Red Blood Cells

Anemia detected in routine preoperative screening should be evaluated with regard to its functional significance and origin. Typically, a preferred preoperative hemoglobin level is >10 g/dL. Although lower intraoperative hemoglobin levels can generally be tolerated by most patients, these values are associated with an increased risk of morbidity and mortality. Additionally, anemia may reflect a previously unsuspected coexisting disease process that could have a significant effect on the perioperative course. Because anemia can be a primary disorder or can occur secondary to other systemic processes, a careful history and physical examination are essential and can provide extensive information about the underlying cause.

Initial diagnostic studies should include reticulocyte count, mean corpuscular volume (MCV), examination of the peripheral blood smear, and a fecal occult blood test. Many urologic conditions can be associated with anemia, including malignancy and chronic renal failure. Iron deficiency anemia has been associated with states of renal cell carcinoma. Direct involvement of the bone marrow by cancer may result in myelofibrosis and subsequent anemia, most often seen in metastatic prostate cancer. Radiation therapy can lead to bone marrow suppression or vitamin B ₁₂ deficiency secondary to radiation ileitis. The use of gastrointestinal segments in the urinary tract is associated with known metabolic derangements including vitamin B ₁₂ deficiency with utilization of the ileum. The body has about 3 years of vitamin B ₁₂ stores, after which the patient can develop megaloblastic anemia. Many chemotherapeutic agents can cause myelosuppression. Commonly used antibiotics in urology, such as nitrofurantoin, sulfa compounds, and quinolones, can produce hemolytic anemia in patients with glucose-6-phosphate dehydrogenase deficiency. Hemolytic anemia has also been reported in association with renal cell carcinoma and seminoma. Finally, hematuria itself can cause anemia if it is chronic or severe.

Understanding the cause of the anemia can dictate the appropriate perioperative course of action to minimize operative morbidity. For patients with an uncorrectable underlying cause of anemia who are judged to be at risk for functional compromise, therapy consists of transfusion. In patients who are undergoing surgical procedures that are deemed elective, it is advisable to proceed after correcting the underlying cause of anemia preoperatively and thereby avoiding transfusion. Preoperative transfusions should ideally be performed 24 hours in advance to allow regeneration of 2,3-diphosphoglycerate, which shifts the oxygen dissociation curve to increase oxygen availability to the tissues. Transfusions incur a potential risk of morbidity, including hemolytic reactions, allergic reactions, and transmission of viral diseases ( Table 4.1 ).

Erythrocytosis, a hematocrit level significantly higher than normal, increases blood viscosity and decreases oxygen transport. Erythrocytosis can significantly increase surgical morbidity and mortality, particularly related to thromboembolic complications. This increase in red blood cell (RBC) mass can be primary, as in polycythemia vera, or secondary. Common causes of secondary erythrocytosis are hypoxic states or paraneoplastic syndromes (as seen in renal cell carcinoma and Wilms’ tumor) likely resulting in increased production of erythropoietin. Patients with polycythemia vera should undergo preoperative phlebotomy to lower hematocrit levels to <45% to reduce the risk of thromboembolic complications. In patients with secondary erythrocytosis, the hematocrit should be lowered to <50%.

Platelets

Normal platelet count can vary greatly among healthy individuals; a platelet count >50,000 is usually adequate for surgical hemostasis. Thrombocytopenia results from decreased production of platelets (radiation, primary marrow disorders, alcohol, drugs), increased peripheral destruction (autoimmune disease, disseminated intravascular coagulation [DIC], sepsis, drugs), sequestration (splenomegaly), or extracorporeal platelet loss (exsanguination). Initial therapy should consist of treating the underlying cause; if this is not possible then the next step is platelet transfusion. One unit of platelets can be expected to raise the platelet count by 5000 to 10,000/mm ³ .

Thrombocytosis can be caused by myeloproliferative disorders and is associated with increased risk of both thrombotic and bleeding complications. Secondary or reactive thrombocytosis leads to an elevation of total number of platelets with normal function caused by underlying inflammation or infection. Patients with reactive thrombocytosis are not at increased risk of thrombotic events and do not require anticoagulation.

