Sedation is often utilized to facilitate care in the ED. PSA has replaced the previous nomenclature of “conscious sedation.” The American College of Emergency Physicians (ACEP) defines PSA as the “administration of sedatives or dissociative agents with or without analgesics to induce a state that allows the patient to tolerate unpleasant procedures while maintaining cardiorespiratory function. Procedural sedation and analgesia is intended to result in a depressed level of consciousness that allows the patient to maintain oxygenation and airway control independently.”
The controversy over nonanesthesiologists providing PSA primarily involves this last statement. Patients can easily progress to each successive stage of sedation to the point of apnea and respiratory arrest. The practitioner's goal should be to avoid progressive unconsciousness and remain capable in managing their cardiopulmonary function when necessary. Despite concerns, the efficacy and safety of ED procedural sedations have been demonstrated in numerous studies, and PSA has become a core skill in emergency medicine training and practice.
PSA is a spectrum involving light, moderate, deep, and general anesthesia levels necessitating the practitioner to be capable of recognizing the levels of sedation, and be prepared to rescue the next level of sedation if necessary. Some experts have proposed adding a separate category for dissociative anesthetics such as ketamine since its performance and side-effect profile differ a great deal from other forms of sedation. Each degree of sedation increases risk of cardiopulmonary instability with a likely need for aggressive intervention.
- Minimal sedation (anxiolysis)
A drug-induced state during which patients respond normally to verbal commands. Although cognitive function and physical coordination may be impaired, airway reflexes, and ventilatory and cardiovascular functions are unaffected.
- Moderate sedation/analgesia (“conscious sedation”)
A drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained.
A drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully following repeated or painful stimulation. Reflex withdrawal from a painful stimulus is not considered a purposeful response. The ability to independently maintain ventilatory function may be impaired. Patients may require assistance in maintaining a patent airway, and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained.
A drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to independently maintain ventilatory function is often impaired. Patients often require assistance in maintaining a patent airway, and positive pressure ventilation may be required because of depressed spontaneous ventilation or drug-induced depression of neuromuscular function. Cardiovascular function may be impaired.
PSA is indicated for the anticipated need of pain relief, amnesia, and anxiolysis required for the patient's comfort. The sedative rugs, the dosage, depth, and duration of sedation must be considered prior to the initiation of the procedure. PSA requires a presedation assessment, sedation monitoring, and postsedation assessment prior to disposition. In the presedation assessment, history of prior anesthesia/sedation complications should be evaluated along with comorbid conditions and allergies. The American Society of Anesthesiologists (ASA) developed a physical status classification system. It describes patients' illness severity as categories I–VI (Table 8–1). Each category involves escalating degrees of progressive systemic disease, and is meant to be used for assessing the illness of the patient prior to surgery.
Table 8–1. ASA Classification System. ||Download (.pdf)
Table 8–1. ASA Classification System.
|ASA 1||A normal healthy patient|
|ASA 2||A patient with mild systemic disease|
|ASA 3||A patient with severe systemic disease|
|ASA 4||A patient with severe systemic disease that is a constant threat to life|
|ASA 5||A moribund patient who is not expected to survive without the operation|
|ASA 6||A declared brain-dead patient whose organs are being removed for donor purposes|
Patients scored as an ASA I–II can be reasonably sedated within the ED without elevating the risk of sequelae from underlying systemic pathology. Once the patient is deemed to be more ill (ie, ASA III–IV), it is often more appropriate to involve anesthesia within the parameters of elective or non-life-threatening scenarios. ASA III classifications have been shown to be an independent risk factor for adverse outcomes in general anesthesia and pediatric sedation cases. Categories V and VI are usually not applicable within the ED setting. The downside to ASA classification is the inherent ambiguity of the definitions and the variable scoring between practitioners.
Patients should be screened for recent illnesses, hospitalizations, smoking, illicit drug use, GERD, CAD, HTN, cirrhosis, and other metabolic disorders as well. Pulmonary diseases such as asthma, cystic fibrosis, pulmonary fibrosis, tracheomalacia, and COPD could all potentially result in profound hypoxemia. Patient using supplemental oxygen at home would indicate an ASA class of III or IV requiring a critical review for the need of ED PSA. A history of GERD may predispose the patient to passive aspiration while sedated, and could result in laryngospasm or aspiration pneumonitis. A history of significant CAD or severe CHF would suggest a higher risk for myocardial events should hypoxemia or hypotension ensue. ED PSA would not be a satisfactory option for these patients.
