Chapter 20 SEDATION, ANALGESIA, AND Neuromuscular BLOCKADE PA srjectives Identify the indications, risks, and monitoring needs of patients undergoing elective sedation. . Ml Describe the benefits and appropriate uses of therapeutic analgesia in critically il patients. i Explain the benefits and side effects associated with commonly used analgesic medications. 1. Outline the benefits and side effects associated with commonly used sedative/ hypnotic medications. lM Determine the benefits and side effects associated with commonly used neuromuscular blockade medications. Know the reversal medications for benzodiazepine, opioid, and neuromuscular blocking agents. Be familiar with the complications of tachyphylaxis and iatrogenic dependence associated with the prolonged usage of benzodiazepine and opioid receptor agonists. BB case Study ‘A4-year-old boy is admitted with a heart rate of 170 beats/min, temperature of 96°F (35.6°C), respiratory rate of 40 breaths/min, and systolic blood pressure of 70 mm Hg. He is mottled, with poor perfusion, and in significant respiratory distress. Several days ago he was diagnosed with influenza A. He is given oxygen by face mask, and fluid resuscitation has begun with isotonic saline. Detection — Whatare the most likely diagnoses? ~ What are the worst possible diagnoses? Intervention ~ What are the most immediate treatment strategies? Reassessment ~ Ifthe decision is made to intubate, which medications should be used? ~ What medications can be given to provide analgesia and sedation before transfer to the pediatric intensive care unit? ~ Which medicines should be avoided?Hil Pediatric Fundamental Critical Care Support Effective Communication - When the patient's clinical status changes, who needs to know and how will this information be disseminated? — Where is the best place to manage the care of this patient? ‘Teamwork — How are you going to implement the treatment strategy? = Who is to do what and when? LANTRODUCTION ‘The treatment of critically ill children would be difficult, if not impossible, without the concurrent use of analgesic, sedative, and neuromuscular blocking agents, When used correctly, these medications not only save lives, they also allow painful and traumatic procedures to be performed on severely ill children, These procedures may include the placement of artificial airways, invasive monitoring devices, central access devices, and even minor surgery. Protection of the child after insertion of these devices may require long-term analgesia and sedation until these treatments are no longer needed. Sedative medications may also be needed for patients undergoing nonpainful procedures like computed tomography scans or magnetic resonance imaging, especially for infants or toddlers who have a difficult time remaining still for prolonged periods. By definition, a patient who receives a medication to decrease stress or anxiety is receiving sedation or being sedated. Anyone receiving a medication or therapy to relieve pain is receiving analgesia. Some medications provide sedation without analgesia whereas others provide analgesia, without sedation; a few provide both. Each practitioner should determine which of these conditions they want to provide and then to choose the appropriate medication, or combination of medications, to accomplish this therapeutic goal. Sedation in the critical care environment reduces ou metabolic demands, mortality, morbidity, and hospital oe mn costs, More importantly, the treatment of critical illness | Basic principles of sedation must be may not only be painful, but may be frightening as | applied by the prudent clinician | well. In fact, the care of critically ill children can lead to Untowardand even fatal complications long-term psychological trauma and stress. Therefore, use of appropriate sedation and analgesia can reduce the negative impact of these factors. However, each a medication has its own indications and side effects, which must be weighed in terms of benefits and risks for each patient on a case-by-case basis. Used correctly, these medications have incredible benefits. Used incorrectly, or without an appropriate level of caution, they can cause significant harm and even death. may accompany any sedation. 20-2Sedation, Analgesia, and Neuromuscular Blockade EX IL. PRE-SEDATION PLANNING Although different medications may have intrinsic benefits, they can also cause significant harm. Determining the correct medication to use, or avoid, requires careful planning based on the particular patient situation. The overriding goal of any sedation plan should be to use the minimal analgesia or sedation needed to accomplish the therapeutic goal. All patients are different and their responses to any medications can vary. These consequences can be reduced or eliminated by careful assessment and preplanning, Several questions must be asked before beginning any sedatio: What is the goal of this sedation? MH What length of sedation is required? i What complications are possible? Likely? First, and most importantly: What is the goal of this particular sedation? If only analgesia is needed, the practitioner must determine how longan effect will be required. If the goal is simply to complete a short painful procedure, perhaps the best choice is a short-acting analgesic with minimal or no sedative component. Alternatively, ifthe procedure requires a prolonged period and is particularly painful or traumatic, perhaps a better choice is a combination of analgesic and sedative medication. What complications are possible? Is the patient at risk of losing the airway during the procedure? If the risk is high, long-acting medications that depress respiration should be avoided, and the practitioner should consider elective intubation before the procedure. Ifthe risk of airway loss is low, a different choice of medications may be made. Is the patient hemodynamically unstable? A radically different choice of medications may be required compared to those used in a patient who is relatively stable, It is recommended that only anesthesiologists or physicians with specialized training perform sedations in hemodynamically unstable patients. Lastly, providers must question themselves and their own skills. What if this child should lose their airway protective reflexes and require an invasive airway? Should a more experienced provider be brought in to help before beginning the sedation? Similarly, how emergent is the procedure? Should an anesthesiologist be performing the sedation? All of these questions must be addressed before any medications are given in order to protect the patient’ life and to prevent unnecessary morbidity. A. American Society of Anesthesiologists Classification System ‘The American Society of Anesthesiologists (ASA) Physical Classification System (Table 20-1) was developed to classify the severity of illness in patients about to undergo anesthesia. The system. has 6 physical status levels, ranging from a healthy individual (ASA P1) to patients who are brain dead (ASA PVD). Although the system is not meant to predict outcomes, it does provide a general assessment of preoperative risk. Most importantly, non-anesthesiologists should be cautious or even avoid electively sedating patients of ASA PIII level and above. Similarly, they should always avoid electively sedating patients of ASA PIV level and above if at all possible. 