Inherited defects of platelet function are rare genetic disorders that result in altered platelet function or morphology, most commonly involving deficiency of glycoprotein mediators that regulate aggregation or adhesions of platelets. Treatment or prevention of bleeding frequently requires platelet transfusion.

Acquired intrinsic platelet dysfunction is most commonly due to medications that affect platelet function, but can also be caused by liver disease, uremia, hypothyroidism, and cardiopulmonary bypass. For acquired defects not related to medication, treatment is directed at the underlying cause.

von Willebrand’s Disease

von Willebrand’s disease (vWD) is the most common inherited bleeding disorder and is a result of dysfunction or deficiency of von Willebrand Factor. vWD is a plasma protein that mediates platelet adhesion and binds to and stabilizes coagulation factor VIII in the circulation. The disease is transmitted in both an autosomal dominant and recessive fashion and affects both men and women. Symptoms are primarily related to platelet dysfunction and are usually manifested in late childhood. Symptoms most commonly include easy bruising and bleeding at skin sites or mucus membranes. Although spontaneous bleeding may be mild, serious gastrointestinal bleeding can occur. Treatment is preferably with cryoprecipitate and desmopressin (DDAVP), which induces endothelial release of vWD and coagulation factor VIII. Desmopressin can result in hyponatremia; very young or elderly patients are at highest risk for this side effect.

Hemophilia A and B

Hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency) are extremely rare inherited disorders. Both deficiencies are typically inherited as a recessive X-linked trait and affect males almost exclusively. The underlying pathophysiology behind both diseases is based on the insufficient generation of thrombin by the factor VIIIa/IXa complex.

Hemophilia A occurs in 1 in 5000–7000 male births. The aPTT is prolonged, whereas PT, fibrinogen level, and platelet count are normal. In severe deficiency, spontaneous bleeding may occur, whereas patients with moderate disease may only have excessive traumatic bleeding. The diagnosis is established by demonstrating a reduction in factor VIII activity. Patients with minor bleeding can generally be treated with factor levels that are 25–30% of normal; surgical patients generally require target levels that reach 75–100% of normal activity. Many different factor VIII preparations can be given; the half-life of factor VIII is 8 to 12 hours, and many administrations may be required to maintain a steady state. Most patients require 2 to 3 weeks of postoperative hematologic support to allow sufficient wound healing and scar formation.

Hemophilia B, also known as Christmas disease, clinically resembles hemophilia A, but is less common with an incidence of 1 in 30,000 male births. Replacement therapy with factor IX, as in hemophilia A, is recommended.

Rare Inherited Factor Deficiencies

Other factor deficiencies are much less common, and not all are associated with coagulopathies. The presentation and management of these disorders are outlined in Table 4.2 . In general, these patients may present with ecchymosis, hematoma, or delayed traumatic bleeding.

Prothrombin deficiency is a very rare autosomal recessive disorder manifested by prolonged PT and variably prolonged aPTT. Prothrombin is usually converted to its active form thrombin (coagulation factor II) leading to fibrin formation. Maintenance of >15% of normal levels should be adequate for surgery and can be achieved with fresh frozen plasma (FFP).

Factor V deficiency, also called parahemophilia, is also a very rare disorder in which the PT and aPTT are prolonged. Approximately 25% of normal activity can be maintained for surgery by treatment with FFP.

Factor VII deficiency is uncommon and is inherited as an autosomal gene with intermediate penetrance. The PT is prolonged and the aPTT is normal. Replacement is achieved by transfusing plasma or factor VII replacement.

Inherited factor X deficiency is autosomal recessive. Maintenance of levels >40% of normal may be achieved with plasma transfusion in preparation for surgery.

Factor XI deficiency is an uncommon disorder inherited in an autosomal dominant fashion. A higher frequency of this deficiency is noted in the Ashkenazi Jewish population. These patients may not have bleeding histories but often present with epistaxis. Severe bleeding may occur with trauma or major surgery. Patients can successfully undergo urologic surgical procedures with adequate FFP therapy.

Factor XII deficiency is not usually associated with bleeding manifestations, although the aPTT is prolonged. Therapy is not needed for this deficiency. Factor XII stabilizes fibrin into a covalent network, and in factor XII deficiency coagulation studies are normal except fibrin stability. Abnormal clot solubility and specific factor XII assay establish the diagnosis, and transfusion of FFP is sufficient for hemostasis.

