The PSA spectrum involves minimal, moderate, deep, and general anesthesia levels necessitating that the practitioner recognizes the levels of sedation, and be prepared to rescue the next level of sedation if necessary. Several experts have recommended a separate category for dissociative anesthetics such as ketamine because the performance and adverse effect profile differs widely from other forms of sedation. Each degree of sedation increases risk of cardiopulmonary instability with likely need for aggressive intervention.
Minimal sedation (anxiolysis): a drug-induced state during which the patient responds 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 the patient responds 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.
Deep sedation/analgesia: a drug-induced depression of consciousness during which the patient cannot be aroused easily but responds purposefully following repeated or painful stimulation. The ability to independently maintain ventilatory function may be impaired. The patient may require assistance in maintaining a patent airway, and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained.
General anesthesia: a drug-induced loss of consciousness during which the patient cannot be aroused, even by painful stimulation. The ability to maintain ventilatory function independently is often impaired. The patient often requires 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.
PROCEDURAL SEDATION & ANALGESIA ASSESSMENT
Indications for PSA include pain relief, amnesia, and anxiolysis required for the patient’s comfort; therefore, drugs, dosages, 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) classifies patient illness severity as categories I, II, III, IV, V, and VI (Table 4–1) using a grading system created in 1941. Each category involves escalating degrees of progressive systemic disease, and is meant to be used for assessment of the illness of the patient prior to surgery. A patient scored as ASA I–II can be reasonably sedated in the emergency department without elevating the risk of sequelae from underlying systemic pathology. When a patient is deemed to be more ill (ASA III-IV), it is often more appropriate to involve anesthesia within the parameters of elective or non–life-threatening scenarios. Category III classifications have shown to be an independent risk factor for adverse outcomes in general anesthesia and pediatric sedation patients. Categories V and VI are usually not applicable within the emergency department setting. The downside to ASA classification is the ambiguity of the category definitions and variable scoring among practitioners.
The patient should be screened for recent illnesses, hospitalizations, birth complications, gastroesophageal reflux disease (GERD), liver or kidney disease, as well as metabolic disorders. Pulmonary diseases such as asthma, cystic fibrosis, pulmonary fibrosis, and tracheomalacia could potentially result in profound hypoxemia. Patient history of supplemental oxygen at home would indicate that ASA category III or IV requires a critical review for the need of emergency department PSA. The pediatric patient with prior history of cardiac surgery (transposition of the great vessels, tetralogy of Fallot, left hypoplastic heart syndrome) requires consultation with an anesthesiologist as well. The patient with GERD may require passive aspiration while sedated, which could result in laryngospasm or aspiration pneumonitis. Food and medication allergies should be documented because egg and soy allergies preclude the option to utilize propofol. Liver disease may indicate a decreased ability to metabolize barbituates and benzodiazepenes potentially prolonging sedation, and methohexital may induce seizure activity in a patient with history of 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 (oral laceration repairs, GI endoscopy)? Does the patient have a large tongue, an overbite, or micrognathia? Patients with a Mallampati classification less than III, inability to open the mouth greater than 4 cm, a thyromental distance less than 6 cm, history of cervical spinal inflexibility, or history of previous difficult intubation indicate a high risk for intubation failure. If the patient is identified as high risk for airway failure, appropriate precautions should be implemented, and decision to abort the PSA should be considered.
The patient should 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 emergency department studies evaluating pediatric fasting regimens have shown no significant adverse events with known oral intake prior to procedures, ASA guidelines recommend safety parameters of liquids requiring 2 hours, and solids requiring 6 hours prior to procedure. Aspiration under general anesthesia has been estimated to have an incidence of 1:3420 with mortality in 1:125,109 patients with little data to suggest long-term sequelae. General anesthesia is at the 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 emergency department, it is imperative to consider gastric contents and depth of sedation. A patient presenting with a full stomach would benefit from observation and procedural delay for gastric emptying. Care needs be taken to minimize the likelihood of aspiration and precautions made to manage aspiration should it occur with wall suction, suction catheter, as well as additional personnel should the patient need to be log-rolled into the lateral decubitus position.
