PART I
PRINCIPLES, TECHNIQUES, AND BASIC SCIENCE
CHAPTER 11 PRINCIPLES OF OFFICE SEDATION FOR COSMETIC SURGERY
MAXIMILIAN W. B. HARTMANNSGRUBER, DOMINICK CANNAVO, AND NIKOLAUS GRAVENSTEIN
The integrity of defense: “A defense that is expecting an attack has an advantage. If the element of surprise is added, it is usually because the defenders ignored warnings and did not take the attackers seriously”
–Samurai: “The Art of War” 2,500 years ago by the Chinese general Sun Tzu1
While the standard of care theoretically allows for complications related to sedation for cosmetic surgery, everyone’s expectation is for perfect results. After all, cosmetic procedures, especially office-based, are the most elective of all procedures. Worse still, complications are not only debated in grand rounds or journals but rather in newspapers and on television. Careful intra- and postoperative care in an accredited, properly equipped facility by adequately trained practitioners is assumed. When complications do occur, they are often the result of inadequate planning and/or improper patient selection.
PREOPERATIVE EVALUATION AND OPTIMIZATION
The purpose of preoperative evaluation is not simply to provide “medical clearance,” but rather to identify and modify any risk factors. A comprehensive discussion of every possible risk factor is beyond the scope of this chapter; we limit the discussion to cardiovascular and pulmonary/smoking, obesity, and the risk of deep vein thrombosis (DVT).
Cardiac
The American Heart Association and the American College of Cardiology guidelines advocate an approach that relates major, intermediate, and minor cardiovascular risk factors to the planned procedure.2 For example, if a major cardiovascular predictor is present, nonemergency surgery should be delayed until risk factor modification has been accomplished.
Clinical predictors for a major adverse cardiac event include recent (<1 month) myocardial infarction, unstable angina, decompensated congestive heart failure, severe valvular heart disease, and significant arrhythmias. The presence of one of these major clinical predictors mandates postponement of any cosmetic surgical procedure.
Intermediate predictors include mild stable angina, previous myocardial infarction, compensated congestive heart failure, diabetes mellitus (especially type I), renal insufficiency, and poor exertional capacity. Adequate cardiovascular fitness to undergo an elective procedure, especially office-based, can be estimated by the patient’s ability to climb one flight of stairs or walk one block on level ground without shortness of breath and/or angina. This equates to 4 METs (metabolic equivalents) in a completed exercise test.2
With respect to ischemic heart disease, it is advisable to wait at least 6 months after a myocardial infarction and/or revascularization, angioplasty, stent placement, or bypass before considering elective surgery.2 Patients with a coronary stent(s) are universally on at least one and often two platelet inhibitors (e.g., aspirin and clopidogrel). This therapy is important for the stents but is a contraindication to many surgical procedures. These platelet-active drugs should not be modified without involving the patient’s cardiologist/internist as acute perioperative stent thrombosis has been reported after discontinuation of antiplatelet therapy.3 On the other hand, if the patient has had coronary revascularization within 5 years and is asymptomatic, the risk of a cardiac event is decreased and does not normally require additional workup. If revascularization was performed more than 5 years previously or the patient is symptomatic, cardiac risk is increased and a more extensive evaluation is mandated.
Cardiac risk factor modification frequently includes beta blockade and cholesterol statin therapy throughout the perioperative period.4
Pulmonary
With respect to pulmonary status, smoking, chronic obstructive pulmonary disease (COPD), reactive airway disease, and obesity are the major risk factors. As with cardiac evaluation, patients should be screened based on symptoms and exertional capacity. If they are asthmatic, the goal is to stabilize them and avoid an exacerbation. Pulmonary function tests are rarely indicated or useful for preoperative screening. Because cosmetic surgery is elective, there is an opportunity to implement smoking cessation in order to reduce pulmonary and thromboembolic complications and improve wound healing and flap perfusion. Maximum benefit, however, is probably not achieved until at least a month after smoking cessation. Shorter term smoking cessation actually causes some increase in pulmonary secretions.
