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166
Capillary Length
Pressure
Volume
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of le heart failure or overload on echocardiography, and
elevated pulmonary artery wedge pressure. Anesthetized
Filtration
Absorption
patients who develop pulmonary edema may present with
frothy pink sputum in the endotracheal tube and with
increased airway pressures.
6
Oncotic Hydrostatic
HEMOPTYSIS
Hemoptysis is the expectoration of blood originating from
the lung or the bronchial tree.7 e lungs are perfused with
a dual circulation system— the pulmonary and bronchial
Figu re21.1 As uid passes along the length of the capillaries, there is
a shift in oncotic and hydrostatic pressure. At the proximal portion of
the capillaries there is an increase in capillary hydrostatic pressure,
favoring net ltration of uid from the capillary to the interstitial uid.
As ow through the capillary progresses and uid extravasates out of
the capillary lumen, there is a relative decrease in capillary hydrostatic
pressure, increasing reabsorption of uid back into the capillaries.
vessels.8 Any disruption in the blood ow of these systems, leading to leakage of the alveolar capillaries into the
airspaces can lead to hemoptysis. e most common cause
of hemoptysis in adults is pneumonia or infection, where
inammation and edema of the supercial mucosal surface
leads to rupture of supercial blood vessels.7 Tumors can
also invade the supercial mucosa of blood vessels or other
Π
is the capillary oncotic pressure, Πis is the interstitial
cap
oncotic pressure, Kf is the ltration coecient, and σ is the
reection coecient.
Pulmonary edema forms when there is an imbalance
between the Starling forces and the lymphatic drainage system (see Figure21.1).
Clinically signicant pulmonary edema is usually
classied as cardiogenic or noncardiogenic in origin.
Cardiogenic pulmonary edema is due to elevations of le
atrial pressure, resulting in marked increases in pulmonary
capillary hydrostatic pressure. Coronary artery disease,
myocardiopathies, or aortic or mitral valve abnormalities
can lead to excess ltration, lling the peribronchovascular
interstitium and eventually ooding the alveolar spaces.6
In contrast, noncardiogenic pulmonary edema is oen due
to increased endothelial permeability of the pulmonary
capillaries, which causes extravasation. is change in permeability may be due to direct insults to the lung, such as
inhalation of corrosive gases or gastric aspiration or indirect insults involving systemic inammatory states such as
sepsis, pulmonary aspiration, anaphylaxis, pancreatitis, and
vascular lesions. e dierential diagnosis for hemoptysis
is large and includes infections, such as pneumonia, tuberculosis, and lung abscesses; neoplasms, particularly bronchogenic carcinoma; bronchiectasis; foreign bodies; lung
trauma and contusions; vasculitides such as Goodpasture’s
and Wegener’s granulomatosis. Primary vascular sources
such as ateriovenous malformations, pulmonary embolisms,
and elevated pulmonary venous pressures from mitral stenosis are also a consideration. Anticoagulants can increase a
predilection for hemoptysis and should be considered during the initial evaluation. Iatrogenic causes such pulmonary
artery rupture from a pulmonary artery catheter are also
possible etiologies.
7
Hemoptysis is usually classied as massive or nonmassive, depending on the amount of blood lost per day. ere
is no consensus on the exact denition of massive hemoptysis, with values ranging from 200 mL to 1000 mL of
blood loss in 24 hours.7 Massive hemoptysis is oen a lethal
condition with up to 80% mortality.7 It requires emergent
evaluation, securement of the airway and control of the
underlyingcause.
multiple organ failure.6 In the operating room, negativepressure pulmonary edema can be seen if a patient inspires
against a closed glottis, as can occur during laryngospasm.
Patients with pulmonary edema oen present with a
constellation of symptoms including shortness of breath,
tachypnea, hypoxia, and rales, crepitus, or wheezes on physical exam. ose with cardiogenic pulmonary edema will
also have signs of right heart failure including an enlarged
heart, with Kerly B lines and the presence of pleural eusions on chest x- ray, elevated brain natriuretic peptide, signs
POSTOPERATIVE PULMONARY COMPLICATIONS
Approximately 5%– 10% of all patients undergoing general
anesthesia for nonthoracic surgery and 22% of high- risk
patients are at risk for postoperative pulmonary complications (POPC) including pneumonia, bronchospasm,
respiratory failure, and prolonged mechanical ventilation,
increasing morbidity, length of stay, and mortality.1 Risk
factors for POPC include age > 70years, > 40- pack- year
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167
smoking history, ASA score > 2, COPD, the inability to
walk >2 blocks or climb >1 ight of stairs, malnutrition,
and BMI > 30. Neck, thoracic, upper abdominal, aortic,
and neurologic surgeries are associated with higher risk of
POPC, as is the use of general anesthesia with an endotracheal tube (ETT) and surgical duration of more than 2
hours.9 If a case is elective, it is important to stabilize the
patient, investigate, and treat the underlying pulmonary
problem prior to the operation.
