Chapter 129. Procedural Sedation and Analgesia (Conscious Sedation)

Procedural sedation and analgesia (PSA) techniques are an essential skill for any Emergency Physician. The daily practice of Emergency Medicine employs painful and anxiety-provoking measures to perform diagnostic testing or therapeutic interventions. These skills not only apply to the Emergency Physician, but to the individual healthcare provider monitoring the procedure as well. PSA is a skill that may require a credentialing process at some institutions. It probably has evoked a written procedural guide in most hospitals and Emergency Departments, with or without the input from a hospital-wide PSA committee or the Department of Anesthesiology. PSA certification may require annual competency assessments in the form of a written examination or practical scenarios. PSA is a technique that probably receives a great deal of attention from the continuous quality improvement committee as a result of The Joint Commission's directive. It is a skill that, with proper training and well-designed application principles, will provide the patient and their families with a sense of compassion and caring for their physical and emotional distress. PSA is a skill that may also result in horrific outcomes when performed without appropriate training, knowledge, risk–benefit analysis, and anticipation of complications.

An extensive spectrum of painful and anxiety-provoking clinical presentations arrive in an Emergency Department on any given day. There may be a dislocation reduction, a fracture reduction, a diagnostic lumbar puncture, a sexual assault examination on a child, or neuro-imaging on a combative, head-injured patient. Each presentation has a separate subset of variables to consider prior to PSA. While Anesthesiologists are still considered the “experts” in sedation, they are not readily available to the Emergency Department's beck and call. Multiple specialties have developed guidelines for the use of PSA to account for these limitations and to ensure that safe, effective care can be rendered to their respective patient populations.1–3

The environment of the Emergency Department is unique in many facets of PSA due to the fact that situations are nonelective. Procedures are relatively brief, thereby making Operating Room time neither timely nor cost effective. Intrinsic to PSA is the core training and frequent exposure that Emergency Physicians have to this particular skill. Who better to handle an untoward cardiopulmonary complication of a procedure than a specialist in the area of airway management and resuscitation?

It is critical to the technique of PSA, including drug selection, to take a variety of parameters into consideration before the first medication is administered. The potency and effectiveness of today's newer agents is a double-edged sword. They are invaluable with the correct selection and administration. They are also a recipe for disaster if risks are not appropriately identified and minimized. Monitoring techniques, including pulse oximetry and capnography, are effective adjuncts to procedural monitoring. However, they are no substitute for a trained, dedicated observer.

Textbooks and review articles use various definitions to define components of PSA, formerly known as conscious sedation. Terms such as light and deep sedation are often applied to the extremes of the sedation continuum. The important thing to realize is that sedation is a continuum.2 At the far left of the continuum is the alert and anxious patient. Eye opening, speech, and motor responses diminish as the sedation process proceeds. At the opposite end of the spectrum are CO2 retention, hypoxia, hypotension, and finally death. These later endpoints are obviously not desirable. Anxiolysis and analgesia are other terms that need definition. The following terminology is representative of current PSA jargon.

Analgesia equates to pain relief without alteration in mental status. Analgesia is required in a variety of procedures in which painful manipulation or instrumentation is anticipated. Most potent pain medications will also have a component of sedation, especially the opioids. This sedation component needs to be carefully considered during drug selection and dosing calculations to minimize the risk of overshooting the desired sedation endpoint.

Anxiolysis means to relieve apprehension. Patients may be anxious for any variety of reasons besides the thought of a painful forthcoming procedure. Anxiolysis involves allaying the patient's fears. The agents used for anxiolysis are pure sedatives and provide no pain relief. Although some degree of sedation is to be expected, it should be minimized with appropriate drug and dosing selection.

Sedation blunts the patient's perception of the surroundings and pain with a depression in their state of wakefulness. Levels of procedural sedation do not follow a discrete stepwise progression. Rather, sedation proceeds along a continuum. This continuum ranges from a mild sedation through deep sedation into general anesthesia. The level of sedation is determined by a patient's state of anxiety, wakefulness, and mobility in addition to their ability to retain protective reflexes.

Dissociative sedation implies sedation, analgesia, amnesia, and the induction of a cataleptic state. This state preserves ventilatory drive and maintains protective reflexes while maintaining cardiovascular stability. Ketamine is the primary agent used to induce this state.

Neurolepsis is a reduced motor activity state in which the patient has reduced anxiety and indifference to their surroundings. Neurolepsis is best achieved with major tranquilizers such as haloperidol or droperidol. Its application is best suited to the agitated or violent patient whose behavior places either themself or others at risk for harm.

General anesthesia represents the extreme right of this continuum. The patient has no awareness of the environment and has lost the ability to self-maintain protective reflexes. This is not a desirable endpoint during PSA in the Emergency Department.

PSA is a technique of administering sedation or dissociative agents with or without analgesics to induce a state that allows the patient to tolerate unpleasant procedures while maintaining cardiorespiratory function. PSA produces a depressed level of consciousness, which allows the patient to maintain airway control independently and continuously. Specifically, the drugs, doses, and techniques used are not likely to produce a loss of protective reflexes according to the American College of Emergency Physicians Clinical Policy for PSA in the Emergency Department.1

Standardizing levels of sedation along a continuum has been attempted with various scoring systems.4 The Ramsay scale was specifically devoted to providing objective determinations of sedation during drug-induced sedation practices. Scoring consists of six sequential scoring levels (Table 129-1).

Another scoring system is the Observer's Assessment of Alertness/Sedation (OAA/S) Scale. It was designed as a research tool for studies incorporating pharmacologic studies with benzodiazepines.4 The scoring system was based upon the assessment of the patient for responsiveness, speech, facial expressions, and ocular appearance. The OAA/S scale incorporates the patients' responsiveness to the effects of the agents given, in contrast to the similar observational scoring used in the Ramsay scale.

A wide variety of clinical presentations and procedures would entail the appropriate use of anxiolysis, sedation, analgesia, or dissociation for case management (Table 129-2). PSA is particularly suited to pediatric patients requiring multiple painful procedures in the Emergency Department, especially if they can be done simultaneously or one after another. An example is the young child with a fever undergoing a septic work-up requiring vascular access, urethral catheterization, and a lumbar puncture.

There are four goals of PSA. The first and foremost is to assure patient safety. This is accomplished with a careful risk–benefit assessment and a well-defined clinical procedure to maximize benefit, limit risk, and foresee potential complications. Second is to appropriately assess and deliver adequate analgesia, anxiolysis, sedation, and amnesia as dictated by the patient's needs. Third is to consider the psychological impact of the forthcoming procedure and minimize the impact of these events. Fourth is to provide a fluid transition to the preprocedural physical and mental status while assuring a safe discharge and postprocedural observation.

