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saturation or heart rate, an eort may be made to deepen
the level of anesthesia by administering 0.25– 0.8 mg/ kg of
IV propofol.
26,27
is has been reported to be eective in
76% of cases, although it has not been thoroughly studied
in children less than 3years old.
23,26,27
Due to the nature of
laryngospasm.
time in the range of 3 minutes and a duration of about
1.5 hours.34 Similarly, transtracheal lidocaine injection36
has also been used to treat stridor and prevent recurrent
laryngospasm.
34,35
is has been shown to have an onset
the crisis, with little to no air movement, it is ineective to
attempt to deepen the anesthetic with an inhalation agent.
SUBSEQUENT TREATMENTSTEPS
24
FOLLOW- UP
Patients who experience laryngospasm should be observed
If the initial treatment steps fail to result in adequate gas
exchange, then denitive treatment should not be delayed.
At this time the administration of succinylcholine is still
considered the “gold standard” treatment for laryngo-
3,4
spasm.
Concomitant administration of atropine at 20
mcq/ kg has been advocated in children, specically with
regard to potential for bradycardia induced by hypox-
3,28
emia.
cardia induced by the succinylcholine is less frequent than
previously thought and recommend administration of atropine only with repeated dosing of succinylcholine.
However, several authors have noted that brady-
29– 31
While it may be clear that succinylcholine is the drug of
choice to achieve rapid laryngeal relaxation, there is much
discussion as to the route of administration and dosage.
With the preferred intravenous route, recommended dosages range from 0.1 to 0.3 mg/ kg,
4,32
which consistently
resolves the laryngospasm within 30– 60 seconds. e
intraosseous route is equivalent to the intravenous route
with regard to dosing and onset times,
3,33
however intraosseous needles are oen not available at the time of the emergency, and experience with using them may be lacking. If
either of these routes is not available, then the alternative
methods listed in order of rapidity of onset are the intralingual, submental, or intramuscular approaches. Intralingual
dosing at 1.1 mg/ kg via direct injection into the tongue
via an open mouth results in relaxation within 60– 75 sec-
4,33
onds.
Submental dosing through the so tissue underneath the mandible and into the tongue has been described
with doses of 3 mg/ kg and an onset time of 265 sec, which
can be decreased to 133 sec with digital massage following injection.
intramuscular route of 295 sec at a dose of 4 mg/ kg.
4,33
is compares with an onset time of the
3,4,33
note, most measures of onset times used 90%– 100% twitch
depression and it is likely that laryngospasm will break prior
to maximal twitch depression.
33
for a longer period of time in the recovery room in order
to monitor for complications such as further episodes or
negative pressure pulmonary edema.37 Clear documentation of the events in the anesthesia record and consideration toward giving the patient a note about the diculty
encountered may help future anesthetists take adequate
precautions.
CASE- BASED LEARNING DISCUSSION
1. Is the anesthesia plan acceptable? What would you
change in the original plan?Why?
2. e case proceeds with the original plan. General
anesthesia is induced, the patient is le spontaneously
breathing, and the head of the table is turned 90 degrees
toward the surgeon. Aer turning the table, there is no
ETCO2 detected and the pulse oximeter starts to drop
intone.
• What are likely diagnoses at thistime?
• What would you do to remedy this situation?
• Are physical airway maneuvers indicated?
• Are there any drugs that would be benecial at
thistime?
3. You have the surgeon provide jaw thrust and conrm
that the mask seal is adequate. CPAP 5– 10cmH2O is
instituted, which results in adequate gas exchange and
improving oxygen saturation.
Of
4. Suspended laryngoscopy begins and the patient
becomes stridorous.
• What should be donenow?
REFRACTORY/ RECURRENT LARYNGOSPASM
Lastly, it has been reported that bilateral superior
laryngeal nerve blocks have been useful for recurrent
136 PART IV. PULMONARY CRISES
5. Once the laser resection begins, the cords close under
observation through the microscope and the monitors.
• List the drugs and dosages that would be benecial in
relieving this condition.
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137
• Should you change your anesthetic technique at
this time? If so,how?
6. e resection is over, and the patient is taken
spontaneously breathing to the PACU. While you
are giving report to the PACU nurse, the pulse
oximeter drops in tone and the patient’s chest
appears to be “rocking.”
• What are likely diagnoses at thistime?
• What would you do to remedy this situation?
• Are physical airway maneuvers indicated?
• Are there any drugs that would be benecial at
thistime?
• How are your answers dierent now that you are in a
new location?
• Do you have the resources to actually carry out your
plan in a timely fashion?
7. You are able to break the recurrent laryngospam and
the patient is now stable, awake, oriented, and able to
converse.
• What can be done to help ensure that this condition
does not recur in the future?
• Are there any studies that may be benecial? Is this
patient still able to be considered an outpatient?
Why or whynot?
