Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 911 - файл
.pdf
146
https://t.me/medicina_free
TABLE18.1 GLOBAL INITIATIVE ONOBSTRUCTIVE LUNG DISEASE CLASSIFICATION (GOLD) OFCOPD BASED ONSEVERITY
OFPOSTBRONCHODILATORFEV
1
Stages Severity Predicted FEV
Stage 1 Mild
Stage 2 Moderate 50%- 80% Inuenza vaccine
Stage 3 Severe 30%- 50% Inuenza vaccine
Stage 4 Very severe <30 %
Suggested treatment plans present. Short- acting bronchodilators=beta- 2 agonists or anticholinergics.
≥ 80%
Or < 50% but with chronic
respiratory distress
1
and prolonged ventilation.1 Previous anesthetic history and
comorbidities should also be considered.3 Patients with airow disruption oen present with dyspnea, cough, chest
tightness, and sputum production. Afocused physical exam
may detect wheezing, rhonci, a prolonged expiratory phase,
or, in the case of severe airway obstruction, diminished or
absent breath sounds.
1
A postbronchodilator FEV1/ FVC < 0.70 is indicative
obstructive disease. Patients with asthma have a reversible
airway obstruction with more than 12% improvement in
FEV1 postbronchodilator administration. Of note, PFTs
can normalize in between asthma attacks and therefore can
appear deceptively normal at the time of testing. Spirometric
classication of COPD is listed in Table 18.1. If the patient
is intubated, capnography can demonstrate an obstructive pattern and the ventilator may display air stacking and
elevated peak airway pressures. In extreme cases, dynamic
hyperination and cardiovascular collapse can be observed.
Treatment
Inuenza vaccine, short- acting bronchodilator (PRN)
Respiratory rehabilitation
Short- acting and ≥ 1 long- acting bronchodilator
Respiratory rehabilitation
Short- acting and ≥ 1 long- acting bronchodilator
Inhaled glucocorticoid
Inuenza vaccine
Respiratory rehabilitation
Short- acting and ≥ 1 long- acting bronchodilator, oxygen
dependence, lung transplant or lung volume reduction surgery
during tracheal intubation of the asthmatic,3 as it has been
shown to relax airway smooth muscle and is a superior bronchodilator in comparison to thiopental and etomidate.10
Ketamine has bronchodilatory eects as well, making it
useful for induction,1 however it can also cause an increase
in airway secretions. e addition of opioids on induction
can blunt the stimulation caused by tracheal intubation and
decrease airway resistance.3 Certain inhaled anesthetics, in
particular sevourane and isourane, have inherent bronchodilator eects.
1,3
Desurane has however been shown to
cause bronchoconstriction.1 Inhaled gases should be warm
and humidied at all times.1 Special consideration should
be taken when using neuromuscular blockers in asthmatics. e use of histamine- releasing neuromuscular blockers,
such as atracurium and mivacurium, can cause histaminemediated bronchoconstriction.3 In addition, neuromuscular blocking agents are the most common cause of allergic
reaction in the operating room and anaphylaxis- induced
bronchospasm should always be a consideration following
ASTHMA AND CHRONIC OBSTRUCTIVE
PULMONARY DISEASE— MANAGEMENT OF
THE PATIENT
Patients should be encouraged to take their daily asthma
medications on the day of surgery. Preoperatively, a shortacting beta- 2 agonist can decrease airway resistance, particularly in patients with evidence of wheezing on exam.3
ere is no denitive evidence that one anesthetic strategy
is superior to another in preventing bronchospasm in the
asthmatic. While regional and neuraxial techniques can
avoid instrumentation of the airway, anxiety or pain during
these procedures can precipitate bronchospasm.1 In terms of
induction medications, propofol is the most suitable agent
their administration.2 e use of anticholinesterase medications such as neostigmine is safe in conjunction with an
anticholinergic, such as glycopyrrolate, to balance the bronchoconstriction seen with anticholinesterase medications.3
Of note, Suggamadex has no anticholinesterase eect, and
can be used safely in asthma.
3
Ventilation strategies should focus on avoiding barotrauma. In addition, one should be conservative with the
use of PEEP, replacing 50%– 75% of intrinsic PEEP with
extrinsic PEEP in order to minimize air trapping.3 e use
of prolonged expiratory times can aid in preventing air trapping.1 Upon induction and initiation of positive pressure
ventilation, the patient can be at signicant risk of developing dynamic hyperination and cardiovascular collapse.
