Download chapter 37 flexible bronchoscopy

P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
CHAPTER 37 ■ FLEXIBLE BRONCHOSCOPY
MICHAEL A. JANTZ
Flexible bronchoscopy is an essential diagnostic and therapeutic tool in the intensive care unit (ICU). Potential indications for
flexible bronchoscopy in the ICU include airway management
(intubation, changing of endotracheal tubes, and extubation);
diagnosis of respiratory infections, parenchymal lung disease,
acute inhalational injury, or airway injury from intubation or
chest trauma; and treatment of hemoptysis, atelectasis, foreign
bodies, obstructing airway lesions, and bronchopleural fistulae. From a diagnostic standpoint, flexible bronchoscopy can
identify the etiology of hemoptysis and the cause of pulmonary
infection.
Compared with rigid bronchoscopy, flexible bronchoscopy
offers enhanced visualization of the proximal and distal airways, is associated with fewer complications, and can be performed at the bedside, averting the need for general anesthesia
and operating room resources. However, for management of
massive hemoptysis, difficult-to-extract foreign bodies, bronchoscopic laser resection, and benign or malignant obstruction of the trachea or bilateral mainstem bronchi, rigid bronchoscopy may be the procedure of choice.
Both fiberoptic and video bronchoscopes are utilized for
flexible bronchoscopy in the ICU. Video bronchoscopy allows
for better resolution of the image because of the greater number
of pixels on the charge-coupled device for image acquisition. In
contrast, the resolution of the traditional fiberoptic bronchoscope is determined by the diameter of the optical fibers and
seems to have reached its technological limit. With the video
bronchoscope, as well as with attachment of a camera head to
the fiberoptic bronchoscope, observation by multiple parties
is possible, which decreases the possibility of missed findings
and facilitates teaching and education. Compared with video
bronchoscopes, the fiberoptic bronchoscope is less expensive,
although improper use and care can result in broken optical
fibers and thus higher repair costs over time.
PROCEDURE
General Considerations
In nonintubated patients, flexible bronchoscopy can be performed by the transnasal or transoral route with a bite block.
In the mechanically ventilated patient, gas exchange abnormalities may occur due to the bronchoscope occupying a significant
portion of the internal diameter of the endotracheal tube (ET)
(1). This reduction in the cross-sectional area of the ET may
lead to hypoventilation, hypoxemia, and air trapping with intrinsic positive end-expiratory pressure (auto-PEEP). The outer
diameter of the bronchoscope should be at least 2 mm smaller
than the lumen of the ET to minimize these effects. As most
adult bronchoscopes have an outer diameter of 5 to 6 mm,
an 8-mm ET is generally recommended for performing bronchoscopy safely in the intubated patient. A pediatric bronchoscope with an outer diameter of 3 to 4 mm should be used if
the ET is smaller.
Informed consent for the procedure should be obtained
prior to starting bronchoscopy. Enteral feeding or oral intake
should be discontinued for 4 hours before and 2 hours after the
procedure. Patients with asthma should receive bronchodilators prior to bronchoscopy. Platelet counts and coagulation
studies should be obtained in those patients with risk factors for
bleeding if the bronchoscopic procedure will include biopsies.
In the ICU setting, most patients will be monitored with a continuous electrocardiogram, pulse oximetry, and intra-arterial
blood pressure or intermittent cuff blood pressure every 3 to
5 minutes. Monitoring intracranial pressure (ICP) and endtidal CO2 has been suggested for patients with a serious head
injury (2).
Equipment for reintubation and bag-valve-mask ventilation
should be readily available, and suctioning equipment, including Yankauer and endotracheal catheters, should be accessible
at the bedside. In addition to sedatives and analgesics, resuscitation medications should also be on hand. It is prudent to have
materials for chest tube thoracostomy located in the ICU.
Premedication
Topical anesthesia is typically used to suppress the gag reflex and coughing. Nonintubated patients will undergo topical anesthesia of the nares and oropharynx with lidocaine jelly
and nebulized or sprayed lidocaine. The tracheal and bronchial
mucosa is anesthetized with 1% lidocaine solution. In intubated patients, the 1% lidocaine can be administered through
the endotracheal tube or through the working channel of the
bronchoscope after insertion into the ET. Lidocaine is absorbed
through the mucous membranes and achieves peak serum concentrations that are similar to that of intravenous administration. The total dose of lidocaine should not exceed 3 to
4 mg/kg. Patients with cardiac or hepatic insufficiency have
reduced clearance of lidocaine, and thus the dose should not
exceed 2 to 3 mg/kg. The use of lidocaine should be kept to a
minimum if samples for culture are to be obtained, as bacteriostatic lidocaine preparations may decrease culture yields. The
administration of antisialagogues, such as atropine or glycopyrrolate, has been recommended in the past to reduce secretions
and prevent bradycardia, although recent studies suggest no
benefit from use of these drugs (3).
Sedation and analgesic agents are often used during bronchoscopy to provide anxiolysis, antegrade amnesia, analgesia, and cough suppression. A combination of opiates and
benzodiazepines is typically used. The most commonly used
505
13:42
P1: OSO/OVY
GRBT291-37-39
506
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Section III: Techniques, Procedures, and Treatments
benzodiazepine is midazolam, given its short elimination halflife and rapid onset of action. Fentanyl is the most commonly
used opiate, again due to a short elimination half-life. Meperidine has also been used for bronchoscopy, although clearance is
decreased with hepatic and renal failure, and accumulation of
a toxic metabolite, normeperidine, may cause seizures. Propofol may also be used in intubated patients and patients with
adjunctive airway support (4); advantages include rapid onset
and offset of action, with the potential disadvantage of druginduced hypotension. The type and level of sedation required
depend on the clinical status. Nonintubated patients, particularly with borderline oxygenation and ventilation or with central airway obstruction, should likely receive light or moderate
sedation. Unstable hypoxic patients with acute respiratory distress syndrome (ARDS) and patients with brain injury may require deep sedation, or even neuromuscular blockade, to safely
perform the procedure (5).
Mechanical Ventilation
In mechanically ventilated patients, a special swivel adapter,
with a perforated diaphragm through which the bronchoscope
is passed, is used to prevent loss of delivered tidal volumes (6).
As previously noted, bronchoscopy in the mechanically ventilated patient may cause hypoxemia, hypoventilation, generation of auto-PEEP, and potential barotrauma. The lumen of
the ET should be 2 mm larger than the external diameter of
the bronchoscope. Decreases in delivered tidal volumes will
occur during pressure-limited, time-cycled ventilator modes, as
well as when flow-limited, volume-cycled breaths become pressure limited. To reliably ensure tidal volume delivery, volumecycled breaths should be used during bronchoscopy. Because
the increase in peak pressure is dissipated along the endotracheal tube and does not represent an increased risk for barotrauma, the peak pressure limit on the ventilator can be significantly elevated to ensure delivery of tidal volume. The high
peak pressures seen during bronchoscopy are not reflective of
pressures distal to the endotracheal tube. The problem with
high peak pressures is ventilator pressure limiting, resulting in
decreased effective tidal volume. Decreasing inspiratory flow
rate decreases peak pressures and pressure limiting, but may
paradoxically increase predisposition to auto-PEEP by decreasing the expiratory time. Set tidal volumes may need to be increased by 40% to 50% in some patients to achieve adequate
tidal volumes. Barotrauma and hypotension may occur if the
bronchoscope-added expiratory resistance leads to auto-PEEP.
Some authors advocate reducing set PEEP or discontinuing
PEEP prior to bronchoscopy (1). The fraction of inspired oxygen (FiO2 ) should be increased to 1.0 prior to and during the
procedure to ensure adequate oxygenation. Exhaled tidal volumes should be monitored during the procedure. The bronchoscope should be withdrawn periodically to allow for adequate
ventilation; prolonged suctioning through the bronchoscope
can decrease delivered tidal volumes and oxygenation.
Bronchoalveolar Lavage
Bronchoalveolar lavage (BAL) allows for sampling of cellular
and noncellular components from the lower respiratory tract.
The tip of the bronchoscope is wedged into a distal airway, and
sterile saline solution is instilled through the bronchoscope and
then aspirated with the syringe or suctioned into a sterile trap.
Aliquots of 20 mL to 60 mL are generally used. Infusions of
120 mL to 240 mL are needed to ensure adequate sampling of
secretions in the distal respiratory bronchioles and alveoli (7–
9). Aspiration of aliquots by syringes in a serial fashion allows
for detection of progressively bloodier aliquots, which strongly
suggests the presence of alveolar hemorrhage. The first aliquot
of aspirated fluid is likely to contain a significant amount of
material from the proximal airways. As such, some authors
recommend discarding this aliquot or analyzing the aliquot
separately from the remainder of the fluid (7). In patients with
emphysema, collapse of the airways with negative pressure during aspiration or suctioning may limit the amount of fluid obtained. The very small fluid return in these patients may contain
only diluted material from the proximal bronchi rather than the
alveoli, and thus may give rise to false-negative results (10).
Suctioning prior to having the bronchoscope in the appropriate wedged position should be minimized to avoid contamination with upper airway secretions and potential false-positive
results.
In addition to quantitative bacterial cultures for the diagnosis of ventilator-associated pneumonia, BAL samples may
also be sent for cytology, antigen tests, and polymerase chain
reaction tests, which provide additional information for the diagnosis of noninfectious and infectious etiologies of pulmonary
disease as compared to the protected specimen brush.
Protected Specimen Brush
The protected specimen brush (PSB) is used to obtain a lower
respiratory tract specimen for microbiology that is not contaminated by organisms in the proximal airways. The PSB consists of a retractable brush within a double-sheathed catheter
that has a distal dissolvable plug occluding the outer catheter
(11,12). After the tip of the bronchoscope is positioned in
the desired area, the catheter is advanced through the working channel and situated 1 to 3 cm beyond the distal end of
the bronchoscope to prevent collection of secretions pooled
around the distal end of the bronchoscope. The inner cannula
containing the brush is advanced to eject the distal plug, and
the brush is then advanced into the desired subsegment under
direct visualization. Once the sample is obtained, the brush
is retracted into the inner cannula, the inner cannula is then
withdrawn into the outer sheath, and the entire catheter is removed from the bronchoscope. The distal ends of the outer
and inner cannula are wiped with alcohol, cut with sterile scissors, and discarded. The brush is advanced beyond the remaining portion of the inner cannula, cut with sterile scissors, and
placed in 1 mL of nonbacteriostatic sterile saline or transport
media.
Quantitative Bronchoalveolar Lavage and
Protected Specimen Brush Cultures
Specimens for culture should be rapidly processed to prevent a
decrease in pathogen viability or contaminant overgrowth. The
BAL sample should be transported in a sterile, leakproof container. The initial aliquot, which is thought to be representative
of proximal airway secretions, should be discarded or analyzed
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 37: Flexible Bronchoscopy
separately from the remaining pooled fractions. It is recommended that specimens for microbiologic analysis be processed
within 30 minutes, although refrigeration can be used when
the specimens cannot be immediately processed (7,13). The
specimens should be processed according to clearly defined
protocols (14). Pathogens are present in lower respiratory tract
secretions, at concentrations of at least 105 to 106 colony forming units (CFU)/mL, in patients with pneumonia, while contaminant bacteria are present at concentrations of less than 104
CFU/mL (15,16). The diagnostic thresholds proposed for BAL
and PSB are based on these concentrations with 104 CFU/mL
for BAL, which collects 1 mL of secretions in 10 to 100
mL of saline and represents 105 to 106 CFU/mL, which is
considered supportive of the diagnosis of ventilator-associated
pneumonia. Similarly, the concentration of 103 CFU/mL
for PSB, which collects 0.001 to 0.01 mL of secretions in
1 mL of saline, is considered supportive of the diagnosis of
ventilator-associated pneumonia.
507
increased risk for hemorrhage with biopsy procedures (20). Patients with pulmonary hypertension have also been noted to be
at risk for greater bleeding with transbronchial biopsies.
Patients with stable COPD may safely undergo flexible
bronchoscopy. Sedation during the procedure should be used
cautiously, and the possibility of supplemental oxygen-induced
hypoventilation should be considered.
Patients with increased ICP should be carefully monitored
during flexible bronchoscopy. Bronchoscopy has been noted to
increase ICP by at least 50% in 88% of patients with head
trauma, despite the use of deep sedation and paralysis (5).
Cerebral perfusion pressure may not change, however, due to
concurrent increases in mean arterial pressure during bronchoscopy. Despite an increase in ICP, no significant neurologic
complications were noted in studies of patients with severe
head trauma or space-occupying lesions who were undergoing
flexible bronchoscopy (2,5,21). In spite of these observations,
caution is warranted in performing bronchoscopy in patients
with markedly elevated ICP.
Transbronchial and Endobronchial Biopsies
Histologic samples of lung parenchyma may be obtained with
transbronchial lung biopsies. In patients with diffuse or localized parenchymal diseases, transbronchial lung biopsies may
be useful and offer a less invasive option to open lung biopsy.
It should be noted, however, that for some interstitial lung
diseases and pulmonary vasculitides, transbronchial biopsy
specimens are inadequate to make a definitive diagnosis. The
major risks of transbronchial biopsies are bleeding and pneumothorax. The risk of pneumothorax is higher when performing transbronchial biopsies in the mechanically ventilated
patient (17). Fluoroscopy may not be required to perform
transbronchial biopsies in mechanically ventilated patients
with diffuse parenchymal disease; however, I would recommend the use of fluoroscopy, if available, to minimize the risk of
a life-threatening pneumothorax. A chest radiograph should be
obtained in all critically ill or mechanically ventilated patients
after transbronchial lung biopsy.
Samples of bronchial mucosa and endobronchial abnormalities may be obtained with endobronchial biopsies. Transbronchial and endobronchial biopsies may be sent for bacterial,
mycobacterial, and fungal cultures as indicated, in addition to
histology.
CONTRAINDICATIONS
Only a few absolute contraindications to flexible bronchoscopy
exist in critically ill patients. Flexible bronchoscopy should not
be performed in the absence of informed consent, if trained
personnel are not available, if adequate oxygenation cannot
be maintained during the procedure, if unstable cardiac conditions are present, or if uncontrolled bronchospasm is present
(18,19). The inability to normalize the platelet count and coagulation parameters if biopsy or PSB is planned is a relative
contraindication. Airway inspection and BAL may likely be
done safely despite thrombocytopenia or coagulopathy unless
the abnormalities are profound. The general recommendation
is that the platelet count should be at least 50,000 cells/μL
if biopsies are going to be performed. Performing biopsies or
PSB in patients on antiplatelet agents is controversial. Patients
with uremia, which causes a functional platelet defect, are at
COMPLICATIONS
With appropriate care, flexible bronchoscopy is an extremely
safe procedure. The incidence rate of major complications
ranges from 0.08% to 0.15%, and the mortality rate ranges
from 0.01% to 0.04%. Minor complications (e.g., vasovagal reaction, fever, bleeding, nausea, and vomiting) occur in
as many as 6.5% of these patients (22–24). Flexible bronchoscopy in mechanically ventilated patients has the potential for life-threatening complications including hypoxemia,
hypercapnia, barotrauma, cardiac arrhythmias, myocardial ischemia, intracranial hypertension, local anesthetic toxicity, and
pulmonary hemorrhage. Careful patient selection, meticulous
preparation before the procedure, and vigilant physiologic
monitoring during the procedure limit complications and mortality. The characteristics of high-risk patients are summarized
in Table 37.1.
A prospective clinical trial in critically ill, mechanically ventilated patients with ARDS provides important information
with regard to the safety of BAL in this patient population.
Careful attention was directed toward maintenance of minute
ventilation and the limitation of auto-PEEP during the procedure. Severe hypoxemia and hypotension were seen in 4.5%
and 3.6% of patients, respectively. No significant reduction
occurred in postprocedure pulmonary function, such as static
compliance or PaO2 /FiO2 ratio. No deaths were attributed to
the procedure. The incidence of pneumothorax was 0.9% (1
of 110 patients) (25).
These results are in contrast to other investigators who
have shown the potential for significant decline in oxygenation, which can persist for up to 2 hours after the procedure
(26). In healthy patients, the arterial partial pressure of oxygen (PaO2 ) may decline by 20 to 30 mm Hg during flexible
bronchoscopy (26). In critically ill patients, the decrement in
PaO2 can exceed 30 to 60 mm Hg (27,28). In a more recent
study of bronchoscopy in critically ill patients, hypoxemia was
observed in 29 of 147 procedures (19.7%) (29). The greater
the amount of normal saline instilled for lavage during bronchoscopy, the more frequent the hypoxemia—seen in as many
as 23% of patients—and the longer its duration, up to 8 hours
(30,31). Hypoxemia- and hypercapnia-induced increased
13:42
P1: OSO/OVY
GRBT291-37-39
508
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Section III: Techniques, Procedures, and Treatments
TA B L E 3 7 . 1
CHARACTERISTICS OF INCREASED-RISK PATIENTS
FOR BRONCHOSCOPY ON MECHANICAL
VENTILATION
PULMONARY
PaO2 <70 mm Hg with FiO2 >0.70
PEEP >10 cm H2 O
Auto-PEEP >15 cm H2 O
Active bronchospasm
CARDIAC
Recent myocardial infarction (<48 h)
Unstable dysrhythmia
Mean arterial pressure <65 mm Hg on vasopressor therapy
COAGULOPATHY
Platelet count <20,000 cells/μL
Increase of prothrombin time or partial thromboplastin time
2.0 times control
CENTRAL NERVOUS SYSTEM
Increased intracranial pressure
FiO2 , fraction of inspired oxygen; PEEP, positive end-expiratory
pressure.
sympathetic tone can result in dysrhythmias, myocardial ischemia, hypotension, and cardiac arrest.
Bronchoscopy-associated hypoxemia may be minimized by
providing 100% oxygen during the procedure, shortening
bronchoscopy time, and frequently withdrawing the bronchoscope from the airway to allow adequate ventilation. Adequate
tidal volume delivery should be monitored by observing chest
excursions and exhaled tidal volumes in patients undergoing
mechanical ventilation. Tidal volume and flow rates must be
adjusted to provide adequate ventilation (1,26,32).
Complications associated with the administration of sedation, analgesia, and topical anesthesia include hypotension and
allergic reactions, as well as hypoventilation, and hypoxemia
from oversedation and respiratory depression. The overzealous
use of local anesthetic agents within the airways has potential
for toxicity with the rapid uptake of these agents into the systemic circulation from the bronchial mucosa (33). Lidocaine is
the most commonly used airway anesthetic. The risks of toxicity are decreased with total doses of less than 4 mg/kg of body
weight. The duration of airway anesthesia induced by lidocaine is approximately 20 to 40 minutes. Lidocaine in excessive
doses can cause sinus arrest and atrial ventricular block, especially in patients with underlying heart disease. Other potential adverse reactions include respiratory arrest, seizures, laryngospasm, and, rarely, hypersensitivity reactions. Although not
as commonly used for topical anesthesia, benzocaine has been
associated with the development of methemoglobinemia (34).
Although rarely associated with bronchoscopy, dysrhythmias are more likely to occur in critically ill patients (35). Major cardiac dysrhythmias occur in 3% to 11% of all patients
undergoing bronchoscopy. Hypoxemia is the major risk factor
for the development of dysrhythmias (36,37).
Laryngospasm (in the nonintubated patient) or bronchospasm can occur in any patient undergoing flexible bronchoscopy, but are more common in patients with pre-existing
reactive airway disease. Preoperative bronchodilator therapy
significantly reduces the risk of bronchoscopy-induced bronchospasm in most patients with reactive airway disease (38).
Although transbronchial biopsy is a relatively safe procedure in patients with normal hemostasis and pulmonary vascular pressures, it is associated with a 2.7% and 0.12% risk of
morbidity and mortality, respectively (39). Hemorrhage (more
than 50 mL of blood) is more likely to occur in patients
who undergo transbronchial biopsy. Risk factors for hemorrhage include thrombocytopenia, coagulopathy, uremia, and
pulmonary hypertension. Transbronchial biopsy should be restricted to nonuremic patients with platelet counts greater than
50,000 cells/μL and prothrombin times and activated partial
thromboplastin times less than twice that of controls (22, 39,
40). The incidence rate of bronchoscopy-related hemorrhage
in normal hosts approaches 1.4%. In immunocompromised
hosts, the rate of hemorrhage ranges from 25% to 29%, while
hemorrhage occurs in as many as 45% of uremic patients
(22,41,42). Administration of desmopressin, 0.3 μg/kg, can
reverse the uremic effect on platelet function, although no controlled study evaluating the safety of performing transbronchial
biopsies after treatment with desmopressin exists (43). Pneumothorax occurs in fewer than 5% of nonventilated patients
undergoing transbronchial biopsy. Tube thoracostomy is required in approximately half of these patients (22). A major risk factor for pneumothorax is positive pressure ventilation, especially if PEEP is used. Rates of pneumothorax after
transbronchial lung biopsy in mechanically ventilated patients
have been reported up to 7% and 23% (44–46). Fluoroscopic
guidance may diminish the risk of pneumothorax. No patient
should undergo bilateral transbronchial biopsy procedures during the same bronchoscopic episode because of the small risk
of bilateral pneumothorax.
Postbronchoscopy fever occurs in as many as 16% of patients. Bronchoscopy-related pneumonia is rare, occurring in
fewer than 5%, and bacteremia is exceedingly rare (47,48). In
general, endocarditis prophylaxis is not required with flexible
bronchoscopy (49).
Neurosurgical patients are at risk for intracranial hypertension as a result of bronchoscopy-induced elevation of intrathoracic pressure, arterial hypertension, and hypercapnia.
Bronchoscopy-associated cough or retching must therefore be
avoided. Deep sedation with or without neuromuscular blockade may be utilized if bronchoscopy is deemed necessary.
DIAGNOSTIC AND THERAPEUTIC
BRONCHOSCOPY
Airway Management
Flexible bronchoscopy can provide an efficient and effective
means to secure a difficult airway, change an endotracheal
tube, and inspect an airway during extubation (50,51). Endotracheal intubation can be technically difficult in select patient
groups (Table 37.2). Intubation using flexible bronchoscopy
under topical anesthesia, with or without conscious sedation,
is an important technique in these patients with compromised
airways, particularly if the airway is obstructed or if the trachea is extrinsically compressed by a mediastinal mass. Spontaneous ventilation keeps the airway open and assists the
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 37: Flexible Bronchoscopy
509
TA B L E 3 7 . 2
FACTORS ASSOCIATED WITH DIFFICULT ENDOTRACHEAL INTUBATIONS
ANATOMIC
Short muscular neck
Receding mandible
Prominent upper incisors
Microglossia
Limited mandible movement
Large breasts
Cervical rigidity
CONGENITAL ABNORMALITIES
Absence of nose
Choanal atresia
Macroglossia
INFECTIOUS
Bacterial retropharyngeal abscess
Epiglotitis
Diphtheria
Infectious mononucleosis
Croup
Leprosy
NEOPLASIA
Laryngeal papillomatosis
Stylohyoid ligament calcification
Laryngeal carcinoma
Mediastinal carcinoma
TRAUMA
Mandibular fracture
Maxillary fracture
Laryngeal and tracheal trauma
Mediastinal carcinoma
ENDOCRINE
Obesity
Acromegaly
Thyromegaly
NONINFECTIVE INFLAMMATION
Rheumatoid arthritis
Instability of cervical spine
Cervical fixation
Temporomandibular disease
Cricoarytenoid disorders
Hypoplastic mandible
Ankylosing spondylitis
bronchoscopist in locating the glottis when airway anatomy is
distorted (50,52). Bronchoscopic examination of the airway
also identifies the nature of the obstructed airway and helps to
plan for additional therapeutic maneuvers to relieve the airway
obstruction.
Bronchoscopic endotracheal intubation can be performed
using either a nasal or oral approach. With the nasal approach,
after preparation of the nasal mucosa with a local anesthetic
such as lidocaine and a mucosal vasoconstrictor such as 1%
phenylephrine, the bronchoscope is passed through the nares
and situated directly above the glottic opening. It is then passed
into the trachea and the ET is passed over the bronchoscope
into the trachea. The major limitation of this approach in many
ICU patients with concomitant abnormalities of coagulation is
epistaxis and the potential for sinusitis with prolonged nasal
intubation. The development of epistaxis can significantly impair the bronchoscopic examination and can seriously hamper subsequent nasal or laryngoscopic attempts at intubation.
Other difficulties associated with nasal intubation include adenoid dislocation and difficulty passing the ET in patients with
a limited diameter of the nares.
Oral flexible bronchoscopic intubation effectively avoids
these difficulties associated with nasal intubation. Topical anesthesia of the oropharynx is achieved with spraying of 4% lidocaine. Translaryngeal injection of 3 mL of 4% lidocaine
through the cricothyroid membrane to provide topical anesthesia to the larynx and trachea, in addition to lidocaine sprays
to the oropharynx, is favored by some practitioners. Others fa-
vor a “spray as you go” technique, with injection of lidocaine
through the working channel of the bronchoscope to provide
laryngeal and tracheal topical anesthesia. Alternatively, nebulization of 6 to 8 mL of 4% lidocaine is used for topical anesthesia in some institutions (50). A bite block should be in place
to prevent scope damage from the patient biting. In some patients, the use of an oral intubating airway, such as the Williams
Airway Intubator, the Ovassapian Airway, or the Berman Airway, may be helpful in successfully intubating the patient with
a difficult airway (53). The oral intubating airway directs the
flexible bronchoscopy past the tongue and directly over the
larynx, facilitating endotracheal intubation. Use of these airways in the completely awake patient with inadequate topical
anesthesia may be problematic due to gagging and vomiting.
This is less of a problem in the sedated or unconscious patient.
After exposure of the vocal cords, the bronchoscope is passed
into the trachea and the ET is then passed over the bronchoscope into the airway. In some patients, the endotracheal tube
impinges on laryngeal structures despite the smooth entrance
of the bronchoscope into the trachea. In this situation, the ET
may be withdrawn back over the bronchoscope, rotated 90 degrees clockwise or counterclockwise to change the position of
the tube bevel relative to the larynx, and readvanced during
inspiration (50). Mild to moderate conscious sedation may be
used in some patients to improve patient comfort and tolerance of nasal or oral bronchoscopic intubation. Great caution
should be taken in patients with highly compromised airways,
however, and sedatives may need to be completely avoided.
13:42
P1: OSO/OVY
GRBT291-37-39
510
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Section III: Techniques, Procedures, and Treatments
In addition to the oral intubating airway, other airway adjuncts have been used in combination with the flexible bronchoscope for intubation of patients with a difficult airway. A
special facial mask with a diaphragm for the bronchoscope has
been developed for the critically ill and for use in the operating
room (54). The mask is useful for bronchoscopic intubation in
sedated or comatose patients with limited respiratory reserve,
providing a tight seal for assisted ventilation during the procedure. The intubating laryngeal mask airway (LMA) has also
been used successfully in combination with the flexible bronchoscope (55).
Flexible bronchoscopy allows for ET changes in patients
with endotracheal tube cuff leaks, inadequate ET internal diameters, and nasotracheal tube–associated sinusitis. Before
bronchoscopy, the oropharynx should be suctioned thoroughly.
For oral tracheal intubation, the endotracheal tube should be
shortened 2 to 3 cm at its proximal end and advanced over the
bronchoscope before its placement in the pharynx. The bronchoscope tip is advanced to the level of the cuff of the existing
endotracheal tube, and secretions are aspirated through the
suction channel. If necessary, the cuff is deflated and the bronchoscope advanced into the tracheal lumen. The endotracheal
tube is then withdrawn with the cuff fully deflated, the bronchoscope tip advanced to the carina, and the new endotracheal
tube advanced over the bronchoscope into the trachea. Adequate positioning of the tube 3 to 4 cm proximal to the carina
is confirmed by visual inspection, and the cuff is inflated. After
intubation, a chest radiograph is not required to confirm adequate placement of the endotracheal tube (56). Tube changes
by the oral or nasal routes are possible. Contralateral nasal
reintubation, however, may be difficult because of the lateral
displacement of the septum by the existing nasotracheal tube.
Percutaneous dilatational tracheostomy (PDT) has become
a well-accepted method for performing bedside tracheostomy
in the ICU. While not universally utilized, flexible bronchoscopy is routinely used in performing PDT (57). Bronchoscopy facilitates proximal positioning of the ET prior to
introducing the guidewire needle into the trachea, reducing the
risk of ET impalement by the needle, and facilitates reintubation if the ET is dislodged out of the airway. Bronchoscopic
visualization ensures that the guidewire needle is introduced in
the appropriate interspace in a midline position and that the
needle does not penetrate the membranous posterior tracheal
wall, thereby decreasing the risk of misplacement of the tracheostomy tube and creation of a false paratracheal passage.
Bronchoscopy also provides feedback to the operator during
dilator passage so that pressure on the posterior wall is minimized and the potential for posterior wall tears is reduced.
Flexible bronchoscopy can be extremely useful in the placement of a double-lumen ET. If a right-sided tube is used, adequate positioning of the tube with the tracheal port proximal
to the carina and bronchial port proximal to the right upper
lobe orifice can be confirmed by using a small-diameter (3.5mm outer diameter) flexible bronchoscope to inspect the airway through each lumen (58,59). Positioning of left-sided tubes
is not as problematic given the longer length of the left mainstem bronchus relative to the right mainstem bronchus and less
likelihood of obstructing the left upper or left lower lobe. In
general, bronchoscopic confirmation of proper bronchial port
positioning should be performed after all double-lumen ET intubations, given the significant rate of malpositioning with a
blind technique (60).
Flexible bronchoscopy provides an excellent opportunity to
inspect the airways at the time of extubation in patients at risk
for airway compromise, including those intubated for inhalation injury, trauma, subglottic stenosis, and laryngeal edema.
The bronchoscope is advanced through the ET to its most distal
aspect, and the ET and bronchoscope are withdrawn slowly together to allow inspection of the airway. If bronchoscopy confirms persistent mucosal edema or airway obstruction, the endotracheal tube can be readvanced over the bronchoscope into
the tracheal lumen and secured, with extubation postponed
until a later time.
Atelectasis
Segmental or lobar atelectasis presents radiographically as a
parenchymal density associated with a combination of shift of
an interlobar fissure, crowding of vessels or bronchi, ipsilateral
mediastinal shift, or elevation of the diaphragm. Complete lung
atelectasis will produce opacification of the hemithorax and
usually ipsilateral mediastinal shift. Atelectasis is most commonly due to mucous plugging; however, in patients who do
not improve after chest physiotherapy, endobronchial obstruction due to endobronchial tumor, foreign body, or blood clot
should be excluded by bronchoscopy. Predisposing conditions
for mucous plugging and atelectasis include inadequate inspiratory effort (pain, sedation, and muscle weakness), immobility,
obesity, excessive airway secretions, pre-existing airway disease, and endobronchial obstructing lesions. Lobar or whole
lung atelectasis produces hypoxemia by right-to-left vascular
shunting and ventilation/perfusion mismatching. The clinical
significance of atelectasis is directly related to its extent and to
the pre-existing pulmonary reserve of the patient.
Much of the evidence supporting the role of flexible bronchoscopy in the treatment of atelectasis is anecdotal. Success
rates for bronchoscopy range from 19% to 89% (61). One
randomized trial comparing bronchoscopy to aggressive chest
physiotherapy and nebulizer therapy found no advantage for
bronchoscopy, although the study methodology has been criticized (62–64). Patients with whole lung or lobar atelectasis
tend to respond better than those with segmental atelectasis.
With the exception of large, obstructing central airway mucous
plugs, the radiographic response to successful removal of secretions is delayed from 6 to 24 hours. Therapeutic bronchoscopy
is, in general, indicated for patients with life-threatening whole
lung or lobar atelectasis and for patients who have not responded to chest physiotherapy measures. Chest physiotherapy should be continued after successful bronchoscopy to prevent new airway obstructions. Instillation of saline or a dilute
10% solution of acetylcysteine through the working channel
may help to clear thick, tenacious secretions. Acetylcysteine is a
bronchial irritant, however, and may exacerbate bronchospasm
in patients with reactive airway disease. Typically 10- to 20-mL
aliquots of saline are used as the irrigant to facilitate clearing of mucous plugs. If saline irrigation fails, then instillation
of acetylcysteine or rhDNase (Pulmozyme) may be considered
(65–67). In some patients, holding continuous suction while
withdrawing the bronchoscope through the ET allows removal
of large mucous plugs that cannot be suctioned directly through
the working channel. Extremely tenacious mucous plugs may
require the use of biopsy forceps or a foreign body basket to
be successfully extracted. Blood clots may similarly be removed
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 37: Flexible Bronchoscopy
with saline irrigation. Instillation of acetylcysteine may be helpful in more difficult to remove blood clots. The use of biopsy
forceps or a foreign body basket may be needed to remove
blood clots that cannot be removed with irrigation and suction
extraction.
Selective intrabronchial insufflation by the flexible bronchoscope, preceded by suctioning of mucus from large airways,
has been used in patients with refractory atelectasis (61). One
study in a surgical ICU study using air insufflation for lobar
collapse reported an overall effectiveness of 82%, with 92%
effectiveness when collapse was less than 72 hours’ duration
(68). Although only minor clinically insignificant complications have been described, selective positive pressure insufflation does carry the potential risk of barotrauma (69–71).
Hemoptysis
Flexible bronchoscopy plays a central role in the evaluation
of hemoptysis. Bronchoscopy should be considered in all critically ill patients with hemoptysis, regardless of the degree of
hemoptysis, to localize the site of bleeding and attempt to determine the underlying etiology. Localization of the site of bleeding is important to guide temporizing therapy such as angiographic embolization and definitive therapy such as surgical
resection. Early rather than delayed bronchoscopy should be
performed to increase the likelihood of localizing the source of
bleeding. Bronchoscopy performed within 48 hours of bleeding onset successfully localized bleeding in 34% to 91% of
patients, depending on the case series, as compared to successful localization in 11% to 52% of patients if bronchoscopy
was delayed (72). Bronchoscopy performed within 12 to
24 hours may provide an even higher yield.
Massive hemoptysis is defined as expectoration of blood
exceeding 200 to 1,000 mL over a 24-hour period, with expectoration of greater than 600 mL in 24 hours as the most commonly used definition (73). In practice, the rapidity of bleeding
and ability to maintain a patent airway are critical factors, and
life-threatening hemoptysis can alternatively be defined as the
amount of bleeding that compromises ventilation. Only 3%
to 5% of patients with hemoptysis have massive hemoptysis,
with the mortality rates approaching 80% in various case series. Most patients who die from massive hemoptysis do so
from asphyxiation secondary to airway occlusion by clot and
blood, not exsanguination. The causes of massive hemoptysis
are listed in Table 37.3. Infections associated with bronchiectasis, tuberculosis, lung abscess, and necrotizing pneumonia are
commonly responsible for the massive bleeding. Other common causes include bronchogenic carcinoma, mycetoma, invasive fungal diseases, chest trauma, cystic fibrosis, pulmonary
infarction, coagulopathy, and alveolar hemorrhage due to Wegener granulomatosis and Goodpasture syndrome.
Airway patency must be ensured in patients with massive
hemoptysis. While preparing for intubation and bronchoscopy,
the patient may be positioned in the lateral decubitus position with the bleeding side down. Most patients with massive
hemoptysis will require intubation and mechanical ventilation.
While intubation generally preserves oxygenation and facilitates blood removal from the lower respiratory tract, the ET
may become obstructed by blood clots with inability to oxygenate and ventilate the patient. The largest possible ET should
be inserted to allow for use of bronchoscopes with a 2.8- to
511
TA B L E 3 7 . 3
POTENTIAL CAUSES OF MASSIVE HEMOPTYSIS
NEOPLASM
Bronchogenic cancer
Metastasis (parenchymal or endobronchial)
Carcinoid
Leukemia
INFECTIOUS
Lung abscess
Bronchiectasis
Tuberculosis
Necrotizing pneumonia
Fungal pneumonia
Septic pulmonary emboli
Mycetoma (aspergilloma)
PULMONARY
Bronchiectasis
Cystic fibrosis
Sarcoidosis (fibrocavitary)
Diffuse alveolar hemorrhage
Airway foreign body
CARDIAC/VASCULAR
Mitral stenosis
Pulmonary embolism/infarction
Arteriovenous malformation
Bronchoarterial fistula
Ruptured aortic aneurysm
Congestive heart failure
Pulmonary arteriovenous fistula
IATROGENIC/TRAUMATIC
Blunt or penetrating chest trauma
Tracheal/bronchial tear or rupture
Tracheoinnominate artery fistula
Bronchoscopy
Pulmonary artery rupture from Swan-Ganz catheter
Endotracheal tube suctioning trauma
HEMATOLOGIC
Coagulopathy
Disseminated intravascular coagulation
Thrombocytopenia
DRUGS/TOXINS
Anticoagulants
Antiplatelet agents
Thrombolytic agents
Crack cocaine
3.0-mm working channel for more effective suctioning and to
allow for better ventilation with the bronchoscope in the airway for prolonged periods of time. In severe cases, the mainstem bronchus of the nonbleeding lung can be selectively intubated under bronchoscopic guidance to preserve oxygenation
and ventilation from the normal lung.
Some authors have recommended the use of a double-lumen
ET to isolate the normal lung and permit selective intubation.
While double-lumen endotracheal tubes have been used successfully in the airway management of massive hemoptysis,
there are a number of potential pitfalls. First, placement of
13:42
P1: OSO/OVY
GRBT291-37-39
512
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Section III: Techniques, Procedures, and Treatments
a double-lumen ET is difficult for less experienced operators,
particularly with a large amount of blood in the larynx and
oropharynx. Second, the individual lumens of the ET are significantly smaller than a standard ET and are at significant
risk of being occluded by blood and blood clots. Lastly, positioning of the double-lumen ET and subsequent bronchoscopic
suctioning of the distal airways require a small pediatric bronchoscope with working channels of 1.2 to 1.4 mm. Adequate
suctioning of large amounts of blood and blood clots through
such bronchoscopes is extremely problematic. In one series of
62 patients with massive hemoptysis, death occurred in four of
seven patients managed with a double-lumen ET due to loss of
tube positioning and aspiration (74). I do not recommend the
use of double-lumen ETs for airway management in massive
hemoptysis. As an alternative to selective mainstem bronchial
intubation or intubation with a double-lumen ET, an ET that
incorporates a bronchial blocker, such as the Univent tube, may
be used.
Endobronchial tamponade with flexible bronchoscopy can
prevent aspiration of blood into the contralateral lung and
preserve gas exchange in patients with massive hemoptysis.
Endobronchial tamponade can be achieved with a 4-French
Fogarty balloon-tipped catheter. The catheter may be passed
directly through the working channel of the bronchoscope or
the catheter can be grasped by biopsy forceps placed though
the working channel of the bronchoscope prior to introduction into the airway. The bronchoscope and catheter—with
the latter held in place adjacent to the bronchoscope by the
biopsy forceps—are then inserted as a unit into the airway.
Care must be taken not to perforate the catheter or balloon by
the forceps. The catheter tip is inserted into the bleeding segmental orifice, and the balloon is inflated. If passed through the
suction channel, the proximal end of the catheter is clamped
with a hemostat, the hub cut off, and a straight pin inserted
into the catheter channel proximal to the hemostat to maintain
inflation of the balloon catheter. The clamp is removed, and the
bronchoscope is carefully withdrawn from the bronchus with
the Fogarty catheter remaining in position, to provide endobronchial hemostasis (75–77). The catheter can safely remain
in position until hemostasis is ensured by surgical resection of
the bleeding segment or bronchial artery embolization. Right
heart balloon catheters have been used in a similar fashion (78).
A modified technique for placement of a balloon catheter has
been described using a guidewire for insertion. A 0.035-inch
soft-tipped guidewire is inserted through the working channel
of the bronchoscope into the bleeding segment. The bronchoscope is withdrawn, leaving the guidewire in place. A balloon
catheter is then inserted over the guidewire and placed under
direct visualization after reintroduction of the bronchoscope
(79). The use of endobronchial blockers developed for unilateral lung ventilation during surgery may hold promise for management of massive hemoptysis in tamponading bleeding and
preventing contralateral aspiration of blood (80). The Arndt
endobronchial blocker is placed through a standard ET and
directly positioned with a pediatric bronchoscope. Suctioning
and injection of medications can be performed through the lumen of the catheter after placement. The Cohen tip-deflecting
endobronchial blocker is also placed through a standard ET
and directed into place with a self-contained steering mechanism under bronchoscopic visualization. At this time, there
is limited published experience with these blockers in the setting of massive hemoptysis, although the author has success-
fully used them for this application. The prolonged use of endobronchial blockers may cause mucosal ischemic injury and
postobstructive pneumonia.
Additional bronchoscopic techniques may be useful as
a temporizing measure in patients with massive hemoptysis. Bronchoscopically administered topical therapies such as
iced sterile saline lavage or topical 1:10,000 or 1:20,000
epinephrine solution may be helpful (81). Direct application of
a solution of thrombin or a fibrinogen–thrombin combination
solution has been used (82). The use of bronchoscopy-guided
topical hemostatic tamponade therapy using oxidized regenerated cellulose mesh has recently been described (83). Although
anecdotal, the author has had success with topical application
of 5 to 10 mL of a 1 mEq/mL (8.4%) sodium bicarbonate solution.
For patients who have hemoptysis due to endobronchial
lesions, particularly endobronchial tumors, hemostasis may be
achieved with the use of neodymium-yttrium-aluminum-garnet
(Nd:YAG) laser phototherapy, electrocautery, or cryotherapy
via the bronchoscope.
Diagnosis of Ventilator-associated
Pneumonia
For the diagnosis of ventilator-associated pneumonia (VAP),
the use of bronchoscopic modalities remains controversial and
is often institution dependent. Although commonly attributed
to pneumonia, the chest radiographic finding of alveolar infiltrates in the ICU patient can represent a broad differential diagnosis, requiring a wide range of therapies. The use of standard
clinical criteria for the diagnosis of pneumonia such as new
pulmonary infiltrates, hypoxemia, leukocytosis or leukopenia,
fever, and pathogenic bacteria in respiratory secretions has been
associated with a significant rate of misdiagnosis (84). Bacterial
colonization of the upper airways and endotracheal tube can
confound the reliability of the Gram stain and cultures from
tracheal aspirates obtained in the intubated patient. Concern
about the inaccuracy of clinical approaches to the diagnosis
of VAP and the possibility of antibiotic overprescribing with
a clinical strategy has led some investigators to postulate that
bronchoscopic methods such as PSB and BAL would improve
the diagnosis of VAP and treatment outcomes (15,16).
The methodology for performing PSB and BAL quantitative
cultures is outlined in a previous section of this chapter. PSB and
BAL should be performed in the most abnormal segment as determined by radiographic studies or where endobronchial abnormalities are most pronounced. Alternatively, samples may
be obtained from the right lower lobe, as this is the most commonly affected area on autopsy studies. A quantitative culture
result of more than 104 CFU/mL is considered diagnostic for
pneumonia with BAL, while more than 103 CFU/mL is considered diagnostic for pneumonia with PSB. An evidence-based review of 23 prospective studies of BAL in suspected VAP showed
a sensitivity of 42% to 93% with a mean of 73% ± 18%, and
a specificity of 45% to 100% with a mean of 82% ± 19%
(85). In 12 studies, the detection of intracellular organisms in
2% to 5% of recovered cells was used to diagnose pneumonia,
with a mean sensitivity of 69% ± 20% and a specificity of
75% ± 28% (85). An advantage of looking for intracellular
organisms is the ability to obtain information of high predictive value in a rapid time frame without waiting for the results
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 37: Flexible Bronchoscopy
of cultures to define the presence of pneumonia, although not
the specific identity of the etiologic pathogen (84).
In a review of studies evaluating PSB, the sensitivity ranged
from 33% to 100% with a median sensitivity of 67%, while the
specificity ranged from 50% to 100% with a median specificity
of 95% (86). It is unclear if BAL is superior to PSB or vice versa
in the diagnosis of VAP. In a meta-analysis of 18 studies on PSB
(795 patients) and 11 studies on BAL (435 patients), there was
no difference in the accuracy of the two tests (87). BAL does offer an advantage in that additional microbiologic tests beyond
routine bacterial cultures, as well as cytologic analysis, can be
performed on the sample if an infectious process is suspected
other than typical bacterial pneumonia. PSB may potentially
have a greater complication rate compared with BAL, but this
has not been formally compared.
Despite studies of BAL and PSB showing a greater accuracy
than tracheal aspirates, the routine use of bronchoscopy for establishing the diagnosis of VAP remains controversial (84,88).
This controversy is in part due to critiques in study methodologies and in part due to some studies showing a benefit in
patient outcomes while others have not. One prospective, nonrandomized study noted a difference in mortality between patients managed with an invasive bacteriologic strategy (19%)
versus those managed with a clinical strategy (35%) (89). One
large, prospective randomized trial did show an advantage to
the quantitative bronchoscopic approach when compared with
a clinical approach in a multicenter study of 413 patients suspected of having VAP. Compared with patients managed clinically, those receiving invasive management had a lower mortality rate on day 14 (16% vs. 25%; p <0.02), but not on day 28,
and lower mean sepsis-related organ failure assessment scores
on days 3 and 7. At 28 days, the quantitative culture group had
significantly more antibiotic-free days (11 ± 9 vs. 7 ± 7 days;
p <0.001), but only a multivariate analysis showed a significant difference in mortality (hazard ratio 1.54; 95% confidence
interval [CI] 1.10–2.16) (90). No differences in mortality were
observed in three randomized single-center studies when invasive techniques (PSB and/or BAL) were compared with either
quantitative or semiquantitative endotracheal aspirate culture
techniques (91–93). However, these studies included few patients (51, 76, and 88, respectively), and antibiotics were continued in all patients, even those with negative cultures, thereby
negating one of the potential advantages of the bacteriologic
strategy. A meta-analysis of these randomized controlled trials
noted that an invasive approach did not alter mortality (odds
ratio 0.89, 95% CI 0.56–1.41), although invasive testing affected antibiotic utilization (odds ratio for change in antibiotic
management after invasive sampling 2.85, 95% CI 1.45–5.59)
(94).
Performing microbiologic cultures of pulmonary secretions
for diagnostic purposes after initiating new antibiotic therapy
can lead to false-negative results and is likely of little value regardless of the manner in which the secretions are sampled.
Studies have demonstrated that culture positivity at 24 and
48 hours after the onset of antimicrobial treatment is markedly
diminished (95,96). The decrease in positive cultures after initiation of antibiotic therapy appears to affect PSB more so than
BAL. If patients have been treated with antibiotics but did not
have a change in antibiotic class prior to bronchoscopy for a
suspected new episode of VAP, the yield of BAL and PSB appears to be similar to that in patients who have not received
antibiotics (97). If an invasive bronchoscopy strategy is used
513
to establish a diagnosis of VAP, BAL and/or PSB should be performed prior to administration of antibiotics or administration
of new antibiotics if the patient was previously on antimicrobial therapy.
Diagnosis of Other Respiratory Infections
Flexible bronchoscopy is an essential modality in evaluating
the critically ill, immunocompromised patient with pulmonary
infiltrates. These patients are at risk for fungal, viral, protozoal, mycobacterial, and atypical bacterial pulmonary infections. Critically ill patients who have no underlying immunocompromised condition, such as acquired immunodeficiency
syndrome (AIDS), leukemia, neutropenia, hematopoietic stem
cell/bone marrow transplant, or solid organ transplant, may
also develop respiratory infections other than bacterial pneumonias, such as fungal and viral infections. In addition to these
patients, those who present with acute respiratory failure and
apparent community-acquired pneumonia, but fail to respond
appropriately to antibiotic therapy, may benefit from bronchoscopy to evaluate for more unusual infections and noninfectious causes of acute respiratory failure with infiltrates. Bronchoscopy is not recommended for routine community-acquired
pneumonia.
