Anesth Analg 2003;96:88-90
© 2003 International Anesthesia Research Society
PEDIATRIC ANESTHESIA
Hemodynamic Response to Caudal Epidural Clonidine in a Pediatric Cardiac Patient
Laura K. Diaz, MD, and
Fernando Cantu, MD
Department of Anesthesiology, Cook Children’s Medical Center, Fort Worth, Texas
Address correspondence to Laura K. Diaz, MD, Baylor College of Medicine, Pediatric Cardiovascular Anesthesiology, Texas Children’s Hospital, 6621 Fannin St., WT19345H, Houston, TX 77030-2399. Address e-mail to lkdiaz{at}bcm.tmc.edu Reprints will not be available.
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Abstract
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IMPLICATIONS: Postoperative management of sedation and analgesia in pediatric cardiac patients presents many challenges. This case report describes a child who experienced dramatic clinical improvement with the postoperative use of caudal morphine and clonidine after conventional therapy had failed.
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Introduction
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The need for prolonged analgesia and sedation after open-heart surgery in children is common after complex palliative procedures and repairs. Children can rapidly develop tolerance to opioid and/or benzodiazepine infusions and may develop withdrawal when these drugs are discontinued. Numerous reports have found caudal morphine to be a safe and effective method for control of postoperative pain in children, including those who have had open-heart surgery (1–3). Clonidine, an 
2-adrenergic agonist, is a useful adjunct in caudal analgesia and prolongs the duration of analgesic effects (4), as well as providing dose-dependent sedation (5,6). This case report describes a child who experienced dramatic clinical improvement with caudal administration of morphine and clonidine after conventional therapy had failed.
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Case Report
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A 3-yr-old, 14.1-kg girl presented for augmentation of central and branch pulmonary arteries (PAs) and reconstruction of her right ventricular outflow tract (RVOT). Her medical history was significant for a history of tetralogy of Fallot. Initial surgical correction at age 5 mo consisted of a pulmonary valvectomy, transannular pericardial patch enlargement of the RVOT, and perforated patch closure of the ventricular septal defect. At the time of her initial surgery, her branch PAs were found to be hypoplastic. Right ventricular pressures were suprasystemic and did not improve despite subsequent interventional catheterizations and dilation of the PAs. No issues with drug tolerance or dependence were noted during her surgery or catheterizations.
Surgical augmentation of the central PAs and reconstruction of the RVOT with muscle resection were planned. Anesthesia was induced with sevoflurane and maintained with sevoflurane, remifentanil, rocuronium, and midazolam. Before surgical incision, a single-shot caudal block was performed with 0.2% ropivacaine 1 mL/kg and preservative-free morphine (0.5 mg/mL) 75 µg/kg. Dopamine 5 µg · kg-1 · min-1 and milrinone 0.5 µg · kg-1 · min-1 were used to support hemodynamics after separation from cardiopulmonary bypass. An initial loading dose of milrinone was administered.
After surgery, in the pediatric intensive care unit, right ventricular pressures remained suprasystemic, and over the next few hours, the patient’s extremities became increasingly cool and her urine output decreased. An epinephrine infusion was begun but discontinued because of the onset of dysrhythmias. On postoperative day (POD) 2, the patient became tachycardic and hypertensive despite a fentanyl infusion of 15 µg · kg-1 · h-1. Frequent as-needed doses of fentanyl 20 µg and midazolam 1 mg were given IV, with little effect on hemodynamics. A midazolam infusion was begun at 0.2 mg · kg-1 · h-1. Dopamine was discontinued, and milrinone was increased to 0.75 µg · kg-1 · min-1. With persistent hypertension and tachycardia on POD 3, milrinone was tapered. Additionally, a nitroprusside infusion was started and gradually increased to 5 µg · kg-1 · min-1, with little improvement. The fentanyl infusion was discontinued, and a morphine infusion was substituted at 0.1 mg · kg-1 · h-1. A persistent mild metabolic acidosis was noted on arterial blood gases.
