“…The two patients in which the low-voltage pattern persisted showed normal blood pressure and renal function at the time of fentanyl administration. Despite normal vital parameters in our patients, variability of pharmacokinetics in newborn has been demonstrated in several studies (22)(23)(24)(25)(26). Opiates are metabolized in the liver by nonspecific monoamine oxidases, and inactive metabolites are excreted in urine (27)(28).…”
ABSTRACT:The aim of this study is to describe the effect of sedation and analgesia on postoperative amplitude-integrated EEG (aEEG) in newborns with congenital heart disease (CHD) undergoing heart surgery. This is a consecutive series of 26 newborns with CHD of which 16 patients underwent cardiopulmonary bypass (CPB) surgery and 10 patients did not. aEEG was monitored for at least 12 h preoperatively and started within the first 6 h postoperatively for 48 h. Outcome was assessed at 1 year of age. All 26 patients showed a normal preoperative continuous cerebral activity with sleep-wake cycles (SWC). The postoperative duration to return to normal background activity with SWC was similar for both groups. Independent of group assignment, patients requiring midazolam had a significantly later onset of a normal SWC than those without midazolam (p ϭ 0.03). Three patients in the CPB group and two in the non-CPB group showed continuous low voltage or flat trace after administration of fentanyl. These changes did not correlate with neurodevelopmental outcome. Sedation with midazolam has a transient effect on the background activity, whereas fentanyl can induce a severe pathologic background pattern. The significance of these changes on outcome is not yet clear. Thus, more attention should be paid to these effects when interpreting aEEG in this population. (Pediatr Res 67: 650-655, 2010)
“…The two patients in which the low-voltage pattern persisted showed normal blood pressure and renal function at the time of fentanyl administration. Despite normal vital parameters in our patients, variability of pharmacokinetics in newborn has been demonstrated in several studies (22)(23)(24)(25)(26). Opiates are metabolized in the liver by nonspecific monoamine oxidases, and inactive metabolites are excreted in urine (27)(28).…”
ABSTRACT:The aim of this study is to describe the effect of sedation and analgesia on postoperative amplitude-integrated EEG (aEEG) in newborns with congenital heart disease (CHD) undergoing heart surgery. This is a consecutive series of 26 newborns with CHD of which 16 patients underwent cardiopulmonary bypass (CPB) surgery and 10 patients did not. aEEG was monitored for at least 12 h preoperatively and started within the first 6 h postoperatively for 48 h. Outcome was assessed at 1 year of age. All 26 patients showed a normal preoperative continuous cerebral activity with sleep-wake cycles (SWC). The postoperative duration to return to normal background activity with SWC was similar for both groups. Independent of group assignment, patients requiring midazolam had a significantly later onset of a normal SWC than those without midazolam (p ϭ 0.03). Three patients in the CPB group and two in the non-CPB group showed continuous low voltage or flat trace after administration of fentanyl. These changes did not correlate with neurodevelopmental outcome. Sedation with midazolam has a transient effect on the background activity, whereas fentanyl can induce a severe pathologic background pattern. The significance of these changes on outcome is not yet clear. Thus, more attention should be paid to these effects when interpreting aEEG in this population. (Pediatr Res 67: 650-655, 2010)
“…Greeley et al [15] have investigated age- since the plasma was sampled during the first elimination phase. In addition, since only 3 plasma determinations were made during the elimination phase, it is unclear whether the premature infant's prolonged half-life is related to differences in Vd, Cl or both.…”
Because developmental pharmacokinetics appear to be closely associated with
anatomic and physiologic changes that occur with growth, we were interested in determining
the disposition and elimination of alfentanil in premature infants and older children. The
pharmacokinetic profile of alfentanil was determined in 6 premature infants requiring sedation
for medical management or analgesia for stressful intensive-care procedures. These
pharmacokinetic profiles were compared with pharmacokinetic profiles determined in 9
older infants and children undergoing operative procedures that required invasive monitoring.
In both groups the plasma decay curves best fit a 2-compartment model. Compared with
older children, premature infants demonstrated a significantly larger apparent volume of
distribution (1.0 ± 0.39 vs. 0.48 ± 0.19 l/kg), a smaller clearance (2.2 ± 2.4 vs. 5.6 ±
2.4 ml/kg/min) and a markedly prolonged elimination half-life (525 ± 305 vs. 60 ±
11 min).
“…In contrast, the terminal elimination half-life (16 h) was longer than reported after bolus administration (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12) h) [14][15][16][17] and the Vs, value (10 1 kg-') was higher (2-9 1 kg-') [14][15][16][17][18][19][20][21]. These differences may be related to differences in the underlying disease states and to the duration of plasma sampling (24 h in our study).…”
Ten patients with head trauma received an intravenous bolus of sufentanil (2 jg kg-1) followed at 30 min by infusion of sufentanil (median 150 jg h-1) and midazolam (median 9.0 mg h-1) over 48 h. Median (range) values of pharmacokinetic parameters for sufentanil were: tih,z = 16 (7-49) h; CL = 1215 (519-2550) ml min-1; CLR = 7 (2-38) ml min-; Vss = 10.0 (6.8-24.2) 1 kg-. Decreases in intracranial pressure (ICP) (from 16.1 ± 1.7 to 10.8 ± 1.3 mm Hg; P < 0.05) and mean arterial blood pressure (MAP) (from 85.5 ± 3.9 to 80.2 ± 4.9 mm Hg; P < 0.05) were observed within 15 min of the bolus injection of sufentanil and remained unchanged thereafter. Thus, cerebral perfusion pressure (CPP = MAP-ICP) was stable.
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