Chapter 53. Acute Pain Management in Infants and Children

Pain in children has been historically undertreated. This was in part the result of misguided assumptions, such as children’s inability to experience pain because of an immature nervous system and the innocuous effects of untreated pain in children. In addition, limited knowledge of pediatric drug metabolism prevented a clear understanding of how to dose analgesics in children. Over the past two decades, there has been significant progress in the understanding of neuroanatomy, physiology, and pharmacology of analgesics in children, which has led to considerable advancements in pain management. This chapter discusses developmental anatomy and neurochemistry, pain assessment, pharmacologic treatment of pain, and regional techniques in pediatric patients.

The late fetus and infant are neurologically sophisticated in their ability to transmit pain signals and respond to stress.1 Cutaneous sensory nerve terminals are present in the perioral region at 7 weeks’ gestation and spread to all body areas by 20 weeks’ gestation. Nerve growth factors regulate the extension of peripheral nociceptive fibers into the dorsal spinal cord, with the larger A fibers entering prior to the C fibers at 8 to 12 weeks. At birth, A and C fiber territories overlap in the developing substantia gelatinosa.2 Therefore, the neonatal response to a nonspecific sensory stimulus is low threshold, nonspecific, and poorly organized. Noxious and non-noxious stimuli produce similar physiologic and behavioral infant responses, complicating an accurate assessment of pain.

In the central nervous system (CNS), the full complement of cortical neurons, approximately 1000 million, are present at 20 weeks’ gestation. Pain transmission pathways complete myelination in the spine and brain stem between 22 and 30 weeks’ gestation. Myelination extends up to the thalamus by 30 weeks, and to the cortex by 37 weeks or term. Cortical descending inhibition develops post-term.

Excitatory and inhibitory neurotransmitters and neuromodulators are present in the fetus, with the balance favoring excitation. Calcitonin gene-related peptide (CGRP), substance P, and the glutamate-NMDA systems are present at 8 to 10 weeks’ gestation. Enkephalin and vasoactive intestinal peptide (VIP) appear at 10 to 14 weeks. Catecholamines are present in late gestation, and serotonin at 6 weeks’ postnatal. Of note, the receptors for excitatory neurotransmitters are numerous and widely distributed in the neonate, regressing toward an adult system in the postnatal months. As well, in the developing nervous system, inhibitory chemicals, such as gamma-amino butyric acid (GABA) and glycine, may act as excitatory transmitters. In an experimental murine model, the spinal cord concentration of NMDA receptors, and their ligand-affinity, is greater in neonates than in older animals. NK-1 receptor density is also maximal in late fetal and early postnatal life; however, substance P levels are lower than adult levels at birth.3

Regarding stress responses, the functional neuroendocrine pathways between hypothalamus and pituitary are present at 21 weeks’ gestation. Corticotrophin-releasing factor (CRF) may stimulate fetal ACTH and β-endorphin from that time, and cortisol and β-endorphin increases have been assayed following intrauterine sampling for exchange transfusion. Norepinephrine is present in paravertebral ganglia and adrenal chromaffin cells at 10 weeks’ gestation and is released with intrauterine stress (asphyxia). Epinephrine is present, in smaller amount, after 23 weeks’ gestation.3

The long-term consequences of untreated pain in the developing organism are not yet defined, but some studies suggest that early pain responses influence later pain behaviors.4 In one murine model, skin wounds on rat pups caused increased innervation and lowered pain thresholds in the area of injury for 3 months post-injury. In the rats that had recurrent painful stimuli from birth, the changes in the receptive fields of the dorsal horn neurons were persistent.5 Another study exposed rat pups to repeated hindpaw injections over several days. When compared with control pups and at adult age, the rats that experienced repeated noxious stimuli showed increased responses to painful and nonpainful stimuli relative to their controls. Pathologically, the experimental group showed a loss of nociceptive primary afferents.6 A third study found that the pain-conditioned behaviors of rats differed according to the timing of the stimulus. Rat pups exposed to early, repetitive noxious stimulation had a decrease in pain threshold compared with control rats. Adult rats given repetitive painful stimuli showed greater stress responses, such as freezing and digging, than controls.7

