**2. Direct cerebral cortical (brain) monitoring**

*When you can MEASURE what you are speaking about, and express it in NUMBERS, you know something about it; but when you cannot measure it, when you cannot express it in numbers, your knowledge is of a meager and unsatisfactory kind; it may be the beginning of knowledge, but you have scarcely, in your thoughts, advanced to the stage of SCIENCE.*

*William Thompson, knighted Lord Kelvin Popular lectures and addresses 1891–1894.*

What was true for temperature measurement more than a century ago is also true for the direct measurement of patient's cortical response to anesthetics. Without such measurement, there can be no science. Without science, there can be no reproducibility across the broad, and often unpredictable yet well-recognized, spectrum of individual patient response to medications.

Brain weight does not vary with body weight (i.e. the brain weight of a 100-kg male is **NOT** twice that of a 50-kg female). Traditional anesthetic dosing based on body weight does not account for individual sensitivities to medications and is, therefore, frequently in error.

Further adding to the possibility of dosing error is the twentieth century practice of relying on heart rate (HR) and blood pressure (BP) changes to ascertain cortical drug response. **HR and BP changes primarily reflect brain stem response but are unreliable to accurately determine cortical response.** Prior to the ability to measure cortical response, the knowledge gap between brain stem and cortical response led to routine overmedication (to avoid under medication with awareness and recall).

Pain and consciousness are processed at higher cortical levels (**Figure 2**). Fifty percent of patients experiencing awareness with recall under anesthesia had no HR or BP changes with which to alert their anesthesiologist [1]. Preventing anesthesia awareness is the *least* important value of direct brain monitoring. No deaths have yet been reported from anesthesia awareness. However, one American overmedication death occurs daily! [2]. **Preventing over medication** is the major value of direct brain monitoring (**Figure 3**).

Complex mathematical modeling, i.e. pharmacodynamics (PD) and pharmacokinetics (PK), is based on body weight that may not accurately reflect individual cortical sensitivities. While currently unavailable in the US, target controlled infusion (TCI) only infers cortical response based on blood drug concentrations, again with possible error.

With the Federal Drug Administration (FDA) 1996 approval of the bispectral index™ (BIS) brain monitor, the promise of *direct measurement* of cortical hypnotic response to anesthetic drugs was made available to the anesthesia community. Competing cortical monitors have been introduced since 1996, but the BIS monitor remains the most well-validated brain monitor on the market to date.

Anesthesia may be defined as the sum of hypnosis plus analgesia (**Figure 4**). Implicit in "hypnosis" is amnesia for surgery and within "analgesia" is sufficient muscle relaxation to imbricate the rectus abdominis sheath for classical abdominoplasty. Measured hypnosis enables differentiation of cortical- versus spinal cord–originated patient movement. As opposed to cortically originating patient movement, spinal cord–originated patient movement is devoid of awareness with recall concerns. Knowledge of the origin of patient movement facilitates origin-appropriate treatment of patient movement, thus assuring adequate local anesthesia during sedation (**Table 1**).

As an index, the BIS scale is from 0 to 100. The lower the number, the deeper the level of hypnosis (**Table 2**). Although validated in over 3500 published papers, the promise of direct

**Figure 2.** Cortex and brain stem.

simulates GA conditions (nonverbal, predominantly immobile patients) while *trespassing the least* on patient physiology, satisfying both patient and surgeon desires. "Goldilocks" anesthesia is **numerically reproducible**. "Goldilocks" anesthesia embodies Friedberg's triad; i.e.

*When you can MEASURE what you are speaking about, and express it in NUMBERS, you know something about it; but when you cannot measure it, when you cannot express it in numbers, your knowledge is of a meager and unsatisfactory kind; it may be the beginning of knowledge, but you have* 

What was true for temperature measurement more than a century ago is also true for the direct measurement of patient's cortical response to anesthetics. Without such measurement, there can be no science. Without science, there can be no reproducibility across the broad, and often unpredictable yet well-recognized, spectrum of individual patient response to

Brain weight does not vary with body weight (i.e. the brain weight of a 100-kg male is **NOT** twice that of a 50-kg female). Traditional anesthetic dosing based on body weight does not account for individual sensitivities to medications and is, therefore, frequently in error.