Obesity
The comorbidities in obese patients include atherosclerotic heart disease, adult-onset diabetes, congestive heart failure, systemic hypertension, cardiac arrhythmias, pulmonary hypertension, obstructive sleep apnea, gastroesophageal reflux (GERD), a predisposition to DVT, and sensitivity to narcotic analgesics. The excess adipose tissue on the chest and abdominal wall compresses the lungs. The resultant increased intrathoracic pressure is magnified by excessive adipose tissues within the peritoneal cavity leading to a further reduction in the functional residual capacity and total lung capacity. Asthma, chronic cough, and pulmonary fibrosis may be manifestations of GERD, another common accompanying effect of the increased intra-abdominal pressure of obesity. It is important to appreciate that following an abdominoplasty, with plication of the rectus abdominis muscles, intra-abdominal pressure is acutely increased, which exacerbates any preexisting pulmonary compromise. In addition, lower extremity venous flow is impeded by increased intra-abdominal pressure, creating venous stasis and an environment conducive to venous thrombosis. The physiologic changes imposed by rectus plication are often underappreciated and persist without concomitant weight loss. While the cosmetic result obtained with an abdominoplasty might give the perception of actual weight loss, the intraperitoneal fat remains and is compressed into a smaller space, exacerbating all the underlying pulmonary and venous stasis aberrations.5
Deep Vein Thrombosis
As with cardiac risk factor stratification/modification, the risk of DVT is considered and mechanical and/or pharmacologic prophylaxis implemented as indicated. Risk factors for DVT include birth control pills or hormone replacement therapy, protein C or S deficiency, antithrombin III deficiency, lupus anticoagulant, factor V Leiden along with acquired risk factors that include smoking, diabetes, congestive heart failure, obesity, and history of prior DVT. A history of DVT superimposes additional risk on the intrinsic thromboembolic risk of the procedure.
Surgery-specific risks can also be stratified as high, medium, and low. High risks for DVT are prolonged procedures and those associated with significant blood loss or fluid shifts. Examples in plastic surgery include major flap procedures, abdominoplasties and/or lower body lifts, and large volume liposuction. Intermediate-risk procedures include facelifts. Blepharoplasty and excision of small lesions present a low risk for DVT.
The aggressiveness of DVT prophylaxis is dictated by preexisting risk factors superimposed on the inherent risk of the procedure. Using Virchow’s triad (endothelial damage, stasis of blood flow, and hypercoagulability) as a model, the latter two components of the triad can be addressed. Sequential compression devices are utilized when possible to prevent stasis and ideally are applied prior to initiation of the sedation/anesthetic. Neuraxial anesthesia (spinal and/or epidural) should be considered for abdominoplasty. Neuraxial anesthesia provides a sympathetic block that promotes venous return and decreases the likelihood of stasis and an environment conducive to thrombosis. In terms of hypercoagulability, pharmacologic prophylaxis is achieved with pre-incision prophylactic administration of subcutaneous heparin or factor Xa inhibitors such as enoxaparin (Lovenox) and fondaparinux (Arixtra).
Preoperative NPO Guidelines
Fasting from solid food should be at least 8 hours. Milk is allowable up to 6 hours before initiation of sedation. Oral medications may be taken with a sip of water up to the time of surgery. To increase patient satisfaction, decrease gastric liquid volume, and to decrease the risk of dehydration or hypoglycemia from fasting, we encourage clear liquids up to 2 hours before the anticipated anesthesia start time in the first patient of the day and 3 hours for all following patients. Even though the minimum fast time for clear liquid is 2 hours, this allows for timely induction of the subsequent patients should the earlier procedures be shorter than anticipated. Examples of clear liquids include water, fruit juices without pulp, carbonated beverages, clear tea, and black coffee. Gatorade or other clear liquid electrolyte sports drinks are attractive because the stomach empties many times faster after these than after water alone because they contain sugar and salt that accelerate absorption from the proximal gastrointestinal tract and the sugar also prevents hypoglycemia in patients who are on a diabetes medication.6
Pretreatment beginning the night before with H2 blockers such as ranitidine (150 mg po), especially in obese patients, should be considered. This class of drugs is inexpensive, available over the counter, and well tolerated.
CONSCIOUS AND DEEP SEDATION
The goal of both conscious and deep sedation is to provide safe, titrated sedation and analgesia to a patient undergoing a surgical procedure.
