Intraoperative Hyperthermia: A Harbinger of Hypothalamic Injury

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To JNA Readers:
Intraoperative hyperthermia portends some of the most dreaded anesthetic emergencies.1,2 We report an unusual case of sudden-onset, rapidly worsening hyperthermia, a probable manifestation of intraoperative hypothalamic injury.
A 5-year-old boy presenting for surgical excision of a craniopharyngioma underwent standard induction and maintenance of anesthesia with routine monitoring as for a regular craniotomy. Toward the end of surgical resection, the child developed a malignant rise in temperature from a baseline of 36.2°C to 40.1°C over a period of 20 minutes, accompanied by tachycardia and hypertension. Inhalational anesthetic was discontinued and propofol infusion was started as malignant hyperthermia was suspected. The end-tidal carbon dioxide remained constant and arterial blood gas did not reveal any abnormality. Administration of intravenous cold saline and IV paracetamol at 15 mg/kg did not control the hyperthermia. Serum potassium was 4.8 meq/L, and an elevated sodium of 152 meq/L compared with normal preoperative values, with a concomitant increase in urine output from 2 to about 25 mL/kg/h, was noted, arousing a suspicion of diabetes insipidus. As the tumor had already been excised, immediate hemostasis was achieved and closure initiated. After surgery, after shifting to the neurosurgical ICU, the temperature subsided to 38°C over 4 hours but tachycardia persisted. The trachea was extubated after he was fully awake and obeying commands. The diagnosis of diabetes insipidus (DI) was confirmed by an increase in serum osmolality, decreased urine-specific gravity, and increased serum sodium levels of 158 meq/L, which was managed with fluid replacement and intranasal desmopressin.
The possible etiologies of intraoperative hyperthermia, including malignant hyperthermia, septicemia, neuroleptic malignant syndrome, thyroid storm, and transfusion reactions, were ruled out by clinical evaluation and laboratory investigations. As the rise in temperature was temporally related to the time of resection and manipulation of the tumor in the region of the hypothalamus, we infer that intraoperative hypothalamic injury was probably the cause of this sudden rapid and uncontrollable hyperthermia. The advent of intraoperative DI during this episode corroborates with this plausible explanation for hyperthermia. Hypothalamus has the greatest concentration of nuclei at which set points are coded for, controlled, and monitored, for the control of homeostasis and temperature. Injury to the hypothalamus results in hyperthermia, and alterations in the functions of the autonomic nervous system and endocrine and immune systems.3,4 Perioperative physicians should be prepared to differentiate this cause of “central fever” from other causes of intraoperative hyperthermia that have an overlapping symptomatology.5 The diagnosis of hypothalamic injury can be zeroed on if the onset of hyperthermia occurs during perihypothalamic tumor manipulation, with hemodynamic dysfunction, and is not associated with a rise in the end-tidal carbon dioxide levels or muscle rigidity. Furthermore, this central fever will be relatively resistant to pharmacological management. Hyperthermia in such cases serves as a harbinger of hypothalamic injury and should alert the anesthetist regarding other more ominous problems associated with hypothalamic injury, such as autonomic dysfunction and DI, which require careful monitoring and management.

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