REFERENCES
1. Arslan IB, etal. Does topical anesthesia using aerosolized lidocaine
inhibit the superior laryngeal nerve reex? Otolaryngology– Head
and Neck Surgery. 2013;149(3):466– 72.
2. Fink BR. e etiology and treatment of laryngeal spasm.
Anesthesiology. 1956;17(4):569– 77.
3. Hampson- Evans D, Morgan P, Farrar M. Pediatric laryngospasm.
Paediatric Anaesthesia. 2008;18(4):303– 7.
4. Al- alami AA, Zestos MM, Baraka AS. Pediatric laryngospasm:pre-
vention and treatment. Current Opinion in Anaesthesiology.
2009;22(3):388– 95.
5. Flick RP, etal. Risk factors for laryngospasm in children during
general anesthesia. Paediatric Anaesthesia. 2008;18(4):289– 96.
6. Lakshmipathy N, et al. Environmental tobacco smoke:a risk fac-
tor for pediatric laryngospasm. Anesthesia & Analgesia. 1996;
82(4):724– 7.
7. Schreiner MS, etal. Do children who experience laryngospasm have
an increased risk of upper respiratory tract infection? Anesthesiology.
1996;85(3):475– 80.
8. Cohen MM, Cameron CB. Should you cancel the operation when
a child has an upper respiratory tract infection? Anesthesia &
Analgesia. 1991;72(3):282– 8.
9. Mamie C, et al. Incidence and risk factors of perioperative respiratory adverse events in children undergoing elective surgery.
Paediatric Anaesthesia. 2004;14(3):218– 24.
10. von Ungern- Sternberg BS, etal. Laryngeal mask airway is associated
with an increased incidence of adverse respiratory events in children with recent upper respiratory tract infections. Anesthesiology.
2007;107(5):714– 9.
11. Tait AR, Knight PR. Intraoperative respiratory complications in
patients with upper respiratory tract infections. Canadian Journal of
Anesthesia. 1987;34(3 Pt 1):300– 3.
12. Tait AR, etal. Use of the laryngeal mask airway in children with
upper respiratory tract infections:a comparison with endotracheal
intubation. Anesthesia & Analgesia. 1998;86(4):706– 11.
13. Tartari S, etal. [Laryngeal mask vs tracheal tube in pediatric anesthesia in the presence of upper respiratory tract infection]. Minerva
Anestesiologica. 2000;66(6):439– 43.
14. Yu SH, Beirne OR. Laryngeal mask airways have a lower risk of
airway complications compared with endotracheal intubation: a
systematic review. Journal of Oral and Maxillofacial Surgery.
2010;68(10):2359– 76.
15. Jamil SN, etal. A study of the use of laryngeal mask airway (LMA)
in children and its comparison with endotracheal intubation. Indian
Journal of Anaesthesia. 2009;53(2):174– 8.
16. Gharaei B, etal. Use of laryngeal mask airway in children with upper
respiratory tract infection, compared with face mask: randomized, single blind, clinical trial. Acta Anaesthesiologica Taiwanica.
2011;49(4):136– 40.
17. Olsson G L, Hallen B. Laryngospasm during anaesthesia:a computeraided incidence study in 136,929 patients. Acta Anaesthesiologica
Scandinavica. 1984;28(5):567– 75.
18. Cohen VG, Krauss B. Recurrent episodes of intractable laryngospasm during dissociative sedation with intramuscular ketamine.
Pediatric Emergency Care. 2006;22(4):247– 9.
19. Zwass MS, etal. Induction and maintenance characteristics of anesthesia with desurane and nitrous oxide in infants and children.
Anesthesiology. 1992;76(3):373– 8.
20. Roy WL, Lerman J. Laryngospasm in paediatric anaesthesia.
Canadian Journal of Anesthesia. 1988;35(1):93– 8.
21. Doi M, Ikeda K. Airway irritation produced by volatile anaesthetics during brief inhalation: comparison of halothane, enurane, isourane and sevourane. Canadian Journal of Anesthesia.
1993;40(2):122– 6.
22. Fisher DM, etal. Comparison of enurane, halothane, and isourane for diagnostic and therapeutic procedures in children with
malignancies. Anesthesiology. 1985;63(6):647– 50.
23. Batra YK, et al. e ecacy of a subhypnotic dose of propofol
in preventing laryngospasm following tonsillectomy and adenoidectomy in children. Paediatric Anaesthesia. 2005;15(12):
1094– 7.
24. Holzki J, Laschat M. Laryngospasm. Paediatric Anaesthesia.
2008;18(11):1144– 6.
25. Shbeeb A, et al. Postanesthesia care unit simulation:acute upper
airway obstruction secondary to laryngospasm. Simulation in
Healthcare. 2013;8(2):124– 30.
