Moderate Sedation and Emergency Medicine for Periodontists 303035749X, 9783030357498

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Moderate Sedation and Emergency Medicine for Periodontists Joseph A. Giovannitti Jr.

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Moderate Sedation and Emergency Medicine for Periodontists

Joseph A. Giovannitti Jr.

Moderate Sedation and Emergency Medicine for Periodontists

Joseph A. Giovannitti Jr., DMD Dental Anesthesiology University of Pittsburgh Pittsburgh, PA USA

ISBN 978-3-030-35749-8    ISBN 978-3-030-35750-4 (eBook) https://doi.org/10.1007/978-3-030-35750-4 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Preface

The inspiration for this text began with an invitation to speak at the 104th Annual Meeting of the American Academy of Periodontology held in Vancouver, British Columbia, Canada, in 2018. The Commission on Dental Accreditation had recently mandated that periodontal training programs train their residents to competency in moderate sedation. As I began my outline, I could see that each segment of the talk resembled a distinct chapter, and the idea for a book was formed. This book is intended for periodontal residents and practicing periodontists who wish to incorporate the principles of moderate sedation into daily practice. A history of the development of sedation in dental practice sets the stage for understanding the need for a comprehensive preanesthetic evaluation to identify potentially reactive patients prior to treatment. Useful drugs for moderate sedation and reversal agents in the office setting are reviewed to ensure proper perioperative usage. Comprehensive airway management and rescue skills are documented in detail so that the patient may be properly managed in the event that the sedation progresses beyond the intended level. A key aim is to equip the reader with sufficient knowledge and preparedness to overcome the patient management challenges associated with common and uncommon deviations from intraoperative norms. Finally, for those academicians interested in teaching the principles of sedation to periodontal residents, a curriculum development tool is provided to ensure comprehensive training leading to competency. In a special way, this book is an homage to my teacher, mentor, and friend, Dr. C. Richard Bennett. His seminal text, Conscious-Sedation in Dental Practice, set forth the principles and philosophy of what we now call moderate sedation. These principles have stood the test of time, and I have done little to improve upon them. I also owe much to my friends and colleagues, Drs. James C.  Phero, William A. MacDonnell, and Morton B. Rosenberg. Their constant support and encouragement has empowered me. Finally, I am eternally grateful to my wife Christine, my greatest supporter and lifesaver in every way. Pittsburgh, PA

Joseph A. Giovannitti Jr., DMD

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Contents

1 Principles and the Development of Sedation in Dentistry������������������������  1 1.1 It All Began with Nitrous Oxide ����������������������������������������������������������  1 1.2 Intravenous Anesthesia ������������������������������������������������������������������������  3 References������������������������������������������������������������������������������������������������������  4 2 Sedation in Dental Practice ������������������������������������������������������������������������  5 2.1 Nature of Pain ��������������������������������������������������������������������������������������  6 2.2 Fear and Anxiety ����������������������������������������������������������������������������������  7 2.3 Spectrum of Pain Control����������������������������������������������������������������������  8 2.4 Cardiovascular Stress Response ����������������������������������������������������������  9 2.5 Objectives of Moderate Sedation ��������������������������������������������������������  9 2.6 Indications and Contraindications�������������������������������������������������������� 10 2.7 Definitions�������������������������������������������������������������������������������������������� 11 2.7.1 Minimal Sedation���������������������������������������������������������������������� 11 2.7.2 Minimal Sedation via the Enteral Route���������������������������������� 12 2.7.3 Moderate Sedation�������������������������������������������������������������������� 12 2.7.4 Deep Sedation �������������������������������������������������������������������������� 12 2.7.5 General Anesthesia������������������������������������������������������������������� 12 References������������������������������������������������������������������������������������������������������ 13 3 Preanesthetic Evaluation for Periodontal Sedation���������������������������������� 15 3.1 Components of a Preanesthetic Evaluation������������������������������������������ 16 3.2 Review of Systems�������������������������������������������������������������������������������� 18 3.2.1 Cardiovascular System�������������������������������������������������������������� 18 3.2.2 Respiratory System ������������������������������������������������������������������ 22 3.2.3 Diabetes Mellitus���������������������������������������������������������������������� 26 3.2.4 Neurological and Developmental Disorders ���������������������������� 29 References������������������������������������������������������������������������������������������������������ 34 4 Drugs Suitable for Moderate Periodontal Sedation���������������������������������� 35 4.1 Opioids�������������������������������������������������������������������������������������������������� 35 4.1.1 Adverse Effects ������������������������������������������������������������������������ 36 4.1.2 Tolerance and Opioid-Induced Hyperalgesia���������������������������� 37 4.1.3 Useful Opioids for Moderate Sedation ������������������������������������ 38

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4.2 Benzodiazepines ���������������������������������������������������������������������������������� 39 4.2.1 Precautions for Use ������������������������������������������������������������������ 40 4.2.2 Useful Benzodiazepines for Moderate Sedation���������������������� 40 4.3 Alpha-2 Adrenergic Receptor Agonists������������������������������������������������ 41 4.3.1 Dexmedetomidine �������������������������������������������������������������������� 42 4.4 Moderate Sedation Technique�������������������������������������������������������������� 42 References������������������������������������������������������������������������������������������������������ 44 5 Periodontal Airway Management Strategies�������������������������������������������� 45 5.1 Preoperative Airway Evaluation����������������������������������������������������������� 45 5.2 Airway Management���������������������������������������������������������������������������� 46 5.3 Difficult Mask Ventilation and Airway Considerations in Obesity �������������������������������������������������������������������� 51 5.4 Key Point to Remember������������������������������������������������������������������������ 51 References������������������������������������������������������������������������������������������������������ 52 6 Monitoring During Periodontal Sedation�������������������������������������������������� 53 6.1 Monitoring Consciousness�������������������������������������������������������������������� 54 6.2 Monitoring Respiratory Function �������������������������������������������������������� 55 6.2.1 Monitoring Oxygenation���������������������������������������������������������� 56 6.2.2 Monitoring Ventilation�������������������������������������������������������������� 58 6.3 Monitoring Circulation ������������������������������������������������������������������������ 60 Reference ������������������������������������������������������������������������������������������������������ 62 7 Emergency Medicine for Periodontists������������������������������������������������������ 63 7.1 Airway Complications�������������������������������������������������������������������������� 67 7.1.1 Obstruction�������������������������������������������������������������������������������� 67 7.1.2 Laryngospasm �������������������������������������������������������������������������� 67 7.1.3 Bronchospasm�������������������������������������������������������������������������� 69 7.1.4 Negative-Pressure Pulmonary Edema�������������������������������������� 70 7.1.5 Emesis/Aspiration �������������������������������������������������������������������� 70 7.2 Cardiovascular Complications�������������������������������������������������������������� 72 7.2.1 Hypertension ���������������������������������������������������������������������������� 72 7.2.2 Hypotension������������������������������������������������������������������������������ 73 7.2.3 Dysrhythmias���������������������������������������������������������������������������� 74 7.2.4 Acute Coronary Syndromes������������������������������������������������������ 75 7.2.5 Stroke���������������������������������������������������������������������������������������� 76 7.3 Miscellaneous Complications �������������������������������������������������������������� 77 7.3.1 Delayed Awakening and Readiness for Discharge�������������������� 77 7.3.2 Local Anesthetic Toxicity �������������������������������������������������������� 78 References������������������������������������������������������������������������������������������������������ 81 8 Curricular Development and Training Requirements for Periodontal Sedation������������������������������������������������������������������������������ 83 8.1 Moderate Sedation for Periodontal Residents�������������������������������������� 84 8.1.1 Course Syllabus������������������������������������������������������������������������ 84 References������������������������������������������������������������������������������������������������������ 86

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Principles and the Development of Sedation in Dentistry

A new era in tooth pulling! —Horace Wells

1.1

It All Began with Nitrous Oxide

In late eighteenth-century England pneumatic medicine was all the rage, treating a variety of diseases with the inhalation of various gases. Humphry Davy, a self-­ taught chemist and employee of the Pneumatic Institute in Oxford, began researching the properties of nitrous oxide which had been discovered by Joseph Priestley in 1792. Thus, in the year 1800, Davy published his findings in Researches, Chemical and Philosophical, Chiefly Concerning Nitrous Oxide, or Dephlogisticated Nitrous Air and Its Respiration. In this report he noted the exhilarating effects of the gas and suggested, “As nitrous oxide in its extensive operation appears capable of destroying physical pain, it may probably be used with advantage during surgical operations in which no great effusion of blood takes place” [1]. This statement was essentially ignored, and Davy went on to become one of England’s most prominent chemists and discoverers of many other chemical compounds. Nitrous oxide was relegated to use as a recreational drug, rising in popularity during the many “frolics” of the 1830s during which revelers engaged in various behaviors while under the influence of the gas. Fast-forward 40  years to the United States, where Gardner Quincy Colton, a medical school dropout and self-proclaimed “Professor,” began public demonstrations of nitrous oxide across New England purely for entertainment, and a fee. Horace Wells, a prominent Hartford, CT dentist, decided to attend one of these demonstrations on December 10, 1844. A handbill distributed by Colton told the tale:

© Springer Nature Switzerland AG 2020 J. A. Giovannitti Jr., Moderate Sedation and Emergency Medicine for Periodontists, https://doi.org/10.1007/978-3-030-35750-4_1

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1  Principles and the Development of Sedation in Dentistry A Grand Exhibition of the effects produced by inhaling Nitrous Oxide, Exhilarating or Laughing Gas! will be given at Union Hall, this (Tuesday) Evening, Dec. 10th, 1844. Forty Gallons of Gas will be prepared and administered to all in the audience who desire to inhale it. Twelve Young Men have volunteered to inhale the Gas, to commence the entertainment. The entertainment will close with a few of the most surprising Chemical Experiments. Entertainment to commence at 7 o’clock. Tickets 25 cents—for sale at the principal Bookstores and at the Door. Eight Strong Men are engaged to occupy the front seats, to protect those under the influence of the Gas from injuring themselves or others. This course is adopted that no apprehension of danger may be entertained. Probably no one will attempt to fight. The effect of the Gas is to make those who inhale it either Laugh, Sing, Dance, Speak, or Fight, and so forth, according to the leading trait of their character. They seem to retain consciousness enough not to say or do that which they would have occasion to regret. The Gas will be administered only to gentlemen of the first respectability. The object is to make the entertainment in every respect a genteel affair [2].

Wells and his wife were enjoying the festivities when one of the volunteers, Sam Cooley, took the gas and careened about the stage, suddenly spying someone in the audience that he decided had done him wrong. He leaped off the stage and began to chase the unfortunate victim around the hall. The audience was delighted and clapped loudly at the spectacle. During the chase, Cooley leapt over a bench, knocking it over. After the effects of the gas have dissipated, he came to his senses and sheepishly got back into his seat, which happened to be near Dr. Wells. Wells watched as he rolled up his pants leg, surprised to reveal an abraded and bloody leg. Immediately recognizing the potential of nitrous oxide to alleviate pain, Wells met Colton backstage after the show and asked him to come to his office the next day. Wells himself had a painful wisdom tooth and wondered if Colton would give him the nitrous oxide while he had his tooth extracted. Wells’ colleague, Dr. John Riggs, painlessly extracted the offending tooth while Wells was under the influence of nitrous oxide. Riggs later wrote: Wells and I had a … conference that night & determination to try the gas on Wells the next morning. Wells went to the Hall & asked Colton to let him have a bag of gas as he wanted to take it and have a tooth pulled--& he invited the party, Colton, Cooley, and two others to come up and witness the operation. I was attending to a patient but was awaiting Wells’ return. When I entered Wells’ office, the said parties were there. Wells took his seat in the operating chair. I examined the tooth so as to be ready to operate without delay. Wells took the bag in his lap-held the tube to his mouth & inhaled till insensibility relaxed the muscles of his arms -his hands fell on his breast-his head dropped on the head-rest & I instantly, passed the forceps into the mouth onto the tooth and extracted it. Mr. Colton, Cooley and the two there stood by the open door ready to run out if Wells jumped up from the chair & made any hostile demonstrations. You may ask-Why did he not get up? Simply because he could not. Our agreement, the night previous was, to push the administration to a point hitherto unknown. We knew not whether death or success confronted us. It was terra incognito we were bound to explore-the result is known to the world. No one but Wells and myself knew to what point the inhalation was to be carried-the result was painfully problematical to us but the great law of Nature, hitherto unknown, was kind to us & a grand discovery was born into the world [3].

When Wells recovered, he said that he hadn’t felt as much as a pinprick and proclaimed “a new era in tooth pulling!” making December 11, 1844, the day that the

1.2  Intravenous Anesthesia

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discovery of anesthesia was made. Nearly 2 years later, on October 16, 1846, Wells’ apprentice, William T.G. Morton, successfully introduced ether into medical practice. Thus, two dentists became responsible for discovering and bringing anesthesia into the world. Nitrous oxide was well suited for shorter operations, such as the extraction of teeth. A common technique was to administer 100% nitrous oxide by facemask until the patient became cyanotic and unconscious. The mask would be removed, and the teeth would be extracted as rapidly as possible. The stimulation of the surgery caused the patients to inhale room air and reoxygenate themselves until they recovered. Occasionally they did not, however, leading to the concomitant administration of oxygen along with the nitrous oxide. Thus, the best surgeons were the fastest surgeons.