Conscious sedation is characterized by:
1. depressed consciousness
2. independent airway
3. responsiveness to verbal stimuli
4. preserved protective airway reflexes and
5. amnesia
In contrast, unconscious or deep sedation is a state in which the patient’s airway may require support and, although the patient may be arousable, the stimulus required to generate a patient response is more vigorous or even noxious. Given the variability to patient response with respect to sedation, careful monitoring is essential.
Monitoring
Basic monitoring calls for compliance with the American Society of Anesthesiologists Monitoring Standards.7
1. Standard I
Qualified anesthesia personnel present throughout the procedure.
2. Standard II
Patient’s oxygenation, ventilation, circulation, and temperature shall be continually evaluated.
2.1 Oxygenation
Inspired gas: When an anesthesia machine is used, the concentration of oxygen in the breathing system shall be measured by an oxygen analyzer with a low oxygen concentration limit alarm in use.
Blood oxygenation: During all anesthetics, a quantitative method of assessing oxygenation such as pulse oximetry shall be employed. When the pulse oximeter is utilized, the variable pitch pulse tone and the low threshold alarm shall be audible.
3. Ventilation
During regional anesthesia (with no sedation) or local anesthesia (with no sedation), the adequacy of ventilation shall be evaluated by continual observation of qualitative clinical signs. During moderate or deep sedation, the adequacy of ventilation shall be evaluated by continual observation of qualitative clinical signs and monitoring for the presence of exhaled carbon dioxide unless precluded or invalidated by the nature of the patient, procedure, or equipment. If invoking the preclusion option, a statement in the record to explain why is recommended.
4. Circulation
4.1 Continuous display of the electrocardiogram (ECG). A helpful intraoperative ECG montage is to use at least one precordial electrode (except in breast surgery). If the ECG monitor has only three leads, this is readily accomplished by placing the left leg lead into the V5 position—anterior axillary line in the fifth intercostal space—and monitoring lead two (right shoulder-left leg). This configuration results in a modified V5 lead and is considerably more sensitive for identifying ischemia than any other single lead.
4.2 Arterial blood pressure and heart rate determination and evaluation at least every 5 minutes. Cautious interpretation of the patient’s blood pressure is essential, especially when the blood pressure cuff is placed lower than the heart (e.g., around the calf in a patient who is in a semi-sitting position).8 Conversely, hypertension secondary to stimulation or inadvertent intravascular injection of local anesthetics with epinephrine can lead to intra- and post-op bleeding and wound hematoma as well as myocardial ischemia. Perioperative treatment of blood pressure can help avoid ischemia as well as reduce intra- and post-op bleeding as well as bruising. In general, it is desirable to continue all cardiac and antihypertensive medications according to the patient’s normal regimen, as hypertension is much more likely to occur than hypotension during procedures performed under local anesthesia with intravenous sedation.
5. Body temperature
To aid in the maintenance of appropriate body temperature during all anesthetics, every patient receiving anesthesia should have temperature monitored when clinically significant changes in body temperature are anticipated or suspected.
Sedation Principles
Clinical experience has shown that even small amounts of benzodiazepines, narcotics, or propofol may result in unconsciousness. As an example, the minimum effective plasma concentration for midazolam (Versed) ranges from 30 to 1,000 ng/mL between individuals and generally decreases with age (Figure 11.1). Paradoxically, at identical plasma concentrations of midazolam, an oral dose induces more marked effects than an intravenous administration, presumably because of the active α-hydroxy metabolite.9 Given that there is such wide inter-patient response variability, the administration of sedatives is therefore titrated to effect.
An important cause of unintended, unconscious sedation is drug interaction. When benzodiazepines, propofol, and narcotics are used in combination, a potent drug synergy occurs, i.e., the drug effect is many times greater than if the drugs’ effects were simply additive. It is important to appreciate that narcotics in conjunction with either propofol or midazolam disproportionately enhance the independent sedative effect of either drug alone (Figure 11.2).
Conscious sedation may easily progress to unconscious sedation following incremental dosing of sedative or as painful stimulation diminishes or ends. The loss of the painful stimulus that serves as an arousal mechanism results in deeper sedation. Clinically, sedation should be considered a continuum from conscious to unconscious with both monitoring and vigilance being employed to achieve the desired state.
