Bleeding and/or thrombosis may occur as a result of a decrease in or imbalance of coagulation factors such as fibrinogen; factors II, VI, VII, and VIII; antithrombin III; and protein-C. Although routine laboratory values such as prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, antithrombin III, and/or protein-C are often monitored, there are no standard or reliable parameters for predicting or preventing complications related to coagulatory alterations. In an effort to address thromboembolic complications, a study was conducted to evaluate the role of fresh frozen plasma.10 Findings did not support improved plasma levels of coagulation proteins.10 Treating low fibrinogen levels with cryoprecipitate is controversial. In the absence of bleeding, there is no documented clinical benefit.
Hyperglycemia may be noted following the asparaginase administration due to a decreased serum concentration of insulin. Because concomitant use of high-dose corticosteroids is common, determining the exact etiology of elevated glucose levels may be difficult. Monitoring blood glucose levels along with careful dosing of insulin is necessary to avoid hypoglycemia upon recovery of the synthesis of endogenous insulin.
Hypoalbuminemia, caused by a decrease in albumin production, may result in third spacing of fluid with mild peripheral edema to massive anasarca (in rare instances). Cholesterol-carrying proteins may also be depressed, resulting in hyperlipidemia. This may be evidenced by a milky white substance noted when drawing a blood sample, and the elevated lipids may hinder laboratory evaluation.
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Hepatic toxicities usually resolve spontaneously, allowing the patient to continue chemotherapy.5 Elevated AST, ALT, and bilirubin levels are common during treatment with asparaginase, especially when administered in combination with other antineoplastic agents. Other supportive therapies such as antibiotics also increase the risk of hepatic toxicity. However, severe hepatic dysfunction is rare.
Acute pancreatitis occurs in 2% to 5% of patients.11 Symptoms may be mild and noted only as some nausea, anorexia, and/or vomiting. Abdominal pain may be mild to severe. In rare instances, pancreatitis may progress to hemorrhagic pancreatitis and pseudocyst formation. Lipase and amylase levels may not be elevated due to decreased protein synthesis; therefore, routine monitoring of lipase and amylase levels may have little to no benefit. The actual etiology has not been identified. The hemorrhagic component may implicate an association with coagulopathy issues. Any patient who develops symptomatic pancreatitis should not receive further doses of asparaginase. Treatment is the same as pancreatitis from any cause; it is based on the severity of symptoms and consists of bowel rest, IV fluids, nutrition support, and pain management.
Neurologic symptoms such as headache, lethargy, and somnolence were reported in patients receiving asparaginase. These symptoms are more common in adult patients. Although many patients receiving asparaginase may have elevated ammonia levels, a correlation between ammonia levels and degree of toxicity has not been made.11
CONCLUSION
Asparaginase therapy presents a challenge for the oncology nurse both during and after administration. Comprehensive patient education and astute clinical assessment are imperative when managing treatment of patients with ALL who are receiving complicated and intensive chemotherapy regimens. These components provide the patient with the best opportunity to survive treatment, allow for the possibility of achieving remission, and ultimately, hope for cure. ONA
Barbara Tripp works at the Cleveland Clinic, Cleveland, Ohio.
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