20-3Wi Pediatric Fundamental Critical Care Support American Society of Anesthesialopists Classification System Normal heelthy patient Mid systemic disease, with no functional imitations ‘Severe systemic disease which nits acivty buts not incapacitating Incapacitating disease thats constant threat ote Patents not expected to survive 24 hours with or without an operation Bran dead pation boing proparod for organ donation “tis recommended that these patients receive sedation administered by appropriately trained anesthesiologists and intensivists. Reproduced with permission, © 2008 Macmillan Publishers Ltd. Wilson K. Vital guide to conscious sedation, Vital B. Depth of Sedation Current classification divides sedation into four levels (Table 20-2). The levels are defined by four different parameters corresponding to the presumed “depth” of sedation: responsiveness, airway maintenance, spontaneous respiration, and cardiovascular function. The level of sedation, and the corresponding patient response, is a continuum without clear delineation of transition from Level to the next. Likewise, a weight-based drug dosage that provides minimal sedation in 1 patient may cause general anesthesia in another. Similarly, a weight-based dosage that provided minimal sedation to a patient when healthy may cause general anesthesia or cardiovascular collapse in the same patient who develops a critical illness, renal dysfunction, or hepatic failure. For these reasons, providers should attempt to provide the minimum level of sedation required to accomplish the therapeutic goal in each patient. The policy of “start low and go slow" (use Jow doses and slowly increase as needed) allows the practitioner to titrate to the required, but minimum, level of sedation. While trying to achieve the minimal level, itis also important to use therapeutic dosages. A common mistake is to use sub-therapeutic doses. This results in inadequate sedation but still exposes the patient to potential side effects. A patient can always drift into a deeper than intended level of sedation despite best efforts, and the practitioner must always be prepared to actively manage the airway and ventilation. C. Risks of Encountering a Difficult Airway Anyone performing sedation must be prepared for the patient to lose airway protective reflexes at any time, regardless of the targeted level of sedation. Therefore, the practitioner must always, have a plan for advanced airway management in any patient undergoing sedation, as well as the ability and training to execute that plan. For this reason, the provider must attempt to predict how likely any patient is to have a difficult airway prior to administration of any medication. A difficult airway, by definition, is challenging or impossible to maintain by routine or straightforward measures. Any patient, regardless of history, may have a difficult airway. This may result in an increased number of attempts at airway insertion or difficulties with mask ventilation or oxygenation. This cannot be definitively determined until advanced airway management is attempted, but several factors can suggest a high, or at Jeast increased, risk of encountering a difficult airway (Table 20-3). 20-4Sedation, Analgesia, and Neuromuscular Blocka | Levels Sedation Response. Winina sedten Nama epost eral smal | Moderate satiation Responds prposey to verbal commands | onalesatrmery ort ight tact stinlton ‘constous sedation) | Deep seston Not easily srouse, tt responds urposoy to repeated or painful stimu General anesthesia Unsonsciousness, unresponsive to physical or verbal commands ‘Adapted from Kalinowski M, Wagner HJ. Sedation and pain management in interventional radiology. C212. 2005;3:14-18. Cardi pulmonary Effects Veatiation/airway rfexes ntact Nocardiovascular eect [Maintains patient aiway, ventilation adequate Minimal cardiovascular effects May require assistance to maintain airway nde ventilation Cardiovascular function usually maitained Loss of airway reflec, requires assistance to suppor entiation (Cardiovascular function may be impaied Clinical Conditions and Syndromes Associated with Difficult Airway’ } «Histor of cfu intubation ‘+ Histor of complications with anesthesia. ‘+Family istry of cificuity with imubation or anesthesia * Histor of obstructive sleep apnea, soring. vecheomalaia of laryngomatacia| ‘© Pharyngeal and laryngeal pathology Bronchospasm © Stidorat est © Chromosomal abnermaltis[uisomy 13,1 oF 21) Pie Robin soquence *Beclvih- Wiedemann syndrome ‘Treacher Calins sdrome *Bag-valve mask ventilation and/or intubation, Micrognattia or retrograthia Obesity Short neck Poor neck extension or fused cervical vertebrae igh arched palate Macroglossia. Hemifacial mirosomia Small thytomental orhyomental distance “Tacha deviation Facial or convial rau, mass, or ifection Tiss ‘Malmpatilclasication or greater i Reproduced with permission. © 2002 Wolters Kluwer Health. American Society of Anesthesiologists Task Force ‘on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology. 2002,96:1004-1017. ‘The Mallampati classification (Figure 20-1) is a simple airway assessment technique that involves looking in the patient’s open mouth with and without phonation, Higher levels of ‘Mallampati classification are frequently associated with higher grade (level of difficulty) airways found during laryngoscopy. Ifany features suggestive ofa difficult airway are present (Table 20-3 and Figure 20-1), the provider should consider involving an anesthesiologist before sedating a patient, especially if the sedation is elective. In addition, the provider should be familiar with the use of the difficult airway algorithm (Appendix 8), regardless of the presence or absence of risk factors. Once a difficult airway is discovered, especially if the patient has received 20-5Hi Pediatric Fundamental Critical Care Support neuromuscular blockade, time is no longer available and a crisis can rapidly ensue. It is far better to plan for a controlled intubation in a patient with a potentially difficult airway than to emergently intubate a child during a procedure. Figure 20-1, Mallampati Classification and Associated Airway Grade Class Grade | Grace it Class Grade v D. Pre-sedation History A thorough pre-sedation history should be taken prior to every sedation event to decrease the risk of avoidable complications. Does the patient have any history of difficulty with anesthesia? This may include sensitivity to particular drugs, difficulty with obtaining an airway, prolonged effects of anesthesia medications, or any other significant history that may impact safety. Wi Is there a history of difficulty with anesthesia or sedation in the parents or other family members? This may uncover common drug allergies or a history suggestive ofa difficult airway, Is the patient allergic to any drugs that may be given during sedation procedures? Without knowing the history, those medications cannot be avoided. 1 Are there other known allergies? This is critical because medications such as propofol cannot be given to people who are allergic to eggs or egg products. 20-6Sadation, Analgesia, and Neuromuscular Blockade EXY I Have there been any recent illnesses? Especially in elective cases, concurrent upper airway infections can cause prolonged, or difficulties with, ventilation. A positive history may indicate that sedation should not be performed, if possible, until the patient is over the acute illness. Mi Does the patient have known renal or hepatic dysfunction? Several medications used in analgesia and sedation utilize liver or kidney metabolism and must be avoided, or have their dosages reduced, in patients with dysfunction. Mi Have all available laboratory results been reviewed? Finding a low platelet count or severe coagulopathy after attempted placement of an invasive line can be disastrous. Mi Have all imaging studies been reviewed? If the patient is symptomatic because of a large intracranial mass, many drugs should be avoided, Likewise, the presence of a chest mass dictates that even minimal sedation is contraindicated by anyone except a qualified anesthesiologist. Patients should have no foods or infant? {formula 6 hours before sedation Clear liquids o breast milk can be M How long has the patient been fasting? ASA. guidelines suggest that patients should have no foods or infant formula 6 hours before sedation. Glear liquids or breast milk can be given up to 4 hours before sedation. The patient should ingest nothing by mouth in the 2 hours before sedation. Vomiting during sedation can turn a routine en tb Bes Before eto procedure into a life-threatening event. ASA but nothing by mouth in the 2 hours guidelines apply to elective sedations only. Insome | before sedation. | situations, emergent sedation may be needed. “ When the guidelines cannot be followed because of emergent needs, the provider must balance the increased risk of vomiting and aspiration versus the benefit of sedation. Clearly a small number of targeted questions can avoid a number of life-threatening complications when attempting to provide sedation. IIL. PRE-SEDATION SETUP AND MONITORING. Once a sedation goal has been determined and alll risks that can be easily discovered have been found, a successful sedation requires extensive setup before giving any medication. The ASA has carefully defined the minimum equipment and monitoring required prior to any sedation by non-anesthesiologists (Table 20-4). Although non-invasive ETCO, monitoring is only a recommendation, it will signal apnea well before pulse oximetry indicates a fall in Spo,. Ifall required equipment is not available and set up for use, the sedation induction should not be initiated. 