Neurogenik Fever

There was an increased risk of development of NF among patients with severe TBI who had experienced either diffuse axonal injury (DAI) or frontal lobe injury of any form.
Other risk factors predicting early hyperthermia include Glasgow Coma Scale score in the emergency department ≤ 8, paediatric trauma score ≤ 8, cerebral oedema or DAI on initial head computed tomography, admission blood glucose > 150mg/dL ,    white cell count   > 14,300cells/mm3, and systolic hypotension

Critical care management of severeTBI in adults

TBI is divided into two discrete periods:

The primary brain injury is the physical damage to parenchyma (tissue, vessels) that occurs during traumatic event, resulting in shearing and compression of the surrounding brain tissue.

The secondary brain injury is the result of a complex process, following and complicating the primary brain injury in the ensuing hours and days.
Secondary, intracranial brain insults include cerebral edema, hematomas, hydrocephalus, intracranial hypertension, vasospasm, metabolic derangement, excitotoxicity, calcium ions toxicity, infection, and seizures

Secondary, systemic brain insults are mainly ischemic in nature , such as:

• TTV : Hypotension, Hypertension (SBP > 160 mm Hg, or mean arterial pressure [MAP] > 110 mm Hg), Fever (temperature > 36.5°C), Hypothermia (temperature < 35.5°C)
• BGA : Hypoxemia, Hypocapnia, Hypercapnia, Hypo-osmolality (plasma osmolality [P Osm] < 290 mOsm/Kg H₂O, Acid-base disorders (acidemia: pH < 7.35; alkalemia: pH > 7.45)
• DL : Anemia, 
• SE : Hyponatremia (serum sodium < 142 mEq/L)
• GDA : Hyperglycemia, Hypoglycemia

General monitoring

• electrocardiography (ECG monitoring)
• arterial oxygen saturation (pulse oxymetry, SpO₂), capnography (end-tidal CO₂, PetCO₂)
• arterial blood pressure (arterial catheter)
• central venous pressure (CVP)
• systemic temperature
• urine output
• serum electrolytes and osmolality