prevent dehydration.11 Humidied facemasks can be used
in the pre- or postoperative setting in a patient who is spontaneously breathing. Intraoperatively, decreasing fresh gas
ows in an intubated patient to the minimal allowable to
meet the patient’s oxygenation demands and provide for
adequate removal of inhaled anesthetics can also be used to
limit dehydration.
Expectorants, such as guaifenesin and hydration, are
medications meant to increase the volume of airway water
in order to improve the eectiveness of coughing. ey do
TREATING THEUNDERLYINGCAUSE
In emergency situations, the patient’s pulmonary status
should be maximized preoperatively with anti- infective
agents, as well as the optimization of uid status and gasexchange strategies. It is important not to wait for initial
cultures to return before initiating therapy for pneumonia, taking into consideration the patient’s risk factors for
community- acquired versus healthcare- associated pneumonia as well as atypical pathogens such as tuberculosis.
Broadening antibiotic coverage may be appropriate. e
risk for pneumonia is increased with decreased mucociliary
clearance and persistent atelectasis, and, thus, treatment of
these factors should be maximized.
Cardiogenic pulmonary edema is oen responsive to
diuresis. Active cardiac conditions such as myocardial infarction, acute valvular disease, and arrythmias should be considered in a patient with new- onset cardiogenic pulmonary
edema and should be evaluated appropriately. Treatment of
noncardiogenic pulmonary edema should largely focus on
supportive management and treatment of the underlying
cause (e.g., sepsis, anaphylaxis, pancreatitis,etc.).
not alter the function of the cilia. In contrast to expectorants, mucolytics degrade components of mucus such as
mucin polymers, DNA, brin, and actin to decrease the
viscosity of secretions. N- acetylcysteine (NAC) is one of
the best- known mucolytics. Although they have theoretical
benets, there is no evidence of supporting the ecacy of
guaifenesin, NAC, or simple hydration alone in improving
expectoration.
10
Incentive spirometry is a simple mechanical device
designed to remind and assist patients to take deep slow
breaths. ere is evidence that preoperative education on
how to use IS has been shown to decrease the rate of postoperative pulmonary complications.12 Patients’ ability to
perform IS has been shown to correlate with their inspiratory reserve volume and forced vital capacity, and a decline
from baseline performance may also be an early indicator of
ensuing pulmonary decline.11 Other devices used to clear
secretions include positive expiratory vibratory devices,
such as Acapella or utter valves, which intermittently
occlude during exhalation, causing a vibration of the airways. is is thought to facilitate coughing.
Chest physiotherapy, including postural drainage, percussion and vibration, and incentive to cough has been
CLEARING SECRETIONS
e inability to clear secretions can lead to pneumonia/
pulmonary infections and atelectasis, which can further
exacerbate V/ Q mismatch. Clearance of secretions primarily depends on the viscoelastic properties of the mucus,
adequate function of the ciliary system, and an individual’s
ability to generate enough forward ow by coughing to
remove the mucus.10 us, it is not surprising that expectorants and mucolytics, deep breathing exercises, incentive
spirometry (IS), and positive expiratory pressure (PEP)
have all been proposed as ways to improve the problem of
retained secretions.
Decreased mucociliary clearance can be caused by
dehydration of the tracheobronchial airways, resulting in
thick adhesive mucus. Humidied oxygen can be used to
shown to lower the incidence of postoperative pulmonary complications. Notably, care involvement by a respiratory therapist, regardless of the exact treatment given
(intermittent positive pressure breathing, IS, deep breathing exercises), lowers the incidence of post- op pulmonary
complications in patients undergoing abdominal surgery.12
Mobilization also improves functional residual capacity.
Patients should be encouraged to get out of bed to chair or
to ambulate as soon as possible to enhance their pulmonary
function.