BAL, as compared to PSB, provides the opportunity for
more extended microbiologic studies and for cytology. It is
unclear if the addition of transbronchial biopsy to BAL improves diagnostic accuracy in immunocompromised patients
with pulmonary infiltrates. Transbronchial biopsy may increase
the yield for the diagnosis of infectious etiologies, but more
commonly establishes an alternate noninfectious cause of infiltrates in these patients (98). The benefits versus risks, including
life-threatening pneumothorax and bleeding, need to be individualized in the critically ill immunocompromised patient.
In immunocompromised and critically ill patients who are
suspected to have an atypical infection, BAL fluid should be
sent for cytopathology to evaluate for viral cytologic changes,
as well as Gomori methenamine silver staining (GMS) to evaluate for fungal organisms and Pneumocystis jiroveci. Alternatively, Papanicolaou, Giemsa, toluidine blue O, or direct
fluorescent antibody staining may be used for detection of
Pneumocystis.
For Pneumocystis in AIDS patients, BAL has a sensitivity rate in diagnosing Pneumocystis pneumonia of approximately 85% to 90%, and for transbronchial biopsy, the diagnostic yield approaches 87% to 95%. When BAL and transbronchial biopsy are performed in AIDS patients with Pneumocystis pneumonia, the diagnostic yield is 95% to 98% (99–
102). Given the high yield of BAL and the potential risk of
transbronchial biopsy in critically ill patients, transbronchial
biopsy is not recommended in AIDS patients for diagnosing
Pneumocystis. In immunocompromised patients without HIV,
the yield of BAL is lower, and transbronchial biopsies to establish a diagnosis may be required. Although not used routinely in clinical practice, polymerase chain reaction (PCR) for
Pneumocystis on BAL specimens may increase diagnostic rates
(103).
For the diagnosis of pulmonary fungal infections in immunocompromised patients, BAL fluid should be sent for fungal stains and cultures in addition to cytology stains. It is unclear if the addition of transbronchial biopsy to BAL increases
13:42
P1: OSO/OVY
GRBT291-37-39
514
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Section III: Techniques, Procedures, and Treatments
the diagnostic yield for fungal infections. If transbronchial
biopsies are obtained, the samples should be sent for culture
in addition to histology. Some fungi, such as Mucor and Rhizopus, are difficult to grow on culture, and diagnosis relies on
BAL cytology or biopsy specimens. Aspergillus is the most commonly encountered pulmonary fungal infection. BAL cytology
and culture are diagnostic in approximately 50% to 60% of
cases of invasive pulmonary aspergillosis. The diagnostic yield
from BAL appears to be increased with the use of galactomannan antigen and PCR testing, although galactomannan antigen
testing is more readily available (104–106). Antigen testing for
histoplasmosis and blastomycosis on BAL samples is now available (107).
To evaluate for viral infections, respiratory viral cultures
and a respiratory syncytial virus antigen assay should be obtained. BAL cytology may demonstrate characteristic intracytoplasmic inclusions, but sensitivity is lacking. Immunofluorescence and PCR for cytomegalovirus (CMV) may be performed
on BAL specimens (108).
If there is suspicion for tuberculosis or nontuberculous mycobacteria, BAL samples should be sent for acid-fast bacillus stains and mycobacterial culture. BAL samples of sputum
smear–negative patients with tuberculosis are smear positive
in 12% to 42% of patients and culture positive in 66% to
95% (109). In one third to one half of initially sputum smear–
negative patients, bronchoscopy specimens yield the only positive source of mycobacterial tuberculosis (110–112). Although
not routinely used, PCR for tuberculosis may be obtained on
BAL to provide a more rapid diagnosis (113,114).
For atypical bacterial infections, additional stains and cultures may be required. Legionella requires specific culture media. A direct fluorescence antibody stain is also available for
Legionella. Some laboratories utilize specific media if Nocardia
is suspected. Nocardia can often be identified with a combination of Gram stain and modified Ziehl-Neelsen stains, and are
observed as delicately branched, weakly Gram-positive, variably acid-fast bacilli. Methenamine-silver stains may demonstrate the organisms in tissue specimens.
Diagnosis of Noninfectious
Pulmonary Infiltrates
Although most helpful in excluding infectious etiologies for
pulmonary infiltrates in ICU patients, bronchoscopy with BAL
and/or transbronchial biopsy may be able to establish the etiology of noninfectious infiltrates in some patients (115,116).
In some cases, surgical lung biopsy will be required to make
a definitive diagnosis. The appearance of the BAL and a cell
count and differential on the BAL fluid can be helpful in suggesting a diagnosis. A bloody BAL that does not decrease, or
increases in the degree of blood return with serial fluid aliquots,
is diagnostic of alveolar hemorrhage. This can be confirmed
with iron staining that demonstrates hemosiderin-laden alveolar macrophages. BAL fluid that has a milky or whitish, cloudy
appearance with flocculent debris that settles to the bottom of
the container is suggestive of pulmonary alveolar proteinosis.
Additional support for this diagnosis is provided with a positive
periodic acid–Schiff (PAS) stain. The diagnosis of pulmonary
alveolar proteinosis can be confirmed with transbronchial or
surgical lung biopsy. A BAL with a differential count greater
than 25% eosinophils is virtually diagnostic of eosinophilic
lung disease. In the patient with acute respiratory failure, this
finding will most commonly be due to acute eosinophilic pneumonia, although parasitic lung infections such as strongyloidiasis rarely have a similar presentation. A finding of greater
than 25% lymphocytes on BAL differential is suggestive of sarcoidosis, hypersensitivity pneumonitis, drug reaction, or viral
infection.
Transbronchial biopsy can confirm the above diagnoses in
most cases. In addition, transbronchial biopsy may be able
to establish other noninfectious diagnoses of pulmonary infiltrates in the ICU including idiopathic interstitial pneumonia
and graft versus host disease in stem cell or bone marrow transplant patients, leukemic infiltrates, drug-induced pneumonitis, bronchiolitis obliterans organizing pneumonia/cryptogenic
organizing pneumonia (BOOP/COP), bronchoalveolar carcinoma, lymphangitic carcinomatosis, and acute rejection after
lung transplantation.
Traumatic Airway Injury
The classic signs of tracheobronchial disruption include shortness of breath, massive subcutaneous emphysema, persistent
pneumothorax despite chest tube insertion, and a large air
leak after tube thoracoscopy. On occasion, however, only subtle signs exist, even in the presence of significant injury. Flexible
bronchoscopy should be performed early in any patient with
chest trauma in whom airway injury may have occurred (117).
Signs and symptoms of tracheobronchial injury are listed in
Table 37.4. Tracheobronchial disruption rarely occurs as an
isolated injury (118). A history of a rapid deceleration injury,
such as a motor vehicle accident with the patient’s chest striking
the steering wheel or dashboard, is typical. The pathogenesis
of tracheobronchial rupture in blunt chest trauma is caused by
shearing, wrenching, or compressive forces, acting alone or in
concert. Rapid deceleration results in shearing forces, acting
predominantly at the distal trachea near the carina where the
relatively fixed trachea joins the more mobile distal airways
(119,120). If the trachea and mainstem bronchi are crushed
TA B L E 3 7 . 4
SIGNS AND SYMPTOMS OF TRACHEOBRONCHIAL
INJURY
Fracture of upper ribs
Fracture of clavicle or sternum
Chest wall contusions
Chest radiograph showing:
Subcutaneous emphysema
Pneumothorax
“Sagging” lung
Pneumomediastinum
Atelectasis
Pulmonary contusion
Hemoptysis
Bronchopleural fistula
Dyspnea
Cough
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 37: Flexible Bronchoscopy
between the chest wall and vertebral column and the glottis
closed, airway pressure suddenly increases, and resultant rupture of the airway may occur (118).
In patients with tracheal or bronchial disruption, early bronchoscopy can reliably detect the site of airway injury (121–
126). Prompt diagnosis and surgical correction or tracheobronchial disruption produce a better outcome, and delay in
diagnosis is usually detrimental to the patient (118). Patients
with partial tracheal or bronchial disruption may be relatively
asymptomatic and present with a paucity of physical findings.
Delays in diagnosis unfortunately are common and have been
associated with decreased frequency of successful repair. Failure to diagnose disruption may result in a delayed stricture
formation at the site of injury, resulting in dyspnea, distal atelectasis, and chronic recurrent infections.
If an airway injury is suspected, flexible bronchoscopy
should be performed through an endotracheal tube prepositioned on the bronchoscope to assess tracheal or bronchial disruption. If a persistent bronchopleural fistula exists because
of proximal airway trauma, the cuff of the endotracheal tube
sometimes can be positioned just distal to the rupture site and
inflated, and adequate ventilation can be established before
surgical repair. Cervical tracheal rupture is less common than
rupture of the intrathoracic trachea. Cervical tracheal rupture,
however, may be more difficult to diagnose once the patient
is intubated because of the proximal location of the tear, and
may itself be an impediment to intubation (127).
Bronchopleural Fistula
In patients who are not candidates for surgical management
of a bronchopleural fistula (BPF), flexible bronchoscopic techniques may offer alternative methods for closure of the BPF. Detection of a proximal BPF due to stump breakdown after lobectomy or pneumonectomy or a BPF due to bronchial dehiscence
is usually relatively straightforward, as these abnormalities can
be directly visualized. In the setting of a BPF due to a rent or
tear on the lung periphery, locating the bronchial segment that
provides ventilation to that area of the lung can be more difficult. Several techniques can be employed by bronchoscopy to
localize the proximal endobronchial site of the fistulous tract.
Occasionally, air bubbles can be seen emanating from the segmental bronchus. Washing the suspected segment with normal
saline and coughing may accentuate the bubbling. A balloontipped catheter, such as a Fogarty catheter or a single-lumen
right heart catheter, can be passed through the working channel of the bronchoscope and selectively positioned in suspect
segmental bronchial orifices that lead to the peripheral fistula.
After positioning the catheter in the suspect segment, the balloon is inflated to occlude the orifice, and the bronchoscopist
then looks for cessation of bubbling in the water seal chamber
of the pleural drainage unit (121). The lack of bubbling after
balloon inflation confirms that the bronchial segment has been
occluded and allows the BPF to heal.
Successful endobronchial occlusion of BPFs has been reported with cyanoacrylate-based tissue adhesives (Histoacryl,
Bucrylate), fibrin sealants (Tisseal, Hemaseal, thrombin plus
fibrinogen or cryoprecipitate), absorbable gelatin sponge
(Gelfoam), vascular occlusion coils, doxycycline and blood,
Nd:YAG laser, silver nitrate, and lead shot (128–130). The
515
agent initially seals the leak by acting as a plug and subsequently induces an inflammatory process with fibrosis and mucosal proliferation permanently sealing the area. Of these techniques, the uses of cyanoacrylate tissue adhesives and fibrin
sealants have been most widely reported.
Airway stents may be used to cover and seal the fistula in
selected patients, depending on the location of the fistula. BPFs
due to breakdown of a stump after lobectomy or pneumonectomy or bronchial dehiscence after lung transplantation or
bronchoplastic procedures are the most amenable to successful
closure with airway stenting. More recently, the successful closure of BPFs using bronchoscopic placement of endobronchial
valves designed for emphysema has been described (131–133).
Foreign Body Removal
Risk factors for foreign body aspiration include age younger
than 3 years, altered consciousness, trauma, and disordered
swallowing mechanisms. Although occurring less frequently
in adults than in children, tracheobronchial foreign bodies are
problematic in adults (134,135). Patients may present with dyspnea, coughing, wheezing, or stridor. Foreign body aspiration
may be relatively occult, with no obvious history for aspiration. Radiographically, there may be evidence of atelectasis,
bronchiectasis, or recurrent pneumonitis.
Bronchoscopy to remove an aspirated foreign body should
be performed by an experienced bronchoscopist. For pediatric
patients, the foreign body may be successfully extracted via
flexible bronchoscopy. For most situations, however, the rigid
bronchoscope remains the instrument of choice in young children and infants (135). In adults, flexible bronchoscopy has
clearly been shown to be an effective diagnostic and therapeutic tool in cases of suspected foreign body aspiration
(134,136,137). Several extraction devices are available for
use through the flexible bronchoscope (138). Biopsy forceps,
graspers, and foreign body baskets are most commonly employed. Large foreign bodies may be extracted by applying
continuous suction and withdrawing the bronchoscope with
the foreign body adhered to the tip of the scope. Compared
with rigid bronchoscopy, flexible bronchoscopy offers an enhanced visualization of the more peripheral airways, can be
performed at the bedside, and averts the need for general anesthesia and operating room facilities. Occasionally, combined
flexible and rigid bronchoscopy are required to enhance retrieval of the foreign body.
Inhalation Injury
Exposure to fire or smoke in an enclosed environment puts
the patient at risk for thermal airway injury. Patients with
singed nasal hairs, facial burns around the nose or mouth,
oral/nasopharyngeal burns, carbonaceous sputum, or hoarseness should be suspected of having an upper airway injury.
Stridor, wheezing, or other manifestations of upper airway
symptomatology may imply impending ventilatory failure. In
patients with suspected inhalation injury, flexible bronchoscopy should be performed early by an experienced bronchoscopist to identify evidence of thermal airway injury. Flexible
13:42
P1: OSO/OVY
GRBT291-37-39
516
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Section III: Techniques, Procedures, and Treatments
bronchoscopy allows direct examination of the supraglottic
and infraglottic areas. The need for intubation should be anticipated and an endotracheal tube placed over the bronchoscope
before examining the airways. If intubation is deemed necessary, the bronchoscope can function as a guide for endotracheal
tube placement. Serial examinations may be necessary in patients with apparent minimal thermal airway injury on initial
evaluation (139). Signs indicating impending airway obstruction include inflammation, edema, ulceration, or hemorrhage
of the upper airway mucosa (140–143).
By using flexible bronchoscopy, inhalation injury can be
classified into acute, subacute, and chronic phases. In the acute
stage, upper airway obstruction from mucosal edema and respiratory failure from pulmonary edema and hemorrhage are
the main characteristics. Soot deposition in the airways and
carbon monoxide poisoning also may be found. The subacute
stage, which lasts from hours to several days, is manifested
by necrosis of the tracheobronchial mucosa, hemorrhagic tracheal bronchitis, persistent pulmonary edema with or without
hemorrhage, and secondary infection. Scarring and stenosis of
the tracheobronchial tree with formation of granulation tissue, as well as bronchiectasis due to bronchiolitis obliterans,
are the hallmarks of the chronic stage. Flexible bronchoscopy
may offer significant utility in identifying these three stages of
significant injury (144).
In the intubated patient, repeat airway examination by
bronchoscopy may be necessary before extubation to ensure
airway patency and resolution of the supraglottic or laryngeal
edema. The endotracheal tube can be withdrawn over the bronchoscope while inspecting the airway mucosa and replaced if
the airway is compromised (145).
Acute Upper Airway Obstruction
Causes of upper airway obstruction include epiglottitis, bilateral vocal cord paralysis, laryngeal edema, and foreign
body. In the pediatric patient, subglottic stenosis secondary to
croup should also be considered. Flexible bronchoscopy can
be helpful to make a diagnosis in these circumstances. Flexible
bronchoscopy may be particularly helpful for diagnosis and
therapeutic intubation in upper airway obstruction after burn
and smoke inhalation injury and trauma to the face and neck.
The flexible bronchoscope affords immediate direct visualization of the upper airway and, if performed with an ET placed
over the bronchoscope, affords visualization and guidance for
endotracheal intubation. If epiglottitis is suspected, it may be
prudent to perform bronchoscopy in the surgical suite, with
the surgical team available for emergency tracheostomy in case
of failure. When performing bronchoscopic intubation in suspected upper airway obstruction, the nasotracheal approach
may be preferable because the turbinates offer stabilization and
a more controlled approach to the area of acute airway obstruction (146). Flexible bronchoscopic intubation in upper airway
obstruction may be performed in the sitting position with decreased posterior displacement of the epiglottis over the compromised upper airway as compared with laryngoscopic examination in the supine position. If foreign body obstruction is
known or suspected as the cause of the upper airway obstruction, rigid bronchoscopy may be the bronchoscopy method of
choice.
Central Airway Obstruction
Patients may develop impending or acute respiratory failure
due to central airway obstruction from primary lung cancer
or metastatic malignancies. Treatment for malignant airway
obstruction from endoluminal tumor has typically consisted of
Nd:YAG laser photoresection and metal or silicone stent placement, although endobronchial electrocautery or argon plasma
coagulation has more recently been used in lieu of the Nd:YAG
laser (147–149). Other modalities such as cryotherapy, photodynamic therapy, and brachytherapy have been used to treat
malignant airway obstruction; however, there is a delay in airway patency after treatment with these therapies and, as such,
they may be less satisfactory in treating the patient with acute
respiratory failure who would benefit from immediate airway
patency. Airway obstruction from extrinsic tumor compression is typically treated with placement of metal or silicone
stents.
Patients may also develop respiratory failure from benign
causes, most commonly previous intubation or tracheostomy
tube placement, causing a cicatricial stenosis with or without granulation tissue. Patients who have an indwelling tracheostomy tube may also develop a fibrous stenosis or granulation tissue just beyond the tip of the tracheostomy tube, thereby
causing airway obstruction. The granulation tissue may be resected with laser electrocautery therapy. The stenosis may be dilated with a rigid bronchoscope or balloon dilatation catheters.
In selected patients, silicone stents may be placed after dilatation. In general, metal stents should not be used for tracheal
stenosis due to a higher complication rate and difficulty in removing the stent should problems develop.
Status Asthmaticus
The usefulness of bronchoscopy in patients with status asthmaticus is the subject of controversy (32,150). Success has been
reported with bronchial lavage in patients with obstructive airway disease who could not be weaned from ventilatory support
(151,152). Bronchial lavage may benefit selected mechanically
ventilated patients with thick, tenacious secretions who are unresponsive to aggressive bronchodilator therapy (65,153). Mucous plugs impacted in airways may be extracted using the flexible bronchoscope for lavage, thus improving ventilation and
oxygenation (65,154). Critically ill, mechanically ventilated
asthmatic patients are, however, poor candidates for bronchial
lavage; the procedure is likely to produce a significant increase
in auto-PEEP and worsening of hypoxemia. The extolled benefits of lung lavage are limited to case reports (155–157). Normal saline lavage solution has been traditionally used, but diluted acetylcysteine may enhance mucous clearance from the
airways by a mucolytic effect (65,155). Acetylcysteine should
be used with caution because it may provoke bronchospasm in
patients with reactive airway disease. Asthmatics should receive
aggressive bronchodilator therapy before bronchoscopy.
References
1. Lindholm CE, Oilman B, Snyder JV, et al. Cardiorespiratory effects of flexible fiberoptic bronchoscopy in critically ill patients. Chest. 1978;74:363.
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 37: Flexible Bronchoscopy
2. Peerless J, Snow N, Likavec M, et al. The effect of fiberoptic bronchoscopy
on intracranial pressure in patients with brain injury. Chest. 1995;108:
962.
3. Cowl CT, Prakash UB, Kruger BR. The role of anticholinergics in bronchoscopy: a randomized clinical trial. Chest. 2000;118:188.
4. Clarkson K, Power CK, O’Connell F, et al. A comparative evaluation of
propofol and midazolam as sedative agents in fiberoptic bronchoscopy.
Chest. 1993;104:1029.
5. Kerwin AJ, Croce MA, Timmons SD, et al. Effects of fiberoptic bronchoscopy on intracranial pressure in patients with brain injury: a prospective clinical study. J Trauma. 2000;48:878.
6. Reichert WW, Hall WJ, Hyde RW. A simple disposable device for performing fiberoptic bronchoscopy on patients requiring continuous artificial
ventilation. Am Rev Respir Dis. 1974;109:394.
7. Meduri GU, Chastre J. The standardization of bronchoscopic techniques
for ventilator-associated pneumonia. Chest. 1992;102(Suppl 1):557S.
8. American Thoracic Society. Clinical role of bronchoalveolar lavage in adults
with pulmonary disease. Am Rev Respir Dis. 1990;142:481.
9. Klech H, Pohl W. Technical recommendations and guidelines for bronchoalveolar lavage (BAL). Eur Respir J. 1989;2:561.
10. Rennard SI, Aalbers R, Bleecker E, et al. Bronchoalveolar lavage: performance, sampling procedure, processing and assessment. Eur Respir J.
1998;26(Suppl):13S.
11. Wimberley N, Faling LJ, Bartlett JG. A fiberoptic bronchoscopy technique
to obtain uncontaminated lower airway secretions for bacterial culture. Am
Rev Respir Dis. 1979;119:337.
12. Wimberley NW, Bass JB Jr, Boyd BW, et al. Use of a bronchoscopic protected catheter brush for the diagnosis of pulmonary infections. Chest.
1982;81:556.
13. de Lassence A, Joly-Guillou ML, Martin-Lefevre L, et al. Accuracy of delayed cultures of plugged telescoping catheter samples for diagnosing bacterial pneumonia. Crit Care Med. 2001;29:1311.
14. Baselski VS, Wunderink RG. Bronchoscopic diagnosis of pneumonia. Clin
Microbiol Rev. 1994;7:533.
15. Chastre J, Combes A, Luyt CE. The invasive (quantitative) diagnosis of
ventilator-associated pneumonia. Respir Care. 2005;50:797.
16. Fagon JY. Diagnosis and treatment of ventilator-associated pneumonia:
fiberoptic bronchoscopy with bronchoalveolar lavage is essential. Semin
Respir Crit Care Med. 2006;27:35.
17. O’Brien JD, Ettinger NA, Shevlin D, et al. Safety and yield of transbronchial
biopsy in mechanically ventilated patients. Crit Care Med. 1997;25:440.
18. British Thoracic Society Bronchoscopy Guidelines Committee, a Subcommittee of Standards of Care Committee of British Thoracic Society. British
Thoracic Society guidelines on diagnostic flexible bronchoscopy. Thorax.
2001;56(Suppl 1):i1.
19. Guidelines for fiberoptic bronchoscopy in adults. American Thoracic Society. Am Rev Respir Dis. 1987;136:1066.
20. Hanson RR, Zavala DC, Rhodes ML, et al. Transbronchial biopsy via
flexible fiberoptic bronchoscope; results in 164 patients. Am Rev Respir
Dis. 1976;114:67.
21. Bajwa MK, Henein S, Kamholz SL. Fiberoptic bronchoscopy in the presence
of space-occupying intracranial lesions. Chest. 1993;104:101.
22. Credle WF, Smiddy JF, Elliott RC. Complications of fiberoptic bronchoscopy. Am Rev Respir Dis. 1974;109:67.
23. Udaya BS, Prakash MD, Stubbs SE. Bronchoscopy: indications and technique. Semin Respir Med. 1981;3:17.
24. Pereira W, Kovnat DM, Snider GL. A prospective cooperative study of
complications following flexible fiberoptic bronchoscopy. Chest. 1978;73:
813.
25. Steinberg KP, Mitchell DR, Maunder RJ, et al. Safety of bronchoalveolar
lavage in patients with adult respiratory distress syndrome. Am Rev Respir
Dis. 1993;148:556.
26. Albertini RE, Harrell JH, Kurihara N. Arterial hypoxemia induced by
fiberoptic bronchoscopy. JAMA. 1974;230:1666.
27. Albertini R, Harrell JH, Moser KM. Hypoxemia during fiberoptic bronchoscopy. Chest. 1974;65:117.
28. Ghows MB, Rosen MJ, Chuang MT, et al. Transcutaneous oxygen monitoring during fiberoptic bronchoscopy. Chest. 1986;89:543.
29. Turner JS, Willcox PA, Hayhurst MD, et al. Fiberoptic bronchoscopy in the
intensive care unit—a prospective study of 147 procedures in 107 patients.
Crit Care Med. 1994;22:259.
30. Trouillet JL, Guiguet M, Gibert C, et al. Fiberoptic bronchoscopy in ventilated patients. Evaluation of cardiopulmonary risk under midazolam sedation. Chest. 1990;97:927.
31. Weinstein HJ, Bone RC, Ruth WE. Pulmonary lavage in patients treated
with mechanical ventilation. Chest. 1977;72:583.
32. Dubrawsky C, Awe RJ, Jenkins DE. The effect of bronchofiberscopic examination on oxygenation status. Chest. 1976;67:137.
33. Wu FL, Razzaghi A, Souney PF. Seizure after lidocaine for bronchoscopy:
case report and review of the use of lidocaine in airway anesthesia. Pharmacotherapy. 1993;13:72.
34. Khan NA, Kruse JA. Methemoglobinemia induced by topical anesthesia: a
case report and review. Am J Med Sci. 1999;318:415.
35. Barrett CR. Flexible fiberoptic bronchoscopy in the critically ill patient.
Chest. 1978;73:746.
517
36. Shrader DL. The effect of fiberoptic bronchoscopy on cardiac rhythm.
Chest. 1978;73:821.
37. Katz AS, Michelson EL, Stawick J, et al. Cardiac arrhythmias: frequency
during fiberoptic bronchoscopy and correlation with hypoxemia. Arch Intern Med. 1981;141:603.
38. Belen J, Neuhaus A, Markowitz D, at al. Modification of the effect
of fiberoptic bronchoscopy on pulmonary mechanics. Chest. 1981;79:
516.
39. Zavala DC. Pulmonary hemorrhage in fiberoptic transbronchial biopsy.
Chest. 1976;70:584.
40. Fulkerson WJ. Current concepts: fiberoptic bronchoscopy. N Engl J Med.
1984;311:511.
41. Landa JF. Indications for bronchoscopy. Chest. 1978;73:687.
42. Johnston H, Reisz G. Changing spectrum of hemoptysis: underlying causes
in 148 patients undergoing diagnostic flexible fiberoptic bronchoscopy.
Arch Intern Med. 1989;149:1666.
43. Kobrinsky NL, Israels ED, Gerrard JM, et al. Shortening of bleeding time by
1-deamino-8-D-arginine vasopressin in various bleeding disorders. Lancet.
1984;1:1145.
44. Pincus PS, Kallenbach JM, Hurwitz MD, et al. Transbronchial biopsy during mechanical ventilation. Crit Care Med. 1987;15:1136.
45. O’Brien JD, Ettinger NA, Shevlin D, et al. Safety and yield of transbronchial
biopsy in mechanically ventilated patients. Crit Care Med. 1997;25:440.
46. Bulpa PA, Dive AM, Mertens L, et al. Combined bronchoalveolar lavage
and transbronchial lung biopsy: safety and yield in ventilated patients. Eur
Respir J. 2003;21:489.
47. Pereira W, Kovnat DM, Khan MA, et al. Fever and pneumonia after flexible
fiberoptic bronchoscopy. Am Rev Respir Dis. 1975;112:59.
48. Kane RC, Cohen MH, Fossieck BE, et al. Absence of bacteremia after
fiberoptic bronchoscopy. Am Rev Respir Dis. 1975;111:102.
49. Dajani AS, Bisno AL, Chung KJ, et al. Antimicrobial prophylaxis for the
prevention of bacterial endocarditis in patients with underlying cardiac
conditions. JAMA. 1990;264:2919.
50. Ovassapian A. The flexible bronchoscope: a tool for anesthesiologists. Clin
Chest Med. 2001;22:281.
51. Weiss YG, Deutschman CS. The role of fiberoptic bronchoscopy in airway
management of the critically ill patient. Crit Care Clin. 2000;16:445.
52. Ovassapian A. Flexible bronchoscopic intubation of awake patients. J Bronchol. 1994;1:240.
53. Greenland KB, Irwin MG. The Williams Airway Intubator, the Ovassapian
Airway and the Berman Airway as upper airway conduits for fiberoptic
bronchoscopy in patients with difficult airways. Curr Opin Anaesthesiol.
2004;17:505.
54. Ovassapian A, Randel GI. The role of the fiberscope in the critically ill
patient. Crit Care Clin. 1995;11:29.
55. Caponas G. Intubating laryngeal mask airway. Anaesth Intensive Care.
2002;30:551.
56. O’Brien D, Registrar S, Curran J, et al. Fiberoptic assessment of tracheal
tube position: a comparison of tracheal tube position as estimated by
fiberoptic bronchoscopy and by chest x-ray. Anaesthesia. 1985;40:73.
57. deBloisblanc BP. Percutaneous dilational tracheostomy techniques. Clin
Chest Med. 2003;24:399.
58. Shinnick JP, Freedman AP. Bronchofiberscopic placement of a doublelumen endotracheal tube. Crit Care Med. 1981;10:544.
59. Ovassapian A. Fiberoptic bronchoscope and double-lumen tracheal tubes.
Anesthesia. 1983;38:1104.
60. Klein U, Karzai W, Bloos F, et al. Role of fiberoptic bronchoscopy in
conjunction with the use of double-lumen tubes for thoracic anesthesia:
a prospective study. Anesthesiology. 1998;88:346.
61. Kreider ME, Lipson DA. Bronchoscopy for atelectasis in the ICU: a case
report and review of the literature. Chest. 2003;124:344.
62. Marini JJ, Pierson DJ, Hudson LD. Acute lobar atelectasis: a prospective
comparison of fiberoptic bronchoscopy and respiratory therapy. Am Rev
Respir Dis. 1979;119:971.
63. Mehrishi S. Is bronchoscopy indicated in the management of atelectasis?
Pro bronchoscopy. J Bronchol. 2002;9:46.
64. Raoof S. Is bronchoscopy indicated in the management of atelectasis? Con
bronchoscopy. J Bronchol. 2002;9:52.
65. Millman M, Goodman AH, Goldstein IM, et al. Status asthmaticus: use of
acetylcysteine during bronchoscopy and lavage to remove mucous plugs.
Ann Allergy. 1983;50:85.
66. Perruchoud A, Ehrsam R, Heitz M, et al. Atelectasis of the lung: bronchoscopic lavage with acetylcysteine: experience in 51 patients. Eur J Respir
Dis Suppl. 1980;111:163.
67. Slattery DM, Waltz DA, Denham B, et al. Bronchoscopically administered
recombinant human DNase for lobar atelectasis in cystic fibrosis. Pediatr
Pulmonol. 2001;31:38.
68. Haenel JB, Moore FA, Moore EE, et al. Efficacy of selective intrabronchial
air insufflation in acute lobar collapse. Am J Surg. 1992;164:501.
69. Harada K, Mutsuda T, Saoyama N, et al. Re-expansion of refractory atelectasis using a bronchofiberscope with a balloon cuff. Chest. 1983;84:
725.
70. Millen JE, Vandree J, Glauser FL. Fiberoptic bronchoscopic balloon occlusion and re-expansion of refractory unilateral atelectasis. Crit Care Med.
1978;6:50.
13:42
P1: OSO/OVY
GRBT291-37-39
518
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Section III: Techniques, Procedures, and Treatments
71. Tsao TC, Tsai YH, Lan RS, et al. Treatment for collapsed lung in critically
ill patients. Chest. 1990;97:435.
72. Dweik RA, Stoller JK. Role of bronchoscopy in massive hemoptysis. Clin
Chest Med. 1999;20:89.
73. Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med. 2000;28:1642.
74. Gourin A, Garzon AA. Operative treatment of massive hemoptysis. Ann
Thorac Surg. 1974;18:52.
75. Gottlieb LS, Hillberg R. Endobronchial tamponade therapy for intractable
hemoptysis. Chest. 1975;67:482.
76. Saw EC, Gottlieb LS, Yokoyama T, et al. Flexible fiberoptic bronchoscopy
and endobronchial tamponade in the management of massive hemoptysis.
Chest. 1976;70:589.
77. Lee SM, Kim HY, Ahn Y. Parallel technique of endobronchial balloon
catheter tamponade for transient alleviation of massive hemoptysis. J Korean Med Sci. 2002;17:823.
78. Jolliet P, Soccal P, Chevrolet JC. Control of massive hemoptysis by endobronchial tamponade with a pulmonary artery balloon catheter. Crit Care
Med. 1992;20:1730.
79. Kato R, Sawafuji M, Kawamura M, et al. Massive hemoptysis successfully
treated by modified bronchoscopic balloon tamponade technique. Chest.
1996;109:842.
80. Kabon B, Waltl B, Leitgeb J, et al. First experience with fiberoptically directed wire-guided endobronchial blockade in severe pulmonary bleeding
in an emergency setting. Chest. 2001;120:1399.
81. Conlan AA, Hurwitz SS. Management of massive haemoptysis with the
rigid bronchoscope and cold saline lavage. Thorax. 1980;35:901.
82. Tsukamoto T, Sasaki H, Nakamura H. Treatment of hemoptysis patients
by thrombin and fibrinogen-thrombin infusion therapy using a fiberoptic
bronchoscope. Chest. 1989;96:473.
83. Valipour A, Kreuzer A, Koller H, et al. Bronchoscopy-guided topical hemostatic tamponade therapy for the management of life-threatening hemoptysis. Chest. 2005;127:2113.
84. American Thoracic Society; Infectious Diseases Society of America. Guidelines for the management of adults with hospital-acquired, ventilatorassociated, and healthcare-associated pneumonia. Am J Respir Crit Care
Med. 2005;171:388.
85. Torres A, El-Ebiary M. Bronchoscopic BAL in the diagnosis of ventilatorassociated pneumonia. Chest. 2000;117(Suppl 2):198S.
86. Baughman RP. Protected-specimen brush technique in the diagnosis of
ventilator-associated pneumonia. Chest. 2000;117(Suppl 2):203.
87. de Jaeger A, Litalien C, Lacroix J, et al. Protected specimen brush or bronchoalveolar lavage to diagnose bacterial nosocomial pneumonia in ventilated adults: a meta-analysis. Crit Care Med. 1999;27:2548.
88. Fujitani S, Yu VL. Quantitative cultures for diagnosing ventilator-associated
pneumonia: a critique. Clin Infect Dis. 2006;43(Suppl 2):S106.
89. Heyland DK, Cook DJ, Marshall J, et al. The clinical utility of invasive diagnostic techniques in the setting of ventilator-associated pneumonia. Canadian Critical Care Trials Group. Chest. 1999;115:1076.
90. Fagon JY, Chastre J, Wolff M, et al. Invasive and noninvasive strategies for
management of suspected ventilator-associated pneumonia: a randomized
trial. Ann Intern Med. 2000;132:621.
91. Sanchez-Nieto JM, Torres A, Garcia-Cordoba F, et al. Impact of invasive and noninvasive quantitative culture sampling on outcome of
ventilator-associated pneumonia: a pilot study. Am J Respir Crit Care Med.
1998;157:371.
92. Ruiz M, Torres A, Ewig S, et al. Noninvasive versus invasive microbial
investigation in ventilator-associated pneumonia: evaluation of outcome.
Am J Respir Crit Care Med. 2000;162:119.
93. Sole Violan J, Fernandez JA, Benitez AB, et al. Impact of quantitative
invasive diagnostic techniques in the management and outcome of mechanically ventilated patients with suspected pneumonia. Crit Care Med.
2000;28:2737.
94. Shorr AF, Sherner JH, Jackson WL, et al. Invasive approaches to the diagnosis of ventilator-associated pneumonia: a meta-analysis. Crit Care Med.
2005;33:46.
95. Prats E, Dorca J, Pujol M, et al. Effects of antibiotics on protected specimen brush sampling in ventilator-associated pneumonia. Eur Respir J.
2002;19:944.
96. Montravers P, Fagon JY, Chastre J, et al. Follow-up protected specimen
brushes to assess treatment in nosocomial pneumonia. Am Rev Respir Dis.
1993;147:38.
97. Souweine B, Veber B, Bedos JP, et al. Diagnostic accuracy of protected
specimen brush and bronchoalveolar lavage in nosocomial pneumonia:
impact of previous antimicrobial treatments. Crit Care Med. 1998;26:
236.
98. Jain P, Sandur S, Meli Y, et al. Role of flexible bronchoscopy in immunocompromised patients with lung infiltrates. Chest. 2004;125:712.
99. Ognibene FP, Shelhamer J, Gill V, et al. The diagnosis of Pneumocystis
carinii pneumonia in patients with the acquired immunodeficiency syndrome using subsegmental bronchoalveolar lavage. Am Rev Respir Dis.
1984;129:929.
100. Stover DE, White DA, Romano PA, et al. Diagnosis of pulmonary disease in acquired immune deficiency syndrome (AIDS). Am Rev Respir Dis.
1984;130:659.
101. Wollschlager C, Khan F. Diagnostic value of fiberoptic bronchoscopy in
acquired immunodeficiency syndrome. Cleve Clin Q. 1985;52:489.
102. Broaddus C, Dake MD, Stulbarg MS, et al. Bronchoalveolar lavage and
transbronchial biopsy for the diagnosis of pulmonary infections in the acquired immunodeficiency syndrome. Ann Intern Med. 1985;102:747.
103. Flori P, Bellete B, Durand F, et al. Comparison between real-time PCR,
conventional PCR and different staining techniques for diagnosing Pneumocystis jiroveci pneumonia from bronchoalveolar lavage specimens. J Med
Microbiol. 2004;53:603.
104. Musher B, Fredricks D, Leisenring W, et al. Aspergillus galactomannan
enzyme immunoassay and quantitative PCR for diagnosis of invasive aspergillosis with bronchoalveolar lavage fluid. J Clin Microbiol. 2004;42:
5517.
105. Klont RR, Mennink-Kersten MA, Verweij PE. Utility of Aspergillus antigen detection in specimens other than serum specimens. Clin Infect Dis.
2004;39:1467.
106. Sanguinetti M, Posteraro B, Pagano L, et al. Comparison of real-time
PCR, conventional PCR, and galactomannan antigen detection by enzymelinked immunosorbent assay using bronchoalveolar lavage fluid samples
from hematology patients for diagnosis of invasive pulmonary aspergillosis.
J Clin Microbiol. 2003;41:3922.
107. Hage CA, Davis TE, Egan L, et al. Diagnosis of pulmonary histoplasmosis
and blastomycosis by detection of antigen in bronchoalveolar lavage fluid
using an improved second-generation enzyme-linked immunoassay. Respir
Med. 2007;101:43.
108. Ison MG, Fishman JA. Cytomegalovirus pneumonia in transplant recipients. Clin Chest Med. 2005;26:691.
109. Danek JJ, Bower JS. Diagnosis of pulmonary tuberculosis by fiberoptic
bronchoscopy. Am Rev Respir Dis. 1979;119:677.
110. Jett JR, Cortese DA, Dines DE. The value of bronchoscopy in the diagnosis
of mycobacterial disease. Chest. 1981;80:575.
111. Pant K, Chawla R, Mann PS, et al. Fiberbronchoscopy in smear-negative
miliary tuberculosis. Chest. 1989;95:1151.
112. de Gracia J, Curull V, Vidal R, et al. Diagnostic value of bronchoalveolar
lavage in suspected pulmonary tuberculosis. Chest. 1988;93:329.
113. Tueller C, Chhajed PN, Buitrago-Tellez C, et al. Value of smear and PCR
in bronchoalveolar lavage fluid in culture positive pulmonary tuberculosis.
Eur Respir J. 2005;26:767.
114. Chen NH, Liu YC, Tsao TC, et al. Combined bronchoalveolar lavage and
polymerase chain reaction in the diagnosis of pulmonary tuberculosis in
smear-negative patients. Int J Tuberc Lung Dis. 2002;6:350.
115. Meyer KC. Bronchoalveolar lavage as a diagnostic tool. Semin Respir Crit
Care Med. 2007;28:546.
116. Meyer KC. Bronchoalveolar lavage in the diagnosis and management of
interstitial lung diseases. Clin Pulm Med. 2007;14:148.
117. Barmada H, Gibbons JR. Tracheobronchial injury in blunt and penetrating
chest trauma. Chest. 1994;106:74.
118. Baumgartner F, Sheppard B, de Virgilio C, et al. Tracheal and main
bronchial disruptions after blunt chest trauma: presentation and management. Ann Thorac Surg. 1990;50:569.
119. Caster R, Wareham EE, Brewer LA. Rupture of the bronchus following
closed chest trauma. Am J Surg. 1962;104:212.
120. Kirsh MM, Orringer MB, Douglas MB, et al. Management of tracheobronchial disruption secondary to nonpenetrating trauma. Current review:
tracheobronchial disruption from blunt trauma. Ann Thorac Surg. 1976;
22:93.
121. Hara KS, Prakash UBS. Fiberoptic bronchoscopy in the evaluation of acute
chest and upper airway trauma. Chest. 1989;96:627.
122. Ecker RR, Libertini RV, Rea WJ, et al. Injuries of the trachea and bronchi.
Ann Thorac Surg. 1971;11:280.
123. Grover FL, Ellestad C, Arom KV, et al. Diagnosis and management of major
tracheobronchial injuries. Ann Thorac Surg. 1979;28:384.
124. Kelly JP, Webb WR, Moulder PV, et al. Management of airway trauma:
combined injuries of the trachea and esophagus. Ann Thorac Surg. 1987;
43:160.
125. Jones WS, Mavroudis C, Richardson JD, et al. Management of tracheobronchial disruption resulting from blunt trauma. Surgery. 1984;95:
319.
126. Roxburgh JC. Rupture of the tracheobronchial tree. Thorax. 1987;42:681.
127. Major CP, Floresguerra CA, Messerschmidt WH, et al. Traumatic disruption of the cervical trachea. J Tenn Med Assoc. 1992;85:517.
128. Sippel JM, Chesnutt MS. Bronchoscopic therapy for bronchopleural fistulas. J Bronchol. 1998;5:61.
129. McManigle JE, Fletcher GL, Tenholder MF. Bronchoscopy in the management of bronchopleural fistula. Chest. 1990;97:1235.
130. Lois M, Noppen M. Bronchopleural fistulas: an overview of the problem
with special focus on endoscopic management. Chest. 2005;128:395.
131. Toma TP, Kon OM, Oldfield W, et al. Reduction of persistent air leak with
endoscopic valve implants. Thorax. 2007;62:830.
132. Feller-Kopman D, Bechara R, Garland R, et al. Use of a removable endobronchial valve for the treatment of bronchopleural fistula. Chest. 2006;
130:273.
133. Ferguson JS, Sprenger K, Van Natta T. Closure of a bronchopleural fistula
using bronchoscopic placement of an endobronchial valve designed for the
treatment of emphysema. Chest. 2006;129:479.
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
134. Limper AH, Prakash UBS. Tracheobronchial foreign bodies in adults. Ann
Intern Med. 1990;112:604.
135. Swanson KL, Edell ES. Tracheobronchial foreign bodies. Chest Surg Clin
N Am. 2001;11:861.
136. Cunanan OS. The flexible fiberoptic bronchoscope in foreign body removal.
Chest. 1978;73:725.
137. Lan RS, Lee CH, Chiang YC, et al. Use of fiberoptic bronchoscopy
to retrieve bronchial foreign bodies in adults. Am Rev Respir Dis.
1989;140:1734.
138. Atul MC, Rafanan AL. Extraction of airway foreign body in adults. J Bronchol. 2001;8:123.
139. Hunt JL, Agee RN, Pruitt BA Jr. Fiberoptic bronchoscopy in acute inhalation injury. J Trauma. 1975;15:641.
140. Wald PH, Balmes JR. Respiratory effects of short-term, high-intensity toxic
inhalations: smoke, gases, and fumes. J Intensive Care Med. 1987;2:260.
141. Crapo RO. Smoke-inhalation injuries. JAMA. 1981;246:1694.
142. Hunt JL, Agec RN, Pruitt BA Jr. Fiberoptic bronchoscopy in acute inhalation injury. J Trauma. 1975;15:641.
143. Williams DO, Vanecko RM, Glassroth J. Endobronchial polyposis following smoke inhalation. Chest. 1983;84:774.
144. Sueoka N, Kato O, Aoki Y, et al. Fiberoptic bronchoscopy in inhalation
injury. J Jpn Soc Bronchol. 1994;16:454.
145. Dellinger RP. Fiberoptic bronchoscopy in adult airway management. Crit
Care Med. 1990;18:882.
146. Giudice JC, Komansky H, Gordon R, et al. Acute upper airway obstruction: fiberoptic bronchoscopy in diagnosis and therapy. Crit Care Med.
1981;9:878.
519
147. Seijo LM, Sterman DH. Interventional pulmonology. N Engl J Med. 2001;
344:740.
148. Beamis J. Interventional pulmonology techniques for treating malignant
large airway obstruction: an update. Curr Opin Pulm Med. 2005;11:
292.
149. Wahidi MM, Herth FJ, Ernst A. State of the art: interventional pulmonology. Chest. 2007;131:261.
150. Satin SA, Scoggin C. Fiberoptic bronchoscopy in bronchial asthma: a word
of caution. Chest. 1976;69:39.
151. Lang DM, Simon RA, Mathison DA, et al. Safety and possible efficacy
of fiberoptic bronchoscopy with lavage in the management of refractory
asthma with mucous impaction. Ann Allergy. 1991;67:324.
152. Henke CA, Hertz M, Gustafson P. Combined bronchoscopy and mucolytic
therapy for patients with severe refractory status asthmaticus on mechanical ventilation: a case report and review of the literature. Crit Care Med.
1994;22:1880.
153. Shridharani M, Maxson TR. Pulmonary lavage in a patient in status
asthmaticus receiving mechanical ventilation: a case report. Ann Allergy.
1982;49:157.
154. Weinstein HJ, Bone RC, Ruth WE. Pulmonary lavage in patients treated
with mechanical ventilation. Chest. 1977;72:583.
155. Niederman MS, Gambino A, Lichter J, et al. Tension ball valve mucus plug
in asthma. Am J Med. 1985;79:131.
156. Millman M, Goodman AH, Goldstein IM, et al. Bronchoscopy and lavage
for chronic bronchial asthma. Immunol Allerg Pract. 1981;3:10.
157. Brashear RE, Meyer SC, Manion MW. Unilateral atelectasis in asthma.
Chest. 1973;63:847.
CHAPTER 38 ■ AIRWAY MANAGEMENT
THOMAS C. MORT r ANDREA GABRIELLI r TIMOTHY J. COONS r ELIZABETH CORDES BEHRINGER
r A. JOSEPH LAYON
IMMEDIATE CONCERNS
Major Problems
Maintenance of the airway must be one of the most essential
goals of critical care. Critical care personnel apply their expertise in resuscitating the critically ill patient by volume infusion,
invasive line placement, titration of vasoactive medications,
analysis of laboratory studies, and performing radiographic
examinations, but may neglect the “A” of the ABCs until further clinical deterioration turns the need for airway management into an emergency. Airway functions are numerous and,
though it primarily supports the exchange of oxygen and carbon dioxide, the airway assists in the regulation of temperature,
contributes to the warming and humidification of inspired gas,
traps and expels foreign particles, and protects against foreign
body entry into the lungs through a complex array of reflex
responses.
Many of these functions are altered or lost in critically ill
patients. Airway obstruction can result from infection, trauma,
laryngospasm, soft tissue edema, and aspiration of gastric or
other noxious materials. Protective reflexes may be lost as a
result of disease and depression with narcotics, sedatives, or
paralytic agents. Humidification can also be lost as various appliances that bypass the nose, pharynx, and upper airway are
inserted to maintain airway patency. Clinicians must then em-
ploy methods to maintain airway hydration, including humidifiers, nebulizers, and heat–moisture exchangers. These devices
introduce additional problems such as nosocomial infections
and increased work of breathing.
GENERAL PRINCIPLES
Primum non nocere (first do no harm) applies most fittingly
to the airways of critically ill patients. The intensivist must
not only be knowledgeable of respiratory pathophysiology,
but also must possess technical skill and sound judgment in
airway management. Various options are available, including
bag-valve-mask ventilation, translaryngeal intubation (oral or
nasal), tracheotomy, and cricothyroidotomy. Adjunctive drugs
such as local anesthetics, narcotics, benzodiazepines, barbiturates, muscle relaxants, ketamine, and propofol play an important role. Their use facilitates airway control and improves
respiratory support.