1.2

Intravenous Anesthesia

The ultrashort-acting barbiturate, thiopental, was first administered by Dr. Ralph Waters in 1934. This led to the use of thiopental, and later methohexital, by dental surgeons Drummond-Jackson, Foreman, and Hubbell, for dental extractions. It was used in a similar manner as nitrous oxide; that is, a bolus dose of the drug was given intravenously until the patient became unconscious and the teeth were extracted rapidly as the patient recovered. Dr. Hubbell pioneered a crude pump device whereby he could readminister the drug incrementally when needed for longer cases or if the patient aroused prematurely. Along with local anesthetics, nitrous oxide, ether, and barbiturate anesthesia became the only available options for dental surgical procedures. Dentists recognized the need for longer acting sedatives that would enable them to perform dental procedures other than quick extractions. This led to two dentists, working independently, to develop intravenous sedative techniques that would permit the performance of longer dental procedures. Dr. Niels Jorgensen, in Loma Linda, CA, and Dr. Leonard Monheim, in Pittsburgh, PA, developed unique sedative techniques using a combination of opioids, psychosedatives, and barbiturates. These drugs were titrated incrementally until the patients were relaxed and cooperative, yet conscious. With patients in this state, dentists were able to accomplish procedures that took much longer than the extraction of teeth. Monheim’s successor, Dr. C. Richard Bennett, honed his technique by incorporating the new benzodiazepine, diazepam, into the treatment regimen. Bennett’s major contribution came with his seminal text, Conscious-Sedation in Dental Practice [4], in which he outlined the philosophy of what he termed “conscious-­ sedation.” He stated that maintenance of consciousness was the key to patient safety since patients in the conscious state are constantly capable of independently maintaining and protecting their own airway. Because of the inherent safety of conscious-­ sedation, it has become the backbone of sedation in dentistry in what has now become known as moderate sedation. Moderate sedation is the most common anesthetic modality practiced in dentistry by a variety of providers and is the level of sedation indicated for periodontal practice. It may be achieved by the administration of nitrous oxide and enteral and/or parenteral agents.

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1  Principles and the Development of Sedation in Dentistry

With the advent of newer and more potent agents such as remifentanil and propofol, deep sedation, such as that practiced by earlier pioneers, has enjoyed a resurgence. This level of sedation has a much-improved safety record due to advances in drug pharmacology, technology, and monitoring devices. However, it should only be attempted by those with advanced training in general anesthesia, and is beyond the scope of this text.

References 1. Davy H. Researches, chemical and philosophical, chiefly concerning nitrous oxide, or dephlogisticated nitrous air and its respiration. Bristol: Printed for J. Johnson, St. Paul’s Church-Yard, by Biggs and Cottle; 1800. 2. Archer WH.  Life and letters of Horace Wells Discoverer of Anesthesia. J Am Coll Dent. 1944;11:81–210. 3. Smith WDA. A history of nitrous oxide and oxygen anaesthesia. Part V: The crucial experiment, its eclipse, and its revival. Br J Anaesth. 1966;38:143–56. 4. Bennett CR. Conscious-sedation in dental practice. St. Louis, MO: CV Mosby; 1978.

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Sedation in Dental Practice

No one ever died in a conscious state. —Dr. Leonard M. Monheim

Moderate sedation is more than a technique to be learned, but rather is a philosophy of pain and anxiety control coupled with patient safety. The hallmark of moderate sedation is the continuous maintenance of consciousness while reducing or eliminating stress and anxiety. Conscious patients are capable of rational response to command and have all protective reflexes intact, including the ability to clear and maintain the airway in a patent state [1]. All aspects of consciousness must be maintained at all times to ensure patient safety. Loss of consciousness, even momentarily, can result in severe adverse consequences that must be avoided at all costs. The preservation of upper airway protective reflexes and the integrity of the cardiorespiratory system during moderate sedation are the key to safe practice. It is important to note that moderate sedation cannot be accomplished via a “cookbook” approach, but rather through individual titration of one or more drugs to a defined clinical endpoint. In addition to didactic training, significant clinical experience is required to achieve mastery of the technique. The American Dental Association has produced two documents, Guidelines for Teaching Pain Control and Sedation to Dentists and Dental Students [2] and Guidelines for the Use of Sedation and General Anesthesia by Dentists [3]. These documents outline curricular development and clinical requirements needed for comprehensive training and propose guidelines for the safe incorporation into practice.

© Springer Nature Switzerland AG 2020 J. A. Giovannitti Jr., Moderate Sedation and Emergency Medicine for Periodontists, https://doi.org/10.1007/978-3-030-35750-4_2

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2.1

2  Sedation in Dental Practice

Nature of Pain

Pain has been described as the bane of mankind’s existence, and we have been searching for methods to alleviate this curse since the dawn of man. However protective pain might be when a tissue insult occurs, it is not something to be desired in dental practice. In fact, pain or fear of pain is one of the primary reasons for dental avoidance. In the realm of periodontal practice, this may be exacerbated by procedures such as deep scaling and curettage, gingival grafting, and implant or flap surgery. An understanding of the nature of pain is fundamental to understanding the indications for, and the utility of, moderate sedation. Pain is perceived in a similar way by all individuals. When tissue injury occurs, mediators are released causing transmission of the stimulus to the central nervous system (CNS) via specific anatomic pathways where it is perceived as such. The interpretation of this signal differs in all individuals and is responsible for wide variations in pain response. Patients with a high pain threshold are said to have a low pain reaction, while patients with a low pain threshold may react violently to what others may perceive to be mild stimulation. This extreme variation in pain reaction among individuals highlights the need for a method to modulate these responses. Variations in pain reaction are due to a host of mitigating factors. Patients who are emotionally stressed due to underlying psychological issues or life stresses tend to have a heightened pain reaction. Likewise, patients who are fatigued due to overwork, stress, or chronic illness often have a lowered pain threshold. In general, older patients respond more stoically to adverse stimuli, whereas children or adolescents may exhibit an exaggerated response due to an overactive sympathetic nervous system response or lack of previous experience. Fear and anxiety, as well as adverse past experiences, play a major role in lowering the pain threshold. Patients with dental phobias are much more likely to experience unpleasantness in the dental setting due to an unreasonable perception of their surroundings. It is essential to identify the level of patient anxiety prior to attempting any type of periodontal treatment in order to ensure that proper measures of stress reduction are applied prior to treatment. This should always include nonpharmacological methods such as the establishment of rapport and gaining of the patient’s trust and confidence. Fear and anxiety constitute one of the most important indications for moderate sedation. The concomitant use of certain chronic medications may alter the pain reaction threshold. While opioid use in the short term could raise the pain threshold, chronic opioid usage may result in what is known as opioid-induced hyperalgesia. As opioid receptors become tolerant to the presence of opioid drugs, there is a compensatory release of proinflammatory cytokines that result in an increase in pronociceptive activity [4]. The result is a significant reduction in the patient’s pain threshold. While anxiolytics or antidepressant medications do not alter the pain threshold per se, they may help control the pain response through the reduction of fear and anxiety.

2.2  Fear and Anxiety

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One of the oldest and most common ways to alleviate pain is to remove the cause. For example, if a patient has a painful tooth abscess, the pain can easily be managed by extracting the offending tooth. More commonly, the dentist may block the pain pathway prior to the application of a noxious stimulus through the use of local anesthetics. The practitioner may choose to alter the pain reaction threshold by using moderate sedation to allay fear and anxiety. Alternatively, non-­pharmacological means may be used alone or in combination with moderate sedation to achieve a reduction in pain reaction. If these methods fail, general anesthesia may be used to completely prevent the pain response.

2.2

Fear and Anxiety

Anxiety has been described as worry gone out of control. It is an anticipatory, internalized emotional response resulting in an unpleasurable state of tension indicative of some impending danger. Fear is a short-lived physiologic response that occurs when the patient is finally confronted with the anticipated danger. This results in a sympathetic nervous system response that produces heightened awareness, shakiness, palpitations, hypertension, and tachycardia. This is known as the cardiovascular stress response which may have severe adverse consequences in susceptible patients. Certain fears are universal, in that everyone is susceptible (Fig. 2.1). Many, if not all, of these fears are magnified in the dental setting. These, coupled with fears specific to the practice of dentistry such as fear of the drill, needle and syringe, instruments, or just sitting in the waiting room, can make dental treatment anathema to many. While some patients may verbalize their fear, many will not. The dentist must be adept at recognizing the signs of fear and anxiety. Failure to make eye contact, stony silences, perspiration, body stiffness, tremors, chronic tardiness or failed appointments, and outstanding balances are all signs of fear and anxiety. As a pretreatment adjunct to moderate sedation, it is very important to actually quantify the patient’s anxiety level. The Modified Dental Anxiety Scale (Fig. 2.2) is a validated tool that has been shown to be invaluable in determining preoperative anxiety. Quantification aids in choosing the proper level of sedation required to meet the patients’ needs. Patients receiving 19 or more points on the scale are considered to have severe dental phobia. While moderate sedation may be effective in many of these individuals, some severe phobics may require general anesthesia for successful management.

Fig. 2.1  Universal fears

• Pain • The Unknown • Helplessness, dependency • Bodily change, mutilation • Death

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2  Sedation in Dental Practice • If you went to your dentist for TREATMENT TOMORROW, how would you feel? • Not anxious (1) Slightly anxious (2) Fairly anxious (3) Very anxious (4) Extremely anxious (5) • If you were sitting in the WAITING ROOM (waiting for treatment), how would you feel? • Not anxious (1) Slightly anxious (2) Fairly anxious (3) Very anxious (4) Extremely anxious (5) • If you were about to have a TOOTH DRILLED, how would you feel? • Not anxious (1) Slightly anxious (2) Fairly anxious (3) Very anxious (4) Extremely anxious (5) • If you were about to have your TEETH SCALED AND POLISHED, how would you feel? • Not anxious (1) Slightly anxious (2) Fairly anxious (3) Very anxious (4) Extremely anxious (5) • If you were about to have a LOCAL ANESTHETIC INJECTION in your gum, above an upper back tooth, how would you feel? • Not anxious (1) Slightly anxious (2) Fairly anxious (3) Very anxious (4) Extremely anxious (5) • TOTAL SCORE: 5–25

No anesthesia

latrosedation

Local anesthesia

Hypnosis

N2O-O2

Oral/ rectal

IV

Intramuscular/ intranasal

General anesthesia Inhalation general anesthesia Tracheal intubation

Conscious

General anesthesia

Fig. 2.2  Modified Dental Anxiety Scale. Quantifying Dental Anxiety. A score ≥19 indicates severe dental phobia

Unconscious

Fig. 2.3  Spectrum of pain control

2.3

Spectrum of Pain Control

It is obvious that patients present with varying degrees of anxiety, ranging from none to severe phobia. Quantification of preoperative anxiety enables customization of the anesthetic technique. This concept is known as the spectrum of pain control (Fig.  2.3). Anxiety-free individuals require nothing more than rapport, trust, and local anesthesia to accomplish treatment. Patients with mild-to-moderate levels of apprehension may require modalities such as nitrous oxide and/or enteral sedation to improve comfort. Moderate-to-severe levels of apprehension may require parenteral forms of sedation. Severe phobia may require deep sedation or general anesthesia. Anesthesia is thus a continuum, moving from the unmedicated to the unconscious. The ADA Guidelines recognize this continuum as a state of flux in

2.5  Objectives of Moderate Sedation Fig. 2.4 Cardiovascular stress response

9 • Catecholamine release • Increased cardiac output • Increased myocardial oxygen demand • Myocardial ischemia • Acute congestive heart failure • Cardiac dysrhythmias

which a patient may move unintentionally to a level of sedation beyond that which is desired. The Guidelines state, “Because sedation and general anesthesia are a continuum, it is not always possible to predict how an individual patient will respond. Hence, practitioners intending to produce a given level of sedation should be able to diagnose and manage the physiologic consequences (rescue) for patients whose level of sedation becomes deeper than initially intended” [2, 3].

2.4

Cardiovascular Stress Response (Fig. 2.4)

During stress the body initiates the fight or flight response by releasing substantial amounts of catecholamines from the adrenal medulla. Epinephrine and norepinephrine are vasoactive substances that activate alpha- and beta-receptors. This is manifested physiologically by increases in heart rate, blood pressure, cardiac output, and thus blood flow to skeletal muscle. These changes are necessary to evoke the appropriate fight or flight response. However, these changes are not protective when occurring in the dental setting. Rather stimulation of the cardiovascular system can be detrimental and even life threatening in patients with underlying cardiovascular disease. For example, tachycardia and hypertension may be well tolerated in healthy individuals, but may precipitate a profound medical emergency in affected patients. Increases in myocardial oxygen demand may result in myocardial ischemia, chest pain, myocardial infarction, significant cardiac dysrhythmias, or acute heart failure. Similarly, unchecked hypertension may result in heart failure or stroke. It goes without saying that tachycardia and hypertension are to be avoided in patients with underlying cardiovascular system impairments. Moderate levels of sedation are indicated for these patients because sedation will serve to attenuate the cardiovascular stress response and reduce the risk of these untoward events. Thus, increasing medical complexity constitutes a medical indication for the administration of moderate sedation.

2.5

Objectives of Moderate Sedation (Fig. 2.5)

Moderate sedation now becomes an integral part of periodontal practice because it serves many purposes to facilitate safe treatment. The patient’s mood is altered through the diminution or elimination of anxiety to the point where a previously objectionable event (periodontal treatment) now becomes acceptable. Consciousness is maintained. This is vital to the success and safety of moderate sedation. Conscious patients maintain all of their protective reflexes at all times. This ensures stability of

10

2  Sedation in Dental Practice

Fig. 2.5  Objectives of moderate sedation

• Mood alteration • • • • •

Fig. 2.6  Advantages of moderate sedation

• • • • •

Consciousness maintained Cooperation Stabilization of vital signs Pain threshold elevated Amnesia

Eliminates or diminishes fear and anxiety Altered time perception Reduced incidence of medical emergencies Effective time management Improved quality of dental care

vital functions and results in attenuation of the cardiovascular stress response. Since conscious patients respond rationally to verbal command, loss of this ability is the prime indicator that the patient has gone beyond the desired level of sedation and must be rescued. Mood alteration and maintenance of consciousness will result in a cooperative patient. Cooperation is a major objective of moderate sedation, since an uncooperative or fidgety patient precludes quality treatment. If a patient cannot cooperate when moderate sedation is applied, he or she may be a candidate for deep sedation or general anesthesia and should be reappointed. Finally, the pain threshold should be elevated, and amnesia is a desirable, although not required, outcome. The latter will aid in the patient’s overall positive perception of the event and help to reduce the need for sedation in the future. As one can see, moderate sedation offers many advantages to enhance productivity and promote safety in periodontal practice (Fig.  2.6). A high percentage of patients exhibit dental anxiety and many periodontal procedures have the potential to exacerbate these feelings. Alleviating these fears promotes patient comfort and cooperation and enables the practitioner to provide a higher quality of care. Additionally, sedation affords more effective time management and increases productivity by allowing more work to be accomplished during a single treatment cycle. Since some periodontal procedures are time consuming, patients may become uncomfortable in the dental chair over a long period of time. This has the potential to increase stress and promote the onset of pain and/or anxiety. Moderate sedation enables the patient to relax in a state in which there is no real perception of time passage, allowing he or she to undergo longer procedures without complaint. Finally, as previously discussed, moderate sedation attenuates the cardiovascular stress response and minimizes the chance of an untoward perioperative event.

