Implications of Electronic Cigarettes on the Safe Administration of Sedation and General Anesthesia in the Outpatient Dental Setting
Today the number of electronic cigarette users continues to rise as electronic cigarettes slowly, yet steadily overtake conventional cigarettes in popularity. This shift is often attributed to the misconception that electronic cigarettes are “safer” or “less dangerous” than conventional cigarettes. Recent studies have shown that electronic cigarettes are far from safe and that the inhaled agents and byproducts within vaping aerosols can have adverse effects on systemic and oral health like combustible tobacco products. The first electronic cigarettes were originally introduced as a tool for smoking cessation. However, newer iterations of electronic cigarette devices have been modified to allow the user to consume tetrahydrocannabinol (THC), the psychoactive component of cannabis, in addition to nicotine. As the popularity of these devices continues to rise, the number of patients seeking dental treatment who also consume electronic cigarettes will too. This article aims to shed light on the deleterious effects electronic cigarettes can have on systemic and oral health, as well as the special considerations for sedation and anesthesia providers treating patients who use electronic cigarettes.
Vaping devices, also known as electronic cigarettes (e-cigarettes) or electronic nicotine delivery systems, were first introduced to the US market in 2007 as aids for smoking cessation. Use of these devices rapidly grew in popularity as users perceived them as safe alternatives to conventional cigarettes and other smoked tobacco products.1 When initially introduced, the effects that e-cigarettes had on one's health were unknown, and the number of users has continued to grow over time. Now there are many prospective and retrospective studies documenting the deleterious systemic effects of e-cigarette use.2 An area of interest for providers of sedation and general anesthesia is the effect of e-cigarettes on multiple organ systems. Just like conventional cigarette users, patients who use vaping devices often require a more extensive preoperative workup and potentially alternative approaches to safely provide deep sedation or general anesthesia in the outpatient dental setting.
HISTORY AND BACKGROUND
Electronic cigarettes are composed of a battery, a reservoir for holding a vaporizable solution that typically contains nicotine, a heating element or an atomizer, and a mouthpiece through which the user inhales or “puffs” (Figures 1 and 2).3 Electronic cigarettes create aerosols when the user draws in air through the mouthpiece. This triggers the device to begin drawing liquid solution from the tank or reservoir and pass it over the internal heating element. The liquid is then vaporized by the heating element, which operates at temperatures ranging between 100°C and 300°C depending on the device's construction and power output. As the device heats the liquid solution (often called “e-liquid” or “e-juice”), an aerosol or vapor is produced that is inhaled by the user.
Citation: Anesthesia Progress 69, 2; 10.2344/anpr-69-02-16
Citation: Anesthesia Progress 69, 2; 10.2344/anpr-69-02-16
Upon their introduction, electronic cigarettes were novel devices with no literature to document their safety. Subsequently, electronic cigarette manufacturers were able to market their products to the public as “safe” since they did not contain any tobacco nor used combustion to produce aerosols. Most of the well-known effects of tobacco are understood from combustion reactions rather than the vaporization of “e-liquids” with electronic cigarettes.4 Due to the quantitative lack of published research on vaporization products, the widespread misconception that using vaping devices is safer than smoking conventional cigarettes permeated its way into the mainstream.
The largest and most rapidly growing demographic of e-cigarette users are teenagers and young adults who view using these devices as benign compared with conventional cigarettes.5 The adoption of electronic cigarettes over conventional cigarettes in this patient population is also appealing because many e-liquids are flavored (eg, fruit, cotton candy, or chocolate). The US Centers for Disease Control and Prevention (CDC) has reported an increase in the use of electronic cigarette devices among both US middle and high school students, and the proportion of young adults (18–24 years) who are current e-cigarette users exceeds that of older adults (>25 years).6 Additionally, the CDC reported the use of electronic cigarette devices by teenagers increased from 1.5% in 2011 to 20.8% in 2018, surpassing conventional cigarette use in this population.7 The growing popularity of electronic cigarettes within younger populations is an important consideration for providers of sedation and general anesthesia for dentistry since third molar extraction, one of the most common outpatient surgeries performed in office-based settings, typically occurs during the second and third decade of life.8 As such, the usual preoperative assessments that are performed in traditional smokers should ideally include users of electronic cigarettes.