Tracheal suctioning can directly and mechanically
remove secretions, mucus plugging, and consolidation. is
can be done in the awake patient with blind nasal suctioning or in an intubated patient. Ideally, the patient should
be preoxygenated with high FiO2; the catheter should
be advanced without suction and then intermittently
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suctioned on the way out. Adverse eects of suctioning
include mucosal damage, bronchospasm, laryngospasm,
cardioarrhythmias, and worsening atelectasis. If airway
obstruction is severe, beroptic bronchoscopy can also be
used to help clear blood or secretions under direct visualization; complications include laryngospasm, bronchospasm,
pneumothorax, and pulmonary hemorrhage.
11
of the patient and to cause bronchodilation. Racemic epinephrine can also be used if bronchoconstriction is severe
and the ability to ventilate is compromised. Steroids are
useful for inammatory mediated bronchospasm, but not
during an acute episode.11 However, there is no evidence
for harm (i.e., increased respiratory or wound infection) in
administering corticosteroids and, if using them prophylactically, it is recommended to administer steroids at least 48
ALLEVIATING BRONCHOSPASM
Bronchospasm can worsen airway obstruction from mucus.
While patients with obstructive lung disease, such as
asthma and COPD, are at increased risk of bronchospasm,
this may be seen in any patient undergoing general anesthesia. Inhaled bronchodilators, including beta- agonists
(e.g., albuterol) and anticholinergics (e.g., ipratropium),
should be considered perioperatively, in all patients with
bronchospastic disease. In the intubated patient, bronchospasm oen presents with increased peak airway pressures
indicated by an upslope of the end- tidal carbon monoxide
waveform. If this is seen in the operating room, it is important to evaluate for obstruction in the breathing circuit,
including the endotracheal tube (ETT); deepen the anesthetic; and treat bronchospasm (see Box21.1).
Inhaled anesthetics, propofol and ketamine have bronchodilating properties that can be used in an acute case of
intraoperative bronchospasm to deepen the anesthetic level
hours in advance for maximal eect.
ATELECTASIS
In addition to mucus plugging, atelectasis can also be caused
by inhibition of surfactant, gas reabsorption, and compression of lung tissue. Atelectasis itself is associated with
increased bacterial overgrowth and increased lung permeability, further increasing the risk for edema and pneumonia.
Loss of intercostal muscle tone and cephalad displacement of
the diaphragm are known physiological changes during anesthesia that worsen airway closure. Interestingly, increased
FiO2, such as during preoxygenation with 100% oxygen, is
also associated with an increase in reabsorption atelectasis.
Minimal atelectasis usually requires little treatment and
is oen responsive to increased O2. It should improve as the
anesthetic medications wear o and the patient is able to
take deeper breaths. In more severe forms, atelectasis may
present with decreased compliance, impaired oxygenation,
increased pulmonary vascular resistance, and development
of lung injury.
11
12
11
Prevention of atelectasis, like retained secretions, is traditionally done with deep- breathing exercises and cough-
BOX 21.1 INTRAOPERATIVE MANAGEMENT OF
AN ACUTE RISE INPEAK INSPIRATORY PRESSURE IN
AN INTUBATED PATIENT
Acute rise in peak inspiratory pressure
• Switch to manual ventilation and assess resistance to
airow
• Check airway for external signs of obstruction (kinked
tube,etc.)
• Listen to breath sounds for wheezing (upper vs. lower
airway obstruction)
• Make sure patient is paralyzed
• Increase depth of anesthesia
• Give bronchodilators:albuterol, propofol, ketamine, inhaled
anesthetics
ing to clear secretions, reopening the airways. Especially in
thoracic or abdominal surgery, one should make sure that
pain issues are well addressed to prevent splinting, with a
reduction in cough eort and deep breathing. Respiratory
depression from systemic opioids may be limited with use
of epidural or regional anesthesia techniques.
Also, CPAP or BiPAP may be benecial in atelectatic
lung and either is less invasive than endotracheal intubation. Extreme forms of atelectasis such as lobar collapse may
require bronchoscopy and mechanical ventilation.
VENTILATION STRATEGIES
Ventilation strategies that can be used to limit atelectasis
include recruitment breaths (which involve inating the
lungs with a pressure of 30– 40cmH2O for 10– 20 seconds),
application of positive end- expiratory pressure (PEEP), and
lung- protective ventilation strategies.
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Positive end- expiratory pressure provides increased
CASE- BASED LEARNING DISCUSSION
intrathoracic pressure, providing resistance to exhalation
and minimizing alveolar collapse, atelectasis, and V/ Q
mismatch. When PEEP is used in patients with one- lung
ventilation in individuals without COPD, it has been associated with decreased incidence of acute lung injury and
atelectasis, decreased shunt formation, and improved oxygenation.11 e only absolute contraindication to PEEP is
the presence of a bronchopleural stula.