In humans, few empiric studies also show late effects of painful stimuli. One report describes that neonatal males who received a eutetic mixture of topical local anesthetic (Emla Cream; Astra Pharmaceuticals) prior to circumcision had 12% to 25% less facial grimacing and tachycardia than randomized control infants without treatment.8 An earlier study observed that males circumcised within 2 days of age had longer periods of crying and higher pain ratings than uncircumcised males.9 Another report compared 18 preterm infants, subject to repeated painful procedures in the neonatal intensive care unit (NICU), with matched full-term infants regarding their somatic complaints at 18 months. Twenty-five percent of mothers of preterm infants with prolonged neonatal intensive care unit stays noted a significantly increased number of somatic complaints in their toddlers as compared with mothers of full-term infants briefly managed in the normal nursery.10 Alternatively, a recent study of 24 preterm infants compared with matched full-term infants had similar behavioral pain scores when exposed to a finger prick at 4 months of age.11

In summary, the neonatal pain transmission system is adequately developed, centrally hyperexcitable, with the necessary components of central sensitization, but generally nonspecific in its response to stimuli. Neonates and infants feel pain, but assessment of this phenomenon remains challenging.12–14 The long-term effects of neonatal pain are now being investigated.

Pain assessment is a fundamental and essential part of pain treatment. The ability to reliably assess pain facilitates the diagnosis of painful conditions and helps to evaluate efficacy of pain relief methods. The assessment of pain in infants and children, however, is one of the most difficult challenges faced by health care providers. The subjective nature of pain, cognitive and language limitations, and differences in pain expression and perception account for the difficulty in assessing pain in pediatric patients. As discussed earlier, there is growing evidence to suggest that inadequately treated pain can have both short-term and long-term consequences. For example, it is well established that full-term and preterm infants develop physiologic stress responses to pain and inadequate anesthesia that can result in greater postoperative complications.1,15,16 Pain is most commonly assessed by asking patients about the quality, location, and severity of their pain. Self-report methods are considered to be the most reliable guides to pain assessment for most patients. However, infants and preverbal children are unable to communicate their experience of pain and must rely on caregivers to interpret signs of pain and distress. Pain assessment methods that combine self-report with other measures, such as behavioral and physiologic responses, may provide more accurate measures of pain. There can be limitations in the use of behavioral and physiologic indices for pain assessment. Distinguishing between pain and distress may be difficult in young children. For example, a young child may cry and exhibit characteristic facial grimacing during an ear examination because of fear and anxiety rather than pain. Physiologic signs may also mislead measures of pain in certain situations. For example, patients who are septic, hypoxic, or receiving vasopressors may have increases in heart rate or blood pressure that reflect other processes not related to pain. Most pain scales have been designed for assessment of acute pain and tend to underestimate pain in children with persistent or chronic pain.

Most pain assessment scales used for infants and preverbal children rely on behavioral observation and physiologic parameters to guide assessment. Observational measures alone may not accurately represent pain intensity since health care workers tend to underestimate pain when compared to a patient or parent report.17,18 The parent report also tends to underestimate children’s pain but to a lesser extent than a report by health care workers.19 Behavioral parameters typically used are facial grimacing, cry, body movement, and sleep pattern. Facial expression measures appear to be most useful and specific in neonates.20,21 The typical pain facial expression of eyes tightly closed, furrowed brows, and square mouth is considered to be one of the most consistent signals of pain in infants. Pain cries in infants have been shown to be spectographically different from cries due to hunger or anger and can be recognized by experienced caregivers.22 Physiologic parameters such as heart rate, oxygen saturation, blood pressure, and palmar sweating provide more objective evidence of pain.

