Robert J. Vissers and James R. Miner
The care of patients with painful conditions and the performance of painful diagnostic and therapeutic procedures are routine aspects of emergency care. Approximately half of emergency department (ED) visits are for pain-related chief complaints. Many of these conditions are also associated with anxiety. Accordingly, procedural sedation and analgesia (PSA) has become a fundamental skill of emergency physicians and an important part of emergency medicine residency training (1).
Despite the emphasis on PSA, oligoanalgesia has been well described in emergency care. Inadequate pain control has been ascribed to underestimation of patient pain, concern for patient safety, fear of delays associated with oversedation, and the alteration of physical findings (1,2). PSA can improve quality of care and patient satisfaction through the relief of pain and anxiety and the facilitation of therapeutic or diagnostic procedures such as cardioversion, incision and drainage of abscesses, tube thoracostomy, lumbar punctures, fracture reduction, complex suturing, and imaging studies (1,3–5). Many drugs used for sedation and analgesia have the potential to cause respiratory, cardiovascular, and central nervous system (CNS) depression. The introduction of protocols using shorter-acting, more effective drugs, the development of noninvasive monitoring devices, and published clinical policies for PSA have made it an extremely safe, practical procedure. The airway and critical care expertise of emergency physicians make them ideal providers of safe PSA (1).
The wide variety of procedures and patient types requires the ability to individualize PSA. This can be achieved only through a comprehensive understanding of the drugs used and by proper patient assessment. Protocols delineating staffing responsibilities, monitoring guidelines, medications, observation periods, and discharge criteria and instructions are recommended before implementing PSA in the ED.
DEFINITIONS
The term conscious sedation has previously been used to describe the process of providing analgesia, sedation, and amnesia for patients undergoing painful procedures. However, this term may be misleading. A more precise and preferred term is PSA. In a recent clinical policy published by the American College of Emergency Physicians, PSA was defined as a technique of administering sedatives or dissociative agents with or without analgesics to induce a state that allows the patient to tolerate unpleasant procedures without undue pain or anxiety while maintaining cardiorespiratory function. PSA is intended to result in a depressed level of consciousness that allows the patient to maintain oxygenation and airway control independently and continuously (1).
The Joint Commission on Accreditation of Healthcare Organizations (JCAHO), in its 2003 Comprehensive Accreditation Manual for Hospitals, states that “the standards for sedation and anesthesia care apply when patients receive, in any setting, for any purpose, by any route, moderate or deep sedation and general, spinal, or other major regional anesthesia” (6). JCAHO has adopted the American Society of Anesthesiologists (ASA) definitions of sedation and analgesia created in 1999 to better describe the continuum of sedation and analgesia. Moderate sedation most closely approximates the replaced term conscious sedation.
Minimal sedation is primarily anxiolysis for a procedure, during which patients respond normally to verbal commands. Ventilatory and cardiovascular function remains unaffected.
Moderate sedation/analgesia is a drug-induced depression of consciousness during which the patient responds purposefully to verbal commands, alone or accompanied by tactile stimulation. Typically, no interventions are required to maintain a patent airway. Spontaneous ventilation is adequate, and cardiovascular function is maintained; therefore, this is associated with less respiratory depression than deep sedation. At this level of sedation, patients generally are amnestic, even to painful procedures, but moderate sedation should be used only when the procedure is likely to be successful on a more responsive patient rather than a deeply sedated patient (7–9).
Deep sedation/analgesia is a drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully following repeated or painful stimulation. Assistance may be needed to maintain a patent airway, and independent ventilation may be inadequate. Cardiovascular function is usually maintained. This level of sedation is associated with a greater degree of respiratory depression than moderate sedation but is often necessary for the successful completion of procedures for which patient relaxation and amnesia is required (9–11).
General anesthesia is a drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. Independent ventilatory function is often impaired, and ventilatory and airway support is often required. Cardiovascular function may be impaired.
The response to medications can vary greatly between individuals and may be unpredictable. Therefore, it is recommended that clinicians be competent in the skills required to manage patients at least one level greater than the intended sedation (12). The management of impaired ventilatory function is a usual part of the practice of emergency medicine and represents a critical skill for the management of procedural sedation in the ED.
ED EVALUATION
Careful patient selection is necessary to provide safe and effective PSA. The comorbid illness or injury, any underlying medical problems, patient age, the procedure, and the ability to manage the airway are important considerations in determining the indication for and the method of PSA. Not all patients or procedures are appropriate candidates for PSA and may be best served in the operating room.