PREOPERATIVE ASSESSMENT CONSIDERATIONS
Oral Effects
A commonly overlooked aspect of vaping devices are their effects upon the oral cavity. Many users believe inhaling aerosols from electronic cigarettes has minimal sequelae on the oral cavity due to the aerosols being generated through a noncombustion reaction, which renders the “vapor” smokeless. Since there is no combustion, users often discount the many epidemiological studies that have shown a positive correlation between the use of combustible tobacco products and increased risks of periodontitis, oral cancer, tooth loss, and dental implant failures.9 Although the vapor is produced through a noncombustion reaction, there are many dangers associated with the generation of aerosols from electronic cigarette devices. Recent studies are beginning to highlight the harmful effects of electronic cigarettes on both the hard and soft tissues of the oral cavity.
The elevated temperatures produced during vaporization facilitate transfer of heavy metals with high atomic density and toxicity to humans (eg, nickel, cadmium, chromium, and lead), from the coil into the e-liquid.10 In addition to the presence of heavy metals in electronic cigarette aerosols, other known carcinogens and mutagens like formaldehyde, acetaldehyde, and acrolein have been recorded in the vapor produced by the device.11
Consumption of and exposure to these heavy metals and carcinogens has detrimental effects on the periodontium of the oral cavity. Like the reactive oxygen species from cigarette smoke and its deleterious effects on the periodontium and increased risk of periodontitis, recent research has shown that the noxious chemicals found in e-liquid aerosols causes increased oxidative and carbonyl stress with inflammatory cytokine release in human periodontal ligament fibroblasts.12 Additionally, increased oxidative stress and inflammatory cytokine release can lead to gingival recession and crestal bone loss.13 The chemicals found in e-liquids and e-cigarette aerosols are also detrimental to the health and long-term prognosis of the osseointegration of dental implants. The use of electronic cigarette devices increases the levels of tumor necrosis factor-α and interleukin-1β in peri-implant sulcular fluid causing an increased local inflammatory response around the implant, which leads to bleeding with probing, increased probing depths, and ultimately, implant failure.14
E-liquids with or without nicotine also demonstrated cytotoxic and genotoxic effects on human oropharyngeal mucosa.10 Oral epithelial cell lines that have been exposed to electronic cigarette aerosols have shown significantly reduced cell viability and increased rates of apoptosis and necrosis, regardless of whether the e-liquid contained nicotine.15 The toxicants in the aerosols appear to be retained in intraoral fluids and tissues at levels often approximating 90% of baseline levels found originally in the inhaled aerosol. These water-soluble reactive toxins can challenge the oral cavity constituents, potentially contributing to alterations in the native oral microbiome and host cells critical for maintaining oral homeostasis.10 Disruption of the normal oral flora may further perpetuate the user's risk of developing periodontitis and/or opportunistic oral infections. Additionally, it has been found that nicotine in e-liquids facilitates increased adhesion of Streptococcus mutans on intraoral hard tissues, doubling the production of oral biofilms and increasing the caries potential.2 Like combustible tobacco products, electronic cigarettes can clearly contribute to the development of periodontitis, tooth loss, implant failure, and oropharyngeal cancer.
