ONC O L O GY NURSING 101 DEBRA L. WINKELJ O HN , RN, MSN, AOCN®, CNS—ASS O CIATE ED IT O R At an Increased Risk: Tumor Lysis Syndrome Beth McGraw, RN, BSN, OCN® Patients at highest risk for tumor lysis hyperphosphatemia, hypocalcemia, and Gastrointestinal syndrome (TLS) often are diagnosed with hyperkalemia. Hyperuricemia occurs Hyperkalemia causes nausea, vomit- bulky, rapidly proliferating hematologic when the liver converts nucleic acids ing, and diarrhea (Cope, 2004). Anorexia, tumors, such as acute leukemia and non- into uric acid; hypocalcemia develops as abdominal cramping, and pain also may Hodgkin lymphoma (Kaplow & Hardin, serum calcium binds to elevated amounts occur because of the elevated potassium 2007). Patients with solid tumors, such of phosphorus within the bloodstream (McCance & Heuther, 2006). Decreased as mediastinal masses which are highly (Kaplow & Hardin). levels of serum calcium may cause in- sensitive to chemotherapy, also may de- testinal cramping and increased bowel velop TLS, although it is more common activity (McCance & Heuther). in patients undergoing treatment for leu- Clinical Findings kemia and lymphoma. TLS occurs from Laboratory findings will demonstrate the effect of chemotherapy or radiation electrolyte imbalances such as hyper- Cardiac on rapidly dividing cells. Patients with uricemia (more than 6.0 mg/dl), hyper- Serum potassium levels more than elevated lactic dehydrogenase (LDH), phosphatemia (more than 4.5 mg/dl), 5.3 mEq/l may cause irregular heart dehydration, and renal insufficiency are hypocalcemia (less than 8.5 mg/dl), and arrythmias and hypotension (Murphy- at greatest risk for developing TLS (Brant, hyperkalemia (more than 5.5 mEq/l) Ende & Chernecky, 2002). Often the 2002). Advances in cancer treatment, such (McCance & Heuther, 2006). Hyper- dysrhythmias are atrial in origin (Kaplow as those in bone marrow transplantation, kalemia generally is the first electro- & Hardin, 2007). Hyperkalemia causes require the use of high-dose chemother- lyte imbalance, followed by hyperphos- electrocardiogram changes such as tall T apy, which may demonstrate an increase phatemia, and leads to hypocalcemia and waves, flattened P waves, prolonged PR in the incidence of TLS. hyperuricemia (Agnani, Gupta, Atray, & intervals, widened QRS complexes, and TLS is a rapidly developing oncologic Vachharajani, 2006). Multisystem organ depressed ST segments (Murphy-Ende & emergency characterized by electrolyte failure may occur because of these meta- Chernecky). The presence of a prolonged and metabolic disturbances that are fatal bolic findings. TLS has the ability to affect QT interval may indicate hypocalcemia. without timely identification and man- the renal, gastrointestinal, cardiac, and agement. Patients present with hype- neuromuscular systems. Neuromuscular ruricemia, hyperphosphatemia, hypocal- cemia, and hyperkalemia. Electrolyte Renal Hyperkalemia causes neuromuscular disturbances can cause acute renal and irritability, muscle weakness, or paralysis, Hyperuricemia occurs when uric acid multisystem organ failure (see Figure 1). and hypocalcemia causes neuromuscular crystals and calcium phosphate salts excitability (McCance & Heuther, 2006). obstruct renal flow, causing renal failure A decreased level of serum calcium also Pathophysiology (Kaplow & Hardin, 2007). Patients will may cause seizures and tetany (McCance have increased uric acid and creatinine TLS occurs from the rapid release of & Heuther). levels, indicating renal failure. Physical intracellular components during cell symptoms consist of flank pain, gross death. Cancer cells have an abnormally hematuria, cloudy urine, oliguria, leth- Medical Management high amount of potassium, phosphorus, argy, nausea, and vomiting (Murphy-Ende and nucleic acid (Kaplow & Hardin, To prevent morbidity and mortality, & Chernecky, 2002). Weight gain and 2007). When cancer cells are destroyed early recognition and management of edema also may be present. by chemotherapy or radiation, they spill TLS are of primary concern. Patients at their intracellular components into the bloodstream, causing an influx of potassi- um, phosphorus, and nucleic acid which Beth McCraw, RN, BSN, OCN®, is a graduate nursing student in the clinical nurse specialist track the kidneys are not able to efficient- in the College of Health Sciences and Human Services at Murray State University in Kentucky. ly excrete, leading to hyperuricemia, Digital Object Identifier: 10.1188/08.CJON.563-565 Clinical Journal of Oncology Nursing • Volume 12, Number 4 • Oncology Nursing 101 563 through the kidneys (Brant, 2002). Maintain hydration by administration of normal or 1/2 normal saline at 3,000 ml/m2 Aggressive hydration and the addition per day of diuretics enhance urinary