Further adding to the possibility of dosing error is the twentieth century practice of relying on heart rate (HR) and blood pressure (BP) changes to ascertain cortical drug response. **HR and BP changes primarily reflect brain stem response but are unreliable to accurately determine cortical response.** Prior to the ability to measure cortical response, the knowledge gap between brain stem and cortical response led to routine overmedication (to avoid under

*William Thompson, knighted Lord Kelvin Popular lectures and addresses 1891–1894.*

Measure the brain, Preempt the pain, Emetic drugs abstain (**Figure 1**).

**2. Direct cerebral cortical (brain) monitoring**

*scarcely, in your thoughts, advanced to the stage of SCIENCE.*

medications.

**Figure 1.** Friedberg's triad.

36 Anesthesia Topics for Plastic and Reconstructive Surgery

medication with awareness and recall).

**Figure 3.** Hypnosis + analgesia = anesthesia.

brain monitoring has remained unrealized for several reasons. First, the BIS only measures response to hypnotic, not analgesic, drugs primarily acting of the cerebral cortex like propofol and inhalation agents like isoflurane, sevoflurane and desflurane. Drugs that act at lower brain centers are benzodiazepines (i.e. diazepam and midazolam), opioids (i.e. morphine, meperidine, hydromorphone, fentanyl, sufentanil, alfentanil, remifentanil), and N<sup>2</sup> O. One cannot depend on reliable BIS cortical measurement from subcortically acting agents.

Second, the original factory default setting included only the BIS value and horizontally displayed BIS trend. BIS values are calculated by an algorithm that delays data by 15–30 s from real time. This delay puts the anesthesiologist in the unfavorable position of catching up to dynamically changing patient hypnotic requirements as opposed to having real-time information with which to formulate a response ahead of patient movement. BIS without EMG is *not useful* and is akin to trying to drive a car with only the rearview mirror information.

The electromyogram (EMG) is the electrical activity of the *frontalis* muscle between the eyebrows. This EMG is as real time and as instantaneous a signal as that of the EKG of the cardiac muscle. Unfortunately, the EMG was originally perceived as a "contaminant" of the BIS signal and not understood as a useful piece of information. *Prompt attention* to EMG spikes during sedation by increasing sedation to return the activity to baseline precludes "contamination" of the BIS value. Trending EMG spike activity enables the anesthesiologist to proactively respond to rapidly changing patient needs, providing a stable level of hypnosis throughout a case. BIS **with** EMG trending is very useful and is akin to driving a car looking through the forward-facing windshield.

Anesthesiologists process information most consistently on the horizontal sweep as displayed

vertical column. Contained in the software of every free-standing BIS unit is the option to select EMG and save it to trend below the BIS trend on a horizontal sweep display. As of 2017, the factory default setting now displays both BIS and EMG trends. However, the lower EMG

There are two vertical numerical scales on either side of the BIS monitor display (**Figure 5**). The left side scale (yellow) for the BIS is from 0 to 100. The right side scale (red) is from 30 to

trend as pictured by the recent company literature is without important EMG spikes.

trends. EMG is displayed on the original factory default, but only as a

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in the EKG and SpO<sup>2</sup>

**Figure 4.** The value proposition of direct cortical monitoring.

98–100 Awake

**Table 1.** BIS values and hypnotic sedation/anesthesia levels.

78–82 Minimal sedation 70–80 Moderate sedation 60–70 Deep sedation 45–60 + systemic analgesia General anesthesia <45 **OVERMEDICATED**

**BIS values Hypnotic sedation/anesthesia levels**

brain monitoring has remained unrealized for several reasons. First, the BIS only measures response to hypnotic, not analgesic, drugs primarily acting of the cerebral cortex like propofol and inhalation agents like isoflurane, sevoflurane and desflurane. Drugs that act at lower brain centers are benzodiazepines (i.e. diazepam and midazolam), opioids (i.e. morphine,

Second, the original factory default setting included only the BIS value and horizontally displayed BIS trend. BIS values are calculated by an algorithm that delays data by 15–30 s from real time. This delay puts the anesthesiologist in the unfavorable position of catching up to dynamically changing patient hypnotic requirements as opposed to having real-time information with which to formulate a response ahead of patient movement. BIS without EMG is *not useful* and is akin to trying to drive a car with only the rearview mirror information.

