Pediatric Procedural Sedation
Pediatric Procedural Sedation
Author: Mark D. Lopez, MD, FACEP, FAAEM, Associate Professor of Emergency Medicine and Pediatrics, Department of Emergency Medicine, Medical College of Georgia, Augusta; and Gerald Beltran, DO, Resident, Department of Emergency Medicine, Medical College of Georgia, Augusta.
Peer Reviewer: George Foltin, MD, Associate Professor of Pediatrics and Emergency Medicine, Director of Pediatric Emergency Service, Bellevue Hospital, New York, NY.
Procedural sedation is an important tool for the emergency department physician, especially when faced with a child who requires a painful procedure. The ability to adequately address the pain and anxiety of the child and safely complete the procedure is rewarding to both the physician and the family of the child. The use of procedural sedation is not without risks, and the clinician must select appropriate agents and monitoring to safely complete the procedure. This article reviews the process of procedural sedation and agents that may be utilized in a variety of common scenarios.
The Editor
Introduction
Pain management is an important part of patient treatment in the ED. Common misperceptions by healthcare professionals are that children do not experience pain and only have short-term memory of it. This has led to pediatric patients receiving less pain medicine than adults for similar conditions.1-4 Selbst and Clark found that children were less likely than adults to receive pain medications in EDs for similar painful conditions.1 This misperception has been called into question with recent research.5-7 The concern has been significant enough for the American College of Emergency Physicians (ACEP) to issue a clinical policy on pediatric pain management and to discuss the importance of addressing pediatric pain in the preface of the clinical policy.8 Additionally, a rapidly expanding body of literature also discusses the importance of pain management in pediatric patients.9-11
The ideal sedation protocol would allow for rapid induction and emergence, maintain effective spontaneous ventilation and airway control, and have minimal to no side-effects.12 No such agent has been identified to date. Many different forms of procedural sedation have been tried, with each having its own risks and benefits.
Originally called "conscious sedation" as published by the American Academy of Pediatrics back in 1992, the currently preferred term is procedural sedation. The term procedural sedation replaced conscious sedation to reflect the concept that effective sedation can alter consciousness. It is a commonly needed tool in the emergency department, as it allows for diagnostic and therapeutic procedures to be performed while minimizing and controlling patient pain and anxiety. It has even more importance in pediatrics, as children cannot fully understand the medical interventions that must be performed, and the child's anxiety can heighten his or her discomfort.
The goal of procedural sedation is to provide effective sedation so that the child can tolerate the procedure and the clinician can complete the procedure in a controlled manner that increases patient safety and minimizes complications.
Sedation of pediatric patients has potential serious associated risks, such as hypoventilation, apnea, airway obstruction, laryngospasm, and cardiopulmonary impairment. Appropriate drug selections for the intended procedure as well as the presence of an individual with the skills needed to rescue a patient from an adverse response are essential. This is the purview of the emergency medicine practitioner. Appropriate physiologic monitoring and continuous observation by personnel not directly involved with the procedure allow for accurate and rapid diagnosis of complications and initiation of appropriate rescue interventions.13
The sedation of children is different from the sedation of adults. Sedation in children frequently is administered to control behavior that will allow for the safe completion of a procedure. A child's developmental and chronological age will determine the ability to control his or her own behavior to cooperate for a procedure. Often, children younger than 6 years of age and those with developmental delay require deep levels of sedation to control their behavior. Therefore, the need for deep sedation should be expected.13
The goals of sedation in the pediatric patient for diagnostic and therapeutic procedures are to guard the patient's safety and welfare; minimize physical discomfort and pain; control anxiety, minimize psychological trauma, and maximize the potential for amnesia; control behavior and/or movement to allow the safe completion of the procedure; and return the patient to a state for safe discharge from medical supervision, as determined by recognized criteria.13
Indications for Conscious Sedation
The purpose of procedural sedation is to induce a state that allows the patient to tolerate an unpleasant procedure while maintaining cardiorespiratory function.13 Sedation may be used for a variety of reasons in children, including inhibition of respiratory drive, promotion of synchrony with mechanical ventilation, reduction of oxygen consumption, reduction of the stress response, and performance of a wide variety of procedures.14 The most common specified pediatric procedures performed in the ProSCED Registry study included laceration repairs (n = 86, 25%), shoulder relocations (n = 78, 23%), and fracture care of the upper extremity (n = 56, 16%).15 (See Table 1.)
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Physiology of Pain
Acute pain is produced by stimulation significant enough to possibly cause tissue damage. Its utility is in warning a person of a potentially serious injury or illness. This encourages the person to stop the task that initiated the painful stimulus or to seek treatment for the underlying disorder.16
Pain is a process that involves multiple steps: activation of receptors, pain signal transmission, modification of the pain signal, and perception of pain. Activation of the ubiquitous nociceptors permits a person to sense the noxious stimulus. These types of receptors change chemical, mechanical, and thermal stimulation into an electrical impulse. They can be found throughout the body in places such as the skin, teeth, joints, muscles, periosteum, and arterial walls. There are many chemical mediators involved in the perception of pain including bradykinin, serotonin, histamine, leukotrienes, platelet aggregating factor, acetylcholine, substance P, and thromboxanes.