The agents used in procedural sedation, to some degree, all cause hypoventilation and diminished airway reflexes. The principle complication of procedural sedation associated with significant morbidity is aspiration pneumonia from the loss of airway reflexes (3,13–15). Luckily, this is a rare complication, but a principle goal of sedation must be to avoid situations where a patient is at risk of its occurrence. Other complications include hypoxia, hypotension, and paradoxical agitation reactions from the sedative agents.
A patient’s physical status can be conveniently described using the ASA’s classification (Table 17.1) (16). This is frequently incorporated into the documentation of the preprocedure assessment. Patients with ASA physical status scores of 3 and 4 are more likely to have complications from hypoventilation and hypotension than patients with scores of 1 and 2, and the risk/benefit ratio of performing PSA in these patients must be considered (17).
TABLE 17.1
American Society of Anesthesiologists Physical Status Classification
A history of prior problems with anesthesia or PSA should be elicited. Particular attention should be paid to underlying hypovolemia, cardiorespiratory diseases, neurologic diseases, medications, and intoxicants. Physical examination should focus on the cardiovascular, respiratory, and neurologic systems and performing an assessment of airway difficulty. There is no evidence to support the need for specific diagnostic testing before PSA. A discussion including the risks, benefits, and potential side effects of PSA should take place before the procedure. Written consent is recommended when possible; however, patient condition may preclude this (12).
There is insufficient literature to recommend a necessary period of fasting prior to PSA. The combination of vomiting and loss of protective reflexes during PSA causing aspiration is considered to be a rare event (13). There is no evidence that gastric emptying or antacids reduces the incidence of PSA-associated complications. It is likely, however, that increasing depth and duration of PSA is associated with an increased risk of aspiration, and it may be beneficial in patients who have recently taken more than clear liquids and require nonurgent procedures to delay until 3 hours after the last oral intake. For patients needing a procedure urgently (fracture reductions, intractable pain, etc.) recent intake should be considered in the choice of the target sedation level and duration of the planned PSA. The complimentary use of local anesthesia when appropriate, such as a regional block, can reduce the amount of sedation required. Patients at high risk for aspiration may benefit from the lightest level of sedation for the shortest amount of time that will allow successful completion of the procedure. Recent food ingestion is not a contraindication but rather a consideration when choosing the targeted level of sedation (13,17,18).
KEY TESTING
• Interactive monitoring
• Airway assessment
• Physical status score
• Procedural plan
• Sedation plan
• Mechanical monitoring
• Capnography
• Pulse oximetry
• Cardiac monitor
• Blood pressure
ED MANAGEMENT
Preparation
The necessary equipment and supplies should be gathered in an appropriate setting prior to the initiation of PSA. There does not have to be a specific dedicated area for PSA. However, the capability to provide cardiovascular and respiratory support and availability of personnel may dictate the location. Monitoring equipment, oxygen, suction, advanced life support equipment and medications, a bag-valve-mask, and intubation equipment must be readily available. IV access should be established and maintained before PSA with IV agents. The antagonists naloxone and flumazenil should be available when opioids and benzodiazepines are being used (19).
The Joint Commission and compliant institutions insist that the PSA provider demonstrate adequate training to administer the agents effectively and safely and have the skills to manage all potential complications (6). These are all within the scope of the emergency physician’s expertise, especially in the unpredictable setting of the ED, which is unique to the practice of emergency medicine. There is no clear guideline in the literature or organizational policies regarding the required number of support personnel. It is essential that an individual is present who is capable of recognizing the respiratory and hemodynamic responses to the medications and is able to perform interactive monitoring without interruption throughout the procedure. The performance of a procedure often precludes the continual clinical assessment of the patient. Therefore, one individual provider not performing the procedure is usually recommended to monitor and document patient status when providing deep sedation (15). Moderate sedation using a single provider has been described (20).
The use of supplemental oxygen during PSA is somewhat controversial. Although its routine use may prevent hypoxemia in some patients, there is concern that it will delay the recognition of respiratory compromise and hypercarbia, due to its effect on the sensitivity of pulse oximetry to changes in ventilation (21,22). Evidence supports the use of supplemental oxygen in patients undergoing PSA to reduce episodes of hypoxia; but care must be taken to use monitoring modalities other than pulse oximetry, such as close interactive monitoring, when supplemental oxygen is used (11,23).