26. Nawfal M, Baraka A. Propofol for relief of extubation laryngospasm. Anaesthesia. 2002;57(10):1036.
27. Afshan G, etal. Is there a role of a small dose of propofol in the
treatment of laryngeal spasm? Paediatric Anaesthesia. 2002;12(7):
625– 8.
28. Visvanathan T, etal. Crisis management during anaesthesia:laryngospasm. uality and Safety in Health Care. 2005;14(3):e3.
29. Fleming B, McCollough M, Henderson HO. Myth: atropine
should be administered before succinylcholine for neonatal and
pediatric intubation. Canadian Journal of Emergency Medicine.
2005;7(2):114– 7.
LARYNGOSPASM 137
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30. McAulie G, Bissonnette B, Boutin C. Should the routine use
of atropine before succinylcholine in children be reconsidered?
Canadian Journal of Anesthesia. 1995;42(8):724– 9.
31. Parnis SJ, van der Walt JH. A national survey of atropine use
by Australian anaesthetists. Anaesthesia and Intensive Care.
1994;22(1):61– 5.
32. Chung DC, Rowbottom SJ. A very small dose of suxamethonium
relieves laryngospasm. Anaesthesia. 1993;48(3):229– 30.
33. Walker RW, Sutton RS. Which port in a storm? Use of suxamethonium without intravenous access for severe laryngospasm.
Anaesthesia. 2007;62(8):757– 9.
34. Monso A, et al. A new application for superior laryngeal nerve
block: treatment or prevention of laryngospasm and stridor.
Regional Anesthesia and Pain Medicine. 1999;24(2):186– 7.
35. Mevorach DL. e management and treatment of recurrent postoperative laryngospasm. Anesthesia & Analgesia. 1996;83(5):
1110– 1.
36. Lewis KE. Transtracheal lignocaine:eective treatment for postextubation stridor. Anaesthesia and Intensive Care. 2007;35(1):
128– 31.
37. Ead H. Post- anesthesia tracheal extubation. Dynamics. 2004;
15(3):20– 5.
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139
17.
ASPIRATION PNEUMONITIS
Agnieszka Trzcinka
CLINICALCASE
demonstrated a biphasic model in acute acid aspiration lung
injury. e rst phase of lung injury occurs 1 hour aer aspiA 50- year- old woman with a history of poorly controlled
diabetes is scheduled for emergent exploratory laparotomy due to bowel perforation. She is 5’5” and weighs 250
pounds. Physical examination reveals Mallampati classII
airway and a thyromental distance of three nger breadths.
She denies any history of problems with general anesthesia.
Plan is general anesthesia with rapid sequence intubation.
ration and is due to direct chemical injury from the acidic
aspirate, leading to increased capillary permeability. e sec-
ond phase occurs 4 hours aer aspiration and is character-
ized by a marked increase in inammatory cells (neutrophils)
and erythrocytes in alveoli.6 e lung injury mechanism is
mediated by neutrophils and inammatory cytokines such as
tumor necrosis factor α and interleukin (IL)- 8.
7– 10
Although
the gastric contents are presumed to be sterile due to the low
PATHOPHYSIOLOGY OFDISEASESTATE
pH, bacterial infection may complicate later stages of aspira-
tion pneumonitis, the incidence of which is unclear.
10
Aspiration pneumonitis during the perioperative period
involves passage of sterile gastric contents into the airway,
RISK
resulting in alveolar damage. It is also referred to as chemical
pneumonitis, and the extent of resulting lung injury is related
to the pH and volume of the aspirated gastric contents.1
is phenomenon was rst presented in a classic article by
Mendelson in 1946, in which he analyzed 44,016 women
who underwent Cesarean delivery under nitrous oxide and
ether anesthesia. Overall, 66 of these patients aspirated gastric contents. Within that subgroup, 61 patients aspirated
liquid gastric contents and developed symptoms of cyanosis
and dyspnea. ese patients recovered within 24– 36 hours.
Experiments by Mendelson suggested that the observed
symptoms of chemical pneumonitis are due to passage of
acid into the airways. He instilled hydrochloric acid and
vomitus into rabbit airways and demonstrated that both
instillations resulted in severe pneumonitis.2 Subsequent
studies focused on both the pH and volume of the gastric
aspirate, and revealed that aspiration pneumonitis occurs
when the liquid gastric aspirate pH is less than 2.5 and the
volume is at least 0.3 mL/ kg.
MECHANISM
2– 5
e risk of pulmonary aspiration is highest when the upper
and lower esophageal sphincters are unable to prevent passage of gastric contents into the pharynx.11 e sphincters’
tone can be aected by a patient’s comorbidities, previous
esophageal and gastric procedures, as well as medications
that are administered. In general, anesthesiologists deem
patients unable to “protect the airway” when they are
not conscious. In this state, the protective cough and gag
2
reexes are absent.