There are two types of pain receptors or nociceptors.17 They are A-delta fibers and C fibers. The A-delta fibers are associated with thinly myelinated fibers that pass through the contralateral spinothalamic tract. These neurons pass the neuronal impulse faster than their counterpart, the C fibers, and provide the sensation of sharp or burning pain. The C fibers are not myelinated and therefore are slower than the A-delta fibers. These C fibers provide impulses relating to dull and aching pain and also pass through the contralateral spinothalamic tract. Both fibers carry impulses to the lateral and medial thalamus. From there, the signal is relayed to the cerebral cortex.
In the central nervous system (CNS) the pain stimulus is modified by neuromodulators, which can be excitatory or inhibitory to the pain signal. Some of these modulators include: opioid (e.g. mu, kappa, delta), serotonin, GABA (gamma-aminobutyric acid), adenosine, glutamate, and alpha adrenergic.
Goals of Sedation
As discussed previously, the purpose of procedural sedation is to address the pediatric patient's pain while allowing an uncomfortable procedure to be completed. While analgesics such as acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDs), and opiates provide relief from pain, they do not address the need for sedation. The goals for procedural sedation include minimizing pain, reducing patient anxiety and fear, and controlling the patient to allow successful performance of the needed procedure.
Definitions
Terms commonly associated with procedural sedation include pain, analgesia, anesthesia, sedation, minimal sedation, moderate sedation, deep sedation, general anesthesia, and dissociative sedation.16 Each of these terms should be understood to allow for clear communication of level of sedation and the effects of each sedative agent.
Pain is defined as having both a sensory and emotional component. The unpleasant stimulus has the potential to cause tissue damage and is exacerbated by fear and anxiety. The purpose of procedural sedation is to control the emotional component while at the same time allowing for analgesia from the uncomfortable stimulus.
Analgesia is a reduction in or relief from pain. This reduction is accomplished without a loss of consciousness.
Anesthesia is usually a drug that is administered to provide amnesia, reduced level of consciousness, analgesia, and relaxation of the body's musculature without having a detrimental affect on the patient's physiologic or cardiorespiratory stability.
Sedation simply reflects a reduction of anxiety, fear, or excitement through administration of a pharmacologic agent. Minimal sedation refers to a level of sedation where the patient responds appropriately to verbal command. Cognitive processing may be affected while the pulmonary and cardiovascular functions are not. Moderate sedation is a level of sedation in which the patient responds appropriately to verbal commands or with the addition of mild stimulus. A patient with moderate sedation maintains his or her airway and ventilates without any intervention being required. With this level of sedation, cardiopulmonary function is maintained near baseline. Deep sedation is a level of sedation in which the patient is not easily aroused but does respond purposefully with a significantly uncomfortable stimulus. A patient with this level of sedation may require medical intervention to maintain an airway and ventilation. This patient also maintains his or her baseline cardiovascular function.1
General anesthesia refers to a patient who is unable to be aroused with a verbal or painful stimulus. These patients often need help in maintaining their airway and may require positive pressure ventilation. Additionally, the patient's cardiovascular function may be negatively affected.
Dissociative sedation is a state in which the patient maintains protective airway reflexes, spontaneous respiratory drive, and cardiovascular stability. In this level of sedation, the patient is placed into a trance-like state in which he or she experiences significant analgesia and amnesia.
Pre-procedural Fasting
The issue of fasting is often considered when determining the risk-benefit ratio for procedural sedation. Traditionally, the recommendations for both pediatric and adult procedural sedation have included pre-procedural fasting. This has been based on the real but rare risk of aspiration. The recent clinical policy on procedural sedation of pediatric patients from the American College of Emergency Physicians states that definitive sedation guidelines based on sound evidence are lacking because of a paucity of ED studies about pre-procedural fasting.8 The American Society of Anesthesiologists (ASA) published guidelines that were based on consensus from patients undergoing general anesthesia.18 Dissociative agents such as ketamine and inhalational agents such as nitrous oxide have a different mechanism of action and do not blunt the airway reflexes to the same extent as other sedatives. The sedation practitioner needs to be aware of the range of sedation from anxiolysis to general anesthesia and the effect the selected agent chosen will have on protective airway mechanisms, but in general, procedural sedation may be safely administered to patients who have had recent oral intake.