Medications
The most commonly used sedatives are midazolam, fentanyl, ketamine, propofol, and recently dexmedetomidine. Local anesthesia is used to provide the analgesia and occasionally narcotic is added as a supplement. If the sedatives are used to anesthetize (i.e., provide the analgesia), then it is no longer “sedation.” Each of the sedative drugs listed with the exception of dexmedetomidine is also capable of inducing general anesthesia when given in larger doses.
Midazolam (Versed) is a water-soluble benzodiazepine agonist characterized by rapid onset (30 to 60 seconds), with peak effect (2 to 3 minutes) and, after small doses, also rapid recovery (10 to 20 minutes). It provides antegrade, dose-dependent amnesia and is reversible with the specific benzodiazepine antagonist flumazenil. When implemented, the pharmacologic antagonism is effective quickly and only takes approximately one arm-brain circulation time (i.e., 30 to 60 seconds). Midazolam causes less compromise of airway tone than propofol and less respiratory depression than narcotics like fentanyl. Even though 1 mg of intravenous midazolam in the elderly patient may cause severe respiratory depression and prolonged hypnosis, younger patients typically receive 5 mg intravenous (IV) midazolam once intravenous access has been established. The clinical response ranges from no apparent effect to sleep. The response to this initial bolus gives important clues to the anticipated drug requirement during the remainder of the procedure.
FIGURE 11.1. Inter-patient variability of minimum effective plasma concentration in individual subjects and decrease with age. From Jacobs JR, Reves JG, Marty J, et al. Aging increases pharmacodynamic sensitivity to the hypnotic effects of midazolam. Anesth Analg. 1995;80:143-148.
FIGURE 11.2. Drug synergy: by combining drugs, their effect is many times greater than if the drugs’ effects were simply additive. From Ben-Shlomo I, Abd-El-Khalim H, Ezry J, et al. Midazolam acts synergistically with fentanyl for induction of anesthesia. Br J Anaesth. 1990;64(1):45-47.
Fentanyl is a synthetic opioid agonist also characterized by rapid onset (30 to 60 seconds) and recovery (15 to 20 minutes). Its peak effect is reached at approximately 10 minutes. Other synthetic opioids include, from short to longer acting, remifentanil (3 to 5 minutes), alfentanil and sufentanil (5 to 10 minutes). Fentanyl when given as an infusion via an electronic pump at 2 µg/kg/h decreases the requirement for other sedative agents by approximately 50% but increases the likelihood of postoperative nausea and vomiting. To decrease the incidence of nausea, the complete avoidance of narcotics should be given serious consideration because a large percentage of patients will be substantially free of pain due to residual local anesthetic effects at the end of the procedure and during their recovery room period. This strategy markedly decreases motion-induced nausea during the patient’s trip home or to the hotel.
While propofol was developed as an induction agent for general anesthesia, it has become the mainstay for most moderate and deep sedation protocols where it is given as a titrated infusion. Commonly, a level of sedation is initially achieved with midazolam and then titrated small incremental bolus or continuous infusion propofol is added to facilitate the progression from mild sedation to deeper sleep. Propofol has a very rapid onset of effect <1 minute. When titrating to the desired effect, about 2 minutes should be allowed after bolus administration for peak drug effect to occur. Propofolis a profound depressant of central respiratory drive and decreases airway tone and as a result further interferes with respiration. In terms of pharmacokinetics, the elimination half-life of propofol is 30 to 60 minutes, while its duration of action is much shorter, <10 minutes, as a result of redistribution to muscle and fat. This short duration of action makes propofol given as a continuous infusion an ideal drug for providing moderate to deep sedation. It is important to appreciate that with a continuous infusion, as the volume of redistribution becomes saturated over time, a progressively greater portion of infused drug becomes bioavailable and the level of anesthesia deepens. A steady-state propofol infusion will continue to progressively increase the plasma and effect site concentration of the drug for over 25 minutes before a relative steady state tends to be reached.10 This requires constant assessment of the patient and then tapering of the rate of infusion. The concept of titration to effect does not simply apply to achieving an appropriate level of sedation but maintenance of that level as well.
It is also important to appreciate the resultant synergy when propofol, benzodiazepines, and narcotics are used in combination.