In most instances, bag-valve-mask (Fig. 38.1) ventilation
precedes tracheal intubation. Immediate correction of hypoxemia should be attempted by application of a mask and
initiation of bag ventilation with an increased FiO2 while equipment for intubation is prepared. An appropriate mask provides a tight seal around the nose and mouth, and the colorless
plastic with soft and pliable edges allows visualization of the
11:53
P1: OSO/OVY
GRBT291-37-39
520
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
TA B L E 3 8 . 1
INDICATIONS FOR TRACHEAL INTUBATION
Open an obstructed airway
Provide airway pressure support to treat hypoxemia
PaO2 less than 60 mm Hg with an FiO2 greater than 0.5
Alveolar-to-arterial oxygen gradient 300 mm Hg
Intrapulmonary shunt more than 15%–20%
Provide mechanical ventilation
Respiratory acidosis
Inadequate respiratory mechanics
Respiratory rate more than 30 breaths/min
FVC less than 10 mL/kg
NIF more than –20 cm H2 O
VD /VT more than 0.6
FIGURE 38.1. Standard bag-valve-mask setup. Note that the bag is
self-inflating, so it can be used with (usual) or without (in emergencies) an external gas supply. The “tail” of the bag serves as an oxygen
reservoir.
mouth and secretions. The mask is attached to the resuscitation (self-inflating or collapsible) bag with a high-flow oxygen source. Various systems will supply an FiO2 between 0.60
and 1.0, depending upon the mask fit, the manufacturer, the
oxygen flow rate, and the style of bag design based on the
Mapleson (Fig. 38.2) designation (1–3). Proper inflation requires two hands: One to hold the mask firmly in place against
FIGURE 38.2. A Mapleson D bag. Note that this is not a self-inflating
bag, and hence must be used with an external gas source. The positioning of the fresh gas inlet—designating the Mapleson bag class—and the
fresh gas flow impact the amount of rebreathing. It is possible, in an
inadvertent situation, if the fresh gas runs out and the pressure regulating (“pop off”) valve is closed, to continuously rebreathe exhaled
gas. This would ultimately result in injury or death.
Facilitate suctioning, instillation of medications, and
bronchoscopy
Prevent aspiration
Gag and swallow reflexes absent
FiO2 , fraction of inspired oxygen; FVC, forced vital capacity; NIF,
negative inspiratory force; VD /VT , dead space/tidal volume ratio.
the patient’s face, and the other to compress the bag (4). The
mandible must be lifted to create a seal without airway occlusion. An oropharyngeal or nasal airway facilitates oxygen delivery by bypassing or retracting the tongue (5,6). Forceful bag
compression should be avoided to prevent gastric distention
and possible pulmonary aspiration. Gentle insufflation allows
clinical assessment of lung compliance and minimizes complications. Contraindications to bag-valve-mask ventilation include airway obstruction, pooling of blood or secretions in the
pharynx, and severe facial trauma (7,8).
Critically ill patients require tracheal intubation (Table
38.1) for several reasons (7). When inadequate ventilation is
observed, tracheal intubation becomes necessary. It provides
airway patency, facilitates tracheobronchial suctioning, and
minimizes aspiration of blood, gastric contents, or secretions
into the pulmonary tree. Oxygen administration and mechanical ventilation correct hypoxemia and hypercapnia, improve
the alveolar-to-arterial oxygen partial pressure gradient, and
reduce intrapulmonary shunting. In emergency situations in
which intravascular access is absent, drug administration into
the endotracheal tube can be life saving. Epinephrine, atropine,
lidocaine, and naloxone exert their pharmacologic effects after
tracheal administration (9–12).
Relative or absolute contraindications to conventional tracheal intubation exist in patients with traumatic or severe degenerative disorders of the cervical spine; in those with acute
infectious processes such as acute supraglottitis or intrapharyngeal abscess; and in patients with extensive facial injury
and basal skull fracture (13–15). Blind nasal intubation may
be contraindicated in upper airway foreign body obstruction
because the tube may push the foreign body distally and exacerbate airway compromise (13–16).
ANATOMIC CONSIDERATIONS
Adult
Specific anatomic characteristics may determine the ease or difficulty of intubation. The intensivist sometimes does not have
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
521
FIGURE 38.3. Demonstration of the “sniffing position” for optimal visualization of the glottic opening.
the flexibility to examine and assess the airway at leisure but
must act quickly with skill and confidence. A good working
knowledge of the anatomy of the mouth, neck, cervical spine,
and pulmonary tree is mandatory for a successful and safe intubation. Examination of cervical spine mobility includes flexion
and extension. Neck flexion aligns the pharyngeal and tracheal
axes, whereas head extension on the neck and opening of the
mouth align the oral passage with the pharyngeal and tracheal
axes. This maneuver places the patient in a “sniffing position”
(17) (Fig. 38.3). Incorrect positioning of the head and neck accounts for one of the common errors in orotracheal intubation.
Flexion and extension of the head decreases 20% by 75 years
of age. Degenerative arthritis limits cervical spine motion, more
so with extension than flexion. Movement of the spine is contraindicated in the presence of potential cervical spine injury;
hence, patients are maintained in a neutral position with in-line
stabilization. Barring the edentulous patient, the front component of the hard cervical collar is commonly removed to allow
full mandibular movement and optimize mouth opening. This
maneuver removes the standard flexion and extension movements used to optimize the line of sight and therefore reduces
one’s ability to see “around the corner” in many cases (18–22).
Each technique, maneuver, or accessory airway device available
may alter the alignment of the cervical spine to a small degree
based on the device itself, combined with the force and maneuvering performed by the operator, despite in-line stabilization
(18,23–25). The available data and accumulated clinical experience do not dictate one method over another, especially when
many practitioners who suggest an awake fiberoptic intubation is the “best” approach may themselves have reservations
and concerns regarding their own comfort and competency at
performing such a technique (18,26,27). The most appropriate technique is debatable but it would be prudent that the
practitioner do his or her best with familiar equipment and
approaches. This would not be the time to attempt to use a
newly purchased item (e.g., rigid fiberscope), since one has not
become competent and familiar with its use on a manikin and
elective “easy” patients. Other diseases may place the patient
at risk for atlantoaxial and cervical spine instability, and reduced mouth opening beyond those with known or suspected
neck pathology (28).
Important anatomic landmarks may help the physician during direct laryngoscopy (Fig. 38.4). The cricoid, a circle of cartilage above the first tracheal ring, can be compressed to occlude
the esophagus (Sellick maneuver), thereby preventing passive
gastric regurgitation into the trachea during intubation (29).
The epiglottis, a large cartilaginous structure, lies in the anterior pharynx. The vallecula, a furrow between the epiglottis
and base of the tongue, is the placement site for the tip of a
FIGURE 38.4. Laryngoscopic landmarks. Panel shows the cricoid
cartilage.
11:53
P1: OSO/OVY
GRBT291-37-39
522
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
curved laryngoscope blade. The larynx is located anterior and
superior to the trachea and contains the vocal cords.
Pediatric
Several anatomic differences exist between the adult and the
pediatric airways. Pediatric patients have a relatively large head
and flexible neck. The air passages are small, the tongue is large,
the epiglottis is floppy, and the glottis is typically slanted at a
40- to 50-degree angle, making intubation more difficult. Mucous membranes are softer, looser, and more fragile, and readily
become edematous when an oversized endotracheal tube is
used.
Adenoids and tonsils in a child are relatively larger than
those in the adult. The epiglottis and larynx of infants lie more
cephalad and anterior, and the cricoid cartilage ring is the narrowest portion of the upper airway. In contrast, the adult glottic
opening is narrowest. Additionally, the pediatric vocal cords
have a shorter distance from the carina, with the mainstem
bronchus angulating symmetrically at the level of the carina at
about 55 degrees. In adults, the right mainstem angulates at
about 25 degrees and the left at about 45 degrees. The cupulae
of the lungs are higher in the infant’s neck, increasing the risk
of lung trauma.
To avoid delay and minimize complications, all anticipated
equipment and drugs must be available for the planned intubation technique (Table 38.2, Fig. 38.5). Additionally, a difficult
airway cart or bag with a variety of airway rescue devices—
as well as a bronchoscope and/or fiberoptic laryngoscope—
should be readily available (30,31). It is far better to have
a limited assortment of airway devices with which personnel
are familiar and competent to handle than to have an expensive, well-stocked cart containing a plethora of devices that
FIGURE 38.5. Demonstration of the equipment and drugs that must
be available for the planned intubation technique.
the airway personnel have not practiced with nor have gained
competence.
MEDICATIONS
The pharynx, larynx, and trachea contain a rich network of
sensory innervation, necessitating the use of anesthesia, analgesia, sedation, and sometimes muscular paralysis during intubation of a spontaneously breathing, awake, or semiconscious
patient. Drugs commonly used are local anesthetics, sedativehypnotics (sodium thiopental, propofol, etomidate), narcotics
(fentanyl, morphine sulfate, hydromorphone, remifentanil),
sedative-anxiolytics (benzodiazepine class—midazolam), muscle relaxants (depolarizing and nondepolarizing agents), and
miscellaneous agents such as ketamine and dexmedetomidine.
Local Anesthetics
TA B L E 3 8 . 2
STANDARD EQUIPMENT AND DRUGS FOR
TRANSLARYNGEAL INTUBATION
Bag-valve-mask resuscitation bag
LMA-type device
Oxygen source
Suction apparatus
Selection of oral and nasal airways
Magill forceps
Assortment of laryngoscope blades and endotracheal tubes
Tape, stylet, lubricant, syringes, and tongue depressors
Monitors (ECG, blood pressure monitor, pulse oximeter,
capnography, or similar device) and defibrillatora
Fiberoptic bronchoscope,a rigid fiberscope,a and specialty
bladesa
A drug tray or cart with vasoconstrictors, topical anesthetics,
induction agents, muscle relaxants, and emergency
medications
14-Gauge IV, scalpel, assortment of supraglottic airways,a
bougie,a Combitube,a ET exchanger,a and Melker-type
cricothyrotomy kit
a
Immediately available.
LMA, laryngeal mask airway; ECG, electrocardiograph; ET,
endotracheal tube.
The use of local anesthetics is often overlooked in the intensive care unit (ICU) setting for a number of reasons: (a) it is
far easier to administer an intravenous agent than to take the
time to prepare the patient with topical anesthetics or local
nerve blocks; (b) the urgency of the situation may preclude
their timely use; (c) the patient’s anatomic/physical characteristics may limit their effective application (poor or nonexistent
landmarks, coagulopathy, excessively dry mucosa, excessive secretions, patient uncooperation); and (d) the underappreciation
of their value in managing the airway and the underestimation
of airway difficulty in the ICU setting. Moreover, access to
the proper local anesthetic agents and the accessories for their
accurate delivery (nebulizer, atomizer, Krause forceps, cotton
balls, Abraham laryngeal cannula, etc.) may be limited in the
ICU setting unless they have been prepared and gathered in
advance (difficult airway cart).
Aerosolized or nebulized 1% to 4% lidocaine can readily
achieve nasopharyngeal and oropharyngeal anesthesia if the
patient is cooperative and capable of deep inhalation, thus
limiting its usefulness in the ICU. The author has found this
method less desirable due to its time-consuming application
process and its limited effectiveness when compared to topically applied local anesthetics or local blocks. Transtracheal
(cricothyroid membrane) instillation of 2 to 4 mL of 1% to
4% lidocaine with a 22- to 25-gauge needle causes sufficient
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
coughing-induced reflex to afford ample distribution to anesthetize the subglottic and supraglottic regions plus the posterior pharynx in 90% of patients (32–34). Cocaine provides
excellent conditions for facilitating intubation through the
nasopharynx due to its outstanding topical anesthetic and mucosal and vascular shrinkage capabilities (33). However, inhospital availability may limit its use in favor of phenylephrine
or oxymetazoline combined with readily available local anesthetics. Lidocaine ointment applied to the base of the tongue
with a tongue blade or similar device allows performance of
direct laryngoscopy in many patients. If time permits, nasal
spraying with a vasoconstrictor followed by passing a progressively larger nasal airway trumpet from 24 French to 32 French
that is coated/lubricated with lidocaine gel/ointment provides
exceptional coverage of the nasocavity in preparing for a nasal
intubation. Instillation of liquid lidocaine via the in situ nasal
trumpet offers an excellent conduit to distribute additional topical anesthetic to the orohypopharynx. It is best performed in
the sitting-up position to enhance coverage of the airway structures.
Barbiturates
Sodium thiopental, an ultra-short-acting barbiturate, decreases
the level of consciousness and provides amnesia without analgesia after an intubation dose of 4 to 7 mg/kg ideal body weight
(IBW) dose over 20 to 50 seconds (administered via a peripheral
IV) in the otherwise healthy patient. Its short duration of action (5–10 minutes) makes it ideal for short procedures such as
intubation. Thiopental has an excellent cerebral metabolic profile in regards to lowering cerebral metabolic rate while maintaining cerebral blood flow as long as systemic blood pressure
is maintained within an adequate range. However, thiopental
may lead to hypotension in critically ill patients due to its vasodilatation properties, especially in the face of hypovolemia
(34). Though inexpensive, its use in the operating room has
declined in favor of propofol. Unfortunately, many upcoming
personnel do not develop a working knowledge of the barbiturates. In the ICU setting, reducing the dose of thiopental to
1 to 2 mg/kg IBW is very useful for preparing the patient for
tracheal intubation with or without a muscle relaxant.
Narcotics
Narcotics such as morphine, hydromorphone, fentanyl, and
remifentanil reduce pain perception and allay anxiety, making
intubation less stressful. In addition, they have some sedative
effect, suppress cough, and relieve dyspnea (35,36). Fentanyl
and the ultra-short-acting remifentanil have a more rapid onset
and shorter duration of action than the conventional narcotics
used in the ICU setting for analgesia (37–39). Morphine may
lead to histamine release and its potential sequelae. Though
all narcotics cause respiratory depression, the newer synthetic
narcotics may lead to muscular chest wall rigidity that may
hamper ventilation and may contribute to episodes of bradycardia. Narcotics, titrated to effect, are quite effective in settling
the patient undergoing an awake intubation. Their analgesic,
antitussive, and antihypertensive qualities are extremely valuable especially in light of the ability to rapidly reverse excessive
narcotization.
523
Benzodiazepines
Benzodiazepines such as lorazepam and midazolam have excellent amnestic and sedative properties (40). Diazepam has seen
its use decline markedly due to its less favorable distribution
and clearance characteristics. This drug class does not provide
analgesia and may be combined with an analgesic agent during intubation, especially if an awake or semiconscious state
with maintenance of spontaneous ventilation is the goal. Midazolam largely has replaced diazepam for intubation because
of its more rapid onset and shorter duration of action. Lorazepam use for intubation is possible, but it is hampered by a
slower pharmacodynamic onset (2–6 minutes) as compared to
midazolam. Hypotension may occur in hypovolemic patients,
and benzodiazepines potentiate narcotic-induced respiratory
depression.
Muscle Relaxants
The clinician may desire or need to administer a muscle relaxant to optimize intubation conditions, but the vast majority
of ICU intubations may be accomplished without such agents.
There are basically two perspectives regarding the use of muscle
relaxants in the critically ill patient:
1. The administration of a sedative-hypnotic agent with a
rapid-acting muscle relaxant, typically succinylcholine, as
the standard technique for tracheal intubation is often cited
as improving intubation conditions and leading to fewer
complications (41). Though this recommendation has much
merit, the ubiquitous acceptance of this approach has fallen
into the hands of practitioners who frequently do not fully
contemplate the patient’s risk for airway management difficulties and may not have access or a good working knowledge of airway rescue devices to bail them out if conventional laryngoscopy techniques fail (42–46). Many who use
this approach may do so regardless of their patient assessment. This is akin to a “shoot first, ask questions later”
approach. One may expect outcomes with this approach
akin to those noted when it is used in social situations.
2. The alternative approach is to assess the patient’s airwayrelated risk factors, the patent’s potential needs, and the
patient’s ability to tolerate methods of preparation (e.g.,
topical, light sedation, and then proceed with induction)
followed by customization of the preparation of the patient
rather than a “one size fits all” mentality. Though the decision for their use is the clinician’s to make, one must be
a patient advocate since he or she rarely ever has any say
in the matter. It is our opinion that any clinician who administers drugs such as induction agents, including paralytics, thus rendering the patient entirely dependent on the
airway management team, must have developed a rescue
strategy coupled with the equipment to deploy such a strategy (43,45,46).
The indications for muscle relaxants include agitation or
lack of cooperation not related to inadequate or no sedation, increased muscle tone (seizures, tetanus, and neurologic
diseases), avoidance of intracranial hypertension, limiting patient movement (potential cervical spine injury), and the need
for shortening the time frame from an awake state with
11:53
P1: OSO/OVY
GRBT291-37-39
524
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
protective reflexes to an asleep state with the goal of rapid
tracheal intubation (upper gastrointestinal bleed).
Neuromuscular blocking agents may cause depolarization
of the motor end-plate (succinylcholine, a depolarizing agent)
or prevent depolarization (nondepolarizer: pancuronium, vecuronium, rocuronium). Succinylcholine has a rapid onset and
short duration of effect, making it useful in the critical care setting; however, it may raise serum potassium levels by 0.5 to 1.0
mEq/L. It is contraindicated in bedridden patients and in those
with pre-existing hyperkalemia, burns, or recent or long-term
neurologic deficits (47–49). Other side effects are elevation
of intragastric and intraocular pressures, muscle fasciculation,
myalgia, malignant hyperthermia, cardiac bradyarrhythmias,
and myoglobinuria. Depending on the initial dose—our recommendation is 0.25 mg/kg IBW—and systemic conditions, succinylcholine has a relatively short duration of 3 to 10 minutes.
However, if airway management difficulties exist, one should
never presume the muscle relaxant will wear off in time to
“save” the patient and allow spontaneous patient-initiated ventilation. Emergency rescue techniques should be deployed as
early as possible when conventional intubation methods prove
unsuccessful.
Nondepolarizing muscle relaxants have a longer time to
onset and duration of action as compared to succinylcholine.
Rocuronium (typical operating room dose, 0.6 mg/kg) can approach succinylcholine in rapid time of onset if dosed accordingly (1.2 mg/kg), but the increased dosage requirements to
meet this objective come with some cost: extended duration of
drug action and increased cost.
One controversy to consider when faced with a known or
suspected difficult airway: If the practitioner is contemplating
the use of a muscle relaxant, which agent is most advantageous?
Standard dosing of succinylcholine potentially offers the awake
option earlier than a nondepolarizing agent, but if it wears
off too soon, then a period of poor or marginal ventilation
may hamper patient care and require a transition to a rescue
option. Conversely, a short-acting nondepolarizer offers good
transition to a rescue plan if mask ventilation is adequate, but
does not allow an early-awaken option (46).
Ketamine
Ketamine, a phencyclidine derivative, provides profound analgesia, amnesia, and dissociative anesthesia (50,51). The patient
may appear awake but is uncommunicative. Airway reflexes
are often, but not always, preserved. Ketamine has a rapid onset and relatively short duration of action. Its profile is unique:
it is a myocardial depressant, but this is often countered by
its sympathomimetic properties, thus leading to hypertension
and tachycardia in many patients. Its use in the critically ill patient with ongoing activation of his or her sympathetic outflow
could lead to profound hemodynamic instability since the underlying myocardial depression may not be successfully countered. Though it offers favorable bronchodilatory properties,
it promotes bronchorrhea, salivation, and a high incidence of
dreams, hallucinations, and emergence delirium (50,51).
Propofol
Propofol also is useful during intubation, especially if titrated
to the desired effect rather than simply administering a one-
time bolus (52–55). After intravenous administration via a peripheral IV (1–3 mg/kg IBW), unconsciousness occurs within
30 to 60 seconds. Awakening is observed in 4 to 6 minutes
with a lower lingering level of sedation compared to other
induction agents (52,53,55). Side effects include pain on injection, involuntary muscle movement, coughing, and hiccups.
Hypotension, cardiovascular collapse, and, rarely, bradycardia may complicate its use, especially if administered in rapid
single-bolus dosing in the critically ill patient with relative or
absolute hypovolemia, a systemic capillary leak syndrome, or
pre-existing vasodilatation (e.g., sepsis, systemic inflammatory
response syndrome [SIRS]). It, however, is an excellent agent
that may be titrated to a desired effect while maintaining spontaneous ventilation.
Etomidate
Etomidate is considered by many to be the preferred induction
agent in the critically ill patient due to its favorable hemodynamic profile, as compared to the other available induction
agents. The hemodynamic stabilization offered by etomidate,
however, should not be considered a panacea since it too may
lead to hemodynamic deterioration (56,57). Currently, its role
as a single-dose induction agent is in question due to its transient depression of the adrenal axis. Once regarded as a minor
concern, this adrenal suppression may be much more influential in the outcome of the critically ill. Some have expressed
caution with etomidate’s use as a single-dose induction agent,
especially in the septic or trauma populations. A variety of
opinions exist, ranging from an opinion that etomidate should
be avoided completely, to its avoidance in select populations
such as the septic population, to its use—if at all—with empiric steroid replacement therapy for at least 24 hours (58–
60). Perhaps well-designed clinical trials should be performed
to determine the relevance of these published precautions. Until more information is available, the practitioner who chooses
to use etomidate would be wise and prudent to consider communicating with the ICU care team so they are aware of its
use and may act accordingly if hemodynamic instability occurs
within 24 hours of administration.
Dexmedetomidine
Dexmedetomidine is an ultra-short-acting α 2 agonist that,
when administered intravenously, provides analgesia and mild
to moderate sedation with relatively minimal respiratory depression while affording tolerance of “awake” fiberoptic and
conventional tracheal intubation (61,62). While a most useful
drug, its cost prevents its use in many centers.
EQUIPMENT FOR ACCESSING
THE AIRWAY
Esophageal Tracheal Combitube
The esophagotracheal airway (Combitube, ETC) (Fig. 38.6),
recommended by the American Heart Association (AHA) Advanced Cardiovascular Life Support (ACLS) course and other
national guidelines (30,63,64), is an advanced variant of the
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
525
B
FIGURE 38.6. The esophagotracheal double-lumen airway, the Combitube.
A
older esophageal obturator airway and the pharyngeal tracheal
lumen airway (PTLA). The double lumens with proximal and
distal cuffs allow ventilation and oxygenation in a majority
of nonawake patients whether placed in the esophagus (95%
of all insertions) or the trachea (65,66). Its proximal cuff is
placed between the base of the tongue and the hard palate and
the distal cuff within the trachea or upper esophagus (67,68).
The ETC is inserted blindly, assisted by a jaw thrust or laryngoscopic assistance. Its role in emergency airway management
is well recognized and though less popular than the laryngeal
mask airway (LMA) or fiberoptic bronchoscope, it may serve a
vital role in offering airway rescue when laryngoscopy, bougie
insertion, or LMA-assisted ventilation/intubation fails (69). A
recent latex-free modification of the Combitube, the Easytuber (Teleflex Ruesch; www.teleflexmedical.com) has a shorter
and thinner pharyngeal section, which allows the passage of a
fiberscope via an opening of the pharyngeal lumen to inspect
the trachea while ventilating.
Tracheal Intubation
When the decision has been made to provide mechanical ventilatory support or airway control, the second question to answer is the route of tracheal intubation: oral versus nasal (unless a surgical airway is clinically indicated). Most commonly,
orotracheal intubation is the preferred procedure to establish
an airway because it usually can be performed more rapidly,
offers a direct view of the glottis, has fewer bleeding complications, avoids nasal necrosis and sinus infection, and allows
a larger tracheal tube to be placed as compared to the nasal
approach. Finally, the blind nasal approach is particularly benefited by spontaneous ventilation. Airway vigilance should be
a goal of the critical care practitioner; thus, conventional and
advanced airway rescue equipment must be immediately available during any attempts at airway management. Before attempting to intubate, all anticipated equipment and drugs must
be prepared. This may best be provided by an organized “intubation box” containing conventional intubation equipment,
with a selection of lubricants, local/topical anesthetics, intravenous induction agents, and medications to assist in treating peri-intubation hemodynamic alterations (heart rate, blood
pressure). The box should have a visible lock with handbreakable deterrent devices to reduce the problem of “missing” equipment. The wide spectrum of patient preparation for
tracheal intubation ranges from an unconscious and paralyzed
patient, to preparation with mild to moderate dosing of sedatives and analgesics, to the other extreme of topical anesthetics
or no medication at all.
Critically ill patients often require only a fraction of the
drug doses provided to their elective operating room counterparts. Careful intravenous titration may attenuate hemodynamic alterations, loss of consciousness, apnea, and aspiration.
Controversy lies in whether or not to preserve spontaneous
ventilation: In essence, should one administer pharmacologic
paralyzing agents to the critically ill patient, thus placing the
patient in a state in which the practitioner is solely responsible
for ventilation, oxygenation, and tracheal intubation? Advocates for paralysis, the majority of which practice in the emergency department locale, cite a low rate of complications and
11:53
P1: OSO/OVY
GRBT291-37-39
526
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 30, 2008
Section III: Techniques, Procedures, and Treatments
FIGURE 38.7. Examples of fiberoptic laryngoscope handle and blades,
in which the bulb is in the handle and the light is transmitted through
fiberoptic bundles.
ease of intubation. Conversely, critical care databases suggest
that emergency tracheal intubation is far from “safe” and devoid of complications whether or not paralyzing agents are administered (41,43–45,70). From a patient advocate standpoint,
any practitioner who ablates the patient’s ability to spontaneously ventilate via neuromuscular blocking agents must be
properly trained and experienced in basic and advanced airway management so that the depth of his or her ability to
provide airway control lies well beyond simply conventional
laryngoscopy and intubation (45).
Equipment
Laryngoscopes. A laryngoscope (Fig. 38.7) (fiberoptic vs. conventional) is used to expose the glottis to facilitate passage of
the tracheal tube. Unfortunately, proper skill and experience using this standard airway management technique varies widely
among critical care practitioners. The utility of the laryngoscope under elective circumstances, with otherwise healthy surgical patients, is essentially limited to individuals with a grade
I or II view that can be easily intubated (22). Though a difficult
view is mentioned by many as being uncommon (22), Kaplan
et al. (71) documented a 14% incidence of grade III or IV views
despite optimizing maneuvers such as the optimal external laryngeal manipulation (OELM) and the backward upward right
pressure (BURP) technique (Fig. 38.8). This is further complicated, as up to 33% of critically ill patients have a limited view
with laryngoscopy (epiglottis only or no view at all) (44,45,72).
This is why the critical care practitioner responsible for airway
management must be prepared to embark on a Plan B or Plan
C immediately if conventional direct laryngoscopy fails to offer a reasonable glottic view that allows timely and accurate
intubation.
Blades. Laryngoscope blades are of two principal kinds,
curved and straight, varying in size for use in infants, children,
or adults (Fig. 38.9). Many varieties of both the curved and
straight blades have been redesigned in the hopes of augmenting visualization to facilitate passage of an endotracheal tube.
Innovations to improve laryngeal exposure include a hinged
blade tip to augment epiglottic lifting during laryngoscopy (73),
FIGURE 38.8. Diagrammatic representation of the optimal external
laryngeal movement (OELM) and backward upward rightward pressure (BURP) maneuvers for optimal visualization of the glottis.
rigid fiberscopes, and video-assisted laryngoscopy (74–80).
These innovations may, depending on the individual patient
airway characteristics, offer an improved view of the glottis
to improve the first-pass success rate, reduce intubation attempts, potentially reduce the time to intubation in the difficult airway, and potentially result in a reduction in esophageal
intubation and other airway-related complications that are relatively commonplace with standard techniques. The future lies
with visualizing “around the corner” in the hopes of improving
patient airway safety (74–80).
Endotracheal Tubes. Most endotracheal tubes (ETs) are disposable and are made of clear, pliable polyvinylchloride, with
FIGURE 38.9. Various types of laryngoscope blades in common use.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
527
The primary reasons for tracheal intubation will vary from
patient to patient and by practitioner, related to not only the
patient’s pathophysiology, but also the physician’s judgment
and experience in caring for the critically ill. The main goals
of tracheal intubation include protecting the airway from contamination, providing positive-pressure ventilation, providing
a patent airway, and permitting access to the tracheobronchial
tree for suctioning, instillation of medications, or diagnostic/therapeutic bronchoscopy. While the vast majority of tracheal intubations are via the oral route, the choice between the
oral and the nasal—or the transcricoid/transtracheal route—
will again be primarily determined by the patient’s physical
and airway conditions, the expected duration of mechanical
support, and the judgment and skills of the practitioner.
FIGURE 38.10. The Malinkrodt Hi-Lo Evacuation tube. While it
comes in various sizes, it is not optimal for all patients. There is level 1
evidence that, with proper use, it decreases risk of ventilator-associated
pneumonia. (From American Thoracic Society. Guidelines for the
management of adults with hospital-acquired, ventilator-associated
and healthcare-associated pneumonia. Am J Respir Crit Care Med.
2005;171:388–416.)
little tendency to kink until they attain body temperature.
Though the ETs mold to the contour of the upper airway
and present a smooth interior, affording easy passage of suction catheters or a flexible bronchoscope, they may become
encrusted with secretions, biofilm, and concretions that may
decrease luminal patency and endanger patient care.
In adults, all commonly used ETs are of the cuffed variety,
and many now used are types that allow suctioning of subglottic secretions—the Hi-Lo Evacuation ET (Fig. 38.10). The
ET cuff ensures a closed system, permitting control of ventilation and reducing the possibility of silent or active aspiration
of oronasal secretions, vomitus, or blood, although microaspiration is well recognized. Commonly, ET cuffs are the high
volume–low pressure models that offer a broad contact with
the tracheal wall and potentially limit ischemic damage to the
mucosa. The tube size used depends upon the size of the patient
(Table 38.3).
TA B L E 3 8 . 3
RECOMMENDED SIZES FOR ENDOTRACHEAL TUBES
Patient age
Newborn
6 mo
18 mo
3y
5y
6y
8y
12 y
16 y
Adult female
Adult male
a
Internal diameter of tube (mm)a
3.0
3.5
4.0
4.5
5.0
5.5
6.0
6.5
7.0
7.0–7.5
8.0–9.0
One size larger and one size smaller should be allowed for individual
intra-age variations and shorter-stature individuals. Where possible,
the subglottic suction endotracheal tube should be used.
Malleable Stylet. A well-lubricated malleable stylet (Fig.
38.11) is preferred by many to preform the ET into a shape that
may expedite passing through the glottis. The stylet should be
viewed as a guide, not a “spear,” and its tip should be safely
inside the ET, never distal to the ET tip (81,82). It should not
be used to force the ET into the airway or ram its way through
the vocal cords when they are closed or otherwise inaccessible.
Also, the popular “hockey stick”–shaped tip used by many is
useful, yet its angle must be appreciated by the operator. The
angle often will impede advancement into the airway since the
ET tip may impinge on the anterior tracheal wall and the sharp
angulations of the stylet may impede its own removal from the
ET (81–83). Ideally, the styleted ET tip should be placed at the
entrance of the glottis, and then, with stylet removal, the ET
will advance into the trachea less traumatically. Unfortunately,
many practitioners unknowingly advance the styleted ET deep
into the trachea without appreciating the potential damage the
stylet-stiffened ET tip may cause to the tracheal wall.
HOW MIGHT THE AIRWAY
BE ACCESSED?
General Indications and Contraindications
The oral approach is the standard method for tracheal intubation today. The indications are numerous and it may be best
to focus on the contraindications. The oral route would not
be a reasonable choice when there is limited access to the oral
cavity due to trauma, edema, or anatomic difficulties. These
contraindications for the oral route would presume that the
nasal approach is feasible from both the patient’s and clinician’s standpoint. If not, a surgical approach via the cricothyroid membrane or a formal tracheostomy would be clinically
indicated. Though nasal intubations were a mainstay in earlier
decades, the oral approach has displaced it due to the popularity of the “rapid sequence intubation” and the better appreciation of the potential detriments of long-term nasal intubation.
Orotracheal Intubation
The airway care team members should expediently prepare
both the patient and the equipment for the airway management procedure. While bag ventilation (preoxygenation) is being provided, obtaining appropriate towels for optimizing head
11:53
P1: OSO/OVY
GRBT291-37-39
528
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
FIGURE 38.11. Malleable stylet for
use with insertion of an endotracheal
tube.
and neck position or blankets for ramping the obese patient
and adjusting the bed height and angulation should be carried
out (Fig. 38.12, left panel); how not to position is noted in the
right panel of Figure 38.12. Assembling the necessary equipment, such as the ET, syringes, suction equipment, lubricant,
CO2 detector, and a stylet if desired, should be quickly carried out for the primary airway manager. During this time, a
rapid medical-surgical history is obtained, the review of previous intubation procedures sought, and an airway examination
completed (30,42). Intravenous access is ensured and a primary plan for induction developed. Access to airway rescue
devices should be addressed and, of course, it is best if they are
at the bedside. Clear communication among team members is
imperative as well as discussion of the plan with the patient, if
appropriate. Chaos is to be avoided and, in this context, the individual managing the procedure must insist that unnecessary
talking and agitation be limited.
A tube of appropriate diameter and length should be selected and, though gender is an important factor in size selection, patient height is equally important as there is a linear relationship between the latter and glottic size. Typically, the choice
in a woman would be a 7.0 to 8.0 mm ET, and in males an 8
to 9 mm ET would be used. Nonetheless, smaller-diameter ETs
should be readily available for any eventuality. A team member should examine the ET for patency and cuff integrity. The
15-mm proximal adapter should fit snugly and the ET kept in
its sterile wrapper and not handled until insertion. It may be
placed in warm water to soften the PVC tubing, which may
assist with passing the ET over a stylet, a tracheal introducing
catheter (bougie), or a fiberscope, or during an ET exchange.
Based on the patient history and physical examination, combined with the practitioner’s judgment, past experience, available equipment, and the needs of the patient, a determination is
made as to what induction method is best. Patient preparation
for tracheal intubation may range from little to no medication
to the other extreme of unconsciousness with muscle relaxation (41,84,85). Considering the earlier discussion involving
airway risk assessment, the practitioner will need to determine
if preservation of spontaneous ventilation is in the patient’s best
interest, as well as the depths of amnesia, hypnosis, and analgesia the patient may require so that airway manipulation is tolerated (30,63,64). Titration of a sedative-hypnotic or analgesic
to render the patient tolerant of airway manipulation is often
based on the practitioner’s knowledge and experience of the
available induction agents, combined with the perceived needs
of the patient plus the predicted tolerance of their administration. The pharmacodynamic effects following administration
via an IV site will depend on the IV location (central vs. peripheral, hand vs. antecubital fossa), vein patency, catheter diameter and length, IV flow rate, and the patient’s cardiac output.
FIGURE 38.12. Ramping of an obese patient’s torso to improve glottic visualization is noted on the left
panel. The right panel shows the patient position without proper ramping.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
529
FIGURE 38.13. Equipment used to
topicalize the airway prior to instrumentation: Tongue blade with lidocaine jelly, nebulizer with 4% lidocaine, and nasal dilators of various
sizes.
Central IV access may speed administration and time to onset
plus potentially deliver a more concentrated medication bolus
as compared to an equal dose administered through an IV on
the dorsum of the hand.
The practitioner has several choices for patient preparation: (a) awake with no medication; (b) awake with topical
anesthesia or local nerve blocks, and with or without light
sedation; (c) sedation/analgesia only with the option of neuromuscular blocker use; and (d) a set induction regimen for a
rapid sequence intubation (e.g., etomidate and succinylcholine)
(41,77,84,85). Faced with a variety of preparation choices and
a wide breadth of patient circumstances, the critical care physician will need to decide what approach to pursue based on
the medical, surgical, and airway situation; the patient’s needs
and level of tolerance, balanced by the practitioner’s judgment; and access to and experience with airway equipment
(41,44,45,84,85).
Awake Intubation
Awake intubation techniques comprise both nasal and oral
routes and, most often, involve topically applied local anesthetics (Fig. 38.13) or local nerve blocks. Conversely, if the
patient’s mental status and response to oropharyngeal stimulation are depressed, no medication may be needed to accomplish intubation. The application of topical anesthesia and
a local nerve block requires more time and effort, expanded
access to such agents and equipment, more patience, and finesse combined with a broader familiarity of head and neck
anatomy (24,86). If done properly, the patient’s airway may
be managed with nearly all conventional and accessory devices with the exception of the Combitube. Practitioners may
prefer to maintain spontaneous ventilation during emergency
airway management by avoiding excessive sedative-hypnotic
agents and/or muscle relaxants (87). Light sedation and analgesics, however, are typically administered despite the label
of being “awake.” Awake intubation techniques have been
largely supplanted by induction of unconsciousness or deep
sedation with or without muscle relaxation (87,88). Though
the “awake intubation” is an extremely useful approach, its
reduced utilization means that practitioners and their students
will be less comfortable with this method through lack of experience and confidence. Its subsequent use by less experienced
practitioners may complicate patient care due to poorly administered topical anesthesia, ineffective local nerve block techniques, and the lack of judicious and creative sedative/analgesic
measures.
Awake intubation may benefit from the addition of a narcotic agent by providing analgesia, antitussive action, and better hemodynamic control. Many reserve an awake approach
for the known or suspected difficult airway to avoid “burning
any bridges” and for those with severe cardiopulmonary compromise, pre-existing unconsciousness, or marked mental or
neurologic depression. However, if the patient is a poor candidate for an awake approach, or preparation for an awake approach is suboptimal, patient injury and difficult management
may still ensue since an awake approach does not guarantee
successful intubation nor is it devoid of morbidity or mortality
(89–91).
Following proper preparation, unless the patient is unconscious or has markedly depressed mental status, the “awake
look” technique incorporates conventional laryngoscopy to
evaluate the patient’s airway to gauge the feasibility and ease
of intubation (46); explanation to the patient (if applicable) is
imperative for cooperation. If viewing the airway structures
during an “awake look” proves fruitful, intubation should
be performed during the same laryngoscopic attempt either
directly—grade I or II view—or by bougie assistance—grade
I, II, or III—or by other means (92,93). Many “awake look”
procedures that yield a reasonable view, but in which intubation is not performed, are followed by anesthetic induction with
the potential for a worse view due to airway tissue collapse and
obstruction by redundant tissue due to loss of pharyngeal tone.
Too often, patient comfort is placed well above patient safety.
The critically ill patient is often tolerant of bougie-assisted intubation (Fig. 38.14), supraglottic airway placement (e.g., LMA)
(Fig. 38.15), or the placement of specialty airway devices such
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
530
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
Single use bougie
Gum-elastic bougie
FIGURE 38.14. Array of tracheal “bougies” used to access the airway in difficult situations.
as the rigid fiberscopes following topical anesthetic application,
local nerve blocks, or even light sedation (24,93–96).
Sedated to Asleep Techniques
Titration of medication to provide amnesia, analgesia, anxiolysis, sedation, or a combination of these desirable effects with
the goal of providing comfort while preserving spontaneous
ventilation is possible (44,97). Muscle relaxants may be added
as an option if pharmacologic attempts to render the patient
accepting of airway manipulation prove suboptimal or unsatisfactory. Sedation and amnesia are mandatory when paralysis is induced (43,44,87,88). The variety of agents available
to render the patient accepting of airway manipulation and
ultimately tracheal intubation have been outlined previously.
Though more physical effort is required when spontaneous
ventilation is maintained, allowing continued respiratory efforts may assist the practitioner in navigating the ET successfully into the trachea by the appreciation of audible breaths
via the ET, coughing after intubation, ventilation bag expansion/contraction, vocalization with esophageal intubation, following the pathway of bubbles percolating around the other-
A
wise hidden glottis, or the “up and down” movement of secretions that may offer direction in the difficult-to-visualize
airway (43,44,76,87,88). Breath-holding, glottic closure,
laryngospasm, swallowing, biting, jaw clenching, and gagging
may contribute adversely to the intubation process, but most
of these are overcome with patience and the acceptance that
these are “signs of life.” In difficult situations, titration techniques that provide sedation/analgesia offer the opportunity
to abort such “signs of life” with the hope of returning the
patient to his or her previous state at a later time (30,63,64).
The “awake” approach is accomplished by the application of
topical local anesthetics and/or local nerve blocks or simply
proceeding without medication based on the concurrent suppression of mental status and gag reflexes.
Rapid Sequence Intubation
Rapid sequence intubation (RSI) refers to the administration
of an induction agent followed by a neuromuscular blocking agent, with the goal of hastening the time needed to induce unconsciousness and muscle paralysis based on a concern for aspiration of orogastric secretions. By minimizing the
B
FIGURE 38.15. Laryngeal mask airways for emergent/difficult intubation. A: The intubating laryngeal
mask airway (LMA). B: Various sized LMAs for patients of different sizes and ages.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
time the airway is unprotected, the risk of aspiration theoretically should be reduced. Preoxygenation is paramount since
oxygenation/ventilation efforts via a bag-mask during the induction process are not typically carried out, thus hypothetically avoiding esophagogastric insufflation (41,98,99). Cricoid
pressure is applied, in theory, to reduce the risk of passive regurgitation of any stomach contents (29). These practices during an RSI may not always be practical nor able to be carried
out, since patients do desaturate during the apneic phase of
the RSI, particularly in obesity, pregnancy, poor or suboptimal preoxygenation efforts or the presence of cardiopulmonary
pathology.
If needed, bag-mask support should be delivered despite the
concern about esophagogastric insufflation and subsequent regurgitation/aspiration. Additionally, the application of cricoid
pressure—both quantitative and qualitative—is so variable
that concerns with its ubiquitous use and overall effectiveness
have been raised (100–104). Cricoid pressure may actually improve or worsen the laryngoscopic view, plus impede mask
ventilation; hence, adjustment or release of cricoid pressure
should be considered in these circumstances. Further, cricoid
pressure may alter the ability to place accessory devices, such
as the LMA, and impede fiberoptic viewing (105–108). Despite these potential limitations of cricoid pressure, no desaturating patient—high risk for aspiration or not—should have
bag-mask ventilation support withheld because of the fear of
aspiration.
When performing an RSI or, for that matter, any induction
method involving a neuromuscular blocking agent, an understanding of ventilation, and intubation options in the event conventional methods fail, and a preplanned strategy to assist the
patient must be in place prior to induction. The development
of such strategies during a crisis is difficult, often short-sighted
and incomplete, and may be counterproductive and destructive
to patient care. Education, training, and immediate access to
airway rescue equipment that the practitioner can competently
incorporate in an airway crisis is a goal worthy of expanded
effort, time, and finances (30,41,43,45,46,63,64).
The proponents of rapidly controlling the airway using RSI
cite a reduction in the risk of aspiration as a main thrust for
this technique. Moreover, an RSI is said to be associated with a
lower incidence of complications and higher first-pass intubation success rate as compared to the “sedation only” method
(41,43,98,99). A predetermined induction regimen, such as
etomidate and succinylcholine, is popular, easy to teach and
replicate, easy to administer (e.g., 0.25 mg/kg IBW etomidate and 0.25 mg/kg IBW of succinylcholine), requires little
planning or forethought, can be standardized, and, most importantly, generally works well for most critically ill patients.
Though the standard dosing regimen of succinylcholine is 1 to
1.5 mg/kg, the authors find that a variety of doses may fit the
needs of the operator. One should consider that the higher the
dose administered, the longer the duration to recover (patientinitiated spontaneous ventilation).
Nevertheless, it appears that this approach is so commonly
practiced by some individuals that it becomes the chosen induction regimen, with little regard for the patient’s individual
clinical condition and airway status. Several authors tout nearperfect success rates with RSI coupled with a minimum number
of complications (41,43,98,99). This “slam-dunk” approach
may not be the best for a significant number of the critically
ill patients, namely the obese, the known or suspected diffi-
531
cult airway patient, the hemodynamically unstable patient, or
those with significant cardiopulmonary compromise, such as
pulmonary embolism, cardiac tamponade, and/or myocardial
ischemia. Though there is little argument that many intubations
may be made easier by the administration of a muscle relaxant,
selective use based on the patient evaluation and clinical circumstances is the best option (30,44–46,63,64,70,72,87,88).
Positioning the Patient
One of the most important factors in improving the success
rate of orotracheal intubation is positioning the patient properly (Fig. 38.3). Classically, the sniffing position, namely cervical flexion combined with atlanto-occipital extension, will
assist in improving the line of sight of the intubator. Bringing the three axes into alignment (oral, pharyngeal, and laryngeal) is commonly optimized by placing a firm towel or
pillow beneath the head (providing mild cervical flexion) combined with physical backward movement of the head at the
atlanto-occipital joint via manual extension. This, when combined with oral laryngoscopy, will improve the “line of sight”
for the intubator to better visualize the laryngeal structures in
most patients (46). Optimizing bed position is imperative, as
is the angle at which the patient lies on the bed. The variety of
mattress material (air, water, foam, gel) provides a challenge to
the practitioner since these mattresses may worsen positioning
characteristics in an emergency setting. Optimizing the position
of the obese (Fig. 38.12, left panel) patient is an absolute requirement to assist with (a) spontaneous ventilation and mask
ventilation; (b) opening the mouth; (c) gaining access to the
neck for cricoid application, manipulation of laryngeal structures, or invasive procedures; (d) improving the “line of sight”
with laryngoscopy; and (e) prolonging oxygen saturation after induction (109–113). A ramp is constructed with blankets,
a preformed wedge, or angulation of the mechanical bed to
bring the ear and the sternal notch into alignment by ramping
the patient’s head, shoulders, and upper torso, thus facilitating
spontaneous ventilation, mask ventilation, and laryngoscopy.
The extra time spent to properly position the patient will reap
great benefits (77,110,113).
Blade Use
The Curved Blade. Following opening of the mouth, either by
the extraoral technique (finger pressing downward on chin) or
the intraoral method (the finger scissor technique to spread the
dentition), the laryngoscope blade is introduced at the right
side of the mouth and advanced to the midline, displacing
the tongue to the left. The epiglottis is seen at the base of the
tongue and the tip of the blade inserted into the vallecula. If the
oropharynx is dry, lubricating the blade is helpful; otherwise,
suctioning out excessive secretions may assist greatly in visualizing airway structures. The laryngoscope blade should be
lifted toward an imaginary point in the corner of the wall opposite the patient to avoid using the upper teeth as a fulcrum for
the laryngoscope blade. Moreover, a forward and upward lift
of the laryngoscope and blade stretches the hyoepiglottic ligament, thus folding the epiglottis upward and further exposing
the glottis. As a result, the larynx is suspended on the tip of the
blade by the hyoid bone. The practitioner’s right hand, prior
to picking up the ET, should be used to apply external pressure on the laryngeal cartilage (thyroid cartilage) to potentially
afford better visualization of the glottis. OELM (Fig. 38.8),
as this maneuver is called, is optimized and turned over to an
11:53
P1: OSO/OVY
GRBT291-37-39
532
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
assistant who attempts to replicate the optimal position for the
operator’s viewing. This description, while obviously optimal,
is not always feasible.
With visualization of the glottic structures, the ET is passed
to the right of the laryngoscope through the glottis into the
trachea until the cuff passes 2 to 3 cm beyond the vocal cords.
As described earlier, a Lehane-Cormack grade II or III airway
may preclude easy placement of the tracheal tube. Thus, a
blind guide underneath the epiglottis (tracheal tube introducer,
bougie) or a rigid fiberoptic stylet may be incorporated to improve the insertion success rate.
The Straight Blade. Intubation with a straight blade involves
the same maneuvers but with one major difference. The blade
is slipped beneath the epiglottis, and exposure of the larynx
is accomplished by an upward and forward lift at a 45-degree
angle toward the corner of the wall opposite the patient. Again,
leverage must not be applied against the upper teeth.
With either technique, the common causes of failure to intubate include inadequate position of the head, misplacement of
the laryngoscope blade, inadequate muscle relaxation, insufficient depth of sedation/analgesia or general anesthesia, obscuring of the glottis by the tongue, and lack of familiarity with
the anatomy, especially where pathologic changes are present.
Inserting a laryngoscope blade too deeply, usually past the larynx and into the cricopharyngeal area, results in lifting of the
entire larynx. If familiar landmarks are not appreciated, stop
advancing the scope, withdraw the blade, and start over. If
more than 30 seconds have passed or there is evidence that
the oxygen saturation has dropped from the prelaryngoscopy
level, bag-mask support to reoxygenate the patient is imperative. There is now evidence that repetitive laryngoscopies are
not in the best interest of patient care and may place the patient
at extreme risk for potentially life-threatening airway-related
complications (44,45). Unless the first one to two laryngoscopy
attempts were performed by less experienced members of the
team, attempts at conventional laryngoscopy alone to intubate
the trachea should be abandoned in favor of incorporating an
airway adjunct to assist the clinician in hastening the process
of gaining airway control (30,44,45,63,64,114,115).