Fibrinogen deficiency, or dysfibrinogenemia, is uncommon, and FFP or cryoprecipitate may be given to maintain a level of fibrinogen adequate for normal hemostasis.

Renal Failure

Uremia can cause a coagulopathic state that can place patients in renal failure at risk for severe hemorrhage. The main hemostatic defect is complex and multifactorial but is primarily the result of impaired platelet function, which can manifest as an elevated bleeding time in laboratory testing. Investigations of the hemorrhagic tendency associated with uremia have mostly been performed in patients with chronic renal failure, and whether these findings can be extrapolated to acute renal failure is unclear.

Uremic bleeding is mainly the result of impaired platelet–vessel wall interaction. Observed changes that are thought to contribute to this dysfunction include increased prostacyclin and nitric oxide production by the endothelium, abnormalities in vWF, and biochemical and functional platelet abnormalities.

Anemia, often associated with renal failure, also plays a role in platelet dysfunction. Correction of anemia in uremic patients has been shown to improve or correct the prolongation of bleeding time. Improvement in coagulation studies was seen when the hematocrit was increased to 27–32% by transfusion of packed red blood cells or by stimulation of erythropoiesis with recombinant human erythropoietin. Anemia related bleeding diathesis is not exclusive to uremia and can be found in anemia from other etiologies.

The finding that acquired platelet dysfunction is partially corrected by hemodialysis suggests that accumulation of uremic toxins in the blood may contribute to the observed effects. Despite the hemorrhagic tendency, activation of coagulation has been demonstrated in uremic patients and is more prominent in those who are being treated with hemodialysis. The safest treatment to relieve uremic bleeding is administration of desmopressin (DDAVP), but its effect is often short-lived. High-dose intravenous (IV) conjugated estrogens can significantly improve the bleeding time and have a longer duration of action in most uremic patients.

Disseminated Intravascular Coagulation

DIC is a clinicopathologic syndrome characterized by systemic activation of the coagulation system. Of all acute causes of coagulopathy, it is potentially the most life-threatening. DIC is not a single entity, but rather the end product of a variety of underlying disorders, most commonly bacterial sepsis and malignancy in the urologic patient.

Central to the pathogenesis of DIC is the unregulated and excessive generation of thrombin. Normally, the cumulative effect of clot production, clot dissolution (fibrinolysis), and inhibition of clot activation is to produce a steady-state equilibrium of hemostasis. In DIC, excess thrombin is generated, resulting in the inappropriate activation of fibrinolysis and the shifting of the steady state to excessive clot dissolution. A secondary result is that fibrin thrombi are formed in the microvasculature, and platelets and RBCs are trapped and consumed. As the cycle continues, platelets, fibrinogen, and other clotting factors are consumed beyond the body’s ability to compensate, and excessive bleeding ensues. It should be clear from this description that DIC is initially a thrombotic process with secondary hemorrhage occurring only when platelets and clotting factors are sufficiently consumed and depleted. Approximately 10% of patients with DIC present with only thrombotic manifestations.

Patients in whom DIC is suspected generally present with diffuse bleeding from several sites, petechiae or ecchymosis, hypoxemia, hypotension, or oliguria. In acute DIC, laboratory evaluation demonstrates variable degrees of thrombocytopenia, hypofibrinogenemia, and prolongation of PT and aPTT. Assays for fibrin split products (FSPs), fibrin degradation products (FDPs), or the D-dimer fragments of fibrin are generally markedly elevated. The D-dimer assay is theoretically more specific for DIC because this fragment is produced by the action of plasmin on polymerized fibrin. Patients with malignant disease often have chronic, compensated DIC in which bleeding is minimal in the steady state, and these patients often present with normal PT/PTT, platelet, and fibrinogen test results. Patients in this subset demonstrate an elevation of FDPs, FSPs, or D-dimer. These patients are also at increased risk for significant bleeding following an insult resulting in activation of their clotting system, such as relatively minor surgical procedures.

The diagnosis of DIC relies heavily on laboratory results, but overall the clinical picture must be considered. Of all the laboratory findings, thrombocytopenia, hypofibrinogenemia, and D-dimer fragments appear to be the most sensitive in making a laboratory diagnosis. In addition to the coagulation abnormalities, microangiopathic hemolytic anemia is present with fragmented RBCs (schistocytes) on the peripheral blood smear.