There are three contraindications to the use of PSA. First, a known allergy to the individual drugs(s) being considered is an absolute contraindication. Ketamine and nitrous oxide have agent specific contraindications. Second is the lack of experienced or credentialed personnel. PSA requires personnel appropriately trained in airway management. Finally, appropriate monitoring capabilities must be available. This includes appropriate equipment monitors as well as personnel to observe the monitors, record procedural flow, and monitor postprocedural recovery.

Issues such as the time of the last oral intake should be considered in the risk–benefit analysis. However, a full stomach does not constitute an absolute contraindication.5–7 Concomitant drug or alcohol use is a complicating variable that needs to be recognized and accounted for prior to the procedure. Complicated airway anatomy should also receive particular attention in case emergent airway management is necessary.

• Crash cart with resuscitation equipment
• Defibrillator
• Oxygen source
• Oxygen masks
• Nasal oxygen cannulas
• Oral airways
• Nasal airways
• Bag-valve-mask device
• Continuous pulse oximetry
• Capnography, if available
• Continuous cardiac monitoring
• Intravenous access supplies (catheters, tubing, fluids, etc.)
• Suction source
• Suction catheters
• Pharmaceutical agents
• Reversal agents (naloxone, flumazenil)
• Succinylcholine

It is imperative that resuscitation equipment be immediately available prior to the onset of PSA. Such requirements should be part of the preprocedural checklist. Age-appropriate equipment must be immediately available. The immediate availability of reversal agents is a prerequisite to the administration of opioids or benzodiazepines. Succinylcholine should be readily available in case of laryngospasm or opioid-induced chest wall tightness.

Informed Consent

The issue of informed consent is institution specific. Most institutions function under the premise that if a particular procedure has any significant level of risk inherent in its application, informed consent regarding the risks and benefits of the procedure be undertaken with the patient and/or their representative. The benefit to the patient is a careful calculated means at reducing the pain and anxiety associated with a planned diagnostic or therapeutic intervention. The risks are inherent in the medications selected, the patient's current state of physical condition, and complicating conditions (such as time of last meal, recent drug use, or recent alcohol use).

Personnel Competency/Credentialing

Any Emergency Physician practicing PSA must be competent in airway management and resuscitation.8 Competency credentialing is institution specific. Emergency Physicians may be granted privileges on the basis of their residency training or current practice. Other institutions may mandate a written competency examination or advanced airway/resuscitation training such as ACLS certification.

Nursing personnel must be proficient in medication profiles, medication administration, and patient monitoring. The staff needs to be aware of the department's policies and procedures. Competency testing may be a prerequisite to providing PSA. All personnel involved must meet these departmental/institutional requirements prior to initiation of PSA.

Risk–Benefit Assessment

The preprocedural assessment constitutes both a risk assessment and a preprocedural baseline determination. Assessment requires a determination of the patient's current health and an evaluation of potential risk, adverse reactions, and procedural complications. The old adage “an ounce of prevention is worth a pound of cure” certainly applies with PSA. Thorough preparation is critical to minimize patient risk. Department procedural flowsheets, complete with preprocedural assessment checklists, can be a valuable adjunct.

Assign patients an American Society of Anesthesiologists (ASA) Physical Status Classification (Table 129-3). Emergency Department PSA would normally be limited to class I or class II patients. Class III or class IV patients are best served in consultation with an Anesthesiologist. Never perform PSA on class V patients.

Perform a complete history and physical examination prior to the application of PSA. Special emphasis should be directed toward allergies to any analgesic or sedation agent. Previous anesthesia and related complications may be critical to drug selection and/or the involvement of an Anesthesiologist. Conduct a separate assessment of the patient's airway, including dentition. Age-appropriate airway management equipment must be immediately available in the event airway control becomes necessary. A patient's breathing is an important continuous determinate that needs to be observed and recorded before the procedure, throughout the procedure, and during recovery. Hypoventilation or bronchospasm may be clinically evident with observation before an alteration in heart rate or pulse oximetry is detected. The patient's state of wakefulness and the ability to follow commands are markers for sedation. Depending on the procedure, a patient's mental status may be minimally depressed whereby they may respond to environmental stimuli, whereas deep sedation requires moderate stimulation to arouse the patient.

A full meal less than 6 hours, or liquids less than 2 to 3 hours, prior to the procedure places adults at risk for aspiration if sedation inadvertently results in loss of protective airway reflexes. These time requirements are not a contraindication to the use of PSA. Agents used to promote gastric emptying or altering gastric pH to minimize the effects of aspiration are typically impractical in the Emergency Department setting due to their delayed onset for effectiveness. These procedures cannot usually be delayed due to the urgency of the matter.

Obtain baseline measurements of the patient's weight, blood pressure, heart rate, oxygen saturation, and capnography (if available). PSA can result in both hypoxia and hypercapnia. The underlying mechanism is opioid/sedative-induced hypoventilation. While pulse oximetry is routinely used, the degree of desaturation does not correlate alone with poor outcomes.9 It would stand to reason that capnography would provide an earlier warning to a hypoventilatory condition, and for this reason it is slowly becoming standard care in PSA. Oxygen application is considered routine, yet its value has not been established.10,11 Furthermore, the routine application of oxygen may delay recognition of a profound hypoventilatory state if capnography is not used.

The use of capnography is common practice in patients undergoing general anesthesia.12 It is not routinely used for PSA in the Emergency Department. Capnography can identify respiratory depression early or that is undetected by the Emergency Physician.13–15 By evaluating the absolute end-tidal CO2 (ETCO2) level or the ETCO2 waveform, one can better evaluate a patient's respiratory status. Pulse oximetry measures oxygen saturation but not ventilation. It is the ventilation that often is affected before oxygen saturation in cases of respiratory decompensation. A patient's oxygen saturation may not actually drop until late into their respiratory decline. Direct observation of chest rise and respiratory rate is not sensitive to identify respiratory decompensation during PSA when compared to capnography.16,17 An ETCO2 >50 mmHg or a change of >10 mmHg should alert the Emergency Physician that the patient may not be achieving adequate ventilation. A loss of the ETCO2 waveform implies that the patient is apneic.

A patient may present with a number of conditions that may require sedation, analgesia, or a combination of both. The first step is to determine exactly what is needed. Levels of sedation range from light or minimal depression of mental status to deep or heavy sedation where protective airway reflexes or hemodynamic stability may be compromised. The goal of PSA is to achieve the desired endpoint with minimal risk of cardiorespiratory compromise.

Light sedation is aimed at blunting the patient's level of awareness to environmental stimuli and painful perceptions. Anxiety is alleviated and the patient maintains their responsiveness to verbal and physical stimuli. Protective airway reflexes are maintained. Deep sedation produces profound depression of awareness with the inability to respond to verbal stimuli. Careful monitoring of the cardiorespiratory status is essential in this setting as protective airway reflexes may be lost.

