CC
A 45-year-old female presents to your office for cosmetic eyelid surgery (blepharoplasty).
HPI
The patient is an otherwise healthy female for whom treatment was planned for bilateral upper and lower eyelid blepharoplasties with intravenous (IV) sedation. After the incision lines had been marked in the usual manner, electrocardiography, blood pressure, pulse oximeter, and a sidestream capnograph monitor were applied. The patient was administered 4 L of oxygen and 2 L of nitrous oxide via nasal hood. (Nitrous oxide decreases the amount of IV sedatives needed.) Sedation was achieved using 5 mg of midazolam, 100 μg of fentanyl, and a propofol drip titrated to effect. Verrill’s sign (50% upper eyelid ptosis, indicating adequate sedation) was observed. Before administration of local anesthesia, 40 mg of propofol was administered as a bolus. (Propofol may cause a 20%–25% drop in systolic blood pressure when given as a bolus.) Upon administration of local anesthesia, loss of the capnogram, with no chest wall movement, was observed. (This indicates the presence of central apnea. Capnography is considered to be more sensitive than clinical assessment of ventilation in the detection of apnea. In a study by Soto and colleagues [2004], 10 of 39 patients [26%] experienced 20-second periods of apnea during procedural sedation and analgesia. All 10 episodes of apnea were detected by capnography but not by the anesthesia providers.) The apnea was attributed to the propofol bolus (combined with the respiratory depressant effects of fentanyl), which was anticipated to resolve shortly. However, the patient continued to be apneic, and her oxygen saturation decreased from 99% to 80%. (Pulse oximeter readings are about 30 seconds behind the real-time oxygen saturation.) Nasal flaring, tracheal tug, and paradoxical chest wall motion were not observed. (These would be signs of upper airway obstruction and inspiratory efforts. An increase in sonorous breath sounds may also be a sign of increasing airway obstruction.) The patient began to appear cyanotic (bluish hue to facial skin and lips caused by prolonged hypoxemia).
PMHX/PDHX/medications/allergies/SH/FH
A thorough medical history is important during the preoperative evaluation of all patients undergoing IV sedation or general anesthesia to identify potential risk factors of intra- or postoperative anesthetic complications.
The past medical and surgical histories are noncontributory. This patient is categorized as American Society of Anesthesiologist (ASA) Class I ( Table 19.1 ). She does not use any medications and has no known drug allergies. She denies previous problems with local anesthetics (e.g., methemoglobinemia), IV sedation, or general anesthetics. (Problems with previous anesthesia or adverse drug reactions should alert clinicians to possible complications that may require modification of anesthetic techniques.) There is no family history of complications with general anesthetics (e.g., malignant hyperthermia). She denies a history of drug or alcohol use (patients with a previous drug history or alcohol abuse may require higher doses of sedative–hypnotic drugs), and she does not smoke. (Smoking decreases oxyhemoglobin concentrations and increases pulmonary secretions.)
| ASA Category | Patient’s Health | Status of Underlying Disease | Limitations on Activities | Risk of Adverse Effects |
|---|---|---|---|---|
| I | Excellent; no systemic disease; excludes persons at extremes of age | None | None | Minimal |
| II | Disease of one body system | Well controlled | None | Minimal |
| III | Disease of more than one body system or one major system | Controlled | Present but not incapacitated | No immediate danger |
| IV | Poor with at least one severe disease | Poorly controlled or end stage | Incapacitated | Possible |
| V | Very poor, moribund | Incapacitated | Imminent |
Examination
Preoperative. A thorough preoperative evaluation is important to identify potential risk factors for negative anesthetic outcomes, with an emphasis on airway anatomy.
General. The patient is a well-developed and well-nourished female in no apparent distress. Her body mass index (BMI) is 24 kg/m 2 . (A BMI >30 kg/m 2 is considered obese and >40 kg/m 2 is considered morbidly obese.)
Airway. Maximal interincisal opening (MIO) is within normal limits. (Difficult intubation occurs with decreased MIO.) Her oropharynx is Mallampati class I (soft palate, tonsillar pillars, and uvula completely visualized), and the thyromental distance (TMD) is three fingerbreadths (intubation is more difficult with retrognathia, a short TMD, and/or a higher Mallampati classification). The cervical spine has a full range of motion. Airway evalauation helps formulate the anesthetic plan for the patient. Other airway assements that signal diffuclt ventilation/intubation include sternomental distance less than 12.5 cm, neck circumference greater than 17 cm, and enlarged tonsils.
Cardiovascular. Heart is regular rate and rhythm without murmurs, rubs, or gallops.
Pulmonary. Lung fields are clear to auscultation bilaterally. (Preoperative wheezing may increase the risk of intraoperative bronchospasm.)
