AIRWAY ISSUES IN ANESTHESIA
Educational Objectives
| The goals of this program are to review guidelines of the American Society of Anesthesiologists (ASA) on obstructive
sleep apnea (OSA) and difficult airway, and to improve asthma management in the operating room (OR). After
hearing and assimilating this program, the participant will be better able to:
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 | 1. Discuss the systemic pathophysiology of sleep-disordered breathing.
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| 2. Review the fundamental questions to ask that will allow the anesthesia provider to rule in or rule out a presumptive
clinical diagnosis of OSA in patients with conditions known to cause OSA.
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| 3. Summarize specifics of the ASA OSA and difficult airway guidelines.
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| 4. Assess the cost of implementing the ASA OSA guideline in the first year.
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| 5. Identify strategies to reduce and/or manage asthma in the OR.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning
committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts
of interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health
care and not a proprietary business or commercial interest. For this program, the faculty and planning committee reported
nothing to disclose.
Acknowledgements
Dr. Benumof spoke in San Diego, CA, at Anesthesia Update 2008, held January 9-12, 2008, and sponsored by the
University of California, San Diego, School of Medicine, Department of Anesthesiology; Dr. Wetzel, in Anaheim,
CA, at the 46th Clinical Conference in Pediatric Anesthesiology, held January 25-27, 2008, and sponsored by the Pediatric
Anesthesiology Foundation, Childrens Hospital Los Angeles. The Audio-Digest Foundation thanks the speakers
and the sponsors for their cooperation in the production of this program.
| OBSTRUCTIVE SLEEP APNEA AND THE DIFFICULT AIRWAY —Jonathan L. Benumof, MD, Professor of Anesthesia,
Department of Anesthesiology, University of California, San Diego, School of Medicine, La Jolla, CA
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| Sleep: during deep and restorative sleep, loss of muscle tone throughout body; loss of pharyngeal muscle tone causes pharyngeal
collapse and increases airway resistance; loss great enough to cause inspired air to flutter around uvula, tongue, and epiglottis
leads to snoring and hypopnea; loss great enough to cause complete obstruction leads to silence and apnea; narcotics,
sedatives, alcohol, and anesthetics also cause loss of pharyngeal muscle tone and pharyngeal collapse
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| Sleep-disordered breathing (SDB): to survive each apneic episode, patient must have some arousal; majority of instances
involve mini arousal; expressed internally as burst on electroencephalography (EEG) and externally as either vocalization,
and/or extremity movement, and/or turning side-to-side; activates pharyngeal muscles and opens pharyngeal airway;
reopened airway allows patient to return to deep sleep and more pharyngeal muscle relaxation, pharyngeal collapse, and
pharyngeal obstruction; because of repetitive and innumerable arousals that fragment sleep, daytime somnolence results;
continued apnea and hypopnea leads to hypoxemia and hypercapnia; chemical changes cause increased ventilatory effort
and increased negative airway pressure; any of these mechanisms can cause brain arousal
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| Arousal: repetitive arousals fragment sleep and rob patient of deep restorative sleep; patient therefore has somnolence
during quiet times of day, and is at high risk for motor vehicle accidents and personality, behavior, and cognitive changes;
patient undesirable bed partner because of noise and movement during sleep; may result in nocturnal social isolation
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| Treatment: one-third of patients with moderate obstructive sleep apnea (OSA) who receive no treatment will die within 8
yr (vs 4% with mild OSA); continuous positive-airway pressure (CPAP) gold standard; can reverse dual-circulation dysfunction
if applied early; other treatments (eg, losing weight, stopping drinking, avoiding sedatives, oral appliances, and
various surgeries) effective in selected patients
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| Presumptive clinical diagnosis of OSA: necessary components include, 1) history or observation of apnea or snoring
with hypopnea during sleep, 2) history or observation of arousal from sleep (ie, vocalization, twitching, turning during
sleep), and 3) history or observation of daytime somnolence; if presumptive clinical diagnosis of OSA made, health
care provider should confirm and quantitate with sleep study
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| Sleep study: provides raw data that allow diagnosis of OSA vs central sleep apnea and determines effect on oxygenation;
in typical patient with OSA, 85% to 95% of apneas obstructive, few central, and few mixed
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| Raw data gathered into clinical report: report of interest to anesthesia provider; apnea equals no air flow for >10 sec; hypopnea
equals tidal volume <50% of control awake value for >10 sec; desaturation equals decrease in SpO2 >4%;
arousal can be clinical or burst on EEG; indexes are events per hour; apnea-hypopnea index (AHI) equals number of