2.6

Indications and Contraindications (Fig. 2.7)

A key to the efficacy of moderate sedation is the identification of those patients in whom sedation will have the greatest chance for success. Fear and anxiety constitute a major indication for moderate sedation. However, in patients presenting with severe dental phobia, extreme behavioral management issues, or severe intellectual

2.7 Definitions Indications

11 Contraindications

• Psychological considerations

• Severe physical/intellectual disability

• Medical history considerations

• Extreme behavioral management problem

• Procedural requirements

• Prior history of adverse experiences

• Special considerations

• Severe emotional handicap • Lack of proper facilities or trained personnel

Fig. 2.7  Indications and contraindications for moderate sedation

disability, the success of moderate sedation is significantly diminished. These patients require deep sedation or general anesthesia to accomplish treatment successfully. Stress reduction through moderate sedation should always be considered when managing patients with cardiovascular disease, reactive airway diseases, and diabetes in order to modulate and/or prevent perioperative emergent responses. The planned periodontal procedure itself may provide the indication for moderate sedation. Patients faced with the prospect of deep scaling or surgical procedures will welcome the opportunity to have sedation as an adjunct to their treatment. The periodontist should always consider the use of moderate sedation when planning these types of procedures. Special consideration should be given to the use of sedation when faced with patients with gagging problems, inability to achieve profound local anesthesia, pediatric patients, or when the procedure is known to be time consuming. Severe gagging is often psychogenically mediated and sedation can easily mitigate this response. In like manner, anxious patients may respond to stimuli as painful even in the presence of profound local anesthesia. Again, sedation will reduce anxiety and magically enhance the success of local anesthesia. Pediatric patients may be seen in periodontal practice when in need of gingival grafting. These patients often have short attention spans and may not provide the necessary cooperation needed for this type of surgery. Thus, moderate sedation is utilized in this setting. Finally, many periodontal procedures can require prolonged chair time, and sedation will enhance the patient’s ability to remain comfortable in the chair during these procedures.

2.7

Definitions

The ADA Guidelines provide precise definitions of every level of sedation and anesthesia, and outline the training requirements for each level. State dental boards use these definitions and training requirements to develop rules and regulations that govern the use of sedation and anesthesia and the issuance of permits. It behooves the periodontist to have an intimate knowledge of these definitions and their state regulations.

2.7.1 Minimal Sedation A minimally depressed level of consciousness, produced by a pharmacological method, retains the patient’s ability to independently and continuously maintain an airway and respond normally to tactile stimulation and verbal command. Although

12

2  Sedation in Dental Practice

cognitive function and coordination may be modestly impaired, ventilatory and cardiovascular functions are unaffected. Patients whose only response is reflex withdrawal from repeated painful stimuli would not be considered to be in a state of minimal sedation.

2.7.2 Minimal Sedation via the Enteral Route Minimal sedation may be achieved by the administration of a drug, either singly or in divided doses, by the enteral route to achieve the desired clinical effect, not to exceed the maximum recommended dose (MRD). The administration of enteral drugs exceeding the maximum recommended dose during a single appointment is considered to be moderate sedation and the moderate sedation guidelines apply. Nitrous oxide/oxygen when used in combination with sedative agent(s) may produce minimal, moderate, or deep sedation or general anesthesia. If more than one enteral drug is administered to achieve the desired sedation effect, with or without the concomitant use of nitrous oxide, the guidelines for moderate sedation must apply.

2.7.3 Moderate Sedation A drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained. In accord with this particular definition, the drugs and/or techniques used should carry a margin of safety wide enough to render unintended loss of consciousness unlikely.

2.7.4 Deep Sedation A drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully following repeated or painful stimulation. The ability to independently maintain ventilatory function may be impaired. Patients may require assistance in maintaining a patent airway, and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained.

2.7.5 General Anesthesia A drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to independently maintain ventilatory function is

References

13

often impaired. Patients often require assistance in maintaining a patent airway, and positive pressure ventilation may be required because of depressed spontaneous ventilation or drug-induced depression of neuromuscular function. Cardiovascular function may be impaired. Close scrutiny of the moderate sedation definition states that drugs used for moderate sedation should have a wide margin of safety to prevent unintentional unconsciousness. The drugs amenable to this definition are described in detail in Chap. 4. It is also important to recognize the differences between moderate and deep sedation. It is possible during moderate sedation for patients to drift into a level of deep sedation. If this occurs, the patient should not be allowed to linger there, but must be immediately returned to a moderate sedation state. Practicing in the deep sedation realm is beyond the scope and training of a moderate sedation-trained dentist that places the patient in a compromised state, and would be a violation of state regulations. Intraoperative monitoring guidelines and rescue tactics will be discussed in Chaps. 6 and 7.

References 1. Bennett CR. Conscious-sedation in dental practice. St. Louis, MO: CV Mosby; 1978. 2. Guidelines for teaching pain control and sedation to dentists and dental students. Adopted by the ADA House of Delegates; 2016. 3. Guidelines for the use of sedation and general anesthesia by dentists. Adopted by the ADA House of Delegates; 2016. 4. Chang L, Ye F, Luo Q, et  al. Increased hyperalgesia and proinflammatory cytokines in the spinal cord and dorsal root ganglion after surgery and/or fentanyl administration in rats. Anesth Analg. 2018;126:289–97.

3

Preanesthetic Evaluation for Periodontal Sedation

Everybody Ought to Treat a Stranger Right —Blind Willie Johnson

The preanesthetic evaluation identifies potentially reactive patients with the sole purpose of preventing, recognizing, and managing perioperative anesthetic urgencies and emergencies. In the not too distant past, the majority of patients presenting for elective dental treatment were essentially healthy, American Society of Anesthesiologists (ASA) Risk Classification I or II (Fig.  3.1). However, as medicine has advanced over the years, it is now commonplace for ASA III and IV patients to routinely seek dental care. Patients are living longer, are taking more prescription and over-the-counter medications, and have been • ASA Class I • Healthy patient who is free of organic disease

• ASA Class II • Patient with mild systemic disease that does not limit activity

• ASA Class III • Patient with severe systemic disease that limits activity, but is not incapacitating

• ASA Class IV • Patient with an incapacitating systemic disease that is a constant threat to life

• ASA Class V • Moribund patient not expected to survive 24h with or without surgery.

Fig. 3.1  American society of anesthesiologists (ASA) risk classification

© Springer Nature Switzerland AG 2020 J. A. Giovannitti Jr., Moderate Sedation and Emergency Medicine for Periodontists, https://doi.org/10.1007/978-3-030-35750-4_3

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3  Preanesthetic Evaluation for Periodontal Sedation

medically optimized to the point where they may seek dental services that previously would have been difficult to achieve. Therefore, periodontists must be more medically astute than ever, with a thorough understanding of their patients’ underlying medical complexities. They must be able to adequately assess whether or not their patient has been optimally managed, what further testing may be necessary, and what type and length of procedure could be safely tolerated. Moderate sedation can play an important role in the overall safe management of the medically compromised patient through its ability to alleviate stress and reduce anxiety.

3.1

Components of a Preanesthetic Evaluation

A comprehensive preanesthetic evaluation begins with a thorough assessment of the patient’s medical status. After a series of general health questions, major systems are reviewed with special attention to the cardiovascular, respiratory, neurologic, and metabolic and endocrine systems. Since perioperative reactivity is likely to involve one or more of these systems, the periodontist should be very familiar with the vagaries of each impairment. Once the underlying issues have been identified, a dialog between patient and periodontist must occur in order to elicit more detailed information. For example, a patient may indicate that they are diabetic. Verbal interaction will determine how the diabetes is being controlled, whether or not the patient checks his or her blood glucose levels regularly, whether they know their hemoglobin A1C level, or whether they have ever been hospitalized because of their condition. A patient who is unaware of things such as blood glucose or A1C values will require medical consultation by the periodontist prior to the initiation of treatment. A comprehensive list of the patient’s current medications, including prescription, over-the-counter, and illicit drugs, is essential to aid in the diagnosis of underlying medical conditions and to alert the periodontist to possible drug interactions with sedative medications. Additionally, a patient’s previous surgical, anesthetic, social, and family histories, and for females of childbearing age, the possibility of pregnancy, will all provide insight into the possible operative course, necessary treatment adjustments, and/or reasons to postpone treatment. Next a physical examination tailored to identify statistical information such as age, sex, height, weight, body mass index (BMI), and baseline vital signs is fundamental. Auscultation of the heart and lungs must be completed as well as a comprehensive airway examination and risk assessment (see Chap. 5). In addition to assigning a Mallampati Classification, mouth opening, dentition, and range of motion of the head and neck must be evaluated and noted. Patients should be questioned about the possibility of sleep apnea, since this could significantly affect sedation outcomes. Laboratory and other testing should be ordered where indicated. For example, it would be prudent to know a diabetic patient’s current A1C value, to

3.1  Components of a Preanesthetic Evaluation

17

determine whether a patient’s seizure medication is in the therapeutic range, or to see the findings of an echocardiogram or stress test prior to initiating treatment. The final component of a comprehensive preanesthetic evaluation is the medical consultation, when indicated. As mentioned previously, it is now common for ASA III and IV patients to seek elective dental and periodontal care. One must determine if the patient’s medical conditions have been optimized and stabilized. If not, treatment must be postponed until this can be accomplished. In some instances, treatment may only be accomplished in a hospital setting with tight medical oversight, or rarely not at all. Requests for medical clearance rarely result in altered or modified therapy. Therefore, it is unreasonable to ask for or accept medical clearance as a free pass to treatment. The periodontist is obligated to direct the consultant to address specific questions and issues pertinent to the patient and procedure. For example, if a patient presents with a history of coronary artery disease, chest pain, or heart failure the clinician should direct the consulting physician to provide the results of a recent cardiac stress test, echocardiogram, and/or electrocardiogram so that an accurate assessment of the patient’s functional cardiac capacity can be determined. Conditions that require medical consultation are provided in Fig. 3.2.

Cardiovascular: • Unstable coronary syndromes (i.e. unstable angina) • Severe heart failure (i.e. ankle edema, ascites, shortness of breath) • Significant arrhythmias (i.e. atrial fibrillation, heart block) • Severe valvular disease (i.e. audible murmur, decompensation with exertion) • MI, bypass surgery, cardiac stenting within the past 6 months • Stroke within the past 6 months • Blood pressure >160/100 • Blood pressure 10.5, history of hospitalizations or diabetic ketoacidosis) Clinically evident hyperthyroidism Pituitary disorders

• • • Adrenal suppression/insufficiency (i.e. Addison’s disease) • Morbid obesity (i.e. BMI >40) Hepatic: • Cirrhosis • Jaundice Renal: • •

Renal failure Dialysis

GI: • Bleeding within the past 6 months Transplants: •

History of organ transplant

Symptomatic Infectious Diseases: • • •

Hepatitis C TB HIV/AIDS

Hematology: • • • •

Bleeding disorders Sickle cell disease Thrombocytopenia INR >3.0

Allergy: •

Local anesthetics

Fig. 3.2 (continued)

3.2

Review of Systems

3.2.1 Cardiovascular System Conditions of concern in the cardiovascular system include coronary artery disease, hypertension, infarction, valvular disease, dysrhythmias, and heart failure. When the cardiovascular system is stressed, catecholamines are released producing tachycardia and hypertension. In patients with coronary artery disease, myocardial oxygen demand will outstrip supply, resulting in myocardial ischemia,

3.2  Review of Systems

19

angina, or infarction. Lack of oxygen to cardiac muscle may also result in serious dysrhythmias such as atrial fibrillation, ventricular tachycardia, or ventricular fibrillation. Tachycardia and hypertension may lead to acute heart failure in patients with aortic stenosis or congestive heart failure histories. Severe hypertension may result in stroke. It would be helpful to determine the degree of risk one is faced with prior to initiating treatment. In a seminal study, Goldman and Caldera [1] created a cardiac risk index point system designed to quantify perioperative risk for cardiac patients undergoing noncardiac procedures (Fig. 3.3). An accumulation of 25 or more points significantly increases cardiac risk for these patients. Twenty-two percent of these patients may develop a cardiac complication during treatment, with a 56% mortality rate (Fig. 3.4). Patients presenting with such an unacceptable risk must only be managed in a hospital under close medical supervision. The periodontist must assess the risk/benefit ratio to determine if treatment is absolutely necessary. One of the most important parameters to measure prior to initiating treatment in a patient with cardiovascular system impairments is the cardiac functional capacity. It has been stated anecdotally that the reason dental offices were traditionally located on the second floor was that a patient’s presence in the waiting room meant that they were healthy enough to receive treatment. This observation holds true to this day. A patient able to walk up a flight of stairs carrying a bag of groceries without stopping to catch his or her breath, or can walk two city blocks, has enough cardiac reserve to withstand a stressful situation. This can be quantified by assessing the patient’s metabolic equivalent, or MET, level (Fig. 3.5). A MET is a measure of a patient’s oxygen consumption and is related to their ability to perform daily activities or exercise without coronary compromise. The critical threshold for an adequate Fig. 3.3  Cardiac risk index

Fig. 3.4  Point score vs. risk

• Age >70 • • • •

5

MI within 6 months 3rd heart sound/jugular venous distention Aortic stenosis Rhythm other than sinus or premature atrial contraction

10 11 3 7

• >5 premature ventricular beats/min

7

• Poor general medical condition • Intraperitoneal, aortic, intrathoracic surgery • Emergency

3 3

Points 0-5 6-12 13-24 25

Life-threatening complication 0.7% 5% 11% 22%

4

Mortality 0.2% 2% 2% 56%

20

3  Preanesthetic Evaluation for Periodontal Sedation

• Metabolic Equivalencies (METS) • Perioperative cardiac risk is increased in patients unable to meet a 4MET demand during most daily activities • 1– 4

• Eating, dressing, walking about home, moderate housework

• 4–10

• Stairs, walking briskly, light yard work, golf

• >10 • Strenuous sports

Fig. 3.5  Cardiac functional capacity. A 4-MET threshold is required to ensure adequate cardiac functional capacity

functional capacity or exercise tolerance is 4 METs. Patients unable to perform at a 4-MET level are poor candidates for office-based procedures due to their inability to tolerate stress without the risk of cardiac decompensation.