Cardiovascular Effects
Although vaping devices were originally touted to be safe in comparison to conventional cigarettes, recent literature has begun to highlight how electronic cigarettes can negatively impact the cardiovascular system like conventional cigarette use. A hallmark finding in cardiovascular diseases is heightened platelet aggregation and increased risk of thromboses. In a study conducted by Hom et al,16 an increase in the platelet aggregation rate and percentage aggregation was noticeable in as little as 15 minutes after exposure to vaping aerosols, independent of whether the aerosol contained nicotine. The platelet aggregation rate continued to rise, peaking at 1 hour after initial aerosol exposure. The enhanced platelet aggregation is believed to be caused by the inhalation of fine particulate matter, which is a byproduct of electronic cigarette aerosol generation.16
E-cigarettes can negatively affect a patient's preoperative vital signs. Acute inhalation of aerosols from an electronic cigarette can increase a patient's heart rate and elevate their systolic blood pressure.17 An increase in blood pressure after acute inhalation of vaping aerosols can partly be attributed to nicotine within some e-liquids. Nicotine activates the renin-angiotensin-aldosterone system by upregulating angiotensin converting enzyme, which converts angiotensin I to angiotensin II and thus increases blood pressure, stimulates the release of norepinephrine, and promotes fluid retention. These changes can lead to a 79% greater risk of an acute myocardial infarction over non-nicotine vaping users and individuals who never use any form of electronic or conventional cigarettes. Overall, a chronic electronic cigarette user has a 1.7× greater chance of sustaining a myocardial infarction over the course of their life.18,19
When propylene glycol and glycerin in e-liquids are heated, they subsequently degrade and form carbonyl compounds. These compounds include the following: acrolein, formaldehyde, and acetaldehyde. Carbonyl compounds have been found to cause oxidative stress and inflammation throughout the body, specifically in the cardiovascular system.20 Exposure to acrolein is linked to an increase in the indices of platelet activation, such as the formation of platelet-leukocyte aggregates in the blood, increased plasma PF4 levels, and increased platelet-fibrinogen binding. This indicates inhalation of electronic cigarette aerosols can predispose the user to thrombotic events.21 In addition to increasing the risk of thrombotic events, the fine particulate matter found in electronic cigarette aerosols has been linked to global vascular endothelial dysfunction. Altered vascular endothelial permeability can lead to the development of atherosclerosis, hypertension, and eventual heart failure.22
According to the CDC, men are more likely than women to have ever tried vaping devices. When analyzing the gender distribution of current electronic cigarette users, men are twice as likely as women to be current users.23 Interestingly, the use of electronic cigarette devices has been linked to male erectile dysfunction, and the link was found to be independent of the male's age and cardiovascular disease status.24 Erectile dysfunction in vaping device users is thought to be caused by impaired vasodilation and reduced penile circulation due to the elevated nicotine levels found in vaping aerosols. Nicotine is not thought to be the only cause of erectile dysfunction in male electronic cigarette users. Research shows e-liquids with and without nicotine can cause a reduction in circulating testosterone levels, which leads to reduced mRNA expression of steroidogenesis enzymes responsible for normal erectile function.25
Respiratory Effects
There is an ever-growing body of literature from in-vitro animal and human studies documenting the deleterious effects of inhaling vaping aerosols on the respiratory system. One of the most widely publicized consequences of chronic electronic cigarette use is bronchiolitis obliterans, more commonly known as “popcorn lung.” The nickname arose in the early 2000s after 8 cases of severe bronchiolitis obliterans were recorded in workers at a microwave popcorn factory. The disease cluster was later traced back to the inhalation of volatile flavoring agents used in the production process. The identified aerosolized flavoring agents were diacetyl (2,3-butanedione) diketone, and 2,3-pentanedione and are used in the manufacturing process to increase aroma and flavor intensity.26 These same flavoring agents are also regularly found in e-liquids. Likewise, the pathophysiology of the popcorn lung secondary to vaping is believed to be initiated by the epithelial damage caused by diacetyl (2,3-butanedione) diketone and 2,3-pentanedione.27 The airway surface liquid and mucociliary clearance is regulated in epithelial cells through absorption of Na+ and Cl− secretion in epithelial cells. These chemicals disrupt the transepithelial Na+ transporters, which causes the proliferation of granulation tissue within the bronchiolar epithelium leading to complete and partial obstruction of the bronchioles (Figure 3).28 Prolonged exposure to diacetyl (2,3-butanedione), diketone, and 2,3-pentanedione can lead to fixed airflow obstruction, gas exchange impairment, and obstructive lung disease. The disease process can become so severe that the only treatment may be lung transplantation.29