times per hour patient either apneic or hypopneic; O2 desaturation index (ODI) equals number of times per hour patient
had decrease in SpO2 >4%; arousal index equals number of times per hour patient aroused; severity of OSA most universally
expressed as function of AHI, in which score of 6 to 20 equals mild, 21 to 40 equals moderate, and >40 equals
severe; SpO2 data also reported as number of events per 10% epochs of SpO2
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| American Society of Anesthesiologists’ OSA guidelines
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| Logic: causes of OSA must be known; ask questions that allow anesthesia provider to rule in or rule out presumptive clinical
diagnosis of OSA; after making diagnosis, determine severity; perioperative risk determines perioperative management
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| Causes: include obesity (body mass index >35), thick neck, small receding mandible (posteriorly positioned tongue), nasal
obstruction, large tonsils, and large tongue
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| Presumptive clinical diagnosis: if one or more causes of OSA present; questions include history or observation of SDB,
history or observation of arousals during sleep, and history or observation of daytime somnolence
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| Severity: determined clinically or with sleep study; patient with mild OSA described as obese, snores most of time during
sleep, has not had definite episodes of apnea or arousal, and falls asleep during some quiet times each day; patient
with severe OSA described as morbidly obese, snores continually during sleep, has definite apneic episodes and frequent
arousals, but occasionally has apnea unaccompanied by arousals and becomes cyanotic, and falls asleep during
most or many of quiet times during day; patient also has significant cardiovascular disease; in between these 2 extremes,
health care provider has to exercise judgment; always desirable to determine severity with sleep study; guideline
encourages anesthesia provider to understand severity of OSA
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| Perioperative risk: determinants include severity of OSA, invasiveness of anesthesia and surgery, and postoperative opioid
requirement
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| Postoperative opioid requirement: scoring scale same as for severity of OSA; low-dose oral opioid (mild, score of 1),
moderate-dose oral opioid (moderate, score of 2), and high-dose oral, parenteral, or neuraxial opioid (severe, score of
3)
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| Calculating perioperative risk: equal to severity of OSA plus either invasiveness of anesthesia and surgery or postoperative
opioid dose, whichever greater; guideline defines increased risk as risk score of 4, and significantly increased risk
as risk score of 5
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| Perioperative management: if patient at increased risk, facility performing case should have emergency difficult airway
equipment, respiratory care equipment, portable chest x-ray and electrocardiography (ECG) capability, laboratory for
arterial blood gases (ABGs), and arrangements for transfer to inpatient facility; no outpatient surgery for uvulopalatopharyngoplasty
(UPPP), tonsillectomy in child <3 yr of age, and upper abdominal laparoscopy; if evidence of
significantly increased risk from OSA, then, according to guidelines, patient generally not good candidate for surgery
in free-standing unit
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| Preoperative and intraoperative care: preoperative preparation with CPAP or bilevel intermittent positive-airway pressure
(BiPAP) improves physical condition; ASA OSA guideline defers to ASA difficult-airway guidelines for airway management;
encourages awake extubation (in upright position when possible); use respiratory CO2 monitoring during moderate
or deep sedation; regional anesthesia for peripheral surgery better than general anesthesia and/or excess opioids
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| Discharge from postanesthesia care unit (PACU) to unmonitored setting: patient with OSA should be monitored for median
of 3 hr longer than non-OSA counterpart; if significant obstruction or hypoxemia in PACU, then monitor for median
of 7 hr longer than non-OSA counterpart
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| Postoperative management: use of regional analgesia decreases adverse outcomes, compared to narcotics and sedatives; consider
exclusion of opioids from neuraxis; nonsteroidal anti-inflammatory drugs (NSAIDs) have opioid-sparing effect and
therefore decrease opioid use and adverse outcomes; avoid basal patient-controlled analgesia (PCA) rates; administer
CPAP as soon as feasible if patient on CPAP preoperatively, but not immediately postextubation; CPAP treatment indicated
for natural sleep, not drug-induced sleep; when problems abate, apply CPAP in PACU, not on hospital floor; guideline
equivocal on whether CPAP should be in place when patient awake but not ambulating; continuous pulse oximetry
decreases risk for complications in OSA
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| ASTHMA MANAGEMENT IN THE OPERATING ROOM (OR)—Randall C. Wetzel, MB,BS, Professor of Pediatrics
and Anesthesiology, Keck School of Medicine of the University of Southern California; Chair, Department of Anesthesiology
Critical Care Medicine, Anne O’M Wilson Professor of Critical Care Medicine, and Director, Laura P. and Leland K.