Certain agents, themselves or in combination, produce varied results in different patient subgroups. Each patient requires individual consideration. Selecting the appropriate agent requires knowledge of the agent's potency, duration to onset, duration of drug effect, titratability, interaction with other drugs, and adverse effects profile. Increasing dosages of an agent reduces its drug-specific effect in exchange for a nonspecific sedative effect complete with cardiorespiratory compromise. The most common mistake in sedation is choosing the wrong agent for the specific goal. For example, sedating a patient does not relieve pain. Sedation must be accompanied by analgesia if a patient is undergoing a painful procedure. This agent should ideally be titratable. The only reliable and precise means of this is via intravenous administration. Deep sedation should be provided only via the intravenous route. Intravenous access is required if the patient undergoes deep sedation in case cardiorespiratory support is required or in the event that reversal agents must be administered. Anxiolysis or mild sedation does not necessarily require intravenous access. Patients may be assessed on an individual basis as to whether intravenous access is deemed appropriate.

Synergistic effects must be considered when choosing a dosing schedule. For example, combining a benzodiazepine with a narcotic analgesic increases the potential effect of either agent alone.10 For this reason, it may become very difficult to titrate a sedative and an analgesic concurrently. Some practitioners advocate the use of a sedative alone initially followed by the addition of a narcotic analgesic as the patient's sedation is resolving. This works well for procedures that are extremely short, and where muscle relaxation is key, such as simple reductions. The anterograde amnesia provided by most sedative agents is usually adequate to prevent the recollection of pain during the procedure. When used in combination, however, physicians should reduce the initial doses of multiple agents owing to the additive sedative effects. Small and incremental dosing enables a controlled titration to effect. Physicians must have a fundamental knowledge of the pharmacological profiles of these agents. Allow the medications to reach peak effect before administering additional medication. Physicians are best served with a thorough knowledge of a few drugs as opposed to little knowledge over the entire procedural sedation agent spectrum.

It would behoove an Emergency Physician to develop and practice four PSA drug regimens: sedative plus analgesic, pure sedation, dissociative analgesia and sedation (ketamine), and inhalation anesthesia (nitrous oxide). Become well versed in the applications of these regimens and do not stray from your routine unless circumstances dictate a different regimen. At that time, identify your limitations and obtain peer or Anesthesiology backup prior to procedural initiation. Provide adequate analgesia first when performing a painful procedure. Some degree of sedation will have already been established. Provide sedation with a pure sedative to obtain the endpoint of relaxation/sedation required to complete the procedure.

Table 129-4 provides a summary review of the agents routinely employed during PSA. It is critical that the Emergency Physician is well versed on both the individual agent and its effect in combination with other medications. Medication routes, dosing parameters, side effects, contraindications, and anticipated complication management must be well known in advance.

The ideal agent is a single drug that has amnestic, anxiolytic, analgesic, and sedative properties. It should have a predictable and rapid onset of action. It should have a predictable and short duration of action with a rapid recovery. The ideal agent should be inexpensive, easy to administer, and have a wide safety margin to make loss of consciousness extremely unlikely. It should have little or no side effects, especially cardiovascular and respiratory. It must be easily reversible if necessary. There should be no residual effects at the end of the procedure. It is obvious that no agent meets all these criteria. We hope to minimize side effects, maximize benefit, allow quick recovery and dispositions, and produce reliable effects using small doses of multiple agents.

Benzodiazepines produce anterograde amnesia, anxiolysis, sedation, and muscle relaxation. They have no analgesic activity and must be used in conjunction with other agents for painful procedures. The use of a benzodiazepine allows less analgesic agent to be administered and may reduce the severity of adverse reactions. The major adverse effects of benzodiazepines are respiratory depression and hypotension. Benzodiazepine-associated respiratory depression is usually transient but can be reversed with flumazenil. Prevent hypotension by ensuring that the patient is euvolemic, using the minimum amount of narcotics to produce analgesia, and carefully titrating the benzodiazepine.

Midazolam (Versed)

Midazolam is an ultra-short-acting benzodiazepine that is metabolized by the liver and excreted by the kidney. Intravenous midazolam in dose ranges from 0.02 to 0.10 mg/kg will produce sedation within 2 to 3 minutes, redistribute rapidly, and provide a 20 to 30 minute duration of action. Most adults have adequate sedation and anxiolysis by a total dose of 5 to 7 mg; administered in 0.05 mg/kg or 1 to 2 mg increments every 3 to 5 minutes. It is important to note the 2 minute delay in the peak CNS effect. Allow midazolam time to work before additional dosing. It may be used intranasally in children (0.3 to 0.5 mg/kg) as an effective means of sedation. It is water-soluble and does not cause vascular irritation on injection, as found in its relative diazepam. Midazolam is three to four times more potent than diazepam. It has anxiolytic and anticonvulsive properties. It is a potent amnestic agent that has the added advantage of providing both antegrade and retrograde amnesia. Like all benzodiazepines, midazolam alters the response to pain but does not reduce pain perception. The addition of an analgesic agent is required when midazolam is administered for a painful procedure.

Midazolam is a potent respiratory depressant, like all sedative agents. Midazolam can cause apnea by depressing the sensitivity of the hypothalamus to hypercapnia. It shifts the CO2 response curve to the right and depresses its slope. Its respiratory depressant effects are augmented in patients receiving opioids, with underlying lung disease (e.g., COPD), and with concomitant circulating CNS depressants (including opioids, alcohol, and barbiturates). Patients may become hypoxic, even with normal respiratory rates.

Pulse oximetry is warranted when administering midazolam. Deaths related to the use of midazolam for sedation during endoscopy prompted the FDA to recommend increased monitoring and particular caution with elderly or debilitated patients. There is a particular propensity for apnea when even very small doses of midazolam are given in conjunction with fentanyl.18 Midazolam may cause hypotension that is related to the dose and to the rate of administration. This effect is more likely to occur in hypovolemic patients or elderly patients.

Diazepam (Valium) and Lorazepam (Ativan)

Both diazepam and lorazepam have longer half-lives than midazolam. While either agent may be used for PSA, they are more difficult to titrate and have a longer duration of action. Neither of these characteristics is well suited to PSA. Midazolam has greater earlier sedation, less recall, less pain upon injection, higher 90 minute alertness scores, and more patients ready for discharge at 90 minutes postprocedure than diazepam. Diazepam results in more respiratory depression, hypotension, and phlebitis than midazolam. Diazepam and lorazepam have no advantage over midazolam if the goal is to produce a short, titratable state of anxiolysis and sedation. These agents are therefore not often used for PSA.

Opiates provide analgesia with minimal sedation and no anxiolysis. They have a long track record showing a predictable performance. The respiratory and central nervous system depression can be readily reversed with naloxone and nalmefene. Opiates are relatively inexpensive and often used in a balanced approach to PSA. Agents in this class include morphine, fentanyl, meperidine, sufentanil, and alfentanil.

