Intranasal midazolam and fentanyl for procedural sedation and analgesia in infants in the neonatal intensive care unit.

BACKGROUND: The intranasal route is a minimally invasive method for rapidly delivering midazolam and fentanyl to provide short-term analgesia and sedation in infants. However, intranasal use of midazolam and fentanyl is not labeled for infants and safety data are sparse. The objective of this study is to evaluate the safety of intranasal midazolam and intranasal fentanyl in infants admitted to the Neonatal Intensive Care Unit (NICU). METHODS: We retrospectively identified all infants receiving intranasal midazolam or fentanyl in the NICU from 2009 to 2015. We recorded indication for use and vital signs and determined the proportion of infants experiencing the following adverse events: death within 24 hours, hypotension, bradycardia, worsening respiratory status, and chest wall rigidity. Vital signs 4 hours before and after each dose were compared using the Wilcoxon signed-rank test. RESULTS: We identified 17 infants (gestational ages 23- 41 weeks) receiving 25 intranasal doses. None of the infants died or developed hypotension, bradycardia, or chest wall rigidity. Intranasal delivery was most commonly used for sedation during magnetic resonance imaging studies. Other indications include analgesia or sedation for retinopathy of prematurity surgery, intubation, and peripherally inserted central catheter placement. One infant receiving intranasal midazolam experienced worsening respiratory status. Vital signs before and after dosing were not significantly different. CONCLUSIONS: Intranasal midazolam and fentanyl use in term and preterm infants appeared safe and well-tolerated in this small cohort of infants. Larger, prospective studies evaluating the safety and efficacy of intranasal midazolam and fentanyl use in infants are warranted.

Congenital diaphragmatic hernia: a systematic review and summary of best-evidence practice strategies.

OBJECTIVES: Recent reports suggest that specific care strategies improve survival of infants with congenital diaphragmatic hernia (CDH). This review presents details of care from centers reporting high rates of survival among CDH infants. STUDY DESIGN: We conducted a MEDLINE search (1995 to 2006) and searched all citations in the Cochrane Central Register of Controlled Trials. Studies were included if they contained reports of >20 infants with symptomatic CDH, and >75% survival of isolated CDH. RESULT: Thirteen reports from 11 centers met inclusion criteria. Overall survival, including infants with multiple anomalies, was 603/763 (79%; range: 69 to 93%). Survival for isolated CDH was 560/661 (85%; range: 78 to 96%). The frequency of extracorporeal membrane oxygenation (ECMO) use for isolated CDH varied widely among reporting centers 251/622 (40%; range: 11 to 61%), as did survival for infants with isolated CDH placed on ECMO: 149/206 (73%; range: 33 to 86%). There was no suggestion of benefit from use of antenatal glucocorticoids given after 34 weeks gestation or use of postnatal surfactant. Low mortality was frequently attributed to minimizing lung injury and adhering to center-specific criteria for ECMO. CONCLUSION: Use of strategies aimed at minimizing lung injury, tolerance of postductal acidosis and hypoxemia, and adhering to center-specific criteria for ECMO were strategies most consistently reported by successful centers. The literature lacks randomized clinical trials of these or other care strategies in this complex patient population; prospective studies of safety and long-term outcome are needed.

Impact of a palliative care program on end-of-life care in a neonatal intensive care unit.

OBJECTIVE: Evaluate changes in end-of-life care following initiation of a palliative care program in a neonatal intensive care unit. STUDY DESIGN: Retrospective study comparing infant deaths before and after implementation of a Palliative Care Program comprised of medication guidelines, an individualized order set, a nursing care plan and staff education. RESULT: Eighty-two infants died before (Era 1) and 68 infants died after implementation of the program (Era 2). Morphine use was similar (88% vs 81%; P =0.17), whereas benzodiazepines use increased in Era 2 (26% vs 43%; P=0.03). Withdrawal of life support (73% vs 63%; P=0.17) and do-not-resuscitate orders (46% vs 53%; P=0.42) were similar. Do-not-resuscitate orders and family meetings were more frequent among Era 2 infants with activated palliative care orders (n=21) compared with infants without activated orders (n=47). CONCLUSION: End-of-life family meetings and benzodiazepine use increased following implementation of our program, likely reflecting adherence to guidelines and improved communication.

Sustained arterial blood pressure elevation associated with pneumothoraces: early detection via continuous monitoring.