The primary management strategy in patients with DIC consists of aggressive basic supportive measures and prompt treatment of the underlying process causing the DIC. When this is not possible, treatment of the underlying disease accentuates the DIC, or the DIC is progressing despite appropriate treatment of the underlying process, the general approach is to support the patient’s hemostatic system with the transfusion of FFP, cryoprecipitate, or platelets. The idea that this approach will add to the consumption coagulopathy has never been clinically proven. If hemorrhage is excessive, replacement with packed RBCs is advised. Use of heparin in DIC is controversial. Therapeutic heparin can be considered if thrombosis is the predominate manifestation and there is no significant bleeding that may be exacerbated by anticoagulation.

Primary Fibrinolysis

Primary fibrinolysis is a condition in which the fibrinolytic pathway is activated independent of the activation of coagulation resulting in the pathologic degradation of fibrinogen and fibrin by plasmin. Fibrinolysis is associated with advanced and often metastatic prostate cancer and portends a very poor prognosis, even if significant bleeding is not present. In patients with metastatic carcinoma, the tumor cells are presumed to release a substance that directly activates fibrinolysis.

Patients do not typically present with gross bleeding but are at significant risk for hemorrhage resulting from hypofibrinogenemia. Marked thrombocytopenia should raise the suspicion of the development of DIC. The major laboratory discriminant between primary fibrinogenolysis and DIC is a normal level of D-dimer. Once active bleeding develops, it is very difficult to distinguish the two entities because fibrin is generated through the action of thrombin and lysis of fibrin produces D-dimer.

Unlike in DIC, the treatment of choice of primary fibrinogenolysis is the use of antifibrinolytic agents, such as ε-aminocaproic acid or tranexamic acid. Transfusion support with cryoprecipitate may also be given for severe hypofibrinogenemia. If DIC has developed, the use of antifibrinolytic agents in the absence of systemic anticoagulation (heparin) is contraindicated because of the risk of increased microvascular thrombosis. The best approach in individuals with primary hyperfibrinogenolysis secondary to malignant disease is often aggressive treatment of the underlying malignant condition. Caution should be used in balancing chemotherapy-related bone-marrow suppression with bleeding complications resulting from fibrinogenolysis.

Vitamin K–related Disorders

Liver disease and vitamin K deficiency are common causes of abnormal coagulation test results and clinical coagulopathy. The pathophysiology of these disorders is the decreased production of vitamin K–dependent clotting factors (factors II, VII, IX, X), protein C, and protein S. The liver is the major source of all coagulation proteins except factor VIII and vWF. Liver disorders may also produce abnormalities in fibrinolysis. Primary vitamin K deficiency is extremely rare in healthy people. A wide variety of animal and plant sources can provide sufficient vitamin K, and the bacterial flora in the intestine is able to synthesize a significant portion of the required dietary vitamin K. Vitamin K is fat soluble, and therefore adequate bile salt circulation is necessary for absorption.

Vitamin K deficiencies can result from a wide range of conditions. These include, but are not limited to, the following:

• 1.
  

  Newborns, owing to poor transfer of vitamin K by the placenta and lack of vitamin K synthesis in the initially sterile intestine

  
  
• 2.
  

  Severe malnutrition or total parenteral nutrition

  
  
• 3.
  

  Extrahepatic biliary obstruction

  
  
• 4.
  

  Intestinal malabsorption syndromes

  
  
• 5.
  

  Broad-spectrum antibiotic use.

The liver also synthesizes factor V, which plays a critical role in fibrin generation. Significant impairment of hepatic synthetic function may result in the decreased production of any of these clotting factors despite normal vitamin K status.

Patients with liver disease or vitamin K deficiency initially have isolated prolongation of the PT resulting from a depletion of factor VII without any signs of clinically significant bleeding. Factor VII has the shortest half-life (6–10 hours) of the coagulation factors. In more severe deficiencies, the PTT can also be elevated because of depletion of factors II, IX, and X. A marked reduction in fibrinogen solely on the basis of decreased synthesis is an ominous sign and suggests very severe liver disease. Patients with long-standing liver disease develop portal hypertension, which may result in splenic pooling of platelets. A valuable assessment of liver synthetic function is the measurement of albumin or cholesterol.