Whittier Virtual Pediatric Intensive Care Unit, Childrens Hospital, Los Angeles, CA
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| Risk categories: asthmatic with history of mechanical ventilation; 2 hospitalizations within previous year; 3 visits to
emergency department within previous year; current or recent long-term use of steroids; history of seizures or loss of consciousness
at any time with asthma (associated with intraoperative complications); hospital visits within previous month;
asthmatic patient with no symptoms, signs, or medications at low risk; however, risk increased in patient on medications
for acute exacerbation at time of surgery, patient experiencing recent bronchospasm or exacerbation of symptoms within
previous 6 wk, and patient who has recently visited hospital (within previous 2 mo) for asthma
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| Airway stimulation: parasympathetic reflex airway constriction occurs with mechanical stimulation of upper airway,
trachea, and larynx; asthma triggered by microaspiration and laryngeal stimulation; bronchoconstriction increases vascular
permeability and vasodilation in small airways; intubation in asthmatic reduces forced expiratory volume in 1 sec
(FEV1 ) by median of 50%
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| Anesthesia: consider regional anesthesia; use mask anesthetic when possible; however, aspiration and asthma bad combination;
severe wheezing without airway control can be lethal; laryngeal mask airway (LMA) probably no advantage over
endotracheal intubation; depth of anesthesia always important (deep anesthesia equals less airway reactivity)
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| Optimize therapy: if patient fits into above risk categories, and opportunity present, always add steroids; for patient at
low risk, current recommendation to give prednisone, 40 to 60 mg/day, divided q8h, for 24 hr before anesthesia (speaker
gives 10 mg/kg q8h [3 doses], before surgery); reduces complications by >90%; if FEV1 <80% of predicted for age and
size, “absolutely” use steroids before induction; β-agonist used to treat active bronchospasm (little reason to give increased
salbutamol [albuterol in United States] if not wheezing on day leading up to surgery); salbutamol, before induction
in patient with upper respiratory infection, does not decrease complications but blunts loss of FEV1 and increased
airway resistance on induction and intubation; if steroids and salbutamol have not resolved wheezing, consider ipratropium
or disodium chromoglycate preinduction; theophyllines—probably do not help if patient already optimized on ipratropium;
infection often overlooked; often worsen asthmatic symptoms and increase likelihood of intraoperative complications
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| Induction: use of intravenous (IV) lidocaine controversial; reports demonstrate 1 to 2 mg/kg IV bolus, 3 to 5 min before
intubation, blocks histamine-induced bronchospasm; inhaled lidocaine also effective, but anesthetizes upper airway and
tastes bad; inhalational anesthetics work through β-adrenergic mechanisms to increase release of intracellular cyclic adenosine
monophosphate (cAMP); intracellular cAMP decreases intracellular ionized calcium, binds intracellular calcium,
and causes bronchial relaxation; may also inhibit release of histamine from mast cells; atropine or glycopyrrolate recommended
before induction in asthmatics; sevoflurane and halothane useful; avoid desflurane; ketamine acts as direct bronchial
muscle relaxant; deep propofol anesthesia blocks mechanically induced bronchospasm; avoid morphine (histamine
release); deep anesthesia before intubation deepens inhalational anesthetic; give lidocaine topically or IV; risk for profound
bronchospasm greatest during induction
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| Emergence: benefits of deep extubation must be weighed against risk associated with no airway reflexes; good asthma
control may obviate need for deep extubation; consider β-agonist in patient who had no wheezing intraoperatively; deep
extubation, laryngospasm, and aspiration may exacerbate asthma; “take your time waking up the patient”
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| Therapy: β-agonists (continuously inhaled)—useful and indicated; complications include tachycardia and increased
basal metabolic rate (when used continuously in large amounts; may increase O2 consumption; can contribute to acidosis);
be attentive to fluid maintenance; give additional steroids (no immediate effect); anticholinergic medications (eg,
ipratropium)—“are worth one or two administrations” (repeat hourly); theophyllines—“probably don’t help that