While morphine has been the mainstay narcotic analgesic, the use of potent synthetic short-acting opioids for analgesia and sedation has been common practice for PSA. These drugs are particularly appealing for their short half-lives, rapid onset of action, limited cardiovascular side effects, ease of controlled administration, and the availability of a rapidly acting reversal agent. The use of these agents requires a thorough familiarity with their pharmacological properties and side effects. A PSA repertoire should include one of the potent synthetic narcotics. It is better to master one drug than dabble in the pharmacology and administration of three different drugs with different dosing regimens.

Morphine

Morphine is a “good old” potent analgesic with a lot of clinical experience. It is the prototype opioid to which all others are compared. Incremental intravenous dosing of 0.05 to 0.20 mg/kg every 3 to 5 minutes provides a nice range over which to carefully titrate to an individual analgesia requirement. It begins working in 1 to 3 minutes and peaks within 15 to 20 minutes. Morphine has a duration of activity of 3 to 4 hours, thereby providing often-needed pain relief even after the procedure has been completed. It is metabolized by the liver and excreted by the kidney. Morphine, as with all opioids, decreases the medullary response thereby promoting hypercapnia and hypoxia. Histamine release with hypotension, nausea, vomiting, itching, bronchospasm, and loss of vascular tone are all too common side effects of morphine administration. Morphine has steadily lost ground to the newer, designer opioids with better cardiovascular stability such as fentanyl, sufentanil, and alfentanil.

Fentanyl (Sublimaze)

Fentanyl is highly lipid soluble and 75 to 125 times more potent than morphine. Peak analgesia is achieved in 2 to 3 minutes after intravenous administration. Although its terminal half-life is 130 to 220 minutes, its clinical effectiveness is limited to approximately 30 minutes due to rapid tissue redistribution. Fentanyl is a “20 minute drug for a 20 minute procedure.” It is metabolized in the liver with renal and hepatic excretion. Approximately 20% is excreted as the unmetabolized parent compound. The major side effect of fentanyl is respiratory depression. Hypotension is less common than with morphine because fentanyl does not induce histamine release.

Administer fentanyl very slowly and in small increments. Patients may experience rigidity of their chest muscles, coined the “rigid chest syndrome,” when it is administered intravenously too rapidly. This syndrome can severely impact ventilation to the point that the patient must be paralyzed to facilitate adequate ventilation. Administer incremental doses of 0.5 to 1.0 μg/kg or 10 to 100 μg boluses slowly intravenously until adequate analgesia is achieved.

Fentanyl may be administered intranasally at a dose of 0.7 to 1.5 μg/kg.19 Concentrated fentanyl at a dose of 1.7 μg/kg is equivalent to 0.1 mg/kg of morphine.22 Its advantages include simple rapid administration, limited training required to administer it intranasally, and it provides faster analgesia when compared to establishing intravenous access and administering an intravenous opioid.19 The disadvantages include having to restrain the child's head for the administration and the time it takes to administer the medication. Atomizer devices can minimize or eliminate these issues.

An alternative method is to administer fentanyl through a nebulizer mask.20,21 Nebulized fentanyl (3 μg/kg) through a breath-actuated mask is effective.20 This study only used children over the age of 3 years because younger children have difficulty triggering the mask. Another study used a standardized nebulizer system to deliver 4 μg/kg of fentanyl, a dose equivalent to 0.1 mg/kg of morphine, to children between 4 and 13 years of age.21 Appropriate analgesia was achieved with this dose and administration system.

Fentanyl is contraindicated in children less than 6 months of age. It stimulates the central vagus nucleus in the brainstem. This can result in a prolongation of the refractory period of the atrioventricular (AV) node and significant bradycardia.

The rigid chest syndrome may occur to the point at which the patient may not be ventilating and attempts at assisted ventilation with a bag-valve-mask device are unsuccessful. The patient may then become hypoxic, bradycardic, and eventually expire. This phenomenon has been well documented in children. The rigid chest syndrome is the reason many Physicians are reluctant to administer fentanyl. It occurs during rapid intravenous administration, so give it slowly. It only occurs at high doses (>15 μg/kg) to anesthetic doses (50 to 100 μg/kg) ranges. The doses used for PSA are safe and do not result in the rigid chest syndrome. Immediately administer naloxone intravenously if the rigid chest syndrome develops. Unfortunately, naloxone does not often work to overcome the rigid chest syndrome. The patient may require paralysis and orotracheal intubation to overcome the rigid chest syndrome.

Sufentanil (Sufenta)

Sufentanil is an extremely potent narcotic analgesic. It is 5 to 10 times more potent than fentanyl and 500 to 1000 times more potent than morphine. It is metabolized and eliminated more rapidly than fentanyl. There is no significant advantage to using sufentanil over fentanyl for most PSA applications.

The one advantage is that its potency and small volume dosing enables it to be delivered intranasally in the pediatric population. ACEP's Guideline to Pediatric Sedation is a proponent of this particular application.23 Sufentanil has an onset of action in 5 to 15 minutes and a duration of action lasting 1 to 2 hours when administered intranasally. It provides exceptional cardiovascular stability but maintains the profound respiratory depressive effects inherent in the opioid class of agents. Careful patient selection is well advised when considering sufentanil.

Alfentanil (Alfenta)

Alfentanil is less lipid soluble than fentanyl. It is therefore less likely to accumulate if multiple doses are required. It is 10 to 20 times more potent than morphine. It is one-tenth to one-fifth as potent as fentanyl. The duration of analgesia is ultrashort. Its onset of action is within seconds and lasts only 2 minutes. Alfentanil is too short-acting to use for PSA. Total dosing is 8 to 10 μg/kg delivered in small repeated dosing aliquots. Its half-life is only 80 minutes. The adverse effect profile is similar to fentanyl except that it may cause more respiratory depression.24 The rigid chest syndrome may also be seen with alfentanil. Alfentanil is more appropriate to use for the induction of general anesthesia.

Meperidine (Demerol)

Meperidine is one-tenth as potent as morphine. It is the most commonly administered opioid agent for pain in the United States. It is not used for PSA because it is hard to titrate and takes a long time to reach peak activity.

Ketamine (Ketalar)

Ketamine is a unique pharmaceutical agent in that it provides sedation, amnesia, analgesia, and anxiolysis. Its safe and effective use in pediatric PSA is well studied.25 It is the most commonly used anesthetic agent throughout the world. It has the best safety profile in terms of cardiorespiratory complications of any agent. Ketamine is a derivative of PCP that generates a functional and electrophysical dissociation between the brain's cortical and limbic systems. This results in a dissociative state whereby the patient is in a trance-like cataleptic condition in which sensory perceptions and memory are blunted. Although the patient appears awake, they are dissociated from their environment. Random tonic movements will occur and gentle physical restraint may be required.