The Joint Commission on Accreditation of Healthcare Organizations (JCAHO) addresses this issue by mandating that each facility develop a standardized protocol that is utilized during procedural sedation. The amount of time a patient must fast before a procedure is not defined by JCAHO; rather, they expect each facility to develop its own standards. The vast majority of literature concerning this subject is from general anesthesia and its applicability to emergency procedural data is limited.19,20 Of studies performed using a pediatric emergency department, the risk of adverse outcomes with limited pre-sedation fasting, including pulmonary aspiration, was extremely low.21-23 This suggests that fasting prior to procedural sedation is not mandatory. However, it is a consideration when contemplating the depth of sedation the physician selects.
Commonly Used Drugs
Ketamine. Ketamine is a dissociative agent, which induces a state of catalepsy that provides sedation, analgesia, and amnesia. The advantages of ketamine include: administration intramuscularly or intravenously, and reliability in production of potent analgesia, sedation, and amnesia.24
Ketamine does not affect pharyngeal-laryngeal reflexes and, therefore, allows a patent airway as well as spontaneous respiration to maintain intact; making it particularly useful for emergency procedures when fasting is not assured. The unique dissociative action permits painful procedures to be performed in a consistent state of sedation. The onset of action for intravenous (IV) administration is within 1 min, and duration of action lasts about 5-10 min. If administered intramuscularly (IM), the onset of action is observed between 3-5 min, and duration of procedural conditions lasts about 20-30 min.
Ketamine acts by inhibiting reuptake of catecholamines and, therefore, can produce mild to moderate increases in blood pressure, heart rate, cardiac output, and myocardial oxygen consumption.25 Administration of ketamine stimulates salivary, tracheal, and bronchial secretions, causing potential airway obstruction, laryngospasm, and tracheal aspiration of secretions. Excessive secretions can be prevented effectively with prior administration of an antisialagogue like atropine or glycopyrrolate.25
The most common adverse reactions are nightmares and unpleasant recovery agitation (mostly in adults up to 30%), emesis (6-7%), laryngospasm (0.4%), and apnea (0.002%).24
The unpleasant hallucinations and dreams that occur during the recovery period may be reduced with benzodiazepines. They occur with less frequency in children than in adults. The use of ketamine and midazolam together has been found to reduce the incidence of hallucinations as well as provide faster onset of analgesia and more effective amnesia.26 However, benzodiazepines suppress ketamine metabolism through competition for hepatic-degradation enzymes and may prolong ketamine recovery time.27,28
In a study by Karapinar et al., 4.8% of patients had potentially serious respiratory complications. All were treated with airway management.25 In a study by Green et al., studying intramuscular ketamine, seven subjects demonstrated transient laryngospasm, apnea, or respiratory depression. None of these children had any contraindications to ketamine, and all had received concurrent atropine. None required endotracheal intubation and, in all cases, the procedure was completed and recovery was uneventful.24
The dosing for ketamine is 1-2 mg/kg intravenously or 2-5 mg/kg (usually 4 mg/kg) for intramuscular use in ED procedural sedation. (See Table 2.)
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Propofol. Propofol (2,6-diisopropylphenol) is an intravenous hypnotic that is produced in a soy-based emulsion. The emulsion contains soybean oil, egg lecithin, and glycerol. It has a rapid onset of action with a loading dose of 2 to 2.5 mg/kg, achieving unconsciousness within 10-50 seconds of intravenous administration. The drug has certain properties that make it attractive for both anesthesia and sedation: rapid redistribution and elimination following a single bolus injection, or during and after continuous infusion; antioxidant and anti-inflammatory properties; mild bronchodilating capabilities; and action on N-methyl-D-aspartate and [gamma]-aminobutyric acid type A receptors that has demonstrated usefulness in the management of refractory seizures and severe delirium tremens.29,30
Its mechanism of action is poorly understood but is likely caused by action on the lipid membrane sodium channel function and potentiation of the stimulatory effect of [gamma]-aminobutyric acid on coupled chloride channels. It is highly protein-bound and undergoes rapid distribution into the brain and other tissues. It is metabolized by the liver by glucuronidation and sulfation, and then it is excreted in the urine. Its distribution half-life is between 1 and 8 minutes with metabolic clearance in 30-50 minutes. Children have a more rapid metabolism than adults, averaging about 9.3 minutes after a single 2.5 mg/kg intravenous dose.29
Propofol is a hypnotic agent with no analgesic properties. Propofol has been used on its own or with a pre-sedation dose of narcotic (fentanyl or morphine) with similar outcomes. Analgesia should be administered during painful procedures either during or soon after sedation for the procedure.29