In 2006, Neelakanta etal. reported the rate of gastric
content aspiration as 1 in 8,600 procedures under anesthesia, with the greatest risk occurring at the time of anesthesia
induction but also, secondarily, during emergence and extubation.12 Previous studies have reported a higher incidence
of aspiration; for example, Warner etal. found the rate of
pulmonary aspiration to be 1 in 3,216 anesthetics.13 In their
series, the incidence was further classied as 1 in 895 for
emergency surgery and 1 in 3,886 for elective surgery.
Olsson etal. sought to clarify the risks of aspiration.
ey found an increase in risk for patients with delayed
gastric emptying, emergency surgery, upper abdominal
e mechanism of aspiration pneumonitis is characterized by a signicant inammatory reaction. Kennedy etal.
surgery, and in patients with noted diculty securing the
airway. Children and the elderly were also at higher risk
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for aspiration. 14 e most important patient risk factors
are pregnancy (during the second and third trimesters)
and active gastrointestinal pathology (such as small bowel
obstruction). 11 Delayed gastric emptying may be worsened
by trauma, obesity, diabetes, and medications such as opioids (single dose administration in healthy patients did not
change gastric volume or pH).
15,16
Certain surgical patient
positions (e.g., lithotomy) may also worsen regurgitation
11
risk.
antacid should be administered, and the airway should be
topicalized in a stepwise fashion that preserves the cough
reex until just prior to endotracheal tube insertion. e
procedure should take place with the patient in a seated
position in order to prevent the passive reux of gastric contents, and minimal sedation should be used. is technique
ensures that the patient is conscious and protective reexes
are maintained as long as is feasibly possible.
In patients with a risk for pulmonary aspiration but
without concern for dicult endotracheal tube placement,
MANAGEMENT OFTHE PATIENT
rapid sequence intubation (RSI) should be performed. is
technique utilizes application of cricoid pressure, rapid
infusion of intravenous induction anesthetics, and a fastAnesthesiologists should focus on the prevention of pulmonary aspiration during the perioperative period. Athorough
history and physical examination will provide critical information about a patient’s pulmonary aspiration risk factors.
Intake of food shortly before anesthesia induction certainly
increases the risk of regurgitation and aspiration of gastric
contents. ere have been many studies analyzing the optimal NPO period (nil per os, withholding oral liquids and
food). In 2011, the American Society of Anesthesiologists
(ASA) published “Practice Guidelines for Preoperative
Fasting and the Use of Pharmacologic Agents to Reduce
the Risk of Pulmonary Aspiration:Application to Healthy
Patients Undergoing Elective Procedures.” e recommendations for fasting prior to elective procedures under
anesthesia for healthy infants, children, and adults are as
follows:2 hours for clear liquids; 4 hours for breast milk; 6
onset neuromuscular blocker, followed by placement of
an endotracheal tube. Cricoid pressure, also known as the
Sellick maneuver, involves application of 30 Newtons of
pressure to the cricoid cartilage, theoretically resulting in
occlusion of the esophagus.11 Awake patients may not toler-
ate such pressure, and the Sellick maneuver may obstruct
the view of direct laryngoscopy or make placement of the
endotracheal tube dicult. 19 In such instances, the cri-
coid pressure should be decreased to prevent esophageal
intubation resulting from poor intubating conditions. e
Sellick maneuver may not eectively prevent pulmonary
aspiration. Smith etal. demonstrated that cricoid pressure
resulted in lateral esophagus displacement in a majority of
studied patients. 20 In- dwelling nasogastric tubes should be
placed on suction, but the patient’s stomach may still not be
completely empty prior to induction of anesthesia.
hours for infant formula, light meals, and nonhuman milk;
and 8 hours for fried or fatty foods and meat. In addition
to guidelines on NPO status, recommendations regarding various pharmacologic interventions were included
ASSESSMENT OFTHE PATIENT:PRESENTING
SIGNS AND SYMPTOMS
as well. For patients without increased risk for aspiration,
routine preoperative use of gastrointestinal stimulants (i.e.,
metoclopramide), gastric acid secretion blockers, antiemetics, anticholinergics, or antacids is not recommended. For
patients at increased risk for aspiration, use of these pharmacologic agents is at the anesthesiologist’s discretion. In a
patient at high risk for aspiration, neutralization of gastric
contents may be benecial, but only nonparticulate antacids
are recommended for preoperative use. 17 Obstetric patients
require special attention, and the ASA guidelines for that
patient population can be found in ASA 2007 “Practice
Guidelines for Obstetric Anesthesia.”