Monitoring
The most important aspects of monitoring during PSA are the interactive observation and assessment of physiologic changes and the level of consciousness. The patient’s ability to follow commands and the response to varied levels of stimulation are useful in quantifying the level of consciousness. Direct observation of the patient’s airway and breathing (interactive monitoring) are likely to be the most accurate monitors of a patient’s ability to maintain adequate ventilations and airway protection and to assess the safety of giving further medication to patients who have not yet achieved the desired level of sedation, and are therefore critical to the safe titration of sedatives and the avoidance of oversedation and its associated adverse effects (15,24,25). Interactive monitoring can be augmented by blood pressure, oxygen saturation, capnometry, and cardiac rhythm monitors.
The use of pulse oximetry is widely recommended in national and institutional PSA guidelines. Many studies have demonstrated its utility in monitoring oxygenation; however, there is no clear demonstration that its use during PSA affects patient outcome other than decreasing episodes of transient hypoxia (1,26). This may be as a result of the extremely low risk of morbidity and mortality during PSA when the patient’s respiratory efforts and level of consciousness are clinically monitored. Furthermore, the clinical significance of transient decreases in oxygen saturation is not known (26), but we at least assume it is a marker of ventilatory depression and therefore a marker of risk for aspiration. Pulse oximetry measures oxygenation, not ventilation. A patient breathing supplemental oxygen may not exhibit changes in the oxygen saturation until several minutes after the onset of hypoventilation. In a patient breathing room air with a normal oxygenation prior to PSA, however, decreases in oxygenation correlate with decreases in ventilatory effort. In either case, it represents useful information and should be utilized during PSA. However, it should not be a substitute for continuous clinical assessment.
Capnometry can be used to monitor ventilation. Capnographs measure expired CO2 and display a waveform that represents the patient’s ventilation. The peak of each wave represents the end-tidal CO2, or the maximum concentration of CO2 in the expired air. Large changes in the end-tidal CO2 values and in the shape of the waveform have been associated with respiratory depression in sedated patients and may allow earlier identification of hypoventilation than oximetry (21,22,26,27). An increasing end-tidal CO2 value can represent CO2 retention from hypoventilation. A decreasing end-tidal CO2 value can represent hyperventilation and decreasing arterial CO2 levels, or increased mixing of room air and expired air in the upper airway owing to airway obstruction. An absent waveform on the capnograph can represent apnea or possibly upper airway obstruction if respiratory effort is present. The earlier detection of hypoventilation associated with the use of capnographic monitoring has been shown to decrease episodes of hypoxia during procedural sedation in the ED (26). Capnographic monitoring of end-tidal CO2improves the detection of hypoventilation, even in patients receiving supplemental oxygen, and decreases episodes of hypoxia. It should be considered in patients undergoing deep sedation who are receiving supplemental oxygen.
Blood pressure, heart rate, and respiratory rate should be assessed at regular intervals throughout PSA. Patients are at the highest risk for complications when they are at their deepest level of sedation, primarily within 90 seconds to 3 minutes of receiving IV sedatives, and when noxious stimuli are removed (immediately after the procedure). Continuous electrocardiographic monitoring is not routinely recommended. However, it should be used in older patients or those with a history of cardiovascular or pulmonary disease. Documentation of the level of sedation can be quantified using a predefined sedation score, such as the Aldrete score or a simplified version suggested in Table 17.2.
TABLE 17.2
Assessment of Sedation
Drug Selection and Administration
The ideal agent for PSA would provide analgesia, anxiolysis, amnesia, and somnolence rapidly and predictably with no adverse effects. Unfortunately this drug does not exist. As a result, multiple sedative hypnotics, opioids, and various anesthetic agents have been employed, singly and in combination, in an attempt to achieve the desired level of PSA (Table 17.3) (2). The agent selected, and its dose and route of administration, should be guided by the type of procedure and by the specific patient. Drug availability and physician experience are also important determinants.
TABLE 17.3
Agents Commonly Used in Procedural Sedation and Analgesia
Prior to PSA, patients with pain should receive pain medications titrated to pain relief. Morphine 0.1 mg/kg, followed by 0.05 mg/kg every 2 to 3 minutes until pain is relieved, is a common approach. For situations in which the patient is likely to have much less pain after PSA owing to the nature of the procedure (the reduction of a severely comminuted fracture, e.g.,), fentanyl 1.5 μg/kg followed by 0.75 μg/kg may be preferable. Fentanyl is short-acting, with a duration of action of 30 to 45 minutes (25,28). It does not cause histamine release and has minimal cardiovascular effects. Like all opioids, fentanyl is reversed by naloxone. Respiratory depression is more likely at higher doses, when given rapidly IV push, or when combined with other CNS depressants, such as benzodiazepines or alcohol. Lower doses should be used in elderly patients and when other CNS depressants may have been previously ingested. Side effects of fentanyl include hypoxemia, apnea, vomiting, and pruritus. Hypotension is rare. Bradycardia may occur with high doses. Truncal rigidity and glottic spasm, which make ventilation difficult, are unique complications seen with doses above 10 μg/kg, or at lower doses if the drug is given rapidly.