The electromyogram (EMG) is the electrical activity of the *frontalis* muscle between the eyebrows. This EMG is as real time and as instantaneous a signal as that of the EKG of the cardiac muscle. Unfortunately, the EMG was originally perceived as a "contaminant" of the BIS signal and not understood as a useful piece of information. *Prompt attention* to EMG spikes during sedation by increasing sedation to return the activity to baseline precludes "contamination" of the BIS value. Trending EMG spike activity enables the anesthesiologist to proactively respond to rapidly changing patient needs, providing a stable level of hypnosis throughout a case. BIS **with** EMG trending is very useful and is akin to driving a car looking through the

forward-facing windshield.

**Figure 3.** Hypnosis + analgesia = anesthesia.

38 Anesthesia Topics for Plastic and Reconstructive Surgery

O. One

meperidine, hydromorphone, fentanyl, sufentanil, alfentanil, remifentanil), and N<sup>2</sup>

cannot depend on reliable BIS cortical measurement from subcortically acting agents.

**Figure 4.** The value proposition of direct cortical monitoring.


**Table 1.** BIS values and hypnotic sedation/anesthesia levels.

Anesthesiologists process information most consistently on the horizontal sweep as displayed in the EKG and SpO<sup>2</sup> trends. EMG is displayed on the original factory default, but only as a vertical column. Contained in the software of every free-standing BIS unit is the option to select EMG and save it to trend below the BIS trend on a horizontal sweep display. As of 2017, the factory default setting now displays both BIS and EMG trends. However, the lower EMG trend as pictured by the recent company literature is without important EMG spikes.

There are two vertical numerical scales on either side of the BIS monitor display (**Figure 5**). The left side scale (yellow) for the BIS is from 0 to 100. The right side scale (red) is from 30 to Propofol titrated to 60 < BIS < 75 with baseline EMG indicated an asleep, amnestic patient.

A blanched surgical field does not equal adequate local analgesia.

Surgery below the clavicles with patient movement without EMG activity indicates more local analgesia in the immediate area of stimulation.

Once sedated, the brain cannot differentiate the signal from a well-intentioned surgeon's scalpel (or trocar) and the malevolent intentions of a mugger's knife. Success with preemptive analgesia makes it imperative to prevent the brain from receiving the noxious input from the violation of the integument's barrier to the outside world of danger. Although other pain receptors exist within the body, the most significant information to prevent the wind-up phe-

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The N-methyl, D-aspartate (NMDA) receptors in the midbrain are the final gatekeepers of noxious input to the cortex. Ketamine is a major NMDA antagonist (propofol has substantially less NMDA antagonism than ketamine). When the initial local anesthetic injection is performed (common to virtually all elective cosmetic surgeries), the **absence of an EMG spike** with multiple local anesthetic injections defines midbrain NMDA receptor saturation

Absent the ability to differentiate cortical- from spinal cord–originating movement during sedation forced anesthesiologists to treat every patient movement "as if" the patient might be awake and recall his or her surgery. All patient movement does not have the same significance. Like GA, "Goldilocks" anesthesia requires patients to be retrained on the operating table. Patient movement per se can be generated without cortical input, i.e. from spinal cord

No spinal cord pathways exist to activate the facial *frontalis* muscle. During the case, patient movement without an EMG spike is an indication for additional local anesthesia in the immediate area of surgical stimulation. Only after two attempts of reinjection after the initial injection (three total injections) fails to eliminate patient movement should additional ketamine be given. Conversely, if patient movement is accompanied by an EMG spike, both additional local anesthesia **and** additional propofol should be administered. Additional local anesthetics should cause the patient movement to cease in the overwhelming majority of cases. Additional propofol must be administered in sufficient amounts to **return the EMG to base-**