20-7Wi Pediatric Fundamental Critical Care Support cessary for Sedation Minimal Equipment and Monitoring ECardiae monitor Endotracheal we + 10 ead eecnecaiog phy + Corectsiee Pulse oximetry 1 sie lager and sie slr Respir apnea monitor Drugs appropiate fr seation awn and labeled | eroo,moiter Sueton with Yankaur ti, on ae uring | Workng access (ie, peripheral intravenous cent ETC, detector fo endotracheal tubo placsment {1 vanous ine) preerbiy2 Laryngeal mask airsay a ober backup ay even | Resuscitation id rnning (normal saline or etatod Oa pharrgeal srway | ‘Ringer solution) '* Nasopharyngeal airway i Oral pharyngeal airway Laryngosoope blade |) Nasogosie be « Agproprit sine for th cil undergoing sedation iiqaoakeaiiaiai + Macinshr Miler lade 1 © Appropriate size ‘Stylet, size appropriate for endotracheal tube 1+ oxygen towing Reproduced with permission. © 2002 Wolters Kluwer Health. American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by non- anesthesiologists. Anesthesiology. 2002;96:1004-1017. A.useful mnemonic for airway equipment setup in all patients is ON BED SCABS: Oral pharyngeal airway Nasogastric tube Bag and mask appropriate for this child, with oxygen flowing Endotracheal tube of appropriate size, I size above and 1 size below Drugs appropriate for sedation and reversal, drawn up and labeled ‘Suction on and running with Yankauer tip attached CO, detector for endotracheal tube placement Alternate airway and alternate plan (i.e., laryngeal mask airway) Blade (laryngoscope) appropriate for this patient, with light working Stylet appropriate for endotracheal tube choice Ora more familiar mnemonic is SOAPME: Suction Oxygen (2 sources) Advanced airway equipment Pharmacy to provide emergency medications and antagonists Monitoring for the level of sedation Equipment for emergency resuscitation All equipment should be set up for use at bedside and checked before sedation begins. “Nearby” isnot close enough and can lead to complications if the equipment and rescue medications are not where they can be immediately used. A conscious effort should be made to administer 20-8Sedation, Analgesia, and Neuromuscular Blockade resuscitation crystalloids (lactated Ringer solution or normal saline) during the procedure so that appropriate boluses can be administered immediately if needed. Likewise, a 3-way stopcock/tap with a 60-mL syringe should be inline so that “pull-push’ resuscitation can take place with little Joss of time. An adequate amount of fluid should also be prepared so that 20 mL/kg fluid boluses can be immediately administered. No potassium-containing fluids should be in the room as they may be inadvertently used during resuscitation. Lastly, the person monitoring sedation should never be the person performing the procedure. Failure to follow this recommendation can lead to a critical delay in recognizing a change in vital signs requiring immediate intervention. Although this setup may seem excessive to some, planning for every possible contingency can be the difference between life and death in an emergency. WV. DRUG ADMINISTRATION DURING SEDATION OW INTUBATION Medication administration during all sedation and intubation procedures should use a rational and consistent methodology including pre-oxygenation, premedication, sedation, and relaxation. A, Pre-oxygenation Pre-oxygenation is essential for decreasing the risk of hypoxia during intubation or sedation. Not only does this fill all alveoli with oxygen prior to interruption or alteration of ventilation, it also allows for nitrogen washout and maximizes the time available for restoring normal ventilation should that become necessary. Oxygen should be provided, ideally Fio, 1.0 via face mask, for 3 105 minutes before administration of any medications. Oxygen flow should then be maintained throughout the procedure. B. Premedication - Premedication of some type is required for most intubations and some sedations, As the term implies, these are medications given before sedatives to optimize sedation, avoid pain, and prevent complications. Selection of premedications is based on the individual patient, clinical situation, and sedation goals determined during pre-sedation planning. The most common premedication agent Is atropine, a vagolytic that can prevent bradycardia induced by sudden increases in vagal tone. These sudden increases may occur during laryngoscopy, airway manipulation, or with increased airway secretions. Most infants maintain cardiac output via an increase in heart rate rather than an increase in stroke volume. Therefore, any drop in heart rate, especially in unstable patients, may result in a catastrophic drop in cardiac output, Because atropine also has drying properties, it prevents secretions from entering the airway during the sedation, possibly decreasing the incidence of micro-aspiration as well as the occurrence of laryngospasm. Atropine, 0.02 mg/kg, should be considered in all infants younger than 1 year. It should never be given below the minimum dose of 0.1 mg as it can cause paradoxical bradycardia. Atropine should also be given prior to the use of succinylcholine as it frequently causes an increase in vagal tone. Glycopyrrolate (4 j1g/kg) decreases secretions to a level similar to 20-9Mi Pediatric Fundamental Critical Care Support that of atropine without consequent central nervous system (CNS) effects. It should be considered in all patients undergoing sedation especially when using drugs (such as ketamine) that increase oral or airway secretions. Analgesia is frequently required as a premedication. This is especially important before painful procedures where sedatives without analgesia (i.e., propofol) are used. Laryngoscopy should be considered a painful procedure; the insertion of a laryngoscope is known to cause transient increased intracranial pressure (ICP). Fentanyl (1 ng/kg) is a good first-line choice because of its rapid onset, short duration, and relatively benign effect on myocardial activity. Lastly, intravenous (IV) lidocaine (1. mg/kg) is known to blunt the transient increases in ICP that occur with laryngoscopy and should be considered for premedication in all patients with presumed or known intracranial pathology. Although its mechanism is unclear, lidocaine administration before laryngoscopy is considered the standard of care in patients with elevated ICP IV lidocaine can also suppress the cough reflex and mitigate bronchospasm, and may therefore be beneficial for intubation of the asthmatic patient. Lidocaine is an antiarrhythmic medication, and its benefits must be weighed against potential side effects in each individual patient. C. Sedation After premedication, the sedative chosen during pre-sedation planning can be given. There are numerous medications, each of which has advantages and disadvantages. All medications given for sedation should have a rapid onset, relatively short duration of action, and minimal side effects. As several of the choices can cause vasodilation (.e., benzodiazepines, propofol, and