The Premature Infant Pain Profile (PIPP) and CRIES are pain scales used for preterm and full-term infants, respectively, that combine behavioral observations and physiologic criteria to assess pain.23,24 The PIPP was specifically designed to assess acute pain in preterm infants with consideration to gestational age (Table 53-1). The CRIES is an acronym that refers to Crying, Requires O2, Increased vital signs, Expression, and Sleepless and consists of five behavioral and physiologic parameters designed to rate postoperative pain in neonates (Table 53-2).

Children ages 3 to 7 years old become increasingly able to communicate their experience of pain to parents and caregivers. Children in this age group may not understand the abstract concept of pain, but they are able to report “hurt” or “owie” and in general are able to indicate pain intensity. Although self-report measures are most reliable, a variety of factors may alter a child’s report of pain.25 For example, children with inadequately treated persistent pain from cancer or surgery may appear very quiet, still, and withdrawn, giving a false impression of adequate analgesia. Some children may underreport or deny pain for fear of receiving a painful analgesic “shot.” Young children are unable to use standard visual analog scales used by older children and adults. Several self-report methods have been developed that are validated and reliable in children as young as 4 years of age.26,28 The Bieri faces scale is a series of facial expressions depicting degrees of pain and was found to be preferred by most children (Fig. 53-1).28,29 The Color Continuum Scale is a ruler with numerical anchors where increasing intensity of red signifies more pain (Fig. 53-2).

Children aged 8 years and older generally can use standard “0 to 10” visual analog scales accurately, but many of the scales used in younger children such as the Bieri faces can also be used. Children in this age group may have concerns over loss of control, or may fear painful injections of analgesics that can distort their self-report. Older children and adolescents have the cognitive ability to understand the meaning of pain and tend to use behavioral coping strategies for pain.

Pain assessment in severely cognitively impaired children is particularly challenging for parents and caregivers. As in preverbal children, behavioral observation scales combined with physiologic parameters can be helpful. In some cases when assessment is unclear, therapeutic trials of comfort measures and analgesics can help clarify the situation.

In general, pain assessment is best accomplished by correlating self-report, behavioral, and physiologic measures with the child’s overall clinical picture. The choice of pain assessment scale should be individualized and based on a child’s age, clinical condition, environment, cognitive abilities, and coping style. Often, explaining and practicing a pain assessment scale to a child during the preoperative visit can help facilitate use after surgery. Table 53-3 summarizes common pain scales used in children and infants.

• Neonates have an immature cytochrome P450 hepatic enzyme system, and therefore conjugate opioids and local anesthetics slowly. Delayed toxicity with prolonged infusions is possible.
• Renal function, including glomerular filtration and renal tubular secretion, is decreased in the first few weeks of life (longer for premature infants) compared with adults. The half-life of opioids and, more significantly, their metabolites (MSO4-6-glucuronide) may be increased. Delayed sedation and respiratory depression are limited by increased dosing intervals and decreased doses.
• Neonatal total body water is increased compared with adults. Fat is minimal. Analgesics with high-water solubility have a large volume of distribution.
• Neonates have decreased plasma-protein binding, albumen and α1 acid glycoprotein, resulting in increased free-drug and greater first-pass toxicity.
• Ventilatory reflexes are immature in the neonate. Infants have a low threshold for hypoventilation secondary to opioids.30

Acetaminophen and Nonsteroidal Anti-Inflammatory Drugs

Acetaminophen (paracetamol) is the most commonly and widely used analgesic and antipyretic in children. It has no peripheral anti-inflammatory effects and it putatively acts on cyclooxygenase (COX-1 more than COX-2) through CNS mechanisms. Although a weak analgesic, it is a generally safe agent, if proper pediatric doses are administered (Table 53-4). It is a useful adjuvant for acute pain therapy and is often combined, synergistically, with weak opioids. The recommended single doses are 15 to 20 mg/kg, 10 to 15mg/kg with repeated dosing. Toxicity occurs at 90 mg/kg in children and adolescents, 60 mg/kg in infants, and 45 mg/kg in preterm infants. Excess acetominophen is metabolized in the liver to reactive nucleophilic benzoquinones, which bind DNA, leading to parenchymal necrosis. Treatment of overdose must occur within 12 hours of intake in adult patients, with the use of N-acetylcysteine or glutathion. Acetaminophen is available in multiple routes of administration—tablets, capsules, suspensions, and suppositories. The rectal dose is 35 to 40 mg/kg every 6 to 8 hours, because of slow absorption and plasma clearance. Rectal absorption peaks at 70 minutes.31,32