Propofol has a rapid onset of action, inducing unconsciousness within minutes of intravenous administration. Its advantage over other agents is that it has a brief duration of action with a very rapid return to pre-sedation levels. Thus, is it ideal for ED sedation. Until recently it was used exclusively in the operating room, but there are now more studies that have demonstrated its successful use in the ED and outpatient setting (e.g. procedural sedation units).29 There have been two methods by which propofol has been administered for sedation. Due to its short half-life, both methods require an initial bolus followed by either repeated boluses or a continuous infusion. Guenther, et al. used 1 mg/kg propofol (with fentanyl 1-2 mcg/kg) followed by a bolus of 0.5 mg/kg every 1-2 minutes, as required. The mean dose was 3.8 mg/kg with a range of 1-15 mg.31 The advantage of this system is that oversedation is less likely to occur because it is up to the physician to administer subsequent doses when the patient is felt to be under-sedated. Vardi, et al. and other studies have used propofol bolus 2 to 2.5 mg/kg followed by a continuous infusion of between 0.05 and 0.1 mg/kg/min.32 This has the advantage of keeping the patient at a steady state of sedation but has an increased risk of oversedation.29
The onset of action is dependent on the speed of injection. Slower injection is recommended since rapid injection has been associated with hypotension and apnea. Injection of propofol causes pain in a significant number of patients (up to 70%). The addition of lidocaine 1% (20-40 mg) to propofol does decrease this incidence, but it is more effective to inject 0.5 mg/kg of lidocaine into the forearm with a rubber tourniquet applied well above the injection site approximately 30-120 seconds before propofol infusion. This prevents pain in approximately 60% of patients.29
Propofol is similar to all sedative agents in that the depth of sedation is variable. Propofol is more likely than other sedative agents to produce general anesthesia at some stage during the procedure. Barbi, et al. reported on more than 1,000 sedations of children using propofol and reported that level of sedation down to general anesthesia occurred in 91% of patients.33 This study was performed by non-anesthetists and non-ED staff and these doctors were given an intense training procedure before they were able to use propofol.29
Propofol can have significant cardiovascular side effects. A decrease in preload, heart rate, systolic blood pressure, diastolic blood pressure, mean arterial blood pressure, stroke volume, cardiac index, left ventricular stroke work index, systemic vascular resistance, myocardial contractility, myocardial blood flow, myocardial oxygen consumption, cardiac output, end systolic pressure-volume relationship, and cardiac arrest with electromechanical dissociation have been described. The cardiorespiratory depressant effect of propofol can be minimized by titrating the dose to produce the desired clinical effect, rather than administering a fixed dose based on body weight.34
The most common adverse effect of propofol is dosage-dependent hypotension as a result of direct smooth muscle vasodilation, blunted sympathetic activity, and reduced tachycardia as a result of diminished baroreceptor response. More than 30% of the children in a study developed hypotension.35 Propofol-induced hypotension seems to be transient and of little physiologic relevance in the relatively healthy child who remains well perfused with peripheral warmth and excellent capillary refill during a sedation intervention.35
In the dosages required for deep sedation, propofol can result in respiratory instability. Oxygen desaturation occurred in almost 5% and airway obstruction that required an oral airway or nasal trumpet occurred in 2% in a study by Vapasiano, et al. Approximately 2.6% of the patients required some form of airway/respiratory intervention (e.g., oral airway, nasal trumpet, rescue breaths, intubation).35 Oxygen desaturation in sedated patients who receive oxygen supplementation is a late sign of alveolar hypoventilation. Propofol also appears to have less nausea and vomiting than other sedation agents (e.g., ketamine and nitrous oxide). The risk of nausea and vomiting is related both to the agent used (e.g., higher with nitrous oxide and opioids) and the type of procedure undertaken (e.g., ophthalmic or ears, nose, and throat surgery).29
Other less common complications during procedural sedation have been laryngospasm, bronchospasm, regurgitation, and aspiration. Complications associated with long-term infusion propofol administration have included hypertriglyceridemia, pancreatitis, green-colored urine (secondary to the production of a phenolic green chromophore), and hemodynamic instability, especially in the presence of hypovolemia.30
In 1992, case reports described fatalities in children undergoing sedation with propofol that came to be known as the "propofol infusion syndrome" (PRIS). The reports were mainly about children with upper respiratory tract infections who received high and escalating doses of propofol. The patients developed metabolic acidosis, refractory bradycardia (even after high doses of positive inotropic agents), lipidemia, rhabdomyolysis, fever, and refractory heart failure.30
The occurrence of PRIS has been associated with long-term propofol infusions (> 48 hours) at doses higher than 4 mg/kg/h (60 mcg/kg/min), and in children younger than 4 years of age. The mechanism for the constellation of metabolic derangements noted in this disorder has been postulated to be related to a defect in the mitochondrial respiratory chain that leads to impaired fatty acid oxidation due to reduced mitochondrial entry of long-chain fatty acids causing respiratory chain failure. Low carbohydrate supply may be a contributing factor in PRIS because energy demand is maintained by lipolysis if carbohydrate supply is low and thus results in an accumulation of free fatty acids. Patients with a mitochondrial disorder and patients who are allergic to eggs, sulfites, or soy products should not be considered candidates for sedation with propofol.30