3.2.1.1 Cardiac Testing Three preoperative tests are indicated for patients with significant cardiac disease, a 12-lead electrocardiogram (EKG), an echocardiogram, and a stress test. An EKG can diagnose cardiac hypertrophy or enlargement secondary to valvular disease, sustained systemic hypertension, or cardiac muscle disorders. Additionally, it may show rhythm and conduction abnormalities, myocardial ischemia or previous infarction, and electrolyte disturbances. An echocardiogram is a noninvasive test that uses sound waves to create moving pictures of the heart. It looks at the size, shape, and functionality of the heart’s chambers and valves. An important parameter is the ejection fraction, the percentage of blood that is ejected from the left ventricle after each contraction. An ejection fraction >50% is considered to be normal, while an ejection fraction 35 kg/m2

Yes No

Age

>50 years

Yes No

Neck circumference

>40 cm

Yes No

Gender

Male

Yes No

Fewer than 3 Yes = low risk of OSA; 3 or more Yes = high risk of OSA; 5-8 Yes = high probability of moderate-to-severe OSA

Fig. 3.10  STOP BANG (screening for OSA)

3.2  Review of Systems

25

risk, and patients with 5–8 yes answers have a high probability of moderate-to-­ severe OSA. Severity may then be quantified through the performance of polysomnography, or sleep study examination. OSA cannot be definitively diagnosed without the completion of a sleep study during which multiple parameters are evaluated during sleep. Electroencephalogram (EEG), electrocardiogram (EKG), submental electromyogram (EMG), nasal airflow, chest and abdominal movement, oxygen saturation, end-tidal carbon dioxide, and blood pressure are monitored continuously throughout sleep. The number of apneic, hypopneic, or other respiratory disturbances per hour is recorded. An apnea/hypopnea index is calculated that represents the degree of severity of the disease. Patients with severe OSA are not candidates for office-based sedation. They should be treated in an ambulatory facility or hospital setting where medical management is available if needed.

3.2.2.2 Treatment Considerations Patients with COPD should be appointed in the afternoon hours. Poor ciliary activity coupled with a reactive airway allows for the buildup of mucus secretions in the tracheobronchial tree during the overnight hours. The presence of mucus in the airways impairs air and gas exchange, and the cough reflex is heightened as the patient attempts to clear the secretions. The airway will be as optimal as possible during the afternoon, allowing for initiation of treatment. If the patient is a smoker, he or she should be instructed to refrain for at least 48 h, and ideally for 6 weeks prior to treatment. Preemptive prophylactic bronchodilation should be provided to ensure that the lower airways remain as open as possible prior to treatment. The use of moderate sedation is advised to alleviate stress and anxiety in order to reduce the possibility of bronchospasm. Since these patients have reactive airways, it is essential to prevent the buildup of irrigation, blood, or surgical debris. Accumulation of foreign substances in the airway will inevitably lead to coughing, choking, and bronchospasm. As with all emergencies, it is better to take preventative precautions rather than managing potentially life-threatening sequelae. Supplemental oxygen must be administered, and the patient monitored closely for early signs of hypoxia. Duration of sedation and surgery should be under 2.5 h in order to minimize the chance of a pulmonary complication. Patients with OSA should be optimized as much as possible prior to treatment. Effective strategies include weight loss, dental repositioning devices, continuous positive airway pressure (CPAP), and in extreme cases surgery. CPAP is the “gold standard” for the treatment of OSA. Continuous airway pressure acts as a pneumatic splint to prevent airway collapse during sleep. It has been used successfully to decrease daytime sleepiness, improve hypertension and symptoms of right-sided heart failure, improve cognitive function, and increase pharyngeal space. If used postoperatively it protects against opioid-induced respiratory depression. However, many patients do not tolerate CPAP and compliance is poor. Sedation for patients with COPD and OSA should be maintained in the minimal to moderate level. The patient must remain conscious at all times, since deepening levels of sedation result in early airway collapse. There is an increased sensitivity to CNS-depressant drugs, especially opioids. Opioids promote respiratory depression

26

3  Preanesthetic Evaluation for Periodontal Sedation

and airway collapse, which are exacerbated in COPD and OSA.  They may also produce hypoxia that extends into the postoperative period and sleep fragmentation may occur for up to a week following surgery. Sensitivity to benzodiazepines, such as diazepam and midazolam, is relevant in this patient population especially when opioids are included in the sedation regimen. It is therefore essential that all sedative medications be slowly titrated to a defined clinical endpoint. The alpha-2 agonist drug, dexmedetomidine, is a valuable adjunct in these patients since it does not produce respiratory depression. Other treatment considerations include treating the patient in the semi-upright (Semi-Fowler) position, maintaining neck extension, providing supplemental oxygen, having appropriate reversal agents readily available, as well as appropriately sized airway adjuncts. Patients should be fully recovered to a baseline level prior to discharge and be able to maintain baseline oxygen saturation levels. Recovery time may need to be extended to ensure that the patient meets discharge criteria. Because normal sleep patterns may be disrupted, the continued use of CPAP is recommended for OSA patients for 1 week posttreatment.

3.2.3 Diabetes Mellitus The diagnosis of diabetes (fasting blood glucose ≥126 mg/dl) has increased dramatically in the past several decades and is closely tied to the worldwide obesity epidemic. Type I diabetes is an autoimmune process resulting in pancreatic beta-cell destruction with resultant insulin deficiency. It accounts for about 10% of the cases. Type II diabetics have functional pancreatic beta-cells that produce insulin in relative deficiency leading to insulin resistance. It is ten times more common than type I and 80% of the cases are associated with obesity. Risk factors for type II diabetes are listed in Fig. 3.11. Chronically elevated blood glucose levels lead to systemic inflammation that adversely affects the cardiovascular, autonomic, and peripheral nervous systems, and increases the propensity for infection and impaired wound healing. Patients with a history of diabetes should be questioned extensively preoperatively concerning the severity of the disease and the degree of control should be ascertained. A history of emergent hospitalizations may indicate labile disease and/ or lack of control. Extreme hyperglycemia and hypoglycemia are acute medical emergencies that may be life threatening. Severe hyperglycemia resulting from Fig. 3.11  Risk factors for type II diabetes

• • • • • • • •

Age >45 years Overweight or obese Parent, brother, or sister with diabetes African American, American Indian, Asian American, Pacific Islander, or Hispanic American/Latino Gestational diabetes, or birth to at least one baby weighing more than 9 pounds Blood pressure 140/90 or higher High cholesterol Inactivity, exercise fewer than three times a week

3.2  Review of Systems Fig. 3.12  Systemic comorbidities associated with diabetes

27

• Microvascular disease • Retinopathy • Nephropathy

• Macrovascular disease • • • •

Coronary artery disease Cerebrovascular disease Peripheral vascular disease Hypertension

• Neuropathic disease • Foot ulcers • Infections trauma, stress, infection, and lack of insulin leads to the breakdown of ketone bodies for fuel. The result is osmotic diuresis, dehydration, hyperketonemia, and metabolic acidosis. The fulminant state is called diabetic ketoacidosis and may lead to coma and death without aggressive treatment. Severe hypoglycemia results when insulin or other antihyperglycemic medication is taken in the absence of food. Low blood glucose produces mental confusion, irritability, inappropriate affect, abnormal behavior, and eventually coma. Catecholamines are released in an attempt to increase blood glucose and may result in diaphoresis, tremor, palpitations, anxiety, and weakness. Hypoglycemia must be corrected immediately to prevent life-­ threatening consequences. The effects of chronic inflammation make patients with diabetes prone to a wide range of systemic complications (Fig. 3.12). A major cause of death among diabetics is due to heart disease and stroke. The risk of death from either cause is 2–4 times greater than that of the general population. Approximately 75% of patients with diabetes have hypertension or are being treated for hypertension. Diabetes is a leading cause of kidney failure, blindness, claudication, and lower limb amputations. Peripheral neuropathies occur in up to 70% of patients, resulting in sometimes incapacitating nerve pain. Poorly controlled diabetes during pregnancy may lead to the development of birth defects and possibly miscarriage. Severe periodontal disease is common in patients with diabetes, so the periodontist must be aware of the possible ramifications of office-based treatment in this compromised group.

3.2.3.1 Preoperative Testing Preoperative evaluation of patients with diabetes involves an assessment of all possible impaired systems. Assessing the adequacy of glucoregulation is paramount. While a blood glucose determination provides a valid snapshot of glucose control at the time of the test, it is the determination of the hemoglobin A1C (HbA1C) that gives the best indication of the patient’s overall degree of control. Glycated, or glycosylated, hemoglobin is formed when glucose in the blood binds irreversibly to hemoglobin to form a stable glycated hemoglobin complex. Since the normal life span of red blood cells is 90–120 days, HbA1C will only be eliminated when the red cells are replaced. Thus, HbA1C values are proportional to the concentration of glucose in the blood over the full life span of the red blood cell. Unlike the blood

28

3  Preanesthetic Evaluation for Periodontal Sedation HbA1C 4 5 6 7

Mean blood glucose (mg/dl) 61 100 124 156

8 9 10 11 12

188 219 251 283 314

Interpretation Nondiabetic range Target for control Action suggested

Fig. 3.13  HbA1C values indicate the average blood glucose levels over a 3-month period. The target for good control is an HbA1C = 7

glucose determination, the HbA1C value gives the average degree of control over the past 3 months. This gives the practitioner a better idea of the patient’s compliance with treatment and its effectiveness. A patient who does not regularly check his or her blood glucose levels and is unaware of HbA1C will require medical consultation prior to treatment. Normal HbA1C values are between 4.8% and 5.7%. The goal of successful therapy for patients with diabetes is at or below 7.0%. HbA1C values and corresponding average blood glucose levels are shown in Fig. 3.13. Since patients with diabetes are at risk for cardiovascular diseases such as hypertension, hyperlipidemia, coronary artery disease, cerebral vascular disease, and kidney disease, it is extremely important to evaluate them in the same manner as patients with heart disease as previously discussed. It is necessary to determine the adequacy of blood pressure control, and depending upon the degree of impairment to assess the patient’s functional capacity through activity levels, EKG, echocardiogram, and stress testing. In addition to ensuring adequate glucose control, any underlying cardiac conditions must be optimized prior to treatment.

3.2.3.2 Treatment Considerations Optimal glucose control is essential to prevent a myriad of perioperative complications and will be of benefit to patients with either type I or type II diabetes. For every percentage point drop in A1C levels (e.g., from 8% to 7%), the risk of eye, kidney, and nerve diseases is reduced by 40%. Blood glucose levels ≤200 mg/dl can significantly reduce the incidence of perioperative cardiac complications. Control of blood pressure and blood lipids will decrease the risk of cardiovascular disease and improve renal function. In addition to antihyperglycemic drugs, diabetic patients commonly take angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB), and statin drugs. Once good glucoregulation has been established and the patient’s underlying comorbidities have been optimized through medical consultation, it is desirable to appoint the patient during the morning hours when glucose control is optimal. Moderate sedation is indicated for patients with diabetes for a variety of reasons. Stress and anxiety cause a catecholamine release (cardiac stress response) that

3.2  Review of Systems

29

results in increased blood glucose levels. Additionally, it is important to reduce stress in order to reduce perioperative cardiac risk. Moderate sedation acts to keep blood glucose levels in check and to keep cardiovascular system parameters near baseline. Since patients undergoing moderate sedation will be following NPO guidelines, adjustments must be made in their antihyperglycemic drug schedule preoperatively. This may be done in consultation with the patient’s physician. Generally, insulin-dependent patients are taking two types of insulin, a long-acting basal insulin and a rapid-acting insulin with meals. Since the patient will be instructed not to have solid foods for at least 6 h prior to treatment, the basal insulin will be reduced by 20–50% and the rapid-acting insulin will be withheld. Patients taking oral antihyperglycemics will be instructed to withhold their medication prior to morning treatment. A baseline blood glucose measurement must be taken immediately prior to initiation of sedation and treatment. Measurements greater than 250 mg/dl are cause for cancellation and reappointment. Blood glucose should be measured periodically during treatment and again upon discharge. The patient should be instructed to resume their usual meal and medication schedule as soon as possible after treatment, and to monitor their blood glucose frequently for 24–48 h postoperatively.