NSAIDs act peripherally, without significantly crossing the blood-brain barrier, and have a prominent anti-inflammatory effect as well as analgesia and antipyresis. They are generally used for mild to moderate postoperative pain, sickle cell crisis, symptomatic headache, and arthritis. Opioids remain the first choice for moderate to severe pain, such as cancer-related pain, with NSAIDs as adjuvants. Their use is guided as well by their adverse effects, including gastritis, potential gastrointestinal bleeding, and platelet and renal dysfunction. Respiratory depression and dysphoria, often seen with opioid use, are not concerns with these agents.31–34 In some studies of postoperative pediatric pain, NSAIDs reduce opioid requirements and side effects.35,36

The major mechanism of action of nonsteroidal anti-inflammatory drugs (NSAIDs) is through inhibition of prostaglandin synthesis by blockade of constitutive and expressed cyclooxygenase (COX). The pharmacology of most NSAIDs has been studied in children 2 years old and older, in which population the elimination half-life is similar to adults. In children 3 months to 2.5 years, the volume of distribution and clearance of ibuprofen and ketorolac are increased, suggesting a possible need for higher loading and maintenance dosing in children.30,31

Aspirin (acetylsalicylic acid), although used for acute pain and fever for more than 100 years, is contraindicated for fever in pediatric patients because of its association with Reye’s syndrome, described 20 years ago. Therefore, acetaminophen and ibuprofen are the primary agents for fever and mild to moderate pain.30,31 For severe pain, parenteral ketorolac is effective. The oral formulation is similar in stength and efficacy to older NSAIDs. Ketololac has been studied as a single dose in postoperative pediatric patients and is well-tolerated and opioid-sparing. Its use postoperatively may be limited in tonsillectomy and other procedures associated with significant bleeding. It is generally prescribed every 6 hours over a period of 24 to 48 hours, with frequent reevaluation and a maximum period of 5 days.37 The newer COX 2 inhibitors, celecoxib and rofecoxeb, are currently being studied in pediatric multicenter pharmacokinetic and postoperative efficacy trials.38

Opioids

As in other clinical populations, opioids are also the standard of care for pediatric patients with severe pain. Historically inadequate use is now increasingly replaced by appropriate use, guided by attention to physiologic immaturity, dosing corrected for age and weight, and awareness of potential adverse effects (Table 53-5). In general, as in adults, the use of opioids for the pediatric population is best guided by the adult acute and cancer pain literature. Exceptional patients are premature infants, neonates, and opioid-naïve children requiring high initial bolusing of medication.30,31

Pharmacokinetic studies of opioids in children are available for morphine, fentanyl, sufentanil, methadone, and hydromorphone, and in process for such newer oral agents as oxycodone and oxycontin.

In neonates and premature infants, the major concern is respiratory depression, even, at times, with sub-anesthetic dosing. A single large bolus dose in a neonate may result in apnea due to rapid CNS absorption. Adjustment in dosage and dosage interval is necessary in this population. For example, the half-life of parenteral morphine in adults and children is 2 hours, in neonates, 6 to 8 hours, and in premature infants, 10 hours. Pharmacokinetic studies of opioid infusions in neonates suggest the use of lower doses of opioids, monitoring for hypoxemia and hypoventilation, and larger but controlled loading doses because of increased volume of distribution. In healthy infants, 3 months and older, renal clearance of opioids and secondary respiratory suppression is similar to adults.30,39