Citation: Anesthesia Progress 69, 2; 10.2344/anpr-69-02-16
The most common and major components of e-liquids are propylene glycol or 1,2-propanediol and glycerol or glycerin (propane-1,2,3-triol). Both types of compounds act as solvents for nicotine and flavoring compounds.4 These compounds are generally well tolerated as food additives and are classified by the US Food and Drug Administration as “generally recognized as safe.”30 However, when inhaled, these solvents have been shown to adversely affect pulmonary tissues.31 During the generation of vaping aerosols, propylene glycol and glycerin are heated and subsequently form aldehydes as byproducts. When inhaled, these aldehydes are known to induce coughing, asthma exacerbations, and alterations in pulmonary function test results that mimic those of obstructive pulmonary disease, like a decreased forced expiratory volume in the first one second to the forced vital capacity of the lungs (FEV1/FVC) ratio.32
In e-liquids that contain tetrahydrocannabinol (THC), vitamin E is used as a thickening agent to permit vaping of the THC.33 The inhalation of vitamin E has been found to cause lung surfactant to lose its ability to maintain the surface tension that is necessary to facilitate pulmonary gas exchange.34 Additionally, when vitamin E is heated to generate aerosols, it creates ketene gas. This gas is highly toxic to pulmonary tissues and has been linked to e-cigarette or vaping use-associated lung injury.35
Pulmonary homeostasis is maintained by a multitude of physiological mechanisms including lung surfactants, mucociliary clearance, and phagocytosis of inhaled particulates. Alveolar macrophages are the primary cell line responsible for protecting pulmonary tissues from further injury after they have received an insult. Whether tissue damage is of infectious or inflammatory origin, alveolar macrophages respond to reduce inflammation and limit the extent of injury. Alveolar macrophages are effectors of resolution of inflammation through phagocytosis of apoptotic cells (efferocytosis), preventing dying cells from releasing pro-inflammatory and toxic contents into the environment while triggering the release of anti-inflammatory and repair factors.36 Exposure to vaping aerosols has been found to change the phenotype and function of alveolar macrophages, suppressing their efferocytotic activity leading to impaired resolution of pulmonary epithelial inflammation.37 Inhalation of electronic cigarette aerosols also suppresses host response to viral infections. With or without nicotine, these aerosols have been shown to inhibit expression of SPLUNC1 (short palate, lung, and nasal epithelial clone 1), a molecule required for host defense against human rhinovirus.38
When e-liquids are heated to generate aerosols, the fine particulate matter byproduct produced creates a pro-inflammatory state within bronchial and alveolar cell lines. This pro-inflammatory state has been linked to the increased generation of reactive oxygen species in response to e-cigarette aerosol inhalation. The generation of reactive oxygen species secondary to electronic cigarette aerosols is capable of triggering apoptosis and programmed necrosis in pulmonary cell lines.39 Compared with conventional cigarette smoke produced via combustion, vaping aerosols do not produce carbon monoxide. Thus, the use of electronic cigarettes is not associated with an increase in carboxyhemoglobin levels.40
Aerosols from electronic cigarette devices affect multiple respiratory system functions including altering airflow, increasing oxidative stress, and interfering with lung development.32 A recent animal model demonstrated long-term exposure (daily 1-hour exposure for 4 months) to nicotine-containing vapor induced COPD-like features in mice lungs. These findings included increased airway hyper-reactivity, distal airspace enlargement, mucin production, and cytokine and protease expression.41 Electronic cigarettes have also been linked to suppression of the protective cough reflex. Research has shown that in a group of healthy adult nonsmokers, a single exposure to electronic cigarette aerosols, approximating the nicotine delivery of 1 tobacco cigarette, significantly inhibits cough reflex sensitivity.42 Therefore, it is not without reason for a sedation/anesthesia provider to consider treating patients who endorse any electronic cigarette use with the same management principles as a COPD or reactive airway patient.