146 PART IV. PULMONARY CRISES
https://t.me/medicina_free
147
Dynamic hyperination is triggered when the inspired tidal
volume occurs before the previous volume is fully exhaled.
is leads to an increase in intrathoracic volume and generates intrinsic PEEP. Venous return is subsequently impaired,
resulting in a decrease in cardiac output, possibly to the point
of pulseless electrical activity and cardiac arrest.11 To decrease
the likelihood of this catastrophic event, preinduction hydra-
predictor of risk of developing status asthmaticus. Other
risk factors include noncompliance or untreated asthma,
history of glucocorticoid use, psychiatric disease, comorbidities, low socioeconomic status, urban residence, and
illicit drug use. Poor perception of dyspnea is also a risk
factor that can increase the likelihood of going into a
major acute exacerbation.
tion and bronchodilator administration is imperative.
Short- acting beta- 2 agonists, such as albuterol and levabuterol, are the quickest way to rapidly reverse airow
obstruction, with an onset time of 5 minutes or less and
peak eect in 30– 60 minutes.1 Anticholinergic bronchodilators, such as ipratropium, should be added in the case
of beta- blocker- induced asthmatic attack.7 Parenteral steroids can be used in acute asthma exacerbations, however
their benecial eect on acute bronchospasm can take 4– 6
hours.1 Treatment of dynamic hyperination involves cessation of ventilation, while maintaining a patent airway, in
order to allow for complete exhalation and a decrease in
intrathoracic pressure. In refractory cases, IV epinephrine
(0.25– 0.5 mg/ min) may be indicated to resolve the airow
STATUS ASTHMATICUS— ASSESSMENT OFTHE
PATIENT
Patients present with severe shortness of breath and
tachypnea. Status asthmaticus is associated with the presence of hypocapnia, which progresses to hypercapnia
secondary to fatigue due to increased work of breathing,
and ultimately acidemia (both respiratory and metabolic), altered level of consciousness, and cardiovascular
collapse. Patients in status asthmaticus are at increased
risk of death secondary to cardiac arrhythmias as well
as complications of mechanical ventilation, specically
barotrauma and pneumonia.
13
obstruction. Antibiotics should be considered if there is any
indication of an active infection.
STATUS ASTHMATICUS— MANAGEMENT
ASTHMA AND CHRONIC OBSTRUCTIVE
PULMONARY DISEASE— FOLLOW- UP
Every eort should be made to extubate the patients at the
end of the case. However, if airow disruption is severe,
mechanical ventilation may be necessary until the patient
is appropriately managed with medications to help control inammation and decrease bronchoconstriction.12 In
COPD patients, noninvasive mechanical ventilation can
provide respiratory support and help maintain an appropriate arterial CO2, therefore avoiding acidosis.
Patients need to be intubated and started on a mechanical
ventilation when they have refractory hypoxemia (PaO2
< 60 mmHG) and progressively worsening hypercapnia
(PaCO2 > 55– 77 mmHg). Other signs that point to the
need for mechanical ventilation include patient exhaustion,
worsening mental status, hemodynamic instability, loss of
consciousness, or apnea. An experienced provider should
perform the intubation. A large- size endotracheal tube is
indicated in order to aid in the clearance of secretions and
to minimize airway resistance. Ventilator settings should
be thoughtfully set with the goal of avoiding barotrauma,
maintaining oxygen saturation above 90%, and permis-
STATUS ASTHMATICUS— MECHANISM
Status asthmaticus is associated with severe smooth muscle
bronchoconstriction, inammation, edema, and mucus
plugging. is contributes to intrapulmonary shunting
that leads to various degrees of hypoxemia. Severe airway obstruction can lead to dynamic hyperination and
decreased cardiac output as previously reviewed in this
chapter. is can lead to a near fatal asthma attack.
13
sive hypercapnia. e mode of ventilation should adapt
to any compliance changes in order to minimize elevated
airway pressures. Inspiratory/ expiratory ratio should be set
at ≥ 1:3, and tidal volumes should fall in the range of 6– 8
mL/ kg with a respiratory rate of 10– 12 breaths/ minute.
Inspiratory ow should be set at ≥100L/ min.
Oxygen therapy is the primary treatment, with the goal
of maintaining an oxygen saturation of greater than 90%
(greater 95% in patients with cardiac disease and pregnant
women). First line pharmacotherapy is a short- acting beta-
STATUS ASTHMATICUS— RISK FACTORS
A history of recurrent asthma exacerbations requiring
hospitalization and mechanical ventilation is a major
2 agonist, most commonly albuterol. Usual dose is four to
eight pus every 10 minutes, or 5.0 to 7.5 mg of nebulized
albuterol. Levalbuterol should be considered in refractory asthma or in patients with coronary artery disease.
PHYSIOLOGIC AIRFLOW DISRUPTION 147
148
https://t.me/medicina_free
Anticholinergic agents can be used, especially if FEV1 is less
than 50% predicted.