The use of patient-controlled analgesia (PCA) in children has been well studied and is safe and effective, with no increased total opioid administration nor adverse effects. Ages 6 years and older are generally able to comprehend the use of the self-administered bolus dose. Younger children and those with developmental delay may be considered for nurse-administered analgesia (NCA) or continuous infusion. Parent-administered dosing is generally only used in the palliative care setting.40

The choice of a specific opioid is based on potency, desired route of administration, and adverse effects. Morphine is the first choice for parenteral boluses and infusions. Children with reactive airway disease may, rarely, be more sensitive to the histaminergic effects of morphine, but generally tolerate this agent well. Rash and pruritis are occasionally present in atopic individuals as well as idiosyncratically. All opioids affect visceral sphincters equally. Meperidine is minimally used secondary to its excitatory effects on the cardiac and central nervous system with repetitive dosing. Hydromorphone is anecdotally preferred in patients with incipient renal failure, putatively due to less accumulation of toxic metabolites compared with morphine (3,6-diglucuronide). Fentanyl is an alternative parenteral opioid, with a short half-life that is useful for painful procedures. It is often a choice in neonates with congenital heart disease because it has little cardiac effect except bradycardia. High doses, and rarely low doses, may produce glottic and chest wall rigidity, treated with naloxone and /or neuromuscular blockade. For older patients with chronic pain, fentanyl may be administered rapidly and transmucosally, in a candy matrix, or over 72 hours transdermally via patch placement and subdermal release following deposition. Methadone provides a form of sustained-release administration, with attention to the accumulation of effect, from 3 to 4 hours to 24 hours, with repetitive dosing. It is often used to wean opioids after sustained parenteral infusion. Sufentanil is used primarily as a general anesthetic. Intermittent intramuscular dosing is contraindicated in pediatric patients because of common needle aversion and often incomprehensible pain with injection in this population. As a rough dosing guide, premature infants and neonates require 1/10 the usual adult dosage; 1 month olds, 1/8; 1 year olds, [1/4]; and 7 year olds, [1/2].30,31,39

Oral opioid preparations (codeine, oxycodone, morphine elixir, and rapid-release tablets) and opioid / NSAID combination (acetaminophen with codeine, oxycodone with acetaminophen) are often used for the pediatric patients following recovery from acute surgery or trauma for mild to moderate pain.31 Tramadol is an unusual opioid, recently studied regarding pediatric pharmacokinetics, with morphine-like μ1-receptor agonism, incompletely antagonized by naloxone, and some additional reuptake blockade of norepinephrine and serotonin.41,42

Rectal suppositories of morphine and hydromorphone are available for patients who cannot tolerate oral drugs and who are not neutropenic or immunosuppressed. Neuroaxial opioids, well-tolerated and commonly used in pediatrics, are fentanyl and hydromophone.

Adverse effects of opioids are treated as in adult patients, with the exception of the use of compazine and other dopaminergic agents for nausea and vomiting. These agents may result in frightening dystonic reactions in children. Recommended agents are ondansetron, hydroxyzine, and diphenhydramine.31

Regional anesthesia techniques are widely used in infants and children for acute postoperative pain management and for diagnosis and treatment of a variety of chronic pain conditions. Because of fear and anxiety of needles and procedures, most children will require general anesthesia for most regional techniques. Some motivated, older children may only require sedation for certain blocks. Regional blockade is typically combined with general anesthesia for most operative procedures. However, patients with neuromuscular diseases requiring muscle biopsy, patients with significant pulmonary disease, or those with a risk for postoperative apnea are often considered for regional techniques without general anesthesia. The regional technique should be explained to the parents and to the child in age-appropriate terms and informed consent should be obtained. Some children become frightened postoperatively with a dense motor or sensory block, and a preoperative discussion about what to expect after surgery can be helpful. Contraindications to the use of regional techniques in children are similar to contraindications for adult patients. These include refusal by patient or parents, infection at the site of needle entry, and clinically significant bleeding disorders.