barbiturates), adequate intravascular volume must be assured before administration. Similarly, isotonic fluids should be immediately available for resuscitation in the event of a rapid drop in blood pressure. Other medications (ie., benzodiazepines and barbiturates) can cause myocardial depression and should be avoided in patients with marginal cardiac output or shock. Medications that have no intrinsic analgesia (i.e., propofol) must be used in conjunction with adequate analgesia for painful procedures. Lastly, medications with unique side-effect profiles (i., ketamine) should only be used after considering the consequences of those side effects in a given patient. There are usually several appropriate choices in every clinical scenario, The agent selected is dependent on the relative balance of positive and negative effects it may, or will, have on a particular patient ina specific situation. O. Neuromuscular Blockade Skeletal muscle relaxation, or neuromuscular blockade (NMB), may or may not be required depending on the clinical situation. These agents may be needed to ensure that the patient remains motionless during a critical procedure, to prevent vocal cord damage during intubation, or to allow ventilation in problematic situations. When needed, these medications have no substitute, but they can also be lethal. If advanced airway management cannot be assured, NMB must be avoided until the airway is secured. In some patients for example, those with an anterior chest mass ~NMB is specifically contraindicated, Each of the paralytic agents has a specific indication and side-effect profile. Careful consideration of the patient, the clinical goal, and the potential side effects of each medication is needed during pre-sedation planning. The dangers associated with these medications cannot be overstated. 20-10Sedation, Analgesia, and Neuromuscular Blockad V. SPECIFIC SEDATIVE AND ANALGESIC MEDICATION ‘SIDE EFFECTS AND CONTRAINDICATIONS Every drug used for sedation and analgesia has a specific indication, side-effect profile, and contraindication. Knowledge of these factors is essential before, during, and after a procedure. The risks and benefits of each medication should be weighed during pre-sedation planning, and the agent chosen should be Individualized to each patient and clinical situation. Failure to do so can result in avoidable morbidity and death. This overview is not meant to be all inclusive but rather to highlight aspects of several commonly used medications (Appendix 7). A. Nonsteroidal Anti-inflammatory Drugs ‘Nonsteroidal anti-inflammatory drugs (NSAIDs) are highly effective analgesics with numerous applications in clinical practice. All of these medications block inflammation by inhibition of cyclo-oxygenase pathways. In most cases, itis this reduction in inflammation that relieves pain rather than a ditect inhibition of pain perception or pain fiber transmission, Because these medications are anti-inflammatory agents, they are also powerful antipyretics. The combination of these effects makes NSAIDs highly desirable in the treatment of postoperative pain. Because they do not cause respiratory depression, constipation, or itching, they are a near-perfect primary or adjunct medication in the treatment of moderate to severe pain. However, several side effects of these drugs limit their usefulness. First, most NSAIDs can inhibit platelet function either directly or indirectly, leading to an increased risk of perioperative and gastric bleeding, In addition, they can cause, or contribute to, renal failure in patients with preexisting renal insufficiency or other predisposing factors, such as concomitant nephrotoxic medications, liver dysfunction, or heart failure, NSAIDs should be used with caution in these patients. For most patients, the use or addition of NSAIDs to nearly every pain regimen will inctease pain control and decrease the dosage of other agents needed to treat that pain, Aspirin (salicylic acid) was the first NSAID developed. Although an effective agent, its use (5 to 10 mg/kg) in most pediatric patients is discouraged secondary to the increased risk of Reye syndrome in those with concurrent viral illness. The “side effect” of platelet inhibition is now the primary reason that aspirin is prescribed. Itis the first choice for a daily oral medication for mild anticoagulation in patients at risk for thrombosis, including children. Acetaminophen/paracetamol (15 mg/kg) is the most commonly used NSAID in pediatric patients. It differs from most NSAIDs in that itis a poor anti-inflammatory agent peripherally, but a powerful anti-inflammatory agent centrally. This makes acetaminophen an ideal antipyretic agent in children because it does not have the associated bleeding and nephrotoxic risks associated with other NSAIDs. In addition, tt also appears to have direct central pain-reducing effects independent of its anti-inflammatory properties. Therefore, acetaminophen/ paracetamol can be tsed in conjunction with other NSAIDs to improve pain and fever control via multiple pathways, In hospitalized patients, acetaminophen/paracetamol is now available in oral, rectal, and TV formulations. Ibuprofen (10 mg/kg) is used frequently to treat fever and pain in children. Itis available in several liquid oral preparations, which make it particularly useful in children, Its also available as an IV preparation, primarily used for the closure of a patent ductus arteriosus. 20-11Wi Pediatric Fundamental Critical Care Support Naproxen is another oral NSAID effective in treating postoperative pain. Ithas a longer half-life than ibuprofen and is given every 12 hours instead of every 6 hours. It is a useful alternative to ibuprofen butis not available in as many different preparations. In addition, no IV formulation is available, which limits its clinical use. Ketorolac is a powerful NSAID available in both IV and oral formulations. It has been shown, effective in the treatment of postoperative pain even in the absence of adjunctive medications. Concerns of hypersensitivity, renal failure, and increased bleeding in patients younger than 16 ‘years of age have limited its use in pediatrics. However, administration for less than 5 days in patients with no other contraindications to NSAID use is generally accepted as safe, even in the youngest patients. B. Opioids Narcotics are used frequently to prevent pain. All narcotics have similar mechanisms of action. The opioids work as agonists at 3 primary opioid receptors: mu, kappa, and delta. Each medication blocks transmission of pain fiber signals to the brain and thereby prevents the sensation of pain. In choosing the appropriate narcotic agent to use, the practitioner must first determine the clinical goal: Ml Is the agent going to be used for short- or long-term pain management? 1 Will a continuous infusion be required, or will intermittent dosing be sufficient? 