Table 4–1.American Society of Anesthesiologists (ASA) classification. |Favorite Table|Download (.pdf) Table 4–1. American Society of Anesthesiologists (ASA) classification.
ASA category I: Normal healthy patient
ASA category II: Patient with mild systemic disease
ASA category III: Patient with severe systemic disease
ASA category IV: Patient with severe systemic disease that is a constant threat to life
ASA category V: Moribund patient who is not expected to survive without the operation
ASA category VI: Declared brain-dead patient whose organs are being removed for donor purposes
When the need for PSA has been confirmed, informed consent should follow, and preparations made for proper monitoring. In the setting of pediatric PSA, the legal guardian should be informed of the risks and benefits, and documented for consent. Patients should have mental status and function documented prior to and following the procedural initiation. Pediatric patients 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 than pulse oximetry in identification of patients with respiratory depression, although there was no significant difference in outcome. Patients with deep sedation resulting in respiratory depression will demonstrate increase in ETCO2 greater than 10 mm Hg from baseline or greater than 50 mm Hg total before they demonstrate decrease in oxygen saturation. Although the ETCO2 does not differentiate 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.
Airway adjuncts beyond direct laryngoscopy, such as an intubating laryngeal mask airway (LMA), glide scope, light wand, or fiber-optic scope, should remain at the bedside. Supplemental oxygen may need to be delivered via non-rebreather, or nasal trumpet if the patient becomes unexpectedly obtunded. Above all, protection of the patient’s airway, and avoidance of respiratory depression is tantamount to a successful sedation.
Hemodynamic stability must be maintained. Many sedative agents and regimens result in vasodilation, and once patients develop a depressed level of consciousness their sympathetic output may also decrease further potentiating bradycardia and decreased mean arterial pressure. Patients with a history of dehydration or acute blood loss anemia should be volume resuscitated prior to PSA. Pressor agents such as norepinephrine, epinephrine, phenylephrine, dopamine, and ephedrine should be available in the event that fluid refractory shock takes place.
Adverse events should be documented with additional descriptions of executed interventions. Standard reporting of adverse events include apnea, oxygen saturation less than 90%, ETCO2 greater than 50, bradycardia, hypotension, and emesis. Continuous cardiac monitoring is important to detect adverse rhythms, and can help determine pain response when the patient develops an increased sinus tachycardia. Additional tools that can prove to be vital during sedations include ACLS medication access, advanced airway equipment, and supplemental oxygen via nasal cannula, non-rebreather, or bag valve mask (Table 4–2).
Table 4–2.Equipment for sedation. |Favorite Table|Download (.pdf) Table 4–2. Equipment for sedation.
|High flow oxygen |
|Ambu bag |
|Nasal trumpet |
|Advanced airway equipment |
|Cardiac monitor |
|Blood pressure monitor |
|Pulse oximetry/ETCO2 |
|Reversal agents (naloxone, flumazenil) |
|ACLS medications |
|Suction device with suction catheter |
|IV capabilities |
A number of sedation scales measure patient levels of comfort, agitation, and sedation in the intensive care unit (ICU), operating room (OR), and emergency department environments. The scales provide a guide for practitioners to determine depth of sedation and the need for smaller titrations, reversal, or additional medications. Most sedation scales include monitoring agitation which does not directly relate to elective procedural sedation in the emergency department. The Ramsay sedation scale (RSS) has been utilized in studies on emergency department PSA to describe levels of sedation. The RSS is a simple 6-score system with 1 being anxious or restless, and 6 being no response to stimulus (Table 4–3). It has been validated for inter-rater reliability, and simplifies the PSA assessment in the emergency department.
Table 4–3.Ramsay sedation scale. |Favorite Table|Download (.pdf) Table 4–3. Ramsay sedation scale.
|Score ||Responsiveness |
|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 sluggish response to light glabellar tap, or loud auditory stimulus |
|6 ||Patient exhibits no response |
SEDATION CONCLUSION & PATIENT DISPOSITION
Care should be taken toward the conclusion of the PSA to limit additional medication administration. Should noxious stimuli cease (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 (propofol, dexmedetomidine, etomidate). Long-acting agents such as fentanyl and midazolam can create overt sedation 20–30 minutes beyond the last dose and completion of the emergency department procedure. The patient should respond verbally once sedation has worn off and, after assessment is completed, should return to baseline mental status documented prior to the PSA. Postprocedural emesis may be common following agents such as ketamine; therefore, 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 resolved by that time. Upon successful completion of the post-PSA observation period, the patient may be discharged from the emergency department.