Nitrous Oxide. Nitrous oxide is a dissociative gas that provides mild to moderate procedural anxiolysis, analgesia, and amnesia in a linear dose-response pattern. It is typically blended with oxygen and is recommended as a level A recommendation by the clinical policy from ACEP at a concentration of 50%.14 Nitrous oxide has both opioid agonist and N-methyl-D-aspartate (NDMA) glutamate receptor agonist effects. Most healthy patients have minimal cardiovascular or respiratory effects. Its advantages include an onset and offset occurrence within 5 minutes and it does not require IV access. It does, however, require a special delivery device for administration, or it can be used through an anesthetic machine, which already may be present in the ED.29
Adverse effects include emesis, nausea and, to a lesser extent, dizziness, euphoria, and dysphoria. Babl, et al. found that vomiting occurred in 7% of pediatric patients during nitrous oxide use in the ED.36 The emesis, however, did not appear to be associated with the length of fasting, type of procedure, depth of sedation, or length of administration. Since nitrous oxide is commonly blended with oxygen, hypoxemia is rare. Diffusion hypoxia with the cessation of nitrous oxide or "wash out" is a concern. A study by Dunn-Russell, et al. in 1993 found clinically significant difference in oxygen saturation after 30 minutes of 40% nitrous oxygen blended with oxygen.37
Midazolam. Midazolam is currently one of the most commonly used sedative drugs for premedication in children. Midazolam is a short-acting agent with rapid onset, and is associated with anxiolytic, sedative, and amnestic properties. Its mechanism of action is by interacting with g-aminobutyric acid (GABA) receptors in the brain.38 It has been attributed several beneficial effects such as anxiolysis, rapid onset of sedation, and profound anterograde amnesia. This may not be of benefit in the anxious patient requiring routine treatment, but it can be beneficial in those undergoing unpleasant procedures.39 Benzodiazepine sedation does not provide an analgesic effect and is inadequate to prevent pain induced by more aggressive procedures.25
The problem with the parenteral use of sedative and analgesic agents is the disturbances in respiratory function and hypoxemia. This was observed in 4.8% of patients in one study.25 Other adverse postoperative behavior changes observed have been hiccups and paradoxical reactions.40
Intranasal midazolam has been found to be effective in doses ranging from 0.2 to 0.6 mg/kg when used for conscious sedation. This technique has advantages when compared with oral administration as the bioavailability of intranasally administered midazolam is approximately 55%, compared with 15% when administered orally. The rate of onset and recovery are more rapid and patients are not required to actively swallow or hold the bitter preparation in their mouths.39
Fentanyl. Oral transmucosal fentanyl has been used in adults and children as a preanesthetic medication, for postoperative pain, and for cancer pain. More recently it has been used in children for sedation and analgesia during painful procedures. Success rates for anxiolysis have ranged from 56% to 100% in published randomized clinical trials.41 Two studies have examined the use of oral transmucosal fentanyl for premedication of children undergoing laceration repair. In a randomized, unblinded study involving 30 children, sedation with oral transmucosal fentanyl was found to be adequate in 52% of those receiving 10-15 mcg/kg compared with 60% of those receiving 15-20 mcg/kg. Vomiting and facial pruritus occurred in 20% and 67% of the low-dose group, respectively, compared with 47% and 60% of the high-dose group. One patient (in the low-dose group) experienced oxygen saturation < 95%, which was treated only with supplemental oxygen. The authors concluded that efficacy at the 2 doses was comparable; but that side effects are higher when higher doses were used.42
The main complications of oral transmucosal fentanyl include vomiting and pruritus (mainly facial). Vomiting occurs in approximately 40% of patients (range: 0%-65%), usually in the postoperative or postprocedure period, and pruritus occurs in approximately 60% of patients (range: 3%-81%). Oxygen desaturation below 94% has been rare (range: 0%-24%) and never required more than blow by oxygen or brief stimulation.41
Preparatory Activities to Procedural Sedation
Prior to performing the actual procedural sedation, several preparatory activities should be performed. These activities reduce risk to the patient, provide for a more smooth sedation, and reduce patient anxiety.
First, the patient should have a pre-sedation evaluation. This encompasses taking a history from the patient or patient's family, discussing allergies (including drug allergies), medications used, previous medical history, previous surgical history, prior hospitalizations, prior sedation or general anesthesia, family history, and last meal or last oral intake.
A physical examination should also be included as part of the pre-sedation evaluation. This should include examination of the lungs, heart, neck, mouth, and airway for conditions that would complicate procedural sedation, intubation, or resuscitation. Included in this examination should be an estimation of intubation difficulty. The most commonly referenced scale is the Mallampati scale, which assesses oral access for intubation. (See Figure 1.) Mallampati Class I is the easiest intubation and allows for views of the soft palate, uvula, fauces, and pillars. Class II is still a fairly easy intubation and permits views of the soft palate, uvula, and fauces. Class III is a moderately difficult airway and the soft palate and base of the uvula are visible when the patient opens his or her mouth. Class IV is a very difficult airway and the hard palate only is visible as the patient opens his or her mouth.