1 Are there specific patient factors to consider? Morphine (0.05 to 0.1 mg/kg) is a good general purpose analgesic. It has a relatively long halt-life (2 hours) in most children, but this can increase signfficantly in small or immature infants. Morphine is metabolized in the liver to generate active metabolites, which are excreted in the urine. For these reasons, morphine must be used cautiously in patients with hepatic or renal dysfunction. Morphine is known to cause vasodilation and hypotension in an immunoglobulin E-independent fashion and should be used with caution in patients with asthma. Additionally, many patients will complain of urticaria due to the associated histamine release. Morphine is also known to cause cardiac depression and should not be used in patients with low cardiac output or shock. Like all narcotics, morphine can cause significant respiratory depression by decreasing minute ventilation and blunting the CNS response to carbon dioxide. Overall, morphine is a good choice for intermittent or patient-controlled analgesia in patients with significant pain. Accumulation of active metabolites and poor clearance in small infants makes it a less desirable agent for continuous infusion in such children. Fentanyl (1 to 2 pg/kg) is a synthetic opioid with rapid onset (90 seconds) and clearance (ty, 30 minutes), but it is stored in fat and can havea significantly longer half-life in obese children, Itis 100 times more powerful than morphine and must be used ata correspondingly lower dose. Fentanyl is inactivated by the liver and should be used with caution in patients with significant hepatopathy. Like all narcotics, fentanyl causes respiratory depression. Although it does not cause significant myocardial depression, it can cause moderate bradycardia, especially when used with muscle relaxation agents. Unlike morphine, fentanyl does not cause histamine release and is therefore a better choice than morphine for patients with asthma or hypotension. Practitioners should be aware of “rigid chest phenomenon,” which can make ventilation difficult 20-12Sedation, Analgesia, and Neuromuscular Blockade or impossible without muscle relaxation. This only occurs with rapid administration and therefore rapid bolus dosing should never be employed. This phenomenon can be reversed Very significant respiratory by paralysis with NMB, but advanced airway management will be required. Fentanyl does not react with most other medications and is therefore a good choice for continuous infusion analgesia, In addition, its fast onset makes it an : excellent choice for rapid sequence intubation or induction. | simultaneously. depression and hypotension can occur in patients who receive narcotics and benzodiazepines Meperidine (pethidine) (0.5 mg/kg) isa synthetic opioid with a approximately one-tenth the activity of morphine. It has ~ numerous CNS side effects, including seizures and muscle tremors. For these reasons, it should be avoided when other options are available. In addition, it should not be used as a continuous infusion because of active metabolite accumulation, especially in patients with renal dysfunction. Methadone (0.1 mg/kg) is frequently used to prevent narcotic withdrawal but can also be used for chronic or intractable pain. It has an extremely long, but frequently variable, half-life (19 hours) and is available in both IV and oral forms. In very small children, the volume per dose in the IV form can be extremely small. Because ofits long half-life, the sedative effects of any particular dosage may not be fully appreciated for 1 or 2 days; therefore, its dosage must be adjusted very slowly and the effect of that dosage change must be followed 224 hours. For these reasons, methadone should be considered in the prevention of narcotic withdrawal, primarily in its oral form, and caution should be used in very small children. There are better choices for “as needed” pain relief and short-term analgesia. Codeine (0.5 to 1 mg/kg) is frequently used as an alternative to morphine in patients who can take medications by mouth. Itis a synthetic narcotic with approximately one-tenth the potency of morphine. It is rarely given IV as it has led to cardiovascular collapse in some case reports. Its primary usage should remain as an oral, first-line analgesic with intermittent dosing. Hydrocodone is a synthetic opioid similar to codeine. It appears to be slightly more powerful than codeine, but it is less active than morphine. It is used to alleviate moderate to severe pain in patients who can take oral medications. Like codeine, it can be used as a first-line analgesic with intermittent dosing. ‘Tramadol, a synthetic opioid available in both oral (1 mg/kg) and IV forms, binds to opioid receptors and blocks pain transmission using the same mechanism of action that all narcotics do, However, it also blocks the effect of the pain-modifying neurotransmitters serotonin and norepinephrine. Itis rarely used in pediatrics in the United States as itis not recommended by the Food and Drug Administration in patients younger than 16 years. Tramadol is also known to cause seizures and to lower seizure thresholds in patients who have epilepsy or are taking neuroleptics. For this reason, it must be avoided in these patients. Tramadol is habit forming and will cause respiratory depression if recommended dosing is exceeded. 20-13atric Fundamental Critical Care Support C. Benzodiazepines Benzodiazepines are the most commonly used sedatives in critical care. All benzodiazepines increase CNS gamma-aminobutyric acid (GABA) receptor activity causing global CNS depression and consequently sedation. They are excellent first-choice sedatives in clinical situations ranging from anxiolysis to deep Appropriate benzodiazepine selection requires a carefiul assessment of the patient's condit cand clinical goals: sas the agent going to be used for short or sedation. They are also useful anticonvulsants long-term sedation? and potent amnestics. However, like opioids, | m Willa continuous infission be required or will benzodiazepines cause dose-dependent intermittent boluses be sufficient? respiratory depression. Unlike opioids, | mAre there specific patient factors to consider? benzodiazepines blunt both hypoxic and hypercarbic respiratory drive. The concurrent use of benzodiazepines and narcotics can result in a profound depression of respiratory drive secondary to the synergistic effect of these medications. This respiratory depression is much more severe than the predicted effect of cumulative doses for the 2 agents when used independently. In addition, some benzodiazepines can cause substantial myocardial depression and would be contraindicated in patients with borderline cardiac output or shock. As with the narcotics, the appropriate benzodiazepine choice requites a careful assessment of the patient's condition and the clinical goals: Is the agent going to be used for short- or long-term sedation? @ Will acontinuous infusion be required or will intermittent boluses be sufficient? @ Are there specific patient factors to consider? Midazolam (0.1 mg/kg) is one of the most common benzodiazepines used. It has a rapid onset and relatively short half-life (2 hours). It has extensive metabolism in the liver and is eliminated in the urine. It should be used cautiously in patients with renal or hepatic dysfunction as its half-life can be profoundly increased. Midazolam is a good choice for anxiolysis and long-term sedation by continuous infusion. In addition, it can be titrated rapidly to treat refractory seizures. Midazolam appears to cause the least amount of cardiac depression of the benzodiazepine family and is the best choice of a GABA-nergic agent in patients with unclear cardiac output. Lorazepam (0.1 mg/kg) has a slower onset than midazolam but has an extremely long half-life (14 hours). For this reason, itis a first-line agent for stopping seizures (Chapter 15) and is often used for prolonged sedation. Like midazolam, it undergoes significant liver metabolism and is cleared by the kidneys. With its long half-life, its a poor choice for use in patients with liver or renal failure. In addition, itis felt to cause more significant cardiac depression than midazolam and should be avoided in patients with persistent shock or low cardiac output. Lorazepam may work well for intermittent dosing in patients requiring long-term sedation. However, itis formulated with propylene glycol and can cause significant lactic acidosis if used for an extended period, especially as a continuous infusion. In addition, its numerous interactions with other medications make Ita poor choice for a continuous infusion. 20-14Sedation, Analgesia, and Neuromuscular Blockade BX Diazepam (0.2 mg/kg) has an extremely long half-life. Itis extensively metabolized in the liver and should not be used in patients with hepatic or renal failure. Like lorazepam, it is also formulated ‘with propylene glycol and may cause pain with peripheral IV administration and contribute to lactic acidosis. For these reasons, diazepam is best used as an oral agent, primarily in the amelioration of benzodiazepine withdrawal. 