In a patient with vitamin K deficiency and no evidence of active bleeding, observation with repletion of vitamin K is indicated. Vitamin K may be administered orally, subcutaneously, intramuscularly, or intravenously. Subcutaneous injection is not favored due to variable response and absorption. The fastest route is intravenous injection (1 mg/day), but this carries a risk of anaphylaxis and therefore should be done slowly and in a monitored setting. Oral vitamin k is given at a dose of 5–10 mg/day; improvement is usually seen within 24 hours.

The response to vitamin K may be poor in the presence of liver disease. Patients who fail to respond to vitamin K, who demonstrate increasing abnormalities of PT or PTT, or who are to undergo an invasive procedure may be treated with FFP infusions. Given the short half-life of factor VII, aggressive support with FFP every 6 hours in the perioperative period is generally necessary to produce sustained correction in clotting.

Massive Transfusion Syndrome

Massive transfusion syndrome results from the replacement of total body blood volume in less than 24 hours without the concomitant transfusion of platelets and FFP, usually in the setting of trauma. This situation leads to dilutional coagulopathy because stored RBCs contain no viable platelets and are usually deficient in coagulation factors. This dilution results in a clinical and laboratory picture resembling DIC. This diagnosis should be suspected in any patient who presents with bleeding, prolonged PT, prolonged PTT, and thrombocytopenia after receiving >5 units of blood. The key element in making the diagnosis is the transfusion history.

Treatment of this disorder is accomplished by replenishment of clotting factors and platelets through administration of FFP and platelet transfusions. The best treatment is prevention by transfusion of 1 unit of FFP and platelets for every 5 units of packed RBCs given. In individuals with continued or excessive blood loss, empirical treatment with FFP or platelets may be advisable. In the absence of uncontrolled or continued bleeding, it is acceptable to hold the use of FFP and platelets unless they are clinically indicated for postoperative bleeding.

Antiplatelet Therapy

The most commonly encountered antiplatelet medications include aspirin (ASA) and the P2Y ₁₂ receptor blocking agents (e.g., clopidogrel and prasugrel). See Table 4.3 for an overview of antiplatelet medications. These drugs are used for secondary prevention in patients with cerebrovascular, coronary, and peripheral vascular disease. Antiplatelet medications are also used after percutaneous coronary intervention (PCI) with placement of endovascular stent to prevent stent thrombosis.

ASA exerts its anticoagulant effect by irreversibly inhibiting platelet cyclooxygenase 1 (COX-1), which inhibits thromboxane A production and reduces platelet aggregation. This effect is irreversible and lasts for the life of the platelet, which is approximately 7 to 10 days. Therefore patients taking ASA who are undergoing an elective procedure should discontinue ASA for approximately 7–10 days before the procedure. The most common side effects of aspirin are gastrointestinal and can manifest as minor dyspepsia or major gastritis, ulcers, and bleeding.

The thienopyridines or P2Y ₁₂ receptor blockers target an integral ADP receptor on the surface of platelets. The thienopyridines include ticlopidine, clopidogrel, and prasugrel ( Table 4.4 ). This potent irreversible blockade prevents ADP-induced platelet aggregation. The thienopyridines can also cause gastrointestinal side effects, but also major hematologic complications (neutropenia, thrombocytopenia, and thrombotic thrombocyptopenic purpura). These major effects usually manifest within the first 3 months of initiation of these medications. P2Y ₁₂ receptor blockers should be stopped 5–7 days prior to a procedure to reduce the risk of bleeding.