Intraoperative. During the course of IV sedation (conscious sedation, deep sedation, or general anesthesia), it is important to continuously monitor the patient’s level of sedation and anesthesia (to prevent oversedation and respiratory depression) and to survey the ABCs (airway, breathing, and circulation; the ABC assesment for this patient is shown in Box 19.1 ).
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A (airway): The upper airway is rapidly evaluated and found to be clear of any obstruction. The patient’s oropharynx is clear (secretions are suctioned with a tonsillar suction), and no inspiratory or expiratory noises are heard (stridor or gurgling noises may indicate upper airway obstruction). No tracheal tug is present. Chin tilt–jaw thrust maneuvers are applied.
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B (breathing): There are no inspiratory efforts, and no chest wall or abdominal motion (apnea) is seen. Breath sounds are not heard with the precordial stethoscope (placed above the suprasternal notch), and the reservoir bag is motionless. The pulse oximetry (Sp o 2 ) reading has been steadily falling from 99% to 80%. (An Sp o 2 of 90% correlates with a Pa o 2 of 60 mm Hg; values below this correspond to the steep portion of the oxygen-hemoglobin dissociation curve.)
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C (circulation): Blood pressure and heart rate are stable. (Bradycardia and hypotension resulting from an extended period of hypoxemia are ominous signs of impending circulatory collapse.) The electrocardiogram shows normal sinus rhythm without any ST changes. (Leads II and V 5 are most sensitive in detecting myocardial hypoxia.)
General. The patient is sedated, unconscious, and unresponsive to painful stimulus (a state of general anesthesia).
Imaging
Preoperative and serial postoperative photoimaging is mandatory for cosmetic procedures. A preoperative chest radiograph has a limited role in healthy individuals and is not warranted unless dictated by other medical factors.
Labs
Routine laboratory tests are not indicated in healthy patients undergoing cosmetic blepharoplasty with IV sedation. Females of childbearing age who are sexually active or have missed their last menstrual period may require a urine pregnancy test.
Assessment
Central apnea secondary to oversedation during IV sedation for cosmetic upper and lower eyelid blepharoplasties.
Treatment
Before the diagnosis of respiratory depression (apnea or hypopnea) as the cause of hypoxemia, possible causes of upper airway obstruction need to be rapidly ruled out by evaluating the airway, jaw position, and possibility of foreign body aspiration. Subsequently, the procedure should be stopped, any open or bleeding wounds should be packed, and necessary assistance should be elicited. Attempts to arouse the patient with verbal command and painful stimulus should be made. Unresponsiveness to painful stimulus is considered to be a state of general anesthesia.
Respiratory depression secondary to oversedation is a self-limiting process that requires adequate supportive measures or pharmacologic interventions until spontaneous respirations resume. Respiratory depression causes a reduction in alveolar ventilation through a decrease in the respiratory rate or tidal volume, which in turn is caused by a decrease in respiratory drive. All sedatives, opioids, and potent inhalation general anesthesia agents have the potential to depress central hypercapnic and peripheral hypoxemic drives. Opioids primarily depress the central chemosensitive area (i.e., hypercapnic drive), whereas inhalation anesthetics and benzodiazepines exert greater influence on the chemoreceptors in the carotid and aortic bodies (i.e., hypoxemic drive). At high doses, all classes can depress both these mechanisms.
Nitrous oxide is not a respiratory depressant; however, when it is combined with sedatives or opioids that depress ventilation, a more pronounced and clinically important depression may result. Therefore, it should be discontinued to allow more rapid arousal from anesthesia and delivery of 100% oxygen, with subsequent resolution of spontaneous respirations. Any anesthetic IV drips should be discontinued immediately. Jaw-thrust maneuvers or tugging on the tongue anteriorly will improve the opening of the airway for more effective oxygen delivery. The anesthesia circuit should be flushed to evacuate residual nitrous oxide and to deliver a higher flow of oxygen. If these measures fail, the patient’s breathing can be assisted with positive-pressure ventilation (PPV) at one breath every 5 seconds (coordinated with any apparent shallow breathing). If oxygenation proves to be successful with PPV, continued ventilatory support is maintained until the sedation lightens and respiratory depression resolves. However, if ventilation is not achieved, rapid reevaluation for other causes (laryngospasm, bronchospasm, foreign body aspiration, chest wall rigidity) should be considered. The airway is reassessed, and chin lift–jaw thrust maneuvers should be optimized. Oral and/or nasal airways can be inserted if there is continued difficulty with PPV. If laryngospasm or bronchospasm is diagnosed, it should be treated promptly (see the discussion of laryngospasm earlier in this chapter). If these measures fail to reestablish ventilation, more advanced airway interventions may be necessary. These include the use of a laryngeal mask airway, endotracheal intubation, or establishment of a surgical airway (cricothyrotomy). Despite the infrequency of the latter scenario, the clinician should be prepared to establish an airway as soon as possible (see the discussion of emergent surgical airway later in this chapter). When the oxygen saturation returns above 95%, the clinician can decide whether to cautiously continue with the procedure and intermittently apply PPV as needed or to abort the procedure for further evaluation.
