Anesthetic Management for a Patient with Congenital Insensitivity to Pain with Anhidrosis (CIPA): A case report / 대한마취과학회지

Congenital insensitivity to pain with anhidrosis (CIPA) is a rare, autosomal-recessive disorder characterized by the clinical triad of indifference of pain, anhidrosis and heat intolerance.Because of their lack of autonomic response to noxious stimuli, the determination of adequate depth of anesthesia in the CIPA patient undergoing surgery is a major challenge.We experienced a patient with CIPA who had minor procedures three times under the general anesthesia, in which bispectral index (BIS) was maintained at 40-50 by adjusting sevoflurane concentrations with 50% nitrous oxide.The low end-tidal sevoflurane concentrations (<1.2 vol%) were required to keep the target BIS while vital signs remained stable throughout the surgery in each operation.BIS monitor may be a valuable tool to guide the depth of anesthesia in patients with CIPA.

Effects of Nitrous Oxide and Remifentanil on Cardiovascular Response to Endotracheal Intubation during Desflurane Anesthesia

BACKGROUND: Desflurane is known to causes hypertension and tachycardia when its inspired concentration is rapidly increased. We determined whether nitrous oxide (N2O) or remifentanil alters cardiovascular responses to intubation and/or inhalation of high concentrations of desflurane during induction of anesthesia. METHODS: Sixty patients were assigned randomly into three groups (n = 20 each). Anesthesia was induced with thiopental 5 mg/kg followed by saline (control and N2O groups) or remifentanil 1microg/kg (remifentanil group). Tracheal intubation was facilitated with intravenous vecuronium 0.12 mg/kg and 12% desflurane was given soon after the intubation. In addition, 75% N2O was given beginning 3 min before the intubation in the N2O group. Systolic arterial pressure (SAP), heart rate (HR), and plasma catecholamine concentrations were determined. RESULTS: The intubation resulted in an immediate increase and an additional second increase of SAP and HR at 3 to 5 min after intubation in all groups. SAP but not HR in the N2O group and both SAP and HR in the remifentanil group at first and second peak responses were lower than in the control group. Norepinephrine increased at 1 min after intubation and increased further at 5 min in the control and N2O groups but only increased at 5 min in the remifentanil group. CONCLUSIONS: A biphasic pressor and tachycardiac response in response to intubation and desflurane were noted. Although N2O did not affect tachycardiac response, it suppressed the pressor responses and augmented norepinephrine release. However, remifentanil significantly attenuated hemodynamic and catecholamine responses to endotracheal intubation and desflurane.