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The physical examination also encompasses patient evaluation according to the ASA classification to determine the overall health of the patient. (See Table 3.) Class I describes a normal healthy patient. An example would be a patient with an unremarkable history. Class II is a patient with mild systemic disease or no functional limitation. An example would be a patient with controlled diabetes mellitus, anemia, mild asthma, or controlled seizures. Class III is defined as a patient with significant or severe systemic disease causing a functional limitation. Patients in this ASA classification could have moderate to severe asthma, moderate obesity, pneumonia, poorly controlled diabetes, or poorly controlled seizures, for example. An ASA classification of IV describes a patient with severe systemic disease that is a constant threat to life. Examples of this classification include severe sepsis, blood pressure disease, advanced pulmonary, endocrine, cardiac, renal, or hepatic disease.
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The ASA classification is important as part of the initial assessment, as it generally is recommended that pediatric patients from ASA class I and class II are acceptable candidates for mild, moderate, and deep sedation outside of the operating room.1 Children who are ASA class III, IV, or V, who have abnormal airways, or who have special needs are not ideal candidates for procedural sedation in the emergency department. If possible, the procedure should be deferred.
Procedural sedation also should be avoided or deferred with patients who are hemodynamically unstable or who are compromised in their respiratory status. These patients should be stabilized first, prior to procedural sedation or preferably sent to the operating room for the sedation.
Second, once the determination has been made to perform procedural sedation, appropriate monitoring should occur. This allows for continuous observation of the patient's cardiopulmonary status. The hemoglobin oxygen saturation can be monitored with pulse oximetry. This non-invasive tool measures absorption of infrared light to provide information on the patient's hemoglobin oxygen saturation. It renders accurate measures of arterial oxygen greater than 70-80%.43-45
Capnography is a tool available to monitor end tidal carbon dioxide. It has been observed that end tidal carbon dioxide increases with deeper sedation, which may occur if the sedation produces hypoventilation.46-49 Its utility has been in providing objective measures demonstrating subclinical respiratory depression and/or obstruction of the airway.
Third, personnel should be present who are familiar with procedural sedation and are also comfortable with resuscitations. A physician should be one of the people on the team who understands the pharmacokinetics and mechanism of action of the procedural sedation drugs. This same individual should be capable of rendering emergency airway management if the sedation is deeper than anticipated or complications occur. Additionally, the physician can assist with management of any adverse reaction to any of the medications used.
Last, resuscitation equipment should be made ready and functionality tested prior to procedural sedation being initiated. Equipment that should be considered includes: suction, bag-valve-mask, oxygen, advanced airway equipment, and advanced airway drugs. This equipment should be kept ready and available until the procedural sedation has been completed. (See Table 4.)
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Reversal agent availability at the bedside should be considered until the patient is discharged. Naloxone (0.005-0.01 mg/kg/dose every 2-3 minutes) is able to reverse sedation and respiratory depression due to opiate medication effects. Flumazenil (0.01 mg/kg every 2-3 minutes with max total dose of 1 mg) is able to reverse the sedation and respiratory depression secondary to benzodiazepine usage during procedural sedation. (See Table 5.)
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Post-procedural Sedation Activities
After the procedural sedation has been completed, the patient should continue to be monitored as there may be an increase in sedation once the uncomfortable stimulus of the procedure is removed. Cessation of monitoring may occur once the patient has returned to his or her baseline status. Characteristics evaluated for return to baseline may include: cardiovascular function, pulmonary function (especially airway maintenance), arousability, hydration, and speech. Some have suggested that discharge after 30 minutes may be acceptable, but patient characteristics are far more important than a set or delineated time.50 (See Table 6.)
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Discharge instructions to the patient and family should include information that sedation can be prolonged. The patient and family should be made aware that coordination may be affected for some time after the procedure and that the patient may experience agitation and gastrointestinal affects for some time after the procedure.
Conclusion
In summary, pediatric pain and anxiety needs are often not addressed appropriately in the emergency department. When a painful procedure is needed to correct an ailment, procedural sedation can be utilized to help reduce patient pain and anxiety. The agent to be used should be determined by the type of procedure being performed, underlying patient co-morbidities, staff familiarity, onset of action, duration of action, and risk of complications. Common activities for procedural sedation include: obtaining a patient history and performing a physical examination, identification of the ASA classification, appropriate selection of drug, placement of monitors, preparation of resuscitation equipment and drugs (including reversal agents), completion of the procedure, post-procedural monitoring, and discharge with appropriate instructions to the family. The patient may be safely discharged home once baseline function and mental status are achieved. When performed in a pre-planned fashion, the risks associated with procedural sedation can be reduced while maintaining patient comfort and minimizing patient anxiety.