13
In cases where beta- 2 agonist therapy does not work,
systemic subcutaneous epinephrine (0.3– 0.5 mL, 1:1000)
every 20 minutes is indicated. is should not exceed three
consecutive doses. In pregnant patients, subcutaneous terbutaline (0.25– 0.5 mg) is the drug of choice. Intravenous epinephrine boluses or infusions should be initiated if patient
does not respond to the above therapies. Systemic corticosteroids should be initiated as soon as possible in patients
presenting in status asthmaticus. Patients need to be started
on 80– 125 mg IV methylprednisolone every 6 hours for
the rst 24 hours. is dose should be tapered over time.
In refractory cases, a trial of IV ketamine or magnesium can
help relieve symptoms. Methylxanthines, such as theophylline, have a very narrow therapeutic range and should only
is easy. e anesthesia monitor now displays a mean
arterial blood pressure of 30mmHg. What is the
dierential? What are the rst steps in management?
3. You stabilize your patient and secure the airway. What
size ETT will you choose (height 70inches, weight 200
pounds)? Why? What size DLT will you place? Will
you inate the bronchial cu? Why or whynot?
4. Aer DLT placement, you notice the peak airway
pressure to be 40cmH2O. What is the dierential?
5. Airway pressures have now dropped to 28cmH2O.
Patient is ipped and in the le lateral decubitus
position. Airway pressures increase back to mid 40s,
and blood pressure drops to a MAP of 50mmHg.
Oxygen saturation is 85% on 100% FiO2. What is the
rst step you willtake?
be used in exceptional circumstances. To decrease the work
of breathing and ow resistance in a severely obstructed airway, a low- density helium- oxygen (Heliox) gas mixture can
be initiated.13 Inhaled sevourane has also been reported
to help with bronchodilation, in cases where patients were
resistant to conservative therapy.14 Extracorporeal CO2
removers have been successful, and in extreme cases, extracorporeal membrane oxygenation (ECMO) support can be
used to bridge cases with near fatal asthma attacks until the
severe airway obstruction resolves.
15,16
6. e patient undergoes an uneventful thoracoscopic
right middle lobectomy. How do you calculate the
predicted postoperative FEV1? Assume your patient’s
predicted postoperative FEV1 is 50%. Will the patient
likely extubate? What if his predicted FEV1 was35%?
7. How will you manage this patient’s COPD in the
postoperative stage? Will you administer O2 in the
recovery room? In the PACU, his respiratory status
deteriorates and patient is hypercapnic. Will you
reintubate? What is another alternative to intubation?
STATUS ASTHMATICUS— FOLLOW- UP
What are the potential contraindications to this
alternative therapy?
Aer an episode of status asthmaticus, if there is no
improvement to baseline aer 4 to 6 hours, patients should
be admitted, observed, and medically optimized in a hos-
REFERENCES
pital setting. Upon discharge, patients need to be able to
assess their peak expiratory ow at home, practice medicine
compliance, and be familiar with the symptoms and signs of
acute exacerbation.
CASE- BASED LEARNING DISCUSSION
1. What is the single best test to predict whether or
not this patient will be extubated at the end of the
case? Apreoperative cardiac echo showed normal
le ventricular function with mildly decreased
right ventricular function and moderately elevated
pulmonary pressures. Is a pulmonary artery catheter
indicated in this case? Why or whynot?
2. Induction was completed with an IV agent and
nondepolarizing muscle relaxant. Mask ventilation
1. Woods B, Sladen R. Perioperative considerations for the patient
with asthma and bronchospasm. British Journal of Anaesthesia.
2009;103(Suppl 1):i57– i65.
2. Dewachter P, Mouton- Faivre C, Emala C, Beloucif S. Case scenario:bronchospasm during anesthetic induction. Anesthesiology.
2011;114(5):1200– 10.
3. Yamakage M, Iwasaki S, Namiki A. Guideline- oriented perioperative
management of patients with bronchial asthma and chronic obstructive pulmonary disease. Journal of Anesthesia. 2008;22(4):412– 28.
4. Kodali B. Capnography.com. 2001. Available at http:// www.capnography.com.
5. Alter H, Koepsell T, Hilty W. Intravenous magnesium as an adjuvant in acute bronchospasm:a meta- analysis. Annals of Emergency
Medicine. 2000;36(3):191– 7.
6. Olin J, Wechsler M. Asthma:pathogenesis and novel drugs for treatment. British Medical Journal. 2014;349(8):g5517– g5517.
7. Fanta C. Asthma. New England Journal of Medicine. 2009;
360(10):1002– 14.
8. Decramer M, Janssens W, Miravitlles M. Chronic obstructive
pulmonary disease. Lancet. 2012;379(9823):1341– 51
9. Rabe KF, Hurd S, Anzueto A, et al. Global strategy for the
diagnosis, management, and prevention of chronic obstructive
148 PART IV. PULMONARY CRISES
https://t.me/medicina_free
149
pulmonary disease: GOLD executive summary. American Journal
of Respiratory and Critical Care Medicine. 2007;176(6):532– 55.