Ketamine is a positive inotrope. It increases the heart rate, blood pressure, cardiac output, and intracranial pressure. The blood pressure and heart rate may slightly increase with the use of ketamine. The systolic and diastolic blood pressure may increase up to 30 mmHg (average 15 mmHg). The heart rate may increase up to 30 beats per minute with an average of 15 beats per minute. These effects are believed due to decreased uptake of catecholamines at neural endplates.

Ketamine's effect on the respiratory system includes bronchodilation, a slight increased respiratory rate, increased secretions, and potential laryngospasm. Ketamine is a potent bronchodilator. It does not depress airway reflexes like narcotics or benzodiazepines. The side effects of increased respiratory secretions can be blocked with atropine or glycopyrrolate. Administer atropine prior to or concurrently with ketamine in a dose of 0.01 mg/kg to a maximum of 0.3 to 0.5 mg. Administer glycopyrrolate before ketamine in a dose of 0.005 mg/kg to a maximum of 0.25 mg. Atropine administration is associated with less adverse respiratory events, less recovery agitation, and less vomiting during recovery than glycopyrrolate.26 Atropine also causes more side effects, compared to glycopyrrolate, because it crosses the blood–brain barrier.27,28 A recent trend is to not use an antisialogue as excessive respiratory secretions are uncommon and not associated with adverse respiratory events.29

Ketamine may be administered by several routes. Rapid predictable effects are best seen with parenteral administration. Intravenous dosing (0.5 to 1.0 mg/kg slowly, up to 2 mg/kg) is approximately one-fourth of the intramuscular dosing (1 to 6 mg/kg, usually 2 to 4 mg/kg). A dissociative state is produced in less than a minute with intravenous administration and 2 to 10 minutes via the intramuscular route. Intravenous dosing may be repeated at 5 minutes with an additional 1 to 2 mg/kg. Intramuscular dosing may be repeated at 10 minutes with an additional 2 to 4 mg/kg if adequate sedation has not been achieved. Although ketamine may be given orally (5 to 6 mg/kg) or rectally (5 to 10 mg/kg), its titratability is poor, which makes its effectiveness much less predictable. Intramuscular dosing may be more commonly associated with laryngospasm when compared to intravenous administration.30

Due to its safety profile, ketamine may be administered intravenously or intramuscularly. Intramuscular administration is preferable when intravenous access is difficult to establish, intravenous access is not required for another reason, and for procedures lasting 15 to 25 minutes due to its longer effects. Intravenous administration is preferable if intravenous access is required for another reason, intravenous access is easily obtained, for procedures lasting less than 10 minutes, and to decrease recovery time.31

The lack of cardiorespiratory compromise of ketamine and the effectiveness of intramuscular administration make it an excellent agent for pediatric PSA. Patients tend to remain hemodynamically stable when using ketamine, reducing the need for intravenous access for fluid boluses and reversal agents. This is especially true in children where intravenous access can be a difficult procedure. A medication that can be safely administered intramuscularly not only simplifies PSA, but also improves patient and family satisfaction.

Contraindications to the use of ketamine include age less than 3 months, procedures involving pharyngeal stimulation, known cardiovascular disease, concurrent head trauma with altered mental status, airway compromise including previous tracheal surgery/stenosis, glaucoma, known CNS mass lesions, increased intracranial pressure, penetrating globe injuries, active upper or lower respiratory disease, and porphyria. Preliminary information suggests that ketamine is safe to administer in head injury patients in the pediatric intensive care unit.32 Further study is required before this can become general practice in the Emergency Department.

Patients will exhibit a slow emergence from the effects of ketamine over the course of 1 to 2 hours. Ketamine is metabolized and excreted by hepatic mechanisms. Place the patient in a quiet room that is free of excessive external stimuli to minimize the possibility of them becoming hyperactive or overstimulated by their surroundings. Ketamine-associated emesis is a commonly seen side effect.30,33–35 The rate of emesis is higher with intramuscular administration, with initial intravenous doses over 2.5 mg/kg, and with total doses ≥5.0 mg/kg.30,33 Although, a study of over 1000 children refuted this theory.34 The use of intravenous ondansetron (0.15 mg/kg, maximum 4 mg) decreased the rate of ketamine-associated emesis.35

Emergence reactions are hallucinations that occur as the ketamine wears off and the patient awakens. They may be seen in up to 50% of adults and up to 10% of children given ketamine. The etiology of these emergence reactions is unknown. There is an association of emergence reactions with an age over 10 years, females, rapid intravenous administration, stimulation during the recovery period, and personality disorders. Rarely will a child less than 10 years of age develop an emergence reaction with hallucinations.

The incidence of emergence reactions can be decreased. Administer the ketamine slowly intravenously. Place the patient in a dark, quiet room with minimal sensory stimulation during the recovery period. Treatment with benzodiazepines is indicated if an emergence reaction develops. The concurrent administration of midazolam in a dose of 0.025 to 0.050 mg/kg can reduce emergence reactions. One study found no advantage of combining midazolam with ketamine in preventing an emergence reaction.36 Another study found midazolam significantly reduced emergence reactions in adults.37 A recent review found no benefit and no harm in coadministering benzodiazepines.33 The concurrent use of midazolam is Physician-dependent, has no serious sequelae, and may reduce emergence reactions.

Ketamine–Propofol

The use of ketamine and propofol in combination has been coined “ketofol.” The reason these agents were combined was to provide appropriate sedation and analgesia while decreasing adverse events by using less of each individual agent. The combination of ketamine and propofol is effective for PSA.38–44 It provides a more rapid recovery than ketamine alone. The combination has similar complication rates, less adverse effects, and higher satisfaction scores than using higher doses of ketamine as a single agent.

There is no established standard dosing. Prepare both the ketamine and the propofol as a 10 mg/mL solution. These agents can then be administered intravenously in a 1:1 ratio in aliquots of 1 to 3 mL every 2 minutes until the desired effect is achieved. Another option is to mix equal parts of both solutions into one syringe and administer the appropriate volume to deliver 0.5 mg/kg of each agent. Additional boluses can be administered to deliver 0.25 mg/kg of each agent every 2 to 3 minutes until the desired effect is achieved.

The sedative hypnotics are a diverse category of agents that include thiopental, methohexital, etomidate, and propofol. These agents provide anxiolysis and sedation with various degrees of amnesia. They provide no analgesia.