AGENTS FOR PROCEDURAL SEDATION & ANALGESIA
The ideal procedural agent for the emergency department patient acts quickly, creates excellent comfort, and resolves soon thereafter with little to no adverse effects. No sedative agent is perfect, but a number of agents exist tailored to each patient encounter (Table 4–4). Analgesia can often be controlled with narcotics, but procedural sedation requires the addition of an amnestic to reach a steady state of comfort. Benzodiazepines are often included with narcotics to facilitate adequate sedation. Ketamine can serve as the sole agent in short-term procedures, whereas midazolam and fentanyl regimens remain the mainstay in a number of emergency departments. Propofol, although a strong agent for moderate to deep sedation, does not satisfy analgesic requirements; however, in multiple studies it is often used solely for the entire PSA.
Table 4–4.Sedation and reversal agent dosages. |Favorite Table|Download (.pdf) Table 4–4. Sedation and reversal agent dosages.
|Agent ||Dosage ||Onset ||Duration |
|Fentanyl || |
Nasal: 1.5-2 mcg/kg
|Ketamine || |
IV: 1-2 mg/kg
IM: 3-5 mg/kg
|Dexmedetomidine || |
IV: 1 mcg/kg bolus
then 0.5-0.7 mcg/kg/h
|15-30 min ||240 min |
|Midazolam || |
IV: 0.05-0.1 mg/kg(6 mo-5 y) q2-3min prn (max 0.6 mg/kg) 0.025-0.05 mg/kg (6-12 y) q2-3min prn (max 0.4 mg/kg)
IM: 1-0.15 mg/kg
Nasal: 0.2-0.6 mg/kg
|Propofol || |
IV: 1 mg/kg then 0.5 mg/kg prn
IV drip: 5-50 mcg/kg/min
|30-60 sec ||2-5 min |
|Etomidate ||IV: 0.1-0.2 mg/kg ||30-60 sec ||3-5 min |
|Naloxone ||IV: 0.01 mg/kg q 2-3 min prn ||1-5 min ||30-60 min |
|Flumazenil ||IV: 0.01 mg/kg/min to max 0.05 mg/kg ||1-5 min ||20-75 min |
Fentanyl is a strong synthetic opiate with potency nearly 100 times that of morphine. Fentanyl lacks amnestic properties, so it is often used in combination with midazolam or propofol. The likelihood of respiratory depression increases greatly when fentanyl is administered with the aforementioned sedatives. It is renally excreted with a half-life of 3.5 hours. Dosing for analgesia is 1-2 mcg/kg IV, but is more optimal if administered as 0.5-2 mcg/kg IV aliquots every 2-3 minutes. Time of onset is 1-2 minutes, and it has a duration of action of 30-45 minutes.
Intranasal fentanyl is dosed 1.5–2 mcg/kg. A number of studies demonstrate efficacy at 2-mcg/kg dosing. Bioavailability is 71% of the IV dose, and typical formulation is 50 mcg/mL. The time of onset is 2–5 minutes. Fentanyl does not induce histamine release, and is less likely to induce hypotension. Fentanyl is also unlikely to cause a cross-reaction allergic response in patients with a known allergy to morphine. Adverse events include bradycardia, hypotension, increased intracranial pressure (ICP), and the potential for chest wall rigidity with high doses.
Ketamine is a dissociative anesthetic which produces analgesic, amnestic, and sedative effects. Ketamine increases endogenous catecholamines by blocking the reuptake pathway facilitating sympathomimetic effects. It maintains protective airway reflexes, and can increase the heart rate and blood pressure as well as intracranial and intraocular pressure (IOP). Patients with head or ocular trauma should be given an alternative agent. Ketamine can cause laryngospasm which may present as persistent cough to complete occlusion with resultant hypoxemia. Recent history of a viral upper respiratory infection (URI), infant younger than 3 months, croup, and stimulation of the posterior pharynx (aggressive suctioning, endoscopy, bronchoscopy) have been demonstrated to increase the likelihood of laryngospasm.
