“Acute pain” in the pediatric setting is generally nociceptive pain arising from tissue injury, inflammation, or infection. It is typically most pronounced immediately after the insult and gradually improves as the tissues repair. This type of pain usually responds to regional techniques, opioid medications, nonsteroidal antiinflammatory drugs (NSAIDs) and nonpharmacologic interventions, such as cognitive behavioral therapy and acupuncture; it rarely progresses to chronic pain.
Nociception involves the transduction of an inflammatory, mechanical, or thermal stimulus into a neural impulse, the transmission of the neural impulse from the periphery to the central nervous system (CNS), the modulation of that impulse, and the perception of the stimulus. The patient’s perception of pain is the most variable of the above components and relies heavily on a combination of psychological, behavioral, and environmental factors.
Pathophysiology of Acute Pain
Trauma to tissue results in the release of arachidonic acid from cellular membranes and its conversion by cyclooxygenase and lipoxygenase into multiple inflammatory substances. These pain-inducing substances include: substance P, histamine, bradykinin, serotonin, leukotrienes, potassium, and hydrogen ions. Substance P is a neurotransmitter and neuromodulator of key importance in the pain response. It is a peptide compound produced in the spinal and Gasserian ganglia which is stored in somatic and visceral neurons. Its release results in nitric oxide dependent vasodilation, bronchoconstriction, further cytokine release, resultant inflammation, and an increase in vascular permeability, which leads to increased edema and erythema at the site of injury. Substance P is associated with the development of denervation hypersensitivity, which is a state of postsynaptic overactivity caused by the increased formation of postsynaptic receptors in response to decreased neurotransmitter release after trauma-associated denervation of substance P nerve terminals. This cascade results in an increased response to any release of substance P into the synaptic cleft.
Nociceptors are sensors located at the sensory neurons axonal terminus, which responds to a variety of noxious mechanical and thermal stimuli. These noxious impulses are carried by A-δ (thinly myelinated) and C (unmyelinated) afferent nerve fibers to the CNS for processing. These are different from other sensory nerves in that periods of prolonged nociceptor stimulation result in a reduction of the excitatory threshold and, consequentially, peripheral sensitization.
A-α and A-β fibers transmit nonnoxious afferent signals, which then have the potential to be transformed in the CNS into pain signals through various mechanisms. This can result in peripheral or central sensitization. Peripheral sensitization includes the phenomena of hyperalgesia (an increased response to normally noxious stimuli) and allodynia (a painful response to a typically nonnoxious stimulus).
Central sensitization, or “wind-up,” is the result of repeated stimulation of C fibers in the peripheral nervous system that results in increased electrical activity. There is also an associated dysfunctional remodeling that occurs at the convergence of peripheral afferent nerve fibers where signals are typically processed and modified. This activity is most concentrated at the dorsal horn of the spinal cord and involves NMDA receptor response priming. This priming results in an amplification of pain intensity and duration. For this reason, patients who undergo repeated, painful procedures may experience an increased perception of pain in the absence of increased stimulation.
The spinal cord is separated into multiple layers, referred to as the Rexed laminae. Most pain signal transmission—via A-δ and C fibers—involves laminae I and V, with a lesser degree of involvement from laminae III, IIo, and II (substantia gelatinosa). Lamina I is the most dorsal aspect of the dorsal horn of the spinal cord. It receives pain and temperature signals primarily from the dorsolateral tract. The sensation relayed at this level is not modulated.
Lamina V is located at the neck of the dorsal horn and receives signals from cutaneous, muscular, and joint mechanoreceptors, and from visceral afferents. This layer contains a large number of wide dynamic range neurons which are involved in sensory discrimination and associated with the wind-up phenomenon, viscerosomatic pain referral, and chronic neuropathic pain.