FIGURE 38.16. Magill forceps for manipulating the endotracheal tube
into the glottis. These come in several sizes.
a small-caliber tube (e.g., a 6.0-mm diameter in an individual
taller than about 69 inches), as the nasal tracheal tube may
end up as an elongated nasal trumpet, without entrance into
the trachea (116–118).
The method of intubation via the nasal approach is variable. It may be placed blindly during spontaneous ventilation,
combined with oral laryngoscopic assistance to aid with ET advancement utilizing Magill forceps (Fig. 38.16); utilize indirect
visualization through the nares via an optical stylet (Fig. 38.17)
or a flexible (Fig. 38.18) or rigid fiberscope (Fig. 38.19); or incorporate a lighted stylet (Fig. 38.20) for transillumination of
the laryngeal structures (78,119,120).
Technique
Nasotracheal Intubation
Nasotracheal intubation, once the mainstay approach in the
emergency setting, is still commonly used in oral and maxillofacial operative interventions, but less commonly in emergency situations outside the operating room. Nasotracheal intubation is an alternative to the oral route for patients with
trismus, mandibular fracture, a large tongue, or edema of the
oral cavity or oropharynx, and is a useful approach for the
spontaneously breathing patient who refuses to lie supine or
in the presence of excessive secretions. The presence of midfacial or posterior fossa trauma and coagulopathy are absolute
contraindications to this technique. Thus, it is best avoided in
patients with a basilar skull fracture, a fractured nose, or nasal
obstruction. It is also contraindicated in the presence of acute
sinusitis or mastoiditis. Additionally, as the nasal portal dictates a smaller-diameter tracheal tube, it must be remembered
that as downsizing takes place, the length of the tracheal tube is
shortened; hence, the length must be considered when placing
The patient may be prepared for the nasal approach by pretreatment of the mucosa of both nostrils with a solution
of 0.1% phenylephrine and a decongestant spray such as
FIGURE 38.17. An optical stylet, allowing visualization of the glottis
as the endotracheal tube is advanced.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
533
Bronchoscope
Video-monitor
Bronchoscope-mounted
camera. Actual device
is to left
Light source
Video-capture
device
FIGURE 38.18. A fiberoptic bronchoscope with associated cart as used at Shands Hospital at the University of Florida.
oxymetazoline for 3 to 10 minutes. This is followed by progressive dilation, starting with either a 26 French or 28 French
nasal trumpet, and progressing to a 30 French to 32 French
trumpet lubricated with 2% lidocaine jelly (Fig. 38.13). The
method is relatively expedient. Conversely, placement of cotton pledgets soaked in a mixture of vasoconstrictor agent and
local anesthetic is equally effective if one is experienced with
the nasal anatomy and the proper equipment is available. Sup-
plemental oxygen may be provided by nasal cannulae placed
between the lips or via a face mask. The patient is best intubated
with spontaneous ventilation maintained, yet incremental sedation/analgesia may be provided to optimize patient comfort
and cooperation. Sitting upright has the advantage of maximizing the oropharyngeal diameter (116,121).
Orientation of the tracheal tube bevel is important for patient comfort and to reduce the risk of epistaxis and tearing or
11:53
P1: OSO/OVY
GRBT291-37-39
534
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 30, 2008
Section III: Techniques, Procedures, and Treatments
FIGURE 38.19. A rigid bronchoscope.
dislocation of the nasal turbinates. On either side of the nose,
the bevel should face the turbinate (away from the septum).
Due to bevel orientation, the tracheal tube’s manufactured
curve (concavity) may be facing posterior “toward the patient’s
face” (left nares) or anterior (right nares); once the ET reaches
the nasopharynx, the concavity of the tube should face posteriorly.
In the ICU setting, this approach may be helpful in those
with restricted cervical spine motion, trismus, and oral cavity
swelling/obstruction, to name but a few conditions of interest.
Awake, sitting upright with spontaneous ventilation is an ideal
setting for nasal intubation. The blind approach is best accomplished with ventilation preserved. Topically applied local
anesthetics, local nerve blocks, and judicious sedation and analgesia supplement the awake approach. Warming the tracheal
tube combined with generous lubrication will assist rotation
and advancement while providing a soft and pliable airway
Airway lightwand. The
ET slips over the wand,
with the light at
the tip of the ET. It is held
in position by the
“stop” (arrow).
to reduce injury to the nasal mucosa or turbinates. Tube advancement should be slow and gentle, with rotation when resistance is encountered. Excessive force, rough maneuvers, poor
lubrication, and use of force against an obstruction should be
discouraged. If advancement is met with resistance from glottic/anterior tissues, helpful maneuvers to overcome these obstacles include sitting the patient upright, flexing the head forward on the neck, and manually pulling the larynx anteriorly.
Conversely, if advancement is met with posterior displacement
into the esophagus, sitting the patient upright, extending the
head on the neck, and applying posterior-directed pressure on
the thyrocricoid complex may assist in intubation. Rotation
of the tube and manual depression or elevation of the larynx
may be required to succeed. Voluntary or hypercapnic-induced
hyperpnea helps if the patient is awake because maximal abduction of the cords is present during inspiration. Entry into
the trachea is signified by consistent breath sounds transmitted by the tube and inability to speak if the patient is breathing, as well as by lack of resistance, often accompanied by
cough. Often one can then feel the inflation of the tracheal cuff
below the larynx and above the manubrium sterni, followed
by connecting the tube to the rebreathing system and expanding the lungs (122). Confirmation with end-tidal CO2 measurement or fiberoptic viewing is imperative. Application of a
specially designed airway “whistle” that assists the clinician
with spontaneous ventilation intubation may be advantageous
(123).
Nasotracheal intubation may also be accomplished with
fiberoptic assistance. When the blind approach is met with
difficulty, the fiberoptic adjunct may expedite intubation, but
may be of limited assistance if secretion control is poor or if
relied upon as a salvage method following nasal trauma. However, use of a fiberoptic bronchoscope is an excellent choice
for the primary nasal approach with the patient sitting upright and the intubator preferentially standing in front or to
the side of the patient as opposed to “over the top” (124,125).
Advancement of the ET into the glottis may be impeded by
hang-up on the laryngeal structures: The vocal cord, the posterior glottis, or, typically, the right arytenoid (126,127). When
resistance is met, a helpful tip is as follows: withdrawing the
tube 1 to 2 cm, rotate the tube counterclockwise 90 degrees,
then readvance with the bevel facing posteriorly (126,127).
Matching the tracheal tube to the fiberscope to minimize the
gap between the internal diameter of the tube and the scope
may also improve advancement (126). Tracheal confirmation
and tip positioning are added advantages to fiberoptic-assisted
intubation.
Complications of Nasal Intubation
FIGURE 38.20. A lighted stylet (Lightwand) for blind insertion of
an endotracheal tube. Utilization of this technique requires significant
practice.
Though the nasally placed ET has the advantage of overall stability, the nasal approach has decreased in popularity due to
a restriction of tube size, the potential to add epistaxis to an
already tenuous airway situation, the potential for sinus obstruction and infection beyond 48 hours, nasal tissue damage,
and perceived discomfort during insertion. Nasotracheal intubation can cause avulsion of the turbinate bone when the tube
engages the anterior end of the middle turbinate’s lateral attachment in the nose and forces the avulsed turbinate into the
nasopharynx (116–118,128,129). Additionally, prolonged nasotracheal intubation may contribute to sinusitis, ulceration,
and tissue breakdown (117,130,131).
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
INTUBATION ADJUNCTS
Indirect Visualization of the Airway
Fiberoptic Bronchoscopy
There is an immense amount of interest in advancing airway
management well beyond simply placing a laryngoscope blade
into the oropharynx in the hopes that tracheal intubation can
be quickly and easily accomplished. It is the critically ill ICU patient who precisely would benefit from improving the “line of
sight,” a straight line from the operator’s eyes to the level of the
glottic opening (71,72,80,132). Being able to see “around the
corner” is immensely important when one’s goal is to minimize
intubation attempts and hasten the time to securing the airway
(74,77–79,83). Flexible bronchoscopy is the gold standard in
indirect visualization of the airway. Its role in the critically ill
ICU patient is as broad as it is adaptable to various clinical scenarios, and serves many life-saving roles, both diagnostic and
therapeutic. Flexible bronchoscopy does require expertise and
patience and may be limited by secretions and edema (124). Its
role in tracheal intubation in the critically ill patient probably
best lies in its use as a first-line technique (124), rather than
as a rescue technique (26,115,132,133) (Table 38.4). Edema,
secretions, and bleeding often complicate visualization of the
airway following multiple failed conventional laryngoscopies,
thus leaving fiberoptic capabilities limited.
Incorporating a portable TV monitor to broadcast the
fiberoptic view (Fig. 38.18) to the airway team is an excellent
teaching modality, plus it allows input by other team members
to optimize communication, positioning, and other maneuvers
to hasten the intubation process (124,134). Fiberoptic intubation effectiveness is reduced by inadequate patient preparation
(e.g., topical local anesthesia application when mucosal desiccation or excessive secretions are present, or excessive sedation
in an attempt to counter poorly functioning topical anesthesia
coverage or inadequate local anesthesia blocks). An inexperienced practitioner, one of the prime reasons for failure or
suboptimal or no assistance (hence the inability to provide adequate jaw thrust or lingual retraction); improper choice of
equipment (using a pediatric-sized bronchoscope to place a 9.0
ET); and improper positioning (utilizing the supine approach
in a morbidly obese patient) all will impact negatively on success. An awake technique chosen in an uncooperative patient,
TA B L E 3 8 . 4
CLINICAL USES OF FIBEROPTIC BRONCHOSCOPY
IN THE INTENSIVE CARE UNIT
Primary tracheal intubation
Intubation adjunct for LMA-type airway device
Confirmation of intubation
Airway evaluation for extubation
ET/tracheostomy evaluation of position and patency
Diagnostic/therapeutic interventions for a cuff leak
Bronchial lavage for diagnostic/therapeutic reasons
ET exchange
LMA, laryngeal mask airway; ET, endotracheal tube.
535
TA B L E 3 8 . 5
KEYS TO FIBEROPTIC INTUBATION SUCCESS
Patient preparation
Sedatives, narcotics, topical, local blocks, secretion control.
Is patient cooperative?
Is fiberoptic approach a reasonable choice for intubation?
Choice of approach
Oral vs. nasal
Position
Supine, upright, elevated head of bed
Choice of fiberoptic equipment
Diameter, pediatric vs. adult
Other
Adequacy of light source, lubrication, assistance, ET
warming capabilities, proper ET size
ET, endotracheal tube.
the lack of bronchoscope defogging, inadequate lubrication,
and poor judgment in the approach (e.g., a nasal fiberoptic approach in the face of a coagulopathy or nasofacial abnormalities, or a fiberoptic approach when patient has excessive, uncontrollable secretions or bleeding) further contribute to failure
and frustration. Inadequate patient preparation with medication (e.g., too light sedation leading to discomfort or an uncooperative patient, or excessive sedation leading to hypoventilation, airway obstruction, or excessive coughing or procedural
pain due to lack of narcotic administration) will place an undue
and likely uncorrectable burden on the fiberoptic technique.
Successful fiberoptic intubation is dependent on a wide
range of factors, each being performed in a timely manner (Table 38.5). Any single factor that is neglected or improperly executed may hamper the fiberoptic effort; hence, the practitioner’s
inexperience is a primary factor in both failures and difficulty
encountered. A properly prepared and positioned patient undergoing fiberoptic nasal intubation may become a challenge—
or the procedure may even fail—if too large an ET is chosen
to pass through the nasal cavity or when arytenoid hang-up is
encountered upon advancing the ET without counterclockwise
rotation (124).
Video-laryngoscopy and Rigid Fiberscopes
In an effort to overcome the difficulty of “seeing around the
corner,” various advancements have been made to the standard
laryngoscope. Though a difficult-to-visualize glottis is reported
to be uncommon (22), Kaplan et al. reported that direct laryngoscopy in a large cohort of elective general anesthesia patients
had a Lehane-Cormack view of III or IV in 14% despite maneuvers to optimize viewing with a curved laryngoscope blade
(71). The incidence of a grade III/IV view in the emergency intubation population is more than double this rate; hence the
need to improve visualization capabilities “around the corner”
(44,135).
The addition of optical fibers or mirrors plus design alterations have improved one’s line of sight over conventional blades. Devices such as the Bullard (20,22,76) (Fig.
38.21) and the Wu scopes (25,136–138) and the UpsherScope rigid fiberscopes (138) provide unparalleled visualization of the airway in most instances and may be particularly
11:53
P1: OSO/OVY
GRBT291-37-39
536
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
FIGURE 38.21. Bullard intubating laryngoscope.
understanding of their proper use, preparation, and restrictions, as well as practice on a normal airway before one ventures to use one in an emergency situation or a potentially
difficult airway.
A recent addition to advanced airway management is a disposable, low cost, J-shaped rigid optical laryngoscope utilizing
mirrors and lenses, and which offers a clear and panoramic
view of the glottic structures when placed midline in the lower
airway (143). The Airtraq laryngoscope (Fig. 38.22) is an excellent adjunct for tracheal intubation, for evaluating the difficult
airway for extubation, and for providing impressive indirect
viewing of the glottic structures of the difficult airway during ET exchange (144). For advancement into the airway, a
minimum amount of mouth opening must exist; its bulky dimensions may limit its use in the presence of a Halovest and
restricted mouth opening.
useful in the presence of restricted cervical mobility (18,74,75).
Each has an eyepiece for viewing via fiberoptic bundles for a
single operator but may be attached to a teaching video head
for team viewing and instruction (124,134). Video capabilities allow viewing on a television monitor, pushing videolaryngoscopy to a new and higher level of sophistication.
The Macintosh (curved) video-laryngoscope (Karl Storz Endoscopy) was developed and produced by modifying a standard laryngoscope to contain a small video camera (71,139).
Currently, improvements in video screen resolution, portable
power sources, and the refinement in optics have afforded a
new class of airway devices to assist in management of the difficult airway in the operating room, the ICU, and even remote
floor locations (78,135,137,140). Alterations of the curved
blade with an approximate 60-degree tip deflection separate
the GlideScope and McGrath scope from the others. Though
visualization is excellent, a principal observation to appreciate is that these instruments allow visualization, but they do
not perform intubation of the trachea. Visualization of structures with failure to intubate is uncommon (less than 4%)
(140,141), though various ET maneuvers and the use of a
bougie may overcome many of these failures (142). The effectiveness and efficiency of these advanced devices require an
Another class of intubation adjuncts that are very useful in
improving success in the difficult-to-visualize airway (LehaneCormack grade III/IV) is the fiberoptic tracheal tube introducer
or stylet. Typically fashioned like a stylet, the ET is loaded onto
the fiberoptic shaft and then the stylet is maneuvered into the
trachea. Visualization via an eyepiece on the scope or from a
video screen affords a view of the airway structures that would
otherwise remain restricted or blind (18,19,77,78,135). The
ability to navigate the ET-loaded stylet past airway structures
and visually confirm entrance into the trachea may hasten intubation in the difficult airway that otherwise would be considered difficult or impossible with conventional laryngoscopy
(77,135,145). Again, edema, secretions, mucosal swelling, and
limited mouth opening, as well as operator inexperience, may
limit visualization capabilities (135). Several manufacturers
produce relatively inexpensive hand-held rigid fiberoptic stylets
that facilitate “seeing around the corner”; hence, they can be
transported to the bedside in the ICU or to remote locations
throughout the hospital (77,78,135). The use of these devices
is improved by optimal positioning, lubrication, defogging,
warming the ET/scope, secretion control, and, above all, practice under controlled conditions prior to deployment in the
emergency setting (77,78,80,135).
Optical Stylets
FIGURE 38.22. The Airtraq laryngoscope.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
537
Tracheal Tube Introducer/Bougie
The tracheal tube introducer (TTI, or bougie) (Fig. 38.14) has
earned a position in anesthesia care as an effective airway adjunct by assisting navigation of the ET into the trachea when
anatomic constraints and/or an overhanging epiglottis limit the
view of the glottic opening. A grade II (arytenoids and posterior
cords only) or grade III laryngeal view (epiglottis only) is ideal
for bougie-assisted intubation (93,146). The TTI is listed as a
rescue option in national guidelines and should be included in a
difficult airway cart or portable bag (30,31,63,64). The advantages of the bougie include low cost, no power supply, portability, a rapid learning curve, minimal set-up time, and a relatively
high success rate and its immediate use reduces intubationrelated complications (93,146). Placement involves passing it
underneath the epiglottis with further navigation through the
glottis to a depth of 20 to 24 cm, with potential tactile feedback
as the curved tip bounces over the cartilaginous trachea rings.
The tracheal ring “clicks” may not be appreciated in all cases.
Further gentle advancement to 28 to 34 cm leads to the “hangup test” or Cheney test. This maneuver is useful not only for
bougie-assisted intubation itself, but also when ET verification
maneuvers and devices are imprecise or confusing. Passing the
ET is assisted by laryngoscopy to clear the airway of obstacles, lubricating the ET, and counterclockwise rotation to limit
arytenoid hang-up of the ET tip. The bougie’s role in difficult
airway management is underappreciated and, given its potentially prominent role as a simple “no frills” airway tool, more
attention to its position in an airway management strategy is
warranted (114,115,147).
CONFIRMATION OF TRACHEAL
INTUBATION
FIGURE 38.23. Disposable colorimetric CO2 detector. Yellow signifies the presence of CO2 , violet its absence.
Capnography
Physical Examination
Confirmation of ET location following intubation is imperative
to optimize patient safety (30,46,63,64,89,91,92,148,149). Indirect clinical indicators of intubation such as chest excursions,
breath sounds, tactile ET placement test, ET condensation, observing abdominal distension or auscultating the epigastrium,
and oxygen saturation monitoring are considered nonfail-safe
methods since each may be lacking, misinterpreted, or falsely
negative or positive in the elective setting, and this fallibility
is exaggerated in the emergency setting (149). Clinician interpretation of these and many other clinical findings in an
acutely ill patient in a noisy environment under adverse conditions is marginal at best (149). Even experienced personnel
are plagued by inadequacies of their interpretation and understanding (89,91,92). Nonetheless, and notwithstanding these
limitations, our practice for initial confirmation of ET placement is as follows:
1.
2.
3.
4.
5.
6.
Observation of the ET passing through the vocal cords
Chest rise with bagging
Presence of condensation upon exhalation
Absence of gurgling over the stomach
Presence of breath sounds over the lateral midhemithoraces
Presence of CO2 (Fig. 38.23)
To supplement the clinician’s skill of accurately assessing ET
location, the identification of exhaled CO2 via disposable colorimetric devices or capnography should be considered an accepted standard of practice for elective as well as out-of-theoperating-room intubation (30,46,148). Considered “almost
fail-safe,” these methods may fail due to a variety of causes,
namely the disposable colorimetric devices may fail in lowflow or no-flow cardiac states (no pulmonary blood flow as a
source of exhaled carbon dioxide), or the color change may
fail or confuse the clinician due to simple misinterpretation or
more commonly by soilage from secretions, pulmonary edema
fluid, or blood. Conversely, capnography may fail due to temperature alterations (outside, helicopter rescue), soilage of the
detector, battery or electrical failure, or equipment failure due
to age, missing accessories, or lack of maintenance.
Other Devices
Esophageal detector devices, either the syringe or the selfinflating bulb (Fig. 38.24) models, assist in the detection of
ET location based on the anatomic difference between the trachea (an air-filled column) and the esophagus (a closed and
collapsible column) (150). Applying a 60-mL syringe to the
11:53
P1: OSO/OVY
GRBT291-37-39
538
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 30, 2008
Section III: Techniques, Procedures, and Treatments
tures as compared to unrestricted advancement if the ET is in
the esophagus (153).
DEPTH OF ENDOTRACHEAL
TUBE INSERTION
FIGURE 38.24. Esophageal detector devices, either the syringe or the
self-inflating bulb models, assist in the detection of endotracheal tube
location based on the anatomic difference between the trachea (an airfilled column) and the esophagus (a closed and collapsible column).
Note that a 15 mm adaptor inserts onto the tip of the bulb syringe so
that the connection may be made.
ET and withdrawing air should collapse the esophagus, while
the trachea should remain patent. This concept was simplified by replacing the syringe with a self-inflating bulb that can
be attached to the ET following placement. Either compression of the bulb prior to attachment to the ET or following
attachment may still lead to false-negative results (no reinflation even though the ET is in the trachea) in less than 4%
of cases (150). Failures of this technique include ET soilage,
carinal or bronchial intubation in the obese, and those with severe pulmonary disease (chronic obstructive pulmonary disease
[COPD], bronchospasm, thick secretions, or aspiration), and
gastric insufflation. This technique is not affected by a low-flow
or arrest state and, hence, it may be useful when capnography
or colorimetric devices fail (150–152).
Two techniques considered infallible or fail-safe when used
under optimal conditions are extremely accurate in detecting and confirming ET position: (a) visualizing the ET within
the glottis and (b) fiberoptic visualization of tracheal/carinal
anatomy (46). However, the critically ill population may have
limited glottic visualization on laryngoscopy in up to 33% of
cases (44,135). Following intubation, visualization of laryngeal structures may be obscured due to the presence of the ET.
Likewise, fiberoptic visualization may be hampered by secretions and blood, as well as access to and the expertise to use
such equipment.
Cheney Test
A clinically useful adjunct for assisting in the verification of
the ET location includes the hang-up test, consisting of passing a bougie or similar catheterlike device for the purpose of
detecting tip impingement on the carinal or bronchial lumen.
Typically, gently advancing a bougie to 27 to 35 cm depth may
allow the practitioner to appreciate hang-up on distal struc-
Classic depth of insertion is height and gender based, as well
as impacted by the route of ET placement (i.e., oral vs. nasal)
and the patient’s intrinsic anatomy. The depth will vary with
head extension/flexion and lateral movement. Final tip position
is best at about 2 to 4 cm above the carina to limit irritation
with head movement and patient repositioning. Typically, the
height of the patient is most specific in determining ET tip
depth. ET depth in the adult patient less than or equal to 62
inches (157 cm) in height should be approximately 18 to 20
cm; otherwise, 22 to 26 cm may be the appropriate depth.
Chest radiography only determines the tip depth at the time
of film exposure. Fiberoptic depth assessment is the real-time
method that garners the most clinical data for diagnostic and
therapeutic purposes (123,154).
AMERICAN SOCIETY OF
ANESTHESIOLOGISTS PRACTICE
GUIDELINES
These guidelines and others specifically suggest that airway
management procedures should be accompanied by capnography or similar technology to reduce the incidence of unrecognized esophageal intubation, hypoxia, brain injury, and death
(30,63,64). We can think of no reason, in the economically advanced countries, why these recommendations would not be
followed.
AMERICAN SOCIETY OF
ANESTHESIOLOGISTS DIFFICULT
AIRWAY PRACTICE GUIDELINES
Though reviewed earlier in this chapter, the salient points of
the algorithm (Table 38.6) as they relate to the critically ill patient requiring emergency airway management are well worth
repeating. Preintubation evaluation in the hopes of recognizing the difficult airway is paramount, yet is meshed with the
understanding that the unrecognized or underappreciated difficult airway (mask ventilation, intubation, or both) occurs
frequently. Examination of the patient, however, may be restricted due to emergent conditions, and the medical record
may provide little to no useful data, especially when the patient previously had an easily managed airway but the airway
status has changed substantially. When difficulty is known or
predicted, patient preparation and access to airway equipment
become primary focal points. This is not the case with the unrecognized or underestimated difficult airway. The induction
technique is obviously not customized to the known difficulty;
hence, the practitioner must counter this “surprise” by a preplanned rescue strategy, immediate access to advanced airway
equipment, and personnel assistance combined with the expertise and competence to initiate and accomplish such a rescue
strategy (30,63,64).
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
TA B L E 3 8 . 6
AMERICAN SOCIETY OF ANESTHESIOLOGISTS DIFFICULT AIRWAY ALGORITHM
Source: http://www.asahq.org/publicationsAndServices/Difficult%20Airway.pdf.
539
11:53
P1: OSO/OVY
GRBT291-37-39
540
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
FIGURE 38.25. Large-bore IV catheter and tubing for emergency airway. This is useful for emergency jet
ventilation.
Primary questions for the practitioner when accessing the
patient are:
1. Is there a reasonable expectation for successful mask ventilation?
2. Is intubation of the trachea expected to be problematic?
3. Should the airway approach be nonsurgical or surgical?
4. Should an awake or a sedated/unconsciousness approach be
pursued?
5. Should spontaneous ventilation be maintained?
6. Should paralysis be pursued (30)?
With forethought and experience, these considerations may
be answered rapidly following patient assessment. Conversely,
a predetermined strategy that dictates an RSI “will be easy” to
pursue and thus requires minimal assessment, since the technique has been predestined rather than modeled around the
findings of the above considerations, is fraught with risk to the
patient (30,63,64).
patient deteriorates, prompting rapid intervention, the rescue
strategy must be pursued immediately (6,46,155,156).
Asleep Pathway
Following induction in the patient with a known or suspected
difficult airway who is uncooperative or agitated, or in the
unrecognized difficult airway, the ability to provide adequate
mask ventilation will determine the direction of management.
If mask ventilation is adequate but conventional intubation is
difficult, incorporating the nonemergency pathway is appropriate, utilizing the bougie, specialty blades, supraglottic airway, flexible or rigid fiberoptic technique, or surgical airway
(30,46). If mask ventilation is suboptimal or impossible, intubation of the trachea may be attempted, but immediate placement of a supraglottic airway such as the LMA is the treatment
of choice. When entering the emergent pathway, if the supraglottic device fails, then an extraglottic device such as the Combitube or similar device may be placed; otherwise, transtracheal
Awake Pathway
If difficulty is recognized, an awake approach may be appropriate, barring lack of cooperation or patient refusal and given
the practitioner’s familiarity with this approach. Patient preparation with an antisialogogue, assembling equipment and personnel, discussion with the patient, and optimal positioning
should be pursued unless the patient conditions dictate immediate awake intervention due to respiratory distress and hypoxemia. The awake choices, following optimal preparation, may
allow the practitioner to take an “awake look” with conventional laryngoscopy; utilize bougie-assisted intubation, LMA
insertion, or indirect fiberoptic techniques (rigid and flexible);
or proceed with a surgical airway. The Combitube would not be
indicated in the awake state. Access to the airway via cricothyroid membrane puncture via large-bore catheter insertion (Fig.
38.25A) with either modified tubing or a jet device (Fig.38.25B)
to ventilate, or Melker cricothyrotomy kit (Fig. 38.26) is an option prior to other awake or asleep methods, but is often forgotten and rarely executed. If the awake approach fails or the
FIGURE 38.26. The Melker cricothyrotomy kit for emergency subglottic access to the airway.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
TA B L E 3 8 . 7
STRATEGY FOR EMERGENCY AIRWAY
MANAGEMENT OF THE CRITICALLY ILL PATIENT
1. Conventional intubation—grade I or II view
2. Bougie—grade III view
a. May use for grade I and II if needed
3. LMA/supraglottic device—grade III or IV view
a. LMA/supraglottic rescue for bougie failure
b. Or use the LMA/supraglottic device as a primary device
(i.e., known difficult airway, cervical spine limitations,
Halo-vest)
4. Combitube—rescue device for any failure or as a primary
device if clinically appropriate
5. Fiberscope (optical/video-assisted rigid or flexible
models)—primary mode of intubation, an adjunct for
intubation via the LMA
LMA, laryngeal mask airway.
jet ventilation may be pursued by personnel knowledgeable
in its application and execution, or a surgical airway placed
(30,46).
A recently suggested strategy for emergency airway management of the critically ill patient outside the operating room
is shown in Table 38.7 (114,115). Patient care was compared
before (no immediate access to rescue equipment or ETCO2
monitoring) and after (immediate access to rescue equipment
and ETCO2 monitoring) the management strategy was in place.
A substantial improvement in patient care was realized with
the following strategy: Hypoxemia, defined as SpO2 <90%,
was reduced from 28% to 12%; severe hypoxemia, defined
as SpO2 <70%, was reduced by 50%; esophageal intubation
was reduced by 66%; multiple esophageal intubations were
reduced by 50%; regurgitation and aspiration were reduced
541
by 87%; and the rate of bradycardia fell by 60%. Any rescue
strategy, however, should be customized to the practitioner’s
skill level, his or her access to rescue equipment, and his or
her knowledge and competence of using such equipment (113,
114). Similar strategies have been used in the operating room
with an improved margin of safety for airway management
(84,85,147).
COMPLICATIONS RELATED TO
ACCESSING THE AIRWAY
Tracheal intubation is an important source of morbidity and,
occasionally, of mortality (30,43–46,89,91,92,148). Complications occur in four time periods: during intubation,
after placement, during extubation, and after extubation
(Table 38.8). Patients with smaller airways, especially infants
and children, have a higher incidence of complications, combined with an increased risk of upper airway obstruction secondary to glottic edema and subglottic stenosis.
Cuffed tube usage for prolonged intubation and artificial
ventilation substantially increases the rate of tracheal and laryngeal injury. The extent of injury is dependent on duration
of exposure, the presence of infected secretions, and severity of
respiratory failure. Cuff pressures above 25 to 35 mm Hg further add to risk by compressing tracheal capillaries, which predisposes to ischemic mucosal damage despite the high-volume,
low-pressure cuffs that are standard today (157–160). Other
factors of importance include the duration of intubation, reintubation, and route of intubation, with nasal intubation producing more complications than oral; patient-initiated selfextubation; excessive tracheal tube movement; trauma during
procedures; and poor tube care. As one might expect, clinicians
unskilled in intubation techniques increase the complication
rate.
TA B L E 3 8 . 8
RISKS OF TRACHEAL INTUBATION
Time
Tissue injury
Mechanical problems
Other
Tube placement
Corneal abrasion; nasal polyp
dislodgement; bruise/laceration
of lips/tongue; tooth extraction;
retropharyngeal perforation;
vocal cord tear; cervical spine
subluxation or fracture;
hemorrhage; turbinate bone
avulsion
Tear/abrasion of larynx, trachea,
bronchi
Esophageal/endobronchial
intubation; delay in
cardiopulmonary
resuscitation; ET
obstruction; accidental
extubation
Dysrhythmia; pulmonary
aspiration; hypertension;
hypotension; cardiac arrest
Airway obstruction; proximal
or distal migration of ET;
complete or partial
extubation; cuff leak
Tear/abrasion of larynx, trachea,
bronchi
Difficult extubation; airway
obstruction from blood,
foreign bodies, dentures, or
throat packs
Bacterial infection (secondary);
gastric aspiration; paranasal
sinusitis; problems related to
mechanical ventilation (e.g.,
pulmonary barotrauma)
Pulmonary aspiration; laryngeal
edema; laryngospasm;
tracheomalacia; intolerance of
extubated state
Tube in place
Extubation
ET, endotracheal tube.
11:53
P1: OSO/OVY
GRBT291-37-39
542
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
Airway-related Complications
During Intubation
Trauma
Tracheal intubation dangers begin at the time of initial tube
insertion. Direct airway trauma depends on operator skill and
the degree of difficulty encountered during intubation (27). Injuries include bruised or lacerated lips and tongue, inadvertent tooth extraction, upper airway hemorrhage, vocal cord
tears, and nasal polyp dislodgement. Inadvertent contact of
the cornea by the operator’s hand may cause a corneal abrasion. Nasopharyngeal mucosa perforation can create a false
passage, whereas a tear in the pyriform fossa mucosal lining
may lead to mediastinal emphysema, tension pneumothorax,
and infectious complications (27,89,91,92). Fracture or subluxation of the cervical spine, though rare, may result from
careless movement of the head or forceful hyperextension during attempts to improve laryngeal exposure (18). Laryngoscopy
may lead to swelling, edema, and bleeding of the oropharyngolaryngeal complex. Pre-existing edema or a coagulopathy
will only exaggerate further swelling and bleeding. Continued efforts to control the airway with conventional laryngoscopic attempts may prove detrimental if supraglottic-glottic
edema/swelling/closure results from repetitive trauma. Accessory devices such as the LMA and Combitube are dependent
on a patent glottic opening; thus, exacerbating tissue damage
with repetitive attempts may reduce rescue success with these
devices (46).
Delay
Excessive delay in cardiopulmonary resuscitation may occur
while an inexperienced practitioner tries to visualize the vocal cords. If intubation cannot be accomplished within 30 seconds, a more experienced person should make the attempt
whenever possible. Multiple intubation attempts by any practitioner, unskilled or skilled, may make subsequent attempts
more problematic and markedly increase the risk of hypoxemia, esophageal intubation, regurgitation, aspiration, bradycardia, cardiovascular collapse, and arrest (44–46). If effective
mask ventilation and oxygen delivery are not possible during
cardiopulmonary resuscitation (CPR), then prompt placement
of an accessory device (LMA, Combitube) to support ventilation and oxygenation should be pursued (30,46,63,64). The
LMA may assist with tracheal intubation itself and/or support
ventilation and oxygenation in lieu of intubation.
Airway-related complications in the emergency setting are
similar in variety but outflank their elective counterpart in
magnitude, occurrence, and consequence. Excessive secretions,
edema, and bleeding, especially from repetitive instrumentation, may plague these interventions. The incidences of laryngospasm, bronchospasm, bleeding, tissue trauma, aspiration,
inadequate ventilation, and difficult intubation remain relatively poorly documented.
Hypoxemia. Hypoxemia during emergency intubation has a
variable incidence, ranging from 2% to 28% (12,44,89,90,
140,161–163). Currently, there is little specific literature reporting the influence of age, comorbid conditions, and pathologic states on the incidence of hypoxemia during emergency
airway management, yet the risk increases as the patient’s clinical situation worsens (Table 38.9) (70,163). Moreover, the patient’s oxygenation reserves, obesity-related pulmonary limitations, and difficulty with airway management will influence the
incidence of hypoxemia (112,164–167).
Hypoxemia-related concerns for emergency airway management include:
1. The limits of preoxygenation in the critically ill
2. The increased incidence of multiple intubation attempts
3. The increased incidence of encountering a “difficult airway”
in the emergency setting (30,44,45,72,85,90)
Esophageal Intubation. Delayed recognition of esophageal intubation (EI) is a leading adverse event contributing to hypoxemia, aspiration, central neurologic system damage, and
death (27,30,89–92,148,149). Failure to recognize EI is not
limited to inexperienced trainees and, despite the use of verification devices, EI-related catastrophes persist (88,90,91). Indirect
clinical signs of detecting tracheal tube location are imprecise
and their interpretation is further restricted under emergent circumstances (Fig. 38.27) (46,89,91,149). Curbing the ill effects
of EI by vigilant monitoring and rapid detection is warranted
(148,149). Viewing the tube between the vocal cords, considered fail-safe, is impractical in 10% to 30% of patients due to
anatomic limitations (44,168). Fiberoptic verification is failsafe, yet is limited by blood and secretions, the operator’s skill,
and equipment access (124).
Regurgitation and Aspiration. Perioperative pulmonary aspiration is uncommon, occurring in approximately 1 in every 2,600 cases, but is magnified in the emergency surgical
TA B L E 3 8 . 9
AIRWAY COMPLICATIONS CONTRIBUTING TO HYPOXEMIA
Esophageal intubation
Mainstem bronchial intubation
Inadequate or no preoxygenation
Failure to “reoxygenate” between attempts
Tracheal tube occlusion: Biting, angulation
Tracheal tube obstruction after intubation
Due to:
Particulate matter
Blood clots
Thick, tenacious secretions
Regurgitation/aspiration
Multiple attempts
Duration of laryngoscopy attempt
Airway obstruction, unable to ventilate
Accidental extubation after intubation
Bronchospasm, coughing, bucking
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
543
30%
20%
10%
0%
Regurgitation
Aspiration
Bradycardia
Non-EI
Dysrhythmia
Cardiac Arrest
EI
FIGURE 38.27. Incidence of complications with (EI) and without (non-EI, i.e., tracheal intubation)
esophageal intubation detected by indirect clinical signs. (From Mort TC. Esophageal intubation with
indirect clinical tests during emergency tracheal intubation: a report on patient morbidity. J Clin Anesth.
2005;17[4]:255.)
setting (169). Regurgitation during emergency intubation
varies widely, ranging between 1.6% and 8.5%, with aspiration of the regurgitated material ranging between 0.4% and 5%
(44,45,90,170). Emergently, there is little control over NPO
status, ileus, upper gastrointestinal bleeding, or altered airway
reflexes. Hypoxemia, bradycardia, and arrest may be magnified during regurgitation/aspiration (44,45,84,170). Immediate access to, and use of, accessory devices and ET-placement
verifying equipment has reduced regurgitation and aspiration
by 43% and 75%, respectively (148,149). Upper gastrointestinal bleeding is particularly risky, as it increases regurgitation
by a factor of 4 and aspiration by a factor of 7 when compared to nonbleeding patients undergoing emergency intubation (95,171).
Airway Injury. The “airway” may sustain minor, nondisabling
to catastrophic, life-threatening degrees of trauma during emergency intubation unbeknown to the practitioner. Difficult intubation is a factor in many, but not all, cases; for example,
in several series, 50% of intubations resulting in esophageal
perforations were believed to have been atraumatic intubations (27,89,91,92). Injury, shrouded by generalized nonspecific signs and symptoms combined with sedated, intubated
patients unable to communicate, may limit the consideration
of any injury (27,92). Pneumothorax, subcutaneous emphysema, pneumomediastinum, dysphasia, chest pain, coughing,
or deep cervical pain advancing to a febrile state should be
investigated (27,92).
Bronchial Intubation. Undetected bronchial intubation discovered by a postintubation chest radiograph is common,
being seen in between 3.5% and 15.5% of cases. This
undetected event increases substantially following difficult
intubation, often leading to hypoxemia, atelectasis, bronchospasm, lobar collapse, and barotrauma if left uncorrected
(44,45,172–176). Lung auscultation and palpation of the
inflated cuff above the sternal notch may decrease bronchial
intubation or carinal impingement, but are not fail-safe (122).
Fiberoptic evaluation is definitive; thus, access to this modality
in the ICU is important to allow for investigation of any
unexplained oxygen desaturation, coughing, bronchospasm,
or changes in peak inspiratory pressures, or an abrupt or
gradual reduction in tidal volume (174–178).
Multiple Intubation Attempts. National guidelines define a difficult intubation as the inability to intubate within three attempts, at which point alternative airway techniques should
be incorporated (30). Repeated interventions increase tissue
trauma, bleeding, and edema, and may transform a “ventilatable” airway to one that is not (44–46). The number of laryngoscopic attempts directly increases complications, increasing
with the second laryngoscopic attempt and accelerating rapidly
with three or more attempts (44,45). All critically ill patients
who require emergency airway management likely should be
regarded as a potentially unanticipated difficult airway. Hence,
observing the one or two attempts “rule” under “optimal conditions” before rapidly moving to an alternative strategy is prudent (27,43–46,85).
Though the literature has recommended a rapid sequence
intubation technique as the definitive method of patient preparation, airways are as individual as their owners, and practitioner skills are variable. Thus, patients may benefit from an
individualized approach (41,97,98). Incorporating a strategy
that is adaptable to the practitioner and the patient (and his
or her airway) may lead to a lower incidence of complications
(27,44,45,85–88,114,115).
After Intubation
Acute Endotracheal Tube Obstruction
Following Intubation
Acute ET obstruction has a differential diagnostic list that is
long but, in most cases, can be discerned rapidly. Biting may be
from an awake, agitated, or delirious patient or, on the other
11:53
P1: OSO/OVY
GRBT291-37-39
544
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
The incidence of such events is not precisely known, but
the most devastating consequence of such airway obstruction,
hypoxia-driven cardiac arrest, was noted in the Hartford Hospital database (5 arrests in over 3,000 emergently intubated patients, 0.17%) (148). One of us (TCM) with an airway database
composed of over 1,800 patients who underwent primary tracheal intubation or ET exchange over a 16-year period has
noted acute airway obstruction leading to arrest in four cases
(0.2%) and near arrest (severe desaturation, bradycardia) in 16
cases (0.9%). Swift suction removal following irrigation of the
tracheobronchial tree, ET removal, or fiberoptic evacuation of
the obstruction was paramount in limiting patient injury.
Bradycardia
FIGURE 38.28. Obstruction of the endotracheal tube by intraluminal
material, in this case, a bloody mucous plug.
hand, the ET tip may abut the tracheal wall. A bite block in
the patient’s mouth, additional sedation/analgesic agents, or
slight rotation of the tube may correct the obstruction. Kinking of the tube or herniation of the cuff can occlude the airway and compromise ventilation, as can blood clots, tissue,
dried secretions, tube lubricants, and foreign bodies. Partial or
complete obstruction (Fig. 38.28) of a newly placed ET or tracheostomy tube by intraluminal or extraluminal sources may
present as a life-threatening emergency requiring immediate
corrective measures to reduce the risk of hypoxia-related morbidity and mortality (155,179).
Signs of ET or tracheobronchial obstruction are high inflation pressures, absent or impaired chest excursion, marked respiratory effort with paradoxical movement, cyanosis, hypoxemia, and venous congestion. Acute severe bronchospasm following primary tracheal intubation or during a tube exchange
may mimic acute obstruction.
The rescue therapy differs between the in situ ET
obstruction—depending upon its degree—and obstruction distal to the ET tip. Rapid removal of a completely obstructed ET
may be life saving and, conversely, partial obstruction of the ET
or tracheobronchial tree by inspissated mucus, blood, or tissue
may require rapid irrigation and suctioning, either blindly via
a suction catheter or utilizing a fiberoptic bronchoscope.
The etiology of the airway obstruction following intubation
in the emergency setting in the ICU is often related to thick
secretions. The patient undergoing emergency tracheal intubation may require mechanical support based on respiratory
insufficiency due to poor secretion-clearing capabilities, poor
cough, retained secretions, and shallow respirations. Once the
trachea is intubated and positive pressure is delivered, the retained and dormant secretions mobilize more proximally toward the upper tracheobronchial tree, potentially contributing to airway obstruction. Conversely, during an ET exchange
in a patient maintained on positive end-expiratory pressure
(PEEP), especially when the level is approximately 8 cm H2 O
or above, the sudden loss of expiratory pressure during the
exchange appears to allow proximal movement of retained secretions, previously undetected or unreachable by standard ET
suction techniques, to rapidly migrate toward the tracheocarinal region, potentially leading to very difficult or impossible
ventilation.
The response to laryngoscopy intubation is typically hyperdynamic, but in a small number of patients, slowing of the
heart rate may accompany airway manipulation. Patients receiving medications which slow sinoatrial (SA) node, atrioventricular (AV) node, or ventricular conduction, in addition to
the aggressive use of fentanyl or other vagotonic medications,
may be at increased risk for a further slowing of the heart
rate. Preintubation bradycardia due to medication, an intrinsically slow heart rate in hypertensive disease of the elderly
and the physically fit, and occasionally severe hypoxemia or
the Cushing reflex in elevated intracranial pressure (ICP) may
place the patient at a lower threshold to experience bradycardia. Vigorous laryngoscopy and tracheal intubation, inadvertent EI, and airway-related complications with severe or prolonged hypoxemia have led to bradycardia and cardiac arrest
(44,45,148,149). Moreover, progressive bradycardia has been
noted to precede intraoperative cardiac arrests in the majority
of cases (146,148,180–182). Propofol’s role in bradycardia remains ill-defined, but may be more relevant in the ICU patient
on a continuous intravenous infusion rather than when using
the agent in a single dose for intubation.
Vagotonic influences related to airway manipulation and hypoxemia appear to be primary factors. While an uncomplicated
laryngoscopy may reduce the heart rate, airway-associated
complications during difficult laryngoscopy and intubation
with concurrent hypoxemia increase the incidence of bradycardia dramatically (148,170). The sympathetic outflow stimulated by a moderate reduction in oxygen tension may be overwhelmed by the parasympathetic influence with ongoing or
worsening hypoxemia, thus leading to medullary ischemia. In
addition, the drop in heart rate is typically associated with a significant reduction in blood pressure, often requiring aggressive
therapy. When confronted with bradycardia, it behooves the
practitioner to optimize oxygen delivery via the rapid deployment of accessory devices, call for the code cart, and provide
pharmacologic intervention as well as interventions for potentially catastrophic pathology such as a tension pneumothorax,
unrecognized esophageal intubation, or mainstem bronchus intubation.
Dysrhythmias
The acute onset of a new dysrhythmia during the manipulation of the airway or immediately after completion of securing
the airway is infrequently reported. Pre-existing rhythm disturbances may be exaggerated by even rapid, straightforward airway manipulation, but may pale in comparison to the response
initiated by a vigorous laryngoscopy, especially if it is associated with multiple attempts, inadequate sedation, or additional
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
myocardial compromise. Bradycardia (see above), supraventricular tachycardia, atrial fibrillation or flutter with a rapid
ventricular response, and ventricular disturbances are usually
poorly tolerated by the critically ill patient, often complicated
by varying degrees of hypotension. Further, succinylcholine—
often used in RSI—is a well-known causative factor in contributing to a multitude of atrial and ventricular rhythm disturbances. Ongoing myocardial injury or a prolonged, vigorous, or traumatic manipulation of the airway can potentiate
life-threatening dysrhythmias (44,183).
Cardiac Arrest
Anesthesia-related cardiac arrest in the operating room is relatively infrequent (0.01%), with the majority related to airway
mishaps/difficulties (146,180–182). The risk of cardiac arrest
in the ICU patient during emergency airway management may
be as high as 2% (44,45,148,170). Specific risk factors contributing to cardiac arrest during airway manipulation included
three or more intubation attempts, hypoxemia, regurgitation
with aspiration, bradycardia, and esophageal intubation, often with one or more of these complications cascading from
one to another (148,149). Nonairway-related cardiac arrests
may result from ET obstruction, tension pneumothoraces, massive pulmonary thromboembolism, induction medication, and
deterioration in patients suffering from acute myocardial infarction with cardiogenic shock (148). The varied list of etiologic factors that may contribute, singly or in combination, to
the risk of cardiopulmonary arrest and cardiovascular collapse
related to tracheal intubation is noted in Table 38.10 (170).
Immediate access and use of advanced airway equipment and
airway-placement verifying devices appear to have a significant
impact on the incidence of hypoxemia-driven cardiac arrest
(148).
545
The Hyperdynamic Response
to Airway Management
A brief or prolonged hyperdynamic response frequently accompanies direct laryngoscopy and intubation, and may reflect a
number of physiologic factors, including wakefulness; the magnitude, vigor, and extent of the airway manipulation; underlying hypertension and cardiovascular disease; intravascular volume status; underlying sympathetic outflow; any related renal
and cerebral pathology; induction medication; and the functional reserve of the patient among other clinical causes. Patients with central nervous system (CNS) pathology (stroke,
intracerebral hemorrhage, seizure disorder) will have a higher
likelihood of hypertension and/or tachycardia with airway
manipulation (184–186). A persistent hyperdynamic response
post intubation may reflect ongoing pain, anxiety, and/or wakefulness that may respond to additional anesthetic induction
agents, or may reflect an exaggerated response seen in the highrisk individual with diabetes mellitus, renal or cardiovascular
disease, or a CNS insult, and may also be seen in the intoxicated and the traumatized patient (184,185,187,188). Treatment with additional induction agents or vasodilators, diltiazem, or β antagonists may suffice, but overly aggressive treatment may quickly introduce further hemodynamic compromise
when the therapy outlasts the self-limited phase of postintubation hypertension (186,187). Pathologic conditions which dictate aggressive therapy include head injury, intracerebral bleed,
cerebral vascular accident, or seizure disorder.
Recognizable causes of an exaggerated hyperdynamic response may include balloon inflation, ET suctioning, mainstem
bronchial/carinal impingement, coughing, bucking, or “fighting” the ventilator. The aggressive administration of anesthesia induction agents is literally a double-edged sword: capable
of limiting the hyperdynamic response during airway manipulation but the quiescent, stimulation-free period that usually
follows securing the airway may lead to a sharp reduction in
the blood pressure (184,186).
