by alloimmunization to red blood cell and leukocyte antigens. Compatibility testing virtually has eliminated immediate hemolytic transfusion reactions; however, if they occur, they are largely due to human error. Nonhemolytic febrile reactions occur in 1% to 2% of recipients due to sensitization to leukocyte antigens but may be reduced by the use of leukocyte reduction filters (<5 × 106).

It is important for gynecologic surgeons to discuss with their patients the possible need for transfusion of blood products and review the risks, benefits, and alternatives of such treatment. The most common transfusion-related viral infection, however, is non-A, non-B hepatitis, which accounts for 90% to 95% of cases of previous transfusion-acquired hepatitis and possibly as many as 3,000 deaths per year in the United States. When mortality or significant morbidity occurs with blood transfusion, the gynecologic surgeon must be able to show that the transfusion was indicated.

There are alternatives to blood and blood component transfusion that may be considered in critically ill patients such as those with sepsis and DIC. The drug-activated protein C, drotrecogin alfa (Xigris), is recombinant human-activated protein C (drotrecogin alfa, activated). It is used in replacement therapy in sepsis and holds a great promise in the management and survival in sepsis. By replacing this essential naturally occurring anticoagulant, there is reversal of the bleeding and thrombosis seen with sepsis. Its specific application in septic gynecologic surgical patients has not been reported in any large study.

Recombinant-activated factor VII (FVII) (NovoSeven) has been clinically demonstrated to successfully manage patients with FVIII and FIX inhibitors. It has also been used in the management of bleeding in cardiovascular surgery, liver failure, Coumadin overdose, and DIC. It has significantly reduced the use of blood components in these disorders, and although expensive, it has the potential to greatly improve patient outcomes.

By reducing the need for blood and blood components with the use of activated protein C (drotrecogin alfa), and recombinant-activated FVII, one can reduce the infectious disease exposure of blood as well as the generation of allogeneic antibodies.


AUTOLOGOUS BLOOD TRANSFUSION

Blood collected from a patient for retransfusion at a later time into the same patient is called autologous blood. Autologous blood transfusions account for over 5% of blood donated in the United States, with the majority obtained by preoperative donation, and have been endorsed by the Council on Scientific Affairs of the American Medical Association and by the Committee on Hospital Transfusion Practice of the American Association of Blood Banks.

The American Association of Blood Banks’ standards for elective preoperative autologous blood donation include the following guidelines:



  • A hemoglobin of no less than 11 g/dL or a packed cell volume of no less than 34%.


  • Phlebotomy no more frequently than every 3 days and not within 72 hours of surgery.

Preoperative autologous donation is generally discouraged in patients over the age of 80 and absolutely contraindicated in patients with an active infection, and any of the following conditions would also preclude a patient from undergoing preoperative autologous donation: unstable angina or angina at rest, a myocardial infarction within the last 3 months, heart failure, aortic stenosis, ventricular arrhythmias, transient ischemic attacks, or marked hypertension.

If established screening and administration guidelines are followed, autologous blood has potential to be the safest type of blood for transfusion. It minimizes the risks of immunologically mediated hemolytic, febrile, or allergic reactions as well as viral transmissions such as hepatitis, malaria, cytomegalovirus, and HIV. In patients with rare blood types who
have antibodies to common blood antigens, it may be the only blood available for transfusion. Autologous blood transfusion may be acceptable to Jehovah’s Witnesses and should be offered preoperatively if a patient meets criteria for donation and based on the indicated procedure.

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Jun 4, 2016 | Posted by in GYNECOLOGY | Comments Off on Control of Pelvic Hemorrhage

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