The original factory default setting of the BIS only included the BIS trend on the screen. Since the BIS value displayed is delayed by 15–30 seconds resulting in the need to “catch up” to patient need for increased hypnosis and/or analgesia. Without a BIS/EMG monitor, differentiating cortically generated movement (suggesting awareness or recall) from spinal cord generated movement (devoid of either awareness or recall issues) was very frustrating, and because of its perceived lack of utility, most anesthesiologists abandoned the device.
The frontalis muscle EMG is a directly measured, not algorithm derived, physiologic parameter that is a real-time signal akin that of the EKG of cardiac muscle. Trending EMG transforms the BIS device into a real-time, very useful monitor for 2 specific reasons (Fig. 3).
First, by responding to EMG spikes (as if they were HR or BP changes), the anesthesiologist stays ahead of patient need and avoids the need to catch up. (One tends to observe far fewer HR or BP changes when conducting anesthesia this way, perhaps giving greater credence to the notion that vital signs are indeed a brain stem effect but consciousness, memory, and pain processing occur at higher, cortical levels).
Second, EMG spikes persist, even with Botox or neuromuscular block (NMB). EMG spikes signal incipient arousal and the need to proactively increase sedation to return the EMG to baseline with additional propofol while avoiding the loss of spontaneous ventilation.10 To display the EMG, use the existing software to select and save it as the secondary trend.
Most patients achieve propofol sedation enough to prevent awareness and recall at 60 < BIS < 75 (with baseline EMG) level of with 25–50 micrograms/kg/min. Over 18 years’ experience titrating propofol with BIS/EMG, variation of as little as 2.5 micrograms/kg/min and as much as 200 micrograms/kg/min has been observed to achieve the same 60 < BIS < 75 (with baseline EMG) with amnesia and sedation. “Apples” to “apples” comparisons between patients, despite the nearly hundred-fold observed variation in propofol requirements to achieve, become more meaningful when using numerically based definitions of similar levels of consciousness achieved.10 When propofol is measured with BIS/EMG, amnesia was observed, avoiding midazolam premedication.
Postoperative brain fog likely is a multi-factorial problem. Until universal BIS/EMG monitoring becomes a standard of care, it may not be possible to clarify the degree routine over-medication plays.11 It may be beneficial for elderly patients to receive a statistically significant 30% less propofol than what is needed to achieve 60 < BIS < 75 with baseline EMG.12
Most people know it does no good to close the barn door after the horses have escaped. However, too many anesthesiologists still need to be convinced that it’s futile to try to prevent postoperative pain by allowing surgeons to cut without first blocking the midbrain N-methyl, D-aspartate (NMDA) receptors13,14 (Fig. 4).
Local anesthetic skin injection or incision is an extremely potent signal to the brain that the “world of danger” has invaded the “protected world of self.” The sedated brain cannot differentiate between the mugger’s knife and the surgeon’s scalpel (or trocar). Although there are certainly other internal pain receptors, no signal is more determinant of postoperative pain than of skin incision (or skin injection). An unprotected incision sets off the major cortical alarms that initiate the wind-up phenomenon.
Surgery is a painful experience. Most anesthesiologists believe a cardinal function is the prevention of pain during surgery. From 1975 through 1993, this author had never once considered why there was a need for postoperative opioid rescue for many, if not most, patients.
In 1992, a clinical trial began using 50 mg IV ketamine, 2–3 minutes before stimulation AFTER propofol hypnosis to dissociate patients for preincisional local anesthesia injection.15
When propofol is incrementally titrated, ketamine hallucinations are eliminated.16 For elective surgery, customary propofol increments are 50–100 micrograms/kg repeated either to loss of lid reflex/loss of verbal response or to 60 < BIS < 75 with baseline EMG. This BIS level is usually attained within 2–3 minutes. Starting with such an apparently homeopathic propofol dose quickly allows the anesthesiologist to quickly identify an extremely sensitive patient, avoid prolonged emergence, and, likely, less brain fog.
The benefit of incremental induction is creating a stable CNS level of propofol to protect from ketamine side effects, preservation of spontaneous ventilation, maintenance of SpO2, and not creating the difficult airway.17 Incremental propofol induction most commonly preserves the tone in the masseter, genioglossus, and orbicularis oris muscles, commonly maintaining a patent airway. Absent a propofol bolus induction, baseline BP is also maintained.
After observing the first 50 cases emerge without opioid rescue, it was reasonable to conclude the principle reason patients have pain after surgery is that they have had pain during surgery. The lack of opioid rescue continued over the next 1,214 patients18 and through to the present day of > 6,000 cosmetic surgery patients including very painful classical abdominoplasty and subpectoral breast augmentation. Skeptics may elect to discount a consistent, 25-year record of consistent clinical success without a level I randomized controlled trial to support this large, yet numerically reproducible anecdote. All this author respectfully asks is to try it.19 Dissociation, or immobility to noxious stimulation, appears to result from mid-brain NMDA blockade. Immobility (i.e., dissociation) to the stimulus of local anesthetic injection or incision has been consistently observed in 45 kg female patients and 114 kg male patients with the same 50 mg ketamine dose.