10. Eames W, Rooke A, Sai- Chuen Wu R, Bishop M. Comparison
of the eects of etomidate, propofol, and thiopental on respiratory resistance aer tracheal intubation. Anesthesiology. 1996;
84(6):1307– 11.
11. Berlin D. Hemodynamic consequences of auto- PEEP. Journal of
Intensive Care Medicine. 2014;29(2):81– 6.
12. Uddin M, Levy BD. Resolvins: natural agonists for resolution
of pulmonary inammation. Progress in Lipid Research. 2011;
50(1):75– 88.
13. Restrepo RD, Peters J. Near- fatal asthma:recognition and management. Current opinion in pulmonary medicine. 2008;14(1):13– 23.
14. Ng D, Fahimi J, Hern HG. Sevourane administration initiated out
of the ED for life- threatening status asthmaticus. American Journal
of Emergency Medicine. 33(8):1110 e1113– 1116.
15. Brenner K, Abrams DC, Agerstrand CL, Brodie D. Extracorporeal
carbon dioxide removal for refractory status asthmaticus:experience
in distinct exacerbation phenotypes. Perfusion. 2014;29(1):26– 8.
16. Alzeer AH, Al Otair HA, Khurshid SM, Badrawy SE, Bakir BM.
A case of near fatal asthma:the role of ECMO as rescue therapy.
Annals of oracic Medicine. 2015;10(2):143– 5.
PHYSIOLOGIC AIRFLOW DISRUPTION 149
150
https://t.me/medicina_free
19.
MECHANICAL AIRFLOW DISRUPTION
Alissa Sodickson and JamesHardy
CLINICALCASE
A 45- year- old man presents to the operating room for a laparoscopic cholecystectomy. e patient has a history of hypertension, hyperlipidemia, and mild intermittent asthma.
OVERVIEW OFAIRWAY ANATOMY
e anatomical structures that constitute the airway are
typically divided into upper airway structures and lower
airway structures. e upper airway includes structures
to the level of the glottis. e lower airway is made up of
structures from the glottis to the alveoli and includes the
trachea, mainstem bronchi, and generations of bronchi
down to bronchioles, alveolar ducts, and nally alveolar
sacs (Figure 19.1). e average length of the adult trachea,
which extends from the larynx to the carina, is 10 to 12cm,
and the distance from the upper incisors to the carina ranges
from 22 to 30cm. is distance changes with changes in
reported an incidence of roughly 5% to 13% based on
chest x- ray
1– 3
and an analysis of the Australian Incident
Monitoring Study (AIMS) database showed a reported
incidence of 2.36%– 6.1% over a 7- year period, with right
mainstem intubation accounting for approximately 97% of
the total endobronchial intubations.
1
Risk factors for endobronchial intubation include surgeries of the head and neck as well as laparoscopic procedures, where the position of the endotracheal tube tip in
relation to the carina can change during the procedure. In
the case of head and neck surgery, repositioning into prone
or lateral positions can cause inadvertent movement of the
endotracheal tube. In addition, movement from an extended
neck, as oen is the case during intubation, to a state of neck
exion is associated with forward movement of the endotracheal tube anywhere from 2.0 to 5.2cm.
4,5
Insuation of the
abdomen to a pressure of 10mmHg during laparoscopy has
been associated with upward displacement of the carina of
up to 1.5cm.6 e use of RAE tubes has also been associated
with an increased incidence of endobronchial intubations.
1
neck position as discussed below. e right and le mainstem bronchi branch o the carina with the right mainstem
bronchi being shorter (average length 2.5cm) and slightly
wider than the le mainstem bronchus (average length
5cm). e angle at which the main bronchi branch from
the carina diers; the right mainstem bronchi branches at
an angle of 20– 30 degrees from midline and the le mainstem bronchi branches more horizontally at an angle of
40- 50 degrees. is dierence accounts for the tendency of
endotracheal tubes and aspirated contents to preferentially
travel down the right main bronchus.