It is not the absolute value (or spike) of any individual BIS reading that may determine recall. Rather, it is the area under the trend curve. Three to five minutes of a BIS >80 will more likely produce recall than less area under the curve. Restraint from the surgeon or operating room staff making loud, negative comments with patient movement deprives the unconscious patient subliminal input with which to process memories. One cannot control the emotional maturity of the personnel in the operating room. Many times, demonstrating to both the surgeon and his staff of an objective numerical measure of the patient's level of consciousness (i.e. BIS < 75 with baseline EMG) can calm otherwise overanxious personalities and preserve

The use of EMG spike activity enables the differentiation between cortically generated patient movement and that originating from the spinal cord. Conducting a cosmetic surgery case in this fashion assures the patient receives critical adequate local anesthesia for the case and sets

nomenon and postoperative pain is that of skin incision.

and creates nonopioid, preemptive analgesia.

reflexes. A headless chicken still generates movement.

**line** to maintain the patient unconscious and amnestic.

the stage for minimal postoperative pain management.

a peaceful operating room.

**Table 2.** The surgeon's golden rules for success with brain monitored propofol ketamine.

100 for the EMG. Spikes in EMG signify incipient patient arousal demanding an increase in propofol (or inhalational agent) sufficient to return the EMG to baseline (i.e. 0 on the top BIS scale and 30 on the bottom EMG scale). (**Figure 6**).

In the pre-BIS era, anesthesiologists considered the absence of HR and BP changes with skin incision to define adequate depth of anesthesia. Nondissociative attempts at preemptive anesthesia have met with variable successes. Postoperative pain management continues to be an issue. HR and BP primarily reflect brain stem changes, while pain and consciousness are processed at higher cortical levels. Twenty-first century standard of care anesthesia monitoring demands cortical monitoring as a standard of care. It is an untenable assertion that 16 million of the 40 million (40%) American patients every year emerge from anesthesia with "brain fog" caused by a previously undiagnosed, underlying condition. Without numerically measuring the depth of sedation/anesthesia, discovering the role of routine overmedication in postoperative "brain fog" will be problematic [3].

**Figure 5.** BIS VISTA monitor.

Once sedated, the brain cannot differentiate the signal from a well-intentioned surgeon's scalpel (or trocar) and the malevolent intentions of a mugger's knife. Success with preemptive analgesia makes it imperative to prevent the brain from receiving the noxious input from the violation of the integument's barrier to the outside world of danger. Although other pain receptors exist within the body, the most significant information to prevent the wind-up phenomenon and postoperative pain is that of skin incision.

The N-methyl, D-aspartate (NMDA) receptors in the midbrain are the final gatekeepers of noxious input to the cortex. Ketamine is a major NMDA antagonist (propofol has substantially less NMDA antagonism than ketamine). When the initial local anesthetic injection is performed (common to virtually all elective cosmetic surgeries), the **absence of an EMG spike** with multiple local anesthetic injections defines midbrain NMDA receptor saturation and creates nonopioid, preemptive analgesia.

100 for the EMG. Spikes in EMG signify incipient patient arousal demanding an increase in propofol (or inhalational agent) sufficient to return the EMG to baseline (i.e. 0 on the top BIS

Surgery below the clavicles with patient movement without EMG activity indicates more local analgesia in the

In the pre-BIS era, anesthesiologists considered the absence of HR and BP changes with skin incision to define adequate depth of anesthesia. Nondissociative attempts at preemptive anesthesia have met with variable successes. Postoperative pain management continues to be an issue. HR and BP primarily reflect brain stem changes, while pain and consciousness are processed at higher cortical levels. Twenty-first century standard of care anesthesia monitoring demands cortical monitoring as a standard of care. It is an untenable assertion that 16 million of the 40 million (40%) American patients every year emerge from anesthesia with "brain fog" caused by a previously undiagnosed, underlying condition. Without numerically measuring the depth of sedation/anesthesia, discovering the role of routine overmedication in postopera-

scale and 30 on the bottom EMG scale). (**Figure 6**).

A blanched surgical field does not equal adequate local analgesia.

40 Anesthesia Topics for Plastic and Reconstructive Surgery

immediate area of stimulation.