Drug-to-Drug Effects
Patients who regularly use vaping devices are potentially at risk for metabolic interactions between compounds found in electronic cigarette aerosols and anesthetic agents. Electronic cigarettes have been shown to produce volatile organic compounds, including toluene, in every sample of aerosol detected in a study conducted by Zhang et al.43 Evidence has shown that toluene shares the same effect as many central nervous system (CNS) depressant agents like opioids and barbiturates.
Many patients seeking dental treatment require and/or desire sedative agents when having dental procedures due to dental anxiety or pain. In addition to enjoying the taste of e-liquids, many users endorse consumption of e-liquids with nicotine for its anxiolytic effects. The acute consumption of nicotine has been shown to have anxiolytic properties by altering neurotransmitter secretion within the CNS.44 It is not without reason to anticipate a patient who uses electronic cigarettes and has dental anxiety to utilize their device prior to sedation or general anesthesia. Consumption of nicotine has also been linked to analgesic and antinociceptive effects that are caused by nicotine interacting with endogenous opioid pathways and binding to central and peripheral nicotine acetylcholine receptors.45 Subsequently, chronic nicotine use has been associated with patients having an increased opioid requirement postoperatively. A proposed mechanism for the increased opioid requirement postoperatively is alteration in pain thresholds secondary to nicotine abstinence in the preoperative period combined with a receptor-mediated tolerance that develops from chronic nicotine use.46 In a study conducted by Chiang et al,47 abstinence for 1 day in nicotine-dependent patients resulted in hyperalgesia and lowered pain thresholds after surgical procedures.
Furthermore, volatile organic compounds and nicotine have been shown to exert CNS depressive effects similar to many sedative agents. Prior to performing a procedure under sedation, the provider should be mindful of these interactions and take a thorough history during their preoperative assessment. In patients who endorse using electronic cigarettes, the sedation and anesthesia provider should inquire about the frequency of use, when the patient last used their device, and what substances they inhale using their device. It is important for the provider to make the distinction between patients inhaling substances other than nicotine (ie, THC products), as patients who vape THC products are at potentially higher risk for perioperative lung injury.48
SURGICAL CONSIDERATIONS
Wound Healing
It has been well documented that smoking conventional cigarettes in the perioperative period negatively impacts surgical outcomes. In soft tissue procedures, nicotine has been found to increase the risk of skin flap necrosis and surgical site infection.49 An animal study found that rats exposed to vaping aerosols have the same rates of skin flap necrosis as those exposed to traditional cigarettes and significantly higher rates of skin flap necrosis compared with a control group.50 For many years, cigarette smoke has been known to cause local tissue ischemia from combustion-produced carbon monoxide-induced vasoconstriction. In a study conducted by Page et al,51 which used a thermal imaging camera, a reduction in cutaneous blood flow to the hands and upper extremities was observed in participants less than 10 minutes after inhalation of electronic cigarette aerosols. A reduction in blood flow to a surgical site secondary to aerosol inhalation increases the length of the tissue repair process by prolonging the 4 phases of healing (coagulation/hemostasis; inflammation; proliferation; and wound remodeling).52
Nicotine can impair the wound healing process in the oral cavity, has been shown to have antiproliferative properties, and affects gingival fibroblasts in vitro. Gingival fibroblasts actively participate in the tissue repair process by proliferating, migrating, and filling the wound beyond the synthesis of growth factors and extracellular matrix molecules.53 When gingival fibroblasts are exposed to vaping aerosols, cell migration and wound healing are delayed.54 Electronic cigarette devices containing nicotine can affect oral myofibroblast differentiation, leading to decreased wound contraction, which also impairs the healing process.55
DISCUSSION
Vaping devices remain largely unregulated and are inexpensive to manufacture. Pair this with the widely held misconception that these devices are less dangerous than conventional cigarettes and it is unlikely that there will be a decline in the number of electronic cigarette users for the foreseeable future. Use of vaping devices poses an equal, if not arguably greater threat to one's systemic and oral health than conventional cigarettes. Just like conventional cigarettes, electronic cigarette devices have been linked to the development of a litany of diseases, including but not limited to hypertension, atherosclerosis, asthma, emphysema, and oropharyngeal carcinoma. The use of vaping devices is becoming a public health crisis that is depleting valuable medical resources. Therefore, it is the responsibility of clinicians and anesthesia providers alike to educate the public regarding the true dangers associated with using these devices.