If prolonged respiratory depression occurs, the sedative effects of some agents can be pharmacologically reversed. Flumazenil (Romazicon) reverses the sedative effects of benzodiazepines. It is given at 0.2 mg intravenously (or 0.01–0.02 mg/kg in small children) every minute up to five doses (maximum total dose, 1 or 3 mg/hr) until reversal of sedation is accomplished. It may be repeated every 20 minutes for resedation. Naloxone (Narcan) is an opioid antagonist that reverses the sedative, respiratory depressant, and analgesic effects of opiates. Low doses are recommended (to prevent adverse effects of reversal). IV naloxone dosing can vary depending on the situation, ranging from 0.04 to 0.08 mg for nonemergent oversedation to 0.4 to 2 mg for emergent opioid toxicity. (A higher dosing schedule is used in narcotic overdose.) After sedation has been reversed, the patient needs to be monitored for resedation because the half-lives of naloxone and flumazenil are shorter than those of their sedative counterparts, potentially requiring redosing of the reversal agent(s). There are no reversal agents for barbiturates or propofol. Reversal of sedation from these agents relies on rapid redistribution of the drugs. It is important to remember that hypoxemia and hypercarbia can further contribute to central nervous system (CNS) depression.
In the current patient, supportive measures included 100% oxygen delivered via PPV with a bag-valve-mask device. PPV was easily accomplished, and the patient’s oxygen saturation steadily increased to 99%. After sufficient ventilation and oxygenation, the surgery was resumed. The propofol IV drip was discontinued during the apnea–hypopnea episode and was subsequently titrated down as the procedure was completed. The patient began to have spontaneous respirations and maintained a normal capnogram and an adequate oxygen saturation, and she arose from sedation shortly after completion of the procedure. Reversal agents were not required.
Complications
Oversedation and respiratory depression can have devastating outcomes if not promptly treated as outlined here. In most circumstances, the patient’s airway and breathing can be easily supported. However, it is important to identify patients at higher risk of difficult mask ventilation and endotracheal intubation (see the discussion of emergent surgical airway later in this chapter) before administering deep sedation. The loss of the patient’s airway (cannot intubate and cannot ventilate scenario) can lead to prolonged hypoxemia, which can in turn lead to cardiovascular collapse, cerebral anoxia, and death if not managed promptly.
Precipitous reversal of sedation and respiratory depression with opioid antagonists is not without adverse side effects. Naloxone (Narcan) may cause cardiac arrhythmias, pulmonary edema, severe hypotension, and cardiac arrest when given at higher doses. The analgesic effects are also reversed, which may cause the patient to experience profound surgical pain accompanied by hypertension and tachycardia. Patients with acute or chronic opioid dependence can experience acute withdrawal symptoms. Naloxone and flumazenil have short half-lives and may require redosing every 20 to 30 minutes if resedation occurs; therefore, close patient observation is paramount.
Discussion
Various levels of IV sedation can be administered by oral and maxillofacial surgeons. The American Society of Anesthesiologists Continuum of Depth of Sedation, and Definition of General Anesthesia and Levels of Sedation/Analgesia are discussed below. These definitions were approved by the ASA House of Delegates on October 13, 1999, and last amended on October 23, 2019.
Minimal sedation (anxiolysis) is defined as “a drug-induced state during which patients respond normally to verbal commands. Although cognitive function and physical coordination may be impaired, airway reflexes, and ventilatory and cardiovascular functions are unaffected.”
Conscious sedation (moderate sedation and analgesia) is defined as “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.”
Deep sedation is defined as “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.”
General anesthesia is defined as “a drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to independently maintain ventilatory function is 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.”
Because sedation is 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 rescue patients whose level of sedation becomes deeper than initially intended. Individuals administering moderate sedation and analgesia (“conscious sedation”) should be able to rescue patients who enter a state of deep sedation and analgesia, and those administering deep sedation and analgesia should be able to rescue patients who enter a state of general anesthesia.
Rescue of a patient from a deeper level of sedation than intended is an intervention by a practitioner proficient in airway management and advanced life support. The qualified practitioner corrects adverse physiologic consequences of the deeper-than-intended level of sedation (e.g., hypoventilation, hypoxia, and hypotension) and returns the patient to the originally intended level of sedation. It is not appropriate to continue the procedure at an unintended level of sedation.