ENDOBRONCHIAL INTUBATION— DIAGNOSIS
Clinical signs and symptoms of endobronchial intubation
can be subtle and nonspecic, oen resulting in delayed detection. Observation of symmetrical chest rise and auscultation
of breath sounds have low sensitivity for the detection of
endobronchial intubation.7 e end- tidal CO2 can increase,
decrease, or remain unchanged, and the waveform may
appear biphasic, obstructive, or normal.8 If using a volumecontrolled mode of mechanical ventilation, endobronchial
intubation will result in an increase in peak inspiratory pres-
ENDOBRONCHIAL INTUBATION— INCIDENCE AND
RISK FACTORS
e incidence of inadvertent endobronchial intubation is
largely unknown because it is oen unrecognized. Studies
done on intubated patients admitted to the ICU have
sure and potential for barotrauma, while during pressurecontrolled ventilation, endobronchial intubation will result
in a drop in tidal volumes and hypoventilation. Several studies have found a decrease in oxygen saturation to be the most
sensitive sign of endobronchial intubation,
1,9
though this
may be harder to recognize if using an FiO2 greater than 0.5.10
150
Superior thyroid notch
lobar bronchus
lobar bronchus
Branches of left
Tracheal mucosa
https://t.me/medicina_free
151
Superior horn of thyroid cartilage
(anterior view)
Branches of
right superior
Branches of
right middle
Right lamina of thyroid cartilage
Cricothyroid ligament
Arch of cricothyroid cartilage
Longitudinal folds of mucosa
Tracheal cartilage (cut)
Cut edge of mucosa
Annular ligaments of trachea
Cricotracheal ligament
Tracheal bifurcation
Right main bronchus
Branches of
right inferior
lobar bronchus
Branches of left
inferior lobar
bronchus
Left lamina of thyroid cartilage
Inferior horn of
thyroid cartilage
Cricothyroid articular capsule
Fibromuscular posterior wall
Tracheal cartilages
Tracheal cartilages
Left main bronchus
Bronchial
cartilages
Tracheal mucosa
Trachea
(posterior view)
superior lobar
bronchus
Figure19.1 Anatomy of the lower airways. The angle of the right main bronchus takeoff is more vertical than the left as 20– 30 degrees versus 40– 50 degrees from
midline. The right main bronchus is shorter and wider than the left main bronchus. SOURCE:Reproduced with permission from Drake RL, Vogl W, Mitchel A.Gray’s Atlas of
Anatomy. 2nd ed. Thorax; Figure86.
Interestingly, one study found that the most sensitive and
specic means for detection was simply estimation of depth
using tube markings. is group suggested using a depth at
the corner of the mouth of 20cm for women and 22cm for
men, except at extremes of height, in order to position the
tube tip safely above the carina.7 Bronchoscopy can be used
where there is ongoing doubt about endotracheal tube posi-
ENDOBRONCHIAL INTUBATION— MANAGEMENT
Once recognized, management of endobronchial intubation is straightforward and involves movement of the endotracheal tube back into the tracheal position. Arecruitment
maneuver should be considered to reexpand the nonventilated lung. and one should monitor for pneumothorax as a
consequence of barotrauma to the ventilatedlung.
tion. Chest x- ray can also denitively assess endotracheal tube
position in relation to the carina (Figure 19.2). Ultrasound
is emerging as a versatile bedside imaging tool that has also
been described in the conrmation of appropriate endotracheal tube position. is is generally accomplished by visualizing bilateral diaphragm movement or pleural sliding,
though some have reported visualization of the cu itself
when inated with saline.
MECHANICAL AIRFLOW DISRUPTION 151
11
AIRWAY FOREIGN BODY— INCIDENCE/
EPIDEMIOLOGY
Tracheobronchial foreign- body aspiration has a bimodal
distribution of incidence, with most episodes occurring
in children under 4years of age but a second increase in
incidence in adults over the age of 75years. Other than
152
AB
https://t.me/medicina_free
Figure19.2 Endobronchial intubation with left lung collapse (A). There is resolution of the collapse with repositioning of the endotracheal tube (B). While
this demonstrates severe collapse as a result of endobronchial intubation, many cases present with more subtle ndings of atelectasis in the poorly
ventilatedlung.
age, risk factors include altered mental status, trauma,
neuromuscular disorders, and dysphagia. Classically,
most aspirated foreign bodies lodge in right main or
lobar bronchi, though several studies have shown equal
distribution between right and le bronchi.
12– 15
Food is
the most common foreign body aspirated, oen nuts or
seeds. Inorganic objects include teeth, dental appliances,
and pills (Figure 19.3).
AIRWAY FOREIGN BODY— DIAGNOSIS
13,14,16– 19
e clinical presentation of tracheobronchial foreign
body can range from acute asphyxia to chronic cough
depending on the degree of obstruction caused by
the object and the inammatory reaction it triggers.
Auscultation may reveal unilateral wheezing or ronchi,
or a discrepancy in breath sounds.
17,18
Children are more
likely to present with acute, life- threatening symptoms
caused by obstruction of the upper or proximal lower
is not elicited and patients are misdiagnosed with pneumonia or asthma. Ahigh degree of clinical suspicion is
therefore necessary, and the presence of a foreign body
should be considered in the case of persistent or recurrent
symptoms.
19,20
Most foreign bodies are radiolucent and therefore do
not show up on chest x- ray.