The growing number of electronic cigarette users has serious implications for providers of moderate and deep sedation and general anesthesia in the outpatient dental setting. Sedation and general anesthesia providers should be aware of the acute and chronic systemic effects of electronic cigarette device use to aid in preventing, identifying, and managing adverse events that can occur perioperatively. The adverse event providers will most commonly encounter and that is of greatest concern is airway obstruction. Electronic cigarette devices have been proven to increase airway reactivity and have been linked to the development of asthma in chronic users.56
Furthermore, patients with reversible and irreversible obstructive lung disease are at an increased risk of perioperative pulmonary complications. Due to the potential risks associated with the administration of anesthetic agents in all patient populations, the preoperative consultation period is critical to determine if a patient is a suitable candidate for sedation in the office setting. There are 3 key factors to take into consideration when evaluating a patient with a suspected reactive airway for an office-based sedation or general anesthesia: (1) Identify risk factors contributing to a reactive airway or obstructive/restrictive disease; (2) If present, evaluate the severity of diminished lung function; (3) Determine whether the patient's condition can be improved or further optimized prior to the procedure. Assessing these 3 factors will aid in deciding the appropriate anesthetic plan and venue for care (office-based versus hospital-based).
Commonly encountered reactive airway risk factors include active smoking history or electronic cigarette use, active upper respiratory infection, symptomatic poorly controlled asthma, and COPD requiring supplemental oxygen. Patients with positive risk factors should have their pulmonary function tested in the preoperative period to assess severity of their disease. Peak expiratory flow rate (PEFR) and spirometry are 2 commonly used methods to assess pulmonary function. PEFR can be measured in an outpatient setting with a handheld peak flow meter. A PEFR >80% of predicted indicates the patient's pulmonary function is stable and/or well controlled. In the patient with a repeated PEFR ≤80% of predicted, further evaluation should be performed with spirometry.
In patients who admit to or with whom there is warranted suspicion of electronic cigarette use, careful attention should be paid to the respiratory component of the primary survey. This includes monitoring the patient's respiratory effort at rest, examining their airway, and auscultation of breath sounds. Patients who are chronic electronic cigarette device users will likely show physical exam findings similar to asthmatic patients, including wheezing and rhonchi. In asthmatic patients, spirometry can be used in the office setting to evaluate if the patient's asthma is well controlled. An FEV1 >80% of predicted indicates the asthmatic is well controlled. In any patients with repeated FEV1 <80% of predicted, the sedation or anesthesia provider should consider having the patient's pulmonary function optimized prior to the procedure, regardless of whether there is a documented history of asthma.
