During general anaesthesia, endotracheal intubation of patients with pre-eclampsia causes stimulation of the sympathetic nervous system and catecholamine release, which may lead to maternal and neonatal complications.
To attenuate both the stress response and the haemodynamic response to tracheal intubation in patients with pre-eclampsia.
A randomised, double-blind, controlled study.
Single University Hospital.
Sixty patients aged 18 to 45 years with pre-eclampsia receiving general anaesthesia for caesarean section.
The patients were randomly allocated to three groups. Groups D1and D2 received an infusion of dexmedetomidine 1 μg kg−1 over the 10 min before induction of general anaesthesia, then 0.4 and 0.6 μg kg−1 h−1 dexmedetomidine, respectively. Group C received equivalent volumes of 0.9% saline.
The primary outcome was the effect of dexmedetomidine on mean arterial blood pressure measured before induction of general anaesthesia at 1 and 5 min after intubation, and then every 5 min until 10 min after extubation. The secondary outcomes were blood glucose and serum cortisol (measured before induction of general anaesthesia, and at 1 and 5 min after intubation), postoperative visual analogue pain scores, time to first request for analgesia, the total consumption of analgesia, Ramsay sedation score, maternal and placental vein blood serum levels of dexmedetomidine and neonatal Apgar score at 1 and 5 min.
At all assessment times, the mean arterial pressures were significantly lower in the dexmedetomidine groups than in the control group. Compared with group C, the heart rate was significantly lower in both groups D1 and D2. In group D2, the heart rate was lower than in group D1. Serum glucose and cortisol were significantly higher in the controls than in either group D1 or D2. Group D2 patients were significantly more sedated on arrival in the recovery room followed by D1. Time to first analgesia was significantly longer in groups D2 and D1 than in group C, and the visual analogue pain scores were significantly lower in groups D1 and D2 than in group C at 1, 2, 3 and 5 h. Total morphine consumption was significantly lower in groups D1 and D2 than in the control group. There was no difference in Apgar scores across the three groups despite significantly higher dexmedetomidine concentrations in group D2 (both maternal and placental vein) than in group D1.
Administration of dexmedetomidine in doses 0.4 and 0.6 μg kg−1 h−1 was associated with haemodynamic and hormonal stability, without causing significant adverse neonatal outcome.
Pan African Clinical Trial Registry (PACTR201706002303170), (www.pactr.org).
From the Department of Anesthesia, ICU and Pain Therapy, Faculty of Medicine (AME, AAM, A-EAA, EME, IME), Department of Biochemistry, National Liver Institute, Menoufiya University, Shibin El-koom (MAO) and Department of Bioequivalence, Egyptian Centre for Research and Development, Cairo, Egypt (OAA-E)
Correspondence to Ashraf M. Eskandr, MD, Department of Anesthesia, ICU and Pain Therapy, Faculty of Medicine, Menoufiya University, 3 Yassin Abd-Elghafar Street, Shibin El-koom, Egypt E-mail: email@example.com
Published online 10 February 2018