The diagnosis of pneumothorax in the neonate is often heralded by such signs as deterioration of arterial blood gases, arterial hypotension, and cardiac arrest. An awareness of more subtle clinical signs of accumulating extra-alveolar gas may lead to earlier intervention and a decrease in morbidity. Fourteen episodes of pneumothorax developed in seven of 69 neonates who received ventilatory assistance (mean birth weight 1,828 +/- 295 gm), of whom six were ventilated for hyaline membrane disease and one for pneumonia. Instantaneous heart rate and arterial blood pressure (ABP) were monitored continuously in all patients. Changes in vital signs were noted at a mean of 48 minutes (range 12 to 116 minutes) prior to thoracentesis. There was an increase in systolic ABP (7 to 26 mm Hg) associated with 70% of the episodes, and an increase in heart rate and pulse pressure associated with 57% of the episodes. By 20 minutes after thoracentesis there was a rapid decrease in ABP values toward levels not significantly different from base line. A sustained increase in ABP may be an early sign of accumulating extra-alveolar gas. Continuous monitoring and graphic representation of vital signs in the ventilated neonate may suggest the diagnosis of pneumothorax before clinical decompensation occurs.

Detection of seizure activity in the paralyzed neonate using continuous monitoring.

In experimental animals neurologic damage may occur during seizure activity whether the seizure is accompanied by motor activity and hypoxemia or whether the animal is paralyzed and normoxemic. These findings suggest that it may be important to detect seizure activity in the paralyzed neonate. Nine infants who were mechanically ventilated and paralyzed with pancuronium had their condition diagnosed as seizure activity. Vital signs were continuously monitored and six infants had either oxygen saturation or transcutaneous oxygen measured during seizure activity. For the group as a whole, rhythmic fluctuations in vital signs, cardiac rhythm, and oxygenation occurred every four minutes (range one to seven minutes) and lasted two minutes (range one to four minutes). In seven patients whose seizures were not accompanied by cardiac arrhythmias the following mean increases were noted: systolic arterial blood pressure, 15 mm Hg (range 7 to 36 mm Hg); heart rate, ten beats per minute (-11 to 30/min); oxygen saturation, 12% (range 4% to 20%); and transcutaneous oxygen, 31 mm Hg (range 14 to 45 mm Hg). Seizures in the two patients with cardiac arrhythmias were accompanied by a decrease in systolic arterial blood pressure of 27 mm Hg (range 15 to 40 mm Hg) and in oxygen saturation of 24% (range 20% to 28%). The presence of rhythmic fluctuation in vital signs and oxygenation should alert the physician to the possibility of seizure activity in the paralyzed neonate.

Hyperammonemia associated with perinatal asphyxia.

Twelve infants with severe perinatal asphyxia were found to have elevated blood ammonia levels (302 to 960 microgram/100 ml). In the seven survivors, hyperammonemia was associated with CNS irritability, hyperthermia, hypertension, and wide neonatal heart rate oscillations. Follow-up examinations revealed severe neurologic dysfunction in five of seven infants. CNS depression, hyperthermia, hypertension, and a nonreactive, fixed heart rate characterized the infants that died. These findings suggest a clinical entity secondary to perinatal asphyxia whose signs and symptoms may be related to hyperammonemia.

Prophylactic indomethacin for prevention of intraventricular hemorrhage in premature infants.

The impact of early prophylactic use of intravenous indomethacin on the incidence and severity of periventricular-intraventricular hemorrhage and patent ductus arteriosus in 199 oxygen-requiring premature infants (less than or equal to 1300 g birth weight) was prospectively investigated. The trial was controlled, the infants were randomized, and the investigators were unaware of the group assignments. Patients with minimal (grade I) or no periventricular-intraventricular hemorrhage determined by prestudy echoencephalography were randomized within two birth weight subgroups (500 to 899 and 900 to 1300 g) to receive either prophylactic indomethacin (n = 99) or an equal volume of saline-vehicle placebo (n = 100). The first dose (0.2 mg/kg) was given within 12 hours of delivery and two subsequent doses (0.1 mg/kg) were administered at 12 hourly intervals. Prophylactic indomethacin significantly reduced the incidence of grades II to IV periventricular-intraventricular hemorrhage. Intraventricular hemorrhage was half as common in infants given prophylactic indomethacin as in control infants (23% v 46%, P less than .002). The reduction was manifested in both birth weight subgroups. Results of this study also confirmed a lower incidence of clinically significant patent ductus arteriosus in infants who received prophylactic indomethacin in contrast to those who received placebo (11% v 42%, P less than .001). No significant differences were found between treatment and control groups in the duration of oxygen therapy, mechanical ventilation, or hospitalization or in the incidence of pneumothorax, chronic lung disease, sepsis, necrotizing enterocolitis, retinopathy of prematurity, or death. Early prophylactic indomethacin initiated within 12 hours of delivery is effective in reducing the incidence of intraventricular hemorrhage as well as clinically significant patent ductus arteriosus in very low birth weight premature infants.