Barbiturates

Short-acting barbiturates (i.e., thiopental, pentobarbital, and methohexital) are effective PSA agents. They provide good titratability with a rapid onset of action. Barbiturates provide sedation, hypnosis, and amnesia. They are highly lipophilic and cross the blood–brain barrier readily, resulting in an onset of action in less than 1 minute. They have short half-lives that promote a rapid recovery and minimize the risks inherent in prolonged sedation. Their major drawbacks are respiratory depression, apnea, occasional transient hypotension, and lack of a reversing agent. The window between PSA, deep sedation, and general anesthesia is extremely narrow. These agents are rarely used for PSA in the Emergency Department.

Thiopental (Pentothal)

Thiopental is one of the more commonly used barbiturates. It has an extremely rapid onset of action in 10 to 20 seconds with a peak activity in 1 minute. Its sedative effect lasts 3 to 10 minutes. Thiopental is titratable in doses of 0.5 to 1.0 mg/kg intravenously. Rarely is more than 2 mg/kg required.

It may be administered rectally (20 to 25 mg/kg) in children who require sedation without intravenous access. Sedation is achieved within 5 to 8 minutes. Rectal administration does not result in apnea or respiratory depression. Thiopental is often administered rectally for laceration repairs in children.

Methohexital (Brevital)

Methohexital has a profile very similar to thiopental with a few noted exceptions. It is twice as potent as thiopental. It has much less of an effect on decreasing myocardial contractility and decreasing vascular tone. A single study has convinced most people not to use this drug in the Emergency Department.45 A total of 102 patients were given methohexital with a mean cumulative dose of 1.6 mg/kg. Three patients developed hypotension. Twenty-two patients developed respiratory depression requiring bag-valve-mask assistance. Five of the 22 patients with respiratory depression developed transient apnea.

Methohexital may be administered as either repeated incremental bolus dosing or via a titratable continuous infusion. Begin with a 0.5 to 1.0 mg/kg bolus followed by an infusion at 50 μg/kg/min. Titrate infusion rates upward to effect, with a maximum rate of 75 μg/kg/min. Bolus dosing is best delivered as 0.5 to 1.0 mg/kg (maximum 20 mg) every 45 to 60 seconds until the desired endpoint is attained. Maximum sedation is achieved at 40 seconds.

Respiratory depression is common and independent of the dose or concomitant administration of a narcotic or benzodiazepine. Patients may require assisted ventilation with a bag-valve-mask device or ventilator assistance until the effect of the drug clears. Respiratory depression is minimized by first administering the analgesic agent to control pain followed by methohexital to effect. Do not use methohexital in children younger than 12 years of age.

Pentobarbital (Nembutal)

Pentobarbital is a short-acting barbiturate that is effective for pediatric sedation during nonpainful diagnostic procedures such as computed tomography or magnetic resonance imaging. Controlled sedation levels are best achieved with titrated small incremental intravenous dosing. It may also be administered intramuscularly, orally, and rectally. Intravenous administration will induce sleepiness within 30 seconds with a duration of action up to 15 minutes. Other dosing methods take longer to work, with a duration of action ranging from 1 to 4 hours.

It is primarily administered intravenously or rectally. Initial intravenous dosing at 2.5 mg/kg may be sufficient. Subsequent doses of 1.25 mg/kg every 30 seconds to effect will minimize oversedation and limit hypoxia. Other side effects are nausea, vomiting, and paradoxical hyperactivity. A maximum total dose of 6 mg/kg or 100 mg should mark the dosing endpoint. Older children may exceed this limit with due caution. Rectal dosing is age-dependent. Administer 3 to 6 mg/kg (maximum 100 mg) to children younger than 4 years of age and 1.5 to 3 mg/kg (maximum 100 mg) to children older than 4 years of age.

Etomidate (Amidate)

Etomidate is an imidazole derivative that is commonly used for the induction of anesthesia or rapid sequence induction. It produces anxiolysis, sedation, and amnesia equal to that of the barbiturates but with fewer hemodynamic affects. It is ultra-short-acting and in a class of its own. It may produce unconscious sedation similar to the barbiturates. There is a narrow window for the use of etomidate in PSA. It can be used when a procedure has to be completed emergently in a patient with a borderline low blood pressure and ketamine is contraindicated. It is often used when there may be contraindications to other sedating agents due to hypotension and/or other injuries.

There is evidence showing that ICU patients given etomidate are at greater risk for the development of adrenal insufficiency. Etomidate inhibits 11-beta-hydroxylase causing a decrease in serum cortisol levels. This was initially found in patients who were receiving continuous intravenous administration of etomidate. There is some evidence that adrenal insufficiency may occur even after a single dose of etomidate.46 These studies were conducted on patients receiving etomidate for induction prior to intubation. The study populations have higher injury severity scores and are receiving higher doses of etomidate when compared to PSA doses. Furthermore, this effect on the adrenal gland is usually transient and resolves after 24 hours. The actual effect on morbidity and mortality is still not clear.58 Adrenal suppression in the Emergency Department patient undergoing PSA for a short procedure then being discharged is probably of little to no consequence.

Etomidate is rapidly becoming one of the more frequently used agents for sedation and PSA. It has a shorter onset and faster recovery time than midazolam.47,48 Myoclonus is a well-described adverse effect that is unique to etomidate.49,50 This myoclonus can be severe enough to result in a decreased oxygen saturation and full body rigidity requiring a brief period of respiratory support. A rare adverse event is agitation or an “emergence-type reaction” as the effects of etomidate wear off.51 These few adverse effects do not outweigh its benefit of a minimal effect on the cardiovascular system.

Propofol (Diprivan)

Propofol is a highly lipid soluble compound with ultra-short sedative hypnotic properties. It can produce profound sedation, hypnosis, anxiolysis, and amnesia.52 Propofol has no analgesic properties. It is unrelated to the barbiturate or benzodiazepine classes. The onset of action is extremely rapid and within 15 to 30 seconds, with a maximal effect seen within 30 to 45 seconds. The duration of effect is typically only 8 to 15 minutes, even after prolonged administration. Propofol is contraindicated if the patient has a known sensitivity or allergy to egg or soy products.

Dosing can be delivered intravenously via repeated small 20 mg doses at 2 minute intervals or initial loading of 0.5 to 2.0 mg/kg followed by infusion rates of 25 to 130 μg/kg/min. For short procedures, a simple method of titrating propofol is to administer 1 mg/kg initially with repeat boluses of 0.5 mg/kg every 1 to 2 minutes as needed to achieve or maintain adequate sedation. Effective total doses may range from 20 to 150 mg. A continuous infusion of 50 to 70 μg/kg/min can be used to produce a sleep-like state with minimal respiratory depression. Continuous infusions allow the patient to be easily aroused by verbal stimuli and recover within 2 to 3 minutes of stopping the infusion. Induction dosing or rapid bolus injection can result in profound respiratory depression and hypotension, especially in the hypovolemic patient. It can be associated with bronchospasm and laryngospasm in rare cases. Propofol can be coadministered with fentanyl or ketamine for painful procedures requiring a combination of sedation and analgesia.