0. Barbiturates Barbiturates are used much less frequently now than in the past because several agents with less, significant side-effect profiles are available, However, barbiturates can be ideal agents in some clinical situations, especially with head injury, elevated ICP, and refractory seizures. All barbiturates are powerful GABA agonists, inducing global CNS depression and concomitant decreased cerebral perfusion. These agents can cause profound respiratory depression and the need for advanced. airway management should be anticipated whenever they are used. All barbiturates cause cardiac depression as well as vasodilation and should never be used in patients with decreased cardiac, output, shock, or volume depletion. Individuals with minimal cardiac reserve may become profoundly hypotensive after only a single dose. Phenobarbital (loading dose of 20 mg/kg, which may be given in divided doses; maintenance dosing, 5 mg/kg/day divided every 12 h) is frequently used as a third-line agent in the control of refractory seizures. However, itis a second-line agent in patients with refractory seizures who are younger than 6 months due to their immature hepatic metabolism (Chapter 15). Phenobarbital has a relatively slow onset but a very long half-life (24 to 96h). Iis clinical use should be restricted to the treatment of refractory seizures, treatment of barbiturate dependence, or as an adjunct in difficult-to-sedate patients who are hemodynamically stable. Pentobarbital (1 mg/kg) is a fourth-line agent used in the treatment of refractory seizures, usually with the clinical intention of temporary coma induction. Ithas a half-life of nearly 20 hours, and continuous infusion requires advanced cerebral monitoring such as bispectral index or continuous electroencephalography. It can cause neutrophil inactivation and associated increased infectious risks, as well as profound myocardial depression and should only be used with continuous arterial pressure monitoring, Midazolam infusions have supplanted pentobarbital usage to a large extent, but pentobarbital can still be considered for intubation induction in patients with elevated ICP or for maintenance of medical coma. E. Propofol Propofol (bolus dose, 1-2 mg/kg; continuous infusion, 50-150 yg/kg/min) is an extremely useful short-term medication that avoids many of the problems associated with other drugs described above. Propofol is unrelated to other general use anesthetics but appears to manifest its activity through the potentiation of CNS GABA receptors, similar to benzodiazepines and barbiturates. Propofol has an extremely rapid onset, is cleared quickly by the liver, and exhibits very little respiratory depression, making it ideal for short procedures or anesthesia induction. However, like all medications, propofol has several properties which need to be carefully considered during pre-sedation planning. First, it is compounded in a mixture that contains both egg and soybean products, so it cannot be administered to patients with these allergies. Second, propofol induces 20-15[i Pediatric Fundamental Critical Care Support vasodilation and significant hypotension in dehydrated patients; therefore, it should never be used in under-resuscitated patients, patients with shock, or those with questionable cardiac output. ‘Third, propofol has been associated with myoclonic movements at low doses but, interestingly, isan effective adjuvant in the treatment of refractory seizures. Fourth, propofol has no intrinsic analgesic properties and must be used in conjunction with narcotics, such as fentanyl, for painful procedures. Lastly, an increased risk of propofol infusion syndrome is associated with long-term use and high doses. This syndrome causes refractory lactic acidosis, cardiac arrhythmia, and hypotension, likely caused by mitochondrial “poisoning.” It is possibly not reversible. Propofol is still an excellent drug in several clinical situations. It is ideal for short procedures in relatively healthy individuals (.¢., setting/reduction of isolated fractures and central line placement) in conjunetion with low-dose narcotics. It should also be considered in the initial treatment of refractory status epilepticus. Similarly, it is an excellent intubation induction agent in patients with traumatic brain injury after adequate resuscitation. Practitioners using propofol should have training and experience in its administration, as well as expertise in airway management, as it may cause profound hypotension, transient apnea, and rapid induction of general anesthesia. F. Ketamine Ketamine (1-2 mg/kg IV, 3-4 mg/kg intramuscularly) has several properties that make it an ideal agent in certain clinical scenarios. It is an N-methyl-D-aspartate antagonist providing both analgesia and sedation while preserving both blood pressure and respiratory status. It is metabolized by the liver and is secreted with its metabolites in the urine. It has a rapid onset and is quickly eliminated. Ketamine is a powerful sialagogue and may require concurrent use of an anticholinergic agent (i.e., glycopyrtolate or atropine) to prevent laryngospasm. In addition, its profound dissociative properties and resultant emergence phenomenon may require concurrent usage of low-dose benzodiazepines, such as midazolam. Ketamine can lower seizure thresholds and should be used with caution in patients with known seizure disorders. Although it has been reported to cause a transient rise in ICP during infusion, recent studies suggest that it may in fact decrease ICP without lowering blood pressure and therefore maintain cerebral perfusion pressure. These studies suggest that ketamine may be safe to use in patients with both traumatic brain injury and intracranial hypertension. Ketamine will also cause a transient rise in catecholamine release, which is useful in the maintenance of blood pressure. In addition, this catecholamine surge results in direct B, stimulation and consequent bronchodilation. Its airway preserving properties, along with its f,-stimulation properties, make it an excellent choice for sedation in asthmatic “uatn patients. However, its increased a- and 6-1 stimulation ou contraindicate its use in patients with hypertension. Lastly, ketamine is felt to be a negative inotrope and | Ketamine isthe drug of choice for requires its catecholamine surge to maintain blood | intubating patients with acute severe pressure; failure to recognize this principle can lead | asthma or septic shock. to profound hypotension in catecholamine-depleted patients, such as those with catecholamine refractory septic shock. 20-16Sedation, Analgesia, and Neuromuscular Blockad Ketamine should be considered as a first-line agent for intubation of children with asthma and as both short- and long-term sedation in those children. It is also an ideal agent for short, painful procedures in patients with potentially difficult airways but stable respiratory status. 