Influence of transcutaneous oxygen monitoring on the incidence of retinopathy of prematurity.

This study was performed to determine whether the use of continuous transcutaneous oxygen tension (tcPO2) monitoring could reduce the incidence of retinopathy of prematurity in preterm infants receiving oxygen therapy. A total of 296 infants with birth weights less than or equal to 1,300 g were randomly assigned to a continuous monitoring or a standard care group. Infants in the continuous monitoring group had tcPO2 monitored continuously as long as they required supplemental oxygen, and infants in the standard care group had tcPO2 monitored only during the more acute state of their illness. Management of both groups was otherwise identical. Of 148 infants in the continuous monitoring group, 101 survived; of the 148 patients in the standard care group, 113 survived. Mean birth weights and gestational ages were similar for both groups. Duration of mechanical ventilation and oxygen therapy was also similar. The overall incidence of retinopathy of prematurity was 51% in the continuous monitoring group and 59% in the standard care group. As birth weight for infants greater than or equal to 1,000 g increased, a higher risk of retinopathy of prematurity developing was noted in the standard care group. Cicatricial retinopathy of prematurity developed in four infants in the continuous monitoring group and five in the standard care group. These results suggest that continuous tcPO2 monitoring may reduce the incidence of retinopathy of prematurity in infants with birth weights greater than 1,000 g but not in the smaller infants in whom this complication occurs more frequently and is more severe.

Influence of group B streptococci on piglet pulmonary artery response to bradykinin.

To study whether a sepsis-induced increase in des-Arg9-bradykinin (des-Arg9-BK) and bradykinin (BK) B1-receptor activity participates in the observed increase in pulmonary vascular resistance in neonatal group B streptococcal sepsis (GBS), isometric force bioassays of pulmonary artery (PA) rings were studied, after 4-h exposure to either Krebs or GBS, by using the following protocols: 1) BK dose-response curve, 2) vascular response to BK with NG-nitro-L-arginine methyl ester (L-NAME), and 3) response to des-Arg9-BK (BK metabolite and B1 agonist). PA rings exposed to BK resulted in contraction in the GBS group and a decrease in resting tension in the Control group (P = 0.034) at a concentration of 10(-5) M. GBS-treated PA rings contracted more to des-Arg9-BK than did Controls (P < 0.001). BK (10(-6) M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls (P < 0.001), and preincubation with L-NAME decreased relaxation in both. These results suggest that GBS decreased endothelium-dependent BK relaxation and increased contractile response to des-Arg9-BK. We speculate that this occurs secondary to upregulation of B1 receptors reflected by B1-agonist-mediated PA contraction.

The role of leukotrienes in the late hemodynamic manifestations of group B streptococcal sepsis in piglets.

In order to evaluate the role of leukotrienes in group B streptococcal (GBS) sepsis we studied the effect of a leukotriene receptor antagonist, FPL 57231, on the late hemodynamic changes occurring secondary to an infusion of live GBS. Paralyzed, mechanically ventilated piglets received a continuous intravenous infusion of bacteria (5 x 10(7) org/kg/min) while systemic arterial (Psa) and pulmonary artery pressures (Ppa) were measured. To separate the effects of the lipoxygenase products of arachidonic acid from those of the cyclooxygenase by-products, animals in control and treatment groups received indomethacin, a cyclooxygenase blocking agent, 15 min after the infusion of GBS was begun. In addition to GBS and indomethacin, treatment animals received a 30 min infusion of FPL 57231 starting 120 min after the bacterial infusion was begun. All study animals responded to bacteria within 15 min with marked elevation in pulmonary artery pressure (X +/- SD) (12 +/- 3 to 49 +/- 5 mmHg; p less than .01), and a decline in PaO2 (84 +/- 9 to 49 +/- 5 mmHg; p less than .01) and cardiac output (0.29 +/- 0.04 to 0.18 +/- .07 liter/min/kg; p less than .01). These changes were reversed by indomethacin. Subsequent values remained relatively stable until approximately 90 min when a gradual decrease in cardiac output (CO) and PaO2, and an increase in Ppa, and calculated systemic (SVR) and pulmonary (PVR) vascular resistances occurred. After the initial increase in TxB2 and 6-keto-PGF1 alpha, indomethacin treatment resulted in return of these values to baseline with no further increase throughout the study period.(ABSTRACT TRUNCATED AT 250 WORDS)