11
If high enough, PEEP can impede venous return to the
right heart. us, while PEEP may reduce atelectasis, it
can also have adverse eects such as reduced cardiac output and redistribution of blood ow toward dependent,
still- collapsed lung regions. Also, PEEP can accentuate lung
injury, especially in individuals with COPD. If the patient
is not allowed to adequately exhale, they may accumulate
their end- expiratory pressures (“stacking”), creating what is
1. Based on the patient’s presentation, would you continue
with plans for surgery? Can the case be postponed?
2. e decision is made with the surgeon to proceed
with the case given the risk of bowel ischemia. What
could you do preoperatively to maximize the patient’s
respiratory status?
3. e patient is brought to the operating room, and
you notice his oxygen saturation aer preoxygenation
with 100% oxygen is 96%. General endotracheal
tube anesthesia is induced with lidocaine, propofol,
fentanyl, and rocuronium. Soon aer intubation you
notice his saturation remains in the low 90s on 50%
FiO2 and 5 PEEP. What would you do to remedy this
situation?
known as auto- PEEP. Patients without signicant obstructive lung disease should be able to tolerate 5– 10mmHg of
PEEP. It is important to monitor end- tidal CO2 tracings
and airway pressure while increasingPEEP.
Lung- protective strategies should be employed to limit
damage to the lung parenchyma during mechanical ventilation. is includes using smaller tidal volumes of 5– 8 mL/
kg, and adjusting the respiratory rate accordingly for a goal
pH >7.3. Goal PaO2 should be >55 or SpO2 > 88% with
titration of PEEP as needed. Additionally, plateau pressure
should be less than 30cmH2O, with an inspiratory to expira-
a. Is there a downside to increasing FiO2 or PEEP in
this situation? What if you increased PEEP and
noted a progressive decrease in his blood pressure?
What should you consider in your dierential
diagnosis?
4. e patient marginally improves with these maneuvers,
and he remains hemodynamically stable. However, his
peak airway pressures remain in the 30s despite low
tidal volumes. You examine his endotracheal tube and
note yellowish frothy sputum. What is your nextstep?
tory ratio of 1:1– 1:3.11 ese parameters are not always feasible in every patient, but should be optimized when possible.
5. You are able to suction the patient’s airway and his
peak airway pressures initially improve. However,
BRONCHOSCOPY
Rigid or exible bronchoscopy has both diagnostic and
therapeutic indications. e anesthetic plan for bronchoscopy should include an endotracheal tube or supraglottic
airway large enough for both scope and ventilation. Rigid
bronchoscopes allow for dynamic examination of the airways from the oropharynx to the subsegmental bronchi,
as well as ventilation through the side port of the bronchoscope. e most common adverse events during these
procedures are transient desaturations and, less frequently,
laryngospasm and bronchospasm.
While bronchoscopy can be used in hemoptysis cases
to biopsy areas suspicious for malignancy or other pathologies, in the case of a massive hemorrhage, it plays a pivotal
role in identifying the source of bleeding. Once this is done,
a double lumen tube can be used to isolate the bleeding and
preferentially ventilate the lung which is not bleeding.
moments later, the ventilator starts to alarm for peak
inspiratory pressures >40. ere is an up- sloping of
the patient’s end- tidal carbon dioxide tracing and
audible wheezes coming from the patient. His oxygen
saturation starts to slowly decrease. You ensure that
there is no kinking in the ETT or the airway circuit.
What should youdo?
6. What alternative bronchodilators could you use in the
operating room if albuterol were unavailable? How
should albuterol be best delivered in this situation?
7. e surgeon nishes the procedure and asks you to
extubate the patient. What are you concerned about
with extubation?
8. e patient is extubated and brought to the recovery
room with a facemask on 6 L O2. What can you do
postoperatively to reduce the risk of postoperative
pulmonary complications?
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REFERENCES
7. Bidwell JL, Pachner RW. Hemoptysis:diagnosis and management.
American Family Physician. 2005;72(7):1253– 60.
1. Hedenstierna G. Respiratory physiology. In: Miller RD, et al.,
eds., Miller’s Anesthesia. 7th ed. Philadelphia, PA: Churchill
Livingstone/ Elsevier; 2010:361– 92.
2. Rogers DF. Physiology of airway mucus secretion and pathophysiology of hypersecretion. Respiratory Care. 2007;52(9):1134– 46;
discussion 1146– 9.