Why does the effective dissociative dose of ketamine not appear to be related to body weight? The adult brain weighs approximately 1.4–1.8 kg and does not vary with body weight. The midbrain is a very small part of the adult brain, and the NMDA receptors are a very small part of the midbrain. Prestimulation NMDA block denies the cortex the knowledge of the intrusion of the outside world of danger, avoiding the windup phenomenon.
What ortho-, neuro-, gynecologic surgery and cosmetic surgery have in common is the violation of the skin barrier. Violating the skin without an EMG spike response is empiric evidence of NMDA receptor saturation and preemptive analgesia. Once the brain protection is measured with BIS/EMG, there is very little downside and, considerable upside, to the nifty fifty.
Cognitive dissonance generated by the lack of or dramatically reduced opioid rescue with prestimulation ketamine dose is so great that many, if not most, anesthesiologists will need to observe 10–20 cases to believe them. However, the post anesthesia care unit nurses will notice more quickly and ask what is being done differently. Surgeons and patients’ family members will be as impressed as the recovery personnel. Once the patient is protected as described above, the nonopioid, 50 mg ketamine “miracle” is reproducible with propofol sedation, regional analgesia/propofol sedation, and general inhalational anesthesia.
POSTOPERATIVE NAUSEA AND VOMITING (PONV)
Much has been written about PONV. In 1996, Apfel et al.20 identified the 4 most predictive PONV factors, namely, nonsmoking, females, history of PONV, planned use of postoperative opioids. Apfel21,22 subsequently referenced Friedberg’s 1999 study18 in his PONV chapters.
PONV chapter by Apfel21 is 86 of 89 chapters in Millers’ Anesthesia. PONV is not lethal to patients, but they, especially abdominoplasty patients, may wish for lethality. Greater importance to PONV needs to be heeded by our profession as patient satisfaction now plays a role in government and other third party reimbursement.
The data for this 5-year review documenting a 0.6% PONV rate (i.e., 7 of 1,264 patients) were collected by 1997 but not published until 1999.19 These patients turned out to be an Apfel-defined high PONV risk patient population that received no antiemetics! No intraoperative opioids or inhalational (“stinky gases”) agent were used.23 Postoperative opioids were routinely prescribed but rarely used.
Analgesia was provided with adequate local analgesia.8 Assuring good local analgesia is facilitated with BIS/EMG monitoring to assure the surgeon the patient only needs more local, and not more hypnosis, to eliminate movement without concomitant EMG spike. Spontaneous ventilation was preserved using only a single respiratory depressant, propofol, and scrupulously avoiding intraoperative opioids. No patients received neuromuscular blocking medications although the use of NMB does not eliminate useful EMG spikes. Spontaneous ventilation allows the possibility of patient movement.
Patient movement under sedation in cosmetic or other surgery is usually the cause for great stress on all involved in the operating room, especially the surgeon who may have preoperatively injected the operative field with syringes of lidocaine and epinephrine. Observing vasoconstriction, the surgeon (but incorrectly) surmises adequate analgesia is present and clamors for more sedation (Table 2). The anesthesiologist usually responds with a request for additional analgesia. Tempers rise leading to the inappropriate addition of opioids, benzodiazepines, and so on, or worse the abandonment of sedation in favor of general anesthesia (GA) with NMBs. These added maneuvers may placate the surgeon but fail to treat the cause of the movement, inadequate analgesia.
The presence or absence of an EMG spike on the BIS monitor enables a dispassionate discussion of what the patient most accurately (and minimally) needs to return the patient to the desired motionless condition. In the pre-BIS era, all patient movement was treated lest it might signify be awareness and recall. As with the headless chicken, a brain is not necessary to generate movement.
No spinal reflex can stimulate the EMG of the forehead frontalis muscle. Patient movement without an EMG spike can only be generated by subcortical areas. The Surgeon’s Golden Rules needs the anesthesiologist’s time preoperatively with the surgeon to assure success without increasing the known risks of GA. This author believes it is very difficult to accept GA risks for patients having surgery without medical indication, that is, elective cosmetic surgery. A more enlightened approach is possible using the absence of the EMG spike with patient movement to refute the notion that the patient is “too light.”
Less is more. – Mies van Der Rohe
Without direct cortical measurement of anesthetic effect, neither reproducible science nor minimally trespassing on patients’ physiology will occur. Predictably, problems like over and under-medication, postoperative pain management, and PONV will continue to plague anesthesiologists and their patients while incurring avoidable costs.
