# A nurse is caring for a client with acute myeloid leukemia (AML) who has developed tumor lysis syndrome following chemotherapy initiation. The client's laboratory results show: potassium 7.2 mEq/L, phosphorus 9.0 mg/dL, calcium 6.8 mg/dL, and uric acid 14.0 mg/dL. Which nursing intervention should be the priority?

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## 문제

A nurse is caring for a client with acute myeloid leukemia (AML) who has developed tumor lysis syndrome following chemotherapy initiation. The client's laboratory results show: potassium 7.2 mEq/L, phosphorus 9.0 mg/dL, calcium 6.8 mg/dL, and uric acid 14.0 mg/dL. Which nursing intervention should be the priority?

## 보기

1. Administer calcium gluconate as prescribed to correct hypocalcemia
2. Increase fluid intake to promote uric acid excretion through the kidneys
3. Prepare for immediate cardiac monitoring and potential emergency interventions for hyperkalemia **✔ 정답**
4. Administer phosphate binders to reduce elevated phosphorus levels

**정답: 3**

## 해설

Tumor lysis syndrome is a life-threatening oncological emergency. The priority intervention is cardiac monitoring for hyperkalemia (K+ 7.2 mEq/L), as severe hyperkalemia can cause fatal cardiac arrhythmias. Other interventions like fluid intake or phosphate binders are important but secondary to managing the immediate cardiac risk.

## 심화 해설

Understanding the Priority in Tumor Lysis Syndrome

The client’s laboratory values reveal the classic metabolic derangements of tumor lysis syndrome (TLS): severe hyperkalemia (potassium 7.2 mEq/L), hyperphosphatemia (phosphorus 9.0 mg/dL), hypocalcemia (calcium 6.8 mg/dL), and hyperuricemia (uric acid 14.0 mg/dL). TLS is an oncologic emergency characterized by severe metabolic derangements resulting from rapid tumor cell breakdown, which releases massive amounts of intracellular contents into the bloodstream [1]. When prioritizing nursing interventions, the immediate threat to life is the most critical consideration.

A potassium level of 7.2 mEq/L constitutes a life-threatening emergency due to its direct effect on cardiac electrophysiology. Hyperkalemia-induced arrhythmias can be rapidly fatal, and prompt recognition and treatment is vital [2]. The elevated potassium alters the resting membrane potential of cardiac cells, leading to a progression of ECG changes from peaked T-waves to widened QRS complexes, and ultimately to ventricular fibrillation or asystole. The simulation-based literature emphasizes that severe hyperkalemia in TLS, if untreated, may lead to renal failure, arrhythmias, or multi-organ failure [2]. Therefore, preparing for immediate cardiac monitoring and potential emergency interventions—such as administering intravenous calcium gluconate to stabilize the cardiac membrane (which is distinct from correcting the potassium level itself) and initiating therapies to shift potassium—is the absolute priority.

While the other options address real and significant TLS abnormalities, they do not target the most immediate threat. Administering calcium gluconate (Option 1) is a critical component of treating hyperkalemia’s cardiac effects, but the stated goal of "correcting hypocalcemia" is a secondary concern. The hypocalcemia in TLS is a direct consequence of hyperphosphatemia, as calcium binds to the excess phosphorus; the priority is to manage the life-threatening hyperkalemia, and calcium gluconate given for cardiac membrane stabilization serves that purpose, not primarily to normalize the serum calcium. Increasing fluid intake (Option 2) is essential for promoting uric acid excretion and preventing acute kidney injury, a known complication of TLS [1], but it does not provide immediate protection against a fatal arrhythmia. Administering phosphate binders (Option 4) is a longer-term strategy to lower phosphorus levels, which will secondarily help correct hypocalcemia, but it has no immediate impact on the hyperkalemia that poses a clear and present danger. The clinical reasoning must follow the "ABC" (Airway, Breathing, Circulation) framework, where a potassium-induced cardiac conduction defect is a direct threat to circulation.References (research sources)

- [1]When Rapid Response Becomes Catastrophic: Tumor Lysis Syndrome Following Cisplatin-Etoposide Therapy in Extensive-Stage Small Cell Lung Cancer.Research articleCruz Figueroa NA, Martinez Arroyo G, Martinez Ruiz G, Rivera JC, Delgado P, Hernandez M, Torres Cintron J. (2026) · DOI: 10.7759/cureus.109632

- [2]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

Tumor Lysis Syndrome: Emergency Priority SettingIdentifying and managing the most immediate life threat
In TLS, the priority intervention targets the most immediately fatal abnormality. A potassium level of 7.2 mEq/L represents severe hyperkalemia with a high risk of cardiac arrest.

The first action is immediate cardiac monitoring and preparing for emergency interventions. Administering IV calcium gluconate or calcium chloride is the critical first drug therapy to stabilize the cardiac membrane, preventing ventricular fibrillation.

CautionIV calcium does not lower the serum potassium level; it only protects the heart. Definitive treatments like insulin and dextrose, beta-agonists, or dialysis must follow immediately to shift or remove potassium.

## 핵심 개념

- **Tumor Lysis Syndrome** — An oncologic emergency characterized by severe metabolic derangements (hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia) resulting from rapid tumor cell breakdown after chemotherapy.
- **Hyperkalemia** — An elevated serum potassium level; a level >7.0 mEq/L is a life-threatening emergency due to the risk of fatal cardiac arrhythmias.
- **Cardiac Membrane Stabilization** — An emergency intervention for severe hyperkalemia using intravenous calcium gluconate or calcium chloride to protect the heart, which does not lower the serum potassium level.

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