3. Watkins RR, Lemonovich TL. Diagnosis and management of
community- acquired pneumonia in adults. American Family
Physician. 20111;83(11):1299– 306.
4. Centers for Disease Control and Prevention. Fast Stats. Deaths and
mortality. http:// www.cdc.gov/ nchs/ fastats/ deaths.htm. Accessed
April 28th2015.
5. Pulmonary edema. Atlas of Pathology. 3rd edition. http:// www.
pathologyatlas.ro/ pulmonary- edema- pathology.php. Accessed
April 28,2015.
6. Murray JF. Pulmonary edema: pathophysiology and diagnosis.
International Journal of Tubercular Lung Disease. 2011;15(2):
8. Corey R. Hemoptysis. In: Walker HK, Hall WD, Hurst JW,
eds. Clinical Methods: e History, Physical, and Laboratory
Examinations. 3rd ed. Boston: Butterworths; 1990. Chapter39.
Available from:http:// www.ncbi.nlm.nih.gov/ books/ NBK360/
9. Michael F, Roizen MF, Fleisher LA. Anesthetic implications of
concurrent diseases. In:Miller RD, etal., eds., Miller’s Anesthesia.
7th ed. Philadelphia, PA: Churchill Livingstone/ Elsevier; 2010:
1067– 1150.
10. Rubin BK. Mucolytics, expectorants, and mucokinetic medications.
Respiratory Care. 2007;52(7):859– 65.
11. Ramsay A, Finley A. Postoperative respiratory failure and treatment. In:Slinger P, etal., eds. Principles and Practice of Anesthesia
for oracic Surgery. New York, NY: Springer Science+Business
Media; 2011:609– 634.
12. Fischer SP, Bader AM, Sweitzer BJ. Preoperative evaluation.
In:Miller RD, etal., eds., Miller’s Anesthesia. 7th ed. Philadelphia,
PA:Churchill Livingstone/ Elsevier; 2010:1001– 1066.
155– 60,i.
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171
22.
PNEUMOTHORAX
Jennifer Oliver and K. Annette Mizuguchi
CLINICALCASE
placement, bronchoscopy, central venous line insertion,
upper- extremity brachial plexus peripheral nerve blocks,
A 26- year- old otherwise healthy male presents for an arthroscopic repair of a torn rotator cu from a tennis injury. He
admits to smoking 4 cigarettes a day for 8years. An intrascalene peripheral nerve block is placed under ultrasound
guidance and general anesthesia is induced with placement
of a supraglottic airway. Surgery proceeds in the beach chair
position. Shortly aer incision the patient becomes hypotensive and tachycardic. Vital signs are as follows:temperature 36.5°C, heart rate 117 beats/ min, blood pressure 80/
45mmHg, oxygen saturation 84% on 50% inspired oxygen
concentration.
neuraxial anesthesia, or foreign- body aspiration.4 According
to the American Society of Anesthesiologists (ASA) Closed
Claims Project, which specically reported on adverse res-
piratory events that lead to malpractice suits using data
from 1974 to 1987, pneumothorax accounted for 3% of the
suits led out of 2,046 cases.5 Although this data is old, it
has helped to identify some of the most common causes of
pneumothorax during anesthesia (Table 22.2).
5
In a minority of cases, a tension pneumothorax may
develop as a consequence of the development of a one- way
valve, which allows air to enter the pleural space with each
breath without allowing air to ow back out. As more air is
PATHOPHYSIOLOGY OFDISEASESTATE
Pneumothorax is dened as a collection of gas inappropriately located between the visceral and parietal pleura resulting in compression of the lung.1 Pneumothorax is classied
as spontaneous (primary or secondary), traumatic, or iatrogenic2 (Table 22.1). Primary spontaneous pneumothorax
added, pressure in the pleural space builds quickly and compresses the lung on the eected side, resulting in hypoxia.
Further increases in this pressure lead to a mediastinal shi
toward the contralateral side and compression of the contralateral lung and the vena cava, with a subsequent decrease
in venous return. If unrecognized, tension pneumothorax
can lead to signicant circulatory impairment, respiratory
distress, cardiovascular collapse, and cardiac arrest.
3,4
occurs without a precipitating event. It frequently results
from rupture of a subpleural bleb in a patient with otherwise unrecognized lung disease. Secondary spontaneous
pneumothorax occurs in persons with recognized preexisting lung disease, and the consequences of a pneumothorax
in this patient group can be devastating as they may already
have poor reserve.
Traumatic pneumothoraces are common aer stab
wounds, gunshot wounds, blast injuries, and other injuries that result in penetration of the chest wall. e most
common mechanism is due to a rib fracture in which a
sharp bony prominence causes direct injury to the pleura.