Pharmacology of Local Anesthetics

The pharmacology of local anesthetics in pediatric patients differs from adult patients. Neonates and infants have delayed hepatic degradation of amide local anesthetics for the first 3 to 6 months of life.43,44 In addition, infants younger than 3 months old have prolonged elimination half-lives of amide local anesthetics.43,45 Delayed hepatic degradation and prolonged elimination half-lives may result in higher systemic amide local anesthetic levels with increased risk of toxic effects. Neonates and young infants have reduced serum levels of albumin and α1-acid glycoproteins involved in protein binding of local anesthetics.46,47 This may lead to increased levels of free unbound drug and higher risk of systemic toxicity in neonates and young infants.45,48 Neonates, however, have larger volumes of distribution that may lead to decreases in serum drug levels and may help reduce systemic toxicity.49

Ester local anesthetics are metabolized by plasma cholinesterase. Neonates and infants up to 6 months of age have approximately one half the levels of plasma cholinesterase found in adult patients.50 Therefore, the clearance of ester local anesthetics such as choloroprocaine may be prolonged in infants. However, because of the rapidity with which chloroprocaine is metabolized, even in infants, it is often used for continuous epidural infusions.

Spinal Anesthesia

The use of spinal anesthesia for surgical procedures below the T10 dermatome has been shown to reduce the incidence of postoperative apnea and bradycardia in former preterm infants <55 weeks postconceptual age and full-term infants <44 weeks postconceptual age.51,52 Short procedures lasting less than 1½ to 2 hours, such as inguinal herniorraphy, circumcision, and hypospadius repair are commonly performed under spinal anesthesia in preterm and full-term infants who may otherwise be at increased risk for postoperative apnea and bradycardia after general anesthesia. Even with the use of spinal anesthesia, patients should continue to be closely monitored for apnea and bradycardia overnight.53,54

Hyperbaric tetracaine and bupivacaine are most commonly used for spinal blocks (Table 53-6). In infants, 0.8 to 1 mg/kg of tetracaine provides effective surgical motor block and sensory block to T2-4. Inadequate dosing results in higher failure rates. The level of blockade to T2-4 may lead to motor block of intercostal and abdominal muscles. However, infants are able to maintain adequate tidal volume through diaphragmatic breathing.55,56 Patients in this age group remain stable with respect to heart rate and blood pressure with this level of blockade.57

Spinal block can be performed with the patient positioned in either a sitting or lateral decubitus position (Fig. 53-3). Careful head positioning is required to avoid airway obstruction, particularly in the sitting position.58 Because the conus medullaris ends at L3 in infants, the dural puncture should be performed at L3 or lower. After aseptic skin preparation and draping, the skin is usually infiltrated with local anesthetic. A 25-gauge 1-in. or 22-gauge 1.5-in. spinal needle is slowly inserted. The characteristic loss of resistance felt when puncturing the dura may not be appreciated in infants. The local anesthetic solution should be slowly injected after free flow of CSF is confirmed. Patients may require brief positioning in reverse Trendelenburg if cephalad spread of local anesthetic appears too great. After testing the level of blockade with a light pinprick, the blood pressure cuff and pulse oximetry probe can be moved to the leg to help ensure a still infant during the procedure. A pacifier dipped in glucose solution and a quiet environment may also be helpful. Typically, no sedatives or analgesics are administered, especially with concerns of postoperative apnea.56

Caudal Epidural Analgesia

Caudal epidural analgesia is a safe, technically successful, and easily performed block in pediatric patients.59,60 A “single shot” caudal block is commonly used for outpatient surgical procedures below the T10 dermatome, such as lower extremity orthopedic procedures, herniorraphy, or circumcision. It can be used as continuous catheter infusion for longer and more extensive procedures. Continuous caudal catheter infusions are discussed in the following section on lumbar and thoracic epidural infusions.