Benzodiazapines do not compromises airway tone to nearly the same extent as propofol but clinically the combination of the two facilitates deep sedation with relative preservation of airway tone. The combination of the two drugs is not fixed in terms of dose. Obese patients or patients with a history of sleep apnea should generally receive relatively more benzodiazepine and less proprofol. The addition of dexmedetomidine (Precedex) is useful to consider in these patients as well. It is a highly specific α2-adrenoceptor agonist with centrally mediated sympatholytic effects.11 Onset of effect can be expected at 5 to 8 minutes, with a peak effect at 10 to 20 minutes, and a duration of effect of 2 to 4 hours. It has sedative and analgesic effects without respiratory depression and when titrated at rates between 0.4 and 0.1 µg/kg/h allows an approximately 30% to 40% reduction in anesthetic requirements.
Ketamine is also an attractive medication in that it is both an analgesic and a sedative and is essentially devoid of respiratory depressant effects. It is important to be aware that ketamine can cause dysphoria and increases salivation. These side effects are mitigated if a benzodiazepine such as midazolam and an antisialagogue such as glycopyrrolate (0.2 mg) are used in combination. Intramuscular effects peak at 10 minutes, intravenous effects at 2 to 3 minutes. Intravenous ketamine in doses of 10 to 20 mg has a short duration of action (5 to 10 minutes) and is a potent integumental analgesic, so its administration should be timed to anticipate any particularly painful stimuli such as the infiltration of local anesthetic.
Monitoring
Monitoring the level of sedation includes both subjective and objective assessments. With respect to subjective assessment, does the patient appear comfortable, anxious, or drowsy? Thus, a critical first element of monitoring conscious sedation is inspection and conversation to allow titration. A common sedation endpoint is when the patient feels a drug effect, manifests a change in speech, or the appearance of lateral nystagmus. The same monitoring technique (i.e., conversation) is also used to establish the second goal, namely verifying that the sedation is still of a conscious nature. It is prudent to document conversation on the case record in the list of monitors used.
Respiration consists of two components, oxygenation and ventilation. It is important to understand that with oversedation, desaturation occurs secondary to decreased ventilation and shallow breathing. In the conscious patient, ventilation is somewhat more difficult to monitor continuously than in the unconscious, intubated patient.
Pulse oximetry is the method by which oxygenation is objectively, continuously, and noninvasively assessed, and its use, as previously noted, is the standard of care during sedation. The pulse oximeter is best utilized in the fastest response (usually not the factory default setting) and applied to a finger rather than a toe.
Ventilation is the other component of respiration. A coherently talking patient is adequately ventilating. With rare exceptions, therefore, provided the presence of an adequate surgical block, reducing sedation and thereby getting the patient to follow complex commands (i.e., hold still) may be a safer choice than deepening a squirming/restless patient. If lightening the patient is not an option, a pre-tracheal stethoscope is helpful to identify airway obstruction, wheezing, as well as the presence or absence and frequency of ventilatory efforts.
Ventilation can be simply monitored by chest wall impedance in which the ECG transduces a respiratory waveform, allowing assessment of both rate and quality of respiration. Specifically, chest wall impedance utilizes an electrical current transmitted between the ECG electrodes through the thorax. Gas is a poor conductor of electrical current and with inspiration, the volume of gas increases in the chest and conduction falls. This change in conduction or increasing impedance with inspiration is transduced into a waveform and rate so that respiration can be qualitatively and semiquantitatively assessed simply and noninvasively. Impedance monitoring does not work in all patients and may fail to differentiate a patient who has chest movement but an obstructed airway from one who is not obstructed.