However, traumatic pneumothorax may occur even in the
absence of apparent chest wall injury.
1,3
Iatrogenic pneumothorax can occur during routine
hospital procedures such as nasogastric or orogastric tube
RISK
A recent study analyzing British national databases
between 1991 and 1995 showed that the annual incidence
of pneumothorax is estimated at 24 cases per 100,000 persons for men and 9.8 cases per 100,000 for women.6 e
majority of pneumothoraces occur at rest, but can occur
during an acute increase in transpulmonary pressure such
as with an episode of coughing or Valsalva maneuver.7 Risk
factors for primary spontaneous pneumothorax include
smoking and family history of pneumothorax.
2,8
Smoking
increases the relative risk of spontaneous pneumothorax
up to 102 times in those who smoke greater than a pack per
day.9 Pneumothorax has also been reported with marijuana
smoking and cocaine inhalation. Primary spontaneous
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TABLE22.1 CLASSIFICATION OFPNEUMOTHORACES AND ASSOCIATED PRECIPITATING FACTORS
Spontaneous Pneumothorax Traumatic Pneumothorax
Primary
Secondary Penetrating Blunt
Iatrogenic
Subpleural blebs Airway disease (COPD, cystic brosis,
status asthmaticus)
Smoking Infectious lung disease (P.carinii
pneumonia, Necrotizing pneumonias)
Interstitial lung disease Foreign body Thoracentesis
Cancer (sarcoma, lung cancer) Cardiopulmonary resuscitation
Thoracic endometriosis Thoracic acupuncture
COPD, chronic obstructive pulmonary disease; P.carinii, pneumocystis carinii
Stab wounds Rib fracture Transthoracic needle aspiration
Gunshot wounds Central venous cannulation
pneumothorax is three to six times more common in males
than females, and the aected typically have a tall, thin
body habitus.
Secondary spontaneous pneumothorax occurs in those
with signicant underlying lung disease and is due to rupture of an apical bleb. Apneumothorax in these patients
TABLE22.2 COMMON CAUSES OFANESTHESIA- RELATED
PNEUMOTHORAX
Causes % of total cases
Regional Nerve Block 40
• Supraclavicular Brachial Plexus 37
• Intercostal 33
• Interscalene 11
• Stellate Ganglion 11
• Suprascapular 7
Airway instrumentation 19
Barotrauma 16
Mechanical ventilation (barotrauma)
Regional nerve blocks
Radical neck dissection, thyroid
surgery, breast surgery, kidney surgery
who have underlying lung disease can be potentially lifethreatening.2 e most common underlying lung diseases
are chronic obstructive pulmonary disease (COPD), cystic brosis, lung malignancy, interstitial lung disease, connective tissue disease, and necrotizing pneumonia. Other
known lung diseases that may increase the incidence for
pneumothorax are tuberculosis, pneumonocystis carinii,
lung cancer, sarcoma involving the lung, sarcoidosis, endometriosis, cystic brosis, acute severe asthma, idiopathic
pulmonary brosis, rheumatoid arthritis, ankylosing spondylitis, polymyositis and dermatomyositis, systemic sclerosis, Marfan s syndrome and Ehlers- Danlos syndrome,
histiocytosis X, and lymphangioleiomyomatosis (LAM).
10
Traumatic pneumothorax can be caused penetrating or blunt trauma. Oen, penetrating trauma injures
the peripheral lung and causes both a hemothorax and
pneumothorax. Blunt trauma can occur secondary to a
rib fracture that causes increased intrathoracic pressure
and bronchial rupture.3 Iatrogenic pneumothorax can
occur as a complication of a diagnostic or therapeutic
intervention.
2
Central line placement 7
Spontaneous/ unknown 7
Other 9
SOURCE:This table is adapted from the results of the ASA Closed Claims Projects that
specically reported on adverse respirator y events that lead to malpractice suits in the
United States from 1974 to1987.