Dilute solutions of bupivacaine are frequently used for caudal blocks.61,62 Doses of 0.75 to 1 mg/kg of 0.25% bupivacaine when combined with general anesthesia provides effective postoperative analgesia, and when placed at the beginning of the procedure, can reduce general anesthetic requirements. This dose is within the recommended maximum safe level of bupivacaine of 2.5 mg/kg.63,64 The duration of postoperative pain control varies with caudal epidural analgesia. Some studies estimate the duration of analgesia with caudal blockade with bupivacaine at 5 hours, whereas other studies report that 50% of patients required no analgesics 12 hours after placement of the caudal block.63,65 The addition of clonidine to the bupivacaine solution may enhance the analgesic effect of the block and prolong duration.66,68 Although the optimal dose has not been clearly established, we use 1 to 1.5 μg/kg for children older than 1 year of age, up to a maximum dose of 30 μg.

Caudal epidural block is most frequently performed with the patient positioned in a lateral decubitus position. The sacral hiatus is easily palpated between the sacral cornu (Figs. 53-4 and 53-5). Using aseptic technique, the needle is inserted through the sacrococcygeal ligament into the epidural space. Our practice is to use a short-bevel needle. A loss of resistance is typically felt on entering the epidural space. The angle of the needle is lowered and the needle is advanced no further than 2 to 4 mm to avoid intravascular placement. After aspiration for blood and CSF, a test dose of local anesthetic and epinephrine is injected to detect tachycardia or hypertension associated with an intravascular injection.

Lumbar and Thoracic Epidural Analgesia

Lumbar and thoracic epidural analgesia is widely used for infants and children in a variety of surgical procedures, such as lower extremity and pelvic orthopedic surgery, major abdominal surgery, and thoracic procedures. There is evidence to support that epidural analgesia helps with early postoperative extubation and helps to improve postoperative pulmonary function.69 Because of the need for general anesthesia in performing this technique, children with chronic pain disorders often have continuous epidural catheter infusions rather than repeated epidural injections for treatment of their underlying pain.

Bupivacaine and, in select cases, chloroprocaine are frequently used local anesthetics for continuous epidural infusions in infants and children (Table 53-7). Because of age-related differences in hepatic degradation and clearance of amide local anesthetics, it is recommended that epidural bupivacaine infusions should not exceed 0.2 mg/kg/hour in infants younger than 3 months of age and 0.4 mg/kg/hour in children.43-45,70,71 The addition of opioid and/or clonidine to the bupivacaine solution can provide optimal analgesia while allowing a safe range of bupivacaine infusion rates. We typically use 0.1% bupivacaine combined with fentanyl 2 μg/mL with or without clonidine 0.4 μg/mL, or 0.1% bupivacaine combined with hydromorphone 10 μg/mL. We recommend reduced initial infusion rates when using solutions containing hydromorphone or in cases where the epidural catheter tip is in the thoracic region. Clonidine has less depression of CO2-response curves in infants compared to fentanyl. Bupivacaine-hydromorphone infusions are rarely used in infants younger than 6 months due to increased risk of respiratory depression. Chloroprocaine 1.5% can be used as a continuous epidural infusion in children younger than 6 months of age, however it can lower the seizure threshold in some patients.

With the patient in a lateral decubitus position, the epidural space is generally located using continuous loss of resistance technique (Fig. 53-6). An 18-gauge 2-in Tuohy needle and a standard 20-gauge catheter are typically used. Loss of resistance to saline rather than air is recommended because of the risk of venous air embolism in infants and small children.72,73 Because of concerns regarding the risks of direct placement of thoracic epidural catheters in anesthetized children, studies have examined the effectiveness of advancing epidural catheters from the caudal and lumbar regions to a thoracic dermatome.74–76 Evidence suggests fairly good success rates in caudal to thoracic advancement in infants compared with lumbar to thoracic level. Catheter advancement to the thoracic region should be performed using fluoroscopy, particularly for patients in whom correct catheter placement is crucial, such as for patients with congenital diphragmatic hernia or for patients requiring palliative care. Our preference is to use styletted 20-gauge catheters with fluroscopic guidance for all thoracic epidural catheters, whether directly placed or advanced from lower levels. Direct thoracic epidural catheters should be placed only in selected patients and by anesthesiologists with considerable expertise in pediatric regional techniques.