Capnography, end tidal carbon dioxide sampling with a carbon dioxide waveform display, is a more definitive form of monitoring ventilation and can be accomplished with capnograph attached to a specially designed CO2 sampling nasal cannula or one that has been modified with a sampling catheter inserted through one of the nasal prongs. Capnography allows the most accurate monitoring of both rate and quality of ventilation. This technique will often underestimate but never overestimate arterial CO2. Capnography has recently also become a formally stated standard of care during moderate or deep sedation.7
Contrary to the knowledge of many anesthesiologists, pulse oximetry (the monitor of oxygenation) can function as a monitor of ventilation as well. During normal ventilation, while breathing room air, a person typically has a PaO2 ≈ 75 mmHg, which translates to a saturation (SpO2) of ≈ 98% as displayed by the pulse oximeter. This places the PaO2 and SpO2 at the point on the oxyhemoglobin saturation curve where there is a nearly linear relationship between PaO2 decrease and O2 saturation (Figure 11.3). At normal and low PaO2 values, there is great resolution for PaO2 changes via the accompanying SpO2 changes. This has considerable impact in relation to PaCO2. Consider the simplified alveolar gas equation:
PaO2 ≈ PIO2 − PaCO2/R
(PIO2 = partial pressure of inspired oxygen; R = respiratory quotient calculated from the ratio of CO2 eliminated/O2 consumed—typically 0.8)
In the patient breathing room air, a 10 torr increase in PaCO2, as commonly occurs with narcotic administration, therefore results in an approximately 12 mmHg decrease in PaO2. In the patient who is significantly hypercarbic, the increase in PaCO2 will, therefore, result in a significant decrease in SpO2, but only if the patient is breathing room air. Thus, when applied in this context (without administration of supplemental O2 oxygen), ventilation can be monitored with a single device—the pulse oximeter. The pulse oximeter’s ability to detect changes in ventilation disappears when PaO2 is increased to >75 mmHg and the patient is on the flat part of the oxyhemoglobin curve (Figure 11.3). It is therefore advisable in our opinion to avoid routine use of supplemental oxygen in patients receiving conscious sedation so that the pulse oximeter is a more sensitive monitor of ventilation—not just oxygenation. In overview, it is preferable to think of supplemental oxygen as a method to treat desaturation. One needs to be cognizant that supplemental oxygen masks oversedation with hypoventilation and makes desaturation a late and precipitous sequel of oversedation.Besides the clinical advantage of converting the pulse oximeter from a pure oxygenation monitor into both a ventilation and oxygenation monitor, the withholding of oxygen (when it is not necessary) has additional advantages: 1) improved individual titration by early feedback via minor desaturations; 2) less likelihood of combustion with the use of electrocautery and laser as is common during head and neck cosmetic procedures.12 To reduce the incidence of airway fire, provided a patient has a normal saturation on room air, it is acceptable practice to abandon CO2 monitoring with head and neck procedures, because the required plastic components would increase the chance for combustion in the field. If supplemental oxygen is used during procedures on the head or thorax done with sedation, then either the airway should be protected (e.g., laryngeal mask or endotracheal tube) or the oxygen concentration coming out of the nasal cannula should not exceed 30%. The latter approach requires an air oxygen blender or separate flow meters.
FIGURE 11.3. Oxyhemoglobin dissociation curve. Y-axis = percent of arterial blood saturated with oxygen, X-axis = partial pressure of oxygen in arterial blood.
If a patient manifests decreased oxygen saturation and cannot be encouraged to ventilate, the initial intervention is that of airway optimization followed by adding supplemental oxygen and alerting the surgeon. This can include jaw lift, neck extension, and insertion of an oral or nasal airway. After the airway has been optimized, supplemental O2 can be phased out while sedation is titrated downward. During the use of supplemental O2, the drop in oxygenation is delayed in relation to the hypoventilation, but once it occurs, the speed of deterioration is independent of the presence or absence of supplemental oxygen. Quite simply, supplemental oxygen masks oversedation until it is late and intervention then must be faster and more definitive, which often involves violating the surgical field. Because CO2 has an anesthetic potency about four times that of N2O,13 by the time desaturation occurs in the presence of oxygen, the patient may already be in CO2 narcosis and therefore less likely to respond to complex commands or to stimulation. Severe consequences may ensue if the patient subsequently is difficult to mask or intubate. It is useful to stress several observations:
1. Above a PaO2 of 75 mmHg supplemental oxygen creates a false sense of security.
2. Provided the SpO2 is normal and the patient is on room air, the PaCO2 must be essentially normal.
3. When even a small amount of oxygen is administered, the pulse oximeter no longer functions as a monitor of ventilation.
4. With the titration of benzodiazepines and/or opioids in the context of a saturation of >90% on room air, the patient cannot be in CO2 narcosis.
5. Should desaturation occur, the airway is optimized and supplemental oxygen is utilized while the level of sedation is titrated downward.