TA B L E 3 8 . 1 0
FACTORS CONTRIBUTING TO POSTINTUBATION
HEMODYNAMIC INSTABILITY
Anesthetic medications
Sympathetic surge, vasovagal response
Excessive parasympathetic tone
Loss of spontaneous respirations
Positive pressure ventilation
Positive end-expiratory pressure (PEEP)
Auto- or intrinsic PEEP
Hyperventilation with pre-existing hypercarbia
Decrease in patient work
Underlying disease process (i.e., myocardial insufficiency)
Volume imbalances (sepsis, diuretics, hypovolemia,
hemorrhage)
Preload dependent physiology
Valvular heart disease, congestive heart failure, pulmonary
embolus, right ventricular failure, restrictive pericarditis,
cardiac tamponade
Hypoxia-related hemodynamic deterioration
Hyperkalemia-induced deterioration (succinylcholine)
Modified from Schwab TM, Greaves TH. Cardiac arrest as a possible
sequela of critical airway management and intubation. Am J Emerg
Med. 1998;16:609.
Hypotension
The incidence of postintubation hypotension in the emergency setting is the most common of the hemodynamic alterations stemming from a variety of single and multiple etiologies (44,45,148,189,190). Being mindful of the pre-existing
comorbidities and the current clinical deterioration prompting intubation, the airway manager’s judgment and experience will influence the medication choices and techniques to
prepare the patient for airway instrumentation. The major
challenge is to select the agents that will achieve the goal of
blunting, attenuating, or blocking the postlaryngoscopy hyperdynamic response, typically lasting for only a brief amount
of time, with minimal subsequent influence or contribution
to postintubation hypotension. Strategies are best tailored to
the individual patient’s needs based on the experience and
judgment of the airway manager rather than, as we have commented several times previously, a standard intubation protocol such as etomidate and succinylcholine being administered
to each and every patient (43,45). The addition of a neuromuscular blocking agent may impact the dosing of induction
agents and the subsequent need for vasoactive medications,
especially when blood pressure is maintained by agitation,
struggling, straining, and muscle contraction of the critically ill
patient.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
546
T1: OSO
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
The aggressive use of induction agents may potentiate the
reduction in blood pressure following airway manipulation,
particularly if no additional stimulation is provided post intubation. The institution of positive-pressure ventilation with
PEEP plus any vasodilatation and myocardial depression from
anesthetic agents may contribute to postintubation hypotension (189,190). This response is accentuated in incidence and
magnitude in the critically ill patient who is struggling with
underlying cardiopulmonary deterioration, acid-base imbalance, sepsis, hemorrhage, hypovolemia, and other maladies
(44,148,189,190). Postintubation hypotension may require
crystalloid resuscitation and/or a vasoactive agent such as
ephedrine, Neo-Synephrine, vasopressin, or norepinephrine.
Postintubation hypotension, per se, has not been studied in detail, though brief hypotension, in general, has been suggested as
a significant contributing factor to patient morbidity and poor
outcomes, especially in the traumatized and the neurologically
injured patient (191).
Published reports that mention postintubation hypotension
suggest that it is a rare occurrence despite the disposition of
the critically ill patient. For example, two emergency department studies of nearly 1,200 patients reported less than 0.3%
(four patients) developed hypotension (systolic less than 90
mm Hg) (98,99). Conversely, emergency intubation outside
the operating room—including the emergency department—
by anesthesiologists reported that four of every ten patients
suffered hypotension requiring vasoactive medications to supplement crystalloid administration in one half of the victims
(44,45,148). Nonetheless, the extent and degree of hypotension will be influenced by the induction agent, volume status,
pre-existing comorbidities, and reason for the clinical deterioration, plus numerous other factors. Sepsis and cardiovascular injury such as myocardial infarction, congestive cardiomyopathy, pulmonary embolism, or cardiac tamponade appear to
place the patient at greater risk for postintubation hypotension
and the subsequent need for vasoactive medications.1
Age appears to play a prominent role in the incidence
of postintubation hypotension: The octogenarian (52%) and
nonagenarian (61%) are at higher risk as compared to those
younger than 30 years old (22%) and the group between 30
and 60 years (35%). The need for vasoactive agents to counter
the hypotension is twice as likely in the octogenarian and older
groups when compared to those younger than 50 years old
(62% vs. 30%) (192).
Endotracheal Tube Displacement/Extubation
Tube displacement out of the trachea or migration of the tube
tip into a bronchus may compromise the airway (177,178). Appropriate securing and notation of tube markings in relation
to the lip may minimize this complication, but the location of
the markings at the dentition level has little bearing on the position of the ET tip (178,193). A chest radiograph may assist
in confirming tip location, but only at the time of the filming.
Fiberoptic evaluation of the tracheal tube positions offer realtime information that a chest radiograph taken 4 hours earlier
cannot offer (154). Hyperextension of the head may cause migration of the tracheal tube tip away from the carina toward
the pharynx; conversely, head flexion may advance the tube
tip, with an average 1.9 cm movement of the tube (158).
1 Data
Printer: Yet to come
from the Hartford Hospital emergency intubation database.
Lateral rotation of the head may move the tube to 0.7 to
1 cm away from the carina. If tube tip position is in question
and there is any clinical sign or symptom suggesting a problem
(e.g., desaturation, tachypnea, and so forth), then one should
consider aggressively pursuing a fiberoptically assisted determination of the tube placement rather than awaiting the call
for a chest radiograph or waiting until an emergent situation
has developed.
Accidental Extubation
Accidental extubation is a well-known clinical problem with
the potential of significant patient morbidity and mortality (193). Accidental extubation, either patient-initiated selfextubation or resultant from external forces (nurse/physician
moving patient, radiology team, transport, etc.), is another potential complication after intubation, occurring in 8% to 13%
of intubated, critically ill patients (194). To prevent unplanned
extubation, secure the tube by taping circumferentially around
the upper neck. A variety of manufactured ET securing devices
are available for purchase in lieu of the taping option. Tincture of benzoin improves adhesiveness of the tape to the skin
and the tube. Restraining the patient’s hands, care in turning
and moving the patient, and good nursing practices minimize—
but do not eliminate—this complication. Proper sedation regimens, close observation, and hastening extubation in those
who meet criteria may reduce patient-initiated self-extubations
(195,196).
Complete extubation of the trachea is most obvious when
the patient self-extubates. However, the trachea may only be
partially extubated when the ET cuff-tip complex is displaced
proximally between or above the cords (193). An audible cuff
leak is common, regardless of whether the final position of the
ET cuff is just below, between, or proximal to the vocal cords.
Moreover, complete extubation of the trachea—the cuff and
ET tip lying in the hypopharynx—may present with a continuous or intermittent leak, or none at all (193). An ET secured
at the lips/dentition at a level of 21 to 26 cm does not always equate to a correct tip position within the trachea (193).
ET thermolability at body temperature may result in a coiled,
kinked, or spirally misshaped (S-shaped) tube. If a cuff leak
is heard, an attempt at remediation on a repetitive basis by
adding air to the cuff may lead to further cuff-tip displacement
(herniation). The hypopharynx may accommodate an ET with
an overinflated cuff containing as much as 30 to 150 mL of
air. Repetitive “fixing” of a cuff leak with small increments of
air over several hours to days may lead to a stretched, highly
compliant cuff positioned in the hypopharynx with continued
ventilation and oxygenation. Cuff pressure measurements may
be misleading due to altered cuff compliance and its position
in the upper airway (193).
If a cuff leak—either intermittent or continuous—is noted,
the pilot balloon should be checked for integrity. If inflated,
the cuff-tip complex may be displaced at or above the glottic opening. Cuff deflation with blind advancement toward the
airway should be discouraged by personnel not fully capable
of managing the airway in the event of ET displacement, kinking, esophageal intubation, or loss of the airway. Evaluating
the airway with direct laryngoscopy (DL) may be very helpful
in assessing the location and status of the ET, but ET thermolability reduces one’s ability to advance the softened, floppy, or
deformed ET (193).
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
Conversely, a more proximal displaced ET (visible cuff in the
hypopharynx) should not be advanced by hand unless the view
of the airway is clear. Diagnostic/therapeutic bronchoscopy is
the optimal choice. Diagnosing the location and deformity of
the ET is possible coupled with its unparalleled utility for advancing the ET into the trachea. Secretions, operator skill, lack
of immediate access to such equipment, and an ET tip abutting on the glottic, supraglottic, or hypopharyngeal structures
may present reintubation challenges (193). If cuff hyperinflation is noted, complete deflation must be done prior to advancement over the fiberoptic bronchoscope (FOB). Once the
airway is resecured, changing the deformed ET to a new one
(via an airway exchanger cannula) may be considered (193).
This clinical problem is common and life threatening; therefore,
equipping the ICU with advanced airway devices is imperative
(27,31,44,46).
The Failed Intubation
In the clinical situation in which the patient has been positioned to the best of the practitioner’s abilities, the operator is
experienced at performing the airway management intervention, and optimal efforts at conventional mask ventilation and
tracheal intubation have been attempted but are unsuccessful
(a CVCI [can’t ventilate, can’t intubate] situation), the practitioner will need to rapidly deploy his or her rescue plan in
an attempt to salvage the airway and to save the patient’s
life. Following failure of conventional mask ventilation (no
ventilation or oxygen delivery) or when mask ventilation is
failing (inadequate gas exchange, SpO2 less than 90%, or a
falling SpO2 ), a supraglottic airway (LMA) should be placed
(30,46,63,64). In some instances in which mask ventilation and
oxygen delivery fail, or are failing—yet prior to any intubation attempt—intubation could be attempted if it is reasonably
assumed to be straightforward and can likely be rapidly completed, as in the case of a patient with a slender habitus, who
is edentulous, with no obvious difficult airway risk factors. If
unsuccessful, placement of the LMA or a Combitube should
proceed immediately (30,46). Conversely, the Combitube may
serve as a backup for LMA failure (69). Both devices have
a high rate of success for ventilation, are placed rapidly and
blindly, and require a relatively simple skill set. However,
in the situation described, most practitioners would choose
the LMA due to its wider familiarity and because it readily
serves as an intubation conduit, whereas the Combitube does
not (46).
Limiting intubation attempts is a key to successful management, since repeated attempts that are probably futile (e.g., a
grade IV view with conventional methods) waste time; increase
trauma, edema, and bleeding; and markedly increase the risk
of hypoxemia and other potentially devastating complications
(27,30,44,45,63,64). It must be stressed that conventional intubation failure should be supplemented by an airway adjunct
such as the bougie, specialty blades, or fiberscopes if immediately available. A key point is: Use them early, and use them
often.
The American Society of Anesthesiologists (ASA) guidelines
list both the LMA and the Combitube as ventilatory devices in
the CVCI situation as less invasive options (30,46). More invasively, transtracheal jet ventilation (TTJV) via a large-gauge (12
or 14 gauge) IV catheter through the cricothyroid membrane
may be an appropriate alternative, but advanced planning with
ready access to the proper equipment and a sound understand-
547
ing of “jetting” principles (lowest PSI setting to maintain SpO2
in the 80%–90% range, prolonged inspiration-to-expiration
ratio [i.e., 1:5], 6–12 quick breaths per minute, allowing a path
for exhalation, constant catheter stabilization, and barotrauma
vigilance) must be followed; otherwise, the consequences may
be very serious, indeed (46,197).
It is imperative to appreciate the difference between an
upper airway CVCI and a lower airway CVCI. A lower airway CVCI due to glottic abnormalities such as spasm, tumor,
abscess, massive swelling, or subglottic pathology cannot be
solved with a device dependent on glottic patency such as the
LMA or Combitube (46). Only a subglottic approach, such as
TTJV or a surgical airway, will suffice. Likewise, repetitive intubation attempts leading to airway trauma, bleeding, and edema
not only markedly reduce the effectiveness of many intubation
adjuncts, but also the once ventilatable airway may deteriorate
into one that cannot be managed effectively, thus transforming the airway to a CVCI situation. If, however, management
of an upper airway CVCI with noninvasive techniques fails,
then rapid transition to TTJV or a surgical approach must be
rendered (30,46,63,64). Conversely, successful ventilation and
oxygen delivery via a supraglottic device does allow time to
gain surgical access if intubation via the supraglottic device is
difficult or fails.
All these life-saving maneuvers cannot be accomplished
by carrying a laryngoscope in our back pocket or by grabbing the bare essential airway management equipment from
a plastic storage bin in the ICU. Advanced planning to acquire and properly deploy conventional and advanced airway equipment, coupled with the education to execute a rescue strategy, is warranted given the precarious airway status
of many critically ill patients who require airway management (30,31,46,63,64). Availability of personnel is imperative, as intubation is a team activity. The CVCI situation is
very terrifying—indeed, bloodcurdling—so planning ahead to
reduce the risks of airway management is both a justifiable and
sound endeavor.
Laryngeal/Tracheal Damage
Prolonged intubation may cause laryngeal or tracheal injury
(110,112–115,164). Excessive cuff pressure and prolonged intubation can initiate mucosal erosion, cartilage necrosis, and
eventually tracheal stenosis. Movement of the tube during assisted ventilation may erode the trachea, usually in the posterior membranous portion. Blood-tinged sputum or any degree of new-onset hemoptysis should prompt evaluation of
the ET or tracheostomy tube position. Erosions, granulation
tissue growth, mucosal tears, and suction catheter–related
trauma may contribute to bloody secretions, as may an undiagnosed lung tumor or necrotizing infectious process. Tracheal or
bronchial rupture occurs more frequently in infants, the elderly,
or patients with chronic obstructive lung disease. Because signs
and symptoms may be delayed, chest radiographs and prompt
endoscopy may confirm the diagnosis.
Miscellaneous
Other problems encountered during intubation are aspiration
of gastric contents secondary to passive (silent) regurgitation,
and leakage of orogastric secretions past the cuff. Regimens
to cleanse the nasal and oropharyngeal cavity suggest a potential reduction in nosocomial pneumonia in the ICU setting.
Paranasal sinusitis develops in 2% to 5% of nasally intubated
11:53
P1: OSO/OVY
GRBT291-37-39
548
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
patients and commonly involves the maxillary sinus (119–121).
Signs and symptoms include fever and purulent nasal discharge,
often appearing 2 to 4 days after nasal intubation. Infrequently,
a middle ear infection results from bacterial reflux into the eustachian tube, followed by contiguous spread into the middle
ear (122,123).
TA B L E 3 8 . 1 1
TRACHEAL INTUBATION COMPLICATIONS SEEN
AFTER EXTUBATION
Time of occurrence
Complications
Early (0–72 h)
Numbness of tongue
Sore throat
Laryngitis
Glottic edema
Vocal cord paralysis
Late (>72 h)
Nostril stricture
Laryngeal ulcer, granuloma, or polyp
Laryngotracheal webs
Laryngeal or tracheal stenosis
Vocal cord synechiae
During Extubation
Problems during extubation arise secondary to mechanical
damage, which develops while the tube is in place or in response to tissue injury. Failure to deflate the cuff, adhesion
of the tube to the tracheal wall, or transfixation of the tube
by a suture to a nearby structure may result in a difficult or
impossible extubation. Laryngospasm and acute airway obstruction represent the most serious complications during the
immediate postextubation period. Positive-pressure ventilation
via a bag-mask assembly may assist in oxygen exchange, but
prompt relief may require reintubation or rapid administration
of a quick-onset muscle relaxant for laryngospasm. Collapse of
redundant supraglottic tissue postextubation combined with
rapid accumulation of laryngeal edema may occur immediately upon extubation of the trachea. Moreover, edema formation occurs in two other phases of the postextubation period:
Acutely during the first 5 to 20 minutes post extubation or on a
delayed basis, within 30 minutes to 8 hours of extubation. Laryngeal edema may involve the supraglottic, retroarytenoidal,
and subglottic areas. Severe respiratory obstruction may occur
after extubation, and frequently requires urgent reintubation
or tracheotomy. Steroid use in the treatment of laryngeal edema
is controversial, but may reduce postextubation stridor, reduce
the need for reintubation in select patients, and hasten the resolution of existing traumatic edema. Utilization of bilevel positive airway pressure (BiPAP) or heliox (helium–oxygen mixture) may also be of use in the postextubation patient with
stridor.
Other causes of airway obstruction after extubation are
blood clots, foreign bodies, dentures, traumatized dentition,
and throat packs inadvertently left in the airway. Passive regurgitation or active vomiting at extubation may result in gastric content aspiration; stridor may be the presenting clinical
sign if air movement is possible. Rapid deployment of therapy
is imperative; nebulized racemic epinephrine, heliox, judicious
use of anxiolytics, noninvasive positive pressure modalities, or
tracheal intubation may be in order.
After Extubation
Complications after extubation are divided into early (up to 72
hours) and late (more than 72 hours).
Early Complications
Early complications are listed in Table 38.11. Mechanical irritation to the pharyngeal mucosa causes sore throat. Shortlived or prolonged aphonia—a weakened voice—is common,
especially following prolonged intubation. Laryngeal incompetence following extubation is the rule; hence, resumption of an
oral diet must be timed appropriately to the patient’s ability to
cough, control secretions, and competently and safely swallow
liquids and solids.
Vocal cord paralysis and arytenoid dislocation and dysfunction may be appreciated following extubation (198–204).
Paralysis may be unilateral or bilateral, with the left cord twice
as frequently affected as the right, and males predominating
with this complication. Damage to the external laryngeal nerve
may cause lasting voice change, with unilateral nerve injury
usually causing hoarseness. Paralysis can result and, if the injury is bilateral, may lead to airway obstruction.
Late Complications
Late postextubation complications include laryngeal ulcer,
granuloma, polyp, synechiae (fusion) of the vocal cords, laryngotracheal membrane webs, laryngeal or tracheal fibrosis, and
nostril stricture from damage to the alae (202,203,205). Laryngeal ulcerations or granulomata are more commonly located at
the posterior region of the vocal cords where the endotracheal
tube tends to have more continual contact. The patient may
complain of foreign body sensation, fullness or discomfort at
the back of the throat, and persistent hoarseness. Any patient
complaining of airway-related pain, discomfort, fever, or systemic signs of infection following difficult airway management
should be evaluated for tissue injury in the upper and lower
airway and pharyngoesophageal region (27,92).
EXTUBATION OF THE DIFFICULT
AIRWAY IN THE INTENSIVE
CARE UNIT
Airway management also constitutes maintaining control of
the airway into the postextubation period. The known or suspected difficult airway patient should be evaluated in regard to
factors that may contribute to his or her inability to tolerate
extubation. A comprehensive review of medical and surgical
conditions and previous airway interventions, an evaluation
of the airway, and formulation of a primary plan for extubation as well as a rescue plan for intolerance are essential
for optimizing safety (206–208). Reintubation, immediately or
within 24 hours, may be required in up to 25% of ICU patients
(209–211). Measures to avert reintubation such as noninvasive
ventilation for those at highest risk for extubation failure are
effective in preventing reintubation and may reduce mortality
rate if done so upon extubation (212). However, a delay in the
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
TA B L E 3 8 . 1 2
549
TA B L E 3 8 . 1 3
RISK FACTORS FOR DIFFICULT EXTUBATION
Known difficult airway
Suspected difficult airway based on the following factors:
Restricted access to airway
Cervical collar, Halo-vest
Head and neck trauma, procedures, or surgery
ET size, duration of intubation
Head and neck positioning (i.e., prone vs. supine)
Traumatic intubation, self-extubation
Patient bucking or coughing
Drug or systemic reactions
Angioedema
Anaphylaxis
Sepsis-related syndromes
Excessive volume resuscitation
THE DIFFICULT EXTUBATION: TWO CATEGORIES
FOR EVALUATION
1. Evaluate the patient’s inability to tolerate extubation
a. Airway obstruction (partial or complete)
b. Hypoventilation syndromes
c. Hypoxemic respiratory failure
d. Failure of pulmonary toilet
e. Inability to protect airway
2. Evaluate for potential difficulty re-establishing the airway
a. Difficult airway
b. Limited access to the airway
c. Inexperienced personnel pertaining to airway skills
d. Airway injury, edema formation
Modified from Cooper RM. Extubation and changing endotracheal
tube. In Benumof J, ed. Airway Management. St. Louis: Mosby; 1995.
ET, endotracheal tube.
The Cuff Leak
application of noninvasive ventilation when the patient displays signs of early or late postextubation respiratory distress
or failure results in a less effective application in most patients,
except those with COPD (213–216). Factors beyond routine
extubation criteria that may be helpful in predicting failure include neurologic impairment, previous extubation failure, secretion control, and alterations in metabolic, renal, systemic,
or cardiopulmonary issues (209–211).
“Difficult extubation” is defined as the clinical situation
when a patient presents with known or presumed risk factors
that may contribute to difficulty re-establishing access to the
airway (Table 38.12). The extubation of the patient with a
known or presumed difficult airway and the potential for subsequent intolerance of the extubated state poses an increased
risk to patient safety. An extubation strategy should be developed that allows the airway manager to (a) replace the ET in
a timely manner and (b) ventilate and oxygenate the patient
while he or she is being prepared for reintubation, as well as
during the reintubation itself (30).
The practitioner should assess the patient’s risk on two levels: The patient’s predicted ability to tolerate the extubated
state and the ability (or inability) to re-establish the airway if
reintubation becomes necessary (206–208). Weaning criteria
and extubation parameters will not be discussed as they vary
by locale, practitioner, and the patient’s clinical situation. Table 38.13 outlines two categories for pre-extubation evaluation
(208).
NPO Status
The NPO status of the patient to be extubated and the subsequent need for reintubation has not been thoroughly studied,
but it makes clinical sense to consider 2 to 4 hours off of distal
enteral feeds prior to extubation while maintaining the NPO
status post extubation until the patient appears at low risk for
failing the extubation “trial.” Unfortunately, the ICU patient
may succumb to reintubation based on a multitude of factors;
hence, predictability of failure and when it will occur is difficult
to discern.
Hypopharyngeal narrowing from edema or redundant tissues, supraglottic edema, vocal cord swelling, and narrowing
in the subglottic region of any etiology may contribute to the
lack of a cuff leak (217–222). Too large of a tracheal tube
in a small airway should, of course, be considered. A higher
risk of post extubation stridor or the need for reintubation is
prevalent in those without a cuff leak, in women, and in patients with a low Glasgow coma score (217–222). Attempting
to determine the etiology for the lack of a cuff leak may impact
patient care, as individuals may remain intubated longer than is
required or receive an unneeded tracheostomy. If airway edema
is the culprit, steps to decrease airway edema include elevation of the head, diuresis, steroid administration, minimizing
further airway manipulation, and “time” (223–225). The cuff
leak test as an indicator for predicting postextubation stridor
is helpful, but the performance of a cuff leak test varies by
institution and protocol, as does its interpretation by the individual physician. Testing to predict successful extubation is
inconclusive (223–225). A relatively crude yet effective method
of cuff leak test involves auscultation for cuff leak with or
without a stethoscope. A more precise method is to take an
indirect measurement of the volume of gas escaping around
the ET following cuff deflation, determined by calculating the
average difference between inspiratory and expiratory volume while on assisted ventilation (218,225). Cuff leak volume (CLV) may be measured as the difference of tidal volume delivered with and without cuff deflation and stated as
a percentage of leak, or as an absolute volume. The percentage CLV will vary with the tidal volume administered during
the test (8 mL/kg vs. 10–12 mL/kg), but several authors have
found an absolute CLV less than 110 to 130 mL (218,219) or
10% to 24% of delivered tidal volume as helpful in predicting postextubation stridor (219–221,225). Stridor increases the
risk of reintubation. Single- or multiple-dose steroids may reduce postextubation airway obstruction in pediatric patients,
depending on dosing protocols, patient age, and duration of
intubation (223). Steroid use in adults administered 6 hours
prior to extubation—rather than 1 hour prior—may reduce
postextubation stridor and decrease the need for reintubation
in critically ill patients (210,223–225).
11:53
P1: OSO/OVY
GRBT291-37-39
550
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
Risk Assessment: Direct Inspection
of the Airway
Garnering useful information about the airway status may need
to go well beyond the cuff leak test since it is relatively crude,
provides little direct data regarding one’s ability to access the
airway in the event of a need for reintubation, and is relatively
uninformative as to the actual status of the glottis. While it
is mandatory that the records of the known difficult airway
patient be reviewed, it is also the case that a record of previous airway interventions in a patient who may have undergone
a marked alteration in their airway status could be less than
informative. Practitioners should weigh the pros and cons of
evaluating such an airway to determine ease or difficulty in the
ability to gain access via conventional or advanced techniques.
Additionally, some patients may need evaluation of their hypopharyngeal structures and supraglottic airway to assess airway patency and resolution of edema, swelling, and tissue
injury. Conventional laryngoscopy is a standard choice for evaluation, but often fails due to a poor “line of sight.” Additionally, the relationship of grading and comparing the laryngeal
view of a nonintubated to an intubated glottis is inconsistent
(226). Flexible fiberoptic evaluation is useful but may be limited
by secretions and edema (124). Video-laryngoscopy and other
indirect visualization techniques that allow one to see “around
the corner” are especially helpful. The Airtraq, as may other
optical or video-laryngoscopy devices, has been found to be
particularly useful by offering outstanding wide-angle visualization of the periglottic structures in the critically ill patient
with a known difficult airway (144).
American Society of Anesthesiologists
Practice Guidelines Statement Regarding
Extubation of the Difficult Airway
The ASA guidelines (30) have suggested that a preformulated
extubation strategy should include:
1. A consideration of the relative merits of awake extubation
versus extubation before the return of consciousness; this is
clearly more applicable to the operating room setting than
to the ICU
2. An evaluation for general clinical factors that may produce
an adverse impact on ventilation after the patient has been
extubated
3. The formulation of an airway management plan that can be
implemented if the patient is not able to maintain adequate
ventilation after tracheal decannulation
4. Consideration of the short-term use of a device that can serve
as a guide to facilitate intubation and/or provide a conduit
for ventilation/oxygenation
Clinical Decision Plan for the
Difficult Extubation
A variety of methods are available to assist the practitioner’s
ability to maintain continuous access to the airway following extubation, each with limitations and restrictions. Though
no method guarantees control and the ability to re-secure the
TA B L E 3 8 . 1 4
AIRWAY EXCHANGE CATHETER (AEC)-ASSISTED
EXTUBATION: TIPS FOR SUCCESS
1. Access to advanced airway equipment
2. Personnel
a. Respiratory therapist
b. Individual competent with surgical airway?
3. Prepare circumferential tape to secure the airway catheter
after extubation
4. Sit patient upright; discuss with patient
5. Suction ET, nasopharynx, and oropharynx
6. Pass lubricated AEC to 23–26 cm depth
7. Remove the ET while maintaining the AEC in its original
position
8. Secure the AEC with the tape (circumferential); mark
AEC “airway only”
9. Administer oxygen:
a. Nasal cannula
b. Face mask
c. Humidified O2 via AEC (1–2 L/min)
10. Maintain NPO
11. Aggressive pulmonary toilet
ET, endotracheal tube.
airway at all times, the LMA offers the ability for fiberopticassisted visualization of the supraglottic structures while serving as a ventilating and reintubating conduit; it is hampered
by a limited time frame in which it may be left in place. The
bronchoscope is useful for periglottic assessment following extubation, but requires advanced skills and minimal secretions.
Moreover, it offers only a brief moment for airway assessment and access to the airway following extubation (124).
Conversely, the airway exchange catheter (AEC, Fig. 38.14) allows continuous control of the airway after extubation, is well
tolerated in most patients, and serves as an adjunct for reintubation and oxygen administration (206,227–229). Patient
intolerance, accidental dislodgment, and mucosal and tracheobronchial wall injury have been reported, but are rare (230–
234). Carinal irritation may be treated with proximal repositioning, the instillation of topical agents to anesthetize the
airway, and explanation and reassurance. Dislodgment may
occur, resultant from an uncooperative patient or a poorly secured catheter. Observation in a monitored environment with
experienced personnel should be given top priority, as should
the immediate availability of difficult airway equipment in the
event of intolerance to tracheal decannulation (206–208). Tips
for success with the use of this device are shown in Table 38.14.
Clinical judgment and the patient’s cardiopulmonary and
other systemic conditions, combined with the airway status,
should guide the clinician in establishing a reasonable time period for maintaining a state of “reversible extubation” with the
indwelling AEC (Table 38.15) (206).
EXCHANGING AN
ENDOTRACHEAL TUBE
Exchanging an ET due to cuff rupture, occlusion, damage, kinking, a change in surgical or postoperative plans,
or self-extubation masquerading as a cuff leak, or when the
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
TA B L E 3 8 . 1 5
Airway Exchange Catheter
SUGGESTED GUIDELINES FOR MAINTAINING
PRESENCE OF AIRWAY EXCHANGE CATHETER
Difficult airway only, no respiratory issues, no
anticipated airway swelling
Difficult airway, no direct respiratory issues,
potential for airway swelling
Difficult airway, respiratory issues, multiple
extubation failures
551
1–2 h
>2 h
>4 h
requesting team prefers a different size or alteration in location, is a common procedure. Preparation for the possible failure of the exchange technique and appreciation of the potential
complications is imperative (30).
Four methods typify the airway manager’s armamentarium
of exchanging an ET: Direct laryngoscopy, a flexible or rigid
fiberscope, the airway exchange catheter, or a combination of
these techniques (2). Proper preparation is imperative and patients should undergo a comprehensive airway exam. Access to
a variety of airway rescue devices is of paramount importance
in the event of difficulty with ET exchange (208).
Direct Laryngoscopy
DL is the most common and easiest technique for exchanging an ET, but has several pitfalls and limitations. Airway collapse following removal of the ET may impede visualization
and, thus, reintubation. This method leaves the patient without continuous access to the airway and should be restricted
to the uncomplicated “easy” airway (94).
The AEC incorporates the Seldinger technique for maintaining continuous access to the airway. Strategy and preparation
are the keys to successful and safe exchange (Table 38.16).
Proper sizing of the AEC to best approximate the inner diameter of the ET will allow a smoother replacement. A chin lift–jaw
thrust maneuver and/or laryngoscopy will assist the passing of a
well-lubricated warmed ET that may need to be rotated counterclockwise by 90 degrees to reduce glottic impingement. A
larger-diameter (19 French is the size we most often use) AEC
is best in passing an adult-sized ET. Exchanging a tracheostomy
tube over an AEC is especially valuable when the peristomal
tissues are immature. The use of a tracheal hook to elevate the
tracheal cartilage and proper head/neck positioning (shoulder
roll) will optimize the exchange. The exchange is often performed “blindly” since laryngoscopy in the ICU patient often
reveals little to no view of the supraglottic airway. Thus, incorporation of any of the advanced laryngoscopes that assist
in “seeing around the corner” (Bullard, Wu, Glidescope, McGrath, Airtraq, etc.) offer certain advantages to the operator
and the patient: (a) assessment of the airway is improved; (b)
there is better estimation of what size ET the glottis will accept;
(c) visualization during the exchange offers the ability to direct
the new ET into the trachea and reduce arytenoid hang-up or
impingement; (d) it confirms that the AEC remains in the trachea during the exchange; and (e) it allows visual confirmation
that the ET is placed in the trachea and the ET cuff is lowered
below the glottis. Finally, the advanced airway device would be
in position to assist in reintubation if any unforeseen difficulties
arise during the exchange.
TA B L E 3 8 . 1 6
Fiberscopic Bronchoscope–assisted
Exchange
Fiberscopic bronchoscope–assisted exchange (FBAE) is useful
for nasal to oral or vice versa exchanges and oral-to-oral exchanges, as well as for immediate confirmation of ET placement
within the trachea and positioning precision (3–5). Though difficult in the edematous or secretion-filled airway, FBAE allows
continuous airway access in skilled hands. Passing the flexible
fiberscope through the glottis along the side of the existing ET,
although not without significant difficulty, the old ET can be
backed out, followed by advancing the ET—preloaded onto
the fiberoptic bronchoscope—into the trachea. Conversely, the
preloaded flexible fiberscope may be placed immediately adjacent to the glottis. The old ET is then backed out over an
AEC and the glottis is intubated with the FOB-ET complex.
A larger flexible model is better maneuvered than a pediatricsized scope. Passing a lubricated, warmed ET that is rotated
90 degrees will reduce arytenoid-glottic impingement. Rigid
fiberscopes such as the Bullard, the Wu scope, the Upsher, and
the Airtraq are very useful for visualizing the otherwise difficult airway during the exchange by offering the ability to “see
around the corner” (124,235–238). The fiberscope may be rendered useless by unrecognizable airway landmarks, edema, and
secretions as well as operator inexperience.
STRATEGY AND PREPARATION FOR
ENDOTRACHEAL TUBE (ET) EXCHANGE
1. Place on 100% oxygen
2. Review patient history, problem list, medications, and
level of ventilatory support
3. Assemble conventional and rescue airway equipment
including capnography
4. Assemble personnel (nursing, respiratory therapy,
surgeon, airway colleagues)
5. Prepare sedation/analgesia ± neuromuscular blocking
agents
6. Optimal positioning; consider DL of airway
7. Discuss primary/rescue strategies and role of team
members; choose new ET (soften in warm water)
8. Suction airway; advance lubricated large AEC via ET to
22–26 cm depth
9. Elevate airway tissues with laryngoscope/hand, remove
old ET, and pass new ET
10. Remove AEC and check ET with capnography/
bronchoscope or use a closed system and place small
bronchoscope through swivel adapter while at the same
time ventilating, checking for CO2 , with the AEC still in
place
DL, direct laryngoscopy; AEC, airway exchange catheter.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
552
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
Minimizing the gap between the ET and the AEC is important for ease of exchange. If, due to luminal size restrictions,
the smaller-sized AEC (4 mm, 11 French) is used when going
from, for example, a double-lumen to a single-lumen ET in
a high-risk ICU patient, then temporary reintubation with a
smaller warmed (6.5 mm) ET as opposed to a larger (8–9 mm)
ET may ease passage into the trachea. Once secured, a larger
AEC may be passed via the indwelling ET with subsequent exchange to a larger ET. Various AEC exchange techniques are
practiced, and customized variations of the standard methods
assist the practitioner to tackle individual patient characteristics (94,235–238).
ET exchange, while simple conceptually, is not a simple procedure as hypoxemia, esophageal intubation, and loss of the
airway may occur. The decision on the method of exchange is
based on known or suspected airway difficulty, edema and secretions, and most significantly, the experience and judgment of
the clinician. It is recommended that continuous airway access
be maintained in all but the simplest and most straightforward
airway situations (94).
Follow-up Care
Following a life-threatening airway encounter with a patient,
dissemination of such information is often overlooked and
there is currently no standard method of relaying information
from one caregiver to another (30,89). Notes written in the
chart are a start, as is a discernible or highly visible label on
the outside of the medical chart, but these may be inadequate.
Informative and accurate medical records of airway interventions should be promoted as a potentially life-saving exercise;
hence, detailed accounting of an intubation with more information written in the chart—not less—is best for patient care.
However, a caveat to note is as follows:
If the chart states difficulty was encountered, assume it will again be
difficult; if the notes states it was “easy” or no details are provided,
assume and plan on the potential for difficulty.
Discussing difficulties with the patient in this setting is certainly different from the elective surgical case in the operating
room. For the future care of the patient, opening a Medic Alert
file has many advantages for improved dissemination of patient
care information, especially in our mobile society. Obtaining
medical records in a timely fashion is a constant deterrent.
However, the Medic Alert file will not assist the care for the
current hospitalization, only in future ones (27,30,89). Hence,
steps for the current hospitalization can be taken to improve
communication for efficient transfer of needed information to
the airway team. Initially identifying the patient by a colorful wrist bracelet, analogous to a medication or latex allergy
bracelet, is a simple but effective trigger for the airway team to
investigate the patient’s airway status. A computerized medical record may allow a “Difficult Airway Alert” to be readily
and prominently displayed, thus allowing identification of the
patient on the current and possibly future hospitalizations—
although only at the current hospital. Future airway interventions in the unrecognizable or unanticipated difficult airway are particularly benefited by “flagging” the patient. The
Medic Alert system is dependent on patient compliance and
payment.
References
1. Campbell TP, Stewart RD. Oxygen enrichment of bag valve mask units
during positive pressure ventilation: a comparison of various techniques.
Ann Emerg Med. 1988;17:232.
2. Dorges V, Wenzel V, Knacke P, et al. Comparison of different airway
management strategies to ventilate apneic, nonpreoxygenated patients. Crit
Care Med. 2003;31:800.
3. Mazzolini DG, Marshall NA. Evaluation of 16 adult disposable manual
resuscitators. Respir Care. 2004;49:1509.
4. Hayes H. Cardiopulmonary resuscitation. In: Wilkens EW, ed. Emergency
Medicine. Baltimore: Williams & Wilkins; 1989:10.
5. Hocbaum SR. Emergency airway management. Emerg Clin North Am.
1986;4:411.
6. Jorden RC. Airway management. Emerg Clin North Am. 1988;6:671.
7. Florete OG. Airway management. In: Civetta JM, Taylor RW, Kirby RR,
eds. Critical Care. 2nd ed. Philadelphia: JB Lippincott; 1992:1419.
8. Yokoyama T, Yamashita K, Manabe M. Airway obstruction caused by
nasal airway. Anesth Analg. 2006;103(2):508.
9. Hasegawa EA. The endotracheal use of emergency drugs. Heart Lung.
1986;15:66.
10. Greenberg MI. Endotracheal drugs: state of the art. Ann Emerg Med.
1984;13:789.
11. Greenberg MI, Mayeda DV, Chrzanowski R, et al. Endotracheal administration of atropine sulfate. Ann Emerg Med. 1982;10:546.
12. Powers RD, Donowitz LG. Endotracheal administration of emergency medications. South Med J. 1983;77:340.
13. Dauphine K. Nasotracheal intubation. Emerg Clin North Am. 1988;6:715.
14. Moore EE, Eiseman B, Vanuy CW. Critical Decisions in Trauma. St. Louis:
CV Mosby; 1984:30.
15. Donlon JV. Anesthetic management of patients with compromised airways.
Anesth Rev. 1980;VII:22.
16. Linscott MS, Horton WC. Management of upper airway obstruction. Otolaryngol Clin North Am. 1979;12:351.
17. Stone DJ, Gal TJ. Airway management. In: Miller RD, ed. Anesthesia. 4th
ed, Vol. 2. New York: Churchill Livingstone; 1994.
18. Crosby ET. Airway management in adults after cervical spine trauma. Anesthesiology. 2006;104(6):1293.
19. Rudolph C, Schneider JP, Wallenborn J, et al. Movement of the upper
cervical spine during laryngoscopy: a comparison of the Bonfils intubation
fiberscope and the Macintosh laryngoscope. Anaesthesia. 2005;60:668.
20. Agro F, Barzoi G, Montechia F. Tracheal intubation using a Macintosh
laryngoscope or a Glidescope in 15 patients with cervical spine immobilization. Br J Anaesth. 2003;90:705.
21. Turkstra TP, Craen RA, Pelz DM, et al. Cervical spine motion: A fluoroscopic comparison during intubation with lighted stylet, Glidescope, and
Macintosh laryngoscope. Anesth Analg. 2005;101:910.
22. Rose DK, Cohen MM. The airway: problems and predictions in 18,500
patients. Can J Anaesth. 1994;41:372.
23. McGuire G, El-Beheiry H. Complete upper airway obstruction during
awake fiberoptic intubation in patients with unstable cervical spine fractures. Can J Anesth. 1999;46:176.
24. Cohn AI, Zornow MH. Awake endotracheal intubation in patients with
cervical spine disease: a comparison of the Bullard laryngoscope and the
fiberoptic bronchoscope. Anesth Analg. 1995;81:1283.
25. Smith CE, DeJoy SJ. New equipment and techniques for airway management in trauma. Curr Opin Anaesth. 2001;14(2):197.
26. Fuchs G, Schwarz G, Baumgartner A, et al. Fiberoptic intubation in 327
patients with lesions of the cervical spine. J Neurosurg Anesth. 1999;11:11.
27. Peterson GN, Domino KB, Caplan RA, et al. Management of the difficult
airway: a closed claims analysis. Anesthesiology. 2005;103:33.
28. Tokunaga D. Atlantoaxial subluxation in different intraoperative
head positions in patients with rheumatoid arthritis. Anesthesiology.
2006;104(4):675.
29. Sellick BA. Cricoid pressure to control regurgitation of stomach contents
during induction of anesthesia. Lancet. 1961:404.
30. 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. 2003;98:1269.
31. Kane BG, Bond WF, Worrilow CC, et al. Airway carts: a systems-based
approach to airway safety. J Patient Saf. 2006;2(3):154.
32. Stoelting RK. Local anesthetics. In: Pharmacology and Physiology in Anesthetic Practice. 2nd ed. Philadelphia: JB Lippincott; 1991:148.
33. Gross JB, Hartigan ML. A suitable substitute for 4% cocaine before blind
nasotracheal intubation: 3% lidocaine-0.25% phenylephrine nasal spray.
Anesth Analg. 1984;63:915.
34. Marshall BE, Wollman H. General anesthetics. In: Gilman AG, Goodman
RS, Rall RW, eds. The Pharmacologic Basis of Therapeutics. New York:
Macmillan; 1985:276.
35. Flacke JW, Bloor BC, Kripke E-A, et al. Comparison of morphine, meperidine, fentanyl and sufentanil in balanced anesthesia: a double blind study.
Anesth Analg. 1985;64:897.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
36. Stanski DR, Hug CC. Alfentanil: aldnetically predictable narcotic analgesic.
Anesthesiology. 1982;87:435.
37. Drover DR. Determination of the pharmacodynamic interaction of propofol and remifentanil during esophagogastroduodenoscopy in children.
Anesthesiology. 2004;100(6):1382.
38. Bouillon TW. Pharmacodynamic interaction between propofol and
remifentanil regarding hypnosis, tolerance of laryngoscopy, bispectral index, and electroencephalographic approximate entropy. Anesthesiology.
2004;100(6):1353.
39. Warner OJ, Rai MR, Parry TM. Is remifentanil better than propofol at
providing optimal conditions for an awake intubation? Anesthesiology.
2006;105:A824.
40. Reves JG, Fragen RJ, Vinik HR, et al. Midazolam: pharmacology and uses.
Anesthesiology. 1981;54:66.
41. Reynolds SF. Airway management of the critically ill patient: rapid-sequence
intubation. Chest. 2005;127(4):1397.
42. Levitan RM. Limitations of difficult airway prediction in patients intubated
in the emergency department. Ann Emerg Med. 2004;44(4):307.
43. Levitan R. The importance of a laryngoscopy strategy and optimal conditions in emergency intubation. Anesth Analg. 2005;100(3):899.
44. Mort TC. Emergency tracheal intubation: complications associated with
repeated laryngoscopic attempts. Anesth Analg. 2004;99:607.
45. Mort TC. The importance of a laryngoscopy strategy and optimal conditions in emergency intubation. Anesth Analg. 2005;100(3):900.
46. Benumof JL. The ASA management of the difficult airway algorithm and
explanation. In: Benumof JL, ed. Airway Management Principles and Practice. St. Louis: Mosby-Year Book; 1996:151.
47. Cooperman LH, Strobel GE, Kennel EM. Massive hyperkalemia after administration of succinylcholine. Anesthesiology. 1970;32:161.
48. Gronert GA, Theye RA. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology. 1975;65:89.
49. Levitan R. Safety of succinylcholine in myasthenia gravis. Ann Emerg Med.
2005;45(2):225.
50. Green SM. Incidence and severity of recovery agitation after ketamine sedation in young adults. Am J Emerg Med. 2005;23(2):142.
51. Berkenbosch JW. Safety and efficacy of ketamine sedation for infant flexible
fiberoptic bronchoscopy. Chest. 2004;125(3):1132.
52. Sebel PS, Lowdon JD. Propofol: a new intravenous anesthetic. Anesthesiology. 1989;71:260.
53. Taylor MB, Grounds RM, Dulrooney PD, et al. Ventilatory effects of propofol during induction of anaesthesia: comparison with thiopentone. Anaesthesia. 1986;41:816.
54. Eastwood PR. Collapsibility of the upper airway at different concentrations
of propofol anesthesia. Anesthesiology. 2005;103(3):470.
55. Doufas AG. Induction speed is not a determinant of propofol pharmacodynamics. Anesthesiology. 2004;101(5):1112.
56. Jacoby J. Etomidate versus midazolam for out-of-hospital intubation: a
prospective, randomized trial. Ann Emerg Med. 2006;47(6):525.
57. Cone D. Etomidate as a sole agent for endotracheal intubation in the prehospital air medical setting. Ann Emerg Med. 2004;43(1):147.
58. Jackson WL. Should we use etomidate as an induction agent for endotracheal intubation in patients with septic shock? — a critical appraisal. Chest.
2005;127(3):1031.
59. Murray H. Etomidate for endotracheal intubation in sepsis: acknowledging
the good while accepting the bad. Chest. 2005;127(3):707.
60. Bloomfield R. Exploring the role of etomidate in septic shock and acute
respiratory distress syndrome. Crit Care Med. 2006;34(6):1858.
61. Cortinez LI. Dexmedetomidine pharmacodynamics: part II: crossover comparison of the analgesic effect of dexmedetomidine and remifentanil in
healthy volunteers. Anesthesiology. 2004;101(5):1077.
62. Jooste EH, Ohkawa S, Sun LS. Fiberoptic intubation with dexmedetomidine in two children with spinal cord impingements. Anesth Analg.
2005;101(4):1248.
63. Henderson JJ, Popat MT, Latto IP, et al. Difficult Airway Society Guidelines for management of the unanticipated difficult intubation. Anaesthesia.
2004;59(7):675.
64. Crosby ET, Cooper RM, Douglas MJ, et al. The unanticipated difficult airway with recommendations for management. Can J Anaesth.
1998;45(8):757.
65. Frass M, Frenzer R, Zdrahl F, et al. The esophageal tracheal Combitube: preliminary results with a new airway for CPR. Ann Emerg Med.
1987;16:768.
66. Cady CE. The effect of Combitube use on paramedic experience in endotracheal intubation. Am J Emerg Med. 2005;23(7):868.
67. Gaitini LA. The esophageal-tracheal Combitube resistance and ventilatory
pressures. J Clin Anesth. 2005;17(1):26.
68. McGlinch B. Recommendation of the minimal volume technique to avoid
tongue engorgement with prolonged use of the esophageal-tracheal Combitube. Ann Emerg Med. 2005;45(5):566.
69. Mort TC. Laryngeal mask airway and bougie intubation failures: the Combitube as a secondary rescue device for in-hospital emergency airway management. Anesth Analg. 2006;103(5):1264.
70. Leibowitz AB. Tracheal intubation in the intensive care unit: extremely
hazardous even in the best of hands. Crit Care Med. 2006;34(9):2497.
553
71. Kaplan MB, Hagberg CA, Ward D, et al. Comparison of direct and videoassisted views of the larynx during routine intubation. J Clin Anesth
2006;18(5):357–362.
72. Ali AK, Trottier SJ, Christopher V, et al. Prevalence of difficult/failed airway: medical-surgical intensive care unit. Crit Care Med.
2006;34(12)S:A135.
73. Sugiyama K, Yokoyama K. Head extension angle required for direct laryngoscopy with the mccoy laryngoscope blade. Anesthesiology.
2001;94(5):939.
74. Smith CE, Pinchak AB, Sidhu TS, et al. Evaluation of tracheal intubation
difficulty in patients with cervical spine immobilization: fiberoptic (WuScope) versus conventional laryngoscopy. Anesthesiology. 1999;91(5):1253.
75. Hastings RH, Vigil AC, Hanna R, et al. Cervical spine movement during
laryngoscopy with the Bullard, Macintosh and Miller laryngoscopes. Anesthesiology. 1995;82:859.
76. Cooper SD, Benumof JL, Ozaki GT. Evaluation of the Bullard laryngoscope using the new intubating stylet: comparison with conventional laryngoscopy. Anesth Analg. 1994;79:965.