Food and medication allergies should also be documented since egg and soy allergies would preclude the option to utilize propofol. Liver disease may indicate a decreased ability to metabolize barbiturates and benzodiazepenes, potentially prolonging sedation. Methohexital may induce seizure activity in patients with a history of a seizure disorder.
Airway assessment is integral in establishing an adequate sedation plan should aggressive maneuvers be necessary. Will the planned procedure involve occluding the airway (ie, oral laceration repairs, GI endoscopy)? Does the patient wear dentures, or have a large tongue, an overbite, or micrognathia? Patients with a Mallampati classification greater than III, inability to open the mouth more than 4 cm, a thyromental distance less than 6 cm, history of cervical spinal inflexibility, or history of previous difficult intubation all indicate a high risk for intubation failure. Should the patient be deemed at a high risk for airway failure, appropriate precautions should be implemented and the decision to abort the PSA should be entertained.
Airway adjuncts beyond direct laryngoscopy such as an intubating LMA, GlideScope, light wand, or fiberoptic scope should remain at the bedside. Supplemental oxygen may need to be delivered via non-rebreather (NRB) or nasal trumpet if the patient becomes unexpectedly obtunded. Above all else, protection of the patient's airway, and avoidance of respiratory depression, is tantamount to a successful sedation.
Hemodynamic stability must also be maintained. Many sedative agents and regimens result in vasodilatation, and once the patient develops a depressed level of consciousness, his or her sympathetic output may also decrease further potentiating bradycardia and decreased mean arterial pressure. Patients taking antihypertensive medications and those with dehydration or acute blood loss anemia should be volume resuscitated prior to PSA. Cardiac patients taking calcium channel blockers or beta-blockers have been shown to have a higher incidence of bradycardia and hypotension with PSA. Pressor agents such as norepinephrine, epinephrine, phenylephrine, dopamine, or ephedrine should be available in the event that fluid refractory shock takes place.
Patients should also be assessed for recent oral intake. Patients are at risk for aspiration of gastric contents when they reach deeper levels of sedation and lose their protective airway reflexes. Although small ED studies have shown no significant adverse outcomes with known oral intake prior to procedures, ASA guidelines recommend safety parameters of liquids requiring 2 hours and solids requiring 6 hours prior to a procedure.
Aspiration under general anesthesia has been estimated to have an incidence of 1:3420 with mortality in 1:125,109 cases with little data to suggest long-term sequelae. General anesthesia is at the extreme end of the sedation spectrum, and often mandates advanced airway manipulation; therefore, aspiration is much more likely. Although no study has demonstrated an elevated risk of aspiration for moderate to deep PSA in the ED, it is imperative to consider gastric contents and depth of sedation. Most authors have concluded that their sample sizes were often not large enough to detect statistically significant differences in study subjects. Patients presenting with a full stomach would benefit from observation and procedural delay for gastric emptying. Care should be taken to minimize the likelihood of aspiration, and precautions made to manage aspiration should it occur with wall suction, suction catheter, and additional personnel should the patient need to be log rolled into the lateral decubitus position.
Once the need for procedural sedation has been assessed, informed consent should be obtained from the patient. Patients should have mental status and function documented prior to and following the procedural initiation. Pediatric and adult patients alike should be placed on a cardiac monitor, pulse oximetry, blood pressure cuff, and, if available, end-tidal CO2 (ETCO2). Studies have shown ETCO2 to be more sensitive in detecting patients with respiratory depression than pulse oximetry, although there was no significant difference in outcome. Patients with deep sedation resulting in respiratory depression will show an increase in ETCO2 greater than 10 mm Hg from baseline or a level above 50 mm Hg total before they demonstrate a decrease in oxygen saturation. Although the ETCO2 does not differentiate the level of sedation, it can accurately detect respiratory depression.