18
When caring for patients with a signicant risk for pulmonary aspiration and signs of potentially dicult endotracheal tube placement, awake beroptic intubation is a
preferred technique to secure the airway. Anonparticulate
Following aspiration of gastric contents, the patient may
exhibit a variety of symptoms, with severity based on the
volume and pH of the aspirate. e anesthesiologist may
observe coughing, desaturation on pulse oximetry, and the
pooling of gastric contents in the oropharynx. Severe symptoms may occur, with profound oxygen desaturation and
respiratory distress requiring intubation.11 Warner et al.
analyzed 67 patients with evidence of pulmonary aspiration
under anesthesia. One patient died due to bleeding. Among
the remaining 66 patients who survived surgery, 42 patients
(64%) did not demonstrate any signs or symptoms of aspiration within 2 hours of the event and did not develop any
pulmonary complications. Twenty- four patients developed
symptoms of cough, wheezing, or oxygen desaturation or
evidence of aspiration on chest radiograph evaluation.
140 PART IV. PULMONARY CRISES
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141
Within this subgroup, 13 patients needed mechanical ventilator support for more than 6 hours and 7 of these patients
developed acute respiratory distress syndrome (ARDS)
with a need for mechanical ventilator support for more
management of patients with acute lung injury is beyond
the scope of this chapter. e reader is referred to the disruption of diusion as a result of inammation chapter for
further information on the management ofARDS.
than 24 hours. ree of these patients died due to respiratory failure.
INITIAL TREATMENTSTEPS
13
CASE- BASED LEARNING DISCUSSION
1. Do you agree with the original anesthesia plan in our
case patient? Why or why not? What other aspects of
If aspiration is observed, the patient’s oropharynx and trachea should be suctioned and the aspirate examined for any
evidence of particulate matter. Despite a timely response,
an acidic gastric aspirate may result in an immediate direct
chemical injury as described by Kennedy.
6
Patients with observed or suspected aspiration need
supportive treatment that varies depending on the severity of symptoms. It may include only supplemental oxygen
via facemask and observation for 24– 48 hours, or it may
the patient’s history and physical exam evaluation do
you want to know to make your decision?
2. You bring the patient to the OR and decide to
proceed with general anesthesia and rapid sequence
induction. What medications and doses will you use
for induction? Would you have another anesthesia
provider present during induction? Why or why not?
How would you instruct your assistant to administer
cricoid pressure?
be necessary to intubate the patient and initiate mechanical
ventilatory support and inotropic treatment as needed.
Treatment with glucocorticoids is not recommended
in patients with observed or suspected aspiration. Astudy
by Wolfe et al. demonstrated that patients treated with
steroids aer aspiration had a higher occurrence of gramnegative pneumonia compared with those who did not
receive steroid treatment.21 Furthermore, a meta- analysis by
Peter etal. concluded that there is not enough evidence to
support the use of corticosteroids for ARDS treatment in
adult patients.
22
Treatment with antibiotics is not recommended in
patients with observed or suspected aspiration. However,
prophylactic antibiotic treatment may be considered in
those aspiration patients with small bowel obstruction or
a coexisting condition predisposing to colonization of gastric aspirate.10 ere is evidence from animal models that
bacterial clearance is reduced in lungs sustaining damage
from acid instillation.23 erefore, antibiotic treatment
may be considered in aspiration patients whose symptoms
do not improve within 48 hours of suspected or witnessed
aspirationevent.
3. Aer administration of medications, the patient loses
consciousness. Alarge amount of clear uid is seen
pooling in patient’s mouth. What would youdo?
4. You successfully place an endotracheal tube and
conrm correct placement with chest auscultation and
sustained presence of an EtCO2 tracing on the monitor.
e pulse oximetry reading is 89% on an FiO2 of 100%.
Would you perform bronchoscopy? What is your
dierential diagnosis? What would youdo?
5. e pulse oximetry reading is now 95% and the surgeon
asks if she can proceed with surgery. What do you
tell her? Would you administer any medications? Are
antibiotics or corticosteroids indicated?
6. Surgery is nished. You assess the patient and note the
pulse oximetry reading ranges between 93% and 95%
and there is bilateral wheezing on chest auscultation.
Would you extubate this patient? Why or why not?
e decision is made to leave the patient intubated and
you transport her to the intensive care unit. e intern
orders a chest x- ray. What are likely ndings within 24
hours of the aspirationevent?
SUBSEQUENT TREATMENT STEPS AND
FOLLOW- UP
Patients who develop severe symptoms aer an aspiration
event will need treatment in the intensive care unit with
supportive ventilatory and inotropic care. e literature on
ASPIRATION PNEUMONITIS 141
REFERENCES
1. Grossman RF. Anaerobic and other infectious syndromes. In:Crapo
JD, Glassroth J, Karlinsky J, eds. Baum’s Textbook of Pulmonary
Diseases. 7th ed. Philadelphia: Lippincott, Williams & Wilkins;
2004:406– 23.
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2. Mendelson CL. e aspiration of stomach contents into
the lungs during obstetric anesthesia. Am J Obstet Gynecol.
1946;52:191– 205.
3. Teabeaut JR 2nd. Aspiration of gastric contents; an experimental
study. Am J Pathol. 1952;28:51– 67.