After signals are processed and modified in the dorsal horn, second-order neurons transmit to the CNS after traveling via tracts in the anterior and anterolateral aspects of the spinal cord. With regard to pain signal transmission, the spinothalamic tract is the most important of these tracts. The spinothalamic tract consists of two pathways: the anterior spinothalamic tract (transmitting signals pertaining to crude touch) and the lateral spinothalamic tract (involved in pain and temperature signals). The spinoreticular tract and spinomesencephalic tracts also play a role in pain transmission, presumably to a lesser extent.
Peripheral nociceptive signal transmission is regulated centrally to some degree by the inhibitory descending pathway. This pathway arises in the cerebral cortex and involves motor neurons which are located in the Rexed laminae I, IIo, and V. Serotonin and norepinephrine are the primary neurotransmitters involved in this pathway and the action of medications like tricyclic antidepressants, tramadol, and clonidine are thought to exert their effects, to some degree, by their modification of the activity at the inhibitory descending pathway.
The transduction, transmission, modulation, and perception of pain involves a complex network of nociceptive pathways involving the limbic system, frontal cortex, and medial thalamus. The patient’s pain experience is further influenced by their emotional state, behavior, past experience, and other cultural and societal factors. The successful management of the acute pain patient requires careful consideration of many different variables and a resultantly balanced and appropriately tailored treatment plan.
Setting Pain Expectations
The many modalities of pain management employed in the acute pain setting are enhanced by discussions of expected procedural pain and management strategies before the patient even arrives at the hospital. The surgical visit is the first step in setting a patient’s and family’s expectations for the hospital experience and management of pain. At the author’s institution, a collaboration between the pain team, surgeons, nurses, and staff has resulted in pathways and order sets which reduce a patient’s length of stay while maintaining or decreasing pain scores. These pathways have focused mainly on orthopedic procedures such a posterior spinal fusion, hip procedures, and sports medicine surgeries that use regional anesthesia and opioids through multimodal analgesia and continued home management with a reduced number of prescriptions. Although it is difficult to tease out which particular aspect or medication in the pathway is responsible for the reductions in length of stay, the establishment of the pain expectation for the patient has been translated into other procedures, including the Nuss procedure for pectus excavatum repair. Consistent use of order sets on the pathway reduce practice variation and maintain a uniform pain management plan to the patient and family. This compliance improves the quality of care delivered and can increase patient and family satisfaction.
Patient-Controlled Analgesia
Patient-controlled analgesia (PCA) has been used for the management of pediatric pain since the 1980s and has become the most common mode of analgesia for the treatment of acute, moderate-to-severe pain in children over the age of about 6 years. PCA is most commonly used in the postoperative period when the patient is still NPO and in patients who have experienced trauma or burns. PCAs, in general, are considered to be safe, effective, and highly satisfactory for patients and their families.
The use of a PCA allows for self-titration of IV opioids, which allows for patient-driven tailoring of medication administration based on the individual patient’s pain experience. Because of more frequent, smaller dosing of opioids, this method of administration leads to a narrower range of opioid levels in the blood compared with IV nurse-administered bolus dosing. Patients avoid pronounced peak drug levels that are associated with side effects such as oversedation and respiratory depression and relatively low trough levels, which result in an increase in pain levels.
PCA can also be used for epidural, peripheral nerve catheter, and transdermal medication administration. Compared with IV routes, epidural administration of PCA-delivered opioids has consistently shown to provide more effective analgesia, particularly in situations of severe pain. IV PCA consists of a pump that is attached to a reservoir of medication and controlled by a hand held remote button, by which demand doses are requested. This reservoir is connected to the patient through IV tubing allowing for delivery of medication straight into the patient’s circulation. The pump itself is programmed to record utilization, allowing for monitoring and trending of overall drug usage.
Though the name implies control by the patient, PCA can also be controlled by the parent, nurse, or a combination thereof. Selection relies on a variety of factors which include the patient’s age (school-age is generally the age at which the patient is developmentally appropriate and self-aware enough to begin assisting with their pain control), cognitive ability, physical ability (the patient must be physically able to press the PCA button), and parental involvement in patient care. The immediate analgesic effect offered by PCA provides the administrator some degree of control over the pain experience, which is particularly useful for parents or patients with a high level of pain-associated anxiety.