When evaluating a patient for office-based sedation, a crucial vital sign that should be obtained during the preoperative period in patients who endorse e-cigarette use is room-air oxygen saturation (SpO2) at rest. In the office setting, a patient's SpO2 can be obtained inexpensively and in real time using a finger pulse oximeter. The importance of obtaining a baseline SpO2 in all patients being evaluated for office-based sedation is highlighted by data that show patients with a SpO2 <92%, excluding any other conditions, are at a higher risk for perioperative and postoperative pulmonary complications.57
Of note, although not commonly used to evaluate the stability of a patient's pulmonary function, chest radiographs can be used as an adjuvant to rule out any lower respiratory tract infection prior to the date of the procedure. In patients with an active respiratory tract infection, elective surgery should be postponed until the patient has been asymptomatic for a minimum of 2 weeks or ideally up to 6 weeks.50,58 An active respiratory tract infection can increase the risk of perioperative respiratory complications by a multiple of 7.59
When treating chronic electronic cigarette users showing signs of reversible obstructive lung disease, it is the belief of the authors of this paper that the patient will benefit from having their lung function and airway optimized with the administration of appropriate medications in the days leading up to the procedure as well as during the immediate preoperative period. The authors of this paper recommend prescribing a short course of oral prednisone (40 mg 1 tab PO QD for 5 days) prior to the day of the sedation (Table). In patients with a history of a reactive airway or reversible obstructive lung disease, administration of oral corticosteroids in the preoperative period has been linked to a decreased incidence of peri- and postoperative bronchospasm, as well as decreased oral airway edema and upper airway reactivity.60
Continuing, the authors recommend on the day of the sedation during the immediate preoperative period to administer a prophylactic dose of a suitable short-acting β-adrenergic agonist such as albuterol. The prophylactic albuterol can be administered as 2 to 4 puffs from a multidose inhaler just prior to the procedure start or in nebulized form (albuterol 2.5 mg) 20 to 30 minutes prior to any airway manipulations (Table).61 Administration of an appropriate short-acting β-adrenergic agonist just prior to the procedure start facilitates relaxation of bronchial smooth muscle and increases the mucociliary clearance of sputum, leading to improved perioperative pulmonary function.62
In addition to preoperative optimization, the provider can further reduce the probability of experiencing an adverse airway event by adequately premedicating the patient. An optimal premedication decreases patient anxiety and improves work of breathing, while eschewing oversedation and respiratory depression. Although there may currently be no single ideal drug for the purposes of premedication, the authors recommend using dexmedetomidine, an α-2 adrenergic receptor agonist, due to its favorable pharmacological profile. Administration of dexmedetomidine provides anxiolytic, sympatholytic, and antisialagogue effects without causing respiratory depression.63 Dexmedetomidine can be administered via multiple different routes including intravenous (IV), intramuscular (IM), intranasal, and buccal infiltration. For the purposes of premedication, the authors recommend IV or IM administration. The IV premedication dosage is 0.33–0.67 μg/kg, while the IM premedication dosage is 2.5 μg/kg, either route should be administered 15 minutes prior to procedure start.64
Furthermore, in patients with a difficult airway or who have diminished respiratory functionality, the provider can further reduce the incidence of possible airway obstruction via the anesthetic agents they opt to use perioperatively. The authors of this paper recommend ketamine as one of the agents used in a balanced sedation technique. Ketamine is a phencyclidine derivative that acts as an N-methyl-D-aspartate (NMDA) receptor antagonist to cause its anesthetic effects. Ketamine is an ideal agent in a patient with a potentially reactive airway because it allows maintenance of protective airway reflexes while sedating the patient without causing respiratory depression.65 Using a balanced technique, ketamine should be dosed at 0.5 mg/kg and administered intravenously in small boluses similar to propofol. Ketamine has an onset of 20 to 30 seconds and a duration of 20 to 30 minutes.66 When used in patients with reactive airways, ketamine should not be administered alone due to increased salivation. The authors recommend administering ketamine with a suitable antisialagogue (eg, glycopyrrolate or atropine) to attenuate the excessive salivation that can occur with ketamine.