77. Levitan RM. Emergency airway management in a morbidly obese, noncooperative, rapidly deteriorating patient. Am J Emerg Med. 2006;24(7):894.
78. Levitan RM. Design rationale and intended use of a short optical stylet for
routine fiberoptic augmentation of emergency laryngoscopy. Am J Emerg
Med. 2006;24(4):490.
79. Rudolph C, Schneider JP, Wallenborn J, et al. Movement of the upper
cervical spine during laryngoscopy: a comparison of the Bonfils intubation
fiberscope and the Macintosh laryngoscope. Anaesthesia. 2005;60:668.
80. Bein B, Caliebe D, Romer T, et al. Using the Bonfils intubation fiberscope
with a double-lumen tracheal tube. Anesthesia. 2005;102(6):1290.
81. Borasio P, Ardissone F, Chiampo G. Post-intubation tracheal rupture. A
report on ten cases. Eur J Cardiothoracic Surg. 1997;12:98–100.
82. Massard G, Rougé C, Dabbagh A, et al. Tracheobronchial lacerations after
intubation and tracheostomy. Ann Thorac Surg. 1996;61:1483.
83. Agro FE, Antonelli S, Cataldo R. Use of Shikani flexible seeing stylet
for intubation via the intubating laryngeal mask airway. Can J Anaesth.
2005;52(6):657.
84. Rosenblatt, William HMD. Preoperative planning of airway management
in critical care patients. Crit Care Med. 2004;32:186.
85. Rosenblatt WH. The Airway Approach Algorithm: a decision tree for organizing preoperative airway information. J Clin Anesth. 2004;16(4):312.
86. Sanchez A, Trivedi NS, Morrison DE. Preparation of the patient for awake
intubation. In: Benumof JL, ed. Airway Management: Principles and Practice. St. Louis: Mosby-YearBook; 1996:159.
87. Atlas GM, Mort TC. Attempts at emergent tracheal intubation of inpatients: a retrospective practice analysis comparing adjunct sedation with or
without neuromuscular blockade. Internet J Anesth. 2003;7(2).
88. Vijayakumar E, Bosscher H, Renzi FP, et al. The use of neuromuscular
blocking agents in the emergency department to facilitate tracheal intubation in the trauma patient: help or hindrance? J Crit Care. 1998;13:1.
89. Caplan RA, Posner KL, Ward RJ et al. Adverse respiratory events in anesthesia: a closed claim analysis. Anesthesiology. 1990;72:828.
90. Schwartz DE, Matthay MA, Cohen N. Death and other complications of
emergency airway management in critically ill adults: a prospective investigation of 297 tracheal intubations. Anesthesiology. 1995;82:367.
91. Cheney RW, Posner KL, Caplan RA. Adverse respiratory events infrequently leading to malpractice suits: a closed claim analysis. Anesthesiology.
1991;75:932.
92. Domino KB, Posner KL, Caplan RA, et al. Airway injury during anesthesia:
a closed claims analysis. Anesthesiology. 1999;91(6):1703–1711.
93. Orelup CM, Mort TC. Airway rescue with the bougie in the difficult emergent airway. Crit Care Med. 2004;32(12)S:A118.
94. Sugarman J, Mort TC. Exchange of the endotracheal tube in the “normal”
airway: strategies & complications. Crit Care Med. 2004;32(12)S:A80.
95. Oliwa N, Mort TC. Is a rapid sequence intubation always indicated for
emergency airway management of the upper GI bleeding patient? Crit Care
Med. 2005;33(12)S:A97.
96. Donahue S, Mort TC. LMA placement with light sedation/topical anesthesia in the critically ill. Crit Care Med. 2005;33(12)S:A86.
97. Ikeda H. The effects of head and body positioning on upper airway collapsibility in normal subjects who received midazolam sedation. J Clin Anesth.
2006;18(3):185.
98. Sakles JC, Laurin EG, Rantapaa AA, et al. Airway management in the
emergency department: a one year study of 610 intubations. Ann Em Med.
1998;31(3):325.
99. Tayal VS, Riggs RW, Marx JA, et al. Rapid-sequence intubation at an emergency medicine residency: success rate and adverse events during a two-year
period. Acad Emerg Med. 1999;6:31.
100. Shorten GD, Alfille PH, Gliklich RE. Airway obstruction following application of cricoid pressure. J Clin Anesth. 1991;3:403.
101. Georgescu A, Miller JN, Lecklitner ML. The Sellick maneuver causing complete airway obstruction. Anesth Analg. 1992;74:457.
102. Ho AMH, Wong W, Ling E, et al. Airway difficulties caused by improperly
applied cricoid pressure. J Emerg Med. 2001;20:29.
103. Vanner RG, Clarke P, Moore WJ, et al. The effect of cricoid pressure and
neck support on the view at laryngoscopy. Anaesthesia. 1997;52:896.
11:53
P1: OSO/OVY
GRBT291-37-39
554
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 30, 2008
Section III: Techniques, Procedures, and Treatments
104. Palmer JH, Ball DR. The effect of cricoid pressure on the cricoid cartilage
and vocal cords: an endoscopic study in anaesthetised patients. Anaesthesia.
2000;55:263.
105. Aoyama K, Takenaka I, Sata T, et al. Cricoid pressure impedes positioning and ventilation through the laryngeal mask airway. Can J Anaesth.
1996;43:1035.
106. Harry RM, Nolan JP. The use of cricoid pressure with the intubating laryngeal mask. Anaesthesia. 1999;54:656.
107. Asai T, Murao K, Shingu K. Cricoid pressure applied after placement of
laryngeal mask impedes subsequent fibreoptic tracheal intubation through
mask. Br J Anaesth. 2000;85:256.
108. Brimacombe J, White A, Berry A. Effect of cricoid pressure on the ease of
insertion of the laryngeal mask airway. Br J Anaesth. 1993;71:800.
109. Collins JS, Lemmens HJ, Brodsky JB, et al. Laryngoscopy and morbid
obesity: a comparison of the “sniff” and “ramped” positions. Obes Surg.
2004;14:1171.
110. Brodsky JB, Lemmens HJ, Brock-Utne JG, et al. Morbid obesity and tracheal intubation. Anesth Analg. 2002;94:732.
111. Neill AM, Angus SM, Sajkov D, et al. Effects of sleep posture on upper
airway stability in patients with obstructive sleep apnea. Am J Respir Crit
Care Med. 1997;155:199.
112. Berthoud MC, Peacock JE, Reilly CS. Effectiveness of preoxygenation in
morbidly obese patients. Br J Anaesth. 1991;67:464.
113. Boyce JR, Ness T, Castroman P, et al. A preliminary study of the optimal anesthesia positioning for the morbidly obese patient. Obes Surg.
2003;13:4.
114. Mort TC. Emergency airway management: a strategy to improve the
first pass success rate and improve patient safety. Crit Care Med.
2004;32(12)S:A80.
115. Sugarman J, Mort TC. Efficacy of an emergency airway management algorithm toward improving resident intubation success. Crit Care Med.
2004;32(12)S:A76.
116. Elwood T, Stillions DM, Woo D, et al. Nasotracheal intubation: a randomized trial of two methods. Anesthesiology. 2002;96(1):51.
117. Scamman FL, Babin RW. An unusual complication of nasotracheal intubation. Anesthesiology. 1983;59:352.
118. Sherry KM. Ulceration of the inferior turbinate: a complication of prolonged nasotracheal intubation. Anesthesiology. 1983;59:148.
119. Xue F, Zhang G, Liu J, Li X, et al. A clinical assessment of the Glidescope
videolaryngoscope in Nasotracheal intubation with general anesthesia. J
Clin Anesth. 2006;18(8):611.
120. Agro F, Hung OR, Cataldo R. Lightwand intubation using the Trachlight:
a brief review of current knowledge. Can J Anaesth. 2001;48(6):592.
121. Xue FS, Li CW, Sun HT. The circulatory responses to fiberoptic intubation:
a comparison of oral and nasal routes. Anaesthesia. 2006;61(7):639–645.
122. Pollard RJ, Lobato EB. Endotracheal tube location verified reliably by cuff
palpation. Anesth Analg. 1995;81(1):135.
123. Rich JM. Recognition and management of the difficult airway with special
emphasis on the intubating LMA-Fastrach/whistle technique: a brief review
with case reports. Proc (Bayl Univ Med Cent). 2005;18(3):220.
124. Ovassapian A. Fiberoptic Endoscopy and the Difficult Airway. Philadelphia: Lippincott-Raven; 1996.
125. Randell T, Yli-Hankala A, Valli H, et al. Topical anesthesia of the nasal
mucosa for fiberoptic airway endoscopy. Br J Anaesth. 1991;66:164.
126. Johnson DM. Endoscopic study of mechanisms of failure of endotracheal
tube advancement into the trachea during awake fiberoptic orotracheal
intubation. Anesthesiology. 2005;102(5):910.
127. Katsnelson T, Frost EAM, Farcon E, et al. When the endotracheal tube
will not pass over the flexible fiberoptic bronchoscope. Anesthesiology.
1992;76:152
128. Patiar S, Ho EC, Herdman RC. Partial middle turbinectomy by nasotracheal
intubation Ear Nose Throat J. 2006;85(6):380–382.
129. Prior S. Foreign body obstruction preventing blind nasal intubation. Anesth
Prog. 2006;53(2):49.
130. Gallagher TJ, Civetta JM. Acute maxillary sinusitis complicating nasotracheal intubation: a case report. Anesth Analg. 1976;55:885.
131. Grindlinger GA, Niehoff J, Hughes SL, et al. Acute paranasal sinusitis related to nasotracheal intubation of head-injured patients. Crit Care Med.
1987;15:214.
132. Kerwin AJ, Croce MA, Timmons SD, et al. Effects of fiberoptic bronchoscopy on intracranial pressure in patients with brain injury: a prospective clinical study. J Trauma. 2000;48:878.
133. Tinnesz P, Mort TC. Emergency airway rescue by the 2nd airway team after
failed attempts. Crit Care Med. 2004;32(12)S:A118.
134. Shulman GB, Nordin NG, Connelly NR. Teaching with a video system improves the training period but not subsequent success of tracheal intubation
with the Bullard laryngoscope. Anesthesiology. 2003;98(3):615.
135. Jacobson D, Mort TC. Comparison of direct laryngoscopy and a fiberoptic
stylet for emergency intubation. Anesthesiology. 2006;105(3):A816.
136. Sprung J, Weingarten T, Dilger J. The use of WuScope fiberoptic laryngoscopy for tracheal intubation in complex clinical situations. Anesthesiology. 2003;98(1):263.
137. Smith CE, DeJoy SJ. New equipment and techniques for airway management in trauma. Curr Opin Anaesth. 2001;14(2):197.
138. Connelly NR, Ghandour K, Robbins L, et al. Management of unexpected
difficult airway at a teaching institution over a 7-year period. J Clin Anesth.
2006;18(3):198.
139. Kaplan M, Ward D, Berci G. A new video laryngoscope: an aid to intubation
and teaching. J Clin Anesth. 2002;14:620.
140. Cooper R, Pacey JA, Bishop MJ, et al. Early clinical experience with
a new video laryngoscope (Glidescope) in 728 patients. Can J Anesth.
2005;52:191.
141. Watts ADJ, Gelb AW, Bach DB, et al. Comparison of Bullard and Macintosh laryngoscopes for endotracheal intubation of patients with a potential
cervical spine injury. Anesthesiology. 1997;87:1335–1342.
142. Heitz JW. The use of a gum elastic bougie in combination with a videolaryngoscope. J Clin Anesth. 2005;17(5):408.
143. Maharaj CH, Chonghaile MN, Higgins BD, et al. Tracheal intubation
by inexperienced medical residents using the Airtraq and Macintosh
laryngoscopes—a manikin study. Am J Em Med. 2006;24(7):769.
144. Mort TC. Laryngoscopy vs. optical stylet vs. optical laryngoscope (Airtraq)
for extubation evaluation. Anesthesiology. 2006;105(3):A823.
145. Turkstra T, Pelz D, Shaikh A. Comparison of Shikani optical stylet to macintosh laryngoscope for intubation of patients with potential cervical spine
injury: a randomized controlled fluoroscopic trial. J Neurosurg Anesthesiol.
2006;18(4):327.
146. Jabre P. Use of gum elastic bougie for prehospital difficult intubation. Am
J Emerg Med. 2005;23(4):552.
147. Combes X, Le Roux B, Suen P, et al. Unanticipated difficult airway in
anesthetized patients: prospective validation of a management algorithm.
Anesthesiology. 2004;100(5):1146.
148. Mort TC. The incidence and risk factors for cardiac arrest during emergency
tracheal intubation: a justification for incorporating the ASA Guidelines in
the remote location. J Clin Anesth. 2004;16(7):508.
149. Mort TC. Esophageal intubation with indirect clinical tests during emergency tracheal intubation: a report on patient morbidity. J Clin Anesth.
2005;17(4):255.
150. Salem MR. Verification of endotracheal tube position. Anesth Clin NA.
2001;19(4):813.
151. Andres AH, Langenstein H. The esophageal detector device is unreliable
when the stomach has been ventilated. Anesthesiology. 1999;91(2):566–
568.
152. Wright RS, Burdumy TJ. Acute endotracheal tube occlusion caused by use
of an esophageal detector device: report of a case and a discussion of its
utility. Ann Emerg Med. 2004;43(5):626–629.
153. Bair AE, Laurin EG, Schmitt BJ. An assessment of a tracheal tube introducer
as an endotracheal tube placement confirmation device. Am J Emerg Med.
2005;23(6):754.
154. Ezri T, Khazin V, Szmuk P, et al. Use of the Rapiscope vs. chest auscultation for detection of accidental bronchial intubation in non-obese patients
undergoing laparoscopic cholecystectomy. J Clin Anesth. 2006;18(2):118.
155. Kemmots O. Six cases of endotracheal tube obstruction. Jpn J Anesthesiol.
1971;21:259.
156. Keenan RL, Boyan CP. Decreasing frequency of anesthetic cardiac arrests.
J Clin Anesth. 1991;3:354–357.
157. Hedden M, Erosoz CEJ, Donnelly WH, et al. Laryngotracheal damage after
prolonged use of orotracheal tubes in adults. JAMA. 1969;207:703.
158. Dubick MN, Wright BD. Comparison of laryngeal pathology following long term oral and nasal endotracheal intubation. Anesth Analg.
1978;57:663.
159. Kastanos N, Miro RE, Perez AM, et al. Laryngotracheal injury due to
endotracheal intubation incidence, evolution and predisposing factors: a
prospective long term study. Crit Care Med. 1983;11:362.
160. Esteller-More E, Ibanez J, Matino E, et al. Prognostic factors in laryngotracheal injury following intubation and/or tracheotomy in ICU patients. Eur
Arch Otorhinolaryngol. 2005;262(11):880.
161. Mort TC. When failure to intubate is failure to oxygenate. Crit Care Med.
2006;34:2030.
162. Mort TC. Preoxygenation remains essential before emergency tracheal intubation. Crit Care Med. 2006;34:1860.
163. Mort TC. Preoxygenation in critically ill patients requiring emergency tracheal intubation. Crit Care Med. 2005;33(11):2672–2675.
164. Mort TC. Morbid obesity—risky airway business. Crit Care Med.
2005;33(12)S:A81.
165. Benumof JL. Preoxygenation: best method for both efficacy and efficiency?
Anesthesiology. 1999;91:603.
166. Baraka AS, Taha SK, Aouad MT, et al. Preoxygenation: comparison of
maximal breathing and tidal volume breathing techniques. Anesthesiology.
1999;91:612.
167. Salem MR, Joseph NJ, Crystal GJ, et al. Preoxygenation: comparison of maximal breathing and tidal volume techniques. Anesthesiology.
2000;92:1845.
168. Bair AE, Filbin MR, Kulkarni RG, et al. The failed intubation attempt in
the emergency department: analysis of prevalence, rescue techniques, and
personnel. J Emerg Med. 2002;23:131.
169. Warner MA. Is pulmonary aspiration still an important problem in anesthesia. Curr Opin Anaesth. 2000;13(2):215.
170. Schwab TM, Greaves TH. Cardiac arrest as a possible sequela of
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Chapter 38: Airway Management
171.
172.
173.
174.
175.
176.
177.
178.
179.
180.
181.
182.
183.
184.
185.
186.
187.
188.
189.
190.
191.
192.
193.
194.
195.
196.
197.
198.
199.
200.
201.
202.
203.
critical airway management and intubation. Am J Emerg Med.
1998;16:609.
Oliwa N, Mort TC. Airway management of the upper GI bleeding patient:
are extra measures warranted? Crit Care Med. 2006;33(12)S:A98.
McCoy EP, Russell WJ, Webb RK. Accidental bronchial intubation. An
analysis of AIMS incident reports from 1988 to 1994 inclusive. Anaesthesia.
1997;52(1):24.
Schwartz DE, Liberman JA, Cohen NH. Confirmation of endotracheal tube
position. Crit Care Med. 1995;23(7):1307–1308.
Seto K, Goto H, Hacker DC, et al. Right upper lobe atelectasis after inadvertent right main bronchial intubation. Anesth Analg. 1983;62:851.
Gandhi SK, Munshi CA, Kampine JP. Early warning sign of an accidental endobronchial intubation: A sudden drop or sudden rise in PaCO2 ?
Anesthesiology. 1986;65:114.
Owen RL, Cheney FW. Endobronchial intubation: a preventable complication. Anesthesiology. 1987;67:255.
Greene ER Jr, Gutierez FA. Tip of polyvinyl chloride double-lumen endotracheal inadvertently wedged in left lower lobe bronchus. Anesthesiology.
1986;64:406.
Brodsky JB, Shulman MS, Mark JBD. Malposition of left-sided doublelumen endotracheal tubes. Anesthesiology. 1985;62:667.
Glinsman D, Pavlin EG. Airway obstruction after nasal-tracheal intubation.
Anesthesiology. 1982;56:229.
Keenan RL, Boyan CP. Cardiac arrest due to anesthesia. JAMA.
1985;253:2373–2377.
Chopra V, Bovill JG, Spierdijk H. Accidents, near accidents and complications during anaethesia. Anaethesia. 1990;45:3.
Kubota Y, Toyoda Y, Kubota H, et al. Frequency of anesthetic cardiac
arrest and death in the operating room at a single general hospital over a
30-year period. J Clin Anesth. 1994;6:227.
Kane DM, Mort TC. Emergency intubation in the cardiac catheterization
suite: hemodynamic consequences. Crit Care Med. 2004;32(12)S:A46.
Wintermark M, Chioléro R, van Melle G, et al. Relationship between brain
perfusion computed tomography variables and cerebral perfusion pressure
in severe head trauma patients. Crit Care Med. 2004;32(7):1579.
Jellish WS. Anesthetic issues and perioperative blood pressure management
in patients who have cerebrovascular diseases undergoing surgical procedures. Neurol Clin. 2006;24(4):647.
Yastrebov K. Intraoperative management: carotid endarterectomies. Anesthesiol Clin NA. 2004;22(2):265.
Nicholls TP, Shoemaker WC, Wo CCJ. Survival, hemodynamics, and tissue
oxygenation after head trauma. J Am Coll Surg. 2006;202(1):120.
Rose DK, Cohen MM. The incidence of airway problems depends on the
definition used. Can J Anaesth. 1996;43(1):30–34.
Franklin C, Samuel J, Hu TC. Life-threatening hypotension associated with
emergency intubation and the initiation of mechanical ventilation. Am J
Emerg Med. 1994;12(4):425.
Klinger JR. Hemodynamics and positive end-expiratory pressure in critically ill patients. Crit Care Clin. 1996;12:841.
Demetriades D, Martin M, Ali Salim A, et al. Relationship between American College of Surgeons trauma center designation and mortality in patients
with severe trauma. J Am Coll Surg. 2006;202(2):212–215.
Mort TC. Emergency intubation: octogenarians and beyond. Crit Care
Med. 2005;33(12)S:A85.
Mort TC. ETT cuff leak: a safety strategy. Crit Care Med. 2005;
33(12)S:A85.
Mort TC. Unplanned tracheal extubation outside the operating room: a
quality improvement audit of hemodynamic and tracheal airway complications associated with emergency tracheal reintubation. Anesth Analg.
1998;86:1171.
Jaber S, Chanques G, Altairac C, et al. A prospective study of agitation
in a medical-surgical ICU incidence, risk factors, and outcomes. Chest.
2005;128(4):2749.
Krinsley JS, Barone JE. The drive to survive unplanned extubation in the
ICU. Chest. 2005;128(2):560.
Benumof JL, Scheller MD. The importance of transtracheal jet ventilation in the management of the difficult airway. Anesthesiology. 1989;71:
769.
Cinar SO. Isolated bilateral paralysis of the hypoglossal and recurrent laryngeal nerves (Bilateral Tapia’s syndrome) after transoral intubation for
general anesthesia. Acta Anaesthesiol Scand. 2005;49(1):98.
Rubin AD. Arytenoid cartilage dislocation: a 20-year experience. J Voice.
2005;19(4):687.
Sagawa M. Bilateral vocal cord paralysis after lung cancer surgery with a
double-lumen endotracheal tube: a life-threatening complication. J Cardiothorac Vasc Anesth. 2006;20(2):225.
Dimarakis I. Vocal cord palsy as a complication of adult cardiac
surgery: surgical correlations and analysis. Eur J Cardiothorac Surg.
2004;26(4):773.
Ulrich-Pur H. Comparison of mucosal pressures induced by cuffs of different airway devices. Anesthesiology. 2006;104(5):933.
Gomes Cordeiro AM. Possible risk factors associated with moderate or
severe airway injuries in children who underwent endotracheal intubation.
Pediatr Crit Care Med. 2004;5(4):364.
555
204. Gaylor EB, Greenberg SB. Untoward sequelae of prolonged intubation.
Laryngoscope. 1985;95:1461.
205. Fan CM. Tracheal rupture complicating emergent endotracheal intubation.
Am J Emerg Med. 2004;22(4):289.
206. Cooper RM. The use of an endotracheal ventilation catheter in the management of difficult extubations. Can J Anaesth. 1996;43:90.
207. Benumof JL. Airway exchange catheters: simple concept, potentially great
danger. Anesthesiology. 1999;91(2):342–344.
208. Cooper RM. Extubation and changing endotracheal tube. In: Benumof J,
ed. Airway Management. St. Louis: Mosby; 1995.
209. Frutos-Vivar F, Ferguson ND, Esteban, A, et al. Risk factors for extubation
failure in patients following a successful spontaneous breathing trial. Chest.
2006;130(6):1664.
210. Epstein SK. Preventing postextubation respiratory failure. Crit Care Med.
2006;34(5):1547.
211. Epstein SK, Ciubotaru RL. Independent effects of etiology of failure and
time to reintubation on outcome for patients failing extubation. Am J Respir
Crit Care Med. 1998;158(2):489–493.
212. Ferrer M, Valencia M, Nicolas JM, et al. Early non-invasive ventilation
averts extubation failure in patients at risk. A randomized trial. Am J Respir
Crit Care Med. 2006;173(2):164.
213. Esteban A, Frutos-Vivar F, Ferguson ND, et al. Noninvasive positivepressure ventilation for respiratory failure after extubation. N Engl J Med.
2004;350:2452.
214. Keenan SP, Powers C, McCormack DG, et al. Noninvasive positive-pressure
ventilation for postextubation respiratory distress: a randomized controlled
trial. JAMA. 2002;287:3238.
215. Nava SGC, Fanfulla F, Squadrone E, et al. Noninvasive ventilation to prevent respiratory failure after extubation in high-risk patients. Crit Care
Med. 2005;33:2456.
216. Salam A, Tilluckdharry L, Amoateng-Adjepong Y, et al. Neurologic status, cough, secretions and extubation outcomes. Intensive Care Med.
2004;30:1334.
217. Chung YH, Chao TY, Chiu CT, et al. The cuff-leak test is a simple tool to
verify severe laryngeal edema in patients undergoing long-term mechanical
ventilation. Crit Care Med. 2006;34(2):409.
218. Miller RL, Cole RP. Association between reduced cuff leak volume and
postextubation stridor. Chest. 1996;110:1035.
219. Jaber S, Chanques G, Matecki S, et al. Post-extubation stridor in intensive
care unit patients. Risk factors evaluation and importance of the cuff-leak
test. Intensive Care Med. 2003;29:6.
220. De Bast Y, De Backer D, Moraine JJ, et al. The cuff leak test to predict
failure of tracheal extubation for laryngeal edema. Intensive Care Med.
2002;28:1267–1272.
221. Sandhu RS, Pasquale MD, Miller K, et al. Measurement of endotracheal
tube cuff leak to predict postextubation stridor and need for reintubation.
J Am Coll Surg. 2000;190:682.
222. Kwon B, Yoo JU, Furey CG, et al. Risk factors for delayed extubation
after single-stage, multi-level anterior cervical decompression and posterior
fusion. J Spinal Disord Tech 2006;19(6):389.
223. Markovitz BP, Randolph AG. Corticosteroids for the prevention of reintubation and postextubation stridor in pediatric patients: a meta-analysis.
Pediatr Crit Care Med. 2002;3:223.
224. Meade MO, Guyatt GH, Cook DJ, et al. Trials of corticosteroids to prevent
postextubation airway complications. Chest. 2001;120:464S.
225. Cheng K-C, Hou C-C, Huang H-C, et al. Intravenous injection of methylprednisolone reduces the incidence of postextubation stridor in intensive
care unit patients. Crit Care Med. 2006;34:1345.
226. Dower AM, George RB, Law JA, et al. Comparison of pre & postintubation
Cormack-Lehane and POGO scores using the AirwayCam(r) video system.
Anesthesiology. 2006;105:A527.
227. Dosemeci L, Yilmaz M, Yegin A, et al. The routine use of pediatric airway
exchange catheter after extubation of adult patients who have undergone
maxillofacial or major neck surgery: a clinical observational study. Crit
Care. 2004;8:385.
228. Loudermilk EP, Hartmanngruber M, Stoltfus DP, et al. A prospective
study of the safety of tracheal extubation using a pediatric airway exchange catheter for patients with a known difficult airway. Chest. 1997;111:
1660.
229. Mort TC. Continuous airway access for the difficult extubation: the efficacy of the airway exchange catheter. Anesth Analg. 2007;105(5):1357–
1362.
230. Baraka AS. Tension pneumothorax complicating jet ventilation via Cook
airway exchange catheter. Anesthesiology. 1999;91:557–558.
231. DeLima L, Bishop M. Lung laceration after tracheal extubation over a
plastic tube changer. Anesth Analg. 1991;73:350–351.
232. Seitz PA, Gravenstein N. Endobronchial rupture from endotracheal reintubation with an endotracheal tube guide. J Clin Anesth. 1989;1:214–
217.
233. Benumof JL, Gaughan SD. Concerns regarding barotrauma during jet ventilation. Anesthesiology. 1992;76:1072–1073.
234. Fetterman D, Dubovoy A, Reay M. Unforeseen esophageal misplacement
of airway exchange catheter leading to gastric perforation. Anesthesiology.
2006;104:1111–1112.
11:53
P1: OSO/OVY
GRBT291-37-39
556
P2: OSO/OVY
QC: OSO/OVY
GRBT291-3641G
T1: OSO
Printer: Yet to come
GRBT291-Gabrielli-v2.cls
October 30, 2008
Section III: Techniques, Procedures, and Treatments
235. Mort TC. Exchange of a nasal ETT to the oral position: patient safety vs
method. Crit Care Med. 2005;33(12)S:A114.
236. Smith CE. Exchange of a double-lumen endobronchial tube using fiber-optic
laryngoscopy (WuScope) in a difficult intubation patient. J Clin Anesth.
2006;18(5):398.
237. Muto T, Akizuki K, Wolford LM. Simplified technique to change the endotracheal tube from nasal to oral to facilitate orthognathic and nasal surgery.
J Oral Max Surg. 2006;64(8):1310–1312.
238. Wolpert A, Goto H. Exchanging an endotracheal tube from oral to nasal intubation during continuous ventilation. Anesth Analg. 2006;103(5):1335.
CHAPTER 39 ■ HYPERBARIC OXYGEN THERAPY
RICHARD E. MOON r JOHN PAUL M. LONGPHRE
The first recorded attempt to use hyperbaric therapy was in
1662, when Henshaw in Britain used an organ bellows to manipulate the pressure within an enclosed chamber designed
to seat a patient. He recommended high pressure for acute
diseases and low pressure for chronic diseases (1). The pressure fluctuations in either direction were probably quite small.
Widespread use of hyperbaric therapy began in the 19th century. At that time, powerful pneumatic pumps were designed,
which could be used to compress chambers with air. Physicians
in France and Britain used compressed air treatment for miscellaneous conditions. Junod used pressures of 1.5 atmospheres
absolute (ATA) to treat patients, but did experiments up to 4
ATA (2). Simpson, using pressures in the range of 1.3 to 1.5
ATA, reported treating a variety of complaints, including dysphonia, asthma, tuberculosis, menorrhagia, and deafness (1),
although without any physiologic basis.
Compressed air construction work was also developed in
the 1800s, in which men were exposed to elevated ambient
pressure within compartments for the purpose of excavating
tunnels or bridge piers in muddy soil that was otherwise subject to flooding. Upon decompression at the end of a work shift,
workers often developed joint pains or neurologic manifestations (caisson disease, the bends, or decompression sickness).
Although the pathophysiology (nitrogen bubble formation in
tissues; see below) was not understood, it was observed that recompression of these individuals could relieve the symptoms.
Administration of recompression therapy became routine during construction of the Hudson River tunnel in the 1890s (3).
All of these treatments used compressed air. Although oxygen breathing under pressure had been suggested for the treatment of decompression sickness as early as 1897 (4) and was
used intermittently over the next 30 years, systematic study
and use of hyperbaric oxygen would not occur until much
later.
Oxygen administration during recompression therapy for
decompression sickness increased the efficacy of the treatment
(5,6) and is now routinely used for both decompression sickness and gas embolism. The administration of oxygen at increased ambient pressure became known as hyperbaric oxygen
(HBO) therapy. In the 1950s, pilot investigations were performed of HBO as a therapy for diseases other than those
related to gas bubbles, including carbon monoxide poisoning, clostridial myonecrosis (gas gangrene), and later, selected
chronic wounds.
For many years, the Undersea and Hyperbaric Medical Society has regularly reviewed and published information regarding
the use of HBO in selected diseases (7), and its recommendations have been widely accepted. The list of accepted indications (7) contains a heterogeneous group of conditions (Table
39.1), suggesting that more than one mechanism mediates the
clinical effects of HBO, including the increase in ambient pressure (partly responsible for its efficacy in conditions caused by
gas bubble disease) and pharmacologic effects of supraphysiologic increases in blood and tissue PO2 as discussed below.
EFFECTS OF HYPEROXIA
Blood Gas Values
Under normal clinical HBO therapy conditions (2–3 ATA),
breathing 100% oxygen can lead to arterial PO2 (PaO2 ) values
that are 10 to 17 times higher than normal (8,9). PaO2 levels can rise from the normal of 90 to 100 mm Hg (breathing
air at sea level, i.e., 1 ATA or normobaria) to 1,000 to
1,700 mm Hg in healthy subjects breathing 100% oxygen at
2 to 3 ATA (see Table 39.2).
One effect is an increase in blood oxygen content:
Blood O2 content (mL/dL)
= 1.34 · Hb · SaO2 /100 + 0.003 · PaO2
[1]
where Hb is hemoglobin concentration (g/dL), SaO2 is arterial
Hb-O2 saturation, and PaO2 is arterial oxygen tension.
The second term of Eq. 1 represents the dissolved oxygen
proportion, which under normal circumstances represents a
small fraction of total arterial oxygen content, and is therefore
often disregarded. However, during HBO, this dissolved fraction is substantially increased (see Table 39.2). In fact, mixed
venous Hb-O2 saturation is 100% under resting conditions
while breathing 100% oxygen at 3 ATA. Thus, oxygen delivery can be maintained under these circumstances without
hemoglobin. This was shown by Boerema et al. in a swine
model (10).
PaCO2 is not significantly affected by the increased pressure
(8,9,11), although the venoarterial PCO2 difference is slightly
increased, mostly because of a reduction in cardiac output.
11:53
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 39: Hyperbaric Oxygen Therapy
TA B L E 3 9 . 1
557
Hemodynamics
CONDITIONS AMENABLE TO TREATMENT WITH
HYPERBARIC OXYGEN THERAPY
Gas bubble disease
Air or gas embolisma (236–238)
Decompression sicknessa (237,238)
Poisonings
Carbon monoxide poisoninga (151–153,239)
Cyanide (154,165)
Carbon tetrachloride (176,240)
Hydrogen sulfide (154,168,169)
Necrotizing soft tissue infections
Clostridial myositis and myonecrosisa (181,241–243)
Mixed aerobic/anaerobic necrotizing soft tissue infectionsa
(182,184,243,244)
Mucormycosis (187,245)
Aerobic infections
Refractory osteomyelitisa (7)
Intracranial abscessa (7)
Streptococcal myositis (48)
Acute ischemia
Crush injury, compartment syndrome, and other acute
traumatic ischemic conditionsa (246)
Compromised skin grafts and flapsa (31,33,247,248)
Acute hypoxia
Acute exceptional anemiaa (191)
Support of oxygenation during therapeutic lung lavage
(219,249)
Thermal burnsa (197,198,200,250)
Delayed radiation injury (soft tissue and osteoradionecrosis)a
(7,251–254)
Enhancement of healing in selected problem woundsa (7,255)
Envenomation
Brown recluse spider bite (256,257)
a
Approved by the Undersea and Hyperbaric Medical Society (Gesell
LB, ed. Hyperbaric Oxygen Therapy: A Committee Report. Durham,
NC. Undersea and Hyperbaric Medical Society; 2008; see also:
http://www.uhms.org).
Vasoconstriction
Hyperoxia causes peripheral vasoconstriction (8,9,12), regardless of atmospheric pressure (13). At a mere 2 ATA, systemic
vascular resistance can increase by 30% in dogs (14). The
mechanisms for this include scavenging of nitric oxide (NO)
by superoxide anion (O2 – ) (15) and increased binding of NO
at high PO2 to hemoglobin, forming S-nitrosohemoglobin (9).
Vasoconstriction has the positive effect of reducing edema
in injured tissues and surgical flaps (discussed later). During
HBO, the arterial blood O2 content is sufficiently high that
despite vasoconstriction and reduced blood flow, oxygen delivery is increased (16) (see also Table 39.2). Although peripheral vasoconstriction occurs in normal skin during hyperbaric oxygen exposure, repetitive intermittent HBO appears to increase the microvascular blood flow of healing
wounds (17).
Heart rate and cardiac output both decrease by 13% to 35%
under hyperbaric conditions (Table 39.2) (8,9,14,18,19). Small
changes may occur in systemic and pulmonary artery pressure, with an increase in systemic vascular resistance (SVR)
and a decrease in pulmonary vascular resistance (PVR) (9). Despite the reduced cardiac output, oxygen delivery is increased
(Fig. 39.1).
Organ Blood Flow
Studies in large animals indicate that the decrease in peripheral blood flow is limited primarily to the cerebral and peripheral vascular beds, with other organs unaffected (14). In rats,
HBO has been shown to decrease organ blood flow, including
the myocardium, kidney, brain, ocular globe, and gut (15,20–
22). In autonomically blocked conscious dogs at 3 ATA, coronary blood flow is decreased (23). Another dog study at 2 ATA
revealed no change in coronary, hepatic, renal, or mesenteric
blood flow (14).
Cellular and Tissue Effects
In a myocutaneous flap model during reperfusion following 4
hours of ischemia, Zamboni et al. described a delayed decrease
in blood flow (24). This flow reduction appears to be associated
with adherence of leukocytes to the endothelium of the small
vessels, an effect that is significantly inhibited by HBO. A delayed reduction in cerebral blood flow has also been observed
after arterial gas embolism in the brain (25), which has similarly been attributed to leukocyte accumulation in the capillaries (26). HBO reduces cerebral infarct volume and myeloperoxidase activity, a marker of neutrophil recruitment (27). In
other studies using animal models, it has been observed that
HBO pretreatment reduces ischemia/reperfusion injury to the
liver (28). HBO reduces ischemia/reperfusion injury to the intestine (29,30) and muscle (31), as well as reducing ischemiainduced necrosis in muscle (32–37), brain (38,39), and kidney
(40). One mechanism for this effect of HBO appears to be the
inhibition of leukocyte β 2 -integrin function (41–43). Part of
the beneficial effect of HBO in these settings is speculated to
be due to the prevention of endothelial leukocyte adherence.
After focal ischemia, HBO also reduces postischemic blood–
brain barrier damage and edema (44) and has an antiapoptotic effect (45).
Antibacterial Effects
The increase in PO2 during HBO can be toxic to anaerobic bacteria, which lack antioxidant defense mechanisms. In addition,
HBO has effects on aerobic organisms via neutrophil mechanisms. Killing of aerobic bacteria by leukocytes is related to
the O2 -dependent generation of reactive oxygen species within
the lysosomes. In vitro studies have demonstrated that phagocytic killing of Staphylococcus aureus by polymorphonuclear
leukocytes becomes less effective as ambient PO2 is decreased.
This mechanism appears to be important in vivo when tissue
13:42
558
Cardiac output
(L min−1 )
6.5 ± 1.1
5.9 ± 1.0
HR (bpm)
66.6 ± 8.2
62.7 ± 12.5
Condition
1 ATA, air
3 ATA, 100% O2
8.2 ± 3.9
9.3 ± 2.5
PA wedge
pressure
(mm Hg)
38 ± 3
35 ± 2
PaCO2
(mm Hg)
1,118 ± 235
1,286 ± 309
SVR (dynes
sec cm−5 )
42 ± 3
43 ± 3
P v CO2
(mm Hg)
67 ± 24
41 ± 11
PVR (dynes
sec cm−5 )
12.7 ± 0.8
12.7 ± 0.8
Hb (g/dL)
16.6 ± 1.1
21.1 ± 1.3
Arterial O2
content
(mL/dL)
1.7 ± 0.2
21.2 ± 3.0
Dissolved O2
(%)
ATA, atmospheres absolute; HR, heart rate; SVR, systemic vascular resistance; PVR, pulmonary vascular resistance. These data obtained in part from McMahon TJ, Moon RE, Luschinger BP, et al. Nitric
oxide in the human respiratory cycle. Nat Med. 2002;8:711–717.
13.6 ± 3.4
12.4 ± 2.1
Mean pulmonary
artery pressure
(mm Hg)
Mean arterial
pressure
(mm Hg)
96 ± 2
98 ± 3
93 ± 9
1,493 ± 224
1 ATA, air
3 ATA, 100% O2
92.5 ± 10.5
94.9 ± 9.4
76 ± 3
98 ± 2
42 ± 2
378 ± 164
SaO2 (%)
S v O2
(%)
Condition
P v O2
(mm Hg)
QC: OSO/OVY
PaO2
(mm Hg)
GRBT291-37-39
P2: OSO/OVY
BLOOD GAS AND HEMODYNAMIC VALUES IN 14 HEALTHY ADULTS BREATHING SPONTANEOUSLY (MEAN ± STANDARD DEVIATION)
TA B L E 3 9 . 2
P1: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Arterial O2 Content
(mL/dL)
Chapter 39: Hyperbaric Oxygen Therapy
25
Clinical Effects
20
At sufficiently high PO2 , any organ can be susceptible to oxygen
toxicity. However, within the clinical range of inspired PO2 (1–
3 ATA), the most susceptible tissues are the lung, brain, retina,
lens, and peripheral nerve.
15
1,500
O2 Delivery
(mL/min)
559
1,250
1,000
750
1 ATA
Air
3 ATA
100% O2
FIGURE 39.1. Arterial O2 content and delivery while breathing air at 1
atmosphere absolute (ATA) or 100% oxygen at 3 ATA. Measurements
are shown in a group of normal volunteers. (Data from McMahon TJ,
Moon RE, Luschinger BP, et al. Nitric oxide in the human respiratory
cycle. Nat Med. 2002;8:711–717.)
PO2 is low (e.g., in osteomyelitis) (46). In an animal model
of osteomyelitis, the cidal effect of tobramycin against Pseudomonas was increased when tissue PO2 was raised by the administration of 100% O2 at increased ambient pressure (47).
Published evidence also supports an augmentation of penicillin
by HBO in the treatment of soft tissue streptococcal infections (48).
Oxygen Toxicity
Pharmacology
Exposure of an animal to increased partial pressure of oxygen
results in higher rates of endogenous production of reactive
oxygen species, including superoxide anion (O2 – ), hydroxyl
radical (OH• ), hydrogen peroxide (H2 O2 ), and singlet oxygen, which are responsible for tissue oxygen toxicity (49–51).
Tissue O2 toxicity includes the following: Lipid peroxidation, sulfhydryl group inactivation, oxidation of pyridine nucleotides, inactivation of Na+ –K+ –ATPase and inhibition of
DNA, and protein synthesis. Toxic effects of these species depend upon both dose and duration of O2 exposure. In the central nervous system, HBO initially reduces NO availability and
causes vasoconstriction. HBO stimulates neuronal nitric oxide
production and causes the accumulation of peroxynitrite. Prior
to onset of a seizure, NO levels and blood flow both increase
above control levels (52,53). This, in turn, decreases brain γ aminobutyric acid (GABA) levels, creating an imbalance between glutamatergic and GABAergic synaptic function, which
is believed to be partly responsible for central nervous system
(CNS) O2 toxicity (54).
Brain. Oxygen toxicity of the central nervous system produces
a wide variety of manifestations (55). The most common mild
symptom is nausea; the most dramatic is generalized nonfocal convulsions. These are usually self-limited, even without
pharmacologic treatment, and have no long-term effects. The
occurrence of a hyperoxic seizure does not imply the development of a convulsive disorder. Factors that increase the risk of
CNS oxygen toxicity include hypercapnia and probably fever.
CNS O2 toxicity is uncommon when inspired PO2 is less
than 3 ATA. While in-water convulsions in divers have been
recorded at an inspired PO2 of 1.3 ATA, convulsions during
clinical hyperbaric oxygen therapy occur in only a small fraction of treatments. Approximately 0.02% of treatments at an
inspired PO2 of 2 ATA and 4% at 3 ATA. At an inspired PO2
less than 3 ATA, the risk of convulsions increases markedly, particularly in patients with sepsis. While anecdotal reports suggest that HBO may precipitate seizures in patients who have an
underlying predisposition (56), there are no epidemiologic data
to confirm this. When indicated, HBO should not be withheld
on the basis of an underlying seizure disorder.
Both CNS and pulmonary toxicity can be delayed by the use
of air breaks (a period of a few minutes where air is administered in lieu of 100% oxygen) (57–60). Oftentimes, the aura of
a hyperoxic convulsion occurs in the form of nausea or facial
paresthesias. The patient can be given an air break to avert such
a convulsion. Once the symptoms have resolved (usually within
a few minutes), the oxygen can be restarted without recurrence.
During the tonic-clonic phase of a seizure, the airway may be
obstructed. Therefore, it is imperative that chamber pressure
not be reduced during this time in order to avoid pulmonary
barotrauma and the possibility of arterial gas embolism. After
a convulsion, some practitioners recommend administering
prophylactic medication for the duration of HBO.
Prophylactic anticonvulsants such as phenytoin, phenobarbital, or benzodiazepines can reduce the chance of convulsions
when utilizing clinical treatment schedules with a significant
risk of CNS O2 toxicity (e.g., treatment pressure >3 ATA).
The authors’ practice is to load septic patients intravenously
with phenobarbital as tolerated, up to 12 mg/kg, prior to hyperbaric oxygen treatment at 3 ATA, with doses every 8 hours
to maintain a serum concentration in the therapeutic anticonvulsant range. When using inspired PO2 ≤2.8 ATA, the risk of
CNS toxicity is sufficiently low that prophylactic anticonvulsant therapy is not required.
Hyperoxic seizures and other CNS manifestations in diabetics can be caused by HBO-induced reduction in blood glucose.
Therefore, the occurrence of CNS O2 toxicity in a patient with
diabetes during HBO treatment should prompt the immediate
measurement of plasma glucose. When blood PO2 is extremely
high, bedside glucose measurement devices, particularly those
dependent upon a glucose oxidase reaction, can be inaccurate, producing measurements that significantly underestimate
the true value (61). Laboratory-based glucose measurement is
usually accurate.
13:42
P1: OSO/OVY
GRBT291-37-39
560
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Section III: Techniques, Procedures, and Treatments
Lungs. Pulmonary oxygen toxicity during hyperbaric oxygen
therapy is also PO2 and time dependent. Clinical HBO protocols have been empirically developed to minimize the risk of
pulmonary O2 toxicity, which almost never occurs during routine daily or twice-daily clinical treatments. However, it can
occur during extended treatments that are used for treating gas
embolism or decompression sickness, in which inspired PO2 is
as high as 2.8 ATA. The initial manifestation is usually a burning substernal chest pain and cough (62), which is most likely
due to tracheobronchitis. Continued exposure to oxygen can
produce more severe manifestations such as dyspnea and acute
respiratory distress syndrome (ARDS). Measurable abnormalities include reduced forced vital capacity and carbon monoxide
transfer factor (DLCO). Pulmonary oxygen toxicity symptoms
may not be evident in patients who are sedated and mechanically ventilated. Moreover, such patients often have pulmonary
infiltrates for a variety of reasons and it may be impossible to
distinguish the possible additive effects of pulmonary O2 toxicity.
While the maximum safe inspired PO2 during clinical hyperbaric oxygen therapy is based mainly upon CNS O2 toxicity limits, the safe exposure duration is determined by pulmonary limits. Prediction formulas have been developed that
approximate the average reduction in vital capacity after continuous oxygen exposure (63–65). However, the usefulness
of these algorithms for individual patients is severely limited due to individual variability and comorbid factors that
may affect O2 susceptibility, such as prior exposure, intermittent exposure, and endotoxemia. HBO treatment schedules that include periods of air breathing (“air breaks”)
interspersed between O2 periods reduce the rate of onset
of both pulmonary and CNS toxic manifestations and can
increase the overall dose of oxygen that is tolerated. In
the awake patient, the occurrence of burning, retrosternal
chest pain is a more useful indicator of incipient pulmonary
toxicity.
If standard HBO treatment schedules are used (e.g., 2 ATA/
2 hours, 2.5 ATA/90 minutes one to two times daily, or U.S.
Navy treatment tables), pulmonary O2 toxicity is almost never
clinically evident. It is seen only with the most extreme levels of
hyperbaric exposure such as may be required for severe neurologic decompression illness. Furthermore, most minor pulmonary oxygen toxicity resolves within 12 to 24 hours of air
breathing. Complete reversal of vital capacity (VC) decrements,
as large as 40% of control, has been observed after extended O2
exposure at 2 ATA (66). Therefore, in clinical situations requiring aggressive HBO therapy such as spinal cord decompression
sickness or arterial gas embolism, some degree of pulmonary
O2 toxicity is acceptable.
Supplemental O2 administration at 1 ATA between HBO
treatments can accelerate the onset of symptoms of pulmonary
O2 toxicity during subsequent HBO. Thus, if O2 is absolutely
required between HBO treatments, it is prudent to use the lowest concentration.
Some antineoplastic agents, such as bleomycin (67,68) and
mitomycin C (69), can predispose to fatal pulmonary O2 toxicity, probably due to drug-induced reduction in antioxidant
defenses. The risk of pulmonary O2 toxicity due to HBO therapy in patients with previous exposure to either of these agents
is unknown, although 6 months after the agent has been discontinued, HBO seems to be safe. Even after this point, in some
patients, HBO induces mild pulmonary O2 toxicity symptoms
such as retrosternal burning chest pain, which can be managed
with air breaks.