4. Exarhos ND, Logan WD Jr, Abbott OA, Hatcher CR Jr. e importance of pH and volume in tracheobronchial aspiration. Dis Chest.
1965;47:167– 9.
5. James CF, Modell JH, Gibbs CP, Kuck EJ, Ruiz BC. Pulmonary
aspiration- eects of volume and pH in the rat. Anesth Analg.
1984;63:665– 8.
6. Kennedy TP, Johnson KJ, Kunkel RG, Ward PA, Knight PR, Finch
JS. Acute acid aspiration lung injury in the rat:biphasic pathogenesis. Anesth Analg. 1989;69:87– 92.
7. Yamada H, Kudoh I, Nishizawa H, et al. Complement partially
mediates acid aspiration- induced remote organ injury in the rat.
Acta Anaesthesiol Scand. 1997;41:713– 8.
8. Goldman G, Welb ourn R, Kobzik L, Valeri CR , Shepro D, Hechtman
HB. Tumor necrosis factor- alpha mediates acid aspiration- induced
systemic organ injury. Ann Surg. 1990;212:513– 20.
9. Knight PR, Druskovich G, Tait AR, Johnson KJ. e role of neutrophils, oxidants, and proteases in the pathogenesis of acid pulmonary
injury. Anesthesiology. 1992;77:772– 8.
10. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N
Engl J Med. 2001;344:665– 71.
11. Henderson J. Airway management in the adult. In: Miller RD,
Eriksson LI, Fleisher LA, Wiener- Kronish JP, Young WL, eds.
Miller’s Anesthesia. 7th ed. Philadelphia: Churchill Livingstone,
Elsevier; 2010:1573– 1610.
12. Neelakanta G, Chikyarappa A. A review of patients with pulmonary aspiration of gastric contents during anesthesia reported to
the Departmental uality Assurance Committee. J Clin Anesth.
2006;18:102– 7.
13. Warner MA, Warner ME, Weber JG. Clinical signicance of pulmonary aspiration during the perioperative period. Anesthesiology.
1993;78:56– 62.
14. Olsson GL, Hallen B, Hambraeus Jonzon K. Aspiration during
anesthesia: a computer- aided study of 185,358 anesthetics. Acta
Anaesthesiol Scand. 1986;30:84– 92.
15. Kallar SK, Everett LL. Potential risks and preventive measures for
pulmonary aspiration:new concepts in preoperative fasting guidelines. Anesth Analg. 1993;77:171– 82.
16. Bricker SR, McLuckie A, Nightingale DA. Gastric aspirates aer
trauma in children. Anaesthesia. 1989;44:721– 24.
17. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration:application to
healthy patients undergoing elective procedures:an updated report by
the American Society of Anesthesiologists Committee on Standards
and Practice Parameters. Anesthesiology. 2011;114:495– 511.
18. Practice guidelines for obstetric anesthesia:an updated report by the
American Society of Anesthesiologists Task Force on obstetric anesthesia. Anesthesiology. 2007;106:843– 63.
19. Hocking G, Roberts FL, ew ME. Airway obstruction with cricoid
pressure and lateral tilt. Anaesthesia. 2001;56:825– 8.
20. Smith KJ, Dobranowski J, Yip G, Dauphin A, Choi PT. Cricoid
pressure displaces the esophagus:An observational study using magnetic resonance imaging. Anesthesiology. 2003;99:60– 64.
21. Wolfe JE, Bone RC, Ruth WE. Eects of corticosteroids in the treatment of patients with gastric aspiration. Am J Med. 1977;63:719– 22.
22. Peter JV, John P, Graham PL, Moran JL, George IA, Bersten A.
Corticosteroids in the prevention and treatment of acute respiratory distress syndrome (ARDS) in adults: meta- analysis. BMJ.
2008;336:1006– 9.
23. Johanson WG Jr, Stephen JJ, Pierce AK. Bacterial growth in vivo. An
important determinant of the pulmonary clearance of Diplococcus
pneumoniae in rats. J Clin Invest. 1974;53:1320– 5.
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143
18.
PHYSIOLOGIC AIRFLOW DISRUPTION
BRONCHOSPASM, OBSTRUCTIVE LUNG DISEASE, ASTHMA, AND STATUS ASTHMATICUS
Kinza Sentissi and Stephanie Yacoubian
CLINICALCASE
A 56- year- old male with coronary artery disease and a 45pack- year smoking history presents for thorascopic resection of a right middle lobe lung mass. Patient has a baseline
metabolic equivalent of 3, but reports progressively worsening shortness of breath in the past month. Anesthetic
plan includes a preinduction thoracic epidural, standard
American Society of Anesthesiologists (ASA) monitors
and invasive blood pressure monitoring. Anesthesia will be
maintained with an intravenous anesthetic.
rocuronium and succinylcholine, but antibiotics and latex
are also oen implicated.
