# A nurse is caring for a 60-year-old patient with non-Hodgkin lymphoma who develops tumor lysis syndrome after starting rituximab. Which nursing intervention should be the highest priority?

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## 문제

A nurse is caring for a 60-year-old patient with non-Hodgkin lymphoma who develops tumor lysis syndrome after starting rituximab. Which nursing intervention should be the highest priority?

## 보기

1. Administer IV normal saline and monitor urine output closely **✔ 정답**
2. Prepare for immediate hemodialysis now
3. Administer calcium gluconate for hypocalcemia
4. Give allopurinol to reduce uric acid levels

**정답: 1**

## 해설

The highest priority is aggressive IV hydration with normal saline to maintain urine output and prevent acute kidney injury from uric acid and phosphate crystallization in tumor lysis syndrome. Other interventions (hemodialysis, calcium gluconate, allopurinol) may be needed but are not the immediate priority.

## 심화 해설

Understanding Tumor Lysis Syndrome (TLS) Pathophysiology

When cytotoxic therapy (like rituximab-containing regimens) rapidly kills malignant cells in hematologic cancers such as non-Hodgkin lymphoma, intracellular contents—potassium, phosphate, and nucleic acids—are released into the bloodstream in massive quantities. Nucleic acids are metabolized to uric acid, leading to hyperuricemia, hyperkalemia, and hyperphosphatemia with secondary hypocalcemia. These metabolic derangements can precipitate acute kidney injury (AKI), cardiac arrhythmias, and multiorgan failure [1]. The case report on bendamustine-rituximab in CLL emphasizes that even first-cycle therapy in patients with high disease burden can trigger severe TLS with AKI, underscoring the need for aggressive prophylaxis and close monitoring during early treatment [1].

Priority Nursing Intervention: Rationale

The highest priority intervention is aggressive IV hydration with normal saline and strict monitoring of urine output. This approach directly targets the most critical pathophysiologic mechanism of TLS-related renal injury: uric acid and calcium phosphate crystal deposition in renal tubules. Vigorous hydration promotes high urine flow, which mechanically flushes these crystals and dilutes nephrotoxic solutes, thereby preventing or mitigating AKI. Maintaining adequate renal perfusion and urine output also facilitates excretion of potassium and uric acid, reducing the risk of life-threatening hyperkalemia-induced arrhythmias [3]. The simulation case on pediatric spontaneous TLS highlights that prompt recognition of hyperkalemia is vital because it can rapidly progress to renal failure or fatal arrhythmias, making preservation of renal function through hydration the cornerstone of immediate management [3].

Why Other Options Are Not the Highest Priority

- Preparing for immediate hemodialysis (Option 2) is reserved for patients with refractory hyperkalemia, severe fluid overload unresponsive to diuretics, or symptomatic uremia. While dialysis is a definitive rescue therapy, it is not the first-line nursing priority when the patient first develops TLS; initial management focuses on aggressive hydration and pharmacologic measures to prevent the need for dialysis.

- Administering calcium gluconate (Option 3) is indicated to stabilize the cardiac membrane in the presence of hyperkalemia-induced ECG changes or arrhythmias. However, hypocalcemia in TLS is typically secondary to hyperphosphatemia, and routine calcium administration without addressing the underlying hyperphosphatemia can increase the risk of calcium-phosphate precipitation in tissues. It is not the primary preventive or initial intervention.

- Giving allopurinol (Option 4) reduces uric acid production by inhibiting xanthine oxidase, but it does not degrade existing uric acid and takes time to lower serum levels. A real-world study comparing anti-hyperuricemic therapies in hematologic malignancies found that rasburicase (which rapidly breaks down existing uric acid) may be associated with differences in TLS-related mortality, but allopurinol alone is insufficient as the sole immediate intervention once TLS is established . Hydration remains the foundational step, often initiated concurrently with hypouricemic agents.

Clinical Application and Monitoring

For a patient developing TLS after rituximab, the nurse should initiate IV normal saline at rates typically ranging from 200 to 250 mL/hour, with the goal of maintaining urine output at or above 2 mL/kg/hour. Strict intake and output monitoring, daily weights, and frequent assessment of serum electrolytes (potassium, calcium, phosphate), uric acid, and creatinine are essential. Cardiac monitoring is critical to detect early signs of hyperkalemia, such as peaked T-waves or widened QRS complexes [3]. The case report on bendamustine-rituximab reinforces that individualized prophylaxis, patient education about symptoms, and close monitoring during the early cycles of therapy are essential to prevent progression to multiorgan failure [1].References (research sources)

- [1]Life-Threatening Acute Tumor Lysis Syndrome With Multiorgan Failure Following First Cycle of Bendamustine-Rituximab in Chronic Lymphocytic Leukemia: A Case Report and Brief Review.Case reportGaruma MT, Begna KH, Amare TB, Desta MK, Leilago DS, Ahmed HM. (2026) · DOI: 10.1002/ccr3.72548

- [3]Recognition and Management of Hyperkalemia-Induced Tachyarrhythmia in Pediatric Spontaneous Tumor Lysis Syndrome: A Simulation Case.Research articleSoliman YH, Kochhar M, Petrone G, Wing R, Sojar SH. (2026) · DOI: 10.7759/cureus.107494

## 임상 시나리오

TLS Priority ManagementAggressive Hydration & Output Monitoring
The highest priority for Tumor Lysis Syndrome (TLS) is to prevent acute kidney injury (AKI) caused by uric acid and calcium phosphate crystal deposition in renal tubules. Initiate aggressive IV normal saline to achieve a urine output of at least 2 mL/kg/hr.

Strict intake and output monitoring is essential to assess renal perfusion and response to hydration. High urine flow mechanically flushes nephrotoxic crystals and dilutes solutes, facilitating excretion of potassium and uric acid.

CautionDo not administer calcium gluconate for asymptomatic hypocalcemia in the presence of hyperphosphatemia; this can worsen metastatic calcification. Reserve hemodialysis for refractory hyperkalemia, severe acidosis, or fluid overload unresponsive to hydration.

## 핵심 개념

- **Tumor Lysis Syndrome (TLS)** — An oncologic emergency caused by rapid tumor cell death releasing intracellular contents, leading to hyperuricemia, hyperkalemia, hyperphosphatemia, and secondary hypocalcemia.
- **Acute Kidney Injury (AKI) in TLS** — Renal damage primarily caused by uric acid crystal nephropathy and calcium phosphate deposition in renal tubules, preventable with aggressive hydration.
- **Rituximab** — A monoclonal antibody targeting CD20 used in B-cell non-Hodgkin lymphoma that can induce rapid cell lysis and trigger TLS.
- **Allopurinol** — A xanthine oxidase inhibitor used prophylactically to reduce uric acid production, but ineffective against pre-formed uric acid in established TLS.

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