While monitoring the patient's sedation course, heart rate, blood pressure, and oxygen saturations should be documented in serial timed intervals. Adverse events should be documented with additional descriptions of executed interventions. Standard reporting of adverse events includes apnea, oxygen saturation less than 90%, ETCO2 > 50 mm Hg, bradycardia, hypotension, and emesis. Continuous cardiac monitoring is important to detect adverse rhythms, and can be helpful to determine pain response when the patient develops a sinus tachycardia. Additional tools that can often prove to be vital during sedations include ACLS medication access, advanced airway equipment, and supplemental oxygen via nasal cannula, NRB, or bag valve mask (BVM) (Table 8–2).
Table 8–2. Equipment for Procedural Sedation and Analgesia. ||Download (.pdf)
Table 8–2. Equipment for Procedural Sedation and Analgesia.
|Advanced airway equipment|
|Blood pressure monitor|
|Reversal agents (ie, Narcan, flumazenil) ACLS medications|
|Suction device with suction catheter|
Multiple scales have been created and described for measuring patients' levels of comfort, agitation, and sedation in the ICU, OR, and ED environments. The scales provide practitioners a guide to determine depth of sedation, and need for smaller titrations, reversal, or additional medications. Most of the sedation scales include monitoring agitation that does not directly relate to elective procedural sedation in the ED.
The Ramsay Sedation Scale (RSS) has been utilized in studies on ED PSA to describe levels of sedation. It is a simple 6-score system with 1 being anxious or restless and 6 being no response to stimulus (Table 8–3). It has been validated for inter-rater reliability, and simplifies the PSA assessment.
Table 8–3. Ramsay Sedation Scale. ||Download (.pdf)
Table 8–3. Ramsay Sedation Scale.
|1||Patient is anxious and agitated or restless, or both|
|2||Patient is cooperative, oriented, and tranquil|
|3||Patient responds to commands only|
|4||Patient exhibits brisk response to light glabellar tap or loud auditory stimulus|
|5||Patient exhibits a sluggish response to light glabellar tap or loud auditory stimulus|
|6||Patient exhibits no response|
The Richmond Agitation–Sedation Scale (RASS) is a 10-score system with 4+ (combative) to 1+ (restless) range for grading decreasing agitation, 0 for calmness, and −1 (drowsy) to −5 (unarousable) to quantify degree of responsiveness (Table 8–4). The RASS scale differentiates the varying degrees of agitation, whereas the RSS scale has only one category (1) for anxious, agitated, or restlessness. The RSS scale utilizes a physical stimulus (glabellar tap) to grade responsiveness, but the RASS scale implements both verbal and physical stimuli to grade consciousness.
Table 8–4. Richmond Agitation–Sedation Scale. ||Download (.pdf)
Table 8–4. Richmond Agitation–Sedation Scale.
|+4||Combative||Overtly combative or violent; immediate danger to staff|
|+3||Very agitated||Pulls on or removes tube(s) or catheter(s) or has aggressive behavior toward staff|
|+2||Agitated||Frequent nonpurposeful movement or patient–ventilator dyssynchrony|
|+1||Restless||Anxious or apprehensive but movements not aggressive or vigorous|
| 0||Alert and calm|
|−1||Drowsy||Not fully alert, but has sustained (more than 10 seconds) awakening, with eye contact, to voice|
|−2||Light sedation||Briefly (less than 10 seconds) awakens with eye contact to voice|
|−3||Moderate sedation||Any movement (but no eye contact) to voice|
|−4||Deep sedation||No response to voice, but any movement to physical stimulation|
|−5||Unarousable||No response to voice or physical stimulation|
Sedation Conclusion and Patient Disposition
Care should be taken toward the conclusion of the PSA to limit additional medication administration. Should the noxious stimuli cease (ie, distal radius fracture is reduced and splinted) shortly after the last dose, respiratory depression, hypotension, and bradycardia could likely ensue. Depending on the sedative regimen utilized, rapid degradation would mitigate these effects (ie, propofol, dexmedetomidine, etomidate). Longer-acting agents such as fentanyl and versed could create overt sedation 20–30 minutes beyond the last dose and completion of the ED procedure.
Patients should be capable of responding verbally once sedation has worn off, and once assessed they should return to the baseline mental status documented prior to the PSA. Postprocedural emesis can be common following agents such as ketamine, so complete return to baseline is recommended prior to administering oral intake. Studies suggest that a minimum post-PSA observation period of 30 minutes be exercised. Most adverse events such as hemodynamic instability and emesis should have been resolved by that time. Once the patient has successfully completed the post-PSA observation period, he or she may be safely discharged from the ED.