12,13,16,18,21
Computed tomography is more sensitive for the detection of radiolucent
foreign objects in the airway,
13,14
and three- dimensional
reformatting may oer even more sensitivity and specicity
as well as enhance surgical planning.
13,15,22,23
Indirect signs
of foreign- body aspiration include pneumonia, atelectasis,
unilateral hyperination, or pneumothorax. Several studies have shown that emphysema, or hyperination, is the
most common radiographic sign and is the result of the
object acting as a ball- valve, which eectively allows distal
air entry upon inhalation but prevents air egress with exha-
15,16,21– 23
lation
mon in cases of delayed presentation.
(Figure 19.4). Atelectasis may be more com-
16,18,23
airway (supraglottis, glottis, trachea), while adults more
oen present with nonspecic signs such as cough or
symptoms of pneumonia. Oen a history of aspiration
Figure19.3 Pill seen in right main bronchus on exible bronchoscopy.
152 PART IV. PULMONARY CRISES
Figure19.4 Foreign body in the right mainstem resulting in hyperination of the
right lung. Note the attening of the right hemidiaphragm and splaying of the
right rib spaces. SOURCE:Reproduced with per mission from Digoy G.Diagnosis and
management of upper aerodigestive tract foreign bodies. Otolarngologic Clinics of North
America. 2008;41:485– 96.
https://t.me/medicina_free
153
AIRWAY FOREIGN BODY— MANAGEMENT
Management of foreign- body aspiration depends on clinical urgency. Acute, life- threatening asphyxia should be
managed with attempts to clear the airway via abdominal
thrusts (the Heimlich maneuver), back slaps, and chest
thrusts according to resuscitation guidelines,
24,25
especially
in the prehospital setting. Anger sweep to clear any visible
upper airway material should also be performed, however
a blind nger sweep is not recommended, as it can further
advance unseen material. In an unconscious victim, cardiopulmonary resuscitation should be initiated while continuing to attempt to clear and secure an airway.
In the hospital setting, urgent operative intervention
should occur in any patient with respiratory distress or in
patients suspected to be at risk of complete airway obstruction due to the location or nature of the aspirated foreign
body. If the patient is stable, it is reasonable to delay intervention so that gastric aspiration is potentially reduced by
an overnight fast and so that experienced personnel and
equipment can be made more readily available.
26,21
e
patient should remain in a monitored setting, and the foreign body should be removed as soon possible to reduce
inammation and build up of granulation tissue.
In most cases, foreign body removal above the glottis is
accomplished via laryngoscopy and below the glottis with
rigid or exible bronchoscopy.
Rigid bronchoscopy is generally preferred for the
removal of large obstructing foreign bodies in the central airways, or for complex foreign bodies that cannot be
removed with exible bronchoscopy. e rigid bronchoscope allows for continued ventilation via the side port and
oers a large working channel through which instruments,
suction, and the foreign body can pass (Figure 19.5). Rigid
bronchoscopy requires general anesthesia, since patient
movement and coughing must be avoided to prevent injury
from the instrument. is may be achieved with the use of
paralyzing agents, opioids, or increased depth of anesthesia.
Flexible bronchoscopy can assess both proximal and distal airways and can be done in an awake or sedated patient
with local anesthesia12 or under general anesthesia. e disadvantages are the small working channel, which cannot
support both suction and a retrieval instrument simultaneously, and the possible need to withdraw and reintroduce
the entire apparatus several times if removing pieces of
foreign body. Additionally, there is no side port dedicated
to ventilation, and thus ventilation must occur around the
bronchoscope. Flexible bronchoscopy is preferred over
rigid bronchoscopy in patients with non- life- threatening,
distal foreign bodies; in those being mechanically ventilated; and in situations where the manipulation of the head
and neck that is required for rigid bronchoscopy would be
problematic, such as patients with head and neck injuries
or severe spinal stenosis. Close communication between
the surgeon and the anesthesiologist is necessary, and all
parties should be present upon induction of anesthesia.
Multiple retrieval devices may be required and should be
on hand, as should equipment for emergency tracheotomy
or cricothyroidotomy.
Figure19.5 Rigid bronchoscope. The
rigid bronchoscope is available
in various sizes. Alight source
is connected to the scope, and
ventilation can occur by connecting to
the side port seen here at the top of
the scope. Graspers and long suction
devices pass through the center
barrel/ working channel of thescope.