The patient often demonstrates a persistent nystagmus with nonpurposeful movements, but is unable to communicate. Prior to PSA initiation, it may be helpful to describe the phenomenon to friends or family in the room. Drawbacks of ketamine are emergence phenomena and postprocedural emesis. Benzodiazepines have been shown to marginally decrease both effects. Ketamine dosing is 1–2 mg/kg IV with onset within 1–2 minutes, peak levels within 5 minutes, and total duration at 20–60 minutes. Ketamine is administered IM at 3–5 mg/kg with onset in 5–10 minutes, peak levels at 10–15 minutes, and duration of 1–2 hours. Ketamine is a sialagogue, which can produce an increase in tracheobronchial and salivary secretions. An anticholinergic, such as atropine or glycopyrolate, may be given to mitigate the effects. Glycopyrolate can be given at IM/IV at 0.004 mg/kg (usual injection solution is 0.2 mg/mL). Atropine dosing should be 0.01 mg/kg IM/IV with a minimum dose of 0.1 mg and maximum dose of 0.5 mg.
Dexmedetomidine is a centrally acting α2-adrenergic agonist with sedating and analgesic effects. Few studies have evaluated the use of dexmedetomidine for PSA in the emergency department; however, a number of studies have demonstrated the safety and efficacy of dexmedetomidine for PSA, surgical interventions, and ICU management. Primary concerns with dexmedetomidine involve its ability to mitigate central sympathetic output. Patients can develop profound bradycardia, sinus arrest, heart block, and hypotension. Patients with a history of cardiovascular disease, heart block, or cardiomyopathy should not be administered dexmedetomidine for PSA. The use of anticholinergics are required to preempt adverse cardiac events.
The standard regimen involves utilizing glycopyrolate at 0.004 mg/kg IV prior to initiation of the PSA. Studies have demonstrated that the preventative measure significantly reduced episodes of bradycardia. The loading does for PSA is 1 mcg/kg bolus over 10 minutes, followed by 0.5–0.7 mcg/kg/hr. The loading dose time should not be less than 10 minutes in order to avoid bradycardia. The patient is capable of participating in painful procedures without developing respiratory depression, and once the PSA is completed, the agent is rapidly metabolized with a short recovery time. The patient should be continuously monitored while on dexmedetomidine.
Midazolam is a benzodiazepine with sedating, anxiolytic, and amnestic effects, but no analgesic effects. It functions through GABA receptors resulting in an influx of chloride, and central nervous system (CNS) depression occurs. It is often used in combination with a narcotic such as fentanyl or a dissociative anesthetic such as ketamine. It is more rapid in onset than diazepam or lorazepam. Midazolam can be given PO, PR, IV, IM, and atomized intranasally. Midazolam has been shown to diminish episodes of postprocedural emesis and emergence reactions with ketamine. Midazolam can cause hypotension and respiratory depression. A patient aged 6 months–5 years should be dosed at 0.05–0.1 mg/kg IV; patient 6–12 years dosed at 0.025 mg-0.05 mg/kg IV. A patient who is administered narcotics simultaneously should have the midazolam dose decreased by 30%. Alternate routes of midazolam and doses include:
The pediatric patients requiring gentle anxiolysis for radiologic imaging can receive atomized intranasal midazolam to facilitate the study without the need for parenteral administration. Intranasal midazolam is more effective with atomization versus drip and does tend to burn on administration.