The duration of action of these agents is often much longer than the sedatives typically used in ED PSA; therefore, their titration should be performed prior to the PSA encounter rather than as part of it. Many of the sedative agents used in PSA have amnestic but not analgesic properties, and patients may have a brief transient increase in pain during their procedure. Combining sedatives with opioids for procedural sedation, however, has been associated with an increased risk of hypoventilation (25,29–31). Furthermore, patients receiving moderate or deep sedation, are unlikely to recall the event. The physiologic significance of brief pain that is not recalled is unlikely to outweigh the risk of prolonged or deeper sedation than was intended and the associated hypoventilation (31).
Regardless of the agent used, an important principle in PSA is the titration of drugs to the desired level of sedation with the least possible respiratory depression. Drugs given IV have a rapid onset with a more predictable response than agents given orally, transmucosally, or IM (2). Drugs should be titrated slowly, because rapid administration is more likely to cause hypotension or respiratory depression (32). To avoid oversedation, it is important to allow adequate time to achieve and assess peak effect before a second dose is given. A possible exception to the preferred IV route may exist in children, in whom IV access is often difficult and the IM response to ketamine is very predictable (33,34).
Sedatives
Methohexital is an ultrashort-acting barbiturate with sedative and hypnotic effects. It produces deep sedation but provides no analgesia (35). Methohexital produces a state of deep sedation, which may be preferred for such procedures as cardioversion, chest tube insertion, or complicated orthopedic reductions. It has a rapid onset of action of 30 to 60 seconds, a duration of action of 3 to 5 minutes, and a short recovery phase. Deep sedation is achieved with bolus doses of 1 to 2 mg/kg (35).
Intramuscular doses of 10 mg/kg produce effects that begin in 2 to 3 minutes and last almost 1 hour. Rectal methohexital has been used in children when a motionless state is needed. A dose of 20 to 30 mg/kg induces sleep within 10 minutes and lasts for about 45 to 80 minutes. Cardiorespiratory complications rarely occur with rectal administration. Adverse reactions associated with the use of methohexital include dose-dependent respiratory depression and apnea. Oxygen desaturation is especially common when concomitant respiratory depressants are used. Hypotension is uncommon but can occur, especially in patients with hypovolemia and sepsis. It is easily corrected by giving IV fluids (2). Hiccups can occur, and protective reflexes may be impaired. Methohexital induces epileptiform activity by electroencephalogram in seizure patients and should be avoided in patients with epilepsy.
Midazolam is a benzodiazepine with amnesic and anxiolytic properties. Midazolam has a more rapid onset and shorter duration of action than diazepam and rarely causes phlebitis. Its amnestic properties also appear to be superior to those of diazepam (2). It is eliminated by hepatic metabolism. The IV dose is 0.03 to 0.1 mg/kg, with a starting dose of 1 mg. Onset of sedation is within 3 to 5 minutes, and the duration of action is about 30 to 60 minutes. With IM administration, the same dose is typically used, but the onset of sedation is delayed. Its duration of action is similar to fentanyl; therefore, the two drugs are frequently used together to induce extended PSA. It is often used to provide minimal procedural sedation.
In children, oral, rectal, and intranasal routes are effective alternatives to IV sedation. Oral doses are 0.2 to 0.75 mg/kg, and sedation is achieved within 1 hour. Rectal administration is effective at doses of 0.3 to 0.5 mg/kg, but the response is variable as a result of the unpredictable effect of first-pass hepatic metabolism and it is not well tolerated or accepted by older children. Intranasal administration can be used when an intravenous line is not needed or when sedation is necessary to establish one. Doses of 0.2 to 0.4 mg/kg result in sedation in about 10 to 15 minutes.
Lower doses should be used when analgesic agents are given concomitantly and in elderly patients. Prolonged effects may occur in elderly patients as a result of decreased metabolic clearance and decreased first-pass metabolism.