3.2.4 Neurological and Developmental Disorders 3.2.4.1 Motor Neuron Disease Motor neuron diseases are primarily caused by progressive degeneration of motor nerve fibers in the anterior horn of the spinal cord. The two major motor neuron diseases are spinal muscular atrophy and amyotrophic lateral sclerosis. Spinal muscular atrophy is a genetic disorder of degenerating lower motor neurons, which may manifest in childhood or early adulthood [6]. As the disease progresses, further degeneration characterized by severe scoliosis, respiratory muscle weakness, frequent and recurrent pulmonary infections, and respiratory failure may result. Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease after the New  York Yankee slugger who famously succumbed to this disease, develops between the ages of 30 and 60 years. It is characterized by progressive deterioration of the corticospinal tract, brainstem, and upper and lower motor neurons [7]. Diagnosis is made initially by limb weakness followed by eventual difficulties in swallowing, eating, speaking, and breathing. It is usually fatal within 3–5 years after diagnosis, most often from pneumonia or respiratory failure. Treatment Considerations Patients with motor neuron diseases are susceptible to aspiration during sedation. Care must be taken to ensure the NPO status of the patient because delayed gastric emptying and GERD may predispose to aspiration. An additional concern is the inhalation and/or aspiration of aerosolized water spray from a handpiece or ultrasonic scaler, the result of which may be posttreatment pneumonia. Patients with spinal muscular atrophy and ALS are prone to excessive salivation and may require

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antisialogogues such as glycopyrrolate to reduce salivary flow. Autonomic dysfunction may make patients susceptible to hypotension during sedation, especially with rapid positional changes.

3.2.4.2 Parkinson’s Disease Parkinson’s disease is a disorder of the central nervous system characterized by clinical signs of tremor, muscle rigidity, lack of spontaneous movement (akinesia), slowness of movement (bradykinesia), and problems with walking or postural instability. There is a degeneration of dopaminergic neurons in the substantia nigra of the basal ganglia [8]. Dopamine is an inhibitory neurotransmitter that helps modulate the excitatory activity of acetylcholine in the brain. The resulting overactivity of acetylcholine produces the tremor of Parkinsonism. Dopamine also inhibits GABA transmission. When dopamine is depleted as in Parkinson’s disease, GABA effects become clinically evident as akinesia and bradykinesia, which may become disabling. Treatment of Parkinson’s disease is usually two-pronged, combining dopaminergic and anticholinergic drugs. Treatment Considerations Treatment of Parkinson’s disease with levodopa results in systemic cardiovascular system effects which may have anesthetic consequences. The chronic administration of levodopa, while increasing dopamine levels, may result in depletion of norepinephrine stores in the autonomic nervous system. Depletion of norepinephrine may sensitize adrenergic receptors to the effects of exogenously administered catecholamines such as epinephrine administered with local anesthetics. Hypertension may be the result. The renin-angiotensin system is inhibited by dopamine as well. This effect may result in reduced intravascular fluid volume and make patients susceptible to intraoperative and/or orthostatic hypotension. The provider must be prepared to rapidly restore the blood pressure with fluids or vasopressors. Side effects of levodopa include nausea and vomiting. Prophylaxis or treatment of postoperative nausea and vomiting should include dexamethasone, 5-HT3 receptor antagonists such as ondansetron, and transdermal scopolamine. Traditional antiemetics such as phenothiazines (promethazine) and butyrophenones (droperidol) are dopaminergic blockers and may worsen the patient’s condition.

3.2.4.3 Myasthenia Gravis Myasthenia gravis is an autoimmune disorder of neuromuscular transmission that affects primarily small motor muscles including the ocular, oropharyngeal, and flexor and extensor muscles of the head and neck. Patients with myasthenia gravis present with characteristic eyelid droop and difficulty in maintaining an erect head position. Autoantibodies at the postsynaptic portion of the neuromuscular junction result in a 70–90% reduction in functioning nicotinic receptors, decreasing the ability of the neuromuscular end plate to transmit an impulse [9]. Myasthenia gravis is associated with other autoimmune disorders such as hyperthyroidism, rheumatoid arthritis, systemic lupus erythematosus, pernicious anemia, and thymic disease.

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31

Treatment of myasthenia gravis is geared toward increasing the amount of acetylcholine available at the neuromuscular junction and inhibiting the extent of autoimmune destruction of nicotinic receptors. Cholinesterase inhibitors, such as edrophonium and pyridostigmine, prevent the hydrolysis of acetylcholine and increase the amount of this neurotransmitter. Improved muscle function is the result. Plasmapheresis, corticosteroids, and immunosuppressants may also be effective in reducing the level of autoantibodies. Thymectomy produces remission of the disease in about one-third of affected patients. Treatment Considerations Specific attention should be paid to respiratory muscle strength, which may be significantly impaired as the disease progresses. Pulmonary function tests may be necessary in some cases to assess the severity of impairment. Benzodiazepines and opioids, and other commonly used sedatives, should be slowly titrated to a defined clinical endpoint in order to maintain consciousness and minimize respiratory depression in these susceptible patients. A more prudent sedation regimen would include the administration of dexmedetomidine, an alpha-2 agonist drug that produces sedation without respiratory depression [10]. Since hyperthyroidism is prevalent in patients with myasthenia gravis, pretreatment thyroid function testing may be indicated. Aminoglycoside antibiotics, such as gentamicin, kanamycin, streptomycin, and neomycin, should be avoided in patients with myasthenia gravis since these drugs reduce acetylcholine release and exacerbate the muscle weakness.

3.2.4.4 Muscular Dystrophy Muscular dystrophy is an X-linked recessive genetic disease that results in progressive skeletal muscular weakness and degeneration. The most significant type is known as pseudohypertrophic, or Duchenne’s, muscular dystrophy. The cardiac muscle also progressively degenerates producing decreased myocardial contractility and congestive failure. Weakness of the respiratory muscles causes a loss of pulmonary reserve; the ability to clear secretions and the cough reflex are diminished, and functional residual capacity is reduced. Pulmonary infections may become commonplace. Kyphoscoliosis results from weakness of postural muscles and the resultant restricted lung expansion further decreases pulmonary function residual capacity. Most patients succumb to respiratory failure, pneumonia, and/or congestive heart failure. Treatment Considerations Pulmonology and cardiology consults are indicated for these patients in order to assess the degree of respiratory and cardiac compromise. Patients with poor pulmonary and/or cardiac function are not candidates for office-based sedation procedures. Patients with Duchenne’s muscular dystrophy are primarily at risk when general anesthesia is administered since there is a propensity for the development of malignant hyperthermia when specific triggering agents are used. However, they may also be sensitive to moderate sedation agents that depress respiratory function. Opioids should be drastically limited or eliminated from sedation regimens due to

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the risk of insufficiency. Strict attention must be paid to the patient’s NPO status since gastric emptying is delayed with resultant risk of aspiration and posttreatment respiratory complications.

3.2.4.5 Cerebral Palsy Cerebral palsy is a group of nonprogressive neuromuscular disorders caused by brain damage sustained during the prenatal or perinatal period, or during infancy [11]. Spastic and dyskinetic palsies are the most common, characterized by uncontrollable muscle spasticity, including uncoordinated limb, head, and eye movements. Intellect may be normal, but many patients with cerebral palsy present with intellectual disabilities and seizure disorders. Gastroesophageal reflux is common in cerebral palsy, and patients are at risk for aspiration and pulmonary infections. Treatment Considerations Obtaining vascular access is often a major challenge in patients with cerebral palsy due to uncontrolled spasticity, rigidity, or joint contractures. During moderate sedation, extreme care should be taken to protect the airway from excess irrigation, bleeding, or aerosols. Due to the significant aspiration risk, endotracheal intubation should be considered in cases where significant bleeding or water spray is anticipated or cannot be adequately controlled. Generally speaking, patients with cerebral palsy tolerate sedation well.

3.2.4.6 Seizure Disorders Seizures are caused by the paroxysmal, abnormal synchronous firing of cerebral cortical neurons resulting in transient cognitive impairment, loss of consciousness, and/or tonic-clonic muscle contractions. Epilepsy is characterized by recurrent seizures and may be idiopathic (75%), genetic, or the result of brain injury or metabolic causes. Seizures are classified as either partial (focal) or generalized. Partial seizures are usually caused by focal brain damage or disease, so underlying causes should be examined. Generalized seizures are categorized as either absence or tonic-clonic in nature. Patients with absence seizures encounter brief alterations in consciousness without loss of posture. The episodes are short-lived, and consciousness is not impaired afterward. Tonic-clonic seizures are the characteristic seizure with sudden loss of consciousness, and tonic and clonic muscle contractions, shaking, and twitching. These seizures are usually self-limiting, lasting from 1 to 2 min, followed by several minutes of unconsciousness and a prolonged period of depressed consciousness. Patients actively seizing should be managed with airway support and with an attempt to prevent self-injury. Treatment Considerations Patients with a seizure disorder history should be evaluated to determine the type of seizure, frequency of occurrence, and precipitating factors. Patients should be followed regularly by their physician to ensure an adequate degree of control with therapeutic blood levels of anticonvulsant drugs. Anticonvulsants such as phenytoin, carbamazepine, and phenobarbital induce the liver enzyme, CYP 3A4, which is

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involved in the metabolism of many drugs, especially benzodiazepines. When using benzodiazepines such as diazepam and midazolam during sedation, the practitioner should be aware of a potential drug interaction in which the metabolism of the administered benzodiazepine would be accelerated, resulting in an incomplete, inadequate, or lessened effect. Consideration must be given to patients taking clonazepam for control of their seizure disorder. Clonazepam is a benzodiazepine, and as such is reversed by flumazenil. Flumazenil reversal of a benzodiazepine overdose during anesthesia could therefore potentially trigger a seizure in these patients.

3.2.4.7 Down Syndrome Down syndrome is the result of a deviation from the normal chromosome complement in which there is an extra copy of chromosome 21. Also known as trisomy 21, Down syndrome occurs in 1:800 births [12]. The incidence increases with advancing maternal age and accounts for approximately one-third of cases of intellectual disability. Approximately 50% of patients have congenital heart defects, the most common being atrioventricular septal defects, followed by atrial-septal defects, patent ductus arteriosus, ventricular septal defects, and tetralogy of Fallot [11]. Patients with Down syndrome also have increased incidences of obesity, respiratory infections, seizures, hematological and immunological problems, hypothyroidism, gastroesophageal reflux disease, musculoskeletal problems, obstructive sleep apnea, diabetes, and Alzheimer’s disease [11]. Treatment Considerations The provision of anesthesia and sedation to patients with Down syndrome is complicated by the various anatomic and physiologic deficiencies that may be present. Airway maintenance and security is a major issue due to anatomical changes related to the syndrome. Patients are frequently obese, with a short, thick neck, and a large protruding tongue. Mallampati Class IV airways are common. There is a midface deficiency with a high, vaulted, and constricted palate. Malocclusions are common as well as skeletal class II profiles. Hypotonia and ligament laxity make these patients prone to airway obstruction as they relax during sedation. Nasal passages are narrow, and patients often require the insertion of airway adjuncts such as a nasopharyngeal airway during treatment. Excessive hyperextension or flexion of the neck should be avoided in patients with Down syndrome due to the increased propensity for atlantoaxial subluxation of the cervical spine. These maneuvers could result in severe spinal cord injury resulting in paralysis or death. Atlantoaxial instability should be suspected if patients have a history of declining physical activity and the onset of a sedentary lifestyle. Cervical spine films should be reviewed if any question exists as to the presence of instability. Cervical collars should be considered for neck support, and to prevent hyperextension or flexion in these patients. In severe cases, the airway should be secured with the aid of video or fiber-optic laryngoscopy. A cardiologist should evaluate patients with unrepaired congenital heart defects and testing should include a 12-lead electrocardiogram, echocardiography, and

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evaluation of the patient’s exercise capacity. Consideration should be given for the provision of care in a hospital setting. Medical consultation should also be considered for patients with repaired cardiac defects. Sedation is advisable in these patients to reduce stress on the cardiovascular system. Obstructive sleep apnea is a growing problem in patients with Down syndrome and presents a particular management challenge. Due to the ease of airway obstruction in these patients, moderate levels of sedation are usually advisable. However, this may not be practical if the behavior is unmanageable. When Down syndrome patients present with severe behavioral problems secondary to intellectual disability or dementia, deep levels of sedation may be preferable to control aberrant behavior. In these cases, general anesthesia with the security of endotracheal intubation is advisable. Gastroesophageal reflux disease (GERD) provides another challenge for anesthetic management. Since patients or their caregivers may not always be aware of this condition, the teeth should be examined for the presence of excessive wear or erosive loss of enamel. The existence of GERD makes patients susceptible to perioperative passive regurgitation or active vomiting. Aspiration of gastric contents thus becomes a risk, so care must be taken to ensure the patient’s NPO status. The presence of GERD along with airway hypotonia makes Down syndrome patients prone to aspiration of oral secretions as well. Fine aerosolized spray, as found in dental handpieces or ultrasonic scalers, may be inhaled by the patient during sedation and produce a postoperative respiratory infection which could become severe.

References 1. Goldman L, Caldera DL, Nussbaum SR, et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med. 1977;297:845. 2. Chung F, et al. Society of Anesthesia and Sleep Medicine guidelines on preoperative screening and assessment of adult patients with obstructive sleep apnea. Anesth Analg. 2016;123:452–73. 3. Sateia MJ. International classification of sleep disorders-third edition: highlights and modifications. Chest. 2014;146:1387–94. 4. Hogg JC, Chu F, Utokaparch S, et  al. The nature of small-airway obstruction in chronic obstructive pulmonary disease. N Engl J Med. 2004;350:2645–53. 5. Chino K, Ganzberg S, Mendoza K.  Office-based sedation/general anesthesia for COPD patients, Part 1. Anesth Prog. 2018;65:261–8. 6. Monani UR. Spinal muscular atrophy: a deficiency in a ubiquitous protein; a motor neuron-­ specific disease. Neuron. 2005;48(6):885–95. 7. Hardiman O, van den Berg LH, Kiernan MC. Clinical diagnosis and management of amyotrophic lateral sclerosis. Nat Rev Neurol. 2011;7:639–49. 8. Navailles S, De Deurwaerdère P. Imbalanced dopaminergic transmission mediated by serotonergic neurons in L-DOPA-induced dyskinesia. Parkinsons Dis. 2012;2012:323686. 9. Meriggioli MN, Sanders DB. Autoimmune myasthenia gravis: emerging clinical and biological heterogeneity. Lancet Neurol. 2009;8(5):475–90. 10. Giovannitti JA, Thoms SM, Crawford JJ. Alpha-2 adrenergic receptor agonists: a review of current clinical applications. Anesth Prog. 2015;62:31–8. 11. Odding E, Roebroeck ME, Stam HJ. The epidemiology of cerebral palsy: incidence, impairments and risk factors. Disabil Rehabil. 2006;28:183–91. 12. Abanto J, Ciamponi AL, Francischini E, et al. Medical problems and oral care of patients with Down syndrome: a literature review. Spec Care Dentist. 2011;31(6):197–203.

