# A 45-year-old patient with traumatic brain injury in the ICU develops hyperthermia with a temperature of 104°F (40°C) over 2 hours, despite normal environmental conditions. The patient is unconscious, has increased intracranial pressure, and shows signs of autonomic dysfunction. Which nursing intervention should be implemented first?

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## 문제

A 45-year-old patient with traumatic brain injury in the ICU develops hyperthermia with a temperature of 104°F (40°C) over 2 hours, despite normal environmental conditions. The patient is unconscious, has increased intracranial pressure, and shows signs of autonomic dysfunction. Which nursing intervention should be implemented first?

## 보기

1. Apply cooling blankets and ice packs to major pulse points **✔ 정답**
2. Administer acetaminophen 650 mg orally
3. Increase room ventilation and remove excess bedding
4. Obtain blood cultures and prepare for antibiotic administration

**정답: 1**

## 해설

Neurogenic hyperthermia from hypothalamic dysfunction requires immediate aggressive cooling (e.g., cooling blankets, ice packs to pulse points) for rapid heat dissipation. Antipyretics like acetaminophen are ineffective as it is not prostaglandin-mediated fever.

## 심화 해설

Clinical Context & Pathophysiology

This patient presents with a classic triad of severe traumatic brain injury (TBI), rapid-onset hyperthermia to 104°F (40°C), and signs of autonomic dysfunction. In neurocritical care, this presentation is highly suggestive of paroxysmal sympathetic hyperactivity (PSH), a syndrome of excessive sympathetic nervous system discharge following brain injury. PSH is characterized by episodic hypertension, tachycardia, tachypnea, hyperthermia, diaphoresis, and posturing [3]. The hyperthermia in PSH is not primarily driven by the hypothalamic set-point shift seen in infection, but rather by uncontrolled peripheral sympathetic outflow and increased metabolic heat production. Critically, fever in the injured brain is not a benign event; it is a key determinant of cerebral vulnerability that exacerbates secondary brain injury by increasing cerebral metabolic demand, elevating intracranial pressure (ICP), and worsening cerebral edema [2].

Priority Intervention Analysis

The immediate priority is to halt the ongoing secondary neurological insult. Evidence-based guidelines for targeted temperature management in neurocritical care emphasize that early recognition of fever and prompt induction of controlled normothermia are essential to limit cerebral damage [1][2]. Among the listed options, applying external cooling measures directly addresses the physiological mechanism of heat dissipation and provides the most rapid temperature reduction.

Rationale for Correct Answer: Apply cooling blankets and ice packs to major pulse points

Surface cooling with ice packs applied to major pulse points (axillae, groin, neck) and cooling blankets initiates conductive heat loss, bypassing the dysfunctional central thermoregulatory pathways. This method directly counteracts the peripheral vasoconstriction and heat generation of PSH. The best-practice evidence synthesis for severe neurological illness supports the use of physical cooling devices as a first-line intervention to achieve and maintain normothermia, thereby reducing ICP and improving cerebral perfusion [1]. In the context of PSH, where hyperthermia is sympathetically mediated, antipyretics that act on central prostaglandin pathways are often ineffective, making external cooling the cornerstone of acute management [3].

Analysis of Incorrect Options

**Option 2: Administer acetaminophen 650 mg orally.** Antipyretics like acetaminophen lower the hypothalamic temperature set-point by inhibiting cyclooxygenase. However, in PSH, the hyperthermia is not caused by a pyrogen-induced set-point elevation but by excessive end-organ sympathetic stimulation [3]. Therefore, acetaminophen is unlikely to be effective. Additionally, the patient is unconscious, making oral administration unsafe due to aspiration risk.

**Option 3: Increase room ventilation and remove excess bedding.** While environmental modifications are a component of fever management, they are insufficient as a sole intervention for a temperature of 40°C in a patient with elevated ICP. This passive approach does not provide the rapid, aggressive heat removal required to prevent ongoing secondary brain injury [2].

**Option 4: Obtain blood cultures and prepare for antibiotic administration.** Although infection must be ruled out in any febrile ICU patient, the acute onset over two hours with concurrent autonomic signs (hypertension, tachycardia, diaphoresis) in the setting of TBI makes PSH the more likely etiology. While a septic workup is part of the comprehensive plan, it is not the first nursing intervention. Delaying active cooling to perform diagnostics would prolong the period of hyperthermia-induced cerebral stress [2]. The immediate physiological threat is the elevated temperature and its impact on ICP, which must be addressed first.References (research sources)

- [1]Summary of best evidence for targeted body temperature management in patients with severe neurological illness.Research articleZhang D, Li F, Wen D, Zeng Z, Yan F, He H, Yang X. (2026) · DOI: 10.3389/fmed.2026.1781153

- [2]Temperature control in acute brain injury.Research articleLavinio A, Busl KM, Coles JP, Donadello K, Helbok R, Sekhon MS, Skrifvars MB, Taccone FS, Wahlster S, Robba C. (2026) · DOI: 10.1007/s00134-026-08367-9

- [3]Propranolol monotherapy versus combined propranolol-gabapentin for prevention of paroxysmal sympathetic hyperactivity after moderate-severe traumatic brain injury: a randomized controlled trial.RCT/clinical trialNegm EM, Gouda AM, Khatab MEM, Youssef EME, Eskandr AAF, Fathi OM, Fathi HM. (2026) · DOI: 10.1186/s12871-026-03802-2

## 임상 시나리오

Neurogenic Hyperthermia in TBIRapid Cooling for Paroxysmal Sympathetic Hyperactivity
In paroxysmal sympathetic hyperactivity (PSH), fever is driven by peripheral sympathetic outflow, not a hypothalamic set-point shift. Immediate priority is external cooling (blankets, ice packs to pulse points) to reduce cerebral metabolic demand and intracranial pressure (ICP).

Antipyretics like acetaminophen are ineffective for PSH because the mechanism is not prostaglandin-mediated. Cooling must be rapid to prevent secondary brain injury; a temperature of 104°F (40°C) is a neurological emergency.

CautionAggressively control shivering during cooling to avoid increased metabolic heat and ICP. Do not delay cooling for diagnostic workup like blood cultures; temperature reduction and hemodynamic stability take precedence.

## 핵심 개념

- **Paroxysmal Sympathetic Hyperactivity (PSH)** — A syndrome of excessive sympathetic nervous system discharge following severe brain injury, characterized by episodic hyperthermia, hypertension, tachycardia, and diaphoresis.
- **Targeted Temperature Management (TTM)** — A therapeutic intervention aimed at achieving and maintaining a specific body temperature to minimize secondary brain injury in neurocritical care patients.
- **Cerebral Metabolic Rate of Oxygen (CMRO2)** — The amount of oxygen consumed by the brain tissue; hyperthermia significantly increases CMRO2, exacerbating ischemia and intracranial pressure.

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