Next, acute and chronic electronic cigarette device use has detrimental consequences on the cardiovascular system and centers around nicotine, which causes sympathetic discharge in the autonomic ganglia and adrenal medulla, leading to the release of catecholamines.67 Patients who vape prior to the administration of sedative or anesthetic agents may present with an elevated heart rate, increased systolic blood pressure, and increased cardiac output. Performing a 12-lead electrocardiogram in the preoperative period can aid in evaluating patients with high clinical suspicion for right ventricular hypertrophy, potential conduction disturbances, and to rule out evidence of ischemic heart disease.57 Patients with no history of cardiovascular disease may be able to tolerate nicotine and vaping-associated cardiovascular system changes. For example, the teenager presenting for impacted third molar extractions while tachycardic is unlikely to be at major risk for an acute coronary syndrome. However, the middle-aged patient with some underlying pre-existing medical comorbidities (eg, hypertension or atherosclerosis) may not be able to tolerate these baseline changes, and therefore, perioperative cardiovascular changes in this type of patient may have the potential to significantly increase morbidity during the perioperative administration of sedative and anesthetic agents. Taking this into consideration, the serum half-life of nicotine is ∼2 hours.19 The authors recommend educating the patient and encouraging them to withhold from electronic cigarette device use for at least 10 hours prior to the administration of any sedative or anesthetic agents in order to reduce acute cardiovascular changes perioperatively.
Additionally, the nicotine in cigarette smoke has been found to induce hepatic microsomal enzymes and enhance the activity of cytochrome P-450 mixed oxidase metabolic pathway. Subsequently, nicotine consumption profoundly alters pharmacodynamics and pharmacokinetics of many anesthetic agents undergoing hepatic metabolism. Currently, it is recommended that a smoker abstain for a period of 6 weeks prior to elective surgery in order to allow hepatic enzymes and the immune system to return to baseline levels, thus making drug metabolism more predictable.67 The nicotine content found in vaping aerosols can be 2–3 times that of cigarette smoke depending on the construction of the device and the nicotine concentration within the e-liquid.68 Therefore, the authors recommend an abstinence period of 6 weeks minimum for electronic cigarette device users undergoing elective procedures.
The use of electronic cigarette devices has been linked to decreased wound healing capabilities and increased postoperative surgical complications. In cigarette smokers who are planning to undergo surgery, it is recommended that cessation begin 6 to 8 weeks prior to surgery.69 There are currently no recommendations for when an electronic cigarette user should initiate cessation to improve surgical outcomes. Nevertheless, given how electronic cigarette use causes comparable end-organ effects to conventional cigarettes, it is the author's belief that electronic cigarette users should be treated like cigarette smokers, and a 6- to 8-week cessation period be recommended to patients undergoing dental sedation.
CONCLUSION
Consumption of electronic cigarettes is not free of consequences to one's systemic and oral health. Peer reviewed literature now supports that the aerosols generated by e-cigarettes have detrimental effects on the health of multiple organ systems including the cardiovascular, pulmonary, and CNSs. Even with emerging literature illustrating the harmful effects of e-cigarettes, these devices remain largely unregulated, and given the current statistical trends, the number of e-cigarette users seeking dental care will continue to rise. Providers of sedation and general anesthesia for dentistry must anticipate an increasing number of patients being e-cigarette users. Similar to patients who smoke tobacco, the modern anesthesia provider must be knowledgeable about the systemic effects of e-cigarette aerosols in order to optimize patient care throughout the perioperative period.
Reusable electronic cigarette components. Reusable e-cigarettes are composed of a plastic or glass tank which allows the user to store a greater volume of e-liquid. The heating element is typically an atomizer which allows for greater generation of aerosols. Reusable e-cigarettes contain a larger battery compared with disposable ones. A larger power supply to the heating element allows for a greater volume of aerosol to be generated with each puff.
Components of a disposable electronic cigarette. Disposable e-cigarettes do not contain a tank and instead store their e-liquid in a saturated piece of cotton. Aerosols are generated by a rudimentary wick and coil which is heated by a low voltage battery. The processor recognizes when the user is taking a puff and triggers the battery to supply power to the coil. The processor is set to a predetermined number of puffs. The device will stop generating aerosols once that number is reached or the battery runs out of power, whichever comes first.
Bronchiolitis obliterans or “popcorn lung.” Axial view of a CT chest in a patient who chronically used electronic cigarette devices, suffering from bronchiolitis obliterans. Image provided courtesy of Dr Jeremy S. Breit, MD.
Contributor Notes