Propofol titrated to 60 < BIS < 75 with baseline EMG indicated an asleep, amnestic patient.

**Table 2.** The surgeon's golden rules for success with brain monitored propofol ketamine.

tive "brain fog" will be problematic [3].

**Figure 5.** BIS VISTA monitor.

Absent the ability to differentiate cortical- from spinal cord–originating movement during sedation forced anesthesiologists to treat every patient movement "as if" the patient might be awake and recall his or her surgery. All patient movement does not have the same significance. Like GA, "Goldilocks" anesthesia requires patients to be retrained on the operating table. Patient movement per se can be generated without cortical input, i.e. from spinal cord reflexes. A headless chicken still generates movement.

No spinal cord pathways exist to activate the facial *frontalis* muscle. During the case, patient movement without an EMG spike is an indication for additional local anesthesia in the immediate area of surgical stimulation. Only after two attempts of reinjection after the initial injection (three total injections) fails to eliminate patient movement should additional ketamine be given. Conversely, if patient movement is accompanied by an EMG spike, both additional local anesthesia **and** additional propofol should be administered. Additional local anesthetics should cause the patient movement to cease in the overwhelming majority of cases. Additional propofol must be administered in sufficient amounts to **return the EMG to baseline** to maintain the patient unconscious and amnestic.

It is not the absolute value (or spike) of any individual BIS reading that may determine recall. Rather, it is the area under the trend curve. Three to five minutes of a BIS >80 will more likely produce recall than less area under the curve. Restraint from the surgeon or operating room staff making loud, negative comments with patient movement deprives the unconscious patient subliminal input with which to process memories. One cannot control the emotional maturity of the personnel in the operating room. Many times, demonstrating to both the surgeon and his staff of an objective numerical measure of the patient's level of consciousness (i.e. BIS < 75 with baseline EMG) can calm otherwise overanxious personalities and preserve a peaceful operating room.

The use of EMG spike activity enables the differentiation between cortically generated patient movement and that originating from the spinal cord. Conducting a cosmetic surgery case in this fashion assures the patient receives critical adequate local anesthesia for the case and sets the stage for minimal postoperative pain management.

Prior to BIS/EMG monitoring, treating all movement left many patients overmedicated and unable to quickly emerge from anesthesia to go home or to a recovery center. Patient movement during sedation was generally regarded by the surgeon that the patient was "too light" and needed more sedation. Anesthesiologists often responded to the surgeon's demand with "needs more local." A circular argument ensued, physicians' feelings got bruised, but more importantly, the patient was ill-served, overmedicated, and often, with postoperative pain management issues. The net effect of pre-BIS/EMG sedation attempts resulted in many surgeons encouraging (or even demanding) the abandonment of sedation in preference to GA with neuromuscular blocking agents. GA exposes the elective cosmetic surgery patient to the unnecessary risks of difficult intubation, failed intubation, misplaced endotracheal tube (ET), esophageal or endobronchial intubation, kinked or occluded ET, teeth damage, anesthesia machine mishaps (i.e. empty vaporizer, vaporizer filling error, reversed oxygen and nitrous oxide gases) and, very rarely, malignant hyperthermia (MH). No endotracheal intubations were required in the

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The advent of the use of the laryngeal mask airway (LMA) has greatly reduced or eliminated many ET issues. This author routinely places an armored (or flexible) LMA for rhinoplasty cases both to cover the glottic chink and using the inflatable cuff to prevent blood from entering the esophagus. For nonrhinoplasty cases, airway management is dependent upon patient

The very small MH risk necessitates any GA facility stocking dantrolene, an expensive agent with a 3-year shelf life. Delays in treating MH are prompt recognition due to its rare occurrence and partly due to the difficulty of dissolving the treatment into solution to administer. A newer formulation of dantrolene (i.e. Ryanodex®) is easier to dissolve into solution for

Neither propofol nor ketamine is a triggering agent for MH. The early diagnosis of MH is most often made by unexplained tachycardia. Tachycardia is frequently observed following the injection of epinephrine containing local anesthesia at the beginning of the case. When the injection is temporally associated with the dissociative ketamine dose, some are more apt to believe the ketamine, not the epinephrine, was the source of the tachycardia. Often, in the performance of "Goldilocks" anesthesia, incremental propofol induction followed the ketamine, but the surgeon did not inject the local analgesia by as along as 10 minutes after the

Chin extended, head rotated to the side (initially to the right but sometimes better airway results turning to the left). IV bag (not heated) under the shoulders (not the neck), increasing the force of extension on the genioglossus muscle.