Side effects include dose-dependent hypoventilation and hypoxemia. At high doses, midazolam blunts the central respiratory center’s sensitivity to hypercapnia (2). Apnea is rare, except when other CNS depressants, such as opioids, are used. Hypotension can also occur with high doses.
Etomidate is an ultrashort-acting, nonbarbiturate sedative hypnotic with no analgesic properties. Like methohexital, it causes deep sedation, has a very rapid onset of less than 1 minute, and has a duration of action of 3 to 5 minutes. Etomidate has minimal cardiac effects. Although respiratory depression can occur, it is usually transient and associated with the use of other respiratory depressants (24,36,37). In critically ill patients (ASA physical status 3 and 4), it is associated with less hypotension than propofol (17).
Etomidate is given IV (0.1 to 0.15 mg/kg) and is currently not approved for children younger than age 10. Side effects are uncommon. Transient respiratory depression can occur. Myoclonic jerking occurs in up to 25% of patients and has been mistaken for seizures (17). Adrenal suppression can occur after long-term use but is not an issue in ED PSA (1,30). Published experience with the use and safety of etomidate in the ED suggests a rate of respiratory depression similar to other agents used for moderate and deep PSA (24).
Ketamine is an anesthetic that causes a dissociation between the thalamic and limbic systems. This, in turn, hinders the perception of visual, auditory, and painful stimuli, leaving the patient in a trancelike state (13). After absorption, ketamine is rapidly distributed and taken up by cerebral tissue. Effects are maintained until the drug redistributes into the peripheral tissues and is metabolized by the liver (34).
Ketamine can be given by multiple routes. An IV dose of 1 to 2 mg/kg, an IM dose of 2 to 6 mg/kg, a rectal dose of 5 to 15 mg/kg, or an oral dose of 6 to 10 mg/kg induces a dissociative state (34). Sedation is achieved within 1 minute when the drug is given IV, 5 minutes when given IM, and 5 to 20 minutes by other routes. The duration of action is 15 to 30 minutes for IV dosing and 30 to 40 minutes for IM dosing.
Ketamine’s most common side effect is the emergence phenomenon, in which the patient wakes up hallucinating. This is more common in patients older than age 10, in females, and in those with an underlying psychiatric disorder. It is less common with IM injection and can be attenuated by the concomitant use of benzodiazepines.
Laryngospasm and emesis are infrequent complications. Patients given ketamine may develop nystagmus and muscular hypertonicity. The pharyngeal–laryngeal reflexes remain intact, although laryngospasm sometimes occurs (13). Ketamine has minimal effects on oxygen delivery. Respiratory depression may occur with high doses or rapid IM infusion. The drug stimulates tracheobronchial and salivary secretions, but this effect can be minimized by the concomitant use of an anticholinergic such as atropine. Mild-to-moderate elevations in pulse rate and blood pressure may result from ketamine’s ability to block the reuptake of catecholamines, especially with IV infusion. Twitching, hypertonus, and myoclonic jerking can occur and have been mistaken for seizures. Electroencephalographic studies, however, have shown that ketamine does not cause convulsions.
Ketamine is contraindicated in patients with cardiovascular disease, chronic obstructive pulmonary disease, intracranial and intraocular injuries, and increased intracranial or intraocular pressure. It is not recommended for use in patients with a history of psychiatric illness or children younger than 3 months of age.
Propofol is a very short-acting sedative hypnotic agent, with a rapid onset of action. Propofol is given intravenously as an initial bolus of 1 mg/kg, followed by 0.5 mg/kg bolus injections every 3 minutes until adequate sedation is achieved. It has a duration of action of 5 to 7 minutes following this dosing regimen. The duration of action of propofol increases with the quantity of propofol used, and can extend to 10 to 20 minutes after a prolonged infusion. It is metabolized by the liver and excreted by the kidneys. It is thought to have a secondary form of metabolism, because it can be used safely in patients with liver cirrhosis and renal failure. Propofol is often used in combination with analgesics such as fentanyl.
ED PSA using propofol has been evaluated in multiple studies of adults and children. Hypoxia has been reported in 5% to 30% of patients (10,15,17,28,32). The use of bag-valve-mask assisted ventilations has been reported to be necessary in 3% to 9% of adults, with a much lower rate of oral airway use (0.3% to 0.5%). Hypotension has been reported to occur in 2% to 7% of adult patients, with emesis occurring in 0% to 0.5% (17,32). These rates are not unique to propofol but are typical of moderate and deep PSA. In comparisons with etomidate and methohexital, propofol was found to have similar rates of respiratory depression (15,17,24,32,35). If hypotension occurs, it is easily reversed with fluids or by terminating the infusion. However, propofol should be avoided in patients with pre-existing hypotension or hypovolemia.