BRONCHOSPASM— RISK FACTORS
2
Anesthesiologists should be aware of the increased risk
of bronchospasm in smokers, females, and patients with
chronic bronchitis.2 Airway instrumentation, IgE- mediated
anaphylaxis, a variety of perioperative medications, inadequate depth of anesthesia, pulmonary congestion,
emergence from anesthesia, and complications such as aspiration, infection, or trauma can all potentially precipitate
BRONCHOSPASM— MECHANISM
e incidence of intraoperative bronchospasm is low, at
approximately 1.7 %,1 however the consequences can be
devastating. Bronchospasm can be triggered via intubation
and activation of vagal C- ber aerents. Vagal stimulation
results in the release of acetylcholine, which binds to muscarinic receptors
2,3
in the airway and induces smooth muscle contraction. In addition, noncholinergic, nonadrenergic
nerves release tachykinins, vasoactive intestinal peptides,
and calcitonin gene- related peptides that can cause local
smooth muscle contraction.2 rough histamine release,
mast cells can trigger airway smooth muscle contraction by
increasing intracellular calcium. All of these mechanisms
ultimately lead to airow disruption.
Allergic bronchospasm, secondary to either immunoglobulin E (IgE)- mediated anaphylaxis or anaphylactoid
(direct activation of complement/ bradykinin cascade and
mast/ basophil cells) reactions, is another important etiology of bronchospasm. ese reactions occur within 60
minutes of exposure to the culprit agent. Notably, bronchospasm is only seen in 19% to 40% of patients with anaphylaxis and is more common in patients with underlying
airway obstruction.2 Neuromuscular blocking agents are
the most frequent oending medications; in particular
bronchospasm.
BRONCHOSPASM— ASSESSMENT OFTHE PATIENT
e diagnosis of acute bronchospasm is a clinical one.
In the operating room, bronchospasm most commonly
occurs at induction.2 Clinical signs include elevated
peak inspiratory pressures, lack of chest rise and fall,
and wheezing or absent breath sounds on auscultation.1
Capnography demonstrates prolonged expiratory phase II
and III4 (Figure18.1).
Allergic bronchospasm is a systemic hypersensitivity
response characterized by the presence of cutaneous ndings,
oxygen desaturation, hemodynamic instability, and duration of symptoms greater than 60 minutes. Elevated serum
tryptase levels can conrm the diagnosis2 postoperatively.
e eects of progressive, acute bronchoconstriction have implications on the cardiopulmonary system.
Airow disruption leads to worsening V/ Q mismatch,
and increased pulmonary vascular resistance with right
ventricular overload. In addition, there is a decrease in the
dynamic compliance of the lungs secondary to air trapping.
Worsening dynamic hyperination and air trapping can
potentially lead to decreased cardiac output and subsequent
cardiac arrest.
1,2,3
1
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ET-CO
2
III
II
I
Expiration Inspiration
Figure18.1 Capnography. A) Normal phases of capnography
I=Expiration, anatomical dead space. II=Expiration, anatomical and alveolar dead space. II=Expiration, anatomical and plateau. ET- CO2=end of exhalation.
0=inspiratory phaseB) Airow disruption (e.g., bronchospasm, COPD, asthma). Slanting and prolonged phase II and increased slope of phase III. SOURCE:Used
with permission from Kodali B.Capnography.com.2001.
BRONCHOSPASM— MANAGEMENT OFTHE PATIENT
In the intubated patient, the initial reaction to suspected
bronchospasm should be to increase the inhaled oxygen
concentration to 100%, and manually ventilate to assess
lung compliance.2 In addition, other possible etiologies
should be ruled out, such as mucous plugging, pulmonary
edema, esophageal or endobronchial intubation, foreign
body aspiration, and tension pneumothorax. Deepening
the volatile anesthetic and administering intravenous
(IV) propofol can prevent and modulate bronchospasm.
0
BRONCHOSPASM— FOLLOW- UP
Following an episode of intraoperative bronchospasm, elective surgery should be postponed until the patient is stabilized.2 Postoperative ventilation should be considered to
allow for airway recovery and full neuromuscular reversal.1
Postoperative pain control should be optimized and the
promotion of bronchodilator use, as well as early mobilization and deep breathing,1 should be encouraged. In cases
of suspected allergic bronchospasm, further allergy testing
should be considered on an outpatient basis.
In addition, the provider should give 8– 10 pus of a
short- acting beta- 2 agonist.2 e addition of ipratropium has been shown to produce greater bronchodilation
ASTHMA AND CHRONIC OBSTRUCTIVE
PULMONARY DISEASE— MECHANISM
than beta- 2 agonist alone and can be eective in refractory bronchospasm.2 Parenteral steroids, such as methylprednisolone IV (1 mg/ kg)2 can be given, but will not
Airway changes in asthma are mediated by interactions
between airway cells and immune cells. T- helper cells play a
take maximal benecial eect for 4– 6 hours.1 In refractory cases, magnesium sulfate (1– 2 g IV) can be used and
will induce bronchodilation via calcium antagonism.5
Vigilance is required, as magnesium sulfate can lead to
prolonged muscle weakness and central nervous system
(CNS) depression. e use of epinephrine in nonallergic
bronchospasm is not recommended, as there is no data to
prove its ecacy when compared with beta- 2 agonists.2
Management steps of acute bronchospasm are summarized in Box18.1.