References
1. Selbst SM, Clark M. Analgesic use in the emergency department. Ann Emerg Med 1990t;19:1010-1013.
2. Alexander J, Manno M. Underuse of analagesia in very young pediatric patients with isolated painful injuries. Ann Emerg Med 2003;41:617-622.
3. Brown JC, Klein EJ, Lewis CW, et al. Emergency department analgesia for fracture pain. Ann Emerg Med 2003;42:197-205.
4. Wilson JE, Pendelton JM. Oligoanalgesia in the emergency department. Am J Emerg Med 1989;7:620-623.
5. Taddio A, Katz, J, Illersich AL, et al. Effect of neonatal circumcision on pain response during subsequent routine vaccination. Lancet 1997;349:599-603.
6. Weisman SHJ, Berstein B, Shechter NL. Consequences of inadequate analgesia during painful procedures in children. Arch Pediatr Adolesc Med 1998;152:147-149.
7. Anand KJ. Clinical Importance of pain and stress in preterm neonates. Biol Neonate 1998;73:1-9.
8. Clinical Policy: Critical Issues in the Sedation of Pediatric Patients in the Emergency Department. Approved by the ACEP Board of Directors October 5, 2007.
9. Mace SE, Murphy M. Pain Management and procurdural sedation: Definitions and clinical emergency department management. In: Mace SE, Duchcarme J, Myrphy M, eds. Pain Management and Sedation: Emergency Department Management. New York, NY: McGraw Hill 2006:7-14.
10. American Academy of Pediatrics and American Pain Society. The assessment and management of acute pain in infants, children, and adolescents. Pediatrics 2001;108:793-797.
11. American Acadmeny of Pediatrics and Canadian Paediatric Society. Prevention and management of pain and stress in the neonate. Pediatrics 2000;105:454-461.
12. Bauman LA, Kish I, Bauman RC, et al. Pediatric sedation with analgesia. Am J Emerg Med 1999;17:1-3.
13. Coté J, Wilson S, et al. After sedation for diagnostic and therapeutic procedures: An update guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures: An update. Pediatrics 2006;118;2587-2602.
14. EMSC Panel (Writing Committee) on critical issues in the sedation of pediatric patients in the emergency department. Clinical policy: Critical issues in the sedation of pediatric patients in the emergency department. Ann Emerg Med 2008;51:378-396.
15. Sacchetti A, Stander E, Ferguson N, et al. Pediatric procedural sedation in the community: Emergency department results from the ProSCED Registry. Pediatric Emerg Care 2007;23:218-222.
16. Marx JA, et al. Emergency Medicine Concepts and Clinical Practice. 6th ed. Philadelphia: Elsevier, 2006.
17. Ganong WF. Review of Medical Physiology. 22nd ed. USA: McGraw-Hill Companies;2005.
18. American Society of Anesthesiologists Task Force on Preoperative Fasting. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy patients undergoing elective procedures. Anesthesiology 1999;90:896-905.
19. Green SM, Krauss B. Pulmonary aspiration risk during emergency department procedural sedationAn examination of the role of fasting and sedation depth. Acad Emerg Med 2002;9:35-42.
20. Brady M, Kinn S, O'Rourke K, et al. Preoperative fasting for preventing perioperative complications in children. Cochrane Database Syst Rev 2005;CD005285.
21. Pena BMG, Krauss B. Adverse events of procedural sedation and analgesia in a pediatric emergency department. Ann Emerg Med 1999;34:483-491.
22. Agrawal D, Manzi SF, Gupta R, et al. Preprocedural fasting state and adverse events in children undergoing procedural sedation and analgesia in a pediatric emergency department. Ann Emerg Med 2003;42:636-646.
23. Roback MG, Bajaj L, Wathen JE, et al. Preprocedural fasting and adverse events in children undergoing procedural sedation and analgesia in a pediatric emergency department: Are they related? Ann Emerg Med 2004;44:454-459.
24. Green S, Rothrock S, Lynch E, et al. Intramuscular ketamine for pediatric sedation in the emergency department: Safety profile in 1,022 cases. Ann Emerg Med 1998;31:688-697.
25. Karapinar B, Yilmaz D, Demirag K, et al. Sedation with intravenous ketamine and midazolam for painful procedures in children. Pediatrics International 2006;48:146-151.
26. Moscona R, Ramon I, Ben-David B, et al. A comparison of sedation techniques for outpatient rhinoplasty: Midazolam versus midazolam plus ketamine. Plast Reconstruct Surg 1995;96:1066-1074.
27. Lo JN, Cumming JF. Interaction between sedative premedicants and ketamine in man and in isolated perfused rat livers. Anesthesiology 1975;43:307-312.