Propofol and ketamine have been combined in an attempt to make a new sedation protocol that maximizes the benefits of both drugs while minimizing their adverse events (38,39). Theoretically, by combining the medications, the dose-related respiratory depression of propofol can be avoided with smaller doses due to the effect of ketamine, whereas the dose-related vomiting and emergence phenomena of ketamine could be avoided through the effects of propofol. Combinations ranging from 1:1 to 4:1 mixtures of propofol and ketamine have been described, with research showing a trend toward less respiratory complications than propofol alone. The duration of sedation appears to be longer than propofol alone, resulting in longer patient stays in the ED. More research will be required to determine the role of this combination of medications in the ED, but the practice appears to be a safe alternative to either agent alone.
Nitrous oxide is a colorless gas that, when used in combination with oxygen, provides analgesia and sedation. The gas diffuses rapidly across membranes, providing a rapid onset and elimination (2). The level of sedation is often disproportional to the analgesia provided. The use of analgesics in combination with nitrous oxide appears to synergistically enhance the level of sedation and pain control; however, potential side effects, such as hypoventilation, also are compounded.
Nitrous oxide is given as a 30% to 70% mixture with oxygen by a demand valve-mask or a mouthpiece, held by the patient. A variety of delivery systems are available that allow titration of the concentration of nitrous and ensure adequate scavenging of the gas. Nitrous oxide is a teratogen, and it is important to avoid exposing pregnant patients or staff to the agent. Scavenger devices and adequate room ventilation are important to minimize the escape of the gas into the air, preventing potential acute and chronic adverse effects on providers.
Because the gas rapidly diffuses into gas-filled pockets, it potentially can worsen conditions such as pneumothoraces, small bowel obstructions, decompression sickness, chronic obstructive pulmonary disease, and ear effusions (6). Nitrous oxide has the potential for abuse, and every effort should be made to safeguard against this. Many systems available currently have lock systems that allow for controlled access to the medication.
Reversal Agents
Naloxone is a competitive antagonist of opioids at the μ receptors and is used primarily for the reversal of opioid-induced respiratory depression. The initial dose is 1 to 2 mg IV. However, if the patient is opioid-dependent, a titrated dosing of 0.1 to 0.2 mg IV every 1 to 2 minutes may prevent unpleasant withdrawal symptoms. Naloxone may have a shorter duration of action than the opioid used; therefore, continued observation for delayed respiratory depression is required. It may not reverse the chest wall rigidity occasionally associated with high-dose fentanyl.
Flumazenil is a competitive antagonist of benzodiazepines and is given in titrated doses of 0.1 to 0.2 mg IV, every 1 to 2 minutes to desired effect. It has a half-life of 45 to 100 minutes; therefore, a similar caution must be exercised when used with benzodiazepines having a longer duration of effect. Flumazenil may not be effective at reversing respiratory depression. It should be used with caution in patients with benzodiazepine dependence or a history of seizures.
Elective reversal of PSA remains controversial. It has been proposed that reversal may reduce the time required for postprocedure observation. Several factors caution against this practice. Naloxone has a clinical effect of 30 minutes, which may be shorter than the continued duration of effect for the opioid (2). Flumazenil has not been shown to be effective at reversing the respiratory depression associated with benzodiazepines (9). No effect on discharge time has been demonstrated with reversal in the ED setting. Therefore, elective reversal is not recommended.
CRITICAL INTERVENTIONS
• Assess the patient’s underlying medical conditions and potential airway difficulty prior to the initiation of PSA.
• Continue to monitor the patient after the completion of the procedure until recovery to baseline. Patients may become more sedated after the removal of a painful stimulus.
DISPOSITION
Patients must be observed after PSA, and monitoring and documentation should continue until they have regained their baseline mental and physical status. Complications after this time are very rare. Discharge criteria should include regaining baseline mental and physical status when complications of PSA are no longer expected. Patients may require treatment for pain and nausea after sedation. Discharge instructions should otherwise focus on the care necessary for the disease process that necessitated the PSA.
Common Pitfalls
• Forgetting that the most important aspect of patient monitoring is interactive clinical assessment of the level of sedation and respiratory effort
• Using the “one-drug-fits-all” strategy. The selection and dosing of agents should be individualized to the patient and the procedure.
• Failure to treat pain adequately
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