Propofol is a nonopioid, nonbarbiturate, sedative hypnotic which is delivered via a lipid emulsion vehicle. Because the emulsion is composed of soy and egg products, patients with these food allergies should not receive this agent. Concentration is 10 mg/mL and is given IV. Propofol does have a tendency to burn on initial IV push. This sensation can be mitigated by pushing 0.5–1.0 mL of lidocine into the peripheral vein. Propofol for PSA is administered as a 1-mg/kg IV loading dose followed by 0.5-mg/kg IV maintenance dose. Propofol drips are initiated at 5–50 mcg/kg/min and titrated to appropriate level of awareness. Risk for respiratory depression and apnea is increased if propofol is given in large, rapid boluses, and significantly more likely if given along with narcotics. Because it is often difficult to titrate correctly the level of sedation with propofol, it is imperative that continuous assessment of the patient’s awareness be attained. Should a deeper level of sedation be achieved than warranted, discontinue the agent, observe, and execute rescue maneuvers as needed. Propofol has the benefit of being rapidly metabolized following discontinuation of the PSA or drip, and this enables the practitioner to observe the patient closely for a short period of time until resolution of sedation. Propofol is beneficial in emergent neurologic cases where serial examinations may be necessary to document progression, and it has been shown to decrease ICP. It has been shown to have antiemetic and anticonvulsant properties. Long-term sequelae with propofol are not seen with short-term PSA doses, but include hyperlipidemia, pancreatitis, zinc deficiency, hepatomegaly, rhabdomyolysis, and propofol infusion syndrome. Short-term adverse events include hypotension, hypoxemia, decreased cardiac output, respiratory depression, and apnea.
Etomidate is a short-acting nonbarbiturate hypnotic with GABA-like effects. It has been studied exhaustively in induction of general anesthesia, RSI, and PSA. For PSA, dose is 0.1-0.2 mg/kg IV. Benefits include rapid onset of action, stable hemodynamic effects, and rapid metabolism. Adverse events include laryngospasm, hiccoughs, and myoclonus. Myoclonus can occur in upward of 20-30% of patients which may make the procedure more difficult to complete (shoulder reduction). No long-term sequelae are evidenced from the myoclonus, but the appearance of seizure activity may prompt an unnecessary work up. Etomidate has been shown to blunt response to the adrenocorticotropic hormone (ACTH) stimulation test suggesting an etiology for adrenal suppression; however, studies have not demonstrated a statistically significant difference in outcome with hospitalized patients who received a single dose of etomidate. Greater concern for adrenal suppression is found in patients receiving multiple doses or continuous infusions of etomidate.
Rarely, the physician may need to administer reversal agents in the event that the patient has been deeply sedated to the state of general anesthesia. Although most agents are rapidly metabolized, and no additional medication is necessary, the midazolam and fentanyl regimen could last for 20–30 minutes. Naloxone is given for opiod overdose, and flumazenil is indicated for benzodiazepine overdose. Although naloxone is relatively benign (excluding symptoms of withdrawal), flumazenil can potentially be dangerous in a patient dependent on benzodiazepenes, and may precipitate a refractory seizure.
Naloxone is an opiod antagonist which competes directly with systemic narcotics. It binds all the opiate receptors, but appears to have a higher affinity for the μ receptor. Naloxone may be administered through the endotracheal (ET) tube, IM, IV, IO, or subcutaneously. It is not recommended to administer naloxone via ET tube in newborn infants. Naloxone is dosed at 0.01 mg/kg IV, and it is recommended to give smaller amounts for patients chronically on opiods in order to avoid overt withdrawal. Abrupt reversal in patients chronically administered narcotics may result in seizures, cardiac arrythmias, pulmonary edema, or profound agitation.
Flumazenil competes directly for the benzodiazepine-binding site on the GABA receptor, thereby reversing some aspects of CNS depression (respiratory depression). Flumazenil does not facilitate the metabolism of benzodiazepenes, and resedation can occur when flumazenil wears off. Flumazil is given IV, undergoes hepatic metabolism, and is excreted renally. The systemic half-life ranges from 20-75 minutes. The pediatric patients is dosed at 0.01 mg/kg up to 0.2 mg IV over 15 seconds. Repeat doses may be given in increments of 0.01 mg/kg up to a maximum dose of 0.05 mg/kg total or 1 mg total. Flumazenil can cause refractory seizures in patients on chronic benzodiazepines. Should a patient develop seizure activity following flumazenil administration, benzodiazepines are likely to be ineffective despite large doses for competitive binding.
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