Complications associated with epidural techniques in children are similar to adult complications, such as inadvertent intravascular or intrathecal injection of local anesthetics and infection. A negative aspiration for blood or CSF helps to reduce the incidence of intravascular or intrathecal injection of local anesthetic.60 Although a test dose is always recommended, changes in hemodynamic profile as a result of intravascular epinephrine may not be obvious in an anesthetized child.60,77 A retrospective review of epidural infusions among pediatric patients suggests a very low incidence of infection when used short term for postoperative analgesia.78

All patients with continuous epidural infusions require careful nursing observation and regular assessment of level of sedation and pain score and measurement of vital signs. Infants younger than 6 months of age, patients with increased risk for respiratory compromise, or patients receiving epidural hydrophilic opioids require electronic monitoring in addition to close observation.

Axillary Brachial Plexus Block

Axillary brachial plexus blockade is a safe and easily performed block in children undergoing arm or hand surgery, often in conjunction with general anesthesia. The axillary artery is usually readily palpated in children between the coracobrachilis muscle and the pectoralis major.79 The arm should be flexed and slightly externally rotated. A 22-gauge short-bevel needle is slowly advanced to the perivascular sheath. Proper placement should be confirmed using a nerve stimulator, especially in anesthetized patients. An injection of 0.5 mL/kg of bupivacaine 0.25% provides up to 12 hours of effective postoperative analgesia. Complications with axillary brachial plexus blockade include inadvertent intravascular injection of local anesthetic and direct injury to artery or nerves.79

Fascia Iliaca Compartment Block

The fascia iliaca block allows for blockade of the femoral, lateral femoral cutaneous, obturator, and genitofemoral nerves.80 Proper needle and local anesthetic placement is based on easily identifiable landmarks. The inguinal ligament is identified between the anterior superior iliac spine and the symphysis pubis. A 22-gauge, short-bevel, blunt needle is inserted 0.5 cm caudad to the junction of the lateral one third and medial two thirds of the inguinal ligament (Fig. 53-7). Two distinct “pops” will be appreciated as the blunt needle traverses the fascia lata and the fascia iliaca. There should be a loss of resistance when the iliaca compartment is reached. Aspiration for blood should be checked before and periodically during injection of local anesthetic solution. A solution of 0.8 mL/kg of bupivacaine 0.25% can provide up to 12 hours of postoperative analgesia.81

Penile Block

The distal part of the penis is innervated by the dorsal penile nerves. These nerves can be reliably blocked in patients undergoing circumcision or distal hypospadius repair.82,83 Because “single-shot” caudal blocks sometimes cause significant lower extremity weakness and inability to ambulate postoperatively, penile blocks are sometimes preferred to caudal blocks for these types of outpatient procedures.84,85 The proximal part of the penis and the scrotum are innervated by the genitofemoral and ilioinguinal nerves and are not affected by a penile block.

A penile nerve block is performed by inserting a 25-gauge needles just below the pubic rami, 0.5 to 1 cm on each side of the symphysis pubis (Fig. 53-8).82 The usual dose of 0.1 mL/kg of 0.25% bupivacaine on each side of the symphysis pubis provides long-lasting analgesia postoperatively. Epinephrine-containing solutions should not be used for penile blocks because of the risk of vasoconstriction of end arteries.

Over the past 20 years, there have been significant clinical advances in the treatment of acute pain in children. Improved analgesics, better understanding of pediatric pharmacology and neurodevelopment, and increased experience in regional techniques in children have led to these clinical advances. Optimal management of acute pain requires reliable assessment of pain and aggressive management of pain and side effects with consideration to emotional and social factors contributing to pain.