much”; deepening inhalational anesthetic—may help avoid trouble; talk to intensive care unit (ICU) staff about continued
inhalational anesthesia postoperatively; complications, in ICU or postoperative setting include hypotension, respiratory
depression, and myocardial depression; may be required for several days; delivery modality required outside of OR;
IV magnesium—prevents uptake and release of calcium in airway smooth muscle; reduces membrane excitability; decreases
release of acetylcholine in airway, thus relaxing airway smooth muscle; also inhibits histamine release by mast
cells and may increase release of nitric oxide and prostacyclin; potentiates anesthesia, analgesia, and muscle relaxants;
also potentiates anesthetic effects of propofol, rocuronium (neuromuscular-blocking effects), and fentanyl (decreases effective
dose by ≈30%); inhaled magnesium—does not cause upper-airway numbness or have bad taste; no additional
benefit to inhaled salbutamol
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| Acute respiratory failure during status asthmaticus: may require continued mechanical ventilation; frequently
difficult, requiring high airway pressures and complicated by barotrauma, air leaks, and cardiovascular collapse; severe
patient-ventilator dyssynchrony may occur; may necessitate paralysis; recognition that acute respiratory acidosis can be
tolerated has led to controlled hypoventilation to avoid barotrauma leading to pneumothorax, cardiovascular collapse, air
trapping, and further worsening of disease; older strategy for ventilating asthmatics included paralysis, ventilation with
pressure control, prolonged inspiratory/expiratory (I:E) ratio, and increased lung volumes at end of expiration; leads to
further increase in total end-expiratory lung volume and mechanical problems in lungs; today, goal of mechanical ventilation
in status asthmaticus only prevention of hypoxemia; patient who is asthmatic forces air out (during exhalation) when
breathing spontaneously; during paralysis, elastic recoil of lungs without forced exhalation completely inadequate when
airway resistance increased and end-expiratory lung volumes greater than physiologic functional residual capacity
(FRC); ie, paralysis and control-mode ventilation prevent patient from assisting in exhalation; large negative intrathoracic
pressure, decreased venous return, and increased left ventricular (LV) afterload eventually lead to LV failure
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| Maintaining or enhancing expiration: consider avoiding muscle relaxants; allow spontaneous breathing, and support
ventilation during inspiration; pressure support assists inspiration and does not require paralysis or controlled ventilation;
allows patient to do work of exhalation during expiratory cycle; patient determines flow pattern, respiratory rate, tidal
volume, inspiratory time, expiratory time, total cycle time, and I:E ratio; balances work of ventilation and perfusion,
matching patient’s brain stem and respiratory muscles; inspiratory work of breathing unloaded; patient able to maintain expiratory
function; pressure-support ventilation may be ideal ventilatory mode
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Suggested Reading
American Society of Anesthesiologists Task Force on Management of the Difficult Airway: Practice
guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiologists Task
Force on Management of the Difficult Airway. Anesthesiology 98:1269, 2003; Erratum in: Anesthesiology 101:565, 2004;
Benumof JL: Obesity, sleep apnea, the airway and anesthesia. Curr Opin Anaesthesiol 17:21, 2004; Burburan SM et
al: Anaesthetic management in asthma. Minerva Anestesiol 73:357, 2007; Gross JB et al: American Society of Anesthesiologists
Task Force on Perioperative Management. Practice guidelines for the perioperative management of patients with
obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of
patients with obstructive sleep apnea. Anesthesiology 104:1081, 2006; Mercier FJ et al: Anaesthetic management in patients
with asthma. Can J Anaesth 43:195, 1996; Mulgrew AT et al: Diagnosis and initial management of obstructive
sleep apnea without polysomnography: a randomized validation study. Ann Intern Med 146:157, 2007; Peterson GN et
al: Management of the difficult airway: a closed claims analysis. Anesthesiology 103:33, 2005; Tirumalasetty J et al:
Asthma, surgery, and general anesthesia: a review. J Asthma 43:251, 2006; von Ungern-Sternberg BS et al: Desflurane
but not sevoflurane impairs airway and respiratory tissue mechanics in children with susceptible airways. Anesthesiology
108:216, 2008; Wetzel RC: Pressure-support ventilation in children with severe asthma. Crit Care Med 24:1603,
1996.
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