# The nurse is monitoring a client who received cisplatin chemotherapy 48 hours ago and is now experiencing multiple side effects. Which assessment finding requires the most immediate nursing intervention?

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## 문제

The nurse is monitoring a client who received cisplatin chemotherapy 48 hours ago and is now experiencing multiple side effects. Which assessment finding requires the most immediate nursing intervention?

## 보기

1. Serum creatinine level of 3.2 mg/dL with decreased urine output **✔ 정답**
2. Mild nausea and vomiting controlled with antiemetics
3. Tinnitus and slight hearing loss in high frequencies
4. Numbness and tingling in fingers and toes

**정답: 1**

## 해설

A serum creatinine of 3.2 mg/dL with decreased urine output indicates acute kidney injury, a life-threatening cisplatin side effect requiring immediate intervention. Other options represent less urgent side effects.

## 심화 해설

Clinical Reasoning & Priority Setting

When caring for a client receiving cisplatin, the nurse must recognize that nephrotoxicity is a dose-limiting and potentially life-threatening adverse effect. The assessment finding that demands the most immediate intervention is a serum creatinine level of 3.2 mg/dL accompanied by decreased urine output. This presentation signals acute kidney injury (AKI), which can rapidly progress to fluid overload, electrolyte imbalances, and irreversible renal damage if not promptly addressed.

Pathophysiology of Cisplatin Nephrotoxicity

Cisplatin accumulates in renal tubular epithelial cells, where it triggers a cascade of intracellular injury. The primary mechanisms involve mitochondrial damage, oxidative stress, and activation of apoptotic pathways, leading to tubular cell death and loss of renal function [1][2][3]. Research demonstrates that cisplatin disrupts mitophagy, the selective autophagic degradation of damaged mitochondria, which is a critical quality-control process for cellular survival [1][2]. When mitophagy is impaired, dysfunctional mitochondria accumulate, releasing pro-apoptotic factors that accelerate tubular epithelial injury [1][2]. This mitochondrial catastrophe directly reduces the kidney's ability to filter blood, resulting in a rapid rise in serum creatinine and a decline in urine output. The elevation in creatinine to 3.2 mg/dL reflects a substantial loss of glomerular filtration, placing the client at immediate risk for complications such as hyperkalemia, metabolic acidosis, and pulmonary edema.

Analysis of Other Options

- **Option 2 (Mild nausea and vomiting controlled with antiemetics):** While nausea and vomiting are common acute toxicities of cisplatin, the key descriptor is that symptoms are "controlled." This indicates the current antiemetic regimen is effective, and the situation, though requiring continued monitoring, does not represent a physiological emergency.

- **Option 3 (Tinnitus and slight hearing loss in high frequencies):** This finding is consistent with ototoxicity, a known adverse effect of cisplatin caused by damage to cochlear hair cells. It is a serious concern that warrants an audiology referral and patient education about safety, but it is not acutely life-threatening and does not take priority over a failing organ system.

- **Option 4 (Numbness and tingling in fingers and toes):** This describes a peripheral sensory neuropathy, a common dose-related toxicity of cisplatin. The "stocking-glove" distribution of paresthesia is a chronic, progressive condition that impacts quality of life and requires safety interventions to prevent falls and injury. However, it does not pose the same immediate threat to homeostasis as acute kidney injury.

Nursing Priority & Clinical Connection

Applying the ABC (Airway, Breathing, Circulation) and safety frameworks, renal function is tightly linked to "Circulation" and fluid/electrolyte balance. A serum creatinine of 3.2 mg/dL with oliguria is a critical laboratory and physical assessment finding that demands immediate collaboration with the healthcare provider. The nurse's priority interventions include strict intake and output monitoring, daily weights, assessment for signs of fluid overload, and withholding any further nephrotoxic agents until the renal function is evaluated. The underlying mechanism, as supported by current research, is a profound disruption of mitochondrial quality control and induction of apoptosis in the proximal tubules, which can be further exacerbated by inflammatory cytokines and oxidative stress [3]. Recognizing this cluster of findings as a hallmark of cisplatin-induced AKI allows the nurse to act swiftly to prevent irreversible renal damage.

References (research sources)

- [1]Docosahexaenoic acid attenuates cisplatin nephrotoxicity by restoring mitophagy.Research articleZhuang Y, Zuo Z, Yang C, Li S, Liu H, Jing K. (2026) · DOI: 10.1038/s41598-026-62168-0

- [2]Carnosic acid alleviates cisplatin-induced acute kidney injury by enhancing prohibitin 2-dependent mitophagy.Research articleChen Y, Xu C, Chen Y, Liu Q, Yin W. (2026) · DOI: 10.1016/j.taap.2026.117887

- [3]Quinic acid attenuates cisplatin-induced acute kidney injury by modulating inflammatory cytokines, oxidative stress, apoptosis, and the Nrf2/HO-1/NQO1 pathway in rats.Research articleGoudarzi M, Lamoochi Z, Sabbagh S, Zamani AM, Mousavi Salehi A. (2026) · DOI: 10.1080/08923973.2026.2705914

## 임상 시나리오

Cisplatin-Induced NephrotoxicityEarly Recognition and Immediate Intervention for Acute Kidney Injury
The most critical assessment finding is a serum creatinine of 3.2 mg/dL with decreased urine output, indicating acute kidney injury (AKI). This is a dose-limiting toxicity requiring immediate intervention to prevent irreversible damage.

Cisplatin accumulates in renal tubular cells, causing mitochondrial damage and oxidative stress. This leads to tubular cell death and a rapid decline in glomerular filtration rate (GFR), reflected by rising creatinine and oliguria.

CautionPrioritize AKI over other toxicities like ototoxicity or neuropathy. Ensure aggressive IV hydration before, during, and after cisplatin infusion as a key preventive measure. Monitor strict intake and output and daily weights.

## 핵심 개념

- **Cisplatin Nephrotoxicity** — A dose-limiting adverse effect where cisplatin accumulation in renal tubules causes mitochondrial damage, oxidative stress, and apoptosis, leading to acute kidney injury.
- **Acute Kidney Injury (AKI)** — An abrupt loss of kidney function characterized by a rise in serum creatinine and/or decrease in urine output, which can lead to fluid overload and electrolyte imbalances.
- **Dose-Limiting Toxicity** — A side effect of a drug that is severe enough to prevent an increase in dose or requires a reduction in dose, often determining the maximum tolerated dose.
- **Ototoxicity** — Damage to the inner ear or auditory nerve caused by certain drugs like cisplatin, often presenting initially as high-frequency hearing loss and tinnitus.
- **Peripheral Neuropathy** — A result of damage to peripheral nerves, commonly caused by cisplatin, manifesting as numbness, tingling, and pain in a stocking-glove distribution.

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