In cases of allergic bronchospasm with associated cardiovascular collapse, the rst step should be to discontinue
the oending agent.2 Management also includes administration of epinephrine starting at 5 to 10 mcg IV bolus for
hypotension, and increasing the dose to as high as 0.5 to
1.0 mg IV bolus if cardiovascular collapse occurs. e provider should also administer 2– 4 liters of IV crystalloid,
histamine- 1 and histamine- 2 blockers, along with bronchodilators and corticosteroids as listedabove.
BOX 18.1 TREATMENT STEPS INMANAGEMENT OFACUTE
BRONCHOSPASM
1. Increase FiO2 to100%
2. Turn off ventilator and manually ventilate.
3. Deepen anesthetic (inhaled orIV).
4. Rule out other etiologies and consider allergic
bronchospasm, discontinue offending agents.
5. Administer shor t- acting inhaled B2- agonists.
6. Consider IV glucocorticoids.
7. Consider inhaled anticholingeric.
8. Consider IV magnesium sulfate.
9. If cardiovascular collapse, or in the case of allergic
bronchospasm, consider IV epinephrine.
2
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Senescence
and bronchoconstriction.6 In addition, mucous plugs are
noted, likely due to the increase in airway secretions, desqua-
Regeneration
Immune Control
mated cells, and intraluminal epithelial cells (Figure18.2).
Chronic obstructive pulmonary disease is a progressive airow obstruction that is only partially reversible.
Acomplex interaction exists between the innate immune
Epithelial damage
1
Innate immune defense
Adaptive immune response
defense and the adaptive immune response (Figure 18.2).
Airway inammation involves the proximal and peripheral
airway and the pulmonary vasculature. e uncontrolled
inammation eventually leads to brosis, luminal exudates,
and narrowing of small peripheral airway (Figure 18.3).
Emphysematous changes develop as collagen and elastin
are destroyed and there is a loss of elastic recoil.8 Genetic
Age
Lung growth
Figure18.2 Pathogenesis time course in COPD. Declining FEV
FEV1=forced expiratory volume in 1 sec. SOURCE:Reprinted with permission from
Decramer M, Janssens W, Miravitlles M.Chronic obstructive pulmonary disease. Lancet.
2012;379(9823).
Environmental exposure
Genetic background
over time.
1
susceptibility will determine the extent of obstruction and
declining FEV1 over theyears.
ASTHMA AND CHRONIC OBSTRUCTIVE
PULMONARY DISEASE— RISK FACTORS
Common asthma risk factors include gender, airway hyperreactivity, atopy, environmental allergens, smoking, and
infections.6 Cigarette smoking is the leading risk factor
crucial role in asthma and increase levels of cytokines such
as interleukin (IL)- 4, IL- 5, and IL- 13. is shis the balance to a proinammatory phenotype and leads to endothelial cell damage and remodeling through recruitment of
for developing COPD. Exposure to second- hand tobacco
smoke can also lead to chronic airow obstruction.9 Other
risk factors include exposure to occupational dust, chemicals, and air pollution.
eosinophils.6 B- cells play an important role by activating IgE
and subsequently mast cells along with basophils. Mast cells
release histamine, leukotrienes, and prostaglandins, which
cause bronchoconstriction, vasodilation, and inammation.6
Chronic inammation leads to airway remodeling and epithelial cell injury, causing increased basement membrane thickness; mucosal, submucosal, and adventitial edema; deposition
of excess collagen;7 and dysregulated airway lymphangiogenesis and angiogenesis.6 ere is also an increase in airway
smooth muscle, which contributes to airway hyperreactivity
ASTHMA AND CHRONIC OBSTRUCTIVE
PULMONARY DISEASE— ASSESSMENT OF
THE PATIENT
Preoperative assessment should include evaluation of functional status, recent respiratory infections, common triggers,
changes in medication regimens, presence of late evening
or early morning symptoms, and recent exacerbations—
particularly those resulting in hospital visits, intubations,
Figure18.3 Airway pathology in healthy individual versus patient with COPD. A) Healthy airway tissue, inltrated with inammatory cells and mucosal
hyperplasia. Reprinted with permission from Decramer M, Janssens W, Miravitlles M.Chronic obstructive pulmonary disease. Lancet. 2012 Apr 7; 379(9823)
PHYSIOLOGIC AIRFLOW DISRUPTION 145
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