N.B. 50–60% of brain monitored PK cases/25 years have been performed without airway instrumentation. No

#28 Fr latex (or latex free) lubricated nasal airway, often better tolerated than oral airways.

**Table 3.** Airway management flow chart (assumes incremental propofol induction).

author's 25-year experience.

administration but may not be widely found.

endotracheal intubations required in 25 years, >6000 patients.

response (**Table 3**).

#4 LMA.

**Figure 6.** Why BIS is not commonly utilized.

Over the past two decades of experience in >4000 patients, the infrequent postoperative discomfort was readily managed with intravenous (IV) ketorolac 30–60 mg and/or oral acetaminophen 1000 mg. Rapid propofol emergence allowed patients who did request additional analgesia to safely swallow oral acetaminophen without aspiration risk. Higher acetaminophen blood levels are unquestionably achieved with the IV versus the oral preparation. However, since adequate pain relief was observed with the oral form, cost considerations precluded the use of IV acetaminophen. Very few patients required IV fentanyl (25–100 mcg) for pain management. The author's experience was entirely in the office-based setting. There were no postoperative hospitalizations for postoperative pain management during the period 1992–2017 in >6000 patients.

Prior to BIS/EMG monitoring, treating all movement left many patients overmedicated and unable to quickly emerge from anesthesia to go home or to a recovery center. Patient movement during sedation was generally regarded by the surgeon that the patient was "too light" and needed more sedation. Anesthesiologists often responded to the surgeon's demand with "needs more local." A circular argument ensued, physicians' feelings got bruised, but more importantly, the patient was ill-served, overmedicated, and often, with postoperative pain management issues.

The net effect of pre-BIS/EMG sedation attempts resulted in many surgeons encouraging (or even demanding) the abandonment of sedation in preference to GA with neuromuscular blocking agents. GA exposes the elective cosmetic surgery patient to the unnecessary risks of difficult intubation, failed intubation, misplaced endotracheal tube (ET), esophageal or endobronchial intubation, kinked or occluded ET, teeth damage, anesthesia machine mishaps (i.e. empty vaporizer, vaporizer filling error, reversed oxygen and nitrous oxide gases) and, very rarely, malignant hyperthermia (MH). No endotracheal intubations were required in the author's 25-year experience.

The advent of the use of the laryngeal mask airway (LMA) has greatly reduced or eliminated many ET issues. This author routinely places an armored (or flexible) LMA for rhinoplasty cases both to cover the glottic chink and using the inflatable cuff to prevent blood from entering the esophagus. For nonrhinoplasty cases, airway management is dependent upon patient response (**Table 3**).

The very small MH risk necessitates any GA facility stocking dantrolene, an expensive agent with a 3-year shelf life. Delays in treating MH are prompt recognition due to its rare occurrence and partly due to the difficulty of dissolving the treatment into solution to administer. A newer formulation of dantrolene (i.e. Ryanodex®) is easier to dissolve into solution for administration but may not be widely found.

Neither propofol nor ketamine is a triggering agent for MH. The early diagnosis of MH is most often made by unexplained tachycardia. Tachycardia is frequently observed following the injection of epinephrine containing local anesthesia at the beginning of the case. When the injection is temporally associated with the dissociative ketamine dose, some are more apt to believe the ketamine, not the epinephrine, was the source of the tachycardia. Often, in the performance of "Goldilocks" anesthesia, incremental propofol induction followed the ketamine, but the surgeon did not inject the local analgesia by as along as 10 minutes after the

IV bag (not heated) under the shoulders (not the neck), increasing the force of extension on the genioglossus muscle.

#28 Fr latex (or latex free) lubricated nasal airway, often better tolerated than oral airways.