MECHANICAL AIRFLOW DISRUPTION 153
154
https://t.me/medicina_free
e major anesthetic considerations include the mode
of induction and the maintenance of ventilation during
the procedure. Additional consideration should be given
to possible complications such as the conversion of a partial obstruction to a complete obstruction, and distal airtrapping from ball- valve eect during positive pressure
ventilation. Anesthesia can be induced intravenously or
via an inhalational route, and ventilation during the case
can be spontaneous, assisted, or controlled. Studies have
shown no dierence in outcome when positive pressure is
used,27 though the theoretical risks of distal migration of
the foreign body or air trapping should always be kept in
mind, and maintenance of spontaneous respiration using
an inhalational induction, or cautious intravenous induction, may be optimal for a proximal foreign body that risks
causing complete airway obstruction with migration.21 e
airway may be secured with a supraglottic device, endotra-
Figure19.6 Foreign body with purulence and surrounding granulation tissue.
These objects may be more challenging to remove and steroids may be
considered. SOURCE:Reproduced with per mission from Digoy GP. Diagnosis and
management of upper aerodigestive tract foreign bodies. Otolarngologic Clinics of North
America. 2008;41:485– 96.s
cheal tube, or rigid bronchoscope depending on the surgical plan and clinical context. Muscle relaxants may be used
to prevent patient movement and provide a “quiet” airway
in cases where the maintenance of spontaneous respiration is not desired. Maintenance of anesthesia can occur
via inhalational or intravenous route. An intravenous route
is oen preferred, as it oers the advantage of continuous
anesthetic depth without the interruption of delivery that
occurs with inhalational anesthetic due to leak and airway
manipulation. Propofol and remifentanil provide excellent short- term hypnosis, analgesia, and blunting of airway
reexes and allow for a relatively rapid emergence.
be temporized by advancing the foreign body into a more
distal airway to allow for ventilation of unobstructed airways. Subsequent attempts at removal can occur aer the
patient becomes clinically stable. Unrecognized, the presence of foreign objects in the airway will oen lead to
recurrent pneumonias and bronchiectasis. Antibiotics and
anti- inammatories are not usually given to patients with
foreign- body aspiration. Antibiotics, however, are indicated
in cases of documented respiratory tract infection, and a
short course of steroids may be considered for foreign bodies that are encased in granulation tissue (Figure19.6).
AIRWAY FOREIGN BODY— COMPLICATIONS
CASE- BASED LEARNING DISCUSSION
e aspiration of inorganic objects, such as plastic or
metal, can lead to direct airway injury and, rarely, perforation. Organic material such as grains or vegetable matter
can absorb uid over time resulting in worsening airway
obstruction and clinical deterioration.18 Various organic
and inorganic objects can also trigger a localized inammatory reaction. is is seen commonly with aspiration of
peanuts or sunower seeds secondary to the oil component
and is also seen in the case of pill aspiration with medications such as iron, potassium, and metformin, among others.28 Bronchoscopic evaluation in these cases will initially
reveal signicant granulation tissue, which can subsequently result in airway stenosis.
18,19
Apartial obstruction
can turn into a complete obstruction due to swelling or
to dislodgment of the foreign body spontaneously or during attempted retrieval. If the patient is unstable and the
object is unable to be removed quickly, the situation can
154 PART IV. PULMONARY CRISES
1. Are there any patient- related concerns for anesthesia?
What is your anestheticplan?
2. Aer uneventful induction and endotracheal
intubation, the patient is prepped and draped and
placed in reverse Trendelenberg position for surgery.
Shortly aer insuation begins, there is an increase in
peak airway pressure and a drop in oxygen saturation
from 98% to 90%. End- tidal CO2 remains unchanged,
as does systemic blood pressure. What is the dierential
diagnosis? How would you evaluate the patient? What
are your initial steps in management?
3: Auscultation of the lungs reveals decreased breath
sounds bilaterally without wheezes or crackles.
Evaluation of the circuit and the endotracheal tube
reveals no kinks in tubing. e endotracheal tube is
https://t.me/medicina_free
155
positioned at 23.5cm at the upper incisors. Pulling
the tube back to 22cm results in a decrease in peak
airway pressures and an increase in O2 saturation to
95%. What can you do to increase the O2 saturation?
What are your concerns for the patient?
REFERENCES
1. McCoy EP, Russell WJ, Webb RK. Accidental bronchial intubation:an analysis of AIMS incident reports from 1988 to 1994 inclusive. Anaesthesia. 1997;52:24– 31.
2. Al- Qahtani, AS, Messahel FM, Ouda, WO. Inadvertent endobronchial intubation: a sentinel event. Saudi Journal of Anaesthesia.
2012; 6:259– 62.
3. Brunel W, Coleman DL, Schwartz DE, Peper E, Cohen NH.
Assessment of routine chest roentgenograms and the physical examination to conrm endotracheal tube position. Chest.
1989;96:1043– 5.
4. Conrardy PA, Goodman LR, Lainge F, Singer MM. Alteration of
endotracheal tube position with exion and extension of the neck.
Critical Care Medicine. 1976;4:8– 12.