Percutaneous coronary intervention is now very common in treatment of obstructive coronary artery disease. During PCI either bare metal stents (BMS) or DES are often placed. Dual antiplatelet therapy (DAPT) with ASA and a P2Y ₁₂ receptor blocker are used to decrease risk of stent thrombosis. Risk of stent thrombosis in the perioperative period is highest in the first 4–6 weeks after stent implantation. DES decrease the risk of re-stenosis but have longer periods of increased risk for in-stent thrombosis. The American College of Cardiology (ACC) and the American Heart Association (AHA) task force created practice guidelines in 2014 for perioperative cardiovascular management of patients undergoing noncardiac surgery. Elective noncardiac surgery should be delayed 14 days after PCI with balloon angioplasty (no stent placement), 30 days for BMS implantation, and 365 days after placement of a DES. Elective noncardiac surgery can be considered after 180 days if the risk of surgical delay is greater than the risk of ischemia or stent thrombosis. In patients undergoing urgent noncardiac surgery during the first 4–6 weeks after stent implantation (BMS or DES), DAPT should be continued if the risk of bleeding is not too great. If the bleeding risk is deemed too high, then ASA should be continued if possible and the PG2Y ₁₂ platelet receptor inhibitor should be restarted as soon as possible. The benefit of aspirin use in prevention of perioperative ischemic complications in a patient without previous cardiac stenting is unclear. The continuation of aspirin in a patient with a high-risk coronary artery disease or cerebrovascular disease with no history of coronary stenting may be reasonable if the risks of an ischemic event outweigh the risks of bleeding.

The American Urologic Association (AUA) and the International Consultation on Urological Diseases (ICUD) released a 2014 review paper covering anticoagulation and antiplatelet therapy in urologic practices. Some of the urology-specific recommendations regarding antiplatelet medication will be listed below. Patients with cardiac risk factors on low-dose aspirin by itself can continue the medication in the perioperative period without increased risk of bleeding. Patients taking low-dose aspirin without any specific indication can hold their aspirin for an elective procedure until directed to restart by the surgical team. Prostate biopsy can be performed safely on a patient taking low-dose aspirin, but with an increased risk of minor bleeding. In general, the continuation of aspirin for urologic procedures in the perioperative period is associated with a minor risk of increased bleeding without major consequences and is not associated with an increased risk of transfusion. Transurethral resection of the prostate, shockwave lithotripsy, and percutaneous renal surgery are probable exceptions to this rule.

Anticoagulation Therapy

Full-dose or therapeutic anticoagulation can be achieved with vitamin K antagonists (warfarin) or the novel oral anticoagulants (NOACs), which include direct thrombin inhibitors and factor Xa inhibitors. These medications are used to prevent thrombotic and thromboembolic events in high-risk patients and in treatment or prevention of deep venous thrombosis. Again, perioperative choices for the management of anticoagulation should be made in conjunction with other providers and must weigh the risks of bleeding against the risk of a thrombotic event.

Warfarin exerts its anticoagulant effect by inhibiting vitamin K–dependent procoagulation factors II, VII, IX, and X and anticoagulant proteins C and S. Warfarin’s effect usually occurs 2–3 days after initiation of therapy because of the prolonged half-life of the different procoagulant factors; factor II has the longest half-life (72 hours). In the past, the PT was used to measure the effect of warfarin, but because of variability in PT measurements the INR (international normalized ratio) is currently used. Most procedures can be performed safely when the INR is 1.4 or less. Warfarin is used in patients with prosthetic heart valves, atrial fibrillation, and a history of stroke as well as in preventing recurrent myocardial infarction and death in patients with an acute myocardial infarction. However, the most common indication for warfarin therapy is management of patients with VTE.

The NOACs are new alternatives to warfarin ( Table 4.5 ). These medications target thrombin or factor Xa directly and reversibly bind the active site of the coagulation factor. Unlike warfarin, the onset of action is rapid and routine monitoring is not required. These medications should be discontinued >48 hours prior to a procedure. A longer interval of discontinuation should be used in the setting of renal impairment. Routine monitoring of the levels of anticoagulation are not performed, but qualitative assessment of anticoagulation can be performed with prothrombin time for factor Xa inhibitors and activated partial thromboplastin time for direct thrombin inhibitors. Apixaban has a limited effect on PT; anti-factor Xa assays can be used to determine the anticoagulant activity. There are no current antidotes or reversal agents for these medications. A patient who is experiencing severe hemorrhage while taking a NOAC should be managed with fluid resuscitation and repletion of blood products by transfusion as needed. If the last dose of anticoagulant was taken within a 4–6 hour window, then activated charcoal may help reduce absorption. There is no substantial evidence to support the effectiveness of the use of procoagulant factors at this time. Dialysis may be used to remove dabigatran from the circulation but will not remove the highly protein bound rivaroxaban or apixaban.

Table 4.5

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