6. Dexmedetomidine Dexmedetomidine is an IV, selective, a,-adrenergic receptor agonist. It is similar in activity to clonidine and works as a sympatholytic at both central and peripheral receptors. It directly inhibits norepinephrine/noradrenaline release and produces both analgesia and sedation, It has arapid onset and is quickly metabolized by the liver to inactive metabolites. Dexmedetomidine has minimal respiratory depression but does slightly decrease heart rate and blood pressure secondary to its sympatholytic activity. Dexmedetomidine must be given by continuous infusion or slow bolus as it can cause transient hypertension due to antagonism of a, receptors if given too ‘quickly, It should never be given to patients taking atrioventricular nodal blockers, patients with bradycardia, hypovolemia, or poor cardiac output as it could worsen those conditions by depleting endogenous catecholamines. With these considerations in mind, dexmedetomidine is being used more often in pediatrics as a first-line sedative medication that preserves respiratory function well. VI. SIDE EFFECTS AND CONTRAINOICATIONS OF SPECIFIC NEUROMUSCULAR BLOCKING AGENTS NMB agents are indispensable in several critical care situations. Skeletal muscle paralysis can. prevent vocal cord damage during intubation, maintain absolute immobility during critical procedures, and allow ventilation of patients who cannot be ventilated using deep sedation alone. However, relaxation agents are 100% lethal if advanced airway management cannot be assured, For this reason, if the provider is not completely certain of their ability to maintain a patient’s airway a alter paralysis, relaxation agents should never be given. In addition, NMB does not prevent pain transmission ‘These drugs are lethal if used and would cause significant terror and stress in an | improperly and should be used only undersedated patient. For these reasons, paralytics bb adequately equipped practitioners should never be used without adequate concomitant, | with excellent airnay sills. Assistance sedation and analgesia. Lastly, non-depolarizing NMB. agents, especially in conjunction with steroid usage, can cause a prolonged polyneuropathy of critical illness. ‘This can significantly extend hospitalization and 7 = ~ a increase morbidity. : should be summoned as soon as an | cirvay emergency is detected. A. Depolarizing Agents NMB medications can be classified into two large groups based on their activity at the neuromuscular junction (NMJ). Depolarizing agents open sodium channels at the post-synaptic membrane and cause rapid membrane depolarization, which prevents further neuromuscular 20-17Wi Pediatric Fundam | Critical Care Support transmission. Once the membrane is depolarized, acetylcholine can no longer propagate action potentials throughout the muscle, inducing paralys Succinyicholine (1 mg/kg IV, 3 mg/kg intramuscularly) is the only depolarizing NMB agent in use today. It is an extremely rapid-acting agent (<1 minute) and is completely metabolized by cholinesterases in minutes, independent of liver and kidney function. Its mechanism of action results in a brief period of fasciculation followed by flaccid paralysis. Fasciculation can be blocked by concurrent administration of a partial dose of anon-depolarizing NMB agent. Although its rapid action and short duration are highly desirable, succinylcholine has several side effects which can be significant: Malignant hyperthermia mM Rhabdomyolysis Mm Bradycardia Hyperkalemia Mi Increased intraocular pressure For these reasons, its use is contraindicated in most ‘Significant byperbalemia resulting in traumas, neuromuscular disorders, and in cases of cardiac arrest has occurred in patients elevated ICP, glaucoma, significant acidosis, or metabolic administered succinylcholine. derangement. Outside of these conditions, itis an excellent - . agent, but it should not be used indiscriminately. a ™ Increased ICP B. Non-depolarizing Agents Unlike the depolarizing agents, the non-depolarizing muscle agents block acetylcholine by binding to its receptor. In this manner, they prevent transmission at the NMJ and induce paralysis until they are metabolized. All non-depolarizing agents have a slower onset than succinylcholine and require a significantly longer period for reversal. Rocuronium (1 mg/kg) has the fastest onset of all non-depolarizing agents at | to 2 minutes. It also has the shortest duration of action at about 30 minutes. Although rocuronium is primarily metabolized by the liver, its effects can be prolonged in patients with renal disease. Due to its short uration ofaction, rocuronium is a poor choice for long-term paralysis, but the best substitute for succinylcholine when short-term paralysis is needed (.e., during intubation). Vecuronium (0.1 mg/kg) provides longer NMB when prolonged paralysis is needed. Vecuronium, requires about 60 minutes for reversal, but a single dose may last several hours in infants. Clearance is significantly reduced in patients with liver disease, and renal dysfunction may also ‘compromise its clearance. Vecuronium is probably the best non-depolarizing agent for long-term, continuous sedation. Pancuronium (0.1-0.15 mg/kg) is the longest acting non-depolarizing agent still in dinical use. Asingle dose can cause paralysis for more than 2 hours. Like rocuronium and vecuronium, 20-18Sedation, Analgesia, and Neuromuscular Blockade EXO pancuronium clearance is significantly reduced in patients with liver and kidney disease. Unfortunately, the benefits of its long duration of action are outweighed by its vagolytic. properties. Pancuronium causes significant tachycardia, which may not be well tolerated in some patients. In light of these considerations, pancuronium is probably only a good choice when vecuronium isnot available. Atracurium (0.5 mg/kg) and cisatracurium (0.1 mg/kg) are clinically useful non-depolarizing agents that are cleared by Hoffman degradation and can be used safely in patients with renal or hepatic failure. Atracurium can cause significant histamine release with resultant hypotension and must be avoided in patients with allergies or asthma. This side effect is greatly attenuated in cisatracurium, which can be considered asa paralytic agent in patients with significant hepatopathy or renal failure. VIL. REVERSAL AGENTS Few drugs are available that can reverse the effects of sedative, analgesic, or neuromuscular blocking agents. However, some agents can decrease morbidity or mortality in various clinical situations. They should be immediately available during any sedation, but their usage must be tempered by clinical context. Naloxone (0.1 mg/kg per dose, up to 2 mg) is a specific antagonist for all opiates. Its action is almost immediate as it displaces opiates from their receptors. All opioid effects are reduced simultaneously at high doses, including respiratory depression and analgesia. At lower doses, naloxone may reverse only respiratory depression and spare analgesia. However, since the medication is usually only given in an emergency, there may not be time available to titrate inadequate dosing. Naloxone’s half-life is much shorter than that of most narcotics, and it may need to be re-dosed intermittently until the patient can clear all residual narcotics from the bloodstream. In fact, long-acting narcotics usually require naloxone to be given asa continuous infusion over a prolonged period. Naloxone can be used as an emergency room diagnostic in patients with depressed mental status and poor respiratory effort. When a full reversal dose is given to patients with narcotic overdose, no doubt will remain regarding effect. However, the primary use of naloxone is to reverse narcotic-induced respiratory depression and spare a patient intubation. Flumazenil (flumazepil), a specific antagonist of benzodiazepines, has a relatively long hall-ife, approximately 1 hour, but hepatic failure can greatly increase this. Flumazenil completely reverses both the sedative effects and respiratory depression associated with benzodiazepine overdose. Unlike naloxone, flumazenil has several side effects that make it an undesirable medication choice in almost every situation. First, and most importantly, it can trigger seizures in patients with known, or even unknown, seizure disorders. If the patient seizes afier flumazenilis given, those seizures cannot be stopped by benzodiazepines, and they may even become refractory to second- and third-line medications as well. Second, flumazenil can cause difficult to control arrhythmias, tachycardia, and hypertension. Lastly, flumazenil can unmask the effects of tricyclic antidepressant overdose associated with polypharmacy overdose. For all of these reasons, flumazenil should never be used diagnostically for benzodiazepine overdose in any situation, In fact, due to its myriad and severe complications, flumazenil should probably be avoided even in known benzodiazepine overdose. The safer alternative would be to support the patient’s airway until the benzodiazepines 20-19Wi Pediatric Fun mental Critical Care Support are cleared. The only