4

Drugs Suitable for Moderate Periodontal Sedation

Among the remedies which it has pleased Almighty God to give to man to relieve his sufferings, none is so universal and so efficacious as opium. —Sydenham, 1680

Drugs used for moderate sedation, by necessity, should carry a wide enough margin of safety to make the unintended loss of consciousness unlikely. Therefore, agents such as propofol, methohexital, ketamine, and remifentanil are not recommended for moderate sedation. This chapter focuses upon the three drug groups that have the most utility for the induction and maintenance of moderate sedation: opioids, benzodiazepines, and alpha-2 agonists.

4.1

Opioids

Opioids act primarily in the central nervous system (CNS) and the bowel. This is due to the pattern of distribution of the various types of opioid receptors found at these locations. They produce analgesia, drowsiness, changes in mood, and mental clouding without the loss of consciousness. Opioids relieve most types of pain regardless of origin or intensity, increase the pain threshold, and alter the affective pain response. They are primary and continuous depressants of respiration, obtunding the central ventilatory drive in a dose-dependent manner. Opioids decrease minute ventilation by decreasing both the respiratory rate and tidal volume. As doses increase, respiratory depression continues to the point of apnea. Patients with active hypothyroidism or obstructive sleep apnea, the elderly, and those taking other CNS-­ depressant drugs are more prone to the respiratory depressant effects of opioids. As always, careful titration to a defined clinical endpoint is necessary to avoid unintentional overdose.

© Springer Nature Switzerland AG 2020 J. A. Giovannitti Jr., Moderate Sedation and Emergency Medicine for Periodontists, https://doi.org/10.1007/978-3-030-35750-4_4

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Hypothalamus

Heart Pituitary gland

Cortisol

CRH

Adrenal cortex

Vasculature

ACTH Fig. 4.1  The hypothalamic-pituitary-adrenal axis. Opioids modulate ACTH and thus cortisol release, decreasing sympathetic tone

One of the most significant effects of opioids is their attenuative effect on the cardiovascular stress response. As discussed previously, catecholamine release caused by pain or anxiety can have serious adverse consequences in patients with underlying cardiovascular disease. During stress, corticotropin-releasing hormone (CRH) from the hypothalamus causes the pituitary gland to release adrenocorticotropin hormone (ACTH), which in turn causes cortisol to be released by the adrenal cortex. Among other things, cortisol enhances the ability of alpha- and beta-­receptors to respond to the effects of norepinephrine and epinephrine. Opioids act on the hypothalamic-pituitary-adrenal axis by reducing ACTH release with a resultant reduction in cortisol, thereby decreasing sympathetic tone (Fig. 4.1). This helps to stabilize the cardiovascular system and to keep parameters within their baseline range. Other advantages of opioids in a moderate sedation regimen are their ability to alter mood, elevate the pain threshold, and potentiate the effects of other sedative agents. While pain control with local anesthetics is essential to ensure the success of moderate sedation, opioids increase the pain threshold and can enable patients to tolerate uncomfortable sensations such as pressure or vibration not controlled by local anesthesia. Potentiation is a drug interaction between two drugs in which the total effect of both is much greater than would be predicted by simple addition of the two. We take advantage of this type of drug interaction during moderate sedation by administering drugs from different classifications to produce an enhanced effect above and beyond that which could be produced by the administration of a single agent. Additionally, this polypharmacy approach helps to conserve the total amount of each drug given, achieving the desired clinical effect while avoiding the potential adverse consequences of higher doses necessitated by single-agent techniques.

4.1.1 Adverse Effects In addition to profound dose-dependent respiratory depression, opioids also act in the GI system to decrease gastrointestinal motility. This may produce antidiarrheal effects and lead to constipation. Gastric emptying is delayed as well, which may be

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consequential in patients chronically exposed to opioids due to the possibility of food remaining in the stomach regardless of compliance with standard NPO requirements. Additionally, opioids may cause nausea and vomiting through stimulation of the chemoreceptor trigger zone and the vestibular apparatus. These effects, combined with lower esophageal sphincter activity, make the patient more susceptible to passive regurgitation or active vomiting during sedative procedures while increasing the risk of aspiration. Opioids increase skeletal muscle tone. This is especially true when ultrapotent opioids such as those described below are used. Most concerning is their potential to produce chest wall rigidity, a spasm of the intercostal muscles. This prevents expansion of the chest during respiration and significantly decreases pulmonary compliance and functional residual capacity, with resultant hypoxia. This effect is typically associated with high doses and rapid administration, so it is prudent to administer these drugs slowly and incrementally. Sedation with a benzodiazepine prior to opioid administration may help to prevent this occurrence. A pathognomonic sign of opioid use is miosis, or pupillary constriction. This occurs through parasympathetic stimulation and there is no tolerance to this effect. True allergic reactions to opioids are rare and can often be attributed to the normal pharmacologic properties of the drugs. For example, patients may often report an opioid allergy as the development of nausea and vomiting or constipation. Certain opioids such as morphine and meperidine release histamine, which may result in typical wheal and flare reactions manifesting as dilation of cutaneous blood vessels in the face, neck, and upper thorax. The resultant flushing and itching are consequences of histamine release and not necessarily allergic in nature. Even the non-­ histamine-­releasing opioids produce pruritus, with facial itching seen commonly with drugs such as fentanyl. When administered in the absence of pain, opioids may produce dysphoria and focal neuroexcitation. Therefore, it is advisable again to begin the sedative induction with a benzodiazepine prior to opioid administration in order to avoid this idiosyncrasy.

4.1.2 Tolerance and Opioid-Induced Hyperalgesia Opioid tolerance may be described as an increasing dose requirement needed to achieve the same analgesic effect with chronic exposure over time. However, tolerance to the respiratory depressant effects develops much slower and to a lesser degree than analgesic tolerance. Paradoxically, an opioid-tolerant patient is at an increased risk for respiratory depression when treated with opioids. Hayhurst and Durieux [1] demonstrated that there is differential tolerance to the analgesic and respiratory depressant effects of opioids. In their study, monkeys tolerant to the analgesic effects of opioids still were sensitive to the respiratory depressant effects. Opioid-tolerant patients may therefore be at risk for respiratory depression when opioids are used perioperatively, especially since they may require more opioid than the average patient to produce the same sedative and analgesic effect.

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Opioid-induced hyperalgesia (OIH) is described as an increased sensitivity to painful stimuli. This may result from chronic opioid exposure as well as exposure during the perioperative period. As opioids depress mu-receptors, other protective mechanisms are activated. Proinflammatory cytokines such as interleukin-1β, interleukin-­6, and tumor necrosis factor-X are released along with pronociceptive peptides and activation of NMDA receptors [2]. The development of tolerance and OIH leads to increased pain and escalating doses of opioids. It becomes a vicious spiral that increases the risk of profound respiratory depression. Perhaps the use of perioperative opioids should be reconsidered in this patient population.

4.1.3 Useful Opioids for Moderate Sedation 4.1.3.1 Fentanyl Fentanyl and its relatives in the phenylpiperidine class of opioids have the greatest utility for use during moderate sedation. Fentanyl is a very potent opioid, about 100 times as potent as the opioid prototype, morphine (Fig. 4.2). It is supplied as a 0.05 mg/ml (50 μg/ml) concentration. The onset is very rapid, within 30 s, and its peak effect occurs in about 5 min. Clinical duration of action is 30–45 min. Fentanyl has a high affinity for mu-opioid receptors, and therefore is a potent analgesic as well as respiratory depressant. There is no appreciable euphoric effect, so it is difficult to appreciate the clinical onset. Care should be taken to avoid excessive dosing. The drug should be administered slowly with doses averaging 25–100 μg depending upon the patient’s needs. Bradycardia may result due to enhanced parasympathetic tone.

Drug

Morphine

Fentanyl

Sufentanil

Alfentanil

Comparative potency

1

75-125

500-1000

10-25

Peak effect (min)

20-30

3-5

3-5

1.5-2

Duration (h)

3-4

0.5-1

0.5-1

0.2-0.3

Half-life (h)

2-4

1.5-6

2.5-3

1-2

Fig. 4.2  Comparative potencies, peak effects and durations of opioids. Morphine is the opioid prototype upon which comparisons are made

4.2 Benzodiazepines

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4.1.3.2 Sufentanil Sufentanil is an ultrapotent analgesic and respiratory depressant drug, 10 times as potent as fentanyl and 1000 times as potent as morphine. It is supplied as a 0.05 mg/ ml (50 μg/ml) concentration. It may be used in lieu of fentanyl, but at a much lower concentration than that supplied. It must be diluted to a final usable concentration of 5 μg/ml prior to use. At this dilution, 5 μg of sufentanil would be the equivalent of 50 μg of fentanyl. At this concentration the clinical onset, effect, and duration are similar to fentanyl. 4.1.3.3 Alfentanil Alfentanil is an opioid that is ten times less potent than fentanyl, but ten times more potent than morphine. It is supplied as a 0.5 mg/ml (500 μg/ml) concentration and may be used at full strength without dilution. Thus, 500 μg of alfentanil would be the equivalent of 50 μg of fentanyl. Using the appropriate concentrations and dilutions, sufentanil and alfentanil may be used interchangeably with fentanyl with similar outcomes.

4.2

Benzodiazepines

Benzodiazepines combine with gamma-aminobutyric acid (GABA) receptors in a selective, stereospecific manner. GABA receptors are a conglomerate of several subunits, the activation of which produces sedative, anxiolytic, amnestic, and anticonvulsant effects [3]. Benzodiazepines act to intensify these physiological effects of GABA by interfering with GABA reuptake, causing neuronal membrane hyperpolarization. Unlike opioids, benzodiazepines have specific anxiolytic effects. Thus, their inclusion in a moderate sedation regimen is essential for anxiety reduction. They have a high therapeutic index; that is, the ratio between the therapeutic dose and the toxic dose is vast. Benzodiazepines appear to have minimal effect on the cardiovascular system and may in fact have a stabilizing effect. Slight-to-moderate decreases in mean arterial pressure, cardiac output, stroke volume, and systemic vascular resistance have been noted [4]. Glisson et al. [5] studied the effects of benzodiazepine premedication on plasma epinephrine and norepinephrine levels during induction of general anesthesia. They found that blood levels of epinephrine and norepinephrine were suppressed, and that benzodiazepines may be of value in attenuating catecholamine surges during stress. By contrast, benzodiazepines can produce dose-dependent respiratory depression, especially when given in doses that induce general anesthesia. However, when titrated slowly to a fixed clinical endpoint, as with moderate sedation, there is no clinically significant respiratory depression [6]. Most benzodiazepines are metabolized in the liver by the cytochrome enzyme CYP3A4. Drugs that affect the activity of this enzyme may produce significant drug interactions with benzodiazepines. For example, when benzodiazepines are administered to patients concomitantly taking a drug such as fluvoxamine, which inhibits the activity of CYP3A4, a more profound and prolonged effect may be appreciated.

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Conversely, in patients taking a drug such as carbamazepine, an enzyme inducer, the clinical effects of benzodiazepines may be reduced.

4.2.1 Precautions for Use Caution should be used in the management of elderly patients. The elderly may exhibit extreme sensitivity to the effects of benzodiazepines, especially the development of idiosyncrasy, delirium, and/or oversedation. In general, dosages should be reduced by at least 25% with a less frequent need for readministration. Cardiac output is typically diminished in the elderly patient, thereby delaying the onset of sedation. Reduced plasma volume, protein binding, and CNS function act to increase drug potency. Reduced metabolic rate, hepatic and renal clearance, and a higher percentage of body fat tend to slow metabolism and elimination, allowing for drug accumulation. This increases the duration of action and prolongs the intervals between readministration. Delirium is described as a disturbance of consciousness, characterized by the acute onset of impaired cognitive functioning, significantly impairing one’s ability to process and store information [7]. Pediatric patients, patients with special needs, and the elderly are particularly prone to delirium during or following sedation and anesthesia, especially when benzodiazepines are used. These patients are prone to develop adverse reactions such as agitation, involuntary movements, hyperactivity, and combativeness. When used for moderate sedation, benzodiazepines should not be administered by rapid bolus intravenous administration. This type of rapid bolus injection has resulted in serious adverse cardiorespiratory events predominantly in older, chronically ill patients, especially when given in combination with other sedative agents. These have included respiratory depression, apnea, and/or cardiac arrest, sometimes resulting in death. Therefore, it is always prudent to allow adequate time for the clinical onset of each individual drug administered in the moderate sedation regimen before adding additional medication from the same or a different drug class.

4.2.2 Useful Benzodiazepines for Moderate Sedation 4.2.2.1 Diazepam Diazepam is the prototypical benzodiazepine. When first introduced, its anxiolytic properties significantly advanced the success of the moderate sedation technique. It is highly lipid soluble and has a high affinity for the benzodiazepine receptor complex, producing reliable sedative and anxiolytic effects. As with many prototypical drugs, however, diazepam has several undesirable side effects that have significantly reduced its usefulness as a viable parenteral sedation drug since the introduction of a newer benzodiazepine, midazolam. Diazepam has a slower rate of distribution than most benzodiazepines (distribution half-life  =  30–66  min), and therefore has a somewhat slower (2×) onset than midazolam. The elimination

4.3  Alpha-2 Adrenergic Receptor Agonists

41

half-life for diazepam ranges from 22 to 139 h, which is at least ten times slower than for midazolam [3]. This is because diazepam has three active metabolites, nordiazepam, desmethyldiazepam, and oxazepam, all of which produce sedative effects. Termination of clinical activity for diazepam occurs primarily through redistribution. However, the combination of active metabolites and the long elimination half-­life account for the residual “hangover” effects seen clinically following diazepam administration. Diazepam is water insoluble and must be formulated with propylene glycol for compatibility. This chemical irritant is responsible for such harmful side effects as pain on injection, venous irritation, and venous thrombophlebitis and thrombosis. This, coupled with poor absorption after intramuscular injection, has severely limited the use of diazepam as an intravenous sedative agent. Today, diazepam is primarily used as an oral sedative agent.