Thermodynamics of hexokinase catalyzed reactions. II. Measurement and calculation of enthalpies of reaction as a function of magnesium ion concentration.

Enthalpies of phosphorylation of glucose by adenosine 5'-triphosphate have been measured as a function of concentrations of magnesium chloride in TRIS/TRIS-HCl buffer in the pH range 8.64 to 8.98. These measurements are compared with the results of calculations of these enthalpies that use a coupled equilibrium formalism with equilibrium data and enthalpy values selected from the literature. The experimental results span the range of magnesium ion concentrations 1 X 10(-6) to 0.3 mol alpha-1 and show a total variation in the enthalpy of reaction of almost 10 kJ mol-1, with the most exothermic reaction occurring at a magnesium ion concentration of 6.0 X 10(-4) mol alpha-1. The calculated enthalpies of reaction, except for the magnesium ion concentration range 4 X 10(-6) to 5 X 10(-4) mol alpha-1, are, within estimated uncertainty intervals (0.8 to 10.2 kJ mol-1), in agreement with the measured values.

Thermodynamics of the disproportionation of adenosine 5'-diphosphate to adenosine 5'-triphosphate and adenosine 5'-monophosphate. I. Equilibrium model.

The thermodynamic treatment of the disproportionation reaction of adenosine 5'-diphosphate to adenosine 5'-triphosphate and adenosine 5'-monophosphate is discussed in terms of an equilibrium model which includes the effects of the multiplicity of ionic and metal bound species and the presence of long range electrostatic and short range repulsive interactions. Calculated quantities include equilibrium constants, enthalpies, heat capacities, entropies, and the stoichiometry of the overall reaction. The matter of how these calculations can be made self-consistent with respect to both calculated values of the ionic strength and the molality of the free magnesium ion is discussed. The thermodynamic data involving proton and magnesium-ion binding data for the nucleotides involved in this reaction have been evaluated.

Thermodynamics of the conversion of penicillin G to phenylacetic acid and 6-aminopenicillanic acid.

The thermodynamics of the enzymatic conversion (penicillin acylase) of aqueous penicillin G to phenylacetic acid and 6-aminopenicillanic acid have been studied using both high-pressure liquid-chromatography and microcalorimetry. The reaction was carried out in aqueous phosphate buffer over the pH range 6.0-7.6, at ionic strengths from 0.10 to 0.40 mol kg-1, and at temperatures from 292 to 322 K. The data have been analyzed using a chemical equilibrium model with an extended Debye-Hückel expression for the activity coefficients. For the reference reaction, penicillin G- (aq) + H2O(l) = phenylacetic acid-(aq) + 6-aminopenicillanic acid-(aq) + H+ (aq), the following parameters have been obtained: K = (7.35 +/- 1.5) X 10(-8) mol kg-1, delta G0 = 40.7 +/- 0.5 kJ mol-1, delta H0 = 29.7 +/- 0.6 kJ mol-1, and delta C0p = -240 +/- 50 J mol-1 K-1 at 298.15 K and at the thermochemical standard state. The extent of reaction for the overall conversion is highly dependent upon the pH.

An investigation of the equilibria between aqueous ribose, ribulose, and arabinose.