When the infusion pump is controlled by the patient alone, there is minimal risk for overdose resulting in CNS and respiratory depression. However, with parental or nurse control, this is a potential risk if demands are requested when the patient is already sedated. Though seemingly intuitive, it is important to educate parents and nursing staff on the importance of ensuring that the patient is awake before demands are requested and that the PCA not be used to treat natural sleep-associated movements or vocalizations. With overly concerned parents, it is helpful to affirm that if the patient is asleep, an adequate level of analgesia has been achieved. At the author’s institution, all patients receiving PCA are monitored by heart rate, respiratory rate, and pulse oximetry for at least the first 24 hours and after any increases to the PCA for 24 hours more to ensure continued safety.
The infusion pump used for PCA employs a few basic settings. These include the demand dose, lockout interval, continuous infusion rate, and 1- or 4-hour total medication limits. Additionally, one should administer an initial loading dose of the medication to obtain adequate levels of analgesia before relying solely on the PCA as it can take significant periods of time to obtain these levels when using the low, demand dose from the PCA. This initial bolus should be given in a highly monitored environment in which respiratory resuscitation equipment is immediately available, (e.g., PACU = post-anesthesia care unit). In this way, the physician can ensure proper dosing and absence of medication allergy or intolerance.
The demand dose is the amount of medication delivered via the pump with each push of the PCA button. This is given at a frequency determined by the dosing interval which is a predetermined lockout that typically ranges from 6 to 12 minutes depending on the medication and clinical setting. Because of this safety feature, regardless of how many times the button is pushed, there will only be one demand dose delivered per lockout interval. One can also set a 1-hour or 4-hour limit to predetermine the maximum amount of medication that can be given over that respective time period.
In some situations, such as in the postoperative period after a procedure with anticipated severe levels of pain, a continuous basal infusion can be added to the PCA program. This continuous infusion is administered to the patient independent of demand usage and can be continuous throughout the entire day or adjusted to be given over a specific time period. For instance, a night time infusion can be started to help prevent the troughs associated with decreased button use during sleep. Basal rates are associated with increased side effects and minimal associated improvement in analgesia. Furthermore, there is an association between continuous infusions and sleep disturbances.
A rescue dose should also be assigned—usually a larger dose of the same medication in the PCA—to be administered on an as-needed basis in cases of severe pain for which the demand dose is not sufficient. These are particularly useful in situations where blood drug levels have decreased significantly, such as upon awakening with minimal overnight demand use with no background continuous infusion. Rescue doses are also important for incident pain: periods of time with higher levels of stimulation, such as dressing changes or bodily rotation.
Naloxone, 10 μg/kg, should be immediately available to treat respiratory depression. Because of the high incidence of nausea and vomiting with opioid administration, ondansetron 0.1 mg/kg every 8 hours as needed is also frequently used. Nalbuphine 50 μg/kg can be given every 4 hours for pruritus. Nalbuphine is also effective in the treatment of mild to moderate pain and can be scheduled or used on an as-needed basis. Of note, this and similar mixed agonist-antagonists can precipitate withdrawal symptoms in patients who are on preexisting μ-agonistic opioid therapy.
Selection of the medication for use in patient-controlled analgesia relies on preexisting disease, clinical setting, and patient response ( Table 35.1 ). One must consider the metabolites and routes of elimination of each option. Though morphine is the most well-studied and most commonly used opioid in PCA, hydromorphone is associated with less nausea and vomiting. Furthermore, morphine’s active metabolite, morphine-6-glucuronide, makes it a poor choice in the setting of renal insufficiency. Morphine is also avoided in patients whose neurologic status must be frequently assessed because of its long duration of action. Nalbuphine can be useful in patients with primary GI illness where the maintenance of gut motility is important such as with patients who have Crohn disease.
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