excre- Keep urine pH at 7.0 or greater by administration of sodium bicarbonate tion. IV solutions containing sodium Administer allopurinol at 300 mg/m2 per day bicarbonate help alkalinize urine, in- Monitor serum chemistry creasing uric acid solubility and, therefore, decreasing precipitation in the renal tubules (Kaplow & Hardin, 2007). Serial electrolyte monitoring is If, after 24–48 hours essential once treatment has begun. Electrolyte monitoring should begin prior to treatment initiation and then every 6–12 hours for early TLS iden- Serum uric acid > 8.0 mg/dl Serum uric acid < 8.0 mg/dl tification (Cantril & Haylock, 2004). Serum creatinine > 1.6 mg/dl Serum creatinine < 1.6 mg/dl Urine pH > 7.0 Although symptoms of TLS may occur up to seven days after initial treatment, pa- tients are at greatest risk during the first Correct treatable renal failure 6–48 hours (Gucalp & Dutcher, 2006). (obstruction) Start recombinant urate oxidase, Treatment Measures 0.2 mg/kg IV daily Depending on the severity of the Start chemotherapy electrolyte imbalance, medical manage- Discontinue bicarbonate ment will begin and treatment options administration Delay chemotherapy or start Monitor serum chemistry every initiated (see Table 1). Hyperkalemia is dialysis 6–12 hours managed with the use of sodium polysty- rene sulfonate, diuretics, IV glucose and insulin infusions, IV calcium gluconate, or dialysis (McCance & Heuther, 2006). If Hyperphosphatemia and hypocalcemia can be treated with IV 10% calcium gluconate, oral phosphate binders (alu- minum hydroxide), dietary restriction of Serum K+ > 6.0 mEq/L phosphorus intake, or dialysis (McCance Serum uric acid > 10 mg/dl & Heuther). Management of hyperuri- Serum creatinine > 10 mg/dl Serum phosphate > 10 mg/dl or increasing cemia consists of aggressive hydration Symptomatic hypocalcemia present with D5 1/2 normal saline (3–6 l/m2 per day), 50–100 mEq of sodium bicarbon- ate per liter for urinary alkalinization to keep the urine pH at 7–7.5, diuretics, Begin hemodialysis allopurinol 200–400 mg/m2 IV daily or 300–800 mg per day orally, or rasbu- ricase 0.20mg/kg IV daily (Brant, 2002). Figure 1. Patient Management for Tumor Lysis Syndrome Dialysis would be required if electrolyte Note. From Harrison’s Principles of Internal Medicine (17th ed., p. 1737), by A.S. Fauci, D.L. imbalances continued and renal failure Kasper, E. Braunwald, S.L. Hauser, D.L. Longo, J.L. Jameson, et al., 2008, New York: McGraw-Hill was imminent. Professional. Copyright 2008 by the McGraw-Hill Companies, Inc. Reprinted with permission. Nursing Management Identifying and initiating prevention increased risk for TLS should be identified Preventive Measures measures prior to the first course of early and preventive measures should be Before treatment begins, patients treatment for high-risk patients will help initiated prior to beginning treatment. are given allopurinal orally to prevent avoid TLS. Continued monitoring for At-risk patients often are diagnosed with uric acid formation. Although more side effects related to TLS is essential. acute leukemias, aggressive lymphomas, expensive than allopurinal, rasbu- Maintenance of IV fluids, strict intake and and solid tumors that are highly chemo- ricase also can be given as a pretreat- output monitoring, daily weights, and sensitive (Brant, 2002). Patients with ment one to two days prior to ther- continued assessment for fluid overload baseline renal failure and an elevated apy initiation. Rasburicase converts is required (Kaplow & Hardin, 2007). LDH are at greater risk for developing TLS uric acid into allantoin, which is more Nurses should be familiar with the signs prior to any cancer treatment. soluble in urine and easily excreted and symptoms of hyperuricemia, hyper- 564 August 2008 • Volume 12, Number 4 • Clinical Journal of Oncology Nursing and electrolyte imbalances is essential Table 1. Treatment Measures for Tumor Lysis Syndrome for early identification, treatment, and ELECTROLYTE imbalance Treatment management. Nurses must be competent in their ability to recognize high-risk Hyperkalemia Administration of sodium polystyrene sulfonate, IV diuretics, patients and the signs and symptoms, IV glucose or insulin infusions, IV calcium gluconate, or dialysis treatment options, and management of (McCance & Heuther, 2006) TLS. Nurses are instrumental in prevent- Hyperphosphatemia Infusion of IV 10% calcium gluconate, oral phosphate binders ing morbidity and mortality for patients and hypocalcemia such as aluminum hydroxide, dietary restriction of phosphorus at risk of or suffering from TLS. intake, or dialysis (McCance & Heuther, 2006) Author Contact: Beth McCraw, RN, BSN, Hyperuricemia Aggressive hydration with dopamine receptor-5 1/2 normal saline ® (3–6 l/m2