Core Temperature and Skin-Surface Temperature Gradients of Ketamine and Propofol for Anesthetic Induction in Children.
10.4097/kjae.2004.46.4.397
- Author:
Soo Kyoung LEE
1
;
Soo Chang SON
;
Yoon Hee KIM
;
Hee Suk YOON
;
Jae Ho CHOI
Author Information
1. Department of Anesthesiology, College of Medicine, Ulsan University, Seoul, Korea.
- Publication Type:Original Article ; Randomized Controlled Trial
- Keywords:
core temperature;
skin temperature;
propofol;
ketamine
- MeSH:
Anesthesia;
Anesthetics;
Child*;
Fingers;
Forearm;
Hernia, Inguinal;
Hot Temperature;
Humans;
Hypothermia;
Ketamine*;
Nitrous Oxide;
Oxygen;
Propofol*;
Skin;
Skin Temperature;
Strabismus;
Vasoconstriction;
Vasodilation
- From:Korean Journal of Anesthesiology
2004;46(4):397-401
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Hypothermia after induction of anesthesia results initially from core-to-peripheral redistribution of body heat. Both central inhibition of tonic thermoregulatory vasoconstriction in arteriovenous shunts and anesthetic induced vasodilation contribute to core-to-peripheral redistribution of heat. Ketamine increases peripheral arteriolar resistance uniquely; in contrast, propofol causes profound venodilatation that other anesthetics do not. The aim of the present study is to evaluate core temperature and skin-surface temperature gradients in use of ketamine for anesthetic induction compared with propofol in children. METHODS: Forty pediatric patients of ASA status I or II, undergoing elective surgery for strabismus or inguinal hernia were studied. The patients were allocated randomly to one of two groups: (i) GROUP P (n = 20): Anesthesia was induced with propofol and maintained with sevoflurane in combination with 60% nitrous oxide in oxygen. (ii) GROUP K (n = 20): Anesthesia was induced with ketamine and maintained with sevoflurane in combination with 60% nitrous oxide in oxygen. Core temperature, forearm skin temperature, fingertip skin temperature and Forearm minus fingertip, skin-temperature gradients were recorded before induction of anesthesia, 3 min after administering ketamine or propofol (just before endotracheal intubation), 5 min, and at 5-min intervals after induction of anesthesia. RESULTS: After induction of anesthesia, core temperature in the two groups was decreased but results did not differ significantly between two groups. Forearm skin temperature was increased significantly after 20 min of anesthesia in propofol group and 15 min of anesthesia in ketamine group, but results did not differ significantly between two groups. Finger tip skin temperature was increased significantly after 3 min of anesthesia in the propofol group and 10 min of anesthesia in the ketamine group. Finger tip skin temperature of 5 min of anesthesia in propofol group increased significantly greater than in ketamine group. Forearm minus finger skin surface temperature gradients was decreased statistically significantly at 3 min of anesthesia in the propofol group and 10 min of anesthesia in the ketamine group, gradients of 5 min of anesthesia was presented statistically significant between two groups. CONCLUSIONS: For pediatric patients, after induction of anesthesia with ketamine arteriovenous shunt vasomoter status was well maintained. And maintaining vasoconstriction during induction of anesthesia reduced the magnitude of redistribution hypothermia.