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Chapter 159 Hematologic Problems in the Surgical Patient 2309
100,000/µL for high-risk surgery is usually appropriate. The optimal endothelial function, the pathophysiology of uremic bleeding is
duration of postoperative platelet support has not been carefully complicated by the comorbidities in this patient population, such as
studied, but even for moderate- or high-risk surgery, platelets may be vascular disease and hypertension, and the medical treatment of those
needed for less than 1 week because they are principally required for conditions. 96
primary hemostasis. The platelet count should be monitored closely
during the postoperative period, with the expectation that platelet
survival will be shortened by infection, fever, or bleeding. In addition, Liver Disease
platelet transfusion may be indicated for surgical patients despite an
apparently adequate count in the presence of known or suspected Hemostatic alterations in patients with acute or chronic liver disease
platelet dysfunction, antiplatelet therapy, and microvascular bleeding. (see Chapter 153) are complex and involve both procoagulant and
When thrombocytopenia is caused by increased platelet destruc- anticoagulant pathways. 97,98 Although patients with liver disease are
tion (e.g., immune thrombocytopenic purpura), prophylactic platelet typically felt to have deficient hemostasis, this concept has been
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transfusion is largely ineffective and is indicated only for active, challenged in the recent literature. These patients are not “autoan-
serious bleeding. In preparation for surgery, therapy with steroids ticoagulated”, as often assumed. In fact, they are not protected from
and/or intravenous γ-globulin often will increase the platelet count and may even be at increased risk for thrombosis, particularly in the
to a satisfactory level so that transfusion is not needed. Rho(D) portal venous system. 100-102 The presence of genetic thrombophilic
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immunoglobulin (WinRho ) may also be useful in this setting. mutations may further increase this risk. The procoagulant tendency
associated with chronic liver disease 103,104 suggests that prophylaxis
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against VTE may be warranted in high-risk situations. However,
Platelet Dysfunction the perceived bleeding risk often limits the use of prophylaxis, and
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appropriately designed pharmacologic clinical studies are clearly
Patients with platelet dysfunction represent a large group for whom needed. 100
preoperative consultation is sought, typically because of an abnormal Patients with severe decompensated liver disease and markedly
bleeding history or the discovery of a prolonged bleeding time or abnormal coagulation test results are at increased risk for bleeding,
other laboratory assessment of platelet function with a normal platelet and surgery should be avoided except as a lifesaving measure. In
count. Drugs are the most common cause of acquired platelet dys- evaluating hemostasis in patients with less severe disease, the PT/INR
function. Many commonly used types of medications, including and aPTT may be good indicators of decreased synthesis of clotting
aspirin and other nonsteroidal antiinflammatory drugs, antibiotics, factors and vitamin K deficiency, but they are poor predictors of
antidepressants (selective serotonin reuptake inhibitors), cardiovascu- bleeding risk. Several studies have shown the failure of the PT/INR
lar drugs, and newer antiplatelet agents, including ADP receptor, and aPTT to predict bleeding after liver biopsy. 106,107 Similarly, pre-
GPIIb/IIIa or protease-activated receptor antagonists, can cause operative hemostatic testing has generally not been shown to be
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platelet dysfunction. Ethanol as well as certain foods and herbal useful for predicting bleeding during liver transplantation. A study
supplements can also inhibit platelets; a careful history is therefore in patients with liver disease found that INR values in the range of
essential. Any drugs that interfere with platelet function should be 1.3–2.0 generally correspond to levels of factors II, V, and VII that
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reviewed before surgery and an assessment of their ongoing use be are adequate for hemostasis. A preoperative platelet count is needed
carefully considred. to identify thrombocytopenia, and some assessment of platelet func-
A number of medical conditions can cause acquired platelet tion may be useful to determine whether platelet function is abnormal
dysfunction. The etiology may be fairly obvious in cases of renal or in the setting of a normal or near-normal platelet count. A thrombin
liver disease, myeloproliferative disorders, leukemia, myelodysplastic time or fibrinogen level should also be performed to evaluate for
syndromes, or dysproteinemia, but consideration of undiagnosed dysfibrinogenemia. Tests for fibrinogen/fibrin degradation products,
intrinsic platelet defects (storage pool disease or platelet release D-dimer, euglobulin clot lysis time or thromboelastography may be
defects) or von Willebrand disease may be necessary. Treatment of useful in evaluating for disseminated intravascular coagulation (DIC)
the underlying disease is the most effective approach, if possible. If or accelerated fibrinolysis.
not, platelet transfusion may be indicated, but the dose required to In patients with mild liver disease and mild-moderate INR pro-
achieve hemostasis is difficult to predict and depends in part on the longation (<2.0), serious surgical bleeding is unlikely in the absence
severity of the underlying platelet abnormality. As discussed earlier, of other hemostatic abnormalities, and prophylactic intervention is
treatment with DDAVP may be appropriate in selected patients. The rarely required for low- or moderate-risk surgery. For high-risk
exact mechanism of action of DDAVP in acquired platelet dysfunc- surgery or for patients with markedly abnormal coagulation tests,
tion is not well understood, but one study suggests that DDAVP transfusion of fresh-frozen plasma is the most commonly used
interacts directly with platelets and exerts a priming effect on platelet approach for correcting the coagulation abnormality, although pro-
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aggregation stimulated by ADP or collagen. Expression of GPIb and spective studies demonstrating the value of fresh-frozen plasma
GPIIb/IIIa on platelet membranes is also enhanced following admin- administration in this setting are lacking. There are, however, guide-
istration of DDAVP. 39 lines that caution against the indiscriminate use of plasma before
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invasive procedures. It should be noted that the PT of fresh-frozen
plasma is approximately 15 s, which corresponds to an INR of 1.5,
Renal Disease so complete correction of the PT/INR is unlikely to be achieved.
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Administration of platelets should be considered for more severe
Impaired hemostasis has long been recognized in patients with degrees of thrombocytopenia, although recovery will be decreased in
chronic renal failure and is discussed in greater detail in Chapter 154. the presence of splenomegaly. Administration of DDAVP may be
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The pathogenesis is multifactorial but is due in large part to altera- useful for correcting abnormal platelet function in some cases.
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tions in platelet function. Anemia also contributes to platelet dys- Intravenous administration of 5–10 mg vitamin K will usually
function in chronic renal failure. Red blood cells release ADP, which shorten the PT/INR if vitamin K deficiency is a contributory factor.
in turn inactivates vascular prostacyclin, an inhibitor of platelet func- Antifibrinolytic agents also may be useful for the reduction of peri-
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tion. Correction of anemia, now routinely accomplished through operative hemorrhage in patients with liver disease.
the use of recombinant erythropoietin, also improves the rheologic
factors that facilitate platelet interaction with the vessel wall. An
increase in hematocrit, whether by the use of erythropoietin or INTRAOPERATIVE AND POSTOPERATIVE BLEEDING
transfusion, is accompanied by significant shortening of the bleeding
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time and improvement of platelet adhesion. In addition to platelet Patients with excessive bleeding during or after surgery require rapid
dysfunction and altered balance between mediators of normal evaluation and treatment. The first step is to distinguish between