Eye. Repetitive hyperbaric oxygen therapy causes myopia,
which is due to a reversible refractive change in the lens (70). A
measurable change in visual acuity usually does not occur until
after 20 or so treatments. The myopia usually resolves over several weeks, in about the same time period as the onset; however,
some residual myopia may remain. On the basis of one study, it
has been suggested that HBO treatment may predispose to nuclear cataract formation (71). However, many of the patients
in this study received hundreds of hours of HBO, considerably more than is customary. Furthermore, nuclear cataracts
are more common in diabetes, which is frequently a comorbidity in patients requiring HBO. Extended exposure to PO2 of 3
ATA can also cause retinal toxicity, manifested by tunnel vision
(72,73). However, such exposures are beyond the range used
clinically.
Peripheral Nerve. After hyperbaric oxygen exposure, some patients experience paresthesias, usually in their fingers and toes,
generally after several HBO exposures but occasionally after
a single prolonged treatment. The physical exam is normal,
and the symptoms resolve within a few hours. This manifestation has no known clinical significance and is not a reason to
discontinue hyperbaric therapy.
PHYSICAL EFFECTS OF
COMPRESSION/DECOMPRESSION
Boyle’s Law
Clinically, the complications of HBO therapy that most frequently occur are those related to the body’s gas-containing
spaces (74). Dealing with volume changes in these gascontaining spaces is unique to HBO therapy. For a gas, absolute pressure and volume are inversely related. The increase
in pressure during HBO treatment will therefore decrease the
volume of closed gas-containing spaces within the body, such
as the gastrointestinal tract or middle ear and, in the event of
gas embolism or decompression sickness, bubbles.
EFFECTS OF GASES
OTHER THAN OXYGEN
Nitrogen
The narcotic properties of compressed air were first reported
by Junod in 1835 as described by Bennett and Rostain (75).
Hyperbaric nitrogen causes narcosis or pleasant intoxication
at pressures greater than about 4 ATA in most individuals and
near unconsciousness at greater than 10 ATA (76). Since patients breathe oxygen, nitrogen narcosis is only a problem for
tenders in multiplace hyperbaric chambers. However, most hyperbaric treatments occur between 2 and 3 ATA, where symptoms of nitrogen narcosis are exceedingly mild.
Nitrogen (and other inert breathing gases such as helium) is the major causative agent of decompression sickness. During decompression, excess tissue nitrogen can become
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 39: Hyperbaric Oxygen Therapy
supersaturated, come out of solution, and form bubbles. This
can lead to decompression sickness, with manifestations depending on their location and secondary effects.
Trace Gases
The pharmacologic effects of gases are proportional to their
partial pressures. Although a trace gas may only be present
in minute quantities, as the chamber pressure rises, so does
the partial pressure of a gas. Therefore, gases such as carbon
monoxide or carbon dioxide in concentrations that have no
pharmacologic or toxic effects at 1 ATA may exert measurable
effects in a hyperbaric environment.
USE OF HYPERBARIC OXYGEN
FOR SPECIFIC DISEASES
Gas Embolism and
Decompression Sickness
Gas bubbles in the body can be due to direct gas entry via
veins or arteries (arterial or venous gas embolism) or via in situ
formation due to gas supersaturation in divers, compressed air
workers, or aviators (decompression sickness). Since the two
conditions often both occur in the same patient (particularly in
divers), the principles of treatment of the two are the same. The
syndrome of either or both condition is commonly referred to
as decompression illness (DCI).
Arterial and Venous Gas Embolism
Entry of gas into the circulation can occur via several mechanisms. Gas embolism has recently been reviewed (77,78). In
divers breathing compressed gas, arterial gas embolism (AGE)
can ensue if decompression (ascent) occurs while the diver
holds his or her breath or due to gas trapping caused by focal or generalized airways obstruction. AGE due to this mechanism can result after an ascent to the surface of as little as
1 meter. AGE can also occur during diagnostic or therapeutic
procedures such as angiography.
Venous gas embolism (VGE) can result due to direct injection or entry via an open vein in which ambient pressure
exceeds venous pressure. This can exist during laparoscopic
surgical procedures due to the elevated intra-abdominal pressure, or open procedures in which venous pressure in the surgical wound is subatmospheric. The classic scenario for this is
an intracranial procedure in the sitting position. However, it
has also been described in procedures such as liver resection,
cesarean section, and spine surgery. VGE can also occur due
to oral hydrogen peroxide (H2 O2 ) ingestion. H2 O2 absorbed
into the circulation is broken down by catalase into water and
oxygen bubbles. VGE can result if a central venous catheter is
opened to air, particularly if the patient is breathing spontaneously. It has also been reported in patients with ARDS being ventilated with positive end-expiratory pressure (79). VGE
has been described during orogenital sex after blowing air intravaginally (80). Intravenous injection is better tolerated than
intra-arterial injection because of the pulmonary filter. However, if the rate of entry of gas into the veins is sufficiently
high, bubbles can traverse the pulmonary capillary network
561
and become arterial emboli. Large volumes can obstruct the
right heart or pulmonary artery and cause cardiac arrest.
Large volumes of arterial gas can cause acute obstruction
of large vessels. Small quantities tend to remain in the circulation only transiently; however, they can precipitate a sustained
reduction in local blood flow (25). The mechanism appears
to be endothelial damage (81) and adherence of leukocytes
(26,82–84). Endothelial barrier function is also impaired in
both the brain and lung, resulting in edema (85,86) and impaired endothelial-dependent vasoactivity (87). Animal models of AGE have revealed a significant elevation of intracranial
pressure (ICP) and depression of cerebral PO2 (88,89). In a
pig model, hyperventilation failed to correct these parameters
(90); however, HBO at 2.8 ATA (U.S. Navy Table 6, Fig. 39.4)
restored both ICP and brain PO2 toward normal (Fig. 39.3).
Clinical manifestations of AGE include acute loss of consciousness, confusion, focal neurologic abnormalities, and
cerebral edema. VGE causes acute dyspnea, tachypnea, hypotension, cardiac ischemia or arrest, and pulmonary edema
(86). In monitored patients, VGE is often heralded by a decrease in end-tidal PCO2 (91), although sometimes, with small
volumes of CO2 embolism such as during laparoscopy, it may
be increased. A mill-wheel murmur can be heard in some patients, although this sign is neither sensitive nor specific. Venous
gas bubbles in sufficient quantities can cross into the arterial circulation (producing AGE) either through the pulmonary capillary network or via an intracardiac shunt, such as a patent
foramen ovale.
Imaging is not useful for diagnosing either VGE or AGE.
Gas bubbles are rarely visible on radiographic images (92). Except in cases where associated conditions such as pneumothorax are suspected or neurologic conditions such as hemorrhage
require exclusion, imaging studies are not necessary and tend
to delay definitive treatment.
Decompression Sickness
During diving or exposure to a compressed gas environment
such as a hyperbaric chamber, inert gas (usually nitrogen)
is taken up by tissues. During decompression, inert gas can
become supersaturated and form bubbles in situ in tissues. Certain tissues are more susceptible to in situ bubble formation.
Manifestations of decompression sickness (DCS) can
range from mild to severe (Fig. 39.2). The most common
Skin
Pulmonary
Hemiparesis
Lightheadedness
Memory
Vertigo
Nausea/vomiting
Vision
Headache
Dizziness
Paresthesias
Pain
0
20
40
60
80
100 120 140
Number of Patients Reporting Symptom
160
FIGURE 39.2. Symptoms of decompression illness in a series of recreational divers. (Redrawn from Divers Alert Network. Annual Diving
Report. Durham, NC: Divers Alert Network; 2006.)
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
562
October 23, 2008
Section III: Techniques, Procedures, and Treatments
60
Untreated
ICP (mm Hg)
50
40
HBO at 60 min
30
HBO at 3 min
20
10
0
0
1
2
3
4
5
6
Time After Embolization (h)
PbrO2 (mm Hg)
800
700
600
500
400
300
200
100
0
HBO at 3 min
HBO at 60 min
(min after starting HBO)
HBO at 60 min
(min after embolization)
0
2
4
6
Time (min)
8
10
manifestations are joint pain and paresthesias. Although mild
cases can progress to severe, severe manifestations almost always occur within 12 hours after surfacing.
FIGURE 39.3. Effect of hyperbaric oxygen
(HBO) on intracranial pressure (ICP) and brain
PO2 in pigs after air embolism. Top panel: HBO
initially at 2.8 atmospheres absolute (ATA) (U.S.
Navy Table 6) reduces ICP compared with no
treatment, whether it is started 3 minutes or
60 minutes after embolization. Bottom panel:
Brain tissue PO2 in the two groups of animals.
For the 60-minute group, the closed circles represent PbrO2 in the first 10 minutes after embolization; the open circles represent PbrO2 in
the first 10 minutes after the start of HBO. Values in lower panel are mean ± standard deviation. (Redrawn from van Hulst RA, Drenthen J, Haitsma JJ, et al. Effects of hyperbaric
treatment in cerebral air embolism on intracranial pressure, brain oxygenation, and brain glucose metabolism in the pig. Crit Care Med.
2005;33:841–846.)
tion is therefore recommended, also because patient access and
supportive therapies can be more easily administered in this
position.
Hospital Treatment
Treatment of Decompression Sickness
and Arterial Gas Embolism
Prehospital Treatment
In addition to standard first aid principles, prehospital treatment of DCI consists of the administration of a high concentration of oxygen and fluid resuscitation. Oxygen administration
reduces bubble size and can sometimes abolish symptoms and
signs of decompression illness. A published study has provided
epidemiologic evidence for its efficacy (93). Use of high concentrations of oxygen (preferably 100%) is recommended until
definitive treatment is available. Periodic air breaks to reduce
toxicity may be appropriate (e.g., 5 minutes every 30 minutes).
The administration of oxygen for longer than 12 hours should
be based upon the severity of the injury or the presence of hypoxemia breathing room air.
Both head-down and lateral decubitus positions have been
recommended based on animal studies (94, 95). However,
the hemodynamic response to venous gas embolism is unaffected by body position (96,97), and prolonged head-down
position may exacerbate cerebral edema (98). Supine posi-
Standard treatment of gas embolism includes airway and ventilatory management, maintaining a high PaO2 and normal
PaCO2 (99) (Fig. 39.3), and support of arterial pressure.
Like other forms of neurologic injury, it is recommended that
when managing neurologic DCI, both hyperthermia and hyperglycemia (>140–185 mg/dL, 7.8–10.3 mM/L) should be
avoided or treated (100).
Physical Removal of Gas
Physical removal of gas after massive arterial gas embolism has
been described in cardiopulmonary bypass (101,102). Venous
gas embolism has been successfully treated with chest compression (103) and aspiration through catheters in the right atrium
(104,105) or pulmonary artery (106).
Recompression
Although symptomatic improvement can be obtained with oxygen at 1 ATA, the definitive treatment of both forms of decompression illness is hyperbaric oxygen. The safety and efficacy of HBO for the treatment of divers was initially shown
70 years ago (6). Since then, treatment protocols have been
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 39: Hyperbaric Oxygen Therapy
563
FIGURE 39.4. Top: U.S. Navy (USN) Treatment Table 5. According to USN guidelines, this table may be
used for symptoms involving skin (except for cutis marmorata), the lymphatic system, muscles and joints,
with a normal neurologic exam, and when all symptoms have completely resolved within 10 minutes of
reaching 2.8 atmospheres absolute (ATA). Bottom: USN Treatment Table 6. This table may be used for
all types of decompression illness. Extensions (additional oxygen breathing cycles) can be administered
at either treatment pressure (2.8 and 1.9 ATA). (Data from Navy Department. US Navy Diving Manual.
Revision 4. Vol. 5: Diving Medicine and Recompression Chamber Operations. NAVSEA 0910-LP-103–
8009. Washington, DC: Naval Sea Systems Command; 2005.)
empirically developed that have been shown to have a high
degree of success with a low probability of oxygen toxicity
(107). The most widely used treatment protocols (“tables”)
were developed by the U.S. Navy and promulgated via the Diving Manual (108) (Fig. 39.4). Both U.S. Navy Treatment Tables 5 and 6 use 100% oxygen breathing periods (“O2 cycles”)
interspersed with air breathing periods (“air breaks”) at 2.8
and 1.9 ATA in a two-step pattern (see Fig. 39.4). Guidelines
are available to administer additional O2 cycles (“extensions”)
at both pressures (108). The vast majority, if not all cases,
of DCI can be adequately treated using U.S. Navy treatment
tables.
The U.S. Navy tables were designed for use in multiplace
chambers, where air breaks can easily be administered by discontinuing O2 . Since monoplace chambers were designed to be
compressed with 100% O2 , shorter alternate treatment tables
were designed for their use (109,110) (Fig. 39.5). Although
direct comparisons with U.S. Navy tables have never been performed, case series suggest that these tables are efficacious for
DCI (110). Monoplace chambers fitted with an air supply and
delivery system can be used to administer treatment according
to traditional Navy tables (111).
FIGURE 39.5. Hart-Kindwall monoplace treatment table. This table
was designed for use in monoplace chambers without the capability of
administering air breaks. Except for the lack of air breaks and limited
ability for extension, it is similar to U.S. Navy Table 5, with a shorter
time at 2.8 atmospheres absolute (ATA) and longer time at 1.9 ATA.
(Data from Boerema I, Meyne NG, Brummelkamp WH, et al. Life
without blood. J Cardiovasc Surg [Torino]. 1960;1:133–146.)
13:42
P1: OSO/OVY
GRBT291-37-39
564
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Section III: Techniques, Procedures, and Treatments
Adjunctive Measures
In the 19th and early 20th century, recompression was the only
treatment administered to patients with decompression illness.
While hyperbaric oxygen remains the definitive treatment of
bubble disease, there is increasing recognition that adjunctive
therapies such as correction of hypovolemia may also be important (112).
Fluids. Severe decompression sickness is often associated with
capillary leak, intravascular volume depletion, and hemoconcentration. The Undersea and Hyperbaric Medical Society
(UHMS) recommends (level 1C) fluid administration to replenish intravascular volume, reverse hemoconcentration, and
support blood pressure (113). Measures that augment cardiac
preload such as supine position, head-down tilt, and water
immersion (114) significantly increase the rate of inert gas
washout. Thus, even in divers who are not dehydrated, there
may be some benefit to extra fluid loading. Intravenous isotonic
fluids without glucose (e.g., lactated Ringer solution, normal
saline, or colloids) are recommended for severe DCI. Patients
with mild symptoms may be treated with oral hydration fluids. For “chokes” (cardiorespiratory decompression sickness,
in which high bubble loads cause pulmonary edema), animal
studies suggest that aggressive fluid resuscitation can exacerbate pulmonary edema. Thus, for the patient with chokes,
aggressive fluid resuscitation may not be warranted, particularly if advanced life support modalities such as endotracheal
intubation and mechanical ventilation are not immediately
available. For isolated AGE, in which the pathology is limited
to cerebral infarction, aggressive fluid administration is also
unwarranted.
Anticoagulants. Intravascular bubbles can induce platelet accumulation, adherence, and thrombus formation. Indeed, in
a canine model of arterial gas embolism, therapeutic anticoagulation promoted a return in a short-term outcome: evoked
potential amplitude, but only when heparin was combined with
prostaglandin I2 (PGI2 ) and indomethacin (115). In this model,
heparin alone was ineffective. In other experiments, heparin
given either prophylactically or therapeutically to dogs with
DCI was not beneficial (116). Furthermore, tissue hemorrhage
can occur in decompression illness involving the spinal cord
(117–119), brain (120,121), and inner ear (122,123). Thus,
full therapeutic anticoagulation is not recommended.
Although anticoagulants are not indicated for the primary
injury in DCI, patients with leg immobility due to DCI-induced
spinal cord injury are at increased risk of deep vein thrombosis (DVT) and pulmonary thromboembolism (PE). Standard
prophylactic anticoagulant measures, typically low-molecularweight heparin (LMWH), are therefore recommended as soon
as feasible after the onset of injury. Full anticoagulation is appropriate for established DVT/PE. If LMWH is contraindicated, elastic stockings or intermittent pneumatic calf compression is recommended, although their efficacy in preventing
DVT or thromboembolism in DCI is unknown. Recommendations have been extrapolated from guidelines for traumatic
spinal cord injury; neither their efficacy nor safety in neurologic
DCI has been specifically confirmed. Thus, when facilities exist,
a screening test for DVT a few days after injury is appropriate
(113).
Lidocaine. The administration of lidocaine for arterial gas embolism is supported by several animal studies (124). No controlled human studies in accidental AGE have been performed.
However, gas emboli are frequently observed in cardiopulmonary bypass. In this setting, two studies have demonstrated
a beneficial effect of lidocaine administered in traditional antiarrhythmic doses on postoperative neurocognitive function
(125,126). Another study has shown benefit for nondiabetics
but not for diabetics (127). Human data directly pertinent to
DCI are confined to three cases of decompression sickness or
arterial gas embolism, published as case reports, which appeared to benefit from intravenous lidocaine (128,129). The
UHMS does not recommend the routine use of lidocaine for
DCI; however, recommendations have been made for its dosing (113). An appropriate end point is a serum concentration
suitable for an antiarrhythmic effect (2–6 mg/L).
Nonsteroidal Anti-inflammatory Drugs. These drugs are commonly used empirically for treatment of bends pain that does
not completely resolve with recompression. A randomized,
controlled trial has been published in which tenoxicam, a nonselective cyclo-oxygenase inhibitor, was compared with
placebo. Tenoxicam or placebo was administered during the
first air break of the first hyperbaric treatment and continued
daily for 7 days. Using as an end point the number of hyperbaric
treatments required to achieve complete relief of symptoms or
a clinical “plateau” of effect, the tenoxicam group required a
median of two treatments versus three for the placebo group.
The outcome at 6 weeks was not different (130). The UHMS
guidelines have assigned nonsteroidal anti-inflammatory drugs
a level 2B recommendation (113).
Corticosteroids. Unless given prophylactically, corticosteroids
have not been shown to be of benefit in animal models of DCI
(131–133). In a pig study, methylprednisolone treatment did
not protect against severe DCS, and the treated animals had
a greater mortality (134). In the absence of human trials of
corticosteroids in DCI and the lack of benefit in animal studies,
corticosteroids are not recommended.
Perfluorocarbons. Perfluorocarbons (PFCs) are a family of
chemically inert, water-insoluble, synthetic compounds with
a high solubility for both inert gases and oxygen, which may
eventually become available for human use as blood substitutes. Intravenous injection of PFC emulsions could augment
oxygen delivery to ischemic tissues with impaired circulation
and facilitate inert gas washout from tissues (135). Indeed, beneficial effects have been observed in animal studies of both decompression sickness and gas embolism (136–140). There may
also be a benefit from the surfactant properties in the treatment
of intravascular gas bubbles (141).
Arterial Gas Embolism and Decompression
Sickness Treatment Summary
Immediate treatment of AGE or DCS includes standard principles of first aid, including the administration of oxygen and
fluids during transport to a hyperbaric chamber. If the patient
is in an extremely remote location from which transport is not
feasible and the manifestations are minor, if the patient’s condition does not progress for 24 hours, and if the neurologic
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 39: Hyperbaric Oxygen Therapy
exam is normal, the risk of emergent transport may exceed the
risk of conservative treatment (142).
Carbon Monoxide
Carbon monoxide (CO) is an important cause of unintentional poisoning fatalities in the United States each year (143).
CO binds to hemoproteins, including hemoglobin and myoglobin, interfering with oxygen transport. It also binds to the
mitochondrial cytochrome C oxidase in the electron transport chain (similar to cyanide), impairing oxidative phosphorylation, stopping the cell’s energy production, and resulting in cellular hypoxia (144–146) and oxidative stress
(147). In addition, CO exposure induces intravascular platelet–
neutrophil activation (148). CO-related oxidative stress can
cause chemical alterations in myelin basic protein (149), triggering immune-mediated neurologic deficits.
The symptoms and signs of CO poisoning include headache
(or tightness across forehead), weakness, nausea and vomiting, syncope, tachycardia, tachypnea, and encephalopathy.
Myocardial ischemia is also a common finding.
For survivors of this poisoning, the most debilitating results
can be the late neurologic sequelae. These are often cognitive
problems such as a decrement in short-term memory (150–
152). Some patients improve clinically and then deteriorate
several days after the event.
HBO therapy is known to accelerate the elimination of CO
(153,154). Pace et al. found that the half-life of CO was longest
when breathing air (214 minutes). Half-life decreased to
42 minutes breathing 100% O2 at 1 ATA and further to 18
minutes with 100% O2 at 2.5 ATA (153). The reduction in
half-life may be important in preventing cell death by allowing
mitochondrial adenosine triphosphate (ATP) production to resume before the cell would have otherwise died (144,155). In
animal studies, HBO administration after acute CO exposure
appears to minimize the lipid peroxidation in the brain, which
occurs during or after removal of CO (147), and results in more
rapid repletion of brain energy stores (155).
A double-blind randomized control trial carried out by
Weaver et al. indicates that HBO therapy can prevent the occurrence of the late neurologic sequelae of CO poisoning if the
patients are treated within 24 hours of the exposure (152).
All patients should be initially treated with 100% normobaric oxygen. HBO therapy is usually reserved for patients who
have more severe poisoning, as determined by high HbCO
level (e.g. ≥25%), loss of consciousness, or other neurologic
manifestations, or myocardial ischemia, arrhythmias, or other
cardiac abnormalities (152,154,156–158). A systematic analysis of 163 patients with CO poisoning who did not receive
HBO revealed the following two risk factors for sequelae: older
age and longer CO exposure (159). However, some patients
without these risk factors also developed sequelae. The authors concluded that, in addition to other indications, regardless of HbCO level or loss of consciousness, anyone older than
36 years with symptoms should receive HBO.
Pregnant women should be treated according to maternal
indications. Pregnant women may therefore have an HbCO
level that is 10% to 15% less than that of the fetus. There is
evidence that short periods of HBO therapy are not dangerous
to the fetus or mother (160).
565
Cyanide
Cyanide leads to hypoxia on a cellular level by rapidly binding to mitochondrial cytochrome oxidase. Inhalation of high
concentrations of cyanide (270 ppm) is rapidly fatal in humans (with blood levels reaching 3 μg/mL), whereas ingestion
of cyanide is less rapidly fatal (161). When very low doses of
cyanide are absorbed (whole blood levels of 0.5–2.53 μg/mL),
tachycardia and decreased level of consciousness are possible
(161,162).
There are very few studies and case reports of the use of
HBO therapy in the treatment of cyanide poisoning (163–167).
This is likely due partly to the effectiveness of chemical treatments (with sodium nitrite and thiosulfate) but also possibly
related to the fact that the bonding of cyanide to the mitochondria’s cytochrome C oxidase is not an oxygen-dependent
mechanism. Chemical treatment of cyanide poisoning leads to
the formation of methemoglobin. Utilizing HBO therapy to
increase the amount of circulating dissolved oxygen has been
shown to have both prophylactic and antagonistic effects on
cyanide poisoning in rabbits (166). Human case reports also
hint that HBO therapy may be useful when the response to
chemical antidotes has been incomplete (165).
Hydrogen Sulfide
Like CO and cyanide, hydrogen sulfide (H2 S) reacts with mitochondrial cytochrome C oxidase, impairing electron transport.
This is not an oxygen-dependent mechanism. The rationale for
using HBO therapy is the same as for cyanide poisoning, in
that HBO therapy can increase the dissolved fraction of oxygen. Use of HBO therapy for H2 S poisoning is based on two
case reports suggesting a positive benefit (168,169).
Carbon Tetrachloride
Carbon tetrachloride (CCl4 ) is a CNS depressant, hepatotoxin,
and nephrotoxin, with renal failure being the most common
cause of death from very high-level exposures (170). In the
setting of CCl4 poisoning of the rat, HBO has been shown
to improve survival (171), decrease liver necrosis (172), decrease conversion of CCl4 to toxic free-radical metabolites
(173,174), and decrease CCl4 metabolite-induced lipid peroxidation (175). One case report describes an obtunded patient
treated with HBO for presumed CO poisoning. There was no
historical evidence for CO exposure; the patient improved, regained consciousness, and admitted to ingestion of a normally
lethal dose of 250 mL of CCl4 (176).
NECROTIZING INFECTIONS
Clostridial Infections
This soil-based anaerobic organism causes a type of rapidly
progressive disease known as gas gangrene, which, if left untreated, is almost uniformly fatal. In most cases, it is introduced
to the human via accidental trauma. The most common species
that cause the disease are Clostridium perfringens (80%–90%),
13:42
P1: OSO/OVY
GRBT291-37-39
566
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Section III: Techniques, Procedures, and Treatments
Clostridium oedematiens, and Clostridium septicum. These organisms release α-toxin, which is a lecithinase related to the
form found in snake, bee, and scorpion venoms, causing a liquefaction necrosis (177).
These organisms lack antioxidant defenses and therefore
are susceptible to HBO therapy. The first to report this finding was Brummelkamp et al. in 1961 (178,179). Around the
same time, it was discovered that at 3 ATA, α-toxin production quickly ceases (180); since then, animal studies (181) and
meta-analyses of human case series support the use of HBO
(182). If treatment is initiated within 24 hours of diagnosis,
disease-specific mortality can be as low as 5% (177).
The typical HBO treatment schedule varies between 2.5
and 3 ATA for 90 minutes, with three treatments in the first
24 hours, followed by two treatments per day at 2 to 3 ATA
until clinical stability. Aggressive surgical debridement and antibiotic therapy are also essential.
Nonclostridial Bacterial Infections
These are often necrotizing infections, usually polymicrobial,
including at least one anaerobic species. These infections
often follow local trauma and are enhanced by both local
ischemia and reduced host defenses (many patients are diabetic
with atherosclerosis) (183). The mainstays of therapy are
surgical debridement and antibiotics. Individual case series
and meta-analyses support the use of HBO as an adjunct
(182,184,185). The HBO treatment schedule is similar to that
of clostridial disease.
Mucormycosis
Rhinocerebral mucormycosis is a rare but devastating invasive
disease of the head and neck with 30% to 50% or greater
mortality when treated, often found in immunocompromised
patients such as diabetics in ketoacidosis, or patients receiving antineoplastic agents and/or steroids (186). It is primarily
treated with wide debridement and amphotericin B. Due to
the rarity of this disease, randomized trials have not been performed. Several case reports have suggested that HBO therapy
may be an effective adjunct (187–189). Recommended treatment protocol is 2 to 2.5 ATA for 2 hours, twice daily, for 40
to 80 treatments (190).
tracranial pressure after head injury (194), presumably due to
cerebral vasoconstriction, but it is logistically very difficult to
transport and monitor such patients for HBO. Although randomized studies have demonstrated a reduction in mortality
with HBO treatment, the proportion of patients with good
long-term results is not increased (194,195).
Thermal Injury
In a series of patients with carbon monoxide poisoning due
to coal mine explosions and fire, those treated for CO poisoning with HBO who also had burns showed more rapid healing
and less infection than others who did not receive HBO (196).
Since then, some studies have supported its use (197,198), but
others have failed to demonstrate a significant beneficial effect of HBO (199–202). In the randomized prospective study
by Brannen et al. (202), twice-daily HBO at 2 ATA for 90
minutes had no effect on mortality or length of stay, although
one of the authors reported in the discussion that HBO reduced the fluid loss, and the patients appeared to heal earlier. HBO appeared to reduce the volume of fluid required for
initial resuscitation. A systematic review of the published evidence did not support the routine use of HBO in thermal burns
(203). It should be noted that thermal burns are often accompanied by acute carbon monoxide poisoning for which HBO is
indicated.
Myocardial Infarction
Increasing the blood O2 content using HBO causes bradycardia, as well as a reduction in cardiac output (204) and myocardial O2 consumption (23). HBO has been shown to improve
wall motion abnormalities in patients with resting myocardial
ischemia (205). In a rabbit model after 30 minutes of left coronary occlusion, HBO at 2.5 ATA reduced infarct size when administered either during or immediately after occlusion (206).
A pilot randomized prospective study revealed lower peak creatine phosphokinase (CPK) levels and shorter time to pain relief
with tissue plasminogen activator (tPA) with a single 2 ATA
HBO treatment versus tPA and O2 at 1 ATA delivered via face
mask (207). The complete study revealed small, statistically insignificant differences in favor of HBO, but was underpowered
to detect differences in mortality (208).
Severe Anemia
Hyperbaric oxygen increases dissolved oxygen in the plasma
and thus enhances arterial oxygen content. Tissue oxygen delivery can therefore be supported acutely, even in the absence
of hemoglobin. Therefore, HBO at 2 to 3 ATA can be used
for temporary support of severely anemic patients if definitive
therapy in the form of cross-matched blood is not immediately
available (191). Evidence that intermittent repetitive HBO is
effective therapy for patients who refuse blood has no basis in
controlled outcome studies (192).
Head Injury
Evidence in animal studies suggests that HBO can prevent secondary injury after head trauma (193). HBO does reduce in-
Stroke
A series of 13 patients with stroke treated with HBO at 2 to 3
ATA within 5 hours of onset was published by Heyman et al.
(209). At that time, no imaging was available to exclude hemorrhage. Nevertheless, of 13 patients treated within 5 hours of
symptom onset, nine improved during HBO treatment, and
two stuporous patients with hemiparesis or hemiplegia improved dramatically immediately upon exposure to HBO and
maintained their improvement permanently. The use of HBO in
stroke is supported by animal studies demonstrating smaller infarct volume, reduced edema, and attenuation of hemorrhagic
transformation (38,39,44,210–214). Human studies have not
been encouraging (215–217), possibly because few if any patients since Heyman’s study have been treated within the same
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 39: Hyperbaric Oxygen Therapy
567
short time frame. Routine use of HBO in this context will have
to await further human outcome studies.
Support of Arterial Oxygenation
HBO has been reported as a method of attempting to support
arterial blood oxygenation in respiratory distress syndrome
(RDS) of the newborn, with disastrous results because of pulmonary oxygen toxicity (218). HBO is occasionally used for
short periods to support oxygenation during therapeutic lung
lavage (219–221).
Sedation and General Anesthesia
during Hyperbaric Treatment
Anesthetic agents may be required for surgery while in a saturation diving system (e.g., offshore), for therapeutic lung lavage,
or for sedation during mechanical ventilation. Inhaled agents
can be used with conventional anesthetic vaporizers, which
deliver a constant partial pressure of agent, irrespective of
chamber pressure. Nitrous oxide can be used as a sole agent
at increased pressure, although it induces several disagreeable
side effects, including tachypnea, tachycardia, hypertension, diaphoresis, muscle rigidity, catatonic jerking of the extremities,
eye opening, and opisthotonus. It is also associated with severe
nausea and vomiting after recovery (222). Nitrous oxide must
be avoided entirely in helium atmospheres because its administration induces intravascular bubble formation due to isobaric
counterdiffusion through the skin (223). Nitrous oxide should
also be avoided even at 1 ATA in patients who have recently
scuba dived or experienced decompression illness. In such patients, tissue bubbles may be present, which could enlarge due
to nitrous oxide diffusion and cause symptoms (224).
Inside hyperbaric chambers, intravenous agents such as
propofol, ketamine, midazolam, and narcotics are preferred because their use avoids atmospheric pollution. Pressure-induced
reversal of anesthesia is not significant up to 10 ATA, and if
it occurs at higher pressures, it can be offset by appropriate
titration.
HYPERBARIC CHAMBER
OPERATION
Types of Hyperbaric Chambers
Monoplace
As implied by the name, these chambers have space for only
one average-sized adult. Generally speaking, modern chambers
of this type are cylindrical in shape and made of a large (approximately 0.6–1 m internal diameter and 2.1–2.3 m long)
clear acrylic tube with a cap on one end and entry/exit hatch
on the other. Patients slide into the chamber through the hatch
to rest supine while they receive HBO therapy (Fig. 39.6).
Other than their small size, these chambers differ from their
multiplace counterparts (described below) in that they are pressurized with 100% oxygen (in most cases) and are generally
limited to no more than approximately 3 ATA operating pressure. This limitation makes them unsuitable for some high-
FIGURE 39.6. Monoplace chamber. This type of chamber has room
for one patient or a tender with a small child. Chamber atmosphere
is 100% O2 . The chamber is constructed of transparent Plexiglas to
allow observation. Through-hull penetrators in the door on the left can
be seen and allow monitoring, intravenous fluid administration, and
control of a ventilator inside the chamber. (Photograph courtesy of Dr.
Lindell Weaver.)
pressure treatment tables occasionally used for some types of
decompression illness. Monoplace chambers can be fitted such
that air breaks can be administered using a tight-fitting mask.
A challenge with the use of these chambers is lack of direct
access to the patient. However, almost all monitoring and ventilatory care (invasive blood pressure monitoring, mechanical
ventilation, chest tube management, etc.) previously only available to patients in multiplace chambers can now be delivered
in monoplace chambers (111,225).
Multiplace
These chambers can hold two or more patients/tenders. They
exist in many shapes and sizes, usually large cylindrical or
spherical shapes made of high-quality steel. Most of these
chambers have a personnel lock as well, which allows patients
or medical staff to exit or enter the chamber while it is at pressure. Transfer locks allow medicines, materials, and food to
be moved into or out of the chamber. Patients are generally
accompanied in the chamber by a tender or nurse, who can
attend to the needs of the patient during the treatment. Administration of all critical care modalities is relatively easy inside a
multiplace chamber (Fig. 39.7).
Due to their sturdier construction, multiplace chambers are
generally able to withstand much higher pressures than their
acrylic monoplace counterparts, and thus can be used for a
wider range of treatment pressures.
Minimization of Fire Hazards and
Atmosphere Control
Hyperbaric chambers are unique among medical equipment
in that the nurse, tender, or physician is frequently also inside
the treatment vessel (chamber) with the patient (in the case
of multiplace chambers) and not easily accessible in the event
of an emergency. The environment must be carefully managed
to ensure atmosphere quality, with specified limits for oxygen
13:42
P1: OSO/OVY
GRBT291-37-39
568
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Section III: Techniques, Procedures, and Treatments
of the chamber. This removes any mucous plugs that could
contribute to air trapping.
Chest Tube Management
Conventional water seal or one-way valve pleural drainage systems operate satisfactorily inside hyperbaric chambers, with or
without applied suction. During chamber decompression, expansion of gas volume within the tubing connecting the chest
tube with the drainage system is automatically vented via the
water seal or one-way valve. On the other hand, during chamber compression, the same gas volume is compressed and the
connecting tubing and gas-containing space on the patient side
of the water seal will tend to collapse, therefore producing high
negative intrapleural pressures. Standard commercially available pleural evacuation systems have a manually activated pressure relief valve, which should be activated during the compression phase to relieve this excessive negative pressure.
FIGURE 39.7. Patient treatment in a multiplace chamber.
and carbon dioxide, and to eliminate sources of ignition such
as matches and cigarette lighters. Cotton suits are worn by
patients and staff. Oil-based cosmetics and/or wigs (frequently
made of synthetic materials) are prohibited (226).
Additionally, stretchers and equipment must have the
petroleum-based lubricants removed from their wheels and
other lubricated parts. Any other objects with petroleum-based
lubricants must be cleaned of these lubricants prior to chamber treatment. At the time of this writing, there has not been
a reported fire in a hyperbaric chamber that has resulted in a
loss of life in the United States, although several such incidents
have occurred overseas.
Ventilatory Care
Mechanical Ventilation
Certain precautions must be taken when diving a mechanically ventilated patient in a hyperbaric chamber. First of all, the
ventilator must be approved for hyperbaric use. They should
be fluidically or pneumatically controlled. Electrically driven
ventilators are arguably less safe than ones using pneumatic
or fluidic control. Although not commonly used at very high
chamber pressures (6 ATA), ventilators powered by compressed
oxygen have an inlet PO2 of up to 4,560 mm Hg (227), which
can present a significant fire hazard.
As pressure rises, so does the gas density, which leads to
a corresponding increase in airway resistance. Unless the ventilator is volume cycled, the tidal volumes may drop as pressure rises (227). Therefore, tidal volumes should be monitored
closely (228).
Prior to chamber pressurization, inflating the endotracheal
cuff with water or saline will prevent leakage due to cuff volume
compression.
Suction
Since the chamber is at pressure, suction can be created simply
by venting a hose to the outside world attaching a regulator to
a through-hull penetrator. Normal hospital equipment can be
modified for this use (229). In patients with copious secretions
or ventilated patients, it is preferable to perform deep suctioning immediately prior to both compression and decompression
Intravenous Infusion Devices
Several different IV infusion devices have been tested inside
multiplace hyperbaric chambers and found to deliver fluid accurately. While it is the policy of some facilities not to use
electrical equipment inside a chamber, others minimize a fire
hazard by purging the device with 100% nitrogen. For monoplace use, the IV infusion device must be outside the chamber.
Glass IV bottles should be avoided in order to prevent explosion during decompression due to expansion of any contained
air bubble.
Arterial Blood Gas Measurement
Arterial blood gas analysis can be performed inside a multiplace hyperbaric chamber using an analyzer adapted for hyperbaric use. Alternatively, blood samples can be decompressed
and analyzed at 1 ATA. The latter procedure is simpler, but subject to error. While pH and PCO2 are relatively stable during
decompression, PO2 usually exceeds ambient pressure outside
the chamber, and thus it tends to decline rapidly as oxygen
is released from solution. Reasonably accurate values can be
obtained if the sample is analyzed immediately after decompression (230).
Alternatively, it is possible to predict arterial PO2 during
HBO therapy from a 1 ATA arterial blood gas measurement
using the following equations. All that is needed is a 1 ATA
blood gas measurement (at known FiO2 ), the HBO treatment
pressure in ATA (PATA , usually between 2 and 3 ATA), barometric pressure (Pb , in mm Hg, usually near 760 mm Hg), the
vapor pressure of water at body temperature (PH2O , at or near
47 mm Hg), the respiratory exchange ratio (usually 0.8), and
PaCO2 and the following formulas:
PaO2 (1 ATA) = (Pb − PH2 O) · FiO2
1 − FiO2
− PaCO2 · FiO2 +
R
PaO2 (predicted during HBO)
= PaO2 (1 ATA)/PaO2 (1 ATA)
·[(760 • PATA − 47) − PCO2 ]
[2]
[3]
where Pb is the barometric pressure outside the chamber; PaO2
(1 ATA) is the arterial PO2 at 1 ATA; PaO2 (1 ATA) is the
alveolar PO2 at 1 ATA; FiO2 is the inspired O2 fraction; R is
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
Printer: Yet to come
GRBT291-3641G GRBT291-Gabrielli-v2.cls
October 23, 2008
Chapter 39: Hyperbaric Oxygen Therapy
the respiratory exchange ratio (usually 0.8); PATA is the ambient pressure in the chamber in ATA; and PCO2 is the arterial
PCO2 measured at 1 ATA, assumed to be unchanged during
HBO.
Patient Monitoring
Most monitoring modalities used in hyperbaric chambers are
identical to those used in normobaric situations, with few exceptions. Whenever inflatable pressure bags are used, such as
for invasive blood pressure measurement, as the chamber pressurizes, the volume of air and the pressure in the pressure bag
decreases, and thus one must periodically pump it up during
compression; when decompressing the chamber, the air in the
pressure bag expands, which must be released periodically to
avoid rupture. For the same reason, pulmonary artery catheter
balloons should be left open to the atmosphere during chamber
compression and decompression.
Invasive pressure monitoring (or any monitoring where an
electrical signal is transmitted via cable/wire) can be performed
using through-hull penetrators to connect the transducer inside
the chamber with the preamplifier outside.
Standard stethoscopes and sphygmomanometers can be
used without difficulty in a multiplace chamber. Mercury pressure gauges should be avoided to prevent chamber contamination in the event of breakage.
Cardiac Arrest and Defibrillation
If a patient requires cardioversion or defibrillation while receiving HBO treatment, it is necessary to have through-hull
penetrators for the high-voltage cables connecting an outside
defibrillator with the paddles inside. Use of a low-impedance
gel will prevent sparks or heat buildup at the site of paddle contact. Careful design and testing are necessary to confirm adequacy of energy delivery. The only alternative is
to decompress the chamber and cardiovert or defibrillate at
1 ATA.
Tenders, Nurses, and Other
Chamber Staff Considerations
Inside tenders in a multiplace chamber will take up nitrogen.
While there is no requirement for a decompression stop for
typical 2 ATA/2 hour or 2.5 ATA/90 minute treatments, many
facilities require their staff to breathe 100% oxygen during decompression to reduce the very small risk of DCS. Additionally,
repetitive exposures within a short time to even these low pressures may incur some risk of DCS. Minimum time intervals between hyperbaric exposures for staff are routine. Longer treatments or higher treatment pressures generally mandate specific
decompression or oxygen breathing requirements for the inside
staff. Emergency decompression from such exposures due to
patient instability may therefore place the accompanying tender at risk. In the event of such an emergency, the tender should
be immediately recompressed. The most widely accepted management schedule is described on p. 9–13 of the U.S. Navy
Diving Manual (108).
569
Critical Care in a Hyperbaric
Chamber in the Field
Field chambers are used in the offshore oil industry and at some
remote inland dive sites. Divers injured due to decompression
illness or trauma may require critical care in this setting. This
is particularly the case for divers decompressing from saturation dives, in which an injured diver may require many days of
decompression before he or she can be transferred to a hospital. Tracheal intubation, chest tube insertion, mechanical ventilation, hemodynamic and CNS monitoring, and treatment of
convulsions may all be necessary (231). Portable radiographs
can be obtained by passing an x-ray beam through a Plexiglas
port, with the x-ray plate inside the chamber (232).
HYPERBARIC TREATMENT
COMPLICATIONS
Barotrauma
Otic
As many as 17% of all HBO therapy patients report ear pain
with compression, making otic barotraumas the most common
complication of HBO therapy (74). This is the result of difficulty with middle ear pressure equalization (i.e., eustachian
tube opening). As the chamber is compressed, the increased
pressure on the tympanic membrane can cause it to stretch medially just as when one dives in a swimming pool. Only rarely
does this result in perforation of the tympanic membrane in
awake patients, as they are able to notify the chamber operator of their progressive discomfort. Most often, there is unilateral otic discomfort associated with an erythematous tympanic membrane that heals over the following 5 to 7 days. In
patients who are unable to adequately perform a Valsalva maneuver required to equalize pressure (i.e., sedated, intubated,
with eustachian tube/sinus dysfunction, or with tracheostomy
tube), bilateral myringotomies with or without tube placement
are performed. Because myringotomies heal in 2 to 3 days, for
patients unable to equalize, bilateral tympanostomy tubes are
normally placed in patients who are expected to receive repetitive treatments for longer.
Sinus
Sinus barotrauma (“sinus squeeze”) is a relatively infrequent occurrence, which occurs in patients with active sinus
infection, allergic rhinitis, or nasal polyps. During pressure
change, the patient will feel discomfort in the region of the
affected sinus, particularly if it is the frontal sinus (233). Sinus
squeeze can usually be prevented using topical decongestants
such as oxymetazoline and slow compression of the chamber
(233).
Pulmonary
Although this is far more frequent with scuba diving, it can
also occur rarely in dry hyperbaric chambers, causing AGE
(234), pneumomediastinum, or pneumothorax. Patients with
cystic or bullous disease are presumably at risk; however, many
such patients have received HBO without complication. In patients with a pre-existing pneumothorax, tube decompression
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
570
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Section III: Techniques, Procedures, and Treatments
is recommended, especially if the patient is to be treated in a
monoplace chamber.
Pulmonary Edema
Peripheral vasoconstriction induced by HBO and the resulting increase in afterload can precipitate pulmonary edema in
patients with impaired ventricular function (235).
Evaluation of a Patient for
Hyperbaric Oxygen Therapy
In assessing a patient for hyperbaric therapy, two aspects need
to be evaluated: Potential efficacy of treatment and risk of adverse effects. Indications for hyperbaric oxygen therapy as determined by the Undersea and Hyperbaric Medical Society (7)
are listed in Table 39.1. A second factor is the predicted arterial PO2 , which must be within a therapeutic range during
HBO therapy (>1,000 mm Hg). If a patient has pulmonary
gas exchange impairment that precludes attainment of an arterial PO2 that is sufficiently high, then HBO is unlikely to be
effective. A method for predicting arterial oxygenation during
HBO makes use of the relative constancy of the ratio of arterial to alveolar PO2 (PaO2 /PaO2 ratio) as described above
(Eq. 2 and 3). Finally, the assessment must include evaluating for the risk of pulmonary barotrauma. During decompression, pulmonary cysts or bullae can rupture (234), although
such complications are extremely rare. Patients with untreated
pneumothorax usually require a tube thoracostomy, unless immediate chest decompression can be performed. Patients with
a pneumothorax for whom monoplace treatment is planned require prophylactic chest tube insertion irrespective of the size
of the pneumothorax. Patients in heart failure in whom left
ventricular function may not be able to tolerate an increase in
afterload are also at risk (235).
Susceptibility to otic barotrauma and occasionally to sinus barotrauma also plays a role in determining fitness for
HBO therapy. Obtunded patients are especially at risk of otic
barotrauma, and many practitioners advocate prophylactic
myringotomy.
SUMMARY
Although hyperbaric oxygen therapy has limited indications,
it represents definitive therapy for some critically ill patients,
especially those with gas bubble disease (decompression sickness or gas embolism) and carbon monoxide poisoning. The
available evidence also strongly suggests that it is an effective adjunct in necrotizing soft tissue infections. HBO can be
safely administered to the critically ill patient using an appropriately equipped hyperbaric chamber and implementing standard monitoring and supportive measures.
References
1. Simpson A. Compressed Air, as a Therapeutic Agent, in the Treatment
of Consumption, Asthma, Chronic Bronchitis, and Other Diseases. Edinburgh: Sutherland & Knox; 1857.
2. Junod VT. Recherches physiologiques et thérapeutiques sur les effets de
la compression et de la raréfaction de l’air, tant sur le corps que sur les
membres isolés. Rev Med Fr Étrange. 1834;3:350–368.
3. Phillips JL. The Bends. New Haven, CT: Yale University; 1998.
4. Zuntz N. Zur Pathogenese und Therapie der durch rasche Luftdruckänderungen erzeugten Krankheiten. Fortschr Med. 1897;15:632–
639.
5. Behnke AR, Shaw LA. The use of oxygen in the treatment of compressed
air illness. Navy Med Bull. 1937;35:1–12.
6. Yarbrough OD, Behnke AR. The treatment of compressed air illness using
oxygen. J Ind Hyg Toxicol. 1939;21:213–218.
7. Gesell LB, ed. Hyperbaric Oxygen Therapy: A Committee Report. Durham,
NC: Undersea and Hyperbaric Medical Society; 2008.
8. Whalen RE, Saltzman HA, Holloway DH Jr, et al. Cardiovascular and blood
gas responses to hyperbaric oxygenation. Am J Cardiol. 1965;15:638–646.
9. McMahon TJ, Moon RE, Luschinger BP, et al. Nitric oxide in the human
respiratory cycle. Nat Med. 2002;8:711–717.
10. Boerema I, Meyne NG, Brummelkamp WH, et al. Life without blood. J
Cardiovasc Surg (Torino). 1960;1:133–146.
11. Bergofsky EH, Wang MC, Yamaki T, et al. Tissue oxygen and carbon dioxide tensions during hyperbaric oxygenation. JAMA. 1964;189:841–844.
12. Bergofsky EH, Bertun P. Response of regional circulations to hyperoxia. J
Appl Physiol. 1966;21:567–572.
13. Bird AD, Telfer AB. Effect of hyperbaric oxygen on limb circulation. Lancet.
1965;13:355–356.
14. Berry JM, Doursout MF, Butler BD. Effects of hyperbaric hyperoxia on
cardiac and regional hemodynamics in conscious dogs. Aviat Space Environ
Med. 1998;69:761–765.
15. Demchenko IT, Boso AE, Bennett PB, et al. Hyperbaric oxygen reduces
cerebral blood flow by inactivating nitric oxide. Nitric Oxide. 2000;4:597–
608.
16. Dooley JW, Mehm WJ. Noninvasive assessment of the vasoconstrictive
effects of hyperoxygenation. J Hyperbar Med. 1990;4:177–187.
17. Sheikh AY, Rollins MD, Hopf HW, et al. Hyperoxia improves microvascular perfusion in a murine wound model. Wound Repair Regen. 2005;
13:303–308.