As problems of tachycardia, hypertension, poor peripheral perfusion, and increasing sedation requirements continued, the anesthesia team was consulted. On POD 3, a caudal epidural catheter was placed with sterile technique and threaded to a depth of 4 cm. Because bleeding had not been an issue after surgery, coagulation studies were not obtained before catheter placement. The patient was initially given morphine 75 µg/kg diluted in 15 mL of preservative-free normal saline. All subsequent doses of epidural morphine and/or clonidine were diluted in 10 mL of preservative-free normal saline. Frequent as-needed doses of IV morphine and midazolam continued to be required; thus, the caudal morphine dosage was increased to 135 µg/kg every 12 h for 2 doses. At the request of the surgical team, the child continued to receive a vecuronium infusion until POD 5, making assessment of her pain and sedation level difficult. The patient continued to be severely vasoconstricted, with cold extremities and poor peripheral pulses, despite the use of nitroprusside. Caudal morphine was adjusted to 100 µg/kg every 8 h, and clonidine (0.1 mg/mL) 1 µg/kg was added to provide additional sedation and vasodilatation. Three hours after the initial dose of clonidine, the patient’s systemic pressures decreased, allowing successful weaning from the nitroprusside. Urine output increased dramatically over the following day, and her metabolic acidosis also resolved. With the next administration of caudal morphine 8 h later, the clonidine dosage was decreased to 0.7 µg/kg. Three hours after her second dose of clonidine, she was warm and vasodilated, with excellent peripheral pulses.
On POD 6, the child was responsive to commands and appeared in no distress. Weaning from caudal clonidine began on POD 6, with each subsequent dose halved. Caudal morphine was decreased to 75 µg/kg every 12 h on POD 7, and the child was successfully tracheally extubated. The epidural catheter was removed the following day, with no complications noted. The midazolam infusion was weaned and eventually discontinued on POD 12. Oral clonidine 25 µg every 8 h (5 µg · kg-1 · d-1) was started on POD 9 and subsequently decreased over the following week. Tapering doses of IV methadone and lorazepam were used, with conversion to oral methadone and diazepam on POD 11. One week later, the patient was discharged home on furosemide and digoxin.
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Discussion
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Providing postoperative sedation and analgesia for children after congenital heart surgery poses many challenges, and fentanyl and midazolam infusions are often used for postoperative sedation and analgesia in these children (7,8). Epidural opioids may lessen the need for postoperative narcotic infusions, simplifying postoperative pain management and eventual weaning from these drugs.
Clonidine, a partial 2-adrenergic agonist, has many beneficial hemodynamic and sedative effects. Through the activation of 2-adrenergic receptors in the medulla, sympathetic nervous system outflow from the brain is decreased, resulting in a decrease in blood pressure, heart rate, and adrenergic activity (9). Clonidine also affects 2-adrenoceptors in the dorsal horn of the spinal cord, inhibiting substance P release and central neural transmission. Studies in adults have shown profound analgesia resulting from the epidural administration of clonidine (10). In addition, clonidine possesses powerful sedative and anxiolytic properties as a result of its inhibitory effect on the locus caeruleus (11). Caudal analgesia with either local anesthetics or morphine is potentiated and prolonged when clonidine is added (12,13). Dexmedetomidine, an 2-adrenergic agonist with 8 times the 2 specificity of clonidine, is approved for use as a short-term sedative in adults (14), but pediatric experience is limited (15).
The initial goal in placing a caudal catheter in this patient was to lessen the dependence on narcotic and benzodiazepine infusions and to achieve more effective analgesia and sedation. The caudal route was chosen for its ease of placement and small incidence of complications (16,17). Despite increasing dosages of caudal morphine, however, the patient remained hypertensive and tachycardic, with poor peripheral perfusion. Nitroprusside was ineffective in improving peripheral perfusion or controlling hypertension. The use of caudal clonidine 1–2 µg/kg has been well described in children (18,19): thus, caudal clonidine 1 µg/kg was added, not only to facilitate pain control and sedation, but also to attempt to improve peripheral perfusion, decrease adrenergic tone, and control hypertension without incurring reflex tachycardia. Because this patient had no residual intracardiac shunting, the decrease in afterload provided by clonidine would have been beneficial as well.
Symptomatic hypotension and bradycardia may occur after the administration of clonidine, particularly in patients with high resting sympathetic tone. Inhibition of central sympathetic outflow in a patient dependent on sympathetic tone could result in a precipitate decreasing of blood pressure, requiring treatment with volume expanders or dopamine. After the second caudal injection of clonidine, our patient experienced a decrease in blood pressure, which responded readily to a fluid bolus. The patient’s urine output improved dramatically after the administration of clonidine, and, in addition, her metabolic acidosis resolved.
In summary, we report a case of a child in a hyperadrenergic state who showed remarkable clinical improvement with the administration of caudal clonidine. Although there are no published data at present regarding the use of caudal clonidine in facilitating the management of postoperative pediatric cardiac patients, we are pursuing a controlled study.
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Acknowledgments
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The authors gratefully acknowledge the assistance of Stephen A. Stayer, MD, Department of Anesthesiology, Baylor College of Medicine, Division of Pediatric Cardiovascular Anesthesiology, Texas Children’s Hospital, for his assistance in reviewing the manuscript.
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References
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Accepted for publication September 25, 2002.
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Abstract
Introduction