172 PART IV. PULMONARY CRISES
ASSESSMENT OFTHE PATIENT:
PRESENTING SIGNS AND SYMPTOMS
e clinical manifestations of pneumothorax in the anes-
5
thetized patient can be challenging
11,12
(Table 22.3). In this
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TABLE22.3 SIGNS AND SYMPTOMS OFPNEUMOTHORAX
INTHE ANESTHETIZED PATIENT
Signs and Symptoms Mechanism
Hypoxemia Poorly ventilated collapsed lung continues to
perfuse; thus hypoxia is commonly caused
by a ventilation/ perfusion mismatch
Hypercapnia Unusual since the contralateral lung
maintains ventilation
Unilaterally decreased
breath sounds
Peak airway pressures Increased with progression to tension
Hypocapnia Seen with progression to tension pneumothorax
Bradycardia or
tachycardia
Abdominal distention
Severe hypotension
Respiratory alkalosis
Cardiac arrest/
pulseless electrical
activity
Most common cause is endobronchial
intubation
pneumothorax
as a result of decreased cardiac output
secondary to compromised venous return
2– 4,11
BOX 22.1 CLINICAL SITUATIONS ASSOCIATED WITHTHE
DEVELOPMENT OFTENSION PNEUMOTHORAX
• Mechanically ventilated patients
• Trauma patients
• Post resuscitation (Post CPR) patients
• Lung disease
• Blocked, clamped or displaced chesttubes
• Patients on non- invasive ventilation
• Patients undergoing hyperbaric treatment
• Surgery involving the head and neck and upper chest area
including thyroidectomy, neck dissection, breast surgery
• Surgery involving upper abdominal/ diaphragm area
including nephrectomy, and laparoscopic procedures.
CPR, cardiopulmonary resuscitation
Ultimately, the diagnosis of a pneumothorax/ tension
pneumothorax is a diagnosis of exclusion.4 erefore, it is
important to have a high index of suspicion and to have
a systematic approach in diagnosing or ruling out this
potentially lethal, yet treatable problem.4 Clinical situa-
circumstance, the diagnosis of pneumothorax is dicult for
the following reasons:
tions that have been associated with the development of
a tension pneumothorax are listed in Box 22.1.e differential diagnosis for pneumothorax under anesthesia
1. anesthetized patients will be unable to complain of
sudden pleuritic chest pain and dyspnea;
2. even in the awake patients, small pneumothoraces may
be asymptomatic and self- limited;
2
3. classic ndings in the awake patient including decreased
chest excursion, diminished breath sounds, and a
hyperresonance to percussion are dicult to diagnose
under anesthesia, especially when the surgical eld
limits access to thechest;
4. under general anesthesia, signs and symptoms of a
pneumothorax are nonspecic (Table22.3);
5. under general anesthesia, a small undiagnosed
pneumothorax can quickly evolve into a lifethreatening tension pneumothorax with positive
pressure ventilation;and
6. the pneumothorax is oen not recognized until the
patient progresses to pulseless electrical activity (PEA)
requiring cardiopulmonary resuscitation(CPR).
includes other causes of hypoxia such as endobronchial
intubation, bronchospasm, and laryngospasm. ese may
be quickly ruled out by examining the patient. Pulmonary
embolism may also cause sudden cardiovascular collapse
and hypoxia. Other causes of hypotension and hypoxia
may include cardiac ischemia, congestive heart failure,
pulmonary edema, massive cardiac shunt, and cardiac
tamponade.
DIAGNOSTIC IMAGING
e diagnosis of pneumothorax is made by chest x- ray,
where as little as 50 mL of gas may be visible on upright
lm. e x- ray will show the interface of the lung and
pleural air with absence of pulmonary vessels beyond
the visceral pleural edge. In an adult, a distance of 2cm
between the lung margin and chest wall at the level of
the hilum on upright chest x- ray roughly correlates with
a 50% pneumothorax.13 Contralateral shi of the trachea
and mediastinum, inversion of the hemidiaphragm, and
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widening of intercostal spaces from increased pressure
within the aected hemithorax may suggest a tension
pneumothorax in the presence of clinical symptoms.
8,13
Of note, supine anterior- posterior chest lms commonly
BOX 22.2 MANAGEMENT STEPS WHEN CONSIDERING A
TENSION PNEUMOTHORAX INTHE OPERATINGROOM
1. Call for help; inform the surgeon
taken in the operating room are oen inaccurate because
air spreads out over the anterior chest, making the supine
lm appear normal.
3
Computed tomographic (CT) scan is more sensitive
than a chest radiograph, especially in the evaluation of
small pneumothoraces and pneumomediastinum in the
stable nonintubated patient. It is the gold standard for
2. Turn off nitrousoxide
3. Give 100% oxygen:oxygen accelerates rate of pleural
air absorption in clinical and experimental situations.
By breathing 100% oxygen, alveolar pressure of
nitrogen falls and nitrogen is washed out of tissue and
oxygen taken up by the vascular system
3
detecting occult traumatic pneumothorax not apparent
on supine chest radiograph.14 However, it is not a practical diagnostic tool in the anesthetized patient who is
hemodynamically unstable and located far away from the
CT scanner.