The thermodynamics of the equilibria between aqueous ribose, ribulose, and arabinose were investigated using high-pressure liquid chromatography and microcalorimetry. The reactions were carried out in aqueous phosphate buffer over the pH range 6.8-7.4 and over the temperature range 313.15-343.75 K using solubilized glucose isomerase with either Mg(NO3)2 or MgSO4 as cofactors. The equilibrium constants (K) and the standard state Gibbs energy (delta G degrees) and enthalpy (delta H degrees) changes at 298.15 K for the three equilibria investigated were found to be: ribose(aq) = ribulose(aq) K = 0.317, delta G degrees = 2.85 +/- 0.14 kJ mol-1, delta H degrees = 11.0 +/- 1.5 kJ mol-1; ribose(aq) = arabinose(aq) K = 4.00, delta G degrees = -3.44 +/- 0.30 kJ mol-1, delta H degrees = -9.8 +/- 3.0 kJ mol-1; ribulose(aq) = arabinose(aq) K = 12.6, delta G degrees = -6.29 +/- 0.34 kJ mol-1, delta H degrees = -20.75 +/- 3.4 kJ mol-1. Information on rates of the above reactions was also obtained. The temperature dependencies of the equilibrium constants are conveniently expressed as R in K = -delta G degrees 298.15/298.15 + delta H degrees 298.15[(1/298.15)-(1/T)] where R is the gas constant (8.31441 J mol-1 K-1) and T the thermodynamic temperature.

Calorimetric determination of the standard transformed enthalpy of a biochemical reaction at specified pH and pMg.

In a biochemical reaction there is generally a change in the binding of hydrogen ions and metal ions. Therefore, calorimetric measurements of enthalpies of reaction have to be adjusted for the enthalpies of reaction of the hydrogen ions and metal ions produced or consumed with the buffer. It can be shown that this yields the standard transformed enthalpy of reaction that determines the change in the apparent equilibrium constant K' (written in terms of sums of concentrations of species of a reactant) with temperature at the chosen pH and concentration of free metal ion. The derivations are based on the assumption that the changes in pH and free metal ion concentrations in the calorimetric experiment are small. This assumption is experimentally realized if a solution is well buffered for hydrogen and metal ions. The derived equations are discussed in terms of the implications they have for the performance and interpretation of calorimetric measurements.

Thermodynamics of carbohydrate isomerization reactions. The conversion of aqueous allose to psicose.

The thermodynamics of the conversion of aqueous D-psicose to D-allose has been investigated using high-pressure liquid chromatography. The reaction was carried out in phosphate buffer at pH 7.4 over the temperature range 317.25-349.25 K. The following results are obtained for the conversion process at 298.15 K: DeltaG degrees = - 1.41 +/- 0.09 kJ mol(-1), DeltaH degrees = 7.42 +/- 1.7 kJ mol(-1), and DeltaC(p) degrees = 67 +/- 50 J mol(-1) K(-1). An approximate equilibrium constant of 0.30 is obtained at 333.15 K for the conversion of aqueous D-psicose to D-altrose. Available thermodynamic data for isomerization reactions involving aldohexoses and aldopentoses are summarized.

Thermodynamics of hydrolysis of disaccharides. Lactulose, alpha-D-melibiose, palatinose, D-trehalose, D-turanose and 3-o-beta-D-galactopyranosyl-D-arabinose.

High-pressure liquid chromatography and microcalorimetry have been used to study the thermodynamics of the hydrolysis reactions of a series of disaccharides. The enzymes used to bring about the hydrolyses were: beta-galactosidase for lactulose and 3-o-beta-D-galactopyranosyl-D-arabinose; beta-glucosidase for alpha-D-melibiose; beta-amylase for D-trehalose; isomaltase for palatinose; and alpha-glucosidase for D-turanose. The buffer used was sodium acetate (0.02-0.10 M and pH 4.44-5.65). For the following processes at 298.15 K: lactulose(aq) + H2O(liq) = D-galactose(aq) + D-fructose(aq), K0 = 128 +/- 10 and delta H0 = 2.21 +/- 0.10 kJ mol-1; alpha-D-melibiose(aq) + H2O(liq) = D-galactose(aq) + D-glucose(aq), K0 = 123 +/- 42 and delta H0 = -0.88 +/- 0.50 kJ mol-1; palatinose(aq) + H2O(liq) = D-glucose(aq) + D-fructose(aq), delta H0 = -4.44 +/- 1.1 kJ mol-1; D-trehalose(aq) + H2O(liq) = 2 D-glucose(aq), K0 = 119 +/- 10 and delta H0 = 4.73 +/- 0.41 kJ mol-1; D-turanose(aq) + H2O(liq) = D-glucose(aq) + D-fructose(aq), delta H0 = -2.68 +/- 0.75 kJ mol-1; and 3-o-beta-D-galactopyranosyl-D-arabinose(aq) + H2O(liq) = D-galactose(aq) + D- arabinose(aq),0H0 = 107 +/- 10 and delta H0 = 2.97 +/- 0.10 kJ mol-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Thermodynamics of the conversion of fumarate to L-(-)-malate.