4.2.2.2 Midazolam Since its introduction in the 1980s, midazolam has become the primary benzodiazepine for parenteral sedation and anesthesia. Its extreme lipid solubility produces a very rapid onset. The distribution half-life is 6–15 min, and its short duration of action can be attributed to its fast clearance and rapid rate of elimination. The elimination half-life for midazolam is 1–4 h, which exceeds that of other benzodiazepines. In contrast to diazepam, there are no active metabolites. Midazolam is water soluble, virtually eliminating pain during intravenous injection and venous irritation. Midazolam has a more rapid onset and produces more profound sedation and better amnesia than diazepam [3]. The short elimination half-life and the lack of active metabolites make overall recovery from midazolam sedation rapid when compared with diazepam. In addition, midazolam is well absorbed after intramuscular injection with predictable sedative effects. It is well absorbed orally as well, and is therefore a very useful oral sedative, especially in the pediatric population. The water solubility and short elimination halflife of midazolam make it the superior drug for moderate sedation. When used as a single intravenous sedative agent for moderated sedation, an average dose of midazolam is 0.1 mg/kg (7 mg for a 70 kg individual). When opioids are included in the sedation regimen, the dose of midazolam should be reduced by half. These are guidelines for dosing and are not meant to be used as a targeted goal. A more prudent method of administration of midazolam is slow titration of the drug until a predetermined clinical endpoint is reached. Titration of the drug to desired effect significantly reduces the chance of overdosage.

4.3

Alpha-2 Adrenergic Receptor Agonists

Adrenergic receptors are divided into two subtypes, alpha and beta. Generally speaking, alpha-receptor activation results in vasoconstriction and beta-receptor activation results in increased heart rate and bronchodilation. Alpha-receptors are subdivided into alpha-1 and alpha-2 subunits. The alpha-2 receptors are located centrally in the locus ceruleus and spinal cord, and peripherally in the sympathetic

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nervous system. Activation of the central alpha-2 receptors results in sedation, anxiolysis, and analgesia, while activation of the peripheral alpha-2 receptors results in decreased sympathetic activity and modulation of the sympathetic stress response.

4.3.1 Dexmedetomidine Dexmedetomidine is a highly selective alpha-2 agonist drug with a high affinity for the alpha-2 receptor. Centrally, it produces a noticeable quieting or mellowing effect without respiratory depression. This is a major advantage for a sedative agent, since other sedative drugs commonly produce respiratory depression. Therefore, dexmedetomidine is extremely useful for the sedative management of patients with morbid obesity or obstructive sleep apnea, or those whose airway may be difficult to manage if compromised. Dexmedetomidine administration results in reduction in mean arterial pressure by decreasing heart rate and systemic vascular resistance. These effects aid in modulating the stress response, promote stability, and may protect against radical fluctuations in cardiovascular parameters intraoperatively. This may be particularly useful in patients at risk for cardiac morbidities who might respond adversely to surgical stressors [7]. Dosage modifications of simultaneously administered sedatives may need to be made because of drug potentiation. Adding dexmedetomidine to a moderate sedation regimen can significantly reduce opioid and benzodiazepine requirements. Typical doses of dexmedetomidine range from 0.25 to 0.5 μg/kg, given slowly in divided doses in order to avoid significant bradycardia and/or hypotension. Dexmedetomidine is supplied in a concentration of 100 μg/ml. It must be diluted with normal saline or sterile water for injection to a final usable concentration of 4 μg/ml before use. A major advantage of dexmedetomidine during moderate sedation is the prevention of delirium in susceptible patients. Delirium can be a significant problem following ambulatory sedation because of the potential for serious disruption of the office, and possible injury to the patient or office personnel. Since pediatric patients and the elderly are likely to experience perioperative delirium with benzodiazepines, it may be prudent to minimize or eliminate their use. Patients who develop delirium are more likely to have poor outcomes than those who do not. It has been proposed that the GABA effects of benzodiazepines may alter levels of potentially deliriogenic neurotransmitters, with negative consequences [7]. Patients treated with dexmedetomidine have a better ability to communicate and cooperate than those treated with midazolam, making it the better choice for sedation in this patient population.

4.4

Moderate Sedation Technique

A thorough understanding of the pharmacodynamics and pharmacokinetics of the drugs used for moderate sedation is essential for the success of the technique. A general overview of useful drugs has been presented, but the reader should

4.4  Moderate Sedation Technique Table 4.1  General dosing guidelines for drugs used for moderate sedation. Drugs should be titrated incrementally until the desired effect is achieved

43 Drug Fentanyl Sufentanil Alfentanil Midazolam Dexmedetomidine

Dose 25–100 μg 2.5–10 μg 250–1000 μg 0.1 mg/kg 0.25–0.5 μg/kg

consult standard pharmacology texts for a more detailed description of drug pharmacology. Table 4.1 shows general dosage information for moderate sedation drugs, but the practitioner should use these only as a guide, since there is extreme patient variability in response. Consequently, these drugs should be given until a desired clinical endpoint is achieved, which may be entirely independent of fixed dosing guidelines. After the patient has been appropriately assessed preoperatively, and standard monitors have been applied and vital signs have been measured, it is usually best to begin with an anxiolytic drug such as midazolam. In order to adequately assess the level of sedation, the drug should be given slowly, approximately 1 mg every 30–45 s, until the patient begins to feel the effects of the medication. The patient may begin to feel a noticeable calming effect and exhibit some slurring of speech. At this point, a fixed dose of opioid medication such as fentanyl may be administered. A dose of 25–50  μg may be given depending upon the patient’s response to the benzodiazepine. Sufficient time should be allowed for the potentiating effect of these two drugs to become evident, approximately 3–5 more minutes. At this point the patient’s level of sedation should be assessed. If the patient is deemed to still be very alert, more midazolam, fentanyl, or dexmedetomidine may be added to enhance the sedation. The desired clinical endpoint occurs when the patient’s eyelids begin to droop and he or she may appear to fall asleep when not stimulated. At this point, the patient should still be able to respond appropriately to verbal command or light tactile stimulation. The patient is now ready to receive local anesthesia and begin the procedure. The patient’s level of consciousness should be continually monitored, and drugs should be readministered according to need as the surgery progresses. Drug dosing should be timed so that patients are recovering from the sedation as the end of the procedure nears. Care should be taken to allow adequate time for the optimal level of sedation to be reached before beginning the procedure. A common mistake is to rush the drug administration and begin treatment before the drugs have reached peak effect. This may lead to relative overdosing at the outset, which may not become evident until the treatment has begun. This could result in a level of sedation beyond the desired moderate sedation level. When deep sedation occurs, it must be immediately recognized and managed in order to prevent significant morbidity and possibly mortality. The next three chapters deal with the consequences of deep sedation and perioperative urgencies and emergencies.

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References 1. Hayhurst CJ, Durieux ME.  Differential opioid tolerance and opioid-induced hyperalgesia. Anesthesiology. 2016;124:483–8. 2. Chang L, Ye F, Luo Q, et  al. Increased hyperalgesia and proinflammatory cytokines in the spinal cord and dorsal root ganglion after surgery and/or fentanyl administration in rats. Anesth Analg. 2018;126:289–97. 3. Giovannitti JA.  Midazolam: review of a versatile agent for use in dentistry. Anesth Prog. 1987;34:164–70. 4. Lebowitz PW, Cote ME, Daniels AL, Martyn JAS, Teplick RS, Davison JK, Sunder N. Cardiovascular effects of midazolam and thiopentone for induction of anesthesia in ill surgical patients. Can Anaesth Soc J. 1983;30:19–23. 5. Glisson SN, Belusko RJ, Kubak MA, Hieber MF.  Midazolam on stimulatory responses to hypotension: preinduction vs. during anesthesia (abstr). Anesthesiology. 1982;57:A365. 6. Power SJ, Morgan M, Chokrabarti MK. Carbon dioxide response curve following midazolam and diazepam. Br J Anaesth. 1983;55:837–41. 7. Giovannitti JA, Thoms SM, Crawford JJ.  Alpha-2 adrenergic receptor agonists: a review of current clinical applications. Anesth Prog. 2015;62:31–8.

5

Periodontal Airway Management Strategies

He lives most life whoever breathes most air. —Elizabeth Barrett Browning

A conscious patient is capable of independently maintaining his or her airway in a patent state. Therefore, the key to patient safety is to retain patient consciousness at all times. Unfortunately, patients may be intentionally or unintentionally placed in a state of deep sedation, whereby airway patency becomes suspect and may require intervention for proper maintenance. The consequences of airway obstruction and hypoxemia are the primary causes of anesthetic-related morbidity and mortality. Thus, the ability to accurately predict an airway problem preoperatively would make an important contribution to patient selection and perioperative management.

5.1

Preoperative Airway Evaluation

Thirty to fifty percent of all anesthetic deaths have been attributed to the inability to manage a difficult airway [1]. The American Society of Anesthesiology’s Closed Claims Project evaluated adverse anesthetic outcomes obtained from the closed claim files of 35 US liability insurance companies. This database dates from 1985 and accrues about 300 cases per year. Respiratory events were found to be the single largest class of injury accounting for 34% of all claims, 85% of which resulted in death or brain damage. Critical review found that most outcomes could have been prevented. It is not surprising that 30% of the mortalities in these claims were the result of an inability to manage a difficult airway. It is therefore essential to include airway assessment as an integral part of your preanesthetic workup.

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The patient should be examined from a frontal and profile view to assess mandibular size and skeletal classification. The presence of micrognathia or a skeletal class II profile is associated with difficult mask ventilation and ability to secure the airway with an advanced airway device, such as a supraglottic airway or endotracheal tube. Thyromental distance is measured, and neck rotation, flexion, and extension mobility are evaluated and graded. The thyromental distance is measured between the bony point of the mentum of the mandible and the thyroid notch with the head fully extended. In the average adult, this should measure 6 cm, or approximately 3 fingerbreadths. A short thyromental distance is also associated with difficulty in securing the airway with advanced airway devices. Additionally, one should check for temporomandibular joint mobility, degree of mouth opening, loose or protruding teeth, degree of overbite, size of the tongue, visibility of oropharyngeal structures, and patency of the nares. Obesity (BMI >30 kg/m2) is an independent risk factor for the prediction of a difficult airway. Patients with an increased neck circumference and neck obesity present a greater airway risk due to the increased propensity for sleep-disordered breathing or obstructive sleep apnea. Patients with sleep apnea are at an increased risk for the development of airway obstruction and severe hypoventilation during sedation and anesthesia. In addition, neck obesity limits cervical range of motion and makes it more difficult to perform airway maneuvers. Mallampati described a method to evaluate a difficult airway by visualizing oropharyngeal structures [2]. He correlated the degree of visibility of the oropharyngeal structures with the difficulty of securing the airway. The patient is asked to open his or her mouth as wide as possible and maximally protrude the tongue. The visibility of the tonsillar pillars, soft palate, and uvula is noted, and the airway is classified as follows: class I—soft palate, fauces, uvula, and pillars are visualized; class II—soft palate, fauces, and uvula are visualized; class III—only the soft palate and base of the uvula can be visualized; and class IV—the soft palate cannot be visualized (Fig. 5.1). The degree of airway management difficulty is proportional to the increasing Mallampati Classification. The Mallampati test has become a standard part of a comprehensive airway evaluation that also includes assessment of dentition, thyromental distance, and neck extension. The cardinal signs of a difficult airway are shown in Fig. 5.2 and the procedures for a comprehensive airway evaluation are listed in Fig. 5.3.

5.2

Airway Management

The mere act of performing dental treatment on a sedated patient constitutes a threat to the airway. Airway manipulation during treatment, especially depression of the mandible while working on the lower jaw, can readily obstruct the airway. If improperly positioned, a mouth prop or tongue retractor may impinge upon the tongue to the point of airway compromise. During periodontal surgery it is common practice to use a handpiece with water spray, an ultrasonic scaler, or irrigation. A sedated patient may not be able to tolerate the excessive buildup of water or blood in the airway, which could lead to coughing, choking, laryngospasm, or bronchospasm.

5.2  Airway Management

47

Class I

Class II

Class III

Class IV

Fig. 5.1  Method of Mallampati • Short neck, wide circumference • Receding lower jaw, micrognathia with obtuse mandibular angle • Protruding upper incisors and maxillary overgrowth • Limited opening

• Decreased mobility of head and neck • Decreased thyro-mental distance • 30 kg/m2 • Obstructive sleep apnea

• High arched palate with long narrow mouth

Fig. 5.2  Cardinal signs of a difficult airway • Mallampati classification • Body mass index

• Mouth opening • Receding mandibular profile

• History of snoring or obstructive sleep apnea • Thyromental distance

• Range of motion of the head and neck • Neck circumference

Fig. 5.3  Airway evaluation strategies

Therefore, it is essential that water spray and irrigation are kept to an absolute minimum and that auxiliary personnel are trained to provide focused high-volume suction during treatment.