5. Hartrey R, Kestin IG. Movement of oral and nasal tracheal tubes
as a result of changes in head and neck position. Anaesthesia. 1995;
50:682– 7.
6. Iwama H, Nakane M, Aoki K, Watanabe K, Komatsu T.
Abdominal insuation pressure during laparoscopic cholecystectomy shis the tracheal carina cephalad. Anesthesiology.
1996;84:491– 2.
7. Sitzwohl C, Langheinrich A, Schober A, etal. Endobronchial intubation detected by insertion depth of endotracheal tube, bilateral
auscultation, or observation of chest movements:randomized trial.
British Medical Journal. 2010;341:c5943.
8. Capnography.com.
9. Rolf N, Cote CJ. Diagnosis of clinically unrecognized endobronchial intubation in paediatric anaesthesia: which is more sensitive, pulse oxymetry or capnography? Paediatric Anaesthesia.
1992;2:31– 5.
10 Barker S, Tremper KK, Hyatt J, Heitzmann H. Comparison of three
oxygen monitors in detecting endobronchial intubation. Journal of
Clinical Monitors. 1988;4:240– 3.
11 Sustic A. Role of ultrasound in the airway management of critically
ill patients. Critical Care Medicine. 2007;35(Suppl):S173– 7.
12 Mise K, Savicevic A, Pavlov N, Jankovic S. Removal of tracheobron-
chial foreign bodies in adults using exible bronchoscopy: experience 1995– 2006. Surgical Endoscopy. 2009;23:1360– 4.
13 Kim M, Lee KY, Lee KW, Bae KT. MDCT evaluation of foreign
bodies and liquid aspiration pneumonia in adults. American Journal
of Roentgenology. 2008;190:907– 15.
14 Franquet T, Gimenez A, Roson N, Torrubia S, Sabate J, Perez C.
Aspiration diseases: ndings, pitfalls, and dierential diagnosis.
RadioGraphics. 2000;20:673– 685.
15 Yang C, Hua R, Xu K, etal. e role of 3D computed tomography
(CT) imaging in the diagnosis of foreign body aspiration in children. European Review for Medical and Pharmacological Sciences.
2015;19:265– 73.
16 Tokar B, Ozkan R, Ilhan H. Tracheobronchial foreign bodies in
children: importance of accurate history and chest radiograph in
delayed presentation. Clinical Radiology. 2004;59(7):609– 15.
17 Oncel M, Sunam GS, Ceran S. Tracheobronchial aspiration of
foreign bodies and rigid bronchoscopy in children. Pediatric
International. 2012;54(4):532– 5.
18 Digoy GP. Diagnosis and management of upper aerodigestive
tract foreign bodies. Otolaryngologic Clinics of North America.
2008;41:485– 96.
19. Hu S, Lee JS, Pianosi PT, Ryu JH. Aspiration- related pulmonary
syndromes. Chest. 2015;147:815– 23.
20 Ezer SS, Oguzkurt P, Ince E, Temiz A, Caliskan E, Hicsonmez A.
Foreign body aspiration in children:analysis of diagnostic criteria
and accurate time for bronchoscopy. Pediatric Emergency Care.
2011;27(8):723– 6.
21 Fidowski C, Zheng H, Firth P. e anesthetic considerations of tra-
cheobronchial foreign bodies in children: a literature report and
review of 12,979 cases. Anesthesia and Analgesia. 2010; 111:1016– 25.
22 Tong B, Zhang L, Fang R, Sha Y, Chi F. 3D images based on MDCT
in evaluation of patients with suspected foreign body aspiration.
European Archives of Otorhinolaryngology. 2013;270:1001– 1007.
23 Hedge SV, Hui PKT, Lee EY. Tracheobronchial foreign bodies in
children: imaging assessment. Seminars in ultrasound, CT, and
MRI. 2015;36:8– 20.
24 Koster R. Part5: Adult basic life support 2010 international con-
sensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation.
2010;81S:e48– e70.
25 Heimlich HJ. A life- saving maneuver to prevent food- choking.
Journal of the American Medical Association. 1975;234(4):
398– 401.
26 Mani N, Soma M, Massey S, Albert D, Baily CM. Removal of
inhaled foreign bodies: middle of the night or the next morning?
International Journal of Pediatric Otorhinolaryngology. 2009;
73:1085– 9.
27 Farrell PT. Rigid bronchoscopy for foreign body removal:anaesthe-
sia and ventilation. Paediatric Anaesthesia. 2004;14:84– 89.
28 Kupeli E, Khemasuwan D, Lee P, Mehta A. “Pills” and the air pas-
sages. Chest. 2013;144(2):651– 60.
MECHANICAL AIRFLOW DISRUPTION 155
Соседние файлы в папке @xirurgi_2025