# A 5-year-old child with hemolytic-uremic syndrome (HUS) is admitted to the pediatric intensive care unit. The child has oliguria, hypertension, and laboratory results showing hemoglobin 6.2 g/dL, platelet count 45,000/mm³, and elevated BUN and creatinine. Which nursing intervention should be the highest priority?

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## 문제

A 5-year-old child with hemolytic-uremic syndrome (HUS) is admitted to the pediatric intensive care unit. The child has oliguria, hypertension, and laboratory results showing hemoglobin 6.2 g/dL, platelet count 45,000/mm³, and elevated BUN and creatinine. Which nursing intervention should be the highest priority?

## 보기

1. Encourage increased fluid intake to prevent dehydration
2. Administer aspirin for fever and discomfort management
3. Provide a high-protein diet to support kidney function
4. Monitor for signs of neurological complications and seizures **✔ 정답**

**정답: 4**

## 해설

Neurological monitoring is the highest priority due to the risk of cerebral edema and seizures in HUS patients. Other interventions are less critical or contraindicated in this acute setting.

## 심화 해설

Understanding the Priority in Hemolytic-Uremic Syndrome (HUS)

The clinical presentation of this 5-year-old child—oliguria, hypertension, severe anemia (hemoglobin 6.2 g/dL), thrombocytopenia (platelet count 45,000/mm³), and elevated BUN and creatinine—is classic for Shiga toxin-producing Escherichia coli hemolytic uremic syndrome (STEC-HUS). While HUS is widely recognized as a leading cause of acute kidney injury in children, the systemic nature of the disease means the toxin-mediated endothelial injury is not confined to the renal vasculature [1]. The highest priority nursing intervention must address the most life-threatening potential complication that requires immediate recognition and intervention.

Why Neurological Monitoring is the Priority

The correct answer is to monitor for signs of neurological complications and seizures. The rationale is rooted in the pathophysiology of STEC-HUS. Shiga toxins circulate and bind to globotriaosylceramide (Gb3) receptors, which are highly expressed not only on renal endothelial cells but also on the microvasculature of the brain. This leads to thrombotic microangiopathy in the central nervous system (CNS), manifesting as a spectrum of extrarenal complications. Neurological involvement is one of the most serious and common extrarenal manifestations of STEC-HUS, and it can present acutely with altered mental status, seizures, or focal neurological deficits [1]. Because these CNS events can deteriorate rapidly, leading to irreversible brain injury or death, continuous and vigilant neurological assessment is the nurse's highest priority for early detection and timely escalation of care.

Analyzing the Incorrect Options

Option 1: Encourage increased fluid intake to prevent dehydration

This intervention is contraindicated. The child is in acute kidney injury, evidenced by oliguria and elevated BUN/creatinine. The kidneys are unable to effectively excrete fluid. Encouraging fluid intake would worsen fluid overload, exacerbating hypertension and increasing the risk of pulmonary edema and heart failure. Management in the oliguric phase typically involves strict fluid restriction, not encouragement of intake.

Option 2: Administer aspirin for fever and discomfort management

This is dangerous. The child has severe thrombocytopenia with a platelet count of 45,000/mm³. Aspirin impairs platelet function through irreversible cyclooxygenase inhibition, which would compound the existing bleeding risk. Antipyretics with minimal effects on platelet function, such as acetaminophen, would be the preferred agent if needed, but pain and fever management do not supersede the priority of detecting life-threatening CNS complications.

Option 3: Provide a high-protein diet to support kidney function

This intervention is not appropriate during the acute phase of HUS. In the setting of acute kidney injury with elevated BUN and creatinine, protein intake is typically restricted, not increased. A high-protein diet would increase the production of nitrogenous waste products, which the injured kidneys cannot clear, further elevating the BUN and worsening uremia. The immediate nutritional focus is on providing adequate calories while restricting protein, fluids, and electrolytes like sodium and potassium.

Connecting to the Evidence

The study by Alconcher et al. explicitly highlights that STEC-HUS is a systemic disease where extrarenal complications, particularly neurological ones, are a major concern and can lead to long-term sequelae [1]. The research underscores the need for clinicians to look "beyond the kidney" during the acute phase. Furthermore, the study by Jarosz-Wójcik et al. reinforces the assessment of complications and outcomes in pediatric HUS, confirming that the disease course involves multiple organ systems and requires comprehensive monitoring for complications beyond the renal system . These findings directly support prioritizing the detection of neurological involvement, as it represents an immediate, life-threatening extrarenal manifestation that demands constant nursing vigilance.References (research sources)

- [1]Beyond the kidney: prevalence of extrarenal complications and their long-term sequelae in Shiga toxin-producing Escherichia coli hemolytic uremic syndrome.Research articleAlconcher LF, Lucarelli LI, Bronfen S, Villarreal F. (2026) · DOI: 10.1007/s00467-026-07376-6

## 임상 시나리오

HUS Neurological MonitoringPrioritizing Extrarenal Complications in STEC-HUS
In Shiga toxin-producing E. coli HUS, Shiga toxin binds to Gb3 receptors on CNS endothelium, causing thrombotic microangiopathy. This makes neurological involvement the most critical extrarenal threat.

Perform frequent neurological checks (level of consciousness, pupillary response, motor strength) at least every 1-2 hours. Monitor for subtle changes: irritability, confusion, visual disturbances, or seizure activity.

CautionDo not administer antiplatelet agents like aspirin due to severe thrombocytopenia. Avoid aggressive fluid resuscitation in the setting of oliguria and hypertension to prevent pulmonary edema.

## 핵심 개념

- **Hemolytic-Uremic Syndrome (HUS)** — A clinical syndrome characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury, most commonly caused by Shiga toxin-producing E. coli.
- **Thrombotic Microangiopathy** — A pathological process involving endothelial injury and microvascular thrombosis, leading to organ damage in conditions like HUS.
- **Oliguria** — Reduced urine output (typically
- **Globotriaosylceramide (Gb3)** — A cell surface receptor for Shiga toxin, highly expressed on renal and CNS endothelial cells, explaining the organ tropism in STEC-HUS.

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