What is the recommended management of neurogenic fever in a patient with traumatic brain injury?

Management of Central Fever in Traumatic Brain Injury

Implement controlled normothermia targeting 36.0–37.5°C using automated feedback-controlled temperature management devices immediately upon detection of fever (>37.5°C) in all sedated and ventilated TBI patients, regardless of intracranial pressure status. 1, 2

Pathophysiology and Clinical Significance

Neurogenic fever occurs in 4-37% of TBI survivors and represents core temperature >37.5°C driven by hypothalamic dysregulation without evidence of sepsis or inflammatory processes. 2, 3 This is a diagnosis of exclusion requiring thorough infectious workup first. 2, 3

Uncontrolled fever precipitates secondary brain injury through multiple mechanisms: 1, 2

• Increased metabolic demands on already-injured brain tissue 2
• Enhanced excitatory neurotransmitter release 2
• Increased free radical production 2
• Elevated intracranial pressure 1, 2

The deleterious effects occur regardless of whether fever stems from infection or thermoregulatory dysfunction, making prompt treatment essential even while diagnostic workup proceeds. 1, 3

Diagnostic Approach Before Labeling as Neurogenic

Complete infectious workup must be performed first: 2

• Chest radiograph for all ICU patients with new fever 2
• At least two sets of blood cultures (60 mL total), with simultaneous central and peripheral collection if central venous catheter present 2
• CT imaging for patients with recent thoracic, abdominal, or pelvic surgery 2
• Lumbar puncture if neurological symptoms present and not contraindicated 2

Key distinguishing features of neurogenic fever: 2, 4

• Persistent temperature elevation without cyclic pattern 4
• Core temperature >37.5°C without infectious markers 3
• Negative cultures and no clear infectious source despite thorough workup 3

Temperature Management Protocol

Primary Treatment Strategy

Use automated feedback-controlled temperature management devices as the primary intervention. 1, 2, 3 These devices are superior to antipyretics alone for achieving target temperature control and are strongly recommended by consensus guidelines. 1, 2

Target temperature parameters: 1, 2, 3

• Maintain core temperature 36.0–37.5°C 1, 2, 3
• Maximum temperature variation ≤0.5°C per hour and ≤1°C per 24-hour period 1
• Continue treatment for as long as the brain remains at risk of secondary injury 1, 3

Device specifications: 1

• Intravascular cooling catheters or water-circulating cooling devices with hydrogel-coated energy transfer pads 5, 6
• Automated feedback control using central temperature monitoring 1, 5
• Rapid cooling capability (fever reduced from 38.4°C to 36.9°C within 120 minutes) 5

Role of Antipyretics

Antipyretics have limited efficacy and should only serve as adjuncts during induction phase, not as primary management. 2, 3 Pharmacological strategies (acetaminophen, NSAIDs) are frequently ineffective in controlling fever and minimizing temperature variability in severe TBI. 2, 7, 8

Temperature Monitoring Requirements

Use central temperature monitoring methods: 2, 3

• Bladder catheter, esophageal thermistor, or pulmonary artery catheter preferred 2, 3
• Continuous monitoring preferable to intermittent measurements 3
• When central monitoring unavailable, use oral or rectal temperatures over axillary or tympanic 2

Management of Shivering

Shivering commonly occurs during cooling and requires treatment: 5

• Apply hand warming at treatment onset 5
• Use meperidine for shivering refractory to warming measures 5
• Maintain adequate sedation in mechanically ventilated patients 6

Critical Clinical Pitfalls to Avoid

Do not delay treatment while searching for fever source. 3 The harmful effects of hyperthermia occur immediately regardless of etiology, and waiting for diagnostic clarity worsens outcomes. 1, 3

Do not rely solely on antipyretics for temperature control. 2, 3 Studies demonstrate that despite antipyretic use in 86% of febrile episodes, 57% of fevers lasted longer than 4 hours and 5% lasted longer than 12 hours. 8

Do not tolerate mild-to-moderate fever in TBI patients. 1 Unlike general ICU populations where fever management did not improve mortality, TBI patients specifically benefit from normothermia due to prevention of secondary brain injury. 1, 7

Maintain systolic blood pressure >110 mmHg at all times during fever management. 2 Hypotension worsens neurological outcomes and increases mortality; use vasopressors (phenylephrine, norepinephrine) immediately if hypotension develops during cooling. 2

Duration of Treatment

Continue controlled normothermia for as long as the brain remains at risk of secondary brain damage. 1, 3 This typically extends throughout the acute phase when patients are sedated and ventilated. 1

Before discontinuing treatment: 1

• Obtain interval CT scan and/or alternative assessment of intracranial compliance 1
• Assess absolute ICP values in addition to compliance 1
• Prevent or promptly treat rebound hyperthermia 1

Evidence of Efficacy

Induced normothermia using intravascular cooling reduces fever burden from 10.6% to 1.6% of time in the first 3 days and significantly decreases percentage of time with ICP >25 mmHg compared to conventional fever control. 6 Mean ICP is reduced from 16.37 mmHg with conventional management to 12.74 mmHg with induced normothermia. 6