#4 LMA.

Over the past two decades of experience in >4000 patients, the infrequent postoperative discomfort was readily managed with intravenous (IV) ketorolac 30–60 mg and/or oral acetaminophen 1000 mg. Rapid propofol emergence allowed patients who did request additional analgesia to safely swallow oral acetaminophen without aspiration risk. Higher acetaminophen blood levels are unquestionably achieved with the IV versus the oral preparation. However, since adequate pain relief was observed with the oral form, cost considerations precluded the use of IV acetaminophen. Very few patients required IV fentanyl (25–100 mcg) for pain management. The author's experience was entirely in the office-based setting. There were no postoperative hospitalizations for postoperative pain management during the period

1992–2017 in >6000 patients.

**Figure 6.** Why BIS is not commonly utilized.

42 Anesthesia Topics for Plastic and Reconstructive Surgery

N.B. 50–60% of brain monitored PK cases/25 years have been performed without airway instrumentation. No endotracheal intubations required in 25 years, >6000 patients.

**Table 3.** Airway management flow chart (assumes incremental propofol induction).

Chin extended, head rotated to the side (initially to the right but sometimes better airway results turning to the left).

ketamine administration. No tachycardia or hypertension was observed when ketamine was administered well prior to the lidocaine with epinephrine solution injection. Nontriggering "Goldilocks'" anesthesia also means surgical facilities need not stock dantrolene.

way to administer it, especially for 4–6 hours rhytidectomies with or without browlifts, platysmal plications or blepharoplasties. Five years of data on 1264 patients demonstrated no reduction in propofol requirements with either 2 or 4 mg preoperative midazolam as admin-

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This same paper [6] also published the lowest postoperative nausea and vomiting (PONV) rate (0.6%) in the literature without antiemetic use in an Apfel-defined high-risk patient population, i.e. nonsmoking females with positive PONV and/or motion sickness histories, having emetogenic (cosmetic) surgery. Scrupulous opioid avoidance both during and after surgery

Aspect Medical Systems (Aspect Medical Systems, a venture capital company, was purchased by Medtronic that has subsequently been acquired by Covidien) exhibited their bispectral index monitor™ (BIS) for measuring cortical effect at the 1997 International Anesthesia Research Society (IARS) annual meeting in San Francisco. The author was exhibiting his Society for Office Anesthesiologists (SOFA) at the same meeting and was initially exposed to the BIS monitor there. The BIS monitor appeared to offer more promise reducing propofol requirements than previous efforts with midazolam premedication [6]. Later work validated that promise [7, 8]. Entropy™ is another depth of anesthesia monitor but has not been vali-

In the 1950s, postoperative pain was treated with morphine or meperidine, often undertreated for two reasons: (a) fear of producing opioid addiction and (b) problems of overtreatment, respiratory insufficiency or apnea and death. Naloxone was not introduced until 1971 and

The researchers of the day postulated that, if another class of drugs could be developed that would ameliorate pain without respiratory depression, patients could be better treated for

The first class of drugs explored was the phencyclidines. The parent compound, phencyclidine phosphate, was marketed as Serenyl® by Parke-Davis in 1958 but was quickly withdrawn from the market because of the high percentage of undesirable side effects, i.e. hallucinations, mania, delirium and disorientation. Later, phencyclidine phosphate, as a drug of abuse,

The researchers did not give up quickly on the phencyclidine class. They began experimenting with a modified PCP molecule, ketamine, which received FDA approval in humans in 1971. The drug, like its predecessor, was introduced as the "silver bullet," a complete, total intravenous agent, meaning no other agents were needed. Because it supported both respiration and blood pressure, ketamine quickly gained a reputation as a safe drug but one not good for adult patients. It did become popular in children's burn units, especially for the extremely

has allowed this astounding PONV rate to go unchallenged to date.

dated in nearly as many clinical papers as BIS [9].

pulse oximetry became commercially available in 1983.

postoperative pain with neither under- nor overtreatment.

became better known by the initials, PCP or "angel dust."

istered [6].

**4. Ketamine**

painful dressing changes.