The high lipid content of the propofol solution causes pain upon injection. The administration of intravenous lidocaine immediately prior to the propofol will decrease the injection pain. Inject 0.5 mg/kg up to a maximum of 40 mg of lidocaine.53,54 Be cautious to not exceed the maximum toxic dose of 4.5 mg/kg in small children. An alternative is to add 30 mg of ephedrine to 20 mL of 1% propofol solution to decrease the injection pain.55 An additional advantage of ephedrine is that it counteracts the potential propofol-associated hypotension.

Fospropofol

Fospropofol is a relatively new, water-soluble prodrug of propofol.56,57 This new formulation is not associated with many of the lipid emulsion effects. This formulation results in decreased injection pain, has a wider therapeutic window, and allows long-term sedation without a large lipid load. Fospropofol is currently FDA approved for monitored anesthesia care. Future studies and safety data are required before this agent can be recommended for PSA.

Dexmedetomidine

Dexmedetomidine is an alpha-2 agonist with analgesic, anxiolytic, and sedative properties. It has a delayed onset of action in 15 to 30 minutes and its effects persist up to 3 hours after the infusion is discontinued. It is administered intravenously at 2 μg/kg over 10 minutes followed by a maintenance dose of 1 μg/kg/h. The side effects include hypertension with loading, hypotension with maintenance infusions, bradycardia, and cardiac arrhythmias. This agent is often used in the outpatient setting for elective CT and MRI scans. Its delayed onset, prolonged effects, and adverse effect profile make it an agent not recommended for PSA.

Several agents can be used for the sedation of children in the Emergency Department and outpatient setting. These agents are not used for PSA. These agents include chloral hydrate and DPT. Chloral hydrate is not often used in the Emergency Department. Never use the DPT cocktail in any outpatient setting.

Chloral Hydrate

Chloral hydrate is a time-tested, effective, and pure sedative hypnotic. It has no analgesic properties. Its primary usage has been for sedation during nonpainful diagnostic testing. The oral dose is 20 to 100 mg/kg (maximum 2000 mg). Most children require 50 to 75 mg/kg to achieve proper sedation. It has an onset of action of 15 to 60 minutes and a duration of effect of 1 to 2 hours. Its effects may persist for up to 24 hours. Rectal dosing is not recommended due to erratic absorption. Contraindications include renal impairment, hepatic impairment, or hypersensitivity to the agent itself. The wide dosing range and variability of onset and duration make chloral hydrate a far-from-perfect sedative for use in the Emergency Department. Its primary usage has been with outpatient testing.

DPT

DPT, also known as the “lytic cocktail,” was popularized for the induction of general anesthesia. Unfortunately, it was expanded to use in the outpatient setting and had many adverse events. It consists of Demerol, Phenergan, and Thorazine in a 2:1:1 or 4:1:1 mixture. It is administered intramuscularly at a dose of 1 mg/kg based upon the Demerol component. Intramuscular absorption is erratic, with up to one-third of children never obtaining moderate to adequate sedation. It produces too deep a level of sedation that is difficult to reverse in the other two-thirds of the children. The mean time to Emergency Department discharge is 5 hours due to the prolonged sedation. The mean time for the child's behavior to return to normal is 19 ± 15 hours.

Many children have suffered respiratory depression, hypoxemia, and apnea due to this agent. DPT is an agent of the past due to its prolonged action and significant potential for respiratory depression. The DPT agent has no use in the Emergency Department. Agents now exist that are safer, easier to use, and have a more rapid recovery. Its use is described here only for the purpose of completeness. Do not use this drug combination for PSA.

Nitrous Oxide

Nitrous oxide is an anesthetic gas that has been used in the outpatient procedural arena since the 1950s. It produces anxiolysis, sedation, and amnesia with a variable degree of analgesia. It dissociates a patient from pain and their surroundings. Nitrous oxide is self-delivered via a handheld demand valve mask in a 50–50 mixture with oxygen. The risk of oversedation is minimized with this mode of administration. The patient will drop the mask once they are too sedated to coordinate self-administration.

The onset of action of nitrous oxide is 30 to 60 seconds with a peak in 3 to 5 minutes. It has a similar washout period once delivery is ceased. Nitrous oxide is eliminated unchanged via the lungs, thereby minimizing any drug–drug interactions. Nausea and vomiting are common. The feelings of disorientation and agitation are also common.

Contraindications to the use of nitrous oxide include impaired mental status, concomitant intoxication, pregnancy, potential to expand air-filled cavities (e.g., pneumothorax or bowel obstruction), and coadministration of narcotics within 4 hours (general anesthesia may be induced). Relative contraindications include a full meal within 1 hour of its use and children less than 5 years of age due to delivery system compliance. Refer to Chapter 128 for the complete details regarding nitrous oxide anesthesia.

It should be well recognized that a desired endpoint can be overshot resulting in an apneic and hypotensive patient despite good preprocedural assessments, appropriate agent selection, appropriate dosing, and titration. There are two reversal agents, namely naloxone and flumazenil, that can be of help in these situations. Reversal agents are not routinely required following PSA. They are reserved for the patient who develops apnea, hypoxia, and/or hypoventilation.

Flumazenil (Romazicon)

Flumazenil is a benzodiazepine antagonist that works by competitive inhibition at the GABA receptor. Intravenous administration will rapidly reverse CNS depression and respiratory depression from benzodiazepines within 2 minutes. Begin by administering a dose of 0.02 mg/kg to a maximum of 0.2 mg over 15 seconds. Administer additional 0.2 mg doses at 1 minute intervals until the desired state of consciousness is achieved. Maximum dosing is 1.0 mg over 15 minutes or 3.0 mg over 60 minutes. The benzodiazepine metabolites are active longer than the reversal agent. Therefore, a patient receiving flumazenil must be carefully monitored for resedation. A safe recommendation would require a minimum observation of 2 hours after the last dose is given.

Flumazenil is contraindicated in patients taking benzodiazepines for an extended amount of time or patients with an underlying seizure disorder. These patients are prone to seizure activity with the administration of flumazenil. It is also contraindicated in patients taking tricyclic antidepressants.

Naloxone (Narcan)

Naloxone is a pure opioid antagonist that works by competitively inhibiting narcotics at the opioid receptor. Intravenous administration reverses the respiratory depressive effects of opioids within 1 to 2 minutes. Its clinical duration of effect is approximately 20 to 30 minutes. Therefore, long-acting narcotics may cause resedation. The opioids and their metabolites are active longer than the reversal agent. Therefore, a patient receiving naloxone must be carefully monitored for resedation and respiratory depression. The drug can be delivered via multiple routes (e.g., intravenously, intramuscularly, sublingually, subcutaneously, and endotracheally). The administration of 1 to 2 mg intravenously (0.1 mg/kg in children) will reverse most respiratory arrest situations. Administer additional doses every 2 to 3 minutes to a total of 10 mg. Another etiology of the sedation and respiratory depression, other than narcotics, should be aggressively sought if the respiratory depression is not reversed after 10 mg of naloxone. Use caution as naloxone can result in opioid withdrawal in those with physical dependence or intoxicated with narcotics.