More recently, several case reports have highlighted the
use of intraoperative transthoracic ultrasound to diagnose
pneumothorax.
15,16
Specically, ultrasound can be used to
rule out pneumothorax with a higher sensitivity than a por-
4. Consider ultrasound to help rule out pneumothorax as
a cause of hemodynamic distress
5. Insert intravenous cannula on affected side to
immediately decompress pleural space; do not wait
for diagnostic imaging (chest X- ray) if the patient is
deteriorating quickly
6. Support circulation and ventilation
22
table chest x- ray (95% sensitivity and 100% negative predictive value).
17
Chest tube insertion is the denitive treatment of a
MANAGEMENT OFTHE PATIENT
large pneumothorax.13 e chest tube is typically inserted
in the axilla along a horizontal line at the level of the nipple
between the pectoralis major and latissimus dorsi muscles.
e management of pneumothorax largely depends on
the clinical scenario. A hemodynamically stable patient
with a small pneumothorax can simply be observed and
treated conservatively with supplemental oxygen.18 Small
spontaneous pneumothoraces typically resolve without
treatment. Supplemental oxygen should be administered
regardless of oxygen saturation to facilitate absorption of
e chest tube is usually le in place for 2– 4days or until
there is no longer evidence of an air leak and chest x- ray
shows reexpansion of the lung. oracoscopy or pleurodesis through the chest tube should be considered if an air
leak persists. Video- assisted thoracoscopic surgery (VATS)
with bleb resection and pleurodesis is eective in treating
recurrent pneumothorax.
pleural air. e patient should be observed for at least 6
hours. If aer 6 hours a repeat chest x- ray shows that the
pneumothorax has not progressed, the patient may be dis-
FOLLOW- UP
charged home, provided they have ready access to emergency services.
If the pneumothorax is large or the patient becomes
symptomatic, or develops a tension pneumothorax, then
decompression by needle aspiration or chest tube insertion
is necessary (Box 22.2). In an emergency, needle decompression may be performed by inserting a 14 gauge intravenous cannula into the second or third intercostal space
in the midclavicular line. Alternatively, the fourth or h
intercostal space in the anterior axillary line may be used if
the thickness of the chest wall precludes catheter placement
at the second intercostal space.
8,19
e standard 14 gauge
cannula (4.5cm) may not penetrate the parietal pleura in
chest wall thickness greater than5cm.
Recurrence aer spontaneous pneumothorax is common,
with estimates ranging from 25%– 50%.20 Most recurrent
pneumothoraces occur during the rst year, with the greatest risk of recurrence occuring during the rst 30 days, and
is higher in patients who have blebs or bullae on CT scan.
All smokers should be encouraged to quit smoking, as
smoking cessation reduces the relative risk of developing
recurrent pneumothorax by over 40%.20 Certain patients
as pilots or scuba divers may need additional follow- up
and intervention. Air travel should be avoided for up to
7 days aer the complete resolution of a pneumothorax.21
Underwater diving is considered unsafe aer an episode of
pneumothorax.
8
174 PART IV. PULMONARY CRISES
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175
CASE- BASED LEARNING DISCUSSION
1. What are possible causes of hemodynamic instability
in this otherwise healthy male patient coming for
elective surgery?
2. Even aer increasing the oxygen concentration to
100%, the pulse oximeter is showing a saturation of
78%. Will you consider changing the supraglottic
airway to an endotracheal tube in this patient?
3. As you are contemplating whether to secure this
patient’s airway with an endotracheal tube, you notice
you are having a dicult time ventilating the patient.
You immediately remove the supraglottic airway and
intubate the patient. e end- tidal CO2 reading is
<10mmHg, and you notice you are having a dicult
time ventilating. How will you manage this situation?
4. Should the surgery be discontinued? Why or whynot?
5. e patient was successfully resuscitated and was
taken to the postanesthesia care unit with a chest tube.
What is the benet of giving supplemental oxygen in
this patient as he recovers in the postanesthesia care
unit? How will you decide when to remove the chest
tube in this patient?
6. e patient is now ready to be discharged home. He is
eager to go on a scuba diving vacation to the Bahamas
in 2 weeks. How will you respond to this information?
7. e patient has become nervous and wants to know if
this can happen to him again and if there is anything
he can do to prevent this from happening. What advice
will you give this patient regarding recurrence and
prevention of this disease?
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