exception to this would be a patient with respiratory failure and known benzodiazepine overdose who cannot be ventilated or oxygenated by advanced airway maneuvers. Non-depolarizing NMB agents can also be reversed to some extent, although not directly, as opioids and benzodiazepines. Since non-depolarizing agents work by antagonizing acetylcholine binding to the NMJ, high doses of anticholinesterases, such as neostigmine (0.025-0.1 mg/kg/dose), can be used to reverse their effect. However, neostigmine will increase acetylcholine levels at muscarinic receptors as well as the NMJ. In the high doses of neostigmine given to reverse blockade, the patient would exhibit symptoms of acetylcholinesterase toxicity (increased salivation, hyperpyrexia, miosis, and bradycardia) if given without an anticholinergic agent. Either atropine or glycopytrolate can be given concurrently with neostigmine reversal doses to prevent these side effects. A variable amount of time is required to reverse paralysis, by non-depolarizing agents depending on the percent of acetylcholine receptors occupied by the blocking agent. Therefore, the practitioner must determine that the patient is breathing spontaneously, without assistance, before attempting to remove any advanced airway devices. The method used to reverse non-depolarizing agents will not work with succinylcholine as it has a different mechanism of action. However, itis cleared so rapidly that a reversal agent is usually not needed. This is touted as one of the benefits of succinylcholine, in addition to rapid onset, as compared to non-depolarizing agents. VILL. TACHYPHYLAXIS AND IATROGENIC WITHDRAWAL Tachyphylaxis describes the phenomenon of decreased drug effectiveness as it is used for longer periods of time. This is usually the result of increased drug metabolism or downregulation of the receptor of interest. Most medications exhibit this effect, and each patient will respond differently. Infusion rates or dosages required to obtain adequate levels of sedation and analgesia should be expected to increase the longer the patient is exposed to a drug. In fact, tachyphylaxis can be so significant that the practitioner must add agents to an already complicated drug regimen to achieve the desired clinical goal. This is especially important in the continuously paralyzed patient, as sedation and analgesia levels may become inadequate while the patient is still paralyzed. This would result in an awake, paralyzed patient with significant pain. IX. OPIOID AND BENZODIAZEPINE WITHORAWAL A. Pharmacologic Strategies Opioid and benzodiazepine withdrawal syndromes should be anticipated in all patients requiring 25 days of therapy, particularly when synthetic opioids have been administered as a continuous infusion. A long-acting agent, such as lorazepam, can be started 1 to 2 days before anticipated extubation to prevent withdrawal to benzodiazepines; the midazolam infusion can be tapered and stopped gradually once the child is close to extubation. Likewise, methadone can be started ata dosage that approximates the opioid equivalent (while also accounting for pharmacokinetic differences between the 2 agents). It may be initially administered at intervals of 6 hours for 20-20Key Points Sedation, Analgesia, and Neuromuscular Blockade EX approximately 1 day and subsequently decreased to longer intervals. Smaller doses are often effective with careful titration and consultation with a pediatric intensivist or pain specialist. Although methadone is given in 3 to 4 divided doses the first day, the dosing interval is gradually increased and the total daily dose is tapered to avoid drug accumulation. Lorazepam and methadone are usually tapered on an individualized basis over several days to weeks, depending on the duration of previous treatment with benzodiazepines and opioids, with the goal of preventing physiologically significant complications of withdrawal, such as agitation, seizures, tachycardia, hypertension, diarrhea, and vomiting. Recovery from critical illness and its associated psychological derangements is also expedited by appropriately tapering these agents. B. Nonpharmacologic Strategies to Control Agitation — ‘The pediatric intensive care unit environment may be very upsetting to patients and their families. Units that allow privacy, continuous access to a supportive parent, and controlled sound and lighting may decrease anxiety in young patients. Likewise, promotion of a circadian rhythm by encouraging exposure to sunlight during the day and quiet, dark conditions at night may minimize the need to escalate drug therapy. Child life specialists can be very helpful in distracting and entertaining patients in ways that permit reduced doses or brief daytime holidays from opioid and sedative infusions, Sedation, Analgesia, and Neuromuscular Blockade Sedation, analgesia, and neuromuscular blockade are necessary in caring for critically ill patients but, if used improperly, they can cause significant morbidity or mortality. M Many of the risks associated with sedation, analgesia, and neuromuscular blockade can be eliminated or reduced by careful pre-sedation planning and preparation. 1 Drug choices should be made based on the clinical goals and the individual patient. No drug or drug combination is ideal in all situations, 1 Each drug has its own side effects and contraindications which must be carefully ‘weighed against the clinical goals the practitioner is trying to achieve. A more experienced practitioner should be called for support before initiating sedation. if the clinician is uncertain about the ability to maintain an airway, and to ventilate and oxygenate a patient. Wl Always “start low and go slow” when choosing the sedation level. § Clinicians should recognize their own limitations and not initiate sedation when uncomfortable with any patient or scenario. Likewise, they should not use an agent or combination of agents unless confident in doing so. im Tachyphylaxis should be anticipated with all agents, and dosages should be adjusted for each patient at any time, 20-21Pediatric Fundam BB sucestes Readings 20-22 ital Critical Care Support 1. Bar-Joseph G, Guilburd Y, Tamir A, Guilburd JN. Effectiveness of ketamine in decreasing Intracranial pressure in children with intracranial hypertension. J Neurosurg Pediatr. 2009; 440-46, 2. Cook DR. Neuromuscular blocking agents. In: Fuhrman BP, Zimmerman J, eds, Pediatric Critical Care. Philadelphia, PA: Mosby Elsevier, 2006:1729-1747. 3, Heard CMB, Fletcher JE. Sedation and analgesia. In: Fuhrman BP Zimmerman J, eds. Pediatric Critical Care, Philadelphia, PA: Mosby Elsevier; 2006:1748-1779. 4, Kraemer FW, Rose JB. Pharmacologic management of acute pediatric pain. Anesthesiol Clin, 2009;27:241-268. 5, PlayforS, Jenkins I, Boyles C, et al; United Kingdom Paediatric Intensive Care Society Sedation; Analgesia and Neuromuscular Blockade Working Group. Consensus guidelines on sedation and analgesia in critically il children. intensive Gare Med. 2006;32:1125-1136. 6. Practice advisory for preanesthesia evaluation: a report by the American Society of Anesthesiologists Task Force on Preanesthesia Evaluation. Anesthesiology. 2002;96:485-496. 7. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology. 2003;98:1269-1277, 8. 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: ‘an updated report by the American Society of Anesthesiologists Committee on Standards and Practice Parameters. Anesthesiology. 2011;114:495-511. 9, Practice guidelines for sedation and analgesia by non-anesthesiologists, American Society of ‘Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Anesthesiology. 2002;96:1004-1017. 10. Weingart SD, Levitan RM. Preoxygenation and prevention of desaturation during emergency airway management. Ann Emerg Med, 2012;59:165-175 11. Yaster M, Easley RB, Brady KM. Pain and sedation management in the critically il child. In: Nichols DG, ed. Rogers’ Texthook of Pediatric Intensive Care. Philadelphia, PA: Lippincott Williams and Wilkins; 2008:136-165.