Small aliquots of 40 μg titrated to effect may be delivered in a situation where the patient is slightly oversedated and rapid full reversal of the narcotic is not desired. Mix 0.4 mg of naloxone with 9 mL of normal saline to produce a concentration of 40 μg/mL. Administer 1 to 2 mL aliquots every 1 to 3 minutes to alleviate respiratory depression yet maintain the analgesic effect.

The technique of PSA can be quite variable depending upon the institution and the agents chosen to administer. A sample PSA protocol can be found in Table 129-5. PSA requires two persons at a minimum. One person must monitor the patient while the other administers the medication and performs the procedure. Take the time to do it right! The right time to perform PSA is not when the Emergency Department is full to capacity and/or the acuity of other patients is high. The medications must be titrated to effect, which can take up to 15 minutes.

Nursing personnel managing the care of the patient receiving PSA must continuously monitor the patient's airway, breathing, circulation, and mental status. It is imperative to observe the rise and fall of the chest wall with the focus upon the work of breathing. Relying solely on pulse oximetry may give one a false sense of security. Observation of a progressive slowing in the patient's respiratory effort is a sign of impending hypercapnia or hypoxia that is seen well ahead of any monitoring alerts or cutoffs. Avoid sterile wraps that cover the entire face or chest for this reason. Observe the patient for a decrease in respiratory rate or depth of breathing. Notice any abnormal airway sounds indicative of partial airway obstruction, laryngospasm, bronchospasm, or stridor. Visually monitor the peripheral perfusion of assessments of skin/mucosa color, temperature, and moisture. Assess pulse quality and rate in addition to frequent blood pressure determinations. Blood pressure monitoring may awaken the patient and forgo the ability to complete the diagnostic or therapeutic interventions in cases of mild sedation (e.g., pediatric sedation for neuroimaging). Continually assess the patient's level of consciousness throughout the procedure and recovery period. The aforementioned scoring systems offer one means of determining the level of sedation. Record the patient's responses to verbal stimuli, if applicable.

The patient must meet several criteria to ensure their safety before leaving the Emergency Department. Vital signs must be appropriate to the age of the patient and comparable to preprocedural parameters. The respiratory effort must return to baseline. Mobility must be equal to or better than that before the procedure. The patient must be able to follow commands and discharge instructions. Preprocedural levels of consciousness and mental status must be present. The patient must be able to tolerate oral fluids. The pain of the procedure for which PSA was performed must be controlled. The patient must be discharged in the care of a responsible adult who understands the discharge instructions. All these criteria must be documented in the medical record and timed prior to discharge.

Patients who have received multiple medications or a reversal agent will require a longer recovery period. A 2 hour observation window is prudent. Provide written discharge instructions and explain them to both the patient and the responsible adult who will accompany the patient home. Examples of preprinted pediatric and adult discharge sheets are presented in Tables 129-6 & 129-7.

Respiratory depression and hypoxia are inherent risks of PSA despite efforts to minimize risk with prudent patient risk-benefit assessment, appropriate drug selection, and appropriate dosing. Individual patient responses to hypnotic, sedative, or analgesic agents can be very unpredictable. Part of the preparation included bedside availability of reversal agents in anticipation of these complications.

The first course of action is simply to provide patient stimulation in the event of respiratory depression. If possible, painful stimulation is most easily applied by continued traction or manipulation of the injured extremity. Frequently, patients undergoing PSA will not become apneic until after the procedure is complete and the noxious stimulus is no longer present. The jaw thrust is another method of providing significant stimulation while placing yourself at the patient's head and assisting ventilation by opening the airway. Support the patient's ventilation with a bag-valve-mask device while the appropriate reversal agent(s) are being drawn up if stimulation is inadequate. Naloxone will rapidly reverse the respiratory depression if a narcotic was administered. Flumazenil will reverse the respiratory depression if a benzodiazepine was administered.

There is no way to determine which reversal agent is best suited to reverse the respiratory depression when both a narcotic and benzodiazepine have been administered. A rational approach is to first administer flumazenil. This maintains the needed analgesia while, hopefully, improving the respiratory drive. Administer naloxone if the flumazenil does not reverse the respiratory depression.

Laryngospasm is a real but relatively rare event during PSA provided that the appropriate patient and drug selection was employed. Ketamine, midazolam, fentanyl, and phenobarbital may all cause laryngospasm. This tends to be a brief and self-limited event that can usually be supported with the use of positive-pressure ventilation. Administer succinylcholine (1 to 2 mg/kg intravenously or 4 to 5 mg/kg intramuscularly), support the patient's airway, and provide airway management if laryngospasm is severe or persistent.

Virtually all agents can induce nausea and vomiting. Patients with recent oral intake are at a higher level of risk for aspiration. Always have suction available if required. Hypotension induced by opiates or benzodiazepines is responsive to fluid management and the corresponding reversal agent. Chest wall rigidity from short-acting opioids that cannot be reversed with naloxone requires succinylcholine and airway management to support ventilation and oxygenation.

Allergic reactions can result from the administration of any of the aforementioned procedural agents. Management is similar to other allergic reactions in terms of treatment with epinephrine, diphenhydramine (H1 antagonist), an H2 antagonist, and methylprednisolone.

The use of PSA in pregnant and lactating patients must be undertaken with great caution. The safety of many of the agents is unknown or of concern (Table 129-8). Consult an Obstetrician, Gynecologist, or Anesthesiologist prior to performing PSA on pregnant and lactating women.

Procedural sedation and analgesia is a necessary part of Emergency Medicine practice. Skillful application in the appropriate clinical scenarios will offer patients a world of anxiety and pain relief. We have the necessary pharmaceuticals to control the patient's pain and anxiety. It is essential that we possess the knowledge and training to understand our patients' needs and satisfy this requirement with a careful risk–benefit assessment and appropriate drug selection. It is essential that we maintain the necessary high standards to safely get our patients through these procedures with a minimum of risk and complications. Competency extends beyond the Emergency Physician and includes nursing and support personnel. They too must be knowledgeable as to the content of procedural sedation and analgesia with an uneventful recovery.

Everyone must know their limitations. Become very comfortable with a limited set of medications that will enable one to address 95% of all procedural sedation and analgesia requirements. Secure the assistance of a colleague or backup from an Anesthesiologist in difficult situations. Procedural sedation and analgesia will never be a substitute for a little patience and a soft, gentle mannerism. Reserve its use for the patient who truly needs the intervention.