With respect to respiratory physiology and its relationship with sedation, narcotics and sedatives individually as well as together depress the CO2 response curve. Under normal circumstances, ventilation increases as PaCO2 increases. Sedatives, especially narcotics, desensitize the central respiratory centers to CO2, thereby shifting the CO2 response (threshold) to the right. The practical implication is less increase in ventilation per unit increase in CO2. In addition, the slope (sensitivity) of the CO2 response curve is shallower following sedative or narcotic administration.
All narcotics have similar efficacy, although within the class there are marked differences in potency and duration of action. Specifically with respect to duration of action: morphine > fentanyl > sufentanil > alfentanil > remifentanil. Alexander14 has shown that decreased awareness (sedation) also markedly decreases the slope of ventilation in response to hypoxia following midazolam. Furthermore, the ventilatory response to CO2 in a patient receiving midazolam is diminished to a greater extent and for longer duration in patients with COPD.15 Thus, individual titration to effect with careful monitoring is again the mainstay of sedative dosing.
Amnesia, an additional component of sedation, is predominantly achieved through the use of benzodiazepines. It must be appreciated though that actually achieving amnesia is inconsistent.Specifically, in the absence of pain, little sedation is required to achieve amnesia. Pretreatment with a benzodiazepine, for example, 5 to 10 mg Valium, orally prior to OR entry should be considered. If benzodiazepines are administered after the patient feels pain, amnesia is not predictable. Lastly, it is important to appreciate that while propofol and narcotics are not amnestic agents, they do synergize with benzodiazepines to help achieve this goal.
In terms of monitoring the depth of anesthesia and therefore awareness and amnesia, bifrontal referential EEG (BIS) has been used with variable success.16 The inconsistent results are likely a consequence of the muscle movement electromyogram artifact.
Oversedation
A final consideration with respect to sedation is that of excess drug effect from a drug administration error, drug synergy, or a loss of offsetting noxious stimulus. In such a circumstance, the treatment approach is:
1. stimulate the patient and support the airway;
2. administer supplemental oxygen;
3. discontinue sedative drug administration; and lastly
4. consider an intravenous drug antagonist if the excess effect is not attenuated or resolved by 1 to 3.
Toward that end, it is ideal to preferentially use sedative drugs with a short half-life or for which a specific antagonist is available. Narcotics can be antagonized with naloxone typically only requiring 20 to 40 µg (0.5 to 1 cc of 0.4 mg naloxone drawn up to a total volume of 10 cc). Benzodiazepines are antagonized with flumazenil typically requiring 0.1 to 0.3 mg (1 to 3 cc of standard concentration of 0.1 mg/cc).17 No facility where sedation is performed should be without these antagonists readily available. If only benzodiazepine has been administered, flumazenil should be utilized as naloxone would be of no benefit. If a patient has received both benzodiazepine and narcotic sedation, it is common to use naloxone first as the narcotic component is the more likely cause of the respiratory depression. Two other considerations are important. First, when possible, titrate the antagonist to avoid a sympathetic surge from acute withdrawal. Second, if several rounds of antagonist do not have the desired effect, consider other diagnoses, for example, metabolic derangement or stroke.
Postoperative Nausea and Vomiting
An important consideration with respect to any surgery is postoperative nausea and vomiting (PONV). This is particularly important in cosmetic surgery as PONV can detract from the perception of the overall experience, no matter how ideal the outcome. Beyond the subjective implications, nausea and vomiting can also undermine the outcome, especially in procedures involving the head and neck. Specifically, during vomiting, as the intra-abdominal pressure is increased with a closed glottis, the intrathoracic pressure increases, thus impeding venous return. This may translate into oozing and more significantly the development of a wound hematoma. Vomiting is often accompanied by an increase in the blood pressure as well, which can further predispose to these complications. Prophylactic pretreatment is essential as preventing nausea is more easily accomplished and reliable than treating it. The use of low-dose intraoperative corticosteroids has become routine in plastic surgery and dexamethasone 10 mg has been shown to be efficacious in both preventing and treating PONV. The antiemetic mechanism of action is not well understood. It is thought that dexamethasone may antagonize prostaglandin or release endorphins that elevate mood, improve one’s sense of well-being, and stimulate appetite. A useful multimodal algorithm also includes intraoperative administration of Ondansetron 4 to 8 mg IV along with the Decadron. Diabetes is a relative contraindication to Decadron as even this small amount of Decadron can play havoc with blood glucose control for 12 to 24 hours. A careful history should be taken preoperatively, and if a history of motion sickness is elicited, dimenhydrinate ½ tablet po or a scopolamine patch applied preoperatively can also be very helpful.
