Comparing the Hemodynamic Effects of Epinephrine Versus Dexmedetomidine as an Adjuvant to Bupivacaine in Caudal Anaesthesia Assessed by Cardiometry - Trial NCT05860010

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Primary Outcome

The percentage change in cardiac output after caudal injection

Summary

Electrical cardiometry (EC) is a non-invasive method of estimating cardiac parameters by
 measuring changes in thoracic bioimpedance during the cardiac cycle. The ICON (Cardiotronic
 Osypka Medical, San Diego, California) monitor uses four electrocardiogram electrodes and
 estimates the maximum rate of impedance change to peak aortic blood acceleration. An
 impedance change occurs between diastole and systole as red blood cell orientation is altered
 from random during diastole to align during systole. This device is validated against Fick
 cardiac output and transthoracic echocardiography in infants and children, as well as
 thermodilution in adults with R values of 0.9. This device is approved by the Food and Drug
 Administration (FDA) for use in pediatrics. Hypotension is expected to occur after epidural
 anesthesia (EA) due to the dilatation of venous vessels by sympathetic blockade with a
 subsequent decrease in venous return and cardiac output (CO). Also, the association of
 general anesthesia (GA) to EA can lead to more decrease in CO. The addition of epinephrine to
 local anesthetics (LA) could worsen hypotension through the systemic absorption of
 epinephrine that leads to a vasodilator β effect. Yet, CO may be enhanced by this
 β-adrenergic stimulation. However, it is well known that caudal epidural anesthesia has few
 or no hemodynamic changes in children less than 8 yr old. This could be attributed to the
 immaturity of their sympathetic system and smaller lower-limbs blood volume compared to
 adults. Caudal anesthesia is highly effective in abdominal, urinary tract, and lower
 extremity surgeries in children for intra- and postoperative analgesia. The addition of
 dexmedetomidine to local anesthetics in caudal anesthesia is a frequent practice.
 Dexmedetomidine, a highly selective alpha-2 adrenoreceptor agonist, is used as an intravenous
 sedative and analgesic drug. It has an a2/a1 selectivity ratio of 1600: 1 and is eight times
 more potent than clonidine. Intrathecal and epidural dexmedetomidine have been reported to
 produce analgesic properties, prolonging the duration of local anesthetics without causing
 nerve damage in pediatric patients.
 
 Although basal heart rate is greater than in adults, activation of the parasympathetic
 nervous system, anesthetic overdose, or hypoxia can quickly trigger bradycardia and profound
 reductions in cardiac output. The sympathetic nervous system and baroreceptor reflexes are
 not fully mature and the infant cardiovascular system displays a blunted response to
 exogenous catecholamines. That's why it is very essential to determine the hemodynamic
 effects of any drug used as an adjuvant to local anesthetics for caudal block and to explore
 whether it reduces the child cardiac output or not.
 
 As invasive cardiac monitors are rarely indicated in pediatric patients, and little is known
 about the impact of caudally administered dexmedetomidine on cardiac function, so we aimed to
 investigate its effect on hemodynamic functions measured by EC.

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