Propofol measurement to 60 < BIS < 75 with baseline EMG provides amnesia and the perceived need of the commonly used 2 mg midazolam premedication. Eliminating midazolam also may eliminate prolonged emergence in sensitive and/or elderly patients.
Direct cortical response measurement enables anesthesiologists to treat patient requirements as the individuals they are as opposed to the 80% of patients in the middle of the bell curve. Doing so eliminates outliers, transforms every patients’ “mystery” into an “open book test,” and creates the basis for more humane, cost-effective anesthesia care.
Over 25 years and in more than 6,000 patients, there has not been a single hospital admission for brain fog, postoperative pain management, or PONV. Friedberg’s Triad appears to answer anesthesia’s persistent problems (Fig. 5).
1. Practice Advisory for Intraoperative Awareness and Brain Function Monitoring: a report by the American Society of Anesthesiologists Task Force on Intraoperative Awareness. Anesthesiology. 2006;104:847–864.
2. Li G, Warner M, Lang BH, et al. Epidemiology of anesthesia-related mortality in the United States, 1999-2005. Anesthesiology. 2009;110:759–765.
3. Monk TG, Weldon BC, Garvan CW, et al. Predictors of cognitive dysfunction after major noncardiac surgery. Anesthesiology. 2008;108:18–30.
4. Chan MT, Cheng BC, Lee TM, et al; CODA Trial Group. BIS-guided anesthesia decreases postoperative delirium and cognitive decline. J Neurosurg Anesthesiol. 2013;25:33–42.
5. Radtke FM, Franck M, Lendner J, et al. Monitoring depth of anaesthesia in a randomized trial decreases the rate of postoperative delirium but not postoperative cognitive dysfunction. Br J Anaesth. 2013;110:i98–105.
6. Friedberg BL. Hypnosis first, then dissociation. Anesth Analg. 2003;96:913–914; author reply 914.
7. Coulter FL, Hannam JA, Anderson BJ. Ketofol dosing simulations for procedural sedation. Pediatr Emerg Care. 2014;30:621–630.
8. Klein JA. Tumescent technique for regional anesthesia permits lidocaine doses of 35 mg/kg for liposuction. J Dermatol Surg Oncol. 1990;16:248–263.
9. McMasters JW. Friedberg BL. PK beyond cosmetic surgery: implications for military medicine and mass-casualty anesthesia. In: Anesthesia in Cosmetic Surgery. 2007:New York, N.Y.: Cambridge University Press; 68–71.
10. Friedberg BL. Friedberg BL. Propofol ketamine with bispectral (BIS) index monitoring chapter. In: Anesthesia in Cosmetic Surgery. 2007:New York, N.Y.: Cambridge University Press; 1–13.
12. Friedberg BL. The effect of a dissociative dose of ketamine on the bispectral index (BIS) during propofol hypnosis. J Clin Anesth. 1999;11:4–7.
13. Paquet M, Tremblay M, Soghomonian JJ, et al. AMPA and NMDA glutamate receptor subunits in midbrain dopaminergic neurons in the squirrel monkey: an immunohistochemical and in situ hybridization study. J Neurosci. 1997;17:1377–1396.
14. Friedberg BL. Friedberg BL. The dissociative effect and preemptive analgesia chapter. In: Anesthesia in Cosmetic Surgery. 2007:New York, N.Y.: Cambridge University Press; 39–46.
15. Friedberg BL. Propofol-ketamine technique. Aesthetic Plast Surg. 1993;17:297–300.
16. Friedberg BL. Hypnotic doses of propofol block ketamine-induced hallucinations. Plast Reconstr Surg. 1993;91:196–197.
17. Friedberg BL. The difficult airway in office-based anesthesia. Plast Reconstr Surg. 2010;125:221e–222e.
18. Friedberg BL. Propofol-ketamine technique: dissociative anesthesia for office surgery (a 5-year review of 1264 cases). Aesthetic Plast Surg. 1999;23:70–75.
19. Friedberg BL. One simple trick to preempt post-op pain. Outpatient Surgery Magazine. 2017;3:Paoli, Pa.: Herrin Publishing Partners LP; 16–17.
20. Apfel CC, Läärä E, Koivuranta M, et al. A simplified risk score for predicting postoperative nausea and vomiting: conclusions from cross-validations between two centers. Anesthesiology. 1999;91:693–700.
21. Apfel CC. Postoperative nausea and vomiting. In: Miller’s Anesthesia. 2010:7th ed. Philadelphia, Pa.: Elsevier; 2743.
22. Apfel CC. Postoperative nausea and vomiting. In: Miller’s Anesthesia. 2015:8th ed. Philadelphia, Pa.: Elsevier; 2961.
Copyright © 2017 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the American Society of Plastic Surgeons. All rights reserved.
23. Friedberg BL. Avoiding emetogenic triggers in the first place is more effective than using antiemetics. Anesth Analg. 2008;106:1921–1922; author reply 1922.