Postoperative Pain
While the mainstay of pain management has always been narcotics, this class of drugs is not without side effects such as constipation and more importantly nausea and vomiting. The COX-2 inhibitors as nonsteroidal anti-inflammatory drugs decrease the mediators of pain and inflammation without affecting platelet function. Beginning these drugs preoperatively and continuing them for 3 days postoperatively can greatly decrease narcotic usage and the resultant narcotic-related adverse side effects.
CONCLUSION
A safe outcome from an office procedure performed under IV sedation is predicated on patient preparation, planning, and technique. Further, in the same way that understanding the operation helps the anesthesiologist optimize outcome, understanding the sedation can afford the same benefit to the surgeon. While what we have written may seem unnecessarily detailed in some regards and superficial in others, our goal is to provide a conceptual understanding of procedural sedation beyond a simple knowledge of drug dosage and effect.
References
1. Sun Tzu S. In: Griffith SB, ed. The Art of War. Oxford: Oxford University Press; 1971.
2. Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.Circulation. 2007;116(17):e418-e500.
3. Dalal AR, D’Souza S, Shulman MS. Brief review: coronary drug-eluting stents and anesthesia. Can J Anaesth. 2006;53:1230-1243.
4. Le Manach Y, Ibanez E, Cristina M, et al. Impact of perioperative statin therapy on adverse postoperative outcomes in patients undergoing vascular surgery. Anesthesiology. 2011;114:98-104.
5. Kral JG. Surgical treatment of obesity. In: Bjorntorp P, ed. International Textbook of Obesity. Hoboken, NJ: John Wiley & Sons Ltd; 2001.
6. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to healthy patients undergoing elective procedures. A report by the American Society of Anesthesiologists Task Force on Preoperative Fasting. Anesthesiology. 1999;90:896-905.
7. Basic Anesthetic Monitoring, Standards for (Effective July 1, 2011). www.asahq.org. Accessed December 11, 2012.
8. Papadonilolatis A, Wiesler ER, Olympio MA, et al. Avoiding catastrophic complications of stroke and death related to shoulder surgery in the sitting position. Arthroscopy. 2008;24(4):481-482.
9. Crevoisier C, Ziegler WH, Eckert M, et al. Relationship between plasma concentration and effect of midazolam after oral and intravenous administration. Br J Clin Pharmacol. 1983;16:51S-61S.
10. Simulation of Propofol Pharmacokinetics. http://vam.anest.ufl.edu. Accessed December 11, 2012.
11. Bekker A, Kaufman B, Samir H, et al. The use of dexmedetomidine infusion for awake craniotomy. Anesth Analg. 2001;92:1251-1253.
12. Joint Commission on Accreditation of healthcare organizations: Sentinel Event Alert 29: preventing surgical fires, June 24, 2003. www.jointcommission.org
13. McAleavy J, Way W, Altstatt A, et al. The effect of PCO2 on the depth of anesthesia. Anesthesiology. 1961;22(2):260-264.
14. Alexander CM, Gross JB. Sedative doses of midazolam depress hypoxic ventilatory responses in humans. Anesth Analg. 1988;67:377-382.
15. Gross JB, Zebrowski ME, Carel WD, et al. Time course of ventilatory depression after thiopental and midazolam in normal subjects and in patients with chronic obstructive pulmonary disease. Anesthesiology. 1983;58:540-544.
16. Glass PS, Bloom M, Kense L, et al. Bispectral analysis measures sedation and memory effects of propofol, midazolam, isoflurane, and alfentanil in healthy volunteers Anesthesiology. 1997;86:836-847.
17. Carter AS, Bell GD, Coady T, et al. Speed of reversal of midazolam-induced respiratory depression by flumazenil—a study in patients undergoing upper G.I. endoscopy. Acta Anaesthesiol Scand. 1990;34 (suppl 92):59.