18. Hahnloser PB, Domanig E, Lamphier E, et al. Hyperbaric oxygenation:
alterations in cardiac output and regional blood flow. J Thorac Cardiovasc
Surg. 1966;52:223–231.
19. Villanucci S, Di Marzio GE, Scholl M, et al. Cardiovascular changes induced
by hyperbaric oxygen therapy. Undersea Biomed Res (Suppl). 1990;17:117.
20. Demchenko IT, Boso AE, Natoli MJ, et al. Nitric oxide is involved in the
mechanism of HBO-induced cerebral vasoconstriction. Undersea Hyperb
Med. 1998;25(Suppl):54.
21. Demchenko IT, Oury TD, Crapo JD, et al. Regulation of the brain’s vascular
responses to oxygen. Circ Res. 2002;91:1031–1037.
22. Hordnes C, Tyssebotn I. Effect of high ambient pressure and oxygen tension on organ blood flow in conscious trained rats. Undersea Biomed Res.
1985;12:115–128.
23. Savitt MA, Rankin JS, Elberry JR, et al. Influence of hyperbaric oxygen
on left ventricular contractility, total coronary blood flow, and myocardial
oxygen consumption in the conscious dog. Undersea Hyperb Med. 1994;
21:169–183.
24. Zamboni WA, Roth AC, Russell RC, et al. Morphological analysis of the
microcirculation during reperfusion of ischemic skeletal muscle and the
effect of hyperbaric oxygen. Plast Reconstr Surg. 1993;91:1110–1123.
25. Helps SC, Meyer-Witting M, Rilley PL, et al. Increasing doses of intracarotid air and cerebral blood flow in rabbits. Stroke. 1990;21:1340–
1345.
26. Helps SC, Gorman DF. Air embolism of the brain in rabbits pre-treated
with mechlorethamine. Stroke. 1991;22:351–354.
27. Miljkovic-Lolic M, Silbergleit R, Fiskum G, et al. Neuroprotective effects
of hyperbaric oxygen treatment in experimental focal cerebral ischemia are
associated with reduced brain leukocyte myeloperoxidase activity. Brain
Res. 2003;971:90–94.
28. Chen MF, Chen HM, Ueng SW, et al. Hyperbaric oxygen pretreatment
attenuates hepatic reperfusion injury. Liver. 1998;18:110–116.
29. Tjarnstrom J, Wikstrom T, Bagge U, et al. Effects of hyperbaric oxygen
treatment on neutrophil activation and pulmonary sequestration in intestinal ischemia-reperfusion in rats. Eur Surg Res. 1999;31:147–154.
30. Yamada T, Taguchi T, Hirata Y, et al. The protective effect of hyperbaric
oxygenation on the small intestine in ischemia-reperfusion injury. J Pediatr
Surg. 1995;30:786–790.
31. Zamboni WA, Wong HP, Stephenson LL. Effect of hyperbaric oxygen on
neutrophil concentration and pulmonary sequestration in reperfusion injury. Arch Surg. 1996;131:756–760.
32. Haapaniemi T, Nylander G, Sirsjo A, et al. Hyperbaric oxygen reduces
ischemia-induced skeletal muscle injury. Plast Reconstr Surg. 1996;97:602–
607; discussion 8–9.
33. Zamboni WA, Roth AC, Russell RC, et al. The effect of acute hyperbaric
oxygen therapy on axial pattern skin flap survival when administered during
and after total ischemia. J Reconstr Microsurg. 1989;5:343–347.
34. Hong JP, Kwon H, Chung YK, et al. The effect of hyperbaric oxygen on
ischemia-reperfusion injury: an experimental study in a rat musculocutaneous flap. Ann Plast Surg. 2003;51:478–487.
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Chapter 39: Hyperbaric Oxygen Therapy
35. Bosco G, Yang ZJ, Nandi J, et al. Effects of hyperbaric oxygen on glucose,
lactate, glycerol and anti-oxidant enzymes in the skeletal muscle of rats during ischaemia and reperfusion. Clin Exp Pharmacol Physiol. 2007;34:70–
76.
36. Buras JA, Reenstra WR. Endothelial-neutrophil interactions during ischemia and reperfusion injury: basic mechanisms of hyperbaric oxygen.
Neurol Res. 2007;29:127–131.
37. Riccio M, Pangrazi PP, Campodonico A, et al. Combined use of WEB2170
and HBO therapy can reduce ischemia and reperfusion injury to the skeletal
muscle in a rabbit model. Microsurgery. 2007;27:43–47.
38. Henninger N, Kuppers-Tiedt L, Sicard KM, et al. Neuroprotective effect of
hyperbaric oxygen therapy monitored by MR-imaging after embolic stroke
in rats. Exp Neurol. 2006;201:316–323.
39. Schabitz WR, Schade H, Heiland S, et al. Neuroprotection by hyperbaric
oxygenation after experimental focal cerebral ischemia monitored by MRI.
Stroke. 2004;35:1175–1179.
40. Gurer A, Ozdogan M, Gomceli I, et al. Hyperbaric oxygenation attenuates
renal ischemia-reperfusion injury in rats. Transplant Proc. 2006;38:3337–
3340.
41. Kalns J, Lane J, Delgado A, et al. Hyperbaric oxygen exposure temporarily
reduces Mac-1 mediated functions of human neutrophils. Immunol Lett.
2002;83:125–131.
42. Thom SR. Effects of hyperoxia on neutrophil adhesion. Undersea Hyperb
Med. 2004;31:123–131.
43. Thom SR, Mendiguren I, Hardy K, et al. Inhibition of human neutrophil beta2-integrin-dependent adherence by hyperbaric O2 . Am J Physiol. 1997;272:C770–C777.
44. Veltkamp R, Siebing DA, Sun L, et al. Hyperbaric oxygen reduces bloodbrain barrier damage and edema after transient focal cerebral ischemia.
Stroke. 2005;36:1679–1683.
45. Lou M, Chen Y, Ding M, et al. Involvement of the mitochondrial ATPsensitive potassium channel in the neuroprotective effect of hyperbaric oxygenation after cerebral ischemia. Brain Res Bull. 2006;69:109–116.
46. Mader JT, Brown GL, Guckian JC, et al. A mechanism for the amelioration by hyperbaric oxygen of experimental staphylococcal osteomyelitis in
rabbits. J Infect Dis. 1980;142:915–922.
47. Mader JT, Adams KR, Sutton TE. Infectious diseases: pathophysiology and
mechanisms of hyperbaric oxygen. J Hyperbar Med. 1987;2:133–140.
48. Zamboni WA, Mazolewski PJ, Erdmann D, et al. Evaluation of penicillin
and hyperbaric oxygen in the treatment of streptococcal myositis. Ann Plast
Surg. 1997;39:131–136.
49. Carraway MS, Piantadosi CA. Oxygen toxicity. Respir Care Clin N Am.
1999;5:265–295.
50. Freeman BA, Crapo JD. Biology of disease: Free radicals and tissue injury.
Lab Invest. 1982;47:412–426.
51. Gerschman R, Gilbert DL, Nye SW, et al. Oxygen poisoning and xirradiation: a mechanism in common. Science. 1954;119:623–626.
52. Demchenko IT, Atochin DN, Boso AE, et al. Oxygen seizure latency and
peroxynitrite formation in mice lacking neuronal or endothelial nitric oxide
synthases. Neurosci Lett. 2003;344:53–56.
53. Demchenko IT, Boso AE, Whorton AR, et al. Nitric oxide production
is enhanced in rat brain before oxygen-induced convulsions. Brain Res.
2001;917:253–261.
54. Demchenko IT, Piantadosi CA. Nitric oxide amplifies the excitatory to
inhibitory neurotransmitter imbalance accelerating oxygen seizures. Undersea Hyperb Med. 2006;33:169–174.
55. Donald KW. Oxygen poisoning in man, I & II. BMJ. 1947;1:667–672,
712–717.
56. Doherty MJ, Hampson NB. Partial seizure provoked by hyperbaric oxygen
therapy: possible mechanisms and implications. Epilepsia. 2005;46:974–
976.
57. Bleiberg B, Kerem D. Central nervous system oxygen toxicity in the resting
rat: postponement by intermittent oxygen exposure. Undersea Biomed Res.
1988;15:337–352.
58. Chavko M, McCarron RM. Extension of brain tolerance to hyperbaric O2
by intermittent air breaks is related to the time of CBF increase. Brain Res.
2006;1084:196–201.
59. Harabin AL, Survanshi SS, Weathersby PK, et al. The modulation of oxygen
toxicity by intermittent exposure. Toxicol Appl Pharmacol. 1988;93:298–
311.
60. Lambertsen CJ. Extension of oxygen tolerance in man: philosophy and
significance. Exp Lung Res. 1988;14(Suppl):1035–1058.
61. Vote DA, Doar O, Moon RE, et al. Blood glucose meter performance under
hyperbaric oxygen conditions. Clin Chim Acta. 2001;305:81–87.
62. Clark JM, Lambertsen CJ. Pulmonary oxygen toxicity: a review. Pharmacol
Rev. 1971;23:37–133.
63. Bardin H, Lambertsen CJ. A Quantitative Method for Calculating Cumulative Pulmonary Oxygen Toxicity. Use of the Unit Pulmonary Toxicity Dose
(UPTD). Philadelphia: Institute of Environmental Medicine, University of
Pennsylvania; 1970.
64. Clark JM. Oxygen toxicity. In: Bennett PB, Elliott DH, eds. The Physiology
and Medicine of Diving. Philadelphia: WB Saunders; 1993:121–169.
65. Harabin AL, Homer LD, Weathersby PK, et al. An analysis of decrements
in vital capacity as an index of pulmonary oxygen toxicity. J Appl Physiol.
1987;63:1130–1135.
571
66. Clark JM, Lambertsen CJ. Rate of development of pulmonary O2 toxicity
in man during O2 breathing at 2.0 Ata. J Appl Physiol. 1971;30:739–752.
67. Goldiner PL, Carlon GC, Cvitkovic E, et al. Factors influencing postoperative morbidity and mortality in patients treated with bleomycin. BMJ.
1978;1:1664–1667.
68. Nygaard K, Smith-Erichsen N, Hatlevoll R, et al. Pulmonary complications after bleomycin, irradiation and surgery for esophageal cancer. Cancer. 1978;41:17–22.
69. Thompson CC, Bailey MK, Conroy JM, et al. Postoperative pulmonary
toxicity associated with mitomycin C therapy. South Med J. 1992;85:1257–
1259.
70. Anderson B Jr, Shelton DL. Axial length in hyperoxic myopia. In: Bove AA,
Bachrach AJ, Greenbaum LJ Jr, eds. Underwater and Hyperbaric Physiology IX Proceedings of the Ninth International Symposium on Underwater
and Hyperbaric Physiology. Bethesda, MD: Undersea and Hyperbaric Medical Society; 1987:607–611.
71. Palmquist BM, Philipson B, Barr PO. Nuclear cataract and myopia during
hyperbaric oxygen therapy. Br J Ophthalmol. 1984;68:113–117.
72. Behnke AR, Forbes HS, Motley EP. Circulatory and visual effects of oxygen
at 3 atmospheres pressure. Am J Physiol. 1936;114:436–442.
73. Clark JM, Thom SR. Oxygen under pressure. In: Brubakk AO, Neuman
TS, eds. Physiology and Medicine of Diving. London: Saunders; 2003:376.
74. Plafki C, Peters P, Almeling M, et al. Complications and side effects of
hyperbaric oxygen therapy. Aviat Space Environ Med. 2000;71:119–124.
75. Junod T. Recherches sur les effets physiologiques et thérapeutiques de la
compression et de raréfaction de 1’air, tant sur le corps que les membres
isolés. Ann Gén Med sér 2, 1835;9:157–172.
76. Behnke AR, Thomas RM, Motley EP. The psychologic effects from breathing air at 4 atmospheres pressure. Am J Physiol. 1935;112:554–558.
77. Muth CM, Shank ES. Gas embolism. N Engl J Med. 2000;342:476–482.
78. Fukaya E, Hopf HW. HBO and gas embolism. Neurol Res. 2007;29:142–
145.
79. Morris WP, Butler BD, Tonnesen AS, et al. Continuous venous air embolism
in patients receiving positive end-expiratory pressure. Am Rev Respir Dis.
1993;147:1034–1037.
80. Kaufman BS, Kaminsky SJ, Rackow EC, et al. Adult respiratory distress syndrome following orogenital sex during pregnancy. Crit Care Med.
1987;15:703–704.
81. Nossum V, Koteng S, Brubakk AO. Endothelial damage by bubbles in the
pulmonary artery of the pig. Undersea Hyperb Med. 1999;26:1–8.
82. Dutka AJ, Kochanek PM, Hallenbeck JM. Influence of granulocytopenia
on canine cerebral ischemia induced by air embolism. Stroke. 1989;20:390–
395.
83. Hallenbeck JM, Dutka AJ, Tanishima T, et al. Polymorphonuclear leukocyte accumulation in brain regions with low blood flow during the early
postischemic period. Stroke. 1986;17:246–253.
84. Levin LL, Stewart GJ, Lynch PR, et al. Blood and blood vessel wall changes
induced by decompression sickness in dogs. J Appl Physiol. 1981;50:944–
949.
85. Chryssanthou C, Springer M, Lipschitz S. Blood-brain and blood-lung barrier alteration by dysbaric exposure. Undersea Biomed Res. 1977;4:117–
129.
86. Zwirewich CV, Müller NL, Abboud RT, et al. Noncardiogenic pulmonary
edema caused by decompression sickness: rapid resolution following hyperbaric therapy. Radiology. 1987;163:81–82.
87. Nossum V, Hjelde A, Brubakk AO. Small amounts of venous gas embolism cause delayed impairment of endothelial function and increase polymorphonuclear neutrophil infiltration. Eur J Appl Physiol. 2002;86:209–
214.
88. van Hulst RA, Lameris TW, Haitsma JJ, et al. Brain glucose and lactate
levels during ventilator-induced hypo- and hypercapnia. Clin Physiol Funct
Imaging. 2004;24:243–248.
89. van Hulst RA, Lameris TW, Hasan D, et al. Effects of cerebral air embolism
on brain metabolism in pigs. Acta Neurol Scand. 2003;108:118–124.
90. van Hulst RA, Haitsma JJ, Lameris TW, et al. Hyperventilation impairs
brain function in acute cerebral air embolism in pigs. Intensive Care Med.
2004;30:944–950.
91. Mann C, Boccara G, Fabre JM, et al. The detection of carbon dioxide
embolism during laparoscopy in pigs: a comparison of transesophageal
Doppler and end-tidal carbon dioxide monitoring. Acta Anaesthesiol
Scand. 1997;41:281–286.
92. Benson J, Adkinson C, Collier R. Hyperbaric oxygen therapy of iatrogenic cerebral arterial gas embolism. Undersea Hyperb Med. 2003;30:117–
126.
93. Longphre JM, Denoble PJ, Moon RE, et al. First aid normobaric oxygen
for the treatment of recreational diving injuries. Undersea Hyperb Med.
2007;34:43–49.
94. Atkinson JR. Experimental air embolism. Northwest Med. 1963;62:699–
703.
95. Van Allen CM, Hrdina LS, Clark J. Air embolism from the pulmonary vein.
Arch Surg. 1929;19:567–599.
96. Mehlhorn U, Burke EJ, Butler BD, et al. Body position does not affect
the hemodynamic response to venous air embolism in dogs. Anesth Analg.
1994;79:734–739.
97. Geissler HJ, Allen SJ, Mehlhorn U, et al. Effect of body repositioning
13:42
P1: OSO/OVY
GRBT291-37-39
572
98.
99.
100.
101.
102.
103.
104.
105.
106.
107.
108.
109.
110.
111.
112.
113.
114.
115.
116.
117.
118.
119.
120.
121.
122.
123.
124.
125.
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Section III: Techniques, Procedures, and Treatments
after venous air embolism. An echocardiographic study. Anesthesiology.
1997;86:710–717.
Dutka AJ. Therapy for dysbaric central nervous system ischemia: adjuncts to recompression. In: Bennett PB, Moon RE, eds. Diving Accident
Management. Bethesda, MD: Undersea and Hyperbaric Medical Society;
1990:222–234.
van Hulst RA, Klein J, Lachmann B. Gas embolism: pathophysiology and
treatment. Clin Physiol Funct Imaging. 2003;23:237–246.
Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early
management of adults with ischemic stroke: a guideline from the American
Heart Association/American Stroke Association Stroke Council, Clinical
Cardiology Council, Cardiovascular Radiology and Intervention Council,
and the Atherosclerotic Peripheral Vascular Disease and Quality of Care
Outcomes in Research Interdisciplinary Working Groups: the American
Academy of Neurology affirms the value of this guideline as an educational
tool for neurologists. Stroke. 2007;38:1655–1711.
Brown JW, Dierdorf SF, Moorthy SS, et al. Venoarterial cerebral perfusion
for treatment of massive arterial air embolism. Anesth Analg. 1987;66:673–
674.
Stark J, Hough J. Air in the aorta: treatment by reversed perfusion. Ann
Thorac Surg. 1986;41:337–338.
Ericsson JA, Gottlieb JD, Sweet RB. Closed-chest cardiac massage in the
treatment of venous air embolism. N Engl J Med. 1964;270:1353–1354.
Michenfelder JD, Martin JT, Altenburg BM, et al. Air embolism during
neurosurgery. An evaluation of right-atrial catheters for diagnosis and treatment. JAMA. 1969;208:1353–1358.
Bowdle TA, Artru AA. Treatment of air embolism with a special pulmonary artery catheter introducer sheath in sitting dogs. Anesthesiology.
1988;68:107–110.
Marshall WK, Bedford RF. Use of a pulmonary-artery catheter for detection and treatment of venous air embolism: a prospective study in man.
Anesthesiology. 1980;52:131–134.
Thalmann ED. Principles of US Navy recompression treatments for decompression sickness. In: Moon RE, Sheffield PJ, eds. Treatment of Decompression Illness. Kensington, MD: Undersea and Hyperbaric Medical Society;
1996:75–95.
Navy Department. US Navy Diving Manual. Revision 4. Vol. 5: Diving
Medicine and Recompression Chamber Operations. NAVSEA 0910-LP103-8009. Washington, DC: Naval Sea Systems Command; 2005.
Hart GB, Strauss MB, Lennon PA. The treatment of decompression sickness
and air embolism in a monoplace chamber. J Hyperbar Med. 1986;1:1–7.
Cianci P, Slade JB Jr. Delayed treatment of decompression sickness with
short, no-air-break tables: review of 140 cases. Aviat Space Environ Med.
2006;77:1003–1008.
Weaver LK. Monoplace hyperbaric chamber use of U.S. Navy Table 6: a
20-year experience. Undersea Hyperb Med. 2006;33:85–88.
Moon RE, ed. Adjunctive Therapy for Decompression Illness. Kensington,
MD: Undersea and Hyperbaric Medical Society; 2003.
Undersea and Hyperbaric Medical Society. UHMS Guidelines for Adjunctive Therapy of DCI. In: Moon RE, ed. Adjunctive Therapy for Decompression Illness. Kensington, MD: Undersea and Hyperbaric Medical Society;
2003:184–189.
Balldin UI. Effects of ambient temperature and body position on tissue
nitrogen elimination in man. Aerosp Med. 1973;44:365–3670.
Hallenbeck JM, Leitch DR, Dutka AJ, et al. Prostaglandin I2 , indomethacin
and heparin promote postischemic neuronal recovery in dogs. Ann Neurol.
1982;12:145–156.
Reeves E, Workman RD. Use of heparin for the therapeutic/prophylactic
treatment of decompression sickness. Aerosp Med. 1971;42:20–23.
Broome JR. Association of CNS hemorrhage with failure to respond to recompression treatment—implications for management of refractory cases
of decompression illness. In: Moon RE, Sheffield PJ, eds. Treatment of Decompression Illness. Kensington, MD: Undersea and Hyperbaric Medical
Society; 1996:364–373.
Elliott DH, Hallenbeck JM, Bove AA. Venous infarction of the spinal cord
in decompression sickness. J Roy Nav Med Serv. 1974;60:66–71.
Palmer AC, Blakemore WF, Payne JE, et al. Decompression sickness in the
goat: nature of brain and spinal cord lesions at 48 hours. Undersea Biomed
Res. 1978;5:275–286.
Gorman DF, Browning DN. Cerebral vaso-reactivity and arterial gas embolism. Undersea Biomed Res. 1986;13:317–335.
Waite CL, Mazzone WF, Greenwood ME, et al. Cerebral air embolism
I. Basic studies. US Naval Submarine Medical Center Report No. 493.
Panama City, FL: US Navy Submarine Research Laboratory; 1967. Report
No.: 493.
Landolt JP, Money KE, Topliff ED, et al. Pathophysiology of inner ear
dysfunction in the squirrel monkey in rapid decompression. J Appl Physiol.
1980;49:1070–1082.
McCormick JG, Holland WB, Brauer RW, et al. Sudden hearing loss due
to diving and its prevention with heparin. Otolaryngol Clin North Am.
1975;8:417–430.
Mitchell SJ. Lidocaine in the treatment of decompression illness: a review
of the literature. Undersea Hyperb Med. 2001;28:165–174.
Mitchell SJ, Pellett O, Gorman DF. Cerebral protection by lidocaine during
cardiac operations. Ann Thorac Surg. 1999;67:1117–1124.
126. Wang D, Wu X, Li J, et al. The effect of lidocaine on early postoperative cognitive dysfunction after coronary artery bypass surgery [comment].
Anesth Analg. 2002;95:1134–1141, table of contents.
127. Mathew J, Grocott H, Phillips-Bute B, et al. Lidocaine does not prevent
cognitive dysfunction after cardiac surgery. Anesth Analg. 2004;98(Suppl):
SCA13.
128. Cogar WB. Intravenous lidocaine as adjunctive therapy in the treatment of
decompression illness. Ann Emerg Med. 1997;29:284–286.
129. Mitchell SJ, Benson M, Vadlamudi L, et al. Cerebral arterial gas embolism
by helium: an unusual case successfully treated with hyperbaric oxygen and
lidocaine. Ann Emerg Med. 2000;35:300–303.
130. Bennett M, Mitchell S, Dominguez A. Adjunctive treatment of decompression illness with a non-steroidal anti-inflammatory drug (tenoxicam) reduces compression requirement. Undersea Hyperb Med. 2003;30:195–205.
131. Francis TJR, Dutka AJ, Clark JB. An evaluation of dexamethasone in the
treatment of acute experimental spinal decompression sickness. In: Bove
AA, Bachrach AJ, Greenbaum LJ, Jr, eds. Underwater and Hyperbaric Physiology IX Proceedings of the Ninth International Symposium on Underwater and Hyperbaric Physiology. Bethesda, MD: Undersea and Hyperbaric
Medical Society; 1987:999–1013.
132. Dutka AJ, Mink RB, Pearson RR, et al. Effects of treatment with dexamethasone on recovery from experimental cerebral arterial gas embolism.
Undersea Biomed Res. 1992;19:131–141.
133. Francis TJR, Dutka AJ. Methylprednisolone in the treatment of acute spinal
cord decompression sickness. Undersea Biomed Res. 1989;16:165–174.
134. Dromsky DM, Toner CB, Fahlman A, et al. Prophylactic treatment of severe
decompression sickness with methylprednisolone. Undersea Hyperb Med.
1999;26(Suppl):15.
135. Novotny JA, Bridgewater BJ, Himm JF, et al. Quantifying the effect of
intravascular perfluorocarbon on xenon elimination from canine muscle. J
Appl Physiol. 1993;74:1356–1360.
136. Mahon RT, Dainer HM, Nelson JW. Decompression sickness in a swine
model: isobaric denitrogenation and perfluorocarbon at depth. Aviat Space
Environ Med. 2006;77:8–12.
137. Dainer H, Nelson J, Brass K, et al. Short oxygen prebreathing and intravenous perfluorocarbon emulsion reduces morbidity and mortality in a
swine saturation model of decompression sickness. J Appl Physiol. 2007;
102:1099–1104.
138. Dromsky DM, Spiess BD, Fahlman A. Treatment of decompression sickness
in swine with intravenous perfluorocarbon emulsion. Aviat Space Environ
Med. 2004;75:301–305.
139. Yoshitani K, de Lange F, Ma Q, et al. Reduction in air bubble size using
perfluorocarbons during cardiopulmonary bypass in the rat. Anesth Analg.
2006;103:1089–1093.
140. Zhu J, Hullett JB, Somera L, et al. Intravenous perfluorocarbon emulsion
increases nitrogen washout after venous gas emboli in rabbits. Undersea
Hyperb Med. 2007;34:7–20.
141. Eckmann DM, Armstead SC, Mardini F. Surfactants reduce platelet-bubble
and platelet-platelet binding induced by in vitro air embolism. Anesthesiology. 2005;103:1204–1210.
142. Mitchell SJ, Doolette DJ, Wachholz CJ, et al., eds. Management of Mild
or Marginal Decompression Illness in Remote Locations. Durham, NC:
Divers Alert Network; 2005.
143. Centers for Disease Control and Prevention (CDC). Unintentional poisoning deaths—United States, 1999–2004. MMWR Morb Mortal Wkly
Rep.2007;56:93–96.
144. Brown SD, Piantadosi CA. Reversal of carbon monoxide-cytochrome c oxidase binding by hyperbaric oxygen in vivo. Adv Exp Med Biol. 1989;248:
747–754.
145. Brown SD, Piantadosi CA. In vivo binding of carbon monoxide to cytochrome c oxidase in rat brain. J Appl Physiol. 1990;68:604–610.
146. Chance B, Erecinska M, Wagner M. Mitochondrial responses to carbon
monoxide toxicity. Ann N Y Acad Sci. 1970;174:193–204.
147. Thom S. Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen. Toxicol Appl Pharmacol. 1990;105:340–344.
148. Thom SR, Bhopale VM, Han ST, et al. Intravascular neutrophil activation
due to carbon monoxide poisoning. Am J Respir Crit Care Med. 2006;174:
1239–1248.
149. Thom SR, Bhopale VM, Fisher D. Hyperbaric oxygen reduces delayed
immune-mediated neuropathology in experimental carbon monoxide toxicity. Toxicol Appl Pharmacol. 2006;213:152–159.
150. Werner B, Back W, Akerblom H, et al. Two cases of acute carbon monoxide poisoning with delayed neurological sequelae after a “free” interval. J
Toxicol Clin Toxicol. 1985;23:249–265.
151. Thom S, Taber R, Mendiguren I, et al. Delayed neuropsychologic sequelae
after carbon monoxide poisoning: prevention by treatment with hyperbaric
oxygen. Ann Emerg Med. 1995;25:474–480.
152. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute
carbon monoxide poisoning. N Engl J Med. 2002;347:1057–1067.
153. Pace N, Strajman E, Walker EL. Acceleration of carbon monoxide elimination in man by high pressure oxygen. Science. 1950;111:652–654.
154. Piantadosi CA. Diagnosis and treatment of carbon monoxide poisoning.
Respir Care Clin N Am. 1999;5:183–202.
155. Brown SD, Piantadosi CA. Recovery of energy metabolism in rat brain after
carbon monoxide hypoxia. J Clin Invest. 1992;89:666–672.
13:42
P1: OSO/OVY
P2: OSO/OVY
GRBT291-37-39
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Chapter 39: Hyperbaric Oxygen Therapy
156. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med. 1998;339:
1603–1608.
157. Tibbles PM, Edelsberg JS. Hyperbaric-oxygen therapy. N Engl J Med. 1996;
334:1642–1648.
158. Thom SR. Hyperbaric-oxygen therapy for acute carbon monoxide poisoning. N Engl J Med. 2002;347:1105–1106.
159. Weaver LK, Valentine KJ, Hopkins RO. Carbon monoxide poisoning: risk
factors for cognitive sequelae and the role of hyperbaric oxygen. Am J
Respir Crit Care Med. 2007;176:491–497.
160. Van Hoesen KB, Camporesi EM, Moon RE, et al. Should hyperbaric oxygen
be used to treat the pregnant patient for acute carbon monoxide poisoning?
A case report and literature review. JAMA. 1989;261:1039–1043.
161. Meyers RA, Thom SR. Carbon monoxide and cyanide poisoning. In: Kindwall EP, ed. Hyperbaric Medicine Practice. Flagstaff, AZ: Best Publishing;
1994:344–366.
162. Cope C, Abramowitz S. Respiratory responses to intravenous sodium
cyanide, a function of the oxygen-cyanide relationship. Am Rev Respir
Dis. 1960;81:321–328.
163. Carden E. Hyperbaric oxygen in cyanide poisoning. Anaesthesia. 1970;25:
442–443.
164. Goodhart GL. Patient treated with antidote kit and hyperbaric oxygen survives cyanide poisoning. South Med J. 1994;87:814–816.
165. Litovitz TL, Larkin RF, Myers RA. Cyanide poisoning treated with hyperbaric oxygen. Am J Emerg Med. 1983;1:94–101.
166. Takano T, Miyazaki Y, Nashimoto I, et al. Effect of hyperbaric oxygen on
cyanide intoxication: in situ changes in intracellular oxidation reduction.
Undersea Biomed Res. 1980;7:191–197.
167. Way JL, End E, Sheehy MH, et al. Effect of oxygen on cyanide intoxication. IV. Hyperbaric oxygen. Toxicol Appl Pharmacol. 1972;22:415–
421.
168. Smilkstein MJ, Bronstein AC, Pickett HM, et al. Hyperbaric oxygen therapy
for severe hydrogen sulfide poisoning. J Emerg Med. 1985;3:27–30.
169. Whitcraft DD 3rd, Bailey TD, Hart GB. Hydrogen sulfide poisoning treated
with hyperbaric oxygen. J Emerg Med. 1985;3:23–25.
170. ATSDR. Toxicological Profile for Carbon Tetrachloride. U.S. Dept. of
Health and Human Services PHS, Agency for Toxic Substances and Disease Registry; 2005.
171. Burkhart KK, Hall AH, Gerace R, et al. Hyperbaric oxygen treatment for
carbon tetrachloride poisoning. Drug Saf. 1991;6:332–338.
172. Marzella L, Muhvich K, Myers RA. Effect of hyperoxia on liver necrosis
induced by hepatotoxins. Virchows Arch B Cell Pathol Incl Mol Pathol.
1986;51:497–507.
173. Burk RF, Lane JM, Patel K. Relationship of oxygen and glutathione in
protection against carbon tetrachloride-induced hepatic microsomal lipid
peroxidation and covalent binding in the rat. Rationale for the use of hyperbaric oxygen to treat carbon tetrachloride ingestion. J Clin Invest. 1984;
74:1996–2001.
174. Burk RF, Reiter R, Lane JM. Hyperbaric oxygen protection against carbon
tetrachloride hepatotoxicity in the rat. Association with altered metabolism.
Gastroenterology. 1986;90:812–818.
175. Bernacchi A, Myers R, Trump BF, et al. Protection of hepatocytes with
hyperoxia against carbon tetrachloride-induced injury. Toxicol Pathol.
1984;12:315–323.
176. Truss CD, Killenberg PG. Treatment of carbon tetrachloride poisoning with
hyperbaric oxygen. Gastroenterology. 1982;82:767–769.
177. Heimbach RD. Gas gangrene. In: Kindwall EP, ed. Hyperbaric Medicine
Practice. Flagstaff, AZ: Best Publishing; 1994:374–388.
178. Brummelkamp WH, Boerema I, Hoogendyk L. Treatment of clostridial
infections with hyperbaric oxygen drenching. A report on 26 cases. Lancet.
1963;1:235–238.
179. Brummelkamp WH, Hogendijk J, Boerema I. Treatment of anaerobic infections (clostridial myositis) by drenching tissues with oxygen under high
atmospheric pressure. Surgery. 1961;49:299–302.
180. Van Unnik AJM. Inhibition of toxin production in Clostridium perfringens
in vitro by hyperbaric oxygen. Antoine von Leeuwenhoek. 1965;31:181–
186.
181. Demello FJ, Haglin JJ, Hitchcock CR. Comparative study of experimental
Clostridium perfringens infection in dogs treated with antibiotics, surgery
and hyperbaric oxygen. Surgery. 1973;73:936–941.
182. Clarke LA, Moon RE. Hyperbaric oxygen in the treatment of life threatening soft tissue infections. Respir Care Clin N Am. 1999;5:203–219.
183. Bakker DJ. Selected aerobic and anaerobic soft tissue infections diagnosis and the use of hyperbaric oxygen as an adjunct. In: Kindwall EP, ed.
Hyperbaric Medicine Practice. Flagstaff, AZ: Best Publishing; 1994:396–
415.
184. Riseman JA, Zamboni WA, Curtis A, et al. Hyperbaric oxygen therapy
for necrotizing fasciitis reduces mortality and the need for debridements.
Surgery. 1990;108:847–850.
185. Dahm P, Roland FH, Vaslef SN, et al. Outcome analysis in patients with
primary necrotizing fasciitis of the male genitalia. Urology. 2000;56:31–35;
discussion 5–6.
186. Blitzer A, Lawson W, Meyers BR, et al. Patient survival factors in paranasal
sinus mucormycosis. Laryngoscope. 1980;90:635–648.
187. Price JC, Stevens DL. Hyperbaric oxygen in the treatment of rhinocerebral
mucormycosis. Laryngoscope. 1980;90:737–747.
573
188. Couch L, Theilen F, Mader JT. Rhinocerebral mucormycosis with cerebral
extension successfully treated with adjunctive hyperbaric oxygen therapy.
Arch Otolaryngol Head Neck Surg. 1988;114:791–794.
189. Ferguson BJ, Mitchell TG, Moon R, et al. Adjunctive hyperbaric oxygen
for treatment of rhinocerebral mucormycosis. Rev Infect Dis. 1988;10:551–
559.
190. Farmer JC, Kindwall EP. Use of adjunctive hyperbaric oxygen in the management of fungal disease. In: Kindwall EP, ed. Hyperbaric Medicine Practice. Flagstaff, AZ: Best Publishing; 1994:582–586.
191. Hart GB, Lennon PA, Strauss MD. Hyperbaric oxygen in exceptional acute
blood-loss anemia. J Hyperbar Med. 1987;2:205–210.
192. Van Meter KW. A systematic review of the application of hyperbaric oxygen
in the treatment of severe anemia: an evidence-based approach. Undersea
Hyperb Med. 2005;32:61–83.
193. Palzur E, Vlodavsky E, Mulla H, et al. Hyperbaric oxygen therapy for
reduction of secondary brain damage in head injury: an animal model of
brain contusion. J Neurotrauma. 2004;21:41–48.
194. Rockswold SB, Rockswold GL, Vargo JM, et al. Effects of hyperbaric
oxygenation therapy on cerebral metabolism and intracranial pressure in
severely brain injured patients. J Neurosurg. 2001;94:403–411.
195. Rockswold GL, Ford SE, Anderson DC, et al. Results of a prospective
randomized trial for treatment of severely brain-injured patients with hyperbaric oxygen. J Neurosurg. 1992;76:929–934.
196. Ikeda K, Ajiki H, Nagao H, et al. Experimental and clinical use of hyperbaric oxygen in burns. In: Wada J, Iwa T, eds. Proceedings of the 4th
International Congress on Hyperbaric Medicine. Baltimore, MD: Williams
& Wilkins; 1970:377–380.
197. Hart GB, O’Reilly RR, Broussard ND, et al. Treatment of burns with hyperbaric oxygen. Surg Gynecol Obstet. 1974;139:693–696.
198. Niezgoda JA, Cianci P, Folden BW, et al. The effect of hyperbaric oxygen
therapy on a burn wound model in human volunteers. Plast Reconstr Surg.
1997;99:1620–1625.
199. Perrins DJD. A failed attempt to limit tissue destruction in scalds of pig
skins with hyperbaric oxygen. In: Wada J, Iwa T, eds. Proceedings of the 4th
International Congress on Hyperbaric Medicine. Baltimore, MD: Williams
& Wilkins; 1970:381–387.
200. Cianci P, Lueders HW, Lee H, et al. Adjunctive hyperbaric oxygen therapy
reduces length of hospitalization in thermal burns. J Burn Care Rehabil.
1989;10:432–435.
201. Cianci P, Williams C, Lueders H, et al. Adjunctive hyperbaric oxygen in the
treatment of thermal burns. An economic analysis. J Burn Care Rehabil.
1990;11:140–143.
202. Brannen AL, Still J, Haynes M, et al. A randomized prospective trial of
hyperbaric oxygen in a referral burn center population. Am Surg. 1997;
63:205–208.
203. Villanueva E, Bennett MH, Wasiak J, et al. Hyperbaric oxygen therapy for
thermal burns. Cochrane Database Syst Rev. 2004:CD004727.
204. Whalen R, Saltzman H, Holloway D, et al. Cardiovascular and blood gas
responses to hyperbaric oxygenation. Am J Cardiol. 1965;15:638–646.
205. Swift PC, Turner JH, Oxer HF, et al. Myocardial hibernation identified
by hyperbaric oxygen treatment and echocardiography in postinfarction
patients: comparison with exercise thallium scintigraphy. Am Heart J.
1992;124:1151–1158.
206. Sterling DL. Hyperbaric oxygen limits infarct size in ischemic rabbit myocardium in vivo. Circulation. 1993;88:1931–1936.
207. Shandling AH, Ellestad MH, Hart GB, et al. Hyperbaric oxygen and thrombolysis in myocardial infarction: the “HOT MI” pilot study. Am Heart J.
1997;134:544–550.
208. Stavitsky Y, Shandling AH, Ellestad MH, et al. Hyperbaric oxygen and
thrombolysis in myocardial infarction: the “HOT MI” randomized multicenter study. Cardiology. 1998;90:131–136.
209. Heyman A, Saltzman HA, Whalen RE. The use of hyperbaric oxygenation
in the treatment of cerebral ischemia and infarction. Circulation. 1966;33
(Suppl II):20–27.
210. Veltkamp R, Warner DS, Domoki F, et al. Hyperbaric oxygen decreases
infarct size and behavioral deficit after transient focal cerebral ischemia in
rats. Brain Res. 2000;853:68–73.
211. Gunther A, Kuppers-Tiedt L, Schneider PM, et al. Reduced infarct volume and differential effects on glial cell activation after hyperbaric oxygen treatment in rat permanent focal cerebral ischaemia. Eur J Neurosci.
2005;21:3189–3194.
212. Veltkamp R, Siebing DA, Heiland S, et al. Hyperbaric oxygen induces rapid
protection against focal cerebral ischemia. Brain Res. 2005;1037:134–138.
213. Qin Z, Karabiyikoglu M, Hua Y, et al. Hyperbaric oxygen-induced attenuation of hemorrhagic transformation after experimental focal transient
cerebral ischemia. Stroke. 2007;38:1362–1367.
214. Veltkamp R, Bieber K, Wagner S, et al. Hyperbaric oxygen reduces basal
lamina degradation after transient focal cerebral ischemia in rats. Brain
Res. 2006;1076:231–237.
215. Anderson DC, Bottini AG, Jagiella WM, et al. A pilot study of hyperbaric oxygen in the treatment of human stroke. Stroke. 1991;22:1137–
1142.
216. Nighoghossian N, Trouillas P, Adeleine P, et al. Hyperbaric oxygen in
the treatment of acute ischemic stroke. A double-blind pilot study. Stroke.
1995;26:1369–1372.
13:42
P1: OSO/OVY
GRBT291-37-39
574
P2: OSO/OVY
QC: OSO/OVY
T1: OSO
GRBT291-3641G GRBT291-Gabrielli-v2.cls
Printer: Yet to come
October 23, 2008
Section III: Techniques, Procedures, and Treatments
217. Rusyniak DE, Kirk MA, May JD, et al. Hyperbaric oxygen therapy in acute
ischemic stroke: results of the Hyperbaric Oxygen in Acute Ischemic Stroke
Trial Pilot Study. Stroke. 2003;34:571–574.
218. Cochran WD, Levison H, Muirhead DM Jr, et al. A clinical trial of high
oxygen pressure for the respiratory-distress syndrome. N Engl J Med.
1965;272:347.
219. Camporesi EM, Moon RE. Hyperbaric oxygen as an adjunct to therapeutic lung lavage in pulmonary alveolar proteinosis. In: Bove AA, Bachrach
AJ, Greenbaum LJ Jr, eds. Underwater and Hyperbaric Physiology IX
Proceedings of the Ninth International Symposium on Underwater and
Hyperbaric Physiology. Bethesda, MD: Undersea and Hyperbaric Medical
Society; 1987:955–960.
220. Biervliet JD, Peper JA, Roos CM, et al. Whole lung lavage under hyperbaric
conditions: 1. The monitoring. Adv Exp Med Biol. 1992;317:115–120.
221. van der Kleij AJ, Peper JA, Biervliet JD, et al. Whole lung lavage under
hyperbaric conditions: 2. Monitoring tissue oxygenation. Adv Exp Med
Biol. 1992;317:121–124.
222. Russell JB, Snider MT, Richard RB, et al. Hyperbaric nitrous oxide as a
sole anesthetic agent in humans. Anesth Analg. 1990;70:289–295.
223. Lambertsen CJ, Idicula J. A new gas lesion syndrome in man, induced by
“isobaric gas counterdiffusion.” J Appl Physiol. 1975;39:434–443.
224. Acott CJ, Gorman DF. Decompression illness and nitrous oxide anaesthesia
in a sports diver. Anaesth Intensive Care. 1992;20:249–250.
225. Weaver LK, Howe S. Noninvasive Doppler blood pressure monitoring in
the monoplace hyperbaric chamber. J Clin Monit. 1991;7:304–308.
226. NFPA. National Fire Protection Association, Standards for Healthcare Facilities. Document 99, Chapter 20; 2005.
227. Moon RE, Bergquist LV, Conklin B, et al. Monaghan 225 ventilator use
under hyperbaric conditions. Chest. 1986;89:846–851.
228. Weaver LK, Greenway L, Elliott CG. Performance of the Sechrist 500A
hyperbaric ventilator in a monoplace hyperbaric chamber. J Hyperbar Med.
1988;3:215–225.
229. Weaver LK. Operational use and patient care in the monoplace hyperbaric
chamber. Respir Care Clin N Am. 1999;5:51–92.
230. Weaver LK, Howe S. Normobaric measurement of arterial oxygen tension in subjects exposed to hyperbaric oxygen. Chest. 1992;102:1175–
1181.
231. Van Meter K. Medical field management of the injured diver. Respir Care
Clin N Am. 1999;5:137–177.
232. Booth L. Details of an X-ray system for use in diving medicine. In: Smith
G, ed. Proceedings of the Sixth International Congress on Hyperbaric
Medicine. Aberdeen: Aberdeen University Press; 1979:443–444.
233. Kindwall EP. Contraindications and side effects to hyperbaric oxygen treatment. In: Kindwall EP, ed. Hyperbaric Medicine Practice. Flagstaff, AZ:
Best Publishing; 1994:46–54.
234. Wolf HK, Moon RE, Mitchell PR, et al. Barotrauma and air embolism
in hyperbaric oxygen therapy. Am J Forensic Med Pathol. 1990;11:
149–153.
235. Weaver LK, Churchill S. Pulmonary edema associated with hyperbaric oxygen therapy. Chest. 2001;120:1407–1409.
236. Leitch DR, Green RD. Pulmonary barotrauma in divers and the treatment
of cerebral arterial gas embolism. Aviat Space Environ Med. 1986;57:931–
938.
237. Moon RE, Gorman DF. Treatment of the decompression disorders. In: Neuman TS, Brubakk AO, eds. The Physiology and Medicine of Diving. New
York, NY: Elsevier Science; 2003:600–650.
238. Moon RE, Sheffield PJ. Guidelines for treatment of decompression illness.
Aviat Space Environ Med. 1997;68:234–243.
239. Piantadosi CA. The role of hyperbaric oxygen in carbon monoxide, cyanide
and sulfide intoxication. Prob Resp Care. 1991;4:215–231.
240. Berk RF, Lane JM, Patel K. Relationship of oxygen and glutathione in
protection against carbon tetrachloride-induced hepatic microsomal lipid
peroxidation and covalent binding in the rat. Rationale for the use of hyperbaric oxygen to treat carbon tetrachloride ingestion. J Clin Invest. 1984;
74:1996–2001.
241. Bakker DJ, van der Kleij AJ. Soft tissue infections including clostridial myonecrosis: diagnosis and treatment. In: Oriani G, Marroni A, Wattel F,
eds. Handbook on Hyperbaric Medicine. New York: Springer-Verlag; 1996:
343–361.
242. Bakker DJ, van der Kleij AJ. Clostridial myonecrosis. In: Oriani G, Marroni
A, Wattel F, eds. Handbook on Hyperbaric Medicine. New York: SpringerVerlag; 1996:362–385.
243. Escobar SJ, Slade JB, Jr., Hunt TK, et al. Adjuvant hyperbaric oxygen therapy (HBO2 ) for treatment of necrotizing fasciitis reduces mortality and
amputation rate. Undersea Hyperb Med 2005;32:437–443.
244. Zamboni WA, Kindwall EP. Author’s reply to: still unproved in necrotising
fasciitis. BMJ. 1993;307:936.
245. Yohai RA, Bullock JD, Aziz AA, et al. Survival factors in rhino-orbitalcerebral mucormycosis. Surv Ophthalmol. 1994;39:3–22.
246. Bouachour G, Cronier P, Gouello JP, et al. Hyperbaric oxygen therapy
in the management of crush injuries: a randomized double-blind placebocontrolled clinical trial. J Trauma. 1996;41:333–339.
247. Nemiroff PM. Synergistic effects of pentoxifylline and hyperbaric oxygen
on skin flaps. Arch Otolaryngol Head Neck Surg. 1988;114:977.
248. Zamboni WA, Roth AC, Russell RC, et al. The effect of hyperbaric oxygen
on reperfusion of ischemic axial skin flaps: a laser Doppler analysis. Ann
Plast Surg. 1992;28:339–341.
249. Jansen HM, Zuurmond WW, Roos CM, et al. Whole-lung lavage under hyperbaric oxygen conditions for alveolar proteinosis with respiratory failure.
Chest. 1987;91:829–832.
250. Niu AKC, Yang C, Lee HC, et al. Burns treated with adjunctive hyperbaric
oxygen therapy—a comparative study in humans. J Hyperbar Med. 1987;
2:75–85.
251. Bevers RF, Bakker DJ, Kurth KH. Hyperbaric oxygen treatment for haemorrhagic radiation cystitis. Lancet. 1995;346:803–805.
252. Farmer JC Jr, Shelton DL, Angelillo JD, et al. Treatment of radiationinduced tissue injury by hyperbaric oxygen. Ann Otol Rhinol Laryngol.
1978;87:707–715.
253. Ferguson BJ, Hudson WR, Farmer JC, Jr. Hyperbaric oxygen therapy for
laryngeal radionecrosis. Ann Otol Rhinol Laryngol. 1987;96:1–6.
254. Norkool DM, Hampson NB, Gibbons RP, et al. Hyperbaric oxygen therapy
for radiation-induced hemorrhagic cystitis. J Urol. 1993;150:332–334.
255. Fife CE, Buyukcakir C, Otto GH, et al. The predictive value of transcutaneous oxygen tension measurement in diabetic lower extremity ulcers
treated with hyperbaric oxygen therapy: a retrospective analysis of 1,144
patients. Wound Repair Regen. 2002;10:198–207.
256. Broughton G 2nd. Management of the brown recluse spider bite to the
glans penis. Mil Med. 1996;161:627–629.
257. Maynor ML, Moon RE, Klitzman B, et al. Brown recluse spider envenomation: a prospective trial of hyperbaric oxygen therapy. Acad Emerg Med.
1997;4:184–192.
258. Divers Alert Network. Annual Diving Report. Durham, NC: Divers Alert
Network; 2006.
259. van Hulst RA, Drenthen J, Haitsma JJ, et al. Effects of hyperbaric treatment
in cerebral air embolism on intracranial pressure, brain oxygenation, and
brain glucose metabolism in the pig. Crit Care Med. 2005;33:841–846.
13:42