28. Okamoto GU, Duperon DF, Jedrychowski JR. Clinical evaluation of the effects of ketamine sedation on pediatric dental patients. J Clin Pediatr Dent 1992;16:253-257.
29. Barnett P. Propofol for pediatric sedation. Pediatric Emerg Care 2005;21:111-114; quiz 115-117.
30. Pate M, Steelman R. Questions unanswered: Propofol use in the pediatric intensive care unit. AACN Advanced Critical Care 2007;18:248-252.
31. Guenther E, Pribble CG, Junkins EP Jr, et al. Propofol sedation by emergency physicians for elective pediatric outpatient procedures. Ann Emerg Med 2003;42:783-791.
32. Vardi A, Salem Y, Padeh S, et al. Is propofol safe for procedural sedation in children? A prospective evaluation of propofol versus ketamine in pediatric critical care. Crit Care Med 2002;30:1231-1236.
33. Barbi E, Gerarduzzi T, Marchetti F, et al. Deep sedation with propofol by nonanesthesiologists: A prospective pediatric experience. Arch Pediatr Adolesc Med 2003;157:1097-1103.33. Guenther E, Pribble CG, Junkins EP Jr, et al. Propofol sedation by emergency physicians for elective pediatric outpatient procedures. Ann Emerg Med 2003;42:783-791.
34. Mart CR, Parrish M, Rosen KL, et al. Safety and efficacy of sedation with propofol for transoesophageal echocardiography in children in an outpatient setting. Cardiology in the Young 2006;16:152-156.
35. Vespasiano M, Finkelstein M, Kurachek S. Propofol sedation: Intensivists' experience with 7304 cases in a children's hospital. Pediatrics 2007;120:e1411-1417.
36. Babl P, Puspitadewi A, Barnett p, et al. Preprocedural fasting state and adverse events in children receiving nitrous oxide for procedural sedation and analgesia. Ped Emerg Care 2005;21:736-743.
37. Dunn-Russell T, Adair S, Sams D, et al. Oxygen Saturation and diffusion hypoxia in children following nitrous oxide sedation. Pedatr Dent 1993;15:88-92.
38. Grehn L. Adverse responses to analgesia, sedation, and neuromuscular agents in infants and children. AACN Clinical Issues 1998;9:36-48.
39. Gilchrist F, Cairns AM, Leitch JA. The use of intranasal midazolam in the treatment of paediatric dental patients. Anaesthesia 2007;62:1262-1265.
40. Almenrader N, Passariello M, Coccetti B, et al. Premedication in children: A comparison of oral midazolam and oral clonidine. Paediatric Anaesthesia 2007;17:1143-1149.
41. Klein EJ, Diekema DS, Paris CA, et al. A randomized, clinical trial of oral midazolam plus placebo versus oral midazolam plus oral transmucosal fentanyl for sedation during laceration repair. Pediatrics 2002;109:894-897.
42. Schutzman SA, Burg J, Liebelt E, et al. Oral transmucosal fentanyl citrate for premedication of children undergoing laceration repair. Ann Emerg Med 1994;24:1059-1064.
43. Council on Scientific Affairs, American Medical Association. The use of pulse oximetry during conscious sedation. JAMA 1993;270:1463-1468.
44. Aughey K. An evaluation of pulse oximetry in prehospital care. Ann Emerg Med 1991;20:887-891.
45. Tachibana C, Fukuda T, Hasegawa R, et al. Accuracy of a pulse oximeter during hypoxia. Masue 1996;45:479-482.
46. Hart LS, Berns SD, Houck CS, et al. The value of end-tidal CO2 monitoring when comparing three methods of conscious sedation for children undergoing painful procedures in the emergency department. Pediatr Emerg Care 1997;13:189-193.
47. Tobias JD. End-tidal carbon dioxide monitoring during sedation with a combination of midazolam and ketamine for children undergoing painful, invasive procedures. Pediatr Emerg Care 1999;15173-175.
48. McQuillen KK, Steele DW. Capnography during sedation/analgesia in the pediatric emergency department. Pediatr Emerg Care 2000;6:401-404.
49. Yldzdas D, Yapcoglu H, Ylmaz HL. The value of capnography during sedation or sedation/analgesia in pediatric minor procedures. Pediatr Emerg Care 2004;20:162-165.
50. Newman DH, Azer MM, Petetti RD, et al. When is a patient safe for discharge after procedural sedation? The timing of adverse effect events in 1,367 pediatric procedural sedations. Ann Emerg Med 2003;42;627-635.
Procedural sedation is an important tool for the emergency department physician, especially when faced with a child who requires a painful procedure. The ability to adequately address the pain and anxiety of the child and safely complete the procedure is rewarding to both the physician and the family of the child.Subscribe Now for Access
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