The thermodynamics of the conversion of aqueous fumarate to L-(-)-malate has been investigated using both heat conduction microcalorimetry and a gas chromatographic method for determining equilibrium constants. The reaction was carried out in aqueous Tris-HCl buffer over the pH range 6.3-8.0, the temperature range 25-47 degrees C, and at ionic strengths varying from 0.0005 to 0.62 mol kg-1. Measured enthalpies and equilibrium ratios have been adjusted to zero ionic strength and corrected for ionization effects to obtain the following standard state values for the conversion of aqueous fumarate 2- to malate 2- at 25 degrees C: K = 4.20 +/- 0.05, delta G degrees = -3557 +/- 30 J mol-1, delta H degrees = -15670 +/- 150 J mol-1, and delta C degrees p = -36 +/- J mol-1 K-1. Equations are given which allow one to calculate the combined effects of pH and temperature on equilibrium constants and enthalpies of this reaction.

Thermodynamics of the disproportionation of adenosine 5'-diphosphate to adenosine 5'-triphosphate and adenosine 5'-monophosphate, II. Experimental data.

High-pressure liquid-chromatography and microcalorimetry have been used to determine equilibrium constants and enthalpies of reaction for the disproportionation reaction of adenosine 5'-diphosphate (ADP) to adenosine 5'-triphosphate (ATP) and adenosine 5'-monophosphate (AMP). Adenylate kinase was used to catalyze this reaction. The measurements were carried out over the temperature range 286 to 311 K, at ionic strengths varying from 0.06 to 0.33 mol kg(-1), over the pH range 6.04 to 8.87, and over the pMg range 2.22 to 7.16, where pMg = -log a(Mg2+). The equilibrium model developed by Goldberg and Tewari (see the previous paper in this issue) was used for the analysis of the measurements. Thus, for the reference reaction: 2 ADp(3-) (ao) AMp(2-) (ao)+ ATp- (ao), K degrees = 0.225 +/- 0.010, DeltaG degrees = 3.70 +- 0.11 kJ mol (-1), DeltaH degrees = -1.5 +/- 1. 5 kJ mol (-1), degrees S degrees = -17 +/- 5 J mol(-1)K(-1), and ACP(p) degrees approximately = -46 J mo1l(-1)K(-1) at 298.15 K and 0.1 MPa. These results and the thermodynamic parameters for the auxiliary equilibria in solution have been used to model the thermodynamics of the disproportionation reaction over a wide range of temperature, pH, ionic strength, and magnesium ion morality. Under approximately physiological conditions (311.15 K, pH 6.94, [Mg2+] = 1.35 x 10(-3) mol kg(-1), and I = 0.23 mol kg(-1)) the apparent equilibrium constant (KA' = m(SigmaAMP)m(SigmaATP)/[ m(SigmaADP)]2) for the overall disproportionation reaction is equal to 0.93 +/- 0.02. Thermodynamic data on the disproportionation reaction and literature values for this apparent equilibrium constant in human red blood cells are used to calculate a morality of 1.94 x 10(-4) mol kg(-1) for free magnesium ion in human red blood cells. The results are also discussed in relation to thermochemical cycles and compared with data on the hydrolysis of the guanosine phosphates.

Thermodynamics of the conversion of aqueous xylose to xylulose.

The thermodynamics of the conversion of aqueous xylose to xylulose has been investigated using high-pressure liquid chromatography (HPLC) and microcalorimetry. The reaction was carried out in aqueous phosphate buffer over the pH range 6.8-7.4 using solubilized glucose isomerase with MgSO(4) as a cofactor. The temperature range over which this reaction was investigated was 298.15-342.15 K. A combined analysis of both the HPLC and microcalorimetric data leads to the following results at 298.15 K for the conversion process: DeltaG degrees = 4389 +/- 31 J mol(-1), DeltaH degrees = 16090 +/- 670 J mol(-1), and DeltaC(p) degrees = 40 +/- 23 J mol(-1) K(-1). The temperature dependence of the equilibrium constant for the reaction is expressed as R ln K = -4389/298.15 +16090[(1/298.15)-(1/T)]+40[(298.15/T)-1 + ln(T/298.15)]. Comparisons are made with literature data.