Non-infectious fever following surgery occurs in children undergoing hemispherectomies
and leads to diagnostic dilemma.[1] Early recognition and treatment is vital to avoid unscrupulous use of antibiotics.
This central fever is resistant to routinely used antipyretics while cerebro-spinal
fluid (CSF) release with an external ventricular drain (EVD) has shown benefit.[2]
A 6-year-old girl, weighing 30 kg presented with left-sided limb weakness and difficulty
in walking. Her parents gave 4-year history of seizures refractory to medical management.
She was treated with oxcarbazepine 600 mg/d and sodium-valproate 450 mg/d. Electroencephalogram
(EEG) demonstrated background epileptiform slow-wave discharges with phase-reversal
on right fronto-temporal hemisphere. Magnetic resonance imaging (MRI) showed atrophy
of right hemisphere, ipsilateral lateral ventricle dilatation and signal changes in
subcortical white-matter. A diagnosis of Rasmussen encephalitis was made based on
European consensus criteria.[3] Sodium-valproate dose was increased to 450 mg/d and methylprednisolone 500 mg/d
was administered for 5 days, following which she was able to walk with support. As
seizure persisted, clonazepam and leviteracitam were added. Video-EEG showed seizures
arising from right hemisphere. Right functional hemispherotomy lasting 8 hours was
performed to control intractable seizures under standard anaesthetic management. She
received 300 ml of packed red cells. EVD was placed at the end of surgery and elective
ventilation instituted for 16 hours. At extubation, tracheal secretions were mucoid
and leucocyte count was 11500 cells/mm3. One hundred and fifty millilitres of clear CSF was drained over 24-hour period.
Eighteen hours after surgery, patient had a temperature spike of 106°F with heart
rate of 180 beats/minute and respiratory rate of 26 breaths/minute. Intravenous paracetamol
15 mg/kg administered twice over 6-hours period, nimesulide 75 mg, cold intravenous
fluids and frequent tepid sponging reduced fever but failed to restore normothermia.
Urine, CSF and sputum examinations were negative for infective aetiology. Intramuscular
chlorpromazine 25 mg was added and other anti-fever measures were continued. Following
this, temperature normalised, about 20 hours after manifestation [Figure 1]. Rest of the hospital stay was uneventful.
Figure 1: Temperature trend over the 1st 48 h of surgery
Post-neurosurgical hyperpyrexia is not uncommon and could be due to both infective
and non-infective causes. Blood transfusion, vascular injury, intracranial haemorrhage,
operative site infection, meningitis, drugs or extensive tissue damage are common
causes for new-onset post-neurosurgical fever.[4] Severe hyperpyrexia (106°F) as observed in this patient is generally not seen. Most
fever of non-infectious aetiology subsides on its own or is unresponsive to conventional
anti-pyretics. However, fever in patients with seizure need to be aggressively managed
to prevent adverse outcomes. Kossoff et al.,[4] reported fever in 82% of hemidecortication surgeries of which only 5.8% were infective
in origin. Rest they claim were due to aseptic meningitis. Conventional anti-pyretics
act by inhibiting cyclooxygenase enzyme and reduce prostaglandin E2 levels within hypothalamus. Despite draining the CSF, hyperpyrexia occurred in our
patient necessitating exploration of alternative therapies. When traditional management
failed, chlorpromazine achieved fever control. Chlorpromazine produces antipyretic
action because of its ability to render patient thermolabile and its effect on thermoregulation.[5]
To conclude, defective thermoregulation occurs after hemispherotomy. Conventional
anti-pyretics may be ineffective in controlling fever. Chlorpromazine may have contributed
to reduced severity and duration of hyperthermia along with other measures and can
be considered early in such scenarios.