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When moderate sedation is the objective, deep sedation is to be avoided at all costs. However, deep levels of sedation may develop inadvertently and must be immediately recognized and managed. The periodontist must be extremely adept at recognizing and managing the difficult airway. All office personnel must be trained to recognize and manage an obstructed airway, as this is the leading cause of anesthetic morbidity and mortality. Snoring, labored breathing with use of accessory chest and neck muscles (rocking boat breathing), retraction of the suprasternal notch, tracheal tug, and loss of the end-tidal carbon dioxide waveform on the monitor are all signs of airway obstruction. Maneuvers such as the head tilt and chin lift, jaw thrust, and triple-airway maneuver are lifesaving if done quickly and efficiently (Fig. 5.4). In the event that these maneuvers are inadequate, the insertion of adjunctive airway devices is indicated. These include nasopharyngeal airways, oropharyngeal airways, and supraglottic airways, such as the i-gel and the King LT airway. Nasal airways are available in different sizes and may be inserted through the nose in semiconscious or unconscious patients. The airway provides a patent air passage from the nose to the oropharynx and helps to keep the tongue from obstructing the airway (Fig. 5.5). Oral airways are also available in various sizes and are inserted into the mouth of unconscious patients. These airways act to provide an air passage by moving the tongue from the posterior pharyngeal wall (Fig. 5.6). In the event of nasal or oral airway failure, a supraglottic airway must be inserted to secure the airway. The i-gel supraglottic airway (Intersurgical Ltd., Wokingham, Berkshire, UK) is recommended as an emergency airway due to its ease of insertion (Fig.  5.7). Alternatively, the King LT airway (King Systems, Noblesville, IN, USA) also provides a secure airway while protecting against gastric aspiration (Fig. 5.8). Both of these devices are available in various sizes to accommodate a range of patient types. Once the airway has been adequately addressed, the character of breathing must be immediately evaluated. The patient may be breathing adequately, or more likely be either hypoventilating or completely apneic. Hypoventilation is recognized by assessing the rate and depth of breathing at chairside by matching your own breathing to the patient’s. If your breathing seems to be inadequate, then the patient’s is

Fig. 5.4  Airway maneuvers

5.2  Airway Management

49

Fig. 5.5 Nasopharyngeal airways

Fig. 5.6  Oropharyngeal airways

too. Check the monitor for decreased oxygen saturation and elevated end-tidal carbon dioxide, both indicators of hypoventilation with a patent airway. If the patient can be aroused, encourage deep breathing and add supplemental oxygen if not already present. If ventilation is still inadequate, respiration may be assisted by the application of a bag-valve-mask (BVM) device with an oxygen flow of 10 l/min.

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5  Periodontal Airway Management Strategies

Fig. 5.7  i-gel supraglottic airway. If mask ventilation is found to be difficult or impossible, a supraglottic airway device may provide a means to rapidly correct a deteriorating airway Fig. 5.8  King airway

Every fifth breath should be assisted by sealing the facemask and manually squeezing the bag. Apnea is recognized by the lack of breathing effort, oxygen desaturation, and absence of an end-tidal carbon dioxide waveform. Ventilation must be controlled again by BVM with 100% oxygen at a rate of 1 breath every 5 s, or 12 times per minute. Once the airway has been secured and the patient is adequately ventilating and oxygenated, reversal agents, such as naloxone and flumazenil, may be given to restore consciousness.

5.4  Key Point to Remember

5.3

51

 ifficult Mask Ventilation and Airway Considerations D in Obesity

Occasionally, mask ventilation may prove to be very difficult. Therefore, it is especially important to predict the ease or difficulty of mask ventilation preoperatively since this is one of the first interventions in the event of airway loss. In a general adult population, difficult mask ventilation was seen in 5% of patients studied [3]. Common predictive risk factors for difficult mask ventilation include age greater than 55 years, body mass index above 30 kg/m2, male gender, presence of a beard, edentulism, high Mallampati Classification, history of snoring or obstructive sleep apnea, decreased thyromental distance, and large neck circumference. Airway assessment of the obese patient should be performed with the patient in both the sitting and supine positions. Respiratory function and airway patency can be significantly altered by this change in position [4]. In the supine position, changes in chest compliance and vital capacity may interfere with adequate spontaneous ventilation. The incidence of hiatal hernia, gastric pH of 2.5 or lower, and reduced functional residual capacity found in obese patients place these patients at increased risk for the consequences of hypoxemia and aspiration of gastric contents [5]. There is consensus that airway management is more difficult in morbidly obese patients. Total body weight may not be as critical as the location of excess weight. Excess weight in the lower abdomen and hip area may be less important than when it is distributed in the upper body area. A short, thick, immobile neck caused by cervical spine fat pads will interfere with typical airway opening maneuvers. Furthermore, the redundancy of soft-tissue structures inside the oropharyngeal and supralaryngeal areas may also make airway maintenance during sedation difficult. Mask ventilation is often difficult in the obese patient. Lack of neck extension and redundant oropharyngeal tissues decrease the success of conventional mask ventilation. Airway adjuncts such as nasopharyngeal and oropharyngeal airways are frequently required to assist mask ventilation. High positive pressures may be necessary in order to successfully ventilate the patient. The chance of inflating the stomach and the possibility of passive regurgitation are increased. If airway obstruction or apnea occurs during sedation, rapid oxygen desaturation secondary to reduced functional residual capacity makes timely airway intervention critical.

5.4

Key Point to Remember

If airway maintenance or mask ventilation is anticipated to be difficult in the event of compromise, serious consideration should be given to performance of the surgical procedure in a hospital or ambulatory surgical center where separate anesthesia providers adept at advanced airway management techniques are immediately available. It is important to remember that the majority of anesthetic mishaps are related to the inability to predict or manage a compromised airway. Proper pretreatment assessment will minimize this risk.

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References 1. Caplan RA, Posner KL, Ward RJ, Cheney FW.  Adverse respiratory events in anesthesia: a closed claims analysis. Anesthesiology. 1990;72:828–33. 2. Mallampati SR, Gatt SP, Gugino LD, et al. A clinical sign to predict difficult tracheal intubation: a prospective study. Can Anaesth Soc J. 1985;32:429–34. 3. Langeron O, Masso E, Huraux C, et al. Prediction of difficult mask ventilation. Anesthesiology. 2000;92:1229–36. 4. Paul DR, Hoyt JL, Boutros AR. Cardiovascular and respiratory changes in response to change of posture in the very obese. Anesthesiology. 1976;45:73–8. 5. Phero JC, Rosenberg MB, Giovannitti JA.  Adult airway evaluation in oral surgery. Oral Maxillofac Surg Clin North Am. 2013;25:385–99.

6

Monitoring During Periodontal Sedation

You can’t manage what you don’t measure. —Peter Drucker

Monitoring during moderate sedation is an essential anesthetic management tool that is needed to assess the patient’s current physiologic condition and responses to pain, stress, and sedative medications. Monitoring acts as an early warning system to identify potentially harmful situations before they escalate, and to permit the adequate assessment of responses to intraoperative interventions. For moderate sedation, the monitoring priority has always been continual assessment of the patient’s level of consciousness, comfort, and cooperation. When these three “Cs” are present, the patient is in a clinically stable state. In 2016, the House of Delegates of the American Dental Association adopted the Guidelines for the Use of Sedation and General Anesthesia by Dentists [1]. In addition to providing terminology definitions and educational, personnel, and equipment requirements, these Guidelines outline the monitoring requirements necessary for moderate sedation (Fig.  6.1). These include continual assessment of the patient’s level of consciousness, monitoring of oxygen saturation continuously via pulse oximetry, and continual monitoring of the ventilatory status by observation of chest excursions and through the measurement of end-tidal carbon dioxide. Circulation must be monitored through continual evaluation of blood pressure and heart rate. Continuous electrocardiographic monitoring should be considered in patients with significant cardiovascular disease.

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• Monitoring: A qualified dentist administering moderate sedation must remain in the operatory room to monitor the patient continuously until the patient meets the criteria for recovery. When active treatment concludes and the patient recovers to a minimally sedated level a qualified auxiliary maybe directed by the dentist to remain with the patient and continue to monitor them as explained in the guidelines until they are discharged from the facility. The dentist must not leave the facility until the patient meets the criteria for discharge and is discharged from the facility. Monitoring must include: • Consciousness: Level of sedation (e.g., responsiveness to verbal command) must be continually assessed. • Oxygenation: Oxygen saturation must be evaluated by pulse oximetry continuously. • Ventilation: • The dentist must observe chest excursions continually. • The dentist must monitor ventilation and/or breathing by monitoring end-tidal CO2 unless precluded or invalidated by the nature of the patient, procedure or equipment. In addition, ventilation should be monitored by continual observation of qualitative signs, includingauscultation of breath sounds with a precordial or pretracheal stethoscope.

• Circulation: • The dentist must continually evaluate blood pressure and heart rate unless invalidated by the nature of the patient, procedure or equipment and this is noted in the time-oriented anesthesia record. • Continuous ECG monitoring of patients with significant cardiovascular disease should be considered.

• Documentation: • Appropriate time-oriented anesthetic record must be maintained, including the names of all drugs, dosages and their administration times, including local anesthetics, dosages and monitored physiological parameters. • Pulse oximetry, heart rate, respiratory rate, blood pressure and level of consciousness must be recorded continually.

Fig. 6.1  Moderate sedation monitoring guidelines

Fig. 6.2  Signs of oversedation

• Inability to keep mouth open • Agitation • • • • •

6.1

Failure to respond to verbal command Incoherent speech Uncooperative behavior Excitation Uncoordinated muscular movement

Monitoring Consciousness

The easiest and most practical way to assess a patient’s level of consciousness is through visual and verbal assessment. A conscious patient is capable of rational response to command and/or can respond appropriately to light tactile stimulation, as defined in the Use Guidelines [1]. A conscious patient is therefore, by definition, capable of maintaining his or her own airway in a patent state, without outside intervention. Consciousness ensures patient safety since loss of consciousness is associated with the inability to maintain a patent airway. As described in Chap. 5, airway compromise is the leading cause of anesthetic-related morbidity and mortality. At an appropriate level of moderate sedation, the patient should be relaxed, comfortable, and cooperative, and should be responsive to verbal interaction. If the patient appears to be sleeping, he or she should be easily arousable with a light tactile stimulus such as a tap or shake to the shoulder. Loss of verbal contact and an aversive response to painful stimulus only indicate that the patient is unconscious and has progressed to a level of deep sedation. It is at this level that the patient’s airway and ventilatory status must be assessed and managed and the patient returned to the conscious state as soon as possible. Therefore, it is important that the periodontist be adept at recognizing the signs of oversedation and take corrective action before the progression to deep sedation can occur (Fig. 6.2).

6.2  Monitoring Respiratory Function

55

Fig. 6.3  A bispectral index (BIS) monitor is useful in monitoring the patient’s level of consciousness. Readings less than 60 are associated with unconsciousness

A monitoring device, the bispectral index (BIS) monitor, exists to help assess the patient’s level of consciousness. The BIS monitor averages the EEG tracings through electrodes placed on the forehead (Fig. 6.3). An algorithm converts these results into a numerical value on the monitor screen. A level of 100 relates to a fully conscious, unsedated patient. The level of consciousness decreases as the number decreases. A value of 60 or below is generally associated with unconsciousness. Through the use of this monitor, one can theoretically prevent oversedation. Although it is a useful tool, it has not demonstrated enough utility to mandate its routine use. Visual and verbal assessments remain the gold standard for monitoring consciousness and CNS function.

6.2

Monitoring Respiratory Function

To completely monitor respiratory function, one must continually assess both oxygenation and ventilatory status. This may be done through visual assessment, and the use of monitoring devices such as a pretracheal stethoscope, pulse oximeter, and capnograph. Oxygenation and ventilation are interdependent and must be monitored simultaneously to obtain an accurate picture of the patient’s well-being. As discussed in Chap. 5, the most common causes of anesthetic mishaps are disturbances in air exchange, i.e., airway obstruction and hypoventilation. Both of these conditions result in hypoxemia which ultimately leads to severe morbidity and/or

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mortality. It is therefore imperative that the practitioner understand the inherent causes and consequences of hypoxemia and how to prevent them. The pulse oximeter is an essential tool that provides an early warning system for hypoxemia, allowing for intervention before it can become catastrophic.

6.2.1 Monitoring Oxygenation Causes of hypoxemia are listed in Fig. 6.4. If airway obstruction or severe hypoventilation occurs, the result is a decrease in lung alveolar oxygenation that leads to hypoxemia. Ventilation/perfusion abnormalities occur in lung diseases, especially obstructive lung diseases. Conditions such as asthma, chronic bronchitis, and emphysema result in portions of the lung that are either underventilated or not ventilated at all. Hypermetabolic states such as occur with hyperthyroidism or fever increase oxygen consumption and may result in hypoxemia. Low cardiac output states such as syncope or profound bradycardia or hypotension result in increased tissue extraction of oxygen leading to low oxygen blood levels. Anemia, or low hemoglobin, reduces the oxygen-carrying capacity of the blood and leads to hypoxemia. Another form of anemia, methemoglobinemia, can occur when excessive amounts of local anesthetics, especially prilocaine and articaine, are administered. Finally, breathing an oxygen content less than that of room air (21%) will result in hypoxemia. This is an iatrogenic condition caused by faulty installation of oxygen and nitrous oxide lines in new facility construction. Cases of morbidity and mortality related to hypoxemia have occurred in instances where lines were crossed during installation. Patients received 100% nitrous oxide instead of the intended oxygen. The pulse oximeter came into routine use in the 1980s. Since then, anesthetic morbidity and mortality have been significantly reduced. The utility of pulse oximetry cannot be overestimated. Prior to pulse oximetry, practitioners had to rely upon clinical signs of hypoxemia in order to recognize and treat the condition. Nail beds, lips and oral mucosa, and blood were assessed for the presence of cyanosis. As we shall see, cyanosis is a late occurrence signifying that the patient is in great peril. The only way to determine blood oxygenation was to obtain a sample from the artery and have it measured through mass spectrometry. This was an invasive procedure that did not produce immediate results. The pulse oximeter, by contrast, provides a noninvasive and relatively immediate measurement of the blood oxygenation. Ninety-seven percent of oxygen is carried in the blood by hemoglobin. The other 3% is dissolved in the arterial blood. An arterial sample is used to measure the Fig. 6.4  Causes of hypoxemia

• • • • • • •

Airway obstruction Hypoventilation Breathing 95%)

90

60

Mild (90-94%)

85

55

Moderate (85-89%)

80

50

Severe (