Respiratory depression from oversedation can occur during the course of a procedure or in the recovery period; however, it is relatively uncommon when sedation is administered by an experienced oral and maxillofacial surgeon. (Short half-lives and lack of active metabolites are ideal properties of IV anesthetic agents.) The short duration of action of modern IV anesthetics relies on rapid redistribution (alpha half-life), rapid metabolism, or both. However, repeated doses of opioids, benzodiazepines, or barbiturates for longer procedures may cause accumulation in inactive tissues (especially adipose tissue), which is later released into circulation to cause delayed emergence (beta half-life), thereby on occasion requiring a reversal agent. Naloxone is an opioid antagonist that competitively binds to mu receptors, effectively reversing the sedative, analgesic, and respiratory-depressant effects of any given opioid (e.g., fentanyl, morphine, sufentanil, alfentanil, remifentanil, meperidine). Flumazenil is a competitive antagonist to benzodiazepines (e.g., midazolam, lorazepam, diazepam) at the central benzodiazepine receptor (alpha subunits of the gamma-aminobutyric acid receptor), and it reverses all effects of benzodiazepines (e.g., sedation, respiratory depression, anxiolysis). The respiratory-depressant effects of midazolam (Versed, the most commonly used benzodiazepine) are minimal compared with those of propofol and narcotics.
Inadequate local anesthesia or insufficient time allocation for its onset may make the sedated patient appear uncooperative or undersedated. The clinician may decide to deepen the sedation to control the uncooperative patient and overcome the effects of inadequate local anesthesia. After the painful stimulus is gone or the local anesthesia has set in, the patient may return to a deeper level of sedation or may become oversedated with respiratory depression. The risk of oversedation and respiratory depression can be minimized by using local anesthesia effectively.
Some additional precautions should be noted when administering anesthesia to pediatric and older adult patients. Small doses of benzodiazepines and opioids can cause significant respiratory depression in older adult patients. The changes in physiology and medical comorbidities associated with aging are beyond the scope of this section, but a general precaution used by clinicians is “go low and go slow.” It is important to remember that children have a lower functional residual capacity (FRC) and do not tolerate hypoventilation and hypoxemia well, which is evidenced by a more rapid drop in oxygen saturation. Differences in the pediatric airway (larger tongue; lymphoid hypertrophy; more rostrally positioned larynx; long and floppy epiglottis, narrowest at the cricoid cartilage; more compliant tracheal walls; more caudal anterior cord attachment; underdeveloped accessory muscles) are important to recognize.
Heightened awareness is also required when sedating obese patients (BMI >30 kg/m 2 ). As a result of the increased abdominal fat in obese patients, the FRC is decreased particulary when supine, which leads to shorter desaturation times. Functional Residual Capacity reflects the volume of gas remaining in the lungs at the end of tidal respiration and approximates 2400 mL for the average adult. The oxygen content of the gas mixture in the FRC can be viewed as oxygen reserve. If ventilation ceases, oxygen in this reserve continues to diffuse into the pulmonary capillaries. This impacts the time from onset of apnea until hypoxemia ensues. This is the basis for preoxygenating a patient before the induction of general anesthesia as well as oxygen supplementation during sedation and general anesthesia. By increasing the oxygen content of the FRC, more time will be available for appropriate intervention if hypoventilation or apnea occurs. Desaturation in obese patients can also occur because of increased metabolic demand for oxygen caused by increased tissue mass, decreased respiratory compliance caused by abdominal and chest wall fat, reduced size of the orohypopharyngeal airway secondary to a large tongue and buccal fat pads, or a decreased ability to extend the neck because of cervical fat. Obese patients are also at an increased chance for aspiration.
Capnometry uses infrared technology to analyze carbon dioxide in exhaled gases. It is the measurement of carbon dioxide concentration during the respiratory cycle. Capnography is the proper term for monitors that display a continuous waveform reflecting inspiration and expiration. Whereas capnometers and capnographs both display numeric values for end-tidal carbon dioxide (EtCO 2 ) and respiratory rate, capnography is preferred because visualization of the waveform allows continuous assessment of the depth and frequency of each ventilatory cycle. Capnography is the noninvasive waveform measurement of the partial pressure of CO 2 in the exhaled breath.
The relationship of CO 2 concentration to time is graphically represented by the CO 2 waveform or capnogram ( Fig. 19.1 ). (Time capnograms are more commonly used than volume capnograms, on which CO 2 is plotted against expired volume.) Pulse oximetry provides real-time information about arterial oxygenation, whereas capnography provides breath-to-breath information of three important physiologic functions (1) ventilation (how effectively CO 2 is being eliminated by the pulmonary system), (2) perfusion (how effectively CO 2 is being transported through the vascular system, i.e., a functioning cardiovascular system), and (3) metabolism (how effectively CO 2 is being produced). Capnography provides the most sensitive measurement of ventilation.
